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PMCPatients_common4417 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An 18-day-old female was admitted to the paediatric intensive care unit because of a heart murmur and weak femoral pulses. The patient was in a good clinical condition with spontaneous breathing on room air and normal vital signs, except for a blood pressure gradient of 30 mmHg between the upper and the lower extremities. The left ventricle had a normal ejection fraction without regional wall abnormalities or mitral valve regurgitation. The RPA defect was closed with a xenopericardial patch. On post-operative Day 4, the patient exhibited recurrent episodes of supraventricular tachycardia, which were successfully treated with flecainide. After surgery, routine coronary angiography was performed, showing normal, antegrade flow into the LCA without stenosis (). The girl recovered well from the operation and was discharged home soon with normal troponin values.\nOUTPUT:"
},
{
"from": "agent",
"value": "Coarctation of the aorta, Anomalous left coronary artery from pulmonary artery, Retrograde perfusion of left circumflex artery"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: An 18-day-old female was admitted to the paediatric intensive care unit because of a heart murmur and weak femoral pulses. The patient was in a good clinical condition with spontaneous breathing on room air and normal vital signs, except for a blood pressure gradient of 30 mmHg between the upper and the lower extremities. The left ventricle had a normal ejection fraction without regional wall abnormalities or mitral valve regurgitation. The RPA defect was closed with a xenopericardial patch. On post-operative Day 4, the patient exhibited recurrent episodes of supraventricular tachycardia, which were successfully treated with flecainide. After surgery, routine coronary angiography was performed, showing normal, antegrade flow into the LCA without stenosis (). The girl recovered well from the operation and was discharged home soon with normal troponin values.
OUTPUT: |
PMCPatients_common2459 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The first case was a 62-year-old male with a past medical history of diabetes mellitus, hypertension, and obesity who presented with altered mental status, lower extremity weakness, and falling. On physical examination, patient was confused, had a stiff neck, and had 0/5 strength in the left lower extremity. MRIs of the brain and spine were done, which were both negative for any spinal and intracranial pathology such as hyperdense lesions or tumors. CSF studies showed a white blood cell count of 228 with 79% polymorphonuclear cells and 17% lymphocytes, a protein count of 57, and a glucose count of 87. The previously mentioned studies were performed on the day of admission. His flaccid paralysis did not improve after 30 days.\\nThe next case was a 62-year-old female with a past medical history of diabetes mellitus and hypertension who presented with headache, nausea, vomiting, and altered mental status of one-week duration. Per family, the patient was also incoherent. Her motor examination was within normal limits. Both MRI and EEG were negative for any pathology. CSF studies showed a white blood cell count of 105 with 1% polymorphonuclear cells and 93% lymphocytes, a protein count of 201, and glucose count of 67. The previously mentioned studies were performed on the day of admission.\nOUTPUT:"
},
{
"from": "agent",
"value": "West Nile Encephalitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: The first case was a 62-year-old male with a past medical history of diabetes mellitus, hypertension, and obesity who presented with altered mental status, lower extremity weakness, and falling. On physical examination, patient was confused, had a stiff neck, and had 0/5 strength in the left lower extremity. MRIs of the brain and spine were done, which were both negative for any spinal and intracranial pathology such as hyperdense lesions or tumors. CSF studies showed a white blood cell count of 228 with 79% polymorphonuclear cells and 17% lymphocytes, a protein count of 57, and a glucose count of 87. The previously mentioned studies were performed on the day of admission. His flaccid paralysis did not improve after 30 days.\nThe next case was a 62-year-old female with a past medical history of diabetes mellitus and hypertension who presented with headache, nausea, vomiting, and altered mental status of one-week duration. Per family, the patient was also incoherent. Her motor examination was within normal limits. Both MRI and EEG were negative for any pathology. CSF studies showed a white blood cell count of 105 with 1% polymorphonuclear cells and 93% lymphocytes, a protein count of 201, and glucose count of 67. The previously mentioned studies were performed on the day of admission.
OUTPUT: |
PMCPatients_common404 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 59-year-old man with a tumor in the upper gastric body and cervical and celiac multiple lymphadenopathy was admitted to a local hospital, where a biopsy of the cervical lymph node was carried out. Histopathologically, the tumor tissue was negative for blood cell markers (CD3, CD30, CD45RO, PAX5, CD138) and positive for an epithelial marker (cytokeratin AE1/AE3) and EBER-ISH, consistent with an epithelial malignancy. Upper gastrointestinal endoscopy revealed a submucosal tumor-like lesion, 4–5 cm in diameter, at the posterior wall of the upper gastric body. Histopathological examination of the endoscopic biopsy from this lesion revealed it to be a poorly to moderately differentiated adenocarcinoma. HER2 was negative by immunohistochemistry (IHC), and EBER-ISH was positive. The patient was thus diagnosed with EBVGC (TXN3M1, cStage IV). PD-L1 was positive in both the primary and metastatic lesions by IHC, with 15% PD-L1-positive cells recorded in each lesion. The patient was treated with standard chemotherapy for advanced gastric carcinoma, using S-1 and cisplatin. S-1 was orally administered at 80 mg·m−2·day−1 on days 1–21, and cisplatin was intravenously administered at 60 mg·m−2·day−1 on day 8, followed by a 2-week rest. We then repeated this 5-week therapeutic cycle. A remarkable decrease in the sizes of the primary lesion and metastatic lymph nodes was observed during the course of therapy. After two cycles of therapy, tumor shrinkage was 54%, defined as a partial response according to the Response Evaluation Criteria in Solid Tumors (RECIST version 1.1), and after eight cycles, a complete response had been achieved. S-1 alone was continued after the eighth cycle. After 14 cycles, the endoscopic needle biopsy from the primary lesion showed no proof of malignancy. Fluorodeoxyglucose (FDG)-positron emission tomography also showed no abnormal uptake of FDG. The patient is alive without relapse, 36 months after initiation of treatment.\nOUTPUT:"
},
{
"from": "agent",
"value": "Epstein–Barr virus-associated gastric cancer"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 59-year-old man with a tumor in the upper gastric body and cervical and celiac multiple lymphadenopathy was admitted to a local hospital, where a biopsy of the cervical lymph node was carried out. Histopathologically, the tumor tissue was negative for blood cell markers (CD3, CD30, CD45RO, PAX5, CD138) and positive for an epithelial marker (cytokeratin AE1/AE3) and EBER-ISH, consistent with an epithelial malignancy. Upper gastrointestinal endoscopy revealed a submucosal tumor-like lesion, 4–5 cm in diameter, at the posterior wall of the upper gastric body. Histopathological examination of the endoscopic biopsy from this lesion revealed it to be a poorly to moderately differentiated adenocarcinoma. HER2 was negative by immunohistochemistry (IHC), and EBER-ISH was positive. The patient was thus diagnosed with EBVGC (TXN3M1, cStage IV). PD-L1 was positive in both the primary and metastatic lesions by IHC, with 15% PD-L1-positive cells recorded in each lesion. The patient was treated with standard chemotherapy for advanced gastric carcinoma, using S-1 and cisplatin. S-1 was orally administered at 80 mg·m−2·day−1 on days 1–21, and cisplatin was intravenously administered at 60 mg·m−2·day−1 on day 8, followed by a 2-week rest. We then repeated this 5-week therapeutic cycle. A remarkable decrease in the sizes of the primary lesion and metastatic lymph nodes was observed during the course of therapy. After two cycles of therapy, tumor shrinkage was 54%, defined as a partial response according to the Response Evaluation Criteria in Solid Tumors (RECIST version 1.1), and after eight cycles, a complete response had been achieved. S-1 alone was continued after the eighth cycle. After 14 cycles, the endoscopic needle biopsy from the primary lesion showed no proof of malignancy. Fluorodeoxyglucose (FDG)-positron emission tomography also showed no abnormal uptake of FDG. The patient is alive without relapse, 36 months after initiation of treatment.
OUTPUT: |
PMCPatients_common4156 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Bleeding within the intraperitoneal drainage tube was observed 5 d after surgery. He developed hematemesis and melena 2 d following the removal of the drainage tube. His anemia worsened and his hemoglobin (Hb) level reached 6.3 g/dL, requiring red blood cell (RBC) transfusions for 5 d consecutively. Endoscopic examination revealed intestinal bleeding from the site of the anastomosis (Figure ), and endoscopic hemostasis was performed. Subcutaneous hemorrhage became apparent in both lower extremities over several days. Transfusion with a total of 7 units of packed RBC was performed. The activated partial thromboplastin time (APTT) was prolonged to 74.2 s compared to 23.1 s measured preoperatively, and the patient was transferred to our hospital.\\nOn admission, the patient presented with anemia, an Hb level of 9.0 g/dL and a prolonged APTT of 93.7 s. FVIII activity was reduced to 3.18%, the inhibitor titer was 7.59 BU/mL, and he was diagnosed with AHA. Prednisone (PSL 1 mg/kg per day) and tranexamic acid were administered. Although the patient had developed an intramuscular hematoma in the right iliacus muscle approximately 1 mo after treatment, bypassing agents had not been administered because the hemorrhage was not persistent. The inhibitors were eradicated, and the patient was discharged 9 wk after treatment for AHA. Because the patient remained in remission for AHA, the PSL dose was reduced and stopped.\nOUTPUT:"
},
{
"from": "agent",
"value": "Stage IV Gastric Cancer, Acquired Hemophilia A"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Bleeding within the intraperitoneal drainage tube was observed 5 d after surgery. He developed hematemesis and melena 2 d following the removal of the drainage tube. His anemia worsened and his hemoglobin (Hb) level reached 6.3 g/dL, requiring red blood cell (RBC) transfusions for 5 d consecutively. Endoscopic examination revealed intestinal bleeding from the site of the anastomosis (Figure ), and endoscopic hemostasis was performed. Subcutaneous hemorrhage became apparent in both lower extremities over several days. Transfusion with a total of 7 units of packed RBC was performed. The activated partial thromboplastin time (APTT) was prolonged to 74.2 s compared to 23.1 s measured preoperatively, and the patient was transferred to our hospital.\nOn admission, the patient presented with anemia, an Hb level of 9.0 g/dL and a prolonged APTT of 93.7 s. FVIII activity was reduced to 3.18%, the inhibitor titer was 7.59 BU/mL, and he was diagnosed with AHA. Prednisone (PSL 1 mg/kg per day) and tranexamic acid were administered. Although the patient had developed an intramuscular hematoma in the right iliacus muscle approximately 1 mo after treatment, bypassing agents had not been administered because the hemorrhage was not persistent. The inhibitors were eradicated, and the patient was discharged 9 wk after treatment for AHA. Because the patient remained in remission for AHA, the PSL dose was reduced and stopped.
OUTPUT: |
PMCPatients_common859 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 67-year-old man was referred to our hospital with a left dorsal lump, neglected for 2 years but having recently increased in size.\\nClinical examination identified a huge dorsal mass of 25*22 cm. It was located opposite the left shoulder blade and it was moderately firm with ulcero-necrotic center fistulized to the skin, (Figure ). A chest CT scan revealed multiple pulmonary metastases. A biopsy was performed. Histology identified (Figures and ) epithelial malignant tumor proliferation, with high cell density and monotonic tumor cells arranged in compact trabeculae or acini, with polarized nuclei arranged radially around acinar lumens; and an abundant eosinophilic granular cytoplasm. Immunochemistry showed an intense and diffuse positivity of tumor cells for alpha-antitrypsin (acinic marker; Figure ), a moderate and heterogeneous staining with CD56 (neuroendocrine marker). Other markers such as synaptophysin, chromogranin A, CK19, CK7 were negative. MRI of face and neck to search for a salivary gland origin of the metastases was unremarkable.\\nChemotherapy with Paclitaxel (175 mg/m2 every 3 weeks) and Carboplatin (AUC:5 according to Calvert formula, every 3 weeks) was indicated. After three cycles, the patient experienced disease progression. A second line of chemotherapy by FEC75 (5-fluorouracil at 500 mg/m2 [at day1], epirubicin 75 mg/m2 [at day1], Cyclophosphamide 500 mg/m2 [at day1], every 3 weeks) was administered. A locoregional and metastatic pulmonary progression were diagnosed after four cycles. The patient died 6 weeks later.\nOUTPUT:"
},
{
"from": "agent",
"value": "Acinar cell carcinoma of unknown primary origin, Soft tissue metastasis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 67-year-old man was referred to our hospital with a left dorsal lump, neglected for 2 years but having recently increased in size.\nClinical examination identified a huge dorsal mass of 25*22 cm. It was located opposite the left shoulder blade and it was moderately firm with ulcero-necrotic center fistulized to the skin, (Figure ). A chest CT scan revealed multiple pulmonary metastases. A biopsy was performed. Histology identified (Figures and ) epithelial malignant tumor proliferation, with high cell density and monotonic tumor cells arranged in compact trabeculae or acini, with polarized nuclei arranged radially around acinar lumens; and an abundant eosinophilic granular cytoplasm. Immunochemistry showed an intense and diffuse positivity of tumor cells for alpha-antitrypsin (acinic marker; Figure ), a moderate and heterogeneous staining with CD56 (neuroendocrine marker). Other markers such as synaptophysin, chromogranin A, CK19, CK7 were negative. MRI of face and neck to search for a salivary gland origin of the metastases was unremarkable.\nChemotherapy with Paclitaxel (175 mg/m2 every 3 weeks) and Carboplatin (AUC:5 according to Calvert formula, every 3 weeks) was indicated. After three cycles, the patient experienced disease progression. A second line of chemotherapy by FEC75 (5-fluorouracil at 500 mg/m2 [at day1], epirubicin 75 mg/m2 [at day1], Cyclophosphamide 500 mg/m2 [at day1], every 3 weeks) was administered. A locoregional and metastatic pulmonary progression were diagnosed after four cycles. The patient died 6 weeks later.
OUTPUT: |
PMCPatients_common2636 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: 56-year-old lady with a history of hypertension, dyslipidemia, and gallstones presented to the emergency department (ED) with severe stinging, nonradiating, midsternal chest pain ongoing for 45 minutes. She experienced nausea, vomiting, and diaphoresis. She denied palpitations, orthopnea, or paroxysmal nocturnal dyspnea. On physical exam she was hypotensive with BP of 80/50 mmHg and a heart rate of 117 bpm. Her lungs were clear and cardiac exam showed normal heart sounds with no murmurs or rubs. She had mild epigastric tenderness, but there was no guarding or rigidity and bowel sounds were heard. 12-lead electrocardiogram (EKG) showed 2 mm ST elevation in leads II, III, and AVF, with reciprocal changes in leads I and AVL (). Her labs data returned in the interim with WBC of 12,000 with no shift, hemoglobin of 11 g/dL, hematocrit of 36%, potassium of 2.6 mg/dL, magnesium of 1.4 mg/dL, and calcium of 7.2 mg/dL. Her serial troponins were 6.0, 1.2, and 0.87. Her liver function tests (LFT) were elevated alanine transaminase (ALT), 398 U/L; aspartate transaminase (AST), 863 U/L; alkaline phosphatase (ALP), 328 U/L; and lipase, 9,080 U/L. Computed tomography (CT) of the abdomen showed diffusely edematous and inflamed pancreas (). Over the course of her hospital stay her chest pain improved and her biochemical markers, including LFT and lipase, trended downwards, and she was discharged.\nOUTPUT:"
},
{
"from": "agent",
"value": "Acute inferior ST elevation myocardial infarction, Acute pancreatitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: 56-year-old lady with a history of hypertension, dyslipidemia, and gallstones presented to the emergency department (ED) with severe stinging, nonradiating, midsternal chest pain ongoing for 45 minutes. She experienced nausea, vomiting, and diaphoresis. She denied palpitations, orthopnea, or paroxysmal nocturnal dyspnea. On physical exam she was hypotensive with BP of 80/50 mmHg and a heart rate of 117 bpm. Her lungs were clear and cardiac exam showed normal heart sounds with no murmurs or rubs. She had mild epigastric tenderness, but there was no guarding or rigidity and bowel sounds were heard. 12-lead electrocardiogram (EKG) showed 2 mm ST elevation in leads II, III, and AVF, with reciprocal changes in leads I and AVL (). Her labs data returned in the interim with WBC of 12,000 with no shift, hemoglobin of 11 g/dL, hematocrit of 36%, potassium of 2.6 mg/dL, magnesium of 1.4 mg/dL, and calcium of 7.2 mg/dL. Her serial troponins were 6.0, 1.2, and 0.87. Her liver function tests (LFT) were elevated alanine transaminase (ALT), 398 U/L; aspartate transaminase (AST), 863 U/L; alkaline phosphatase (ALP), 328 U/L; and lipase, 9,080 U/L. Computed tomography (CT) of the abdomen showed diffusely edematous and inflamed pancreas (). Over the course of her hospital stay her chest pain improved and her biochemical markers, including LFT and lipase, trended downwards, and she was discharged.
OUTPUT: |
PMCPatients_common3656 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 55-year-old male patient was admitted to our emergency department with right flank tenderness preceding 4-6 hours. He had no dysuria, hematuria, fever, nausea, or vomiting. Except for the right flank tenderness and 3/6 systolic murmur at the cardiac apex, his physical examination and hemodynamic parameters were normal. His medical history was remarkable for non-ischemic dilated cardiomyopathy, which was diagnosed by coronary angiography (CAG) and cardiac catheterization in another clinic 2 days ago, and the drugs in use were carvedilol, ramipril, furosemide, and acetylsalicylic acid. The abdominal x-ray, urinary ultrasonography (US), and laboratory analysis were all normal. Only mild microscopic hematuria was detected. The patient was clinically diagnosed with renal colic, treated with analgesics, and then discharged home for further ambulatory urologic investigation. A few hours later, the patient returned to the emergency department with severe right flank pain. Globally systolic dysfunction (ejection fraction: 35%), mild-moderate mitral insufficiency, dilated left chamber without thrombi or vegetation, and multiple self-terminating atrial fibrillation (AF) episodes compatible with paroxysmal AF were detected on transthoracic echocardiography and 24-hour Holter monitoring, respectively. CHA2DS2-VASc and HAS-BLED scores were calculated as 3 and 2, respectively. Dabigatran (150 mg, b.i.d. ), analgesics, and hydration were initiated. In 5 days, he recovered and was discharged home on dabigatran. On the control CECT scan performed 1 month later, reperfusion and contrast enhancement were seen at the previously hypodense renal infarct area ().\nOUTPUT:"
},
{
"from": "agent",
"value": "Acute Renal Infarction"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 55-year-old male patient was admitted to our emergency department with right flank tenderness preceding 4-6 hours. He had no dysuria, hematuria, fever, nausea, or vomiting. Except for the right flank tenderness and 3/6 systolic murmur at the cardiac apex, his physical examination and hemodynamic parameters were normal. His medical history was remarkable for non-ischemic dilated cardiomyopathy, which was diagnosed by coronary angiography (CAG) and cardiac catheterization in another clinic 2 days ago, and the drugs in use were carvedilol, ramipril, furosemide, and acetylsalicylic acid. The abdominal x-ray, urinary ultrasonography (US), and laboratory analysis were all normal. Only mild microscopic hematuria was detected. The patient was clinically diagnosed with renal colic, treated with analgesics, and then discharged home for further ambulatory urologic investigation. A few hours later, the patient returned to the emergency department with severe right flank pain. Globally systolic dysfunction (ejection fraction: 35%), mild-moderate mitral insufficiency, dilated left chamber without thrombi or vegetation, and multiple self-terminating atrial fibrillation (AF) episodes compatible with paroxysmal AF were detected on transthoracic echocardiography and 24-hour Holter monitoring, respectively. CHA2DS2-VASc and HAS-BLED scores were calculated as 3 and 2, respectively. Dabigatran (150 mg, b.i.d. ), analgesics, and hydration were initiated. In 5 days, he recovered and was discharged home on dabigatran. On the control CECT scan performed 1 month later, reperfusion and contrast enhancement were seen at the previously hypodense renal infarct area ().
