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hippocrates

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Multicare_common_train

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[ { "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 woman presented at the emergency room in February 2017 with acute pain around the left knee and high fever accompanied by extreme fatigue that had persisted for a week. She had a no medical, smoking or pneumococcal vaccination history. Physical examination indicated the following: temperature of 38.5 C, blood pressure of 90/50 mmHg, respiratory rate of 24 breaths/min, and consciousness level of E3V3M5 on the Glasgow Coma Scale. There were crackles (rhonchi) on both lower lung fields, and chest radiography indicated heart failure with pericardial and pleural effusions. Furthermore, her left knee was swollen and showed inflammation and effusions on magnetic resonance imaging (MRI) (Fig. 1). Her initial white blood cell (WBC) count was 14,400/L and C-reactive protein (CRP) level was 34.95 mg/dL. Rapid urine antigen testing for S. pneumoniae was positive. We punctured her knee and turbid, yellow fluid was drained and neutrophils were found. S. pneumoniae was identified in left knee effusion, pericardial effusion, and blood cultures. The strain was identified as serotype 12F, and minimum inhibitory concentration (MIC) testing according to Clinical and Laboratory Standards Institute breakpoints revealed susceptibility to ampicillin (ABPC), ampicillin/sulbactam (ABPC/SBT), and piperacillin (Table 1). After drainage of knee and pericardial effusions in the intensive care unit, intravenous meropenem (1 g every 8 h daily) for 1 week were started because she was septic status and susceptibility of the pathogen was unknown at first. Then, ABPC/SBT (3 g every 8 h) for 3 weeks improved chest radiograph and knee MRI findings and inflammatory markers, such as WBC (4300/L) and CRP (2.25 mg/dL). She was discharged from the hospital after completing the course of treatment and continued oral amoxicillin administration for 2 additional weeks. Finally, we genetically analyzed the S. pneumoniae isolate from this patient, and sequence typing (ST) profile showed ST4846 (Table 2).\nOUTPUT:" }, { "from": "agent", "value": "Invasive pneumococcal disease (IPD), including arthritis, pericarditis, and bacteremia" } ]

[ { "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 history of hard smoke, coronary artery disease, arterial hypertension, type II diabetes mellitus, chronic renal failure, permanent atrial fibrillation, and a previous right carotid artery stenting. The main symptoms were rest dyspnea and recurrent transient right-side paresthesia and weakness. In consideration of the high surgical risk with a \"Society of Thoracic Surgeon\" risk score of morbidity or mortality of 32%, we planned a transcatheter approach. The key question was: Is it safe to perform carotid stenting before TAVR? After Heart Team discussion, we planned a combined transcatheter procedure. Because of the common development of bradycardia and hypotension after carotid stenting and raised risk of asystole in a patient having small aortic orifice area, we performed the aortic valve replacement first. Heparin was given to achieve a target activating clotting time of 200 seconds. By means of a 14-Fr sheath we implanted via a transfemoral access a 23-mm Edwards SAPIEN S3 bioprosthesis (Edwards Lifesciences; Irvine, California, United States; Fig. 1 ). After hemodynamic normalization, we implanted a 7 x 40 mm Carotid WALLSTENT (Boston Scientific; Massachussets, United States) in the left carotid artery ( Fig. 2 ). The brain was protected by a 3.2-Fr FilterWire EZ (Boston Scientific) device. The postoperative recovery was uneventful. He is alive and well at 2 years of follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Severe symptomatic aortic stenosis, Severe contralateral carotid stenosis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 92-year-old woman was admitted to the intensive care unit with acute onset of pain in the back with radiation to the left shoulder, as well as mild respiratory distress. She had a medical history of similar episodes of chest pain not however investigated with non-invasive or invasive methods of ischemic diagnostic, along with hypertension for about 35 years, and paroxysmal atrial fibrillation. She had no history of any recent major emotional or physical stress. The patient was taking an angiotensin converting enzyme inhibitor, beta-Blocker, Tamoxifen (for three months) and Coumadin. On admission, her blood pressure was 199/119 mmHg and radial pulse rate 90 bpm. Cardiovascular examination revealed soft heart sounds, no gallop rhythm, and an early systolic murmur was heard in the apical region. Echocardiography showed mild mitral regurgitation and wall motion abnormalities including apical dyskinesia, as well as mild hypokinesia in mid-segments of the anterior and lateral walls. Bilateral lung crepitating were heard at auscultation, and chest radiography revealed pulmonary oedema. The initial 12-lead electrocardiogram showed atrial fibrillation with significant ST depression in leads I, aVL and V4-6, and inverted T-waves in leads II, III, V3-6 associated with undervolted QRS, with no R wave progress from V1 to V3 and lengthening of QT interval. Blood tests performed concomitantly revealed severe elevation of cardiac troponin (39.16 ug/L) and creatinine kinase levels 550 U/L (normal range: 12-140 U/L). Emergency coronary angiography showed normal coronary arteries with no luminal narrowings (data not shown); however, left ventriculography revealed an apical sparing with preserved basal and midventricular contractile function and ejection fraction of the left ventricle of 45% (movie). Echocardiography (data not shown) repeated 6 weeks after the index event showed a left ventricular ejection fraction of 64% with complete resolution of wall motion abnormalities in apical segments. TTC is mainly seen in post-menopausal women aged between 50 and 80 years of age precipitate, without risk factors for coronary artery disease.\nOUTPUT:" }, { "from": "agent", "value": "Tako-Tsubo cardiomyopathy" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 70-year-old man was admitted to our hospital because of erythema on the face, trunk, and upper extremities and muscle pain in the proximal limbs. Carcinoma of the penis had been diagnosed at 52 years of age, and carcinoma of the skin at 55 years of age, with surgery performed for both. On admission, his height and weight were 156 cm and 44.2 kg, respectively, and his body temperature was 37.3C. A physical examination showed no abnormal auscultation of the chest and no abnormal signs for the abdomen. The laboratory findings were as follows: WBC count, 9,500 /muL; Hb, 13.7 g/dL; platelet count, 32.0x104/muL; total protein, 6.7 g/dL, albumin, 3.5 g/dL; aspartate aminotransferase (AST), 227 U/L; alanine aminotransferase (ALT), 102 U/L; LDH, 758 U/L; CK, 4,665 U/L; TC, 262 mg/dL; CRP, 0.57 mg/dL; and negative results for anti-Jo-1 antibody. However, his ability to swallow worsened, and he could not eat or take medicine. A gastric fistula was therefore created. On hospital day 100, a physical examination showed a distended abdomen. Abdominal X-ray showed massive gas accumulation in the ascending colon, and abdominal CT showed pneumoderma in the abdominal skin on the right side and gas in the ascending colon (Fig. 2). Nutrition via the gastric fistula was stopped, and he was administered high-dose oxygen, kanamycin, and purgative medicines through the gastric fistula. After these treatments were started, the abdominal abnormalities improved. However, the patient died of systemic fungal infection on hospital day 150. No abnormalities, such as gas or fistula, were evident in the small or large intestines on a histological examination at autopsy.\nOUTPUT:" }, { "from": "agent", "value": "Pneumatosis Cystoides Intestinalis, Connective Tissue Diseases, Dermatomyositis" } ]

[ { "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 with underlying chronic hepatitis B visited our out-patient hospital clinic. His serum alpha-fetoprotein level was within normal limits (3.05 ng/mL, normal limit: ~7.0 ng/mL). An abnormal 1.3 cm mixed echoic hepatic nodule was found in the right lobe incidentally on routine screening ultrasonography. The hepatic nodule had a peripheral hypoechoic halo, mimicking a malignant nodule. Multi-detector computed tomography (MDCT) was performed to characterize the focal liver lesion. The hepatic nodule showed complete enhancement during the early arterial phase of MDCT that then faded to iso-attenuation during the portal venous phase and the delayed phase without definite washout of the contrast enhancement. We proposed several possible diagnoses for this incidental nodule, including a well-differentiated hepatocellular carcinoma (HCC) and a high-grade dysplastic nodule due to the background of chronic hepatitis. FNH and hepatic adenoma were also included in the differential diagnosis. On T2-weighted imaging (T2WI) of MR, the nodule showed a high signal intensity (SI) and mild diffusion restriction on diffusion- weighted imaging (DWI, diffusion b-factor, 800) and apparent diffusion coefficient imaging. On gadoxetic acid-enhanced MR imaging, the mass demonstrated early intense homogeneous enhancement and subtle peripheral washout during the portal venous phase and ring-like peripheral enhancement with a central washout during the equilibrium phase and hepatobiliary phase (20 minutes, Figure 1 A). We hypothesized that the ring-like peripheral enhancement was suggestive of the capsule of a HCC. Ultrasound-guided biopsy was performed, and the biopsy specimens were grossly visualized as yellowish gray soft tissue and proliferating bile ductules with fibrous stroma and normally proliferating hepatocytes (Figure 1 B), which was histopathologically indicative of FNH. The nodule was stable over the 18 months of follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Focal Nodular Hyperplasia" } ]

[ { "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 current study evaluated the efficacy of PRT in two five-year-old children with ASD, using multiple modalities including fMRI, eye tracking, and behavioral outcome to assess treatment response. We anticipated that we would replicate the widespread positive effects of PRT on communication, behavior, and social skills in our two cases, as measured by standardized assessments of social and communicative function and adaptive behavior. In addition, we predicted, with successful treatment, an increased utilization of key nodes of the social brain previously implicated in processing socially salient visual stimuli. The social stimuli we utilized, comprised of point light displays of biological motion, have been repeatedly used to identify neural and eye tracking signatures of disruptions in social motivation in autism. Critically, using these stimuli, a recent fMRI study in our lab identified three categories of brain responses (State, Trait, and Compensatory) in a group of typical children (TD), unaffected siblings (US) and children with ASD. Regions reflecting the State of having ASD showed decreased activation in ASD compared to TD and US and were localized to the left ventrolateral prefrontal cortex, right amygdala, right posterior superior temporal sulcus, ventromedial prefrontal cortex, and bilateral fusiform gyri. Trait regions, reflecting an increased risk for developing ASD, showed decreased activation in children with ASD and US, and were localized to the bilateral fusiform gyrus, left dorsolateral prefrontal cortex, and right inferior temporal gyrus. Compensatory activity, unique to US, suggested a neural system-level mechanism by which US might compensate for an increased genetic risk for developing ASD and was localized to the right posterior superior temporal sulcus and ventromedial prefrontal cortex. The fMRI component of the current study was designed to test whether these, a priori and independently identified brain regions were altered by PRT treatment. We hypothesized that treatment related changes in neural activation would be present in the previously identified State, Trait and Compensatory regions representing areas of atypical activation in children with ASD and unaffected siblings.\nOUTPUT:" }, { "from": "agent", "value": "Autism Spectrum Disorder (ASD)" } ]

[ { "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 61-year-old man weighing 65 kg was referred to the Reference Laboratory at the Kashan University of Medical Sciences, Kashan, Central Iran, in Jan 2022, with a 2-month history of a 1x3 cm lesion on the left ear (Fig.1). A written and signed consent to use the data and results for publication was taken from the patient. The patient had diabetes and had no experience traveling outside Kashan for the past one years ago. He complained that his feature of ear was uncomfortable and scabrous, but has not any pain or any systemic complaints. Direct microscopy examination of the scales by 10% potassium hydroxide (KOH) preparation was negative for fungus elements. The lesion was thoroughly cleaned with 70% alcohol. Specimens were collected from the margin of the lesion by scraping with a scalpel blade. Two prepared smears were fixed by methanol, stained with 10% Giemsa stain for 30 min, and examined microscopically for the presence of amastigote forms of Leishmania spp. In the microscopy examination, many amastigotes forms of Leishmania spp were observed (Fig. 2). The DNA extraction was performed from the stained smear samples using a DNP kit (Cinaclon, Iran), according to the manufacturer's instruction protocol. A single PCR was performed using species-specific primers, LINR4 (Forward: GGG GTT GGT GTA AAA TAG GG) and LIN17 (Reverse: TTT GAA CGG GAT TTC TG), to amplify the variable region of the minicircle kDNA of Leishmania. These primers amplify a 760, and 650 bp fragment for L. tropica and L. major respectively. A positive sample of L. tropica (MHOM/IR/89/AR2) and L. major (MHOM/IR/54/LV39) were used as the positive controls, and distilled water was used as the negative control. PCR product was evaluated by electrophoresis on 1.5% agarose gel, stained by ethidium bromide, and then visualized using ultraviolet light. A 760-bp fragment was amplified using the primers. The PCR products were identical in size to the positive control of L. tropica (Fig. 3). Eventually, the patient was introduced to a physician to begin the treatment protocol. He was treated with glucantime, two vials of muscular, and intra-lesion injections weekly for four weeks. Unfortunately, the patient was lost for post-treatment monitoring.\nOUTPUT:" }, { "from": "agent", "value": "Cutaneous Leishmaniasis" } ]

[ { "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 white, sixty-six-year-old man born and residing in Miracema,Rio de Janeiro, was admitted in August 2014 for having had cough for three months, weight loss of six kg in a month, and febrile episodes over the 10 previous days. The patient underwent renal transplantation in January 2013 and he was using prednisone, 5 mg/day; mesalazine, 1,080 mg/day; and tacrolimus, 8 mg/day. He had systemic arterial hypertension, diabetes mellitus and gout, controlled with oral medications. He used to visit a farm and perform soil management frequently. Physical examination showed good general conditions, there was no palpable lymphadenopathy; dermatological examination revealed shallow ulcerated lesions on the palate surrounded by erythema, measuring about 8 mm; multiple mulberry-like erythematous eroded papules giving to the lesion a cobblestone appearance (Aguiar-Pupo stomatitis); erythematous papule with a central umbilication of about 3 mm located at the left nasal wing (Fig. 1); and an infiltrated erythematous plaque with irregular borders and indistinct boundaries, of approximately 1 cm in diameter, located on the left flank (Fig. 2). Chest x-rays showed bilateral nodular infiltrate, so it was started empirical treatment for tuberculosis and bacterial pneumonia. Biopsies in the described mucocutaneous lesions were performed, including oral ulcers, which were consistent with this diagnosis (Fig. 3). All materials were subjected to culture and there was growth of P. brasiliensis. Itraconazole, 400 mg daily, was started, but after five days of treatment the patient had clinical worsening and liposomal amphotericin B was introduced. The basal serum cortisol was normal and abdominal CT scan showed no specific changes; however, in lung CT (Fig. 4) an extensive involvement with bilateral nodular infiltrates, an excavated area suggestive of necrosis in the middle third of the right lung, and bilateral pleural effusion, largest in the right lung, were seen. Despite the prescribed therapies, the patient died.\nOUTPUT:" }, { "from": "agent", "value": "Paracoccidioidomycosis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 77-year-old obese woman was admitted to our emergency department with septic shock. Her medical history was notable for hypertension, type 2 diabetes and a previous scare of a right trochanteric fracture operated on one month before. Upon admission, the patient's temperature was 39 C, blood pressure was 92/48 mm Hg, heart rate was 125 beats/min, respiratory rate was 24 breaths/min, and oxygen saturation of 91% on room air body. Physical examination disclosed necrosis of the right anterior abdominal wall extended to the genital region and painful palpation in the right iliac fossa with no signs of peritoneal irritation (Fig. 1). There were no clinical signs of surgical wound infection. Biological tests showed an elevated WBC at 41000/mm3 and positive C-reactive protein at 250 mg/dl. An acute renal failure was noticed in creatinine level at 200 mmol/L. After initial resuscitation, an emergent abdominal and pelvic CT associated with Cystography was performed with the aim of excluding an intra-abdominal collection or surgical-site infection after hip fracture surgery. We, as well, found subcutaneous edema extending from the right groin along the right lower abdominal wall with a large amount of subcutaneous gas (Fig. 2). The intraoperative findings reveal extensive necrosis of the right lower abdominal wall tracking into the pubis and right flank. All necrotic tissue was excised (Fig. 3). A permanent urinary catheter was placed for bladder drainage and decompression. Urine and blood culture revealed Klebsiella pneumonia. The patient has received empiric intravenous antibiotic therapy. Additional surgical debridement had been performed in the following days. A refractory septic shock was installed and yet the patient died in the 5 PO day.\nOUTPUT:" }, { "from": "agent", "value": "Emphysematous cystitis, Necrotizing fasciitis" } ]

