Datasets:

hippocrates

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Multicare_common_train

like 0

[ { "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 colonoscopy sample was used to perform RAS BRAF analysis, adopting the Oncomine Solid Tumour panel on Next Generation Sequencing (NGS) Ion Torrent platform, with a limit of detection of 5%. In January 2017, the patient began chemotherapy with mFOLFOX-6 plus panitumumab. During these first 3 months, the patient reported G1 skin rash, G1 peripheral neuropathy, and G2 neutropenia as side-effects, according to CTCAE 4.0. This case was evaluated by a multidisciplinary team. Histopathological findings were compatible with metastasis from intestinal adenocarcinoma and the molecular assessment detected a BRAF V600E mutation that was probably the cause of resistance to panitumumab. After surgery, the patient restarted chemotherapy with mFOLFOX-6 plus panitumumab for another six cycles and then continued with 5-FU/FA (De Gramont schedule) plus panitumumab as maintenance until March 2018. Afterwards, for persistent conjunctivitis (Grade 2, CTCAE 4.0) and considering the disease control, confirmed by a quarterly CT-scan, the patient began a treatment holiday period. On June 2018, CT scan showed lung progression for evidence of two new lesions ( Figures 3A, B ). Therefore, the patient resumed 5-FU/FA + panitumumab until March 2019. During this period, disease stability and response on the new lung metastases were achieved ( Figures 3C, D ) and treatment was stopped temporarily for ocular toxicity (Grade 2, CTCAE 4.0) that was particularly bothersome for the patient. To date, with CT scan performed every two months, after 36 months since the last cycle and nearly 72 months since diagnosis, no evidence of disease progression has been observed and the patient's clinical condition was also preserved.\nOUTPUT:" }, { "from": "agent", "value": "Stage IV RAS BRAF wild-type, poorly differentiated transverse colon adenocarcinoma with subcutaneous, pleural, left axillary, and abdominal lymph-node involvement" } ]

[ { "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: Glasgow Coma Score (GCS) at the scene of accident directly after the trauma was reportedly seven with a normal pupillary response. Prior to transportation to the trauma center the patient was intubated and a cervical collar was applied. She was polytraumatized with multiple injuries; pneumothorax, pulmonary contusions, fractures of the upper and lower extremities. She underwent surgery for the injuries of the extremities. According to the the patient she started noticing hoarseness and difficulties swallowing about six weeks after the accident. At this point she was gradually recovering from sedation and assisted breathing. After hospitalization she was admitted to the rehabilitation-unit. Due to lack of progression and weakness in her left shoulder, despite training, she was referred to an MRI-scan of the neck and thoracal region. MRI was not conclusive in terms of soft tissue injury. Three years after the accident the patient still suffers from paresis of the left trapezius and sternocleidomastoid muscle and insignificant paresis of the throat muscles. She is partly disabled due to pain in the neck and the left shoulder where she has a scapular winging (Figure 3). Our patient has all the expected symptoms of the Collet- Sicard-syndrome except affection of the tongue muscles (CN XII). Thus one has a good basis for the diagnosis of the syndrome in this trauma patient.\nOUTPUT:" }, { "from": "agent", "value": "Occipital condyle fracture, lower cranial nerve palsy, Collet-Sicard-syndrome, brain edema, arachnoid cyst, axonal injury to the left accessory nerve" } ]

[ { "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 man, heavy smoker with no history of ischemic heart disease, developed ventricular fibrillation 30 minutes after the onset of severe retrosternal chest pain. Sinus rhythm was restored after 6 direct-current cardioversions combined with lidocaine infusion. After resuscitation, pulmonary edema developed; the patient had a systolic blood pressure of 60 mm Hg, a pulse rate of 120 beats/min, and frequent premature ventricular contractions. The cardiac index, measured with a thermodilution Swan-Ganz catheter, was 1 liter/min/m2. An intra-aortic counterpulsation balloon (IACPB) was inserted through the right femoral artery and blood pressure increased to 110/70 mm Hg and the cardiac index to 1.9 liters/min/m2. Mechanical assistance was combined with intravenous treatment of glucose-potassium-insulin solutions, oral isosorbide-dinitrate, digoxin, and diuretic agents. Cardiac catheterization and angiography, performed 15 days after admission, revealed a left ventricular end-diastolic pressure of 35 mm Hg, a large aneurysm of the anterior and apical regions, and a normal contraction of the inferior wall. Coronary arteriography demonstrated complete obstruction of the LMCA (Figure 1(a)) while the right coronary artery was normal. There was no collateral filling of the left coronary system. The left ventricular ejection fraction was 16% with mechanical assistance and 5% without assistance. After 26 days, the patient developed a shaking chill and the IACPB was removed. The patient was discharged after 40 days. On discharge, the cardiac index was 1.8 liters/min/m2. Radionuclide angiography showed a left ventricular ejection fraction of 10%. A year later he was in functional class III.\nOUTPUT:" }, { "from": "agent", "value": "Acute Left Main Coronary Artery Occlusion, Acute extensive anterior myocardial infarction, Congestive heart failure" } ]

[ { "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 76-year-old woman with no significant medical history presented with a left upper abdominal mass at a routine medical checkup. Upper gastrointestinal endoscopy demonstrated extrinsic compression in the middle of the gastric body. Computed tomography and magnetic resonance imaging indicated a huge lesion in the spleen (Figure 1). There was no abnormal increase in glucose metabolism in parts other than the spleen according to whole-body 18F-fluorodeoxyglucose positron emission tomography (Figure 2). No other abnormality was revealed on clinical examination; thus, the lesion was thought to be a primary splenic tumor, such as an angiosarcoma. She underwent excision of the spleen for treatment and diagnosis. The tumor was a white-gray, well-defined mass containing necrotic areas and measured approximately 130 x 120 x 90 mm with an expansive growth pattern (Figure 3). It showed infiltration into the surrounding lymph nodes, left lung, diaphragm, and stomach. Histopathological examination of the resected tissue specimens showed pleomorphic and hyperchromatic nuclei, prominent nucleoli, and frequent mitotic activity. The neoplastic cells exhibited a papillary pattern with psammoma bodies. The representative features are shown in Figure 4. On immunohistochemical analysis, the tumor cells were positive for cytokeratin (CK) 7 (Figure 5(a)), PAX-8 (Figure 5(c)), WT-1 (Figure 5(d)), p16, p53 (Figure 5(e)), and Ber-EP4 (Figure 5(f)) but negative for CK20 (Figure 5(b)), thyroid transcription factor-1, carcinoembryonic antigen, CD10, estrogen receptor, calretinin, D2-40, intelectin-1, and sialylated HEG1.\nOUTPUT:" }, { "from": "agent", "value": "Serous carcinoma" } ]

[ { "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 15 years old male presented with the compliant of progressive abdominal swelling since 10 years which had further progressed within the preceding 12 months.\" Furthermore he experienced early satiety, unable to run, difficulty walking, shortness of breath in lying position, and significant subjective weight loss in 3 months duration. He was a grade VII student but discontinued school due to walking difficulty for the last 3 months. Two years prior to the current presentation he was admitted for with chylous ascites diagnosed by abdominal ultrasound at our hospital; however, a CT or MRI was not done at this time and a planned treatment with octreotide could not be performed as the patient left the hospital prior to that. On physical examination he was looking chronically sick, the vital signs were within normal limits. The abdomen was significantly distended ( Fig. 1 ) with dullness on percussion over the whole abdomen with a positive fluid thrill. The right scrotum was empty. The complete blood cell count, renal and liver function tests, and serum albumin and stool examination were normal. 2 ). On exploratory laparotomy through a midline abdominal incision a huge retroperitoneal cyst from duodenum to sacrum was found. The cyst was completely excised and right orchiectomy was done for intra-abdominal testis to prevent testicular germ cell malignancy. Gram stain, culture, and gene expert of the cystic fluid was negative with 7/mm 3 white blood cells. A postoperative abdominal ultrasound postoperative day 7 showed a mild left sided hydronephrosis. The patient recovered uneventfully and was discharged 1 day later. Histology of the resected testis showed an atrophic testis without sign of malignant transformation. Follow-up on 20th post surgery was unremarkable.\nOUTPUT:" }, { "from": "agent", "value": "Giant Mesenteric Cyst, Right Sided Syndrome" } ]

[ { "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 man, who suffered from cerebral palsy due to measles encephalopathy at the age of 6 months, became unable to eat and underwent gastroscopy. No other polypoid lesions were detected. The level of serum gastrin was very high (4100 pg/mL (normal range: <200 pg/mL)) and the antiparietal cell antibody test was positive. No gastrin-producing tumor was detected by radiologic examination. Due to the persistent symptom, they accepted only a reduced surgery, and partial resection of the stomach was performed and metastatic lymph nodes were dissected. The tumor was 2 cm in diameter (Figure 1(b)) with involvement of the muscularis propria (Figure 2(a)). These uniform cells (Figure 2(b)) were strongly positive for chromogranin A and synaptophysin (Figures 2(c) and 2(d)). High lymphatic permeation was observed. Seven months later, follow-up gastroscopy revealed another polypoid lesion in the residual stomach (Figure 3(a)). Total gastrectomy was performed (Figure 3(b)), and microscopic evaluation showed numerous endocrine cell micronests (ECMs; size: 0.1~1.75 mm), which were diffusely observed in the stomach (Figure 3(c)). Regional lymph node metastasis was observed again. Mucosal atrophy was evident in the fundus but not in the antrum. The level of serum gastrin became within normal range.\nOUTPUT:" }, { "from": "agent", "value": "Gastric carcinoid, Hypergastrinemia" } ]

[ { "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 gentleman with end stage renal disease, coronary artery disease, type 2 diabetes, and hypertension was admitted to the hospital for dyspnea due to mild volume overload. On physical exam, he was noted to have a 3 x 3 cm soft tissue mass on the right forehead with superficial ulceration (Figure 1). His medication list did not contain any anti-platelet agents or anticoagulation. The patient described a hematoma since a mechanical fall while walking on the street 6 weeks prior with impact to his forehead. He had developed swelling immediately after the fall but did not lose consciousness. He presented to the emergency department (ED) at that time where CT head was performed showing a 3 cm prominent right prefrontal soft tissue hematoma. A needle aspiration was performed with reportedly over half of the fluid in the hematoma drained. He was discharged from the ED. Given increased swelling and pain at the site of the hematoma, he returned to the ED 1 week later where the soft tissue swelling was noted to be 4 cm. Given persistent pain, a repeat needle aspiration was performed and 7 ml of blood was removed. Incision and drainage was also performed with clotted blood removed and he was discharged. Fluid specimens were not sent for laboratory analysis at either visit. Since the second visit to the ED, the patient reported that the \"hematoma\" had recurred status-post aspiration and drainage but was smaller than it was initially and remained painful. Plastic surgery was consulted who noted palpable thrill at lateral aspect of the mass. CTA was performed which revealed a 7 mm round pool of contrast at the lesion, supplied by an artery with a questionable draining vein, consistent with an AVM or less likely pseudoaneurysm (Figure 3). Given ongoing pain at the site of the soft tissue mass, the patient was planned for outpatient resection of the vascularized soft tissue mass with interventional radiology support.\nOUTPUT:" }, { "from": "agent", "value": "Arteriovenous Malformation" } ]

[ { "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 45-year-old ethnic Kashmiri woman presented in August 2004 with a few-weeks history of pain and discomfort in her lower limbs. For the past one week, she had low back pain radiating to left lower limb and weakness of the left foot. She also complained of distal paresthesias and pin prick-like feeling over her trunk. She had no bladder and bowel symptoms. She had history of chronic sinusitis and difficult-to-treat asthma with frequent exacerbations for the past several years. On examination, she had mild pallor and bilateral wheeze on chest auscultation. Her neurological examination revealed hypoesthesia along the right ulnar distribution and weak interossei of the right hand. Calf muscles of the left limb were wasted with weak dorsiflexion and planter flexion of the foot and diminished knee and ankle jerks on the same side. The rest of the systemic examination was unremarkable. Electrodiagnostic studies revealed severe left peroneal, tibial, and mild right ulnar neuropathies. These findings favoured the diagnosis of mononeuritis multiplex. She had hemoglobin level of 10.8 gm/dL, total leucocyte count (TLC) of 25000/mm3, differential count which revealed 20% eosinophils, and erythrocytic sedimentation rate (ESR) of 10 mm at first hour. Serum concentration of glucose, urea, creatinine, aminotransferases, thyrotropin, and electrolytes were within normal limits. Chest X-ray, electrocardiogram, and MRI of the lumbosacral spine were unremarkable. MRI of the head and CT scan of paranasal sinuses revealed pansinusitis with exuberant mucosal thickening and polyp formation (Figure 1). Perinuclear antineutrophil cytoplasmic antibody (p-ANCA) test was reactive at 34.2 U/mL (reference range < 7.0 U/mL) while tests for rheumatoid factor and antinuclear antibody (ANA) were negative. We administered oral prednisolone for six weeks at a dose of 50 mg/day. She showed a remarkable recovery with minor sensory symptoms persisting. She was seen recently doing well on 5 mg alternate day prednisolone and azathioprine 100 mg daily.\nOUTPUT:" }, { "from": "agent", "value": "Churg-Strauss syndrome" } ]

[ { "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 man presented to the emergency room following a road traffic accident. Computed tomography scan of the brain (plain) revealed frontal hematoma, intraventricular hemorrhage, and subarachnoid hemorrhage with depressed skull fracture. Emergency craniotomy with decompression was performed. On the 4th day of hospitalization, he developed increasing proptosis and conjunctival congestion [Figure 1a]. Magnetic resonance (MR) imaging showed hyperintense signals in the basal cisterns suggestive of subarachnoid hemorrhage on T1-weighted sequence. However, the precise location of the rent was not identified [Figure 1b and c]. There was severe vasospasm seen in all the cerebral vessels. Endovascular treatment was planned in order to occlude the aneurysm and the fistulous communication. Balloon occlusion test was not tolerated and hence we chose to occlude the aneurysm and the fistulous communication (preserving the parent artery) over parent vessel occlusion. Under general anesthesia, 6 French guiding catheter was placed in the left internal carotid artery. Echelon micro catheter with traxcess microwire was inserted into the aneurysm. A gentle steam shaping of the micro catheter tip was done to facilitate the navigation of the distal end of the micro catheter into the sinus [Figure 2c]. Selective micro-catheter angiogram showed high flow through the aneurysm into the cavernous sinus and inferior petrosal sinus. After achieving stable position of the micro-catheter distally, multiple platinum detachable coils were placed occluding the flow into the sinus. Thereafter, the aneurysm was completely packed with multiple coils and complete occlusion was achieved with no flow into the fistulous communication. Post-coiling angiogram showed complete obliteration of the fistula and exclusion of the aneurysm from the circulation [Figure 3a-c]. Patient's proptosis and congestion dramatically decreased over the next few days. Long-term follow-up to assess the coil compaction and recanalization is waiting to be done.\nOUTPUT:" }, { "from": "agent", "value": "Traumatic intradural aneurysm, Carotid cavernous fistula" } ]

[ { "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 primigravida was referred to our unit at 27 weeks' gestation for a neck mass and polyhydramnios. Amniocentesis performed then showed a normal male karyotype. At our unit, we found a clear, nonseptated 4 cm mass in the anterior neck with hydramnios (Figure 1), the amniotic fluid index being 29 cm. The stomach also appeared small. No other fetal anomalies were present. She delivered at term via elective Caesarean section. The second case was also referred to our centre at 26 weeks' gestation when a neck mass was detected incidentally on ultrasound. Her antenatal course had been hitherto uneventful. Our scan found a 5 cm multiloculated anterior neck mass between the lower jaw and upper chest. There were well-defined borders and no increased vascularity (Figure 2). An epignathus was excluded as the tumour was not arising from the mouth. The amniotic fluid index was normal at 14 cm. The patient delivered via elective Caesarean section at term. This patient was admitted with symptoms of preterm labour at 29 weeks'. A scan performed showed all the features of fetal hydrops, namely, ascites, pleural, and pericardial effusions. A large, highly vascular anterolateral neck mass with variable echogenicity and mainly solid areas was also discovered. The amniotic fluid index was 17 cm. The patient delivered a macerated stillborn male baby at 30 weeks' gestation. A postmortem examination was declined.\nOUTPUT:" }, { "from": "agent", "value": "Branchial cyst, Cervical teratoma, Haemangioma" } ]

[ { "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 Caucasian female was transferred from an outside hospital for progressively worsening heart failure (New York Health Association Class IV) and evaluation of cardiac replacement therapy and ventricular assistive device. Her past medical history was significant for SLE diagnosed 50 years prior to our initial encounter. For flares, she reported taking low-dose oral prednisone as needed. Her initial admission vitals were stable. Physical exam showed a cachectic appearing elderly female with ulnar drift across her metacarpal joints which were completely reducible. The exam also revealed lower extremity bunions bilaterally with cock-up deformities. No joint effusions were noted. She had 2+ pedal edema bilaterally and hyper- and hypopigmentation on her lower extremities. Her initial labs were significant for pancytopenia which from outside records seemed chronic. A complete metabolic panel was significant for an elevated creatinine of 1.9 mg/dL but otherwise, normal electrolytes. Transthoracic echocardiogram reported dilated left ventricle with a globally depressed ejection fraction of 15%, grade III diastolic dysfunction, severe mitral regurgitation, severe tricuspid regurgitation, and elevated right ventricular systolic pressure (RVSP). Previous but recent cardiac catheterization findings were consistent with a nonischemic cause for her cardiomyopathy. Right heart catheterization was performed to evaluate for pulmonary artery hypertension and showed a pulmonary artery wedge pressure of 47 mmHg. An endomyocardial biopsy was performed to evaluate the cause of her cardiomyopathy and showed mild ventricular myocyte hypertrophy and focal mild interstitial fibrosis. Myeloid bodies and curvilinear bodies were present on ultrastructural examination (Figure 2). The patient was deemed a poor candidate for a ventricular assistive device due to poor nutritional status and thrombocytopenia. She was discharged home on milrinone infusion and life-vest but passed away shortly after discharge.\nOUTPUT:" }, { "from": "agent", "value": "Hydroxychloroquine toxicity, Fabry Disease" } ]