OUTPUT: |
PMCPatients_common4679 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 40-year-old female admitted with complaint of shortness of breath for last 2-3 day, associated with cough and sputum streaking with blood for last around 15 days. Her condition further deteriorated to the point that the patient was intubated with an endotracheal tube (ETT) number eight and mechanically ventilated with sedation and paralysis.\\nAfter a few hours of mechanical ventilation, her saturation began to drop, and blood pressure increased to more than 200 mmHg systolic with tachycardia. On realizing the problem that tidal volume is not being delivered, endotracheal suction was attempted. However, it was found that the suction catheter could not be passed as an obstruction was encountered. The tube was removed, and the patient was reintubated. On removing the tube, there was no blockage in the tube but now patient was reintubated with a seven number ETT. This was followed by delivery of set tidal volume and normalization of oxygen saturation and blood pressure.\\nFurther into the patient's management, after a few hours, patient developed the same problem of worsening oxygen saturation with rise in blood pressure and tachycardia. Again, the delivered tidal volume was not adequate and less than the predetermined value. It was again not possible to introduce the suction catheter through the ETT. On looking specifically at airway pressure alarm limit nothing relevant found which could be the reason for failure to deliver predetermined tidal volume.\\nNow, it was suspected that there could be impingement of ETT bevel on the tracheal wall after intubation due to the anatomical distortion of trachea. Gradual withdrawal of the ETT tip up to just below the vocal cords did not restore the ventilation. Therefore, another ETT was introduced with its bevel tip shortened. This was followed by adequate tidal volume delivery.\nOUTPUT:"
},
{
"from": "agent",
"value": "Pulmonary Tuberculosis, Destroyed Lung, Pulmonary Infiltrates"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 40-year-old female admitted with complaint of shortness of breath for last 2-3 day, associated with cough and sputum streaking with blood for last around 15 days. Her condition further deteriorated to the point that the patient was intubated with an endotracheal tube (ETT) number eight and mechanically ventilated with sedation and paralysis.\nAfter a few hours of mechanical ventilation, her saturation began to drop, and blood pressure increased to more than 200 mmHg systolic with tachycardia. On realizing the problem that tidal volume is not being delivered, endotracheal suction was attempted. However, it was found that the suction catheter could not be passed as an obstruction was encountered. The tube was removed, and the patient was reintubated. On removing the tube, there was no blockage in the tube but now patient was reintubated with a seven number ETT. This was followed by delivery of set tidal volume and normalization of oxygen saturation and blood pressure.\nFurther into the patient's management, after a few hours, patient developed the same problem of worsening oxygen saturation with rise in blood pressure and tachycardia. Again, the delivered tidal volume was not adequate and less than the predetermined value. It was again not possible to introduce the suction catheter through the ETT. On looking specifically at airway pressure alarm limit nothing relevant found which could be the reason for failure to deliver predetermined tidal volume.\nNow, it was suspected that there could be impingement of ETT bevel on the tracheal wall after intubation due to the anatomical distortion of trachea. Gradual withdrawal of the ETT tip up to just below the vocal cords did not restore the ventilation. Therefore, another ETT was introduced with its bevel tip shortened. This was followed by adequate tidal volume delivery.
OUTPUT: |
PMCPatients_common247 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Patient 6 is a 49-year-old woman who presented to the W-TBI clinic in April 2017 after being injured in a motor vehicle accident in February 2017. The patient could not recall whether she had lost consciousness following the accident. In the days following the accident, the patient started noticing nausea and headaches with reading on the computer, increased somnolence, and worsening discomfort with motion, sound, or lights. The patient had an MRI and CT following the accident which were both read as normal. At her initial appointment, the patient noted that she had enjoyed reading before the accident, but now could use a computer for only five minutes intervals prior to becoming nauseous and experiencing headache. Her past medical history was notable for breast cancer, migraines, rectal bleeding, gastric polyps, and dyspepsia. Her ROS was positive for fatigue, IBS, more headaches since the accident, increased urinary frequency, burning pain in neck and shoulders, sound sensitivity, worse bruxism since the injury, poor balance, insomnia, and cognitive impairments. In June 2017, the patient was re-evaluated and demonstrated little improvement in her symptoms or upon examination. She did report some improvement in her fatigue, sleeping and cognition. Continued orthoptic training was recommended and that patient returned in October 2017 reporting further improvement in reading, driving, and computer use. However she stated she was not yet at her pre-morbid functioning. It was noted that the patient was hypermobile at that visit (Beighton score 4/9). In May 2019, the patient returned to the W-TBI clinic reporting that her symptoms had “plateaued”.\nOUTPUT:"
},
{
"from": "agent",
"value": "Ehlers-Danlos, hypermobility type III, Convergence insufficiency, Postconcussion syndrome, Occipital neuralgia"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Patient 6 is a 49-year-old woman who presented to the W-TBI clinic in April 2017 after being injured in a motor vehicle accident in February 2017. The patient could not recall whether she had lost consciousness following the accident. In the days following the accident, the patient started noticing nausea and headaches with reading on the computer, increased somnolence, and worsening discomfort with motion, sound, or lights. The patient had an MRI and CT following the accident which were both read as normal. At her initial appointment, the patient noted that she had enjoyed reading before the accident, but now could use a computer for only five minutes intervals prior to becoming nauseous and experiencing headache. Her past medical history was notable for breast cancer, migraines, rectal bleeding, gastric polyps, and dyspepsia. Her ROS was positive for fatigue, IBS, more headaches since the accident, increased urinary frequency, burning pain in neck and shoulders, sound sensitivity, worse bruxism since the injury, poor balance, insomnia, and cognitive impairments. In June 2017, the patient was re-evaluated and demonstrated little improvement in her symptoms or upon examination. She did report some improvement in her fatigue, sleeping and cognition. Continued orthoptic training was recommended and that patient returned in October 2017 reporting further improvement in reading, driving, and computer use. However she stated she was not yet at her pre-morbid functioning. It was noted that the patient was hypermobile at that visit (Beighton score 4/9). In May 2019, the patient returned to the W-TBI clinic reporting that her symptoms had “plateaued”.
OUTPUT: |
PMCPatients_common4879 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 54-year-old female presented with a history of exertional breathlessness and dry cough for two months. She was afebrile with SpO2 of 91% on room air and bilateral crepitations on respiratory examination. Chest radiography showed bilateral reticular nodular opacities in upper and mid zones. Lung function test revealed severe restrictive abnormality with FEV1 of 1.2 L (46.4%), FVC of 1.45 L (45.2%), and FEV1/FVC 83% with reduction in DLCO 1.46 mmol/min/kPa (18%) and corrected value with alveolar volume 0.49 mmol/min/kPa (30%). Six-minute walk distance was 170 m and lowest oxygen saturation was 74%. High-resolution computed tomography (HRCT) of chest showed multiple ill-defined nodular opacities in both lung fields showing centrilobular distribution associated with ground glass opacities bilaterally. Fine reticular densities were seen at places with segments of traction bronchiectasis []. Routine complete blood count and biochemistry were normal. Connective tissue markers were negative (RA, Anti-CCP, ANA). Total serum IgE was 145 IU/mL and specific IgE for pigeon droppings (<0.10 k/U) was negative. TBLB showed thickened alveolar septa with mild lymphoplasmacytic inflammatory infiltrate in the interstitium with cross-sections of calcified parasitic larvae with foreign body giant cell reaction around it []. Travel history revealed frequent travels in the Himalayan belts yearly for 20 years during which she had frequent episodes of diarrhea. Stool examination did not show any ova or cyst or trophozoites. She was given albendazole 400 mg for three days and oral corticosteroids for 12 weeks. Bronchoalveolar lavage (BAL) for tuberculosis culture at 6 weeks was negative. At 6 weeks follow up, she had remarkable clinical improvement with SpO2 95% at rest. HRCT chest also showed remarkable improvement after 4 months [].\nOUTPUT:"
},
{
"from": "agent",
"value": "Parasitic infestation of lung, Interstitial pneumonitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 54-year-old female presented with a history of exertional breathlessness and dry cough for two months. She was afebrile with SpO2 of 91% on room air and bilateral crepitations on respiratory examination. Chest radiography showed bilateral reticular nodular opacities in upper and mid zones. Lung function test revealed severe restrictive abnormality with FEV1 of 1.2 L (46.4%), FVC of 1.45 L (45.2%), and FEV1/FVC 83% with reduction in DLCO 1.46 mmol/min/kPa (18%) and corrected value with alveolar volume 0.49 mmol/min/kPa (30%). Six-minute walk distance was 170 m and lowest oxygen saturation was 74%. High-resolution computed tomography (HRCT) of chest showed multiple ill-defined nodular opacities in both lung fields showing centrilobular distribution associated with ground glass opacities bilaterally. Fine reticular densities were seen at places with segments of traction bronchiectasis []. Routine complete blood count and biochemistry were normal. Connective tissue markers were negative (RA, Anti-CCP, ANA). Total serum IgE was 145 IU/mL and specific IgE for pigeon droppings (<0.10 k/U) was negative. TBLB showed thickened alveolar septa with mild lymphoplasmacytic inflammatory infiltrate in the interstitium with cross-sections of calcified parasitic larvae with foreign body giant cell reaction around it []. Travel history revealed frequent travels in the Himalayan belts yearly for 20 years during which she had frequent episodes of diarrhea. Stool examination did not show any ova or cyst or trophozoites. She was given albendazole 400 mg for three days and oral corticosteroids for 12 weeks. Bronchoalveolar lavage (BAL) for tuberculosis culture at 6 weeks was negative. At 6 weeks follow up, she had remarkable clinical improvement with SpO2 95% at rest. HRCT chest also showed remarkable improvement after 4 months [].
OUTPUT: |
PMCPatients_common3837 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 59-year-old female was referred to the Department of Dentistry in July 2013. The lesions were predominantly located on the lower lip in the beginning but subsequently developed also on the buccal mucosa. The lesions were slightly prominent, with a submucosal palpable mass [Figures and ]. There was no erythema in the adjacent mucosa. No systemic symptoms were present, and cervical lymphadenopathy was absent. The involvement of the brain at the time of original diagnosis was suspected (not proven). Medical history of the patient included prednisolone 10 mg daily, omeprazole, and levothyroxine (for hypothyroidism) and telmisartan (for hypertension) at the time of examination.\\nClinical appearance of the lesions did not allow the proper diagnosis. Therefore, the biopsy of one lesion was performed during the first visit.\\nMicroscopically, besides superficial erosions with mixed inflammation, there were several nonnecrotizing epithelioid granulomas deeper in the submucosa, composed of CD68-positive macrophages and surrounded by lymphoplasmacytic infiltrate []. No change of systemic steroid medication was recommended by the responsible specialist, but topical treatment was administered. The patient received 0.1% dexamethasone gel three times daily and one intralesional application of 7 mg of betamethasone.\nOUTPUT:"
},
{
"from": "agent",
"value": "Oral sarcoidosis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 59-year-old female was referred to the Department of Dentistry in July 2013. The lesions were predominantly located on the lower lip in the beginning but subsequently developed also on the buccal mucosa. The lesions were slightly prominent, with a submucosal palpable mass [Figures and ]. There was no erythema in the adjacent mucosa. No systemic symptoms were present, and cervical lymphadenopathy was absent. The involvement of the brain at the time of original diagnosis was suspected (not proven). Medical history of the patient included prednisolone 10 mg daily, omeprazole, and levothyroxine (for hypothyroidism) and telmisartan (for hypertension) at the time of examination.\nClinical appearance of the lesions did not allow the proper diagnosis. Therefore, the biopsy of one lesion was performed during the first visit.\nMicroscopically, besides superficial erosions with mixed inflammation, there were several nonnecrotizing epithelioid granulomas deeper in the submucosa, composed of CD68-positive macrophages and surrounded by lymphoplasmacytic infiltrate []. No change of systemic steroid medication was recommended by the responsible specialist, but topical treatment was administered. The patient received 0.1% dexamethasone gel three times daily and one intralesional application of 7 mg of betamethasone.
OUTPUT: |
PMCPatients_common1173 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A previously well, ten-year-old boy was admitted with progressive cognitive decline, myoclonic jerks, gait unsteadiness, and frequent falls for the past four months. There was no history of measles, fever, or trauma. He had received measles vaccination at nine months of age. On examination, he appeared confused with intermittent lapses in consciousness and periodic myoclonic jerks every 5 to 6 seconds in form of sudden flexion of the neck, trunk, and arms. He had difficulty in sitting, swallowing, drooling of saliva, slurred speech, and poor interaction with the examiner. He had generalized spasticity, hyperreflexia, and bilateral extensor plantar response. Cranial nerves, fundus, and the rest of the physical examination were normal.\\nA clinical diagnosis of SSPE was considered in view of periodic myoclonus and progressive cognitive decline. Scalp electroencephalogram showed disorganized background with generalized spike-wave discharges 2–2.5/second occupying more than 80% of tracing, consistent with NCSE (). Following intravenous diazepam (0.3 mg/kg) administration, transient normalization of background rhythm to 6–8/second along with intermittent, generalized high-voltage slow-wave discharges was seen, but typical periodic complexes were not seen. There was no change in the mental status of the child following diazepam. Magnetic resonance imaging of brain (fluid attenuated inversion recovery sequence) showed periventricular hyperintensities involving bilateral parieto-occipital white matter (). Measles antibody titers by enzyme-immunoassay were raised in both cerebrospinal fluid and serum: 5.24 IU/mL (positive >1.1) and 5.11 IU/mL (positive >1.1), respectively. A diagnosis of SSPE was made with clinical stage IIIA according to Jabbour's criteria []. Child was started on valproic acid (30 mg/kg/day) and clonazepam (0.5 mg/kg/day). At four months follow-up, the child showed some improvement in sensorium and myoclonic jerks with electroencephalogram now showing the typical periodic complexes time locked with periodic myoclonus.\nOUTPUT:"
},
{
"from": "agent",
"value": "Subacute Sclerosing Panencephalitis, Nonconvulsive Status Epilepticus"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A previously well, ten-year-old boy was admitted with progressive cognitive decline, myoclonic jerks, gait unsteadiness, and frequent falls for the past four months. There was no history of measles, fever, or trauma. He had received measles vaccination at nine months of age. On examination, he appeared confused with intermittent lapses in consciousness and periodic myoclonic jerks every 5 to 6 seconds in form of sudden flexion of the neck, trunk, and arms. He had difficulty in sitting, swallowing, drooling of saliva, slurred speech, and poor interaction with the examiner. He had generalized spasticity, hyperreflexia, and bilateral extensor plantar response. Cranial nerves, fundus, and the rest of the physical examination were normal.\nA clinical diagnosis of SSPE was considered in view of periodic myoclonus and progressive cognitive decline. Scalp electroencephalogram showed disorganized background with generalized spike-wave discharges 2–2.5/second occupying more than 80% of tracing, consistent with NCSE (). Following intravenous diazepam (0.3 mg/kg) administration, transient normalization of background rhythm to 6–8/second along with intermittent, generalized high-voltage slow-wave discharges was seen, but typical periodic complexes were not seen. There was no change in the mental status of the child following diazepam. Magnetic resonance imaging of brain (fluid attenuated inversion recovery sequence) showed periventricular hyperintensities involving bilateral parieto-occipital white matter (). Measles antibody titers by enzyme-immunoassay were raised in both cerebrospinal fluid and serum: 5.24 IU/mL (positive >1.1) and 5.11 IU/mL (positive >1.1), respectively. A diagnosis of SSPE was made with clinical stage IIIA according to Jabbour's criteria []. Child was started on valproic acid (30 mg/kg/day) and clonazepam (0.5 mg/kg/day). At four months follow-up, the child showed some improvement in sensorium and myoclonic jerks with electroencephalogram now showing the typical periodic complexes time locked with periodic myoclonus.
OUTPUT: |
PMCPatients_common1719 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 38-year-old postpartum woman, gravida 3, para 2, ab 1, with no history of diabetes, hypertension, or cardiovascular disease was admitted to the hospital for acute dyspnea and leg edema.\\nThe patient had a preterm delivery at 36 weeks of gestation in her first pregnancy 12 years ago, which did not require cervical cerclage or tocolysis. Her father had hypertension. She presented to the obstetric department at 21 weeks of gestation and underwent cerclage after her cervical length was found to be <19 mm. She was given tocolytic therapy with ritodrine, nifedipine, and diclofenac, which continued for 100 days until her delivery. The patient remained healthy until the last week of pregnancy when she developed mild dyspnea and increased leg swelling. She had a vaginal birth at 37 weeks of gestation.\\nThree days after delivery, the patient presented to the emergency department with progressive dyspnea, orthopnea, and significant bilateral leg swelling. Her blood pressure was 161/110 mmHg, respiratory rate 30/min, and tachycardia 118/min. Laboratory data showed her troponin T level at 0.13 ug/l and N-terminal pro-brain natriuretic peptide level at 5,430 pg/ml. Chest imaging revealed pulmonary edema and bilateral pleural effusion (Fig. ). A computed tomography pulmonary angiogram was negative for pulmonary emboli and electrocardiography revealed sinus tachycardia (Fig. ). An echocardiogram showed generalized hypokinesia of left ventricular (LV) wall motion and a low ejection fraction of 34% (Fig. The patient was fully ambulatory and was discharged 6 days after admission. A follow-up echocardiogram at 3 months and 12 months showed normalization of her ejection fraction to 64% and 80%, respectively. The patient showed complete recovery from PPCM and remained asymptomatic.\nOUTPUT:"
},
{
"from": "agent",
"value": "Peripartum cardiomyopathy, Acute heart failure"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 38-year-old postpartum woman, gravida 3, para 2, ab 1, with no history of diabetes, hypertension, or cardiovascular disease was admitted to the hospital for acute dyspnea and leg edema.\nThe patient had a preterm delivery at 36 weeks of gestation in her first pregnancy 12 years ago, which did not require cervical cerclage or tocolysis. Her father had hypertension. She presented to the obstetric department at 21 weeks of gestation and underwent cerclage after her cervical length was found to be <19 mm. She was given tocolytic therapy with ritodrine, nifedipine, and diclofenac, which continued for 100 days until her delivery. The patient remained healthy until the last week of pregnancy when she developed mild dyspnea and increased leg swelling. She had a vaginal birth at 37 weeks of gestation.\nThree days after delivery, the patient presented to the emergency department with progressive dyspnea, orthopnea, and significant bilateral leg swelling. Her blood pressure was 161/110 mmHg, respiratory rate 30/min, and tachycardia 118/min. Laboratory data showed her troponin T level at 0.13 ug/l and N-terminal pro-brain natriuretic peptide level at 5,430 pg/ml. Chest imaging revealed pulmonary edema and bilateral pleural effusion (Fig. ). A computed tomography pulmonary angiogram was negative for pulmonary emboli and electrocardiography revealed sinus tachycardia (Fig. ). An echocardiogram showed generalized hypokinesia of left ventricular (LV) wall motion and a low ejection fraction of 34% (Fig. The patient was fully ambulatory and was discharged 6 days after admission. A follow-up echocardiogram at 3 months and 12 months showed normalization of her ejection fraction to 64% and 80%, respectively. The patient showed complete recovery from PPCM and remained asymptomatic.