[ { "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 male presented to his family physician with a five-week history of nonbloody diarrhea, vomiting, and a 20 lb weight loss. Three days previously he had been seen by ophthalmology with new onset right eye pain, redness, and light sensitivity and diagnosed with severe right nongranulomatous anterior uveitis. He was treated with homatropine, dexamethasone, and prednisolone eye drops. He had no fevers, joint pain, skin changes, or recent travel. Past medical history included kidney stones, hypertension, and bioprosthetic aortic valve replacement three years earlier for severe aortic stenosis. He had been on olmesartan/hydrochlorothiazide 40/12.5 mg daily for 3-4 years. Other medications included ASA 81 mg twice weekly, vitamin C daily, multivitamin daily, cod liver oil daily, and acetaminophen as needed. Blood work ordered by his family physician included an elevated creatinine at 474 mumol/L. Physical examination was unremarkable. He had normocytic anemia (hemoglobin 120 g/L), normal albumin (40 g/L), normal electrolytes, and nonanion gap metabolic acidosis. Creatinine improved to 77 mumol/L with intravenous fluids over 5 days. Stool was negative for culture, parasites, and Clostridium difficile. Anti-tissue transglutaminase (TTG) antibody was negative with normal immunoglobulin A levels. There was an increase in intraepithelial lymphocytes as well as neutrophils in the surface epithelium. The crypts had a prominent increase in apoptosis. In hospital, his uveitis improved considerably and he was reassessed by ophthalmology. The uveitis resolved at 16 weeks with a taper of prednisolone eye drops. The patient's diarrhea resolved within 2 weeks of olmesartan discontinuation. His anemia improved to baseline and he returned to his previous weight within 3 months.\nOUTPUT:" }, { "from": "agent", "value": "Duodenal Villous Atrophy, Acute Kidney Injury, Idiopathic Bilateral Anterior and Intermediate Uveitis" } ]

[ { "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: Patricia was in her early 20s when her parents brought her for therapy. She was an only child, and lived with her parents. Her father was a 56-year-old professional; she described him as severe and judgmental. Her mother was a 50-year-old housewife, described as cold, perfectionist, and controlling. Patricia grew up with a constant fear of mistakes and of disappointing her parents' expectations. Simultaneously, in line with the standards set by her mother, Patricia displayed perfectionistic tendencies and neglected social relations, dedicating herself body and soul to studying. She was studying for her first exam session at the university when she began to manifest an initial psychotic breakdown, in the form of mental confusion, persecutory delusions and auditory verbal hallucinations. She was convinced that during the lessons the teachers told the whole class, through \"a secret communication code,\" that Patricia was \"unreliable and unable to be in the world,\" and she heard whispering voices insulting her. This prompted her to abandon lessons. She gradually lost the ability to concentrate on her studies, and had fallen into severe social withdrawal and apathy. At first, her parents criticized Patricia for neglecting her studies and for the absurdity of her delusional thoughts. When they witnessed the worsening of her condition, they asked for therapeutic help. Patricia started a pharmacological treatment with a public health psychiatrist (Olanzapine, 10 mg). This treatment drastically reduced hallucinations and partially regulated persecutory delusions: even though the patient no longer showed a structured delusion, a recurring doubt that her colleagues and neighbors had malicious intentions toward her persisted. Patricia also started individual psychotherapy, delivered in a private outpatient clinic. Individual sessions were weekly and lasted about 45 min. Patricia attended more than 90% of the scheduled weekly appointments. The psychotherapist, Judy,2 was in her early 40s, she had a cognitive behavioral background, a thorough knowledge of the literature on the relationship between metacognition and psychopathology and about 10 years of clinical experience working with persons with severe mental illnesses. During her training, she had undergone 2 years of cognitive-analytic therapy.\nOUTPUT:" }, { "from": "agent", "value": "Psychosis" } ]

[ { "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 man arrived in the emergency room with progressive erythema of the right thigh, right flank, and scrotum for 1 day after lifting weights and using the stationary bike at the gym. He reported no prior infections, illnesses, hospitalizations, or previous surgeries and was a nonsmoker. The severe infection of the scrotum resulted in complete loss of all of the underlying fascia and left the patient with exposed testes [Figure 1]. Wound cultures and blood cultures were positive for Group A Streptococcus infection. Treatment included intravenous antibiotics and fluid resuscitation, local wound care, serial operative debridements, and subsequent vacuum-assisted closure (VAC) therapy (KCI, Acelity, San Antonio, Texas). Fourteen days later, split-thickness skin grafts were used for coverage of the lower extremity, flank, groin, and penile wounds and Integra was used to cover the anterior scrotum and exposed testes [Figure 2]. A VAC dressing was placed over the skin grafts and scrotal Integra. Antibiotics were maintained until complete wound coverage was achieved. A VAC dressing change was performed at 1 week. Two weeks following Integra placement, the patient was taken back to the operating room and the silicone sheet was removed from the Integra. The Integra appeared fully incorporated by the patient's tissue, and healthy granulation was present at the wound base [Figure 3]. A split-thickness skin graft and overlying VAC dressing were then applied. The skin graft healed well with complete and stable wound coverage [Figures 4 and 5].\nOUTPUT:" }, { "from": "agent", "value": "Necrotizing Fasciitis" } ]

[ { "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 with a chief complaint of rash was admitted at the emergency room of the Sardjito General Hospital in Yogyakarta, Indonesia. His Javanese ethnicity was confirmed from parents and both grandparents of the patient. Upon physical examination, the temperature was 37 C, arterial blood pressure was 130/80 mm Hg, and heart rate was 87 beats/min. Further physical examination revealed diffuse maculopapular erythema on almost the whole body (more than 30%), some erosion, and denuded skin on the chest and lower extremities. Erosion was also found on the mucosal areas, such as lip, conjunctiva, and genital area, including scrotum and external urethral orifice with pain at urination. As the findings of clinical examination, i.e., skin and mucosal involvement and positive Nicolsky's sign, were consistent with SJS, diagnosis of SJS was established. Upon further history taking, the patient had a history of gout arthritis and allopurinol use. He had taken 200 mg/day allopurinol 2 months before skin lesion erupted. He also took metamizole and diazepam 2 months before the occurrence of symptoms. Laboratory examination revealed normal blood counts and hepatic enzymes but markedly elevated ureum and creatinine ratio, suggesting decreased renal function (Table 1). All medications were discontinued, and the patient was administered methylprednisolone of 125 mg/24 h for 4 days. After 2 days, the dosage was tapered off to 62 mg/24 h for 2 days. The patient was also treated with ibuprofen, cetirizine, tramadol, and topical preparation. Dressing with NaCl 0.9% was applied for 15 min on a daily basis. No new erythematous patches or vesiculobullous lesions were observed upon discharge.\nOUTPUT:" }, { "from": "agent", "value": "Stevens-Johnson Syndrome" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 51-year-old female with no history of trauma or knee surgery came to the visit with a chief complaint of bilateral knee pain for several years. She also experienced stiffness over bilateral knees, especially in the morning. The symptoms were worsening until she could not walk without pain. The Patient's body weight was 59 kg, and height was 160 cm (BMI: 23.04 kg/m2). The pain sensation reduced when resting (VAS = 5) and increased when climbing stairs, going down the stair, and even when walking (VAS = 9). The WOMAC index was rated 63. Varus deformity, tenderness, and crepitus on both knees were also identified and grade IV knee OA was showed on the X-Ray (Figure 7A). She underwent PFO procedure on both legs in April 2019 followed by a course of intra-articular dextrose prolotherapy every six months continuously on bilateral knee (one course consisted of six doses, each dose was injected once a month consecutively). A dose dextrose prolotherapy was prepared using 6 mL solution containing 13% hypertonic dextrose and 0.6% lidocaine, injected into the articular. After each injection, the patient was given oral medication of acetaminophen as pain reliever, one tablet three times a day for three days. At the follow-up (24 months post-surgery), she had received two courses of intra-articular dextrose prolotherapy (12 doses). The patient reported that the symptoms were improving. She did not feel knee stiffness anymore, but she still suffered from pain occasionally. Although the Patient still complained of pain, the pain intensity was decreasing, with a VAS score of 5. The WOMAC index was improved with 26. The X-Ray showed bilateral knees after treatment (Figure 7B).\nOUTPUT:" }, { "from": "agent", "value": "Severe Medial Knee Osteoarthritis" } ]

[ { "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 female patient presented with acute symptoms of abdominal and flank pain, nausea, dark red urine, fevers and chills. One month prior to presentation, she had experienced a few days of rhinorrhea and headaches, suggestive of a viral upper respiratory tract infection. Upon presentation, she was found to be pregnant by serum hCG and ultrasound, with an estimated gestational age of 6 weeks. Laboratory evaluation showed hemoglobin 11.2 g/dL, haptoglobin <20 mg/dL, total bilirubin 6.8 mg/dL, direct bilirubin 0.7 mg/dL, lactic acid dehydrogenase (LDH) 735 U/L, and absolute reticulocyte count 49.3 K/muL. Urine analysis demonstrated 3+ blood and the microscopic examination was negative for red blood cells. A direct antiglobulin test was positive for anti-C3d and negative for IgG. The cold agglutinin titer was negative (<2). Donath Landsteiner antibody testing was performed using a blood sample that was immediately immersed into an insulated container filled with water at 37 C, and directly delivered to the testing laboratory. A Donath Landsteiner antibody test was positive (Figure 1), confirming the diagnosis of PCH. Over the next 48 hours, the patient's hemoglobin declined to 7.3 g/dL (Figure 2). She was managed supportively with a prenatal vitamin supplement and encouraged to keep warm. Her hemoglobin and LDH normalized by day 42 (Figure 2). A Donath Landsteiner test on day 77 was negative. Her hemoglobin declined during the third trimester of pregnancy, to 11.0 g/dL on the day of delivery, without any laboratory evidence of recurrent hemolysis. She delivered a healthy female child by Cesarian section at 39 weeks of gestation. The neonate did not have anemia or hemolysis after birth.\nOUTPUT:" }, { "from": "agent", "value": "Paroxysmal cold hemoglobinuria" } ]

[ { "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 81-year-old Turkish woman with a mechanical bowel obstruction was referred to our emergency department. The patient had complained of acute abdominal pain, vomiting, and mechanical obstruction for five days before her admission to our emergency service. Her records confirmed that she had cholecystolithiasis for 15 years; a cholecystectomy was offered to her many times by different surgeons, but she refused to undergo the surgery. At physical examination, her abdomen was moderately distended, and tympanic bowel sounds were auscultated. The rectal examination revealed empty ampulla recti. The laboratory test an elevated total leukocyte count (15.6 x 109 cells/L) and slightly increased renal function test values, which could be considered as an indication of pre-renal azotemia. The liver function test results and serum bilirubin levels were normal. Plain radiographs of the abdomen revealed multiple air-fluid levels in the small intestine. The patient was treated with intravenous fluids and antibiotics in the tertiary hospital. On the fifth day of hospitalization, she was referred to our hospital because of the deterioration of her clinical condition. After the initial examination, computed tomography (CT) was performed, which demonstrated small-bowel obstruction by a 40 mm high-density image in a jejunal loop (Fig. 1). Additionally, the scan showed pneumobilia in the left hepatic biliary branch and thickening between the gallbladder and the duodenal walls (Fig. 2). The contrast liquid was observed in the gallbladder, and the air-fluid levels were detected on the CT scan. A cholecystoduodenal fistula resulting from chronic cholelithiasis was suspected. An exploratory laparoscopy was performed. Moderately dilated jejunal loops proximal to the distal jejunum were observed during the laparoscopy. 3). The patient had an uneventful postoperative course and was discharged on postoperative day 5.\nOUTPUT:" }, { "from": "agent", "value": "Gallstone ileus" } ]

[ { "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 woman suddenly developed involuntary movements of her left arm and leg. The symptom deteriorated rapidly. She was admitted to our hospital two weeks after symptom onset. The patient had papillary thyroid cancer at the age of 67 years. Her medical history included no psychotropic medications or head trauma. There was no family history of neurological diseases. On examination, irregular, seemingly random, semi-directed movements of the left upper and lower extremities were seen. The patient also showed a scowling face and darting tongue. These choreic movements substantially disabled the patient during wakefulness, but they disappeared during sleep. Her muscle tone and tendon reflexes were normal, and no pathological reflexes were observed. Magnetic resonance imaging (MRI) of the brain demonstrated a focal lesion in the right caudate head, which showed hyperintensity on fluid-attenuated inversion recovery (Figure 1) and diffusion-weighted imaging. This lesion showed hypointensity on apparent diffusion coefficient mapping, and it was slightly contrast-enhanced with gadolinium. These findings on MRI indicated an ischemic stroke in the caudate head; however, laboratory findings disclosed that this patient's disease process was not that simple. The blood cell count showed a mild leucopenia. There were high titers of antinuclear antibody, anti-DNA antibody, and anti-SSA antibody on two occasions 12 weeks apart. Cerebrospinal fluid analysis was unremarkable. In coagulation examination, the levels of fibrin degradation product, D-dimer, and thrombin-antithrombin complex were elevated slightly. The patient's chorea improved spontaneously two weeks after admission. Haloperidol (1.5 mg/day) further ameliorated the symptom. We also started antiplatelet therapy using aspirin, which also has an inhibitory effect on endothelial activation and inflammation. Brain MRI performed 2 months after disease onset showed disappearance of the caudate lesion, in keeping with the improvement of the chorea. The patient gave her informed consent before the evaluations and treatment were performed.\nOUTPUT:" }, { "from": "agent", "value": "Elderly-onset systemic lupus erythematosus, Neuropsychiatric syndromes of SLE (NPSLE), APS" } ]

[ { "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: Treatment using clozapine was started in September 1997 when he was hospitalized at Seoul National University Hospital. Considering the distance to the hospital, he was transferred to the Psychiatry Department of Inha University Hospital for treatment in September 1997. Because the administration of clozapine 250 mg/day led to some improvement in his symptoms, and no side effects except sialorrhea were observed, he left the hospital on the 42nd day of hospitalization. During outpatient treatment, persecutory ideation and sialorrhea continued. In August 1999, he experienced a convulsion while taking clozapine 425 mg/day and benztropine 3 mg/day. In August 2000, he had a second convulsion while being treated with clozapine 400 mg/day and benztropine 3 mg/day. Obsessive-compulsive symptoms began in August 2001 and persisted; the patient took fluvoxamine 100 mg/day in August 2002 and discontinued benztropine in November 2002.\nOUTPUT:" }, { "from": "agent", "value": "Paranoid type schizophrenia, Enuresis" } ]

