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PMCPatients_common1004
[ { "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 nasopharyngeal swab test was found positive for SARS-CoV-2 and the patient was treated with non-invasive ventilation due to respiratory distress. After 11 days, the patient became lethargic and showed negative upper limbs myoclonus and random, involuntary, and rapid vertical eye movements. Kidney and liver function biomarkers, serum electrolytes and ammonia were normal, head CT scan and toxicological examination resulted negative. Clinical evaluation (myoclonic positive and negative jerks, and altered mental status) was compatible with NCSE diagnosis, while EEG revealed generalized epileptic discharges with bilateral frontal high amplitude delta waves (Fig. ). At first, intravenous Valproic Acid (2000 mg/24 h iv) and secondarily Levetiracetam infusion (3000 mg/24 h iv) were started but led to no clinical nor EEG improvement. Early diagnostic work-up was performed as follows: contrast-enhanced MRI—negative results; serum VDRL and hepatitis virus panel—negative; CSF analysis—CSF protein concentration was 53.9 mg/dL, glucose 104 mg/dL, 1 mononuclear white blood cell, CSF culture and PCR yielded negative results, as well as serum and CSF onconeural antibody and antineuronal surface antigens antibody. IVIG therapy was initiated at 0.4 g/kg for 5 days. After the first 5-day cycle, due to the scarce response (remission of myoclonic jerks and vigilance partial improvement), a second 5-day IVIG cycle was started with a progressive improvement of both clinical and EEG features (Fig. ) without side effects. The patient was dismissed from the hospital without severe cognitive defects and with a partial decrease of antiepileptic drugs.\nOUTPUT:" }, { "from": "agent", "value": "COVID-19 bilateral pneumonia, seronegative autoimmune encephalitis-related NORSE" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The nasopharyngeal swab test was found positive for SARS-CoV-2 and the patient was treated with non-invasive ventilation due to respiratory distress. After 11 days, the patient became lethargic and showed negative upper limbs myoclonus and random, involuntary, and rapid vertical eye movements. Kidney and liver function biomarkers, serum electrolytes and ammonia were normal, head CT scan and toxicological examination resulted negative. Clinical evaluation (myoclonic positive and negative jerks, and altered mental status) was compatible with NCSE diagnosis, while EEG revealed generalized epileptic discharges with bilateral frontal high amplitude delta waves (Fig. ). At first, intravenous Valproic Acid (2000 mg/24 h iv) and secondarily Levetiracetam infusion (3000 mg/24 h iv) were started but led to no clinical nor EEG improvement. Early diagnostic work-up was performed as follows: contrast-enhanced MRI—negative results; serum VDRL and hepatitis virus panel—negative; CSF analysis—CSF protein concentration was 53.9 mg/dL, glucose 104 mg/dL, 1 mononuclear white blood cell, CSF culture and PCR yielded negative results, as well as serum and CSF onconeural antibody and antineuronal surface antigens antibody. IVIG therapy was initiated at 0.4 g/kg for 5 days. After the first 5-day cycle, due to the scarce response (remission of myoclonic jerks and vigilance partial improvement), a second 5-day IVIG cycle was started with a progressive improvement of both clinical and EEG features (Fig. ) without side effects. The patient was dismissed from the hospital without severe cognitive defects and with a partial decrease of antiepileptic drugs. OUTPUT:
PMCPatients_common2665
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An 18 year old Sri Lankan Muslim female, presented with a 9 month history of colicky right iliac fossa pain and a 5 kg weight loss. Clinical examination was normal.\\nColonoscopy revealed an ulcerated ileocaecal valve and a terminal ileal stricture, while the colon itself was macroscopically normal. Biopsy of these lesions was reported as suggestive of CD. TB polymerase chain reaction (PCR) performed on the specimen was negative. Contrast-enhanced CT abdomen showed a segment of terminal ileum with concentric wall thickening. Mantoux test and Quantiferon gold test for TB were negative and chest X-ray was normal.\\nShe was started on treatment for CD with a short course of oral steroids followed by azathioprine. However, she failed to tolerate azathioprine and subsequently 6-mercaptopurine (6-MP), and therefore was started on intravenous infliximab. Despite 3 dose of infliximab she failed to respond, and a follow up colonoscopy showed persistence of the ileal stricture. Therefore she was referred for surgical resection of the involved ileal segment. During the laparotomy, multiple terminal ileal and cecal strictures were noted and unexpectedly, multiple omental and peritoneal deposits were also seen. A limited right hemicolectomy including resection of the involved terminal ileum was performed.\\nHistology of the resected specimen showed multiple coalescent caseating granulomata involving full thickness of the bowel wall and extending into the mesentery and pericolic fat, suggesting a diagnosis of ITB (Figs. , ). No evidence of dissemination beyond the intestine was found. She was started on anti-TB treatment (ATT), and 2 months later was free of abdominal pain and has regained 3 kg of weight. Three months after commencing ATT a repeat colonoscopy was performed. There were no macroscopic or microscopic changes in the neo-terminal ileum or residual colon. She completed 6 months of ATT and made a full recovery.\nOUTPUT:" }, { "from": "agent", "value": "Intestinal tuberculosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 18 year old Sri Lankan Muslim female, presented with a 9 month history of colicky right iliac fossa pain and a 5 kg weight loss. Clinical examination was normal.\nColonoscopy revealed an ulcerated ileocaecal valve and a terminal ileal stricture, while the colon itself was macroscopically normal. Biopsy of these lesions was reported as suggestive of CD. TB polymerase chain reaction (PCR) performed on the specimen was negative. Contrast-enhanced CT abdomen showed a segment of terminal ileum with concentric wall thickening. Mantoux test and Quantiferon gold test for TB were negative and chest X-ray was normal.\nShe was started on treatment for CD with a short course of oral steroids followed by azathioprine. However, she failed to tolerate azathioprine and subsequently 6-mercaptopurine (6-MP), and therefore was started on intravenous infliximab. Despite 3 dose of infliximab she failed to respond, and a follow up colonoscopy showed persistence of the ileal stricture. Therefore she was referred for surgical resection of the involved ileal segment. During the laparotomy, multiple terminal ileal and cecal strictures were noted and unexpectedly, multiple omental and peritoneal deposits were also seen. A limited right hemicolectomy including resection of the involved terminal ileum was performed.\nHistology of the resected specimen showed multiple coalescent caseating granulomata involving full thickness of the bowel wall and extending into the mesentery and pericolic fat, suggesting a diagnosis of ITB (Figs. , ). No evidence of dissemination beyond the intestine was found. She was started on anti-TB treatment (ATT), and 2 months later was free of abdominal pain and has regained 3 kg of weight. Three months after commencing ATT a repeat colonoscopy was performed. There were no macroscopic or microscopic changes in the neo-terminal ileum or residual colon. She completed 6 months of ATT and made a full recovery. OUTPUT:
PMCPatients_common4081
[ { "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 a 2-year history of idiopathic abdominal pain. Laboratory investigations revealed that renal- and liver-function tests, blood-cell counts, urinalysis, serum electrolytes, aldosterone, free plasma metanephrines, and 24-hour urine levels of catecholamines were all within normal ranges. Renal ultrasound examination of the abdomen was normal, with both kidneys normal size. Doppler-derived renal resistive index revealed elevated values (0.78 on the left and 0.8 on the right). Thoracic and abdominal MR angiogram revealed reduced caliber of the abdominal aorta and celiac trunk, stenosis of the upper mesenteric artery, irregular right renal artery with reduced caliber, and narrowed left renal artery at its emergence (). Ophthalmological findings were unremarkable. This regimen failed to control blood pressure, so angioplasty was scheduled.\nOUTPUT:" }, { "from": "agent", "value": "Neurofibromatosis 1, Middle Aortic Syndrome, Secondary Hypertension, Dextrocardia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: He had a 2-year history of idiopathic abdominal pain. Laboratory investigations revealed that renal- and liver-function tests, blood-cell counts, urinalysis, serum electrolytes, aldosterone, free plasma metanephrines, and 24-hour urine levels of catecholamines were all within normal ranges. Renal ultrasound examination of the abdomen was normal, with both kidneys normal size. Doppler-derived renal resistive index revealed elevated values (0.78 on the left and 0.8 on the right). Thoracic and abdominal MR angiogram revealed reduced caliber of the abdominal aorta and celiac trunk, stenosis of the upper mesenteric artery, irregular right renal artery with reduced caliber, and narrowed left renal artery at its emergence (). Ophthalmological findings were unremarkable. This regimen failed to control blood pressure, so angioplasty was scheduled. OUTPUT:
PMCPatients_common4305
[ { "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 male patient presented to the emergency room 1 hour after the onset of chest pain. He was a current smoker with no history of coronary artery disease, hypertension, or diabetes. He was reported to undergo a diagnostic work-up for possible diagnoses of lymphoma and sarcoidosis in the past 3-month period. He decided to visit the emergency room due to sudden and recurrent chest pain. At admission, his blood pressure (BP) was 95/69 mm Hg, his heart rate was 150 bpm, respiratory rate was 26/min, and oxygen saturation was 94%. An ECG showed a normal sinus rhythm with 75 heart bpm, and negative T-waves at III, aVF, and V4–6 leads (). In the laboratory results, the high-sensitive-troponin-I value was 200 ng/L. He was administered 300 mg of acetylsalicylic acid, 300 mg of clopidogrel, and 5000 U of IV heparin. In the first hour of the intensive care follow-up, the patient had no chest pain, and his hemodynamic parameters were stable. At the time of angiography, BP was 90/60 mm Hg, and the heart rate was 108 bpm. Angiography of the right and left coronary systems showed multiple stenotic images in the right coronary artery, left descending coronary artery, and circumflex coronary artery (). Despite the presence of hypotension, intra-coronary nitrate was given to both coronary systems in sequence on the basis of the suspicion of vasospasm, and this was followed by the flushing of both systems with physiological saline. During the course of his management, analgesics were administered to reduce symptoms and prevent vasospasm. Control angiography showed disappearance of the lesions in all three vessels (). Due to the chest pain resolution and the absence of critical lesions in control angiography, the procedure was terminated. Nitrates and Ca-channel blockers were added to the routine treatment of the patient, and follow-up exams were scheduled.\nOUTPUT:" }, { "from": "agent", "value": "Vasospastic angina, Severe three-vessel disease with critical stenoses, Non-ST elevation myocardial infarction, Acute inferolateral myocardial infarction" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 35-year-old male patient presented to the emergency room 1 hour after the onset of chest pain. He was a current smoker with no history of coronary artery disease, hypertension, or diabetes. He was reported to undergo a diagnostic work-up for possible diagnoses of lymphoma and sarcoidosis in the past 3-month period. He decided to visit the emergency room due to sudden and recurrent chest pain. At admission, his blood pressure (BP) was 95/69 mm Hg, his heart rate was 150 bpm, respiratory rate was 26/min, and oxygen saturation was 94%. An ECG showed a normal sinus rhythm with 75 heart bpm, and negative T-waves at III, aVF, and V4–6 leads (). In the laboratory results, the high-sensitive-troponin-I value was 200 ng/L. He was administered 300 mg of acetylsalicylic acid, 300 mg of clopidogrel, and 5000 U of IV heparin. In the first hour of the intensive care follow-up, the patient had no chest pain, and his hemodynamic parameters were stable. At the time of angiography, BP was 90/60 mm Hg, and the heart rate was 108 bpm. Angiography of the right and left coronary systems showed multiple stenotic images in the right coronary artery, left descending coronary artery, and circumflex coronary artery (). Despite the presence of hypotension, intra-coronary nitrate was given to both coronary systems in sequence on the basis of the suspicion of vasospasm, and this was followed by the flushing of both systems with physiological saline. During the course of his management, analgesics were administered to reduce symptoms and prevent vasospasm. Control angiography showed disappearance of the lesions in all three vessels (). Due to the chest pain resolution and the absence of critical lesions in control angiography, the procedure was terminated. Nitrates and Ca-channel blockers were added to the routine treatment of the patient, and follow-up exams were scheduled. OUTPUT:
PMCPatients_common78
[ { "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 24-year-old female patient presented to the otolaryngology clinic with a six-month history of progressive hoarseness of voice. In addition, she has a recent history of mild dyspnea on exertion and dry cough. The patient did not have any weight loss nor dysphagia. The patient was a cigarette smoker of around one pack per day for five years. There was no past family history of cancer, and she did not have any medical illness of significance. The patient also did not have any prior history of radiotherapy. In the clinic, fiberoptic nasoendoscopy showed a right vocal fold mass reaching the anterior commissure. The vocal fold mobility was normal. The neck examination was unremarkable. Our clinical impression, at this stage, was that the patient had early glottic laryngeal cancer. Consequently, the patient had a computed tomography (CT) scan showing the mass with no cervical lymphadenopathy (Figure ).\\nThe vocal fold mobility was normal. The neck examination was unremarkable. The patient underwent a laryngotracheoscopy under general anesthetic, with a biopsy taken from the lesion, which appeared to be arising from the right vocal fold without a subglottic extension. The options for management were evaluated by the head and neck multidisciplinary team, who preferred a transoral surgical excision as a modality of treatment. We discussed the treatment options with the patient, who refused surgical intervention. Consequently, she received intensity-modulated radiotherapy (IMRT). The patient had followed up at a six-month interval, and she remains free of the disease (Figure ).\nOUTPUT:" }, { "from": "agent", "value": "Sarcomatoid Carcinoma of the Larynx" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 24-year-old female patient presented to the otolaryngology clinic with a six-month history of progressive hoarseness of voice. In addition, she has a recent history of mild dyspnea on exertion and dry cough. The patient did not have any weight loss nor dysphagia. The patient was a cigarette smoker of around one pack per day for five years. There was no past family history of cancer, and she did not have any medical illness of significance. The patient also did not have any prior history of radiotherapy. In the clinic, fiberoptic nasoendoscopy showed a right vocal fold mass reaching the anterior commissure. The vocal fold mobility was normal. The neck examination was unremarkable. Our clinical impression, at this stage, was that the patient had early glottic laryngeal cancer. Consequently, the patient had a computed tomography (CT) scan showing the mass with no cervical lymphadenopathy (Figure ).\nThe vocal fold mobility was normal. The neck examination was unremarkable. The patient underwent a laryngotracheoscopy under general anesthetic, with a biopsy taken from the lesion, which appeared to be arising from the right vocal fold without a subglottic extension. The options for management were evaluated by the head and neck multidisciplinary team, who preferred a transoral surgical excision as a modality of treatment. We discussed the treatment options with the patient, who refused surgical intervention. Consequently, she received intensity-modulated radiotherapy (IMRT). The patient had followed up at a six-month interval, and she remains free of the disease (Figure ). OUTPUT:
PMCPatients_common4996
[ { "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 abdominal drain was left in situ, and postoperatively he made good progress until day nine when he developed fever and diarrhoea. A computerized tomography (CT) scan of the abdomen showed a large 30 × 16 cm collection in the pelvis and the abdominal drain was repositioned to drain the collection. He received a stat dose of intravenous gentamicin 320 mg and vancomycin 1 gm, and was commenced empirically on imipenem 500 mg 6-hourly. The following day, a blood culture yielded gram-negative rods, later identified as R. terrigena sensitive to co-amoxiclavulanic acid, cefotaxime, cefradine, ciprofloxacin, gentamicin and imipenem. The imipenem was changed to piperacillin-tazobactam, in accordance with the local policy, and he responded to therapy. The abdominal drain was removed.\\nHe was finally discharged home 50 days after admission.\nOUTPUT:" }, { "from": "agent", "value": "Sepsis caused by Raoultella terrigena, Pancreatic cancer, Clostridium difficile infection, Klebsiella pneumoniae infection, Candida spp. infection, Bacteremia with Enterococcus durans, Thrombus in the inferior vena cava" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An abdominal drain was left in situ, and postoperatively he made good progress until day nine when he developed fever and diarrhoea. A computerized tomography (CT) scan of the abdomen showed a large 30 × 16 cm collection in the pelvis and the abdominal drain was repositioned to drain the collection. He received a stat dose of intravenous gentamicin 320 mg and vancomycin 1 gm, and was commenced empirically on imipenem 500 mg 6-hourly. The following day, a blood culture yielded gram-negative rods, later identified as R. terrigena sensitive to co-amoxiclavulanic acid, cefotaxime, cefradine, ciprofloxacin, gentamicin and imipenem. The imipenem was changed to piperacillin-tazobactam, in accordance with the local policy, and he responded to therapy. The abdominal drain was removed.\nHe was finally discharged home 50 days after admission. OUTPUT:
PMCPatients_common1983
[ { "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 initial evaluation in the emergency department, she was found to be haemodynamically stable, febrile (39°C), somnolent, with non-comprehensible speech, and with no signs of neurological focalization. The rest of her physical examination was unremarkable. Cerebrospinal fluid (CSF) showed protein levels of 0.66 g/L (normal value < 0.5 g/L), 70 cells (mostly mononuclear), glucose levels of 45 mg/dL (normal value > 60 mg/dL), and adenosine deaminase (ADA) levels of 3.3 U/L (normal value < 7 U/L). Gram stain was negative for bacteria and the bacterial and fungus cultures were negative. Computed tomography (CT) of the brain revealed hydrocephalus without structural lesions. The study was complemented with magnetic resonance imaging (MRI) that revealed non-specific periventricular changes and diffuse meningeal enhancement, quadriventricular hydrocephalus, and diffuse leucoencephalopathy. The image was compatible with NPH (Figs. , ).\\nComplementary studies, including HIV and venereal disease research laboratory (VDRL) tests, were negative. Electroencephalogram (EEG) showed non-specific changes suggesting diffuse encephalopathy due to metabolic abnormalities, and the patient had normal thyroid panel, complement and B12 levels, with negative connective tissue serologies. ).\\nAfter a multidisciplinary evaluation, a ventriculoperitoneal (VP) shunt was installed without complications, and the patient was started on steroid therapy with prednisone of 0.5 mg per kg, with rapid improvement in her symptoms. After 2 years of follow-up, patient recovery was successful, without fever or evidence of infection. Current medication includes prednisone of 5 mg per day and azathioprine of 100 mg per day.\nOUTPUT:" }, { "from": "agent", "value": "Dementia, gait disturbance, urinary incontinence, pulmonary sarcoidosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: At initial evaluation in the emergency department, she was found to be haemodynamically stable, febrile (39°C), somnolent, with non-comprehensible speech, and with no signs of neurological focalization. The rest of her physical examination was unremarkable. Cerebrospinal fluid (CSF) showed protein levels of 0.66 g/L (normal value < 0.5 g/L), 70 cells (mostly mononuclear), glucose levels of 45 mg/dL (normal value > 60 mg/dL), and adenosine deaminase (ADA) levels of 3.3 U/L (normal value < 7 U/L). Gram stain was negative for bacteria and the bacterial and fungus cultures were negative. Computed tomography (CT) of the brain revealed hydrocephalus without structural lesions. The study was complemented with magnetic resonance imaging (MRI) that revealed non-specific periventricular changes and diffuse meningeal enhancement, quadriventricular hydrocephalus, and diffuse leucoencephalopathy. The image was compatible with NPH (Figs. , ).\nComplementary studies, including HIV and venereal disease research laboratory (VDRL) tests, were negative. Electroencephalogram (EEG) showed non-specific changes suggesting diffuse encephalopathy due to metabolic abnormalities, and the patient had normal thyroid panel, complement and B12 levels, with negative connective tissue serologies. ).\nAfter a multidisciplinary evaluation, a ventriculoperitoneal (VP) shunt was installed without complications, and the patient was started on steroid therapy with prednisone of 0.5 mg per kg, with rapid improvement in her symptoms. After 2 years of follow-up, patient recovery was successful, without fever or evidence of infection. Current medication includes prednisone of 5 mg per day and azathioprine of 100 mg per day. OUTPUT:
PMCPatients_common558
[ { "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 75-year-old male was admitted to our dermatology department with a widespread, itchy rash that had developed during five months. The patient did not respond well to oral antihistamine, topical corticosteroid cream, and narrowband ultraviolet B phototherapy (UVB) for 13 sessions. He was on drug-free follow-up for CLL and GD at the time of hospital admission. The patient was otherwise healthy with no family history of diseases.\\nDermatological examination revealed multiple, widespread, dome-shaped umbilicated papules and nodules with an average diameter of ∼4 mm distributed on the trunk, face, and upper and lower extremities (, ). Some of these were located in a linear pattern suggesting the Koebner phenomenon (). Examination of the nails and oral mucosa revealed no abnormalities.\\nLaboratory results of complete hemogram, blood sugar, liver, and kidney function tests were found to be within normal limits. Histopathological evaluation of a representative skin lesion taken from the left leg showed acanthosis, basket weave orthokeratosis, increased number of vessels in the superficial dermis, and perivascular and interstitial inflammatory infiltrate with erythrocyte extravasation. Punched-out ulceration with cellular debris was observed in the crateriform invagination and transepidermal elimination of collagen fibers (, ). ARPC was diagnosed based on the clinical and histological findings and the onset of the disease at the age of 75 years. Treatment with oral acitretin 25 mg/day was planned; however, the patient was lost to follow-up. Later, during a control visit to our clinic, an excellent response to gabapentin 300 mg/day and topical doxepin cream for one month was observed in the patient; these medications were prescribed in another medical center.\nOUTPUT:" }, { "from": "agent", "value": "Acquired reactive perforating collagenosis, Prostate adenocarcinoma, Chronic lymphocytic leukemia, Graves’ disease" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 75-year-old male was admitted to our dermatology department with a widespread, itchy rash that had developed during five months. The patient did not respond well to oral antihistamine, topical corticosteroid cream, and narrowband ultraviolet B phototherapy (UVB) for 13 sessions. He was on drug-free follow-up for CLL and GD at the time of hospital admission. The patient was otherwise healthy with no family history of diseases.\nDermatological examination revealed multiple, widespread, dome-shaped umbilicated papules and nodules with an average diameter of ∼4 mm distributed on the trunk, face, and upper and lower extremities (, ). Some of these were located in a linear pattern suggesting the Koebner phenomenon (). Examination of the nails and oral mucosa revealed no abnormalities.\nLaboratory results of complete hemogram, blood sugar, liver, and kidney function tests were found to be within normal limits. Histopathological evaluation of a representative skin lesion taken from the left leg showed acanthosis, basket weave orthokeratosis, increased number of vessels in the superficial dermis, and perivascular and interstitial inflammatory infiltrate with erythrocyte extravasation. Punched-out ulceration with cellular debris was observed in the crateriform invagination and transepidermal elimination of collagen fibers (, ). ARPC was diagnosed based on the clinical and histological findings and the onset of the disease at the age of 75 years. Treatment with oral acitretin 25 mg/day was planned; however, the patient was lost to follow-up. Later, during a control visit to our clinic, an excellent response to gabapentin 300 mg/day and topical doxepin cream for one month was observed in the patient; these medications were prescribed in another medical center. OUTPUT:
PMCPatients_common3160
[ { "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 44-year-old gentleman, married and unemployed, had a history of bullous lesions over the tongue, buccal mucosa, and palate. Dermatological evaluation revealed bullae and crusted erosions over the forehead spreading toward the chest, abdomen, and ventral aspects of thighs. He responded poorly to dapsone (100 mg/day), azathioprine (100 mg/day), and prednisolone (20 mg/day) for 10 weeks. In view of large areas of erosions with significant pain, he was hospitalized and was started on intravenous (IV) dexamethasone 8 mg once daily, tablet cyclophosphamide 50 mg once daily, and IV immunoglobulin 2 g/kg of total dose for 5 days. Meanwhile, he developed significant dysphoria, pessimistic ideas, death wishes, and fear against two unknown persons that he could see in their absence. Detailed psychiatric evaluation revealed depressed mood, easy fatigability, and crying spells with Lilliputian hallucinations of seeing two small individuals (size of 2 feet) threatening to kill him. On mental status examination (MSE), an interesting phenomenon noted was the evolution of tiny Lilliputian hallucinations into gigantic Brobdingnagian hallucinations (size of 10 feet) on treatment with steroids. The description of the visuals could not fit dysmegalopsia or visual imagery. There was nothing suggestive of delirium or seizures. Neurological and ophthalmic evaluation was normal. His routine blood investigations and computed tomography of the brain were within the normal limits. Within a week of treatment, the size of hallucinations reduced back to tiny people (from 10 feet to 2 feet) while preserving the shape of them and completely resolved by the end of 2 weeks. His depression improved at the time of discharge backed by MSE and drop in the Hamilton Depression Rating Scale scores from 18 to 6.\nOUTPUT:" }, { "from": "agent", "value": "Pemphigus vulgaris, Organic depression with psychotic symptoms" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 44-year-old gentleman, married and unemployed, had a history of bullous lesions over the tongue, buccal mucosa, and palate. Dermatological evaluation revealed bullae and crusted erosions over the forehead spreading toward the chest, abdomen, and ventral aspects of thighs. He responded poorly to dapsone (100 mg/day), azathioprine (100 mg/day), and prednisolone (20 mg/day) for 10 weeks. In view of large areas of erosions with significant pain, he was hospitalized and was started on intravenous (IV) dexamethasone 8 mg once daily, tablet cyclophosphamide 50 mg once daily, and IV immunoglobulin 2 g/kg of total dose for 5 days. Meanwhile, he developed significant dysphoria, pessimistic ideas, death wishes, and fear against two unknown persons that he could see in their absence. Detailed psychiatric evaluation revealed depressed mood, easy fatigability, and crying spells with Lilliputian hallucinations of seeing two small individuals (size of 2 feet) threatening to kill him. On mental status examination (MSE), an interesting phenomenon noted was the evolution of tiny Lilliputian hallucinations into gigantic Brobdingnagian hallucinations (size of 10 feet) on treatment with steroids. The description of the visuals could not fit dysmegalopsia or visual imagery. There was nothing suggestive of delirium or seizures. Neurological and ophthalmic evaluation was normal. His routine blood investigations and computed tomography of the brain were within the normal limits. Within a week of treatment, the size of hallucinations reduced back to tiny people (from 10 feet to 2 feet) while preserving the shape of them and completely resolved by the end of 2 weeks. His depression improved at the time of discharge backed by MSE and drop in the Hamilton Depression Rating Scale scores from 18 to 6. OUTPUT:
PMCPatients_common704
[ { "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 2005, an 81-year-old man with a medical history of smoking, systemic hypertension, and type 2 diabetes mellitus, presented SAH with ventricular irruption secondary to traumatic etiology, treated with a ventriculoperitoneal shunt. After 3, 12, and 24 months, he required shunt replacements for an unspecified etiology, the last was a ventriculopleural shunt.\\nThe patient sought medical attention through his primary care physician complaining of one-month history of attention disturbances, behavior changes, instability and urinary incontinence. With the clinical impression of a new shunt disfunction, the physician referred the patient to the neurosurgery department of our hospital for evaluation and treatment.\\nWhen the patient arrived to admission, he was inattentive and disoriented, with a Glasgow Coma Score of 14. He presented bilateral papilledema, wide-based gait in brief steps, negative Kerning, Brudzinski, and Binda signs and absent of neck stiffness. The shunt reservoir did not expand after applying pressure, showing a proximal obstruction.\\nWe performed blood, and urinary tests obtaining normal results. The CT reported dilation of the ventricular system and interstitial periventricular edema (). The results showed that three aneurysms were identified on the angiography, a small saccular aneurysm in the left medial cerebral artery at M2 segment, a blister aneurysm in the left ophthalmic segment of the internal carotid artery (C6) and a small saccular aneurysm in the right ophthalmic segment of the internal carotid artery (C6) ().\\nWe performed a shunt replacement of the proximal catheter. After two days of follow-up, we discharged the patient with improved gait, attention, and behavior. We referred him to the neurovascular department to treat the aneurysmatic disease.\nOUTPUT:" }, { "from": "agent", "value": "Subarachnoid Hemorrhage" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: In 2005, an 81-year-old man with a medical history of smoking, systemic hypertension, and type 2 diabetes mellitus, presented SAH with ventricular irruption secondary to traumatic etiology, treated with a ventriculoperitoneal shunt. After 3, 12, and 24 months, he required shunt replacements for an unspecified etiology, the last was a ventriculopleural shunt.\nThe patient sought medical attention through his primary care physician complaining of one-month history of attention disturbances, behavior changes, instability and urinary incontinence. With the clinical impression of a new shunt disfunction, the physician referred the patient to the neurosurgery department of our hospital for evaluation and treatment.\nWhen the patient arrived to admission, he was inattentive and disoriented, with a Glasgow Coma Score of 14. He presented bilateral papilledema, wide-based gait in brief steps, negative Kerning, Brudzinski, and Binda signs and absent of neck stiffness. The shunt reservoir did not expand after applying pressure, showing a proximal obstruction.\nWe performed blood, and urinary tests obtaining normal results. The CT reported dilation of the ventricular system and interstitial periventricular edema (). The results showed that three aneurysms were identified on the angiography, a small saccular aneurysm in the left medial cerebral artery at M2 segment, a blister aneurysm in the left ophthalmic segment of the internal carotid artery (C6) and a small saccular aneurysm in the right ophthalmic segment of the internal carotid artery (C6) ().\nWe performed a shunt replacement of the proximal catheter. After two days of follow-up, we discharged the patient with improved gait, attention, and behavior. We referred him to the neurovascular department to treat the aneurysmatic disease. OUTPUT:
PMCPatients_common670
[ { "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 shaping the remnant stomach, esophagogastrostomy was performed in the mediastinum under right thoracotomy. The anastomosis was performed using a circular stapler and was wrapped around the stomach to prevent gastroesophageal reflux disease. a). Since the tube caused pain, the patient repeatedly tried to remove it by himself. We had to restrain his limbs, so that the main drainage tube would not be removed. On POD 25, we performed PTEG and inserted a drainage tube instead of an NGT. He was soon released, after PTEG. c). As enteral feeding was required to start as soon as possible, we exchanged the PTEG tube with a double elementary diet (W-ED) tube with jejunal extension with the side hole located near the anastomosis, on POD43 (Fig. d). We used the 16-Fr W-ED tube, supplied by Japan Covidien Corp., Tokyo, Japan. It measures 150 cm and includes connectors both for drainage and nutrition; one lumen has its openings alongside the tube, 60 cm above the leading edge. The other lumen has its openings at the end of the tube for feeding.\nOUTPUT:" }, { "from": "agent", "value": "Siewert type I esophagogastric junction cancer, mediastinal abscess, anastomotic leakage, dysphagia due to disuse atrophy of the swallowing musculature" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: After shaping the remnant stomach, esophagogastrostomy was performed in the mediastinum under right thoracotomy. The anastomosis was performed using a circular stapler and was wrapped around the stomach to prevent gastroesophageal reflux disease. a). Since the tube caused pain, the patient repeatedly tried to remove it by himself. We had to restrain his limbs, so that the main drainage tube would not be removed. On POD 25, we performed PTEG and inserted a drainage tube instead of an NGT. He was soon released, after PTEG. c). As enteral feeding was required to start as soon as possible, we exchanged the PTEG tube with a double elementary diet (W-ED) tube with jejunal extension with the side hole located near the anastomosis, on POD43 (Fig. d). We used the 16-Fr W-ED tube, supplied by Japan Covidien Corp., Tokyo, Japan. It measures 150 cm and includes connectors both for drainage and nutrition; one lumen has its openings alongside the tube, 60 cm above the leading edge. The other lumen has its openings at the end of the tube for feeding. OUTPUT:
PMCPatients_common721
[ { "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 cardiac electrophysiology (EP) study was scheduled. Right femoral vein access was obtained. As a rule in our lab, after gaining access through the Seldinger technique, we check the position of the guide wires so that they are aligned to the right of the spine which confirms the venous route to the heart before placing sheaths. In our patient, the guide wire was noticed to track to the left of the spine; an inadvertent arterial access had to be excluded. Another femoral venous access was taken and 0.032 inch long J -tipped wire was advanced to track and assess the venous route. The long wire was noticed to cross to the left of the midline, then coursed up and roughly at the level of the renal veins curved back to the right of the spine before finally entering the right atrium through the inferior vena cava (IVC) route. Venography was performed through femoral venous sheath which highlighted the left-sided IVC route to the right atrium. ().\\nNext, we placed three femoral venous sheaths and advanced a steerable ablation catheter for positioning at His bundle region and two quadripolar non-steerable electrophysiology catheters to the right atrium and ventricle. We encountered some difficulty negotiating the tortuous IVC course at the level of the renal veins. (). A decapolar catheter was advanced from the left subclavian vein for coronary sinus cannulation. Successful radio-frequency (RF) ablation of slow pathway region with a 7 F, 4 mm tip Medtronic Marinr MCXL RF ablation catheter at 40 Watts and 60o C was performed. The following day of procedure, abdominal contrast CT scan was performed and that revealed a left-sided IVC draining into the right atrium in this unusual case. ().\nOUTPUT:" }, { "from": "agent", "value": "Supraventricular tachycardia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A cardiac electrophysiology (EP) study was scheduled. Right femoral vein access was obtained. As a rule in our lab, after gaining access through the Seldinger technique, we check the position of the guide wires so that they are aligned to the right of the spine which confirms the venous route to the heart before placing sheaths. In our patient, the guide wire was noticed to track to the left of the spine; an inadvertent arterial access had to be excluded. Another femoral venous access was taken and 0.032 inch long J -tipped wire was advanced to track and assess the venous route. The long wire was noticed to cross to the left of the midline, then coursed up and roughly at the level of the renal veins curved back to the right of the spine before finally entering the right atrium through the inferior vena cava (IVC) route. Venography was performed through femoral venous sheath which highlighted the left-sided IVC route to the right atrium. ().\nNext, we placed three femoral venous sheaths and advanced a steerable ablation catheter for positioning at His bundle region and two quadripolar non-steerable electrophysiology catheters to the right atrium and ventricle. We encountered some difficulty negotiating the tortuous IVC course at the level of the renal veins. (). A decapolar catheter was advanced from the left subclavian vein for coronary sinus cannulation. Successful radio-frequency (RF) ablation of slow pathway region with a 7 F, 4 mm tip Medtronic Marinr MCXL RF ablation catheter at 40 Watts and 60o C was performed. The following day of procedure, abdominal contrast CT scan was performed and that revealed a left-sided IVC draining into the right atrium in this unusual case. (). OUTPUT:
PMCPatients_common3698
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 38 year old female was referred to the Department of Conservative Dentistry at Chonnam National University Dental Hospital for pain control on the upper right side while biting. She had received medical therapy since being diagnosed with XLH at the age of 2 years. She underwent 2 corrective operations for her legs at the age of 32 years. She reported that she had stopped taking medication due to pregnancy and breastfeeding. A physical examination demonstrated a short height and abnormalities of the cranium (flattening of the cranium and prominent frontal bossing) and the lower extremities, which were characterized by bowing of the legs. An intraoral examination showed the absence of caries, dental abrasions, and periodontal inflammation. A radiographic examination showed ample radicular canals, pulp chambers, and pulp horns. General alveolar bone loss causing tooth mobility was observed (). In the clinical examination, the upper right second premolar (tooth #15) was responsive to percussion and nonresponsive to the electric pulp test. Microscopic observation (Carl Zeiss Surgical GmbH) confirmed that no crack was present. The pulp tissue was removed and the working length was established with an apex locator (DentaPort ZX) and the radiographic method. Two canals were cleaned and shaped using ProTaper NiTi rotary instruments with a crown-down technique. During instrumentation, copious irrigation was performed using 5.25% sodium hypochlorite solution and sterile saline. The canals were dried and calcium hydroxide was applied as a medicament for a month. The access cavity was temporarily sealed with Caviton (GC). After 1 month, the canals were filled with gutta-percha and AH26 plus (Dentsply DeTrey) using a continuous wave technique. After root canal therapy, she complained of discomfort during biting.\\nIn this patient, implants were placed after the extraction of the upper right and left central incisors due to hypermobility and discomfort, as was the case for the upper right second premolar. Since the implants showed consistent hypermobility after 1 year and 6 months of implant installation, the final restorations were postponed.\nOUTPUT:" }, { "from": "agent", "value": "X-linked hypophosphatemia, Acute apical periodontitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 38 year old female was referred to the Department of Conservative Dentistry at Chonnam National University Dental Hospital for pain control on the upper right side while biting. She had received medical therapy since being diagnosed with XLH at the age of 2 years. She underwent 2 corrective operations for her legs at the age of 32 years. She reported that she had stopped taking medication due to pregnancy and breastfeeding. A physical examination demonstrated a short height and abnormalities of the cranium (flattening of the cranium and prominent frontal bossing) and the lower extremities, which were characterized by bowing of the legs. An intraoral examination showed the absence of caries, dental abrasions, and periodontal inflammation. A radiographic examination showed ample radicular canals, pulp chambers, and pulp horns. General alveolar bone loss causing tooth mobility was observed (). In the clinical examination, the upper right second premolar (tooth #15) was responsive to percussion and nonresponsive to the electric pulp test. Microscopic observation (Carl Zeiss Surgical GmbH) confirmed that no crack was present. The pulp tissue was removed and the working length was established with an apex locator (DentaPort ZX) and the radiographic method. Two canals were cleaned and shaped using ProTaper NiTi rotary instruments with a crown-down technique. During instrumentation, copious irrigation was performed using 5.25% sodium hypochlorite solution and sterile saline. The canals were dried and calcium hydroxide was applied as a medicament for a month. The access cavity was temporarily sealed with Caviton (GC). After 1 month, the canals were filled with gutta-percha and AH26 plus (Dentsply DeTrey) using a continuous wave technique. After root canal therapy, she complained of discomfort during biting.\nIn this patient, implants were placed after the extraction of the upper right and left central incisors due to hypermobility and discomfort, as was the case for the upper right second premolar. Since the implants showed consistent hypermobility after 1 year and 6 months of implant installation, the final restorations were postponed. OUTPUT:
PMCPatients_common657
[ { "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 11-day-old term male presented to pediatric urology with antenatally diagnosed bilateral hydronephrosis. Renal ultrasound after birth at 11 days of age revealed moderate left hydronephrosis and moderate right hydronephrosis with ureteral dilation (Figure ).\\nFurther evaluation with voiding cystourethrogram (VCUG) demonstrated right grade 5 VUR with a concern for possible secondary UPJO (Figure ).\\nHe was initially managed with prophylactic antibiotics and serial renal ultrasounds. Ultrasound at 8 and 14 months of age demonstrated stable bilateral hydronephrosis. At 27 months of age, follow-up renal ultrasound demonstrated worsening right hydronephrosis with parenchymal thinning and abnormal echogenic renal parenchyma (Figure ).\\nAt 31 months of age, he underwent follow-up VCUG, which demonstrated residual right grade 1 VUR, and a renogram, which demonstrated delayed drainage of the right kidney with 26% differential function, consistent with UPJO (Figure ). No blood studies were obtained. Based on these findings, the decision was made to proceed with surgical intervention.\\nHe underwent surgical repair with an open right dismembered pyeloplasty at 33 months of age. Initial cystoscopy revealed a normal bladder with normal bilateral orthotopic ureteral orifices. Intraoperatively, there was no extrinsic compression of the UPJ. The stenotic UPJ was identified and excised, and the ureter was anastomosed to the renal pelvis. There was no visible lesion noted grossly on the excised urothelium.\\nHis postoperative course was uneventful, and he was discharged home on postoperative day 1. Pathology of the excised segment demonstrated ureteral tissue with subepithelial and epithelial eosinophils (Figure ).\nOUTPUT:" }, { "from": "agent", "value": "Eosinophilic Ureteritis, Ureteropelvic Junction Obstruction, Vesicoureteral Reflux" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 11-day-old term male presented to pediatric urology with antenatally diagnosed bilateral hydronephrosis. Renal ultrasound after birth at 11 days of age revealed moderate left hydronephrosis and moderate right hydronephrosis with ureteral dilation (Figure ).\nFurther evaluation with voiding cystourethrogram (VCUG) demonstrated right grade 5 VUR with a concern for possible secondary UPJO (Figure ).\nHe was initially managed with prophylactic antibiotics and serial renal ultrasounds. Ultrasound at 8 and 14 months of age demonstrated stable bilateral hydronephrosis. At 27 months of age, follow-up renal ultrasound demonstrated worsening right hydronephrosis with parenchymal thinning and abnormal echogenic renal parenchyma (Figure ).\nAt 31 months of age, he underwent follow-up VCUG, which demonstrated residual right grade 1 VUR, and a renogram, which demonstrated delayed drainage of the right kidney with 26% differential function, consistent with UPJO (Figure ). No blood studies were obtained. Based on these findings, the decision was made to proceed with surgical intervention.\nHe underwent surgical repair with an open right dismembered pyeloplasty at 33 months of age. Initial cystoscopy revealed a normal bladder with normal bilateral orthotopic ureteral orifices. Intraoperatively, there was no extrinsic compression of the UPJ. The stenotic UPJ was identified and excised, and the ureter was anastomosed to the renal pelvis. There was no visible lesion noted grossly on the excised urothelium.\nHis postoperative course was uneventful, and he was discharged home on postoperative day 1. Pathology of the excised segment demonstrated ureteral tissue with subepithelial and epithelial eosinophils (Figure ). OUTPUT:
PMCPatients_common2927
[ { "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 had had intermittent diarrhea over the past four weeks but no bleeding or mucous appeared in her stool. Although treated as a rheumatic flare by her general practitioner, and low dose corticosteroids (prednisolone 20 mg daily) had been commenced three weeks prior to admission, she had failed to improve and therefore in-patient assessment was sought. Her past medical history consisted of hypertension and two successful normal vaginal deliveries. There was no significant family history. Apart from prednisolone, her only other medication was bendrofluazide 2.5 mg once daily. On admission to hospital, examination revealed reduced right hip and knee power of 4/5. Her diarrhea had settled by the time of admission to hospital. She was apyrexial, with a white cell count of 22.6×109/dL, neutrophils 18.36, C-reactive protein (CRP) 279 mg/L and her body mass index (BMI) was 27 kg/m2. Hip, pelvic, chest and abdominal X-rays, ultrasound scan of the abdomen, pelvis and stool cultures were unremarkable. Sigmoidoscopy revealed mild active proctitis and diverticulosis. A diagnosis of exacerbation of PMR was made and corticosteroid dosage increased to 40 mg daily. In view of raised inflammatory markers, intravenous broad spectrum antibiotics were also commenced (Tazocin (piperacillin and tazobactam) and gentamicin). Despite this her limb weakness and hip pain became progressively worse and inflammatory markers continued to rise. Magnetic resonance imaging (MRI) of the spine and pelvis was therefore arranged on day five of admission. This revealed a posterior diverticular perforation into the pre-sacral space resulting in large bilateral gluteal abscesses. There was also gas extending around the right femoral head (Figures and ). Although an urgent percutaneous computed tomography (CT)-guided drainage with a view to proceed to laparotomy and Hartmann's procedure was arranged, she became increasingly septic and died.\nOUTPUT:" }, { "from": "agent", "value": "Perforated colonic pathology, Polymyalgia rheumatica" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: She had had intermittent diarrhea over the past four weeks but no bleeding or mucous appeared in her stool. Although treated as a rheumatic flare by her general practitioner, and low dose corticosteroids (prednisolone 20 mg daily) had been commenced three weeks prior to admission, she had failed to improve and therefore in-patient assessment was sought. Her past medical history consisted of hypertension and two successful normal vaginal deliveries. There was no significant family history. Apart from prednisolone, her only other medication was bendrofluazide 2.5 mg once daily. On admission to hospital, examination revealed reduced right hip and knee power of 4/5. Her diarrhea had settled by the time of admission to hospital. She was apyrexial, with a white cell count of 22.6×109/dL, neutrophils 18.36, C-reactive protein (CRP) 279 mg/L and her body mass index (BMI) was 27 kg/m2. Hip, pelvic, chest and abdominal X-rays, ultrasound scan of the abdomen, pelvis and stool cultures were unremarkable. Sigmoidoscopy revealed mild active proctitis and diverticulosis. A diagnosis of exacerbation of PMR was made and corticosteroid dosage increased to 40 mg daily. In view of raised inflammatory markers, intravenous broad spectrum antibiotics were also commenced (Tazocin (piperacillin and tazobactam) and gentamicin). Despite this her limb weakness and hip pain became progressively worse and inflammatory markers continued to rise. Magnetic resonance imaging (MRI) of the spine and pelvis was therefore arranged on day five of admission. This revealed a posterior diverticular perforation into the pre-sacral space resulting in large bilateral gluteal abscesses. There was also gas extending around the right femoral head (Figures and ). Although an urgent percutaneous computed tomography (CT)-guided drainage with a view to proceed to laparotomy and Hartmann's procedure was arranged, she became increasingly septic and died. OUTPUT:
PMCPatients_common4796
[ { "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 man visited hospital with lower back pain, paresthesia, and weakness in his left foot that had been present for one week. When presented in clinics, the paresthesia had disappeared, but he still could not move his left ankle. The sensory exam was normal, as were his deep tendon reflexes (DTR), superficial reflexes, and pathologic reflexes. In the neurologic exam, he was alert and oriented, and his cranial exam responses were intact. Previously, he had undergone surgery for a varicose vein in his right leg ten years ago and endoscopic surgery for a gastric adenoma three years ago. He did not have a history of peripheral neuropathy or systemic diseases, such as hypertension or diabetes. A lumbar spine magnetic resonance imaging (MRI) showed a ruptured disc, which was compressing the nerve root on the left side of L4/5, and degenerative spondylosis in L5/S1 (). The electromyography (EMG) and nerve conduction study (NCS) showed decreased amplitude and prolonged latency in the left peroneal and tibial compound muscle action potential and normal sensory findings. This means that there was lumbar radiculopathy in L4/5 (). The brain CT and plexus MR did not show any specific findings. With several days of daily rehabilitation physiotherapy, his lower back pain partially improved, while his motor power was not recovered. A follow-up NCS and EMG did not show any changes. Surgery for decompression and fusion in the lumbar spine was performed. After the surgery, the weakness still did not change. At postoperative day 8, the deep tendon reflex was increased on the left ankle and ankle clonus was noticed. For a detailed stroke investigation, electrocardiography and echocardiography were performed, and the results showed no specific problems. The patient was treated with a daily antiplatelet and adjuvant physiotherapy for foot drop. A month later, his motor deficit had improving, up to grade III.\nOUTPUT:" }, { "from": "agent", "value": "Cerebral Infarction" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 71-year-old man visited hospital with lower back pain, paresthesia, and weakness in his left foot that had been present for one week. When presented in clinics, the paresthesia had disappeared, but he still could not move his left ankle. The sensory exam was normal, as were his deep tendon reflexes (DTR), superficial reflexes, and pathologic reflexes. In the neurologic exam, he was alert and oriented, and his cranial exam responses were intact. Previously, he had undergone surgery for a varicose vein in his right leg ten years ago and endoscopic surgery for a gastric adenoma three years ago. He did not have a history of peripheral neuropathy or systemic diseases, such as hypertension or diabetes. A lumbar spine magnetic resonance imaging (MRI) showed a ruptured disc, which was compressing the nerve root on the left side of L4/5, and degenerative spondylosis in L5/S1 (). The electromyography (EMG) and nerve conduction study (NCS) showed decreased amplitude and prolonged latency in the left peroneal and tibial compound muscle action potential and normal sensory findings. This means that there was lumbar radiculopathy in L4/5 (). The brain CT and plexus MR did not show any specific findings. With several days of daily rehabilitation physiotherapy, his lower back pain partially improved, while his motor power was not recovered. A follow-up NCS and EMG did not show any changes. Surgery for decompression and fusion in the lumbar spine was performed. After the surgery, the weakness still did not change. At postoperative day 8, the deep tendon reflex was increased on the left ankle and ankle clonus was noticed. For a detailed stroke investigation, electrocardiography and echocardiography were performed, and the results showed no specific problems. The patient was treated with a daily antiplatelet and adjuvant physiotherapy for foot drop. A month later, his motor deficit had improving, up to grade III. OUTPUT:
PMCPatients_common3823
[ { "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 premenopausal female presented with abdominal fullness and vomiting. She had a performance status-1, and clinical examination was suggestive of ascites and decreased air entry in right lower lobe. Blood investigation showed a creatinine of 5.81 mg/dl and uric acid >15 mg/dl. Her cancer antigen (CA)-125 was 3240 U/ml, carcinoembryonic antigen of 0.70 ng/ml, alpha-fetoprotein – 4.80 ng/ml, and beta human chorionic gonadotropin – 5.05 mIU/ml. Noncontrast computed tomography thorax and abdomen showed mild ascites, thickened infiltrated omentum forming omental caking, and the presence of moderate right pleural effusion. Both kidneys, ovary, uterus were normal. Pleural fluid cytology was suggestive of malignant cells. Fine needle aspiration cytology from omental cake was suggestive of metastatic adenocarcinoma. She received a single dose of 1.5 mg rasburicase along with aggressive hydration at 3 L/m2. Urine output and daily creatinine and uric acid were monitored daily. The blood investigation on diagnosis and subsequent to diagnosis are mentioned in . A decision to start neoadjuvant chemotherapy (NACT) was made in view of advanced stage. Paclitaxel and carboplatin could be given postpresentation day 4 after reversal of TLS; however, hydration for 2 days' postchemotherapy and allopurinol for 7 days was given. She underwent cytoreductive surgery post three cycles NACT. Presurgery CA-125 was 24.20 U/ml, and contrast-enhanced computed tomography abdomen showed resolution of pleural effusion and partial response in omental deposits and no ascites. Her surgical pathology report showed marked response to chemotherapy with minimal residual poorly differentiated serous carcinoma involving left ovary and omentum and single pelvic lymph node. The patient then went on to complete three cycles of adjuvant chemotherapy. The patient is now apparently healthy, and her posttreatment ultrasonography abdomen pelvis and CA-125 are normal.\nOUTPUT:" }, { "from": "agent", "value": "Epithelial Ovarian Carcinoma, Spontaneous Tumor Lysis Syndrome, Renal Failure" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 49-year-old premenopausal female presented with abdominal fullness and vomiting. She had a performance status-1, and clinical examination was suggestive of ascites and decreased air entry in right lower lobe. Blood investigation showed a creatinine of 5.81 mg/dl and uric acid >15 mg/dl. Her cancer antigen (CA)-125 was 3240 U/ml, carcinoembryonic antigen of 0.70 ng/ml, alpha-fetoprotein – 4.80 ng/ml, and beta human chorionic gonadotropin – 5.05 mIU/ml. Noncontrast computed tomography thorax and abdomen showed mild ascites, thickened infiltrated omentum forming omental caking, and the presence of moderate right pleural effusion. Both kidneys, ovary, uterus were normal. Pleural fluid cytology was suggestive of malignant cells. Fine needle aspiration cytology from omental cake was suggestive of metastatic adenocarcinoma. She received a single dose of 1.5 mg rasburicase along with aggressive hydration at 3 L/m2. Urine output and daily creatinine and uric acid were monitored daily. The blood investigation on diagnosis and subsequent to diagnosis are mentioned in . A decision to start neoadjuvant chemotherapy (NACT) was made in view of advanced stage. Paclitaxel and carboplatin could be given postpresentation day 4 after reversal of TLS; however, hydration for 2 days' postchemotherapy and allopurinol for 7 days was given. She underwent cytoreductive surgery post three cycles NACT. Presurgery CA-125 was 24.20 U/ml, and contrast-enhanced computed tomography abdomen showed resolution of pleural effusion and partial response in omental deposits and no ascites. Her surgical pathology report showed marked response to chemotherapy with minimal residual poorly differentiated serous carcinoma involving left ovary and omentum and single pelvic lymph node. The patient then went on to complete three cycles of adjuvant chemotherapy. The patient is now apparently healthy, and her posttreatment ultrasonography abdomen pelvis and CA-125 are normal. OUTPUT:
PMCPatients_common4639
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Her creatinine rose to 205 µmol/L from a baseline creatinine of 78 µmol/L over 8 months (MDRD eGFR 67 mL/min/1.73 m2 to 22 mL/min/1.73 m2) in the presence of a donor-specific antibody but no significant proteinuria. She had been compliant with her immunosuppression regimen of prednisolone 5 mg once daily and ciclosporin 35 mg twice daily. She was not receiving diuretic therapy and other medications included alfacalcidol 0.25 µg, aspirin 75 mg, atorvastatin 20 mg, bisoprolol 1.25 mg, co-trimoxazole 480 mg and ranitidine 150 mg twice daily. Her sodium concentration prior to desmopressin use was 129 mmol/L.\\nShe presented for a day-case renal transplant biopsy and was given an infusion of 12 µg intravenous DDAVP over 20 min prior to the procedure. She was discharged following a 6-h observation period. After leaving the hospital, she developed symptoms of nausea, feeling generally weak and unwell. The following day, she was found collapsed at home and had a witnessed self-terminating generalized tonic–clonic seizure. She was found to have a sodium concentration of 124 mmol/L on admission to her local hospital (normal range, 135–145 mmol/L). Sodium levels were <130 mmol/L on pre-admission blood tests prior to DDAVP administration, although they had been previously within the normal range. They had not received clear enough instructions to alter their water intake following the use of DDAVP and both patients continued to consume their standard post-transplant fluid intake.\nOUTPUT:" }, { "from": "agent", "value": "End-stage renal failure secondary to hypertension, Deteriorating graft function, Hyponatraemia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Her creatinine rose to 205 µmol/L from a baseline creatinine of 78 µmol/L over 8 months (MDRD eGFR 67 mL/min/1.73 m2 to 22 mL/min/1.73 m2) in the presence of a donor-specific antibody but no significant proteinuria. She had been compliant with her immunosuppression regimen of prednisolone 5 mg once daily and ciclosporin 35 mg twice daily. She was not receiving diuretic therapy and other medications included alfacalcidol 0.25 µg, aspirin 75 mg, atorvastatin 20 mg, bisoprolol 1.25 mg, co-trimoxazole 480 mg and ranitidine 150 mg twice daily. Her sodium concentration prior to desmopressin use was 129 mmol/L.\nShe presented for a day-case renal transplant biopsy and was given an infusion of 12 µg intravenous DDAVP over 20 min prior to the procedure. She was discharged following a 6-h observation period. After leaving the hospital, she developed symptoms of nausea, feeling generally weak and unwell. The following day, she was found collapsed at home and had a witnessed self-terminating generalized tonic–clonic seizure. She was found to have a sodium concentration of 124 mmol/L on admission to her local hospital (normal range, 135–145 mmol/L). Sodium levels were <130 mmol/L on pre-admission blood tests prior to DDAVP administration, although they had been previously within the normal range. They had not received clear enough instructions to alter their water intake following the use of DDAVP and both patients continued to consume their standard post-transplant fluid intake. OUTPUT:
PMCPatients_common3724
[ { "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 white female with a past medical history of hypertension and bipolar disorder presented with a few hours of severe sharp epigastric abdominal pain radiating to the back associated with nausea and vomiting. No new medication had recently been started, and there was no history of abdominal trauma. She had had a cholecystectomy in 2004. On physical examination, she was afebrile, had a heart rate of 105 beats/min, and a blood pressure of 132/84 mm Hg. She was in severe distress due to pain with severe epigastric tenderness. The remainder of her physical exam was normal.\\nHer laboratory tests on admission revealed a WBC of 22.1 × 103/μL with neutrophils 87%, a hemoglobin level of 14.0 g/dL, and platelets 380 × 103/μL. Her comprehensive metabolic panel was unremarkable except for a potassium level of 2.7 mEq/L. She had a negative pregnancy test and a normal urine drug screen. Her serum amylase was 31 IU/L (normal ref: 20–160) and lipase was 14 IU/L (normal ref: 8–78).\\nSince the patient was in severe pain with no clear diagnosis, a CT scan of her abdomen with intravenous contrast was done in the emergency room. ). The patient was admitted to the floor and kept nothing by mouth. She was treated with intravenous fluids, analgesics, potassium supplement, and antiemetics. On the next morning, repeated measurements of her amylase and lipase were still within normal limits. We checked her triglyceride level and it was 53 mg/dL. Her symptoms continued to improve during her course of hospitalization, and her leukocytosis was resolved without the use of antibiotics. She was discharged home on day 3.\nOUTPUT:" }, { "from": "agent", "value": "Acute Pancreatitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 40-year-old white female with a past medical history of hypertension and bipolar disorder presented with a few hours of severe sharp epigastric abdominal pain radiating to the back associated with nausea and vomiting. No new medication had recently been started, and there was no history of abdominal trauma. She had had a cholecystectomy in 2004. On physical examination, she was afebrile, had a heart rate of 105 beats/min, and a blood pressure of 132/84 mm Hg. She was in severe distress due to pain with severe epigastric tenderness. The remainder of her physical exam was normal.\nHer laboratory tests on admission revealed a WBC of 22.1 × 103/μL with neutrophils 87%, a hemoglobin level of 14.0 g/dL, and platelets 380 × 103/μL. Her comprehensive metabolic panel was unremarkable except for a potassium level of 2.7 mEq/L. She had a negative pregnancy test and a normal urine drug screen. Her serum amylase was 31 IU/L (normal ref: 20–160) and lipase was 14 IU/L (normal ref: 8–78).\nSince the patient was in severe pain with no clear diagnosis, a CT scan of her abdomen with intravenous contrast was done in the emergency room. ). The patient was admitted to the floor and kept nothing by mouth. She was treated with intravenous fluids, analgesics, potassium supplement, and antiemetics. On the next morning, repeated measurements of her amylase and lipase were still within normal limits. We checked her triglyceride level and it was 53 mg/dL. Her symptoms continued to improve during her course of hospitalization, and her leukocytosis was resolved without the use of antibiotics. She was discharged home on day 3. OUTPUT:
PMCPatients_common530
[ { "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 82-year-old African-American woman with a past medical history of diabetes mellitus type II, hypertension, hypothyroidism, and biopsy-confirmed bilateral GCA with anterior ischemic optic neuropathy of the right eye was started on TCZ after developing glucocorticoid-related complications. She was started on 162 milligrams of TCZ subcutaneously once per week in addition to a prednisone taper. After one month of therapy, the patient presented to our emergency department (ED) with complaints of pharyngitis and odynophagia. One day prior to onset of symptoms, she received topical proparacaine eye drops during a routine ophthalmologic visit. She denied any new medications or exposures to any new products. Home medications included alendronate, aspirin, atovaquone, calcium-carbonate-vitamin D, glipizide, metformin, levothyroxine, and olmesartan-amlodipine-hydrochlorothiazide. In the ED, physical examination was significant for drooling and mild tongue and lip swelling, with open sores on oral commissures bilaterally. Inflammatory markers (erythrocyte sedimentation rate and C-reactive protein) were within normal limits. A CT scan of the sinuses displayed edema and mucosal thickening of the wall of nasopharynx and oropharynx. Due to concern for an allergic reaction with possible airway compromise, she was treated with IV steroids and admitted for further observation. Hospital course was complicated by progressive dysphagia, conjunctivitis and mucosal ulcers (Figure ). She also developed new onset erythematous macules on her back and flaccid bullae on her palms, back, and extremities, involving 8% of her skin (Figure ). Her SJS was presumptively due to TCZ, which was thus discontinued. She was transferred to the ICU and managed with IV fluids, steroids, and intravenous gamma globulin (IVIG). She responded well to treatment with no new lesions and resolution of existing lesions after two weeks of supportive care.\nOUTPUT:" }, { "from": "agent", "value": "Stevens Johnson Syndrome, Giant Cell Arteritis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 82-year-old African-American woman with a past medical history of diabetes mellitus type II, hypertension, hypothyroidism, and biopsy-confirmed bilateral GCA with anterior ischemic optic neuropathy of the right eye was started on TCZ after developing glucocorticoid-related complications. She was started on 162 milligrams of TCZ subcutaneously once per week in addition to a prednisone taper. After one month of therapy, the patient presented to our emergency department (ED) with complaints of pharyngitis and odynophagia. One day prior to onset of symptoms, she received topical proparacaine eye drops during a routine ophthalmologic visit. She denied any new medications or exposures to any new products. Home medications included alendronate, aspirin, atovaquone, calcium-carbonate-vitamin D, glipizide, metformin, levothyroxine, and olmesartan-amlodipine-hydrochlorothiazide. In the ED, physical examination was significant for drooling and mild tongue and lip swelling, with open sores on oral commissures bilaterally. Inflammatory markers (erythrocyte sedimentation rate and C-reactive protein) were within normal limits. A CT scan of the sinuses displayed edema and mucosal thickening of the wall of nasopharynx and oropharynx. Due to concern for an allergic reaction with possible airway compromise, she was treated with IV steroids and admitted for further observation. Hospital course was complicated by progressive dysphagia, conjunctivitis and mucosal ulcers (Figure ). She also developed new onset erythematous macules on her back and flaccid bullae on her palms, back, and extremities, involving 8% of her skin (Figure ). Her SJS was presumptively due to TCZ, which was thus discontinued. She was transferred to the ICU and managed with IV fluids, steroids, and intravenous gamma globulin (IVIG). She responded well to treatment with no new lesions and resolution of existing lesions after two weeks of supportive care. OUTPUT:
PMCPatients_common3184
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 67-year-old Caucasian male presented to the emergency department with progressively worsening headache that started 5 weeks prior. He denied having similar symptoms in the past. Four weeks after his headache started, he noted new left eyelid drooping with tearing, redness, double and blurry vision (). The double vision had resolved upon presentation. In addition, he also described myalgias in all four extremities for ~2 weeks, limiting him from lifting his arms above his head or getting up from a squatted position. Past medical history was notable for COPD, hypertension and 80 pack-year smoking history. Physical exam was significant for trace left ptosis, conjunctival injection; visual acuity was 20/70 in the right eye and 20/50 in the left with unremarkable appearance of the optic nerves.\\nLaboratory studies obtained were significant for elevated C-reactive protein: 14.4 [reference range (RR): <1.0 mg/dl] and erythrocyte sedimentation rate: 54 (RR: 0–20 mm/h). Other laboratory work including thyroid stimulating hormone, creatinine kinase, vitamin D level, antinuclear antibody, rheumatoid factor and anti-citrullinated protein antibody were unremarkable. Computed tomography (CT) of the chest showed non-calcified pulmonary nodules without any concerning features. Imaging studies including CT, magnetic resonance imaging, and magnetic resonance angiogram of head and neck were noted to be unremarkable. Giant cells were not seen. Elastic stain highlighted the disruption of internal elastic lamina ( and ).\\nPatient reported improvement in symptoms after 2 days of steroids and he was discharged on a Prednisone taper. Two weeks after discharge, he reported feeling much better with only very mild headache and no visual symptoms at all ().\nOUTPUT:" }, { "from": "agent", "value": "Temporal arteritis, Polymyalgia rheumatica" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 67-year-old Caucasian male presented to the emergency department with progressively worsening headache that started 5 weeks prior. He denied having similar symptoms in the past. Four weeks after his headache started, he noted new left eyelid drooping with tearing, redness, double and blurry vision (). The double vision had resolved upon presentation. In addition, he also described myalgias in all four extremities for ~2 weeks, limiting him from lifting his arms above his head or getting up from a squatted position. Past medical history was notable for COPD, hypertension and 80 pack-year smoking history. Physical exam was significant for trace left ptosis, conjunctival injection; visual acuity was 20/70 in the right eye and 20/50 in the left with unremarkable appearance of the optic nerves.\nLaboratory studies obtained were significant for elevated C-reactive protein: 14.4 [reference range (RR): <1.0 mg/dl] and erythrocyte sedimentation rate: 54 (RR: 0–20 mm/h). Other laboratory work including thyroid stimulating hormone, creatinine kinase, vitamin D level, antinuclear antibody, rheumatoid factor and anti-citrullinated protein antibody were unremarkable. Computed tomography (CT) of the chest showed non-calcified pulmonary nodules without any concerning features. Imaging studies including CT, magnetic resonance imaging, and magnetic resonance angiogram of head and neck were noted to be unremarkable. Giant cells were not seen. Elastic stain highlighted the disruption of internal elastic lamina ( and ).\nPatient reported improvement in symptoms after 2 days of steroids and he was discharged on a Prednisone taper. Two weeks after discharge, he reported feeling much better with only very mild headache and no visual symptoms at all (). OUTPUT:
PMCPatients_common933
[ { "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 91-year-old healthy Taiwanese female presented with a progressing skin lesion on her right forearm. The patient, originally from Taiwan, immigrated to the United States in 1995. Initially, she had mild skin breakdown that matured to erythema, swelling, and rubor. The patient noted some purple spots on her lower extremities, especially around her right knee. The patient denied any swollen lymph nodes, fever, chills, night sweats, or weight loss. The patient stated her cheeks developed redness, but attributed this to high blood pressure. According to the patient’s family, the exact chronicity of the rash was unknown as she usually wore long sleeves and pants. The patient’s home medications included hydrochlorothiazide and meloxicam as well as hydrocodone/acetaminophen as needed.\\nUpon examination, the patient was afebrile and had normal vital signs. There was a large fungated/crusted lesion present on the right forearm with a scabbed area and surrounding erythema without fluctuance or purulence (Figure ). The lesion was mildly warm to the touch. On the patient’s lower extremities there were non-blanching purple macules, the largest located around her right knee and right thigh. No clavicular or inguinal swollen lymph nodes were noted. The initial complete blood count workup was unrevealing: prothrombin time and partial thromboplastin time were within normal range; serum and urine protein electrophoresis were normal; and antineutrophil cytoplasmic antibodies and cryoglobulins were negative. A skin biopsy of the thigh showed non-specific purpura. The nodular erythematous area on her right arm was biopsied. Findings were consistent with Fonsecaea species (Figure ). The infectious disease team was consulted and the patient was started on itraconazole twice a day. Approximately one week later, she was discharged with close clinic follow-up and inflammatory markers were routinely monitored. She had a persistent rash with moderate improvement when evaluated two months later.\nOUTPUT:" }, { "from": "agent", "value": "Chromoblastomycosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 91-year-old healthy Taiwanese female presented with a progressing skin lesion on her right forearm. The patient, originally from Taiwan, immigrated to the United States in 1995. Initially, she had mild skin breakdown that matured to erythema, swelling, and rubor. The patient noted some purple spots on her lower extremities, especially around her right knee. The patient denied any swollen lymph nodes, fever, chills, night sweats, or weight loss. The patient stated her cheeks developed redness, but attributed this to high blood pressure. According to the patient’s family, the exact chronicity of the rash was unknown as she usually wore long sleeves and pants. The patient’s home medications included hydrochlorothiazide and meloxicam as well as hydrocodone/acetaminophen as needed.\nUpon examination, the patient was afebrile and had normal vital signs. There was a large fungated/crusted lesion present on the right forearm with a scabbed area and surrounding erythema without fluctuance or purulence (Figure ). The lesion was mildly warm to the touch. On the patient’s lower extremities there were non-blanching purple macules, the largest located around her right knee and right thigh. No clavicular or inguinal swollen lymph nodes were noted. The initial complete blood count workup was unrevealing: prothrombin time and partial thromboplastin time were within normal range; serum and urine protein electrophoresis were normal; and antineutrophil cytoplasmic antibodies and cryoglobulins were negative. A skin biopsy of the thigh showed non-specific purpura. The nodular erythematous area on her right arm was biopsied. Findings were consistent with Fonsecaea species (Figure ). The infectious disease team was consulted and the patient was started on itraconazole twice a day. Approximately one week later, she was discharged with close clinic follow-up and inflammatory markers were routinely monitored. She had a persistent rash with moderate improvement when evaluated two months later. OUTPUT:
PMCPatients_common3222
[ { "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 female with a strong smoking history (>25 pack years), dyslipidaemia, and increased body mass index, but not on any medical therapy, presented with a 2-h history of typical ischaemic chest pain to the emergency department of a non-PCI centre. Initial ECG showed evidence of a de Winter’s pattern () with slight ST-elevation in the septal leads V1, V2. Initial clinical evaluation revealed a normal cardiovascular examination with no clinical evidence of heart failure. Due to ongoing severe chest pain, the inability to transfer the patient to the closest PCI centre within 120 min and the close association between the de Winter’s and an occluded artery, a pharmacoinvasive strategy for reperfusion was adopted. The patient was given 1.5 million units of streptokinase which was infused over a period of an hour. During the course of thrombolytic therapy, the patient developed a reperfusion rhythm in the form of an accelerated idioventricular rhythm with subsequent resolution of chest pain and disappearance of the de Winter’s pattern on the ECG (). The patient was transferred to our PCI-capable centre with angiography confirming a severe proximal LAD lesion with evidence of plaque rupture which had reperfused and was successfully stented (). Peak highly sensitive troponin I level measured 2834 ng/L (normal < 14 ng/L) and echocardiography revealed an ejection fraction of 30–35% with RWMAs within the LAD territory (). She had an uneventful stay in the ward and was discharged 2 days after PCI on DAPT [oral aspirin (lifelong), oral clopidogrel (6 months)], and lifelong simvastatin enalapril, atenolol, and furosemide. Subsequent follow-up at 3 months revealed an improvement of LVEF to low-normal (50–55%) with discontinuation of diuretic therapy.\nOUTPUT:" }, { "from": "agent", "value": "STEMI" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 34-year-old female with a strong smoking history (>25 pack years), dyslipidaemia, and increased body mass index, but not on any medical therapy, presented with a 2-h history of typical ischaemic chest pain to the emergency department of a non-PCI centre. Initial ECG showed evidence of a de Winter’s pattern () with slight ST-elevation in the septal leads V1, V2. Initial clinical evaluation revealed a normal cardiovascular examination with no clinical evidence of heart failure. Due to ongoing severe chest pain, the inability to transfer the patient to the closest PCI centre within 120 min and the close association between the de Winter’s and an occluded artery, a pharmacoinvasive strategy for reperfusion was adopted. The patient was given 1.5 million units of streptokinase which was infused over a period of an hour. During the course of thrombolytic therapy, the patient developed a reperfusion rhythm in the form of an accelerated idioventricular rhythm with subsequent resolution of chest pain and disappearance of the de Winter’s pattern on the ECG (). The patient was transferred to our PCI-capable centre with angiography confirming a severe proximal LAD lesion with evidence of plaque rupture which had reperfused and was successfully stented (). Peak highly sensitive troponin I level measured 2834 ng/L (normal < 14 ng/L) and echocardiography revealed an ejection fraction of 30–35% with RWMAs within the LAD territory (). She had an uneventful stay in the ward and was discharged 2 days after PCI on DAPT [oral aspirin (lifelong), oral clopidogrel (6 months)], and lifelong simvastatin enalapril, atenolol, and furosemide. Subsequent follow-up at 3 months revealed an improvement of LVEF to low-normal (50–55%) with discontinuation of diuretic therapy. OUTPUT:
PMCPatients_common3448
[ { "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 previously healthy man presented to our institution with a large mass in his left axilla. The mass had been present for several months but had grown significantly in recent weeks. The mass measured 17 cm in maximum dimension and was relatively mobile. The mass had developed superficial skin ulceration and was malodorous (). There was purulent material draining from the ulcerated areas. Of note, the patient was a factory worker in an industrial plant and had been exposed to benzene for over 20 years. A computed tomography (CT) scan of the chest revealed the large axillary mass, multiple bilateral pulmonary nodules and splenomegaly with rounded, hypodense areas ().\\nGiven that the axillary mass was infected, the patient underwent a complete resection of the mass. The mass abutted the axillary vein and thoracodorsal nerve, but these structures were spared. The skin was kept open and had a wound vacuum dressing applied. The patient had an uneventful postoperative course and was discharged on day 4.\\nHistologic analysis of the mass showed a diffuse lymphoid infiltrate of predominantly large atypical lymphoid cells. Staining was negative for CD10, CD5, CD43, CD34, multiple myeloma oncogene 1 (MUM-1) and terminal deoxynucleotidyl transferase (TdT) as well as myelocytomatosis oncogene (c-myc). Fluorescence in situ hybridization (FISH) was positive for both c-myc and BCL-6. The patient was given three cycles of including dose adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab (DA-EPOCH-R). On follow-up in 7 months after surgery, he was asymptomatic and the wound had healed completely.\nOUTPUT:" }, { "from": "agent", "value": "Double-hit, high-grade B-cell lymphoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 45-year-old previously healthy man presented to our institution with a large mass in his left axilla. The mass had been present for several months but had grown significantly in recent weeks. The mass measured 17 cm in maximum dimension and was relatively mobile. The mass had developed superficial skin ulceration and was malodorous (). There was purulent material draining from the ulcerated areas. Of note, the patient was a factory worker in an industrial plant and had been exposed to benzene for over 20 years. A computed tomography (CT) scan of the chest revealed the large axillary mass, multiple bilateral pulmonary nodules and splenomegaly with rounded, hypodense areas ().\nGiven that the axillary mass was infected, the patient underwent a complete resection of the mass. The mass abutted the axillary vein and thoracodorsal nerve, but these structures were spared. The skin was kept open and had a wound vacuum dressing applied. The patient had an uneventful postoperative course and was discharged on day 4.\nHistologic analysis of the mass showed a diffuse lymphoid infiltrate of predominantly large atypical lymphoid cells. Staining was negative for CD10, CD5, CD43, CD34, multiple myeloma oncogene 1 (MUM-1) and terminal deoxynucleotidyl transferase (TdT) as well as myelocytomatosis oncogene (c-myc). Fluorescence in situ hybridization (FISH) was positive for both c-myc and BCL-6. The patient was given three cycles of including dose adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab (DA-EPOCH-R). On follow-up in 7 months after surgery, he was asymptomatic and the wound had healed completely. OUTPUT:
PMCPatients_common4217