OUTPUT: |
PMCPatients_common639 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Our patient is a 36-year-old female with no past medical history. She has never smoked cigarettes and does not consume alcohol. She denied any history of clots, prior miscarriages, or family history of stroke. Her risk factors for stroke are oral contraceptive use, morbid obesity, and the recent use of weight loss supplements. Our patient awoke at approximately 06:30 with symptoms of dizziness, vomiting, head and neck pain, and left lip paresthesia. Her last known normal was 22:30 the previous night. She presented to the emergency department at 08:30, where a focused physical exam also revealed left eye ptosis, right medial gaze palsy, and right upper extremity dysmetria. A non-contrast head CT revealed no acute intracranial abnormality. Upon re-examination of the prior non-contrast CT, a subtle focus of increased density was identified anterior to the pons, representing a possible thrombus. At 13:00, the patient was noted to have developed mild right-sided facial droop. The patient was transferred to a tertiary care center for emergent endovascular thrombectomy at 14:00. Following successful thrombolysis in cerebral infarction (TICI) grade 3 thrombectomy, the patient experienced a significant improvement of her symptoms, with only mild right facial droop and right internuclear ophthalmoplegia noted on physical exam. MRI was remarkable for acute infarcts of the right midbrain, right pons, and left cerebellar hemisphere.\\nOnce the patient was stabilized, a transesophageal echocardiogram (TEE) was ordered, and further history was elicited to evaluate the cause of the patient’s stroke. TEE with agitated saline contrast revealed no evidence of shunt. She was discharged to an acute rehab facility with a 30-day cardiac monitor and instructed to take aspirin 325 mg and atorvastatin 80 mg daily.\nOUTPUT:"
},
{
"from": "agent",
"value": "Basilar Artery Occlusion"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Our patient is a 36-year-old female with no past medical history. She has never smoked cigarettes and does not consume alcohol. She denied any history of clots, prior miscarriages, or family history of stroke. Her risk factors for stroke are oral contraceptive use, morbid obesity, and the recent use of weight loss supplements. Our patient awoke at approximately 06:30 with symptoms of dizziness, vomiting, head and neck pain, and left lip paresthesia. Her last known normal was 22:30 the previous night. She presented to the emergency department at 08:30, where a focused physical exam also revealed left eye ptosis, right medial gaze palsy, and right upper extremity dysmetria. A non-contrast head CT revealed no acute intracranial abnormality. Upon re-examination of the prior non-contrast CT, a subtle focus of increased density was identified anterior to the pons, representing a possible thrombus. At 13:00, the patient was noted to have developed mild right-sided facial droop. The patient was transferred to a tertiary care center for emergent endovascular thrombectomy at 14:00. Following successful thrombolysis in cerebral infarction (TICI) grade 3 thrombectomy, the patient experienced a significant improvement of her symptoms, with only mild right facial droop and right internuclear ophthalmoplegia noted on physical exam. MRI was remarkable for acute infarcts of the right midbrain, right pons, and left cerebellar hemisphere.\nOnce the patient was stabilized, a transesophageal echocardiogram (TEE) was ordered, and further history was elicited to evaluate the cause of the patient’s stroke. TEE with agitated saline contrast revealed no evidence of shunt. She was discharged to an acute rehab facility with a 30-day cardiac monitor and instructed to take aspirin 325 mg and atorvastatin 80 mg daily.
OUTPUT: |
PMCPatients_common5099 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 59-year-old woman who had pre-existing hypertension presented with chest pain and dyspnea. She reported claudication and coldness of the lower extremities that had been becoming more severe. Her medical history included a diagnosis of hypertension.\\nOn physical examination, she was found to be hypertensive in the right arm (170/100 mmHg), normotensive in the left arm (100/60 mmHg), and hypotensive in the thighs (76/45 mmHg). Both femoral pulses were weak and the ankle-brachial index (ABI) was 0.56. There were no remarkable findings in the laboratory tests including the C-reactive protein level and erythrocyte sedimentation rate. A 12-lead electrocardiogram revealed a normal sinus rhythm and left ventricular hypertrophy. The chest X-ray revealed cardiomegaly (cardiothoracic ratio 57.4%) and left ventricular enlargement. The left ventricular ejection fraction assessed by echocardiography was 25%.\\nFor treatment, bypass grafting was performed between the right axillary artery and the right femoral artery using an 8 mm ringed Gore-Tex graft (). Warfarin (2 mg/day) was administered postoperatively. At the time of discharge, the patient showed marked improvement of the dyspnea and chest pain. The ABI became normal (1.0) (). Echocardiography showed early improvement of the left ventricular ejection fraction (range, 23% to 41%) and dimensions (range, 61/69 mm to 52/62 mm) compared with the preoperative values. At 11 months, these indices had improved further according to the echocardiogram; the left ventricular ejection fraction was 57% and the dimensions were 37/52 mm.\nOUTPUT:"
},
{
"from": "agent",
"value": "Takayasu's Arteritis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 59-year-old woman who had pre-existing hypertension presented with chest pain and dyspnea. She reported claudication and coldness of the lower extremities that had been becoming more severe. Her medical history included a diagnosis of hypertension.\nOn physical examination, she was found to be hypertensive in the right arm (170/100 mmHg), normotensive in the left arm (100/60 mmHg), and hypotensive in the thighs (76/45 mmHg). Both femoral pulses were weak and the ankle-brachial index (ABI) was 0.56. There were no remarkable findings in the laboratory tests including the C-reactive protein level and erythrocyte sedimentation rate. A 12-lead electrocardiogram revealed a normal sinus rhythm and left ventricular hypertrophy. The chest X-ray revealed cardiomegaly (cardiothoracic ratio 57.4%) and left ventricular enlargement. The left ventricular ejection fraction assessed by echocardiography was 25%.\nFor treatment, bypass grafting was performed between the right axillary artery and the right femoral artery using an 8 mm ringed Gore-Tex graft (). Warfarin (2 mg/day) was administered postoperatively. At the time of discharge, the patient showed marked improvement of the dyspnea and chest pain. The ABI became normal (1.0) (). Echocardiography showed early improvement of the left ventricular ejection fraction (range, 23% to 41%) and dimensions (range, 61/69 mm to 52/62 mm) compared with the preoperative values. At 11 months, these indices had improved further according to the echocardiogram; the left ventricular ejection fraction was 57% and the dimensions were 37/52 mm.
OUTPUT: |
PMCPatients_common3497 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 32-yr-old gravida 3, para 2 patient was referred at 24 wk gestation for fetal hydrops detected on ultrasound imaging. The mother has two healthy children from a previous relationship. The father of this pregnancy is a healthy 33-yr-old man. The family history was unrevealing and there is no known close consanguinity; however, the couple were of Indigenous descent from the same community. The pregnancy was otherwise unremarkable with no history of exposure to known teratogens. The prenatal ultrasound identified massive ascites and moderate body wall edema in the fetus. The cardiac anatomy and function were normal, and there were no masses to suggest a structural etiology of the hydrops. Maternal viral studies returned without evidence of active infection. An amniocentesis revealed a normal quantitative fluorescent polymerase chain reaction (QF-PCR) result. Chromosomal single-nucleotide polymorphism (SNP) array studies were performed (see the Technical Analysis section).\\nThe patient presented at 34 wk gestation following premature rupture of membranes. Given the breech presentation, her history of having a previous Caesarean section, and parental desire for full fetal/neonatal intervention, she underwent a cesarean section. A 3230-g (97th %ile) male infant was delivered with Apgar scores of 3 at 1 min and 6 at 5 min. His length was 46 cm (50th %ile), and his head circumference was 33 cm (90th %ile). The neonate was edematous with a distended abdomen. He required immediate and ongoing support on the ventilator for respiratory failure, and repeated paracentesis was performed for removal of accumulating ascitic fluid. An abdominal ultrasound on the first day of life revealed a large amount of ascites. The liver was of normal size, shape, and echotexture. The spleen was enlarged measuring ∼6 cm in length. A brain sonogram revealed some abnormalities prompting magnetic resonance imaging (MRI). The MRI revealed hypoplasia of the corpus callosum, interhemispheric cysts demonstrating mass effect on the posterior aspect of the right thalamus, and bilateral periventricular band heterotopia. The infant died at 4 wk of age.\nOUTPUT:"
},
{
"from": "agent",
"value": "Prenatal hydrops fetalis, Infantile free sialic acid storage disease"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 32-yr-old gravida 3, para 2 patient was referred at 24 wk gestation for fetal hydrops detected on ultrasound imaging. The mother has two healthy children from a previous relationship. The father of this pregnancy is a healthy 33-yr-old man. The family history was unrevealing and there is no known close consanguinity; however, the couple were of Indigenous descent from the same community. The pregnancy was otherwise unremarkable with no history of exposure to known teratogens. The prenatal ultrasound identified massive ascites and moderate body wall edema in the fetus. The cardiac anatomy and function were normal, and there were no masses to suggest a structural etiology of the hydrops. Maternal viral studies returned without evidence of active infection. An amniocentesis revealed a normal quantitative fluorescent polymerase chain reaction (QF-PCR) result. Chromosomal single-nucleotide polymorphism (SNP) array studies were performed (see the Technical Analysis section).\nThe patient presented at 34 wk gestation following premature rupture of membranes. Given the breech presentation, her history of having a previous Caesarean section, and parental desire for full fetal/neonatal intervention, she underwent a cesarean section. A 3230-g (97th %ile) male infant was delivered with Apgar scores of 3 at 1 min and 6 at 5 min. His length was 46 cm (50th %ile), and his head circumference was 33 cm (90th %ile). The neonate was edematous with a distended abdomen. He required immediate and ongoing support on the ventilator for respiratory failure, and repeated paracentesis was performed for removal of accumulating ascitic fluid. An abdominal ultrasound on the first day of life revealed a large amount of ascites. The liver was of normal size, shape, and echotexture. The spleen was enlarged measuring ∼6 cm in length. A brain sonogram revealed some abnormalities prompting magnetic resonance imaging (MRI). The MRI revealed hypoplasia of the corpus callosum, interhemispheric cysts demonstrating mass effect on the posterior aspect of the right thalamus, and bilateral periventricular band heterotopia. The infant died at 4 wk of age.
OUTPUT: |
PMCPatients_common1304 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The patient was administered antibiotics and taken to theatre at 11 h post-injury. The wound was debrided and temporarily stabilised with an external fixator (Fig. ). A CT of the extremity was obtained. The soft tissue defect was medial, measuring 8 cm by 4 cm. On day 3, an acute angulation at the fracture site was performed and the fracture stabilised with a Taylor Spatial Frame (Fig. ). The wound was primarily closed without tension (Fig. ), and the leg was held in intentional varus by 35° (Fig. ). The wound was healed by 2 weeks and sutures removed. At 6 weeks, the correction was started and required only occasional morphine analgesics. Correction was completed at 11 weeks and, once achieved, the hindfoot element was removed from the frame and the fast-fix struts were substituted for rods. Four courses of oral antibiotics were required for pin-site infections during the treatment. At 9 months, the fracture gap had consolidated sufficiently for frame removal (Fig. ). The patient had no leg problems following this and radiographs were satisfactory (Fig. ).\\nEighteen months following the injury (Fig. ), he had not returned to his previous physically active job principally due to breathlessness on exertion. This significantly affected his general wellbeing and is reflected in his EQ-5D visual analogue score of 70/100. His ankle was not painful, allowed him to walk, drive and climb stairs using a reciprocating gait. He complained of a degree of ankle stiffness. The range of ankle movement lacked 8° of dorsiflexion compared to the contralateral side, and the subtalar joint had a similar range of motion to the contralateral side. His Iowa knee score was maximal and the Olerud and Molander activity score was 85/100. Overall, he was satisfied with the outcome and would recommend the treatment.\nOUTPUT:"
},
{
"from": "agent",
"value": "IIIb open fracture of his tibia, multiple hereditary exostoses, alveolar microlithiasis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: The patient was administered antibiotics and taken to theatre at 11 h post-injury. The wound was debrided and temporarily stabilised with an external fixator (Fig. ). A CT of the extremity was obtained. The soft tissue defect was medial, measuring 8 cm by 4 cm. On day 3, an acute angulation at the fracture site was performed and the fracture stabilised with a Taylor Spatial Frame (Fig. ). The wound was primarily closed without tension (Fig. ), and the leg was held in intentional varus by 35° (Fig. ). The wound was healed by 2 weeks and sutures removed. At 6 weeks, the correction was started and required only occasional morphine analgesics. Correction was completed at 11 weeks and, once achieved, the hindfoot element was removed from the frame and the fast-fix struts were substituted for rods. Four courses of oral antibiotics were required for pin-site infections during the treatment. At 9 months, the fracture gap had consolidated sufficiently for frame removal (Fig. ). The patient had no leg problems following this and radiographs were satisfactory (Fig. ).\nEighteen months following the injury (Fig. ), he had not returned to his previous physically active job principally due to breathlessness on exertion. This significantly affected his general wellbeing and is reflected in his EQ-5D visual analogue score of 70/100. His ankle was not painful, allowed him to walk, drive and climb stairs using a reciprocating gait. He complained of a degree of ankle stiffness. The range of ankle movement lacked 8° of dorsiflexion compared to the contralateral side, and the subtalar joint had a similar range of motion to the contralateral side. His Iowa knee score was maximal and the Olerud and Molander activity score was 85/100. Overall, he was satisfied with the outcome and would recommend the treatment.
OUTPUT: |
PMCPatients_common1780 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Case 2. A 52-year-old man living in Ananindeua City, Brazil, was clinically examined on the third day of illness and experienced high fever, with episodes of focal seizures persisting for 3 days. Clinical examination revealed altered gait, muscle weakness, and absence of signs of meningeal irritation, but a positive Romberg sign; the CT scans and hemogram results were normal. During examination in the National Reference Laboratory, RT-qPCR using serum tested negative for the RNA of CHIKV (Lanciotti et al. ), DENV (Santiago et al. ), SLEV (Lanciotti and Kerst ), WNV (Lanciotti et al. ), and ZIKV (Lanciotti et al. ), but positive for OROV (Naveca et al. ). Similarly, IgM-ELISA was negative for CHIKV, DENV (Henriques et al. ), SLEV (Henriques et al. ), WNV (Henriques et al. ), and ZIKV (Henriques et al. ), but positive for OROV-IgM. On the 11th day after onset of symptoms, CSF was collected and IgM-ELISA confirmed OROV infection. Moreover, HI test (Clarke and Casals ) showed the presence of total antibodies against OROV in both serum and CSF samples.\\nIt is noteworthy that approximately 30 days before the clinical symptoms mentioned previously, the patient developed another clinical condition of high fever accompanied by headache, myalgia, and arthralgia that persisted for 2 weeks without a clear etiological diagnosis at the time. The patient developed insomnia, right hearing loss, and horizontal nystagmus and thus sought for specialized investigation at the National Reference Laboratory for Arboviruses, as described above. It is important to clarify that sample collection for the second clinical investigation was considered after the appearance of neurological symptoms.\nOUTPUT:"
},
{
"from": "agent",
"value": "OROV-associated encephalitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Case 2. A 52-year-old man living in Ananindeua City, Brazil, was clinically examined on the third day of illness and experienced high fever, with episodes of focal seizures persisting for 3 days. Clinical examination revealed altered gait, muscle weakness, and absence of signs of meningeal irritation, but a positive Romberg sign; the CT scans and hemogram results were normal. During examination in the National Reference Laboratory, RT-qPCR using serum tested negative for the RNA of CHIKV (Lanciotti et al. ), DENV (Santiago et al. ), SLEV (Lanciotti and Kerst ), WNV (Lanciotti et al. ), and ZIKV (Lanciotti et al. ), but positive for OROV (Naveca et al. ). Similarly, IgM-ELISA was negative for CHIKV, DENV (Henriques et al. ), SLEV (Henriques et al. ), WNV (Henriques et al. ), and ZIKV (Henriques et al. ), but positive for OROV-IgM. On the 11th day after onset of symptoms, CSF was collected and IgM-ELISA confirmed OROV infection. Moreover, HI test (Clarke and Casals ) showed the presence of total antibodies against OROV in both serum and CSF samples.\nIt is noteworthy that approximately 30 days before the clinical symptoms mentioned previously, the patient developed another clinical condition of high fever accompanied by headache, myalgia, and arthralgia that persisted for 2 weeks without a clear etiological diagnosis at the time. The patient developed insomnia, right hearing loss, and horizontal nystagmus and thus sought for specialized investigation at the National Reference Laboratory for Arboviruses, as described above. It is important to clarify that sample collection for the second clinical investigation was considered after the appearance of neurological symptoms.
OUTPUT: |
PMCPatients_common785 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: No medical treatment was established.\\nFour years later the patient presented himself without any complaints. The TSH level was still normal at 1.44 mU/l.\\nDiscussing the results of the investigations with the patient, he raised the question of what impact THA would have for him in the short term and long term.\nOUTPUT:"
},
{
"from": "agent",
"value": "Thyroid Hemiagenesis, Iodine Deficiency, Vitamin D Deficiency"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: No medical treatment was established.\nFour years later the patient presented himself without any complaints. The TSH level was still normal at 1.44 mU/l.\nDiscussing the results of the investigations with the patient, he raised the question of what impact THA would have for him in the short term and long term.
OUTPUT: |
PMCPatients_common4934 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 67-year-old Caucasian male presented with a 10-day history of gradually worsening abdominal pain, associated with nausea and episodes of vomiting. His medical history was significant for arterial hypertension. Physical examination revealed a distended abdomen with a palpable tender mass in the left lower quadrant. The hemogram revealed anemia with a hemoglobin level of 9.5 g/dL and a hematocrit of 30%. Biochemical investigations revealed elevated serum levels of C-reactive protein 49 mg/L (reference range < 5) and significantly elevated serum carcinoembryonic antigen levels 500 ng/mL (reference range 0-10). The appendix was distended with a maximum diameter of approximately 2 cm. Liver metastases were also noted. A Hartman's procedure (sigmoid colectomy with end colostomy and oversewing of the rectal stump) along with appendectomy was performed. A transanal local excision of the rectal tumor was also performed. The postoperative course was uneventful. Four out of the twenty resected lymph nodes contained extensive metastases. Although the patient received adjuvant chemotherapy, he unfortunately died of progressive disease 5 months later.\nOUTPUT:"
},
{
"from": "agent",
"value": "Appendiceal mucinous cystadenoma, Colon adenocarcinoma, Tubulovillous rectal adenoma"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 67-year-old Caucasian male presented with a 10-day history of gradually worsening abdominal pain, associated with nausea and episodes of vomiting. His medical history was significant for arterial hypertension. Physical examination revealed a distended abdomen with a palpable tender mass in the left lower quadrant. The hemogram revealed anemia with a hemoglobin level of 9.5 g/dL and a hematocrit of 30%. Biochemical investigations revealed elevated serum levels of C-reactive protein 49 mg/L (reference range < 5) and significantly elevated serum carcinoembryonic antigen levels 500 ng/mL (reference range 0-10). The appendix was distended with a maximum diameter of approximately 2 cm. Liver metastases were also noted. A Hartman's procedure (sigmoid colectomy with end colostomy and oversewing of the rectal stump) along with appendectomy was performed. A transanal local excision of the rectal tumor was also performed. The postoperative course was uneventful. Four out of the twenty resected lymph nodes contained extensive metastases. Although the patient received adjuvant chemotherapy, he unfortunately died of progressive disease 5 months later.