[ { "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 diagnosed in June 2011 at 6 years of age when he presented with partial seizures. He underwent an unrelated donor umbilical cord blood transplant (minor B->O incompatibility) and maintained stable donor chimerism. Post-operative recovery was uneventful and he led a relatively normal seizure free life. He presented on August 2012 with blood-stained urine and chest pain. Physical examination revealed a 46 kg male with pallor, yellow sclera and cushingoid facies. He was confined to the wheelchair and demonstrated hypotonia. The child showed limited interaction with his environment. Pre-operative medications included levitiracetam, fludrocortisone and famotidine. His pre-operative investigations showed a haemoglobin concentration of 3 g/dL, which eventually improved to 6.9 g/dL after several cycles of plasmapheresis and blood transfusion, and a raised total bilirubin of 97 mumol/L. Standard monitoring was attached, and intravenous hydrocortisone 100 mg was administered. The patient was tilted 30 degrees head-up, pre-oxygenated and cricoid pressure was applied. However, ventilation could not be achieved, and decision was made to release cricoid pressure. Anaesthesia was induced with a target propofol concentration of 4 mug/mL and remifentanil infusion rate of 4 ng/mL. Muscle relaxation was provided with rocuronium 0.7 mg/kg. The trachea was intubated orally with a size 6 cuffed tracheal tube. Maintenance of anaesthesia was achieved with a target propofol concentration of 2.5 mug/mL and remifentanil infusion rate of 3 ng/mL. Post-operative analgesia was obtained with 10 mL of lignocaine 1% infiltrated over the surgical site. Following the procedure that lasted 105 minutes, residual neuromuscular blockade was reversed with neostigmine 2.5 mg and glycopyrrolate 0.4 mg. Neuromuscular function was assessed with electromyography. After the patient demonstrated airway protective reflexes, spontaneous eye opening and a regular respiratory pattern, the trachea was extubated. Recovery was uneventful, and he was subsequently discharged to the general ward.\nOUTPUT:" }, { "from": "agent", "value": "X-linked cerebral ALD, Severe autoimmune haemolytic anaemia, Liver dysfunction" } ]

[ { "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 31-year-old male developed weakness of both lower limbs and severe low back pain after lifting a gas cylinder. Four days later he was admitted to Adan Hospital. X-ray of the lumbosacral spine revealed simple fracture at L1 and L2 vertebrae and magnetic resonance imaging of the lumbar spine confirmed the fracture. Within the next few days the weakness gradually progressed to 3/5 power in the upper limbs and 0/5 in the lower limbs bilaterally and bilateral lower motor neuron facial palsy. Deep tendon reflexes were absent in all four limbs and the plantar response was mute. He was assessed by a neurologist and was transferred to the ICU as he developed respiratory distress and bulbar weakness. NCS showed prolonged distal latencies with conduction block, prolonged F waves, reduced M-wave amplitudes, reduced nerve conduction velocities and absent H reflexes. Blink reflex was abnormal with prolonged latencies and reduced amplitudes. Routine blood counts and blood biochemistry were normal. Connective tissue disease and porphyria screening were negative. Serological tests for M. pneumonia, Epstein-Barr virus and hepatitis virus were negative. Cerebrospinal fluid study was not done because the patient refused it as he had back pain. The clinical and electrophysiological features were consistent with GBS. He was treated with a course of IVIG (0.4 g/kg/day for 5 days). While in the ICU he developed aspiration pneumonia and septicaemia which was treated by meropenem and ciprofloxacin. Follow-up electrophysiological studies showed progression of neuropathy with features of mixed axonal and demyelinating neuropathy. As he did not respond to the initial course of IVIG, he was treated with six sessions of plasmapheresis. However, he continued to be febrile in spite of treatment with appropriate antibiotics. He developed cardiovascular instability and renal impairment. Twenty-five days later the patient expired after developing cardiac arrest and resuscitative measures failed. The probable cause of death was septicaemic shock with multi-organ failure secondary to septicaemia.\nOUTPUT:" }, { "from": "agent", "value": "Guillain-Barré syndrome" } ]

[ { "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: This patient underwent 24 exercise sessions in a 22-24 C temperature-controlled gym (conventional exercises) between May and July 2007. After the exercise training program, this patient was invited to continue in our rehabilitation program but opted out. After 6 months, the patient returned to our program to continue the exercise program, and we assigned him to hydrotherapy. Between January and March 2008, he had 24 more exercise sessions in a 30-31 C temperature-controlled swimming pool (hydrotherapy). The exercise training protocol was almost the same for both methods: 5 minutes of warm up exercises (stretching), 30 minutes of aerobic exercise training (90% of ventilatory threshold), 25 minutes of strength exercises (lower and upper limbs) and 5 minutes of cool down exercises (stretching). The medications were not changed during the protocols (150 mg/day Carvedilol, 100 mg/day Losartan, 40 mg/day Furosemide, 25 mg/day Spironolactone and 0.25 mg/day Digoxin). This protocol was approved by the ethical committee of our institution (number 1107/05).\nOUTPUT:" }, { "from": "agent", "value": "Heart failure" } ]

[ { "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: There were 92 health workers participated in this study, 30 responded to the paper questionnaires and 62 responded to electronic questionnaires, for a response rate of 100%. Most were female and 30 to 34 years old. 57.5% were doctors, followed by nurses and nurse aids. The majorities were staff, working in hospitals and interacting with patients. Two third worked in geriatrics, followed by psychiatry palliative care, and general practice. Others worked in various fields of healthcare system for example; home care, maternal and child health, occupational health and safety, school health, emergency and trauma, dental care, health promotion, laboratory, administrative, disability care, end-stage renal disease care, and surgery. Half of them knew how to report when the incident occurred (Table 1). Most of the reported participants were female and doctors, except for racial harassment, the victim was a male support staff (Table 2). The IOC from the 4 experts ranged from 0.75 to 1 for each item. However, the racial and sexual harassment were not reported due to small numbers of responses (Table 3).\nOUTPUT:" }, { "from": "agent", "value": "Workplace violence" } ]

[ { "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 had never travelled to Taiwan or other countries. On examination, chest auscultation revealed discrete inspiratory crackles over the lower lung fields. The leukocyte count was 1.2 G/l, with a neutrophil ratio of 72.5%. The C-reactive protein count was 163 mg/l. Within the first 24 hours, hypoxemia worsened (PaO2/FiO2<100 mm Hg), profound septic shock developed, and the leukocyte count dropped to 0.82 G/l. The HIV test was negative. The patient was treated with teicoplanin (400 mg twice daily for 3 days, followed by 400 mg once daily for 6 days), and then was switched to linezolid (600 mg twice daily). Teicoplanin and linezolid treatment lasted 29 and 15 days, respectively. The patient was successfully weaned after 49 days of mechanical ventilation and was transferred to the medical ward after 76 days in the intensive care unit. He was discharged from the hospital after five months.\nOUTPUT:" }, { "from": "agent", "value": "Community-associated methicillin-resistant Staphylococcus aureus ST59, Human sepsis, Severe pneumonia, Influenza B" } ]

[ { "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 64-year-old male with relapsed diffuse large B-cell lymphoma received anti-CD19 CAR-T cell therapy in 12/2020. His initial treatment course was complicated by severe CRS resulting in spinal cord edema and chronic urinary retention. After 3 months of physical recovery, the patient was found to have rising serum creatinine peaking to 1.4 mg/dL in 3/2022, thrombocytopenia to a nadir of 10,000/muL, and progressive anemia requiring weekly transfusion. A bone marrow biopsy showed a consumptive process without morphologic dysplasia. Treatment of immune thrombocytopenic purpura with intravenous immune globulin (IVIG), steroid, and thrombopoietin receptor agonist romiplostim did not resolve his thrombocytopenia. Serum lactate dehydrogenase (LDH)was found to be > 400 units/L, haptoglobin < 30 mg/dL, and schistocytes demonstrated on peripheral blood smear (> 4/HPF). The nephrology service was consulted for MAHA and kidney injury. Urinalysis demonstrated 1+ protein, with no bacteria or casts present. An initial workup for immune-mediated TTP consisted of a negative ADAMST13 antibody screen. Direct antiglobulin (Coombs) test was negative thereby excluding autoimmune hemolytic anemia. Coagulation assays were found to be normal. Folate, B12, and methylmalonic acid levels were all within normal ranges. Autoimmune testing panels (ANA, ANCA) were unremarkable. Complement C3/C4/CH50 were similarly within normal limits. A send out Genetic and Complement Renal Panel to the University of Iowa, which tests for 13 genes implicated in hereditary disorders associated with atypical HUS and TMA, returned negative. All viral studies were negative. Patient remained normotensive. A diagnostic kidney biopsy was deferred given the patient's marked thrombocytopenia and risk for bleeding. Fortunately, the patient improved over the next year with eventual recovery to baseline creatinine levels and transfusion independent platelet counts by 11/2021.\nOUTPUT:" }, { "from": "agent", "value": "Thrombotic microangiopathy" } ]

[ { "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: Because of obstructive symptoms, it was decided to proceed with a resection up-front without neo-adjuvant treatment. Subsequently, the patient developed an anastomotic leak, which required a diverting loop ileostomy. Following recovery, the patient was treated with adjuvant chemo-radiation therapy, after which, the diverting ileostomy was reversed. A year after the initial diagnosis, the patient was found to have extensive left-sided liver metastases which were treated with chemotherapy, and left-sided liver tri-segmentectomy. As a consequence of all these surgeries, the patient developed a large incisional hernia extending from the site of the Kocher incision to the site of prior ileostomy. The hernia was repaired laparoscopically with a prosthetic mesh. Three years following the initial diagnosis, the patient was referred to our center with an anastomotic recurrence. This recurrence presented as a retroperitoneal perforation forming a recto-cutaneous fistula through the sacrum with extensive adjacent soft tissue infection and necrosis (Fig. 1). The patient's quality of life was poor. The diagnosis and treatment options were reviewed in a multidisciplinary setting and with the patient. Both operative and non-operative options were discussed. An APR with total sacrectomy was offered. With respect to the proposed surgery, the patient was made aware of inevitable loss of bowel, bladder and sexual functions. Other risks discussed included significant blood loss, permanent lower extremity neurological injury, lower body mobility impairment, cerebrospinal fluid leak, persistent infection, hardware failure, structural non-union, tumor recurrence, and death. The surgical team involved colorectal, spinal, and plastic surgery consultants. APR with complete sacrectomy was performed using an anterior-posterior approach with posterior spinal instrumented fusion and pelvic fixation using iliac crest bone graft. Left-sided vertical rectus abdominis and right-sided gracilis muscle flaps were used for closure of the perineal and pelvic defects.\nOUTPUT:" }, { "from": "agent", "value": "Recurrent rectal cancer" } ]

[ { "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: In contrast, changes in body fat between groups were not too dissimilar between finishers. Therefore, the discrepancies in weight lost throughout the South Pole race between groups are likely associated with the differences in fat-free mass (FFM). Sea-level studies indicate that acute caloric restriction (less than 3 weeks) activates AMP-activated protein kinase (AMPKalpha), an inhibitor of the rapamycin pathway. As a consequence of low energy intake, protein availably too is limited. This suggests the importance for ingesting higher amounts of protein during intensive prolonged events. Nevertheless, the dietary protein requirements for men undertaking competitive endurance exercise of this nature are still unclear. Nutritional intakes of 24 adventure racing athletes were profiled. Protein intakes were high for both male and female athletes, respectively (1.9 +- 0.5 g.kg in men and 2.0 +- 0.4 g.kg in women). A previous research concluded that protein requirement in very active individuals may be as high as 160% of the RDA. Whatever the case, protein intake relative to body weight within the current case study was 2.0 +- 0.6 g.kg for faster finisher and 1.1 +- 0.5 g.kg for slower finishers. Despite any significant value, there was a clear positive relationship reported between changes in lean mass and race completion times within the current study. In the absence of sufficient carbohydrate availability during a prolonged endurance race, energy transfer is compromised. In addition, there is an increased risk of becoming hypoglycaemic. To maintain homeostatic functioning regarding the management of blood glucose levels, the body will rely on the process of gluconeogenesis, an alternative means for making new glucose molecules from a non-carbohydrate source.\nOUTPUT:" }, { "from": "agent", "value": "Muscle degradation, Hypoglycaemia" } ]

[ { "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 45-year-old woman, living in Northeastern Pennsylvania, presented to the emergency department with a sudden episode of typical left-sided chest pain radiating to her neck. The pain was described as a pressure sensation being 9/10 in intensity and accompanied by diaphoresis. Two days before, the patient had an intermittent headache attributed to sinus infection for which she took amoxicillin. She did not recall a tick bite or a skin rash. She was not a smoker. Upon admission, the patient was given nitroglycerin with relief of her chest pain. Initial EKG showed normal sinus rhythm with 1 mm concave ST-elevation involving lead II and lead aVF and a 1 mm ST-depression in lead V1 with associated T-wave inversion (Figure 1). A second EKG performed one hour later, did not show any further ST-T changes. She did not have any evidence of cardiac dysrhythmias during her stay in the emergency room. Initial Troponin I (normal <0.4 ng/mL) and CK-MB (normal <7.7 ng/mL) were elevated at 7.82 ng/mL and 55.2 ng/mL, respectively. Six hours later, Troponin I increased to 13.44 ng/mL and CK-MB to 75.7 ng/mL. Echocardiogram did not reveal any pericardial effusion and showed a left ventricular ejection fraction of 55%. Two days later, the patient developed right-sided facial palsy. Treatment with intravenous ceftriaxone and oral steroids was started. Eventually resolution of symptoms and, normalization of cardiac markers and EKG changes, were achieved (Figure 2).\nOUTPUT:" }, { "from": "agent", "value": "Lyme disease" } ]

[ { "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 African American male presents with a chief complaint of right mandibular pain, edema, and intraoral bleeding at night. This condition has persisted for 12 months with a gradual increase in size and pain. This patient has medical history significant for ESRD, for which he undergoes dialysis three times per week for the past 10 years, congestive heart failure, anemia, diabetes mellitus, and atrial fibrillation. He has been prescribed oral calcium and vitamin D supplements which he has not been compliant with. Extraoral examination reveals facial asymmetry with right facial enlargement (Figure 1) which is soft to palpation and mildly tender, no trigeminal nerve paresthesia was noted. Intraoral examination shows a large soft tissue mass measuring 8 cm x 2 cm x 4 cm extending from right mandibular second premolar to 2 cm past right mandibular third molar (Figure 2). There was no buccal or lingual expansion of bone noted clinically. The first molar was mobile and the second and third molars were free floating lingually in the soft tissue mass. Bleeding and pain were noted upon palpation of mass and associated teeth. Panoramic radiograph shows a well-defined multilocular radiolucent lesion in the right mandibular body. This lesion extends from one centimeter posterior to the third molar to the second premolar in a horizontal dimension and from the inferior border of the mandible to the alveolar ridge in a vertical dimension. The mandibular second and third molars are displaced and the inferior alveolar nerve canal is obliterated (Figure 3). H&E stain showed numerous multinucleated giant cells in a hypercellular fibrous background with hemosiderin pigmentation.\nOUTPUT:" }, { "from": "agent", "value": "Brown tumor of hyperparathyroidism" } ]

[ { "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: Thirty-eight studies were identified, including 22 RCTs, one non-RCT, and 15 case series. All the studies were published in Chinese. The details of the characteristics of included trials RCTs and non-RCTs are presented in Table 3. The participants were children and adults, ranging from 4 months to 58 years old. The total sample size of the included clinical studies was 2,015. These included interventions comprising 15 classic Chinese herbal formulas, three self-made prescriptions, and one Chinese patent medicine (Lianhua Qingwen Capsules). Among these, modified Yinqiao powder was applied most frequently (7/15), followed by Xijiao Dihaung decoction (5/15). Shengma Gegen decoction, Baihu decoction, and modified Wuwei Jiedu decoction appeared three times. Modified Qingjie Toubiao decoction, Sanren decoction, and modified Liuyi powder appeared two times. The specific composition of the prescription is shown in Supplementary Table S1. The control group was generally treated with Western medicine. Eighteen RCTs reported the course of Chinese herbal formulas ranging from 3 to 10 days. The main outcome measures included the total effective rate, fever clearance time, time of rash disappearance, rash scab time, and index tested by laboratory serological diagnosis. Twelve clinical studies reported adverse events that occurred, including nausea, vomiting, and bad appetite. Six studies reported that no adverse events occurred, while the others did not report on this aspect.\nOUTPUT:" }, { "from": "agent", "value": "Varicella" } ]

[ { "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 34-year-old woman (gravida 1, para 1) was admitted to our hospital in the 16th week of gestation because of sudden left hemiparesis. CT and MRI revealed an intracerebral hemorrhage in the right frontal lobe. Cerebral angiography showed a right frontal AVM of Spetzler and Martin grade 1 on the same day (Fig. 3A, B). The mother wished to continue the pregnancy and consented to the AVM resection. The surgery was performed in the 18th week of gestation. General anesthesia was induced with rocuronium 50 mg i.v., thiopental 250 mg i.v., fentanyl 0.2 mg i.v., and maintained with remifentanyl 0.20-0.25 mug/kg/min, and 1.0-1.5% sevoflurane in oxygen. During the procedure, FHR was directly monitored using ultrasonography, with a transesophageal echo probe attached to the mother's lower abdomen (Fig. 2B, C). The patient's SBP was maintained between 90 to 100 mmHg during surgery, and the lowest SBP was 84 mmHg during the resection of the nidus. Her oxygenation level was good and no fetal bradycardia occurred during surgery. The FHR remained between 150 and 160 bpm throughout the perioperative period. The surgery was completed without any problems. The amount of blood loss was only 200 ml. The mother complained of no new abnormal neurological symptom. The remaining course of the pregnancy was favorable, and a cesarean section was performed in the 40th week of pregnancy because of macrosomia and a history of cesarean section.\nOUTPUT:" }, { "from": "agent", "value": "Cerebral arteriovenous malformation" } ]

[ { "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 XKUB demonstrated the presence of two urinary calculi, one 8 mm right renal pelvis stone, and one 10 mm stone in the right distal ureter. IVU revealed hydronephrosis of the right kidney and a dilated ureter up to the ureteric stone. The ureter distal of the stone was not opacified on any of the films. After a failed attempt by a colleague to insert a ureteric stent to de-block the right kidney, the patient was referred to our endourology service. The colleague had failed to find the right ureteric orifice. At no point did the patient mention that he underwent bladder surgery as a child for a large bladder diverticulum on the right and had a Cohen ureteric reimplantation on that side. A percutaneous nephrolithotomy (PCNL) and a combined retrograde-anterograde flexible ureteroscopic approach (URS) were planned. Again, an initial attempt to localize the right ureteric orifice on cystoscopy failed. A PCNL was performed and the kidney stone removed. A guidewire was passed anterogradely down the right ureter alongside the stone into the bladder. At that point, it became clear that immediately distal of the stone the right ureter angulated 90 degrees to the left within the posterior wall of the bladder and exited in the left bladder half. The stone was firmly lodged within that bend. The stone could be visualized endoscopically anterogradely and retrogradely, but due to inflammation, bleeding and lack of vision, a safe laser lithotripsy could not be attempted in that session. Finally, a thin anterograde double-J stent was inserted. Only now, questioned again about this most unusual anatomy, the patient remembered his childhood operation. He was scheduled for another retrograde transurethral URS, and this time the operation was successful due to an easy and marked access by the double-J stent. Four weeks later, the patient underwent hyperparathyroidectomy. So far, he is doing well without stone recurrence or complications.\nOUTPUT:" }, { "from": "agent", "value": "Ureterolithiasis, Primary hyperparathyroidism" } ]