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 38-year-old multiparous woman wit previous cesarean delivery at 7th week of gestation was admitted at clinic, due to her medical record, vaginal bleeding. Obstetric history was significant for a one cesarean delivery three years ago. Transvaginal ultrasound was performed and showed two gestational sacks, one was positioned low in uterus (supracervical location) and alive embryo with CRL 11mm. The other one gestational sack was positioned in fundal region of uterus, but with absence of the embryo. According to sonographic finding, the patient underwent dilatation, vacuum aspiration and curettage as a management option. At the time of admittance performed transvaginal ultrasound showed mixed echogenicity formation in isthmico-cervical region, with marked thinning of the anterior and side myometrium. The value of beta-human chorionic gonadotropin serum concentration was 8,418 mU/ml. At the second day after surgery value of beta human chorionic gonadotropin serum concentration dropped to 76,4 mU/ml, patient was well.\nOUTPUT:" }, { "from": "agent", "value": "Cesarean Scar Pregnancy, Placenta Percreta" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 38-year-old multiparous woman wit previous cesarean delivery at 7th week of gestation was admitted at clinic, due to her medical record, vaginal bleeding. Obstetric history was significant for a one cesarean delivery three years ago. Transvaginal ultrasound was performed and showed two gestational sacks, one was positioned low in uterus (supracervical location) and alive embryo with CRL 11mm. The other one gestational sack was positioned in fundal region of uterus, but with absence of the embryo. According to sonographic finding, the patient underwent dilatation, vacuum aspiration and curettage as a management option. At the time of admittance performed transvaginal ultrasound showed mixed echogenicity formation in isthmico-cervical region, with marked thinning of the anterior and side myometrium. The value of beta-human chorionic gonadotropin serum concentration was 8,418 mU/ml. At the second day after surgery value of beta human chorionic gonadotropin serum concentration dropped to 76,4 mU/ml, patient was well. OUTPUT:
PMCPatients_common1653
[ { "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 patient was met with an accident due to collision between bike and truck. Female who was sitting on back seat of bike was fallen. Her face was caught in the rear tyre of a truck. The patient was immediately brought to hospital. The patient had profuse bleeding and was in shock. Initial resuscitation of patient was done in emergency department. A complete physical examination of patient was done. There was no obvious injury over her body except face. Degloving of face was extending from temporal region of scalp, upper and lower conjunctiva, and cheek to upper and lower lip. Patient CT Scan of head and face done. NCCT head was normal. Ophthalmology reference was done for ocular injury. Nasal intubation was done. Thorough wash was given to remove dirt and dead tissue. Anatomical landmarks of avulsed hemifacial flap were identified and matched with its counterparts. Layered closure was performed to achieve oral competence. Left Upper and lower eyelid were avulsed from muco-cutaneus junction. Closure of muco-cutaneus junction was achieved. Closure of scalp wound was done over a suction drain. Dressing done and patient was shifted to intensive care unit for 2 days. Tarsorraphy of right eye was performed. Patient was discharged on postoperative day 9.\nOUTPUT:" }, { "from": "agent", "value": "Hemifacial Degloving of right side of the face, fracture of right condyle of mandible, right zygomatic arch comminuted fracture, fracture of right zygomatic-frontal buttress, right zygomatic-maxillary buttress, nasal bone fracture, fracture alveolar process of maxilla, corneal abrasion" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 45-year-old female patient was met with an accident due to collision between bike and truck. Female who was sitting on back seat of bike was fallen. Her face was caught in the rear tyre of a truck. The patient was immediately brought to hospital. The patient had profuse bleeding and was in shock. Initial resuscitation of patient was done in emergency department. A complete physical examination of patient was done. There was no obvious injury over her body except face. Degloving of face was extending from temporal region of scalp, upper and lower conjunctiva, and cheek to upper and lower lip. Patient CT Scan of head and face done. NCCT head was normal. Ophthalmology reference was done for ocular injury. Nasal intubation was done. Thorough wash was given to remove dirt and dead tissue. Anatomical landmarks of avulsed hemifacial flap were identified and matched with its counterparts. Layered closure was performed to achieve oral competence. Left Upper and lower eyelid were avulsed from muco-cutaneus junction. Closure of muco-cutaneus junction was achieved. Closure of scalp wound was done over a suction drain. Dressing done and patient was shifted to intensive care unit for 2 days. Tarsorraphy of right eye was performed. Patient was discharged on postoperative day 9. OUTPUT:
PMCPatients_common3245
[ { "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 clinical neurological examination revealed a deep coma. The clinical neurological examination revealed a deep coma, with a Glasgow coma scale score of 3/15.\\nOn hospital day 18, laboratory tests showed 105 mg/L of C-reactive protein (CRP), and the white blood cell count (WBC) was 10.37 × 109/L. Additionally, his renal and liver function tests were normal. The cerebral spinal fluid (CSF) obtained through lumbar puncture showed increased WBC, while the glucose level was 0.8 mmol/L, and the total protein was 4.49 g/L. Three sets of sputum, blood, and CSF cultures were obtained, but no bacterial growth was detected in any of the three samples. On hospital day 21, analysis of the sputum and CSF cultures again demonstrated the absence of any bacterial growth. On hospital day 26, the patient's CSF culture tested positive for A. baumannii that was susceptible only to tigecycline, though susceptibility to polymyxin was not tested (Table ). The same strain of XDR A. baumannii was persistently isolated from the CSF until hospital day 35. The results of blood and CSF analysis are shown in Table .\\nOn hospital day 18, head computed tomography (CT) showed normal postoperative changes after the operations (Figure ). On hospital day 24, head CT indicated ventricular empyema (Figure ). On hospital day 29, no ventricular pus was detected on the head CT.\nOUTPUT:" }, { "from": "agent", "value": "Pyogenic ventriculitis caused by extensively drug-resistant Acinetobacter baumannii, Severe traumatic brain injury" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The clinical neurological examination revealed a deep coma. The clinical neurological examination revealed a deep coma, with a Glasgow coma scale score of 3/15.\nOn hospital day 18, laboratory tests showed 105 mg/L of C-reactive protein (CRP), and the white blood cell count (WBC) was 10.37 × 109/L. Additionally, his renal and liver function tests were normal. The cerebral spinal fluid (CSF) obtained through lumbar puncture showed increased WBC, while the glucose level was 0.8 mmol/L, and the total protein was 4.49 g/L. Three sets of sputum, blood, and CSF cultures were obtained, but no bacterial growth was detected in any of the three samples. On hospital day 21, analysis of the sputum and CSF cultures again demonstrated the absence of any bacterial growth. On hospital day 26, the patient's CSF culture tested positive for A. baumannii that was susceptible only to tigecycline, though susceptibility to polymyxin was not tested (Table ). The same strain of XDR A. baumannii was persistently isolated from the CSF until hospital day 35. The results of blood and CSF analysis are shown in Table .\nOn hospital day 18, head computed tomography (CT) showed normal postoperative changes after the operations (Figure ). On hospital day 24, head CT indicated ventricular empyema (Figure ). On hospital day 29, no ventricular pus was detected on the head CT. OUTPUT:
PMCPatients_common2071
[ { "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 had no frothy urine or hematuria. She did not have exertional breathlessness or orthopnea, and she had no history suggestive of a cardiac or hepatic cause of edema. She was not diabetic or hypertensive. She was commenced on methotrexate 10 mg weekly and infrequent nonsteroidal anti-inflammatory drugs, with good symptom control achieved.\\nHer physical examination revealed that she had bilateral pitting leg edema and periorbital edema. She was not pale or icteric. No malar rash, vasculitic rash, or distal gangrene was seen. She had evidence of mild synovitis of the small joints of the hands bilaterally with no deformities. No generalized lymphadenopathy or hepatosplenomegaly was noted. Her pulse rate was 90 beats per minute; her blood pressure was 170/100 mmHg; and her jugular venous pressure was elevated to 7 cm with an undisplaced cardiac apex and normal heart sounds. A fundus examination did not reveal papilledema. Her lungs were clear with equal breath sounds bilaterally. The results of the rest of the examination were normal. The patient was started on atorvastatin, enalapril, and diuretics. Intravenous methylprednisolone 1 g was given for 3 consecutive days, followed by 1 mg/kg oral prednisolone. She was started on intravenous cyclophosphamide 500 mg every 2 weeks for a total of six doses. She gradually had increasing urine output and was symptomatically better, with improving renal function. Her serum creatinine level was 110 μmol/L at her last clinic visit after 3 months of treatment.\nOUTPUT:" }, { "from": "agent", "value": "Crescentic glomerular nephritis, Rheumatoid arthritis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: She had no frothy urine or hematuria. She did not have exertional breathlessness or orthopnea, and she had no history suggestive of a cardiac or hepatic cause of edema. She was not diabetic or hypertensive. She was commenced on methotrexate 10 mg weekly and infrequent nonsteroidal anti-inflammatory drugs, with good symptom control achieved.\nHer physical examination revealed that she had bilateral pitting leg edema and periorbital edema. She was not pale or icteric. No malar rash, vasculitic rash, or distal gangrene was seen. She had evidence of mild synovitis of the small joints of the hands bilaterally with no deformities. No generalized lymphadenopathy or hepatosplenomegaly was noted. Her pulse rate was 90 beats per minute; her blood pressure was 170/100 mmHg; and her jugular venous pressure was elevated to 7 cm with an undisplaced cardiac apex and normal heart sounds. A fundus examination did not reveal papilledema. Her lungs were clear with equal breath sounds bilaterally. The results of the rest of the examination were normal. The patient was started on atorvastatin, enalapril, and diuretics. Intravenous methylprednisolone 1 g was given for 3 consecutive days, followed by 1 mg/kg oral prednisolone. She was started on intravenous cyclophosphamide 500 mg every 2 weeks for a total of six doses. She gradually had increasing urine output and was symptomatically better, with improving renal function. Her serum creatinine level was 110 μmol/L at her last clinic visit after 3 months of treatment. OUTPUT:
PMCPatients_common3043
[ { "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 no symptoms and a blood test only revealed a serum PSA level of over 10 000 ng/mL. A transrectal ultrasound-guided biopsy of his prostate revealed six cores (out of 6) of adenocarcinoma, with a Gleason score of 4 + 5. Bone scintigraphy showed diffuse increased tracer uptake with a pattern compatible with metastatic supercan (Fig. ). Computed tomography also indicated multiple bone metastases and multiple lymphadenopathy. There were no identifiable visceral organ metastases. He received ADT. ADT included LHRH agonist and bicalutamide and his serum PSA level decreased to 0.11 ng/mL (nadir) in 10 months, but his duration of response to initial ADT (time to castration resistance) was 12 months without androgen withdrawal syndrome. His serum PSA level increased to 1.1 ng/mL. The complete blood count was normal. The level of serum lactate dehydrogenase was slightly elevated, which was 242 U/L. The level of serum testosterone was 21 ng/dL, which achieved a castrate level. All other laboratory results including serum cholesterol levels were within normal limits.\\nAbiraterone acetate at a dose of 1000 mg per day along with 10 mg prednisone was administered as a first-line therapy for CRPC. Within 6 months, the patient achieved a complete PSA response. His serum PSA level reached a nadir (undetectable level). Follow-up bone scintigraphy demonstrated no area of intense uptake, suggesting the bone metastasis had disappeared (Fig. ). His serum PSA level remained at the nadir and no bone metastasis appeared for 4 years after starting abiraterone acetate (Fig. ). We reviewed the patient's medical history and medications. The patient's medical chart showed he had a history of hyperlipidemia (his total cholesterol level was 256 mg/dL) and he was started on atorvastatin at home just after starting abiraterone acetate.\nOUTPUT:" }, { "from": "agent", "value": "Metastatic castration-resistant prostate cancer" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: He had no symptoms and a blood test only revealed a serum PSA level of over 10 000 ng/mL. A transrectal ultrasound-guided biopsy of his prostate revealed six cores (out of 6) of adenocarcinoma, with a Gleason score of 4 + 5. Bone scintigraphy showed diffuse increased tracer uptake with a pattern compatible with metastatic supercan (Fig. ). Computed tomography also indicated multiple bone metastases and multiple lymphadenopathy. There were no identifiable visceral organ metastases. He received ADT. ADT included LHRH agonist and bicalutamide and his serum PSA level decreased to 0.11 ng/mL (nadir) in 10 months, but his duration of response to initial ADT (time to castration resistance) was 12 months without androgen withdrawal syndrome. His serum PSA level increased to 1.1 ng/mL. The complete blood count was normal. The level of serum lactate dehydrogenase was slightly elevated, which was 242 U/L. The level of serum testosterone was 21 ng/dL, which achieved a castrate level. All other laboratory results including serum cholesterol levels were within normal limits.\nAbiraterone acetate at a dose of 1000 mg per day along with 10 mg prednisone was administered as a first-line therapy for CRPC. Within 6 months, the patient achieved a complete PSA response. His serum PSA level reached a nadir (undetectable level). Follow-up bone scintigraphy demonstrated no area of intense uptake, suggesting the bone metastasis had disappeared (Fig. ). His serum PSA level remained at the nadir and no bone metastasis appeared for 4 years after starting abiraterone acetate (Fig. ). We reviewed the patient's medical history and medications. The patient's medical chart showed he had a history of hyperlipidemia (his total cholesterol level was 256 mg/dL) and he was started on atorvastatin at home just after starting abiraterone acetate. OUTPUT:
PMCPatients_common3631
[ { "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 been suffering from bizarre psychotic behaviors and inappropriate rearing of the both parents from childhood. While he had not been quite interested in interpersonal relationship or academic achievement, he did not show any clinical symptoms at the time of baseline assessment. A diagnosis of schizoid personality disorder was given. Until 3 years of followed up, despite of stress from his parents' disease and his mother's death, he was free of psychiatric symptoms and at good functional status. He no more felt the need to participate in the follow-up program and he refused follow-up assessments afterwards. Thus, from 2008 till 2011, he had been lost to follow-up, although later retrospective assessment strongly suggested the presence of sustained distress during this period. In Jul 2012, he wanted psychiatric counseling for depressive mood, anger, and communication problem. However, his symptoms were very mild and he was still functioning well in his life. Although there were some psychiatric symptoms, he did not meet the criteria for ultra-high risk for psychosis. In Dec 2013, after 9 years of follow-up, attenuated psychotic symptoms such as idea of reference, suspiciousness occurred, the severity fulfilling the ultra-high risk for psychosis. He was diagnosed as both genetic risk and deterioration and attenuated psychotic symptoms syndrome of ultra-high risk for psychosis and also as depressive disorder not otherwise specified. We tried intensive cognitive behavioral therapy and supportive psychotherapy but his compliance was poor. In Jul 2014, he showed persecutory delusion with a high level of conviction and his transition to a psychotic disorder was suspected. Disorganized speech and negative symptoms were also observed.\nOUTPUT:" }, { "from": "agent", "value": "Schizophrenia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: He had been suffering from bizarre psychotic behaviors and inappropriate rearing of the both parents from childhood. While he had not been quite interested in interpersonal relationship or academic achievement, he did not show any clinical symptoms at the time of baseline assessment. A diagnosis of schizoid personality disorder was given. Until 3 years of followed up, despite of stress from his parents' disease and his mother's death, he was free of psychiatric symptoms and at good functional status. He no more felt the need to participate in the follow-up program and he refused follow-up assessments afterwards. Thus, from 2008 till 2011, he had been lost to follow-up, although later retrospective assessment strongly suggested the presence of sustained distress during this period. In Jul 2012, he wanted psychiatric counseling for depressive mood, anger, and communication problem. However, his symptoms were very mild and he was still functioning well in his life. Although there were some psychiatric symptoms, he did not meet the criteria for ultra-high risk for psychosis. In Dec 2013, after 9 years of follow-up, attenuated psychotic symptoms such as idea of reference, suspiciousness occurred, the severity fulfilling the ultra-high risk for psychosis. He was diagnosed as both genetic risk and deterioration and attenuated psychotic symptoms syndrome of ultra-high risk for psychosis and also as depressive disorder not otherwise specified. We tried intensive cognitive behavioral therapy and supportive psychotherapy but his compliance was poor. In Jul 2014, he showed persecutory delusion with a high level of conviction and his transition to a psychotic disorder was suspected. Disorganized speech and negative symptoms were also observed. OUTPUT:
PMCPatients_common699
[ { "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 42-year-old man with a history of bilateral myopic LASIK surgery 10 years ago complained of right eye pain for 6 days after injured by a twig. Examination revealed a best corrected visual acuity (BCVA) of 20/100 in the right eye and 20/20 in the left eye. Initial slit lamp examination described 2 suspected ulcers with satellite lesions. Scraping for smear and culture was done, and topical 5% natamycin, 1% voriconazole, and levofloxacin were prescribed, but in vain. The patient was referred to our clinic 3 days later. Temporal flap inversion was noted. A, B). C–H). Topical 1% Voriconazole, 0.5% Levofloxacin, and 0.1% Betamethasone were given every hour around the clock. Later, the culture of the 2 dense infiltrates revealed P acnes, and topical antibiotics were shifted to 0.5% levofloxacin and 3% vancomycin Q2H around the clock at daytime. The cornea cleared up under topical antibiotics and steroids. Topography revealed symmetric smooth surface. The visual acuity returned to 20/20.\nOUTPUT:" }, { "from": "agent", "value": "Traumatic laser in situ keratomileusis flap dislocation, Epithelial ingrowth, Propionibacterium acnes infection, Diffuse lamellar keratitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 42-year-old man with a history of bilateral myopic LASIK surgery 10 years ago complained of right eye pain for 6 days after injured by a twig. Examination revealed a best corrected visual acuity (BCVA) of 20/100 in the right eye and 20/20 in the left eye. Initial slit lamp examination described 2 suspected ulcers with satellite lesions. Scraping for smear and culture was done, and topical 5% natamycin, 1% voriconazole, and levofloxacin were prescribed, but in vain. The patient was referred to our clinic 3 days later. Temporal flap inversion was noted. A, B). C–H). Topical 1% Voriconazole, 0.5% Levofloxacin, and 0.1% Betamethasone were given every hour around the clock. Later, the culture of the 2 dense infiltrates revealed P acnes, and topical antibiotics were shifted to 0.5% levofloxacin and 3% vancomycin Q2H around the clock at daytime. The cornea cleared up under topical antibiotics and steroids. Topography revealed symmetric smooth surface. The visual acuity returned to 20/20. OUTPUT:
PMCPatients_common3525
[ { "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-year-old female, educated up to 10th std, unmarried, 22 weeks gravida came to OPD with complaints of gradually progressive low mood, decreased interest in daily activities, feelings of hopelessness, worthlessness, sleep disturbance, and loss of appetite over the span of 4 years with increased intensity for the past 6 months. The patient reported that when she was 17 years old, her stepfather tried to molest her sexually. She was able to save herself by running out of the house. Later, her father threatened her not to tell anyone about the incident with which she got frightened. A month later, her stepfather again tried to force her to engage in sexual activity which she resisted. She complained to her mother when she returned from work, but her mother did not believe her and thought that she was lying. After a month, due to frequent quarrels in the family, she started feeling low. The symptoms increased to such an extent that she had to leave her job. Then by mutual decision, her parents asked her to live separately. The patient shifted with one of her friends who was residing in a rented flat. She found another job where she met a man. They frequently met each other and fell in love with each other. During this period, the patient started feeling well and regained hope of a better and happy life in future. After around 1 year of relationship, she became pregnant. On being informed of this, her boyfriend refused to have anything to do with the child. He even left the job and stopped all communication with her. After this, the patient decided that she will give birth to the child without any support and look after her child on her own. Gradually she started having low mood, began taking frequent leave from job, and used to sit alone at home and do nothing. She had disturbed sleep and poor appetite. She felt hopeless about her future and inability to support her child. On MSE, the patient appeared sad with teary eyes. Talk was relevant and coherent. The mood was depressed; there was no suicidal ideation. She responded satisfactorily to pharmacological treatment and cognitive behavior therapy and delivered a healthy male child.\nOUTPUT:" }, { "from": "agent", "value": "Recurrent depressive disorder" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 25-year-old female, educated up to 10th std, unmarried, 22 weeks gravida came to OPD with complaints of gradually progressive low mood, decreased interest in daily activities, feelings of hopelessness, worthlessness, sleep disturbance, and loss of appetite over the span of 4 years with increased intensity for the past 6 months. The patient reported that when she was 17 years old, her stepfather tried to molest her sexually. She was able to save herself by running out of the house. Later, her father threatened her not to tell anyone about the incident with which she got frightened. A month later, her stepfather again tried to force her to engage in sexual activity which she resisted. She complained to her mother when she returned from work, but her mother did not believe her and thought that she was lying. After a month, due to frequent quarrels in the family, she started feeling low. The symptoms increased to such an extent that she had to leave her job. Then by mutual decision, her parents asked her to live separately. The patient shifted with one of her friends who was residing in a rented flat. She found another job where she met a man. They frequently met each other and fell in love with each other. During this period, the patient started feeling well and regained hope of a better and happy life in future. After around 1 year of relationship, she became pregnant. On being informed of this, her boyfriend refused to have anything to do with the child. He even left the job and stopped all communication with her. After this, the patient decided that she will give birth to the child without any support and look after her child on her own. Gradually she started having low mood, began taking frequent leave from job, and used to sit alone at home and do nothing. She had disturbed sleep and poor appetite. She felt hopeless about her future and inability to support her child. On MSE, the patient appeared sad with teary eyes. Talk was relevant and coherent. The mood was depressed; there was no suicidal ideation. She responded satisfactorily to pharmacological treatment and cognitive behavior therapy and delivered a healthy male child. OUTPUT:
PMCPatients_common270
[ { "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 47-year-old white woman was admitted to our ENT clinic with the suspicion of acute gangrenous pharyngitis. She presented with unilateral pharyngeal discomfort starting 2 days before and precipitating during the previous 3 hours. Later, she also reported dysphagia, position-dependent dyspnea, and a superficial neck swelling. She had no history of trauma, no known coagulopathy, and had not been taking any anticoagulants. Arterial hypertension and obesity were part of her pre-existing conditions. She denied any snoring or any observed apneas. However, her mother was diagnosed as having OSA and was treated by continuous positive airway pressure (CPAP). An endoscopic examination showed a submucosal hemorrhage of the posterior wall of her pharynx, from the nasopharynx to the hypopharynx and extending to her vocal cords. The parameters of her hemostasis were standard with an activated partial thromboplastin time of 21.4 seconds and thrombocytes of 216 per nanoliter. An orotracheal intubation was indicated but rejected by our patient. She was referred to the intensive care unit (ICU) for further monitoring. After 1 day she was moved to a general ward. As snoring was reported by the nurses of the ICU, a subsequent seven-channel polygraphy was conducted, showing an apnea-hypopnea index of 59.5 per hour with an oxygen desaturation index of 69.9 per hour. She was subsequently provided with an automatic CPAP device to treat the newly diagnosed OSA. After 6 days she could be discharged (Fig. ).\\nTwo months after this episode, she presented without any complaints. The OSA remained sufficiently treated every night since the initial stay. A physical examination showed normal findings.\nOUTPUT:" }, { "from": "agent", "value": "Retropharyngeal hematoma, Obstructive sleep apnea" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 47-year-old white woman was admitted to our ENT clinic with the suspicion of acute gangrenous pharyngitis. She presented with unilateral pharyngeal discomfort starting 2 days before and precipitating during the previous 3 hours. Later, she also reported dysphagia, position-dependent dyspnea, and a superficial neck swelling. She had no history of trauma, no known coagulopathy, and had not been taking any anticoagulants. Arterial hypertension and obesity were part of her pre-existing conditions. She denied any snoring or any observed apneas. However, her mother was diagnosed as having OSA and was treated by continuous positive airway pressure (CPAP). An endoscopic examination showed a submucosal hemorrhage of the posterior wall of her pharynx, from the nasopharynx to the hypopharynx and extending to her vocal cords. The parameters of her hemostasis were standard with an activated partial thromboplastin time of 21.4 seconds and thrombocytes of 216 per nanoliter. An orotracheal intubation was indicated but rejected by our patient. She was referred to the intensive care unit (ICU) for further monitoring. After 1 day she was moved to a general ward. As snoring was reported by the nurses of the ICU, a subsequent seven-channel polygraphy was conducted, showing an apnea-hypopnea index of 59.5 per hour with an oxygen desaturation index of 69.9 per hour. She was subsequently provided with an automatic CPAP device to treat the newly diagnosed OSA. After 6 days she could be discharged (Fig. ).\nTwo months after this episode, she presented without any complaints. The OSA remained sufficiently treated every night since the initial stay. A physical examination showed normal findings. OUTPUT:
PMCPatients_common504
[ { "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 29-year-old man visited the memory clinic at Samsung Medical Center for 1 year of progressive memory impairment and visuospatial dysfunction. He was fired from his work due to serious memory problem and lost his way home from the workplace. He had 12 years of formal education and did not have any past history of medical problems. On neurological examination, he showed bradykinesia and tremor on the left side. On neuropsychological examination, he scored 25 on Mini-mental state examination and showed a severe impairment on visuospatial function, verbal memory and visual memory tests (Table ). He had a strong family history of early-onset dementia on his mother's side (Figure ). His mother was diagnosed to have dementia in her twenties and died at the age of 29 (Figure , II-1). His aunt was also demented in her thirties but did not visit the hospital (Figure , II-3). His grandfather was demented as he used to get lost in the neighbourhood in his forties (Figure , I-1). In genetic analysis, a known mutation in PSEN1 (p.S170F, c.509C>T) was identified as heterozygous. The APOE genotype was ε3/ε3. The patient's brain MRI showed an atrophy in the bilateral parietal areas (Figure ), and FDG-PET showed hypometabolism in the bilateral temporo-parietal area, suggestive of AD (Figure ). He showed a rapid cognitive decline and scored 19 on MMSE 6 months after his first visit. He also developed gait disturbance and action induced myoclonus on the bilateral legs. Two years later, he entered nursing home as he became fully dependent on basic daily activities and died at the age of 34. We collected the patient's blood sample when he was 33 years old.\\nThe cognitively normal control showed no atrophy on brain MRI (Figure ), and his 18F-florbetaben amyloid PET showed no significant amyloid deposition in the brain. His APOE genotype was e3/e4. This study was approved by the Institutional Review Board of Samsung Medical Center [1044308-201612-BR-031-05]. We obtained a written consent from each participant and his next of kin.\nOUTPUT:" }, { "from": "agent", "value": "Early-onset Alzheimer's disease" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 29-year-old man visited the memory clinic at Samsung Medical Center for 1 year of progressive memory impairment and visuospatial dysfunction. He was fired from his work due to serious memory problem and lost his way home from the workplace. He had 12 years of formal education and did not have any past history of medical problems. On neurological examination, he showed bradykinesia and tremor on the left side. On neuropsychological examination, he scored 25 on Mini-mental state examination and showed a severe impairment on visuospatial function, verbal memory and visual memory tests (Table ). He had a strong family history of early-onset dementia on his mother's side (Figure ). His mother was diagnosed to have dementia in her twenties and died at the age of 29 (Figure , II-1). His aunt was also demented in her thirties but did not visit the hospital (Figure , II-3). His grandfather was demented as he used to get lost in the neighbourhood in his forties (Figure , I-1). In genetic analysis, a known mutation in PSEN1 (p.S170F, c.509C>T) was identified as heterozygous. The APOE genotype was ε3/ε3. The patient's brain MRI showed an atrophy in the bilateral parietal areas (Figure ), and FDG-PET showed hypometabolism in the bilateral temporo-parietal area, suggestive of AD (Figure ). He showed a rapid cognitive decline and scored 19 on MMSE 6 months after his first visit. He also developed gait disturbance and action induced myoclonus on the bilateral legs. Two years later, he entered nursing home as he became fully dependent on basic daily activities and died at the age of 34. We collected the patient's blood sample when he was 33 years old.\nThe cognitively normal control showed no atrophy on brain MRI (Figure ), and his 18F-florbetaben amyloid PET showed no significant amyloid deposition in the brain. His APOE genotype was e3/e4. This study was approved by the Institutional Review Board of Samsung Medical Center [1044308-201612-BR-031-05]. We obtained a written consent from each participant and his next of kin. OUTPUT:
PMCPatients_common508
[ { "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 woman was admitted with a 3-year history of primary infertility and oligo-anovulation. Her BMI was 19.7 kg/m2 and her total AFC was 27. A low-dose step-up protocol with a daily dosage of 75 IU (Puregon, MSD, İstanbul, Turkey) for ovulation induction was employed. On the 9th day of ovarian stimulation (OS), folliculometry with ultrasonography revealed one follicle of >17 mm, two follicles between 13-14 mm, and two follicles between 11-13 mm with an estradiol level of 2100 pg/mL. We decided to trigger (Ovitrelle, Merck, Istanbul) and perform intrauterine insemination (IUI) 36 hours later because she had only one leading follicle exceeding 17 mm.\\nEight days after triggering, she was admitted to the emergency department with right chest pain, dyspnea, tachypnea, and tachycardia. The heart rate was 110/minute, blood pressure was 105/70 mm Hg, and her body temperature was 37.1°C. In a physical examination, diminished respiration sounds on the right hemi-thorax and a mild abdominal discomfort was noticed. In laboratory tests, the hemoglobin (Hb) was 15.1 g/dL, hematocrit (HCT) was 45.9%, and white blood cell (WBC) count was 16.4x103. The serum electrolytes, liver enzymes, creatinine value, and cardiac panel were within the normal range; there was a slight increase in D-Dimer level up to 2.1 mg/L. Under ultrasonography, there was only minimal fluid accumulation in the recto-uterine pouch. Under fluoroscopy guidance, a total of 1500 mL serous characterized fluid was drained via transthoracic aspiration with a 22-G needle (Cook, Inc., Bloomington, IN, USA). Immediately after intervention, the symptoms were relieved and the HCT declined to 37% one day after the procedure. The patient was discharged from hospital four days later but she failed to conceive.\nOUTPUT:" }, { "from": "agent", "value": "Ovarian hyperstimulation syndrome, Unilateral right-side hydrothorax" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 28-year-old woman was admitted with a 3-year history of primary infertility and oligo-anovulation. Her BMI was 19.7 kg/m2 and her total AFC was 27. A low-dose step-up protocol with a daily dosage of 75 IU (Puregon, MSD, İstanbul, Turkey) for ovulation induction was employed. On the 9th day of ovarian stimulation (OS), folliculometry with ultrasonography revealed one follicle of >17 mm, two follicles between 13-14 mm, and two follicles between 11-13 mm with an estradiol level of 2100 pg/mL. We decided to trigger (Ovitrelle, Merck, Istanbul) and perform intrauterine insemination (IUI) 36 hours later because she had only one leading follicle exceeding 17 mm.\nEight days after triggering, she was admitted to the emergency department with right chest pain, dyspnea, tachypnea, and tachycardia. The heart rate was 110/minute, blood pressure was 105/70 mm Hg, and her body temperature was 37.1°C. In a physical examination, diminished respiration sounds on the right hemi-thorax and a mild abdominal discomfort was noticed. In laboratory tests, the hemoglobin (Hb) was 15.1 g/dL, hematocrit (HCT) was 45.9%, and white blood cell (WBC) count was 16.4x103. The serum electrolytes, liver enzymes, creatinine value, and cardiac panel were within the normal range; there was a slight increase in D-Dimer level up to 2.1 mg/L. Under ultrasonography, there was only minimal fluid accumulation in the recto-uterine pouch. Under fluoroscopy guidance, a total of 1500 mL serous characterized fluid was drained via transthoracic aspiration with a 22-G needle (Cook, Inc., Bloomington, IN, USA). Immediately after intervention, the symptoms were relieved and the HCT declined to 37% one day after the procedure. The patient was discharged from hospital four days later but she failed to conceive. OUTPUT:
PMCPatients_common379
[ { "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 HAART-naive HIV seropositive male weighing 48 kg presented with forgetfulness, irritability and incontinence of urine, along with fever and headache for the last two months. His CD4+ cell counts were 36/μl, and he was seronegative for hepatitis B and C. He did not experience seizure or took anti-epileptic medication. Clinical examination revealed neurocognitive impairment with a mini-mental status score of 14/30. There was no focal neurological deficit. A computed tomography (CT) of the brain (Figure ) showed a hypodense lesion in the left frontal lobe. value>55 mg/dl), cells 32/cmm (lymphocytes) and Cryptococcus Antigen Latex Agglutination System 4+. The rapid CSF Cryptococcus Antigen Latex Agglutination assay was the preferred diagnostic approach. The treatment regimen of amphotericin B in the dose of 0.7 mg/kg of body weight in 5% dextrose IV infusion daily for 12 days and fluconazole (400 mg) orally (in place of flucytosine) per day was initiated. Serum electrolytes were monitored during amphotericin B infusion. Antiretroviral drugs such as tenofovir, lamivudine and efavirenz were started after two weeks of treatment with antifungal drugs. Fluconazole 400 mg/day was continued for 10 weeks. Following the treatment, neurocognitive functions improved markedly with a mini-mental state score of 26/30 and CD+ T-cell counts of 165/μl. However, CT image (Figure ) still showed a heterogeneous hypodense lesion with elements of peripheral enhancement in the left frontal lobe.\\nFluconazole (200 mg per day) was continued along with HAART. At the end of six months, CD4+ cell counts were up to 246/μl and a further CT image (Figure ) showed a resolution of the neurolesion.\nOUTPUT:" }, { "from": "agent", "value": "Cryptococcal Immune Reconstitution Inflammatory Syndrome, Cryptococcal meningitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 32-year-old HAART-naive HIV seropositive male weighing 48 kg presented with forgetfulness, irritability and incontinence of urine, along with fever and headache for the last two months. His CD4+ cell counts were 36/μl, and he was seronegative for hepatitis B and C. He did not experience seizure or took anti-epileptic medication. Clinical examination revealed neurocognitive impairment with a mini-mental status score of 14/30. There was no focal neurological deficit. A computed tomography (CT) of the brain (Figure ) showed a hypodense lesion in the left frontal lobe. value>55 mg/dl), cells 32/cmm (lymphocytes) and Cryptococcus Antigen Latex Agglutination System 4+. The rapid CSF Cryptococcus Antigen Latex Agglutination assay was the preferred diagnostic approach. The treatment regimen of amphotericin B in the dose of 0.7 mg/kg of body weight in 5% dextrose IV infusion daily for 12 days and fluconazole (400 mg) orally (in place of flucytosine) per day was initiated. Serum electrolytes were monitored during amphotericin B infusion. Antiretroviral drugs such as tenofovir, lamivudine and efavirenz were started after two weeks of treatment with antifungal drugs. Fluconazole 400 mg/day was continued for 10 weeks. Following the treatment, neurocognitive functions improved markedly with a mini-mental state score of 26/30 and CD+ T-cell counts of 165/μl. However, CT image (Figure ) still showed a heterogeneous hypodense lesion with elements of peripheral enhancement in the left frontal lobe.\nFluconazole (200 mg per day) was continued along with HAART. At the end of six months, CD4+ cell counts were up to 246/μl and a further CT image (Figure ) showed a resolution of the neurolesion. OUTPUT:
PMCPatients_common306
[ { "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 female patient, a psychiatric nurse, was recommended at 19 years to the outpatient facility specializing in eating disorders (ED). She has a history of long-term repeated vomiting, diets, meat rejection, vegetarianism, abuse of laxatives, drinking of some bleach, and excessive exercise. Always skeptical about the treatment, she expressed the feeling she can live with the disease because without it she would lose her self-image. During the years of illness, she experienced various psychotherapy and pharmacotherapy (venlafaxin, hypnogen, seropram, prothazin, rivotril, prothiaden, fevarin), and had been hospitalized as an inpatient at the day care of a specialized ED center. When she reached 60 kg/173 cm (BMI 20.05), she felt \"fat as a pig\", and focused only on weight loss and gradually increasing somatic difficulties. Despite various antibiotic treatment regimes, and a low saccharide diet, only mild and temporary symptom alleviation was achieved. There were no known contraindications for this procedure. During the study, the authors monitored her psychiatric symptoms, family dynamics, and specific symptoms with eating disorder examination questionnaire (EDEQ).\nOUTPUT:" }, { "from": "agent", "value": "Anorexia Nervosa, Dyspepsia, Malnutrition, Dysmicrobia with dyspeptic syndrome, Mycotic upper esophagitis, Hooked stomach, Stomach evacuation disorder, Duodenogastric reflux, Galactosemia, SIBO" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 37 year old female patient, a psychiatric nurse, was recommended at 19 years to the outpatient facility specializing in eating disorders (ED). She has a history of long-term repeated vomiting, diets, meat rejection, vegetarianism, abuse of laxatives, drinking of some bleach, and excessive exercise. Always skeptical about the treatment, she expressed the feeling she can live with the disease because without it she would lose her self-image. During the years of illness, she experienced various psychotherapy and pharmacotherapy (venlafaxin, hypnogen, seropram, prothazin, rivotril, prothiaden, fevarin), and had been hospitalized as an inpatient at the day care of a specialized ED center. When she reached 60 kg/173 cm (BMI 20.05), she felt "fat as a pig", and focused only on weight loss and gradually increasing somatic difficulties. Despite various antibiotic treatment regimes, and a low saccharide diet, only mild and temporary symptom alleviation was achieved. There were no known contraindications for this procedure. During the study, the authors monitored her psychiatric symptoms, family dynamics, and specific symptoms with eating disorder examination questionnaire (EDEQ). OUTPUT:
PMCPatients_common1334