OUTPUT: |
PMCPatients_common3678 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She denied palpitation, chest pain, syncope, or presyncope. Detailed anamnesis of the patient revealed no history of cardiac disease, hypertension, diabetes mellitus, hyperlipidemia, and smoking and she was a healthy woman otherwise. Her blood tests including liver, kidney, thyroid function tests, and complete blood count were in normal limits. Her pulmonary function test, chest X-ray, and tomography were normal. She had been prescribed bronchodilatator therapy by pulmonologists. Unfortunately, adrenal insufficiency occurred which were thought to be secondary to steroid therapy and was discontinued. Her cardiac examination revealed S1, S2 with a regular rhythm and no murmurs, S3 or S4. Her blood pressure and heart rate were within the normal range. Her electrocardiographic and echocardiographic examinations were normal. Then, the patient was scheduled for electrophysiological study in cardiology clinic. Programmed atrial and ventricular stimulation revealed dual atrioventricular node physiology. Then, successful empirical slow pathway catheter ablation was performed. After successful ablation procedure, acetylsalicylic acid was prescribed to the patient and was discontinued 3 months later. Written informed consent was obtained from the patient.\nOUTPUT:"
},
{
"from": "agent",
"value": "Asthma-like attacks, SVT"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: She denied palpitation, chest pain, syncope, or presyncope. Detailed anamnesis of the patient revealed no history of cardiac disease, hypertension, diabetes mellitus, hyperlipidemia, and smoking and she was a healthy woman otherwise. Her blood tests including liver, kidney, thyroid function tests, and complete blood count were in normal limits. Her pulmonary function test, chest X-ray, and tomography were normal. She had been prescribed bronchodilatator therapy by pulmonologists. Unfortunately, adrenal insufficiency occurred which were thought to be secondary to steroid therapy and was discontinued. Her cardiac examination revealed S1, S2 with a regular rhythm and no murmurs, S3 or S4. Her blood pressure and heart rate were within the normal range. Her electrocardiographic and echocardiographic examinations were normal. Then, the patient was scheduled for electrophysiological study in cardiology clinic. Programmed atrial and ventricular stimulation revealed dual atrioventricular node physiology. Then, successful empirical slow pathway catheter ablation was performed. After successful ablation procedure, acetylsalicylic acid was prescribed to the patient and was discontinued 3 months later. Written informed consent was obtained from the patient.
OUTPUT: |
PMCPatients_common65 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: He voluntarily participated in this study. He first was examined by a physician, who took a complete medical history and administered a dermatological examination. The patient had not used any topical or oral agents to reduce the oiliness of his skin for the previous 10 weeks. He experienced postprandial fullness, excessive belching and upper abdominal bloating. His endoscopic and biopsy evaluations were normal. Sebumetry is a well-accepted method of measuring the casual levels of sebum. Sebumetry was performed on the patient’s vertex region 24 h after shampooing with his usual shampoo without a topical agent. The patient was also asked to record any changes in his GI symptoms in his self-report diary. The severity and frequency of the symptoms were assessed before and at the end of treatment using a Likert scale. During the 8-wk therapeutic period, the patient consumed capsules containing 500 mg of Triphala twice daily (after breakfast and dinner). No restrictions were placed on the frequency of shampooing. He was asked to inform his physician of any adverse effects. He also was visited two times during this period to examine for possible complications. No adverse effects or drug intolerance were detected during treatment. His gastrointestinal complications also improved dramatically noted in .\nOUTPUT:"
},
{
"from": "agent",
"value": "Scalp Seborrhea, Functional Dyspepsia"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: He voluntarily participated in this study. He first was examined by a physician, who took a complete medical history and administered a dermatological examination. The patient had not used any topical or oral agents to reduce the oiliness of his skin for the previous 10 weeks. He experienced postprandial fullness, excessive belching and upper abdominal bloating. His endoscopic and biopsy evaluations were normal. Sebumetry is a well-accepted method of measuring the casual levels of sebum. Sebumetry was performed on the patient’s vertex region 24 h after shampooing with his usual shampoo without a topical agent. The patient was also asked to record any changes in his GI symptoms in his self-report diary. The severity and frequency of the symptoms were assessed before and at the end of treatment using a Likert scale. During the 8-wk therapeutic period, the patient consumed capsules containing 500 mg of Triphala twice daily (after breakfast and dinner). No restrictions were placed on the frequency of shampooing. He was asked to inform his physician of any adverse effects. He also was visited two times during this period to examine for possible complications. No adverse effects or drug intolerance were detected during treatment. His gastrointestinal complications also improved dramatically noted in .
OUTPUT: |
PMCPatients_common1915 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 27-year-old woman presented to the emergency department with nausea, vomiting, and global headache. The admission of non-contrast CT of the head showed a rounded hyperdense lesion in the left Sylvian fissure, without evidence of acute hemorrhage or associated hydrocephalus. A subsequent magnetic resonance angiogram (MRA) was performed showing a giant aneurysm of the left MCA. Before deciding whether to occlude the vessels or not, a balloon-assisted occlusion test (BOT) with a Scepter balloon in the proximal ostium of the aneurysm was performed, which resulted in a transitory facial paralysis. The parent vessel occlusion could not be performed. Therefore, it was decided to perform stent-assisted coil embolization of the aneurysm using both small and large coils. (Figure ) A right femoral artery entry was used with an 8F-introducer, through which a 0.88 Neuronmax catheter was entered up to the right internal carotid artery (ICA). Subsequently, a distal support Vasco microcatheter was catheterized with a 0.014 microwire to the segment of the artery distal to the aneurysm. A Slim-px microcatheter was used to access the proximal M1 segment of the right MCA. A 3D-DSA reconstruction was performed and used as a railroad map.\\nPosteriorly, an Enterprise stent was successfully introduced, and a complete recanalization was achieved. After the placement of the stent, a total of 36 coils (26 conventional and seven large coils) were used. Subsequent one and two-year follow-up MRAs and angiograms showed adequate packaging (Figure ). The patient presented occasional headaches, but there was no hemorrhage or other complications related to the treatment of the aneurysm.\nOUTPUT:"
},
{
"from": "agent",
"value": "Giant Aneurysm of the Middle Cerebral Artery"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 27-year-old woman presented to the emergency department with nausea, vomiting, and global headache. The admission of non-contrast CT of the head showed a rounded hyperdense lesion in the left Sylvian fissure, without evidence of acute hemorrhage or associated hydrocephalus. A subsequent magnetic resonance angiogram (MRA) was performed showing a giant aneurysm of the left MCA. Before deciding whether to occlude the vessels or not, a balloon-assisted occlusion test (BOT) with a Scepter balloon in the proximal ostium of the aneurysm was performed, which resulted in a transitory facial paralysis. The parent vessel occlusion could not be performed. Therefore, it was decided to perform stent-assisted coil embolization of the aneurysm using both small and large coils. (Figure ) A right femoral artery entry was used with an 8F-introducer, through which a 0.88 Neuronmax catheter was entered up to the right internal carotid artery (ICA). Subsequently, a distal support Vasco microcatheter was catheterized with a 0.014 microwire to the segment of the artery distal to the aneurysm. A Slim-px microcatheter was used to access the proximal M1 segment of the right MCA. A 3D-DSA reconstruction was performed and used as a railroad map.\nPosteriorly, an Enterprise stent was successfully introduced, and a complete recanalization was achieved. After the placement of the stent, a total of 36 coils (26 conventional and seven large coils) were used. Subsequent one and two-year follow-up MRAs and angiograms showed adequate packaging (Figure ). The patient presented occasional headaches, but there was no hemorrhage or other complications related to the treatment of the aneurysm.
OUTPUT: |
PMCPatients_common1626 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Her compliance to highly active antiretroviral therapy has been variable with ongoing viremia over the last five years, and consistently low CD4 count of less than 100. She presented to the emergency room with a four-day history of nausea, vomiting, diarrhea, cough, and subjective fevers associated with tenderness on the left side of her neck. There is no history of thyroid dysfunction, neck irradiation, family history of thyroid disease, recent travel, or recent sick contacts.\\nOn examination, she was hypertensive, tachycardic, and later developed fever as high as 101.6 degrees Fahrenheit. The neck was supple with a prominent thyroid gland, more on the left, associated with tenderness on palpation. Thyroid function tests revealed elevated free T4 of 5.5 [0.61-1.12 ng/dl] and T3 of 7.6 [0.87-1.78 ng/ml] with thyroid-stimulating hormone (TSH) level of 0.01 [0.34-5.6 ulU/ML]. The electrocardiogram disclosed sinus tachycardia with ventricular rate of 135 and non-specific T-wave abnormality with no ischemic changes. CT pulmonary angiogram ruled out central pulmonary embolic disease, but incidentally noted a markedly enlarged heterogeneous thyroid gland with prominent cervical lymphadenopathy (Figure ). Thyroid ultrasound revealed enlarged heterogeneous thyroid gland with increased vascularity (Figures , ). Thyroid-stimulating immunoglobulin turned out to be abnormal at 324% of the reference control. The patient was started on methimazole 30 mg daily along with propranolol 40 mg four times a day, with improvement of her clinical symptomatology. At the time, repeat HIV parameters revealed improvement in virologic control while on bictegravir/emtricitabine/tenofovir alafenamide and a CD4 count of 330.\nOUTPUT:"
},
{
"from": "agent",
"value": "Graves’ Disease, Human Immunodeficiency Virus Infection"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Her compliance to highly active antiretroviral therapy has been variable with ongoing viremia over the last five years, and consistently low CD4 count of less than 100. She presented to the emergency room with a four-day history of nausea, vomiting, diarrhea, cough, and subjective fevers associated with tenderness on the left side of her neck. There is no history of thyroid dysfunction, neck irradiation, family history of thyroid disease, recent travel, or recent sick contacts.\nOn examination, she was hypertensive, tachycardic, and later developed fever as high as 101.6 degrees Fahrenheit. The neck was supple with a prominent thyroid gland, more on the left, associated with tenderness on palpation. Thyroid function tests revealed elevated free T4 of 5.5 [0.61-1.12 ng/dl] and T3 of 7.6 [0.87-1.78 ng/ml] with thyroid-stimulating hormone (TSH) level of 0.01 [0.34-5.6 ulU/ML]. The electrocardiogram disclosed sinus tachycardia with ventricular rate of 135 and non-specific T-wave abnormality with no ischemic changes. CT pulmonary angiogram ruled out central pulmonary embolic disease, but incidentally noted a markedly enlarged heterogeneous thyroid gland with prominent cervical lymphadenopathy (Figure ). Thyroid ultrasound revealed enlarged heterogeneous thyroid gland with increased vascularity (Figures , ). Thyroid-stimulating immunoglobulin turned out to be abnormal at 324% of the reference control. The patient was started on methimazole 30 mg daily along with propranolol 40 mg four times a day, with improvement of her clinical symptomatology. At the time, repeat HIV parameters revealed improvement in virologic control while on bictegravir/emtricitabine/tenofovir alafenamide and a CD4 count of 330.
OUTPUT: |
PMCPatients_common3298 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An African American female in her early 90s with a history of diabetes, hypertension, and prior pulmonary embolism presented from a nursing home with recurrent falls. She reported that she had had multiple falls the week prior to presentation, associated with dizziness and feeling of faintness. She reported that she had never had as many episodes of dizziness like this before. On the morning of presentation, she felt dizzy when she got out of bed, but had to use the restroom. As she was walking to the restroom, she felt light headed and fell but did not lose consciousness. She denied chest pain, shortness of breath, palpitations, fevers, chills, cough, sore throat, nausea, vomiting, or abdominal pain. She did report a poor appetite and some loose stools 2 weeks prior to presentation. Notably for potential fall risk medications, she was taking furosemide. Her examination revealed an oxygen saturation of 98% on room air, BP 153/82, Respiratory Rate 17, Pulse 100, Temperature 37.1°C. She demonstrated no orthostasis in her blood pressure readings from the lying to standing position. The rest of her exam was unremarkable. A SARS-CoV-2 screen was positive. Her laboratory results however revealed new abnormal laboratory findings including leukocytosis of 13.2, thrombocytosis of 480, elevated C-reactive protein (CRP) of 114, lactate dehydrogenase (LDH) 374, D-dimer 6,460, folate levels of 4.7. She had a computerized tomography (CT) scan of the chest, abdomen, and pelvis which showed regions of atelectasis within both lungs and no focal consolidation. It also showed mild left lateral compression type pelvic injury, with left inferior pubic ramus, and left lateral superior pubic ramus fractures with left sacral ala fracture. She was seen by orthopedic surgery who recommended non-operative management including pain management and physical therapy. Her hospital course remained unremarkable and her dizziness resolved. She was subsequently discharged to a Subacute Rehabilitation Facility.\nOUTPUT:"
},
{
"from": "agent",
"value": "COVID-19 Disease"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: An African American female in her early 90s with a history of diabetes, hypertension, and prior pulmonary embolism presented from a nursing home with recurrent falls. She reported that she had had multiple falls the week prior to presentation, associated with dizziness and feeling of faintness. She reported that she had never had as many episodes of dizziness like this before. On the morning of presentation, she felt dizzy when she got out of bed, but had to use the restroom. As she was walking to the restroom, she felt light headed and fell but did not lose consciousness. She denied chest pain, shortness of breath, palpitations, fevers, chills, cough, sore throat, nausea, vomiting, or abdominal pain. She did report a poor appetite and some loose stools 2 weeks prior to presentation. Notably for potential fall risk medications, she was taking furosemide. Her examination revealed an oxygen saturation of 98% on room air, BP 153/82, Respiratory Rate 17, Pulse 100, Temperature 37.1°C. She demonstrated no orthostasis in her blood pressure readings from the lying to standing position. The rest of her exam was unremarkable. A SARS-CoV-2 screen was positive. Her laboratory results however revealed new abnormal laboratory findings including leukocytosis of 13.2, thrombocytosis of 480, elevated C-reactive protein (CRP) of 114, lactate dehydrogenase (LDH) 374, D-dimer 6,460, folate levels of 4.7. She had a computerized tomography (CT) scan of the chest, abdomen, and pelvis which showed regions of atelectasis within both lungs and no focal consolidation. It also showed mild left lateral compression type pelvic injury, with left inferior pubic ramus, and left lateral superior pubic ramus fractures with left sacral ala fracture. She was seen by orthopedic surgery who recommended non-operative management including pain management and physical therapy. Her hospital course remained unremarkable and her dizziness resolved. She was subsequently discharged to a Subacute Rehabilitation Facility.
OUTPUT: |
PMCPatients_common107 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 55 year old female patient was being treated at local hospital for 3 days symptoms suggestive of acute exacerbation of COPD. She was referred to our center for further management after she developed multiple episodes of seizure followed by loss of consciousness on the first day of hospital admission. The patient’s relatives revealed that she had history of COPD for last 5 years but was not compliant to inhaler medications. Her family history was unremarkable. She has been a smoker for the last 30 years. No other significant history was available.\\nOn examination, the patient was drowsy, and was not obeying commands. She had a temperature of 37.6 °C, blood pressure of 130/80 mmHg, pulse rate of 96/min and respiratory rate of 26/min. She had widespread expiratory wheeze. While the patient was regaining consciousness, she reported of headache and a decreased vision. An ocular examination revealed normally reactive pupil and fundus. Cranial nerves examination was unremarkable. Motor and sensory function examination was normal. There was no any clinical sign of meningeal irritation.\\nHer laboratory tests on admission were as follows: hemoglobin, 17 g/dl; white blood cells, 12640 /Cumm; platelets, 155000 /Cumm; urea, 37 mg/ dl; creatinine 0.3 mg/dl; Na, 132 meq/L; K,4.6 meq/L. Chest X-radiography revealed emphysematous changes. Arterial blood gas finding showed the pH, 7.56; pCO2, 46.2; pO2, 81.0; HCO3, 41.5. Magnetic Resonance Imaging (MRI) demonstrated hyperintense lesions in the bilateral parieto-occipital region consistent with PRES (Fig. ).\\nOur patient was treated with salbutamol and ipratropium nebulisation, hydrocortisone, levetiracetam and other supportive care. The patient was continuously monitored for hemodynamic stability in Intensive Care Unit (ICU) for 2 days and was later transferred to a general ward. The patient continued to improve clinically and was discharged home on the sixth day of hospitalization without any respiratory and neurological symptom.\nOUTPUT:"
},
{
"from": "agent",
"value": "Posterior reversible encephalopathy syndrome, Exacerbation of chronic obstructive pulmonary disease"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 55 year old female patient was being treated at local hospital for 3 days symptoms suggestive of acute exacerbation of COPD. She was referred to our center for further management after she developed multiple episodes of seizure followed by loss of consciousness on the first day of hospital admission. The patient’s relatives revealed that she had history of COPD for last 5 years but was not compliant to inhaler medications. Her family history was unremarkable. She has been a smoker for the last 30 years. No other significant history was available.\nOn examination, the patient was drowsy, and was not obeying commands. She had a temperature of 37.6 °C, blood pressure of 130/80 mmHg, pulse rate of 96/min and respiratory rate of 26/min. She had widespread expiratory wheeze. While the patient was regaining consciousness, she reported of headache and a decreased vision. An ocular examination revealed normally reactive pupil and fundus. Cranial nerves examination was unremarkable. Motor and sensory function examination was normal. There was no any clinical sign of meningeal irritation.\nHer laboratory tests on admission were as follows: hemoglobin, 17 g/dl; white blood cells, 12640 /Cumm; platelets, 155000 /Cumm; urea, 37 mg/ dl; creatinine 0.3 mg/dl; Na, 132 meq/L; K,4.6 meq/L. Chest X-radiography revealed emphysematous changes. Arterial blood gas finding showed the pH, 7.56; pCO2, 46.2; pO2, 81.0; HCO3, 41.5. Magnetic Resonance Imaging (MRI) demonstrated hyperintense lesions in the bilateral parieto-occipital region consistent with PRES (Fig. ).\nOur patient was treated with salbutamol and ipratropium nebulisation, hydrocortisone, levetiracetam and other supportive care. The patient was continuously monitored for hemodynamic stability in Intensive Care Unit (ICU) for 2 days and was later transferred to a general ward. The patient continued to improve clinically and was discharged home on the sixth day of hospitalization without any respiratory and neurological symptom.