[ { "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 histological findings showed fragments of colonic mucosa with an intense and acute inflammatory cell infiltrate (presence of polymorphonuclear neutrophils) in the lamina propria, with formation of cryptitis. There was also mucin depletion but no granulomas were seen. He presented with a severe episode of bloody diarrhea (12 to 15 bowel movements daily), pallor, abdominal pain and serum hemoglobin of 10.7 g/dL, leukocyte count 11,000 cells/mm3, platelet count 531,000 cells/mm3, serum CRP 134.6 mg/dL and serological p-ANCA was negative. He was treated with full doses of i.v. corticosteroids and oral and topical 5-aminosalicylic acid. 1). A good response was initially obtained after surgical debridement of the abscess and seton placement. Infliximab was started at 5 mg/kg as an induction dose (at 0, 2 and 6 weeks) followed by maintenance doses every two months.\nOUTPUT:" }, { "from": "agent", "value": "Ulcerative colitis, Perianal fistulas" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: On the 5th of August, 2020, a 58-year-old woman presented in our emergency department with seizures and hemiparesis. She had a prior fever, malaise, and dry cough a week before admission. She has had a history of hypertension since a year ago. The vital sign is within normal limit except the blood pressure is 170/110 mmHg. The results of the laboratory test were high blood glucose 254 mg/dL and HbA1C 6.5%. Leukocytosis with white blood cells (WBC) was 14/L and neutrophil-lymphocyte ratio (NLR) was 33. Increase level of erythrocyte sedimentation rate (ESR) 93 mm/h, D-dimer 21,176 ng/mL, and fibrinogen 446 mg/dL. The result of the reverse transcription-polymerase chain reaction (rt-PCR) test from the nasal swab was observed to be positive for SARS-CoV-2. The completed laboratory results are listed in Table 1\nHead contrast computed tomography (HCCT) showed cerebral edema at the right parietal lobe (Fig. 1B). 1B-D), with a sign of venal hypertension. CT venography (CTV) was also confirmed CSVT at SSS, bilateral TS, and bilateral sigmoid sinus (Fig. 1E, F). Furthermore, the thorax CT scan showed ground-glass opacity and subpleural bilateral, with a fibrotic appearance in the left lung (Fig. 1A). On the 5th day of treatment, D-dimer was decreased to 2092 ng/ml. Other clinical manifestations also improved and the patient was discharged from the hospital on the 10th day.\nOUTPUT:" }, { "from": "agent", "value": "Cerebral Sinus Venous Thrombosis, COVID-19" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Four consecutive treatments with ipilimumab (3 mg/kg body weight) were well tolerated apart from a slight decrease in thyroid-stimulating hormone (TSH) (0.3 mU/l; normal range: 0.4-4.9 mU/l) with normal fT4 before the third treatment. Fourteen weeks after initiation of ipilimumab, the patient presented with acute onset of nausea, dizziness and ataxia. On examination, a blurred speech was noticed, prolactin was elevated with 30.7 ng/ml (normal range 3.5-19.5 ng/ml), cortisol and TSH were decreased with <1.0 microg/dl (normal range 4.3-22.4 microg/dl) and 0.27 mU/l (normal range 0.4-4.9 mU/l), respectively. CT scan showed the previously described irradiated metastases with adjacent edema as well as an increase in volume of the pituitary gland with signs of brain edema. Under i.v. steroid treatment (dexamethasone 16 mg/day) symptoms ameliorated. Ipilimumab-associated neurological symptoms are rare, but may be life-threatening. Common symptoms include headache, dizziness, lethargy, and asthenia. Rarely, patients present with cranial neuropathy and optic nerve ischemia, ataxia, tremor, myoclonia, dysarthria and peripheral neuropathy. Importantly, Guillian-Barre syndrome was described twice with fatal outcome in one patient. In addition, meningo-radiculo-neuritis, enteric neuropathy and cerebral edema with convulsions have been reported. Six out of eleven rare neurological AEs reported in this study required immunosuppression (Table 5, last patient Table 6). In general, steroid treatment was effective although one patient experienced a therapy-refractory neuropathy and eventually died despite additional treatment with intravenous immunoglobulin (IVIG).\nOUTPUT:" }, { "from": "agent", "value": "Metastatic Melanoma, Cerebellar Metastasis, Hypophysitis" } ]

[ { "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 severe pain radiating down his back after lifting a lawn mower into a van. On examination, the only sign was an elevated BP of 240/100 mmHg. DNA sequencing from the peripheral blood of the index case identified a missense variant (c.958C>T) (NM_003238.3) in exon 6 of the TGFB2 gene (NG_027721.1). This variant causes a p.(Arg320Cys) substitution in a highly conserved region of TGFB2 (Figure 1D). The variant was also detected in the uncle (III:1) and two currently asymptomatic teenage family members (IV:3) and (IV:5). Immunofluorescent imaging showed markedly enhanced TGFB1 and TGFB2 expression in the aorta of the index case compared to age and gender-matched controls (Figure 2 and 3). This was confirmed by immunoblotting for both proteins in the aorta of IV:10 versus controls where the upregulation of TGFB1 was particularly striking (Figure 2 and 3).\nOUTPUT:" }, { "from": "agent", "value": "Aortic dissection" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: He was admitted on April 24, 7 days after his last chemotherapy, within 24 hours of abrupt fever onset (40 C/104 F), chills, diaphoresis, headache, malaise, myalgias, and productive cough. Figure 1 shows neutrophils, lymphocytes, and monocytes counts and chest roentgenogram on admission with confluent lower lung air-space opacities. SpO2 was 91% at room air. He was started on oseltamivir 75 mg BID, ceftazidime, and amikacin. A nasopharyngeal-swab for A H1N1 was negative. After 8 days on oseltamivir, he continued with fever; chest CT scan showed bilateral alveolar infiltrates (Figure 1); amphotericin B was started. Forty hours after oseltamivir discontinuation, the lung opacities grew and patient developed respiratory failure, requiring invasive mechanical ventilation. A second nasopharyngeal-swab was positive for H1N1; oseltamivir and rimatadine were started, and patient continued on antibiotics and amphotericin B. The patient was transferred to ICU in septic shock and ARDS; Acute Physiology and Chronic Health Evaluation (APACHE) II and Sequential Organ Failure Assessment (SOFA) scores were 18 and 11 points. A second oseltamivir course was administered for 10 days; 72 hours after discontinuation, the patient developed fever again (39 C/102 F) and breathing difficulty. Oseltamivir and rimantadine were reinitiated and stopped when clinical recovery-associated lymphocyte count reached 500 cells/ml (Figure 1). The patient was discharged after 35 days of hospital stay and 25 days of mechanical ventilation. Genetic study of the virus on sample taken 20th day of illness showed 100% identity for AH1N1SW, and no H274Y mutation for oseltamivir resistance was found. He underwent successful autologous hematopoietic stem cell transplantation (HSCT) on September 2009 with BEAM plus dexametasone conditioning.\nOUTPUT:" }, { "from": "agent", "value": "Lymphoblastic lymphoma, Pandemic influenza A H1N1 2009 virus infection" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: We report a case of a 30-year-old man who presented electively in our clinic with a history of intermittent high grade fever and right lower quadrant non-radiating abdominal pain for 1 year + 6 months duration, for which he consulted and treated in 5 different health facilities with no favourable evolution. On review of his systems; presence of non-productive cough, intermittent night sweat, loss of appetite, nausea but neither vomiting nor altered bowel habit. His past history is remarkable for appendicectomy 10 months ago after he consulted for similar complaints. Also, there is a history of contact with relative diagnose with pulmonary Tuberculosis (TB) 2 years ago. On examination; our patient was normotensive (BP=110\\70mmHg) febrile to touch (Temp=38 c), lost 10% body weight within 6 months, ill-looking, asthenic with moderately pink conjunctivae and anicteric sclera. Nodes were mobile, non-tender with the left cervical node having the largest diameter of 4cm. Presence of fine inspiratory crackles on chest examination. Abdominal examination revealed grid-iron incision mark and mild tenderness around the right lower abdominal quadrant. Patient was then placed on a 6 month Anti-TB regiment under Direct Observational Therapy. Two weeks after onset of treatment evolution was favourable with normal body temperature and gain of appetite. Patient is fine now, has no complaint and has resume work.\nOUTPUT:" }, { "from": "agent", "value": "Lymph node Tuberculosis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Moreover, he smoked shisha and had recovered of COVID-19 infection three months earlier. His blood results showed raised inflammatory markers (Table 2), and his chest X-ray showed pulmonary congestion and infiltrates (Figure 2). The NIV trial in the ED failed to improve his hypercapnia. In the ICU, NIV was associated with an obstructive breathing pattern, low tidal volume, and high peek pressures seen on the ventilator monitor (Drager Evita V800). An immediate resolution of the obstructive breathing pattern was achieved once he was placed in a ramping position using an Oxford HELP pillow (Figure 3). The arterial blood gas showed marked resolution of the hypercapnia and acidosis (Table 2). He received broad-spectrum antibiotics and diuretics (Table 4). Twelve hours later, he was weaned from NIV and placed on humidified oxygen during the day and NIV at night. Oesophageal manometry was not used in both cases to assess the work of breathing (WOB) due to its impracticality during the acute phase in non-intubated patients; however, a WOB scale from 1-7 was used instead (Table 1, Table 2). In both cases, oral feeding was started within the first 24 hours. They received isocaloric high protein diet based on their adjusted body weight. Both patients were transferred to the respiratory ward after their fifth ICU Day for further pulmonary function tests and sleep studies. Afterwards, they were discharged home. Case 1 was given a follow-up appointment with the orthogeriatric nurse, dietitian, and the smoke cessation team. Case 2 was given a home BiPAP machine and a dietitian appointment.\nOUTPUT:" }, { "from": "agent", "value": "Severe type 2 respiratory failure due to community acquired pneumonia, Hypogonadism, Morbid obesity" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 13-year-old football player with a 1-year history of recurrent palpitations during exercise despite beta-blocker therapy attended our Paediatric Arrhythmia Clinic. Despite an aggressive radiofrequency ablation procedure including lesions in the low, middle, and superior aspects of the triangle of Koch as well as in the coronary sinus, we could not induce any junctional response. After a conventional right-sided procedure, there was no modification in the tachycardia characteristics or in the slow pathway conduction (including tachycardia induction, cycle length, and slow pathway refractory period). A decision was made to attempt a left-sided procedure. A steerable decapolar electrode catheter was placed in the coronary sinus, and the His position was again identified on the anterior septum. The transseptal puncture was performed using the usual technique under fluoroscopy guidance without complications, followed by heparin administration. A deflectable catheter with a 4-mm tip was introduced into the left atrium, and the septal aspect of the mitral valve was mapped. A balanced atrioventricular signal with multicomponent atrial electrograms and low amplitude potentials was identified in the posteroseptal aspect of the mitral annulus, 3 mm above the coronary sinus (Figure 1). This left site clearly corresponded with the usual target for a conventional right-sided procedure (Figure 2, Figure 3). At this point, a single radiofrequency application resulted in an immediate accelerated junctional response with stable retrograde ventriculoatrial conduction. This application also resulted in temperatures of 55 -60 and was continued for 60 seconds. The procedure was terminated without complications, and the patient did not show recurrence of palpitations afterward.\nOUTPUT:" }, { "from": "agent", "value": "AVNRT" } ]

[ { "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 cause of spontaneous bowel perforation is unclear. He had been doing well on intravenous immunoglobulin (IVIG) up until this point. A computed tomography scan of the abdomen and pelvis with contrast revealed diffuse small bowel mucosal hyperenhancement consistent with enteritis, with no evidence of free air or recurrent bowel perforation. He underwent EGD and colonoscopy with no complications. Both procedures revealed grossly normal mucosa with the exception of two diminutive sessile polyps at the cecum, which were biopsied. Serum CMV was quantitated by PCR and found to be 9561 IU/ml. He was subsequently started on valgancyclovir with marked improvement in his clinical condition. Results of routine immunological analysis prior to starting immunoglobuline therapy revealed IgG (498 mg/dl; control range 694-1,618 mg/dl), IgA (118 mg/dl; control range 68-378 mg/dl), IgM (92 mg/dl; control range 65-263 mg/dl). Proliferative responses to recall antigens (Candida albicans and tetanus toxoid) and mitogens (phytohemagglutinin, concanavalin A, and pokeweed) were also normal. HIV was negative.\nOUTPUT:" }, { "from": "agent", "value": "Cytomegalovirus Colitis, Primary Hypogammaglobulinemia" } ]

[ { "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 with left nasal alar melanoma post wide excision with a nasolabial flap was admitted due to progressive left side costal pain associated with dyspnea. Physical examination revealed crackle breath sounds over the left lower lung field. A chest X-ray revealed accumulated left pleural effusion and a chest CT scan showed left loculated pleural effusion with pleural thickening. Video-assisted thoracic surgery (VATS) with left side decortication was performed due to poor response to piperacillin/tazobactam and imipenem/cilastatin. The pathological findings showed acute suppurative inflammation composed of dense neutrophilic and eosinophilic infiltration with extensive necrosis which indicated empyema and tissue culture did not yield bacterial or mycobacterial pathogens. Sputum and pleural effusion acid-fast stain also failed to identify specific pathogen. The patient received ciprofloxacin for pneumonia complicated with empyema. The fever episode subsided except dry cough and persistent pneumonia consolidation in the right upper lung field. Progressive bilateral cervical lymphadenopathy was noticed by the patient one month after discharge (Fig. 1A). Additionally, abnormal granular nodules over nasopharynx were found by otolaryngologist during follow up for melanoma. Excisional biopsy of the left-side cervical lymph node was performed. The pathological report showed ill-defined granulomatous inflammation (Fig. 2A), and acid-fast positive bacilli was identified (Fig. 2B). M. szulgai was also grown from the cervical lymph node. M. szulgai was isolated from the following three sets of sputum. HIV screening was negative whereas anti-interferon-gamma autoantibodies were positive. Anti-mycobacterial combination therapies of clarithromycin, ethambutol, and rifampin were administered. Clinical improvement of cervical lymphadenitis was noted during follow up. Sputum culture for mycobacteria turned negative after five months of combination therapies. Follow up chest X-ray showed gradual resolution of consolidation over the right upper lung field. The patient is regularly followed up at the outpatient clinic on the therapy planned for 12 months after the sputum culture turns negative.\nOUTPUT:" }, { "from": "agent", "value": "Disseminated Mycobacterium szulgai infection" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Patient information: a 41-year-old woman with a history of three miscarriages and skin photosensitivity, without other medical, family, psycho-social history or past interventions, who presented with a symptomatology of abrupt onset, admitted in the plateau phase, made up of a synchronous and symmetrical ascending functional impotence of both lower limbs 20 days before admission. Clinical findings: the clinical examination found a dyspneic patient with a motor deficit evaluated at 4/5 proximal and 3/5 distal to the four limbs, a hypotonia more accentuated in the two lower limbs and an osteotendinous areflexia in the four limbs. Sensibility and cranial pairs were intact with a plantar skin reflex in flexion. Dermatological examination revealed generalized myxedema associated with alopecia (Figure 1). Diagnostic assessment: electroneuromyography (ENMG) revealed collapse of motor potential and absence of F waves in all four limbs. The study of the sensory nerve conduction is without abnormality suggesting an acute axonal motor polyradiculoneuropathy more marked in the two lower limbs (Figure 2). Biological abnormalities were in favor of SLE (Table 1). Radiological exploration revealed hepatomegaly and large effusions: peritoneal, pericardial, and bilateral pleural, which explain the severity of the clinical picture. Complete brain and spinal cord magnetic resonance imaging (MRI) were normal as part of the extension workup. Diagnostic/therapeutic intervention: the diagnosis of acute Guillain-Barre type Pro Re Nata (PRN) associated with lupus disease was retained, and a bolus of methyl-prednisolone at a dose of 1g per day was established for five days. The patient benefited from monthly courses of cyclophosphamide 1g, synthetic antimalarials such as hydroxychloroquine (Plaquenil) 400 mg per day, and complementary corticosteroid therapy of 60 mg for six weeks with progressive reduction of 5 mg every 15 days. Follow-up and outcomes: the evolution is marked by a clear clinical improvement with recovery of walking, a markedly improved muscle testing and no side effects related to the treatment. The prognosis of our case is clearly good explained by the therapeutic precocity. The patient's perspective: the patient reports satisfaction following the recovery of motor functions and her autonomy with a marked improvement in her quality of life. The psychological interview of the patient also demonstrates a stable post-therapeutic psychic state.\nOUTPUT:" }, { "from": "agent", "value": "Severe acute polyradiculoneuritis, Systemic lupus erythematosus" } ]

[ { "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 fit-and-healthy ex-army officer presented with a two-day history of a cold, numb, and painful left lower leg; he had been doing vigorous exercises two days prior to admission. Over the past few months, the patient had experienced similar worsening leg pain after running long distances. Apart from smoking (5 pack years), the patient had no other significant cardiovascular risk factors. Physical examination revealed a regular heart rate of 60 beats per minute and a blood pressure of 120/80 mm Hg. There was no palpable abdominal aortic aneurysm. Examination of the right leg was unremarkable. On the left side, there were normal palpable femoral and popliteal pulses, but no palpable distal pulses. The left foot also appeared paler; however, motor and sensory functions were intact. Intraarterial thrombolysis (Alteplase) was commenced. The stricture was accentuated with the foot in dorsiflexion and plantar flexion. At 48 hours, the angiogram demonstrated that the thrombus had largely resolved; however, the stricture was still present. The site of stenosis was angioplastied which resulted in a marked improvement in blood flow. Having excluded bilateral disease on the MRI, the patient underwent surgery-division of the medial head of gastrocnemius with autogenous saphenous vein interposition graft. A postoperative duplex scan showed that the vein graft was patent with pulsatile signals. The patient's recovery was uneventful and he was discharged 3 weeks after hospitalisation.\nOUTPUT:" }, { "from": "agent", "value": "Popliteal artery entrapment syndrome, Acute limb ischaemia" } ]

[ { "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: During our focus groups, all participants answered our query about their perceptions of AL cases and telehealth simulations. Student participants expressed enjoyment in using AL technology and found it reinforced motivation to keep learning. However, faculty participants found the AL platform to be difficult to navigate. The generational gap of faculty participants could have played a role in this discrepancy, as Chica and colleagues speak to this barrier in online nursing programs nationwide. Realism in the AL platform and cases was also appealing to participants, as has also been seen in many studies that utilized Association of Standardized Patient Educators best practices in the delivery of simulations using SPs. Participants reported prebriefing and debriefing of the simulation cases to be most helpful, as well as time outs during the simulations both on the SET-M scores and in their focus groups. Many simulation experts and researchers speak to the importance of prebriefing and debriefing as the most integral components of successful simulations. Prebriefing, an essential step in successfully implementing simulated experiences, was helpful in this study. Similarly, collected SET-M data that showed that prebriefing increased confidence and benefited learning related to telehealth simulations in a NP curriculum. By design, the AL platform used here worked as a quasi-prebriefing tool to better prepare participants for the simulation. As participants worked through the AL case study, they gained essential content necessary to succeed in the telehealth simulation. As evidenced by this study's participant response to the SET-M question indicating that prebriefing increased their confidence, one can assume both the AL platform and discussion with simulation faculty before the start of the simulation were useful. The time-out method utilized in the intraoperative environment to refocus clinicians' clinical judgment and patient safety can be useful in a telehealth simulation like the one used in this feasibility study.\nOUTPUT:" }, { "from": "agent", "value": "The case report does not provide information about a specific diagnosis." } ]

[ { "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: During anamnesis, the patient revealed that she had had a car accident 6 years ago, which was the cause of the fractures. However, the patient did not accept orthodontic treatment. Therefore, following endodontic treatment, fiber post-reinforced composite restorations were planned. An impression was taken, and a mock-up was fabricated on the patient's model. The mock-up was utilized to determine the limits of the predicted restorations. An impression was taken of the provisional restorations to serve as a reference guide for the permanent restorations. Two thirds of the root canal was prepared with a bur (RelyX Fiber Post Drill, 3M ESPE, GmbH Dental Products) to apply the fiber post. The root canal was air dried, and a self-adhesive resin cement (RelyX U200, 3M ESPE, GmbH Dental Products) and a suitable fiber post (RelyX Fiber Post, 3M ESPE, GmbH Dental Products) were applied to the cavity. Photopolymerization was achieved with a LED source (Hilux Ledmax 550, Benlioglu, Ankara, Turkey) (Figure 9). The excessive part of the fiber post was removed, and composite restorations (Filtek Ultimate dentin, body, and enamel, 3M ESPE, St. Paul, MN, ABD) were manipulated to achieve a precise fit. Finishing and polishing were performed with thin-grained burs and disks (Sof-Lex, 3M ESPE, GmbH Dental Products) (Figure 10).\nOUTPUT:" }, { "from": "agent", "value": "Fractured central incisors, Non-vital teeth, Asymmetry and malocclusion between the upper and lower jaws" } ]

[ { "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 patient was admitted to the emergency service with the complaints of a 7-day history of colic-style abdominal pain, nausea and biliary vomiting. The patient whose vital signs were stable at the time of admission was. In laboratory tests, C-reactive protein (CRP): increased as 10 mg / dl, the value of WBC (White blood count) was found as 16,000 mu/L high, and in biochemistry values glucose value was viewed as elevated by 414 mg/dL. There was no significant change in other tests. 1). The patient was taken to the surgical intensive care unit due to her advanced age and dehydration, also having additional disease. After hydration he was operated on the 2nd day of his hospitalization. The operation was performed openly due to the fact that the duration of anesthesia was wanted to be kept short. In the exploration, it was seen that the segment of jejunum which was 80 cm distant from the treitz ligament was totally obstructed with a limited mobile, large mass. Intestinal segment of the mass in the proximal was seen widely. After enterolithotomy, small bowel was repaired double transversely (Fig. 2). When exploration was continued, it was seen that gallbladder was edematous and also there was cholecystoduodenal fistula between gallbladder and duodenum. Cholecystectomy and fistula repair were left for the second session because of the edematous tissues. The operation was terminated by placing a drain into the abdomen. The operation lasted a total of 80 min. Antibiotic treatment was started to the patient before the operation and the treatment was completed in 48 h. The naso gastric catheter, which was inserted for aspiration and decompression, was withdrawn on the second post-operative day because the patient had gas outlet. At the postoperative 5th day, the abdomen drain was withdrawn from the patient who took diet of Regime 1 and tolerated. The patient was discharged with full recovery on the 6th post-operative day.\nOUTPUT:" }, { "from": "agent", "value": "Gallstone ileus" } ]

[ { "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 seven month old baby was referred because of feeding difficulties and failure to thrive since 3 months of age. There was history of bluish discolouration of the body while excessive crying. The antenatal history was unremarkable and the baby was delivered at term normally by a 22 year old primigravida. Physical examination revealed an active baby with weight of 5.5 Kgs, length of 63 cm, heart rate of 120 beats/min, blood pressure of 92/58 mm of Hg, respiratory rate of 40/min and systemic oxygen saturation was 85% at ambient room air. On musculoskeletal examination, left upper limb had foreshortened mid segment associated with flexion deformity at the elbow and wrist joints, rudimentary thumb and clinodactyly [Figure 1a]. Right upper limb had hypoplastic thumb, clinodactyly and flexion deformity of wrist [Figure 1a]. No obvious deformities were observed in lower limbs or elsewhere. Cardiovascular examination revealed ejection systolic murmur of grade III/VI at left parasternal area. Electrocardiogram [Figure 2] showed normal sinus rhythm with right ventricular hypertrophy with right axis deviation. Plain radiograph of both upper limbs revealed absent radius, underdeveloped ulna of left upper limb and absent first metacarpal, hypoplastic thumb pahalanges in both upper limbs [Figure 1b]. There was evidence of aorto-mitral discountinuity. It also revealed persistent left superior vena cava draining into dilated coronary sinus. Complete blood count was normal (no thrombocytopenia). Renal ultrasound and kidney function tests were normal. The baby underwent the complete intracardiac repair. On follow up the baby is thriving well and asymptomatic regarding his cardiac symptoms. He is being followed up in paediatric, cardiology and orthopedic clinics.\nOUTPUT:" }, { "from": "agent", "value": "Holt-oram syndrome, Double outlet right ventricle" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: He was started on prednisolone, which led to an improvement in his renal function with his serum creatinine falling to 160 mmol/L. He was maintained on 5 mg of prednisolone. He re-presented 1 year later with headache, blurred vision and hypercalcaemia. An MRI brain showed a 9 mm lesion in the frontal lobe, which was consistent with a granuloma. The dose of prednisolone was increased to 40 mg and azathioprine 150 mg was added. A repeat scan showed no enhancement of the frontal lobe lesion. In search of other organ involvement, a high resolution CT of the lungs, lungs function tests and cardiac MRI were done, all of which were normal. His renal function continued to deteriorate and a repeat renal biopsy showed a globally scarred kidney. He progressed to end-stage renal failure and was started on haemodialysis at the age of 21 years. He received a heart-beating deceased donor kidney the same year and was given standard immunosuppression with cyclosporin, mycophenolate mofetil (MMF) and prednisolone with no induction. He had stable graft function (serum creatinine ~100 mmol/L) for 4 months when his serum creatinine climbed to 160 mmol/L. The transplant biopsy was negative for C4d staining and no donor-specific antigens were detected in the patient's serum. There was no evidence of infectious causes of granulomatous disease. He was pulsed with methylprednisolone (500 mg) and the subsequent dose of prednisolone was increased to 20 mg. The serum creatinine fell to 139 mmol/L. Due to lack of further improvement in renal function, a biopsy was repeated 2 months later (Figure 2).\nOUTPUT:" }, { "from": "agent", "value": "Sarcoidosis" } ]

[ { "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 3-year-old boy was born to healthy nonconsanguineous parents at 37 weeks of gestation. He was born with a birth weight of 2,494 g (33.2 percentile), a head circumference of 34 cm (84.0 percentile), a length of 44.5 cm (10.9 percentile), and a chest circumference of 28 cm. The Apgar score was 8 at 1 min. The patient was the only child of his parents, and he had no family history. He was born with a congenital omphalocele, which was immediately repaired after birth. Moreover, congenital iris coloboma, astigmatism, and exotropia were diagnosed, and the patient underwent regular check-ups with a pediatric ophthalmologist. Additionally, shortening of the lingual frenulum and upper labial frenulum was observed. The patient was referred to our hospital for genetic testing. An array-based comparative genomic hybridization analysis was performed after obtaining written informed consent from the parents. The deletions encompassed ENPEP, PANCR, PITX2, MIR297, FAM241A, AP1AR, TIFA, ALPK1, NEUROG2, LOC105377372, ZGRF1, LARP7, MIR302CHG, MIR367, MIR302D, MIR302A, MIR302C, MIR302B, and ANK2.\nOUTPUT:" }, { "from": "agent", "value": "4q25 Microdeletion, Axenfeld-Rieger Syndrome, Developmental Delay" } ]

[ { "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: Two siblings, a 13-year-old girl (case 1, Figures 1(a)-1(d)) and a 10-year-old boy (case 2, Figures 2(a)-2(d)) of normal intelligence had come to Chettinad Dental College and Research Institute, Chennai, with a complaint of decayed teeth. The physical appearances were similar, characterized by short stature, short neck, protuberant chest, scoliosis, and a waddling gait. Their facial feature presented frontal bossing and flat nasal bridge. The history revealed that the patients had pain in the hip region on walking that subsides at rest. The parents did not belong to different ethnicity. They had a nonconsanguineous marriage and a family history free from any skeletal disorder. On oral examination, exposed teeth with sharp cusps and rough enamel texture were found (Figures 1(a), 1(b), 2(a), and 2(b)). The orthopantomograph showed thin hypoplastic enamel of normal radiodensity (Figures 1(c) and 2(c)). A multispecialty approach was adopted and medical examination of all major systems revealed no dysfunctional changes. However, the orthopedic and radiographic evaluation indicated gross skeletal deformity. The hand-wrist radiograph showed proximally narrow metacarpals. The anteroposterior view of the spine expressed curvature of the thoracolumbar vertebral segment. The lateral spinal view revealed anterior beaking of the vertebral body (Figure 1(d)). The pelvic view radiograph revealed an irregularly outlined square-shaped head of the femur and coxa valga defect (Figure 2(d)). The diagnosis would need to be confirmed by analysis of GALNS enzyme activity and molecular genetic testing of GALNS gene. Unfortunately, parents' consent could not be obtained for this analysis.\nOUTPUT:" }, { "from": "agent", "value": "Morquio's Syndrome, mucopolysaccharidosis type IVA" } ]

[ { "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 male presented with yellow discoloration of his eyes and urine over for one month; his medical history was notable for HIV infection that was diagnosed 8 years ago. At the time of admission, he had been on antiretroviral therapy treatment for 8 years. The ART regimen consisted of Zidovudine (AZT), Lamivudine (3TC), and Nevirapine (NVP) (Cipla) a single tablet combination; however, 5 months prior to this presentation, his regimen was changed to Tenofovir Disoproxil Fumarate 300 mg (TDF), Lamivudine 300 mg, and Efavirenz 600 mg in a single pill combination tablet (TELURA, Mylan) (TDF, 3TC, and EFV) in May 2016. The CD4 count was 667 cells per mm3 and his viral load was below level of detection at less than 40 copies per millimeter of blood (<40 copies/ml). He had no history of drinking alcohol or use traditional herbal remedies. The physical examination was notable for presence of jaundice, confusion, and excessive somnolence with presence of a hepatic flap. Tests for HBsAg, anti-HCV, anti-HAV IgM, CMV IgM, and EBV, antinuclear antibody (ANA), antimitochondrial antibody (AMA), and anti-smooth muscle antibody (ASMA) were negative. Abdominal ultrasound examination of the liver was normal. His liver function showed marked transaminitis as shown in Table 1. Liver biopsy was done which showed portal tracts with moderately heavy mixed inflammatory cell infiltrates of neutrophils, eosinophils, and lymphocytes. There were no plasma cells. The histological picture was in favor of drug-induced hepatitis. His ART medications were stopped; however, his clinical course was characterized by recurrent episodes of hepatic encephalopathy without much improvement despite treatment with lactulose, metronidazole, and mannitol. His ALT was 339 U/L (normal range 13-40 U/L) at 1 month.\nOUTPUT:" }, { "from": "agent", "value": "Acute Liver Failure" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Samples from these family members were referred to our laboratory for further investigations (Fig. 1). The parents (G106 and G107) were consanguineous and came from the southeast of Iran (Sistan and Baluchestan province) near the Persian Gulf and Oman Sea. At birth, their first affected child (G101) was noted to have anemia, an enlarged spleen and thrombocytopenia. The preliminary workup did not lead to a diagnosis, and the spleen was removed to improve the low platelet count. The second and third children born subsequently (G102 and G103) developed the same symptoms (Table 1). Enzyme replacement therapy (ERT) with recombinant glucocerebrosidase (Imiglurcerase) was begun on the three children, resulting in an improvement of clinical symptoms. In subsequent years, the parents gave birth to two additional children (G104, G105). At age three, anemia was also noted in each of these children. Enzymatic activity was measured in another laboratory in the Middle East and was reported to be deficient, and the two younger children were also begun on ERT. However, in these two, no clinical improvement was noted on treatment, and the cases were referred to us for further investigation. At this point, peripheral blood samples were obtained from all five children and their parents with informed consent. DNA was extracted using a standard method and was shipped to the National Institutes of Health for genotyping. Sequencing of the all exons and flanking intronic regions of the glucocerebrosidase gene (GBA) was performed on the seven genomic DNA samples using a 3130 Genetic Analyzer (Applied Biosystems, Foster City, CA) as previously described. The data was analyzed using Sequencing Analysis v.5.1.1 and SeqScape v.2.1.1 (Applied Biosystems, Foster City, CA). Additionally, the intronic regions of GBA, known to have a high prevalence of polymorphisms, were sequenced to confirm the amplification of both alleles.\nOUTPUT:" }, { "from": "agent", "value": "Gaucher disease, α-thalassemia" } ]