[ { "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 male was admitted to the University of Tsukuba Hospital (Mito, Japan) for an examination of a chest nodule in the right upper lobe of the lung. On admission, the laboratory examination revealed a hemoglobin level of 13.9 g/dl, a hematocrit level of 41.6% and a lactate dehydrogenase level of 139 IU/l. The serum level of neuron-specific enolase (NSE) was 19.9 ng/ml and the pro-gastrin-releasing peptide (proGRP) level was elevated to 522.1 pg/ml. A chest X-ray and computed tomography (CT) scan revealed a poorly-defined mass in the upper lobe of the right lung, with an ipsilateral mediastinal lymph node swelling. A transbronchial biopsy revealed the tumor to be SCLC. As no metastatic lesion was identified, the tumor was diagnosed as limited disease-SCLC. The patient was treated using chemoradiotherapy (chest irradiation up to 65 Gy and four courses of chemotherapy) containing cisplatin (80 mg/m2, day 1 for 4 weeks) and etoposide (100 mg/m2, days 1–3, for 4 weeks), which resulted in a complete response (CR). A requirement for prophylactic cranial irradiation (PCI) was indicated, however, whole brain irradiation was not administered as the patient did not want the therapy. Subsequent to 18 months from the initial diagnosis of SCLC, a metastatic lesion was observed in the right temporal lobe of the cerebral hemisphere during a follow-up magnetic resonance imaging (MRI) scan (). The patient was administered 30 Gy whole grain irradiation and four courses of platinum-containing chemotherapy consisting of cisplatin (80 mg/m2, day 1 for 4 weeks) and etoposide (100 mg/m2, days 1–3 for 4 weeks). The patient eventually succumbed to cardiac disease seven years after the recurrence. However, no further recurrence was observed until the patient succumbed.\nOUTPUT:" }, { "from": "agent", "value": "Isolated solitary brain metastasis, Relapse of small cell lung cancer" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 63-year-old male was admitted to the University of Tsukuba Hospital (Mito, Japan) for an examination of a chest nodule in the right upper lobe of the lung. On admission, the laboratory examination revealed a hemoglobin level of 13.9 g/dl, a hematocrit level of 41.6% and a lactate dehydrogenase level of 139 IU/l. The serum level of neuron-specific enolase (NSE) was 19.9 ng/ml and the pro-gastrin-releasing peptide (proGRP) level was elevated to 522.1 pg/ml. A chest X-ray and computed tomography (CT) scan revealed a poorly-defined mass in the upper lobe of the right lung, with an ipsilateral mediastinal lymph node swelling. A transbronchial biopsy revealed the tumor to be SCLC. As no metastatic lesion was identified, the tumor was diagnosed as limited disease-SCLC. The patient was treated using chemoradiotherapy (chest irradiation up to 65 Gy and four courses of chemotherapy) containing cisplatin (80 mg/m2, day 1 for 4 weeks) and etoposide (100 mg/m2, days 1–3, for 4 weeks), which resulted in a complete response (CR). A requirement for prophylactic cranial irradiation (PCI) was indicated, however, whole brain irradiation was not administered as the patient did not want the therapy. Subsequent to 18 months from the initial diagnosis of SCLC, a metastatic lesion was observed in the right temporal lobe of the cerebral hemisphere during a follow-up magnetic resonance imaging (MRI) scan (). The patient was administered 30 Gy whole grain irradiation and four courses of platinum-containing chemotherapy consisting of cisplatin (80 mg/m2, day 1 for 4 weeks) and etoposide (100 mg/m2, days 1–3 for 4 weeks). The patient eventually succumbed to cardiac disease seven years after the recurrence. However, no further recurrence was observed until the patient succumbed. OUTPUT:
PMCPatients_common3024
[ { "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 patient with a medical history of hypertension and hyperlipidaemia presented to the emergency room with a 3-day history of dyspnoea. His blood pressure at presentation was 85/51 mmHg, heart rate was 80 beats per minute, respiratory rate was 36 breaths per minute and oxygen saturation was 70% on room air. The patient was intubated, mechanically ventilated, started on norepinephrine for hypotension and admitted to the medical intensive care unit (MICU). The patient’s chest x-ray is shown in .\\nA baseline ECG showed non-specific T wave changes but did not demonstrate acute ischaemic changes or arrhythmia (). The patient’s baseline troponin was 0.17 ng/ml. On day 2 of hospitalization, the patient’s hypoxia worsened, requiring maximum ventilatory support and sedation. After administration of loading doses, aspirin 81 mg, clopidogrel 75 mg and a heparin drip were initiated. The patient’s other medications included azithromycin, hydroxychloroquine, meropenem, tocilizumab, norepinephrine, phenylephrine, vasopressin, atracurium, propofol and fentanyl.\\nA transthoracic echocardiogram (TTE) showed a vigorous ejection fraction of 70–75% with no regional wall motion abnormalities ().\\nRepeat troponins obtained 6 hours apart were 0.056 ng/ml, 0.123 ng/ml and 0.11 ng/ml, respectively. Unfortunately, patient did not recover and died 24 hours later.\nOUTPUT:" }, { "from": "agent", "value": "Transient ST Segment Elevation, COVID-19" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 64-year-old male patient with a medical history of hypertension and hyperlipidaemia presented to the emergency room with a 3-day history of dyspnoea. His blood pressure at presentation was 85/51 mmHg, heart rate was 80 beats per minute, respiratory rate was 36 breaths per minute and oxygen saturation was 70% on room air. The patient was intubated, mechanically ventilated, started on norepinephrine for hypotension and admitted to the medical intensive care unit (MICU). The patient’s chest x-ray is shown in .\nA baseline ECG showed non-specific T wave changes but did not demonstrate acute ischaemic changes or arrhythmia (). The patient’s baseline troponin was 0.17 ng/ml. On day 2 of hospitalization, the patient’s hypoxia worsened, requiring maximum ventilatory support and sedation. After administration of loading doses, aspirin 81 mg, clopidogrel 75 mg and a heparin drip were initiated. The patient’s other medications included azithromycin, hydroxychloroquine, meropenem, tocilizumab, norepinephrine, phenylephrine, vasopressin, atracurium, propofol and fentanyl.\nA transthoracic echocardiogram (TTE) showed a vigorous ejection fraction of 70–75% with no regional wall motion abnormalities ().\nRepeat troponins obtained 6 hours apart were 0.056 ng/ml, 0.123 ng/ml and 0.11 ng/ml, respectively. Unfortunately, patient did not recover and died 24 hours later. OUTPUT:
PMCPatients_common4816
[ { "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 21-year-old male with dissociative convulsions and fugue.\\nWhen Mr. F first visited us in March 2013, he was a 21 years old single student into his 2nd year of graduation. There was no past or family history of neuropsychiatric morbidity or substance use. He presented with episodes of tonic stretching of his limb and neck muscles. These episodes occurred in a clear consciousness without any fall, incontinence or injury in a frequency of once-twice a month starting from 2004. These episodes had increased to ten-twelve per day since April 2013 with some correlation of increasing stress after working for a brief period of time in a call center; each episode lasting for around 10-20 min with Mr. F being well aware of the surrounding around him and able to recollect conversations around him during the episode.\\nThere was one episode for around half an hour in which Mr. F had wandered out of the house to an unknown location and had to be traced and when found, was unaware of his whereabouts and how he had got there.\\nHe underwent an awake EEG and a computed tomography scan brain which showed normal results. He had been treated with a combination of antiepileptics and antidepressants with no improvement in his condition.\\nHe was admitted in April 2013 on an involuntary basis and treatment was initiated with a major focus on nonpharmacological strategies, elicitation of stressors, and all his medications were tapered and stopped.\\nThe episodes continued during an inpatient stay. He wondered out of the ward during one of his episodes and was not traceable for 24 h. He returned on his own and recollected that he had boarded a train and had gone to an unknown location, but was unable to recall what he did at that place or how did he maintain himself in those 24 h. He recollected that he was restless and had to go.\\nThe resistance to therapy continued for nearly 3 weeks, until 1 day when he started reported fearfulness, persecutory delusions that a “shaitan” has done black magic on to him and auditory hallucinations of “Allah” calling him. He is maintaining well till June 2013 and had resumed his studies.\nOUTPUT:" }, { "from": "agent", "value": "Paranoid Schizophrenia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 21-year-old male with dissociative convulsions and fugue.\nWhen Mr. F first visited us in March 2013, he was a 21 years old single student into his 2nd year of graduation. There was no past or family history of neuropsychiatric morbidity or substance use. He presented with episodes of tonic stretching of his limb and neck muscles. These episodes occurred in a clear consciousness without any fall, incontinence or injury in a frequency of once-twice a month starting from 2004. These episodes had increased to ten-twelve per day since April 2013 with some correlation of increasing stress after working for a brief period of time in a call center; each episode lasting for around 10-20 min with Mr. F being well aware of the surrounding around him and able to recollect conversations around him during the episode.\nThere was one episode for around half an hour in which Mr. F had wandered out of the house to an unknown location and had to be traced and when found, was unaware of his whereabouts and how he had got there.\nHe underwent an awake EEG and a computed tomography scan brain which showed normal results. He had been treated with a combination of antiepileptics and antidepressants with no improvement in his condition.\nHe was admitted in April 2013 on an involuntary basis and treatment was initiated with a major focus on nonpharmacological strategies, elicitation of stressors, and all his medications were tapered and stopped.\nThe episodes continued during an inpatient stay. He wondered out of the ward during one of his episodes and was not traceable for 24 h. He returned on his own and recollected that he had boarded a train and had gone to an unknown location, but was unable to recall what he did at that place or how did he maintain himself in those 24 h. He recollected that he was restless and had to go.\nThe resistance to therapy continued for nearly 3 weeks, until 1 day when he started reported fearfulness, persecutory delusions that a “shaitan” has done black magic on to him and auditory hallucinations of “Allah” calling him. He is maintaining well till June 2013 and had resumed his studies. OUTPUT:
PMCPatients_common1170
[ { "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: We report the MRI findings of an incidental focal liver lesion, which was detected by ultrasound (US) in a 75-year-old Albanian man treated for benign hypertrophy of the prostate. His physical examination and laboratory test results were unremarkable.\\nMulti-detector chest and abdominal computed tomography (MDCT), with intravenous administration of 100mL iodinated contrast material was performed using a Emotion 6 MDCT device (Siemens Medical Systems, Erlangen, Germany). MDCT scans showed a focal liver lesion in the right lobe, and a mild enlargement of the prostate gland. No other abnormalities were identified in the rest of his chest and abdomen. Subsequently, an MRI scan of the upper abdomen was performed for better characterization of this lesion.\\nAn MRI scan was performed using a 1.5T magnetic resonance unit (Avanto; Siemens Medical Systems, Erlangen, Germany), using a set protocol including unenhanced sequences and enhanced sequences, obtained in early phase at 25 seconds after administration of intravenous contrast gadolinium (Magnevist, Bayer HealthCare) at 2mL/second, 45 and 90 seconds (late phase).\\nTwo-dimensional gradient echo in axial plane was performed using these parameters: TR/TE 140 to 200/2.2 to 2.4ms, flip angle 80, slice thickness 6mm, image matrix 128 × 256 and acquisition time 20 seconds.\\nA three-dimensional gradient echo sequence (VIBE) with a fat saturation was performed before and after administration of intravenous contrast using the following parameters: 5.58/2.38ms, flip angle 10, matrix 320 × 256, slice thickness 3.3mm and acquisition time 20 seconds.\\nA dual T1-weighted spoiled gradient echo (SGE) sequences in phase/out-of-phase was obtained in the axial plane using the following parameters: 113/4.92/2.22ms, flip angle 70, slice thickness 8mm and acquisition time 22 seconds for each sequence.\\nT2-weighted half-Fourier acquisition single-shot turbo spin echo (HASTE) with and without fat saturation was obtained using the following parameters: 1000/94ms, flip angle 15, slice thickness 6mm, matrix 320 × 246 and acquisition time 22 seconds.\nOUTPUT:" }, { "from": "agent", "value": "Primary lymphoma of the liver" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: We report the MRI findings of an incidental focal liver lesion, which was detected by ultrasound (US) in a 75-year-old Albanian man treated for benign hypertrophy of the prostate. His physical examination and laboratory test results were unremarkable.\nMulti-detector chest and abdominal computed tomography (MDCT), with intravenous administration of 100mL iodinated contrast material was performed using a Emotion 6 MDCT device (Siemens Medical Systems, Erlangen, Germany). MDCT scans showed a focal liver lesion in the right lobe, and a mild enlargement of the prostate gland. No other abnormalities were identified in the rest of his chest and abdomen. Subsequently, an MRI scan of the upper abdomen was performed for better characterization of this lesion.\nAn MRI scan was performed using a 1.5T magnetic resonance unit (Avanto; Siemens Medical Systems, Erlangen, Germany), using a set protocol including unenhanced sequences and enhanced sequences, obtained in early phase at 25 seconds after administration of intravenous contrast gadolinium (Magnevist, Bayer HealthCare) at 2mL/second, 45 and 90 seconds (late phase).\nTwo-dimensional gradient echo in axial plane was performed using these parameters: TR/TE 140 to 200/2.2 to 2.4ms, flip angle 80, slice thickness 6mm, image matrix 128 × 256 and acquisition time 20 seconds.\nA three-dimensional gradient echo sequence (VIBE) with a fat saturation was performed before and after administration of intravenous contrast using the following parameters: 5.58/2.38ms, flip angle 10, matrix 320 × 256, slice thickness 3.3mm and acquisition time 20 seconds.\nA dual T1-weighted spoiled gradient echo (SGE) sequences in phase/out-of-phase was obtained in the axial plane using the following parameters: 113/4.92/2.22ms, flip angle 70, slice thickness 8mm and acquisition time 22 seconds for each sequence.\nT2-weighted half-Fourier acquisition single-shot turbo spin echo (HASTE) with and without fat saturation was obtained using the following parameters: 1000/94ms, flip angle 15, slice thickness 6mm, matrix 320 × 246 and acquisition time 22 seconds. OUTPUT:
PMCPatients_common4018
[ { "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 female presented to the OPD with complaints of a gradually progressive, red-colored rash on the neck, trunk, and upper limbs for the past 3 to 4 days. She presented with a history of high-grade fever, malaise, breathlessness (even at rest), excruciating headache, retro-orbital pain, and loss of appetite for a period of 8 to 10 days. On examination, non-palpable purpura was noted over the neck, chest, abdomen, back, upper limbs, and palms with islands of sparing noticed on the back. Pseudo-vesiculation was seen in purpuric lesions on the back [Figures , and ]. A preliminary diagnosis of dengue rash was made. The platelet count was 100,000/mm3, and all other routine investigations were within normal limits. Lactate dehydrogenase, erythrocyte sedimentation rate, D-dimer and C-reactive protein levels were raised. Serum ferritin was within normal limits. NS1 antigen test for dengue was negative. Chest X-ray posterior–anterior view revealed peripheral and lower lobar predominant air space opacities and haziness, suggestive of COVID pneumonitis in the current scenario. RAT was negative, but reverse-transcriptase polymerase chain reaction (RT-PCR) was positive. The patient was referred to an advanced center for hospitalization. For cutaneous lesions, the patient was advised levocetirizine tablet 5 mg HS, betamethasone dipropionate cream, and an emollient for local application twice a day. On reviewing the discharge papers, we found that she was treated using paracetamol tablet 500 mg TDS (thrice a day; till the fever subsided), hydroxychloroquinone tablet 200 mg BD (twice a day), enoxaparin injection 4 mg s.c. (subcutaneous) BD for 2 weeks. Azithromycin tablet (500 mg) OD (once a day) was also given for 5 days. Oxygen support was given for breathlessness and inability to maintain the oxygen saturation (SpO2). She was discharged after 17 days. The rash completely subsided in about 3 weeks from its appearance.\nOUTPUT:" }, { "from": "agent", "value": "COVID-19" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 31-year-old female presented to the OPD with complaints of a gradually progressive, red-colored rash on the neck, trunk, and upper limbs for the past 3 to 4 days. She presented with a history of high-grade fever, malaise, breathlessness (even at rest), excruciating headache, retro-orbital pain, and loss of appetite for a period of 8 to 10 days. On examination, non-palpable purpura was noted over the neck, chest, abdomen, back, upper limbs, and palms with islands of sparing noticed on the back. Pseudo-vesiculation was seen in purpuric lesions on the back [Figures , and ]. A preliminary diagnosis of dengue rash was made. The platelet count was 100,000/mm3, and all other routine investigations were within normal limits. Lactate dehydrogenase, erythrocyte sedimentation rate, D-dimer and C-reactive protein levels were raised. Serum ferritin was within normal limits. NS1 antigen test for dengue was negative. Chest X-ray posterior–anterior view revealed peripheral and lower lobar predominant air space opacities and haziness, suggestive of COVID pneumonitis in the current scenario. RAT was negative, but reverse-transcriptase polymerase chain reaction (RT-PCR) was positive. The patient was referred to an advanced center for hospitalization. For cutaneous lesions, the patient was advised levocetirizine tablet 5 mg HS, betamethasone dipropionate cream, and an emollient for local application twice a day. On reviewing the discharge papers, we found that she was treated using paracetamol tablet 500 mg TDS (thrice a day; till the fever subsided), hydroxychloroquinone tablet 200 mg BD (twice a day), enoxaparin injection 4 mg s.c. (subcutaneous) BD for 2 weeks. Azithromycin tablet (500 mg) OD (once a day) was also given for 5 days. Oxygen support was given for breathlessness and inability to maintain the oxygen saturation (SpO2). She was discharged after 17 days. The rash completely subsided in about 3 weeks from its appearance. OUTPUT:
PMCPatients_common2583
[ { "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 second patient is an otherwise healthy 34-year-old woman referred to nephrology for evaluation of hypokalemia and hypomagnesemia. She was diagnosed with GS after presenting with a serum potassium of 2.6 mEq/L, serum magnesium of 0.9 mg/dL, metabolic alkalosis, modestly low blood pressure, and additional testing that revealed an elevated urine potassium and chloride, increased fractional excretion of magnesium, hypocalciuria, and negative diuretic screen. Interestingly, she had been maintained on an oral contraceptive pill containing drospirenone until shortly prior to her initial presentation for hypokalemia. Genetic testing was not pursued.\\nOne year later, at the time of her first pregnancy, she presented with serum potassium and magnesium levels of 2.9 mEq/L and 1.4 mg/dL, respectively. Her oral repletion was increased to 200 mEq/day of potassium chloride and 640 mg/day (53 mEq) of magnesium chloride. Spontaneous fetal demise occurred at 7 weeks and 6 days. Her serum potassium and magnesium levels were 3.6 mEq/L and 1.0 mg/dL at the time of this event.\\nShe became pregnant again 1 year later. At the time of her second pregnancy, oral potassium and magnesium replacement were increased from pre-pregnancy doses of potassium chloride 160 mEq/day and magnesium chloride 512 mg/day (43 mEq) to potassium chloride 200 mEq/day and magnesium chloride 768 mg/day (64 mEq). Serum potassium and magnesium levels were monitored at 3-week intervals throughout the pregnancy. Goal levels were achieved with a serum potassium of ~ 3.2 meq/L and serum magnesium levels greater than 1.0 – 1.1 mg/dL (normal lab range 1.5 – 2.5 mg/dL). She was asymptomatic throughout her pregnancy and her electrocardiogram was unremarkable. She delivered a healthy infant at 33 weeks gestation via cesarean section.\nOUTPUT:" }, { "from": "agent", "value": "Gitelman’s syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The second patient is an otherwise healthy 34-year-old woman referred to nephrology for evaluation of hypokalemia and hypomagnesemia. She was diagnosed with GS after presenting with a serum potassium of 2.6 mEq/L, serum magnesium of 0.9 mg/dL, metabolic alkalosis, modestly low blood pressure, and additional testing that revealed an elevated urine potassium and chloride, increased fractional excretion of magnesium, hypocalciuria, and negative diuretic screen. Interestingly, she had been maintained on an oral contraceptive pill containing drospirenone until shortly prior to her initial presentation for hypokalemia. Genetic testing was not pursued.\nOne year later, at the time of her first pregnancy, she presented with serum potassium and magnesium levels of 2.9 mEq/L and 1.4 mg/dL, respectively. Her oral repletion was increased to 200 mEq/day of potassium chloride and 640 mg/day (53 mEq) of magnesium chloride. Spontaneous fetal demise occurred at 7 weeks and 6 days. Her serum potassium and magnesium levels were 3.6 mEq/L and 1.0 mg/dL at the time of this event.\nShe became pregnant again 1 year later. At the time of her second pregnancy, oral potassium and magnesium replacement were increased from pre-pregnancy doses of potassium chloride 160 mEq/day and magnesium chloride 512 mg/day (43 mEq) to potassium chloride 200 mEq/day and magnesium chloride 768 mg/day (64 mEq). Serum potassium and magnesium levels were monitored at 3-week intervals throughout the pregnancy. Goal levels were achieved with a serum potassium of ~ 3.2 meq/L and serum magnesium levels greater than 1.0 – 1.1 mg/dL (normal lab range 1.5 – 2.5 mg/dL). She was asymptomatic throughout her pregnancy and her electrocardiogram was unremarkable. She delivered a healthy infant at 33 weeks gestation via cesarean section. OUTPUT:
PMCPatients_common352
[ { "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 then treated with enoxaparin and warfarin and was later discharged with regular followed up in our cardiovascular outpatient clinic. This time, she suffered from shortness of breath for a week and returned to our emergency department. Physical examinations showed tachycardia (101/min) and hypertension (173/104), and her body temperature was 37.4 °C. Her D-dimer level was 2.64 mg/L and troponin level was within the normal range. Electrocardiography revealed sinus tachycardia, and S1Q3T3 pattern was recorded (). No abnormal findings were obtained in her chest roentgenography. Rivaroxaban was administered but her symptoms did not improve. As a result, she had received catheter-directed thrombolytic therapy by Ekosonic Endovascular System (EKOS, BTG International Ltd., London, United Kingdom), together with recombinant tissue plasminogen activator infusion. Abdominal ultrasound also revealed no abnormality. The patient was then discharged under long-term medication of rivaroxaban. Written informed consent was obtained from the patient for this study.\nOUTPUT:" }, { "from": "agent", "value": "Pulmonary Embolism, Severe Asthma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: She was then treated with enoxaparin and warfarin and was later discharged with regular followed up in our cardiovascular outpatient clinic. This time, she suffered from shortness of breath for a week and returned to our emergency department. Physical examinations showed tachycardia (101/min) and hypertension (173/104), and her body temperature was 37.4 °C. Her D-dimer level was 2.64 mg/L and troponin level was within the normal range. Electrocardiography revealed sinus tachycardia, and S1Q3T3 pattern was recorded (). No abnormal findings were obtained in her chest roentgenography. Rivaroxaban was administered but her symptoms did not improve. As a result, she had received catheter-directed thrombolytic therapy by Ekosonic Endovascular System (EKOS, BTG International Ltd., London, United Kingdom), together with recombinant tissue plasminogen activator infusion. Abdominal ultrasound also revealed no abnormality. The patient was then discharged under long-term medication of rivaroxaban. Written informed consent was obtained from the patient for this study. OUTPUT:
PMCPatients_common5175
[ { "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 30-year-old man presented with hypoesthetic, depigmented patches over the skin of the chest and back of 1 year duration. He gave history of recurrent fractures since the age of 4 years with shortening of right leg. The parents gave history of hyperpigmented macules over the trunk since birth and denied similar features in family members. Examination revealed (height 152 cm) asymmetry of the face with expansion of right maxilla and lower jaw and short right leg (82 vs 86 cm) [Figures and ]. Cutaneous examination revealed a large CALM over the back, extending across the midline and multiple anesthetic patches over scapula and lower back []. There was no evidence of goiter, acromegaloid features, and thickened nerves, and the rest of the examination was normal.\\nHormonal profile revealed normal thyroid adrenal and gonadal axes evaluation. Skeletal survey revealed expansile osteolytic lesion over right maxilla, right hip, and shoulder. Skin biopsy specimens were obtained from ear lobes, legs, and depigmented lesions over the back, avoiding areas of CALM. Specimens revealed the presence of acid-fast bacilli along with noncaseating granulomas consistent with the diagnosis of tuberculoid leprosy. The diagnosis of fibrous dysplasia is made by the presence of bone pains, recurrent fractures, deformity of bone, and radiological evidence of fibro-osseous tissue showing expansile lytic lesion. Biopsy and 99mTc-MDP scan of the bone were not considered necessary to establish the diagnosis in this classical case. Other laboratory workup showed elevated alkaline phosphatase (388 U/l) with normal calcium, phosphorus, parathyroid hormone, and 25-hydroxy vitamin D levels. He was treated with triple drug regimen for leprosy and also given oral calcium carbonate 1.5 g daily along with the first dose of zoledronic acid 4 mg as an intravenous infusion. He is under regular follow-up for the skin and bone condition.\nOUTPUT:" }, { "from": "agent", "value": "Hansen's disease, McCune–Albright syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 30-year-old man presented with hypoesthetic, depigmented patches over the skin of the chest and back of 1 year duration. He gave history of recurrent fractures since the age of 4 years with shortening of right leg. The parents gave history of hyperpigmented macules over the trunk since birth and denied similar features in family members. Examination revealed (height 152 cm) asymmetry of the face with expansion of right maxilla and lower jaw and short right leg (82 vs 86 cm) [Figures and ]. Cutaneous examination revealed a large CALM over the back, extending across the midline and multiple anesthetic patches over scapula and lower back []. There was no evidence of goiter, acromegaloid features, and thickened nerves, and the rest of the examination was normal.\nHormonal profile revealed normal thyroid adrenal and gonadal axes evaluation. Skeletal survey revealed expansile osteolytic lesion over right maxilla, right hip, and shoulder. Skin biopsy specimens were obtained from ear lobes, legs, and depigmented lesions over the back, avoiding areas of CALM. Specimens revealed the presence of acid-fast bacilli along with noncaseating granulomas consistent with the diagnosis of tuberculoid leprosy. The diagnosis of fibrous dysplasia is made by the presence of bone pains, recurrent fractures, deformity of bone, and radiological evidence of fibro-osseous tissue showing expansile lytic lesion. Biopsy and 99mTc-MDP scan of the bone were not considered necessary to establish the diagnosis in this classical case. Other laboratory workup showed elevated alkaline phosphatase (388 U/l) with normal calcium, phosphorus, parathyroid hormone, and 25-hydroxy vitamin D levels. He was treated with triple drug regimen for leprosy and also given oral calcium carbonate 1.5 g daily along with the first dose of zoledronic acid 4 mg as an intravenous infusion. He is under regular follow-up for the skin and bone condition. OUTPUT:
PMCPatients_common5302
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 27-year-old man presented with a 9-month history of chest wall pain and a palpable growing mass in the anterior end of the left sixth rib. The mass was hard and fixed to the chest wall. There was mild tenderness. The overlying skin was normal. He had a history of contusion at the left anterior chest wall 9 months earlier. There were no specific pulmonary symptoms.\\nA chest X-ray demonstrated an expansile bony mass in the distal end of the left 6th rib. Computed tomography revealed a large irregular contoured and heterogeneously enhancing soft tissue mass in the anterior arc of the left 6th rib. The tumor contained peripheral calcification and bony destruction (). No abnormality was found on laboratory examinations.\\nA surgical resection was performed. The tumor was completely resected, including surrounding soft tissue. The tumor was adhered to the parietal pleura. There was no visceral pleural invasion. The distance of the margin from the tumor was 3 cm (medial) and 6 cm (lateral). The medial margin of the resected rib was the lateral border of the sternum. Partial resection of the ribs above (5th) and below (7th) the GCT including the intercostal muscle and soft tissue was performed. The lengths of the resected ribs were 10.5 cm, 13.5 cm, and 13 cm (). The chest wall defect was covered with a 2-mmthick Gore-Tex Soft Tissue Patch (W. L. Gore & Associates Inc., Flagstaff, AZ, USA).\\nThe tumor was 6×4.5×4.5 cm in size. There were focal hemorrhage and a yellowish mass-like lesion in gross findings. The pathological diagnosis was a primary GCT of the left sixth rib.\\nNo adjuvant treatment was performed. The patient has been receiving follow-up care for 3 months since the surgery with out evidence of recurrence.\nOUTPUT:" }, { "from": "agent", "value": "Giant Cell Tumor" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 27-year-old man presented with a 9-month history of chest wall pain and a palpable growing mass in the anterior end of the left sixth rib. The mass was hard and fixed to the chest wall. There was mild tenderness. The overlying skin was normal. He had a history of contusion at the left anterior chest wall 9 months earlier. There were no specific pulmonary symptoms.\nA chest X-ray demonstrated an expansile bony mass in the distal end of the left 6th rib. Computed tomography revealed a large irregular contoured and heterogeneously enhancing soft tissue mass in the anterior arc of the left 6th rib. The tumor contained peripheral calcification and bony destruction (). No abnormality was found on laboratory examinations.\nA surgical resection was performed. The tumor was completely resected, including surrounding soft tissue. The tumor was adhered to the parietal pleura. There was no visceral pleural invasion. The distance of the margin from the tumor was 3 cm (medial) and 6 cm (lateral). The medial margin of the resected rib was the lateral border of the sternum. Partial resection of the ribs above (5th) and below (7th) the GCT including the intercostal muscle and soft tissue was performed. The lengths of the resected ribs were 10.5 cm, 13.5 cm, and 13 cm (). The chest wall defect was covered with a 2-mmthick Gore-Tex Soft Tissue Patch (W. L. Gore & Associates Inc., Flagstaff, AZ, USA).\nThe tumor was 6×4.5×4.5 cm in size. There were focal hemorrhage and a yellowish mass-like lesion in gross findings. The pathological diagnosis was a primary GCT of the left sixth rib.\nNo adjuvant treatment was performed. The patient has been receiving follow-up care for 3 months since the surgery with out evidence of recurrence. OUTPUT:
PMCPatients_common3838
[ { "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 51-year-old Japanese man presented at a community hospital with a chief complaint of continuous low-grade fever. The patient had an abnormal chest X-ray and visited our hospital in October 2012. Laboratory evaluations revealed the following findings: hemoglobin, 7.2 g/dL (normal range: 13.5–17.5 g/dL), corrected calcium level, 10.6 mg/dL (normal range: 8.3–10.3 mg/dL), and C-reactive protein, 17.3 mg/dL (normal range: <0.3 mg/dL). Computed tomography (CT) revealed a hypervascular tumor (size, 9 × 8.5 cm) in the upper pole of the left kidney with multiple lung metastases (Fig. , A and B). Pathological analysis identified a pT3a clear cell RCC of Fuhrman grade 3 with hemorrhage and necrotic tissue. In January 2013, the patient received sunitinib at 50 mg/day for 2 weeks of every 3-week cycle for the treatment of multiple lung metastases. After two cycles, a lung CT showed disease progression with lung metastases, which increased in size (Fig. A and B). The patient received axitinib at 10 mg/day starting in March 2013. After 5 months of axitinib treatment, the patient achieved a complete response (CR) with lung metastases . In February 2014, CT showed a mediastinal lymph node metastasis after a year of axitinib treatment (Fig. ). The patient received temsirolimus at 25 mg/week beginning in March 2014. After 3 months of temsirolimus treatment, the patient achieved a CR with a mediastinal lymph node metastasis (Fig. ). In November 2016, the treatment schedule of temsirolimus was changed from weekly to biweekly. To date, CT has shown no evidence of disease and treatment with temsirolimus is still ongoing. The patient did not experience any adverse events.\nOUTPUT:" }, { "from": "agent", "value": "Metastatic renal cell carcinoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 51-year-old Japanese man presented at a community hospital with a chief complaint of continuous low-grade fever. The patient had an abnormal chest X-ray and visited our hospital in October 2012. Laboratory evaluations revealed the following findings: hemoglobin, 7.2 g/dL (normal range: 13.5–17.5 g/dL), corrected calcium level, 10.6 mg/dL (normal range: 8.3–10.3 mg/dL), and C-reactive protein, 17.3 mg/dL (normal range: <0.3 mg/dL). Computed tomography (CT) revealed a hypervascular tumor (size, 9 × 8.5 cm) in the upper pole of the left kidney with multiple lung metastases (Fig. , A and B). Pathological analysis identified a pT3a clear cell RCC of Fuhrman grade 3 with hemorrhage and necrotic tissue. In January 2013, the patient received sunitinib at 50 mg/day for 2 weeks of every 3-week cycle for the treatment of multiple lung metastases. After two cycles, a lung CT showed disease progression with lung metastases, which increased in size (Fig. A and B). The patient received axitinib at 10 mg/day starting in March 2013. After 5 months of axitinib treatment, the patient achieved a complete response (CR) with lung metastases . In February 2014, CT showed a mediastinal lymph node metastasis after a year of axitinib treatment (Fig. ). The patient received temsirolimus at 25 mg/week beginning in March 2014. After 3 months of temsirolimus treatment, the patient achieved a CR with a mediastinal lymph node metastasis (Fig. ). In November 2016, the treatment schedule of temsirolimus was changed from weekly to biweekly. To date, CT has shown no evidence of disease and treatment with temsirolimus is still ongoing. The patient did not experience any adverse events. OUTPUT:
PMCPatients_common4242
[ { "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 male who had a family history of UC visited Daehang Hospital presenting with abdominal pain and frequent (>10/day) bloody diarrhea. He was diagnosed with left-sided UC about 10 years ago. He maintained remission with combination mesalamine therapy. The patient was admitted to our hospital and intravenous corticosteroid (hydrocortisone 300 mg/day) was started. On admission, his body temperature was 38.8°C. Blood test revealed elevation of CRP, leukocytosis and mild anemia as follows; CRP 4.0 mg/dL, white blood cells 12,900/μL, and hemoglobin 10.4 g/dL. The patient also complained of severe epigastric pain and vomiting. We added proton pump inhibitor, but his symptoms did not improve. Simple abdominal radiography was performed and it showed no sign of intestinal obstruction or toxin megacolon. On histopathologic examination, marked inflammatory cell infiltration and cryptitis were noted without evidence of granuloma or inclusion body (intranuclear or intracytoplasmic) (). Helicobacter pylori was not detected. We started standard induction therapy of infliximab (300 mg infusion at 0, 2nd and 6th weeks). His epigastric symptom and bloody diarrhea improved abruptly. Three months later, follow-up colonoscopy and EGD showed mucosal healing with whitish scarring ( and ). On histopathologic examination of duodenal mucosa, there was decreased density of inflammatory cell infiltrates in lamina propria with decreased active inflammation compared to those at prior medical treatment. Instead of prominent inflammatory cell infiltrates, subepithelial fibrosis was noted (). After more than 1 year, the patient is still sustaining clinical remission with infliximab maintenance therapy.\nOUTPUT:" }, { "from": "agent", "value": "Diffuse ulcerative duodenitis, Ulcerative colitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 45-year-old male who had a family history of UC visited Daehang Hospital presenting with abdominal pain and frequent (>10/day) bloody diarrhea. He was diagnosed with left-sided UC about 10 years ago. He maintained remission with combination mesalamine therapy. The patient was admitted to our hospital and intravenous corticosteroid (hydrocortisone 300 mg/day) was started. On admission, his body temperature was 38.8°C. Blood test revealed elevation of CRP, leukocytosis and mild anemia as follows; CRP 4.0 mg/dL, white blood cells 12,900/μL, and hemoglobin 10.4 g/dL. The patient also complained of severe epigastric pain and vomiting. We added proton pump inhibitor, but his symptoms did not improve. Simple abdominal radiography was performed and it showed no sign of intestinal obstruction or toxin megacolon. On histopathologic examination, marked inflammatory cell infiltration and cryptitis were noted without evidence of granuloma or inclusion body (intranuclear or intracytoplasmic) (). Helicobacter pylori was not detected. We started standard induction therapy of infliximab (300 mg infusion at 0, 2nd and 6th weeks). His epigastric symptom and bloody diarrhea improved abruptly. Three months later, follow-up colonoscopy and EGD showed mucosal healing with whitish scarring ( and ). On histopathologic examination of duodenal mucosa, there was decreased density of inflammatory cell infiltrates in lamina propria with decreased active inflammation compared to those at prior medical treatment. Instead of prominent inflammatory cell infiltrates, subepithelial fibrosis was noted (). After more than 1 year, the patient is still sustaining clinical remission with infliximab maintenance therapy. OUTPUT:
PMCPatients_common2896
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 67-year-old man presented with a 6-week history of hiccupping and foul odor. He also complained of difficulty swallowing, diffuse epigastric pain, and weight loss. Panendoscopy revealed a large ulcerated mass at least 8 cm in diameter at the lesser curvature side of the anterior wall of the gastric upper body, with invasion into the lower esophagus. Chest, abdominal and pelvic computed tomography (CT) showed distal esophageal involvement and lymphadenopathy, but no evidence of liver or distal metastasis. A lower esophagectomy, total gastrectomy with Roux-en-Y anastomosis, and feeding jejunostomy were performed. This drainage persisted for 1 month after surgery. After the drain was removed, no intraperitoneal organs (such as small bowel, liver, or spleen) were visible. The patient was treated with suction via a nasogastric tube drain for 5 days. He thereafter had an uneventful recovery.\\nThe patient subsequently was treated with 4 cycles of combination chemotherapy consisting of cisplatin and etoposide (VP-16). Sixteen months after surgery the patient was alive and showed no signs of cancer recurrence. The patient discussed in this report provided informed consent for all treatments rendered and consent for the publication of this case report and the use of radiological images.\nOUTPUT:" }, { "from": "agent", "value": "Gastric small cell carcinoma, Drain tube migration into the anastomotic site of an esophagojejunostomy" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 67-year-old man presented with a 6-week history of hiccupping and foul odor. He also complained of difficulty swallowing, diffuse epigastric pain, and weight loss. Panendoscopy revealed a large ulcerated mass at least 8 cm in diameter at the lesser curvature side of the anterior wall of the gastric upper body, with invasion into the lower esophagus. Chest, abdominal and pelvic computed tomography (CT) showed distal esophageal involvement and lymphadenopathy, but no evidence of liver or distal metastasis. A lower esophagectomy, total gastrectomy with Roux-en-Y anastomosis, and feeding jejunostomy were performed. This drainage persisted for 1 month after surgery. After the drain was removed, no intraperitoneal organs (such as small bowel, liver, or spleen) were visible. The patient was treated with suction via a nasogastric tube drain for 5 days. He thereafter had an uneventful recovery.\nThe patient subsequently was treated with 4 cycles of combination chemotherapy consisting of cisplatin and etoposide (VP-16). Sixteen months after surgery the patient was alive and showed no signs of cancer recurrence. The patient discussed in this report provided informed consent for all treatments rendered and consent for the publication of this case report and the use of radiological images. OUTPUT:
PMCPatients_common2178