OUTPUT: |
PMCPatients_common4375 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 7-year-old boy was referred to our hospital with a chief complaint of tongue enlargement. The degree of symptom was accompanied by his growth. The enlarged tongue was dry and prevented mastication. An enlarged mass in the right submandibular area at birth caused breathing and breastfeeding difficulties. At 5 years old, he underwent sclerotherapy with three injections of 95% alcohol; however, this therapy had no effect on tongue reduction.\\nOn physical examination, the patient had a large globular tongue, 11×8×3 cm in size (). On palpation, the tongue was firm, pebbly, and non-tender with crenation on both sides. The movement of the tongue was almost totally restricted by its texture and stiffness. The patient had no obstructive sleep apnea but was uncomfortable with oral intake and had limited communication due to dysarthria. The patient was not able to close his mouth properly and was constantly drooling. In preoperative facial bone three-dimensional computed tomography (3D-CT), diastema, tooth spacing, prognathism, and class III malocclusion were noted, but other skeletal deformities were not significant (). The incision was executed using a surgical scalpel; hemostasis was completed with electrocautery. The excess tongue muscle tissue was resected. The tongue was closed using absorbable 5-0 Vicryl sutures (Ethicon, Bridgewater, NJ, USA) (). Postoperatively, the reduced tongue was contained completely within the oral cavity, but an open bite remained as the result of increased gonial angle and mandibular plane and disproportionate mandibular growth. Sensory and motor nerves to the tongue appeared to be intact, and circulation was adequate.\nOUTPUT:"
},
{
"from": "agent",
"value": "Lymphangioma, Macroglossia"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 7-year-old boy was referred to our hospital with a chief complaint of tongue enlargement. The degree of symptom was accompanied by his growth. The enlarged tongue was dry and prevented mastication. An enlarged mass in the right submandibular area at birth caused breathing and breastfeeding difficulties. At 5 years old, he underwent sclerotherapy with three injections of 95% alcohol; however, this therapy had no effect on tongue reduction.\nOn physical examination, the patient had a large globular tongue, 11×8×3 cm in size (). On palpation, the tongue was firm, pebbly, and non-tender with crenation on both sides. The movement of the tongue was almost totally restricted by its texture and stiffness. The patient had no obstructive sleep apnea but was uncomfortable with oral intake and had limited communication due to dysarthria. The patient was not able to close his mouth properly and was constantly drooling. In preoperative facial bone three-dimensional computed tomography (3D-CT), diastema, tooth spacing, prognathism, and class III malocclusion were noted, but other skeletal deformities were not significant (). The incision was executed using a surgical scalpel; hemostasis was completed with electrocautery. The excess tongue muscle tissue was resected. The tongue was closed using absorbable 5-0 Vicryl sutures (Ethicon, Bridgewater, NJ, USA) (). Postoperatively, the reduced tongue was contained completely within the oral cavity, but an open bite remained as the result of increased gonial angle and mandibular plane and disproportionate mandibular growth. Sensory and motor nerves to the tongue appeared to be intact, and circulation was adequate.
OUTPUT: |
PMCPatients_common1819 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: 49 year-old Caucasian woman with a history of stage I (T1cN0M0) invasive ductal carcinoma (IDC), ER/PR positive, HER2 non-amplified, treated with lumpectomy and SLN evaluation, followed by adjuvant taxotere/cyclophosphamide (TC) chemotherapy for 4 cycles. Upon loco-regional recurrence, a new biopsy showed TNBC disease, and she subsequently underwent bilateral mastectomies and lymph node evaluation, followed by adriamycin/cyclophosphamide (AC) for 4 cycles, and radiation therapy. She presented shortly after radiation therapy with biopsy-proven high grade mTNBC involving lungs, mediastinal and upper gastrohepatic lymph nodes, right adrenal gland, and bones (Table ). At 14 days after metastatic disease diagnosis, the patient received treatment on study, with a best response of progressive disease (PD). The patient developed rapid progression and passed away after 2 months on therapy. During the course of treatment, the patient did not have elevated serum tumor markers (CA15-5, CA27-29, or CEA). Two lesions remained stable, one decreased and one increased in size (Fig. ). Both pre- and on-olaparib biopsies were acquired from a mediastinal lymph node. H&E staining of both biopsies showed similar histopathological features, with over 90% tumor content and little immune cell infiltration (Fig. ). Pre and on-treatment samples were negative for hormone receptors, except for strong nuclear expression of the androgen receptor (AR) (Fig. ). In addition, the on-treatment sample had 5% estrogen expressing cells. Ki67 decreased from 50% in the pre-treatment sample to 30% in the on-treatment sample. PD-L1 was positive low in both samples (1–10% and 10–20% respectively) (Table ). GeneTrails© Comprehensive Tumor Panel and WES showed mutations in TP53 and FGFR4 variant of unknown significance (VUS) as well as amplification of CCND1 and FGF3 (Table ). The full list of SNVs and CNVs from WES can be found in Supplementary Tables and , respectively.\nOUTPUT:"
},
{
"from": "agent",
"value": "Metastatic TNBC (Triple Negative Breast Cancer)"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: 49 year-old Caucasian woman with a history of stage I (T1cN0M0) invasive ductal carcinoma (IDC), ER/PR positive, HER2 non-amplified, treated with lumpectomy and SLN evaluation, followed by adjuvant taxotere/cyclophosphamide (TC) chemotherapy for 4 cycles. Upon loco-regional recurrence, a new biopsy showed TNBC disease, and she subsequently underwent bilateral mastectomies and lymph node evaluation, followed by adriamycin/cyclophosphamide (AC) for 4 cycles, and radiation therapy. She presented shortly after radiation therapy with biopsy-proven high grade mTNBC involving lungs, mediastinal and upper gastrohepatic lymph nodes, right adrenal gland, and bones (Table ). At 14 days after metastatic disease diagnosis, the patient received treatment on study, with a best response of progressive disease (PD). The patient developed rapid progression and passed away after 2 months on therapy. During the course of treatment, the patient did not have elevated serum tumor markers (CA15-5, CA27-29, or CEA). Two lesions remained stable, one decreased and one increased in size (Fig. ). Both pre- and on-olaparib biopsies were acquired from a mediastinal lymph node. H&E staining of both biopsies showed similar histopathological features, with over 90% tumor content and little immune cell infiltration (Fig. ). Pre and on-treatment samples were negative for hormone receptors, except for strong nuclear expression of the androgen receptor (AR) (Fig. ). In addition, the on-treatment sample had 5% estrogen expressing cells. Ki67 decreased from 50% in the pre-treatment sample to 30% in the on-treatment sample. PD-L1 was positive low in both samples (1–10% and 10–20% respectively) (Table ). GeneTrails© Comprehensive Tumor Panel and WES showed mutations in TP53 and FGFR4 variant of unknown significance (VUS) as well as amplification of CCND1 and FGF3 (Table ). The full list of SNVs and CNVs from WES can be found in Supplementary Tables and , respectively.
OUTPUT: |
PMCPatients_common791 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 35-year-old woman with end-stage kidney disease due to focal segmental glomerulosclerosis underwent an ABO compatible preemptive KT in the right iliac fossa. Her body mass index was 18.7 kg/m2. She had low titer donor specific antibodies. The induction immunosuppression regimen included tacrolimus, mycophenolate mofetil, methylprednisolone, basiliximab, and rituximab. The total operating time was 5 h and 7 min, including a 1 h 31 min wait for the donor kidney. The surgical techniques are described in next part. The graft function after surgery was excellent. However, on postoperative day 1, the patient was not able to straighten her right leg. Physical examination revealed a paresis of her right quadriceps muscle. The patient’s sensation of her right thigh was also impaired. Computed tomography and magnetic resonance imaging showed no significant findings that could lead to FNP including hematoma or spinal disk herniation. We diagnosed her with FNP caused by inappropriate compression from a self-retaining retractor during surgery. Rehabilitation was started immediately. The patient’s motor weakness gradually improved, and the patient became able to walk independently 4 weeks later. The patient began to complain of neuropathic pain as her sensory disturbance recovered. Despite the administration of pregabalin (200 mg/day), her neuropathic pain sustained 6 months after her KT.\\nA lower quadrant curvilinear incision was made. A self-retaining retractor with three blades in the mid-medial, upper-medial, and mid-lateral directions was used. In this case, the mid-lateral blade to the retractor was directed more caudally than usual (Fig. ). Arterial dissection was performed from the proximal common iliac artery to the distal external iliac artery. The internal iliac vein was ligated to mobilize the external iliac vein. The renal artery was anastomosed to the common iliac artery, and the renal vein to the external iliac vein.\nOUTPUT:"
},
{
"from": "agent",
"value": "Femoral nerve palsy"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 35-year-old woman with end-stage kidney disease due to focal segmental glomerulosclerosis underwent an ABO compatible preemptive KT in the right iliac fossa. Her body mass index was 18.7 kg/m2. She had low titer donor specific antibodies. The induction immunosuppression regimen included tacrolimus, mycophenolate mofetil, methylprednisolone, basiliximab, and rituximab. The total operating time was 5 h and 7 min, including a 1 h 31 min wait for the donor kidney. The surgical techniques are described in next part. The graft function after surgery was excellent. However, on postoperative day 1, the patient was not able to straighten her right leg. Physical examination revealed a paresis of her right quadriceps muscle. The patient’s sensation of her right thigh was also impaired. Computed tomography and magnetic resonance imaging showed no significant findings that could lead to FNP including hematoma or spinal disk herniation. We diagnosed her with FNP caused by inappropriate compression from a self-retaining retractor during surgery. Rehabilitation was started immediately. The patient’s motor weakness gradually improved, and the patient became able to walk independently 4 weeks later. The patient began to complain of neuropathic pain as her sensory disturbance recovered. Despite the administration of pregabalin (200 mg/day), her neuropathic pain sustained 6 months after her KT.\nA lower quadrant curvilinear incision was made. A self-retaining retractor with three blades in the mid-medial, upper-medial, and mid-lateral directions was used. In this case, the mid-lateral blade to the retractor was directed more caudally than usual (Fig. ). Arterial dissection was performed from the proximal common iliac artery to the distal external iliac artery. The internal iliac vein was ligated to mobilize the external iliac vein. The renal artery was anastomosed to the common iliac artery, and the renal vein to the external iliac vein.
OUTPUT: |
PMCPatients_common41 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Patient 2 is a 32-year-old male and a younger sibling of patient 1. Given the recently identified CDH1 mutation and HDGC diagnosis in his sibling, patient 2 had a 50% likelihood of being a CDH1 mutation carrier. Subsequent genetic screening at our institution confirmed that similarly to his older sibling, patient 2 had a monoallelic deletion of exons 1–2 of the CDH1 gene, predisposing him to the HDGC like several members of his family.\\nInitial CT scan of the chest, abdomen, and pelvis and EGD biopsy of gastric tissue indicated no sign of active malignancy. However, given the ~ 70% lifetime chance of developing HDGC, the patient was recommended prophylactic gastrectomy despite showing no signs or symptoms of disease. The patient agreed with the recommendation and underwent prophylactic total gastrectomy with Roux-en-Y esophagojejunostomy and feeding j-tube placement. Immunohistochemical analysis of gastric and intestinal tissue identified three microscopic foci of signet ring cells in the lamina propria without invasion of the submucosa (Fig. The rest of the intestinal tract showed no signs of malignancy, and 0 of 30 tested lymph showed positive for metastatic carcinoma. The tumor was pathologically staged as pT1aN0M0.\\nThe patient recovered without complications and was discharged home on post-operative day 7. He returned to the emergency department 5 days later due to diffuse abdominal pain, dark-colored emesis, and no bowel movements for 2 days. Initial CT scan of abdomen and pelvis revealed dilated, gas-filled, small bowel loops. With the presumed diagnoses of ileus vs. partial small bowel obstruction, the patient was re-admitted to the surgical floor for further management. He was subsequently discharged from our institution and continues to do well without evidence of disease at the time of this manuscript.\nOUTPUT:"
},
{
"from": "agent",
"value": "Hereditary Diffuse Gastric Cancer, Poorly Differentiated Adenocarcinoma of the Stomach, Pancreatitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Patient 2 is a 32-year-old male and a younger sibling of patient 1. Given the recently identified CDH1 mutation and HDGC diagnosis in his sibling, patient 2 had a 50% likelihood of being a CDH1 mutation carrier. Subsequent genetic screening at our institution confirmed that similarly to his older sibling, patient 2 had a monoallelic deletion of exons 1–2 of the CDH1 gene, predisposing him to the HDGC like several members of his family.\nInitial CT scan of the chest, abdomen, and pelvis and EGD biopsy of gastric tissue indicated no sign of active malignancy. However, given the ~ 70% lifetime chance of developing HDGC, the patient was recommended prophylactic gastrectomy despite showing no signs or symptoms of disease. The patient agreed with the recommendation and underwent prophylactic total gastrectomy with Roux-en-Y esophagojejunostomy and feeding j-tube placement. Immunohistochemical analysis of gastric and intestinal tissue identified three microscopic foci of signet ring cells in the lamina propria without invasion of the submucosa (Fig. The rest of the intestinal tract showed no signs of malignancy, and 0 of 30 tested lymph showed positive for metastatic carcinoma. The tumor was pathologically staged as pT1aN0M0.\nThe patient recovered without complications and was discharged home on post-operative day 7. He returned to the emergency department 5 days later due to diffuse abdominal pain, dark-colored emesis, and no bowel movements for 2 days. Initial CT scan of abdomen and pelvis revealed dilated, gas-filled, small bowel loops. With the presumed diagnoses of ileus vs. partial small bowel obstruction, the patient was re-admitted to the surgical floor for further management. He was subsequently discharged from our institution and continues to do well without evidence of disease at the time of this manuscript.
OUTPUT: |
PMCPatients_common1362 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 59-year-old Caucasian male presented to our center with a rapidly growing mass in his left axilla. He complained of weight loss, night sweating, and daily fevers. Physical examination revealed lymph node enlargement only in the left axilla, but neither loss of motor function of the left arm nor neurologic deficit presented. A full dermatological examination did not reveal any concerning lesions. Incisional biopsy of the mass demonstrated malignant melanoma metastatic to regional lymph nodes, which stained positively for S100 and MART-1. BRAF mutation status was found to be V600E using Cobas 4800. The patient underwent a total body CT with no further findings, except for the axillary mass, which was observed to be extensive, poorly circumscribed, and infiltrating adjacent structures, and therefore, it was assessed as unresectable (). As he was a good candidate for BRAF inhibition, the patient was treated with vemurafenib tablets, 960 mg BID. From the first week of treatment he reported an immediate improvement in his general condition and shrinkage of the painful, ulcerating axillary mass.\\nAlthough the initial positive results of therapy were optimistic, because such improvement has been shown to be only temporary—often followed by a state of increased resistance and progression of the disease—one month after beginning treatment we decided to operate. Surgical resection revealed a mass of 14 cm in diameter that penetrated the pectoralis major and minor muscles and encircled the axillary artery, vein, and nerve. The entire mass, including the pectoralis muscle and skin above it, was removed. The pathological examination revealed foci of a totally necrotic tumor with no observable traces of viable tissue ().\\nFollowing his recovery, the patient returned to his homeland overseas and stopped treatment, despite medical advice to the contrary.\nOUTPUT:"
},
{
"from": "agent",
"value": "Stage IIIc unresectable melanoma of unknown origin, Brain metastases"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 59-year-old Caucasian male presented to our center with a rapidly growing mass in his left axilla. He complained of weight loss, night sweating, and daily fevers. Physical examination revealed lymph node enlargement only in the left axilla, but neither loss of motor function of the left arm nor neurologic deficit presented. A full dermatological examination did not reveal any concerning lesions. Incisional biopsy of the mass demonstrated malignant melanoma metastatic to regional lymph nodes, which stained positively for S100 and MART-1. BRAF mutation status was found to be V600E using Cobas 4800. The patient underwent a total body CT with no further findings, except for the axillary mass, which was observed to be extensive, poorly circumscribed, and infiltrating adjacent structures, and therefore, it was assessed as unresectable (). As he was a good candidate for BRAF inhibition, the patient was treated with vemurafenib tablets, 960 mg BID. From the first week of treatment he reported an immediate improvement in his general condition and shrinkage of the painful, ulcerating axillary mass.\nAlthough the initial positive results of therapy were optimistic, because such improvement has been shown to be only temporary—often followed by a state of increased resistance and progression of the disease—one month after beginning treatment we decided to operate. Surgical resection revealed a mass of 14 cm in diameter that penetrated the pectoralis major and minor muscles and encircled the axillary artery, vein, and nerve. The entire mass, including the pectoralis muscle and skin above it, was removed. The pathological examination revealed foci of a totally necrotic tumor with no observable traces of viable tissue ().\nFollowing his recovery, the patient returned to his homeland overseas and stopped treatment, despite medical advice to the contrary.
OUTPUT: |
PMCPatients_common1555 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A previously healthy 2-year-old girl presented with a 4-week history of a cutaneous pruritic eruption that initially appeared on her legs and subsequently progressed to affect her soles, arms and face sparing the trunk and palms. The child had already been treated three-times with topical administration of benzyl-benzoate lotion as a trial treatment for scabies without any improvement. History revealed that 2 weeks prior to the eruption, the child had received hepatitis B vaccination. On physical examination, she was afebrile with erythematous papules and vesicles on the cheeks, arms, hands and legs (A & B) with bullous transformation on the soles (C & D). There was no lymphadenopathy or hepatosplenomegaly. The patient experienced intense pruritus causing sleep disturbances. In the view of parents’ demand and atypical clinical presentation, a skin biopsy was performed and histopathologic examination of a specimen from the left buttock revealed the presence of parakeratosis and mild acanthosis in the epidermis. Focally, mild interface dermatitis is noted without apoptosis. Moderately intense perivascular and periadnexial lympho-histiocytic infiltrate is also noted in the superficial and mid-dermis with focal exocytosis of lymphoid cells (). The child was diagnosed with atypical GCS following hepatitis B vaccination. Because symptoms were unresponsive to topical betamethasone 0.05% and oral antihistaminic drug, she received oral administration of dexamethasone 0.5 mg/5 ml for 4 days and the eruption resolved partially.\\nThree months later, the child presented with a similar papulovesicular monomorphic pruritic eruption localized on the face, arms and legs, sparing the trunk as well (A–C). The MMR vaccine (measles, mumps and rubella) was administered 7 days prior to the eruption. A history of intercurrent viral illness was noted by the parents at the time of vaccination. The patient was treated only with topical corticosteroids and an oral antihistaminic drug.\nOUTPUT:"
},
{
"from": "agent",
"value": "Gianotti–Crosti syndrome"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A previously healthy 2-year-old girl presented with a 4-week history of a cutaneous pruritic eruption that initially appeared on her legs and subsequently progressed to affect her soles, arms and face sparing the trunk and palms. The child had already been treated three-times with topical administration of benzyl-benzoate lotion as a trial treatment for scabies without any improvement. History revealed that 2 weeks prior to the eruption, the child had received hepatitis B vaccination. On physical examination, she was afebrile with erythematous papules and vesicles on the cheeks, arms, hands and legs (A & B) with bullous transformation on the soles (C & D). There was no lymphadenopathy or hepatosplenomegaly. The patient experienced intense pruritus causing sleep disturbances. In the view of parents’ demand and atypical clinical presentation, a skin biopsy was performed and histopathologic examination of a specimen from the left buttock revealed the presence of parakeratosis and mild acanthosis in the epidermis. Focally, mild interface dermatitis is noted without apoptosis. Moderately intense perivascular and periadnexial lympho-histiocytic infiltrate is also noted in the superficial and mid-dermis with focal exocytosis of lymphoid cells (). The child was diagnosed with atypical GCS following hepatitis B vaccination. Because symptoms were unresponsive to topical betamethasone 0.05% and oral antihistaminic drug, she received oral administration of dexamethasone 0.5 mg/5 ml for 4 days and the eruption resolved partially.\nThree months later, the child presented with a similar papulovesicular monomorphic pruritic eruption localized on the face, arms and legs, sparing the trunk as well (A–C). The MMR vaccine (measles, mumps and rubella) was administered 7 days prior to the eruption. A history of intercurrent viral illness was noted by the parents at the time of vaccination. The patient was treated only with topical corticosteroids and an oral antihistaminic drug.