[ { "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 epidemic curve shows a gradual increase in the number of cases with symptom onset from 6 May, reaching a peak of 763 cases in EW 29 (15-21 July), then decreasing gradually (Figure 1). The median reporting delay was 1 day (range 0-155 days), considering the difference between the notification and rash onset dates; therefore, the decrease in the number of notifications from the EW 30 onwards does not seem to be explained by the reporting delay. All five districts presented confirmed cases, which indicates the circulation of the virus throughout the municipality (Figure 2). Of 7,602 notified cases, the majority (55.5%) were male; among women, 86 of 3,385 (2.5%) were pregnant. The age group with the highest number of cases (26.6%) was the 20-29-year-olds, followed by those aged 15-19 years (23.3%). Together, these two age groups comprised ca 50% of all notifications (Table 1). Up to week EW 22, most cases were in the age group of 6 months-4 years, from the EW 23 onwards, however, an increase of cases aged 15-29 years was observed (Figure 3A). In addition, the majority of unvaccinated cases were in the age group of 15-29 years (Figure 3B). Of the 7,602 suspected cases, 823 (11.6%) were hospitalised, and the average of the hospitalisation period was 4 days (Table 1).\nOUTPUT:" }, { "from": "agent", "value": "Measles" } ]

[ { "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 37-year-old male patient, with frequent IV drug use, was presented to our institution with fever, chills, left-sided pleuritic chest pain and mild dyspnea. On clinical examination, he was using accessory breathing muscles and a 4/6 systolic murmur was noted in the left parasternal region that increased with inspiration. Basic laboratory studies along with blood cultures were obtained. Laboratory values were remarkable for leukocytosis of 37.000 cells/mul, with a left shift. A Computer topography (CT) of the chest exhibited multiple peripherally based nodules on both lungs, some with cavitation suggestive of septic emboli [Figure 1a]. He was started on empiric antibiotic therapy and a transesophageal echocardiography (TEE) was performed, revealing a 1 x 0.9 cm mobile vegetation in the TV [Figure 1b]. Blood cultures grew two out of two positives for methicillin-sensitive Staphylococcus aureus and the patients'antimicrobial regimen was converted to oxacillin. Despite being on the appropriate antimicrobial therapy for more than 3 days, the patient had persistent fever and leukocytosis. Given that his clinical status was worsening, surgery was indicated to decrease the bacterial burden on the TV vegetation. Traditionally, the next step would have been a TV repair/replacement through a minimally invasive approach through the thoracic cavity. However, given that the patient's clinical status was not optimal for such an invasive procedure, we opted for a less invasive approach: percutaneous mechanical vegetation debulking with an AngioVac system. The patient tolerated the procedure well and he remained hemodynamically stable at all times. He completed a 4-week course of IV oxacillin after the vegetation was removed. Subsequent to the procedure, the patient no longer had episodes of fever and his leukocytosis trended down to normal levels. He was discharged in stable conditions.\nOUTPUT:" }, { "from": "agent", "value": "Infective endocarditis" } ]

[ { "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 45 year-old female, presented with difficulty in walking and speech impairment for 2 years and both these symptoms exacerbated over last 2-3 months. The patient had two episodes of syncope, with clumsiness of movements and was not able to stand without support. Initially, the patient spoke in syllables and later her speech became incomprehensible to attendants. She had no history of weakness, difficulty in swallowing, headaches and blurring of vision or bladder and bowel involvement. On examination she was conscious and oriented to time, place and person. Her vitals were stable. She had pallor but her respiratory, cardiovascular and abdominal examinations were within normal limits. On neurological examination, higher mental functions were intact. Cranial nerve examinations revealed no abnormality. Sensations pertaining to lateral columns and dorsal columns were intact throughout, with no dissociation. Motor testing showed normal muscle tone and power with preserved deep tendon reflexes and bilateral plantar flexor response. Her biochemical investigations profile is summarized in Table 1. Brain and spine MRI were normal. Cerebrospinal fluid examination was normal and nerve conduction studies were also normal. Upper GI endoscopy revealed scalloping of mucosal folds in second part of duodenum (Figure 1). The patient was thereafter put on gluten-free diet along with iron supplementation. Follow-up examinations showed drastic improvement over 2-3 months. Her hemoglobin level rose to 9.2 gm%. Clinically, her speech improved and, to some extent, even her gait showed signs of improvement as she could walk few steps with support.\nOUTPUT:" }, { "from": "agent", "value": "Coeliac disease, Cerebellar ataxia" } ]

[ { "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 12-year-old girl was admitted to the emergency room after having suffered from a fall. She fell from a height of approximately 12 m on her left leg then hit her hip on the ground vertically. So an ethical statement is not required. She had severe thigh and left leg pain. She did not have any neurological deficits or incontinence and her abdominal examination revealed normal findings. Her thigh and left leg pain were increased with movement. The patient was placed on the operating table in the prone position under general anesthesia after the preoperative procedures had been completed. A midline skin incision was performed in the lumbosacral region. The paravertebral muscles between L4 and S3 were stripped subperiosteally. An S1 and S2 total laminectomy was performed and cord nerve decompression was provided. Transpedicular screws were placed at the L5, S1, and S2 vertebrae bilaterally. The pedicle screws were connected with a rod system (Titani-Istanbul). Bilateral iliac wing screws were placed and both iliac wings were attached to the system through a connector (Figure 3). No postoperative problems were observed. She did not have any complaints on the control examination 3 months later and she was able to do her daily activities. An ethical statement is not required.\nOUTPUT:" }, { "from": "agent", "value": "Malgaigne Fracture, zone 3 sacral fracture, subtype 2 fracture, S1-S2 listhesis, right sacroiliac joint dislocation, talus fracture" } ]

[ { "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 50-year-old Filipino man was admitted for allogeneic SCT to treat idiopathic myelofibrosis in which medical management had failed. His history was notable for 2 pruritic plaques on the left arm and right cheek that had been present for 6 months. He underwent induction chemotherapy with fludarabine phosphate and busulfan, followed by a matched sibling donor allogeneic SCT. On day 5 after transplant, he developed neutropenia and fever. On day 6, the dermatology service was consulted to evaluate a new skin lesion on the patient's left forearm. Examination revealed a small, ill-defined, indurated, erythematous plaque on the left forearm (Figure 1A) and an annular erythematous plaque with central clearing and fine scale measuring several centimeters on the left bicep. A biopsy specimen from the left forearm showed a sparse, superficial and deep, perivascular and periadnexal infiltrate for which a specific diagnosis could not be rendered (Figure 1B). Results of tissue cultures for bacteria, fungus, and mycobacteria were negative. The patient was discharged and presented to the outpatient clinic 4 months later with marked induration of the previously noted areas plus new erythematous to violaceous papules and plaques on the right deltoid, cheek, and tragus (Figure 2A and 2B). Examination of a second biopsy specimen revealed clusters of epithelioid and foamy macrophages (Figure 2C) shown by Fite stain to contain many acid-fast bacilli. Acidfast bacilli were seen on a biopsy touch preparation but were not recovered in the tissue culture. A retrospective Fite stain performed on the initial skin biopsy specimen taken 6 days after transplant demonstrated acid-fast bacilli in the perivascular and perineural dermis in a microscopic pattern consistent with an occult undefined leprosy (Figure 1C).\nOUTPUT:" }, { "from": "agent", "value": "Multibacillary leprosy undergoing type 1 reaction, Chronic graft-vs-host disease, Non-mycobacterial pneumonia and sepsis" } ]

[ { "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 underwent a radical left orchiectomy and the pathology of removed testis reported consistently with sex cord stromal tumor in favor of Leydig cell tumor and in immunohistochemically (IHC) evaluation, calretinin was positive and CD99, WT1 and Melan A were weakly positive. The patient has no history of hospitalization in infancy. He states that he was taller than his peers at the age of 7, but he has not increased in height compared to his peers since he was 10 years old. He did not mention the history of allergies to drugs and food and any sort of drug consumption. The parents were not related and his brother died at a young age (possibly a stroke). On examination of the patient, hair growth was sufficient and had a masculine pattern. He did not have gynecomastia on chest examination. The patient did not have a history of hypertension and on examination, the patient's blood pressure was normal. The patient is 154 cm tall and weighs 60 kg. The patient's BMI was measured at 25.2kg/m2. Patient was then diagnosed with TART and was treated with corticosteroids for one year, which reduced the number of right testicular masses. The patient is still in the follow-up period.\nOUTPUT:" }, { "from": "agent", "value": "Congenital adrenal hyperplasia, Bilateral testicular tumor" } ]

[ { "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 second gravida mother was referred to us at 29+5 weeks of gestation for prenatal ultrasonography (USG) findings of polyhydramnios associated with a heterogeneous left renal mass measuring 3.5 x 5.5 x 4.7 cms with solid and cystic components. She had had a previous LSCS at 28 weeks for pre-eclampsia with placenta abruption. During the current pregnancy, she had malaria in the first trimester and varicella in the second trimester. Scans during early pregnancy did not reveal any anomaly. Hence, emergency LSCS was done at 34 weeks and a 3420 G girl baby was born. The newborn required resuscitation for poor APGAR scores which was followed by mechanical ventilation. There was no haematuria or hypertension. Postnatal USG confirmed the large left renal mass crossing the midline associated with ascites. Ascitic tap revealed transudative fluid. Laboratory investigations showed anaemia, leucocytosis and thromcytopenia. Peripheral smear showed the presence of some nucleated red blood cells. She required platelet transfusion for progressive decrease in platelet counts. Following this, left nephroureterectomy was done on day 4 of life (Fig. 1). The opposite kidney was normal. The child was kept on ventilator in the neonatal intensive care unit. Postoperatively, the condition of the baby deteriorated despite all possible measures and she died on the second postoperative day. Histopathology (HPE) (Fig.\nOUTPUT:" }, { "from": "agent", "value": "Wilms' tumour" } ]

[ { "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 43-year-old woman without relevant medical history acutely developed nausea, severe chest pain, and dyspnoea during strenuous mountain-hiking. At a local emergency department, she was immediately intubated and initiated on intravenous nitrates because of severe arterial hypertension. At request of the family, she was transferred to our hospital. On arrival, ECG revealed an ectopic atrial rhythm, poor R-wave progression, and a prolonged corrected QT-interval. Chest X-ray showed pulmonary oedema. The troponin level was 2.42 mug/L (normally <0.005), and NT-proBNP was 39,061 ng/L (normally <125). Echocardiography documented severely impaired left ventricular (LV) function (ejection fraction (EF) 35%) with basal and midsegmental akinesis and preserved contractility of the apex. Coronary angiography ruled out significant coronary disease. Because of refractory high blood pressure, a diagnostic work-up was performed. Contrast-enhanced total body CT scan identified a left adrenal heterogeneous mass measuring 59 x 56 mm (Figure 2). 24-hour fractionated urinary metanephrine and normetanephrine levels were 7483 and 8895 mug, respectively (normally <240 and <600). Adequate alpha-adrenergic and beta-blockade was ensured, and laparoscopic adrenalectomy was performed. Pathological examination revealed nests of polygonal cells with eosinophilic cytoplasm. After surgery, the patient's hemodynamic condition rapidly stabilized. The LV systolic function, evaluated by repeated bedside \"quick look\" cardiac ultrasound, gradually improved during the following weeks. She made a further uneventful recovery and was discharged from the hospital 50 days after admission. Follow-up echocardiography at the cardiology clinic 10 weeks later showed complete normalization of LV function.\nOUTPUT:" }, { "from": "agent", "value": "Acute Heart Failure, Pheochromocytoma, \"Inverted\" Takotsubo Syndrome" } ]

[ { "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 was managed with mesalazine and prednisolone. Her disease was nonremitting. A Doppler ultrasound showed total occlusion of the left carotid artery and a 2-D transesophageal echo showed a normal heart with no intramural thrombus. She was not on thromboprophylaxis. She was started on low-molecular-weight heparin but continued to have hematochezia and a drop in her hemoglobin, so it was decided that an inferior vena cava filter should be inserted. Histopathology was compatible with UC with no dysplasia or cytomegalovirus. Her investigations showed the following: Hb 3.8 g/dL, mean corpuscular volume 61.5, mean corpuscular hemoglobin 17.6, platelets 432,000/mm3, ESR 75, and albumin 27 g/L. Her liver function tests and renal profile were normal. All studies for thrombophilia were negative, including protein S, protein C, antithrombin III, and factor V Leiden. Lupus anticoagulant was negative and JAK2 mutation was ordered. She was started on prednisolone and azathioprine and was titrated up to 100 mg once daily in addition to aspirin 100 mg once daily. She went into remission after that and steroids were discontinued. She was maintained on mesalazine 1 g twice daily and azathioprine 100 mg orally once daily.\nOUTPUT:" }, { "from": "agent", "value": "Ulcerative Pancolitis, Left Cerebrovascular Accident, Right Popliteal Deep Venous Thrombosis, Pulmonary Embolism" } ]

[ { "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 28-year-old male with no known medical illness presented with a history of pain, redness and decreased vision in the right eye for the last 4 months. On examination, his visual acuity was no perception of light with intraocular pressure of 58 mmHg while he was on oral acetazolamide and topical beta blocker/alpha-2 agonist combination in the right eye. 1)). Fundus was not visible. The left eye showed a visual acuity of 20/20 with -0.75 DS correction, an intraocular pressure of 14 mmHg, a normal anterior chamber and normal disc and macula. 2)). After systemic clinical evaluation and ruling out systemic involvement, the enucleation of the right eye was performed. The microscopic examination of the section showed choroid tissue infiltration by a tumour arranged in sheets and fascicles with elongated spindle-shaped vesicular nuclei with prominent nucleoli and abundant melanin pigment (Figure 3 (Fig. 3)). The tumour cells were positive for HMB45, S100 and Melan A. The patient is under regular follow-up in outpatient care and has not shown any evidence of local or systemic relapse 1 year after the diagnosis and treatment.\nOUTPUT:" }, { "from": "agent", "value": "Large choroidal melanoma, Neovascular glaucoma" } ]

[ { "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 83-year-old woman presented to another hospital complaining of sudden headache, dizziness, and nausea. Magnetic resonance imaging (MRI) performed at this hospital 13 days after the onset of symptoms was interpreted as a normal finding. The patient was transferred to our unit. On admission, 15 days after the symptom onset, neurological examination was normal, with the exception of mild confused mentality. We reviewed outside first MRI, which revealed the presence of a thin blood collection along the dural lining of the posterior dorsum sellae, clivus, and occipital bone down to the whole border of the foramen magnum. This blood accumulation extended to the cervical spine level with cerebrospinal fluid intensity inside the subarachnoid space [Figure 1]. We also performed computed tomography (CT)-angiography 15 days after the symptom onset. The medial lobe of the aneurysm was attached to the right dorsum sellae [Figure 2]. Angiographic examination performed 16 days after ictus also showed the aneurysm, which had two lobes with a maximal diameter of 10 mm. Twenty-one days after ictus, the patient underwent stent-assisted coil embolization (using a 4.5 mm x 28 mm Enterprise stent; Cordis Endovascular, Miami Lakes, FL, USA). The aneurysm was embolized successfully [Figure 3]. The postoperative course was uneventful and the patient was discharged with antiplatelet drug (aspirin) from our unit without any neurological deficit 3 weeks after admission. In 3 months after discharge, she demonstrated neither neurological deficit nor headache.\nOUTPUT:" }, { "from": "agent", "value": "Subdural hematoma of the posterior fossa, Posterior communicating artery aneurysm" } ]

[ { "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 77-year-old male, a retired soldier, presented with pain in his lower back, radiating down his right leg in the distribution of L4 dermatome and his left leg in L4, 5 dermatome. He had a 3-year history of symptoms, which became aggravated during the previous three months. He rated his leg pain as 9/10 and his back pain as 4/10. The pain disturbed his sleep, and his Oswestry Disability Index was 52%. Motor strength testing showed 4/5 in both quadriceps and tibialis anterior muscles, suggesting pain-induced reduction of strength. He had a tingling sensation and numbness in his lateral calf and experienced leg pain after walking more than 10 m, making him unable to go to the bathroom in his house. He had been treated with Opalmon 15 mg/day, Lyrica 150 mg/day, Ultracet and a fentanyl patch (25 microg/hour), and had received 17 epidural steroid injections of transforaminal epidural blockers and decompressive neuroplasty. Despite these injections and a further increase in analgesic dosage, he reported no improvements in pain and functional status. We elected to perform a transforaminal balloon decompression procedure. There were no complications throughout the procedure. Over the next 24 weeks, the patient reported moderately reduced leg pain (3-4/10), improved functional status (38-40%) and increased claudication distance (70 m).\nOUTPUT:" }, { "from": "agent", "value": "Spinal stenosis, Degenerative spondylolisthesis of L4 on L5, Stenosis of both lateral recesses and both neural foramens, Retrolisthesis of L5 on S1 with disc bulging and facet arthrosis causing left neural foraminal stenosis" } ]

[ { "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: In August 2012, after self-detection of a left breast lump, a 32 year-old woman underwent fine biopsy of the breast nodule, which was positive for invasive ductal carcinoma. Due to the young age and the presence of a positive FH, BRCA genetic testing was performed with detection of the c.8878C>T germline pathogenic BRCA2 mutation. In October 2012 the patient underwent both left and prophylactic right mastectomy. The left breast pathology report revealed the presence of a pT1cN1M0, stage IIB, G2, BC (ER: 100%, PR: 40%, HER2 negative, ki67: 25%). From December 2012 to March 2013, the patient received adjuvant chemotherapy with FEC for 3 cycles followed by docetaxel for 3 cycles. Then, she started adjuvant endocrine therapy with LHRH analog in combination with tamoxifen. In June 2016, a blood exam showed an increase of CA 15-3 along with CT scan documenting suspicious chest-wall lymph-nodes, liver, and bone lesions. FNB and cytology of lymph-nodes confirmed the presence of BC cells (ER: 100%, PR: 35%, HER2-negative). In July 2016, the patient started first line chemotherapy with capecitabine, with good PR. However, in April 2017, the CT scan showed disease progression in lung, liver, and thoracic lymph-nodes. The patient started second-line chemotherapy with eribulin, which was interrupted after 3 cycles due to pulmonary and liver progression. From August 2017 to February 2018 the patient received 9 cycles of Carboplatin (best response: PR). The treatment was then interrupted for further disease progression (neoplastic lymphangitis with dyspnea). In April 2018, the patient began a new treatment with palbociclib plus letrozole and LHRH analog. After 5 months of treatment, she reported resolution of dyspnea with PS improvement, and a significant response was observed by CT scan [best response by RECIST critera: PR; Figures 1C,D]. At the last visit (April 2019), the patient is currently on treatment with no evidence of disease progression (DOR: 7 months).\nOUTPUT:" }, { "from": "agent", "value": "BRCA-Mutated, Estrogen Receptor-Positive Breast Cancer" } ]

[ { "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: Whole exome sequencing (WES) was performed using next-generation sequencing (NGS) technology for the molecular diagnosis of the patient. A heterozygous pathogenic variant was detected in exon 31 of the CREBBP gene [NM_004380.3; c.5552G > A (p. Argl851His)], which is specific for Rubinstein-Taybi 1. Our patient is married and has a 10-year-old boy. Molecular tests were also applied to other family members so that we could guide their future plans. It was seen that her son also had the same pathogenic variant in one allele of the CREBBP gene. There is just one case with this in the Genome Aggregation Database (GnomAD) and Genomes database. The UniProt database showed that this variant was 63% pathogenic for the CBP_HUMAN region of interest. Pathogenicity prediction was conducted based on 9 different computational methods. A different variant in the same codon was classified as pathogenic in Clinvar Database. That's why, we classified this variant as a \"likely pathogenic variant\" due to ACMG criteria. In direction with the recommendations of international drug agencies, immunoglobulin (IVIG) treatment was initiated at the dose of 600 mg/kg every three weeks due to hypogammaglobulinemia. In addition, oral budesonide, a topically acting synthetic steroid, at three daily doses of 3 mg and oral methylprednisolone (MP) at a single daily dose of 0.5 mg/kg, were used for the treatment of NLH. The dose titrations of these drugs were adjusted according to the patient's clinical response. Vitamin D and Calcium supplements were also given to prevent the adverse effect of glucocorticoid therapy on bone metabolism.\nOUTPUT:" }, { "from": "agent", "value": "Common Variable Immunodeficiency, CREBP Gene Mutation, Gluten Enteropathy" } ]

[ { "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 57-year-old female presented with sudden onset of loss of taste and tongue deviation to the left on protrusion. She had slurring of speech but no limb weakness, no syncopal attack, no headache, no vomiting, and no history of seizure. Underlying medical problems revealed that she suffered from hypertension, psoriasis, and right knee osteoarthritis. She was first seen by the neurosurgery team as the computed tomography (CT) scan showed right posterior frontal-subcortical intraparenchymal bleed with multifocal infarcts. A magnetic resonance imaging (MRI) was also performed and there was an incidental finding of right masticator space lesion following the course of the right mandibular nerve. The patient was then referred to us for further management. On examination, her face was symmetrical. She had slurred speech, tongue deviation to the left but no paresthesia of her tongue or right labiomental region. There was no buccal or lingual bony expansion at the right mandible. However, thick fibrous mucosa was palpable lingually. It had minimal central enhancement seen postcontrast. No evidence of intracranial perineural spread. The patient declined incisional biopsy to establish the diagnosis of the lesion as she was asymptomatic and unwilling to take the risk of paresthesia postbiopsy.\nOUTPUT:" }, { "from": "agent", "value": "Mandibular Canal Enlargement, Schwannoma or Neuroma" } ]

[ { "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: Laboratory results including full blood picture, urea and electrolytes, fasting glucose, thyroid function tests, vitamin B12, folate levels and rheumatoid factor were all normal. Liver function tests were abnormal with an ALP of 515 U/l (35 - 120) and gamma GT of 271 U/L (12 - 58). Hepatitis screening blood tests were normal and ultrasound scanning of her abdomen showed several gallstones with no evidence of biliary dilatation. She was treated empirically with intravenous methyl prednisolone (500 mg daily) for presumed myelitis for 5 days prior to the results of her MRI scan becoming available. Although she did not improve clinically with this regime, there was a striking fall in serum C reactive protein from an initial 118 mg/L to 8.8 mg/L over this period. 10 days after stopping methyl prednisolone, serum C reactive protein was 74.5 mg/L. Yet again this fell to 11.0 mg/L after 2 days resumption of prednisolone and azathioprine (Fig 1). ANCA results became available two days after admission. C-ANCA was positive at 1:320 dilution, PR3-ANCA was positive 42.1 U/ml (< 2 U/ml). This led to a working diagnosis of WG. Nasal septum mucosal biopsy revealed non-specific inflammation with no evidence of a vasculitic process. The patient declined a nerve biopsy. Together with a reducing course of steroids, she was commenced on azathioprine 100 mg daily, twelve days after completing the course of pulsed intravenous methylprednisolone. 12 months after the initiation of treatment she is clinically well, with almost complete resolution of bilateral foot-drop and no overt complications of treatment.\nOUTPUT:" }, { "from": "agent", "value": "WG (Wegener's Granulomatosis)" } ]

[ { "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 presented with fever, fear of cold, dry cough, fatigue, and muscle pain. After being admitted to the hospital, he was administered Chinese herbal compound and western medicine treatments, including nasal oxygen, Pidotimod capsules, compound glycyrrhizin tablets, thymalfasin for injection, interferon alpha2b injection, and umifenovir hydrochloride tablets (Arbidol ) tablets. After treatment, the clinical symptoms disappeared. However, SARS-CoV-2 test results were repeatedly positive. Routine blood, C-reactive protein, and interleukin-6 tests performed on March 10, 2020 were normal. CT results showed flocculent ground glass shadows in both lungs, with fuzzy boundaries, which were present in the middle and outer zones of the lung field. He had no respiratory symptoms. CT of the lungs performed on March 10, 2020 showed that the lung inflammation improved a lot than before. SARS-CoV-2 test result was negative on April 9, 2020. However, it turned positive again a day later. He was therefore transferred to a designated hospital for observation. PTH was administered to the patient from April 19, 2020, while other treatments were stopped. On April 20 and 24, 2020, SARS-CoV-2 RT-PCR test results were negative. Follow-up on July 3, 2020 again showed a negative SARS-CoV-2 test result. The time elapsed from the onset of the disease to when the nucleic acid test results turned negative was 67 days. After 3 months of follow-up, SARS-CoV-2 test results remained negative, and he had no clinical symptom or lung abnormalities on CT.\nOUTPUT:" }, { "from": "agent", "value": "COVID-19" } ]

[ { "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 41-year-old female presented with yellow discoloration of her eyes and urine over 3 weeks; she was diagnosed with HIV infection 9 years ago. She had been on ART treatment since her diagnosis. Her antiretroviral regimen consisted of Zidovudine (AZT) Lamivudine (3TC) and Nevirapine (NVP) (Cipla) a single tablet combination. Her CD4 count is 550 cells per mm3 and her viral load is below level of detection at less than 40 copies per millimeter of blood (<40 copies/ml). Her ART regimen was changed 2 weeks prior to presentation to Tenofovir Disoproxil Fumarate 300 mg (TDF), Lamivudine 300 mg, and Efavirenz 600 mg in a single pill combination tablet (TELURA, Mylan). She had no history of alcohol or any other drug use. Her physical examination was notable for jaundice; there was no evidence of bleeding, no confusion, or other clinical signs of hepatic encephalopathy. Tests for HBsAg, anti-HCV, anti-HAV IgM, CMV IgM, and EBV, antinuclear antibody (ANA), antimitochondrial antibody (AMA), and anti-smooth muscle antibody (ASMA) were negative. Her ALT above 942 U/L (normal range 13-40 U/L) and AST was above 913 U/L (normal range 10-40 U/L). Abdominal ultrasound examination of the liver was normal. Liver biopsy was done which showed normal hepatocytes with portal tracts having heavy mixed inflammatory cell infiltrates with numerous polymorphs and eosinophils. Cholestasis was evident with no granulomas, neoplasm, no fibrosis, or nodular formation. Her ART was stopped and serial liver function testing was done to monitor her response to treatment. The ALT at weeks 2 and 4 of follow-up was 128 U/L and 114 U/l (normal range 13-40 U/L), respectively; the ALP was 153 and 185 U/L and GGT 250 and 310, respectively at weeks 2 and 4 of follow-up. She recovered well and at week two she was switched to a regimen consisting of Abacavir 300 mg twice daily, Lamivudine 150 mg twice daily, and Lopinavir boosted with ritonavir 400 m/100 mg twice daily. She recovered well.\nOUTPUT:" }, { "from": "agent", "value": "Acute Liver Failure" } ]

[ { "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 77-year-old female, an immigrant from Peru 20 years earlier, with interferon-gamma release assay positivity for M. tuberculosis, presented with fevers and decreased oral intake due to poor appetite for the previous 3 weeks. Her review of systems on admission was otherwise negative, and she reported no recent travel. She had been diagnosed with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis approximately 1 year earlier and, after completing a 6-month course of cyclophosphamide, was taking 10 mg of prednisone and 100 mg of azathioprine (AZA) at the time of admission. Even prior to the diagnosis of vasculitis, her chest imaging had revealed fibrocystic and bronchiectatic changes. Physical examination revealed a comfortable but undernourished woman with a temperature of 101.3 F and dry crackles on lung auscultation. There were no other pertinent findings. Laboratory values were significant for serum sodium of 126 meq/L and normocytic anemia with a hemoglobin level of 11 gm/dL. Her admission chest radiograph (CXR) was unchanged from previous radiographs. She was started on ceftriaxone and azithromycin for possible pneumonia. Her immunosuppressants were continued. Fevers persisted despite broadening of her antibiotic regimen first to cefepime and then to imipenem. Her subsequent CXR revealed subtle diffuse reticulonodular densities (Fig. 3A). Chest CT demonstrated a miliary pattern of involvement superimposed on chronic changes (Fig. 3B). Due to concurrent worsening pancytopenia, AZA was discontinued, but the dose of prednisone was not changed. Despite the initiation of empiric anti-tuberculous therapy, she became progressively more hypoxemic and somnolent with a worsening CXR (Fig. 3C). Two sputum mycobacterial smears returned negative. Continued deterioration and pancytopenia prompted a bone marrow biopsy, which revealed rare aggregates of histiocytes (Fig. 4). Stains for acid-fast bacilli and fungi were negative. The patient expired just as she was about to receive the first dose of L-AmB for presumed DH. Post-mortem, her urine and serum Histoplasma antigen titers were reported as above the limit of quantification (>19 ng/ml, Quest Diagnostics, Inc., Teterboro, NJ, USA). Sputum and blood cultures ultimately revealed no growth. The family declined autopsy.\nOUTPUT:" }, { "from": "agent", "value": "Histoplasmosis" } ]

[ { "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 fifty-year-old male presented with a one-month history of left shoulder pain unresponsive to conservative management. The patient was a nonsmoker with a BMI of 27, a history of dyslipidemia, and no prior history of shoulder problems. Upon physical exam the patient had decreased ROM of the left arm as well as a positive Jobe sign, Hawkins sign, and Speed test. On the day of surgery, the patient was given a preoperative, ultrasound-guided, interscalene nerve block with 25 mL of 0.5% ropivacaine administered with a 21 gauge, 90 mm, echogenic short bevel needle. Next the patient underwent induction of general endotracheal anesthesia. The patient was placed in the lateral decubitus position with the head in a neutral position, and a boom was used to apply 15 pounds of traction throughout the arthroscopic procedure. Glenohumeral debridement and subacromial bursectomy were performed arthroscopically, followed by repair of the supraspinatus and infraspinatus rotator cuff tendons. Inspection of the biceps tendons revealed extensive synovitis. Traction was released and an open subpectoral long head biceps tenodesis was performed. The total case time was three hours and twenty-eight minutes. The patient presented seven weeks postoperatively with the inability to flex the left thumb interphalangeal joint or the index DIP joint; he was diagnosed with AIN palsy. The patient also had mildly decreased sensation to light touch along the median nerve distribution in the hand and mildly decreased sensation to light touch and subjective paresthesias along the ulnar nerve distribution. However, according the patient, the findings along the ulnar nerve distribution existed prior to the surgery. He was observed clinically and at twenty-two weeks postoperatively began to show improvement by demonstrating motor recovery of the AIN with flexion of the thumb IP joint; at this time he still lacked index finger DIP flexion. At twenty-eight weeks postoperatively, an electromyography and nerve conduction study was attempted, but the patient did not tolerate and therefore did not complete these studies.\nOUTPUT:" }, { "from": "agent", "value": "Anterior Interosseous Nerve Neuropraxia, Full thickness rotator cuff tear, Severe proximal median neuropathy, Possible C8 radiculopathy" } ]

[ { "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 presented to the outpatient department with complaints of bilateral nasal obstruction for 1 month associated with intermittent blood stained nasal discharge. The patient also gave history of swelling over the dorsum of the nose which developed rapidly over 1 month. There was no history of headache, facial pain, or visual disturbance. There was history of similar swelling in the past over the same site for which she had undergone a minor surgery 5 years back at a different hospital and the records of the biopsy were untraceable. On examination, there was a firm, fixed, and well-defined swelling of size 2 x 2 cm over the root of the nose in the midline. On nasal endoscopy, left nasal cavity showed a fleshy mass filling the entire cavity pushing the septum to right lateral nasal wall. Contrast-enhanced computed tomography of the nose and paranasal sinuses showed a heterogeneously enhancing soft-tissue density over root of the nose with erosion of nasal bone and extension into left nasal cavity and filling left maxillary sinus, anterior, and posterior ethmoid sinuses and extending into right nasal cavity with erosion of bony septum (Figure 1(A) and (B)). There was no skull base or lamina papyracea erosion or any enlarged neck nodes. Patient underwent whole-body positron emission tomography-computed tomography to rule out metastasis in lungs, liver, and skeletal system which failed to show any uptake in the site other than nose and paranasal sinus region. Patient underwent excision of the mass by external approach (lateral rhinotomy incision) along with left medial maxillectomy and excision of the external subcutaneous component (Figure 2). Patient received intensity-modulated radiotherapy 60 Gy/30 fractions, 4 weeks after the surgery. Patient was followed up every month in the first 6 months with diagnostic rigid nasal endoscopy, followed by 6 monthly interval for 2 years and found to have no further recurrence.\nOUTPUT:" }, { "from": "agent", "value": "Malignant Chondroid Syringoma" } ]

[ { "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's fresh sperm was collected at the oocyte retrieval day and semen analysis revealed sperm counts of 84 x 106/ml with 45% motile and 100% round-headed sperm under x 400 magnifications without sperm morphology staining (Figure 1a). Thirteen oocytes were retrieved and 12 were found to be metaphase II. Metaphase II oocytes were divided into two groups and each 6 oocytes were inseminated with either patient's sperm or donor sperm. It was found that 3 out of 6 oocytes injected with round-headed sperm and activated by ionophore fertilized to form 2 pronuclei. All fertilized oocytes cleaved at Day 3 examination, and 2 developed to blastocysts (Figures 1b,c). By contrast, 5 out of 6 oocytes injected with donor sperm fertilized normally, all cleaved at Day 3 examination, and 3 developed to blastocysts. All blastocysts were biopsied for aneuploidy screening with next generation sequencing. As results, one euploid (46, XX) blastocyst with good inner cell mass (ICM)/good trophectoderm (TE) (Figure 1b) and one aneuploid blastocyst [45, X, dup(Y) (p11.2p11.2), del (1) (q31)] with fair ICM/good TE (Figure 1c) were obtained from the oocytes injected with round-headed sperm and activated by ionophore. By contrast, 2 euploid (46, XX) blastocysts (one with good ICM/good TE and the other with fair ICM/good TE) and 1 aneuploid (45, XY, -22) blastocyst with fair ICM/fair TE were obtained from the oocytes injected with donor sperm. Blastocyst morphology classification was based on the standard developed by the Society for Assisted Reproductive Technology. After transfer of one euploid blastocyst resulting from the patient's round-headed sperm and AOA, the blastocyst implanted and a healthy girl (weight 7.13 lb) was delivered at gestation of 40 weeks and 5 days by cesarean section. No neonatal care was recorded and reported.\nOUTPUT:" }, { "from": "agent", "value": "Globozoospermia" } ]

[ { "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 was a 74-year-old man suffering from heart failure, chronic atrial fibrillation, severe venous insufficiency, leg ulcers, type 2 diabetes, chronic obstructive lung disease, and severe obesity (160 kg, BMI 49). At hospital admission the patient was confused with delayed response time. Furthermore he presented with atrial fibrillation (140 beats/minute), hyperthermia (39.0 C), and elevated blood levels of creatinine. He was tachypnoeic with low oxygen saturation (91%). A urine test strip showed presence of blood, protein, and ketone bodies. Initial treatment included fluid therapy and antibiotics on the suspicion of sepsis. The patient was transferred to telemetry in the cardiology department where treatment with digoxin was initiated. During the following days urine output increased, but his level of consciousness decreased and he developed myoclonia. Due to accumulation of carbon dioxide he was transferred to the ICU, where intubation and mechanical ventilation were initiated. At admission GCS score was 3, pupil reactions were sluggish, and muscle spasms in the upper body were observed. Blood tests were normal except an increasing INR. During the first days in the ICU the patient improved with decreasing demand of oxygen and cardiac inotropes. Analysis of the cerebrospinal fluid and a head CT were both normal. Microbiological tests showed no sign of infection. Despite fanning and cold fluids the patient still had an elevated temperature and cooling was intensified using a thermoregulatory device with cooling pads. On day 5 the patient's temperature normalized and he gained consciousness. On day 7 the diagnosis of HS syndrome was suspected. The patient stabilized and was extubated, but he still received intermittent cooling. The patient developed hypercapnia and was reintubated and later a tracheostomy was performed. Due to anuria dialysis was performed until he regained his kidney function on day 23. The patient was again stabile and interacting with family and staff. Unfortunately the patient was infected with pneumonia. His overall condition thereafter gradually declines and he died 55 days after admission.\nOUTPUT:" }, { "from": "agent", "value": "Heat Stroke" } ]

[ { "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 history of travel or surgery was recorded. Over the years, he was treated with cDMARDs (methotrexate) and bDMARDs (certolizumab, ETN, TCZ, abatacept, and adalimumab). Previous treatments provided only a partial clinical benefit; however, the systemic inflammation with CRP ranging from 20 to 40 mg/l persisted. There was not any improvement with the introduction of colchicine. The patient was then treated with steroid 0.5 mg/kg/day, with clinical improvement. Infliximab was started and steroid progressively tapered, but with recurrence of fever and systemic inflammation (CRP 68 mg/l). Despite the PAS negativity in the duodenal biopsy, the patient was then treated with ceftriaxone, showing a dramatic and rapid clinical and laboratory improvement (Figure 4). Finally, the patient was treated with doxycycline 100 mg twice daily and hydroxychloroquine 6 mg/kg/day, with no relapse after 6 months.\nOUTPUT:" }, { "from": "agent", "value": "Seronegative Arthritis, Whipple Disease, Adult onset Still's disease" } ]

[ { "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 peak temperature was 38.1 C. Besides fever, she had a stuffy nose and a mild cough. She did not develop diarrhea and vomiting during the course. She had no complicated perinatal history. Her examination was febrile at 38.1 C with a respiratory rate of 48 breaths/min and oxygen saturation of 98%-100%. She had normal respiratory effort, and coarse breath sounds could be heard in all lung fields. Lab data of the WBC, CRP, blood gas, transaminase levels, and bilirubin levels were all in the normal range. After admission, the baby was given the nebulization treatment of budesonide and ipratropium bromide, using normal saline and nasal drops to relieve nasal congestion and keep the nasal cavity clean (see Table 1). The baby returned to normal temperature and developed frequent coughs over the days. Her lung examination demonstrated scattered crackles on the back side, and then, phlegm and wheezing sounds could be heard in the following days. Chest x-rays showed that bilateral lung markings increased and blurred, with patchy shadows on the right upper lung field (see Figure 1). The piperacillin/tazobactam for pneumonia was administered on the fourth day after admission. Since then, her symptoms and signs of respiratory improved gradually. The baby got better on the 6th day after admission with wild nasal congestion. Laboratory tests showed that ALT and AST increased significantly (see Table 2 and Figure 2). She was also administered hepatoprotective treatment of glycyrrhizin and bicyclol. After a 2-week treatment, the liver function recovered totally.\nOUTPUT:" }, { "from": "agent", "value": "Acute hepatitis, COVID-19" } ]

[ { "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 71-year-old male with a recent history of recurrent episodes of left arm and face paresthesias was admitted to our department after a first generalized convulsive seizure. His past medical history disclosed hypertension, hypercholesterolemia and peripheral arterial disease, but no known epilepsy, cerebrovascular events or cognitive impairment. His usual medication included bisoprolol, sinvastatin and clopidogrel. On admission, his blood pressure was 180/100 mm Hg. A general examination was unremarkable, and a neurological examination revealed mild left facial palsy and left visual and tactile extinction. 1a, b). An electroencephalogram showed no evidence of paroxysmal activity. His antithrombotic medication was stopped, and the patient was started on phenytoin (100 mg t.d.s.) and perindopril (5 mg o.d.). Despite his treatment, the patient remained confused and agitated and his blood pressure values ranged from 160-200 (systolic) and 70-97 mm Hg (diastolic). On day 2 of his hospitalization, the patient suffered a cardiac arrest and was resuscitated. Afterwards, global aphasia and right hemiplegia were noted. 1c, d). His cervical and intracranial CT angiograms were normal. The patient's blood pressure was controlled with a low dose of bisoprolol and furosemide, and then, there were no further events. 1e, f). The patient was discharged at 3 months with a modified Rankin Scale score of 4 but died 1 month later of unknown causes and without any autopsy being performed on him.\nOUTPUT:" }, { "from": "agent", "value": "Cortical subarachnoid hemorrhages, Parenchymal hemorrhage, Superficial siderosis, CAA" } ]

[ { "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 25 day old male baby born at full term gestation, with uneventful antenatal and perinatal period, birth weight of 3.1 kg, was brought to emergency with complaints of poor feeding and respiratory distress for one week. Chest radiograph showed cardiomegaly. Echocardiography revealed bicuspid aortic valve, critical aortic stenosis, small PDA (right to left shunt) and severe left ventricular dysfunction (LVEF 20%). The baby underwent balloon dilatation of the aortic valve successfully. Two days post balloon dilatation, repeat echocardiography while still on oxygen showed a mean gradient across the aortic valve of 18 mmHg, trivial aortic regurgitation, no flow across the PDA and mild tricuspid regurgitation (gradient 28 mmHg) with a left ventricular ejection fraction of 50%. After 3 months, he was readmitted with features of congestive cardiac failure. Echocardiography showed a well opened aortic valve (mean gradient 20 mmHg), trivial aortic regurgitation, normal mitral valve, normal flow in the pulmonary veins and normal LV function. There was right ventricular dysfunction with severe PAH (TR peak gradient 86 mmHg). CT pulmonary angiography was done to profile pulmonary vein anatomy and to rule out any lung malformation contributing to PAH. The child was stabilized with diuretics and oxygen. Repeat echocardiography showed a TR gradient of 50 mmHg (on oxygen by nasal prongs 5 l /minute). Cardiac catheterization was done for hemodynamic assessment. Hemodynamic data (taken on oxygen) is given in table 3. The baby was stabilized on a pulmonary vasodilator (sildenafil) and oral diuretics (frusemide and aldactone). He was discharged in a clinically stable condition. After two months the child returned with acute deterioration. Despite all resuscitative measures, child could not be revived.\nOUTPUT:" }, { "from": "agent", "value": "Pulmonary arterial hypertension" } ]

[ { "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 31 year old woman had a seven year history of complex partial seizures consisting of behavioral arrest, rarely secondarily generalizing to a convulsion. She had no known risk factors for epilepsy. Brain MRI was initially considered normal, though subsequent high-resolution studies showed possible subtle dysplasia of the right frontal lobe (Figure 1A). She was hospitalized for persistent confusion after a seizure and was found to be in complex partial status epilepticus. After treatment and clinical recovery, frequent right frontal electrographic seizures persisted (Figure 1B). 18-FDG Positron Emission Tomography (FDG-PET) performed at this time, considered to be an ictal study, showed intense right frontal hypermetabolism (Figure 2A). A subsequent FDG-PET performed during a seizure-free period after treatment with lorazepam showed right frontal hypometabolism (Figure 2B). As part of an approved research study, the patient provided informed consent to undergo PET using [C11]PK11195, a radiotracer that identifies brain inflammation by binding to the translocator protein expressed by activated microglia. [C11]PK11195 PET (PK-PET) has identified inflammation associated with multiple sclerosis, Alzheimer's Disease, and stroke, but has not yet been applied to epilepsy, except for rare cases of epilepsy due to known inflammatory causes such as vasculitis or encephalitis. Using a two-parameter linearized reference tissue model implemented in PMOD (PMOD Technologies, Zurich, Switzerland), images of tracer uptake (relative to cerebellum) were generated (Figure 2C). Focally increased [C11]PK11195 uptake was apparent in the right frontal lobe in the same region identified as metabolically abnormal by ictal and interictal FDG PET. Because the patient's seizures were difficult to control using medication, she underwent right frontal lobe resection. Surgery was guided by intraoperative electrocorticography, which showed frequent epileptic activity in the right frontal region corresponding to imaging abnormalities. The patient is seizure free one year after surgery.\nOUTPUT:" }, { "from": "agent", "value": "Focal cortical dysplasia" } ]

[ { "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 3 is a 22-year-old woman with a history of EDS who presented with several years of progressive headaches and neck pain. Her pain was accompanied by numbness of her hands and feet, nausea, gait instability, and was aggravated by flexion and extension of her neck. At the initial presentation, her pain was a 3 out of 10 in intensity and nonresponsive to multiple previous medications. A hard cervical collar trial helped alleviate her headaches. Her symptoms worsened over the following 6 months, with pain becoming more constant and reaching a 5 out of 10 intensity. She also developed weakness in her upper extremities, right worse than left, resulting in commonly dropping objects. Her balance and coordination also worsened with associated lower extremity fatigue and feeling that her legs would give out from under her. Her sensation of tingling also spread from her hands to include her shoulders. Following her procedure, she reported improvement in her symptoms which lasted for the first few months. At this point, her symptoms began to return. An external bone stimulator was utilized in an attempt to nonoperatively stimulate fusion, but this did not improve the fusion mass. Her pain returned to the preoperative 5 out of 10 intensity. Following this procedure, the patient's symptoms improved and remained stable. At her most recent follow-up, she continued to have headaches and neck pain, but significantly milder in comparison to preoperative symptoms. Her symptoms and radiographic studies have remained stable at 48 months after her index procedure and 19 months after her revision, with imaging at that time demonstrating adequate fusion and expected postsurgical changes [Figure 3d]. This patient was categorized as having experienced a significant improvement in symptoms.\nOUTPUT:" }, { "from": "agent", "value": "Ehlers-Danlos syndrome, C1-2 rotational subluxation, AAI, pseudoarthrosis at C1-2" } ]

[ { "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: Currently the patient presents malformations of the lower left limb (hip, knee and ankle), evident on the articular and periarticular level, where there are diffuse exostoses. This case discusses the main occupational concerns relating to the patient's workspace at a high floor level that could create critical issues in the event of an emergency exodus. Given the impossibility of placing the patient in heavy manual activities, employment is limited to office activities. Adjustments were carried out at the patient's workstation, and thus the patient has been recognized as fit to work. Increased frequency of breaks were prescribed in order to allow the physiological alternation of postures. Image Caption and Description: \nImage caption: []\nImage description: []\nCase Report: \nMovements at the workplace are very limited and of short duration; however, given the limitations of the patient's movement, the use of the stairs must be limited and the use of a dedicated elevator is required. Therefore, to allow travel to and from the workplace, the patient was reserved a flat parking space, and an elevator located at the parking level to his workstation was provided, as well as to the entire library area and related offices.\nOUTPUT:" }, { "from": "agent", "value": "Overgrowth syndrome" } ]

[ { "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: With a past history of asthma, he was on inhalers on an occasional basis. Having been experiencing disfigurement-related emotional and psychosocial abuse after burn injuries, he expressed a strong desire to have his original appearance restored. Accordingly, a two-stage reconstructive procedure was performed. Accordingly, bilateral pre-expansion of occipito-dorsal flaps was conducted. Under general anaesthesia in the prone position, the shape of the flap was designed in a way to match the recipient site and the occipital arteries were identified and marked on the skin using a portable Doppler ultrasound machine [Figure 2]. Tissue expanders were positioned in a suprafascial plane inferior to the pedicle and deep to the center of the earlier defined occipito-dorsal flap, and the skin was closed directly. The expanders were inflated over a period of 3 months to a volume of 700 ml each. Prior to raising the flap, the occipital arteries were again dopplered and the flap was raised on a narrow isthmus, with precautions taken to ensure the flap remained above the fascial layer over the posterior trunk musculature. Once elevated, the flap was thinned to the layer in which the subdermal vascular network became visible through a layer of fat. Although designed as bilateral flaps, the two cavities converged as one. Upon rising, the expanders were removed. The donor site, measured 20 cm by 15 cm, was closed directly without drains. Two revision procedures were performed; the first one to address the dog ears in the posterior cervical region and the second one to remove excess adipose tissue by liposuction. As shown in Figure 3, these procedures achieved a satisfactory cosmetic result in terms of skin contouring, despite minimal scar hypertrophy.\nOUTPUT:" }, { "from": "agent", "value": "Significant scars, keloids, and contractures in anterior chest and neck due to burn injuries" } ]

[ { "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 sedated and intubated, was transferred to our institution. At the end of the surgical procedure, the patient was transferred to the pediatric intensive care unit (ICU). Nonetheless, during hospitalization, the patient showed a progressive neurological improvement, recovering also cognitive functions. She was discharged on postoperative day 15. She was therefore discharged with a program of hospitalization to another country (England) for neurorehabilitation and cranioplasty planning.\nOUTPUT:" }, { "from": "agent", "value": "Concussive head trauma, left fronto-temporo-parietal lesion, lacerated-contusive trauma of the chest wall, left mammary gland trauma, fracture of the left hand, multiple left frontotemporo-parietal skull fractures, contusive-hemorrhagic lesions, diffuse cerebral damage in the left frontotemporo-parietal lobe, aphasia nominum, right hemiparesis." } ]

[ { "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 63-year-old female presented with iron-deficiency anaemia (haemoglobin 44 g/L, ferritin 190 mcg/L). After unremarkable upper and lower gastrointestinal endoscopies and biopsies, she was referred for wireless capsule endoscopy (WCE). The WCE study demonstrated an area of ulceration and stenosis in the distal jejunum. The capsule failed to pass the pathology within the duration of the capsule's battery life (approximately 14 hours). Four days following ingestion, the patient presented with 48 hours of increasing generalised abdominal pain and nausea, but no vomiting. She had a mild fever of 37.8 C. On examination, the abdomen was distended and tympanic on percussion and generally tender, but there was no guarding. The wireless capsule can be seen in the left lower quadrant of the abdomen. A computed tomography (CT) scan of the abdomen (Figure 2) demonstrated the wireless capsule in the distal ileum, 15 cm proximal to the ileocaecal junction with evidence of perforation at this level. There was diffuse thickening of the terminal ileum distal to site of perforation. At laparotomy, there was four-quadrant feculent peritonitis. The site of terminal ileum perforation was on the antimesenteric border, 15 cm from the ileocaecal valve, with the wireless capsule in situ (Figure 3). There was a 5 cm segment of markedly thickened ileum distal to the site of perforation. The patient recovered well and was discharged from hospital five days after her operation.\nOUTPUT:" }, { "from": "agent", "value": "Small Bowel Obstruction with Perforation, Crohn's disease" } ]

[ { "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 extraoral examination (Fig. 1), she was having a convex profile, asymmetric face slightly increased lower third, and mesofacial pattern. Intraoral examination (Fig. 1) revealed that she was in the mixed dentition stage with Angle's class I in molars and canines. 1). Her radiological exam (Fig. 2) revealed that all permanent second premolars were with the crown completely formed (Nolla stage 5) and developing between primary molars. Treatment plan on the upper arch consisted of RPE with HAAS expander modified with palatal vertical crib to correct SPC AOB (Fig. 3). After RPE, expander was maintained in the mouth for 6 months with retention. At the end of retention time, expander was removed and it was installed removable appliance with palatal crib in the maxilla to finish the AOB correction. The last appliance was used by 12 months. Lingual arch was placed next to exfoliation of the lower second primary molars to harness the E-space (Fig. 3). Treatment results were: SPC correction, AOB closure and overcorrection. At the lower arch, there was the harness of the E-space and improvement of the crowding (Fig. 4). Patient was evaluated until permanent dentition and soon after, it was installed an orthodontic corrective appliance for alignment, leveling, and finalization of the occlusion. By the end, the patient had good facial esthetics, stable, and adequate occlusion (Fig. 5).\nOUTPUT:" }, { "from": "agent", "value": "Crowded teeth, Anterior open bite, Skeletal posterior crossbite, Transverse maxillary deficiency" } ]

[ { "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: 2). A bronchoscopy demonstrated negative Aspergillus cultures, but positive for Penicillium species fungal cultures. The patient shown initially some clinical improvement with trimethoprim/sulfamethoxazole, but over the following six months, he developed a worsening productive cough with brown sputum, hemoptysis, night sweats, fevers, and chills. He was admitted to the hospital for worsening hemoptysis and initially started on meropenem given a history of ESBL E. coli on prior sputum culture. One month later the patient presented with worsening back pain and was found to have multiple sites of poorly differentiated adenocarcinoma in the liver, bone, adrenal gland, and pancreas, likely originating from gastric adenocarcinoma. In individuals who are HIV positive originating from endemic geographical regions presenting with pulmonary or systemic infection, T. marneffei should be considered as one of the differentials. However, without endemic risk factors, the diagnosis of T. marneffei can be overlooked.\nOUTPUT:" }, { "from": "agent", "value": "Talaromyces pneumonia, underlying cancer" } ]

[ { "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: Initial chest (Fig. 1A) and abdominal (Fig. 2B). CT abdomen and pelvis also showed a retained guide wire extending from the inferior vena cava (IVC) to the left iliac and left common femoral vein (Fig. 3). Upon further investigation, patient was involved in a motor vehicle accident necessitating trauma intensive care stay with femoral central venous access placement sixteen years prior to current presentation at an outside facility. Of note, patient was aware of the guide wire presence with initial plan for re-imaging and retrieval but was lost to follow up until current presentation. Interventional radiology were able to remove the IVC portion of the wire but unable to retrieve the right pulmonary artery portion due to its being completely epithelialized. Patient was started on appropriate antibiotic regimen with clearance of bacteremia after source control. Due to resolution of bacteremia and symptoms at the end of his treatment period and lack of exposed hardware, patient did not require chronic lifelong suppression therapy for his retained pulmonary artery fragment of guide wire.\nOUTPUT:" }, { "from": "agent", "value": "Retained foreign objects, MSSA pulmonary septic emboli, Septic shock, Endocarditis with systemic emboli" } ]

[ { "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 woman underwent ESD for a 5.6-cm mixed-nodular type laterally spreading tumor (LST) in the rectum (Fig. 1A, B). Neither a non-lifting sign nor significant submucosal fibrosis was identified. The specimen was fixed in 10% formalin, paraffin-embedded, and evaluated after being cut into 2-mm-thick slices. The histology showed a well-differentiated adenocarcinoma confined to the LP without lymphovascular invasion and with clear resection margins (Fig. 1C). Follow-up sigmoidoscopy at 8 months showed only a scar (Fig. 1D). However, she was admitted with sacral area pain at 17 months after ESD. Sigmoidoscopy showed an extrinsic infiltrative lesion at the previous ESD site (Fig. 1E). CT showed a perirectal mass, enlarged perirectal lymph nodes, and multiple lung nodules. The pathological findings of the previous ESD site lesion revealed a poorly differentiated adenocarcinoma under normal colonic crypts (Fig. 1F). The histology of lung nodules (Fig. Following these findings, the entire original ESD specimen was re-examined after slicing the paraffin-embedded blocks to check for the presence of missed submucosal invasive foci smaller than 2 mm, the routine slice thickness for histologic review of an ESD specimen at our center. At low magnification, the bulky, laterally spreading adenoma contained multiple foci of adenocarcinoma component (Fig. 1C). Higher magnification of the least differentiated area showed solid and cribriform architecture and multiple foci of the invasive front, consisting of small, infiltrative tumor glands (Fig. 1C, inset). However, neither submucosal invasion nor lymphovascular invasion was identified, even with CD34 and D2-40 immunostaining.\nOUTPUT:" }, { "from": "agent", "value": "Local Recurrence of Colorectal Mucosal Cancer, Distant Metastasis" } ]

[ { "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 youngest sibling is a 19-year-old male. Airway cultures through childhood were positive for Pseudomonas aeruginosa and he was maintained on continuous nebulised colistin. The initial sample was co-infected with Pseudomonas spp. and later samples were co-infected with Aspergillus fumigatus, Pseudomonas aeruginosa and Paenibacillus amylolyticus. The subsequent 9 years involved intermittent Inquilinus identification with 8 further isolates (9/19 respiratory samples were Inquilinus-positive, Fig. 1A). Case 1 did not receive intravenous (IV) antibiotics in the twelve months before or after first growth of Inquilinus. Susceptibility patterns were consistent with recent reports, with most isolates resistant to piperacillin-tazobactam, tobramycin, aztreonam and colistin sulfate and susceptible to ertapenem, meropenem and ciprofloxacin (Fig. 1B). Infection was associated with a decline in the ppFEV1 and ppFVC compared to twelve months prior (ppFEV1 from 60.9% to 46.9%, ppFVC from 61.2% to 52.2%). Lung parameters improved twelve months after the first isolate (ppFEV1 64.1%, ppFVC 61.2%) and fluctuated at a higher baseline than pre-Inquilinus levels. The patient's weight at the time of the first isolate was lower than twelve months prior (75th percentile from 80th percentile), but weight increased on transition to adult services.\nOUTPUT:" }, { "from": "agent", "value": "Inquilinus limosus infection, Cystic fibrosis" } ]