[ { "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 wore a bilateral fixed partial denture between the canines and a bilateral removable partial denture in the mandible. The bone shape was examined using the CT images and plaster model, and a thin residual ridge was found around the anterior region.\\nTwo mini-implants (Magfit® MIP, Aichi Steel, Aichi, Japan & Platon Japan, Tokyo, Japan) were placed in the anterior region of the mandible. After local anesthesia, the periosteal flap was opened and minimal osetoplasty was done prior to placement of the implant. The mini-implants were placed at the planned positions according to the manufacturer’s directions using the preoperative examinations, and a dome-type keeper was connected to the mini-implant ( and ).\\nAfter surgical installation, the denture was fixed so that the implant placement region was relieved by the application of a tissue conditioning material ().\\nThree months after the procedure, the final impression and interocclusal record of the duplicated denture were obtained (). A new magnet-retained two-mini-implant overdenture with hard artificial teeth (ENDURA, Shofu, Kyoto, Japan) was manufactured by conventional denture fabrication. Two magnet assemblies with concave surfaces having a complementary relationship with the dome-type keepers were placed on the mini-implant. Both the mucosa and implants provided support, retention, and stability ().\\nThe patient was satisfied with masticatory performance and appearance with the magnet-retained two-mini-implant overdenture.\nOUTPUT:" }, { "from": "agent", "value": "Total edentulism in the mandible, Periodontal disease, Complete denture instability" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The patient wore a bilateral fixed partial denture between the canines and a bilateral removable partial denture in the mandible. The bone shape was examined using the CT images and plaster model, and a thin residual ridge was found around the anterior region.\nTwo mini-implants (Magfit® MIP, Aichi Steel, Aichi, Japan & Platon Japan, Tokyo, Japan) were placed in the anterior region of the mandible. After local anesthesia, the periosteal flap was opened and minimal osetoplasty was done prior to placement of the implant. The mini-implants were placed at the planned positions according to the manufacturer’s directions using the preoperative examinations, and a dome-type keeper was connected to the mini-implant ( and ).\nAfter surgical installation, the denture was fixed so that the implant placement region was relieved by the application of a tissue conditioning material ().\nThree months after the procedure, the final impression and interocclusal record of the duplicated denture were obtained (). A new magnet-retained two-mini-implant overdenture with hard artificial teeth (ENDURA, Shofu, Kyoto, Japan) was manufactured by conventional denture fabrication. Two magnet assemblies with concave surfaces having a complementary relationship with the dome-type keepers were placed on the mini-implant. Both the mucosa and implants provided support, retention, and stability ().\nThe patient was satisfied with masticatory performance and appearance with the magnet-retained two-mini-implant overdenture. OUTPUT:
PMCPatients_common427
[ { "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: Previous treatments of that eye included 2 cycles of systemic chemotherapy (carboplatin, etoposide), 2 intraarterial and 10 intravitreal melphalan injections as well as numerous focal treatments (cryotherapy and thermotherapy). Scleral buckling without drainage but with an intraoperative anterior chamber tap to allow a sufficient tightening of the band was done, resulting in a complete reattachment of the retina. a and c). PPV under melphalan perfusion (5 μg/ml) was performed. To allow the retina to re-applicate, a retinectomy was created around the tumor scar, followed by laser photocoagulation and silicone oil tamponade. Cytologic examination of the vitrectomy fluid did not find any malignant cells. Silicone oil was removed 4 months later. b and d).\nOUTPUT:" }, { "from": "agent", "value": "Retinoblastoma, Rhegmatogenous RD, Cataract, Tractional retinal detachment" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Previous treatments of that eye included 2 cycles of systemic chemotherapy (carboplatin, etoposide), 2 intraarterial and 10 intravitreal melphalan injections as well as numerous focal treatments (cryotherapy and thermotherapy). Scleral buckling without drainage but with an intraoperative anterior chamber tap to allow a sufficient tightening of the band was done, resulting in a complete reattachment of the retina. a and c). PPV under melphalan perfusion (5 μg/ml) was performed. To allow the retina to re-applicate, a retinectomy was created around the tumor scar, followed by laser photocoagulation and silicone oil tamponade. Cytologic examination of the vitrectomy fluid did not find any malignant cells. Silicone oil was removed 4 months later. b and d). OUTPUT:
PMCPatients_common2058
[ { "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 75-year-old woman with a history of surgical intervention for aortic aneurysm showed dilatation of her main pancreatic duct and pancreatic head tumor on CT scan at an annual medical check-up. Endoscopic ultrasound-guided fine needle aspiration of the pancreatic head tumor was performed, and the result was group 4. She was referred to our department for the surgical treatment of suspected pancreatic head cancer.\\nPreoperative enhanced high-resolution CT detected pancreatic head tumor and major posterior segmental branch of RHA (RHA-PB) which originated from posterior inferior pancreaticoduodenal artery (PIPDA) and run through the tumor (Fig. ). The image also demonstrated that there was a junction between RHA-PB and minor anterior segmental branch of RHA (RHA-AB) at the hilar portion (Fig. ).\\nShe received PD combined with regional lymph node dissection. At laparotomy, RHA-PB was isolated from the hepatoduodenal ligament and confirmed that it originated from PIPDA in accordance with the preoperative findings, which revealed to run through the tumor. To preserve RHA-PB, we had to preserve posterior pancreaticoduodenal arcade and the common trunk of PIPDA, which decreased the curability of the tumor. We ensured that the color of the liver did not change after clamping of RHA-PB. Finally, we ligated and divided RHA-PB for complete resection of the pancreatic head tumor because we knew from the preoperative images that there was the junction between RHA-PB and RHA-AB at the hilar portion. We performed the operation without any complication and achieved R0 resection macroscopically (duration of surgery, 355 min; blood loss, 220 mL).\\nHer postoperative course was uneventful, and she was discharged on POD15 without hepatic or biliary ischemia. The tumor invasion was seen near the intraparenchymal vessels (Fig. ), but R0 resection was performed.\\nAlthough she died from chronic heart failure 13 months after the operation, local recurrence had not be seen throughout the whole course.\nOUTPUT:" }, { "from": "agent", "value": "Adenocarcinoma of the pancreas" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 75-year-old woman with a history of surgical intervention for aortic aneurysm showed dilatation of her main pancreatic duct and pancreatic head tumor on CT scan at an annual medical check-up. Endoscopic ultrasound-guided fine needle aspiration of the pancreatic head tumor was performed, and the result was group 4. She was referred to our department for the surgical treatment of suspected pancreatic head cancer.\nPreoperative enhanced high-resolution CT detected pancreatic head tumor and major posterior segmental branch of RHA (RHA-PB) which originated from posterior inferior pancreaticoduodenal artery (PIPDA) and run through the tumor (Fig. ). The image also demonstrated that there was a junction between RHA-PB and minor anterior segmental branch of RHA (RHA-AB) at the hilar portion (Fig. ).\nShe received PD combined with regional lymph node dissection. At laparotomy, RHA-PB was isolated from the hepatoduodenal ligament and confirmed that it originated from PIPDA in accordance with the preoperative findings, which revealed to run through the tumor. To preserve RHA-PB, we had to preserve posterior pancreaticoduodenal arcade and the common trunk of PIPDA, which decreased the curability of the tumor. We ensured that the color of the liver did not change after clamping of RHA-PB. Finally, we ligated and divided RHA-PB for complete resection of the pancreatic head tumor because we knew from the preoperative images that there was the junction between RHA-PB and RHA-AB at the hilar portion. We performed the operation without any complication and achieved R0 resection macroscopically (duration of surgery, 355 min; blood loss, 220 mL).\nHer postoperative course was uneventful, and she was discharged on POD15 without hepatic or biliary ischemia. The tumor invasion was seen near the intraparenchymal vessels (Fig. ), but R0 resection was performed.\nAlthough she died from chronic heart failure 13 months after the operation, local recurrence had not be seen throughout the whole course. OUTPUT:
PMCPatients_common4036
[ { "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: NaF PET in July 2015 showed widespread bone metastasis []. Clinical stage based on PET and radiological studies was T3bN1M1. The patient was placed on chemotherapy. PSA became 4.4 ng/ml with chemotherapy, but it was stopped in February 2016, due to liver toxicity, and hormone therapy (HT) was started. Because of rising PS (10 ng/ml), while on HT, FDG and NaF PET studies were ordered in May 2016. NaF PET/CT study showed widespread bone metastasis with slight reduction in osteoblastic activity of some lesions with overall stability in other lesions as compared to prechemotherapy NaF PET/CT scan []. The patient continued to receive HT, but PSA continued to rise to 99 ng/ml. The patient was referred to another hospital for Lu-177 PSMA treatment.\nOUTPUT:" }, { "from": "agent", "value": "Prostate Cancer, Diffuse Bone Metastases" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: NaF PET in July 2015 showed widespread bone metastasis []. Clinical stage based on PET and radiological studies was T3bN1M1. The patient was placed on chemotherapy. PSA became 4.4 ng/ml with chemotherapy, but it was stopped in February 2016, due to liver toxicity, and hormone therapy (HT) was started. Because of rising PS (10 ng/ml), while on HT, FDG and NaF PET studies were ordered in May 2016. NaF PET/CT study showed widespread bone metastasis with slight reduction in osteoblastic activity of some lesions with overall stability in other lesions as compared to prechemotherapy NaF PET/CT scan []. The patient continued to receive HT, but PSA continued to rise to 99 ng/ml. The patient was referred to another hospital for Lu-177 PSMA treatment. OUTPUT:
PMCPatients_common4216
[ { "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 74-year-old woman was found unresponsive outdoors, and the ambient temperature on the arrival of emergency medical services to the scene was −1.7°C. At that time, she was in shock, with a body temperature of 24.6°C. During her transfer to our hospital, she suffered cardiopulmonary arrest (CPA). On arrival, she was still in CPA, and her cardiac rhythm was ventricular fibrillation. Veno-arterial ECMO was initiated for resuscitation and rewarming, and she became responsive to commands after a few minutes. Rewarming was aimed at increasing her body temperature to 36°C as rapidly as possible with the inclusion of a heater-cooler device with ECMO. Whole-body computed tomography scan with contrast enhancement showed no abnormalities that could explain the cause of CPA. She was admitted to the intensive care unit (ICU), and the return of spontaneous circulation was achieved at the time of admission without adrenaline and defibrillation. The left ventricular (LV) ejection fraction was approximately 60% estimated visually.\\nHer blood pressure suddenly dropped 1 h after the ICU admission, and echocardiography showed severe diffuse hypokinesis of the LV wall and apical akinesis. Coronary angiography undertaken on day 2 indicated that coronary arteries were intact (Fig. A,B). C,D) as well as a T-wave inversion in multiple leads on the electrocardiogram (Fig. ). Left ventricular wall motion gradually improved, and she was taken off ECMO on day 3 (Fig. ) and extubated on day 5. Echocardiography on day 6 showed that abnormalities in the LV wall motion had almost disappeared.\\nShe was discharged from the ICU on day 8. She confessed having ingested several sleeping pills. Therefore, she was moved to the psychiatric ward to receive psychological treatment on day 12 and was discharged on day 43 without neurological deficits.\nOUTPUT:" }, { "from": "agent", "value": "Takotsubo cardiomyopathy" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 74-year-old woman was found unresponsive outdoors, and the ambient temperature on the arrival of emergency medical services to the scene was −1.7°C. At that time, she was in shock, with a body temperature of 24.6°C. During her transfer to our hospital, she suffered cardiopulmonary arrest (CPA). On arrival, she was still in CPA, and her cardiac rhythm was ventricular fibrillation. Veno-arterial ECMO was initiated for resuscitation and rewarming, and she became responsive to commands after a few minutes. Rewarming was aimed at increasing her body temperature to 36°C as rapidly as possible with the inclusion of a heater-cooler device with ECMO. Whole-body computed tomography scan with contrast enhancement showed no abnormalities that could explain the cause of CPA. She was admitted to the intensive care unit (ICU), and the return of spontaneous circulation was achieved at the time of admission without adrenaline and defibrillation. The left ventricular (LV) ejection fraction was approximately 60% estimated visually.\nHer blood pressure suddenly dropped 1 h after the ICU admission, and echocardiography showed severe diffuse hypokinesis of the LV wall and apical akinesis. Coronary angiography undertaken on day 2 indicated that coronary arteries were intact (Fig. A,B). C,D) as well as a T-wave inversion in multiple leads on the electrocardiogram (Fig. ). Left ventricular wall motion gradually improved, and she was taken off ECMO on day 3 (Fig. ) and extubated on day 5. Echocardiography on day 6 showed that abnormalities in the LV wall motion had almost disappeared.\nShe was discharged from the ICU on day 8. She confessed having ingested several sleeping pills. Therefore, she was moved to the psychiatric ward to receive psychological treatment on day 12 and was discharged on day 43 without neurological deficits. OUTPUT:
PMCPatients_common4484
[ { "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 woman, who had taken antihypertensive medications for seven years, complained of intermittent motor aphagia with right hemiparesis (Grade IV/III) for one month. Brain single proton emission computed tomography (SPECT) showed the perfusion defect on the area of both ICAs, especially left (). Digital subtraction angiography (DSA) showed the obstruction of the left ICA, luminal irregularity of the right ICA and right vertebral artery (VA) ().\\nTwo months from the onset of symptoms, the operation was performed. Direct anastomaosis between STA and angular branch of distal MCA was performed uneventfully for the obstruction of the left ICA.\\nThe neurological examination showed no change compared with that of the preoperative state. On the fourth postoperative day (POD), she complained of sudden motor aphagia and deteriorated right hemiparesis (Grade IV/II). The yellowish fluid was drained through the silicon catheter used for trephination.\nOUTPUT:" }, { "from": "agent", "value": "Chronic Cerebral Infarction, Left Internal Carotid Artery Stenosis, Subdural Hygroma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 63-year-old woman, who had taken antihypertensive medications for seven years, complained of intermittent motor aphagia with right hemiparesis (Grade IV/III) for one month. Brain single proton emission computed tomography (SPECT) showed the perfusion defect on the area of both ICAs, especially left (). Digital subtraction angiography (DSA) showed the obstruction of the left ICA, luminal irregularity of the right ICA and right vertebral artery (VA) ().\nTwo months from the onset of symptoms, the operation was performed. Direct anastomaosis between STA and angular branch of distal MCA was performed uneventfully for the obstruction of the left ICA.\nThe neurological examination showed no change compared with that of the preoperative state. On the fourth postoperative day (POD), she complained of sudden motor aphagia and deteriorated right hemiparesis (Grade IV/II). The yellowish fluid was drained through the silicon catheter used for trephination. OUTPUT:
PMCPatients_common3667
[ { "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 male was brought to the emergency department due to inattention and transient episodic memory loss. He was relatively healthy, except for taking medications for a headache that developed a year ago. For 2 weeks prior to admission, he showed excessive daytime sleepiness at work and an indifferent mood noticed by his colleague during a conference. One day before admission, the patient got lost going back home from work. It took more than 2 hours to get home, which normally took 30 minutes. On the day of admission, the patient showed transient episodic memory loss of that day. He had intact remote memory. Neurologic examination demonstrated no other lateralizing of focal deficit. His initial Korean mini mental status exam (K-MMSE) score was 27 out of 30, showing a mild impairment in attention. On the following day, K-MMSE score had fallen to 19 out of 30, showing a worsening of attention and mild impairment in memory recall. The electroencephalogram was normal. A cerebral spinal fluid study showed high opening pressure of 330 mmH2O, but was acellular showing a nonspecific finding. Brain MRI showed a DAVF in right lateral sinus with a bilateral thalamic venous infarction (). The following cerebral angiography confirmed a right transverse sigmoid DAVF with a feeding artery of the right occipital artery and left posterior meningeal artery (). Endovascular embolization was performed three times due to a highly stenotic, compartmentalized sinus and small, tortuous vessels (). After the third intervention, there was a decrease in extent of venous congestion in the bilateral thalami. Follow up Brain MRI taken one month later after embolization showed a remaining DAVF, though with a decreased signal change in the bilateral thalami. At the time of discharge, the follow-up K-MMSE score showed improvement with a score of 27 out of 30 with improvement in attention and memory recall.\\nThe fourth embolization was performed 5 months after initial endovascular therapy. Since there were some thrombus at the sagittal sinus and straight sinus, we decided to maintain warfarin anticoagulation. At the time of discharge, his mental status and mental function was well preserved and the patient had begun his normal daily life. Follow up cerebral angiography performed 1 year later showed no evidence of a residual AVF.\nOUTPUT:" }, { "from": "agent", "value": "Dural Arteriovenous Fistula" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 43-year-old male was brought to the emergency department due to inattention and transient episodic memory loss. He was relatively healthy, except for taking medications for a headache that developed a year ago. For 2 weeks prior to admission, he showed excessive daytime sleepiness at work and an indifferent mood noticed by his colleague during a conference. One day before admission, the patient got lost going back home from work. It took more than 2 hours to get home, which normally took 30 minutes. On the day of admission, the patient showed transient episodic memory loss of that day. He had intact remote memory. Neurologic examination demonstrated no other lateralizing of focal deficit. His initial Korean mini mental status exam (K-MMSE) score was 27 out of 30, showing a mild impairment in attention. On the following day, K-MMSE score had fallen to 19 out of 30, showing a worsening of attention and mild impairment in memory recall. The electroencephalogram was normal. A cerebral spinal fluid study showed high opening pressure of 330 mmH2O, but was acellular showing a nonspecific finding. Brain MRI showed a DAVF in right lateral sinus with a bilateral thalamic venous infarction (). The following cerebral angiography confirmed a right transverse sigmoid DAVF with a feeding artery of the right occipital artery and left posterior meningeal artery (). Endovascular embolization was performed three times due to a highly stenotic, compartmentalized sinus and small, tortuous vessels (). After the third intervention, there was a decrease in extent of venous congestion in the bilateral thalami. Follow up Brain MRI taken one month later after embolization showed a remaining DAVF, though with a decreased signal change in the bilateral thalami. At the time of discharge, the follow-up K-MMSE score showed improvement with a score of 27 out of 30 with improvement in attention and memory recall.\nThe fourth embolization was performed 5 months after initial endovascular therapy. Since there were some thrombus at the sagittal sinus and straight sinus, we decided to maintain warfarin anticoagulation. At the time of discharge, his mental status and mental function was well preserved and the patient had begun his normal daily life. Follow up cerebral angiography performed 1 year later showed no evidence of a residual AVF. OUTPUT:
PMCPatients_common13
[ { "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 transgender male with a history of Guillain Barre Syndrome and heterozygous Factor V Leiden underwent gender reassignment surgery, including phalloplasty, mastectomy, and vaginal eversion. Physical exam revealed tachycardia, holosystolic murmur at the apex, faint bibasilar crackles, and right lower extremity edema. Laboratory work showed leukocytosis (WBC 11.6 K/uL), creatinine 0.7 mg/dL, hemoglobin 8.8 g/dL, B-type natriuretic peptide of 610 pg/mL, and D-dimer of 3469 ng/mL. CT chest revealed cardiomegaly, pulmonary edema, bilateral lower lobe consolidations, and pleural effusions, a large pericardial effusion, and a 5x10 cm perisplenic abscess found to be secondary to septic emboli. Echocardiogram showed a 2.1 cm mobile vegetation on the anterior leaflet of the mitral valve (Figure ), moderate-severe mitral valve insufficiency (Figure ), ejection fraction of 65%, markedly dilated left atrium, elevated peak pulmonary artery pressure at 57 mmHg, and large pericardial effusion without evidence of tamponade. Broad-spectrum IV antibiotics were started for infective endocarditis and diuresis for new-onset heart failure. He underwent subsequent cardiothoracic surgery with an On-X mechanical mitral valve (On-X Life Technologies Inc., Austin, TX). Unfortunately, the postoperative course was complicated by mediastinal thrombus formation and hemothorax requiring surgical exploration. Once stabilized, the patient was discharged and upon discharge was placed in IV penicillin G and ceftriaxone to complete six weeks of antibiotic therapy.\nOUTPUT:" }, { "from": "agent", "value": "Penile Artery Thrombosis, Recurrent Extended-Spectrum Beta-Lactamase (ESBL) Urinary Tract Infection (UTI), Colovesical Fistula, Enterococcus Faecalis Endocarditis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 45-year-old transgender male with a history of Guillain Barre Syndrome and heterozygous Factor V Leiden underwent gender reassignment surgery, including phalloplasty, mastectomy, and vaginal eversion. Physical exam revealed tachycardia, holosystolic murmur at the apex, faint bibasilar crackles, and right lower extremity edema. Laboratory work showed leukocytosis (WBC 11.6 K/uL), creatinine 0.7 mg/dL, hemoglobin 8.8 g/dL, B-type natriuretic peptide of 610 pg/mL, and D-dimer of 3469 ng/mL. CT chest revealed cardiomegaly, pulmonary edema, bilateral lower lobe consolidations, and pleural effusions, a large pericardial effusion, and a 5x10 cm perisplenic abscess found to be secondary to septic emboli. Echocardiogram showed a 2.1 cm mobile vegetation on the anterior leaflet of the mitral valve (Figure ), moderate-severe mitral valve insufficiency (Figure ), ejection fraction of 65%, markedly dilated left atrium, elevated peak pulmonary artery pressure at 57 mmHg, and large pericardial effusion without evidence of tamponade. Broad-spectrum IV antibiotics were started for infective endocarditis and diuresis for new-onset heart failure. He underwent subsequent cardiothoracic surgery with an On-X mechanical mitral valve (On-X Life Technologies Inc., Austin, TX). Unfortunately, the postoperative course was complicated by mediastinal thrombus formation and hemothorax requiring surgical exploration. Once stabilized, the patient was discharged and upon discharge was placed in IV penicillin G and ceftriaxone to complete six weeks of antibiotic therapy. OUTPUT:
PMCPatients_common334
[ { "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 with a history of multiple sclerosis (MS) was admitted to the hospital for low platelet count, after being referred by her primary care physician (PCP). She was placed on alemtuzumab as a part of the treatment for MS. Treatment was initiated two years ago, and she received two doses one year apart, with the last dose administered one year ago. The patient was continuously monitored with monthly complete blood count (CBC). On physical examination, the patient had mucocutaneous manifestations of thrombocytopenia; petechia on the chest and bruises on upper limbs were noticed. The patient did not have a history of Wiskott-Aldrich syndrome, thrombocytopenia - absent radius syndrome, May-Hegglan anomaly, gray platelet syndrome, Upshaw-Shulman syndrome, or Bernard-Soulier syndrome. On the first day of admission, the patient had a platelet count of only 3000/μL. Her medical records from the last three months showed a serial decline of platelet count.\\nFurther investigations were done on the patient, in search for the etiology of thrombocytopenia. Moreover, patient‘s home medications were reviewed, including ampura, oxybutynin, donepezil, baclofen which were not associated with thrombocytopenia. Other labs such as vitamin B12 level, thyroid stimulating hormone (TSH), antinuclear antibody (ANA), rheumatoid factor (RF), human immunodeficiency virus (HIV), Ebstein-Barr virus (EBV), hepatitis serology were unremarkable. After excluding other causes, the patient was treated for ITP secondary to alemtuzumab, with prednisone 1 mg/kg. Soon, the patient showed a good response to treatment; platelet count increased, and bruises and petechiae resolved within a few days.\nOUTPUT:" }, { "from": "agent", "value": "Idiopathic Thrombocytopenic Purpura" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 45-year-old female with a history of multiple sclerosis (MS) was admitted to the hospital for low platelet count, after being referred by her primary care physician (PCP). She was placed on alemtuzumab as a part of the treatment for MS. Treatment was initiated two years ago, and she received two doses one year apart, with the last dose administered one year ago. The patient was continuously monitored with monthly complete blood count (CBC). On physical examination, the patient had mucocutaneous manifestations of thrombocytopenia; petechia on the chest and bruises on upper limbs were noticed. The patient did not have a history of Wiskott-Aldrich syndrome, thrombocytopenia - absent radius syndrome, May-Hegglan anomaly, gray platelet syndrome, Upshaw-Shulman syndrome, or Bernard-Soulier syndrome. On the first day of admission, the patient had a platelet count of only 3000/μL. Her medical records from the last three months showed a serial decline of platelet count.\nFurther investigations were done on the patient, in search for the etiology of thrombocytopenia. Moreover, patient‘s home medications were reviewed, including ampura, oxybutynin, donepezil, baclofen which were not associated with thrombocytopenia. Other labs such as vitamin B12 level, thyroid stimulating hormone (TSH), antinuclear antibody (ANA), rheumatoid factor (RF), human immunodeficiency virus (HIV), Ebstein-Barr virus (EBV), hepatitis serology were unremarkable. After excluding other causes, the patient was treated for ITP secondary to alemtuzumab, with prednisone 1 mg/kg. Soon, the patient showed a good response to treatment; platelet count increased, and bruises and petechiae resolved within a few days. OUTPUT:
PMCPatients_common256
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 55-year-old male with poorly controlled HIV infection (cluster of differentiation (CD)4 count 194) and severe pulmonary hypertension (HTN) due to amphetamine abuse presented with a two-week history of cutaneous nodules (eight to ten nodules on the abdomen with the largest being 2 x 2 cm). He did not have any peripheral lymphadenopathy or hepatosplenomegaly. The scans also suggested bilateral testicular enlargement prompting a testicular ultrasound which showed bilateral testicular masses (Figure ).\\nAt this point, the primary source of malignancy was thought to be testicular. Unfortunately, due to the patient’s severe pulmonary HTN, he was unable to undergo anesthesia for a testicular biopsy as he kept becoming hypoxic. Since this lymphoma has a high risk of relapse in the CNS, a spinal tap was done but the fluid was negative for malignant cells. He was treated with cyclophosphamide, vincristine, and prednisone (CVP) regimen along with high dose methotrexate (to provide CNS prophylaxis). He had a complete response after five cycles of chemotherapy.\\nEight months after his initial diagnosis, he presented to the clinic confused and forgetful. Further work up revealed the involvement of cerebral spinal fluid with lymphoma. He underwent an Ommaya placement with intrathecal chemotherapy. His spinal fluid became negative for malignant cells after three treatments. Bilateral testicular radiation therapy was given (as testes have poor chemotherapy penetration and can act as sanctuary sites). In spite of all this, he developed delirium and acute hypoxic respiratory failure and continued to decline and died ten months after his diagnosis.\nOUTPUT:" }, { "from": "agent", "value": "Testicular Plasmablastic Lymphoma, Human Immunodeficiency Virus" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 55-year-old male with poorly controlled HIV infection (cluster of differentiation (CD)4 count 194) and severe pulmonary hypertension (HTN) due to amphetamine abuse presented with a two-week history of cutaneous nodules (eight to ten nodules on the abdomen with the largest being 2 x 2 cm). He did not have any peripheral lymphadenopathy or hepatosplenomegaly. The scans also suggested bilateral testicular enlargement prompting a testicular ultrasound which showed bilateral testicular masses (Figure ).\nAt this point, the primary source of malignancy was thought to be testicular. Unfortunately, due to the patient’s severe pulmonary HTN, he was unable to undergo anesthesia for a testicular biopsy as he kept becoming hypoxic. Since this lymphoma has a high risk of relapse in the CNS, a spinal tap was done but the fluid was negative for malignant cells. He was treated with cyclophosphamide, vincristine, and prednisone (CVP) regimen along with high dose methotrexate (to provide CNS prophylaxis). He had a complete response after five cycles of chemotherapy.\nEight months after his initial diagnosis, he presented to the clinic confused and forgetful. Further work up revealed the involvement of cerebral spinal fluid with lymphoma. He underwent an Ommaya placement with intrathecal chemotherapy. His spinal fluid became negative for malignant cells after three treatments. Bilateral testicular radiation therapy was given (as testes have poor chemotherapy penetration and can act as sanctuary sites). In spite of all this, he developed delirium and acute hypoxic respiratory failure and continued to decline and died ten months after his diagnosis. OUTPUT:
PMCPatients_common2525
[ { "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 March 2007, a 62-year-old Caucasian male followed for a compensated HCV-correlated liver cirrhosis at the Liver Unit of the Second University of Naples. Due to dyspeptic symptoms and weight loss in the last two months, he was evaluated. At the time of our observation, an abdominal US showed a hypoechoic, irregular-shaped mass of 4 cm in the body of the Pancreas. The laboratory data showed an abnormal serum value of CA 19.9 and a leuko- thrombocytopenia (). The CT scan confirmed the hypovascularity. Subsequently a Radio Frequency Ablation was performed and followed by radiotherapy with systemic and local chemotherapy (infusion of 5-fluorouracil, leucovorin, epirubicin and carboplatin - FLEC regimen).\\nAfter three years, in June 2010, a routinely abdominal US showed a mass of 2 cm in celiac trunk area. The CEUS showed a mass with hypo-enhancement in the arterial phase, confirmed by CT scan. After this diagnostic test, the patient underwent laparotomy surgery. After laparotomy, the patient showed decompensation of liver cirrhosis with ascites. Due to decompensation, never resolved, the patient was not able to undergo a new surgical treatment.\nOUTPUT:" }, { "from": "agent", "value": "Pancreatic Adenocarcinoma, Gastric GIST" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: In March 2007, a 62-year-old Caucasian male followed for a compensated HCV-correlated liver cirrhosis at the Liver Unit of the Second University of Naples. Due to dyspeptic symptoms and weight loss in the last two months, he was evaluated. At the time of our observation, an abdominal US showed a hypoechoic, irregular-shaped mass of 4 cm in the body of the Pancreas. The laboratory data showed an abnormal serum value of CA 19.9 and a leuko- thrombocytopenia (). The CT scan confirmed the hypovascularity. Subsequently a Radio Frequency Ablation was performed and followed by radiotherapy with systemic and local chemotherapy (infusion of 5-fluorouracil, leucovorin, epirubicin and carboplatin - FLEC regimen).\nAfter three years, in June 2010, a routinely abdominal US showed a mass of 2 cm in celiac trunk area. The CEUS showed a mass with hypo-enhancement in the arterial phase, confirmed by CT scan. After this diagnostic test, the patient underwent laparotomy surgery. After laparotomy, the patient showed decompensation of liver cirrhosis with ascites. Due to decompensation, never resolved, the patient was not able to undergo a new surgical treatment. OUTPUT:
PMCPatients_common3306
[ { "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 36-year-old woman presented with a 4-month history of a progressive and painful increase in volume of the parotid. ).\\nIn October 2018, she presented with a de novo macular lesion in the right frontal region, asymmetric and hyperpigmented, with spontaneous bleeding. Subsequently, a combined 2-[18F]-fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography (18FDG-PET/CT) was performed as an extension study, which demonstrated the presence of right cervical lymphadenopathy at levels IIA and IIB, the largest being 25 × 15 mm in size. , B, ).\\nIt was staged IVA, so that adjuvant treatment with radiotherapy at 66 Gy to the right cervical region (total: 33 sessions) and concomitant chemotherapy (carboplatin AUC 2 + paclitaxel 80 mg/m2) was performed. A complete response was reported (Fig. ).\\nTen months after the operation, control 18FDG-PET/CT was performed, in which local recurrence and metastasis to the lung were shown. , F, ).\nOUTPUT:" }, { "from": "agent", "value": "Myoepithelial Carcinoma of the Parotid Gland, Plasmacytoid Myoepithelioma, Melanoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 36-year-old woman presented with a 4-month history of a progressive and painful increase in volume of the parotid. ).\nIn October 2018, she presented with a de novo macular lesion in the right frontal region, asymmetric and hyperpigmented, with spontaneous bleeding. Subsequently, a combined 2-[18F]-fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography (18FDG-PET/CT) was performed as an extension study, which demonstrated the presence of right cervical lymphadenopathy at levels IIA and IIB, the largest being 25 × 15 mm in size. , B, ).\nIt was staged IVA, so that adjuvant treatment with radiotherapy at 66 Gy to the right cervical region (total: 33 sessions) and concomitant chemotherapy (carboplatin AUC 2 + paclitaxel 80 mg/m2) was performed. A complete response was reported (Fig. ).\nTen months after the operation, control 18FDG-PET/CT was performed, in which local recurrence and metastasis to the lung were shown. , F, ). OUTPUT:
PMCPatients_common1229
[ { "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 man confined in a crowded prison presented to our institution due to respiratory symptoms. During hospitalization he was subjected to a standardized diagnostic approach including physical examination and a detailed clinical history. Routine laboratory tests, CD4 T cell count and HIV viral load were performed. Appropriate treatment for these conditions was administrated, and after 13 days in hospital he initiated ART with tenofovir, emtricitabine and efavirenz. His clinical condition improved and 5 days later he was discharged. No skin lesions were visible when he attended a routine visit after 13 days on ART. Interestingly, he presented with disseminated itchy dermatosis characterized by hyperkeratotic, hyperpigmented crusted plaques with hemorrhagic fissures after 20 days on ART (Figure\\n). Microscopic examination of the scale and skin biopsy enabled identification of scabies mites and eggs (Figure\\n). The temporal relation with ART initiation and the rapid progression of infection by Sarcoptes scabiei, in presence of an exaggerated inflammatory reaction and atypical inflammatory response in the affected tissues, supported the diagnosis of IRIS\\n[]. Complete resolution of dermatosis was observed with administration of 3 doses of 12 mg ivermectin given at 1-week intervals, as well as 5-day topical ointment containing balsam of Peru, precipitate sulfur and benzoate butter (Figure\\n). The confinement center received notification of this case, and was also provided with recommendations for the prevention and control of scabies. Days later the patient was discharged home, where he transmitted Sarcoptes scabiei to his mother, father and pregnant sister. They all received appropriate treatment leading to remission of the lesions. After three months on ART the patient had a CD4 T-cell count of 281 cells/μl and a viral load of 86 HIV RNA copies/ml (1.93 log). At this point, the diagnosis of IRIS was confirmed by the ART-induced decrease of more than 4 log in the viral load.\nOUTPUT:" }, { "from": "agent", "value": "Crusted scabies-associated immune reconstitution inflammatory syndrome, late HIV infection, disseminated tuberculosis involving lymph node and central nervous system, cytomegalovirus retinitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 28-year-old man confined in a crowded prison presented to our institution due to respiratory symptoms. During hospitalization he was subjected to a standardized diagnostic approach including physical examination and a detailed clinical history. Routine laboratory tests, CD4 T cell count and HIV viral load were performed. Appropriate treatment for these conditions was administrated, and after 13 days in hospital he initiated ART with tenofovir, emtricitabine and efavirenz. His clinical condition improved and 5 days later he was discharged. No skin lesions were visible when he attended a routine visit after 13 days on ART. Interestingly, he presented with disseminated itchy dermatosis characterized by hyperkeratotic, hyperpigmented crusted plaques with hemorrhagic fissures after 20 days on ART (Figure\n). Microscopic examination of the scale and skin biopsy enabled identification of scabies mites and eggs (Figure\n). The temporal relation with ART initiation and the rapid progression of infection by Sarcoptes scabiei, in presence of an exaggerated inflammatory reaction and atypical inflammatory response in the affected tissues, supported the diagnosis of IRIS\n[]. Complete resolution of dermatosis was observed with administration of 3 doses of 12 mg ivermectin given at 1-week intervals, as well as 5-day topical ointment containing balsam of Peru, precipitate sulfur and benzoate butter (Figure\n). The confinement center received notification of this case, and was also provided with recommendations for the prevention and control of scabies. Days later the patient was discharged home, where he transmitted Sarcoptes scabiei to his mother, father and pregnant sister. They all received appropriate treatment leading to remission of the lesions. After three months on ART the patient had a CD4 T-cell count of 281 cells/μl and a viral load of 86 HIV RNA copies/ml (1.93 log). At this point, the diagnosis of IRIS was confirmed by the ART-induced decrease of more than 4 log in the viral load. OUTPUT:
PMCPatients_common1378
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 58-year-old woman presented to our outpatient clinic with left hip pain with a duration of 15 years. There was no history of trauma or other diseases. Her hip pain usually occurred only on walking and not at rest. Physical examination demonstrated no tenderness in the hip joint, and Patrick's fabere test was negative. The range of motion of both hip joints was almost normal: flexion was 140/140 degrees (right/left), abduction was 35/35 degrees, and adduction was 10/10 degrees. Laxity of other joints was not observed. There was no abnormal value on laboratory examinations. The bone mineral density of the lumbar spine (L2–4, 0.643 g/cm2, T-score: −3.41 S.D.) and proximal femur (0.760 g/cm2, T-score: −1.99 S.D.) Lumbosacral angles (LSA) on lying and standing were 27 and 6 degrees, respectively (). Centre-edge angles (CEA) were 17/17 degrees (right/left), Sharp angles were 36/36 degrees, and acetabular head index (AHI) values were 66/72% () []. Distances from the original hip center to the migrated femoral head center were 10 mm in the right hip and 9 mm in the left hip. We performed right total hip arthroplasty, and she could walk with a cane or walker. No problems were noted in the right hip joint, such as dislocation, at the most recent follow-up 6 years postoperatively.\nOUTPUT:" }, { "from": "agent", "value": "Anterior Hip Subluxation, Lumbar Degenerative Kyphosis, Posterior Pelvic Tilt, Osteoporosis, Severe Osteoarthritis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 58-year-old woman presented to our outpatient clinic with left hip pain with a duration of 15 years. There was no history of trauma or other diseases. Her hip pain usually occurred only on walking and not at rest. Physical examination demonstrated no tenderness in the hip joint, and Patrick's fabere test was negative. The range of motion of both hip joints was almost normal: flexion was 140/140 degrees (right/left), abduction was 35/35 degrees, and adduction was 10/10 degrees. Laxity of other joints was not observed. There was no abnormal value on laboratory examinations. The bone mineral density of the lumbar spine (L2–4, 0.643 g/cm2, T-score: −3.41 S.D.) and proximal femur (0.760 g/cm2, T-score: −1.99 S.D.) Lumbosacral angles (LSA) on lying and standing were 27 and 6 degrees, respectively (). Centre-edge angles (CEA) were 17/17 degrees (right/left), Sharp angles were 36/36 degrees, and acetabular head index (AHI) values were 66/72% () []. Distances from the original hip center to the migrated femoral head center were 10 mm in the right hip and 9 mm in the left hip. We performed right total hip arthroplasty, and she could walk with a cane or walker. No problems were noted in the right hip joint, such as dislocation, at the most recent follow-up 6 years postoperatively. OUTPUT:
PMCPatients_common495
[ { "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: Immunofixation demonstrated immunoglobulin G (IgG) lambda monoclonal gammopathy of 1040 mg/dL. Bone marrow biopsy revealed less than 5% lambda-restricted plasma cells. No evidence of CRAB (hypercalcemia, renal failure, anemia, bone disease) criteria were seen. Hemoglobin was 14 g/dl, calculated glomerular filtration rate (GFR) between 90 to 100 mL/min, corrected calcium of 9.3 mg/dl, and urinalysis demonstrated no evidence of proteinuria. Thyroid-stimulating hormone (TSH) was normal. Monthly intravenous immunoglobulin (IVIg) was started in August 2017 with gradual improvement in his skin lesions, and complete resolution by December 2017. He did not follow up with dermatology and so was not resumed on treatment. Plasmapheresis was also not able to be performed due to the amount of time required to attain treatment effect. Corticosteroids were also avoided due to concerns for impairing surgical wound healing. He suffered no complications postoperatively and his sternal incision site healed well (Figure ).\nOUTPUT:" }, { "from": "agent", "value": "Scleromyxedema, Triple-vessel coronary artery disease" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Immunofixation demonstrated immunoglobulin G (IgG) lambda monoclonal gammopathy of 1040 mg/dL. Bone marrow biopsy revealed less than 5% lambda-restricted plasma cells. No evidence of CRAB (hypercalcemia, renal failure, anemia, bone disease) criteria were seen. Hemoglobin was 14 g/dl, calculated glomerular filtration rate (GFR) between 90 to 100 mL/min, corrected calcium of 9.3 mg/dl, and urinalysis demonstrated no evidence of proteinuria. Thyroid-stimulating hormone (TSH) was normal. Monthly intravenous immunoglobulin (IVIg) was started in August 2017 with gradual improvement in his skin lesions, and complete resolution by December 2017. He did not follow up with dermatology and so was not resumed on treatment. Plasmapheresis was also not able to be performed due to the amount of time required to attain treatment effect. Corticosteroids were also avoided due to concerns for impairing surgical wound healing. He suffered no complications postoperatively and his sternal incision site healed well (Figure ). OUTPUT:
PMCPatients_common2337
[ { "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 man presented with shortness of breath, swollen legs, and dry cough enduring five days. Fine, moist, and subcrepitant inspirations were heard at the left base and diminished breath sounds were present at the right base. The respiratory rate was 32/min. His heart rate was 99/min and his arterial blood pressure was 165/105 mm Hg, and he had a systolic murmur 3/6 over aortic valve projection. Arterial blood gas sampling revealed pH = 7.448, pCO2 = 4.33 kPa, pO2 = 7.67 kPa, HCO3 = 22.0 mmol/L, base excess −1.1 mmol/L, and SaO2 = 91.4%. Laboratory studies were remarkable for a normal complete blood count, a slightly elevated serum creatinine level of 143 μmol/L, and a GGT level threefold elevated. Echocardiogram obtained on admission demonstrated concentric left ventricular hypertrophy, aortic stenosis, and moderate mitral regurgitation accompanied by dilated left atrium and impaired left ventricular systolic function with ejection fraction of 39%.\\nCXR showed massive sharply demarked round/oval homogeneous dense shadow 10 × 7 cm in size in the right inferior lobe (). Archive CXR undergone 1 and 4 years ago revealed intermittent appearance of the similar tumor-like shadows in the same region of the right lobe (). Pulmonary ultrasound examination confirmed collection of the pleural fluid within oblique interlobar fissure of the right pulmonary lobe. The parenteral diuretic therapy was immediately initiated. Due to clinical and subjective improvement during the observation period, the patient was dismissed for a home treatment with a recommendation to raise peroral diuretic therapy with reduction of fluid intake. Three days later, a control CXR revealed complete resolution () of the observed round/oval tumor-like image.\nOUTPUT:" }, { "from": "agent", "value": "Phantom Tumor of the Lung, Localized Interlobar Effusion, Congestive Heart Failure" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 83-year-old man presented with shortness of breath, swollen legs, and dry cough enduring five days. Fine, moist, and subcrepitant inspirations were heard at the left base and diminished breath sounds were present at the right base. The respiratory rate was 32/min. His heart rate was 99/min and his arterial blood pressure was 165/105 mm Hg, and he had a systolic murmur 3/6 over aortic valve projection. Arterial blood gas sampling revealed pH = 7.448, pCO2 = 4.33 kPa, pO2 = 7.67 kPa, HCO3 = 22.0 mmol/L, base excess −1.1 mmol/L, and SaO2 = 91.4%. Laboratory studies were remarkable for a normal complete blood count, a slightly elevated serum creatinine level of 143 μmol/L, and a GGT level threefold elevated. Echocardiogram obtained on admission demonstrated concentric left ventricular hypertrophy, aortic stenosis, and moderate mitral regurgitation accompanied by dilated left atrium and impaired left ventricular systolic function with ejection fraction of 39%.\nCXR showed massive sharply demarked round/oval homogeneous dense shadow 10 × 7 cm in size in the right inferior lobe (). Archive CXR undergone 1 and 4 years ago revealed intermittent appearance of the similar tumor-like shadows in the same region of the right lobe (). Pulmonary ultrasound examination confirmed collection of the pleural fluid within oblique interlobar fissure of the right pulmonary lobe. The parenteral diuretic therapy was immediately initiated. Due to clinical and subjective improvement during the observation period, the patient was dismissed for a home treatment with a recommendation to raise peroral diuretic therapy with reduction of fluid intake. Three days later, a control CXR revealed complete resolution () of the observed round/oval tumor-like image. OUTPUT:
PMCPatients_common1611
[ { "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 69-year-old man was admitted to the hospital for right-sided neck and bilateral upper extremity edema and headache for 1 month. Vital signs showed a heart rate of 70 beats/min, arterial blood pressure of 120/70 mm Hg, a respiratory rate of 20 breaths/min, and body temperature of 37°C. Physical examination revealed swelling along the anterior border of the right sternocleidomastoid muscle and distension of the right jugular vein (). Chest and cardiac physical examination were unremarkable. He had no history of tobacco or intravenous drug use. Abnormal laboratory findings included a high serum level of total bilirubin (23 μg/L), direct bilirubin (6.2 μg/L), and indirect bilirubin (16.8 μg/L). Chest radiography finding revealed two dome-shaped elevations of the right hemidiaphragm suggestive of intra-abdominal masses (). Gram stain, culture, and cytology of the fluid were negative. The patient was treated with 7 days of subcutaneous low–molecular weight heparin (1 mg/kg every 12 hours) followed by a long-term vitamin K antagonist. Postsurgical transthoracic echocardiography demonstrated elimination of compression and recovery of right atrial function (, ). Partial resolution of venous thrombi was seen by carotid ultrasound on day 7 following the anticoagulant therapy (). This was accompanied by a significant alleviation of the patient's symptoms.\nOUTPUT:" }, { "from": "agent", "value": "Hepatic Cyst, Internal Jugular Venous Thrombosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 69-year-old man was admitted to the hospital for right-sided neck and bilateral upper extremity edema and headache for 1 month. Vital signs showed a heart rate of 70 beats/min, arterial blood pressure of 120/70 mm Hg, a respiratory rate of 20 breaths/min, and body temperature of 37°C. Physical examination revealed swelling along the anterior border of the right sternocleidomastoid muscle and distension of the right jugular vein (). Chest and cardiac physical examination were unremarkable. He had no history of tobacco or intravenous drug use. Abnormal laboratory findings included a high serum level of total bilirubin (23 μg/L), direct bilirubin (6.2 μg/L), and indirect bilirubin (16.8 μg/L). Chest radiography finding revealed two dome-shaped elevations of the right hemidiaphragm suggestive of intra-abdominal masses (). Gram stain, culture, and cytology of the fluid were negative. The patient was treated with 7 days of subcutaneous low–molecular weight heparin (1 mg/kg every 12 hours) followed by a long-term vitamin K antagonist. Postsurgical transthoracic echocardiography demonstrated elimination of compression and recovery of right atrial function (, ). Partial resolution of venous thrombi was seen by carotid ultrasound on day 7 following the anticoagulant therapy (). This was accompanied by a significant alleviation of the patient's symptoms. OUTPUT:
PMCPatients_common200
[ { "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 tumor, about 3 cm in diameter, was located on the right side of the lower rectum 3 cm above the anal verge. The pathological analysis of the biopsy sample revealed that the tumor was a moderately differentiated adenocarcinoma. a–c). To achieve complete TME with negative CRM, a hybrid transabdominal-transanal approach for ISR was conducted.\\nFirst, vascular division and mobilization of the left colon were performed laparoscopically. After closure of the anal orifice, the GelPoint Mini was placed to start the transanal approach. Posterior side of the rectum was first dissected until the transanal approach was connected to the dissection layer made by the transabdominal approach. The dissection procedure was extended to the lateral side. Bilateral pelvic splanchnic nerves were identified at the 5 and 7 o’clock positions. At the anterior side, the proper dissection layer cannot be easily identified because of the perineal body and the enlarged prostate. Once the dissection plane between the rectum and the prostate could be identified, it was relatively easy to continue along the same plane. The assistance provided by the laparoscopic approach was useful to determine the appropriate dissection line in the transanal approach.\nOUTPUT:" }, { "from": "agent", "value": "Rectal cancer, Prostatic hypertrophy" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The tumor, about 3 cm in diameter, was located on the right side of the lower rectum 3 cm above the anal verge. The pathological analysis of the biopsy sample revealed that the tumor was a moderately differentiated adenocarcinoma. a–c). To achieve complete TME with negative CRM, a hybrid transabdominal-transanal approach for ISR was conducted.\nFirst, vascular division and mobilization of the left colon were performed laparoscopically. After closure of the anal orifice, the GelPoint Mini was placed to start the transanal approach. Posterior side of the rectum was first dissected until the transanal approach was connected to the dissection layer made by the transabdominal approach. The dissection procedure was extended to the lateral side. Bilateral pelvic splanchnic nerves were identified at the 5 and 7 o’clock positions. At the anterior side, the proper dissection layer cannot be easily identified because of the perineal body and the enlarged prostate. Once the dissection plane between the rectum and the prostate could be identified, it was relatively easy to continue along the same plane. The assistance provided by the laparoscopic approach was useful to determine the appropriate dissection line in the transanal approach. OUTPUT:
PMCPatients_common1837
[ { "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 69-year-old woman was referred to us due to a diagnosis of recurrent SUI while coughing, sneezing, and walking. Eleven years earlier, she underwent a bone anchor sling to treat SUI at another hospital. Although the leakage appeared to issue from the vagina at first, the second round of coughing showed leakage from the external urethral meatus. Retrospectively, coexistent UVF was overlooked as the lighting was poor and a vaginal speculum was not used. A 1-h pad test resulted in 166 g of leakage. Uroflowmetry was normal (maximum flow rate 34 mL/s, voided volume 331 mL, and residual volume 0 mL). Videourodynamic study verified leakage and the bladder neck opening while coughing and straining without detrusor overactivity.\\nAn MUS was planned, but immediately before the procedure, a UVF was found 2 cm proximal to the external urethral meatus (Fig. ). Three months later, a 1-h pad test resulted in 195 g of leakage. Usage of a vaginal speculum and powerful medical lamps during a stress test made it obvious that more leakage occurred from the UVF than from the external urethral meatus (Fig. ). She did not want further treatment for the remaining mild SUI.\nOUTPUT:" }, { "from": "agent", "value": "Urethrovaginal fistula, Recurrent Stress Urinary Incontinence" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 69-year-old woman was referred to us due to a diagnosis of recurrent SUI while coughing, sneezing, and walking. Eleven years earlier, she underwent a bone anchor sling to treat SUI at another hospital. Although the leakage appeared to issue from the vagina at first, the second round of coughing showed leakage from the external urethral meatus. Retrospectively, coexistent UVF was overlooked as the lighting was poor and a vaginal speculum was not used. A 1-h pad test resulted in 166 g of leakage. Uroflowmetry was normal (maximum flow rate 34 mL/s, voided volume 331 mL, and residual volume 0 mL). Videourodynamic study verified leakage and the bladder neck opening while coughing and straining without detrusor overactivity.\nAn MUS was planned, but immediately before the procedure, a UVF was found 2 cm proximal to the external urethral meatus (Fig. ). Three months later, a 1-h pad test resulted in 195 g of leakage. Usage of a vaginal speculum and powerful medical lamps during a stress test made it obvious that more leakage occurred from the UVF than from the external urethral meatus (Fig. ). She did not want further treatment for the remaining mild SUI. OUTPUT:
PMCPatients_common4425
[ { "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 also reported seeing daily images of a little girl playing with blocks, a cat in his window, and men tearing down his neighbor’s roof that he recognized were not real. These visual disturbances were debilitating to the patient and made it difficult to complete work around his home and interact with family members. A trial of atypical antipsychotic therapy including gradually increasing quetiapine to 300 mg twice daily over the course of 3 weeks followed by the addition of pimavanserin 34 mg daily for 3 weeks failed to relieve his hallucinations. Most recently, his dose of carbidopa/levodopa was decreased, and clozapine was initiated and gradually increased to 150 mg twice daily for 3 weeks since the visual disturbances continued to be debilitating. Clozapine, in particular, is a high-risk antipsychotic medication with the potentially serious adverse effect of agranulocytosis along with possible metabolic, neurologic, and cardiac toxicities including hyperglycemia, hyperlipidemia, seizures, myocarditis, and pulmonary embolism. He continued to experience hallucinations while on clozapine when he presented to the ophthalmology service. His ophthalmic exam revealed a best-corrected visual acuity (BCVA) of 20/200 in each eye (OU). Ocular examination was remarkable for mild corneal guttae OU, posterior chamber intraocular lenses (PCIOL) OU, and visually significant PCO OU. The anterior and posterior segments were otherwise unremarkable. He underwent sequential Nd:YAG capsulotomy OU. At his one-month follow-up, the patient reported complete resolution of his hallucinations with BCVA of 20/25 in his right eye (OD) and 20/30 in his left eye (OS). The patient then resumed his previous carbidopa/levodopa dose and was tapered off clozapine with sustained resolution of the visual disturbances.\nOUTPUT:" }, { "from": "agent", "value": "Charles Bonnet Syndrome, Parkinson’s Disease, Bilateral Posterior Capsule Opacification" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: He also reported seeing daily images of a little girl playing with blocks, a cat in his window, and men tearing down his neighbor’s roof that he recognized were not real. These visual disturbances were debilitating to the patient and made it difficult to complete work around his home and interact with family members. A trial of atypical antipsychotic therapy including gradually increasing quetiapine to 300 mg twice daily over the course of 3 weeks followed by the addition of pimavanserin 34 mg daily for 3 weeks failed to relieve his hallucinations. Most recently, his dose of carbidopa/levodopa was decreased, and clozapine was initiated and gradually increased to 150 mg twice daily for 3 weeks since the visual disturbances continued to be debilitating. Clozapine, in particular, is a high-risk antipsychotic medication with the potentially serious adverse effect of agranulocytosis along with possible metabolic, neurologic, and cardiac toxicities including hyperglycemia, hyperlipidemia, seizures, myocarditis, and pulmonary embolism. He continued to experience hallucinations while on clozapine when he presented to the ophthalmology service. His ophthalmic exam revealed a best-corrected visual acuity (BCVA) of 20/200 in each eye (OU). Ocular examination was remarkable for mild corneal guttae OU, posterior chamber intraocular lenses (PCIOL) OU, and visually significant PCO OU. The anterior and posterior segments were otherwise unremarkable. He underwent sequential Nd:YAG capsulotomy OU. At his one-month follow-up, the patient reported complete resolution of his hallucinations with BCVA of 20/25 in his right eye (OD) and 20/30 in his left eye (OS). The patient then resumed his previous carbidopa/levodopa dose and was tapered off clozapine with sustained resolution of the visual disturbances. OUTPUT:
PMCPatients_common4777
[ { "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 26-year-old female was referred to our department of oral and maxillofacial surgery with a chief complaint of deviated nose and smaller nostril on the right side. The surgery was carried out under general anesthesia through orotracheal intubation. An inverted-V transcolumellar incision with bilateral marginal incisions was made, the lower lateral cartilage and septal cartilage were exposed [], the cartilaginous septum was separated from the maxillary crest and secured to the midline using 5–0 PDS suture, deviated portions of the septum were then removed and the excess cartilage is preserved for graft in future use [], while preserving an adequate dorsal and caudal strut. The tip projection and symmetry was increased with a strut graft in the columella in a pocket between medial crura, medial advancement of lower lateral cartilage was done []. Alar hooding was improved and alar collapse was prevented by placing a spreader graft [].\\nPostoperatively the healing was satisfactory with no evidence of infection or wound dehiscence. The results were stable with no evidence of relapse with a period of follow-up of 1-year.\nOUTPUT:" }, { "from": "agent", "value": "Cleft nasal deformity" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 26-year-old female was referred to our department of oral and maxillofacial surgery with a chief complaint of deviated nose and smaller nostril on the right side. The surgery was carried out under general anesthesia through orotracheal intubation. An inverted-V transcolumellar incision with bilateral marginal incisions was made, the lower lateral cartilage and septal cartilage were exposed [], the cartilaginous septum was separated from the maxillary crest and secured to the midline using 5–0 PDS suture, deviated portions of the septum were then removed and the excess cartilage is preserved for graft in future use [], while preserving an adequate dorsal and caudal strut. The tip projection and symmetry was increased with a strut graft in the columella in a pocket between medial crura, medial advancement of lower lateral cartilage was done []. Alar hooding was improved and alar collapse was prevented by placing a spreader graft [].\nPostoperatively the healing was satisfactory with no evidence of infection or wound dehiscence. The results were stable with no evidence of relapse with a period of follow-up of 1-year. OUTPUT:
PMCPatients_common950
[ { "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, an 8 year-4-month-old boy, was referred to the pediatric neurology clinic due to focal seizures with loss of consciousness occurring 8 times within a 12 months period. His cognitive and language milestones were all delayed, and he also presented with constipation, and obesity. On examination, polydactyly and strabismus were noted, and initial workup revealed hypothyroidism. He was the second born of a consanguineous marriage and his older sister was healthy.\\nIn this patient, a rare homozygous mutation impacting BBS1gene was identified using WES (c.1339 G > A[p.Ala447Thr])that causes Alanine to Threonine change at position 447 of BBS1 protein. In very rare cases, seizure has also been found in patients of BBS. The variant c.1339 G > A falls at the last nucleotide of exon 13 of the BBS1 coding sequence, which is part of the consensus splice site for this exon. Nucleotide substitutions within the consensus splice site are relatively common causes of aberrant splicing. This variant was not found in the Genome Aggregation Database (gnomAD) as homozygous state. The heterozygous state of the variant is present in population databases at extremely rare frequencies (rs200116631, gnomAD frequency = 0.00003). Patient 3 meets the major clinical features of BBS with regard to hypothyroidism, polydactyly, obesity, strabismus, impaired intelligence in comparison to peers, and language delay. Therefore, this variant can be classified as ‘likely pathogenic’ in accordance with ACMG guideline. This variant was not screened in the parents’ DNA (Fig. ).\nOUTPUT:" }, { "from": "agent", "value": "Bardet–Biedl Syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Patient 3, an 8 year-4-month-old boy, was referred to the pediatric neurology clinic due to focal seizures with loss of consciousness occurring 8 times within a 12 months period. His cognitive and language milestones were all delayed, and he also presented with constipation, and obesity. On examination, polydactyly and strabismus were noted, and initial workup revealed hypothyroidism. He was the second born of a consanguineous marriage and his older sister was healthy.\nIn this patient, a rare homozygous mutation impacting BBS1gene was identified using WES (c.1339 G > A[p.Ala447Thr])that causes Alanine to Threonine change at position 447 of BBS1 protein. In very rare cases, seizure has also been found in patients of BBS. The variant c.1339 G > A falls at the last nucleotide of exon 13 of the BBS1 coding sequence, which is part of the consensus splice site for this exon. Nucleotide substitutions within the consensus splice site are relatively common causes of aberrant splicing. This variant was not found in the Genome Aggregation Database (gnomAD) as homozygous state. The heterozygous state of the variant is present in population databases at extremely rare frequencies (rs200116631, gnomAD frequency = 0.00003). Patient 3 meets the major clinical features of BBS with regard to hypothyroidism, polydactyly, obesity, strabismus, impaired intelligence in comparison to peers, and language delay. Therefore, this variant can be classified as ‘likely pathogenic’ in accordance with ACMG guideline. This variant was not screened in the parents’ DNA (Fig. ). OUTPUT:
PMCPatients_common230
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 7-year-old male patient began his condition in 2008 with pain and claudication in the left lower limb. He was taken to his Family Medical Unit, where he was referred to the Emergency Unit of the Lomas Verdes High Specialty Medical Unit (UMAE) of Traumatology and Orthopedics of the Mexican Institute of Social Security (IMSS), where they performed a bone biopsy and curettage with bone graft application in lyophilized cadaveric tricortical bone allograft, with a presumptive diagnosis of aneurysmal bone cyst. He remained under surveillance in the private sector; however, pain persisted in the left lower limb. Afterwards, he presented with pain exacerbation, which was why he returned to the emergency department in 2013.\\nAdditional studies were performed showing osteolysis of the left iliac bone. Suspecting a malignant process, he was referred to the UMAE at Pediatrics Hospital National Medical Center “Siglo XXI” to the Oncology Department for study protocol at 11 years, 11 months old. Further studies were performed with pelvic radiographs and computerized tomography with three-dimensional reconstruction (see Figs. , and ). The magnetic resonance showed a neoplastic lesion of the pelvis with edema, suggestive of Ewing’s sarcoma. An incisional biopsy was performed in December 2013, with an initial histopathology report of an aneurysmal bone cyst. However, the observed osteolysis in the radiographic studies created diagnostic doubts.\\nFollow-up was performed through the outpatient clinic, showing slight improvement of his symptoms. In June 2014, a new bone biopsy and curettage was performed, with the use of lyophilized cadaveric tricortical bone grafts fixed with Kirschner wire. The histopathological study reported necrosis and reabsorption of spongy bone tissue and vascularized fibrous connective tissue with some osteoclastic giant cells. Two years later, lyophilized cadaveric tricortical bone grafts were used again. He had appropriate evolution and remitting symptoms; thus, he was discharged from the service (Additional file ).\nOUTPUT:" }, { "from": "agent", "value": "Gorham-Stout disease" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 7-year-old male patient began his condition in 2008 with pain and claudication in the left lower limb. He was taken to his Family Medical Unit, where he was referred to the Emergency Unit of the Lomas Verdes High Specialty Medical Unit (UMAE) of Traumatology and Orthopedics of the Mexican Institute of Social Security (IMSS), where they performed a bone biopsy and curettage with bone graft application in lyophilized cadaveric tricortical bone allograft, with a presumptive diagnosis of aneurysmal bone cyst. He remained under surveillance in the private sector; however, pain persisted in the left lower limb. Afterwards, he presented with pain exacerbation, which was why he returned to the emergency department in 2013.\nAdditional studies were performed showing osteolysis of the left iliac bone. Suspecting a malignant process, he was referred to the UMAE at Pediatrics Hospital National Medical Center “Siglo XXI” to the Oncology Department for study protocol at 11 years, 11 months old. Further studies were performed with pelvic radiographs and computerized tomography with three-dimensional reconstruction (see Figs. , and ). The magnetic resonance showed a neoplastic lesion of the pelvis with edema, suggestive of Ewing’s sarcoma. An incisional biopsy was performed in December 2013, with an initial histopathology report of an aneurysmal bone cyst. However, the observed osteolysis in the radiographic studies created diagnostic doubts.\nFollow-up was performed through the outpatient clinic, showing slight improvement of his symptoms. In June 2014, a new bone biopsy and curettage was performed, with the use of lyophilized cadaveric tricortical bone grafts fixed with Kirschner wire. The histopathological study reported necrosis and reabsorption of spongy bone tissue and vascularized fibrous connective tissue with some osteoclastic giant cells. Two years later, lyophilized cadaveric tricortical bone grafts were used again. He had appropriate evolution and remitting symptoms; thus, he was discharged from the service (Additional file ). OUTPUT:
PMCPatients_common4186
[ { "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 woman with no smoking history was referred to our hospital in November 2017 after an abnormal shadow was detected in the left lower lung on chest X-ray (Fig a). A physical examination revealed no significant abnormalities. Laboratory findings were within the normal ranges, except for a high cytokeratin 19 fragment serum level of 5.1 ng/mL. Hematoxylin and eosin staining of the biopsy specimen revealed medium sized tumor cells of a polygonal shape, with medium cytoplasm and hyperchromatic nuclei (Fig ). Immunohistochemistry revealed that tumor cells were negative for TTF-1 and p40. on day 1). After the first cycle of pembrolizumab, the tumor in the left lung increased in size and atelectasis appeared in the upper lobe as a result of hilar lymph node enlargement (Fig a–c). The patient complained of dyspnea and developed hypoxia. We considered obvious disease progression and introduced second-line chemotherapy of carboplatin (CBDCA, area under the curve = 5) and pemetrexed (PEM, 500 mg/m2 on day 1). These cytotoxic agents were remarkably effective with apparent tumor shrinkage after two cycles of treatment (Fig d–f), representing a partial response. Because the patient was a non-smoker we conducted next-generation sequencing panel analysis, which revealed a MET exon 14 skipping mutation.\nOUTPUT:" }, { "from": "agent", "value": "Non-small cell lung cancer, Poorly differentiated lung adenocarcinoma, Sarcomatoid carcinoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 71-year-old woman with no smoking history was referred to our hospital in November 2017 after an abnormal shadow was detected in the left lower lung on chest X-ray (Fig a). A physical examination revealed no significant abnormalities. Laboratory findings were within the normal ranges, except for a high cytokeratin 19 fragment serum level of 5.1 ng/mL. Hematoxylin and eosin staining of the biopsy specimen revealed medium sized tumor cells of a polygonal shape, with medium cytoplasm and hyperchromatic nuclei (Fig ). Immunohistochemistry revealed that tumor cells were negative for TTF-1 and p40. on day 1). After the first cycle of pembrolizumab, the tumor in the left lung increased in size and atelectasis appeared in the upper lobe as a result of hilar lymph node enlargement (Fig a–c). The patient complained of dyspnea and developed hypoxia. We considered obvious disease progression and introduced second-line chemotherapy of carboplatin (CBDCA, area under the curve = 5) and pemetrexed (PEM, 500 mg/m2 on day 1). These cytotoxic agents were remarkably effective with apparent tumor shrinkage after two cycles of treatment (Fig d–f), representing a partial response. Because the patient was a non-smoker we conducted next-generation sequencing panel analysis, which revealed a MET exon 14 skipping mutation. OUTPUT:
PMCPatients_common5028
[ { "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 75-year-old woman was admitted to our hospital due to general weakness and to check for neurologic deficits. She had been in a bed-ridden state for the previous five months due to right hemiparesis, which was caused by cerebral infarction. She also complained about chronic cough. There was no fever or dyspnea. There was no history of recent trauma. The fibrin D-dimer measurement and other blood analyses were within the normal limits.\\nThe chest radiograph revealed a 3.4-cm well defined right paratracheal mass that was suspected to be mediastinal mass or lymphadenopathy (). Indirect CT venography of both lower extremities (4.8 mSv) showed no definite deep vein thromboses (not shown). Also, ECG-gated MDCT showed the preserved right heart function and morphology ().\\nThe patient was treated with heparin for four days and then she was given warfarin. The warfarin and an international normalized ratio of about 2.0 were maintained for two months.\\nFollow-up MDCT with ECG-gating after one month of medication was performed. She discharged after improvement of her cough and general condition.\nOUTPUT:" }, { "from": "agent", "value": "Thrombosed Azygous Vein Aneurysm, Pulmonary Arterial Thromboembolism" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 75-year-old woman was admitted to our hospital due to general weakness and to check for neurologic deficits. She had been in a bed-ridden state for the previous five months due to right hemiparesis, which was caused by cerebral infarction. She also complained about chronic cough. There was no fever or dyspnea. There was no history of recent trauma. The fibrin D-dimer measurement and other blood analyses were within the normal limits.\nThe chest radiograph revealed a 3.4-cm well defined right paratracheal mass that was suspected to be mediastinal mass or lymphadenopathy (). Indirect CT venography of both lower extremities (4.8 mSv) showed no definite deep vein thromboses (not shown). Also, ECG-gated MDCT showed the preserved right heart function and morphology ().\nThe patient was treated with heparin for four days and then she was given warfarin. The warfarin and an international normalized ratio of about 2.0 were maintained for two months.\nFollow-up MDCT with ECG-gating after one month of medication was performed. She discharged after improvement of her cough and general condition. OUTPUT:
PMCPatients_common3619
[ { "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 woman presented to us with the chief complaint of difficulty in night vision in her right eye. She had no visual complaints in the left eye. She had no history of any systemic disease, malignancy, chronic drug intake, or any inflammatory eye disease in the past. There was no family history of night blindness. The best corrected visual acuity was 20/50 in the right eye and 20/30 in the left eye. There was a relative afferent pupillary defect in the right eye. The intraocular pressure was 10 mmHg in the right eye and 20 mmHg in the left eye. Fundus examination showed waxy pallor of the disc, arteriolar attenuation, bony spicule pigmentation, diagnostic of RP, in the right eye []. The left eye showed a normal pink-colored disc and no attenuation of arterioles or bony spicules. Pigmented atrophic patches were seen along the vessels []. There were no signs of any past inflammation in either eye. Investigations were ordered to confirm these findings. All tests pointed to a diagnosis of RP in the right eye. There was generalized hypoautofluorescence of the retina []. Optical coherence tomography of the macula showed loss of the ellipsoid zone and external limiting membrane with retinal thinning []. Electroretinogram (ERG) of the right eye showed nonrecordable scotopic and photopic responses [] and a multifocal ERG showed nonrecordable foveal, parafoveal, and perifoveal ring responses []. In addition, there was gross peripheral constriction of the visual field []. However, the left eye showed hypoautofluorescence only along the vessels []. The OCT was normal with intact ellipsoid zone and external limiting membrane []. There were normal scotopic and photopic responses on ERG [] and normal foveal, parafoveal, and perifoveal ring responses on multifocal ERG []. The visual field was also normal in the left eye []. The findings were suggestive of PPRCA in the left eye.\nOUTPUT:" }, { "from": "agent", "value": "Retinitis pigmentosa, Pigmented paravenous retinochoroidal atrophy" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 32-year-old woman presented to us with the chief complaint of difficulty in night vision in her right eye. She had no visual complaints in the left eye. She had no history of any systemic disease, malignancy, chronic drug intake, or any inflammatory eye disease in the past. There was no family history of night blindness. The best corrected visual acuity was 20/50 in the right eye and 20/30 in the left eye. There was a relative afferent pupillary defect in the right eye. The intraocular pressure was 10 mmHg in the right eye and 20 mmHg in the left eye. Fundus examination showed waxy pallor of the disc, arteriolar attenuation, bony spicule pigmentation, diagnostic of RP, in the right eye []. The left eye showed a normal pink-colored disc and no attenuation of arterioles or bony spicules. Pigmented atrophic patches were seen along the vessels []. There were no signs of any past inflammation in either eye. Investigations were ordered to confirm these findings. All tests pointed to a diagnosis of RP in the right eye. There was generalized hypoautofluorescence of the retina []. Optical coherence tomography of the macula showed loss of the ellipsoid zone and external limiting membrane with retinal thinning []. Electroretinogram (ERG) of the right eye showed nonrecordable scotopic and photopic responses [] and a multifocal ERG showed nonrecordable foveal, parafoveal, and perifoveal ring responses []. In addition, there was gross peripheral constriction of the visual field []. However, the left eye showed hypoautofluorescence only along the vessels []. The OCT was normal with intact ellipsoid zone and external limiting membrane []. There were normal scotopic and photopic responses on ERG [] and normal foveal, parafoveal, and perifoveal ring responses on multifocal ERG []. The visual field was also normal in the left eye []. The findings were suggestive of PPRCA in the left eye. OUTPUT:
PMCPatients_common1637
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 59-year old female with a history of hypertension presented to the outpatient clinic in East Jeddah Hospital, Saudi Arabia, with sore throat, cough and arthralgia for 2 days. Nine days later, the patient presented to the emergency department with drowsiness, loss of appetite and decreased activities. Patient was admitted and was initiated on prophylaxis enoxaparin 30 mg subcutaneously q12hr.\\nPatient was conscious with normal vital signs on admission and CT brain was unremarkable (Figure ). Her chest radiograph showed bilateral infiltration with extensive peripheral consolidations (Figure ). Laboratory analysis showed markedly elevated D-dimer, fibrinogen and C reactive protein (CRP). Other laboratory values are presented in Table . On day 2 after admission, the patient deteriorated and became unconscious and developed acute renal shutdown. She was started on extensive medical therapy and serial CT angiography. Hematologist was consulted and the patient was shifted from prophylaxis enoxaparin into therapeutic enoxaparin 30 mg IV bolus dose followed 8hr later with maintenance dose enoxaparin 60 mg SC q12hr and monitored with the PTT and fibrinogen level. CT head was obtained on day 2 post admission demonstrating bilateral frontal lobe ischemia (Figure ). While in hospital, she became increasingly hypoxic and required intubation and mechanical ventilation. Serial CT brain showed diffuse ischemic insult involving left cerebral hemisphere, right frontal lobe and right cerebellum (Figure ). Her mental function continued to deteriorate with extensive involvement of anterior, middle and posterior cerebral artery complicated with brain edema (Figure ). The patient remained unresponsive and showed an abnormal breathing pattern on mechanical ventilation.\nOUTPUT:" }, { "from": "agent", "value": "Massive Arterial Cerebral Thrombosis, Severe COVID-19" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 59-year old female with a history of hypertension presented to the outpatient clinic in East Jeddah Hospital, Saudi Arabia, with sore throat, cough and arthralgia for 2 days. Nine days later, the patient presented to the emergency department with drowsiness, loss of appetite and decreased activities. Patient was admitted and was initiated on prophylaxis enoxaparin 30 mg subcutaneously q12hr.\nPatient was conscious with normal vital signs on admission and CT brain was unremarkable (Figure ). Her chest radiograph showed bilateral infiltration with extensive peripheral consolidations (Figure ). Laboratory analysis showed markedly elevated D-dimer, fibrinogen and C reactive protein (CRP). Other laboratory values are presented in Table . On day 2 after admission, the patient deteriorated and became unconscious and developed acute renal shutdown. She was started on extensive medical therapy and serial CT angiography. Hematologist was consulted and the patient was shifted from prophylaxis enoxaparin into therapeutic enoxaparin 30 mg IV bolus dose followed 8hr later with maintenance dose enoxaparin 60 mg SC q12hr and monitored with the PTT and fibrinogen level. CT head was obtained on day 2 post admission demonstrating bilateral frontal lobe ischemia (Figure ). While in hospital, she became increasingly hypoxic and required intubation and mechanical ventilation. Serial CT brain showed diffuse ischemic insult involving left cerebral hemisphere, right frontal lobe and right cerebellum (Figure ). Her mental function continued to deteriorate with extensive involvement of anterior, middle and posterior cerebral artery complicated with brain edema (Figure ). The patient remained unresponsive and showed an abnormal breathing pattern on mechanical ventilation. OUTPUT:
PMCPatients_common2355