OUTPUT: |
PMCPatients_common2220 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 72-year-old female with a history of hypertension, type II diabetes, dyslipidemia, peripheral vascular disease (PVD), and severe chronic obstructive pulmonary disease (COPD) presented with a non-ST elevation myocardial infarction (NSTEMI). Transthoracic echocardiography confirmed mild left ventricular (LV) systolic dysfunction with an ejection fraction of 40%-45% and severe AS with a valve area of 0.6 cm2. An intra-aortic balloon pump (IABP) was unable to be inserted due to severe PVD, which was confirmed on computed tomographic angiography (CTA). After a review by cardiac surgery, the patient was deemed not to be a surgical candidate due to underlying COPD. As the patient developed recurrent ischemic pain with diffuse ST depression across the precordial leads, a multidisciplinary approach with support from interventional radiology, structural cardiology, and interventional cardiology was pursued. Femoral balloon angioplasty to the common iliac artery was performed to facilitate the insertion of an Impella CP device, given the underlying PVD in this patient (Figure , Video ). Using a 14F short catheter and subsequently upgrading to a 14F Cook sheath, balloon aortic valvuloplasty (BAV) was performed to allow the insertion of the Impella device into the LV cavity (Figure , Figure , Videos -). Although the patient had a significant post-procedural femoral bleed requiring an interposition graft within the right femoral artery, she tolerated the procedure well and was subsequently discharged home with no recurrent ischemic symptoms at one year of follow-up.\nOUTPUT:"
},
{
"from": "agent",
"value": "Complex Left Main Coronary Artery Disease"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 72-year-old female with a history of hypertension, type II diabetes, dyslipidemia, peripheral vascular disease (PVD), and severe chronic obstructive pulmonary disease (COPD) presented with a non-ST elevation myocardial infarction (NSTEMI). Transthoracic echocardiography confirmed mild left ventricular (LV) systolic dysfunction with an ejection fraction of 40%-45% and severe AS with a valve area of 0.6 cm2. An intra-aortic balloon pump (IABP) was unable to be inserted due to severe PVD, which was confirmed on computed tomographic angiography (CTA). After a review by cardiac surgery, the patient was deemed not to be a surgical candidate due to underlying COPD. As the patient developed recurrent ischemic pain with diffuse ST depression across the precordial leads, a multidisciplinary approach with support from interventional radiology, structural cardiology, and interventional cardiology was pursued. Femoral balloon angioplasty to the common iliac artery was performed to facilitate the insertion of an Impella CP device, given the underlying PVD in this patient (Figure , Video ). Using a 14F short catheter and subsequently upgrading to a 14F Cook sheath, balloon aortic valvuloplasty (BAV) was performed to allow the insertion of the Impella device into the LV cavity (Figure , Figure , Videos -). Although the patient had a significant post-procedural femoral bleed requiring an interposition graft within the right femoral artery, she tolerated the procedure well and was subsequently discharged home with no recurrent ischemic symptoms at one year of follow-up.
OUTPUT: |
PMCPatients_common4551 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The bleeding was too abrupt and massive to be controlled, and the source could not be identified. Her respiration was relatively stable due to the endotracheal tube. Temporary hemostasis was achieved with manual compression followed by meticulous packing of gauze and pad. Her hemoglobin decreased to 9.6 from 12.4 g/dL.\\nNeck computed tomography (CT) angiogram with three-dimensional reconstruction demonstrated a saccular aneurysm of the right ITA (). The patient was immediately prepared for endovascular intervention because the tentative hemostasis and poor general condition of the patient made surgical exploration risky. After groin site puncture, conventional angiography through the thyrocervical trunk (TCT) revealed an ITA aneurysm 8 mm in diameter (). The right TCT was superselected, and a microcatheter was placed adjacent to the aneurysm. A single pushable embolization coil (18S, 3/2, Tornado Embolization Microcoils Soft, Cook, Bjaeverskov, Denmark) was inserted and placed in the parent artery immediately proximal to the aneurysm (). The aneurysm was no longer visible on angiogram 10 minutes after insertion of the coil (). There was no additional bleeding after removal of the packed materials. Follow-up CT three days after embolization evidenced the complete disappearance of the aneurysmal sac ().\\nDetailed history taking to investigate possible causes of the rare aneurysm did not reveal any history of previous neck surgery, percutaneous procedure, or trauma. There was no history of other connective tissue disorder. Follow-up angiography on the seventh postoperative day confirmed the absence of the aneurysmal sac. The patient's postoperative course was uneventful.\nOUTPUT:"
},
{
"from": "agent",
"value": "Ruptured Inferior Thyroid Artery Aneurysm with Active Bleeding, Subarachnoid hemorrhage, Pneumonia"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: The bleeding was too abrupt and massive to be controlled, and the source could not be identified. Her respiration was relatively stable due to the endotracheal tube. Temporary hemostasis was achieved with manual compression followed by meticulous packing of gauze and pad. Her hemoglobin decreased to 9.6 from 12.4 g/dL.\nNeck computed tomography (CT) angiogram with three-dimensional reconstruction demonstrated a saccular aneurysm of the right ITA (). The patient was immediately prepared for endovascular intervention because the tentative hemostasis and poor general condition of the patient made surgical exploration risky. After groin site puncture, conventional angiography through the thyrocervical trunk (TCT) revealed an ITA aneurysm 8 mm in diameter (). The right TCT was superselected, and a microcatheter was placed adjacent to the aneurysm. A single pushable embolization coil (18S, 3/2, Tornado Embolization Microcoils Soft, Cook, Bjaeverskov, Denmark) was inserted and placed in the parent artery immediately proximal to the aneurysm (). The aneurysm was no longer visible on angiogram 10 minutes after insertion of the coil (). There was no additional bleeding after removal of the packed materials. Follow-up CT three days after embolization evidenced the complete disappearance of the aneurysmal sac ().\nDetailed history taking to investigate possible causes of the rare aneurysm did not reveal any history of previous neck surgery, percutaneous procedure, or trauma. There was no history of other connective tissue disorder. Follow-up angiography on the seventh postoperative day confirmed the absence of the aneurysmal sac. The patient's postoperative course was uneventful.
OUTPUT: |
PMCPatients_common3263 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 58-year-old man presented with complaints of breathlessness and high-grade fever of 15 days duration. There was no history of chest pain or dizziness. He was a known hypertensive for 20 years with a history of coronary artery disease for 17 years. He had a history of tuberculous lymphadenitis, diagnosed and treated 3 years back. He had undergone angioplasty to the left anterior descending artery and right coronary artery 11 years back, coronary artery bypass grafting for triple-vessel disease, and left ventricular (LV) aneurysm repair with native autologous pericardial patch 9 years back. For the past 2 years, he had recurrent episodes of fever secondary to methicillin-resistant Staphylococcus aureus (MRSA) bacteremia, for which he was treated with broad-spectrum antibiotics. He also had a history of one episode of cardioembolic ischemic stroke (right middle cerebral artery infarct) secondary to mobile LV thrombus and pulmonary embolism. Only contrast-enhanced CT chest and abdomen did not reveal any evidence of infection. Hence, 18F-FDG PET-CT was done to rule out any occult infective focus which showed intense abnormal 18F-FDG uptake (five-point visual grading score: 3) in the region of LV apex where the autologous pericardial patch repair for LV aneurysm was performed earlier Figures -]. No other significant metabolically active disease was noted in the whole-body survey. The pericardial patch repair was done 9 years back; hence, the question of postsurgical inflammation/granuloma formation was not considered. The repeat blood culture revealed MRSA bacteremia; hence, cardiac patch repair infection was confirmed, and the patient was treated with appropriate broad-spectrum antibiotics which resolved his symptoms gradually. The follow-up blood culture showed no growth after the treatment. 18F-FDG PET-CT plays a vital role to create an evidence-based localization of the source of infection, to rule out other causes of fever and for accurate management of the patient.\nOUTPUT:"
},
{
"from": "agent",
"value": "Vascular graft infections"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 58-year-old man presented with complaints of breathlessness and high-grade fever of 15 days duration. There was no history of chest pain or dizziness. He was a known hypertensive for 20 years with a history of coronary artery disease for 17 years. He had a history of tuberculous lymphadenitis, diagnosed and treated 3 years back. He had undergone angioplasty to the left anterior descending artery and right coronary artery 11 years back, coronary artery bypass grafting for triple-vessel disease, and left ventricular (LV) aneurysm repair with native autologous pericardial patch 9 years back. For the past 2 years, he had recurrent episodes of fever secondary to methicillin-resistant Staphylococcus aureus (MRSA) bacteremia, for which he was treated with broad-spectrum antibiotics. He also had a history of one episode of cardioembolic ischemic stroke (right middle cerebral artery infarct) secondary to mobile LV thrombus and pulmonary embolism. Only contrast-enhanced CT chest and abdomen did not reveal any evidence of infection. Hence, 18F-FDG PET-CT was done to rule out any occult infective focus which showed intense abnormal 18F-FDG uptake (five-point visual grading score: 3) in the region of LV apex where the autologous pericardial patch repair for LV aneurysm was performed earlier Figures -]. No other significant metabolically active disease was noted in the whole-body survey. The pericardial patch repair was done 9 years back; hence, the question of postsurgical inflammation/granuloma formation was not considered. The repeat blood culture revealed MRSA bacteremia; hence, cardiac patch repair infection was confirmed, and the patient was treated with appropriate broad-spectrum antibiotics which resolved his symptoms gradually. The follow-up blood culture showed no growth after the treatment. 18F-FDG PET-CT plays a vital role to create an evidence-based localization of the source of infection, to rule out other causes of fever and for accurate management of the patient.
OUTPUT: |
PMCPatients_common1727 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: On her routine clinic visit in October 2020, the decision was made to start treatment with systemic isotretinoin (Roaccutane®) with a dose of 20 mg once daily for one month. A baseline platelet count was requested before starting the medication, the results of which are shown in Table .\\nAfter one month (November 2020), the patient returned to the clinic for her routine visit. A new complete blood count was requested to identify any hematological abnormalities induced by isotretinoin. A reticulocyte count and a peripheral blood smear were not done.\\nAccordingly, the medication was discontinued.\\nThe patient also reported other non-hematological side effects. She was not feverish during the physical examination, and we did not observe leukocytosis or any signs of infection. Also, she did not have any known drug allergies. A new complete blood count was requested. The results showed that the platelet count had returned to the normal range, as shown in Table . However, the seizure episodes continued to occur even after one month of isotretinoin discontinuation. The patient was referred to a neurologist to initiate anti-epileptic therapy.\nOUTPUT:"
},
{
"from": "agent",
"value": "Isotretinoin-Induced Thrombocytosis, Acne Vulgaris, Seizures"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: On her routine clinic visit in October 2020, the decision was made to start treatment with systemic isotretinoin (Roaccutane®) with a dose of 20 mg once daily for one month. A baseline platelet count was requested before starting the medication, the results of which are shown in Table .\nAfter one month (November 2020), the patient returned to the clinic for her routine visit. A new complete blood count was requested to identify any hematological abnormalities induced by isotretinoin. A reticulocyte count and a peripheral blood smear were not done.\nAccordingly, the medication was discontinued.\nThe patient also reported other non-hematological side effects. She was not feverish during the physical examination, and we did not observe leukocytosis or any signs of infection. Also, she did not have any known drug allergies. A new complete blood count was requested. The results showed that the platelet count had returned to the normal range, as shown in Table . However, the seizure episodes continued to occur even after one month of isotretinoin discontinuation. The patient was referred to a neurologist to initiate anti-epileptic therapy.
OUTPUT: |
PMCPatients_common2595 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 65-year-old male visited a community hospital complaining of urinary retardation, dysuria, and gross hematuria. The patient had history of hypertension, hyperuricemia, and hyperlipidemia. He had no family history of prostate cancer, and his prostate-specific antigen (PSA) value was 1.6 ng/mL (normal range: 0–4 ng/mL). A physical examination revealed low-grade fever. Administration of 4 mg of alpha blocker did not relieve his symptoms.\\nLaboratory evaluations were as follows: hemoglobin (Hb), 9.6 g/mL, hematocrit (Ht), 28.9%, leukocytes, 8200 cells/mL, glucose, 175 mg/dL, creatinine, 0.65 mg/dL, and C-reactive protein (CRP), 17.96 mg/dL. Urinalysis noted 30–40 WBCs/hpf and 5–9 RBCs/hpf. Urine cytology is Class IIIa.\\nAbdomen and pelvic computed tomography (CT) scan and magnetic resonance imaging (MRI) showed a lobular lesion with irregular edge and fluid collection in the left lobe of prostate ().\\nChest CT scan in the presence of a dye showed bilateral, bizarre pulmonary nodules with cavitation and an enhancing mass of about 6.5 cm at its largest diameter ().\\nThis patient was admitted to a hospital for intensive examination.\\nThus, a transurethral resection of the prostate (TURP) as part of tissue sampling and a bronchoscopic examination were performed. Histologic examination of the prostate revealed accumulation and cellular infiltration of neutrophils and lymphocytes as well as histiocytosis and necrotizing tissues. These findings were consistent with those of GPA (). Histologic examination of lung lesions also showed accumulation and cellular infiltration of neutrophils and lymphocytes as well as histiocytosis with fibrinoid necrosis ().\\nCerebral MRI showed that T2WI high-iso signal occupied the area from right lateral maxillary to ethmoid sinus involving a fluid collection.\\nAn immunologic investigation showed positive c-ANCA with high anti-PR3 activity (296 U/mL).\\nWe diagnosed GPA as the systemic disease considering these results, and the patient was treated in the department of respiratory medicine.\nOUTPUT:"
},
{
"from": "agent",
"value": "Granulomatosis with Polyangiitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 65-year-old male visited a community hospital complaining of urinary retardation, dysuria, and gross hematuria. The patient had history of hypertension, hyperuricemia, and hyperlipidemia. He had no family history of prostate cancer, and his prostate-specific antigen (PSA) value was 1.6 ng/mL (normal range: 0–4 ng/mL). A physical examination revealed low-grade fever. Administration of 4 mg of alpha blocker did not relieve his symptoms.\nLaboratory evaluations were as follows: hemoglobin (Hb), 9.6 g/mL, hematocrit (Ht), 28.9%, leukocytes, 8200 cells/mL, glucose, 175 mg/dL, creatinine, 0.65 mg/dL, and C-reactive protein (CRP), 17.96 mg/dL. Urinalysis noted 30–40 WBCs/hpf and 5–9 RBCs/hpf. Urine cytology is Class IIIa.\nAbdomen and pelvic computed tomography (CT) scan and magnetic resonance imaging (MRI) showed a lobular lesion with irregular edge and fluid collection in the left lobe of prostate ().\nChest CT scan in the presence of a dye showed bilateral, bizarre pulmonary nodules with cavitation and an enhancing mass of about 6.5 cm at its largest diameter ().\nThis patient was admitted to a hospital for intensive examination.\nThus, a transurethral resection of the prostate (TURP) as part of tissue sampling and a bronchoscopic examination were performed. Histologic examination of the prostate revealed accumulation and cellular infiltration of neutrophils and lymphocytes as well as histiocytosis and necrotizing tissues. These findings were consistent with those of GPA (). Histologic examination of lung lesions also showed accumulation and cellular infiltration of neutrophils and lymphocytes as well as histiocytosis with fibrinoid necrosis ().\nCerebral MRI showed that T2WI high-iso signal occupied the area from right lateral maxillary to ethmoid sinus involving a fluid collection.\nAn immunologic investigation showed positive c-ANCA with high anti-PR3 activity (296 U/mL).\nWe diagnosed GPA as the systemic disease considering these results, and the patient was treated in the department of respiratory medicine.
OUTPUT: |
PMCPatients_common4554 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 60-year-old male was diagnosed with lung adenocarcinoma (cT4N3M0, stage IIIB; fig. ). He was a current smoker with a smoking history of 30 pack-years and he had no allergies. Highly sensitive immunohistochemistry using 5A4 monoclonal antibody on a bronchoscopic biopsy specimen was positive for ALK protein []. A subsequent fluorescent in situ hybridization analysis using break-apart probes confirmed the ALK fusion gene. The patient was in a good general condition with an Eastern Cooperative Oncology Group performance status of 1. As first-line therapy, crizotinib was administered orally at a dose of 250 mg twice daily. On day 50, while he had achieved a partial response by hisResponse Evaluation Criteria In Solid Tumors score, a chest computed tomography (CT) revealed a contralateral pulmonary infiltrate in the left lung (fig. ). Pulmonary function test showed a restricted dysfunction pattern. Transbronchial lung biopsy revealed lymphocytic alveolitis and OP (fig. ). No pathogens were found in the bronchoalveolar lavage fluid. The patient was diagnosed with secondary OP induced by crizotinib. Oral corticosteroid therapy was started at 30 mg/ 60 kg body weight (0.5 mg/kg) prednisolone, and the dose was reduced every 2 weeks. He responded well to the corticosteroid therapy and the infiltrate gradually improved. One and a half months after stopping crizotinib and 1 month after starting corticosteroid therapy, we readministered crizotinib at a dose of 250 mg 3 times a week, and the patient showed no signs of interstitial lung disease (ILD) recurrence. His restrictive pulmonary dysfunction improved. The dose of crizotinib was increased to 250 mg once daily, then to 400 mg once daily. He maintained a partial response after crizotinib rechallenge with a gradual improvement of ILD for 4 months and no ILD recurrence thereafter (fig. ).\nOUTPUT:"
},
{
"from": "agent",
"value": "Anaplastic Lymphoma Kinase-Rearranged Non-Small Cell Lung Cancer, Organizing Pneumonia"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 60-year-old male was diagnosed with lung adenocarcinoma (cT4N3M0, stage IIIB; fig. ). He was a current smoker with a smoking history of 30 pack-years and he had no allergies. Highly sensitive immunohistochemistry using 5A4 monoclonal antibody on a bronchoscopic biopsy specimen was positive for ALK protein []. A subsequent fluorescent in situ hybridization analysis using break-apart probes confirmed the ALK fusion gene. The patient was in a good general condition with an Eastern Cooperative Oncology Group performance status of 1. As first-line therapy, crizotinib was administered orally at a dose of 250 mg twice daily. On day 50, while he had achieved a partial response by hisResponse Evaluation Criteria In Solid Tumors score, a chest computed tomography (CT) revealed a contralateral pulmonary infiltrate in the left lung (fig. ). Pulmonary function test showed a restricted dysfunction pattern. Transbronchial lung biopsy revealed lymphocytic alveolitis and OP (fig. ). No pathogens were found in the bronchoalveolar lavage fluid. The patient was diagnosed with secondary OP induced by crizotinib. Oral corticosteroid therapy was started at 30 mg/ 60 kg body weight (0.5 mg/kg) prednisolone, and the dose was reduced every 2 weeks. He responded well to the corticosteroid therapy and the infiltrate gradually improved. One and a half months after stopping crizotinib and 1 month after starting corticosteroid therapy, we readministered crizotinib at a dose of 250 mg 3 times a week, and the patient showed no signs of interstitial lung disease (ILD) recurrence. His restrictive pulmonary dysfunction improved. The dose of crizotinib was increased to 250 mg once daily, then to 400 mg once daily. He maintained a partial response after crizotinib rechallenge with a gradual improvement of ILD for 4 months and no ILD recurrence thereafter (fig. ).