[ { "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 underwent minimally invasive bovine pericardial patch closure of the secundum ASD through a right thoracotomy incision. Post-operatively, there was a moderate left-sided pleural effusion which was drained by thoracentesis. Her vital signs were within normal limits. Physical examination was significant for a thoracotomy incision that was healing well and mild bilateral lower extremity edema. A transthoracic echocardiogram (TTE) obtained 2 days post-operatively again demonstrated the high-velocity jet entering the right atrium (Figure 2), as well as a nonobstructive echodensity in the IVC just proximal to the right atrial junction. Further imaging was performed. The patient initially presented to the cardiology clinic for evaluation of syncope, which was believed to be vasovagal in origin. However, she was noted to have fixed splitting of the second heart sound on physical examination. Electrocardiography showed first-degree atrioventricular block and incomplete right bundle branch block. Cardiac magnetic resonance (CMR) imaging confirmed a large secundum ASD measuring 2.4 x 2.3 cm with left-to-right shunting and pulmonary/systemic flow ratio (Qp:Qs) of 2.3. The CMR also showed moderate-to-severely dilated right ventricle without hypertrophy and unobstructed right ventricular outflow tract, main pulmonary artery, and branch pulmonary arteries. Normal pulmonary and systematic venous connections were noted. Due to evidence of right heart enlargement, she was referred for ASD closure. Computed tomography (CT) angiography of the heart was performed, which confirmed the CMR findings and demonstrated deficient rims for percutaneous device closure, and therefore, surgical ASD closure was planned.\nOUTPUT:" }, { "from": "agent", "value": "Inferior Vena Cava Obstruction, Secundum Atrial Septal Defect" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: After a single round of CPR, central pulses were palpable with a heart rate (HR) of 88. Compressions were discontinued and a cardiac POCUS was performed. Parasternal long axis, parasternal short axis, sub-xiphoid 4 chamber, and sub-xiphoid short axis views were obtained using a phased array probe in a pediatric cardiac preset. Additionally, an inferior vena cava (IVC) view was obtained using a curvilinear probe in EM convention. The POCUS revealed a collapsed IVC (Figure 1, Supplemental Video S1), normal cardiac function, and an absence of a pericardial effusion. While performing the subxiphoid short axis evaluation, with volume resuscitation ongoing via infusion of normal saline through the IO line by means of premeasured 10 milliliter syringes, bubbles were serendipitously appreciated within the right heart (Figure 2, Supplemental Videos S2, S3). The presence of bubbles within the right heart moments after the saline was infused helped to confirm the proper placement and functioning of the patients tibial IO line. As volume resuscitation continued the patient began to exhibit a weak cry and spontaneous movements. After a prolonged hospitalization in the Pediatric Intensive Care Unit, complicated by disseminated intravascular coagulation (DIC), the patient was ultimately discharged home.\nOUTPUT:" }, { "from": "agent", "value": "Hypovolemic shock, Tumor necrosis factor receptor associated factor 3 deficiency leading to a systemic inflammatory syndrome" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: At the age of 5 days, the baby underwent a right thoracotomy. The anomalous communication from the carina to the medial liver dome was identified by direct visualization. The fistula was subsequently opened just below the carina, and the airway was closed with interrupted sutures. The distal portion of the fistula was also explored to below the diaphragm and resected. At the liver dome level, the residual portion of the fistula was closed in a similar fashion. Histological examination of the resected specimen of fistula showed submucosal glands and fibrous soft tissue with fragments of benign cartilage (Fig. 1). Followup CT scan of the abdomen and pelvis, including inferior portion of the chest (parameters: 1.2 mm collimation, 120 kVp, 47 mAs; CT dose index 3.19 mGy; 6 ml of Omnipaque 300 mgI/ml), was performed one month after the surgery. A fluid-filled tubular structure was seen, extending from the cystic structure at the mediastinal base through the esophageal hiatus and into the liver (Fig. 2). This finding was consistent with a residual fistulous tract with cystic dilatation of the proximal stump in the mediastinal base.\nOUTPUT:" }, { "from": "agent", "value": "Congenital tracheobiliary fistula, Hypoplastic common hepatic duct, Biliary atresia" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 20-year-old male presented to the emergency department following increasing lethargy and emesis over a twelve hour period. At presentation, the patient's Glasgow coma scale score was 6. Arterial blood gas demonstrated a pH of 6.96, pCO2 25 mm Hg, pO2 225 mm Hg and HCO3 5 mmol/L. The serum osmolality was 337 mmol/L and the osmolality gap was markedly elevated at 32 mmol/L. Microscopic examination of the urine demonstrated cigar and envelope shaped crystals characteristic of calcium oxalate crystals (Figure 1). The patient was transferred to the intensive care unit for mechanical respiratory support, fluid management, and hemodialysis. Arterial blood gases were monitored from initial presentation through normalization. pO2 levels ranged from 225 mm Hg (elevated due to supplemental oxygen administration as part of resuscitation) to 84 mm Hg (normal at 36 hours into management). No hypoxic or anoxic periods were demonstrated during hospitalization. Due to clinical concern for seizure activity, head computed tomography (CT) was performed which showed diffuse hypodensity within the bilateral basal ganglia and thalami with loss of differentiation with the subjacent white matter, compatible with edema (Figure 2). For further evaluation, magnetic resonance imaging (MRI) was performed (day one of hospitalization) which demonstrated increased signal intensity on T2 and fluid attenuation inversion recovery (FLAIR) sequences within the basal ganglia, thalami, amygdala, hippocampus, and brainstem bilaterally (Figure 3). There was restricted diffusion within the white matter tracks of the corona radiata bilaterally (Figure 4) on diffusion weighted (DWI) and apparent diffusion coefficient (ADC) imaging. On completion of the medical treatment seven days later, the patient's minimental status exam was normal with a score of 27. As the patient's symptoms had resolved, no further imaging was clinically indicated.\nOUTPUT:" }, { "from": "agent", "value": "Ethylene Glycol Toxicity" } ]

[ { "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: Past medical history included gender incongruence for which the patient had been receiving weekly testosterone injection therapy for one year prior to presentation. Gynecological history was unremarkable and menses had stopped approximately one month into gender-affirming therapy. Home medications included intramuscular testosterone enanthate 100 mg weekly, multivitamin, and vitamin D supplement. He had never smoked and denied alcohol or illicit drug use. On physical exam, the patient was a well-appearing male with moderate growth of facial hair. Cardiac, pulmonary, abdominal, neurologic, and musculoskeletal exam were all unremarkable. His lab values included total testosterone ranging over the year from 544 to 970 ng/dL (reference range for men: 270-1,734), hemoglobin and hematocrit of 15.1 g/dL (reference range for men: 12.5-16.3) and 44.2% (reference range for men: 36.7-47.0), and normal hepatic function panel.\nOUTPUT:" }, { "from": "agent", "value": "Breast Cancer" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 7-year-old girl presented to our hospital with fever and tender right cervical lymphadenopathy of 20-day duration. She underwent surgery for Pierre-Robin syndrome when she was 2 years old. She was noted to have a tender right cervical lymphadenopathy of >2 cm in diameter without hepatosplenomegaly. On admission, her CRP level was normal. The complete blood count revealed a WBC count of 4,410 cells/mm3 and an ESR of 92 mm/h. EBV, CMV, and HBV serum tests were negative. An excisional cervical lymph node biopsy was performed, which showed paracortical hyperplasia accompanied by a large number of immunoblastic macrocells revealing KFD. The patient was treated with NSAIDs. After 14 days, her fever resolved with regression of the noted lymphadenopathy. The inflammatory markers remain elevated. The patient was discharged with naproxen, hydroxychloroquine, and a tapering dose of prednisone. Four months later, she had a 30-day history of rapidly progressive hyposthenia, ataxic gait, and urinary retention. The patient was brought to our emergency department due to status epilepticus, which presented as generalized tonic-clonic seizures with unconsciousness, lock-jaw, and blank stare. Oxygen support was provided, and intravenous diazepam and midazolam were administered. Physical and neurological examinations revealed hyperextension of the limbs. No other abnormalities were noted. Head computed tomography on admission revealed decreased white matter density. CSF analysis revealed an elevated number of cells (42/mm3, 82% lymphocytes) and proteins (22.7 mg/dL). The CSF sample was submitted for bacteriologic and viral examination and evaluated with serological and pathological tests. Growth was not observed in the non-specific or mycotic cultures of the CSF sample. IVIG (1 g/kg) and an intravenous bolus dose of methylprednisolone (360 mg/d for 3 days) were administered. Plasma exchange was performed two times. After 4 weeks of treatment, the child was still unable to speak or sit without support. MRI findings showed remaining symmetrical abnormal signals in the bilateral basal ganglia with no apparent changes. The prognosis was poor.\nOUTPUT:" }, { "from": "agent", "value": "Kikuchi-Fujimoto Disease, Encephalopathy" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 60 year old male with idiopathic PAH and morbid obesity (BMI of 40 kg/m2) was using tadalafil 40 mg daily and selexipag 1200 mcg twice daily. Due to nasal congestion, he could not tolerate endothelin receptor antagonists or higher selexipag dosing. He was on stable doses of torsemide and spironolactone without clinical evidence of fluid retention. He had worsening dyspnea on exertion within NYHA Functional Class II. We recommended switching selexipag to oral treprostinil therapy with hospitalization and an IV treprostinil bridge as above. Because of the COVID-19 pandemic, the patient declined admission. He took his last dose of selexipag the evening prior, and the following morning he started treprostinil 0.75 mg every 8 hours. On careful phone follow-up, he denied worsening breathlessness, lightheadedness, presyncope, chest pain, or edema. He was able to titrate up by 0.125 mg every 72 hours until 1.75 mg but stopped further titration because he experienced prostacyclin side effects including flushing and nasal congestion. He reported clear symptom improvement within FC II. His 6MWT increased by 67 m, and his Reveal 2.0 risk score fell to 5. At 6 month follow up, his echocardiogram showed a mildly enlarged right ventricle with preserved systolic function and minimal septal dyskinesis (Table 1).\nOUTPUT:" }, { "from": "agent", "value": "Pulmonary Artery Hypertension" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: No vomiting or changes in bowel movements. Laboratory studies showed WBC 16,000/muL (normal, 4500-11,000/microL), platelets 165,000/muL (normal, 150,000-450,000/microL), creatinine 1.75 mg/dL (normal, 0.6-1.3 mg/dL), blood urea nitrogen 25 mg/dL (normal, 7-18 mg/dL), glucose 135 mg/dL, calcium 9 mg/dL, albumin 3.6 g/dL (normal, 3.5-5 g/dL), alkaline phosphatase 143 U/L (normal, 50-136 U/L), total bilirubin 3.3 mg/dL (normal, 0.3-1.2 mg/dL), aspartate aminotransferase 205 U/L (normal, 10-30 U/L), alanine aminotransferase 99 U/L (normal, 10-40 U/L), lipase 12,883 U/L (normal, 31-210 U/L), amylase 1996 U/L (normal, 25-115 U/L), serum triglyceride, and serum calcium were within normal limits. Abdominal ultrasound showed mildly distended gallbladder with no gallstones.\nOUTPUT:" }, { "from": "agent", "value": "Gastrostomy tube migration, Acute pancreatitis" } ]

[ { "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 symptoms progressed rapidly over past 4days. Physical examination revealed tachypnea (RR- 40cycles/min), tachycardia (PR-108bps), blood pressure of 120/80 mmHg, temperature 101F and SpO2 was 60% in room air. Chest auscultation revealed bilateral coarse crepetations and scattered ronchi. His laboratory investigations showed Leucocytosis(TC- 13000 cells/cumm) with 81% neutrophils, serum creatinine of 1.3mg/dl and normal liver enzymes (Table 1). His arterial blood gases revealed hypoxia (pH- 7.36, pO2-64 with Fio2 80%, pCo2-36.9 and HCO3- 21.1). After a provisional diagnosis of CAP he was started on broad spectrum antibiotics. A chest radiograph at the time of admission revealed dense consolidation involving both the lungs (Fig. 1). The patient deteriorated over next 24hrs with new onset hypotension, hematuria, worsening of symptoms, saturation and laboratory values (Table 1). His sputum and blood culture reports were negative, non-reactive HIV status, CRP was normal and 2D-Echo revealed normal LV function with LVEF of 60%. The patient tested negative for CTD and vasculitis screening (negative ANA and ANCA reflux tests). HRCT thorax revealed bilateral interstitial and alveolar infiltrates with consolidation and ground glass opacities (Fig. 2).\nOUTPUT:" }, { "from": "agent", "value": "Retinoic acid syndrome, Psoriasis" } ]

[ { "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 6-year-old, African American male with a past medical history (PMH) significant for difficult-to-control moderate persistent asthma, eczema, seasonal allergies, and learning delays presented to his primary care physician for evaluation of chronic cough and persistent, thick, nasal discharge. He lacked fevers, facial pain, and otalgia. His cough was productive and limited his activity due to exertional fatigue and frequent interruptions due to breathlessness. Three months prior to presentation, his primary care physician (PCP) started him on a daily inhaled corticosteroid for asthma, without improvement in his cough. His nasal discharge did not improve following a course of amoxicillin-clavulanic acid therapy. Additional PMH was significant for three prior episodes of pneumonia requiring hospitalization for intravenous antibiotic therapy at 7 months, 2 and 4 years of age. He had a history of six sinus infections, which occurred independently of his episodes of pneumonia, that were each treated with antibiotics without improvement. Five months prior to his presentation, he was diagnosed with a disseminated varicella-zoster viral rash that crossed dermatomes which required treatment with antiviral therapy. Due to his learning delays, he was enrolled in a special education program at school and received at home speech therapy twice weekly. On physical exam, he was afebrile and normotensive with a heart rate of 115 beats per minute, a respiratory rate of 20 breaths per minute, and pulse oximeter 100% on room air. His weight was 20.5 kilograms (CDC, 20.93%, Z = -0.81), his height was 111 cm (CDC, 2.62%, Z = -1.94), and his body mass index was 16.64 kg/m2 (75.74%, Z = 0.70). On exam, he had thick, green nasal secretions and bilateral, painless, mobile, cervical lymphadenopathy. He was breathing comfortably and had clear breath sounds. He had no hepatosplenomegaly. He had a healed dermatomal rash along the right lower trunk that crossed midline. He had speech delay with phonological and receptive language disorders. His cranial nerves were grossly intact. He had normal strength, tone, reflexes, and gait. Initial laboratory and imaging studies are reported in Table 1 and Figure 1, respectively. He was admitted to the hospital for further evaluation.\nOUTPUT:" }, { "from": "agent", "value": "Perinatal human immunodeficiency virus infection" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 42-year-old woman complaining of transient blindness in her left eye was referred to our hospital. The patient had a history of SLE and central retinal artery occlusion in her right eye that occurred at the age of 33 years. On initial examination, she had a best-corrected visual acuity of 1.2 in the left eye and no light perception in the right eye. Ocular pressures and anterior segments were normal (fig. 1a, e). Fundus examination showed no specific retinochoroidal abnormalities with the exception of optic disc atrophy due to central retinal artery occlusion in her right eye (fig. 1b) and a peripapillary small hemorrhage in her left eye (fig. 1f). Fluorescein angiography revealed no dye leakage and pooling (fig. 1c, g). However, NIR (Heidelberg Retina Angiograph 2, Heidelberg Engineering, Heidelberg, Germany) showed multiple bright patchy lesions in the choroid of the posterior pole and the mid-periphery of the fundus in both eyes (fig. 1d, h). OCT (RS-3000, NIDEK, Gamagori, Japan) images of these lesions revealed irregular, hyperreflective choroidal foci (fig. 2). Administration of oral steroids was continued and her laboratory values were as follows: hemoglobin 9.1 g/dl, hematocrit 29.3%, WBC count 6,900/mm3 and platelet count 223,000/mm3. No atypical cells were found during a peripheral blood smear. C-reactive protein was 0.97 mg/dl (normal <0.06 mg/dl). Hepatic and renal function tests and electrolytes were within normal limits. Urinalysis was normal. C3 and C4 complement fractions were 64 and 11 mg/dl, respectively (normal values are 86-160 and 17-45 mg/dl, respectively). Anti-double-stranded DNA antibody was 125.1 IU/ml (normal <12.0 IU/ml). Cranial magnetic resonance imaging findings were unremarkable.\nOUTPUT:" }, { "from": "agent", "value": "Systemic lupus erythematosus" } ]

[ { "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 female with a 2-year history of dermatomyositis was referred to our facility for refractory disease. Over the prior 2 years, she experienced multiple disease exacerbations. Treatment included methotrexate, mycophenolate mofetil, rituximab, intravenous immunoglobulin, and high-dose corticosteroids with no significant improvement. Within several months of her diagnosis, her ability to complete basic activities of daily living declined to the point that she required gastrostomy tube placement due to dysphagia and became wheelchair bound. One month prior to this hospitalization, she was diagnosed with splenic vein thrombosis. Physical examination revealed a diffuse macular rash on her torso and extremities. She was profoundly weak on muscle testing in all 4 extremities. Anasarca was also evident. She underwent colonoscopy to evaluate abdominal pain and fecal occult blood. Colonoscopy revealed ischemic colitis. Subsequent biopsies detected cytomegalovirus. Laboratory studies are presented in Table 3. Of note, ferritin and soluble interleukin-2 receptor levels were significantly elevated. She also had profound pancytopenia. Workup for malignancy was negative. Peripheral smear showed pancytopenia as well as schistocytes suggestive of microangiopathy. Given the severity of her illness and poor prognosis, her family asked for palliative care only. She passed away several minutes after being compassionately extubated. The patient had an HScore of 235 suggesting a 98% to 99% likelihood of hemophagocytic syndrome and a disseminated intravascular coagulation (DIC) score of 10 indicating overt DIC. She was thus diagnosed with MAS in the setting of both rheumatic disease and severe infection.\nOUTPUT:" }, { "from": "agent", "value": "Macrophage Activation Syndrome" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Patient A; This is a 40-year-old male patient who came with a non-productive cough for one month and a three-month history of unquantified but significant weight loss. He also had a history of losing his appetite. On initial presentation, he appeared to be chronically ill, and all of his vital signs were within normal limits. The man weighed 52 kilograms and stood 1.74 meters tall, with a BMI of 17.2 kilograms per square meter, indicating that he was underweight. The lymphoglandular system revealed 3 by 4 cm enlarged masses that were mobile, had no overlying skin color change, and were tender in the cervical areas bilaterally, as well as 2 by 3 cm enlarged masses that were soft in consistency, mobile, had no overlying skin color change, and were non-tender on the submental areas. Other findings in the abdomen were a palpable mass in the right upper quadrant, about 5 cm below the right costal border, indicating hepatomegaly, and a soft mass along the line of spleen expansion, suggesting splenomegaly. He was then probed for a possible TB diagnosis, despite the fact that all of the standard TB diagnostic tests were negative. A FNAC biopsy revealed bilateral cervical and submental lymphadenopathies, with a tuberculous abscess as the most likely diagnosis. He was then tested for retrovirus infection and was found to be positive. The CD4 cell count was 14 cells per millimeter squared. He is now on his 7th month and is apparently healthy, and taking his medication regularly. His weight also increased to 63 kilograms, with a BMI of 20.8, which is normal. The viral load was done 2 weeks back, and it was 800 copies, which is below the threshold for viral transmission (greater than 1000 copies).\nOUTPUT:" }, { "from": "agent", "value": "Active Tuberculosis, Human Immuno Deficiency Virus (HIV)" } ]