[ { "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 hemiarthroplasty was converted to general endotracheal anesthesia and completed. While being in the recovery room, patient began complaining of symmetric, bilateral lower extremity weakness with subsequent paraplegia and upper extremity \"heaviness,\" with consequent sensory deficits to the C4-C5 levels. Patient was taken immediately for MRI of cervical, thoracic, and lumbar spine and brain CT, which were negative for spinal hematoma and cord compression. One dose of Methylprednisolone 2500 mg IV was given and patient placed on a Methylprednisolone drip at 5.4 mg/hr for the following 24 hours. Six hours after initiation of drip patient became agitated and confused. At this time, labs remarkable for potassium level 6.4 mEq/L (5.6 mEq/L prior to surgery, baseline 5.2 mEq/L) and digoxin 1.9 ng/ml. ECG showed no acute changes pertaining to digoxin toxicity or hyperkalemia. Patient was given Calcium Gluconate and Regular Insulin with 1 amp of D50W. Urgent hemodialysis was performed and 1.0 L of fluid was removed. Patient began complaining incessantly of dyspnea: ABG: 7.35/42/83/23.2 on 2 L nasal cannula, SpO2 100%. Vital signs were temperature 97.5 F, blood pressure 171/80, pulse 76 beats per minute, and respirations 18. Troponin was negative. Concurrently, patient was also observed to be posturing with a right-sided gaze. Repeat brain CT showed no acute changes. EEG showed no seizure activity. After, patient was noted to be less anxious and breathing comfortably, though not oriented to time, person, or place. Digoxin level noted to be at 1.4 ng/mL. By postoperative day 2, patient was alert and oriented to person and place. On postoperative day 3, patient had 2.5 L of fluid removed through scheduled hemodialysis. Digoxin level was 1.1 ng/mL. By the evening, patient was able to engage in full conversation, was moving all four extremities, and was following simple commands.\nOUTPUT:" }, { "from": "agent", "value": "Accidental Intrathecal Administration of Digoxin, End-Stage Renal Disease" } ]

[ { "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 with a history of HIV AIDS, daily marijuana use, and asthma presented to the hospital for worsening shortness of breath. He had been short of breath for one week. He was working in the kitchen of a restaurant and noticed he was having more difficulty completing tasks he could normally do without issue. His breathing became progressively worse and because of that he presented to the hospital. Medications: atovaquone 10 mL/1500 mg by mouth daily, diphenhydramine 25 mg capsule every 6 h as needed for itching, and Dolutegravir-Rilpivirine 50-25 mg tablet daily. On physical exam his maximum temperature was 102.4 F (39.1C), heart rate ranged from 98 to 116 beats per minute, respiratory rate ranged from 11 to 36 breaths per minute, and blood pressure was 102-136/60-83 mmHg. Otherwise, there was an unremarkable cardiopulmonary exam. No lower extremity edema. His initial ECG revealed coved ST segment elevation >2 mm in V1 and V2 followed by a negative T wave (Fig. 1). Initial chest x-ray showed patchy bilateral opacification concerning for multifocal pneumonia. The initial troponin was <0.03 ng/mL. COVID-19 testing was negative. CD 4 count was 14%. He was started on Vancomycin and Cefepime for pneumonia. His fever overnight was treated with acetaminophen 650 mg every 6 h as needed. Vancomycin was discontinued with negative MRSA nares swab. The second troponin was <0.03 ng/dL. His febrile episodes were treated with acetaminophen. He did continue to have some temperature elevations into the second day. The temperature taken before the second ECG was performed was 37.7C (99.8 F). 2). Several hours after the second ECG, he did have one episode where temperature was 39.1C (102.1 F) but then returned and stayed around 37.1C (98.7). He had a transthoracic echocardiogram (TTE). This showed ejection fraction 61% with normal left ventricular size, thickness, and preserved systolic function. Mild tricuspid regurgitation with elevated estimated pulmonary pressure of 50 mmHg, otherwise structurally normal heart.\nOUTPUT:" }, { "from": "agent", "value": "Brugada Syndrome" } ]

[ { "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 female baby GDG was born at 38 weeks of gestation by spontaneous delivery. No examinations were performed during pregnancy for parental nomadism. Birth weight was 3470 g and Apgar score 1/3/3. After delivery, the baby needed immediate cardiopulmonary resuscitation with intubation, external cardiac massage, ventilatory assistance (A/C with PIP 20, PEEP +5, TI 350 msec, FR 50/minute, MAP 9.9, FiO2 0.80), and an immediate blood transfusion for severe anemia (Hb 2.5 g/dL). Severe metabolic acidosis was present (pH 6.81), with arterial hypotension (41/19 mmHg). Correction of acidosis and treatment with dopamine, dobutamine, hydrocortisone, and furosemide was started. Chest X-ray showed marked cardiomegaly (Figure 1a). On ECG there were small Q waves in D2-3 and marked signs of subendocardial ischemia-lesion:with diffused ST-T segment elevation (Figure 1c). Echocardiography (Figure 1b) showed normal anatomy with the coronary arteries originated from the aorta; dilated and hypocontratile left ventricle (LV), with hypertrophic walls, mitral regurgitation, dilated right ventricle with tricuspid regurgitation and estimated pulmonary pressure of 35 mmHg, left-to-right shunt at atrial and ductal level, and moderate pericardial effusion. Serum enzymes, at 10 hours of life, were: CK = 14.895 U/L, CK-MB = 2.472 U/L and LDH = 3771 U/L. Rh isoimmunization was excluded and no specific infective agents were found by laboratory tests.\nOUTPUT:" }, { "from": "agent", "value": "Massive myocardial infarction" } ]

[ { "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 man presented with a 3-year history of numbness in both arms, with sensory changes in the right arm. Six months before admission, he noticed weakness in his right upper extremity and stiffness in the right lower extremity. No history of major trauma or viral infection was noted. Physical examination at admission revealed grade IV weakness of the right upper extremity, negative bilateral Hoffmann sign, positive Wartenberg sign on the right side, and hypoactive deep tendon reflexes in both the upper extremities. 1-a, b). 1-c, d). Magnetic resonance imaging (MRI) showed a bilaterally compressed spinal cord with an anomalous bony structure at the C2-3 level (Fig. 2-A, b, c). Computed tomography (CT) showed an invaginated abnormal bony structure at the C2-3 level and an abnormal lateral mass on the right side at the C2-3 level (Fig. 3-a, b, c, d, e). We did not perform nerve conduction studies or electromyography. The patient decided to undergo decompression surgery for removing the abnormal portion. During surgery using the conventional posterior open approach, an abnormal bony structure was found at the C2-3 level. The connection between the abnormal bony structure and the C2/C3 laminae was not bony but fibrous. To decompress the dura mater, the abnormal bony structure was removed using a high-speed drill until 50% AP diameter of the dura mater was exposed, and sufficient decompression was confirmed. There were no adhesions between the dura mater and abnormal bony structure. No instability was observed at this level, and instrumented fusion was not performed.\nOUTPUT:" }, { "from": "agent", "value": "Cervical Myelopathy" } ]

[ { "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 years old female with history of mandibular first molarextraction followed by pain left side of face since past 03 months was presented to the department of oral and maxillofacial surgery for consultation. Work up revealed that pain occurred several time in a day. Detailed history was taken. There was no significant medical history. She denied symptoms / history of psychiatry illness. Physical examination revealed no underlying cause. Her vital parameter was within normal limit. Submandibular lymph nodes were non tender. Intra oral examination revealed no abnormal finding in the floor of the mouth and other area of oral cavity. Oral mucosal lining of the floor of mouth, tongue were healthy and intact. Socket of the extracted molar tooth was healed and covered with over lyingmucosa. On palpation there was no tenderness present in first molar region bucally as well lingually. Patient was partially edentulous and remaining teeth were in healthy condition without anyradiographic evidence of disease OPG showed partial obliteration of first molar socket with ill defined radiolucency extending up to inferior alveolar canal (history of traumatic transalveolar extraction healed by secondary intention as by socket dressing). Pain was recorded on visual analogue scale (VAS) and a score of 6was obtained. Initially tablet Pregabalin was started with 75 mg daily for one week followed by 75 mg twice daily. After 07 days patient reported reduction in pain intensity, but not completely relief in pain and her sleep was also improved. Gradually dosage of tab. Pregmate was increased up to 150mg twice daily without any difficulty. After 03 months follow up of drug therapy patient reported complete relieve in pain.\nOUTPUT:" }, { "from": "agent", "value": "Peripheral neuropathic pain" } ]

[ { "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: Of 117 patients suspected with HON, 82 cases (66 males and 16 females) were obtained after the exclusion of cone dystrophy, occult macular degeneration, Leber congenital amaurosis, congenital stationary night blindness, glaucoma, and other common causes of child and adolescent neuropathy, retinopathy, or maculopathy. The mean age of the patients was 19.4 years (range, 5-46 years old). One hundred fifty-eight effected eyes were evaluated, including 6 patients affected with unilateral, 61 bilateral, and 15 sequential neuropathies. The median duration of the visual decrease was 0.5 year (range, 0.1-20 years). The initial visual acuity after the attack was from hand motion to 0.8, while the mean prognosis visual acuity is 0.1. Of 136 eyes from 68 patients that underwent visual field examination, central scotoma accounted for 69.9%, cecocentral scotoma connected with blind spot for 8.0%, paracentral and temporal defect for 6.6%, and diffuse defect for 15.5%. Interestingly, 81.5% of the asymptomatic eyes also demonstrated the central visual field damage. Of the 82 cases, 68 were identified with LHON, accounting for 83% of the cases. Both of them were with optic atrophy. Figure 1 shows the disease spectrum.\nOUTPUT:" }, { "from": "agent", "value": "Hereditary Optic Neuropathy, Leber's Hereditary Optic Neuropathy (LHON), Autosomal Dominant Optic Atrophy (ADOA), OPA1 mutation, OPA3 mutation, Wolfram syndrome, Hereditary Spastic Paraplegia, Spinocerebellar Ataxia Type 28, Polymicrogyria with Optic Nerve Hypoplasia" } ]

[ { "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 Caucasian lady presented to our clinic complaining of decreased vision in her left eye (LE). On presentation, best-corrected visual acuity (BCVA) was 10/10 in the right eye (RE) and 1/20 LE. Anterior segment examination was unremarkable in both eyes and intraocular pressures were within normal limits. Fundus biomicroscopy revealed in the right macula, slightly dilated right-angle veins with RPE hyperplasia beneath them (Figure 1A). Fluorescein angiography (FA) and optical coherence tomography (OCT) were performed and confirmed the above diagnosis (Figures 1C-D, 2, 3A). After a discussion outlining the possible risks and benefits of the treatment, the patient was started on 0.5 mg intravitreal ranibizumab in the LE. Based on the findings of FA and OCT which were performed monthly, the patient underwent three intravitreal injections of ranibizumab every month for three months. Examinations were repeated monthly for another 12 months and showed no recurrence of CNV.\nOUTPUT:" }, { "from": "agent", "value": "Subretinal neovascularization, Idiopathic juxtafoveal retinal telangiectasis" } ]

[ { "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 standard preparation for 20-gauge pars plana vitrectomy was made, including conjunctival peritomy and three sclerotomies. After a core vitrectomy was performed, the nucleus of the lens was initially crushed with a microvitreoretinal blade and a 20-gauge needle introduced through a superotemporal and superonasal sclerotomies, respectively (Figure 1A). The nucleus was then removed with a fragmatome and a vitreous cutter through the pars plana, and cortical cleaning was performed using the active vacuum of the vitreous cutter (Figure 1B). The posterior capsule was removed during the procedure, but care was taken to preserve the anterior capsule. After completion of the vitrectomy, viscoelastic material was introduced into the anterior chamber through a side-port stab incision, and a superior clear corneal incision of 2.8 mm in length was made. After complete replacement of the aqueous humor with viscoelastic material (Figure 1C), a small puncture was made on the preserved anterior capsule with a bent needle (Figure 1D). Then capsulorhexis was performed using capsulorhexis forceps (Figure 1E). After a foldable IOL was inserted into the ciliary sulcus through the corneal incision, one side of the optic was pushed back into the vitreous cavity with a Sinskey hook and then the other side of the optic was pressed in the same manner, 90 from the haptic-optic junction (Figure 1F).\nOUTPUT:" }, { "from": "agent", "value": "Diabetic vitreous hemorrhage, Tractional retinal detachment, Thick posterior polar cataract" } ]

[ { "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: After confirming the diagnosis, patient received five cycles of induction chemotherapy using cisplatin, vincristine, etoposide, cyclophosphamide, and high-dose methotrexate. He underwent second-look surgery after completing induction that showed viable tumor. This was followed by consolidation with a single cycle of myeloablative chemotherapy using thiotepa, carboplatin, and etoposide followed by autologous hematopoietic progenitor cell rescue (AuHPCR). The first follow-up brain and spine MRI after AuHPCR showed no evidence of residual or recurrent tumor. However, as gross residual disease had been confirmed by biopsy at the beginning of consolidation, the patient received craniospinal proton beam irradiation to 30Gy with focal boosts to 54Gy to areas of bulky disease followed by metronomic low-dose temozolomide and cis-retinoic acid for 13 months. On a follow-up MRI scan 19 months after diagnosis, small interval increase was detected in a new nodular enhancement in the region of the lower lumbarsacral spine, described as consistent with tumor recurrence (Figure 1(e)). Patient underwent a biopsy of the lesion at L3, which was reported as leptomeningeal fibrosis with remote hemorrhage and no evidence of malignancy on histopathology (Figure 2(b)). Lumbarsacral MRI at 23 months from diagnosis (1f) remained unchanged. This patient is currently doing well, with no evidence of disease progression 6 years after diagnosis and 57 months after completion of all therapy.\nOUTPUT:" }, { "from": "agent", "value": "Disseminated medulloblastoma with multiple leptomeningeal and parenchymal gross nodular disease in inferior cerebellar hemispheres, medulla, fourth ventricle, posterior optic chiasm, anterior temporal lobes, and thoracic spinal cord." } ]

[ { "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 17-year-old female reported to the Department of Dentistry in Guru Gobind Singh Medical College and Hospital, Faridkot with a chief complaint of growth in the lower jaw [Figure 1]. Medical history of the patient revealed no relevant association with the lesion. The patient denied a history of smoking, ethanol consumption or any other harmful habits. The patient had noticed swelling and dull pain in the mandible 1 year ago and taken medicine from a private practitioner but with no relief. Hence, she was referred to a medical college. On clinical examination, an ulcerative lesion was noticed in the mandible extending from 35-46 crossing the midline. Lower anterior teeth showed Grade III mobility while premolars showed Grade II mobility. Bilateral enlarged submandibular lymph nodes (N2) were noted. The patient was advised orthopantomography and computed tomography (CT) scan [Figures 2 and 3]. CT scan revealed a lytic lesion involving alveolar ridge with erosion of labial and lingual cortices in the anterior region of mandible involving floor of mouth also. The incisional biopsy of the lesion showed dysplastic epithelium with epithelial cells showing distinct nuclear pleomorphism, presence of mitotic activity, including atypical mitotic figures and premature keratinization [Figure 4a]. The dysplastic epithelial islands were seen invading the connective tissue [Figure 4b]. On higher magnification the cells of tumor islands showed cellular and nuclear pleomorphism and nuclear hyperchromatism. The histopathological findings were suggestive of moderately differentiated (G2) SCC [Figure 4c and d]. As the lesion was diagnosed to be at Stage IV, the patient was advised surgery and radiotherapy.\nOUTPUT:" }, { "from": "agent", "value": "Squamous cell carcinoma" } ]

[ { "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: Of the 113 cases in this report, approximately 12%, 79% and 9% of them were detected from prenatal, pediatric and reproductive clinics, respectively. These guidelines were based on data from peer-review scientific literature and on a subsequent holistic summary by a heterogeneous panel of experts. For example, epilepsy should be treated from the onset with anticonvulsive therapy. Advices for taking care of a child with this rare and complex syndrome were offered to parents.\nOUTPUT:" }, { "from": "agent", "value": "Ring chromosome syndrome, Ring chromosome 18, Ring chromosome 14 syndrome" } ]

[ { "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 4-year-old boy was admitted with a history of recurrent respiratory tract infections in the last six months. The parents were second-degree consanguineous and family history was unremarkable for PIDs. Physical examination was normal on admission. Initial immunologic evaluation revealed very low IgG and IgA with very high IgM levels. Flow cytometric lymphocyte subsets analysis revealed very low CD19+ B cells. Specific IgG antibodies against hepatitis A and B vaccines were both undetectable. Other laboratory tests including leukocyte, lymphocyte, haemoglobin counts, liver and kidney function tests, serologic investigations for common viruses, were all normal (Table 1). Abdominal ultrasonography revealed mild hepatosteatosis and chest radiography was normal. Regular IVIG treatment provided IgG serum levels higher than 400 mg/dl. Targeted next-generation sequencing (TNGS) was performed in order to understand the molecular pathology two years after admission to pediatric immunology clinic. This novel BLNK mutation was confirmed by Sanger sequencing. Analysis of familial segregation revealed that his mother and father were heterozygous for the mutation. The patient's parents were healthy and had normal concentrations of serum immunoglobulins and normal number of B cells. The clinical findings of this patient are similar to typical XLA patients and he was followed for two years with XLA diagnosis before TNGS gene analysis. The patient has been treated with IVIG replacements for 4 years, and an excellent response was obtained. To our knowledge, this patient with BLNK mutation is the ninth case in the literature and the first case to be published from Turkey. The patient is doing very well now and no major infectious episodes and autoimmune manifestations were noted up to date.\nOUTPUT:" }, { "from": "agent", "value": "X-Linked Agammaglobulinemia, AR agammaglobulinemia (BLNK defect)" } ]

[ { "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 45-year-old woman was admitted to this hospital because of headaches, epigastric pain, nausea, vomiting, asthenia, dyspnea, loss of appetite, and fever. The patient was taking sulfadiazine and pyrimethamine due to a presumptive diagnosis of neurotoxoplasmosis in a previous recent hospitalization. On the physical examination, the patient was lethargic, with pain at palpation. She presented a severe immunosuppression with a CD4-T lymphocyte count of 23 cells/mm3 and a viral load of 167,580 copies/ml. Cerebral MRI showed mild volume loss with scattered FLAIR hyperintensities and asymmetric lesions without mass effect (Figure 2). The cerebrospinal fluid analysis showed 8 leucocytes/mm3, protein 133 mg/dL, and glucose 40 mg/dl. Cultures for bacteria, mycobacteria, and fungi were negative. PCR testing for herpes simplex virus types 1 and 2, herpes zoster virus, Epstein-Barr virus, and JC virus was negative. She continued to receive empiric treatment for neurotoxoplasmosis. During the hospitalization, she presented impaired renal function, which was attributed to sulfadiazine. The patient was started on HAART (zidovudine, lamivudine, and efavirenz). She was discharged after 62 days of hospitalization with partial neurological improvement.\nOUTPUT:" }, { "from": "agent", "value": "BK Virus Encephalitis, HIV infection" } ]

[ { "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 was lost to follow-up until 2 years later, at 12 years old, when she was admitted at the emergency room for edema, exertional dyspnea, and orthopnea. On physical examination, she was in respiratory distress, tachypneic with alar flaring, and had bilateral crackles. She was initially treated for community-acquired pneumonia and pulmonary tuberculosis, with initial blood cultures yielding Streptococcus viridans. This was treated with Penicillin G. However, despite improvement of pneumonia, she was persistently febrile. Repeat blood cultures were positive for Pseudomonas putida. The IE was then treated with a 6-week course of intravenous meropenem. Furosemide, digoxin, and enalapril were also initiated for the heart failure. Surgery to close the PDA and remove the vegetations was offered but was not done due to the lack of consent and funds. Serial TTE done during the following year did not show a significant decrease in the size of the pulmonary artery masses. She was again lost to follow-up but continued taking furosemide, digoxin, and enalapril. She returned to our institution for prenatal care. She discontinued taking furosemide, enalapril, and digoxin at the start of pregnancy. Given her history of a congenital heart disease, a TTE was ordered as part of the prenatal work-up.\nOUTPUT:" }, { "from": "agent", "value": "Pulmonary Artery and Pulmonic Valve Vegetations, Patent Ductus Arteriosus" } ]

[ { "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 79-year-old woman presented with post-menopausal bleeding and pain in lower abdomen for 2 months. The obstetric history of the patient was P2L2 and the patient had attained menopause 30 years back. The age of menarche was 14 years. On examination, a firm mass was palpable in lower abdomen extending upto umbilicus. On vaginal examination, uterus size could not be made out and a large abdomino pelvic mass was palpable. Left ovary was not seen separately and there was minimal ascites. Patient underwent staging laparotomy which revealed a 20 x 10 cm solid left ovarian tumor. The right ovary was normal and there was minimal ascites which was sent for cytology. On exploration, intestines, liver and biliary tract, pancreas, omentum, and fallopian tubes were without lesions and the uterus was of normal size. The patient underwent total abdominal hysterectomy with bilateral salpingo-oophorectomy, infra-colic omentectomy, and pelvic lymphadenectomy and the specimen was submitted for histopathological examination. Left ovary measured 21 x 14 x 10 cm and the cut section was homogenously fleshy with areas showing yellowish discoloration. The right ovary, omentum, and bilateral fallopian tubes were grossly normal. The tumor comprised mainly of fibroma-thecoma component (more than 90%) with few aggregates of granulosa cells [Figure 2]. These granulosa cell aggregates were immunoreactive for inhibin [Figure 3a] and calretinin [Figure 3b]. The omentum and lymph nodes were free of tumor. The patient did not receive radiotherapy post-operatively and she is on regular follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Ovarian stromal tumor with minor sex cord elements, Endometrial carcinoma" } ]

[ { "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: Despite these difficulties, some general trends are apparent. Under the age of 35, rates are less than 10 in 100 000 people/year (ranging from 0 to 9). Within the 35 to 44 year old age range, rates range from 22 to 45 in 100 000 people/year.\nOUTPUT:" }, { "from": "agent", "value": "Young stroke" } ]

[ { "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: In the present clinical study, we encountered one fatal case, wherein a 72-year-old female had preexisting autoimmune hepatitis with liver cirrhosis. She received daily treatment with 5 mg of prednisolone and 50 mg of azathioprine. Flu-like symptoms had developed 11 hours before she was transferred by ambulance to the National Center for Global Health and Medicine (NCGM) in Tokyo. Upon admission, the patient was conscious and able to respond to the doctor's queries. At that time, the result of the rapid influenza diagnostic test was negative, whereas the RT-SmartAmp assay gave a positive result from her nasopharyngeal swab sample (Figure 4A). Therefore, the treatment with oseltamivir was started immediately. Nine hours later, however, her respiratory condition deteriorated, and she experienced a sudden drop in blood pressure. The patient was admitted to the intensive care unit (ICU) and promptly treated with broad-spectrum antibiotics, fluid resuscitation, norepinephrine, corticosteroids, and double dose oseltamivir. Both nasopharyngeal swab and tracheal fluid samples were taken from the patient and tested with a rapid influenza diagnostic kit and the RT-SmartAmp assay. The rapid influenza diagnostic kit again gave negative results with both swab and tracheal fluid samples. However, the RT-SmartAmp assay clearly detected the 2009 pdm virus in both samples (Figure 4A). In spite of intensive treatments, however, the patient expired 52 hours after the onset of fever. There was no mutation associated with oseltamivir-resistance in the NA segment in this patient (data not shown).\nOUTPUT:" }, { "from": "agent", "value": "2009 pandemic influenza A(H1N1) virus, severe influenza virus pneumonia, septic shock" } ]

[ { "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 sixty years old male presented with 2 months history of abdominal lump, pain and dyspepsia. On clinical examination around 10 cm x 10 cm non-tender, retroperitoneal tumour was palpable. MRI of the abdomen revealed a 15 cm x 12 cm heterogeneous retroperitoneal mass involving right para spinal muscle extending deep into reteroperitoneum, right iliac fossa and right perinephric region with destruction of right transverse process and erosion of adjacent L3 vertebra. Patient was investigated further and found to have a negative metastatic workup. He underwent a wide local excision of the mass with surrounding tissue including muscles and a part of bone. Margins were labelled and sent for a frozen section which revealed negative margins. The excised tumour with labelled margins was sent for final histopathological examination. On gross examination the 15 cm x 12 cm x 7 cm specimen contained a 7 cm x 3.5 cm x 3.1 cm tumour with whitish/pale yellow cut surfaces. Haematoxylin and eosin staining showed a neoplasm with high cellularity and mostly spindle-shaped cells arranged in storiform pattern (Figure 3). All of these IHC panels came negative and increased the complexity and dilemma of diagnosis. Subsequently other immunostainings such as MDM2, cdk4 and p16 were performed (Figures 6-8). FUS-DDIT3 was negative in the tumour on PCR.\nOUTPUT:" }, { "from": "agent", "value": "Dedifferentiated Liposarcoma" } ]

[ { "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 was diagnosed with MM and was treated with five cycles of Cyclophosphamide, Bortezomib, and Dexamethasone (CYBOR-D) prior to undergoing an autologous stem cell transplant (ASCT). After the transplant, he was put on Lenalidomide for maintenance therapy. After CYBOR-D chemotherapy, anti-HBs became negative and ALT was elevated. In February 2013 his anti-HBs was positive and in December 2014 his anti-HBs was found to be negative. His anti-HCV was negative and he remained immune to hepatitis A. An abdominal ultrasound was unremarkable and a FibroScan was consistent with F1 (minimal) fibrosis. At 4 months' follow-up, he remained asymptomatic from a liver perspective.\nOUTPUT:" }, { "from": "agent", "value": "HBV reactivation" } ]

[ { "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 53-year-old asthmatic male with a previous history of carcinoma of tongue subjected to left hemiglossectomy with suprahyoidal neck dissection 10 years back, was presented with right cervical lymphadenopathy and fever. He was normotensive and euglycemic. He denied of any weight loss, night sweats, and cough. C-reactive protein was negative and ultrasonography of neck had showed multiple bilateral cervical lymphadenopathy. Suspecting it to be metastatic disease, a whole body F-18 FDG PET/CT was performed which showed metabolically active cervical, mediastinal, abdominal, pelvic, left inguinal and femoral lymph nodes [Figure 1]. Diffuse low-grade uptake noted in the region of soft palate, base of tongue, and valleculae was considered to be physiological. The pattern of increased FDG uptake is not typical for squamous carcinoma for head and neck metastasis and so it raised the possibility of lymphoma. FNAC showed the Ziehl-Neelsen staining to be strongly positive for acid-fast bacilli [Figure 2]. Tuberculin skin test was positive (15 mm induration after 48 h). The patient was started on first line antitubercular medication. Six months later after the initiation of therapy, a follow-up whole body F18-FDG PET/CT scan showed a significant resolution of previously FDG avid lymph nodes but for residual hypermetabolism at right cervical level I, right paratracheal and right axillary lymph nodes [Figure 3]. The maximum standardized uptake value (SUVmax) of different lymph nodes before and after therapy is depicted in Table 1.\nOUTPUT:" }, { "from": "agent", "value": "Extra-pulmonary tuberculosis" } ]

[ { "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: Clinical and Pharmacokinetic Profile of Lithium Monotherapy in Exclusive Breastfeeding. The variation in transfer is just one reason behind this advice. Objectives: To present clinical and pharmacokinetic data of nine mother-infant pairs exposed to lithium monotherapy during late pregnancy and exclusive breastfeeding at the Perinatal Psychiatric Unit (2006-2018). Methods: We obtained sociodemographic data, medical risk factors, obstetric variables, and family and personal psychiatric history by semi-structured interview, and assessed maternal psychopathology with the Hamilton Depression Rating Scale and Young Mania Rating Scale. A senior neonatologist reviewed neonatal outcomes at birth using the Peripartum Events Scale. Paired maternal and cord blood and infant venous blood samples were collected. During the breastfeeding period, we monitored serum lithium and creatinine concentrations in mother-infant pairs at delivery, and at days 1-5, 7-11, 30, and 60 postpartum, and monthly until 6-months. Results: Lithium equilibrated completely across the placenta [1.13 (0.10), range (1.02-1.30)]. No women presented symptoms of postpartum lithium intoxication, two of the neonates presented transient hypotonia (22%). Lithium exposure was significantly less during breastfeeding than during late pregnancy, and serum lithium concentrations decreased up to 44% overtime from delivery to the first-month, and up to 60% to the third-month postpartum. There was no growth or developmental delay in the follow-up period. One woman had a manic episode with psychotic features at 45 days postpartum. Image Caption and Description: \nImage caption: []\nImage description: []\nCase Report: \nBreastfeeding has many important health advantages for both mothers and their children. recommend exclusive breastfeeding for the first 6 months of life whenever possible, before combining it with complementary foods until the infant is 1-2 years old. Two recent systematic reviews of clinical studies into lithium use during breastfeeding found limited evidence about whether one should initiate, maintain, or discontinue lithium during breastfeeding. The aim of this study was to examine serum lithium concentrations in mothers and their exclusively breastfed term infants from delivery.\nOUTPUT:" }, { "from": "agent", "value": "Bipolar disorder" } ]

[ { "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: Had excessive contraction of orbicularis, while sipping a straw use. She complained of any choking with any type of consistency but especially with liquids. In the second call, she reported improvement of gagging and, as the years to adjust the sensitivity, said it was \"very good nothing to do with his mouth than eat.\" Reported some difficulty with the use of straw as it limited the amount she wanted to consume. On the other hand, she was concerned referring drank much more before the operation. After the procedure, she reported that ingested liquid quickly and felt sense of esophageal stopping, saying it should maintain attention during meals.\nOUTPUT:" }, { "from": "agent", "value": "Deviated septum, muscle tone alterations in lips, tongue, cheeks and chin, incoordination of language movements, swallowing difficulties" } ]

[ { "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 13-yr old boy presented with near-daily attacks of mild to severe paralysis for the past 8 yr. The symptoms mainly appeared in the morning and he usually awakened with weakness of the four limbs to the point of difficulty in sitting and walking. After the paralytic episode in the morning, he was free of symptoms in the afternoon, but eating high-sodium or carbohydrate foods and rest after vigorous exercise made him weak or completely paralyzed again at any time. In family history, his mother (41 yr old), maternal-grandmother (81 yr old), maternal aunt (55 yr old) and her two sons (the patient's cousins, 23 and 27 yr old) were also suffering from similar attacks of weakness or paralysis throughout their lives (Fig. 1). The severity and frequency of attacks of grandmother and mother has decreased with age. Two cousins of the proband were diagnosed HOPP 8 yr ago at our hospital. They were treated with acetazolamide and potassium supplements. Because there is no effect of such treatment, they stopped taking the drugs and they were lost further medical support. On admission, the proband showed non-specific findings in physical examination, radiologic and laboratory findings including muscle enzymes. During paralytic episodes, the patient showed low serum potassium levels (3.2 mEq/L vs. 4.4 mEq/L between attack) and hypokalemic ECG findings, such as ST segment depression and U-wave. There was no myotonia in EMG findings. DNA examination identified a nucleotide 3705 C to G mutation in exon 30 of CACNA1S gene (Table 1). This mutation predicts codon change from arginine to glycine at amino acid position #1239 of axon 30 in the calcium channel gene (Fig. 2). The patient was treated with spironolactone (25 mg b.i.d. ), and he showed a dramatic improvement in his symptoms within 2 days. Other affected members of the family, including two cousins of the proband, have also started taking spironolactone. They could also themselves awaken refresh and move at their will throughout the day.\nOUTPUT:" }, { "from": "agent", "value": "Hypokalemic Periodic Paralysis" } ]

[ { "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 diagnosis, the majority of the patients had normal or slightly increased leukocyte counts, with relative lymphocytopenia and relative neutrophilia, mild hyponatremia, thrombocytopenia, elevated inflammatory markers (CRP to 478.8 mg/l; IL-6 to >5,000 pg/ml; ferritin to 1,250 mug/l, sedimentation rate to >119 mm in the 1st hour, triglycerides to 380 mg/dl), hypoalbuminemia, elevated cardiac enzymes (maximum pro-BNP of 89367 ng/l, maximum high-sensitivity troponin I value of 20,308 ng/l) and elevated D-dimer. SARS-CoV-2 antibodies (IgG) were elevated in all patients (3-9 times above the cut-off; from 42 to 121 U/ml, reference value <12 negative, >15 positive). Viral or bacterial infections were ruled out in all patients. Additional details on laboratory findings, and the course of fever are presented in Figures 1-5. Echocardiography showed significantly impaired left-ventricular (LV) function in two patients [systolic function (SF) 20-25%], and moderately impaired LV function in three patients (SF 33-35%). Two patients had echogenic coronary swelling without evidence of coronary aneurysm, six patients had minor tricuspid valve regurgitation, and four had additional minor mitral valve regurgitation. Ultrasound investigation of the abdomen revealed mesenteric lymphadenitis in three patients, edema of the gallbladder wall in two patients, hepatosplenomegaly in one patient, hepatomegaly with signs of hyperemia in both testicles and epididymis in one patient. One patient underwent surgery due to suspected appendicitis, with intraoperative findings of mesenteric lymphadenitis, an ulcerous appendix and peritonitis. However, the patient's condition deteriorated after 3 days: he had fever, signs of inflammation, and elevated cardiac enzymes. The patient developed Kawasaki-like symptoms including rash, bilateral conjunctivitis, palmar edema, and injected and fissured lips.\nOUTPUT:" }, { "from": "agent", "value": "Multisystem Inflammatory Syndrome in Children (MIS-C)" } ]

[ { "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 man presented to his local emergency department the day after sustaining a fall from a standing height. He complained of back pain but experienced no lower extremity numbness, weakness, or sciatica. On examination he was neurologically intact and ambulated without aids. (1-3). 4). Although surgery was discussed as a treatment option, the patient was not keen on operative stabilization of his fracture. In addition to the patient's wishes, we also took into consideration his age and comorbidities of emphasema and peripheral vascular disease in deciding on nonoperative treatment. Therefore, he was instructed to wear a Jewett back brace while standing or walking. The patient was further instructed to avoid exercises and heavy or repetitive use of his back. His treatment plan was to monitor his progression, both clinically and with xrays, at 5 weeks, 3 months, 6 months, 9 months and 13 months. When the patient presented over time at follow-up clinics, he noted a steady continuous improvement in his back pain and his ability to function. At 3 months he was independent in activities of daily living, and had switched from his back brace to using a lumbosacral corset. At 6 months he was increasing his mobilization and was able to resume playing darts. At 9 months he reported exercising at the gym 3 times per week. At this time he also reported performing his activities of daily living with ease. At the final follow-up visit which occurred at 13 months, the patient had discontinued the use of his brace. He had increased his activity and reported experiencing only minor and transient back pain after using a shovel. He had no signs or symptoms of neurologic dysfunction. At this time his x-rays showed callous formation anteriorly and laterally between the L1 and L2 vertebral bodies Figs. (1 and 3), mature bridging bone across the middle and posterior columns at L1 and L2 on the lateral view Figs. (1 and 2). There was no change in the sagittal or coronal alignments (Figs. 1 & 3).\nOUTPUT:" }, { "from": "agent", "value": "Lumbar Spine Extension Injury, Ankylosing Spondylitis" } ]

[ { "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 Caucasian female patient presented with a painless swelling in the soft palate, breathing and swallowing difficulties, and suffocation feeling. Clinical examination revealed that the lesion was located mostly in the right side, extending from the limit between the hard and soft palate and continuing to the oropharynx. The lesion had smooth surface, hard consistency, and irregular shape (Figure 1(a)). Cervical tomography was requested (Figures 1(b) and 1(c)). Based on clinical and imaging aspects, a hypothesis of benign X malignant salivary gland tumor was formulated. An incisional biopsy was performed under local anesthesia to establish the definitive diagnosis. However, the histopathological examination of the fragment revealed normal mucosa (Figure 2(a)). The professionals decided to perform a second conventional biopsy giving attention to collecting material from a greater depth. Once again, the histopathological analysis revealed normal mucosa (Figure 2(b)). The otorhinolaryngologist team was consulted and the decision was made to perform a CNB. The localization of the lesion was identified during the intraoral exam with no need of imaging guidance (Figure 3). In CNB a needle is activated by an automatic spring system equipped with outer cannula and inner stylet. Under local anesthesia using 1% lidocaine the biopsy area was chosen with palpation of the lump and the tip of the needle was positioned adjacently to the lesion. The handpiece was activated, moving quickly 20 mm back and forth, cutting a sample measuring 17 mm in length. Only one core of tissue was obtained and carefully removed from the biopsy needle. The quality of the specimen was assessed by visual inspection and, with care not to damage the thin tissue, it was put into 10% formalin for fixation. The biopsy site was compressed for five minutes to avoid bleeding and the patient was observed for more 30 minutes and later discharged as no signs or symptoms as bleeding or pain were noted. The patient was referred to the head and neck service for complete resection of the tumor. The specimen was sent to the pathology service and the histopathological analysis confirmed the diagnosis established with CNB (Figure 4(c)). No complications occurred in the postoperative period and no signs of recurrence were found at the 12-month follow-up (Figure 4(d)).\nOUTPUT:" }, { "from": "agent", "value": "Pleomorphic adenoma" } ]