[ { "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 66-year-old female developed a descending aortic dissection and was treated conservatively with medical therapy because there were no complications such as splanchnic ischemia, renal insufficiency, lower extremity ischemia, or focal neurologic deficits. One month later she was admitted via our emergency department (ED) because of recurrent severe back pain. Aortic computed tomography (CT) showed a type B aortic dissection with intramural hematoma and false lumen expansion (Figure ). She underwent TEVAR. Left carotid-subclavian artery bypass was performed by exploration from left low neck for left subclavian artery coverage (Figure A). After surgery, she resumed oral intake and increased left pleural drainage of a milky fluid was noted on postoperative day 2. Aortic CT on postoperative day 4 revealed no endoleak or thrombosis. Persistent pleural drainage of a milky appearing fluid of more than 1000 mL per day continued. The pleural fluid triglyceride concentration was 227 mg/dL. Conservative medical treatment of nothing per oral (NPO) and administration of total parenteral nutrition (TPN) failed to reduce the amount of drainage. Therefore, surgical ligation of the thoracic duct was planned at postoperative day 30. After induction of general anesthesia, the right lung was deflated, and 3 trocar sleeves were inserted at lateral ninth, anterior lateral seventh, and anterior lateral fifth intercostal spaces. The pulmonary ligament was transected, and the lung was retracted. The parietal pleura was incised along the distal part of azygos vein toward diaphragm. The thoracic duct should be found between aorta and azygos vein. Careful dissection exposed the thoracic duct as near as possible to diaphragm, which was then ligated (Figure B). Her recovery was uneventful, and the left Jackson-Pratt drain was removed on postoperative day 5.\nOUTPUT:" }, { "from": "agent", "value": "Chylothorax" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 66-year-old female developed a descending aortic dissection and was treated conservatively with medical therapy because there were no complications such as splanchnic ischemia, renal insufficiency, lower extremity ischemia, or focal neurologic deficits. One month later she was admitted via our emergency department (ED) because of recurrent severe back pain. Aortic computed tomography (CT) showed a type B aortic dissection with intramural hematoma and false lumen expansion (Figure ). She underwent TEVAR. Left carotid-subclavian artery bypass was performed by exploration from left low neck for left subclavian artery coverage (Figure A). After surgery, she resumed oral intake and increased left pleural drainage of a milky fluid was noted on postoperative day 2. Aortic CT on postoperative day 4 revealed no endoleak or thrombosis. Persistent pleural drainage of a milky appearing fluid of more than 1000 mL per day continued. The pleural fluid triglyceride concentration was 227 mg/dL. Conservative medical treatment of nothing per oral (NPO) and administration of total parenteral nutrition (TPN) failed to reduce the amount of drainage. Therefore, surgical ligation of the thoracic duct was planned at postoperative day 30. After induction of general anesthesia, the right lung was deflated, and 3 trocar sleeves were inserted at lateral ninth, anterior lateral seventh, and anterior lateral fifth intercostal spaces. The pulmonary ligament was transected, and the lung was retracted. The parietal pleura was incised along the distal part of azygos vein toward diaphragm. The thoracic duct should be found between aorta and azygos vein. Careful dissection exposed the thoracic duct as near as possible to diaphragm, which was then ligated (Figure B). Her recovery was uneventful, and the left Jackson-Pratt drain was removed on postoperative day 5. OUTPUT:
PMCPatients_common1077
[ { "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 68-year-old Caucasian man presented to our hospital with acute shortness of breath and left-sided chest pain. He had no significant medical history. His physical examination revealed that his chest auscultation was normal and that he was normotensive. The arterial blood gas measurement showed respiratory failure with partial pressure of oxygen (pO2) = 55 mmHg, partial pressure of carbon dioxide (pCO2) = 30 mmHg, pH = 7.42 and alveolar-arterial gradient [p (A-a) O₂] = 57 mmHg on room air. His electrocardiogram revealed sinus tachycardia. The chest radiograph showed left hilar opacity. His serum D-dimer concentration was markedly elevated, and all routine laboratory tests were within normal limits. Subcutaneous administration of low-molecular-weight heparin (LMWH) at a therapeutic dose was started, followed by oral acenocoumarol. Spiral computed angiography of the lower extremities showed no evidence of thrombi. His echocardiogram revealed normal valves, normal atrial and ventricular dimensions and normal systolic and diastolic function. The clinical and laboratory investigations were negative for infections or connective tissue diseases. The lung function tests were also within normal range. Therefore, we classified the PAA as idiopathic. Moreover, no underlying cause for the patient's PE was found. Given the large size of the aneurysm and its potential association with the thrombotic event, surgical intervention was suggested. The patient refused any invasive management, and he was discharged with normal respiratory function on acenocoumarol treatment.\nOUTPUT:" }, { "from": "agent", "value": "Low-pressure pulmonary artery aneurysm, Pulmonary embolism" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 68-year-old Caucasian man presented to our hospital with acute shortness of breath and left-sided chest pain. He had no significant medical history. His physical examination revealed that his chest auscultation was normal and that he was normotensive. The arterial blood gas measurement showed respiratory failure with partial pressure of oxygen (pO2) = 55 mmHg, partial pressure of carbon dioxide (pCO2) = 30 mmHg, pH = 7.42 and alveolar-arterial gradient [p (A-a) O₂] = 57 mmHg on room air. His electrocardiogram revealed sinus tachycardia. The chest radiograph showed left hilar opacity. His serum D-dimer concentration was markedly elevated, and all routine laboratory tests were within normal limits. Subcutaneous administration of low-molecular-weight heparin (LMWH) at a therapeutic dose was started, followed by oral acenocoumarol. Spiral computed angiography of the lower extremities showed no evidence of thrombi. His echocardiogram revealed normal valves, normal atrial and ventricular dimensions and normal systolic and diastolic function. The clinical and laboratory investigations were negative for infections or connective tissue diseases. The lung function tests were also within normal range. Therefore, we classified the PAA as idiopathic. Moreover, no underlying cause for the patient's PE was found. Given the large size of the aneurysm and its potential association with the thrombotic event, surgical intervention was suggested. The patient refused any invasive management, and he was discharged with normal respiratory function on acenocoumarol treatment. OUTPUT:
PMCPatients_common730
[ { "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 presented to the cardiology outpatient clinic for evaluation of recurrent syncope and palpitations. He had a one-month history of intermittent fevers with associated dry mouth and eyes. His physical examination revealed a bilateral parotid gland enlargement, cervical adenopathy, and facial nerve palsy, with eye redness. The patient's medical history was notable for longstanding hypertension. The initial electrocardiogram showed sinus rhythm with bifascicular block (Figure ). Brain natriuretic peptide (BNP) level was slightly elevated at 250 (pg/mL). A transthoracic echocardiogram revealed septal and apical hypokinesis with preserved systolic function. An event monitor was ordered, and revealed symptom correlation with sinus pauses. Serology for tuberculosis, human immunodeficiency virus, antinuclear, anti-Ro, and anti-La antibodies were all negative. Other causes for heart block, such as Lyme disease, were considered but excluded based on geographic distribution. A chest radiograph was performed and negative for hilar adenopathy, infiltrates, or fibrosis. He was initially started on a high dose course of oral corticosteroids with a gradual taper over one year. Due to the frequent sinus pauses with correlation to the patient's syncopal episodes, a dual-chamber pacemaker was implanted. On follow up appointment, a pacemaker device interrogation showed a minimal need for pacing. He reported improvement in his symptoms, and physical exam had complete resolution of uveitis, parotitis, and facial nerve palsy.\nOUTPUT:" }, { "from": "agent", "value": "Heerfordt-Waldenström syndrome, Cardiac sarcoidosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 49-year-old African American male presented to the cardiology outpatient clinic for evaluation of recurrent syncope and palpitations. He had a one-month history of intermittent fevers with associated dry mouth and eyes. His physical examination revealed a bilateral parotid gland enlargement, cervical adenopathy, and facial nerve palsy, with eye redness. The patient's medical history was notable for longstanding hypertension. The initial electrocardiogram showed sinus rhythm with bifascicular block (Figure ). Brain natriuretic peptide (BNP) level was slightly elevated at 250 (pg/mL). A transthoracic echocardiogram revealed septal and apical hypokinesis with preserved systolic function. An event monitor was ordered, and revealed symptom correlation with sinus pauses. Serology for tuberculosis, human immunodeficiency virus, antinuclear, anti-Ro, and anti-La antibodies were all negative. Other causes for heart block, such as Lyme disease, were considered but excluded based on geographic distribution. A chest radiograph was performed and negative for hilar adenopathy, infiltrates, or fibrosis. He was initially started on a high dose course of oral corticosteroids with a gradual taper over one year. Due to the frequent sinus pauses with correlation to the patient's syncopal episodes, a dual-chamber pacemaker was implanted. On follow up appointment, a pacemaker device interrogation showed a minimal need for pacing. He reported improvement in his symptoms, and physical exam had complete resolution of uveitis, parotitis, and facial nerve palsy. OUTPUT:
PMCPatients_common1341
[ { "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 52-year-old woman presenting with a two-week history of epigastric pain and vomiting was referred to our clinic. She had a medical history of cholecystectomy and T-tube drainage operation for choledocholithiasis a year previously. Abdominal pain was of recent onset and mainly in the upper quadrants of her abdomen. Laboratory parameters revealed high levels of leukocyte (13,1×103μL) and cholestatic enzymes; aspartate aminotransferase (AST): 51 U/L, alanine aminotransferase (ALT): 37 U/L, alkaline phospatase (ALP): 143 U/L, gamma glutamyl transferase (GGT): 120 U/L and amylase: 220 U/L. Plain abdominal radiography and ultrasonography (USG) were unremarkable. The preliminary diagnosis was acute pancreatitis until abdominal computed tomography (CT) revealed a 10×8 cm mass located in the stomach which was compatible with a gastric carcinoma. Gastroscopy was performed for diagnosis and treatment. A written informed consent including surgical risks was obtained from the patient. The procedure was performed under sedation in the operation room with regards to possible urgent surgical intervention. On the gastroscopy, a large surgical gas compress which totally migrated and filled two thirds of the stomach was observed (Figure ). The distal side of the compress was located in the bulbus. The surgical compress was loosened up with saline. Subsequently, it was grasped with saw-tooth forceps and pulled into the stomach. The compress was grasped again with a snare followed by releasing from the bulbus, then pulled out through the esophagus to the posterior region of the tongue. The material was then removed with gentle round motions from the mouth (Figure ). No bleeding, fistula or injury was observed. All laboratory parameters were normal after one day following the procedure. The recovery of the patient was uneventful; and she was discharged 4 days following the procedure.\nOUTPUT:" }, { "from": "agent", "value": "Gossypiboma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 52-year-old woman presenting with a two-week history of epigastric pain and vomiting was referred to our clinic. She had a medical history of cholecystectomy and T-tube drainage operation for choledocholithiasis a year previously. Abdominal pain was of recent onset and mainly in the upper quadrants of her abdomen. Laboratory parameters revealed high levels of leukocyte (13,1×103μL) and cholestatic enzymes; aspartate aminotransferase (AST): 51 U/L, alanine aminotransferase (ALT): 37 U/L, alkaline phospatase (ALP): 143 U/L, gamma glutamyl transferase (GGT): 120 U/L and amylase: 220 U/L. Plain abdominal radiography and ultrasonography (USG) were unremarkable. The preliminary diagnosis was acute pancreatitis until abdominal computed tomography (CT) revealed a 10×8 cm mass located in the stomach which was compatible with a gastric carcinoma. Gastroscopy was performed for diagnosis and treatment. A written informed consent including surgical risks was obtained from the patient. The procedure was performed under sedation in the operation room with regards to possible urgent surgical intervention. On the gastroscopy, a large surgical gas compress which totally migrated and filled two thirds of the stomach was observed (Figure ). The distal side of the compress was located in the bulbus. The surgical compress was loosened up with saline. Subsequently, it was grasped with saw-tooth forceps and pulled into the stomach. The compress was grasped again with a snare followed by releasing from the bulbus, then pulled out through the esophagus to the posterior region of the tongue. The material was then removed with gentle round motions from the mouth (Figure ). No bleeding, fistula or injury was observed. All laboratory parameters were normal after one day following the procedure. The recovery of the patient was uneventful; and she was discharged 4 days following the procedure. OUTPUT:
PMCPatients_common1010
[ { "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 G4P1Ab2 refugee woman was referred to our perinatology clinic due to a suspected a fetal heart defect. There was no family history of congenital heart disease nor did she have any risk factors leading to congenital heart disease. Pulmonary valve, main PA, and the branches of the pulmonary valve were in the normal range. The diameters of the pulmonary annulus, right and LPA were 2.49 mm, 1.55 mm, and 1.87 mm, respectively (). The antegrade flow was seen in the main and branch of the PA but DA could not be demonstrated using color Doppler. After a prenatal genetic consultation, amniocentesis for karyotyping and analysis of 22q11 deletion was declined by the parents. The female fetus was delivered by CS due to previous CS at 38 weeks gestation. The neonate did not need any cardiac or respiratory support and weighed 3175 g. There were no findings suggesting any genetic anomaly in the phenotype of the newborn baby. The diameters of the pulmonary annulus, right and LPA were 5.8 mm, 4.5 mm, and 4.8 mm, respectively. The peak pressure gradient at the level of the pulmonary valve was approximately 23 mm Hg at discharge from the hospital. She has remained uneventful for two months at the time of the writing. Surgical correction is delayed until she reaches the appropriate age.\nOUTPUT:" }, { "from": "agent", "value": "Right aortic arch, malalignment ventricular septal defect, and overriding aorta" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 35-year-old G4P1Ab2 refugee woman was referred to our perinatology clinic due to a suspected a fetal heart defect. There was no family history of congenital heart disease nor did she have any risk factors leading to congenital heart disease. Pulmonary valve, main PA, and the branches of the pulmonary valve were in the normal range. The diameters of the pulmonary annulus, right and LPA were 2.49 mm, 1.55 mm, and 1.87 mm, respectively (). The antegrade flow was seen in the main and branch of the PA but DA could not be demonstrated using color Doppler. After a prenatal genetic consultation, amniocentesis for karyotyping and analysis of 22q11 deletion was declined by the parents. The female fetus was delivered by CS due to previous CS at 38 weeks gestation. The neonate did not need any cardiac or respiratory support and weighed 3175 g. There were no findings suggesting any genetic anomaly in the phenotype of the newborn baby. The diameters of the pulmonary annulus, right and LPA were 5.8 mm, 4.5 mm, and 4.8 mm, respectively. The peak pressure gradient at the level of the pulmonary valve was approximately 23 mm Hg at discharge from the hospital. She has remained uneventful for two months at the time of the writing. Surgical correction is delayed until she reaches the appropriate age. OUTPUT:
PMCPatients_common2055
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An 18-year old unmarried illiterate girl presented with dysuria, increased frequency of micturition and occasional mild hematuria. The patient had history of insertion of plastic pen through vagina 6 months earlier for sexual gratification. There was no history of continuous leakage of urine per vagina. She informed history of normal menstruation. There was no associated psychiatric illness. Laboratory investigations such as electrolyte profile and blood count were normal but routine urine analysis showed pyuria and microscopic hematuria. General physical examination revealed no abnormality. On per vaginal and speculum examination, a pointed object was felt at anterior vaginal wall with no continuous leakage of urine from vagina. The digital rectal examination was normal. Plain X-ray pelvis was normal. Contrast enhanced computed tomography showed a 10.2 x 1.2cm hypodense linear object piercing the anterior vaginal wall and left posterior bladder wall with majority of its part lying inside the bladder. The tip of the foreign body pierced right to anterior bladder wall and reached the abdominal wall () with normal upper tracts, uterus and ovaries. Cystoscopy showed encrusted plastic pen inside the bladder extending from right anterior bladder wall up to the left posterior bladder wall () with a small portion of pen (approximately mm) protruding through anterior vaginal wall visualized on vaginoscopy. Patient refused psychiatric evaluation. Foreign body was broken into two parts by transurethral cystolithopaxy using stone punch under regional anesthesia and was removed under cystoscopic guidance (). Foley catheter (16Fr) was inserted per urethra and the patient was discharged on postoperative day 3 with an advice to follow-up after 3 weeks. She did not complain of continuous leakage of urine per vagina in the post-operative period. Foley catheter was removed at 3 weeks and voiding cystourethrogram was performed which revealed intact bladder and complete emptying of bladder in post void film with no dye in vagina (). The patient was fully continent with no urine leakage per vagina. Patient was doing well at 6 months follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Vesicovaginal fistula" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 18-year old unmarried illiterate girl presented with dysuria, increased frequency of micturition and occasional mild hematuria. The patient had history of insertion of plastic pen through vagina 6 months earlier for sexual gratification. There was no history of continuous leakage of urine per vagina. She informed history of normal menstruation. There was no associated psychiatric illness. Laboratory investigations such as electrolyte profile and blood count were normal but routine urine analysis showed pyuria and microscopic hematuria. General physical examination revealed no abnormality. On per vaginal and speculum examination, a pointed object was felt at anterior vaginal wall with no continuous leakage of urine from vagina. The digital rectal examination was normal. Plain X-ray pelvis was normal. Contrast enhanced computed tomography showed a 10.2 x 1.2cm hypodense linear object piercing the anterior vaginal wall and left posterior bladder wall with majority of its part lying inside the bladder. The tip of the foreign body pierced right to anterior bladder wall and reached the abdominal wall () with normal upper tracts, uterus and ovaries. Cystoscopy showed encrusted plastic pen inside the bladder extending from right anterior bladder wall up to the left posterior bladder wall () with a small portion of pen (approximately mm) protruding through anterior vaginal wall visualized on vaginoscopy. Patient refused psychiatric evaluation. Foreign body was broken into two parts by transurethral cystolithopaxy using stone punch under regional anesthesia and was removed under cystoscopic guidance (). Foley catheter (16Fr) was inserted per urethra and the patient was discharged on postoperative day 3 with an advice to follow-up after 3 weeks. She did not complain of continuous leakage of urine per vagina in the post-operative period. Foley catheter was removed at 3 weeks and voiding cystourethrogram was performed which revealed intact bladder and complete emptying of bladder in post void film with no dye in vagina (). The patient was fully continent with no urine leakage per vagina. Patient was doing well at 6 months follow-up. OUTPUT:
PMCPatients_common5366
[ { "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 78-year-old man with ischemic heart disease underwent cardiac catheterization and percutaneous transluminal coronary angioplasty via the femoral artery. His premorbid condition included old age, liver cirrhosis, renal cell carcinoma, diabetes mellitus, and significant ischemic cardiomyopathy. Six days following discharge from the hospital, the patient experienced severe sharp pain in the right groin with no skin discoloration of the right lower extremity. On physical examination, a pulsatile mass was noted in the right groin. Lower-extremity angiography revealed a PA of the superficial femoral artery (). Hematoma removal and bleeder ligation were performed by a vascular surgeon. The affected part of the superficial femoral artery was freed, the aneurysm was opened along its length, and the thrombus was evacuated. A heparin infusion was begun postoperatively.\\nFive days later, the patient developed progressive abdominal pain, fever, vomiting, skin discoloration, and wound induration (). A laboratory study revealed that the white blood cell count was 2000/µL, erythrocyte sedimentation rate (ESR) level was 11 mm/hr, and reactive protein-C (CRP-C) level was 17.91 mg/dL; all these were mildly elevated values. Further, the creatine kinase-MB (CK-MB) level was in the normal range, but the myoglobin level was elevated to 174 ng/mL (normal range, 22-75 ng/mL). The sodium level was found to be 132 mmol/L (normal range, 135-153 mmol/L), a slightly lowered level, and blood urea nitrogen (BUN) was 25.6 mg/dL (normal range, 8-20 mg/dL). Computed tomographic scans of the abdomen and perineal region revealed fluid accumulations involving multiple subcutaneous spaces and the peritoneum. The patient also had ileus of multiple bowel loops (). The necrotic wound was serially excised, and treatment was performed with the VAC device. VAC therapy was conducted for a period of 12 days (). The patient had an uneventful recovery with a normal range of laboratory results and finally underwent wound closure ().\nOUTPUT:" }, { "from": "agent", "value": "Pseudoaneurysm, Necrotizing Fasciitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 78-year-old man with ischemic heart disease underwent cardiac catheterization and percutaneous transluminal coronary angioplasty via the femoral artery. His premorbid condition included old age, liver cirrhosis, renal cell carcinoma, diabetes mellitus, and significant ischemic cardiomyopathy. Six days following discharge from the hospital, the patient experienced severe sharp pain in the right groin with no skin discoloration of the right lower extremity. On physical examination, a pulsatile mass was noted in the right groin. Lower-extremity angiography revealed a PA of the superficial femoral artery (). Hematoma removal and bleeder ligation were performed by a vascular surgeon. The affected part of the superficial femoral artery was freed, the aneurysm was opened along its length, and the thrombus was evacuated. A heparin infusion was begun postoperatively.\nFive days later, the patient developed progressive abdominal pain, fever, vomiting, skin discoloration, and wound induration (). A laboratory study revealed that the white blood cell count was 2000/µL, erythrocyte sedimentation rate (ESR) level was 11 mm/hr, and reactive protein-C (CRP-C) level was 17.91 mg/dL; all these were mildly elevated values. Further, the creatine kinase-MB (CK-MB) level was in the normal range, but the myoglobin level was elevated to 174 ng/mL (normal range, 22-75 ng/mL). The sodium level was found to be 132 mmol/L (normal range, 135-153 mmol/L), a slightly lowered level, and blood urea nitrogen (BUN) was 25.6 mg/dL (normal range, 8-20 mg/dL). Computed tomographic scans of the abdomen and perineal region revealed fluid accumulations involving multiple subcutaneous spaces and the peritoneum. The patient also had ileus of multiple bowel loops (). The necrotic wound was serially excised, and treatment was performed with the VAC device. VAC therapy was conducted for a period of 12 days (). The patient had an uneventful recovery with a normal range of laboratory results and finally underwent wound closure (). OUTPUT:
PMCPatients_common567
[ { "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 73-year-old female patient presented with a history of back pain following a fall. The radiofrequency ablation procedure was performed under general anaesthesia using fluoroscopic image guidance. Bipedicular 10-gauge bone access needles were advanced at the L4 vertebral level, and a bone drill was used to achieve satisfactory ablation probe position within the vertebral body (Figure ).\\nBipolar 17-gauge, 20-mm ablation probes were advanced, with each probe creating an ablation zone of approximately 29 mm x 21 mm. Care was taken to position the ablation probes such that the ablation zone did not extend beyond the posterior margin of the tumour, and a 20-gauge thermocouple was advanced via a transforaminal approach into the anterior epidural space to allow for continuous temperature monitoring to minimise the risk of neural injury during the ablation procedure. Following this, methyl methacrylate was injected into the L4 ablation cavity to augment the vertebral body and maintain stability. The procedure was well tolerated, and there were no immediate complications. No post-procedure neural deficit was elicited, and the patient was discharged home the same day. The patient reported significant improvement in pain at follow-up with his oncology team with reduced opiate medication requirement. Subsequent MRI at two months post-procedure demonstrated significant tumour regression at the L4 level with resolution of the epidural disease and improved canal dimension (Figure ).\\nThe patient had no recurrence of their low back pain. Unfortunately, there was disease progression elsewhere and the patient died the following month following a pulmonary emboli.\nOUTPUT:" }, { "from": "agent", "value": "Metastatic Melanoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 73-year-old female patient presented with a history of back pain following a fall. The radiofrequency ablation procedure was performed under general anaesthesia using fluoroscopic image guidance. Bipedicular 10-gauge bone access needles were advanced at the L4 vertebral level, and a bone drill was used to achieve satisfactory ablation probe position within the vertebral body (Figure ).\nBipolar 17-gauge, 20-mm ablation probes were advanced, with each probe creating an ablation zone of approximately 29 mm x 21 mm. Care was taken to position the ablation probes such that the ablation zone did not extend beyond the posterior margin of the tumour, and a 20-gauge thermocouple was advanced via a transforaminal approach into the anterior epidural space to allow for continuous temperature monitoring to minimise the risk of neural injury during the ablation procedure. Following this, methyl methacrylate was injected into the L4 ablation cavity to augment the vertebral body and maintain stability. The procedure was well tolerated, and there were no immediate complications. No post-procedure neural deficit was elicited, and the patient was discharged home the same day. The patient reported significant improvement in pain at follow-up with his oncology team with reduced opiate medication requirement. Subsequent MRI at two months post-procedure demonstrated significant tumour regression at the L4 level with resolution of the epidural disease and improved canal dimension (Figure ).\nThe patient had no recurrence of their low back pain. Unfortunately, there was disease progression elsewhere and the patient died the following month following a pulmonary emboli. OUTPUT:
PMCPatients_common1058
[ { "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 2-year-old female child with G-6-PD deficiency, weighing 13 kg was admitted to our neurosurgical unit with the complaints of a swelling over the lower back and weakness of both the lower limbs. There was no history haemolysis, jaundice or blood transfusion. All the routine investigations were within normal limits (haemoglobin 13.6 g%, unconjugated bilirubin 0.7 mg%, and reticulocyte count 1%). The child was premedicated with oral atropine and midazolam. In the operating room, inhalational induction with sevoflurane in oxygen was carried out and an intravenous (IV) access was secured, simultaneously. Fentanyl 2 μg/kg was administered and tracheal intubation was facilitated with rocuronium 1mg/kg. The child was placed prone for surgery. Intraoperative monitoring included electrocardiogram (ECG), oxygen saturation (SpO2), non invasive blood pressure (NIBP) and end tidal carbon dioxide (EtCO2), temperature. Anaesthesia was maintained with sevoflurane, O2/N2O mixture and intermittent boluses of rocuronium and fentanyl. Cloxacillin 200 mg and amikacin100 mg were given IV as prophylactic antibiotics. The blood loss was 150 ml, urine output was 90 ml, and 650 ml of Ringers lactate was infused. The uneventful surgery lasted for 4 h. At the end of procedure, the child was placed supine, anaesthetic agents discontinued. Rectal paracetamol 500 mg suppository was given for postoperative analgesia. Residual neuromuscular blockade was reversed with neostigmine and glycopyrrolate and trachea was extubated. On third postoperative day (POD), the child was discharged after ensuring the complete blood count (CBC) to be normal.\nOUTPUT:" }, { "from": "agent", "value": "Glucose-6-phosphate dehydrogenase deficiency, Lumbosacral lipoma, Tethered cord syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 2-year-old female child with G-6-PD deficiency, weighing 13 kg was admitted to our neurosurgical unit with the complaints of a swelling over the lower back and weakness of both the lower limbs. There was no history haemolysis, jaundice or blood transfusion. All the routine investigations were within normal limits (haemoglobin 13.6 g%, unconjugated bilirubin 0.7 mg%, and reticulocyte count 1%). The child was premedicated with oral atropine and midazolam. In the operating room, inhalational induction with sevoflurane in oxygen was carried out and an intravenous (IV) access was secured, simultaneously. Fentanyl 2 μg/kg was administered and tracheal intubation was facilitated with rocuronium 1mg/kg. The child was placed prone for surgery. Intraoperative monitoring included electrocardiogram (ECG), oxygen saturation (SpO2), non invasive blood pressure (NIBP) and end tidal carbon dioxide (EtCO2), temperature. Anaesthesia was maintained with sevoflurane, O2/N2O mixture and intermittent boluses of rocuronium and fentanyl. Cloxacillin 200 mg and amikacin100 mg were given IV as prophylactic antibiotics. The blood loss was 150 ml, urine output was 90 ml, and 650 ml of Ringers lactate was infused. The uneventful surgery lasted for 4 h. At the end of procedure, the child was placed supine, anaesthetic agents discontinued. Rectal paracetamol 500 mg suppository was given for postoperative analgesia. Residual neuromuscular blockade was reversed with neostigmine and glycopyrrolate and trachea was extubated. On third postoperative day (POD), the child was discharged after ensuring the complete blood count (CBC) to be normal. OUTPUT:
PMCPatients_common437
[ { "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 46-year-old female, with no known history of any medical illness, was referred to our surgical outpatient department with complains of mild to moderate intermittent abdominal pain in the right hypochondrium for 5 months. The patient denied any history of anorexia, weight loss, and jaundice. Ultrasonography (US) of abdomen was done in the referral hospital at that time and showed a large oval-shaped hypoechoic focal lesion superior to the right kidney. On physical examination, the patient was well-nourished, in moderate pain, and had no pallor or jaundice. Abdominal examination revealed mild tenderness in the right hypochondrium area with no palpable masses. Laboratory examination revealed the following: haemoglobin: 9.6 g/dl, leucocyte count: 6.06 × 109/L, haematocrit: 30.3%, and platelet count: 359 × 109/L. The liver function test, renal function test, and the coagulation profile were all within normal ranges. Hormonal profiles were all within normal ranges, including the investigations of serum cortisol, aldosterone, metanephrine, normetanephrine, 5 hydroxyindoleacetic acid, adrenocorticotropic hormone, and renin. No other mases were found. The postoperative recovery was uneventful, and the patient was discharged home at post-operative day 2 with regular follow-up in our outpatient department clinic.\nOUTPUT:" }, { "from": "agent", "value": "Adrenal Myelolipoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 46-year-old female, with no known history of any medical illness, was referred to our surgical outpatient department with complains of mild to moderate intermittent abdominal pain in the right hypochondrium for 5 months. The patient denied any history of anorexia, weight loss, and jaundice. Ultrasonography (US) of abdomen was done in the referral hospital at that time and showed a large oval-shaped hypoechoic focal lesion superior to the right kidney. On physical examination, the patient was well-nourished, in moderate pain, and had no pallor or jaundice. Abdominal examination revealed mild tenderness in the right hypochondrium area with no palpable masses. Laboratory examination revealed the following: haemoglobin: 9.6 g/dl, leucocyte count: 6.06 × 109/L, haematocrit: 30.3%, and platelet count: 359 × 109/L. The liver function test, renal function test, and the coagulation profile were all within normal ranges. Hormonal profiles were all within normal ranges, including the investigations of serum cortisol, aldosterone, metanephrine, normetanephrine, 5 hydroxyindoleacetic acid, adrenocorticotropic hormone, and renin. No other mases were found. The postoperative recovery was uneventful, and the patient was discharged home at post-operative day 2 with regular follow-up in our outpatient department clinic. OUTPUT:
PMCPatients_common2042
[ { "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 been seen multiple times in the proceeding 3 weeks by both his GP and the emergency department and had initially been given a course of oral amoxicillin. Swabs from his otorrhoea had grown Proteus mirabilis and meticillin-resistant Staphylococcus aureus (MRSA), and he had also therefore been given a course of oral co-trimoxazole and regular gentamicin/dexamethasone ear drops. There was no history to suggest that he was immunocompromised.\\nOn examination, observations were stable and he was apyrexial with a temperature of 36.7 °C, although his parents reported fevers at home. He was alert and rousable but appeared in significant pain and was 5 % dehydrated. His right ear contained thick pale green exudate and, when microsuctioned, revealed an inflamed auditory canal. The tympanic membrane was intact but with fluid behind it. There was no cervical lymphadenopathy, and examination of the chest and abdomen was normal. Initial neurological examination revealed no focal neurological signs and no evidence of meningism. Intravenous (i.v.) fluids were commenced and oral co-trimoxazole continued. Overnight, nursing staff noted an episode of decerebrate posturing and decreased responsiveness. Upon assessment by the on-call doctor, his Glascow coma score was 13 (E3, M6 and V4) and the posturing had ceased. Pupils were equal and reactive but with a bilateral fixed downward left lateral gaze.\nOUTPUT:" }, { "from": "agent", "value": "Otitis media, Intracranial infection with Actinomyces turicensis, Dehydration, Right cerebellar abscess, Obstructive hydrocephalus" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: He had been seen multiple times in the proceeding 3 weeks by both his GP and the emergency department and had initially been given a course of oral amoxicillin. Swabs from his otorrhoea had grown Proteus mirabilis and meticillin-resistant Staphylococcus aureus (MRSA), and he had also therefore been given a course of oral co-trimoxazole and regular gentamicin/dexamethasone ear drops. There was no history to suggest that he was immunocompromised.\nOn examination, observations were stable and he was apyrexial with a temperature of 36.7 °C, although his parents reported fevers at home. He was alert and rousable but appeared in significant pain and was 5 % dehydrated. His right ear contained thick pale green exudate and, when microsuctioned, revealed an inflamed auditory canal. The tympanic membrane was intact but with fluid behind it. There was no cervical lymphadenopathy, and examination of the chest and abdomen was normal. Initial neurological examination revealed no focal neurological signs and no evidence of meningism. Intravenous (i.v.) fluids were commenced and oral co-trimoxazole continued. Overnight, nursing staff noted an episode of decerebrate posturing and decreased responsiveness. Upon assessment by the on-call doctor, his Glascow coma score was 13 (E3, M6 and V4) and the posturing had ceased. Pupils were equal and reactive but with a bilateral fixed downward left lateral gaze. OUTPUT:
PMCPatients_common580
[ { "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 intracardiac ultrasound proprietary catheter (CARTOSOUND; Biosense Webster) was advanced to the right atrium through femoral vein access. Meanwhile, the CARTO 3 mapping system (Biosense Webster) was applied to reconstruct the ventricle and interventricular septum models. Then, the 3830 lead (Select-Secure™ lead, Medtronic) was connected to the CARTO 3 mapping system and advanced into right ventricle (RV) through sheath 315HIS (Medtronic) under ICE real-time imaging guidance. During the operation, the sector of ICE was adjusted to clearly display both sides of the ventricular septum, and the position of the lead was observed directly (Figure ). The sheath was adjusted to the upper region of the IVS under ICE real-time imaging guidance. At this site, the paced QRS morphology usually demonstrates a “w” pattern in lead V1. The sheath was rotated counterclockwise to maintain the orientation of the lead tip perpendicular to the septal surface. During the time, EMG morphology changes of V1 lead, LBB potential, lead depth, and pacing impedance were closely monitored. Confirmation of the LBB capture was done according to Vijayaraman P and Huang., Including: Paced morphology of right bundle branch block pattern; Identification of the LBB potential; Stim-LVAT (stimulus to left ventricular activation time, defined as the interval from the pacing stimulus to the QRS upstroke in V5/V6) that shortens abruptly with increasing output or remains shortest and constant both at low and high outputs. Then, the pacing and EMG parameters of LBBP were measured. In this case, Stim-LVAT was 68 ms, and paced QRS was 115 ms (Figure ). The sensed R-wave amplitude was 7.1 mV, capture threshold was 0.7 V/0.4 ms, and lead impedance was 726 Ω. Ultrasonic images showed the lead tip was perpendicular to the interventricular septum, with depth of 8 mm (Figure ). LBBP was successfully achieved, with a radioactive exposure time of 1.5 minutes, and total operation time 76 minutes.\nOUTPUT:" }, { "from": "agent", "value": "Bradycardia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An intracardiac ultrasound proprietary catheter (CARTOSOUND; Biosense Webster) was advanced to the right atrium through femoral vein access. Meanwhile, the CARTO 3 mapping system (Biosense Webster) was applied to reconstruct the ventricle and interventricular septum models. Then, the 3830 lead (Select-Secure™ lead, Medtronic) was connected to the CARTO 3 mapping system and advanced into right ventricle (RV) through sheath 315HIS (Medtronic) under ICE real-time imaging guidance. During the operation, the sector of ICE was adjusted to clearly display both sides of the ventricular septum, and the position of the lead was observed directly (Figure ). The sheath was adjusted to the upper region of the IVS under ICE real-time imaging guidance. At this site, the paced QRS morphology usually demonstrates a “w” pattern in lead V1. The sheath was rotated counterclockwise to maintain the orientation of the lead tip perpendicular to the septal surface. During the time, EMG morphology changes of V1 lead, LBB potential, lead depth, and pacing impedance were closely monitored. Confirmation of the LBB capture was done according to Vijayaraman P and Huang., Including: Paced morphology of right bundle branch block pattern; Identification of the LBB potential; Stim-LVAT (stimulus to left ventricular activation time, defined as the interval from the pacing stimulus to the QRS upstroke in V5/V6) that shortens abruptly with increasing output or remains shortest and constant both at low and high outputs. Then, the pacing and EMG parameters of LBBP were measured. In this case, Stim-LVAT was 68 ms, and paced QRS was 115 ms (Figure ). The sensed R-wave amplitude was 7.1 mV, capture threshold was 0.7 V/0.4 ms, and lead impedance was 726 Ω. Ultrasonic images showed the lead tip was perpendicular to the interventricular septum, with depth of 8 mm (Figure ). LBBP was successfully achieved, with a radioactive exposure time of 1.5 minutes, and total operation time 76 minutes. OUTPUT:
PMCPatients_common1401