[ { "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 61-year-old male presented with a 2-year history of progressive distal weakness of the lower limbs. His medical and social history were uninformative. Neurological examination of the patient revealed moderate weakness in both lower limbs with hypotrophy, whereas the upper limb and bulbar function were initially spared. Widespread fasciculations involved all four limbs. Deep tendon reflexes were brisk in all limbs, more pronounced on the left side, and without spasticity. Interestingly, MRI revealed UMN involvement as hypointensity along the bilateral motor cortex on T2-weighted images (Figures 1C, D), with a reduction in the fractional anisotropy (FA) values of the pyramidal bundle in tractography acquisitions. Reduced amplitudes with normal latencies and central motor conduction times were observed in the lower limbs, as measured by transcranial MEPs. Extensive neuropsychological testing revealed normal cognitive profiles. One year later, the weakness had spread to the upper limbs, and NIV was initiated to support respiratory function (Figure 1A). The patient remains alive 48 months after the onset of symptoms. He currently demonstrates weakness in four limbs with predominant LMN signs, respiratory impairment (FVC 25%) without bulbar involvement, and is undergoing treatment with intrathecal Tofersen (early access program).\nOUTPUT:" }, { "from": "agent", "value": "ALS" } ]

[ { "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 33-year-old French-Canadian male was referred for reevaluation of chronic lymphadenopathy and splenomegaly since the age of 4, when he had been diagnosed with \"chronic EBV illness\" based on serology. He had no history of unexplained fever, liver dysfunction, cytopenia, mosquito bite reactions, or hydroa vacciniforme, features that would suggest the nosologic entity \"chronic active EBV.\" Based on elevated serum vitamin B12 level, polyclonal hypergammaglobulinemia and 15% DNTC, the diagnosis of ALPS was confirmed by identification of a heterozygous c.784A>T mutation in TNFRSF6, resulting in p.I262F mutation in the intracellular death domain of FAS (GeneDx). Initial whole blood EBV VL was 0 copies/mL. At 1-year followup, he was noted to have asymptomatic EBV viremia (Figure 1). Serial monitoring of the viral load demonstrated an initial decline and then progressive increase in EBV viremia followed by worsening lymphadenopathy, without constitutional symptoms. PET-CT demonstrated nodal foci with significantly increased metabolic activity.\nOUTPUT:" }, { "from": "agent", "value": "Autoimmune Lymphoproliferative Syndrome, Epstein-Barr Virus-Associated Lymphoma, follicular lymphoma, diffuse large B-cell lymphoma, classical HL" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: On arrival at the hospital, the attending clinician screened the case-patient and diagnosed pneumonia and malaria, and recommended admission. The case patient was admitted to a hospital and treated for malaria and pneumonia. An ambulance was dispatched to transfer the case patient to KGH, but the case patient died before the ambulance arrived. Record review and active case search: the investigation revealed that no suspected cases were found in the general registers, case base forms, rumor logbook, and district database. Additionally, no suspected cases were found in the community where the case patients were living. Contact tracing: eight contacts were listed for case-patient one, four HCWs, and four family members. Ten contacts were listed for case-patient two, four HCWs, and six family members. The case patients did not travel outside their village. Environmental assessment: the two case-patients lived in mud houses without paved floors. The households were in a wetland close to a garbage dumping site. Households were crowded and food was poorly stored. Rodent droppings and boreholes were observed in the homes of each case patient. The surrounding environment was untidy with rubbish scattered around their houses. Rodent trapping: twenty-two traps were set using Sharman trap and bait. One trap was placed in each case patient s residence and ten neighboring houses. We observed rodent droppings in both case patients homes while rodent boreholes were found only in the case-patient one s residence.\nOUTPUT:" }, { "from": "agent", "value": "Lassa fever" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 50-year-old white male physician, born and raised in Rio de Janeiro, was referred to our Dermatology Department for skin cancer screening. On physical examination, we observed a 3 cm blackened macula with an irregular border and more than one color on the right calf (Figure 1). The patient told us that the lesion had appeared 10 years ago, showing progressive growth in recent months. He had a positive family history of melanoma. Dermoscopic examination showed a peripheral atypical pigmented network structure (more marked on the right of the lesion), brownish streaks in the central area and in the right periphery, a peripheral area with a black blotch and some globular structures, an amorphous area with a pseudofollicular opening and pseudocysts on the left of the lesion, beyond the veil in the center of the lesion (Figures 2 e 3). As the lesion had some clinical aspects of seborrheic keratosis and the more suspicious dermoscopic findings were restricted to only a part of the lesion, we chose to perform an incisional biopsy (punch 4) in this area (with streaks). Histological examination showed confluent atypical melanocytes, occupying part of the epidermis and extending into the superficial dermis, several mitotic figures, and an inflammatory reaction in the dermis. The lesion was then removed with a 1 cm margin, and the wound was left to heal by secondary intention. The histological examination of this surgical specimen just showed a residual inflammatory reaction. There were no other melanoma features. The area of the blotch seen on the dermoscopy was histologically related to acanthosis, papilomatosis, and extensive deposition of melanin pigment in the dermis (consistent with partial regression phenomenon) (Figure 5). Thus, we found that the portion of the malignant lesion had been excised with incisional biopsy guided by dermoscopy.\nOUTPUT:" }, { "from": "agent", "value": "Superficial spreading melanoma" } ]

[ { "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 team was contacted by her daughter reporting the patient being suspicious and refusing to take her long-acting injectable antipsychotic that she had last received a few weeks before the earthquake. There was also a lack of information about when the next injection would be received, as there was no communication with her treating psychiatrist. The patient refused to be seen by an EMS team but agreed to meet with members of the CMHT in Petrinja's community health center. During the visit, the patient confided to the team members about her paranoid beliefs. She also complained about pelvic discomfort and vaginal bleeding. Because of the high risk of further illness progression due to medication non-adherence and the lack of support system, all possibly resulting in deterioration of psychic and somatic health, the team indicated a further diagnostic evaluation and treatment, so the patient was transferred to Dr. Ivan Barbot hospital. She was prescribed with haloperidol 7 mg/daily, promazine 25 mg/daily, and biperiden 2 mg/daily upon which her psychotic symptoms diminished. Until the beginning of August 2021, she continued to experience stability in her psychiatric state.\nOUTPUT:" }, { "from": "agent", "value": "Residual schizophrenia, bacterial pneumonia, and cervical polyps" } ]

[ { "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 woman presented to the emergency department with sudden-onset right side chest pain. Physical examination revealed diminished breathing sound in the right chest. Her vital signs were stable, and no respiratory distress was noted. Five months before this event, she visited our outpatient clinic for bilateral heel pain; ankylosing spondylitis was suspected at that time, but examinations showed no sacroiliitis or other evidence of the disease, and she received symptomatic treatment only. However, the symptoms did not resolve. In addition, consolidations and reticular opacities involving the pleural and subpleural regions indicating fibrosis at bilateral upper and middle lung zones were noted (Figure 1(b) and (c)). She was admitted to our hospital for surgical intervention. Eleven days after symptom onset, she received video-assisted thoracoscopic surgery (VATS). During the surgery, multiple blebs and consolidated areas in right upper, middle and lower lobes were noted. The lesions were wedge-biopsied, and mechanical pleurodesis was performed. The patient recovered well after the surgery. Three lung wedge biopsies were received for examination. No obvious blebs were seen on the pleura surface, but the pleura appeared thickened, and the parenchyma immediately below the pleura was consolidated. Microscopically, small blebs and foci of intrapleural hemorrhage were seen in all three wedges. Fibrosis of the visceral pleura was noted in the specimens from all three lobes, more significant in the upper lobe (Figure 2(a) -(c)). Prominent, homogenous subpleural fibrosis was also noted, while the alveolar parenchyma away from the pleura appeared relatively normal. There were a few lymphocytic aggregates in the fibrotic zone, while no fibroblastic focus was observed. Elastic Van Gieson (EVG) stain was performed and showed a pattern of alveolar septal elastosis with intra-alveolar fibrosis (Figure 2(d)). These findings established the diagnosis of PPFE.\nOUTPUT:" }, { "from": "agent", "value": "Pleuroparenchymal fibroelastosis, Pneumothorax" } ]

[ { "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 Caucasian female, with a history of depression and breast fibroadenoma status postresection, presented to the hospital with a one-month history of fatigue, impaired concentration, and remitting slurred speech and right-sided facial droop. Three weeks prior to this admission, she came to the emergency department with the chief complaint of a \"hard time processing thoughts\" and had a normal neurologic examination. She was evaluated by computed tomography (CT) of the head and discharged home as the imaging study was unremarkable and symptoms were presumed to be anxiety related as they involved a strong psychiatric component. She subsequently developed slurred speech and facial droop. On physical examination, her heart rate was 88/min, blood pressure was 139/93, respiratory rate was 15/min, temperature was 98 degrees Fahrenheit, and pulse oxygenation was 96% on room air. On mental status exam, she displayed anxiety regarding her condition. On neurological examination, she had word-finding difficulty and difficulty in repetition; however, her comprehension was intact. She also had a right-sided central facial droop of the upper motor neuron type. Her muscle strength was normal, and sensation was intact in all extremities. Magnetic resonance angiogram (MRA) of the head and neck demonstrated stenosis of the origin of the left middle and anterior cerebral arteries with thrombosis of the former (Figure 1). Cerebral angiogram (CTA) showed high-grade stenosis of the origin of the left middle cerebral artery with associated delayed filling in that territory. A neurologist was consulted, and he started her on aspirin, clopidegrol, and statin. She remained neurologically stable during the hospital course and was discharged with outpatient neurosurgery follow-up. She eventually underwent a direct and indirect bypass of the abnormal cerebral vasculature. She also had rehabilitation for her physical symptoms and had significant clinical improvement on follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Moyamoya Syndrome, Subacute Stroke" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The patient had a history of partial gastrectomy with Billroth II reconstruction due to multiple gastric ulcers 27 years previously, and liver cirrhosis (Child A) of more than 15 years' standing due to a period of alcoholism as well as local breast cancer in 2003. For treatment of portal hypertension and recurrent ascites, she was being treated with propranolol, furosemide and spironolactone. A fasting blood sample taken the morning after admission produced the following results: elevated liver transaminases (GGT 242 U/l [<38], AST 49 U/l [<30]), but unimpaired liver function. Blood count and other parameters were within normal limits. Standardized x-ray of the spine showed hyperkyphosis but no fractures.\nOUTPUT:" }, { "from": "agent", "value": "Vitamin D deficiency, Osteoporosis" } ]

[ { "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 thirteen-year-old female Congolese patient, born in August 2000 and living in Belgium since the age of four, was referred to the Stomatology and Maxillofacial Surgery Department, in January 2014, for swelling of the floor of the mouth associated with a submandibular mass. Both appeared a few days previous, along with dysphagia. The patient had no other symptoms. The patient was in good health, height and weight were in the normal percentile range, and she presented no medical history, nor allergies. The clinical examination showed a soft painless blue swelling of the left side floor of the mouth. Except for the left submandibular mass, no cervical lymphadenopathy was palpated. Medical imaging, including an ultrasound and magnetic resonance (Figure 2), was performed confirming the presence of a cystic lesion of 31 x 31 x 17 mm. The patient had 477 CD4 cells/mm and a viral load of 8310 copies/mL at the time of diagnosis. A marsupialization of the lesion was performed. Unfortunately, relapse of the lesion occurred three months later. The patient benefited from a resection of the cystic lesion and the sublingual gland. The anatomopathological examination of the 4.5 x 1.5 x 1 cm fragment revealed a seromucous salivary gland characterized by canals dilatation, containing mucin and a discreet chronic inflammatory infiltrate without lymphoid formation that could fit in a mucocoele context. The postoperative follow-up was uneventful. No recurrence of the lesion was observed since then. The last blood sample showed an undetectable viral load. The patient is currently treated with an integrase inhibitor.\nOUTPUT:" }, { "from": "agent", "value": "Ranula, HIV Infection" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 57-year-old male with type 2 diabetes mellitus, coronary artery disease (status postcoronary artery bypass grafting), and chronic kidney disease on dialysis for three years underwent a deceased donor transplantation. His immediate posttransplant period was uneventful, and at discharge, he had normal renal functions. He returned to hospital after 2 weeks with high-grade fever, chills, and allograft dysfunction. He was diagnosed to have allograft pyelonephritis. He was treated with 14 days of intravenous colistin with resolution of his clinical symptoms and allograft dysfunction. His second admission 10 days later was with back pain, and on evaluation, there was evidence of lumbar discitis in the MRI of the lumbar spine. A biopsy of the infected disc was noncontributory, and he was empirically started on ATT and carbapenems based on an infectious disease consult. During his follow-up, he complained of the presence of a new-onset subcutaneous maculonodular necrotic lesion on his abdominal wall (Figure 1). At this time, he had symptoms of abdominal discomfort after eating food. He had evidence of mild allograft dysfunction (creatinine: 2.2 mg/dl), low serum albumin (3.2 g/dl), normal calcium levels (8.10 mg/dl), slightly high phosphorus (5.6 mg/dl), high PTH (572 pg/ml), and normal vitamin D levels (33 ng/ml). His PTH level before transplant was 1029 pg/ml. An allograft biopsy was essentially normal with evidence of resolving pyelonephritis. The abdominal CT scan was noncontributory except for extensive calcification of the intra-abdominal vessels. The anterior abdominal wall vessels were also calcified (Figure 2). The biopsy showed extensive tissue necrosis and presence of nonseptate fungi (Figure 3). The culture isolate was identified as Rhizopus spp. (Figure 4). He underwent surgical debridement of the lesion and was treated with 6 weeks of liposomal amphotericin. On completion of therapy, his skin lesion had healed and allograft function was stable (serum creatinine: 1.5 mg/dl).\nOUTPUT:" }, { "from": "agent", "value": "Secondary Subcutaneous Rhizopus Infection, Calcific Uremic Arteriolopathy" } ]

[ { "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 female presented to our SSc clinic with diffuse cutaneous SSc and Raynaud's for 5 years with the onset of rapidly evolving skin thickening over 3 months and a modified Rodnan skin score (mRSS) of 13. Her oral aperture was normal. She had facial telangiectasia. No synovitis or tendon friction rubs were noted. She did not have digital ulcerations or pits but did have abnormal nailfold capillaroscopy. Her antinuclear antibody (ANA) was 1 : 160, but SSc-specific antibodies were negative. At presentation, her University of California Los Angeles Scleroderma Clinical Trials Consortium Gastrointestinal Questionnaire (GIT 2.0) was significant for severe scores for reflux and bloating. Normal upper third of esophagus, middle third of esophagus, and lower third of esophagus were described endoscopically. Biopsies from the stomach and duodenum had no features of Helicobacter pylori gastritis or celiac disease, respectively. She was treated with pneumatic dilatation, but she had not received any other treatment, including steroid, prior to presentation to SSc clinic. After her visit to SSc clinic, the patient was referred to an allergist, and she was diagnosed with allergies to peanuts, milk, chocolate, and wheat by radioallergosorbent test. She eliminated these foods from her diet and returned to SSc two months later. Her mRSS had increased to 15; otherwise her physical exam was unchanged. She reported fatigue and Raynaud's as significantly improved (despite no change in seasonal temperatures). Her GIT 2.0 improved from previously severe to now mild scores for reflux and bloating. Remarkably she had repeat endoscopy, which showed resolution of erythema with a report, which read as \"normal upper third of esophagus, middle third of esophagus, and lower third of esophagus and stomach\". Manometry studies were not done.\nOUTPUT:" }, { "from": "agent", "value": "Eosinophilic Esophagitis, Systemic Sclerosis" } ]

[ { "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 individual in their early 30s presented with fever, photophobia, meningismus and altered level of consciousness 10 days after experiencing a sudden severe headache. A cranial CT scan was negative for subarachnoid hemorrhage; however, a lumbar puncture revealed xanthochromia in the cerebrospinal fluid without evidence of meningitis. On examination the patient was somnolent but arousable with no focal deficits. The Glasgow Coma Scale score was 13. Catheter-based angiography confirmed severe vasospasm in the bilateral internal carotid artery (ICA) termini, A1 segments of the anterior cerebral arteries and M1 segments of the middle cerebral artery. Treatment with intra-arterial verapamil and angioplasty resulted in significant improvement in the patient's vasospasm. In light of the severe spasm, the patient was considered a poor candidate for surgical clipping. Two Galaxy coils (2.5 mm32.5 cm and 2 mm31.5 cm; DePuy/Codman & Shurtleff, Johnson & Johnson, Warsaw, Indiana, USA) were placed through a Prowler select LP ES microcatheter (DePuy/Codman & Shurtleff, Johnson & Johnson). The patient did well and made a full neurologic recovery.\nOUTPUT:" }, { "from": "agent", "value": "Ruptured aneurysm" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Case 2: a 46-year old male patient on tenofovir, lamivudine and efavirenz, presented with intermittent low grade fever for the last four months. This was associated with night sweats, loss of appetite and loss of weight of around five kilograms. He also complained of decrease in urine output and generalized swelling of the body. On general examination, he was febrile and was found to have enlarged right axillary lymph node (1cm x 1cm). On systemic examination, he had ascites and a palpable spleen (8 cm below the left costal margin). Fundus examination was normal. On laboratory investigations, he was found to have pancytopenia, deranged liver function and kidney function tests (Hemoglobin- 7.4g/dl, total leucocyte count-1200/mcl, platelet count-20000/mcl, aspartate transaminase/alanine transaminase-209/117 U/l and urea/creatinine- 78/1.7 mg/dl). His baseline CD4 was 221/mul and the most recent CD4 was 158/mul. Non contrast computed tomography of abdomen revealed multiple enlarged retroperitoneal lymph nodes with the largest measuring 47 x 22 mm. Lymph node biopsy could not be performed due to deranged coagulation parameters. Blood and urine cultures were sterile. Peripheral smear showed normocytic normochromic anemia. Vitamin B12 levels were normal but the folate levels were low (2.2ng/ml). Serum LDH levels were elevated (834 IU/l). Immunochromatography for rk39 antibody was negative. Ascitic fluid analysis revealed a protein of 1.9 g/dl, albumin of 0.9 g/dl, total leucocyte counts of 380/mcl (Lymphocytes 90%, Neutrophils 10%), serum-ascitic albumin gradient of 1.1g/dl and adenosine deaminase levels of 40 IU/l. Ascitic fluid cultures were sterile. His ferritin levels were elevated (>2000 ng/ml) and triglyceride levels were also high (324 mg/dl). A presumptive diagnosis of HLH was made. A lymph node biopsy was performed after correction of coagulation abnormalities to identify the primary pathology. However, he succumbed to his illness before the results of biopsy were available.\nOUTPUT:" }, { "from": "agent", "value": "Haemophagocytic lymphohistiocytosis, Human immunodeficiency virus infection, Disseminated tuberculosis, Hodgkin's lymphoma" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 57-year-old man consulted the orthopaedic surgeon because of atraumatic left shoulder pain that had been present for over five months. He experienced activity-related pain and had trouble carrying out overhead movements. Clinical examination revealed limited shoulder mobility and slightly diminished force exerted by the infraspinatus muscle. A magnetic resonance imaging (MRI) arthrography was performed, which showed tendinopathy and a partial thickness tear of the supraspinatus tendon. Also, T2 weighted images with fat supression (FS T2-WI) showed hyperintense oedematous infiltration of the infraspinatus muscle (Figures 1 and 2). Electromyography (EMG) showed isolated neuropathy of the suprascapular nerve with signs of denervation of the infraspinatus muscle. There were no signs of external compression of the suprascapular nerve on the MRI exam. Treatment by means of physiotherapy and vitamin B supplementation was initiated. MRI examination nine months later showed resolution of the oedematous changes in the infraspinatus muscle with minor muscle atrophy and fat infiltration of the infraspinatus muscle belly (Figure 3). Infraspinatus muscle strength on clinical examination and EMG findings had normalized. It is unclear why only the infraspinatus muscle was involved, since the affected suprascapular nerve also innervated the supraspinatus muscle.\nOUTPUT:" }, { "from": "agent", "value": "Parsonage-Turner Syndrome" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The case was a 41-year-old married male without any medical histories whose right forearm was caught in a conveyor belt at a factory 2 years prior while at work. Therefore, the patient was referred to our hospital. Paroxetine (37.5 mg/day) and eszopiclone (2 mg/day) were prescribed for his depressive state and insomnia. Eszopiclone was stopped 3 days before ECT but paroxetine was continued. A total of 12 sessions of bilateral ECT were performed using a Thymatron (Somatics LLC; Lake Bluff, IL). The validity of the seizures was determined by brain monitoring and looking at motor spasm activity in the extremities with a tourniquet wrapped around the limb prior to succinylcholine injection. Propofol and succinylcholine for muscle relaxation were used for anesthesia. The Ham-D score was reduced to 6, and the NRS score decreased to 3 after the last ECT. After ECT, the patient was subsequently maintained with paroxetine (37.5 mg/day), eszopiclone (2 mg/day), and alprazolam (0.4 mg/day), because the efficacy of ECT has been reported relatively transient. He has not experienced a relapse for at least one year after the last ECT. Time courses of Ham-D and NRS scores and grip strength are shown in Table 1.\nOUTPUT:" }, { "from": "agent", "value": "Neuropathic Pain, Major Depression" } ]

[ { "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 information: a 33-year-old, with no medical history besides 5-pack-year history of tobacco use, has been admitted to our emergency department with melena of 3 weeks duration. He denied hematemesis, abdominal pain, changes in bowel habits or vomiting. Clinical findings: on physical exam, the patient was normotensive, afebrile and has normal heart rate. He had significant pallor. The abdominal exam was benign and the rectal exam showed melena. Diagnostic assessment: laboratory studies showed anemia with Hb of 8.7g/dL. Esophagogastroduodenoscopy was done urgently and showed a gastritis. No active bleeding was seen. A scrotal ultrasound was performed, revealing a left testis measuring 6x5.2x6 cm with a heterogeneous echo texture and multiple nodular lesions suspicious for neoplasm. The patient's beta-human chorionic gonadotrophin level was elevated at 805588IU/mL. Lactate dehydrogenase level was also elevated at 699 U/L, and serum alpha-fetoprotein level was normal at 2.8 ng/ml. The following day, the patient developed serious abdominal pain with bilious vomiting. Therapeutic intervention: the patient underwent left orchiectomy with intestinal resection, removing the umbilicated lesion and biopsy of the liver nodule. Follow-up and outcomes: the multidisciplinary team decision was an aggressive chemotherapy, but unfortunately, the patient died few days after.\nOUTPUT:" }, { "from": "agent", "value": "Testicular choriocarcinoma, Small bowel metastases" } ]

[ { "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: Kreuzer et al. Trains of stimulation at 110% resting MT (1 Hz, 2000 stimuli/session) applied to the left primary auditory cortex for 10 sessions demonstrated a positive effect lasting 3 months after the first treatment series (TQ = 38). Four subsequent treatment series over the course of 3 years demonstrated effects lasting 6 months (TQ = 26 after third session, no ratings taken after fourth session). The fifth and final series followed a modified protocol targeted at the right DLPFC (1 Hz, 1000 pulses/session) followed by stimulation applied to the left primary auditory cortex (1 Hz, 1000 pulses/session) for a duration of 5 days (beginning of fifth session TQ = 50; following treatment TQ = 33).\nOUTPUT:" }, { "from": "agent", "value": "Traumatic Brain Injury, severe tinnitus, post-injury onset depression, severe sleep disorder, alcohol and benzodiazepine abuse, single symptomatic seizure" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 13 year old female had a rigid mass in the oral cortical bone of her maxilla, with mucosa integrity, and lacking teeth 23 and 24 on the affected side. Panorama radiographic study revealed a radiolucent lesion, circumscribed, with few radiopaque areas inside, associated to the canine tooth, which was shifted towards the nasal cavity. We carried out an intraoral surgical intervention through a Neumann's incision, from the alveolar and left central superior incisive gingiva all the way to the first ipsilateral molar, shifting the mucoperiosteum. After that, the tumor mass and the unerupted canine were removed (Figure 1a), and finally we repositioned the tissue and sutured the mucoperiosteal flap. The material removed was then sent to the Pathology Department of the Oral Pathology Division of the Dentistry School of UFRN. After routine histology on the material, under light microscopy they observed fragments of the odontogenic lesion, characterized by the proliferation of fusiform/globular cells, arranged as large islands and solid sheets, as well as numerous structures similar to ducts, lined by low cylindrical or cubic cells, of polarized nuclei (Figure 1b). Occasionally, some detached eosinophylic amorphous material was, together with calcification areas (Figure 1c). After 12 months, the patient returned to our department, not showing clinical or radiographic signs of tumor recurrence. We did notice bone remodeling and neoformation.\nOUTPUT:" }, { "from": "agent", "value": "Adenomatoid Odontogenic tumor, Dentigerous cyst" } ]

[ { "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: Two years after this procedure he returned to hospital with recurrent angina, responsive to sub-lingual nitrates (CCS II), and palpitations, even though on maximal beta-blocker therapy and anti-plated therapy. Coronary angiography was performed as exercise stress test resulted positive with symptomatic ST segment depression in leads V2-V6, associated with ventricular couplets. Right femoral approach with 5 French catheters was used. There was no angiographic evidence of instent restenosis in the previously stented segments. Therefore PCI of LM and LAD was decided. The angiographic control showed complete resolution of the critical stenoses of both LM and LAD (Figure 2) with resolution of symptoms and EKG alterations. Therefore, patient was treated by PCI and a drug eluting stent was implanted on the PDA alone (Figure 4). The patient was discharged with dual anti-plated therapy, ACE-inhibitor, statin and long acting calcium channel blockers. Six months later he was completely asymptomatic; a stress test was performed which resulted negative for myocardial ischemia.\nOUTPUT:" }, { "from": "agent", "value": "Multivessel coronary artery disease" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Sometimes these episodes would result in loss of balance and fall. He denied any chest pain and complete loss of consciousness. The patient was also having PVCs and NSVT on standing up (Figure 1). He would then get disoriented and would be unaware of his surroundings. His echocardiogram revealed a normal ejection fraction without any significant structural heart disease. Given his episodes of NSVT, he underwent a stress test as well. His stress test revealed a medium size and a moderate intensity reversible defect in anteroseptal area. The patient was seen in the follow-up in the arrhythmia clinic and was not having any palpitations.\nOUTPUT:" }, { "from": "agent", "value": "Paroxysmal Orthostatic Ventricular Tachycardia, Supine Hypertension, Orthostatic Hypotension, Triple Vessel Coronary Artery Disease" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: 2). The next day, an explorative laparotomy was performed. Small bowel segmental resection and anastomosis were performed. After the surgery, feeding intolerance did not improve and the scrotum, which collapsed immediately after surgery, gradually swelled the next day, leading to redness and a heating sensation. Vital signs, whole blood cell counts, and serum CRP levels were within normal limits. Because passage disturbance at the anastomosis site or intestinal motility disorder was considered based on the contrast studies, loop ileostomy was planned. 3). The patent processus vaginalis was closed on the peritoneal side. Intravenous vancomycin was administered. Six months later, the patient underwent ileostomy repair and was discharged. He is scheduled to undergo surgery for a buried penis when he is 2 years old.\nOUTPUT:" }, { "from": "agent", "value": "Scrotal pyocele, Gastrointestinal perforation, Ileal atresia, Generalized peritonitis" } ]

[ { "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 56-year-old African male with no known underlying health conditions initially presented to the surgical department with a 2-year history of a progressively enlarging but painless buttock mass. Clinical examination revealed a 15 x 10 cm soft, non-tender, mobile, outer upper quadrant mass of the right buttock. Magnetic resonance imaging (MRI) showed a 15.5 x 10.6 x 6.9 cm (CC x TV x AP) heterogeneous well-defined, right gluteal intermuscular soft tissue mass. The visualized pelvic bones and appendicular skeleton on MRI demonstrated low signal intensity on T1-weighted images with multifocal hypointense lesions suggestive of secondary metastatic disease (Figure 1). Widespread osteoblastic lesions were also identified on 99mTc methylene diphosphonate (MDP) bone scintigraphy (Figure 2). The differential diagnosis at this stage was either a primary soft tissue sarcoma with metastatic disease or an unknown primary elsewhere with soft tissue metastases. Fused glands and nests comprising relatively monotonous neoplastic cells were present, with surrounding fibrosis. The tumoral cells contained moderate amphophilic cytoplasm and small round nuclei with fine chromatin and conspicuous single central nucleoli. Immunohistochemical interrogation of these cells revealed absent staining with cytokeratin (CK) 7, CK20 and prostate-specific antigen (PSA), but NKX3.1 showed a diffuse strong positive labelling. Therefore, it was decided at the Uro-Oncology multi-disciplinary clinic to initiate androgen deprivation therapy (ADT) with long-acting three monthly goserelin with additional short-term cover with bicalutamide for the testosterone flare. In addition, he was commenced on systemic docetaxel. He has shown an excellent PSA response and remains asymptomatic with complete resolution of the size of the gluteal metastasis at the most recent follow-up 9 months later.\nOUTPUT:" }, { "from": "agent", "value": "Metastatic prostate carcinoma" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 73-year-old Hispanic woman with a history of left eye enucleation secondary to endophthalmitis, history of dacryocystitis, and primary open-angle glaucoma presented with persistent right eye conjunctivitis and epithelial defect. On ophthalmic examination, her visual acuity was 20/50 in the right eye. The left eye had prosthesis. Intraocular pressure was within normal limits. The right eyelid showed thickened, telangectatic lid margins, with upper trichiasis and distichiasis. The semilunar fold was keratinized. There was subepithelial fibrosis of the right superior palpebral conjunctiva (Figure 1 (Fig. 1)) and symblepharon in the inferior medial palpebral conjunctiva (Figure 2 (Fig. 2)). The bulbar conjunctiva had notable amount of conjunctival injection. The cornea had superior pannus with diffuse severe punctuate epithelial erosions. Flat-topped polygonal papules were noted on the patient's forearm. The patient was referred to Oral Surgery to perform buccal mucosal biopsy given the suspicion of the chronic conjunctivitis. The patient was started on 0.05% cyclosporine eyedrop twice daily, very frequent lubrication with Artificial Tears, and Genteal Gel at bedtime. Later, 0.1% fluoromethalone acetate twice daily was added. Throughout the fourteen years that the patient was followed in our clinic, she had frequent epilation for her trichiasis. During this time course, she presented with several episodes of corneal abrasion and two episodes of corneal ulcer, which healed with topical antibiotic treatment. The option to start oral cyclosporine was discussed with the patient, but the patient deferred starting the medication due to the potential medication side effects and the very slow progression of her disease.\nOUTPUT:" }, { "from": "agent", "value": "Cicatricial keratoconjunctivitis, Lichen planus" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 28-year-old male with moderate ID who lives in a group home had a history of significant comorbid diagnoses, including autism spectrum disorder (ASD), hypertension, hypothyroidism, and GERD (Table 1). Psychiatric diagnoses included excoriation disorder and schizoaffective disorder, bipolar type. In addition, he was anxious, restless, irritable, easily provoked, and physically aggressive and had begun isolating himself from group activities. The patient's medication history included long-term exposure to quetiapine (200/400/200 mg once daily (QD)). TD symptoms were intermittent chewing movement of the jaw, constant bilateral hand/arm movements (e.g., opening and closing of hands/fingers; finger tapping), repetitive bilateral foot tapping, and truncal rocking (Table 2). The duration of these symptoms is unknown. He was initiated on valbenazine (40 mg QHS for 1 week, then escalated to 80 mg QHS) in February 2018. Due to persistent psychosis, the patient was also tapered off quetiapine and started on clozapine (titrated over 2 weeks to 300 mg daily). Four days after starting valbenazine treatment, improvement in abnormal movements was noted. After 2 months of valbenazine treatment, the patient had no abnormal jaw movements, minimal to no arm/hand/finger movements or foot tapping, and no truncal movements (Table 2). Caregivers reported that the improvements in movements seemed to result in less isolating, aggressive, and confrontative behavior. He was also more cooperative, was less resistant to caregiver assistance with ADLs, and had increased participation in group home activities. The patient remains stable on valbenazine (80 mg QHS) with no changes to his medication regimen and no reported adverse events.\nOUTPUT:" }, { "from": "agent", "value": "Tardive Dyskinesia" } ]

[ { "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 primipara was admitted to clinic at 13 weeks of gestation with severe abdominal pain. 1 A and Fig. 1 B). At 7 and 11 weeks of gestation, the patient had presented with abdominal pain, which was treated by drotaverine, and resolved permanently. The patient had been treated at a public hospital, where a transvaginal scan (TVS) had been performed, yet in the exam report data about both adnexa were unavailable. On admission to our hospital, the patient presented with acute abdomen symptoms. Clinical examination revealed painful, enlarged right appendages. Blood examination revealed anemia with a hemoglobin concentration of 9.1 g/dl. TVS revealed fluid in the pouch of Douglas, as well as two gestational sacs. The second gestational sac with a living fetus was located behind the posterior uterine wall, within the right fallopian tube. This fetus had a CRL of 64 mm, and presented with bradycardia. 1 C). The right fallopian tube was attached to the lower part of the posterior uterine wall by a small adhesion. 1 D). The patient was discharged after 6 days. Follow-up was performed at an outpatient clinic.\nOUTPUT:" }, { "from": "agent", "value": "Heterotopic pregnancy" } ]

[ { "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 woman with no past medical or surgical history presented to the ophthalmology clinic for the first time in September 2019 with unilateral swelling in the right orbit for more than two years. This swelling was associated with ptosis. She denied eye pain, diplopia, chemosis, joint pain, sinusitis, nasal or oral ulcer, nasal discharge, epistaxis, otitis media or hoarseness. None of her family members suffered from a similar condition or history of connective tissue diseases. She was single, a non-smoker, unemployed, and not on any regular or over-the-counter medications. Physical examination revealed proptosis of the right eye and ptosis, with swelling above the eyelid. Left eye examination was unremarkable (Figure 1a). She had no physical findings of an underlying systemic rheumatic disease. Laboratory investigations are shown in Table 1. MRI of the orbit conducted in October 2019 revealed proptotic right eye globe with extra-conal enhancing soft tissue that is possibly involving the lacrimal gland (Figure 2a). For further assessment, biopsy of the right orbit was performed and showed fibrosis with CD20-positive inflammatory infiltrates, vascularized dense connective tissues and striated muscles (Figure 3). Based on clinical, radiologic, and histopathologic assessments, the diagnosis of IOI was confirmed. Following a multidisciplinary discussion between ophthalmology, rheumatology and pathology teams and due to the abundance of the CD20 inflammatory infiltrates in the histopathology slides, RTX was started at a dose of 1000 mg intravenous (IV) infusions on days 1 and 15 (rheumatology protocol: a cycle of two sessions two weeks apart). This cycle was administered in December 2019, followed by two more cycles in June 2020 and December 2020, respectively. Regular follow-up assessment revealed significant reduction in the right orbital swelling and improvement in the ptosis clinically (Figure 1b), resolution of the ptosis and extra-conal enhancement on repeat MRI after treatment (Figure 2b) and sustained clinical and radiologic remission one year post treatment (Figure 2c).\nOUTPUT:" }, { "from": "agent", "value": "Idiopathic Orbital Inflammation" } ]

[ { "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 male, already followed in the Institute, presented at the ophthalmology outpatient clinic with complaints of progressively diminished visual acuity in both eyes. CDVA was 20/200 in the OD and counting fingers in the OS. At the twelfth-month appointment of OD and OS, both corneas were transparent, the grafts were perfectly positioned (Figure 4D-F), and the patient presented a CDVA of 20/63 in his OD and 20/40 in his OS.\nOUTPUT:" }, { "from": "agent", "value": "Failed Penetrating Keratoplasty, Repeated Corneal Ulcers, Autoimmune Disease, PK-induced Glaucoma, Lipid Keratopathy, Corneal Neovascularization, Stromal Fibrosis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 64-year-old Caucasian female presented with sudden onset of unilateral leg weakness, where she experienced great difficulty in hip flexion. She had previously been well but had recently complained of excessive fatigue and episodes of abdominal pain. Examination revealed a vasculitic rash covering extensor surfaces of her knees; proximal left leg weakness was also demonstrated. Unfortunately, this failed to control her weakness, which gradually progressed over 8 weeks to involve both lower limbs. She additionally developed a bulbar palsy and weakness of neck flexion, prompting her transfer to ITU. On admission to ITU, patient was moribund, with bulbar dysarthria, nasal speech, and a nonpruritic, vasculitic rash covering the extensor surfaces of her arms and knees. There was no evidence of Gottron's sign or of a heliotropic rash. Examination of her limbs elicited significant weakness, more severe proximally. An EMG revealed a myodestructive pattern, with reduced amplitudes on NCS. Throughout her admission, the patient had several investigations, including routine bloods, glucose, TFTs, B12 and folate, autoantibodies, iron studies, and tumor markers; the only abnormality appeared to be an elevated Ca-125 (see Figure 1). CT of her pelvis failed to reveal any malignancy on three different occasions. Whilst in ITU, the patient additionally developed complex partial seizures originating from the left occipitotemporal region, though she had a normal CT head and only evidence of small vessel disease on MRI. A maintenance regimen of propofol and phenytoin seemed to control her seizures. She then developed what appeared to be an acute abdomen, for which a laparotomy was arranged; despite exploration revealing inflammatory changes involving her right adnexa, no malignancy was identified, and she was transferred back to ITU and eventually to a ward. The patient's weakness was refractory to immunoglobulins and methotrexate, though it showed a dramatic response to rituximab, and plans were made for her discharge, during which time she developed a DVT with a concurrent PE, despite pharmacological and mechanical measures. Therefore a PET scan was arranged upon her discharge.\nOUTPUT:" }, { "from": "agent", "value": "Paraneoplastic neurological syndromes, Dermatomyositis, Disseminated ovarian carcinoma" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 92-year-old white woman with a history of hypertension and congestive heart failure presented with an erythematous and scaling plaque that enlarged over 15 years. Although not painful, the plaque itched. Topical moisturizing creams and antifungals did not improve the lesion. Physical examination revealed a 27- x 16-cm suprapubic lesion, extending superiorly onto the abdomen and inferiorly onto the right thigh. There was a 12-cm central macerated area. In other areas, there was hyperpigmentation (Fig 1). Shave biopsy revealed a confluent proliferation of pagetoid cells in the epidermis with pleomorphism, hyperchromasia, and irregular nuclear contour. Mitotic activity among the pagetoid cells was observed. No dermal invasion was identified. The pagetoid cells expressed cytokeratin 7, carcinoembryonic antigen, and epithelial membrane antigen but did not mark with Mart1 (Fig 2). Basic laboratory studies were unremarkable, and a positron emission tomography scan identified no other foci of disease. A dermatologic surgeon and general surgeon evaluated the patient, but she was not a candidate for any extensive surgical resection. Topical medications were impractical, at which point radiation therapy was pursued. The patient received 6000 cGy in 30 fractions, delivered as a single en face electron cone field to the lower abdomen and perineum, using 6 MeV electrons and a 1/2-cm bolus (Fig 3). Aquaphor ointment was used to treat the short-term erythema and hyperpigmentation of the skin. After 12 months of follow-up, the patient had an excellent response to radiation therapy (Fig 4). The skin over the treatment area is mildly hyperpigmented, but it is otherwise unaffected. Areas of desquamation, erosion, and bleeding resolved entirely. There is no evidence of treatment failure manifesting as recurrent skin erosions, lymphadenopathy, or visceral metastases, and the patient is asymptomatic and pleased with the result.\nOUTPUT:" }, { "from": "agent", "value": "Extramammary Paget disease" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Initial surgery consisted of ORIF of the medial and lateral columns through a chevron osteotomy of the ulna. She failed to show signs of union at 5 months postoperatively and underwent bone stimulator therapy for 4 months. The patient then underwent removal of hardware, repeat fixation with 90/90 plating and iliac crest bone graft (ICBG). Six months postoperatively she fails to demonstrate union and to avoid yet another failure of fixation the decision was made to use a MFCF. A para-tricipital and anteromedial approach was performed, with dissection and exposure of the brachial artery, median nerve and ulnar nerve. The fracture site at the medial column was debrided and cancellous graft was placed without removing the plate. After harvest of the MFCF as described above, the graft was placed in the medial column crossing the fracture site and secured with two 2.0 mm cortical screws after elevating the periosteum about 5 mm at both ends of the graft. The pedicle was anastomosed to the brachial artery in end-to-side fashion. Five months after surgery, there was no pain, elbow flexion of 110 degrees and her elbow extension lag of 30 degrees. Her left-hand strength was 30 pounds compared with the right side that was 40 pounds. Subsequent radiographs demonstrated signs of consolidation with bone bridging at the medial column and residual radiolucency at the lateral column. The patient reported no complaints, with flexion of 110 degrees, extension lag of 30 degrees and complete prono-supination at the time of her final follow-up visit. The result of a DASH score performed 2 years after her last surgery was 0.8 (Figure 1).\nOUTPUT:" }, { "from": "agent", "value": "Supracondylar fracture of the left elbow, Persistent nonunion, Deep surgical site infection" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An 82-year-old female patient is with a history of chronic arterial hypertension, ischemic stroke without sequelae, and hypothyroidism. She is hospitalized in our institution with a diagnosis of nephrotic syndrome, for study and management. Prednisone 1 mg/kg/day is started at admission. There was a torpid progression with multiple intercurrent infections, right renal infarction, and a progressive deterioration of kidney function, requiring the initiation of hemodialysis. In this context, after 3 weeks of hospitalization, she manifested multiple painful genital and inguinal ulcers, the largest one on the skin of the left labia majora, 1.5 cm in diameter, with a well-defined erythematous border and base with scarce fibrin. There was a rapid progression of the ulcers, with an increase in their size, number, and the extension to the perianal region, thighs, and right leg (Figure 1). Dermatology department was consulted, and polymerase chain reaction (PCR) for herpes simplex viruses 1 and 2, Varicella zoster virus, Epstein barr virus, and Cytomegalovirus, in addition to HIV serology and VDRL, were performed, with negative results. Biopsies of the vulvar and right leg lesions were taken and, on the PAS staining of the latter, septate hyphae were found, some with ramifications at acute angles and with invasion of blood vessels (Figure 2). Cultures of the lesions were negative. The patient presented with respiratory distress, and chest computed tomography showed a cavitated lesion in the upper segment of the left lower lobe, suggestive of aspergilloma. Intravenous antifungal therapy with voriconazole and caspofungin was initiated; however, the patient deteriorated rapidly, with multiorgan failure, and died despite intensive care and twenty days of antifungal treatment.\nOUTPUT:" }, { "from": "agent", "value": "Invasive Aspergillosis" } ]

[ { "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 deceased man was discovered locked inside the bathroom of a rented house. He was a tourist that arrived at the airport the day before and rented a house by the sea. The death scene investigation (Figure 1, Figure 2) found the presence of black plastic bands taped to the inner faces of the window and the door's edges clogging thereby the air inlet. Even the keyhole of the bathroom door was clogged with paper and ribbon tape. Inside, the deceased body was semi-lying on a mattress next to the bathroom wall and holding a paper in his left hand on which was printed his picture accompanied by a young woman. Just below his feet, there was a suicide note in which he indicates that betrayal and a relationship breakup are the reasons behind his suicide. On his right side, there was a cell phone closed by electric charge drop. Even further to the right, we found three barbecue grills and a brazier. It was hardly used and it contained ashes with charred coal residue. However, we did not find any potentially dangerous substances, except for one plastic bottle containing a petroleum product used to make fire. The police investigation confirmed that the deceased arrived alone at the airport. The neighborhood merchant avows that the deceased had purchased barbecue grills, charcoal, soda drink and one liter of petroleum product to prepare a barbecue dinner. The surveillance camera in front of the house did not record any visitors. The examination of the deceased's phone eliminated recent suspect phone contacts. The review of the telephone browser history revealed that he was searching on the internet for terms like <<easy suicide>> and consulting a web-forum about suicide. In this regard, a detailed description of an American famous singer suicide by CO poisoning using charcoal burning in the bathroom was exposed. The external examination carried out during autopsy, 48 hours later, revealed the beginning of putrefaction with rigor mortis resolution, green discoloration at the right flank, cherry red livor mortis on posterior and left sides (Figure 3(A,B)), and particularly blackish incrustations under the fingernails of hands (Figure 3C). Autopsy showed cherry-red coloration of blood and muscles with black soot in the airways (Figure 4), cerebral and pulmonary edema (brain weight=1660g, lungs weight=1180/1025g) and greyish liquid in the stomach without particular odor. Toxicological analyses performed five days later, on samples of peripheral and cardiac blood, urine and gastric contents indicated the only presence of carboxyhemoglobin (COHb) in the blood at the level of 40.05% without any other potentially toxic substances.\nOUTPUT:" }, { "from": "agent", "value": "Carbon monoxide poisoning" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Our third patient was a 17-year-old woman with severe AD since the age of 5 years. She had previously been unsuccessfully treated with topical corticosteroids, phototherapy (narrow-band UVB), oral cyclosporine, methotrexate, and systemic tralokinumab (anti-IL13, clinical trial). She also had a history of anxiety disorder treated with pregabalin. Her baseline results revealed SCORAD 99.4, EASI 72, and DLQI 20. She started dupilumab 300 mg subcutaneously every 2 weeks after a loading dose of 600 mg. Before the fifth dose of dupilumab, similarly to the second patient, due to a laboratory error on that day, a false-negative SARS-CoV2 PCR test was reported, and she was able to collect her medication for another month. The error was corrected the same day after she had had the medication injected. She reported fatigue and a runny nose during the infection, with the symptoms lasting 10 days. She did, however, observe exacerbation of her skin lesions, with more erythema, papules, and scaliness on lower extremities, shoulders, and back. On follow-up after 1 month (3 weeks later, she was still SARS-CoV2-positive), her results were SCORAD 78.3, EASI 45.5, and DLQI 18. One dose of her treatment was omitted during her infection following advice from the department. As her PCR test continued to be positive 3 weeks after initial diagnosis, she was finally cleared for attending the appointment by the infectious disease specialist. All three patients' scores on SCORAD, EASI, and DLQI are presented in Table 1.\nOUTPUT:" }, { "from": "agent", "value": "COVID-19, Atopic Dermatitis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The patient was a 61-year-old, non-smoking, female veteran with a past medical history of hypertension, who presented with a chronic cough, dyspnea, significant 50-pound weight loss, and three weeks of nausea and vomiting. The patient was found to be cachexic with scleral icterus, jaundice, and dry mucous membranes, but had normal bowel sounds without pain, distension, or organomegaly. She was tachycardic and hypotensive and labs were significant for hyponatremia with a sodium level of 131 mEq/L and a bicarbonate level of 32 mEq/L. Liver function labs revealed an elevated alkaline phosphatase level of 215 u/L, a total bilirubin level of 5.8 mg/dL, and an aspartate aminotransferase and alanine aminotransferase level of 58 u/L and 36 u/L, respectively. There was also pleural effusion around the mass as well (Fig. 1). Abdominal ultrasonography was significant for a severely dilated common bile duct and a moderately distended gall bladder, however, follow up imaging with computed tomography showed a large heterogeneous mass in the pancreatic head which measured approximately 4.5 cm. A grossly dilated common bile duct and enlarged retroperitoneal lymph nodes contiguous with the mass were also seen (Fig. 2). Further imaging and work up also revealed the presence of metastases to the brain as well. Due to her widespread tumor burden, radiation therapy and adjunctive chemotherapy were immediately initiated.\nOUTPUT:" }, { "from": "agent", "value": "Lung adenocarcinoma" } ]