OUTPUT: |
PMCPatients_common2294 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Retroauricular pain, hyperacusis, decreased production of tears, or altered taste was also denied. There was no history of previous cold exposure.\\nThe patient was afebrile and her vital signs were within the normal range, namely, her blood pressure which was 110/75 mmHg (below the 90th percentile for gender, age, and height). There were multiple crusted lesions scattered all over the body. She had no vesicular eruption over the external pinna, ear canal, or pharynx. Otoscopy revealed a gray and translucent tympanic membrane in the neutral position. There were no signs of otitis or mastoiditis or evidence of ear trauma. No evidence of dental abscess was found. The ophthalmological examination revealed symmetrical pupillary reflexes, normal eye movements, and preserved convergence. The neurological examination showed asymmetries in the ability to perform eyelid closure and asymmetries in labial movements, which were not evident at rest due to a normal facial symmetry. During follow-up, a complete recovery of the initial deficits and a restoration of normal functions were registered.\nOUTPUT:"
},
{
"from": "agent",
"value": "Acute Peripheral Facial Palsy, Chickenpox"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Retroauricular pain, hyperacusis, decreased production of tears, or altered taste was also denied. There was no history of previous cold exposure.\nThe patient was afebrile and her vital signs were within the normal range, namely, her blood pressure which was 110/75 mmHg (below the 90th percentile for gender, age, and height). There were multiple crusted lesions scattered all over the body. She had no vesicular eruption over the external pinna, ear canal, or pharynx. Otoscopy revealed a gray and translucent tympanic membrane in the neutral position. There were no signs of otitis or mastoiditis or evidence of ear trauma. No evidence of dental abscess was found. The ophthalmological examination revealed symmetrical pupillary reflexes, normal eye movements, and preserved convergence. The neurological examination showed asymmetries in the ability to perform eyelid closure and asymmetries in labial movements, which were not evident at rest due to a normal facial symmetry. During follow-up, a complete recovery of the initial deficits and a restoration of normal functions were registered.
OUTPUT: |
PMCPatients_common1729 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A medically free 30-year-old Saudi male was referred to our setup as a case of urethral stricture. Six months ago, he had gastric sleeve surgery. Since then, he started to have recurrent attacks of urinary retention, a weak urinary stream, and difficulty in urinating. He was not suffering from any suspicious symptoms, such as hematuria and recurrent urinary tract infections. On history acquisition, the patient was not a smoker, had no significant history of trauma, exposure to radiation and chemicals, sexually transmitted diseases, or tumors. He also had no family history of cancers.\\nHe had undergone multiple cystoscopies and urethral dilation procedures with the last one being an optical urethrotomy four months ago, but he kept re-stricturing and his symptoms persisted. His latest ascending urethrogram showed a short annular stricture segment measuring 2 cm at the bulbourethra with no filling defect (Figure ).\\nOn examination, he was active and alert with no distress. He had a body mass index (BMI) of 23.7 kg/m2. Both his cardiovascular and respiratory examinations were normal. The abdomen was soft, non-tender, and non-distended. His baseline examinations and laboratory tests were all unremarkable. The patient was booked for a urethroplasty. During the routine diagnostic cystoscopy, a papillary lesion in the stricture area was detected (Figure ).\\nAn open biopsy from both the spongiosa and the urethral mucosa was obtained by preforming an incision in the urethra and performing dissection. The procedure was aborted, and a cystodilation was done instead. Only benign sclerotic rims in the right iliac bone were found. An in situ hybridization (ISH) was done and showed no evidence for human papillomavirus (HPV) infection. The treatment plan was concluded to be radical cystoprostatectomy along with urethrectomy as it is currently the curative gold standard.\nOUTPUT:"
},
{
"from": "agent",
"value": "Primary Urothelial Carcinoma"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A medically free 30-year-old Saudi male was referred to our setup as a case of urethral stricture. Six months ago, he had gastric sleeve surgery. Since then, he started to have recurrent attacks of urinary retention, a weak urinary stream, and difficulty in urinating. He was not suffering from any suspicious symptoms, such as hematuria and recurrent urinary tract infections. On history acquisition, the patient was not a smoker, had no significant history of trauma, exposure to radiation and chemicals, sexually transmitted diseases, or tumors. He also had no family history of cancers.\nHe had undergone multiple cystoscopies and urethral dilation procedures with the last one being an optical urethrotomy four months ago, but he kept re-stricturing and his symptoms persisted. His latest ascending urethrogram showed a short annular stricture segment measuring 2 cm at the bulbourethra with no filling defect (Figure ).\nOn examination, he was active and alert with no distress. He had a body mass index (BMI) of 23.7 kg/m2. Both his cardiovascular and respiratory examinations were normal. The abdomen was soft, non-tender, and non-distended. His baseline examinations and laboratory tests were all unremarkable. The patient was booked for a urethroplasty. During the routine diagnostic cystoscopy, a papillary lesion in the stricture area was detected (Figure ).\nAn open biopsy from both the spongiosa and the urethral mucosa was obtained by preforming an incision in the urethra and performing dissection. The procedure was aborted, and a cystodilation was done instead. Only benign sclerotic rims in the right iliac bone were found. An in situ hybridization (ISH) was done and showed no evidence for human papillomavirus (HPV) infection. The treatment plan was concluded to be radical cystoprostatectomy along with urethrectomy as it is currently the curative gold standard.
OUTPUT: |
PMCPatients_common1584 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 60-year-old female with a 33-year history of type 1 diabetes mellitus and a 10-year history of renal replacement therapy underwent an SPK in 2015 (Fig. ). One and a half years after the transplantation, the patient presented with lower abdominal pain. Laboratory data revealed that the white blood cell count (4000/μl), serum CRP (< 0.02 mg/dl), and blood glucose (112 mg/dl) were normal. A CT revealed urinary retention (Fig. ). In addition to the treatment with antibiotics and protease inhibitor, a 20 Fr indwelling catheter was inserted to reduce the pressure inside of the bladder. The fistula did not close over 8 weeks of bladder catheter insertion. ). However, the fistula did not completely heal. Therefore, after obtaining informed consent from the patient, NBCA (Histoacryl®, Aesculap, Tuttlingen, Germany) diluted to 50% with iodized oil (Lipiodol, Guerbet, Tokyo, Japan) was percutaneously directly injected at the site of the leak under CT-guided fluoroscopy (Fig. ). The fistula was closed immediately after the injection, with no recurrences of leaks.\nOUTPUT:"
},
{
"from": "agent",
"value": "Pancreatic duodenal stump leak, Acute pancreatitis of the pancreas graft"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 60-year-old female with a 33-year history of type 1 diabetes mellitus and a 10-year history of renal replacement therapy underwent an SPK in 2015 (Fig. ). One and a half years after the transplantation, the patient presented with lower abdominal pain. Laboratory data revealed that the white blood cell count (4000/μl), serum CRP (< 0.02 mg/dl), and blood glucose (112 mg/dl) were normal. A CT revealed urinary retention (Fig. ). In addition to the treatment with antibiotics and protease inhibitor, a 20 Fr indwelling catheter was inserted to reduce the pressure inside of the bladder. The fistula did not close over 8 weeks of bladder catheter insertion. ). However, the fistula did not completely heal. Therefore, after obtaining informed consent from the patient, NBCA (Histoacryl®, Aesculap, Tuttlingen, Germany) diluted to 50% with iodized oil (Lipiodol, Guerbet, Tokyo, Japan) was percutaneously directly injected at the site of the leak under CT-guided fluoroscopy (Fig. ). The fistula was closed immediately after the injection, with no recurrences of leaks.
OUTPUT: |
PMCPatients_common2289 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The teeth present were:\\n16, 55, 54, 53, 52, 51, 61, 62, 63, 64, 65, 26\\n46, 85, 84, 83, 82, 81, 71, 72, 73, 74, 75, 36\\nAnterior and a unilateral right posterior crossbites were\\npresent. The radiographic view of the chest revealed aplasia\\nof clavicles and low placed scapulas with a funnel shaped\\nthorax (Fig. 9). The A-P view of skull concluded wide open\\nsutures and fontanelles along with multiple wormian bones\\n(Fig. 10). The hypoplastic appearance of maxilla was clearly\\nevidenced on the lateral cephalogram. The malrelationship\\nbetween maxilla and mandible could arise through\\ndiscrepancies in the effective horizontal lengths of both the\\narches or due to an abnormal contribution by the projected\\nlength of the cranial base element. The projected lengths\\nwere measured and mandibular length which exceeded the\\nstandard indicated mandibular prognathism. Vertical\\nparameters pointed the increased Y-axis along with an\\nelevated FMA (Fig. 12). These findings ascertained a relative\\nmandibular prognathism. The oral pentamogram findings\\nwere partial anodontia with the absence of 14, 15, and 25\\n(Fig. 11). This relative mandibular prognathism was\\nintercepted by occipital chin cup therapy (Fig. 13).The\\ndermatoglyphic findings were LWLLL (loop, whorl) and\\nLLLLL (loop) sequence patterns in left and right hands\\nrespectively. The total ridge count was 65 (Table 1 and\\nFig. 14).\nOUTPUT:"
},
{
"from": "agent",
"value": "Cleidocranial Dysplasia"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: The teeth present were:\n16, 55, 54, 53, 52, 51, 61, 62, 63, 64, 65, 26\n46, 85, 84, 83, 82, 81, 71, 72, 73, 74, 75, 36\nAnterior and a unilateral right posterior crossbites were\npresent. The radiographic view of the chest revealed aplasia\nof clavicles and low placed scapulas with a funnel shaped\nthorax (Fig. 9). The A-P view of skull concluded wide open\nsutures and fontanelles along with multiple wormian bones\n(Fig. 10). The hypoplastic appearance of maxilla was clearly\nevidenced on the lateral cephalogram. The malrelationship\nbetween maxilla and mandible could arise through\ndiscrepancies in the effective horizontal lengths of both the\narches or due to an abnormal contribution by the projected\nlength of the cranial base element. The projected lengths\nwere measured and mandibular length which exceeded the\nstandard indicated mandibular prognathism. Vertical\nparameters pointed the increased Y-axis along with an\nelevated FMA (Fig. 12). These findings ascertained a relative\nmandibular prognathism. The oral pentamogram findings\nwere partial anodontia with the absence of 14, 15, and 25\n(Fig. 11). This relative mandibular prognathism was\nintercepted by occipital chin cup therapy (Fig. 13).The\ndermatoglyphic findings were LWLLL (loop, whorl) and\nLLLLL (loop) sequence patterns in left and right hands\nrespectively. The total ridge count was 65 (Table 1 and\nFig. 14).
OUTPUT: |
PMCPatients_common3197 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: No significant change in skin color or temperature of both lower limbs was observed after onset. Routine urine analysis showed ERY +++, PRO ++, and LEU negative. Past history showed that 20 years before admission, the patient had an exploratory laparotomy for acute abdomen in a local hospital, but the cause was not determined. He had a smoking history for more than 30 years (approximately 20 cigarettes/day), no drinking, no history of blood transfusion, no history of venereal disease and no relevant family history. Physical examination showed that systemic skin color was dark, a 10 cm surgical scar 3 cm from left side of the umbilicus, a soft intestinal mass in the scar the size of a fist could be pushed into the abdomen. Diffuse erythema and scales in both lower extremities, which manifested as erythema with clear boundaries, different shapes and sizes, covered with multiple layers of silvery white scales, and Auspitz’s sign was positive.\nOUTPUT:"
},
{
"from": "agent",
"value": "Non-transfusion secondary hemochromatosis, Bone tumor, Left knee joint degenerative changes, Abdominal hernia, Psoriasis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: No significant change in skin color or temperature of both lower limbs was observed after onset. Routine urine analysis showed ERY +++, PRO ++, and LEU negative. Past history showed that 20 years before admission, the patient had an exploratory laparotomy for acute abdomen in a local hospital, but the cause was not determined. He had a smoking history for more than 30 years (approximately 20 cigarettes/day), no drinking, no history of blood transfusion, no history of venereal disease and no relevant family history. Physical examination showed that systemic skin color was dark, a 10 cm surgical scar 3 cm from left side of the umbilicus, a soft intestinal mass in the scar the size of a fist could be pushed into the abdomen. Diffuse erythema and scales in both lower extremities, which manifested as erythema with clear boundaries, different shapes and sizes, covered with multiple layers of silvery white scales, and Auspitz’s sign was positive.
OUTPUT: |
PMCPatients_common901 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She received a standard treatment also without effectiveness, showing persistent fluctuation. Her clinical severity scores were improved from 32.9 to 5 after 24 Histobulin injections. The laboratory test results and skin test results before and after treatment are shown in Figure . The MAST results showed that 7 allergens were positive (Dp 100<, Df 100<, shrimp 0.61, Cladosporum hertiarum 1.34, A fumigatus 2.65, A alternata 1.88, and mugwort 4.41) before treatment and 12 allergens were positive (Dp 100<, Df 100<, crab 0.41, shrimp 0., C herbarum 8.89, A fumigatus 5.10, Alternaria alternata 14.19, mugwort 1.13, P notatum 44.23, oxeye daisy 0.74, dandelion 0.57, and goldenrod 0.62) after treatment. In the skin test, 10 allergens (Dp 4+, Df 4+, grey Alder with silver birch 2+, mugwort 4+, short ragweed 2+, black willow pollen 2+, Japanese cedar 2+, milk mix 2+, almond 2+, and peanut 2+) showed a positive reaction before treatment and 7 allergens (C albicans 2+, Dp 4+, Df 4+, mugwort 4+, black willow pollen 3+, Japanese cedar 1+, and peanut 2+) after treatment. The patient frequently suffered from URI 12 times per year, but he did so only twice during and after treatment for a year.\nOUTPUT:"
},
{
"from": "agent",
"value": "Atopic dermatitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: She received a standard treatment also without effectiveness, showing persistent fluctuation. Her clinical severity scores were improved from 32.9 to 5 after 24 Histobulin injections. The laboratory test results and skin test results before and after treatment are shown in Figure . The MAST results showed that 7 allergens were positive (Dp 100<, Df 100<, shrimp 0.61, Cladosporum hertiarum 1.34, A fumigatus 2.65, A alternata 1.88, and mugwort 4.41) before treatment and 12 allergens were positive (Dp 100<, Df 100<, crab 0.41, shrimp 0., C herbarum 8.89, A fumigatus 5.10, Alternaria alternata 14.19, mugwort 1.13, P notatum 44.23, oxeye daisy 0.74, dandelion 0.57, and goldenrod 0.62) after treatment. In the skin test, 10 allergens (Dp 4+, Df 4+, grey Alder with silver birch 2+, mugwort 4+, short ragweed 2+, black willow pollen 2+, Japanese cedar 2+, milk mix 2+, almond 2+, and peanut 2+) showed a positive reaction before treatment and 7 allergens (C albicans 2+, Dp 4+, Df 4+, mugwort 4+, black willow pollen 3+, Japanese cedar 1+, and peanut 2+) after treatment. The patient frequently suffered from URI 12 times per year, but he did so only twice during and after treatment for a year.
OUTPUT: |
PMCPatients_common2851 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 70-year-old British Caucasian man with end stage renal failure (ESRF) secondary to IgA nephropathy received a deceased donor kidney transplant on the 14th January 2008. He had been diagnosed with ESRF 15 years previously, and was initially dialysing via peritoneal dialysis and later via haemodialysis. At the time of transplant, his only remaining vascular access was a long-term intravenous catheter. Many years previously he had undergone a total parathyroidectomy for tertiary hyperparathyroidism and therefore took regular calcium supplements and alfacalcidol at a dose of 0.25 μg/day. Both pre- and post-kidney transplant parathyroid hormone (PTH) and serum calcium levels were within normal ranges with a calcium-phosphate product of less than 4. Post-transplant recovery was complicated by delayed graft function requiring dialysis for 14 days, transplant wound dehiscence requiring V.A.C.® dressing, and bladder outflow obstruction requiring intermittent self-catheterization. Despite these complications, he continued to improve with a good urine output and a glomerular filtration rate of 38.9 ml/min and was discharged home.\\nDuring routine follow-up at the outpatient clinic, the patient's calcium supplements were modified. He was admitted four months later with a complaint of sudden onset of painless lesions bilaterally on the medial aspect of his thighs. They appeared within the 48 hours prior to admission and were not associated with a history of trauma. Serum levels of calcium, phosphate, PTH and calcium-phosphate product were found to be normal. Clinically, both lesions were well demarcated, gangrenous in appearance and foul smelling (Figure ). Peripheral pulses were intact. Swabs taken from this lesion grew Pseudomonas and coliforms sensitive to meropenem. Intravenous antibiotic was immediately introduced and all calcium supplements were stopped. Over a period of one month, the lesions had fully resolved.\nOUTPUT:"
},
{
"from": "agent",
"value": "Calciphylaxis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 70-year-old British Caucasian man with end stage renal failure (ESRF) secondary to IgA nephropathy received a deceased donor kidney transplant on the 14th January 2008. He had been diagnosed with ESRF 15 years previously, and was initially dialysing via peritoneal dialysis and later via haemodialysis. At the time of transplant, his only remaining vascular access was a long-term intravenous catheter. Many years previously he had undergone a total parathyroidectomy for tertiary hyperparathyroidism and therefore took regular calcium supplements and alfacalcidol at a dose of 0.25 μg/day. Both pre- and post-kidney transplant parathyroid hormone (PTH) and serum calcium levels were within normal ranges with a calcium-phosphate product of less than 4. Post-transplant recovery was complicated by delayed graft function requiring dialysis for 14 days, transplant wound dehiscence requiring V.A.C.® dressing, and bladder outflow obstruction requiring intermittent self-catheterization. Despite these complications, he continued to improve with a good urine output and a glomerular filtration rate of 38.9 ml/min and was discharged home.\nDuring routine follow-up at the outpatient clinic, the patient's calcium supplements were modified. He was admitted four months later with a complaint of sudden onset of painless lesions bilaterally on the medial aspect of his thighs. They appeared within the 48 hours prior to admission and were not associated with a history of trauma. Serum levels of calcium, phosphate, PTH and calcium-phosphate product were found to be normal. Clinically, both lesions were well demarcated, gangrenous in appearance and foul smelling (Figure ). Peripheral pulses were intact. Swabs taken from this lesion grew Pseudomonas and coliforms sensitive to meropenem. Intravenous antibiotic was immediately introduced and all calcium supplements were stopped. Over a period of one month, the lesions had fully resolved.
OUTPUT: |
PMCPatients_common2958 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 32-year-old male presented to another Institute with complaints of back pain and left lower limb weakness. The patient was well for a few months. After 10 months of surgery, the patient noticed that he had developed a foot drop and the weakness in his left lower limb had increased. This progressed to a feeling of stiffness and numbness in all his limbs. His symptoms gradually progressed over a period of 3 years, and he additionally developed difficulty in micturition and constipation. When he presented to us, he had spastic quadriparesis with difficulty in walking. The weakness was more pronounced in his left lower limb. He was able to walk with a stick with a limp. His grading was 3 when assessed by Goel's clinical grading scale. [] He had decreased sensations to fine touch in his left leg and to pain and temperature in his right upper limb by 50%. He was catheterized and used laxatives to pass stools. [] Atlantoaxial fixation was now done as per the techniques described in 1994 and 2004 [ and ]. [] Following the surgery, in the immediate postoperative phase, the patient improved significantly in all his complaints. The urinary catheter was removed 4 days after the surgery, and he regained normal urinary and bowel control. Furthermore, he observed improvement in his foot drop. At the follow-up of 10 months, apart from mild walking disability due to foot drop, there was no other neurological symptom. Magnetic resonance imaging repeated 3 months after surgery showed a reduction in the size of syrinx and evidences of fusion of the atlantoaxial joint [].\nOUTPUT:"
},
{
"from": "agent",
"value": "Tethered cord, Chiari formation, Syringomyelia, Basilar invagination with the assimilation of the atlas, Cervicodorsal syringomyelia, Atlantoaxial facets alignment (Goel Type C facetal instability)"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 32-year-old male presented to another Institute with complaints of back pain and left lower limb weakness. The patient was well for a few months. After 10 months of surgery, the patient noticed that he had developed a foot drop and the weakness in his left lower limb had increased. This progressed to a feeling of stiffness and numbness in all his limbs. His symptoms gradually progressed over a period of 3 years, and he additionally developed difficulty in micturition and constipation. When he presented to us, he had spastic quadriparesis with difficulty in walking. The weakness was more pronounced in his left lower limb. He was able to walk with a stick with a limp. His grading was 3 when assessed by Goel's clinical grading scale. [] He had decreased sensations to fine touch in his left leg and to pain and temperature in his right upper limb by 50%. He was catheterized and used laxatives to pass stools. [] Atlantoaxial fixation was now done as per the techniques described in 1994 and 2004 [ and ]. [] Following the surgery, in the immediate postoperative phase, the patient improved significantly in all his complaints. The urinary catheter was removed 4 days after the surgery, and he regained normal urinary and bowel control. Furthermore, he observed improvement in his foot drop. At the follow-up of 10 months, apart from mild walking disability due to foot drop, there was no other neurological symptom. Magnetic resonance imaging repeated 3 months after surgery showed a reduction in the size of syrinx and evidences of fusion of the atlantoaxial joint [].
OUTPUT: |
PMCPatients_common4264 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Visual acuity was 20/20 in the right eye and 20/300 pinhole 20/70 in the left eye. Pupils showed no relative afferent defect, and intraocular pressure was 14 mmHg in each eye. The right eye was normal. Examination of the left eye revealed moderate vitreous cellularity and a large endophytic vascular mass in the inferonasal quadrant, measuring 13 mm × 12 mm in base and 6.3 mm in thickness. There were surrounding subretinal fluid, exudation, and vitreous and subretinal debris [].\\nMinor intratumor hyperreflectivity on ultrasonography, concerning for calcium, was noted. Full physical examination, complete blood count, and blood and urine cultures were unremarkable. The tip of a microcatheter was placed at the orifice of the ophthalmic artery to infuse melphalan (5 mg) and topotecan (1 mg). [] The patient underwent three cycles of IAC, with an interval of 5 weeks between the first and second treatments and a 7-week interval between the second and third treatments, combined with administration of four intravitreal melphalan injections (20 μg/0.1 cc) to the left eye. Each intravitreal injection was given at regular 5-week intervals. Visual acuity improved to 20/30 in the left eye. There were no adverse events from therapy.\nOUTPUT:"
},
{
"from": "agent",
"value": "Retinoblastoma"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Visual acuity was 20/20 in the right eye and 20/300 pinhole 20/70 in the left eye. Pupils showed no relative afferent defect, and intraocular pressure was 14 mmHg in each eye. The right eye was normal. Examination of the left eye revealed moderate vitreous cellularity and a large endophytic vascular mass in the inferonasal quadrant, measuring 13 mm × 12 mm in base and 6.3 mm in thickness. There were surrounding subretinal fluid, exudation, and vitreous and subretinal debris [].\nMinor intratumor hyperreflectivity on ultrasonography, concerning for calcium, was noted. Full physical examination, complete blood count, and blood and urine cultures were unremarkable. The tip of a microcatheter was placed at the orifice of the ophthalmic artery to infuse melphalan (5 mg) and topotecan (1 mg). [] The patient underwent three cycles of IAC, with an interval of 5 weeks between the first and second treatments and a 7-week interval between the second and third treatments, combined with administration of four intravitreal melphalan injections (20 μg/0.1 cc) to the left eye. Each intravitreal injection was given at regular 5-week intervals. Visual acuity improved to 20/30 in the left eye. There were no adverse events from therapy.
OUTPUT: |
PMCPatients_common3845 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Although first-hand information was not available to us from the husband, we were told that the problem started after she was asked to resign her high profile job by her husband to look after his parents in India. She was eating very often in large quantities; she was obsessed with eating nonvegetarian food very frequently. She will plead for the food with her parents as if very hungry. She showed personality change in the sense that she was not wearing matching dresses any more, she was not cooking at all, she showed tendency to wander away whenever the family was less cautious. She was adamant in getting her demands completed and claimed she has divine powers. She was found to be praying often and was not showing interest in the activities of children. Her parents observed a very interesting behavior in their daughter. She was entertaining her visitors whoever it may be by non stop story telling. When one story is over, she will drift to the next. The stories were constructed in English with proper grammar. She could read, write in her mother tongue, and comprehend well and her HMSE score was full. However, she will always drift to storytelling with similar themes and minor change in characters. The heroine was always herself as a nurse with extraordinary talents and integrity. The stories always involved people of great social standing such as the King of Arabia, Ambassador from the USA, and high profile couple from Canada and Delhi, one story lead to the other nonstop even when interrupted and requested to stop. In a day-to-day basis, the members in the storytelling changed. However, all stories expressed grandiose ideas about herself how she had been more efficient than doctors in diagnosis and treatment and how she was offered gifts by her patients who could not forget her timely interventions which saved their lives, but she never accepted anything from them and offered their gifts to the free donation box []. Her children aged 9 years and 8 years are reported to be hostile and violent with mother and physically abusing her. Her magnetic resonance imaging showed diffuse atrophy with significant loss in frontal, temporal regions [].\nOUTPUT:"
},
{
"from": "agent",
"value": "Bipolar affective disorder"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Although first-hand information was not available to us from the husband, we were told that the problem started after she was asked to resign her high profile job by her husband to look after his parents in India. She was eating very often in large quantities; she was obsessed with eating nonvegetarian food very frequently. She will plead for the food with her parents as if very hungry. She showed personality change in the sense that she was not wearing matching dresses any more, she was not cooking at all, she showed tendency to wander away whenever the family was less cautious. She was adamant in getting her demands completed and claimed she has divine powers. She was found to be praying often and was not showing interest in the activities of children. Her parents observed a very interesting behavior in their daughter. She was entertaining her visitors whoever it may be by non stop story telling. When one story is over, she will drift to the next. The stories were constructed in English with proper grammar. She could read, write in her mother tongue, and comprehend well and her HMSE score was full. However, she will always drift to storytelling with similar themes and minor change in characters. The heroine was always herself as a nurse with extraordinary talents and integrity. The stories always involved people of great social standing such as the King of Arabia, Ambassador from the USA, and high profile couple from Canada and Delhi, one story lead to the other nonstop even when interrupted and requested to stop. In a day-to-day basis, the members in the storytelling changed. However, all stories expressed grandiose ideas about herself how she had been more efficient than doctors in diagnosis and treatment and how she was offered gifts by her patients who could not forget her timely interventions which saved their lives, but she never accepted anything from them and offered their gifts to the free donation box []. Her children aged 9 years and 8 years are reported to be hostile and violent with mother and physically abusing her. Her magnetic resonance imaging showed diffuse atrophy with significant loss in frontal, temporal regions [].
OUTPUT: |
PMCPatients_common3001 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: At the time of admission, his vital signs were normal and stable. The results of the complete blood count and serum biochemical test were as follows: white blood cells, 4,700/μL; hemoglobin, 9.9 g/dL; hematocrit, 31.0%; platelets, 118,000/μL; prothrombin time, 1.47 international normalized ratio; activated partial thromboplastin time, 40.7 sec; aspartate aminotransferase, 24 IU/L; alanine aminotransferase, 21 IU/L; albumin, 3.6 g/dL; and total bilirubin, 2.4 mg/dL. Endoscopic band ligation (6 Shooter Saeed Multi-Band Ligator; Cook Medical, Bloomington, IN, USA) was performed without sedation. During additional band ligation, the trigger cord malfunctioned and was inserted between the bands on a single varix (). The trigger cord was stuck between several bands, and the endoscope could not be retrieved. Forcibly moving the endoscope would have meant tearing the varix and potentially causing massive bleeding. Thus, we had to think of another way to solve the problem immediately. After cutting the trigger cord with scissors (it was connected to the ligator handle) (), we pushed the cord out of the endoscope inside the accessory channel using forceps. After selectively grasping the trigger cord between the bands (), we gradually advanced the endoscope and forceps to pull out the trigger cord between the bands (). After the trigger cord was removed from between the bands, the endoscope was released and retrieved. One month after the procedure, the patient did not experience any hemorrhagic events and received an additional EVL procedure.\nOUTPUT:"
},
{
"from": "agent",
"value": "Esophageal Variceal Hemorrhage, Liver Cirrhosis due to Chronic Hepatitis B"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: At the time of admission, his vital signs were normal and stable. The results of the complete blood count and serum biochemical test were as follows: white blood cells, 4,700/μL; hemoglobin, 9.9 g/dL; hematocrit, 31.0%; platelets, 118,000/μL; prothrombin time, 1.47 international normalized ratio; activated partial thromboplastin time, 40.7 sec; aspartate aminotransferase, 24 IU/L; alanine aminotransferase, 21 IU/L; albumin, 3.6 g/dL; and total bilirubin, 2.4 mg/dL. Endoscopic band ligation (6 Shooter Saeed Multi-Band Ligator; Cook Medical, Bloomington, IN, USA) was performed without sedation. During additional band ligation, the trigger cord malfunctioned and was inserted between the bands on a single varix (). The trigger cord was stuck between several bands, and the endoscope could not be retrieved. Forcibly moving the endoscope would have meant tearing the varix and potentially causing massive bleeding. Thus, we had to think of another way to solve the problem immediately. After cutting the trigger cord with scissors (it was connected to the ligator handle) (), we pushed the cord out of the endoscope inside the accessory channel using forceps. After selectively grasping the trigger cord between the bands (), we gradually advanced the endoscope and forceps to pull out the trigger cord between the bands (). After the trigger cord was removed from between the bands, the endoscope was released and retrieved. One month after the procedure, the patient did not experience any hemorrhagic events and received an additional EVL procedure.
OUTPUT: |
PMCPatients_common2186 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 49-year-old woman presented with a 6-week history of pruritic raised wheals on her shins and dorsum of both hands. The lesions appeared suddenly and lasted from between 8 and 12 h, with no association to the time of day. The size varied from between 3 and 15 mm in diameter. The patient was unaware of any triggering factors such as specific foods, cold or hot temperatures, water or emotional stress. However, the patient reported increased lethargy. ).\\nDue to the patient’s associated symptom of lethargy and in accordance with the British Society for Allergy and Clinical Immunology guidelines [], a complete blood count, erythrocyte sedimentation rate (ESR), liver function tests (LFTs) and thyroid function tests were measured to rule out the possibility of any systemic disease. Investigations revealed normal haemoglobin, white cell count, absence of eosonophillia, normal ESR and normal LFTs. However, the T4 and T3 was lower than the normal range (8.6 and 3.2 pmol/L, respectively [normal T4 values: 10–20pmol/L and normal T3 values: 3.5–7.8 pmol/L]) and the thyroid stimulating hormone (TSH) was raised (5.4 mU/L [normal range: 0.4–4 mU/L]). The patient was reviewed 4 weeks later. ).\nOUTPUT:"
},
{
"from": "agent",
"value": "Chronic urticaria, Hypothyroidism, AITD"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 49-year-old woman presented with a 6-week history of pruritic raised wheals on her shins and dorsum of both hands. The lesions appeared suddenly and lasted from between 8 and 12 h, with no association to the time of day. The size varied from between 3 and 15 mm in diameter. The patient was unaware of any triggering factors such as specific foods, cold or hot temperatures, water or emotional stress. However, the patient reported increased lethargy. ).\nDue to the patient’s associated symptom of lethargy and in accordance with the British Society for Allergy and Clinical Immunology guidelines [], a complete blood count, erythrocyte sedimentation rate (ESR), liver function tests (LFTs) and thyroid function tests were measured to rule out the possibility of any systemic disease. Investigations revealed normal haemoglobin, white cell count, absence of eosonophillia, normal ESR and normal LFTs. However, the T4 and T3 was lower than the normal range (8.6 and 3.2 pmol/L, respectively [normal T4 values: 10–20pmol/L and normal T3 values: 3.5–7.8 pmol/L]) and the thyroid stimulating hormone (TSH) was raised (5.4 mU/L [normal range: 0.4–4 mU/L]). The patient was reviewed 4 weeks later. ).
OUTPUT: |
PMCPatients_common1556 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Case 1. 40-year-old female, nurse, with systemic arterial hypertension of 3 years of diagnosis, smoking of 11 years of evolution, at a rate of 3 to 4 cigarettes per day. On 26 April 2020, she started with fever of 38.7 °C, dry cough, and scarce nasal drainage, 3 days later she presented medium effort dyspnea, myalgia, arthralgia, increased cough and headache. The patient developed exacerbation of symptoms and decreased oxygen saturation up to 84%, 7 days after the onset of the symptoms, accompanied by maculopapular rash on the upper and lower limbs, chest, face and neck, anosmia and dysgeusia. Twenty days after the beginning of symptoms, a chest X-ray was performed showing an increase in bronchial tram track, faint left basal opacity, without evidence of pneumonic data. The patient evolved to improvement and was reported asymptomatic 23 days after the onset of symptoms, so she was discharged and went back to work. On 7 September 2020, she presented a sudden general condition attack, sneezing, runny nose, myalgias, arthralgias, followed by fever, dry cough, headache, and dyspnea on medium exertion. On 18 September, a chest computerized tomography (CT) scan with lung window was performed, which reported increased diffuse opacity and central air cystic cavities, data of central-lobular emphysema of the right lung, with no data of alveolar involvement or tumors. On 10 October 2020, she was discharged.\nOUTPUT:"
},
{
"from": "agent",
"value": "SARS-CoV-2 Reinfection, Post-infectious bullae"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Case 1. 40-year-old female, nurse, with systemic arterial hypertension of 3 years of diagnosis, smoking of 11 years of evolution, at a rate of 3 to 4 cigarettes per day. On 26 April 2020, she started with fever of 38.7 °C, dry cough, and scarce nasal drainage, 3 days later she presented medium effort dyspnea, myalgia, arthralgia, increased cough and headache. The patient developed exacerbation of symptoms and decreased oxygen saturation up to 84%, 7 days after the onset of the symptoms, accompanied by maculopapular rash on the upper and lower limbs, chest, face and neck, anosmia and dysgeusia. Twenty days after the beginning of symptoms, a chest X-ray was performed showing an increase in bronchial tram track, faint left basal opacity, without evidence of pneumonic data. The patient evolved to improvement and was reported asymptomatic 23 days after the onset of symptoms, so she was discharged and went back to work. On 7 September 2020, she presented a sudden general condition attack, sneezing, runny nose, myalgias, arthralgias, followed by fever, dry cough, headache, and dyspnea on medium exertion. On 18 September, a chest computerized tomography (CT) scan with lung window was performed, which reported increased diffuse opacity and central air cystic cavities, data of central-lobular emphysema of the right lung, with no data of alveolar involvement or tumors. On 10 October 2020, she was discharged.
OUTPUT: |
PMCPatients_common4154 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 20-year-old female allegedly consumed some tablets with suicidal intention. She initially presented at primary health center with abdominal pain, vomiting, diarrhea, and shock. As the intoxicating agent was not clear, treatment was started for aluminum phosphide poisoning as it is quite prevalent in the area. Initial complete blood count and serum electrolytes were unremarkable. The patient's condition deteriorated and she was referred to our hospital on the 3rd day. At our hospital, she was further investigated; hemoglobin was 9.1 g/dl and total white blood cell count was 11,900/cumm. Liver function tests showed marked elevation in the liver enzymes (aspartate aminotransferase [AST] – 404 IU/L and alanine aminotransferase [ALT] – 1982 IU/L). Other investigations showed total bilirubin – 6.37 mg/dL, direct bilirubin – 4.60 nm/dL, indirect bilirubin – 1.77 mg/dL, total protein – 6.43 g/dL, serum albumin – 3.35 g/dL, alkaline phosphatase – 112 IU/L, and amylase – 465 U/L. Prothrombin time was 56 with international normalized ratio of 5.7. Silver nitrate test was negative for phosphide. Her detailed history was sought again, in which she revealed consumption of many ferrous sulfate tablets. Blood gas analysis showed severe metabolic acidosis. Chelation therapy with desferrioxamine was started, and supportive measures were continued. However, her clinical condition deteriorated further, and she died within 48 h of admission due to multiorgan failure.\\nAutopsy revealed enlarged liver. Histopathology showed periportal necrosis and bile cholestasis [Figure and ]. Other organs were unremarkable on routine hematoxylin and eosin stain.\nOUTPUT:"
},
{
"from": "agent",
"value": "Iron Toxicity"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 20-year-old female allegedly consumed some tablets with suicidal intention. She initially presented at primary health center with abdominal pain, vomiting, diarrhea, and shock. As the intoxicating agent was not clear, treatment was started for aluminum phosphide poisoning as it is quite prevalent in the area. Initial complete blood count and serum electrolytes were unremarkable. The patient's condition deteriorated and she was referred to our hospital on the 3rd day. At our hospital, she was further investigated; hemoglobin was 9.1 g/dl and total white blood cell count was 11,900/cumm. Liver function tests showed marked elevation in the liver enzymes (aspartate aminotransferase [AST] – 404 IU/L and alanine aminotransferase [ALT] – 1982 IU/L). Other investigations showed total bilirubin – 6.37 mg/dL, direct bilirubin – 4.60 nm/dL, indirect bilirubin – 1.77 mg/dL, total protein – 6.43 g/dL, serum albumin – 3.35 g/dL, alkaline phosphatase – 112 IU/L, and amylase – 465 U/L. Prothrombin time was 56 with international normalized ratio of 5.7. Silver nitrate test was negative for phosphide. Her detailed history was sought again, in which she revealed consumption of many ferrous sulfate tablets. Blood gas analysis showed severe metabolic acidosis. Chelation therapy with desferrioxamine was started, and supportive measures were continued. However, her clinical condition deteriorated further, and she died within 48 h of admission due to multiorgan failure.\nAutopsy revealed enlarged liver. Histopathology showed periportal necrosis and bile cholestasis [Figure and ]. Other organs were unremarkable on routine hematoxylin and eosin stain.
OUTPUT: |
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