[ { "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: We observe a 67-year-old man for severe LUTS (IPSS questionnaire score of 23). The patient's medical history reveals right orchidopexy (in childhood) for cryptorchidism with simultaneous contralateral simple orchiectomy performed for unknown reasons, a history of recurrent renal colic (from at least 50 years) always treated with automedication, and infertility. Physical uroandrologic examination shows the presence of glandular hypospadias with slightly painful anterior urethra, normal right didymus and epididymis, and, in accordance with medical history, uninhabited left hemiscrotum. The digital rectal exam shows a prostate volume slightly increased with characters related to adenomatous growth. The blood count, laboratory indices of renal functionality, the hydroelectrolyte balance, and urine examination appear normal. The uroflowmetry tracing appears classically restrictive and the postvoid residual not significant. Renal ultrasonography performed during the office visit shows the presence of bilateral multiple hyperechoic elements with posterior acoustic shadow amenable to urolithiasis and no hydroureteronephrosis (). A pathognomonic appearance on “bouquet of flowers” is evident in a kidney-bladder radiograph that the patient brings into view (). Subsequently, the patient has been subjected to spiral uro-CT to obtain a morphofunctional evaluation of kidney and, also, to get a visualization of the upper urinary tract that has, however, showed no abnormality. The study of the lower urinary tract visualized by retrograde and voiding urethrocystography shows a short but tight stricture of the distal anterior urethra and a proximal ectasia to the stenosis (). The scrotal ultrasound shows normal echogenicity of didymus. The series of blood tests and urine laboratory tests performed in order to assess the phosphocalcium homeostasis are normal. We subjected the patient to internal urethrotomy according to the technique of Sachse with complete resolution of symptomatological condition.\nOUTPUT:" }, { "from": "agent", "value": "Medullary Sponge Kidney, Testicular Dysgenesis Syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: We observe a 67-year-old man for severe LUTS (IPSS questionnaire score of 23). The patient's medical history reveals right orchidopexy (in childhood) for cryptorchidism with simultaneous contralateral simple orchiectomy performed for unknown reasons, a history of recurrent renal colic (from at least 50 years) always treated with automedication, and infertility. Physical uroandrologic examination shows the presence of glandular hypospadias with slightly painful anterior urethra, normal right didymus and epididymis, and, in accordance with medical history, uninhabited left hemiscrotum. The digital rectal exam shows a prostate volume slightly increased with characters related to adenomatous growth. The blood count, laboratory indices of renal functionality, the hydroelectrolyte balance, and urine examination appear normal. The uroflowmetry tracing appears classically restrictive and the postvoid residual not significant. Renal ultrasonography performed during the office visit shows the presence of bilateral multiple hyperechoic elements with posterior acoustic shadow amenable to urolithiasis and no hydroureteronephrosis (). A pathognomonic appearance on “bouquet of flowers” is evident in a kidney-bladder radiograph that the patient brings into view (). Subsequently, the patient has been subjected to spiral uro-CT to obtain a morphofunctional evaluation of kidney and, also, to get a visualization of the upper urinary tract that has, however, showed no abnormality. The study of the lower urinary tract visualized by retrograde and voiding urethrocystography shows a short but tight stricture of the distal anterior urethra and a proximal ectasia to the stenosis (). The scrotal ultrasound shows normal echogenicity of didymus. The series of blood tests and urine laboratory tests performed in order to assess the phosphocalcium homeostasis are normal. We subjected the patient to internal urethrotomy according to the technique of Sachse with complete resolution of symptomatological condition. OUTPUT:
PMCPatients_common1987
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 27-year-old African American female presented to the hospital after a sudden onset of severe retrosternal chest pain. Past medical history was insignificant for hypertension or diabetes mellitus. Patient has a history of smoking cigarettes, beginning at age 9, and frequent marijuana use. The patient was treated with morphine and Percocet for pain. Lab data and urine toxicology screen were negative for troponins and significant for marijuana, respectively. Urine drug screen was negative for cocaine and amphetamines. Drug screen was positive for opiates, but this result is most likely an artifact of morphine and Percocet treatment for chest pain. Initial laboratory findings included hemoglobin 12 g/dL, hematocrit 12.6%, platelets 223 × 103/μL, glucose 156 mg/dL, BUN 9 mg/dL, creatinine 0.8 mg/dL, sodium 135 mEq/L, potassium 4 mEq/L, chloride 101 mEq/L, and bicarbonate 18 mEq/L. In the emergency room, vital signs demonstrated a pulse rate of 98 beats/min, respiratory rate 22 breaths/min, blood pressure 132/89 mm Hg, temperature 98.1 °F, and oxygen saturation 100% on room air. The remainder of the physical examination was unremarkable. Initial electrocardiogram (ECG) demonstrated normal sinus rhythm, and the patient was admitted to telemetry for observation. The subsequent morning, the patient actively experienced chest pain and ECG changes. ECG demonstrated ST segment elevations in leads II and III, and T-wave inversions in V1-V3. Stat troponin level was found to be elevated at 11.07 ng/mL (< 0.30 ng/mL). The patient immediately underwent cardiac catheterization which demonstrated a 99% blockage of the left anterior descending artery and revascularization was performed (, ). Two-dimensional echocardiogram demonstrated a left ventricular ejection fraction of 40% with anterior wall akinesis. Transesophageal echocardiogram ruled out an apical mural thrombus, but confirmed the ejection fraction and wall akinesis from the previous echocardiogram. The patient was also found to have hyperlipidemia after the conduction of a lipid panel. Hypercoaguable state and vasculitis workup was negative.\nOUTPUT:" }, { "from": "agent", "value": "STEMI" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 27-year-old African American female presented to the hospital after a sudden onset of severe retrosternal chest pain. Past medical history was insignificant for hypertension or diabetes mellitus. Patient has a history of smoking cigarettes, beginning at age 9, and frequent marijuana use. The patient was treated with morphine and Percocet for pain. Lab data and urine toxicology screen were negative for troponins and significant for marijuana, respectively. Urine drug screen was negative for cocaine and amphetamines. Drug screen was positive for opiates, but this result is most likely an artifact of morphine and Percocet treatment for chest pain. Initial laboratory findings included hemoglobin 12 g/dL, hematocrit 12.6%, platelets 223 × 103/μL, glucose 156 mg/dL, BUN 9 mg/dL, creatinine 0.8 mg/dL, sodium 135 mEq/L, potassium 4 mEq/L, chloride 101 mEq/L, and bicarbonate 18 mEq/L. In the emergency room, vital signs demonstrated a pulse rate of 98 beats/min, respiratory rate 22 breaths/min, blood pressure 132/89 mm Hg, temperature 98.1 °F, and oxygen saturation 100% on room air. The remainder of the physical examination was unremarkable. Initial electrocardiogram (ECG) demonstrated normal sinus rhythm, and the patient was admitted to telemetry for observation. The subsequent morning, the patient actively experienced chest pain and ECG changes. ECG demonstrated ST segment elevations in leads II and III, and T-wave inversions in V1-V3. Stat troponin level was found to be elevated at 11.07 ng/mL (< 0.30 ng/mL). The patient immediately underwent cardiac catheterization which demonstrated a 99% blockage of the left anterior descending artery and revascularization was performed (, ). Two-dimensional echocardiogram demonstrated a left ventricular ejection fraction of 40% with anterior wall akinesis. Transesophageal echocardiogram ruled out an apical mural thrombus, but confirmed the ejection fraction and wall akinesis from the previous echocardiogram. The patient was also found to have hyperlipidemia after the conduction of a lipid panel. Hypercoaguable state and vasculitis workup was negative. OUTPUT:
PMCPatients_common5014
[ { "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 woman was admitted to the emergency room with right upper quadrant pain with fever over 2 days. Laboratory findings were as follows: white blood cell count 14,400/µL, total/direct bilirubin 2.89/2.09 mg/dL, gamma-glutamyl-transpeptidase 1,470 IU/L, and alkaline phosphatase 1,334 IU/L. After the removal of the impacted stone on the ampullary orifice and nasobiliary drainage, clinical symptoms were improved. On the 3rd hospital day, we performed endoscopic retrograde cholangiography (ERC) to evaluate for remnant stones. ERC showed no remnant stone but duct dilation on left hepatic duct and short segment stricture on the orifice ().\\nWe examined the stricture under endoscopic visualization using intraductal balloon-guided direct POC using an ultra-slim upper endoscope (GIF-XP260N; Olympus, Tokyo, Japan) as our previous report. The endoscope was inserted into the ampulla of Vater. After advancing the 5 F balloon catheter (MTW Endoskopie, Wesel, Germany) through the stricture via the guidewire, the balloon was inflated to anchor it inside the left hepatic duct. We observed the stricture under white light (WL) and NBI (Evis Lucera 260 System; Olympus) examination.\\nThe WL examination showed ill-defined hyperemia at the stricture site. NBI showed better contrast than did the WL examination, with a well-defined margin and prominent, thickened vascular markings (). We performed a target biopsy of the lesion using biopsy forceps (FB-19K-1; Olympus). Histopathological examination revealed a well-differentiated adenocarcinoma. The patient underwent an extended left hepatectomy. Histopathologically, the resected specimen showed focal papillary adenocarcinoma confined to the ductal mucosa ().\nOUTPUT:" }, { "from": "agent", "value": "Bile Duct Cancer" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 63-year-old woman was admitted to the emergency room with right upper quadrant pain with fever over 2 days. Laboratory findings were as follows: white blood cell count 14,400/µL, total/direct bilirubin 2.89/2.09 mg/dL, gamma-glutamyl-transpeptidase 1,470 IU/L, and alkaline phosphatase 1,334 IU/L. After the removal of the impacted stone on the ampullary orifice and nasobiliary drainage, clinical symptoms were improved. On the 3rd hospital day, we performed endoscopic retrograde cholangiography (ERC) to evaluate for remnant stones. ERC showed no remnant stone but duct dilation on left hepatic duct and short segment stricture on the orifice ().\nWe examined the stricture under endoscopic visualization using intraductal balloon-guided direct POC using an ultra-slim upper endoscope (GIF-XP260N; Olympus, Tokyo, Japan) as our previous report. The endoscope was inserted into the ampulla of Vater. After advancing the 5 F balloon catheter (MTW Endoskopie, Wesel, Germany) through the stricture via the guidewire, the balloon was inflated to anchor it inside the left hepatic duct. We observed the stricture under white light (WL) and NBI (Evis Lucera 260 System; Olympus) examination.\nThe WL examination showed ill-defined hyperemia at the stricture site. NBI showed better contrast than did the WL examination, with a well-defined margin and prominent, thickened vascular markings (). We performed a target biopsy of the lesion using biopsy forceps (FB-19K-1; Olympus). Histopathological examination revealed a well-differentiated adenocarcinoma. The patient underwent an extended left hepatectomy. Histopathologically, the resected specimen showed focal papillary adenocarcinoma confined to the ductal mucosa (). OUTPUT:
PMCPatients_common85
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Her daughter reported a three-week history of gradual onset confusion, neck pain, and generalised body weakness. In addition, she had urinary incontinence for several months. She reported no systemic symptoms of TB.\\nShe had been on antiretroviral therapy (ART) and prophylactic cotrimoxazole for 12 years. She had undergone two previous changes to her antiretroviral regimen: the first three years prior due to virologic failure, from zidovudine, lamivudine and nevirapine to second line tenofovir, lamivudine and atazanavir/ritonavir. Her second change three months prior to admission was after having discontinued ART for two weeks when developing urinary incontinence. Thereafter, her tenofovir was switched to abacavir. In addition, she completed treatment for pulmonary TB (confirmed by sputum Xpert) three years prior. She was known to have type II diabetes mellitus, and took regular metformin and glibenclamide.\\nOn admission, she was afebrile with other vital signs within normal range, and a random blood glucose of 7.4 mM (133 mg/dL). On examination, she had a Glasgow coma scale score of 14 (of 15 possible) due to confusion but no focal neurological signs. She had no evidence of wasting and no palpable lymphadenopathy. She had mild generalised abdominal tenderness with no palpable masses or organomegaly, and no abnormalities on thoracic examination.\nOUTPUT:" }, { "from": "agent", "value": "Mycobacterium tuberculosis, HIV" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Her daughter reported a three-week history of gradual onset confusion, neck pain, and generalised body weakness. In addition, she had urinary incontinence for several months. She reported no systemic symptoms of TB.\nShe had been on antiretroviral therapy (ART) and prophylactic cotrimoxazole for 12 years. She had undergone two previous changes to her antiretroviral regimen: the first three years prior due to virologic failure, from zidovudine, lamivudine and nevirapine to second line tenofovir, lamivudine and atazanavir/ritonavir. Her second change three months prior to admission was after having discontinued ART for two weeks when developing urinary incontinence. Thereafter, her tenofovir was switched to abacavir. In addition, she completed treatment for pulmonary TB (confirmed by sputum Xpert) three years prior. She was known to have type II diabetes mellitus, and took regular metformin and glibenclamide.\nOn admission, she was afebrile with other vital signs within normal range, and a random blood glucose of 7.4 mM (133 mg/dL). On examination, she had a Glasgow coma scale score of 14 (of 15 possible) due to confusion but no focal neurological signs. She had no evidence of wasting and no palpable lymphadenopathy. She had mild generalised abdominal tenderness with no palpable masses or organomegaly, and no abnormalities on thoracic examination. OUTPUT:
PMCPatients_common2570
[ { "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 came to our emergency department with pain, swelling, deformity of right thigh, and being unable to bear weight on same limb following slip and fall. She had massive swelling and multiple elevated verrucose-like lesions over thigh, the larger ones along medial and lateral aspect of thigh (). Her distal pulses and neurology were intact. Systemic examination revealed no abnormality. She had undergone hemiepiphysiodesis of right distal femoral physis and upper tibial physis at age of seven years. Contralateral thigh X-ray was taken and obvious differences in bone diameter as well as bone quality were noted.\\nThe patient was kept on upper tibial skeletal traction for two weeks. Swelling gradually subsided. X-ray was taken with traction applied over the limb and it revealed about 15 degrees of valgus and posterior angulation with some callus at fracture site. At this time patient was taken for definitive fixation. We did closed reduction under fluoroscopy and then immobilization with external fixator. While putting the Schanz screws, distal screws were kept without predrilling due to severe osteopenia of bone.\\nGradual range of motion exercise and quadriceps strengthening exercises were started from third postoperative day. Crutch walking was a bit difficult for her as her right limb was about 5 cm longer than the left.\\nFollow-up X-rays showed good amount of callus (). External fixator was removed at two and half months and partial weight bearing was started two weeks thereafter. The fracture finally united at four and half months (Figures and ). At final follow-up, at about eight months, she was doing all her daily activities independently with knee range of motion of about seventy degrees (15-degree extensor deficit and flexion up to 85 degrees) and limb length discrepancy of 5 cm ().\nOUTPUT:" }, { "from": "agent", "value": "Femoral Shaft Fracture, Klippel-Trenaunay Syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 12-year-old girl came to our emergency department with pain, swelling, deformity of right thigh, and being unable to bear weight on same limb following slip and fall. She had massive swelling and multiple elevated verrucose-like lesions over thigh, the larger ones along medial and lateral aspect of thigh (). Her distal pulses and neurology were intact. Systemic examination revealed no abnormality. She had undergone hemiepiphysiodesis of right distal femoral physis and upper tibial physis at age of seven years. Contralateral thigh X-ray was taken and obvious differences in bone diameter as well as bone quality were noted.\nThe patient was kept on upper tibial skeletal traction for two weeks. Swelling gradually subsided. X-ray was taken with traction applied over the limb and it revealed about 15 degrees of valgus and posterior angulation with some callus at fracture site. At this time patient was taken for definitive fixation. We did closed reduction under fluoroscopy and then immobilization with external fixator. While putting the Schanz screws, distal screws were kept without predrilling due to severe osteopenia of bone.\nGradual range of motion exercise and quadriceps strengthening exercises were started from third postoperative day. Crutch walking was a bit difficult for her as her right limb was about 5 cm longer than the left.\nFollow-up X-rays showed good amount of callus (). External fixator was removed at two and half months and partial weight bearing was started two weeks thereafter. The fracture finally united at four and half months (Figures and ). At final follow-up, at about eight months, she was doing all her daily activities independently with knee range of motion of about seventy degrees (15-degree extensor deficit and flexion up to 85 degrees) and limb length discrepancy of 5 cm (). OUTPUT:
PMCPatients_common2279
[ { "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 65-year-old man who received bilateral MoM THA in 2008. He presented for his follow-up visits at 1 and 5 months postoperative. The components were well aligned and he was pain free (Fig. a). The patient presented again for follow-up at 53 months after the index procedure. On the right side, he reported pain in his thigh for the past 3 months. On the left side, he was asymptomatic. The AP pelvis radiograph suggested periprosthetic lucencies in DeLee [] zone 1 and 2 on the right side and in zone 1 on left side, respectively (Fig. b). The CT of the right hip showed an osteolytic lesion extending 5 × 1 cm in the anteromedial acetabulum. On the left hip, CT demonstrated a lesion of 2.2 × 1 cm in the anterolateral acetabulum. The corresponding MARS MRI which was obtained at the same day did not detect any areas of bone resorption in the acetabulum on either side. The patient was scheduled for bilateral hip revision surgery the following months; however, the surgery was postponed because of signs of cardiac ischemia in the preoperative stress test. After successful stent implantation, hip revision surgery was scheduled 3 months later. c). Considering the anticipated difficulty of the surgery and the medical condition of the patient, only the right hip was revised at this point. Intraoperatively, there was a significant amount of fluid collection, but no clear evidence of abnormal soft tissue proliferation. The postoperative radiographs, showed well-aligned components (Fig. d).\nOUTPUT:" }, { "from": "agent", "value": "Acetabular osteolysis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Patient 2 was a 65-year-old man who received bilateral MoM THA in 2008. He presented for his follow-up visits at 1 and 5 months postoperative. The components were well aligned and he was pain free (Fig. a). The patient presented again for follow-up at 53 months after the index procedure. On the right side, he reported pain in his thigh for the past 3 months. On the left side, he was asymptomatic. The AP pelvis radiograph suggested periprosthetic lucencies in DeLee [] zone 1 and 2 on the right side and in zone 1 on left side, respectively (Fig. b). The CT of the right hip showed an osteolytic lesion extending 5 × 1 cm in the anteromedial acetabulum. On the left hip, CT demonstrated a lesion of 2.2 × 1 cm in the anterolateral acetabulum. The corresponding MARS MRI which was obtained at the same day did not detect any areas of bone resorption in the acetabulum on either side. The patient was scheduled for bilateral hip revision surgery the following months; however, the surgery was postponed because of signs of cardiac ischemia in the preoperative stress test. After successful stent implantation, hip revision surgery was scheduled 3 months later. c). Considering the anticipated difficulty of the surgery and the medical condition of the patient, only the right hip was revised at this point. Intraoperatively, there was a significant amount of fluid collection, but no clear evidence of abnormal soft tissue proliferation. The postoperative radiographs, showed well-aligned components (Fig. d). OUTPUT:
PMCPatients_common3808
[ { "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 man was admitted with a positive fecal occult test. He had type 2 diabetes mellitus and a previous open prostatectomy for cancer 7 years ago. Physical examination revealed a lower midline incision scar. Colonoscopy demonstrated normal rectum and multiple colonic polyps that could not be removed endoscopically. The NOSE after laparoscopic TC-IRA combined with cholecystectomy was planned after informed consent from the patient.\\nThe port sites and the position of the patient were as described above. Cholecystectomy was completed and the gall bladder was removed through the 12 mm trocar site. Laparoscopic TC and NOSE were done as described in the surgical technique portion. The rectal stump was re-closed with a 60 mm linear stapler. The IRA was accomplished side-to-side using a 60 mm linear stapler, and the common orifice of the stapler opening was closed by intracorporeal suturing. Oral fluids were started on day one. Postoperative analgesics were required six times (three dosages of paracetamol and three dosages of non-steroid anti-inflammatory analgesics). Defecations started on day one (four per day) and continued at 2–3 times per day. On the 30th day after surgery he was readmitted for oral intolerance in the absence of fever or pain. He had raised white blood cell counts. He was well on the 45th day after surgery.\nOUTPUT:" }, { "from": "agent", "value": "Attenuated familial adenomatous polyposis, Tubulovillous adenoma with high-grade dysplasia, Cholelithiasis, Pneumonia, Pelvic abscess" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 63-year old man was admitted with a positive fecal occult test. He had type 2 diabetes mellitus and a previous open prostatectomy for cancer 7 years ago. Physical examination revealed a lower midline incision scar. Colonoscopy demonstrated normal rectum and multiple colonic polyps that could not be removed endoscopically. The NOSE after laparoscopic TC-IRA combined with cholecystectomy was planned after informed consent from the patient.\nThe port sites and the position of the patient were as described above. Cholecystectomy was completed and the gall bladder was removed through the 12 mm trocar site. Laparoscopic TC and NOSE were done as described in the surgical technique portion. The rectal stump was re-closed with a 60 mm linear stapler. The IRA was accomplished side-to-side using a 60 mm linear stapler, and the common orifice of the stapler opening was closed by intracorporeal suturing. Oral fluids were started on day one. Postoperative analgesics were required six times (three dosages of paracetamol and three dosages of non-steroid anti-inflammatory analgesics). Defecations started on day one (four per day) and continued at 2–3 times per day. On the 30th day after surgery he was readmitted for oral intolerance in the absence of fever or pain. He had raised white blood cell counts. He was well on the 45th day after surgery. OUTPUT:
PMCPatients_common3548
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 54-year-old woman presented with dysarthria and left-sided hemifacial hypoesthesia. The patient underwent digital subtraction angiography (DSA) that revealed a fusiform aneurysm with a dilated portion measuring 7.5×9.3 mm. The diameters of the inflow and outflow were 3.5 mm and 2.9 mm ().\\nBecause the aneurysm was a symptomatic lesion and a vertebrobasilar fusiform aneurysm can potentially cause significant neurological morbidity, we decided to treat the patient with a PED.\\nDual antiplatelet therapy, including 100 mg aspirin and 75 mg clopidogrel, was started 7 days prior to the procedure. Intravenous heparin was given to maintain the activated coagulation time at 250–300 s. Then, under the roadman guidance, a Marksman microcatheter (EV3, Irvine, CA, USA) was advanced into the right posterior cerebral artery (PCA). Subsequently a 3.5×25 mm PED was unsheathed across the target landing zone. Although we required additional manipulations such as repeated 'pull and push' and rotation of the wire, the proximal end of the PED was successfully opened. Until then, the procedure was uneventful and subsequent DSA demonstrated a completely deployed PED with a fully covered fusiform segment (). However, during removal of the PED delivery wire, its distal tip engaged with a small branch of the right PCA and fractured (). Subsequent angiography demonstrated vasospasm and thrombus formation just proximal to the PED. Thrombolysis was performed with abciximab and chemical angioplasty. Fortunately, vasospasm and thrombus were resolved on final DSA and the patient recovered without any further neurological morbidity.\nOUTPUT:" }, { "from": "agent", "value": "Vertebral Artery Dissecting Aneurysm" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 54-year-old woman presented with dysarthria and left-sided hemifacial hypoesthesia. The patient underwent digital subtraction angiography (DSA) that revealed a fusiform aneurysm with a dilated portion measuring 7.5×9.3 mm. The diameters of the inflow and outflow were 3.5 mm and 2.9 mm ().\nBecause the aneurysm was a symptomatic lesion and a vertebrobasilar fusiform aneurysm can potentially cause significant neurological morbidity, we decided to treat the patient with a PED.\nDual antiplatelet therapy, including 100 mg aspirin and 75 mg clopidogrel, was started 7 days prior to the procedure. Intravenous heparin was given to maintain the activated coagulation time at 250–300 s. Then, under the roadman guidance, a Marksman microcatheter (EV3, Irvine, CA, USA) was advanced into the right posterior cerebral artery (PCA). Subsequently a 3.5×25 mm PED was unsheathed across the target landing zone. Although we required additional manipulations such as repeated 'pull and push' and rotation of the wire, the proximal end of the PED was successfully opened. Until then, the procedure was uneventful and subsequent DSA demonstrated a completely deployed PED with a fully covered fusiform segment (). However, during removal of the PED delivery wire, its distal tip engaged with a small branch of the right PCA and fractured (). Subsequent angiography demonstrated vasospasm and thrombus formation just proximal to the PED. Thrombolysis was performed with abciximab and chemical angioplasty. Fortunately, vasospasm and thrombus were resolved on final DSA and the patient recovered without any further neurological morbidity. OUTPUT:
PMCPatients_common2550
[ { "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 24 year old Asian female presented to the surgical clinic with a goitre of eight months duration and recent onset of altered bowel habits (i.e., increased stool frequency) with features of anaemia. Physical examination revealed a multi nodular goitre. Ultrasonically both lobes of the thyroid gland were enlarged with multiple hyper-echoic nodules with central irregularity denoting necrosis. The patient was biochemically euthyroid and antithyroid antibody status was negative.\\nColonoscopy revealed multiple polyps (more than 100) of varying sizes from the caecum extending to the rectum. Histology showed adenomatous polyps with low grade dysplasia rendering the diagnosis of FAP.\\nShe underwent a total thyroidectomy with level VI lymph node dissection and the recovery was uneventful. Macroscopy revealed multiple circumscribed whitish tumours of varying sizes in both thyroid lobes (Fig. ). There were 14 separate tumours in total, the largest measuring 18 × 17 × 14 mm in size. Some of the lesions contained areas of haemorrhages and cystic changes.\\nMicroscopically, all the tumours showed predominant features of encapsulated PTC. However, unlike in the usual PTC, a variety of architectural growth patterns including cribriform, solid and trabecular with morule formation were noted along with the papillary structures (Fig. ). Constituent cells were cuboidal to columnar with amphophilic cytoplasm. Spindle shaped cells were noted in morular structures. Capsular invasion was seen in one tumour but there was no evidence of vascular invasion. The lymph nodes were free of metastases.\\nThe patient was started on high dose thyroxine replacement and referred for radio iodine treatment. Disease involvement of the small bowel was excluded with capsule endoscopy and restorative proctocolectomy is being planned for the colonic polyposis. Colonoscopy screening of her two brothers and parents was found to be negative for FAP.\nOUTPUT:" }, { "from": "agent", "value": "Papillary thyroid carcinoma, Familial adenomatous polyposis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 24 year old Asian female presented to the surgical clinic with a goitre of eight months duration and recent onset of altered bowel habits (i.e., increased stool frequency) with features of anaemia. Physical examination revealed a multi nodular goitre. Ultrasonically both lobes of the thyroid gland were enlarged with multiple hyper-echoic nodules with central irregularity denoting necrosis. The patient was biochemically euthyroid and antithyroid antibody status was negative.\nColonoscopy revealed multiple polyps (more than 100) of varying sizes from the caecum extending to the rectum. Histology showed adenomatous polyps with low grade dysplasia rendering the diagnosis of FAP.\nShe underwent a total thyroidectomy with level VI lymph node dissection and the recovery was uneventful. Macroscopy revealed multiple circumscribed whitish tumours of varying sizes in both thyroid lobes (Fig. ). There were 14 separate tumours in total, the largest measuring 18 × 17 × 14 mm in size. Some of the lesions contained areas of haemorrhages and cystic changes.\nMicroscopically, all the tumours showed predominant features of encapsulated PTC. However, unlike in the usual PTC, a variety of architectural growth patterns including cribriform, solid and trabecular with morule formation were noted along with the papillary structures (Fig. ). Constituent cells were cuboidal to columnar with amphophilic cytoplasm. Spindle shaped cells were noted in morular structures. Capsular invasion was seen in one tumour but there was no evidence of vascular invasion. The lymph nodes were free of metastases.\nThe patient was started on high dose thyroxine replacement and referred for radio iodine treatment. Disease involvement of the small bowel was excluded with capsule endoscopy and restorative proctocolectomy is being planned for the colonic polyposis. Colonoscopy screening of her two brothers and parents was found to be negative for FAP. OUTPUT:
PMCPatients_common3471
[ { "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 female presented with a 1-month history of pruritic crust formation but no history of autoimmune disease or malignancy. The patient had been treated with bee-venom acupuncture in the way of subcutaneous injection twice a week for 2 months at an oriental medicine hospital due to back pain. The exact concentration or the entire contents of the bee-venom acupuncture were unknown. A month after starting the alternative bee-venom therapy, her skin lesions started to develop, then she stopped the bee-venom therapy. Physical examination revealed pruritic erythematous erosive and crusted patches and plaques on the scalp and trunk, which was not in accordance with the acupuncture site (). The oral mucosa was not affected. Laboratory findings revealed that there were no bee-venom-specific immunoglobulin E (IgE) or wasp-venom-specific IgE in her serum. Tzanck smear on trunk lesion was negative finding. A punch-biopsy specimen from the trunk revealed intraepidermal acantholysis just below the stratum corneum containing neutrophils and lymphocytes (). In the dermis, perivascular infiltration of lymphocytes and histiocytes was observed. A direct immunofluorescence study showed immunoglobulin G (IgG) and complement 3 deposition in the intercellular space of keratinocytes (). In addition, an indirect immunofluorescence study revealed IgG deposition in the intercellular space at a 1:160 dilution (). Based on these clinical, histopathological, and immunological findings, the patient was diagnosed with PF. In addition, we concluded that it was most likely triggered by the bee-venom, based on correlation with the time of onset and clinical manifestations. She was treated with oral methylprednisolone (16 mg/day for 2 weeks, subsequently tapered by 4 mg per week) and azathioprine (100 mg/day); the patient achieved partial remission at 2 months after initial treatment. We received the patient's consent form about publishing all photographic materials.\nOUTPUT:" }, { "from": "agent", "value": "Pemphigus Foliaceus" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 64-year-old female presented with a 1-month history of pruritic crust formation but no history of autoimmune disease or malignancy. The patient had been treated with bee-venom acupuncture in the way of subcutaneous injection twice a week for 2 months at an oriental medicine hospital due to back pain. The exact concentration or the entire contents of the bee-venom acupuncture were unknown. A month after starting the alternative bee-venom therapy, her skin lesions started to develop, then she stopped the bee-venom therapy. Physical examination revealed pruritic erythematous erosive and crusted patches and plaques on the scalp and trunk, which was not in accordance with the acupuncture site (). The oral mucosa was not affected. Laboratory findings revealed that there were no bee-venom-specific immunoglobulin E (IgE) or wasp-venom-specific IgE in her serum. Tzanck smear on trunk lesion was negative finding. A punch-biopsy specimen from the trunk revealed intraepidermal acantholysis just below the stratum corneum containing neutrophils and lymphocytes (). In the dermis, perivascular infiltration of lymphocytes and histiocytes was observed. A direct immunofluorescence study showed immunoglobulin G (IgG) and complement 3 deposition in the intercellular space of keratinocytes (). In addition, an indirect immunofluorescence study revealed IgG deposition in the intercellular space at a 1:160 dilution (). Based on these clinical, histopathological, and immunological findings, the patient was diagnosed with PF. In addition, we concluded that it was most likely triggered by the bee-venom, based on correlation with the time of onset and clinical manifestations. She was treated with oral methylprednisolone (16 mg/day for 2 weeks, subsequently tapered by 4 mg per week) and azathioprine (100 mg/day); the patient achieved partial remission at 2 months after initial treatment. We received the patient's consent form about publishing all photographic materials. OUTPUT:
PMCPatients_common927
[ { "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 is a 33-year-old female who presented with a two-year history of left HS that began with intermittent left eye twitching and progressed to involve the entire left side of her face. Other past medical history included hypertension and bicuspid aortic valve. She denied a family history of HS. High-resolution, thin cut magnetic resonance imaging (MRI) demonstrated an obvious arterial vessel loop contacting the inferior portion of the cisternal segment of the facial nerve. Her symptoms were causing intolerable distraction at work and in her personal life, thus she ultimately opted to undergo a left-sided microvascular decompression of cranial nerve (CN) VII for relief.\\nThe patient underwent a small retrosigmoid craniotomy and after careful microdissection, the cerebellopontine angle and flocculonodular lobe of the cerebellum and adjacent seventh and eighth nerve complex were identified. The superior petrosal vein was identified superiorly and preserved. Careful retraction over the flocculonodular lobe of the cerebellum facilitated exposure of the facial REZ medially. We hypothesize that the venous tethering aggravated the arterial compression of the seventh nerve by preventing natural movement away from the arterial vascular loop. A standard retrosigmoid craniotomy was performed and microvascular decompression was carried out not only on the artery but also on the vein with careful dissection and mobilization. The vein was preserved as major complications have been associated with venous sacrifice. Nonresorbable Teflon patties were interposed at the nerve REZ both cranially and caudally, displacing the adjacent arterial and venous loops. Video depicts the intraoperative view demonstrating careful microdissection of the offending artery and vein away from the facial nerve.\\nThe patient tolerated the surgery well without complications. She was discharged home on postoperative day one in stable condition. At her follow-up visit six weeks later, she endorsed the complete resolution of her HS.\nOUTPUT:" }, { "from": "agent", "value": "Double Crush Syndrome, Hemifacial Spasm" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The patient is a 33-year-old female who presented with a two-year history of left HS that began with intermittent left eye twitching and progressed to involve the entire left side of her face. Other past medical history included hypertension and bicuspid aortic valve. She denied a family history of HS. High-resolution, thin cut magnetic resonance imaging (MRI) demonstrated an obvious arterial vessel loop contacting the inferior portion of the cisternal segment of the facial nerve. Her symptoms were causing intolerable distraction at work and in her personal life, thus she ultimately opted to undergo a left-sided microvascular decompression of cranial nerve (CN) VII for relief.\nThe patient underwent a small retrosigmoid craniotomy and after careful microdissection, the cerebellopontine angle and flocculonodular lobe of the cerebellum and adjacent seventh and eighth nerve complex were identified. The superior petrosal vein was identified superiorly and preserved. Careful retraction over the flocculonodular lobe of the cerebellum facilitated exposure of the facial REZ medially. We hypothesize that the venous tethering aggravated the arterial compression of the seventh nerve by preventing natural movement away from the arterial vascular loop. A standard retrosigmoid craniotomy was performed and microvascular decompression was carried out not only on the artery but also on the vein with careful dissection and mobilization. The vein was preserved as major complications have been associated with venous sacrifice. Nonresorbable Teflon patties were interposed at the nerve REZ both cranially and caudally, displacing the adjacent arterial and venous loops. Video depicts the intraoperative view demonstrating careful microdissection of the offending artery and vein away from the facial nerve.\nThe patient tolerated the surgery well without complications. She was discharged home on postoperative day one in stable condition. At her follow-up visit six weeks later, she endorsed the complete resolution of her HS. OUTPUT:
PMCPatients_common29
[ { "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 48-year-old woman complained of constipation for 5 days, and then turned into diarrhea with discontinuous abdominal distension. She was hospitalized because of severe diarrhea (7 times/ d) with muco-bloody stools for one week. The stool frequency was five times a day. Her previous medical history revealed exposure to trichloroethylene (TCE) for one year. (Table ) Physical examination at admission revealed extensive abdominal tenderness. Fecal occult blood tests were positive. Other serological markers for autoimmunity and viral serology were normal, as was stool examination for bacteria and parasites. However, abdominal X-ray showed multiple intraluminal gas pockets in the left colon (Fig. ). Coronal reconstruction confirmed the widespread serosal intestinal air cysts involving long segment of colon (Fig. ). Colonoscopy revealed grape-like or beaded subepithelial lesions, and some with erythematous mucosa distributed in the sigmoid. Given the narrowing of the lumen secondary to these lesions the colonoscopy was incomplete (Fig. ). The endoscopic ultrasonography showed low echo of cystic below the mucosal layer (Fig. ). We used high frequency electrosurgical resection of the gas cysts; But considering that extensive endoscopic therapy might lead to infection, we used only partial treatment. Since the narrow lumen of the patient, we restricted her food intake and used parenteral nutrition. One week later, the patient started to have a half-fluid diet. Ornidazole (500 mg/bid) and vitamin B2 (10 mg/bid) were given to regulate intestinal anaerobes, while bifidobacterium (420 mg/bid) was given at intervals of half an hour. We also advised him to eat less gas-producing foods. The patients’ condition improved after 2 weeks (Table ). One month later the lesions disappeared completely (Fig. ) and NBI demonstrated visible patchy erythema and yellow nodules (Fig. ). After four months of follow up, the patient was still no symptoms, and findings at colonoscopy were normal.\nOUTPUT:" }, { "from": "agent", "value": "Pneumatosis cystoides intestinalis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 48-year-old woman complained of constipation for 5 days, and then turned into diarrhea with discontinuous abdominal distension. She was hospitalized because of severe diarrhea (7 times/ d) with muco-bloody stools for one week. The stool frequency was five times a day. Her previous medical history revealed exposure to trichloroethylene (TCE) for one year. (Table ) Physical examination at admission revealed extensive abdominal tenderness. Fecal occult blood tests were positive. Other serological markers for autoimmunity and viral serology were normal, as was stool examination for bacteria and parasites. However, abdominal X-ray showed multiple intraluminal gas pockets in the left colon (Fig. ). Coronal reconstruction confirmed the widespread serosal intestinal air cysts involving long segment of colon (Fig. ). Colonoscopy revealed grape-like or beaded subepithelial lesions, and some with erythematous mucosa distributed in the sigmoid. Given the narrowing of the lumen secondary to these lesions the colonoscopy was incomplete (Fig. ). The endoscopic ultrasonography showed low echo of cystic below the mucosal layer (Fig. ). We used high frequency electrosurgical resection of the gas cysts; But considering that extensive endoscopic therapy might lead to infection, we used only partial treatment. Since the narrow lumen of the patient, we restricted her food intake and used parenteral nutrition. One week later, the patient started to have a half-fluid diet. Ornidazole (500 mg/bid) and vitamin B2 (10 mg/bid) were given to regulate intestinal anaerobes, while bifidobacterium (420 mg/bid) was given at intervals of half an hour. We also advised him to eat less gas-producing foods. The patients’ condition improved after 2 weeks (Table ). One month later the lesions disappeared completely (Fig. ) and NBI demonstrated visible patchy erythema and yellow nodules (Fig. ). After four months of follow up, the patient was still no symptoms, and findings at colonoscopy were normal. OUTPUT: