Datasets:

hippocrates

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Multicare_common_train

like 0

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 35-year-old Caucasian man went to an urgent care clinic twice before being admitted to the hospital with fever as high as 39.4 C, myalgias, and renal insufficiency later. Additional symptoms included headache, photophobia, nausea, and anorexia, starting 10 days after returning from the boating trip. Signs included subtle diffuse flushing and conjunctival suffusions. Initial laboratory values showed a mild hepatitis with a rising creatinine that increased daily to peak at 4.0 mg/dL. Liver enzymes were elevated with peak values of alanine aminotransferase (ALT) 258 U/L, alkaline phosphatase 189 U/L, and bilirubin 3.5 mg/dL. Results of examination of the cerebrospinal fluid were normal. Leukocyte count was within normal range at 4.7 k/muL. By the third day of hospitalization, after IV rehydration and broad-spectrum antimicrobial agents, the patient's fever subsided with improvement of his myalgias and headache. He was discharged and given doxycyline 100 mg twice daily for 10 days. He had no clinical sequelae. Serologic tests for infectious hepatitis A, B, C, and brucella, and a Monospot test were negative. Titers from serum drawn 15 days after the initial exposure were negative; however, convalescent-phase serum drawn 17 days later tested positive for leptospira by IgM-ELISA at CDHS, and MAT at CDC showed the strongest reaction with serovars from L. interrogans serogroups Australis and Mini (Table 2).\nOUTPUT:" }, { "from": "agent", "value": "Leptospirosis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 44-year-old male patient presented with bilateral renal colic pain. Renal ultrasound showed mild hydroureteronephrosis on the left side. Blood analysis showed normal leukocytes counts, normal C-reactive protein, and normal creatinine and urea. Renal colic pain persisted despite adequate analgesic therapy. Therefore, the patient was admitted to the hospital and DJS was placed bilaterally. During placement of the DJS on the right side, some resistance was felt. Perioperative kidneys, ureters, and bladder radioscopy showed a somewhat medial position of the right stent, but a nice proximal curl was noted [Figure 1]. During hospitalization, right renal colic pain persisted, gross hematuria occurred, and kidney function decreased. The next-day follow-up NECT was performed. Inferior venocavagraphy was performed which confirmed the intravascular position of the stent and excluded the formation of significant thrombus at its tip [Figure 3a]. The DJS was removed cystoscopically. Immediate inferior venocavagraphy after DJS removal showed limited contrast leakage at the perforation site, and a fully clear image was noted after 10 min [Figure 3b]. Another 4 weeks later, the DJS were removed. Follow-up was uneventful, and as far as, we know the patient had no stone remission.\nOUTPUT:" }, { "from": "agent", "value": "Intravascular migration of the double J stent, Ureteral stones, Hydronephrosis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 69-year old woman, previous smoker (30 pack years (PY)) presented with dry cough, headache, dyspnoea at rest and general malaise. The symptoms appeared 21/2 weeks prior to admission, and. Six days treatment with antibiotics and corticosteroids did not have any effect. Before admission, the patient had never experienced pulmonary symptoms. At admission, the patient had a temperature of 39.5 C, normal blood pressure, saturation of 92% and basal crackles at lung auscultation. Blood samples showed a mild anaemia, elevated C-reactive protein 174.5 mg/ml (CRP) and normal leucocytes (LKC). No deep venous thromboembolism was present on clinical examination. Echocardiography showed a normal left ventricular ejection fraction of 60%, a borderline dilated and hypertrophic left ventricle and no signs indicating increased pulmonary pressure. Tests for atypical pneumonia, tuberculosis and fungal infections were negative. Intravenous broad-spectrum antibiotics were initiated but due to continuing fever and an elevated CRP, a chest X-ray and an HRCT were performed. On the chest radiograph, blurry bilateral less than 1 cm large consolidations were present predominantly on the left side. HRCT revealed diffuse ground glass opacities, thickening of interlobular septae, traction bronchiectasis, localized subpleural honeycombing, mosaic perfusion pattern in the apical areas of the lung parenchyma and mediastinal lymphadenopathy. Radiologically, a diagnosis of pulmonary fibrosis and infection was made (Fig. 1A and 1B). CT angiography did not demonstrate pulmonary embolisms. Chronic eosinophilic pneumonia (CEP) or fibrotic non-specific interstitial pneumonia (NSIP) was suggested as an underlying interstitial lung disease with simultaneous infection. Prophylactic low-molecular-weight-heparin was administered together with oxygen, intermittent continuous positive airway pressure (CPAP) and high dose corticosteroid. Despite treatment, the patient's condition deteriorated and respiratory support including high frequency oscillation and NO treatment was started at the intensive care unit, where, as a consequence of multi-organ failure, she succumbed after 21 days of hospitalisation.\nOUTPUT:" }, { "from": "agent", "value": "Emphysema, Haemorrhagic pulmonary infarction, Widespread bilateral pulmonary thrombosis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: They were prematurely delivered by cesarean section on July 6, 2012, at the Provincial Maternity and Child Care Center (Guangzhou, China). The boy (patient 1, Apgar score 9-10/1-10 min) had a birthweight of 2.3 kg, and the girl (patient 2, Apgar score 9-10/1-10 min) had a birthweight of 1.8 kg. They received standard care for preterm neonates at the hospital. They were discharged once their weight reached 2.5 kg; this happened for patient 1 at 3 weeks of age and for patient 2 at 4 weeks of age (July 29 and August 3, 2012, respectively). On October 2, 2012, the boy was examined at the hospital for irregular fever up to 39 C. On October 9, he was readmitted to the hospital with a fever of 38 C and weight of 5.0 kg. Chest radiograph showed signs of increased bronchovascular shadows. Mezlocillin sodium and sulbactam sodium (4:1) and ribavirin were administered, but the patient did not improve. On the same day, the girl had a cough and low-level fever (37-37.5 C) but was not hospitalized. On October 17, the twins were transferred to an infectious disease hospital, where they had extensive physical and laboratory examinations (Table 1). At the time of discharge (December 12), the twins were well and without fever. They left the hospital for home care, which was supervised by a local general practitioner who provided rifampin and sulfamethoxazole for up to 6 weeks.\nOUTPUT:" }, { "from": "agent", "value": "Congenital brucellosis, brucellosis with alveobronchiolitis, abnormal hepatic function, moderate anemia, glucose-6-phosphate dehydrogenase deficiency" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Sir: A 52-year-old man, a non-smoker and previously healthy, presented to the hospital with fever, cough and dyspnea. Five days after intubation (six from symptoms onset), the patient was still markedly hypoxemic (PaO2/FiO2 ratio of 148 mmHg on a positive end-expiratory pressure of 18 cmH2O) while ventilated with a protective ventilatory strategy (tidal volume 5.2 ml/kg PBW, plateau pressure 27 cmH2O). In the context of a clinical trial ongoing in our center, he underwent a positron emission tomography (PET) scan with [18F]fluoro-2-deoxy-d-glucose combined with computed tomography (CT). As shown by Fig. 1, the PET scan disclosed an abnormally high uptake of [18F]FDG, which, in the course of lung inflammatory processes, has been shown to indicate the presence of activated neutrophils. The increased [18F]FDG uptake not only involved the areas characterized by a loss of aeration on the CT scan (black arrow, standardized uptake value 11.2), but also areas with preserved aeration, or showing only a modest ground-glass opacification (white arrows, SUV 6.8). The patient recovered; he was extubated after 8 days and discharged alive from the ICU. The presence of inflammation in normally aerated lung regions has already been shown in patients with ARDS or in patients at risk for ARDS and subsequently developing the disease.\nOUTPUT:" }, { "from": "agent", "value": "Influenza A: H1N1, Acute respiratory distress syndrome (ARDS), Viral pneumonia" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Numerous breakdowns in communication occurred between the referring providers and palliative care consult team in this case study. Perhaps foremost, the palliative care clinician did not insist on a direct conversation with the appropriate referring provider so that a more nuanced consult question could have been better articulated or negotiated in real time.12 The pace of inpatient care and the complexity of care teams involved contributed to the substandard interteam communication and likely compelled both teams to pursue shortcuts with the consultation intake process.12 Another structural issue was a lack of a clear understanding of the phrase \"goals of care.\" Without a clear operational consensus on the meaning of the phrase within the medical community, \"goals of care\" often is used as a vaguely defined \"buzz phrase\" to connote that a patient is not doing well clinically. Although one clinician may employ the phrase to connote that code status needs to be addressed, another may interpret it to mean that employing life prolongation as the fundamental goal of medical interventions needs to be reconsidered. Bern-Klug argued that the implicit goal of medical care is cure or life prolongation, and when either of these aims is no longer possible, more reasonable medical goals of care are often not explicitly stated by clinicians.13 Weissman and Meier defined \"goals of care\" as physical, social, spiritual, or other patient-centered goals that arise after an informed discussion of the disease(s), prognosis, and treatment options.14 Stone offered a list of over nine potential goals of care for medical treatment including avoidance of premature death, optimized quality of life, or relief of suffering.15 Stanek utilized a concept clarification process in hopes of assimilating these disparate definitions in the literature. Through this methodology, she defined \"goals of care\" as desired health expectations formulated through thoughtful interactions between the health care team and a human being. Although Stanek's definition offers a potentially unified concept for \"goals of care,\" in our experience, there still is not a uniformly accepted definition that is applied reliably throughout clinical situations, nor a standardized process for establishing goals of care, which are essential in the current culture of inpatient practice involving multiple clinicians and care teams. Although having a standardized and uniformly accepted definition for \"goals of care\" certainly would not replace the need for direct communication between referring and consulting providers, we do believe it could potentially reduce communication misadventures between care services, or even with patients, knowing that time pressures to complete consultations efficiently and communication challenges in dealing with increasingly complex care teams are likely to continue in inpatient care environments.\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: A 45-year-old man presented to a walk-in clinic in our hospital with a 3-day history of severe sudden-onset posterior headache, which was exacerbated in the upright position. A tentative diagnosis of tension headache or cerebrospinal fluid hypovolemia was made and he was sent home. Three days later, he was transported to another hospital after experiencing a generalized tonic-clonic seizure and wasreferred back to our hospital. On examination, he had mild consciousness disturbance and increased deep tendon reflexes. A blood test showed an elevated D-dimer level of 2.7 mug/mL. Contrast-enhanced head CT revealed a low density lesion of the parietal lobe (Fig. 1) and brain MRI indicated brain edema and thrombosis of the cortical veins (Fig. 2, 3). The day after admission, his consciousness improved and he claimed that he had personally imported tadalafil and that he had occasionally taken it at a larger dose (40 mg per day) than the recommend daily dose (20 mg per day) in the 6 months prior to the onset of his symptoms. He had been using tadalafil to treat erectile dysfunction. The patient reported that he did not have sexual contact on the day prior to the onset of his headache. His anti-cardiolipin (aCL) antibody (14 U/mL; normal range <10 U/mL) and anti-caldiolipin-beta2-glycoprotein-I (aCL beta2GPI) complex antibody (11 U/mL; normal range <3.5 U/mL) levels were elevated. He was discharged on day 15 after a full recovery from his symptoms. At the 3-month follow-up clinic visit, his aCL antibody and aCL beta2GPI complex antibody levels remained elevated at 7.8 U/mL and 15 U/mL, respectively. Warfarin treatment was initiated. At the time of his most recent follow-up visit, there had been no recurrence of thrombosis and he had not experienced any complications.\nOUTPUT:" }, { "from": "agent", "value": "Cerebral Venous Thrombosis, Antiphospholipid 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 first patient was a 53-year-old woman who was diagnosed with T2DM at 47 years of age. She had been on 7.5 mg glibenclamide, 1000 mg metformin, and 150 mg miglitol for the previous 3 years, during which time her HbA1c levels never went below 8.9%. The patient was advised to start insulin therapy on many occasions, but she refused because of a fear of injections and hypoglycemia. In December 2009, the patient's body mass index was 24.4 kg/m2 and she had no diabetic microangiopathy (Table 1). She had 2.5 mg of amlodipine besilate for hypertention. A peripheral blood count revealed that the patient was not anemic, and blood chemistry evaluations indicated normal liver and renal function, including estimated glomerular filtration rate (Table 1). Because the patient's HbA1c level deteriorated to 11.1% and she still refused to initiate insulin therapy, 50 mg sitagliptin was added to ongoing glibenclamide, metformin, and miglitol. The patient's HbA1c level decreased gradually, reaching 6.1% over a period of 24 weeks from starting sitagliptin (Fig. 1A). The patient's fasting plasma glucose improved from 147 mg/dL to 127 mg/dL, whereas there were no significant changes in C-peptide immunoreactivity and body mass index (from 1.10 to 1.17 ng/mL and from 24.4 to 24.6 kg/m2, respectively, Table 1). The patient's HbA1c levels were maintained between 6.6% and 7.4% over period of 60 weeks after starting sitagliptin, despite a reduction in the daily dose of glibenclamide to 5 mg (Fig. 1A).\nOUTPUT:" }, { "from": "agent", "value": "Type 2 Diabetes Mellitus" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 49-year-old female presented with nausea, vomiting, and weight loss. Full blood count revealed a white blood cell count of 238.0 x 109/L, hemoglobin of 7.7 g/dL, and platelets of 746 x 109/L. Bone marrow morphology revealed granulocytic hyperplasia with increased megakaryocytes and <1% myeloblasts. Cytogenetics detected the t(9;22) translocation with molecular analysis demonstrating high levels of e13a2 BCR-ABL1 transcripts, consistent with a diagnosis of chronic-phase CML with a low-risk Sokal score. She commenced imatinib 400 mg oral daily with transient toxicities of nausea and increased susceptibility to infections but overall tolerated imatinib well, achieving a major molecular response (MMR) of BCR-ABL1/ABL1 0.09% on the International Scale (IS) at 20 months (Figure 1). BCR-ABL1 transcripts became undetectable (<0.001% IS) at 40 months with optimal adherence and a good quality of life. After BCR-ABL1 transcripts became undetectable, monitoring intervals were extended to six months. Rising transcript levels resulted in loss of MMR at 105 months, peaking at a BCR-ABL1/ABL1 IS of 3.43%, almost nine years after starting imatinib (Figure 1). After adherence was assured, ABL1 KD mutation analysis was performed as previously described and detected the Y253H (c.757T > C; NM_005157.5) mutation. The time between loss of MMR and mutation detection was six months. The patient then switched to bosutinib 500 mg oral daily, reduced to 400 mg oral daily after gastrointestinal toxicities, which resulted in an MMR within three months (BCR-ABL1/ABL1 IS 0.02%). The BCR-ABL1 transcript level continues to decline (Figure 1) with continued frequent monitoring advocated.\nOUTPUT:" }, { "from": "agent", "value": "Chronic Myeloid Leukemia" } ]

[ { "from": "human", "value": "As a physician engaged 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 39-year-old male, Caucasian, smoker who was usually fit and well presented with a 4-month history of progressive headache and new onset vomiting leading to attendance at the emergency department. Headaches were suggestive of raised intracranial pressure, worse on lying flat and bending forward. The patient reported blurriness of his vision when the headaches were severe, but there were no lower cranial nerve signs. Blood pressure on arrival was 241/151 mmHg. Fundoscopy demonstrated Grade III papilledema in the right eye. The rest of the neurological examination was normal. The patient was commenced on antihypertensive medications (amlodipine and bisoprolol) before a magnetic resonance imaging (MRI) scan was performed. MRI demonstrated T2 hyperintensity involving the cerebellum, midbrain, pons, and medulla [Figure 2]. Cerebellar edema was once again demonstrated. There were also multiple small T2 hyperintensities in the supratentorial white matter, suggestive of microvascular changes. Microhemorrhages were evident within the left cerebellar hemisphere, brainstem, putamen, and temporal lobe; deemed to be due to profound hypertension. There was no restricted diffusion or abnormal enhancement in relation to the abnormalities described above. The patient was admitted under neurosurgery and underwent frequent neurological examinations in case of any deterioration requiring surgical intervention. Investigations for secondary causes of hypertension were negative. Following optimization of blood pressure with oral calcium channel blockers, the patient was subsequently discharged as clinical symptoms had improved. The patient remained well with complete resolution of headaches at outpatient review 6 months later.\nOUTPUT:" }, { "from": "agent", "value": "Hypertensive posterior reversible encephalopathy, Obstructive hydrocephalus" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 46-year-old female with symptoms of hoarseness and Horner's syndrome presented with a left cervical mass that was diagnosed to be undifferentiated carcinoma based on the findings of aspiration cytology (Figure 1). The patient's chest computed tomography (CT) findings showed a mass measuring 5.0 cm in size spreading from the left upper mediastinum to the left supraclavicular area, which pressed against both the trachea and esophagus and it seemed to involve the left common carotid artery (Figure 2). Based on these findings, and cytology findings a clinical diagnosis of stage IIIB (T4N3M0) non-small cell lung cancer (NSCLC) originating from the apex of the left lung involving both the mediastinum and the supraclavicular lymph nodes was made. The patient received concurrent chemo-radiotherapy (cisplatin 80 mg/m2 for days 8 and 36 + UFT 400 mg/m2, both on days 1-14 and on days 29-42 plus radiotherapy, 2 Gy/day on days 1-20 for a total of 40 Gy). After this treatment regimen, the tumor size decreased by 35.0%. Thereafter, the patient underwent a surgical resection though a median sternotomy with a combined resection of the left clavicle. During the operation, an encapsulated tumor was detected in the mediastinum. Although the tumor was easily ablated from the left common carotid artery, it involved both the left vagus and the sympathetic nerves. As a result, both nerves had to be sacrificed in order to achieve a complete resection of the tumor. Grossly, the tumor was in continuity of the vagus nerve was whitish in color and oval shaped measuring 5 x 3 cm in diameter (Figure 3). Both cytological and histological examinations revealed 1) Continuity between the vagus nerve and tumor was seen, while the no continuity between the tumor and the sympathetic nerve was found. 2) The findings of aspiration cytology of the tumor diagnosing it to be undifferentiated carcinoma before the treatment included an atypical spindle cell. (Figure 1). 3) The predominantly tumor consisted of necrotic tissue and a few viable atypical spindle cells (Figure 4A) which were positive for S-100 protein (Figure 4B). At present, the patient has survived for about 2 years since operation without any recurrence.\nOUTPUT:" }, { "from": "agent", "value": "Malignant schwannoma" } ]

[ { "from": "human", "value": "As a physician engaged 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 woman visited a local hospital with cough and vomiting. She had episodes of periodic headaches and paroxysmal palpitations. Bilateral adrenal tumors were identified by abdominal CT scan (maximum diameter of 4 cm for right mass and 9 cm for left mass) (Fig. 1a). 1b), along with elevated urinary catecholamine and metabolite concentrations (Table 1), and she was, therefore, transferred to the Fujita Health University Hospital for surgical management. On admission, blood pressure was 111/68 mmHg. Although her basal serum calcitonin level was normal(37.0 pg/ml), elevated levels were recorded following stimulation with 2 mg/kg of Ca2+ infusion (330 pg/ml). However, neither ultrasonography nor 99mTc-methoxy-isobutyl-isonitrile (MIBI) scan showed any cervical lesions. Although serum PTH level was elevated (340.5 pg/ml), serum calcium and phosphorus were within normal range (9.3, 3.8 mg/dl), and urinary Ca excretion was not elevated (Ca/creatinine = 0.163). Finally, screening for the RET gene was performed after appropriate informed consent was obtained (approved by the Ethical Review Board for Human Genome Studies at Fujita Health University), and, unexpectedly, the S891A mutation was identified. 2a). One year later, the patient underwent prophylactic total thyroidectomy. Histological examination demonstrated that multiple nodal lesions were scattered, indicating the presence of C-cell hyperplasia without any evidence of MTC (Fig. 2b, c). Regarding the four resected parathyroid glands (Fig. 3a), two right glands were slightly enlarged (231 mg for superior and 118 mg for inferior glands) compared with the two left glands (48 mg for superior and 15 mg for inferior glands). However, no specific histological change was observed even in the enlarged glands (Fig. 3b). Approximately, one-third of the resected parathyroid glands were implanted into the muscle of the left forearm.\nOUTPUT:" }, { "from": "agent", "value": "Pheochromocytomas, MEN2A" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Periods of altered mental status were also reported. Outpatient fever workup including echocardiogram, blood cultures, and HIV testing were negative. On admission vital signs were normal except a blood pressure of 145/95. Physical and neurologic exam revealed an awake male who was slow to answer questions, able to name some objects, and repeat words. Motor and sensation were intact. No dysmetria was noted. CT of the head revealed a new focal hypodensity involving the posterior limb of the left internal capsule and medial aspect of the left globus pallidus concerning for infarct. Given the concern for a CNS infection a lumbar puncture (LP) was obtained. Treatment with ceftriaxone and acyclovir was initiated. Admission blood and urine cultures were eventually negative. LP revealed a total nucleated cell (TNC) count of 350 cells/muL, with a lymphocytic pleocytosis (84%), protein 169 mg/dL, glucose 15 mg/dL. MRI of the brain revealed a basilar leptomeningeal process and multiple small left thalamocapsular (Fig. 3) and superior cerebellar infarcts concerning for an arterial vasculitis secondary to the leptomeningitic process. Bacterial culture, fungal culture, acid fast bacilli, herpes simplex virus, enterovirus, and VDRL were all negative from the CSF. CSF cryptococcal antigen was positive with a titer of 1:16. Treatment with amphotericin and flucytosine was initiated on hospital day 3,other antimicrobials were discontinued. Repeat HIV testing was negative. Amphotericin and flucytosine were later discontinued and IV fluconazole was started on day 11 due to elevated creatinine. On hospital day 13 the patient was discharged on IV fluconazole to finish a 3 week course. Repeat serum cryptococcal antigen was negative and repeat MRI showed evolution of the original infarcts. After 3 months of treatment, the fluconazole was discontinued.\nOUTPUT:" }, { "from": "agent", "value": "Central nervous system infection, Renal cell carcinoma" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 68-year-old male presented to the urology out-patient department of our institution with a painless nodular lesion over glans penis of two weeks duration. He had also noticed a small swelling on his right groin in the preceding one week. He denied the presence of any lower urinary tract symptoms. There was no history of hematuria or pyuria. On direct enquiry, he admitted that he was having mild low back pain for some time, to which he did not give much attention. On examination, he was in good general condition. There was a well circumscribed erythematous nodular lesion over the glans penis at the parameatal position [Figure 1]. Genital examination did not reveal any other abnormality. A single 1.5 cm, mobile, hard, non-tender right superficial inguinal lymph node was detected [Figure 1]. On digital rectal examination, the prostate was found to be hard and nodular. There was no vertebral or pelvic tenderness. No other abnormality was detected on physical examination. His serum PSA was 50 ng/ml. Radionuclide scintigraphic bone scan revealed diffuse skeletal metastasis. He did not come back to our hospital for follow-up but on telephonic conversation he reported that there was no change in the size of the lymph node or of the penile lesion nine months after orchiectomy.\nOUTPUT:" }, { "from": "agent", "value": "Metastatic prostatic adenocarcinoma" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Camrelizumab is an anti-PD-1 antibody being developed by Jiangsu Hengrui Pharmaceuticals Co., Ltd. We reported a case of an adult critical Chinese patient with primary hepatocellular carcinoma and lung metastasis completely responding to Camrelizumab, most of the lesions were stable and no new lesions occurred after 1-year treatment, which provides us to reconsider the therapeutic effect of Camrelizumab on such patients. Camrelizumab had a safety profile for the patient in our case report, except for the occurrence of RCCEP. Image Caption and Description: \nImage caption: []\nImage description: []\nCase Report: \nOn November 6, 2020, the patient accepted one course of Camrelizumab treatment with 200 mg once daily in 21-day cycles. Afterward, the patient presented with the prodromal symptoms of hepatic encephalopathy, including irritability, irrelevant answer, lethargy, and disturbance of consciousness. Then deamination treatment with arginine did improve this critically severe patient. Subsequently, the patient underwent second round of Camrelizumab treatment on December 4, 2020. Later, he refused to continue immunotherapy due to economic reasons. The patient was given best supportive care using oral antiviral entecavir tablets (0.5mg qd) and glycyrrhizin tablets (75mg tid). On February 25, 2021, on MRI of the abdomen, dense masses were seen in the right posterior lobe of the liver, multiple nodules and increased lesions were observed in the liver. Multiple enlarged high-density nodules were observed in both lungs, significantly increased in number and volume.\nOUTPUT:" }, { "from": "agent", "value": "Advanced hepatocarcinoma" } ]

[ { "from": "human", "value": "As a physician engaged 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 presented with abdominal distention, lower extremity edema and severe dyspnea. Informed consent was taken from the patient. On physical examination, tension ascites but no any collateral veins were noted on the abdomen. Respiratory sounds were normal at the bases of both lungs. The abdominal ultra-sound revealed venous outflow obstruction caused by HC occupying supra hepatic veins of an IVC segment of the hepatic dome and measuring 8 cm on average (Fig. 1). There was no flow viewed in the left hepatic vein and IVC on abdominal portal Doppler ultrasound. The portal vein was 20 mm, and the splenic vein was 18 mm in diameter and hepatofugal flow was noted. It was occluding the IVC and left hepatic vein at the level where the hepatic veins poured into the IVC. TTE also revealed a large thrombosis in the right atrium that came out from IVC orifice. The thrombosis was mobile however, no any clot was found in the main pulmonary artery or its left and right major branches (Fig. 2). With para centhesis, the intra peritoneal fluid was not clear and total leukocyte count was, 90% of lympho-monocyts. The intra peritoneal fluid was exudates with high albumin (0.6 g/dl) and protein 5.6 g/dl. There was no other pathology found in the Gram staining and culture of the intra peritoneal fluid. According to these findings, the patient was diagnosed with secondary (BCS) developmental due to HC. The patient scheduled for emergency removal of right atrial clot and possible pulmonary embolectomy. The standard median sternotomy was carried out and CPB was constituted by the aorta, SVC and femoral vein cannulation. Following cardiac arrest by cardioplegin, right atrium and main pulmonary arteries were opened. A long segment of the clot was removed from IVC as a small piece of clot suctioned from the left pulmonary artery (Fig. 3). The IVC was repeatedly suctioned to sure that no thrombosis was remained in its wall and its accessory branches. Surgical treatment successfully restored venous out-flow in our patient. The operation had an uneventful postoperative course and the patient discharged on the 14th day of hospitalization and referred to a general surgery center for the management of his liver HC.\nOUTPUT:" }, { "from": "agent", "value": "Budd Chiary Syndrome, Hydatid 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: A 28-year-old man presented to the Department of Neuroradiology, UConn Health, with complaints of left-sided extremity numbness, altered mental status, and swelling of the forehead on the right side (supraorbital region). The mass and edema compressed the adjacent portion of the right lateral ventricle and caused an approximately two cm right-to-left midline shift. There was partial opacification of the right frontal sinus with erosion through the anterior wall of the sinus (Figures 1-2). MRI confirmed the findings of the CT scan (Figures 3-4). A right frontal craniectomy was performed. The midline shift decreased from 1.5 to 1 cm. In the region of vasogenic edema, there was mild parenchymal enhancement at the gray-white junction. In addition, interval improvement in aeration of the right ethmoidal and maxillary sinus with a small amount of residual mucosal thickening of the maxillary sinus was noted. Case report 2\nOUTPUT:" }, { "from": "agent", "value": "Pott's Puffy Tumor, Sinusitis, Cerebral Abscess" } ]

[ { "from": "human", "value": "As a physician engaged 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 16-year-old girl was referred for a brain MR scan to the Department of Diagnostic Imaging of the Institute of Mother and Child. She remained without verbal contact, responded only to simple verbal commands and to pain, and showed no neurological improvement over time. Her previous brain MR studies were performed outside our institution prior to and shortly after surgery. The early postoperative scan (five days post-surgery) showed no clear evidence of a residual enhancing tumour (Figure 2). The subsequent MRI performed at our institution, apart from postoperative changes in the posterior fossa, revealed a region of volume increase and high signal intensity on T2-weighted (T2W) fast-spin echo (FSE) and fluid attenuation inversion recovery (FLAIR) images involving the right anterolateral aspect of the medulla at the level of ION (Figure 3). This lesion was absent on both previous studies (Figures 1 and 2). Taking into account the patient's history, the above-mentioned imaging features raised at first the suspicion of tumour recurrence on a late postoperative scan. However, the typical location and MR morphology, as well as the time of occurrence in the patient, who underwent brainstem surgery several months earlier, contributed to the diagnosis of HOD. Additionally, there was no evidence of restricted diffusion and of contrast enhancement. Two months later, the girl came out of the coma and was discharged home in full verbal and logical contact, with no intellectual disabilities and only mild spastic quadriparesis. She returned to normal life and continued her education at school.\nOUTPUT:" }, { "from": "agent", "value": "Hypertrophic olivary degeneration, Brainstem pilocytic astrocytoma" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Prior ophthalmic history included radial keratotomy and LASIK in both eyes (OU). He also had uneventful cataract surgery with intraocular lens implantation OD and YAG capsulotomy. Best-corrected visual acuity was 20/50 OD and 20/20 in the left eye (OS). Manifest refraction was -1.00 + 1.50 x 52 OD and +1.50 + 1.75 x 42 OS. Intraocular pressure was 17 mmHg in both eyes (OU). Pupils were equally round and equally reactive to light. Anterior segment examination was remarkable for radial keratotomy with pseudophakia OD and nuclear sclerosis +1 OS. No evidence of intraocular inflammation was seen. Fundus examination was remarkable for foveal pigment mottling OU. No diabetic or hypertensive retinopathy was present. SDOCT revealed atrophic cysts and ellipsoid zone disruption OU (Figure 1). Macular OCTA was performed bilaterally. OCTA OS reveals microvascular abnormalities in the deep capillary plexus of the retina most prominent temporally.\nOUTPUT:" }, { "from": "agent", "value": "Macular Telangiectasia Type 2, Subretinal Neovascular Membrane" } ]

[ { "from": "human", "value": "As a physician engaged 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 male patient was brought to our emergency department by his neighbor after sustaining a single stab wound to the neck and finding himself unable to walk. Physical examination found him fully conscious, hemodynamically stable and without any neck restraint. A single right-sided stab wound was noted in the lower anterior triangle of the neck (Figure 1), and air entry was reduced over the right hemithorax. He could not move his lower limbs or feel sensation below the waist, and his cervical spine was immobilized forthwith. A chest x-ray revealed a right-sided pneumothorax, and an intercostal drain was inserted. A multidetector helical computed tomography (CT) with angiography and contrast swallow ruled out vascular, laryngotracheal, and pharyngo-oesophageal injuries. Our urology department was consulted 5 h after admission with a complaint of persistent erection of 4-h duration. He denied the use of antipsychotics, recreational drugs, or any oral medication or self-injection for erectile dysfunction. He gave no history of hematological diseases such as sickle cell anemia or leukemia. Further, examination revealed no evidence of trauma to the pelvis, perineal, or genital area. A full blood count, liver, renal and thyroid function tests and serum electrolytes were normal. No sickle cells were detected on the peripheral smear. A tox screen was negative. The patient reported two further episodes of unwanted erections, each lasting 30 min over the next 24 h. He was transferred to a rehabilitation unit.\nOUTPUT:" }, { "from": "agent", "value": "Priapism, Spinal cord injury" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: AngioCT revealed a right ICCA aneurysm with signs of partial thrombosis without evidence of rupture [Figure 1a]. Angiography on admission confirmed the presence of a giant aneurysm of the anterior portion of the right ICCA [Figure 2a-c]. Since endovascular techniques seemed inappropriate due to the partially intraluminal thrombosis and very wide neck, PAO was considered as the optimal treatment choice. A balloon test occlusion (BTO) was performed to evaluate the preoperative risk of ischemia without relevant findings and no evidence of retrograde filling of the aneurysm by anterior or posterior communicating arteries [Figure 2d and e]. Then, the patient underwent surgical ligation of the cervical CCA at the level of C6 with a 3/0-silk, and anticoagulation was started 3 days after surgery. A cerebral magnetic resonance angiography (MRA) revealed decrease of the size of the aneurysm lumen and no ischemic lesions were detected [Figure 3a]. Nine months later, and without new neurological symptoms, signs of aneurysm growth were detected in a serial MRA [Figure 3b], and a new angiography was planned. Right CCA angiogram showed the therapeutic occlusion of the right ICA, but the right vertebral angiogram demonstrated proximal partial recanalization of the ICCA aneurysm. Collateral supply was explained from the external carotid artery (ECA) through the occipital artery with an inverse flow to the ICA [Figure 4a]. Therefore, surgical occlusion of the cervical ICA at the level of the ansa cervicalis of the hypoglossal nerve with a 0-silk was performed, and intraoperative Doppler ultrasound revealed no efferent flow in ICA. Postoperative new angiography confirmed the total occlusion of the aneurysm [Figure 4b]. After 6 years of follow-up, we have not detected refilling or thromboembolic events [Figure 5].\nOUTPUT:" }, { "from": "agent", "value": "Giant intracavernous carotid artery aneurysm, Arterial hypertension, Right 6th nerve palsy, Cavernous sinus syndrome" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She presented to gynaecology clinic at Bugando Medical Centre, Mwanza, Tanzania, with seven-month history of progressive growths around genital region. The growths were of insidious onset, initially painless, although they later became painful. The lesion was initially noted on the edges of vaginal introitus; however they continued to spread to involve the perianal region. The growths were associated with foul smelling yellowish discharge. She has no history of receiving HPV vaccine. On examination, there were huge multiple masses, friable, cauliflower-like in appearance, dark grayish-pink in colour on her vulva involving both labia majora, extending anteriorly to the mons pubis and posteriorly to the perianal region, completely obliterating the urethral orifice, vaginal introitus, and anal opening (Figure 1). Masses were firm, edge growth, well-demarcated margins with rough surface. There were also some small satellite lesions on labia minora and the perianal region. There was also a foul smelling yellow vaginal discharge draining from multiple contoured margin areas on the masses. There was no peripheral lymph node enlargement. The vitals were blood pressure 110/65 mmHg, pulse rate of 78 beats per minute, respiratory rate of 20 cycles per minute, and temperature of 37 C. The diagnosis of GCA was reached. Due to the extensive nature of the lesions, surgical excision was planned and done successfully (Figure 2). The wounds healed by primary intention approximately one week after the procedure. Pap smear of the excised lesions was negative. Histological evaluation showed hyperkeratotic squamous epithelium underlying fibrous connective tissue stroma with nonspecific chronic inflammatory cells. There were no features of malignancy. The patient was seen at one month and two months at which point she was doing fine, still on her ART with no recurrence of the vulval lesions. She was counseled on safe sex and other preventive measures for STIs. She was then lost to follow-up after six months of follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Giant Condyloma Acuminatum of Vulva, 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 25-year-old male, resident of Srinagar, businessman by occupation returned to Srinagar after a weeklong trip to Delhi in October 2012. Physical examination was unremarkable and haemogram revealed a normal study except for a low platelet count of 86,000/mm3. His renal and liver function tests, spot urine examination, chest X-ray, and USG abdomen were ordered and all parameters were within normal limits. The patient was put on 600 mg of oral Chloroquine Phosphate followed by 300 mg after six hours and then 300 mg daily for two days. Patient responded well to the treatment.\nOUTPUT:" }, { "from": "agent", "value": "Dengue fever, Malaria" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 77 year old male with the past medical history of diabetes mellitus type 2 complicated by a right BKA, hypertension, hypercholesterolemia, and chronic kidney disease presents to the ED for shortness of breath and abdominal pain. Three days prior to admission he noted a sudden onset of crampy and aching pain across his lower abdomen, constant in nature, relieved somewhat with over-the-counter Maalox and Pepcid, but never completely subsiding. The same evening the pain started, he experienced nausea, but no vomiting. He had no history of biliary colic, or abdominal angina. The patient also noted increasing dyspnea, and was found sitting on the edge of his bed trying to catch his breath. He denied any recent fever or chills, hematochezia, or melena. In the ED, he was afebrile with a BP 101/50 mmHg, pulse of 93/min, and oxygen saturation of 92% on 2 liters nasal cannula, and respirations of 24/min. His cardiac exam was regular. His lungs revealed bibasilar crackles. His abdomen exam revealed an obese abdomen with some pain to deep palpation in the lower quadrants, but overall fairly benign. Bowel sounds were normoactive, and there was no hepatosplenomegaly. Rectal exam was guaic negative without any masses. Laboratory data was significant for a creatinine 3.6 mg/dl, with normal liver function tests and coagulation tests. His abdominal pain was never clarified on admission, but was still concerning and a CT scan of the abdomen without contrast because of renal insufficiency was ordered in the morning. STAT surgical consultation was obtained and after discussion with the family regarding the high operative risk of mortality versus certain sepsis and mortality without surgery, the patient and family decided to become comfort care. The patient's pain was controlled, and comfort measures were initiated with his family at the bedside. The patient ultimately demised after two days. A higher clinical suspicion may have led to earlier diagnosis.\nOUTPUT:" }, { "from": "agent", "value": "Hepatic Portal Venous Gas, Pneumatosis Intestinalis, Acute Mesenteric Ischemia, Pulmonary Embolism" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 73-yr-old male presented to us with a pulsating abdominal mass. His past medical history was positive for smoking, hypertension, benign prostatic hypertrophy, and parkinsonism. On physical examination, a pulsating non-tender abdominal mass of about 8 cm in diameter was palpable around the umbilicus. Lower extremity pulses were palpable without evidence of aneurysmal dilatation. Laboratory tests, chest radiography, and electrocardiography were normal. The patient underwent a transfemoral aortogram (Fig. 1) to evaluate the renal arterial anatomy. One pelvis and one ureter for each kidney were also identified. Operation was conducted. The retroperitoneal cavity was approached transperitoneally. The ureter of the lower (crossover left) kidney crossed the midline at the level of the bifurcation and entered the bladder. To minimize renal ischemic injury, we dissected the lower two renal arteries (one from the aneurysm itself and the other from the left common iliac artery) and anastomosed the lowest renal artery (from the left common iliac artery) to middle renal artery (from the aneurysm itself) in a side-to-end fashion before aneurysm resection. We administered mannitol before the aortic cross clamping. After the proximal anastomosis of the bifurcated graft, two renal arteries were individually reimplanted and blood flow was resumed to renal arteries. The renal arteries were reperfused within 20 min after the aortic cross clamping. Anastomosis of the two iliac limbs of the bifurcated graft to common iliac arteries was performed without concern of the time. The patient recovered uneventfully and was discharged on postoperative 7th day. Magnetic resonance (MR) angiogram (Fig. 2) was taken two weeks after the operation and showed patent renal arteries and well perfused kidneys.\nOUTPUT:" }, { "from": "agent", "value": "Abdominal aortic aneurysm, Crossed ectopia with fusion anomaly of the kidney" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: This imaging procedure (Toshiba Aplio XG, using a curved 3.5-MHz probe) showed intense hyperechoic, homogenous and well-defined nodules in segment VII/VIII (3.1 x 2 cm, 0.9 x 0.6 cm and 0.7 x 0.7 cm), segment V/VI (1.5 x 1.5 cm) and another in the caudate lobe (1.8 x 2.2 cm) (fig. 1). 2). A follow-up ultrasound at 3 months demonstrated all lesions with a typical hypo- to isoechoic pattern (fig. 3a). These ultrasound images from the referral hospital were available, demonstrating identical sonographic features (fig. An additional contrast-enhanced ultrasound on Aplio XG using low mechanical index after injection of 1.4 ml of the contrast agent SonoVue showed for the lesion in segment VIII a typical peripheral nodular arterial enhancement with a portal venous centripetal filling consistent with typical hemangioma.\nOUTPUT:" }, { "from": "agent", "value": "Liver Hemangiomas, Pneumonia, Systemic Inflammatory Response Syndrome (SIRS)" } ]

[ { "from": "human", "value": "As a physician engaged 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 adolescent was referred to the outpatient child and adolescent psychiatry clinic for odd affect, cognitive blunting and psychomotor retardation by a pediatric neurologist who ruled out an underlying neurologic condition upon the request of the patient's legal guardian. The legal guardian was a significantly older sibling who had been independently raising the patient over the last several years. As the adolescent was unaccompanied to the psychiatric appointment it was not possible to elucidate the development of the clinical findings over time. Further assessment was delayed due to a missed follow-up appointment and unreturned phone calls by the guardian. Case management was established after a report concerning for medical neglect was filed by the outpatient CAP. Adequate food availability at home was confirmed by the case manager. Behavioral interventions and guidelines for close monitoring were outlined by the CAP; however, these were not adhered to at home despite numerous care conferences between the CAP, legal guardian, case manager, and school counselor. The patient demonstrated lack of insight into the illness and endorsed a lack of motivation for change. Psychiatric symptoms progressed to social withdrawal, and self-imposed seclusion in the context of minimal oral intake. The guardian repeatedly vocalized hopelessness considering the patient's unwillingness to eat and hesitation to follow through with the treatment plan due to concern that the patient may run away from home, although the patient had never expressed this intention. Over the course of treatment, the patient was medically hospitalized on multiple occasions due to malnutrition and unstable vital signs. While weight restoration in the hospital occurred without difficulty, weight drastically plummeted soon after discharge home. Reports of concern for ongoing medical neglect were raised to CPS but were not substantiated by the agency.\nOUTPUT:" }, { "from": "agent", "value": "Eating disorder" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She was cared by a maid at home; however, her children were busy and seldom visited her during weekdays. She had repeated admission for anemic and uremic symptoms. Her blood transfusion requirement was 2-3 U of pack cells per 2 months. In July 2014, she was admitted to our unit because of dizziness again. This time, her hemoglobin level was dropped to only 3.4 g/dL. Thus, urgent blood transfusion was required, and RBRS was utilized by the on-call nursing officer who successfully collected the red cells. The whole procedure only took about 5 min. The patient's condition improved after blood transfusion with most of her symptoms reduced. However, she was deteriorated gradually because of declining of renal function and finally passed away peacefully. He finally decided for blood transfusion only. Once, he was admitted to our unit because of anemic symptoms and was found to pass tarry stool for few days at home. Since he refused for further investigations including endoscopy and biopsy, he was planned for supportive treatment including rehydration, blood/blood products transfusion, and proton-pump inhibitor injection. After baseline investigation, his hemoglobin level was only 5.1 g/dL. Our on-duty nursing officer was informed about the management plan and then decided to use the RBRS when our blood bank was closed during that holiday. Again, he could easily handle the operation of RBRS and collect the red cells successfully. After transfusion, the patient became well and then discharged uneventful after the holiday. There was no adverse report or incident as noted from these two cases.\nOUTPUT:" }, { "from": "agent", "value": "ESRD, Anemia, Hypertension, Diabetes Mellitus, Hyperlipidemia, Multiple Myeloma, Gastrointestinal Bleeding" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: It is estimated that 1 to 6% of hospitalized patients due to COVID-19 will develop a stroke. For example, Quenzer et al. Rajae et al. described an ischemic stroke in frontal, temporal, and parietal regions presenting as the primary manifestation of COVID-19. Prasad et al. reported a patient that developed ischemic stroke in several vascular territories after recovering from hypoxic respiratory failure due to COVID-19. One promising rehabilitation strategy is comprised by brain-computer interface (BCI) interventions since they have shown evidence of efficacy for the upper limb motor recovery of stroke patients. A BCI decodes information from the central nervous system and translates this information into commands for external devices, such as rehabilitation robots. The rehabilitation was provided as part of the patient's participation in a clinical trial for stroke neurorehabilitation with a BCI.\nOUTPUT:" }, { "from": "agent", "value": "Stroke related to SARS-CoV-2 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: The authors report a case of a 36-year-old active man with no relevant medical history, who went to the emergency department due to a diffuse headache and dizziness, with a 3-day course after a long bicycle ride. The patient referred that these symptoms were usual after an intense physical activity as he regularly performed in cycle races. He was admitted to Neurology observation in the Emergency Room (ER). On examination, there were no evident de novo neurological signs. A cerebral CT was performed, and it was normal. He was then referred to Ear, Nose, and Throat (ENT) observation due to suspicion of peripheral vertigo. The ENT examination revealed a horizontal-rotatory nystagmus, with rapid phase to the right, that was exhaustible in the gaze, however with a normal head impulse test. The Neurology ER team assumed noncentral vertigo since at this time there was no evidence of any signs of a central cause, neither in physical examination nor in the imaging test performed. This diagnosis seemed the most likely to the team. He was admitted to the ENT ward, and symptomatic and medical treatment was initiated. There was clinical stabilization until the 3rd day, when sudden symptoms and signs emerged: ipsilateral downward fall, right hemifacial paresthesia, right hemifacial pain, ipsilateral limb ataxia with ataxic gait, and diplopia. An emergent magnetic resonance angiography revealed \"(...) hyperintense area in T2 and T2 FLAIR in the dorsal lateral aspect of the right bulb that in the diffusion study showed a marked restriction (...).\" The patient was transferred to the Cerebrovascular Accidents Unit (CVAU) and started treatment with antiplatelet therapy, rehabilitation with obvious improvement. At the time of hospital discharge (15 days after admission), he had just a slight alteration in gait and left eye ophthalmoparesis.\nOUTPUT:" }, { "from": "agent", "value": "Vertebral Artery Dissection, Posterior Inferior Cerebellar Artery Infarction" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The patient complained of bilateral orbital pain with gradual protrusion of eyes since 30 years old. Thyroid function tests, including T3, T4, thyroid-stimulating hormone and free T4, showed normal results. Magnetic resonance imaging (MRI) of the eyes revealed increases in retrobulbar space with fat-like density and mild hypertrophy of extra-ocular muscles (Fig. 1A). She received enzyme replacement therapy (ERT) with imiglucerase (Cerezyme) at a dose of 60 U/kg every two weeks since 32 years old. Exposure conjunctivitis still bothered her currently. The patient suffered from intermittent dyspnea at age 34 years. She became cyanotic and had an oxygen saturation of 85% as measured by pulse oximeter. Arterial blood gas analysis revealed a pH of 7.41, carbon dioxide tension of 27.9 mmHg, and oxygen tension of 61.2 mmHg in room air. A grade III/VI bruit was audible over the right lower chest, and a chest x-ray revealed prominent pulmonary conus and increased infiltration over the right lower lung field (Fig. 1B). A high-resolution computed tomography (HRCT) of the chest suspected an AVM with engorged right inferior pulmonary artery and its draining veins (Fig. 1C); but no focal lesions were found in the lung parenchyma. Right pulmonary artery angiogram showed several dilated and tortuous vessels from the right pulmonary artery, which directly connected to vessels draining into the right pulmonary vein over the right lower lobe of the lung (Fig. 1D). The patient's pulmonary artery pressures were 48/19 mmHg (mean, 33 mmHg). Embolization was achieved with 6 coils, and resulted in a rise of oxygen saturation to 96%, although residual shunt was still present. Unfortunately, two months later, dyspnea and cyanosis recurred, and her oxygen saturation dropped to 85% in room air. A pulmonary function test at that time revealed moderately severe restrictive lung disease.\nOUTPUT:" }, { "from": "agent", "value": "Type I Gaucher disease, Exophthalmos, Pulmonary arteriovenous malformation" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A more detailed description of disease progression is presented in case reports, some of which are summarized in Table 1. Fever was present in all patients described in these reports. Edema, predominantly on the face, was observed with a relatively high frequency, as were lymphadenopathy, hypereosinophilia, and atypical lymphocytes. Internal organ involvement manifested itself largely as liver dysfunction, with elevated levels of liver enzymes and cholestatic hepatitis with hepatocellular insufficiency. Kidney failure was observed in a 75-year-old lamotrigine patient. Multiple organ failure was observed in a couple of studies, one of which resulted in death. Hypogammaglobulinemia, another symptom of DIHS, was observed in a number of studies as well. The offensive drug is immediately interrupted in DIHS patients, and treatment with prednisolone is often used to reverse the condition. Symptoms begin to improve gradually, but both fever and skin manifestations often relapse approximately 2-3 weeks after the onset of DIHS. There is a delay until antibodies to the virus are generated. Therefore, there is a delay until the peak of the infection is detected. Symptoms relapse coincides with detection of HHV-6 reactivation, measured by circulating anti-HHV-6 antibodies and HHV-6 DNA. Anti-HHV-6 IgG levels are elevated after 3 weeks following the onset of the reaction (time of drug withdrawal), but not after 2 weeks. Increases in HHV-6 DNA in PBMCs were found to precede the increases in anti-HHV-6 IgG levels in anticonvulsant HSR patients and were absent in controls. The presence of HHV-6 DNA in PBMCs was found to correlate with the magnitude of anti-HHV-6 antibody titers (P = 0.0002). Intermittent detection of HHV-6 DNA in PBMCs was not indicative of illness, such that HHV-6 DNA can be found in the PBMCs at low levels in immunocompetent children, with and without symptoms. Significant increases in anti-HHV-6 IgG titers were noted in all 6 patients included in a study. HHV-6 infection was confirmed in all 6 patients by PCR in PBMCs. HHV-6 reactivation was observed between 17 and 27 days after the onset of the reaction.\nOUTPUT:" }, { "from": "agent", "value": "Hypersensitivity Syndrome Reaction, Human Herpes Virus-6 Reactivation" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 33 year old male presented with a fifteen-hour history of vomiting, diarrhoea, and lower abdominal pain one week after a holiday in Portugal. He had no significant past medical history. On examination he had a tanned appearance, and was tender with guarding and rebound in the right iliac fossa. Rovsing's sign was positive. Over the next 24 hours he had persisting pyrexia and became tachycardic and hypotensive. Examination revealed decreased chest air entry bilaterally and abdominal distension. C reactive protein was increased to 369ug/L, from 5.0ug/L on admission. Electrolyte profile confirmed hyponatraemia. Arterial blood gas sampling showed a metabolic acidosis. He was thought to be septic. The following morning a CT scan of chest and abdomen showed, bilateral pleural effusions with collapse at both lung bases. There was free fluid in the abdomen with dilatation of the small bowel throughout its length. He was thought to have a postoperative ileus, but an atypical pneumonia was also considered. He was transferred to ICU. Over the next 24 hours the abdominal distention increased and in view of this he returned to theatre. At laparotomy, an inflammatory mass was found in the caecum and terminal ileum, causing small bowel obstruction. A limited right hemicolectomy was done. His general postoperative condition remained poor. Further discussions with the family revealed that the patient had been of a tanned appearance since he had returned from holiday in a hot climate 10 years previous. The tanned appearance, hyponatraemia, and polyuria raised the possibility of adrenal insufficiency and a Synacthen test was undertaken. Treatment with intravenous hydrocortisone and fludrocortisone lead to an immediate clinical improvement. He was discharged home well five days later.\nOUTPUT:" }, { "from": "agent", "value": "Acute appendicitis, Addison's disease" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The second case (GS0155) is a 27-year-old female. She had had some episodes of right hemiparesis and a bowel volvulus in pediatric age. She was studied in the Neurology Unit after an episode of right hemiparesis, paresthesia and a visual field deficit. Imaging studies did not show any significant alteration. Biochemical analysis showed calcium values in the lower limit of normality (8.5-9.3mg/dl) and elevated PTH (200-300pg/ml), so she was diagnosed of pseudohypoparathyroidism. She did not present any symptom of Albright's hereditary osteodystrophy (height 1.65m; weight 68.5kg; BMI: 25.1). No other hormone deficit was detected (TSH, 3muU/ml). She referred regular periods. Calcium and vitamin D supplements (both cholecalciferol and calcifediol) were prescribed, although she is not properly following the treatment. In the last visit, she referred paresthesia in upper extremities with no calcium supplementation for a month. She brought a report with analytical levels: Ca, 8.7mg/dl; P, 3.9mg/dl; Mg, 2.4mg/dl, TSH, 4.15muU/ml; PTH, 349pg/dl; 25(OH)D, 37.2 ng/ml; urine Ca, 76mg/day; CLcr, 177ml/min; Dual-energy X-ray absorptiometry (DXA) with a lumbar T score of -0.7 SD and a femoral T score of -0.3 SD. She is clinically stable, with no symptoms of latent tetany. Biochemical analysis were performed: Ca, 8.9mg/dl; P, 3.7mg/dl; HbA1c 5.4%, PTH, 417pg/dl; 25(OH)D, 44 ng/ml. Her mother was diagnosed at age 48 years with a multinodular toxic goitre. She was treated with I131 that caused iatrogenic hypothyroidism, so she was prescribed levothyroxine 125mug/day. Her past clinical history showed symptoms of generalized anxiety, being followed in the Mental Health Unit. She does not present any characteristic phenotype, with a normal physic exploration (height 1.64m; weight 70kg; BMI: 26).\nOUTPUT:" }, { "from": "agent", "value": "Pseudohypoparathyroidism type Ib" } ]

[ { "from": "human", "value": "As a physician engaged 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 male patient presented to our out-patient department with a history of injecting about 5 ml of kerosene to his left hand at two sites following an argument with his family members 2 days prior to presentation, with an intention to commit suicide. Initially he experienced mild pain and redness at the injected sites. After 2 days, the pain became intolerable leading to disturbed sleep, with multiple blisters and swelling of the left hand. He is a chronic alcoholic, but he has had no psychiatric problems. No other significant medical history was noted. On examination, he was an alert middle-aged man, moderately built and nourished, and well oriented to time, place, and person. He was in agonizing pain with a temperature of 38 C. Systemic examination was within normal limits. Multiple vesicles and blisters were present over the left forearm and few over the dorsal aspect of the left hand. Few erosions were also present. Black discoloration extending from the hand up to the lower third of the arm was present. Local rise of temperature and tenderness was present from the hand up to lower third of arm. Patient was unable to flex the hand. Peripheral pulses (radial, ulnar, and brachial arteries) were feeble. Capillary refilling could not be elicited [Figures 1 and 2]. There were no other lesions. Examination of the mucus membranes, hair, and nails was normal. The patient was admitted to the ward; intravenous (IV) amoxycillin with clavulinic acid, IV steroid, and IV fluids were started. The patient was referred to Department of Surgery and Psychiatry for an opinion. But the patient refused to take further treatment and left against medical advice.\nOUTPUT:" }, { "from": "agent", "value": "Irritant contact dermatitis, Cellulitis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Testolactone (200 mg/day) therapy was initiated. After the first year of treatment, testolactone was discontinued. Anastrazole was started and used for four years. On this treatment, serum E2 levels ranged between 29 and 59.3 pg/mL, LH - 0.15 and 0.2 mIU/mL, and FSH between 0.1 and 2 mIU/mL. Pelvic ultrasonography revealed uterine volume between 6.2 and 10.2 ml with persisting follicular cysts of 23-32 mm in diameter. Growth rate was 6 cm/year during this period. Anastrozole treatment was discontinued when the patient reached 11 years of age. At this time, she was at pubertal stage 3, with a bone age of 12 years. She started to have spontaneous menses six months after discontinuation of anastrazole therapy. Her menstruation periods were irregular at the beginning, but she has had regular menses in the past three years. She was 153.8 cm (-0.9 SD), 50.1 kg (-0.1 SD) and had achieved Tanner stage B5 in her recent control when she was 14 years old. Our patient was in euthyroid status without any treatment during the last four years. Thyroid ultrasound and fine-needle aspiration biopsy were planned to be annually performed. During the follow-up period, no other endocrinopathies (e.g. hypercortisolism, hyperprolactinoma or growth hormone excess) that may accompany MAS were noted. There was no pathology on the MR images of the sella either.\nOUTPUT:" }, { "from": "agent", "value": "McCune-Albright syndrome, Subclinic hyperthyrodism, Multinodular goiter" } ]

[ { "from": "human", "value": "As a physician engaged 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 underwent deceased donor renal transplant (DDRT) in 2018. Her transplant was initially complicated by delayed graft function. Two consecutive renal biopsies showed mild acute tubular injury without any evidence of antibody-mediated or cell-mediated rejection. Patient continued the hemodialysis for a few more months until graft function returned to normal. Her creatinine level changed from 1.89 mg/dL to current baseline level of 1.1-1.2 mg/dL. In 2019, an incidental mass was found in her left native kidney during routine post renal transplant workup. An abdominal magnetic resonance imaging (MRI) with and without contrast showed a subtle T2 hypointense, T1 intermediate lesion at the interpolar renal hilum measuring up to 2.6 cm demonstrating mild early enhancement, diffusion restriction, and delayed washout, concerning for renal cell carcinoma or less likely urothelial carcinoma of renal pelvis (Figure 1(a)). CT urogram showed a questionable heterogeneous enhancement within the left renal pelvis (Figure 1(b)). Given the concern of urothelial carcinoma, diagnostic ureteroscopy was performed but did not show any mass in the renal pelvis. Due to anatomic location of the mass and major imaging and clinical concern for malignant process, like renal cell carcinoma, endoscopic ultrasound-guided needle biopsy of mass was performed. Histopathological examination was not conclusive for definite pathologic diagnosis due to inadequate tumor sampling. Considering high risk of renal cell carcinoma in patient due to years on dialysis and chronic immunosuppression, the patient subsequently underwent laparoscopic nephrectomy of native kidney. Patient had an uneventful postoperative and recovery phase.\nOUTPUT:" }, { "from": "agent", "value": "Myelolipoma of renal sinus, End-stage renal disease" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 44-year-old Zimbabwean-born male was referred with a 12-month history of cough, areas of patchy sub-pleural consolidation on thoracic Computed Tomography (CT) (Fig. 1), and a significantly elevated serum Immunoglobulin subclass 4 (IgG4) level (4.61 g/L; normal range 0.08-1.4 g/L). He was a lifelong non-smoker with no significant prior medical history and, particularly, no history of pancreatitis. He was not on any regular medications. Physical examination was unremarkable, and lung function testing revealed an isolated mild reduction in forced vital capacity (3.3 L, 78% predicted) with normal gas transfer. Connective tissue disease and vasculitic serology was negative, and C-reactive protein (CRP) was 2.7 mg/L (normal <5 mg/L). Absolute blood eosinophil count of 0.47 X 109/L (normal <0.60 X 109/L), however, was elevated as a proportion of white cells at 8%. Bronchoscopy with bronchoalveolar lavage and trans-bronchial lung biopsy was non-diagnostic, and he proceeded to a surgical lung biopsy. 2). Subsequent stool microscopy confirmed the presence of Schistosoma mansoni ova; microscopy of urine did not reveal any schistosome ova. He was treated with praziquantel at a total dose of 40 mg/kg (3600 mg), split into two doses administered 4 h apart. At three- and 12-month follow up, his cough had resolved, and serum IgG4 levels had reduced significantly (from 4.61 to 1.59 g/L). Stool microscopy became negative for schistosome ova, and the eosinophil percentage of total white cells normalized (4%).\nOUTPUT:" }, { "from": "agent", "value": "Pulmonary schistosomiasis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Physical examination at our hospital when he was re-evaluated at 12 years old revealed his weight was 44.1 kg (+0.42 SDS), height 148.4 cm (-0.32 SDS, MPH 175 cm, -0.21 SDS), arm span of 147.8 cm, body mass index 20.2 kg/m2 (+1.03 SDS) with broad hips. There was mild gynaecomastia (similar to breast Tanner stage 3) but no galactorrhoea. His right scrotum was empty and there was only a palpable 2mls testis in the left scrotum. Penile size was 5.2 cm x 2.0 cm with no pubic or axillary hair. Examination of both his upper limbs revealed reduced range of movement on pronation and supination which led him to having difficulty in opening bottle-caps and door-knobs. The rest of his physical examination was normal. X-ray of the right forearm including the elbow joint showed a proximal radio-ulnar fusion/synostosis (Fig. 1). The bone age was 12 years, similar to his chronological age. Baseline laboratory data were LH < 0.1 mIU/ml, FSH 1.4 mIU/ml and testosterone 0.6 nmol/L with estradiol 96 pmol/L. HCG stimulation test showed a minimal rise of testosterone from 0.6 nmol/L on day 0 to 3.0 nmol/L on day 4. Chromosome study based on 76 cells revealed 47 XXY [9, 12 %]/46 XX [67, 88 %] with positivity of SRY determined by FISH. Laparoscopic examination of the abdomen and pelvis confirmed absence of Mullerian structures with small left testis within the scrotal sac, epididymis and vas deferens. He received 50 mg intramuscular testosterone injection every 4-weeks at the age of 13 years to initiate his pubertal development. At the age of 14.5 years, his repeat baseline laboratory data taken on the day of intramuscular testosterone 100 mg every 4-weeks, showed LH 6.3 mIU/ml, FSH 9.2 mIU/ml, testosterone 4.3 nmol/L, consistent with partial hypergonadotropic hypogonadism.\nOUTPUT:" }, { "from": "agent", "value": "Klinefelter 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: An 18-year-old male patient presented for orthodontic retreatment with the chief complaint of unaesthetic facial appearance (Figs 1- 4). Previous treatment lasted 24 months and afterwards a retention period of 19 months. Lastly, mandible and maxilla alignment, to correct dental and facial midlines.\nOUTPUT:" }, { "from": "agent", "value": "Severe skeletal Class III malocclusion, Mandibular prognathism, Anterior crossbite, Retroclination of the mandibular incisors, Transverse asymmetry, Root resorption in the maxillary incisors, Mild horizontal bone loss in the mandibular incisors" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Table 1 displays the selected caregivers. Age ranged from a minimum of 20 years to a maximum of 53 years. Of note, a 20-year-old caregiver was looking after her father, because the parents separated long ago. The sample consisted of more female caregivers (five) than male caregivers (one). There were four married and two single caregivers. Most of them (five) had no income and only one was receiving a monthly income of about R6000-R10 000, because he had a job. The majority of participants had no monthly income, because they were not employed and were earlier dependent on the CKD patients before the onset of illness. Table 2 reveals the summary of the main and emerging themes from the perspective of caregivers regarding engagement with integrated management of CKD patients. Hypertension and diabetes mellitus were the most highlighted risk factors of CKD confirmed by the caregivers. Unemployment, changes in lifestyle and limited social interaction were cited as negative effects of CKD. Consequences of non-engagement with integrated management included difficulty in breathing, swollen lower and upper limbs, readmissions, abnormal blood results, additional treatment and faster progression of CKD to late stages that require dialysis. Barriers to engagement with integrated management were side effects of diet and haemodialysis, hot weather, unemployment, false perception of good health and shortage of kidneys for transplantation. The literature was linked to the themes identified and reconstructing interpretations into something meaningful. This process was influenced both by the original research objectives and new concepts generated inductively from the data. The emerged themes were made into narrative passages and the findings emerged logically from the participants' responses. Verbatim quotes were set as extracts and they were used to give the reader an idea of how main and emerging themes evolved during the process of data analysis in this case study.\nOUTPUT:" }, { "from": "agent", "value": "Chronic Kidney Disease" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Abnormal urine sediment was revealed in one child. As for inflammatory markers, all children apart from one with leukopenia had normal white blood cell count and all the patients had CRP level within normal limits. Kidney function was normal in all 4 children. Two children had hypoalbuminemia. Positive result of QuantiFERON-TB test was found in all the patients. In 2 children (cases No. 2 and 3) bronchoalveolar lavage was performed and 3 children were tested with Gen-Probe and BACTEC MGIT system (cases No. 2, 3, 4). In none of the patients positive results of genetic tests, bacterioscopy or culture were found. Chest X-ray and ultrasonography of the urinary tract were performed in all these 4 children and revealed no abnormalities. Chest CT examination was performed in 3 children (cases No. 1, 2, 4). At the moment of diagnosis, 3 children were treated with GCS. Three patients were diagnosed with LTBI. One child (case No. 2) was diagnosed with lymph node TB after exclusion of other possible causes of lymphadenopathy (Mycoplasma pneumoniae, Chlamydophila pneumoniae, Toxoplasma gondii, and neoplasms). LTBI was treated with 6-month therapy with isoniazid. In the child with proteinuria and erythrocyturia (patient No. 4), chemoprophylaxis with isoniazid and renoprotective treatment with enalapril was used. Proteinuria subsided during antituberculous treatment and concomitant nephrological treatment in all the patients.\nOUTPUT:" }, { "from": "agent", "value": "Tuberculosis infection, Proteinuria/Nephrotic 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: Currently the patient presents malformations of the lower left limb (hip, knee and ankle), evident on the articular and periarticular level, where there are diffuse exostoses. This case discusses the main occupational concerns relating to the patient's workspace at a high floor level that could create critical issues in the event of an emergency exodus. Given the impossibility of placing the patient in heavy manual activities, employment is limited to office activities. Adjustments were carried out at the patient's workstation, and thus the patient has been recognized as fit to work. Increased frequency of breaks were prescribed in order to allow the physiological alternation of postures. Image Caption and Description: \nImage caption: []\nImage description: []\nCase Report: \nFor our patient, the maximum distance between a safe place to go to in event of an evacuation (as determined by the fire department, which was on a level) and the patient's workstation or other places of work the patient occasionally frequented, such as reading room and book store, was <30 meters. A simulation was carried out at the patient's workplace by the patient to assess the time taken for arrival at the safe place from the usual workstation (30 seconds) and from a more distant location (45 seconds), which seem to be acceptable times for the worker to keep in safe.\nOUTPUT:" }, { "from": "agent", "value": "Overgrowth syndrome" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Few hours later, the patient collapsed again and referred immediately to angio-suite for TAE. 3a). 3b,c). TAE was then performed using gelatin sponge until arterial occlusion obtained (Fig. 3d). After embolization, the patient remained hemodynamically stable and did not require further transfusion. A follow-up CECT was performed 5 days later and showed no more extravasation of contrast media and confirmed the presence of CA stenosis by cMAL (Fig. 4a,b). This case series has been reported in line with the PROCESS criteria and has been registered at ResearchRegistry.com (researchregistry3605).\nOUTPUT:" }, { "from": "agent", "value": "Severe celiac axis stenosis, Hepatic hemorrhage, Grade 4 liver injury" } ]

[ { "from": "human", "value": "As a physician engaged 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 39 years old pre-menopausal woman came to our attention with a locally advanced BC. The pathological evaluation revealed the presence of HR-/HER2+ IDC (cT3N2). The patient initially received 3 cycles of neoadjuvant FEC followed by docetaxel concurrent with trastuzumab; docetaxel was discontinued due to anaphylactic reaction. She then underwent left mastectomy plus AND. The pathological study of the surgical specimen reported the presence of scattered foci of residual IDC in the breast and the presence of metastasis in four axillary nodes (ypT1micN2). After surgery, 1 year of trastuzumab treatment was completed. The patient also underwent RT to the chest wall and sovra-clavicular fossa. After 12 months from the end of adjuvant trastuzumab, the patient experienced isolated skin relapse. In particular, she presented with itchy erythematous skin lesions on her left chest wall. Since a restaging PET did not reported any sign of distant metastatic disease, a wide cutaneous surgical excision was performed. Pathological study of the surgical specimen confirmed the presence of HR-/HER2+ skin recurrence. The patient was then offered systemic therapy with CT plus an anti HER2 agent. However, she refused treatment. The patient was therefore strictly followed-up. However, after a disease-free interval (DFI) of 4 months, the patient experienced a second skin relapse, with a wide erythematous rash appearing on her trunk. Systemic therapy with trastuzumab plus vinorelbine was therefore administered. Unfortunately, 5 months later, the patient experienced a cutaneous disease progression, consisting in an increasing in size of pre-existing skin lesions and appearance of new skin lesions on the antero-lateral abdominal wall. TDM1 was then initiated. Two months later, a complete response was achieved. After 17 cycles of TDM1, the patient decided to stop treatment. After 9 months since TDM1 had been discontinued the patient was still disease free (Figure 2).\nOUTPUT:" }, { "from": "agent", "value": "Breast Cancer Skin 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: This 48-year-old female was a front passenger in a van involved in a head-on collision with a car and was subsequently trapped in a sitting position for 75 minutes. She was given high-flow oxygen via an NRBM which initially maintained her SpO2 around 98%. However, bleeding into the airway became an increasing problem despite frequent suctioning, and her SpO2 was seen to fall to 88%. Extrication and transport in a supine position were considered to carry a major risk of aspiration if undertaken with an uncontrolled airway. Consequently, an iLMA was inserted after sedation with midazolam (two 5 mg IV boluses) with the patient still trapped in a sitting position (Figure 1). Spontaneous respiration was augmented with a bag-valve-mask device (BVMD) fitted with an oxygen reservoir and the SpO2 rose rapidly to 100%. In view of the good response, it was judged unnecessary to intubate the patient via the iLMA either at the scene or en route to the nearby hospital. On arrival at hospital the duty anaesthesiologist requested removal of the iLMA in order that RSI could be performed under direct laryngoscopy. The iLMA was therefore reinserted and, following a period of reoxygenation, the author intubated the patient via the iLMA at the first attempt. The patient went on to make a full recovery.\nOUTPUT:" }, { "from": "agent", "value": "Severe polytrauma, Extensive facial injuries, Low platelet count due to idiopathic thrombocytopenic purpura, Open fracture of the left wrist, Fracture dislocation of the left elbow, Anatomical anomaly (recession of the mandible)" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: He also monitored the dirty electricity in his home using a Protek 506 Digital Multimeter connected to a ubiquitous filter to remove the 60-Hz signal and its harmonics. Measurements were taken in the morning and randomly throughout the day. Low or no readings of dirty electricity were taken in an electromagnetic clean environment far from power lines and cell phone antennas (Fig. 1 upper graph). Three years later, the microsurge meter became available and Case 1 monitored his blood sugar levels once more (Fig. 1 lower graph). This meter provides a digital readout of the absolute changing voltage as a function of time (|dv/dt|, expressed as GS units) for the frequency range 4-100 kHz and with an accuracy of +-5%. Figure 1 shows a positive correlation between dirty electricity and plasma glucose levels taken randomly during the day (upper graph) and first thing in the morning (lower graph). His elevated plasma glucose is unrelated to eating. Working on a computer increases blood sugar, but these values decrease as much as 0.11 mmol/L* [2 mg/dL] per minute after moving away from the computer. Blood viscosity decreased as his plasma glucose levels dropped. Case 1 also documented rapid changes in blood sugar as he moved from a medical clinic (environment with dirty electricity), to his parked vehicle (no dirty electricity), and back to the medical clinic. His blood sugar levels changed significantly within 20 min. Measurement of blood sugar needs to be done in an electromagnetically clean environment to prevent misdiagnosis and to accurately determine the severity of the disease.\nOUTPUT:" }, { "from": "agent", "value": "Type 2 diabetes" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: 1). 2). Physiologic pulse and blood pressure responses were noted: blood pressure rose from 130/70 to 160/75, and heart rate dropped from maximal rate of 150 down to 100 within 2 min after exercise. No other wall motion abnormalities were noted. Coronary angiography was advised. The right coronary artery (RCA) revealed minimal disease. Coronary artery bypass grafting was performed, with a left internal mammary graft to the LAD and saphenous vein grafts to two obtuse marginal branches.\nOUTPUT:" }, { "from": "agent", "value": "ST elevation, Anteroseptal infarction, 60-70% eccentric stenosis of the left main coronary artery, 70% long proximal stenosis of the left anterior descending (LAD), 99% mid-LAD stenosis, Total occlusion of a small LAD diagonal, 70% heavily calcified obtuse marginal branch stenosis, Antero-apical hypokinesis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She had previously received intramuscular interferon beta-1a, intravenous immunoglobulin, baclofen for spasticity, steroids, and rehabilitation therapy, but had not been treated with compounded 4-AP. The patient had sensory impairment, imbalance, limitations in leg muscle strength, and bilateral visual impairment that together contributed to a severe walking impairment and made it difficult for her to walk a great distance. She reported that she could walk a maximum of 20 m using two walking crutches. Clinical assessment revealed that she had severe walking impairment due to spastic paraparesis and ataxia (see Supplementary Video Patient #3), an EDSS score of 6.5, severe spasticity in both legs, proximal and distal paraparesis (LEMMT grades 4 out of 5 and 2 out of 5, respectively), and a T25FW time of 29.4 seconds (walking speed, 0.26 m/second). After 4 weeks of treatment with PR-fampridine, patient #3 reported experiencing dizziness, confusion, and difficulties with short-term memory tasks after initiating PR-fampridine. She continued to have severe spasticity in both legs, and her paraparesis remained unchanged proximally but worsened distally (LEMMT grade 1 out of 5). Interestingly, this patient did report an improvement in her vision and physician assessment at the 4-week visit found no detectable nystagmus. Based on physician assessment and patient report, this patient was considered to have no clinical benefit with PR-fampridine treatment and she reported potentially treatment-related side effects. Treatment with PR-fampridine was stopped and the patient was no longer followed-up on.\nOUTPUT:" }, { "from": "agent", "value": "MS and secondary-progressive MS" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Biochemically the patient had no clinical signs or symptoms of Cushing disease and the ACTH and cortisol tests were within the normal range (ACTH 83pg/ml; cortisol 2,17mug/100ml). Histological analysis showed an ACTH-secreting adenoma, with a Ki-67 less than 3%. As the postoperative MRI showed a millimetric remnant, the patient was treated with adjuvant radiotherapy. In 2002, he suddenly developed a left fourth-nerve palsy due to compression of the cavernous sinus by a multilobulated cyst. A transsphenoidal endoscopic drainage of the cyst was performed, which resulted in a complete recovery of the fourth-nerve palsy but induced a panhypopituitarism. In 2014, he developed an asymptomatic retroclival extra-axial mass encasing both vertebral arteries and compressing the medulla oblongata. In absence of other malignancies this lesion was most likely a metastasis. Because of the challenging location, the absence of clinical symptoms or biochemical abnormalities the decision for watchful waiting was made. In 2015, this lesion caused a mass-effect on the medulla oblongata ( Figure 3B ) and a second lesion in the left cerebellar tonsil was diagnosed. Therefore, a surgical resection of the two lesions was performed. The histopathological analysis confirmed the metastasis of an ACTH-expressing adenoma. Neither obvious nuclear atypia nor mitotic activity was observed. The Ki-67 was less than 3% and p53 was negative. A follow-up cerebral MRI 6 months postoperatively showed multiple new tumoral lesions at different intracranial locations. Due to the disseminated disease a treatment with temozolomide was initiated. After 12 cycles there was a slight decrease in size of the cerebellar and supratentorial lesions, the other lesions remained stable. Treatment was halted and at last follow-up in September 2021 there was no further clinical, biochemical or radiological progression.\nOUTPUT:" }, { "from": "agent", "value": "Pituitary 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 20-year-old male presented with alleged history of assault having stab injury with a knife over the front of neck. Victim arrived within 1 h of penetrating trauma. On initial assessment as per the Advanced Trauma Life Support (ATLS) principles in Emergency Department, primary survey was unremarkable without any abnormality. However, secondary survey revealed a 1 x 0.5 cm in length penetrating wound situated in zone II of the neck, 1 cm left of midline, anterior to sternocleidomastoid muscle (Figure 1), without any neurovascular deficit. Duplex ultrasound of neck revealed triphasic flow with normal calibre left sided common carotid artery; however, intimal flap visualized in right sided common carotid artery with eccentric partial thrombus (Figure 2). Patient immediately shifted for computed tomography (CT) angiography of neck as per the existing protocol of our institute. CT angiography revealed narrowing of lumen with eccentric thrombus in right common carotid artery about 5 cm proximal to bifurcation (Figure 3). Left sided carotid arteries and brain were unremarkable. Patient planned for surgical exploration of the neck wound under general anaesthesia. There was a through and through tangential rent of 0.5 cm in the right common carotid artery (CCA) with contused segment, situated about 5 cm proximal to carotid bifurcation (Figure 4). Resection of contused segment of about 3 cm done and interposition prosthetic polytetrafluoroethylene (PTFE) graft was placed (Figure 5). Postoperative hospital stay was uneventful and patient was discharged on postoperative day five. Anticoagulants were given for 6 months and then discontinued. Follow-up Duplex ultrasound at 1, 6 and 12 months were normal without any flow abnormality.\nOUTPUT:" }, { "from": "agent", "value": "Central vascular injury" } ]

[ { "from": "human", "value": "As a physician engaged 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 insisted on having the option to hasten death with the help of an organisation that provides assisted suicide (EXIT). At the request of the patient, her physician completed a medical report to be sent to EXIT in case she decided to contact them. However, she said that her spiritual beliefs would hold her back: \"Because I feel, after you have died, you could be punished for it\". She felt ambivalent. In the course of one discussion with her physician she confirmed her wish to hasten death but also asked fearfully whether her continuous nausea and inability to eat would make her starve to death. She had a complex, highly emotional family situation: although all her family members were members of EXIT themselves they were strictly opposed to her hastening her own death, and expressed their disapproval to her. Although when completing the medical report this patient undertook concrete steps to make a hastened death possible (intention type 9: \"Acting towards dying\"), we interpreted her main intention as belonging to type 4: \"Hypothetically considering hastening death (in future if certain things happen),\" since during the interview she expressed her wish as follows: \"When I feel very, very, very wretched, this thought always returns: If you can't bear it any more, you can actually cut it short. Right at the last I just could [pause]... if it's even worse than it isnow...\"\nAs reasons for her WTD she indicated her frequent stomach cramping, nausea, incontinence and feelings of shame, and her poor eyesight, which made it impossible for her to read. We interpreted the intention of her WTD to be based on three wider meanings: to let death put an end to severe suffering: see quote in the text under meaning 2; to end a situation that is seen as an unreasonable demand (meaning 3): \"It is hard this fate [...] it is cruel, I can tell you\"; to preserve self-determination in the last moments of life (meaning 5): \"I am glad to be still so clear in my head. I still can make my own decisions myself.\" Her WTD had also the function of re-establishing agency (function 3): \"But it [WTD] is a ray of hope. You can say, if nothing works anymore and things are only getting worse, then you'd still have some way of shortening it.\" We also interpreted the emphasis with which she expressed her WTD in part as an appeal for moral support for her own position vis-a-vis her family (function 1).\nOUTPUT:" }, { "from": "agent", "value": "Advanced rectal adenocarcinoma" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: In Barbiero and Lio, the authors proposed a computational tool for running simulations integrating a variety of mechanistic and phenomenological models describing the human body with ordinary differential equations (ODEs). This computational framework is hereby used to generate two clinical case studies. The main difference of the proposed approach with respect to the computational tool proposed in Barbiero and Lio consists of a different modeling approach based on state-of-the-art AI models instead of ODEs. Her lifestyle is mainly sedentary and her diet is rich in carbohydrates. The task for the clinician is to personalize the therapy assigning a proper daily dosage of benazepril. This case study is used to show how the digital patient model can be employed to simulate the evolution over time of clinical endpoints under a set of possible therapeutic plans and to choose the best option. For this case study, the model can be used to constantly monitor and forecast clinical endpoints to prevent complications threatening patient's life. The decreased oxygenation caused by flu may have detrimental effects on both heart and brain activities indeed. Studies have reported that SARS-CoV infections can activate the blood clotting pathway by impairing left heart pumping performance, which results in a blood back up in the lungs and in a increased blood pressure. High blood pressure can reduce blood vessel's compliance decreasing blood and oxygen flows and leading to a higher risk of developing systemic conditions. For this reason, heparin-based therapies have been recommended to prevent clot formation or tissue plasminogen activator (tPA) (Sardu et al.,; Tang et al.,). Although some variation in blood pressure throughout the day is normal, a high blood pressure variability is associated with a higher risk of cardiovascular disease (O'Rourke and Nichols,; Mitchell et al.,; Wen et al.,; Clark et al.,; Bangalore et al.,) and all-cause mortality (Tao et al.,; Kim et al.,). Clogged arteries, fibrosis, and strokes caused by blood pressure spikes are among the main complications threatening patient's life and calling for the foremost necessity for treatment. Hence, blood pressure is one of the most relevant clinical endpoints that need to be constantly monitored in real time and accurately forecast.\nOUTPUT:" }, { "from": "agent", "value": "Hypertension, Type 2 Diabetes with Diabetic Nephropathy, Mild Flu caused by SARS-CoV infection" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She had a four-year history of neurological symptoms due to autoimmune processes and spinal compression from degenerative changes. She described numbness in her hands and lower extremities, weakness limited to her lower extremities, sensation of abdominal tightness, and occasional urinary and fecal incontinence. She was anti-glutamic acid decarboxylase (GAD) antibody positive and she reported symptoms as having progressed in the previous year. However, symptoms were mild and pre-operative medications only included oxycodone and tramadol. It works against the GAD enzyme, involved in the formation of gamma aminobutyric acid (GABA). Surgery was performed with general endotracheal anesthesia. On induction, 1mg of midazolam, 60mg of lidocaine, 50mcg of fentanyl, 150mg of propofol and 50mg of rocuronium were administered. After the airway was secured, the patient was maintained on sevoflurane and a dexmedetomidine infusion was started at 0.4mcg/kg/hr for the duration of the case. The patient was placed in lithotomy, and care was taken not to excessively raise the patient's legs in this position so as not to exacerbate lower extremity symptoms postoperatively. An additional 20mg of rocuronium was administered during the case while monitoring train of four (TOF), and the patient was reversed with 200mg of sugammadex at the conclusion of surgery. The patient emerged from anesthesia and had an uneventful recovery in the post-anesthesia care unit. She was monitored overnight and discharged home uneventfully without worsening of any preoperative SPS symptoms the next day.\nOUTPUT:" }, { "from": "agent", "value": "Stiff-Person Syndrome, Endometrial 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 39-year-old Saudi woman presented in our oncology clinic for her routine visit with left lower neck swelling. She had noticed this swelling for 2 months, and it had been rapidly increasing in size over a month causing pain, for which she was taking nonsteroidal anti-inflammatory drugs (NSAIDs), but no benefit. Her previous medical history revealed that three years ago she was treated with total abdominal hysterectomy and bilateral salpingo-oophorectomy (TAH and BSO) followed by adjuvant chemoradiation for bulky FIGO stage IB. She had no history comorbid conditions and no history of smoking, and her weight was stable. On physical examination, her vitals were stable. A fixed, solitary, hard neck mass of size 4 x 4 cm was palpable in the left supraclavicular region. There was no other palpable cervical lymphadenopathy, and the examination of chest, heart, nervous system, abdomen, and pelvis was normal. Clinical differential diagnosis was tuberculosis or carcinoma of breast or lung. Computed tomography (CT) neck showed left supraclavicular solid mass of size 3.2 x 2.5 cm encasing the vessels (Figure 1). The mammogram of both breasts was normal with no solid or cystic lesion. Hematological, renal, and liver function tests, tuberculin, and serum electrolytes were within normal limits. CT of chest, abdomen, and pelvis revealed para-aortic lymphadenopathy and lytic lesion in dorsal spine however, no local recurrence. Bone scintigraphy confirmed bone metastasis in skull, dorsal spine, left femur, distal right femur, and proximal right tibia (Figure 3). Patient was started on duplet chemotherapy (cisplatin and paclitaxel). After four cycles, she has responded well to the treatment with a reported decrease in the size of the supraclavicular nodes (Figure 4).\nOUTPUT:" }, { "from": "agent", "value": "Metastasis in carcinoma of cervix" } ]

[ { "from": "human", "value": "As a physician engaged 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 Japanese woman without a medical history expatriated to Jakarta, Indonesia, for 5 years. She lived in an upper-class residential area, in a clean environment. Around the time she returned to Japan, 1.5 months prior to her visit to our clinic, the patient started experiencing a dry cough, which subsided after several days. One month prior to her visit, she developed a fever of 40 C that persisted for several days accompanied by malaise, followed by fever and malaise every week. Two days prior to her visit, the patient experienced fever and epigastric pain. The patient had no history of consumption of raw seafood; however, the patient had been eating organic raw vegetables on a daily basis, including watercress. At admission, her body temperature was 35 C, vital signs were stable, and the liver was enlarged and tender. She had eosinophilia (eosinophil count, 3,465 cells/microL) and mild hepatic dysfunction (aspartate transaminase, 37 U/L; alanine transaminase, 60 U/L; gamma-glutamyl transpeptidase, 70 U/L; and alkaline phosphatase, 398 U/L). Hyperbilirubinemia was absent. Three of the stool specimens were negative, the latter for ova, cysts, and parasites, examined under a microscope. Enhanced CT showed multiple microabscesses arranged in a tractlike pattern with ring enhancement in the right lobe of the liver (Fig. 1). Endoscopic retrograde cholangiopancreatography did not show worms in the bile duct, and no ova were detected in the bile examined under a microscope. using the Ouchterlony double-diffusion test (Fig. 2). For treatment, 500 mg (10 mg/kg) triclabendazole (Egaten , Novartis Pharma AG, Switzerland) was orally administered two times at 12-h intervals. After the initiation of triclabendazole administration, the fever and malaise resolved immediately. Her eosinophil count decreased to 1,966/microL in 1 month, 624/microL in 2 months, and 273/microL in 3 months, reaching the normal range. Contrast-enhanced CT performed a year later showed almost complete disappearance of the multiple nodular lesions (Fig. 3).\nOUTPUT:" }, { "from": "agent", "value": "Fascioliasis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 7-year-old male child (weight: 21 kg) was diagnosed with a large left-side MFAC by a CT scan of the head in community hospitals. There was no history of traumas. After 1 month, the patient developed severe headaches, dizziness, nausea, and vomiting. The patient recovered well; any postoperative headaches dissipated within X days after the surgery. No neurological dysfunction was observed. However, 26 days after surgery, the patient experienced headaches and repeated nausea and vomiting. A CT scan of the head showed a left subdural hematoma in the frontal and temporal-parietal regions ( Supplementary Figure 1E and F ). A burr-hole craniotomy (BHC) was performed in the emergency department to remove the hematoma. The postoperative symptoms of the patient's caused by cranial hypertension related to the subdural hematoma resolved and the patient recovered well ( Supplementary Figure 1G and H ). On the 27th day after surgery, the patient's headaches reemerged along with double vision, and mild strabismus in the left eye. General physical and neurological examinations revealed no abnormalities. Laboratory findings were within normal limits except for an alkaline phosphatase of 239 U/L. The patient received atorvastatin monotherapy once daily for eight weeks, with an initial dose of 5 mg daily for the first week, followed by 10 mg a day for 7 weeks. Follow-up monitoring was done monthly for 12 months after the initial atorvastatin treatment ( Figure 1C ). Laboratory tests and physical examination were thoroughly conducted and MRI follow-up was performed regularly. The patient experienced improvements in symptoms and a significant decrease in hematoma volume within the first month of the treatment ( Supplementary Figure 3A and B ). By the third month after the initial treatment, neurological function had fully recovered and the hematoma had completely resolved ( Figure 1B ).\nOUTPUT:" }, { "from": "agent", "value": "Arachnoid Cyst, Spontaneous Hemorrhage" } ]

[ { "from": "human", "value": "As a physician engaged 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 woman was admitted in 2010 for investigation of hypercalcemia discovered during recurrent nephrolithiasis. Her family history was noteworthy with cardiac arrhythmia in two dead sisters and nephrolithiasis in another sister. Her son was diagnosed with MD at the age of 24 years. Five years ago, an arrhythmia was diagnosed and required the implantation of a pacemaker. She was noted to have a bilateral cataract. She complained of muscle weakness, diffuse myalgia, and palpitation. The weakness was gradually progressive in arms. Physical examination revealed percussion myotonia and the typical emaciated face of MD, hollow cheeks, drooping jaw, a peripheral neurogenic syndrome, and multinodular goiter. There was no exophthalmia. The electrocardiogram was normal. Hypercalcaemia was confirmed 2.83 mmol/L. There were no symptoms directly attributable to hypercalcemia. Other laboratory tests showed serum phosphate 1.2 mmol/L, urinary calcium 0.153 mmol/kg/day, creatinine level 52 mumol/L, alkaline phosphatase 97 IU/L (normal range: 45-245 IU/L), parathormone 362.5 pg/mL (normal range: 15-65 pg/mL), thyroid stimulating hormone TSH 0.02 mIU/L (normal range: 0.34-5.6 mIU/L), FT4 21.17 ng/mL (normal range: 6.09-12.2 ng/mL), and negative anti-thyroperoxidase antibodies. Cervical ultrasound revealed a multinodular goiter with isoechogenic homogenic nodules with clear border and cystic cavities (8*6 mm). The 99mTc-MIBI scintigraphy localized a lower right parathyroid adenoma. The bone mineral density (BMD) was normal. The patient was treated with benzylthiouracil, propranolol, and vitamin E. Euthyroidism was obtained after 2 years and the antithyroid drug was stopped. Four years later, MD is still in remission, and the alkaline phosphatase levels, serum creatinine and calcium, urinary calcium, and BMD are normal during follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Primary Hyperparathyroidism, Hyperthyroidism, Myotonic Dystrophy" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Also the patient had a history of anorexia, nausea, pallor, disseminated bone pain, abdominal distention and severe generalized edema since 7 days prior to this admission. Pallor, generalized petechial lesions all over his body and face, huge peripheral lymphadenopathies (each one 4*3 cm ), a mild splenomegally, and a grade 4/6 systolic heart murmur with radiation to the left side of his chest wall were the remarkable points in physical examination. Growth percentiles of the patient were all in normal ranges. Complete blood count (CBC) showed, white blood cells (WBC) 1.8x103/microl with 80% lymphocyte and 20% neutrophil, red blood cells (RBC) 2.7x106/ microl, platelet count (Plt) 90x103/microl, hemoglobin (Hb) 6.4 gr/dl and erythrocyte sedimentation rate (ESR) 146 mm/hr. Other abnormal tests were urine calcium level 18.1 mg/dl, Ca 9.3 mg/dl, P 4.1 mg/dl and Alk-ph 1500 IU/L. Bone marrow aspiration was done and showed a hypocellular marrow containing more than 90% lymphoblasts and immunophenotyping showed B-cell ALL. B-cell ALL induction chemotherapy was started as follows: Prednisolone, vincristine, asparginase, daunorubicin, methotroxate and cytosin arabnoside. The patient developed complete remission. Then it has been a maintenance therapy as well as two courses of consolidation therapy. According to type of fractures (green stick) any workups for management of fractures not done for him. In follow up X-rays, callus formation was seen.\nOUTPUT:" }, { "from": "agent", "value": "Acute lymphoblastic leukemia, Osteoporosis, Multiple spontaneous bone fractures" } ]

[ { "from": "human", "value": "As a physician engaged 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 admitted to consuming 2-4 alcoholic drinks weekly and had just recently resumed B12 supplementation. Complete blood count revealed a severe macrocytic anemia (6.6 g/dL), MCV (108 fl), and neutropenia (ANC 520/muL). She had an elevated vitamin B12 level reflective of recent intramuscular supplementation (Table 1). Bone marrow biopsy was performed and revealed a hypercellular marrow for age (75%) and dyserythropoiesis but without cytogenetic and dysplastic changes characteristic of MDS. However, early MDS could not be ruled out. Despite two months of B12 supplementation, her anemia and leukopenia did not improve, and she required further transfusion. Direct Coombs testing, lactate dehydrogenase, reticulocyte count, haptoglobin, and methylmalonic acid testing revealed no significant abnormalities. Daily prednisone (40 mg) was started as empiric treatment for potential occult autoimmune condition with no efficacy. The patient's anemia continued to worsen (5.7 g/dL) requiring further transfusion with progressive neutropenia. Additionally, she developed bilateral foot paresthesias, which were felt to be due to Raynaud's phenomena. A repeat bone marrow biopsy now revealed a hypocellular bone marrow (20-30%) with erythroid hyperplasia and dyserythropoiesis. A presumptive diagnosis of MDS (R-IPSS 3) was made, and the patient was referred for allo-HCT evaluation. Accordingly, the patient was started on IV cupric chloride (2 g) daily for 5 days and then once weekly for four weeks. At one-month follow-up, the patient's anemia improved and leukopenia resolved (Table 1). Although her energy level improved, her paresthesia remained.\nOUTPUT:" }, { "from": "agent", "value": "Copper deficiency" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She also gives a history of loss of appetite for 4 months, no history of weight loss, any bladder or bowel complaint, or any hormonal pill intake. Vaginal examination suggested the same mass in the left adnexa with bulky uterus. EA HPE reported as endometrial adenocarcinoma. Considering both ovarian and uterine malignancy with no idea of the primary tumor, an exploratory laparotomy with ascitic fluid cytology, total abdominal hysterectomy, bilateral salpingo-ovariotomy, infracolic omentectomy, and bilateral pelvic lymphadenectomy was performed. Ascitic fluid cytology was positive for malignant cells. The patient received adjuvant chemoradiation and currently in remission, on regular follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Synchronous independent primary malignancies arising from endometrium and ovary. Endometrioid adenocarcinoma of endometrium Stage 1A, Grade 3, and endometrioid carcinoma of ovary Stage 1c, Grade 1." } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Eleven years postresection, a surveillance X-ray computed tomography (CT) scan revealed two pancreatic lesions, consistent with disease relapse. On the appearance of malignant lymphadenopathy on further imaging, the patient commenced treatment with oral sunitinib. A dose reduction was required at cycle three due to mucositis, but otherwise the treatment was generally well tolerated with minimal toxicity. Serial CT scans showed evidence of objective disease response and subsequent disease stabilization [Figure 1]. Five years after commencing sunitinib, the patient developed stiffness of the jaw and difficulty opening his mouth, which worsened over the subsequent 2 weeks. Eventually, his symptoms were so severe that he was only able to open his mouth wide enough to use a straw for drinking. Speech and swallowing were unaffected, and there was no evidence of mucositis in the oral cavity. No other neuromuscular symptoms, muscle stiffness spasm were present. The patient had no history of jaw or dental problems and was not taking any other regular medication. Head and neck imaging was unremarkable with no evidence of metastatic disease or other pathology. The patient initially continued with sunitinib treatment, but when he commenced his scheduled 2-week treatment break, his symptoms spontaneously resolved. On commencing the next cycle 2 weeks later, the same symptoms recurred, and once again resolved spontaneously on stopping treatment. A further staging CT scan revealed only a new adrenal metastasis, which was resected. Several months later, on further disease progression, pazopanib was commenced.\nOUTPUT:" }, { "from": "agent", "value": "Trismus, Metastatic renal cell carcinoma" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: He had been taking zidovudine-lamivudine and efavirenz for the past 8 years. On physical examination, he was afebrile, anicteric, and without rash. His arterial pressure was 70/40 with a heart rate of 120 beats per minute. There was no prominent lymphadenopathy. The lungs were clear, but on cardiac auscultation a grade IV systolic murmur was auscultated at the left sternal border. On abdominal examination, a pulsatile epigastric mass was palpated. Cardiac enzymes were not elevated. The EKG was consistent with left ventricular hypertrophy without signs of cardiac ischemia. A chest radiograph demonstrated mediastinal widening (Figure 1(a)) and prompted a 3D computed tomography of the aorta (Figures 1(b) and 1(c)), which revealed an aortic aneurism extending from the ascending aorta to the iliac vessels. Further laboratory studies were notable for a strongly positive Venereal Disease Research Laboratory (VDRL) titer of 1 : 128 and a positive fluorescent treponemal antibody absorption (FTA-ABS) test. The patient denied any knowledge of prior syphilis infection or testing. Waiting for cardiovascular surgery consultation, during the following 24 hours, the patient was started on aqueous crystalline penicillin and volume resuscitated with a crystalloid infusion. During the second hospital day, the patient developed sudden abdominal pain and hypovolemic shock. He died 30 minutes later despite resuscitation. An autopsy was performed on the following day, and 3500 cc of blood was encountered within the peritoneum as well as a ruptured abdominal aneurysm.\nOUTPUT:" }, { "from": "agent", "value": "Syphilitic Aortic Aneurysm, 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: There was neither history of trauma before the appearance of lesions nor pruritus or other symptoms. The lesions first appeared at the age of 6, involving the left foot only, later developing to involve the left leg. Over the last 7 years, lesions began to appear on the right leg. On examination, scaly erythematous plaques were found exclusively on the left side of the lower limbs, in lines running on the left leg from the anterior aspect to the dorsum of the foot, with silvery, scaly plaque and papule over the right leg, and with multiple psoriatic plaques over both elbows (Fig. 1a, b). The patient was treated with subcutaneous injections of adalimumab for 8 months, with inadequate response. A skin biopsy was taken from both legs to better understand the clinical condition, with the histopathologic examination of both showing similar features. Sections showed confluent hyperparakeratosis, loss of granular layer (agranulocytosis), papillomatosis with thin suprapapillary plate, and dilated papillary dermal vessels. Frequent mitoses were identified in the stratum basalis. In the dermis, mild, superficial perivascular lymphohistiocytic infiltrate was appreciated (Fig. 2a, b, c, d). A subcutaneous injection of 50 mg etanercept was prescribed twice weekly for 24 weeks, with PASI 75 reduction, followed by a weekly maintenance dosage of 50 mg by subcutaneous injection. The plaques on the legs and elbow had either disappeared completely or thinned and faded (Fig. 3a, b) after 52 weeks of treatment.\nOUTPUT:" }, { "from": "agent", "value": "Inflammatory Linear Verrucous Epidermal Nevus, 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 55-year-old female presented an erythematous, asymptomatic papule of 0.5cm in diameter on her left anterior neck, just above a midline transverse scar caused by a thyroidectomy. (figure1) Excisional biopsy was performed. The histopathological examination showed a well-demarcated lesion of cells in trabecular and glandular arrangement (Figure 2). The cells displayed enlarged and hyperchromatic nuclei and frequent mitotic figures, including atypical ones (Figure 3). Occasionally, there was eosinophilic secretion in the lumen (Figure 4). The cells did not show nuclear grooves or pseudoinclusions. The tissue was submitted to immunohistochemical analysis which was positive for anti-cytokeratin and anti-thyroglobulin - cytokeratin markers of 40, 48, 50 and 50.6 kDa and AE1/AE3 clones - confirming the diagnosis of a primary thyroid tumor (Figure 5). She also had a maternal family history of ovarian cancer. Therefore, she was referred to the genetic service for testing of PTEN mutation, which result was negative for allelic variants, deletion or duplication of exons.\nOUTPUT:" }, { "from": "agent", "value": "Follicular thyroid carcinoma metastatic to skin, Cowden 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: Whilst defects in type I IFN pathways have been described in association with severe coronavirus disease 2019 (COVID-19), less is known about the outcomes of upregulation. Our patient was initially managed with systemic steroid therapy, but due to relapse of symptoms on weaning, an alternative therapy was sought. In this case, a novel use of ruxolitinib, a JAK inhibitor, has resulted in lasting remission without complications. Image Caption and Description: \nImage caption: []\nImage description: []\nCase Report: \nOur patient was born to consanguineous parents from Pakistan and had a confirmed diagnosis of AGS with previous genetic testing confirming homozygous SAMHD1 mutations (c. 427C > T). She had an older sibling who was confirmed to have the same genotype and who displayed an almost identical phenotype, manifesting in severe neurological deficit, spastic quadriplegia, and dystonia. Her regular medication consisted of sodium valproate (160 mg twice daily) and baclofen. Although the older sibling had developed cutaneous manifestations in the form of acral perniosis and periungual necrosis at the age of 8 years, there were no prior cutaneous changes in our patient.\nOUTPUT:" }, { "from": "agent", "value": "Generalised Panniculitis, Post-COVID-19, Aicardi-Goutières Syndrome" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She presented to the district hospital with the clinical picture of fluid overload, necessitating urgent dialysis. A double lumen dialysis catheter was inserted into the left femoral vein. The neck veins were avoided due to the presence of the brachiocephalic AVF. She underwent dialysis via the left femoral catheter for two weeks but subsequently developed a purulent peri-catheter discharge and bleeding that necessitated its removal. She was hemodynamically stable, but the entire lower extremity was severely swollen, cold, numb, and paralyzed (her left knee and ankle joints were graded 1 on the Medical Research Council muscle power scale). She had a palpable femoral pulse, but the popliteal and pedal pulses were absent. Both Duplex ultrasound and CT angiography confirmed an AVF between the right superficial femoral artery (SFA) and femoral vein. Imaging further revealed a thrombus in the SFA just distal to the AVF (Figure 2). However, the distal vascular tree remained patent down to the foot on CT.\nOwing to the presence of intraluminal thrombus in the SFA, open surgical thrombectomy and vessel repair was embarked upon after confirming the viability of muscles at fasciotomy. Following femoral vascular control, the AVF was discontinued, and the femoral vein was closed primarily. The catheter-inflicted SFA injury was such that a 4 cm segment was excised and repaired with an interposed reversed vein graft (Figure 3). Postoperatively, she became severely septic, the groin wound dehisced, and the vascular repair was disrupted necessitating common femoral ligation and high above knee amputation.\nOUTPUT:" }, { "from": "agent", "value": "Femoral arteriovenous fistula, Acute limb ischemia, End-stage renal failure, Diabetes mellitus, Hypertension, Acute ileo-femoral deep vein thrombosis, Systemic sepsis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She was treated with interferon alpha in the adjuvant setting, but two years letter an in-transit lesion on her left thigh emerged and was excised. She was then treated with ipilimumab, but treatment was discontinued due to hypophysitis. A year later, she developed a subcutaneous nodule on her chest, the histologic examination of which was consistent with a metastasis. She was treated with nivolumab, at 240 mg every two weeks, but six months later she experienced a grade-3 increase of the liver enzymes [serum glutamic oxaloacetic transaminase (SGOT)/serum glutamic pyruvic transaminase (SGPT)] and nivolumab was permanently discontinued. She was then started with dabrafenib at 150 mg twice a day and trametinib at 2 mg once a day in the adjuvant setting. The patient experienced recurrent panniculitis lesions on both lower limbs and the abdominal wall during the first four months of treatment; nine months after treatment initiation, upon her 3rd imaging assessment of response, several enlarged paratracheal, subcarinal, aortopulmonary window, and hilar lymph nodes were found without any parenchymal lung lesions. No other signs of disease progression were found. The patient underwent a bronchoscopy and an endobronchial ultrasound-guided biopsy (EBUS-TBNA) of one of the subcarinal lymph nodes. The histologic evaluation of the lesions revealed epithelioid non-caseating granulomas without multinucleated giant cells, suggestive of a SLR. Her complete blood count, biochemistry profile, and serum angiotensin-converting enzyme (sACE) levels were within normal limits while an interferon gamma release assay (IGRA) was found to be negative. The patient received no treatment for these lesions and continued treatment with dabrafenib and trametinib without any dose reduction. Eight months later, she is still in complete remission, with no change in the number and/or size of the lymph nodes. Scarce erythema nodosum lesions still come up on her legs but are well-tolerated.\nOUTPUT:" }, { "from": "agent", "value": "Sarcoid-like reactions, 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: No complications were observed during the procedure or in the immediate post-operative period. During the immediate post-operative follow-up, the patient reported a feeling of malaise and anxiety, interpreted initially as mixed anxiety-depressive syndrome. Psychotherapy was proposed to the patient. Due to a persistent state of malaise, PTSD was finally diagnosed by a psychiatrist. The patient experienced intense PTSD symptoms one month after surgery. He complained of repetitive intrusive memories of abuse. He described seeing a family member entering his bedroom to abuse him, generating repetitive, involuntary, and invasive memories of sustained abuse. He felt as if these episodes of abuse were starting again, thus, exacerbating his feelings of distress. He reported a history of abuse between the ages of 9 and 23 years. The Childhood Trauma Questionnaire revealed emotional abuse (score = 22), severe physical abuse (score = 18) and severe emotional negligence (score = 19). No sexual abuse was reported, and no other history was recorded. Interestingly, he had never complained about PTSD symptoms linked to these events before surgery. Various environmental clues triggered the sudden involuntary retrieval of memories. \"When I hear my wife's keys in the door, I have flashbacks from when I used to be abused with keys by somebody entering the house.\" He reported nightmares associated with these events and avoided situations that could make those memories resurface. Neurovegetative signs of fear (tachycardia, excessive perspiration) and hypervigilance accompanied these reviviscences. He described a persistent negative, emotional state with feelings of anger and fear, resulting in a diminished interest in his daily activities. He also experienced difficulties in falling asleep, irritability, attention disorder, and poor concentration. The PTSD checklist score (PCL-5) was equal to 62/80 (score >= 32: \"probable\" PTSD).\nOUTPUT:" }, { "from": "agent", "value": "Post-traumatic Stress Disorder, Right Temporal Lobe Epilepsy" } ]

[ { "from": "human", "value": "As a physician engaged 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 23-year-old woman charged with attempted manslaughter. She was ordered by the court to undergo a pre-trial forensic psychiatric examination which took place in a maximum security state mental hospital. The trial records and all available background information were reviewed. Her grandmother suffered from schizophrenia and her mother had been in a psychiatric hospital after a suicide attempt. The patient used to shoplift before the age of 15 and later she stole money from time to time. She also worked as a prostitute to earn money. She had several boyfriends but has never married and has no children. Her personality was noticed to change before the age of 17. She started to have obsessive-compulsive behaviour, paranoid thoughts as well as depressive symptoms. She tried to kill herself by hanging and by several drug intoxications. She brutally killed her own pet. She was never hospitalized before the forensic mental examination but she irregularly visited an outpatient clinic. Despite psychiatric treatment, she impulsively tried to kill her male friend with whom she was drinking. Neither waking EEG nor brain MRI (1.5T) disclosed any abnormality. She had no somatic disorders. She had finished high school and vocational school, and was within average intelligence (WAIS-IQ total 109). She was not sentenced, but was ordered by the Finnish National Board of Medico-Legal Affairs to stay in the state mental hospital as a criminally insane patient.\nOUTPUT:" }, { "from": "agent", "value": "Schizophrenia paranoid type, alcohol dependence, features of antisocial personality disorder" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 45-year-old woman referred to the emergency room of our ophthalmology center with the chief complaint of abrupt vision loss and periorbital edema in her right eye. The patient reported that she was stung by a scorpion on her right eyebrow 2 days prior to admission and she had not received anti-venom. The patient brought the dead scorpion picture, and the species was confirmed by an entomologist as yellow scorpion (Mesobuthus Eupeus). The patient reported that she had not referred to the treatment center during the scorpion bite and had not presented with systematic symptoms; she also had not received an anti-venom. At emergency admission, the patient's vital signs were within normal range (BP:130/70mmHg, HR: 78bpm in the sinus rhythm, RR: 21 bpm, T:37.1oC oral temperature). The patient had no past history of systemic diseases such as hypertension, diabetes and coagulative disorders. External eye examination showed the site of scorpion bite had redness and swelling (Figure 1). Visual acuity was 4/10 in the right eye and 10/10 in the left eye. No relative afferent pupillary defect was detected. There was no disturbance in the extraocular muscle function. The slit lamp examination had no remarkable finding. The examination of the fundus showed retinal edema and retinal hemorrhage in the superior arcade of the macula. Spectral Domain Optical Coherence Tomography (SD; OCT) revealed that retinal thickness had increased in the temporal side and there were some hyper-reflective dots in the thickness of the retina in favor of retinal hemorrhage. Intravitreal injection of bevacizumab resolved the macular edema and vision recovery was achieved 2 weeks after the injection.\nOUTPUT:" }, { "from": "agent", "value": "Macular Branch Retinal Vein Occlusion" } ]

[ { "from": "human", "value": "As a physician engaged 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 participant (C.S.) is a 74 year old, left-handed female with 16 years of education. Her past medical history is notable for hypertension, gastric reflux, osteoarthritis, headaches, benign essential tremor, glaucoma, anxiety, and depression. Concurrent medications upon initiation of the trial were omeprazole, sertraline, trazadone, Miralax, calcium, fish oil, and baby aspirin. The researchers had access to the participants' medical records and previous neuropsychological evaluations in 2011 and 2013, which were negative for neurodegenerative disease diagnosis but noted mild cognitive changes due to anxiety and depression. Symptoms included disorientation to time, repetitive speech, mild word finding difficulty, difficulty following conversations, confusability, and difficulties with attention and concentration. The patient had mild, stable symptoms of depression and anxiety and had very minor dilapidation of instrumental activities of daily living (IADL's) such as driving and financial management. The patient had also become more socially withdrawn as a result of conversational difficulties and lost ~25 pounds over the 2 years preceding presentation. After diagnosis, the participant began a regimen of donepezil 5 mg, but this was discontinued due to GI problems and excessive weight loss. The patient's inability to tolerate a cholinesterase inhibitor resulted in application for a compassionate use IND for eflornithine (DFMO).\nOUTPUT:" }, { "from": "agent", "value": "Early Alzheimer's Disease" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An 80-year-old woman was admitted to our hospital for evaluation of progressive difficulty in swallowing to solids and liquids. Prior to this admission timing, her ascitic fluid was totally removed and showed malignant cells with estrogen receptor expression. Serum cancer antigen 27.29 was 5.126 U/mL (normal range; 0-38 U/mL) at the time of admission. Barium swallow showed moderate fixed narrowing in the distal thoracic esophagus (Fig. 1). Distal esophageal stricture was found on upper endoscopy at 35 cm from the incisors extending to esophago-gastric junction at 40 cm with modest resistance to passage of the standard gastroscope (9.8 mm in diameter). Esophageal mucosa appeared to be normal (Fig. 2). Biopsy obtained from the esophageal stricture revealed no malignancy. Computed tomography showed thickened distal esophagus and proximal stomach wall, mild intrahepatic biliary dilatation, massive ascites and right-sided hydronephrosis (Fig. 3). EUS with a 12 MHz mini-probe that was passed through the upper endoscope into the stricture was performed. It showed approximately 10 mm thickened esophageal wall disruption of the normal esophageal wall layer pattern (Fig. 4). Then, the linear echoendoscope was passed to the level of the stricture which also showed thickened esophageal wall consistent with an infiltrating process involving all the layers and penetrating into the adventitia. No extraluminal mass which might cause compression was observed. After confirming the absence of major blood vessels, EUS-FNA of thickened esophageal wall was performed with a 22- and 25-G needle (Fig. 5). Considering her poor performance status mainly due to inability to eat, chemotherapy was not indicated at that time. Therefore, we performed esophageal metallic stent placement and successfully relieved her symptoms.\nOUTPUT:" }, { "from": "agent", "value": "Metastatic 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: This is a case of a 56-year-old female patient reporting symptoms of low back pain, buttock pain, shoulder pain, arthralgias, and limited spinal mobility. The intensity of the pain that the patient experienced was described by her as a severe stabbing and shooting pain, splitting and exhausting, and sickening and very fearful, causing her severe discomfort. She had been suffering from back pain since the age of 51. The patient reported that during the last 2 years, she had been prescribed a combination of various medications for pain relief with only transient improvement. The patient was complaining of walking difficulties and presented with sudden right buttock pain, right inguinal fold pain, and low back pain for 2 months, with inability to walk and to sit down. At levels 04-05 and 05-I1, small-scale circular projection of the intervertebral discs is observed, with no appreciable narrowing of the intervertebral tracts. On the Short-Form McGill Pain Questionnaire, she scored I-a = 24, II = worst possible pain, and III =2, while on the Beck Depression Inventory (BDI) she had a score of 24. Her score on BDI was mainly shaped from her reported symptoms in the subscale that measures somatic-vegetative performance complaints (consisting from the last eight items of the BDI). She was prescribed duloxetine (30 mg/day), and the dosage of duloxetine was escalated to 60 mg/day after 2 weeks of titration and then 120 mg/day after 4 weeks with satisfactory results.\nOUTPUT:" }, { "from": "agent", "value": "Depressive symptomatology, Tarlov 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: Patient 1, BP, is an 84-year-old man who presented for outpatient evaluation on 6/2/2020 for proteinuria (albumin/creatinine ratio of 1,501 mg/g) and reduced eGFR (serum creatinine 1.68 mg/dl) (see Table 3 ). There was a history of type 2 diabetes, hypertension, hyperlipidemia, and heart failure with preserved ejection fraction. He was receiving apixaban following thromboembolectomy of a femoral artery clot thought to be secondary to atrial fibrillation in a patient not on anticoagulation. Review of symptoms revealed lower extremity swelling and was otherwise unremarkable. There was no constitutional symptoms, purpura, or diarrhea. Physical exam was remarkable for blood pressure 150/50 mm/Hg and lower extremity edema. Serologic evaluation revealed an IgGkappa paraprotein detectable in serum, but not in urine. A kidney biopsy was obtained on 9/30/2020 to differentiate possible diabetic kidney disease (DKD) from MGRS. TMA was diagnosed (see Table 4 and Figure 1 ) and subsequent assessment for MAHA and secondary causes of TMA was unremarkable. Analysis of the genes for complement Factor H (CFH), complement Factor I (CFI), C3, and thrombomodulin was negative for pathogenic mutations. However, due to financial constraints, we could not assess the genes for membrane cofactor protein (MCP, CD46) or complement Factor B (CFB) for genetic mutations, or the genes for CFH and MCP for at risk haplotypes (vide infra). This same limitation for genetic testing applies to Patients 2 and 3 below. Bone marrow biopsy revealed a 5% plasma cell clone. C5 inhibition (eculizumab or ravulizumab) was not immediately offered since there was no evidence of MAHA and renal function was not acutely deteriorating. Also, the urine protein/creatinine ratio spontaneously improved prior to any treatment (see Table 3 ) and serum creatinine remained stable through 6/2021, precluding a potential C5 inhibitor indication for chronic smoldering disease. Clone directed therapy was initiated with dexamethasone and bortezomib. Despite the apparent clinical stabilization, clone directed therapy was still pursued due to the obvious detectable plasma cell clone and the fear that any relapse could lead to end stage kidney disease. We suspect that the paraprotein in this case was more of a susceptibility factor requiring a \"second hit\", perhaps an infection, to manifest disease.\nOUTPUT:" }, { "from": "agent", "value": "Thrombotic Microangiopathy, Monoclonal Gammopathy of Renal Significance" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 55 year old male with low GCS was intubated and transferred to our level 1 trauma centre following a single shotgun bullet wound to the right anterior neck and supraclavicular region. He had been documented to be hypotensive post injury by ambulance first responders. CT was performed approximately three hours after the injury and demonstrated scores of spherical metallic shot pellets scattered over a 15 cm x 15 cm area of the neck and supraclavicular region. The CT head lateral scout revealed a single intracranial pellet, projected over the pterion (Figure 1 arrow). Subsequent CT angiography of intracranial vessels confirmed an intra-arterial 3 mm pellet within the M1 segment of the right middle cerebral artery resulting in moderate flow reduction. Follow-up CT angiography performed 24 hours after arrival showed complete reperfusion of the right middle cerebral artery (Figure 3) with the shot fragment seemingly unchanged in position (arrow). CT angiography of the neck revealed a focal dissection (Figure 4 arrow) and linear focus of thrombus within the right common carotid artery 5 cm inferior to the bifurcation, at the presumed arterial entry point of the embolised pellet. A large surrounding haematoma, but no active arterial extravasation of contrast, was present. The pulmonary venous system, a second potential entry site described, was unremarkable. Craniectomy was performed to reduce intracranial hypertension and mass effect due to profound parenchymal swelling. An enterostomy tube was required for feeding and the patient remained an inpatient several months after admission.\nOUTPUT:" }, { "from": "agent", "value": "Arterial and venous intravascular embolisation following shotgun injury, acute MCA infarct, right-sided MCA territory infarct" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: There was a history of non-recordable blood pressure and pulse, following which the medical officer proceeded with resuscitation maneuvers. On admission, the patient was unresponsive, hyperventilating without spontaneously opening his eyes or responding to pain. Pupils were bilaterally equal with sluggish response to light. Pulse was 100/min, Blood pressure was 110/60 mmHg, and respiratory rate was 42 breaths per minute. Systemic examination revealed normal cardiovascular and chest findings. An arterial blood gas analysis showed a marked anion gap metabolic acidosis (pH 6.61, lactate 24.59, anion gap 30.4mmol/L, HCO3 4 mmol/L, pCO2 41.4 mmHg, sPO2 94%). Random blood sugar was 246 mg/dL. Electrocardiogram (ECG) showed features of hyperkalemia. The patient remained disoriented and started presenting a tense tender abdomen and decreased bowel sounds with dilated stomach, with distended bowel loops at the plain abdominal X-Ray. Despite fluid resuscitation, he continued to be anuric. The abdominal contrast-enhanced computed tomogram showed acute renal cortical necrosis with and distended bowels. A bedside 2D echogram was normal. Investigations revealed normal hemoglobin level, elevated total leukocyte counts (peripheral smear was characterized by normocytic normochromic red cells and neutrophil leukocytosis), deranged coagulation profile, hyperkalemia, markedly elevated liver enzymes, lactate dehydrogenase, and creatine kinase (Table 1). Blood cultures failed to detect bacterial growth. The patient was managed with continuous renal replacement therapy. However, he desaturated, had a cardiac arrest, and died 18 hours after admission. On perusal of medical documents of the patient, it was found that, in the past, there had been a history of two similar episodes. The patient had presented with presyncope following organized battle preparedness efficiency test (BPET) as a part of military training. He had been hospitalized following one such episode during which tall T waves on ECG and hyperkalemia had been documented. However, his cardiac evaluation, including electrocardiogram, Holter, and treadmill test, had been normal.\nOUTPUT:" }, { "from": "agent", "value": "Fatal sickling-associated microvascular occlusive crisis, Sickle cell trait" } ]

[ { "from": "human", "value": "As a physician engaged 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 man with nocturia and urge incontinence was referred to the Department of Urology, Atsugi City Hospital, Japan. He experienced right inguinal painless swelling that gradually increased in size for 30 years. His medical history was unremarkable. A right scrotal mass was detected (20 cm in diameter). The mass was soft, non-transilluminated, and nonreducible without bowel sounds. His body mass index was 29.43 kg/m2, and PSA level was 4.17 ng/mL. PCa was diagnosed with a transrectal prostate needle biopsy, and the Gleason score was 3 + 4. His CT, magnetic resonance imaging (MRI), and bone scintigraphy (BS) demonstrated a right IBH without metastasis (Figures 3(a)-3(c)). Simultaneous IBH repair and RRP were performed. Subsequently, radical prostatectomy with pelvic extended lymph node dissection was performed. Finally, a right inguinal incision was made. The enlarged inguinal ring was repaired using a polypropylene mesh (Lichtenstein technique, PerFix Light Plug; Bard Davol Inc., NJ, USA) after concealment with the endopelvic fascia. The operative time was 243 minutes. The patient ambulated and ingested food the next postoperative day. He received intravenously 2 g cefotiam dihydrochloride twice daily until the first postoperative Cystogram. The bladder catheter was removed after this postoperative normal Cystogram on postoperative day 7. The patient's postoperative course was uneventful, and the histopathological findings of the prostate revealed adenocarcinoma. Three months later, neither IBH relapse nor PCa recurrence was observed.\nOUTPUT:" }, { "from": "agent", "value": "Inguinal Bladder Hernia, Localized Prostate 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 4-year-old boy was referred for the continuation of follow-up for CT after completing his anti-Toxoplasma treatment in his first year of life. He was born at 37 weeks of gestational age after an uneventful pregnancy. His birth weight was 3000 grams. After presenting with increased head size with a head circumference of 42 cm (between +2 and + 3 SD for his age) and abnormal body movements at 2 months of age, he underwent an MRI of the brain which showed communicating hydrocephalus. Subsequent workup showed positive Toxoplasma IgM and elevated Toxoplasma IgG of 21 IU/mL (normal <3 IU/mL). Details of the commercial test kit could not be extracted. He was initiated on oral levetiracetam and underwent ventriculostomy. An ophthalmologic assessment showed bilateral strabismus (esotropia). A lumbar puncture was deferred. He was treated with oral pyrimethamine, sulfadiazine, and leucovorin for 1 year. He started wearing corrective eyeglasses at 6 months of age. With control of seizures, levetiracetam was discontinued at one year of age but was restarted after the reappearance of generalized tonic seizures at 3 years and 5 months of age. He achieved his developmental milestones in comparable time to his peers. An audiogram done at 3 years of age showed normal hearing ranges. At 4 years of age (start of follow-up at our clinic), he was asymptomatic and had good seizure control. His anthropometric measurements showed a height of 111 cm (50th-75th centile for age), a weight of 17 kg (25th-50th centile), and a head circumference of 52 cm (+1 SD). He remained wearing glasses for his bilateral strabismus.\nOUTPUT:" }, { "from": "agent", "value": "Congenital Toxoplasmosis" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Despite the existence of best practice guidelines for the diagnosis of DMD, implementation of these recommendations in different parts of the world is challenging. Here, we present 4 unique case studies which illustrate the different diagnostic pathways of patients with DMD in Middle Eastern countries and highlight region-specific challenges to achieving timely and accurate genetic diagnosis of DMD. A lack of disease awareness and consequential failure to recognize the signs and symptoms of DMD significantly contributed to the delayed diagnoses of these patients. Additional challenges included limited available funding for genetic testing and a lack of local specialist and genetic testing centers, causing patients and their families to travel vast distances for appointments in some countries. Earlier and more accurate genetic diagnosis of DMD in this region would allow patients to benefit from effective disease management, leading to improvements in health-related quality of life. Image Caption and Description: \nImage caption: []\nImage description: []\nCase Report: \nBy the time the patient was 8 years old, her family had noticed increasing fatigue, enlarged calves, and frequent falls. The PCP referred the patient to a clinical geneticist at a Lebanese medical genetic center ~120 km away. Upon examination, the patient had mild psychomotor delay, intellectual disability, hyperlordosis, and muscle weakness. Even at this stage, DMD was not suspected because of the rarity of disease in female individuals. Another blood test revealed CK levels of ~8,000 U/L, prompting a series of genetic tests. For each test, the family had to complete an ~240 km roundtrip. Because there were no Lebanese or Syrian government reimbursement schemes available, the patient's family paid for the genetic tests themselves, leading to delays in the transfer of payments and ultimately obtaining the results.\nOUTPUT:" }, { "from": "agent", "value": "Duchenne Muscular Dystrophy" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: It is almost exclusively a pediatric neoplasm : the median age at diagnosis is 2 years, and more than 90% of patients are diagnosed under ten years of age . In patients over 30 years, it is rare (0.2 cases per million inhabitants per year) and its incidence becomes increasingly scarce in the elderly population . It was first described by Dr. Rudolf Virchow as a \"glioma\" in the abdominal cavity in 1864 . By 1910, Dr. Homer-Wright determined that this tumor originates from primitive neural cells based on the histological rosettes it forms within the bone marrow . In well-differentiated tumors, cells are approximately 7 to 10 microns in diameter, have hyperchromatic nuclei and scant cytoplasm, and may form Homer-Wright rosettes. These rosettes are characterized by a central lumen filled with neuropil, a delicate fibrillary material consisting of neuronal processes, which are surrounded by a halo of tumor cells . Given that Homer-Wright rosettes are also found in medulloblastomas and peripheral primitive neuroectodermal tumors (PNET), it is believed that their presence indicates neuronal differentiation . Yet, the cellular mechanisms responsible for the formation of rosettes are not fully understood.\nOUTPUT:" }, { "from": "agent", "value": "Neuroblastoma" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Their curricular level was equivalent to the 1st to 4th year of primary education (6-9 years old). They participate in DLG together with another transition to adult life course class, so they were finally about 15 participants in these sessions. Within this group there is more variability in terms of cognitive and communicative levels. They have been 2 years implementing DLGs once a week. Qualitative data collection techniques were used with a communicative orientation (Puigvert et al.,). The data collection techniques used were in depth interviews and focus groups. These interviews and focus groups encompass different issues such as: strategies that facilitate implementing DLGs with children with disabilities, the characteristics of the implementation, results that emerged, etc. and were structured previously. Data was gathered from teachers of three different educational levels comprised in the school: primary education, secondary education and the transition to adult life course. This strategy allows to analyse teachers' different perspectives since they have different experiences and professional careers and encompass the overall educational intervention and impacts achieved. Specifically, two semi-structured interviews were conducted (to the school principal and a teacher of the transition to adult life course) and four focus groups, one with two secondary education teachers, one with three primary education teachers, one with two secondary education and a transition to adult life course students, and one with four primary education students. In the case of the focus groups with students, the conversation was always facilitated by a teacher familiar with the students to facilitate their expression and overall communication with them. Table 1 summarizes the information on the data collection techniques implemented. To ensure the research process's ethical integrity full details of the study objectives and procedures were explained to the participants, teachers and families prior to the start of the study. They were informed about the anonymous and voluntary participation and the confidentiality of the data collected of all participants. Informed consents were signed by all the participants or legal guardians after being properly informed. Ethical requirements were addressed following the Ethics Review Procedure established by the European Commission for EU research. The study was fully approved by the Ethics Board of the Community of Researchers on Excellence for All (CREA). After data collection, interviews and focus groups were transcribed verbatim and subsequently analyzed. Drawing from the research questions, two main categories of analysis were stablished, which referred respectively to the strategies that were used in DLGs implementation and the improvements shown among participants. Within these two main categories, subcategories were created inductively based on the specific themes that emerged from the data. All names have been changed to pseudonyms to ensure the anonymity of the participants.\nOUTPUT:" }, { "from": "agent", "value": "Intellectual disability" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She had a two-month history of throat discomfort but no voice dysfunction or difficulty breathing. She had never had any thyroid hormone dysfunction and there was no family history of thyroid disease. On examination, she was clinically euthyroid. There was a visible 3cm nodule in the lower pole of the left lobe of the thyroid. There was no associated lymphadenopathy. Thyroid function tests were normal. Ultrasonography demonstrated a 3.75cm circumscribed, solid, echogenic nodule in the lower pole of the left lobe of the thyroid and radiological appearances suggested a follicular lesion. There was regrowth of the right thyroid remnant. Fine needle aspiration showed follicular cells that were graded as Thy3 (intermediate risk of malignancy). After discussion with the patient about the alternative management options and in light of the undiagnosed lung lesion, she underwent an urgent left hemithyroidectomy and excision of the right thyroid remnant. There were no post-operative complications. This was completely encapsulated and not adjacent to the thyroid capsule. The presenting lung lesion was ultimately determined to be unrelated to the thyroid lesion. Resection of the lung nodule revealed an area of necrotising granulomatous inflammation. There were no acid-fast bacilli or fungal bodies seen and there was no clear clinical indication of tuberculosis.\nOUTPUT:" }, { "from": "agent", "value": "Benign thyroid adenoma, Incidental microcarcinoma" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Written informed consent was obtained from the patient to publish this paper. A 54-year-old Japanese woman presented with depressed mood, psychomotor retardation, and loss of interest. In around May 2013, the patient experienced gastric discomfort and visited the Department of Internal Medicine. The depressed mood and psychomotor retardation subsequently worsened to a degree such that they interfered with daily activities. The gastric discomfort also gradually worsened; thus, beginning on June 4, 2013, the patient was given metoclopramide, 10 mg intravenously, twice per week in the outpatient emergency care unit. On the seventh day after beginning metoclopramide, facial hot flushes, increased sweating, muscle rigidity, and galactorrhea were observed. Blood biochemical tests revealed an elevated serum prolactin level of 44 ng/mL. Metoclopramide was thus discontinued, and the dose of paroxetine was increased to 40 mg/d. The Hamilton Rating Scale for Depression score also improved to 5, and the serum prolactin level decreased to 15 ng/mL after 4 weeks.\nOUTPUT:" }, { "from": "agent", "value": "Major depressive disorder, Extrapyramidal symptoms, Hyperprolactinemia" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An 11-year-old male presented at the University Hospital with painful macroscopic hematuria for 3 months. A urinary tract ultrasound showed a heterogeneous intravesical mass measuring 23 x 21 mm with papillary projections on the surface. Abdominal and pelvic CT scans with contrast showed a 20 mm mass in the right posterolateral bladder wall. The CT scan was unable to determine whether there was tumor extravesical extension, so the patient underwent an MRI with contrast that showed that tumor was restricted to the bladder mucosa (Figure 1). There was no history of passive smoking or industrial exposure due to proximity of residence. Cystoscopy demonstrated a vegetative lesion in the right lateral bladder wall. Incisional biopsy was performed and histopathology revealed urothelial papilloma. Subsequently the patient was lost to follow-up and returned after 1 year with sporadic painless hematuria. A new CT scan with contrast identified a 29 x 22 mm solitary lesion in the same topography (Figure 2). The patient underwent a cystoscopic transurethral resection of the lesion (TURB). The specimen was positive for p53 mutation on immunohistochemistry. On follow-up, ultrasound was performed every 3 months and cystoscopy every 6 months. Two and a half years after the resection, the patient is cancer free. The tumor genetic profile presented a pathogenic variant in the BRAF gene (c.1894C> T p.P632S), a probably pathogenic variant KRAS (c.97G> A p.D33N), and nine variants of uncertain significance in the ALK, EGFR, ERBB2, ERBB3, KIT, and PIK3CA (Table 1).\nOUTPUT:" }, { "from": "agent", "value": "Bladder Urothelial 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 37-year-old woman was referred to us with epigastric discomfort. She had gone to a different hospital over a year before and had been taking iron supplementation for anemia ever since. 1). There were no signs of H.pylori infection such as atrophic gastritis. H.pylori was negative. She had no mucocutaneous pigmentation and no family history of polyps. Laboratory findings showed a slightly depressed serum iron level. The tumor markers CEA and CA19-9 were within normal limits. Contrast CT showed a stalk-like structure at the root portion of the polyp (Fig. 2). Lymph node swelling and distant metastasis were not found. The serosal surfaces of the tumor were indented. The tumor was nodular and a stalk was evident at the root of the tumor. Histopathological assessment revealed foveolar hyperplasia on the surface of the polyp and cystically dilated glands (Fig. 3a and b), with cells at the base that resembled those in the fundic glands (Fig. 3c). Desmin staining showed arborizing smooth muscle bundles extending up to the superficial lamina propria (Fig. 3d). Only the neck of enlarged glands was immunostained for Ki 67 like normal glands. All of these features supported a differential diagnosis as a PJ hamartomatous polyp. The overlying epithelium did not contain any atypical cells (Fig. 3a, b and c). The postoperative course was uneventful and the patient was discharged after six days. Colonoscopy and capsule endoscopy of the intestine proceeded considering the histological judgement, but neither the intestine nor the colon contained any polyps.\nOUTPUT:" }, { "from": "agent", "value": "solitary gastric Peutz-Jeghers-type polyp, stomach cancer" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: In September, a 45-year-old Tunisian woman, with no personal or familiar medical history, was admitted to internal medicine unit for fever associated with a bilateral lower extremity erythematous rash with an edema extending from the knees to the ankles, evolving over two weeks. Initial examination showed multiple tender nodules consistent with the diagnosis of erythema nodosum (Figure 1). Further examination revealed maculopapular generalized rash involving palms and soles (Figure 2), malar rash, and arthritis of the knees, the ankles, the wrists and the proximal interphalangeal joints. Blood pressure was 120/70 mmHg and pulse rate 80/min. Complete blood count (CBC) revealed normocytic anemia, lymphopenia, and no thrombopenia. Further lab testing showed accelerated sedimentation rate (110mm/h), and elevated C-reactive protein (73mg/dl). Blood tests for urea, creatinine, electrolytes, and liver function did not reveal any abnormality. Serological set of bacterial and viral causes yielded positive for Rickettsia conorii. Rickettsia conorii serology by indirect immunofluorescence showed positivity of immunoglobulin G at 1: 200, and immunoglobulin M at 1: 100. Computed tomography (CT) scan was normal. Subsequently, the diagnosis of MSF was made. She was initially treated with colchicines, and had a course of doxycycline 200 mg for 5 days on an empirical basis. There was a prompt improvement with recovery of the fever, the maculopapular rash, and the erythema nodosum within a week. However, despite treatment, the patient had persistent malar rash, polyarthritis, and lymphopenia. The diagnosis of SLE was established since the immunological profile was positive for antinuclear antibodies (ANA), anti-DNA antibodies, anti-nucleosomes antibodies, and anti-citrullinated protein antibodies (ACPA). X-ray radiography of both hands and feet were normal. The patient received Hydroxychloroquine (5mg/kg/day), and a low dose of prednisone (10mg daily) with clinical improvement of both cutaneous and articular symptoms.\nOUTPUT:" }, { "from": "agent", "value": "Mediterranean spotted fever, 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: Patient 2, a boy, was the only child to a healthy, non-consanguineous Norwegian couple. He was delivered at term by an unplanned caesarean section due to his large size. Birth weight was 4600 g (97th centile), length 56 cm (>97th centile), and OFC was not recorded. Norwegian consensus anthropometric measures were used for this patient. He gained weight adequately, and walked at 16 months. Lack of interest in the surrounding was noticed by the kindergarten staff. He had impaired hearing due to recurrent middle ear infections, which normalized after he received drainage tubes bilaterally at 4 years of age. Neuropsychological testing with an extensive panel of tests performed at age 8.5 years showed an overall score in the lower normal range. He showed deficits in attention and executive functions. Cerebral MRI and EEG examinations were normal. At the clinical examination at age 9, his height was 125.5 cm (3rd centile), weight 25.7 kg (10th centile) and OFC 52 cm (10th centile). He received special tutoring at school. 1b-d). He also had mild divergent strabismus and hypermetropia. Testing for fragile X syndrome was negative. Metabolic screening of urine was normal.\nOUTPUT:" }, { "from": "agent", "value": "Developmental delay, Mild facial dysmorphisms, Pervasive developmental disorder not otherwise specified (PDD-NOS)" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: In 2018, a 73-year-old woman was referred due to persistent leukocytosis for 1 year. Medical therapy comprised acetylsalicylic acid (80 mg QD), bisoprolol (2.5 mg QD), and rosuvastatin (10 mg QD). Besides significant weight loss (>10% within 12 months), no B-symptoms were present. Blood film analysis confirmed the presence of left-shifted neutrophilia with toxic granulations and Dohle bodies. Bone marrow biopsy showed hypercellularity (>95%) with myeloid hyperplasia, plasmacytosis of 10%-15% (lambda positive), and bone marrow fibrosis grade 1. Karyotyping resulted normal. NGS revealed mutated ASXL1 (c.1934dup;p.Gly646Trpfs*12)(VAF 26%); CSF3R appeared normal ( Table 2 ). The tentative diagnosis of CNL was made. No therapy was initiated. Biochemical analysis revealed neutrophilic leukocytosis, hypogammaglobulinemia, and a normal beta2-microglobulin concentration. Serum lambda FLCs were significantly increased (free lambda: 276 mg/L (ref. 10-34) ( Table 1 )). There was significant proteinuria (6.79 g/24 h) with prominent lambda excretion (9816 mg/24 h). Bone marrow biopsy showed hypercellularity with segmented neutrophils (36.3% ANC) and increased central plasmocytosis (13.7% ANC) without blastosis. Congo Red staining resulted normal. Karyotyping revealed hyperdiploidy with gain on chromosomes 5, 7, 9, and 15. FISH detected IGH/14q32 rearrangement. Bortezomib-melphalan-prednisone (VMP) was initiated and halted after nine cycles as biochemical CR and minimal residual disease on PET-CT were obtained. Currently, more than 4 years after CNL and MM diagnosis, the patient is stable. Peripheral blood leukocyte count is <25 x 109/L.\nOUTPUT:" }, { "from": "agent", "value": "Chronic neutrophilic leukemia, Monoclonal gammopathies, Lambda light chain multiple myeloma" } ]

[ { "from": "human", "value": "As a physician engaged 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 presented with a 5-month history of horizontal binocular diplopia, after which he found a lump on the left side of his neck and developed epistaxis and tinnitus. He had no headache, eye pain, nasal obstruction, or hyposmia. He had experienced no significant weight loss or brain injury during this period. He had no systemic diseases and no history of smoking. Ophthalmic examination revealed a BCVA of 20/25 in both eyes. The anterior segment and posterior segment examination findings were normal. He had absent RAPD with normal pupillary responses and the pupil size was equal in both eyes. Orthoptic examination showed right esotropia of 30 PD at distance and 40 PD at near. The right esotropia and diplopia were worse in the right gaze. Ocular motility was normal in the left eye, but markedly limited abduction was noted in the right eye (unable to cross the midline). The cranial nerve areas V1-V3 were intact. Two weeks later the patient reported markedly blurred vision in his right eye. The ophthalmic examination showed a BCVA of hand motion in the right eye and 20/25 in the left eye. He developed grade III RAPD in the right eye. Posterior segment examination demonstrated a mildly pale optic disc in the right eye and normal optic disc in the left eye. Orthoptic examination revealed orthotropia in the primary position due to total ophthalmoplegia in the right eye and normal eye movement in the left eye. Sensation at V1-V3 distribution was reduced on the right side. Rhinoscopy showed a tumor in the right nasopharynx. Pathological examination revealed a non-keratinizing NPC. Postcontrast axial brain MRI showed an enhancing infiltrative mass that involved the right ethmoid and bilateral sphenoid sinuses with extension into the right orbit. The mass also encased the right cavernous ICA (Figure 4). The patient was treated with CCRT. Two months after treatment his symptoms of diplopia, epistaxis, and tinnitus significantly improved. Orthoptic examination demonstrated right esotropia of 16 PD at distance and 20 PD at near. The ocular motility in his right eye showed marked improvement (ability to abduct 80%).\nOUTPUT:" }, { "from": "agent", "value": "Nasopharyngeal 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 66-year-old man underwent percutaneous coronary intervention on a stenosis of the ramus intermedius for worsening dyspnea and positive exercise testing (Fig. 1A). Weight-adjusted heparin (a total of 8000 IU) was administered as per standard practice. Two drug-eluting stents were implanted at the ostial and proximal segments of the vessel. Final angiography demonstrated a flow-limiting dissection, which was covered with a stent. 1B). A balloon was inflated proximal to the CAP. Pericardiocentesis was performed, with complete resolution of the effusion. A right femoral artery access was secured, and a second guide catheter engaged the left coronary artery (ping-pong technique) (Fig. 1C). Three 3-mm MicroNester 18 (Cook Medical, Bloomington, Indiana) coils were delivered to seal the perforation through the second guide catheter (Fig. 1D, E). The patient was transferred to the intensive care unit. No anticoagulation reversal with protamine was deemed necessary since CAP sealing with coils was considered adequate. Two hours later, de novo formation of pericardial effusion was documented, and additional 150 mL of blood were extracted from the pericardial drainage. 1F). Contrast-enhanced TTE was performed after intravenous injection of 10 mL of sodium hexafluoride-based ultrasound contrast (SonoVue, Bracco Imaging, San Donato Milanese, Italy). Echocardiographic contrast is strictly intravascular, and is visualized as hyperechoic spots using dedicated imaging protocols. The identification of contrast in the pericardial space implies active extravasation. 1G, H). The patient remained subsequently stable until hospital discharge. The Supplementary Movie 1 presents the key passages of this case, including CAP management and contrast-enhanced echocardiography.\nOUTPUT:" }, { "from": "agent", "value": "Ellis type 3 coronary artery perforation, Cardiac tamponade, Active intrapericardial bleeding" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: For 5 years, the lesions gained a cauliflower appearance. The local examination demonstrated a vegetant perianal tumor by 12/8 cm, with an ulcerated, bleeding and anfractous surface, crossed by deep grooves. On palpation is detected a hard consistency and the tumor is fixed by the deep infiltration of the underlying tissues. Peritumoral are present many condylomas acuminati (Fig.13). The patient was treated on surgery department where an ellaptical incision was performed, circumscribing the perianal tumor mass. During excizion, using the electric surgical knife, was noticed the tumor extension in deepness, to the ischiorectal fossa, on 7-8 cm. After tumor removal, hemostasis was made by transfixing surgical sutures and a hemostatic bud of the residual cavity was performed (Fig.14). Histopathological examination relieved an epidermis with marked papillomatosis, acantholysis and parakeratosis hyperkeratosis. Many keratinocytes were showing a koilocytotic figure with perinuclear vacuolization and the irregularity of the nuclear contour (\"raisin\"-like aspect) (Fig.15). The epidermis sometimes express pseudoepitheliomatous hyperplasia changes, but those areas were not areas of clear invasion of the underlying tissue because the cell islands were limited by a basal cells layer. Within the dermis was noticed a massive chronic inflammatory infiltrate (Fig.16).\nOUTPUT:" }, { "from": "agent", "value": "Verrucous Carcinoma, Perianal giant condyloma Buschke-Lowenstein" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Pain was localized to the lower back, leg above knee, head, neck, and around scapula edge. This pain first started when he became ill with flu-like symptoms for three weeks. He experienced recurrent bouts of illness throughout the following year that seemed to increase during stressful times. He was treated successfully by the UCLA Pediatric Pain Program for fibromyalgia seven years prior to this study, and that specific pain had since resolved. At that time he received biofeedback and physical therapy, both of which were useful in managing fibromyalgia, but they had not been tried yet for his most recent pain condition. The mentee had a close group of friends but, at times, felt uncomfortable in large groups. He got along with most people and was well-liked by peers, but did not feel comfortable discussing his pain with his peers. His pain prevented him from seeing friends as much as he would like, although he tried to see them once every week. He preferred to stay home when having pain flare-ups. He reported that his friends tried to be supportive, but he felt that they did not really understand the pain he was experiencing and how it affected him. His pain prevented him from interacting with peers because it limited his physical abilities, and also affected his mood. He was also limited in his ability to travel. The mentee had attended the same school since kindergarten. He had extensive hobbies and interests, including teaching an after school class to elementary school students and being president of a local club. He was also involved with the school newspaper, wrote his own blog, and was passionate about photography. He volunteered with community service in foreign countries. He was very ambitious and academically driven. However, pain interfered with his education by causing extensive school absence and impaired concentration on studies. He also expressed his difficulty concentrating on exams because of his pain.\nOUTPUT:" }, { "from": "agent", "value": "Diffuse chronic pain, Sleep problems" } ]

[ { "from": "human", "value": "As a physician engaged 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 C618G mutation in exon 10 of the RET gene was demonstrated in DNA extracted from blood. Due to weight loss a French 4.2 BC catheter (Bard , Bard Access Systems, reference 0600060CE, Salt Lake City, Utah, USA) had been inserted 15 months previously to allow administration of home parenteral nutrition by infusion pump (Abbott Laboratories GEMSTAR, Reference 13000-15-05/06, North Chicago, Ill, USA) 14 hours a day. Because of the occurrence of HIT in this patient the BC was blocked each morning using lepirudin. Three months before the described event occurred, the BC had to be replaced surgically because of thrombus formation in the superior vena cava adjacent to the tip of the BC. An attempt at inducing thrombolysis using Urokinase proved to be ineffective. An X-ray taken after the previous repair demonstrated the correct position of the CVC (Figure 4). Seven weeks after the last repair, malfunction of the catheter with increased resistance when applying the home parenteral nutrition solution was noted by outpatient nurses and the patient's mother at home. During inspection of the former BC repair region, we noticed a missing central metallic tube (MT, Figure 3), together with a transparent appearing repair site area. By gentle palpation of the proximal BC, migration of the central MT was suspected, and a palpable resistance within the BC at the skin entrance level was noted. By gentle milking maneuvers the MT was manipulated distally and the MT was removed after transection of the BC 5 cm above skin level.\nOUTPUT:" }, { "from": "agent", "value": "Mechanical Complication with Broviac Repair Kit, MEN 2a" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 55-year-old male, with chronic liver disease, long-standing diabetes mellitus, and obesity (body mass index of 30), was admitted to the Intensive Care Unit (ICU) with altered sensorium, upper gastrointestinal bleed, and hemodynamic instability. His Child-Turcotte-Pugh score was seven. He was intubated and put on ventilatory support for airway protection. An upper gastrointestinal endoscopy showed bleeding from a gastric varix which was appropriately controlled. There were no esophageal varices. His hemoglobin was stabilized to 12 g% after transfusion of packed red blood cells. Despite control of bleed, the patient required rapid escalation of vasopressors over several hours. He had developed fever after 24 h of ICU admission. He developed a temperature of 39 C (axillary temperature) with circulatory shock and increasing lactate levels. His 24 h culture (blood, urine, and mini bronchoalveolar lavage) reports sent on ICU admission were sterile. He developed atrial fibrillation, which required cardioversion. His bedside echocardiogram showed a very poor window with a provisionally normal report. In view of long-standing diabetes mellitus, obesity, and poor transthoracic images, a bedside TEE was planned to rule out a cardiac cause of poor hemodynamics. After appropriate consent, the transesophageal probe (MyLab 30Gold Esaote, TE 022) was inserted orally into the esophagus. It was examined physically for any defects before insertion. Within seconds of the probe insertion, the TEE monitor showed a rapid rise in temperature to 42.5 C. The probe stopped functioning, indicating a high temperature. The examination was withheld and a cold saline lavage was given through the nasogastric tube to reduce the local temperature. The lavage reduced the local temperature down to 38 C after which examination was resumed. After obtaining images for 5 min, there was a rise in temperature and the above procedure was repeated twice before we could satisfactorily complete the examination. The probe was re-examined after removal to rule out any mechanical damage.\nOUTPUT:" }, { "from": "agent", "value": "Hyperthermia" } ]

[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: CASE 1: Mrs. ZNA, a 29-year-old Malay housewife, Gravida 4 Para 2+1, came for antenatal booking at the primary care clinic, complaining of polyuria, polydipsia and lethargy for the past one week. Dating ultrasound revealed 11 weeks fetus. She was subsequently treated appropriately. The serology tests for hepatitis B and HIV were negative. However, the rapid plasma reagin (RPR) was reactive at 1:16 titration. She was given three doses of intramuscular penicillin. Her other medical problems were managed accordingly. She was discharged from the ward once the blood sugar level was optimized and continued her follow up in the clinic. The second and third trimester ultrasounds revealed no abnormalities. Repeated RPR at 33 weeks of gestation was non-reactive. She delivered a baby boy at 38 weeks of gestation through LSCS with birth weight of 4.0 kg. Rapid Plasma Reagin (RPR) result for the baby was non-reactive. She was discharged after three days in the ward. Post-natal follow up was scheduled for them but she requested to be seen in another hospital at her hometown.\nOUTPUT:" }, { "from": "agent", "value": "Syphilis in pregnancy, Gestational diabetes mellitus, Candida infection, Syphilis re-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 62-year-old woman presented with bilateral blurred vision that had persisted for 1 week and metamorphopsia that had emerged the day before. On her first visit, the patient's BCVA was 0.8 in her right eye and 0.5 in her left eye. She also suffered from headaches and tinnitus for 1 week. Funduscopic examination revealed serous retinal detachment in both eyes without optic disc swelling (fig. 4a, b). SD-OCT showed remarkable choroidal folds and mutilobular serous retinal detachment in both eyes with the presence of subretinal septa (fig. 4c, d). After VKH diagnosis, systemic steroid therapy consisting of 250 mg methylprednisolone was initiated and tapered (fig. 5). After systemic steroid therapy initiation, SD-OCT showed that choroidal folds disappeared and the amount of serous retinal detachment remarkably reduced in both eyes. At the time of recurrence, choroidal folds were detected by OCT and funduscopic examination, and the patient again started complaining of metamorphopsia (fig. 4e, f). The amount of methylprednisolone was increased to 40 mg per day and was tapered again. After the increase in steroids administered, the patient recovered from metamorphopsia, and SD-OCT showed disappearance of the choroidal folds. The patient is now stabilized with 5 mg methylprednisolone and observed periodically.\nOUTPUT:" }, { "from": "agent", "value": "Vogt-Koyanagi-Harada 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: An 80-year-old male had an elective admission for an anterior resection for adenocarcinoma of the rectum. Initially, he had a laparoscopic approach but because of the poor bowel preparation (despite preoperative enemas) and the tumour being unable to be seen with either on-table rigid sigmoidoscopy or with the laparoscope, the operation was converted to an open procedure. During dissection, both ureters were clearly seen and reflected. The patient had a small pelvis with relatively bulky contents. An anastomosis was formed with a covering loop ileostomy. During both laparoscopic and open phases, LigaSure was used for dissection and to secure haemostasis. Postoperatively, he initially progressed well; however, his urinary catheter output gradually dropped, and his peritoneal drainage output increased over the first three days. The patient was taken back to theatre where cystoscopy, bilateral retrograde ureterograms and insertion of JJ stent on the right side were done. He was returned to HDU and had problems with fluid overload, type II NSTEMI, CHF, and fast atrial fibrillation over the next few days. Following all of this, he recovered well and was discharged home. More likely, it was the result of the conduction of thermal energy from tissues within the jaws of LigaSure during dissection close to the right ureter on its medial side.\nOUTPUT:" }, { "from": "agent", "value": "Ureteric Injury" } ]

[ { "from": "human", "value": "As a physician engaged 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 62 year-old man was referred to our urology unit with a history of painless intermittent hematuria for 3 months. His occupation was long-distance driver; he had no chronic illness and a history of smoking for 45 years. In his physical examination, there were no significant findings such as hepatosplenomegaly, lymphadenopathy, fever or weight loss. Leukocytosis (15700 103/ ul) was determined in the blood cell count and thought to be related to the pyuria in the urinalysis. The left kidney was found at grade three hydronephrosis and a heterogeneous hypoechoic solid mass with irregular borders on the left side of the bladder wall were reported in the abdominal ultrasonography. All papillary masses in the left side of the bladder wall and in the prostatic urethra were resected transurethrally. The transurethral resection specimen was fixed in 10% buffered formaldehyde and routine hematoxylin and eosin preparation was performed for histological examination. Immunohistochemistry was performed on the formalin-fixed, paraffin-embedded tissue sections. Light microscopic examination revealed high grade urothelial carcinoma extending into the muscularis propria. The urothelium of the surrounding bladder mucosa showed carcinoma in situ. Diffuse small lymphocytic infiltration was found along the periphery of the tumor. Immunohistochemical studies revealed that the lymphocytes present in the region were positive for CD20, CD5 and CD43 and transitional cell carcinoma (TCC) [Figures 1 and 2]. After the pathological report the patient was investigated for hematological malignancies. Computer tomography scan of the abdomen, pelvic and chest regions demonstrated asymmetric wall thickening in the left side of the bladder and multiple lymphadenopathies in the pelvis and upper abdomen [Figure 3]. A peripheral blood smear and flow cytometry were performed and resulted in a diagnosis of CLL. CLL was followed conservatively. The patient died six months after diagnosis as a result of heart attack.\nOUTPUT:" }, { "from": "agent", "value": "Chronic Lymphocytic Leukemia, Invasive Bladder 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: The Second Patient. The second patient is a 29-year-old man, single, having secondary education. He started substance abuse since he was 15 and has consumed all kinds of illegal drugs in Iran. However, he was affected by psychosis for the first time due to methamphetamine abuse since 6 months ago. In last 3 months, however, despite methamphetamine withdrawal, psychosis continued to remain. In the patient's first visit to psychiatry clinic, persecutory delusion, reference delusion, somatic hallucinations (in a way that the patient felt an outer thing under his hand skin), and olfactory hallucinations (in a way that he felt the smell of opium) as well as anxiety, irritation, and loss of libido were seen. Due to being aggressive, the patient was hospitalized in psychiatric emergency department. Then, clonazepam (6 mg daily) was prescribed for him. In 24 hours, he was seen to be much calmer. However, he was unaware of his psychotic states. In last 6 months, despite treatment with the medications mentioned below (each lasting for 3 weeks), in spite of controlling aggression, psychosis was not removed: olanzapine: 15 mg daily; risperidone: 5 mg daily; quetiapine 600 mg daily; and haloperidol: 10 mg daily. Eventually, all drugs prescribed previously were avoided and clozapine (with a dosage of 100 mg daily), together with clonazepam (2 mg daily), started to be prescribed. One week after clozapine prescription, clonazepam was discontinued. In a 9-month follow-up and with the continuance of clozapine consumption, no signs of psychosis relapse were seen. Concerning drug abuse, he had no other abuse experience; and the patient returned to his work. So, he was in \"early full remission\" based on DSM-IV-TR criteria despite the fact that he was not in a controlled environment. The patient's familial and personal backgrounds, regarding axis-I psychiatric disorders were negative. Moreover, similar to the previous patient, all paraclinical examinations proved to be negative.\nOUTPUT:" }, { "from": "agent", "value": "Methamphetamine-induced resistant psychosis, Antisocial personality disorder" } ]