[ { "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: Following disease progression despite doxorubicin, the decision was made to treat with ifosfamide. Chemotherapy was delivered as outlined in Table 1, Case 2. Each cycle of ifosfamide was given as one dose, three weeks apart. Escalating doses of ifosfamide were administered over three cycles as follows: 1.5 g/m2, 1.8 g/m2, and 2 g/m2. The first cycle was administered as an inpatient and was followed by hemodialysis approximately 3 hours after ifosfamide infusion. Cycles 2-3 were given as an inpatient and the patient then received her regular hemodialysis at her local outpatient dialysis unit 2-3 hours later. The patient did report some softening of her intraabdominal masses and decreased abdominal distension following the first two cycles. A repeat scan done after cycle 2 showed no interval increase in tumor size. Two weeks after the final cycle, she reported painful neuropathy in the left lower extremity. A consulting neurologist felt that this presentation and distribution of symptoms was more consistent with a plexopathy as opposed to a toxin mediated neuropathy. No spinal involvement with tumor was noted on MRI or CT of the abdomen and pelvis. Imaging performed after the third cycle showed interval decrease in the size of some intraabdominal nodules with additional nodes in the retroperitoneum and peritoneal cavity and new hydronephrosis and hydroureter. Due to chronic pain and progressive disease, the patient opted for palliative care. She expired 8 months later.\nOUTPUT:" }, { "from": "agent", "value": "Metastatic leiomyosarcoma, End stage kidney disease" } ]

[ { "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 57 year old lady presented to a peripheral hospital with complaints of penetrating epigastric pain of a week's duration. There was no vomiting or weight loss. Bowel movements were normal. Clinical examination at the time was unrevealing. An abdominal ultrasound examination was reported as normal. The patient's insistence on full investigation of the persistent epigastric pain led to a computed tomographic examination and discovery of a pancreatic tumour subsequent to which she was referred to our institution. The CT scan (Figure 1) showed a large tumour (6cm in largest diameter) in the body and tail of pancreas with no evidence of metastasis. She was prepared for exploratory laparotomy. The pancreas was explored through the gastrocolic omentum. The body and tail of the pancreas including the tumour were resected (Figure 2). The spleen was also removed. The end of the pancreas was suture ligated. Her post-operative recovery was uneventful. Histological examination of the specimen (Figure 3) showed a well circumscribed ovoid tumour 60mm x 50mm across. Sections revealed islands and trabeculae of regular cells with variable amounts of eosinophilic cytoplasm, mostly regular nuclei with indistinct nucleoli. Areas of necrosis were present with hemorrhage. A fibrous pseudo-capsule was noted around the tumour and the resection of the tumour appeared complete. No capsular of vascular invasion was seen. Immuno-peroxidase staining was positive for chromogranin A. Synaptophysin was strongly positive (Figure 4), CD10 was negative, Ki-67 was less than 2% positive and the mitotic count was between 2-20 per 10 hpf. The staining reactions were confirmatory of a neuroendocrine carcinoma of the pancreas. The final staging of the completely excised tumour was T3 N0 M0. Following discharge, she was followed up regularly and remains symptom free. A CT Scan performed 2 years after surgery (Figure 5) showed no evidence of tumour recurrence.\nOUTPUT:" }, { "from": "agent", "value": "Pancreatic neuroendocrine neoplasm" } ]

[ { "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 41-year-old Japanese man became aware of abdominal swelling in December 2008 but did not seek a medical opinion until he developed marked leg edema, a 30 kg weight gain, and cough. He was hospitalized the same day after a retroperitoneal tumor was detected by computed tomography (CT). On admission his body surface area was 2.18 m2. A CT scan detected a 43 x 37 x 31 cm tumor in the right retroperitoneum, with the right kidney significantly displaced to the left and anterior side (Figure 1). Whole-body CT scan detected no metastasis. We concluded that surgical resection was the only option for saving the patient's life, so we performed a tumorectomy 3 weeks later through a midline incision. The operation took 3 hours and 20 minutes, and the estimated blood loss was 3990 mL requiring 800 mL blood transfusion. During surgery, the tumor and right kidney were completely resected. Pathological examination showed that the resected mass weighed 22 kg and was 45 x 40 x 30 cm in size (Figure 3). Grossly, the tumor was well encapsulated and transverse sectioning revealed a solid multinodular tumor mass. Microscopically, no tumor cells were identified in the right kidney and this was an R0 resection. He declined adjuvant therapy. The patient was discharged from our hospital after 18 days. His body surface area at discharge was 1.66 m2. A CT scan performed 12 months after surgery detected no recurrence.\nOUTPUT:" }, { "from": "agent", "value": "Giant Liposarcoma, Respiratory Failure" } ]

[ { "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 a 33-year-old nulligravida female whose husband had asthenoteratospermia. Tubal patency had been demonstrated with hysterosalpingography. The day 3 FSH level was 2.6 IU/mL, and LH level was 2.1 IU/mL. The long protocol of pituitary desensitization was commenced and maintained with daily injection of 0.1 mg of triptorelin (Arvekap, Ipsen) administered on day 21 of the preceding menstrual cycle, for 2 weeks. Ovulation induction was achieved with daily subcutaneous injections of 300 IU of recombinant human FSH (Gonal F, Serono). On day 13 of stimulation, sonography of the left ovary showed 10 follicles of 19 mm in mean diameter and 5 smaller follicles (16 mm in mean diameter); the right ovary had 12 follicles of 19 mm in mean diameter and 6 smaller follicles. Estradiol level was 1741 pg/mL. A dose of 5,000 IU of hCG was administered intramuscularly on day 13, and oocyte retrieval was scheduled at 36 hours later on day 15. Late in the afternoon on day 14, the patient had a sudden onset of lower left abdominal pain with nausea. A physical examination revealed lower abdominal tenderness especially on the left side and signs of peritonitis on day 15. Transvaginal oocyte retrieval was undertaken. No oocytes were retrieved from the left ovary; 18 oocytes were obtained from the right ovary. After the procedure was completed, the patient's symptoms worsened. The ovary was detorsed under laparoscopic control and peritoneal lavage was performed. Antibiotics were given for 10 days. The patient's clinical symptoms resolved 2 days later, and transcervical transfer of 4 embryos, created from retrieved oocytes of the right ovary, was performed on day 18. Unfortunately, pregnancy did not ensue.\nOUTPUT:" }, { "from": "agent", "value": "Empty follicle syndrome, Ovarian torsion" } ]

[ { "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 male with splenomegaly and asthma presented with 2 months of progressive abdominal distension. His initial laboratory tests were notable for INR 1.6, platelets 139/microL, and total bilirubin 3.9 mg/dL. Peritoneal fluid studies revealed a serum-ascites albumin gradient (SAAG) of 1.3 and total protein of 3.8. The patient was started on a heparin infusion. His hypercoaguable work-up was negative. Venography demonstrated multiple spider collaterals and a clot in the right hepatic vein with a hepatic venous pressure gradient (HVPG) of 24 mm Hg. Liver biopsy showed centrilobular necrosis with marked congestion of zone 3. The patient underwent TIPS placement with a decrease in HVPG from 18 mm Hg to 5 mm Hg (Figure 1). After TIPS placement, he was noted to have elevated liver enzymes in a cholestatic pattern. ERCP showed stenosis at the takeoff of the left intrahepatic duct due to extrinsic compression from the TIPS (Figure 3). The stenosis was dilated (Figure 4), and a 7-French x 15-cm plastic stent was deployed without complications (Figure 5). His liver enzymes improved and his ascites resolved. A larger 10-French x 15-cm plastic stent was placed upstream of the stenosis, with plan for removal in 6 to 9 weeks.\nOUTPUT:" }, { "from": "agent", "value": "Budd-Chiari Syndrome, Biliary Obstruction" } ]

[ { "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 30-year-old patient presented with 2 days history of fever and dyspnea. His initial assessment showed high inflammatory markers (CRP 141 mg/L) accompanied with mild disturbance in his hepatic profile. He was diagnosed with SARS-CoV-2 infection on nasopharyngeal swab. On day two, he was admitted to the ICU for severe hypoxia and acute hepatic cytolysis. In the setting of severe ARDS, he was intubated for 12 days, placed on ECMO for 29 days, and sedated with ketamine (total 6 g) for 8 days. Six sessions of prone positioning were performed. His hospitalization was complicated by venous thrombosis and acute kidney injury that required 30 sessions of haemodialysis. He was treated with dexamethasone, lopinavir /ritonavir, tocilizumab, anakinra, and therapeutic anticoagulation. During his stay, the patient had abnormal liver function tests (Fig. 1). He had neither active HIV nor viral hepatitis (A, B, C, and E) infections. He had EBV reactivation with spontaneous resolution and CMV reactivation with viremia (3.3Log) treated with ganciclovir for 14 days. Plasma CMV viral load was undetectable on day 60. No autoimmune antibodies were detectable. Hepatic ultrasound was normal. Histology of liver biopsy done on day 62 showed cholestatic hepatitis lesions and bile ducts dystrophy suggesting a viral cytopathic effect. Viral panel performed on liver biopsy was negative (SARS-CoV-2, CMV, EBV, HSV-1, HSV-2, VZV, adenovirus and enterovirus). Throughout his hospital stay, his hepatic profile showed only persistent cholestatic disturbance. After nine months from his CoVID-19 illness, he developed liver failure with ascites and prolonged prothrombin time (54 s). He ended up having a liver transplant 11 months after his admission for CoVID-19. Histology report of hepatic explant showed extensive portal fibrosis, biliary infarction, and cholangitic lesions. Also, there was atrophy of central areas suggesting an ischemic etiology.\nOUTPUT:" }, { "from": "agent", "value": "Cholangitis" } ]

[ { "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 17-year-old girl presented with hand tremors at rest and worsened by stress. Tracing back her medical history, it was found that the onset of the tremors in both hands had occurred for 6 months. The patient's handwriting was atrocious and illegible. Her daily activities and learning became more problematic and difficult. Clinical examination revealed the features of extrapyramidal symptoms included tremors with a frequency of about 4-6 Hz, mainly in the upper extremities, slow and scribbled writing. Furthermore, there were no signs of pyramidal tract lesions, ophthalmoplegia or hallucinations, and behavior disorders. Although the patient had malaise, she could still manage to walk independently. The clinical features of slowly progressing extrapyramidal symptoms in a young patient suspected that a metabolic disorder or intoxication affecting central gray nuclei. With respect to laboratory findings, that diagnosis was supported. The elevated 24 h ceruloplasmin level (224 mug/day [<40 mug/day]) and the decreased serum ceruloplasmin level (3 mg/dL [20-40 mg/dL]) were identified. Complete blood count biochemistry and urinary routine were within normal limits. Brain MRI showed high signal intensities of both basal ganglia, head of caudate nucleus in T2W, fluid-attenuated inversion recovery, and diffuse-weighted imaging [Figure 1]. Abdominal ultrasound revealed morphological changes in the liver with regenerative nodules, consistent with cirrhotic image. Serum transaminase (AST and ALT) and prothrombin time were normal. A slit-lamp examination revealed a typical Kayser-Fleischer ring. Therefore, the patient has performed sequencing of 21 exons on the ATP7B gene and detected two pathogenic mutations c.2333G>T (p.R778L) and c.314C>A (p.S105X). The patient has received trihexyphenidyl (10 mg/day) and trientine (1.5 g/day) and had no significant side effects. After about 6 months of treatment, the movement function has partially improved, her writing and movement have been more flexible.\nOUTPUT:" }, { "from": "agent", "value": "Wilson disease" } ]

[ { "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 lady presented to our emergency department with a one-week history of fever and localised RIF pain. CT scan performed on admission delineated a dilated and ill-defined appendix with focal perforation at its tip (Figure 3). There was an adjacent abscess with surrounding fat-stranding as well as reactive thickening of the caecum and terminal ileum with prominent ileocolic lymph nodes. The patient was initially treated conservatively with intravenous antibiotics. She represented approximately 2 weeks later due to worsening symptoms. Repeat CT scan (Figure 4) demonstrated a stable collection and CT-guided drainage was performed. As the drain output progressively decreased, this tube was removed after 7 days. She returned another two and a half months later for nonresolving symptoms. The repeat CT scan (Figure 5) revealed an irregular lobulated mass with central necrosis at the ileocaecal junction associated with small bowel obstruction. New small soft-tissue nodules were observed adjacent to the mass and along the track of previous drain insertion. The adjacent mesenteric lymph nodes were enlarged and necrotic. A new hypodense lesion in the caudate lobe of the liver was also identified, suspicious for a metastasis (Figure 6). The patient underwent an open right hemicolectomy with en bloc right salpingooophorectomy. Intraoperative findings revealed a mass involving and encasing the terminal ileum as well as involving the right fallopian tube, ovary, and ureter and extending into the pelvic side wall. A separate appendix was not identified within the mass. Multiple peritoneal nodules were evident in the omentum and as far up as the hepatic dome.\nOUTPUT:" }, { "from": "agent", "value": "Adenocarcinoma" } ]

[ { "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 woman was admitted to the hospital because of shortness of breath. The symptoms started one month before admission and worsened over the following weeks. On the day before admission, the patient's condition worsened, and she experienced substernal chest pain and palpitations. She had a history of hypertension and type 2 diabetes mellitus. On physical examination, mild distress, tachypnea, and tachycardia were observed. There was a pulsus paradoxus of 10 mmHg (110 mmHg decreasing to 100 mmHg). She was normoxemic while breathing ambient air. Mild jugular venous distention was also observed. Heart auscultation revealed mildly diminished heart sounds. A 12-lead electrocardiogram revealed sinus tachycardia. Bedside echocardiogram showed circumferential pericardial effusion and respiratory variation in the intracardiac flows; all findings were consistent with increased intrapericardial pressure (Figure 1A). Chest computed tomography (CT) showed mild left pleural effusion and signs of circumferential pericardial effusion (Figure 1B). The patient underwent an urgent surgical pericardial window with a pericardial biopsy. Approximately 550 mL of bloodstained fluid with exudative properties was removed from the pericardium. Fluid analysis revealed three leukocytes. The adenosine deaminase level was 37 IU/mL. Polymerase chain reaction for Mycobacterium tuberculosis complex showed negative results. Histological analysis of the pericardium did not reveal any granulomas; however, acid-fast bacilli were identified (Figure 2). The patient had a favorable evolution and was discharged after one week. Posterior culture from the pericardial tissue was negative.\nOUTPUT:" }, { "from": "agent", "value": "Tuberculous pericarditis" } ]

[ { "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 43-year-old woman with migraines, anxiety, and a vague history of irritable bowel syndrome complained of excessive postprandial pharyngeal secretions for six months, which were associated with cough, nausea, and vomiting. She also endorsed abdominal pain following ingestion of spicy foods but denied hematemesis, melena, weight changes, or rectal bleeding. A Helicobacter pylori breath test was negative, and she was empirically treated for gastroesophageal reflux disease with rabeprazole, resulting in the resolution of only her abdominal discomfort. The patient then underwent EGD and colonoscopy, which demonstrated mild reflux esophagitis, a sessile serrated adenoma of the cecum, a tubular adenoma of the sigmoid colon, as well as erythematous, congested, and nodular gastric mucosa (Figure 1(b)). These findings were most consistent with CG. Human leukocyte antigen (HLA) testing was not performed, but her duodenal biopsy had also shown no disruption of normal villous architecture. She was ultimately recommended to avoid nonsteroid anti-inflammatory drugs (NSAIDs) and to begin a low-gluten diet, resulting in complete symptom resolution. One and one-half years later, the patient developed diffuse myalgias. Extensive rheumatologic laboratory testing provided no evidence for a connective tissue disease or inflammatory myopathy. At four years of follow-up, the patient continued to deny gastrointestinal complaints despite unchanged gastric mucosal findings observed by EGD/colonoscopy.\nOUTPUT:" }, { "from": "agent", "value": "Collagenous Gastritis, Myofascial pain syndrome/fibromyalgia" } ]

[ { "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 50-year-old male was referred to the Department of General Surgery at Jordan University Hospital, Amman, Jordan, complaining of right lower lip paresthesia and right facial pain radiating to the right ear of five-month duration. The patient was diagnosed in the private sector to have trigeminal neuralgia and was treated by Carbamazepine for two months. A month prior to admission, the patient started developing right facial swelling. Physical examination revealed right non-tender immobile parotid swelling without overlying skin changes. Trismus, right cervical and supraclavicular lymphadenopathy were also noted. There was no facial weakness. The patient has lost 20 kg over the last 2 months prior to admission. Lab tests were performed and revealed hypercalcemia (calcium 12.20 mg/dL), hypoparathyroidism (PTH 5.6pg/mL), elevated aspartate aminotransferase (AST 110 u/lit) and lactate dehydrogenase (LDH 349 u/lit) were also noted. Right parotid glandfine-needle aspirationcytology(FNA) was conducted twice due to inadequacy and showed multilayered sheets of cells with eccentric nuclei, granular cytoplasm, occasional prominent nucleoli and occasional mitotic figures, suspicious for malignancy. The cells were diffusely positive for CD-10 and AMACR with focal positivity for CK7. They were negative for C-kit immunostains. This immune profile favors RCC over the others. Microscopically all the slides show a hemorrhagic smear containing scattered sheets and clusters of plasmacytoid and cuboidal cells having abundant cytoplasm and showing mild nuclear pleomorphism. The cytoplasm is granular and occasionally containing few vacuoles (Fig. 1). 2-6).\nOUTPUT:" }, { "from": "agent", "value": "Renal Cell Carcinoma" } ]

[ { "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 was a 68-year-old woman with a history of chronic ulcerative colitis refractory to medical therapy who underwent total colectomy three years prior to presentation. She also had a history of paroxysmal nocturnal hemoglobinuria requiring long-term corticosteroid therapy, aplastic anemia, and diabetes mellitus. She had no previous history of opportunistic infections. The patient presented initially with a left proximal radial fracture, a left intertrochanteric femoral fracture, and hypothermia having fallen on ice with prolonged environmental exposure. Prior to undergoing operative repair of her fractures, she developed disseminated intravascular coagulation, sepsis, and multiorgan system failure (including pulmonary, renal, and hepatic). Despite appropriate antibiotic coverage for positive blood cultures for Enterobacter cloacae and tracheal secretion cultures positive for Staphylococcus aureus and Klebsiella pneumoniae, the patient developed persistent fever and clinical deterioration. Two weeks after initial presentation, the patient developed a 5 by 6 cm ecchymotic wound of the dorsum of the right hand that progressed rapidly to epidermolysis and necrosis extending to the extensor tendons; it was conjectured at the time that the site was a previous peripheral IV access site, but no clinical documentation confirmed that possibility. Cultures of debrided tissue grew many Rhizopus spp. Patient's WBC was elevated at 28,000 WBC/microlitre (4,500-10,000 white blood cells per microlitre around the time she presented with the lesion. Despite surgical debridement and treatment with intravenous amphotericin B deoxycholate the wound infection progressed, with aerial hyphae visible on exam 4 days after initial clinical manifestation. The patient died of progressive multiorgan failure one week later. An autopsy was refused.\nOUTPUT:" }, { "from": "agent", "value": "Mucormycosis" } ]