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Multicare_common4249
[ { "from": "human", "value": "As a physician engaged 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 started on inotropes and vasopressors, and intra-aortic balloon pump and LVAD were placed through heparinization. However, the patient continued to deteriorate requiring an urgent transplant. On day 6, a fall in platelets from 113,000 to 26,000 was noticed. Heparin was discontinued, and the patient was started on argatroban to attain aPTT 2-3 times baseline. After availability of a suitable donor, the patient was scheduled for heart transplant on day 10. Preoperatively, the labs were as follows: hemoglobin: 8 g/dl; platelets: 110000; creatinine: 2 mg/dl; PT: 10.9; and aPTT: 60.1. Given the timing and magnitude of the platelet count decline, along with its resolution after heparin cessation, the need for further laboratory investigation was deemed not necessary, and the patient was diagnosed with HIT. Two peripheral intravenous lines, 16G and 18G, and a 20G right radial arterial line were placed, followed by central venous catheterization. Intraoperatively, induction and intubation were uneventful. After sternotomy, a loading dose of argatroban 200 mcg/kg was administered to reach the target ACT > 400 (activated clotting time). ACT values were derived utilizing the point-of-care Hemochron Signature Elite, whole blood microcoagulation system. Once ACT >400, the patient was placed on CPB. This was followed with an infusion of argatroban at 3.5 mcg/kg/min initially and then titrated to 3 mcg/kg/min as guided by ACT. The infusion was continued until the patient was successfully weaned from CPB. During surgery, no clots were noted in the extracorporeal circuit, and postoperatively, there were no thrombotic and hemorrhagic complications. aPTT normalized 23 hours after stopping argatroban. The postoperative course was significant only for line sepsis requiring a prolonged course of antibiotic therapy and oliguria for which the patient was being hemodialyzed prior to surgery.\nOUTPUT:" }, { "from": "agent", "value": "Heparin-Induced Thrombocytopenia, Renal Insufficiency, Postpartum Cardiomyopathy, Severe Decompensated Heart Failure" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: She was started on inotropes and vasopressors, and intra-aortic balloon pump and LVAD were placed through heparinization. However, the patient continued to deteriorate requiring an urgent transplant. On day 6, a fall in platelets from 113,000 to 26,000 was noticed. Heparin was discontinued, and the patient was started on argatroban to attain aPTT 2-3 times baseline. After availability of a suitable donor, the patient was scheduled for heart transplant on day 10. Preoperatively, the labs were as follows: hemoglobin: 8 g/dl; platelets: 110000; creatinine: 2 mg/dl; PT: 10.9; and aPTT: 60.1. Given the timing and magnitude of the platelet count decline, along with its resolution after heparin cessation, the need for further laboratory investigation was deemed not necessary, and the patient was diagnosed with HIT. Two peripheral intravenous lines, 16G and 18G, and a 20G right radial arterial line were placed, followed by central venous catheterization. Intraoperatively, induction and intubation were uneventful. After sternotomy, a loading dose of argatroban 200 mcg/kg was administered to reach the target ACT > 400 (activated clotting time). ACT values were derived utilizing the point-of-care Hemochron Signature Elite, whole blood microcoagulation system. Once ACT >400, the patient was placed on CPB. This was followed with an infusion of argatroban at 3.5 mcg/kg/min initially and then titrated to 3 mcg/kg/min as guided by ACT. The infusion was continued until the patient was successfully weaned from CPB. During surgery, no clots were noted in the extracorporeal circuit, and postoperatively, there were no thrombotic and hemorrhagic complications. aPTT normalized 23 hours after stopping argatroban. The postoperative course was significant only for line sepsis requiring a prolonged course of antibiotic therapy and oliguria for which the patient was being hemodialyzed prior to surgery. OUTPUT:
Multicare_common2158
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 28-year-old male was referred to our clinic for an ulcerated, hyperemic, and nodular mass on his right upper eyelid that grew rapidly within 2 weeks (Fig. 1a). There was no pathological finding in systemic examination. Best-corrected visual acuity was 20/20 bilaterally. Both anterior and dilated posterior segment examinations were normal in both eyes. On detailed anamnesis, it was learned that he experienced a sudden pain that occurred during drying his face with a towel a few weeks ago. When he admitted to our clinic, empirical topical and systemic antibiotics and anti-inflammatory medications were initiated as the lesion resembled an eyelid granulomatous lesion related to meibomian glands. Hence, the symptoms of the patient progressed despite treatment, a punch biopsy from the lesion was performed which did not distinguish infective pathologies or malignancy (Fig. 1b). In histopathological examination, there was ulceration in epidermis. Abundant eosinophils, histiocytes, and lymphoid infiltrate were detected in dermis (Figures 2a-c). There were enlarged CD30-positive lymphocytes in immunohistochemical analysis (Fig. 2d). As the punch biopsy histopathology did not discriminate the lesion, an incisional biopsy was scheduled. On immunohistochemical examination of the incisional biopsy specimen, no CD30-positive cells were detected. Histopathological examination revealed post-biopsy findings such as lymphocytes, histiocytes, increased vascularity, myofibroblasts, and fibrosis in the dermis. After the incisional biopsy, the patient did not receive any treatment other than prophylactic topical antibiotic ointment. However, following incisional biopsy, the lesion rapidly regressed in 7 days (Figs. 3a-b).\nOUTPUT:" }, { "from": "agent", "value": "Insect bite reaction" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 28-year-old male was referred to our clinic for an ulcerated, hyperemic, and nodular mass on his right upper eyelid that grew rapidly within 2 weeks (Fig. 1a). There was no pathological finding in systemic examination. Best-corrected visual acuity was 20/20 bilaterally. Both anterior and dilated posterior segment examinations were normal in both eyes. On detailed anamnesis, it was learned that he experienced a sudden pain that occurred during drying his face with a towel a few weeks ago. When he admitted to our clinic, empirical topical and systemic antibiotics and anti-inflammatory medications were initiated as the lesion resembled an eyelid granulomatous lesion related to meibomian glands. Hence, the symptoms of the patient progressed despite treatment, a punch biopsy from the lesion was performed which did not distinguish infective pathologies or malignancy (Fig. 1b). In histopathological examination, there was ulceration in epidermis. Abundant eosinophils, histiocytes, and lymphoid infiltrate were detected in dermis (Figures 2a-c). There were enlarged CD30-positive lymphocytes in immunohistochemical analysis (Fig. 2d). As the punch biopsy histopathology did not discriminate the lesion, an incisional biopsy was scheduled. On immunohistochemical examination of the incisional biopsy specimen, no CD30-positive cells were detected. Histopathological examination revealed post-biopsy findings such as lymphocytes, histiocytes, increased vascularity, myofibroblasts, and fibrosis in the dermis. After the incisional biopsy, the patient did not receive any treatment other than prophylactic topical antibiotic ointment. However, following incisional biopsy, the lesion rapidly regressed in 7 days (Figs. 3a-b). OUTPUT:
Multicare_common1889
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 71-year-old diabetic woman was admitted to the emergency center because of loss of consciousness. She had new onset headache, nausea, and vomiting a few hours before her admission. She had a history of controlled hypertension and previous myocardial infarction. On neurological examination GCS (Glasgow Coma Scale) was 9, and no neurologic localizing signs were detected. A brain CT scan was performed which revealed the presence of hyperdense lesions in right cerebellum and ventricles corresponding to cerebellar and intraventricular hemorrhage. A large hyperdense mass-like lesion was also noticed in left vitreous cavity which was assumed to be a vitreous hemorrhage (Figure 1). Based on initial brain CT scan findings, a simultaneous intracranial and vitreous hemorrhage was assumed. With a diagnosis of Terson syndrome, an ophthalmology consultation was requested. Handheld slit-lamp examination and indirect funduscopy revealed that the left eye was pseudophakic and had evidence of regressed diabetic retinopathy with extensive photocoagulation laser scars. There was no sign of vitreous or subhyaloid hemorrhage. The right eye was pseudophakic with severe posterior capsule opacification making the fundus invisible. 48 hours later a brain MRI was performed as a routine diagnostic procedure. The follow-up MRI confirmed the presence of intracranial hemorrhage.\nOUTPUT:" }, { "from": "agent", "value": "Intraocular Silicone Oil" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 71-year-old diabetic woman was admitted to the emergency center because of loss of consciousness. She had new onset headache, nausea, and vomiting a few hours before her admission. She had a history of controlled hypertension and previous myocardial infarction. On neurological examination GCS (Glasgow Coma Scale) was 9, and no neurologic localizing signs were detected. A brain CT scan was performed which revealed the presence of hyperdense lesions in right cerebellum and ventricles corresponding to cerebellar and intraventricular hemorrhage. A large hyperdense mass-like lesion was also noticed in left vitreous cavity which was assumed to be a vitreous hemorrhage (Figure 1). Based on initial brain CT scan findings, a simultaneous intracranial and vitreous hemorrhage was assumed. With a diagnosis of Terson syndrome, an ophthalmology consultation was requested. Handheld slit-lamp examination and indirect funduscopy revealed that the left eye was pseudophakic and had evidence of regressed diabetic retinopathy with extensive photocoagulation laser scars. There was no sign of vitreous or subhyaloid hemorrhage. The right eye was pseudophakic with severe posterior capsule opacification making the fundus invisible. 48 hours later a brain MRI was performed as a routine diagnostic procedure. The follow-up MRI confirmed the presence of intracranial hemorrhage. OUTPUT:
Multicare_common7711
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 21-year-old Caucasian woman presented to an outside facility with altered mental status after being found lethargic by family. On arrival to the emergency department, plasma glucose was 20 mg/dl. The patient was hospitalized and started on dextrose infusion, including 10% dextrose in water but remained hypoglycemic with capillary glucose ranging between 50 and 60 mg/dl. She was transferred to our facility on suspicion of an insulinoma as the patient was unable to recall her prior diagnosis. Medical records from our hospital revealed treatment for hypoglycemia as a neonate. The patient reported repeated episodes of seizures, syncope, dizziness, headaches, palpitations, and sweating around age 12; however, symptoms were never formally investigated as she did not seek expert care. These symptoms were also reported to have been present since birth but had been intermittent and of varying severity. She remained seizure-free and without syncopal episodes until 17 when she experienced another syncopal episode. At that time, she underwent extensive inpatient hypoglycemia evaluation with the following results: blood glucose of 47 mg/dl after 2 h of fasting, proinsulin levels varying from 10.4 to 84.1 pmol/l (normal range 0-10 pmol/l), C-peptide level 3.1 ng/ml (normal range 1.1-4.4 ng/ml), negative insulin antibodies and sulfonylurea screen. She was successfully treated with diazoxide and discharged home on oral diazoxide 250 mg daily, which she discontinued due to side effects of hirsutism and fluid retention. On current admission, the patient was treated with dextrose boluses initially. Her blood glucose level remained low in spite of a continuous infusion of 5% dextrose necessitating transfer to an intensive care unit. Both fasting and postprandial blood glucose levels were low. As review of her medication list did not show any implicating drugs, no additional work-up was pursued. She was then placed on octreotide 200 microg subcutaneously twice daily and diazoxide suspension 100 mg three times a day on consultation with the pediatric endocrinologist. Neuroglycopenic symptoms of hypoglycemia improved. The patient's hypoglycemia improved with capillary glucose of 55-110 mg/dl by the time of discharge. Importance of compliance with the treatment and follow-up with an endocrinologist was emphasized.\nOUTPUT:" }, { "from": "agent", "value": "Glucokinase mutation" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 21-year-old Caucasian woman presented to an outside facility with altered mental status after being found lethargic by family. On arrival to the emergency department, plasma glucose was 20 mg/dl. The patient was hospitalized and started on dextrose infusion, including 10% dextrose in water but remained hypoglycemic with capillary glucose ranging between 50 and 60 mg/dl. She was transferred to our facility on suspicion of an insulinoma as the patient was unable to recall her prior diagnosis. Medical records from our hospital revealed treatment for hypoglycemia as a neonate. The patient reported repeated episodes of seizures, syncope, dizziness, headaches, palpitations, and sweating around age 12; however, symptoms were never formally investigated as she did not seek expert care. These symptoms were also reported to have been present since birth but had been intermittent and of varying severity. She remained seizure-free and without syncopal episodes until 17 when she experienced another syncopal episode. At that time, she underwent extensive inpatient hypoglycemia evaluation with the following results: blood glucose of 47 mg/dl after 2 h of fasting, proinsulin levels varying from 10.4 to 84.1 pmol/l (normal range 0-10 pmol/l), C-peptide level 3.1 ng/ml (normal range 1.1-4.4 ng/ml), negative insulin antibodies and sulfonylurea screen. She was successfully treated with diazoxide and discharged home on oral diazoxide 250 mg daily, which she discontinued due to side effects of hirsutism and fluid retention. On current admission, the patient was treated with dextrose boluses initially. Her blood glucose level remained low in spite of a continuous infusion of 5% dextrose necessitating transfer to an intensive care unit. Both fasting and postprandial blood glucose levels were low. As review of her medication list did not show any implicating drugs, no additional work-up was pursued. She was then placed on octreotide 200 microg subcutaneously twice daily and diazoxide suspension 100 mg three times a day on consultation with the pediatric endocrinologist. Neuroglycopenic symptoms of hypoglycemia improved. The patient's hypoglycemia improved with capillary glucose of 55-110 mg/dl by the time of discharge. Importance of compliance with the treatment and follow-up with an endocrinologist was emphasized. OUTPUT:
Multicare_common9525
[ { "from": "human", "value": "As a physician engaged 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 stated that he had not experienced FBTCs in a decade. The FIASs occurred a few times per month and consisted of, \"not being aware of what's happening to me\" and \"my mind is vibrating\". He was treated successfully in the past with multiple antiseizure medications including phenobarbital and phenytoin. At the time of his initial presentation in 2014, he was reporting between 2 and 4 FIASs per month. Electroencephalographic results were obtained from an admission for long-term video-EEG monitoring (LTVEM) in 2015. Interictal EEG demonstrated right temporal sharp discharges and focal attenuation and delta slowing involving the right temporal region. Brain MRI in 2014 showed atrophy and abnormal signal within the right hippocampus with slight atrophy of the right mammillary body (see Fig. This finding was unchanged, based on a previous imaging report. Neuropsychological test scores from winter 2015 are summarized in Table 1. His performance was in the average range of general intellectual ability with no signs of any general cognitive decline. Cognitive functions were normal on many tasks, with performance decrements observed on tests of working memory, processing speed, cognitive flexibility, problem solving, naming, semantic fluency, and episodic memory. The short form of the Wisconsin Card Sorting Test (WCST-64) was discontinued due to conceptual difficulties and perseveration. He exhibited relative strengths on measures of visual and spatial functions.\nOUTPUT:" }, { "from": "agent", "value": "Focal to bilateral tonic-clonic seizures, Focal impaired awareness seizures, Mesial temporal sclerosis, Chronic small vessel ischemic disease, Posterior cerebral artery territory infarction, Focal cortical atrophy" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: He stated that he had not experienced FBTCs in a decade. The FIASs occurred a few times per month and consisted of, "not being aware of what's happening to me" and "my mind is vibrating". He was treated successfully in the past with multiple antiseizure medications including phenobarbital and phenytoin. At the time of his initial presentation in 2014, he was reporting between 2 and 4 FIASs per month. Electroencephalographic results were obtained from an admission for long-term video-EEG monitoring (LTVEM) in 2015. Interictal EEG demonstrated right temporal sharp discharges and focal attenuation and delta slowing involving the right temporal region. Brain MRI in 2014 showed atrophy and abnormal signal within the right hippocampus with slight atrophy of the right mammillary body (see Fig. This finding was unchanged, based on a previous imaging report. Neuropsychological test scores from winter 2015 are summarized in Table 1. His performance was in the average range of general intellectual ability with no signs of any general cognitive decline. Cognitive functions were normal on many tasks, with performance decrements observed on tests of working memory, processing speed, cognitive flexibility, problem solving, naming, semantic fluency, and episodic memory. The short form of the Wisconsin Card Sorting Test (WCST-64) was discontinued due to conceptual difficulties and perseveration. He exhibited relative strengths on measures of visual and spatial functions. OUTPUT:
Multicare_common9418
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: After operation, he received a course of chemotherapy. From then on, he did not accept any treatment or follow-up examinations related to RCC. In 2008, 2 years after nephrectomy, he received a rectal polyp resection by colonoscopy, and the pathologic examination revealed primary rectal benign polyps. Since then, he received an electronic colonoscopy every 1 to 2 years until the year 2016, when a protruded lesion was found in his rectum. The electronic colonoscope examination showed a hyperemic mass covered with sphacelus, approximately 1.2 cm x 1.5 cm size, which was protruded from rectal mucosa (Fig. 1). The mass was fragile and tended to hemorrhage. Biopsy tissue was confirmed as metastatic RCC to rectum by the result of histopathology and immunohistochemical examination. Under the microscope, there were amounts of large and anomalously shaped clear cells with abundant clear cytoplasm and nuclear atypia consistent with RCCC, forming nests or aciniform structure surrounded with slender small vascular tissues (Fig. 2). Immunohistochemical examination revealed cytokeratin pan (AE1/AE3) (+), paired box (PAX)-8 (+), Vimentin (+), caudal typehomebox transcription factor (CDX)-2 (-), Melan-A (-), and alpha-inhibin (-) (Fig. 2). Positron emission tomography-computed tomography with fluorodeoxyglucose (FDG-PET/CT) examination was performed, which showed an abnormal increased radioactive uptake in the upper rectum, 1.6 cm x 2.8 cm x 1.8 cm size, with an average standardized uptake value (SUV) of 5.0 and SUVmax of 10.0, indicating possibility of malignancy (Figs. 3 and 4). In consideration of the existence of multiple metastatic lesions, the patient received targeted therapies by using sunitinib. After 3 months of treatment with sunitinib, the CT images showed that the metastatic lesion of rectum was stable, as well as other metastasis, and the patient is still being followed-up now. The patient is informed consent, and the timeline is listed in Table 1.\nOUTPUT:" }, { "from": "agent", "value": "Metastatic renal clear cell carcinoma to the rectum, lungs, ilium, and lymph nodes" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: After operation, he received a course of chemotherapy. From then on, he did not accept any treatment or follow-up examinations related to RCC. In 2008, 2 years after nephrectomy, he received a rectal polyp resection by colonoscopy, and the pathologic examination revealed primary rectal benign polyps. Since then, he received an electronic colonoscopy every 1 to 2 years until the year 2016, when a protruded lesion was found in his rectum. The electronic colonoscope examination showed a hyperemic mass covered with sphacelus, approximately 1.2 cm x 1.5 cm size, which was protruded from rectal mucosa (Fig. 1). The mass was fragile and tended to hemorrhage. Biopsy tissue was confirmed as metastatic RCC to rectum by the result of histopathology and immunohistochemical examination. Under the microscope, there were amounts of large and anomalously shaped clear cells with abundant clear cytoplasm and nuclear atypia consistent with RCCC, forming nests or aciniform structure surrounded with slender small vascular tissues (Fig. 2). Immunohistochemical examination revealed cytokeratin pan (AE1/AE3) (+), paired box (PAX)-8 (+), Vimentin (+), caudal typehomebox transcription factor (CDX)-2 (-), Melan-A (-), and alpha-inhibin (-) (Fig. 2). Positron emission tomography-computed tomography with fluorodeoxyglucose (FDG-PET/CT) examination was performed, which showed an abnormal increased radioactive uptake in the upper rectum, 1.6 cm x 2.8 cm x 1.8 cm size, with an average standardized uptake value (SUV) of 5.0 and SUVmax of 10.0, indicating possibility of malignancy (Figs. 3 and 4). In consideration of the existence of multiple metastatic lesions, the patient received targeted therapies by using sunitinib. After 3 months of treatment with sunitinib, the CT images showed that the metastatic lesion of rectum was stable, as well as other metastasis, and the patient is still being followed-up now. The patient is informed consent, and the timeline is listed in Table 1. OUTPUT:
Multicare_common138
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: indicating a weight loss of 8% since birth. The patient's general condition was poor. Marked dehydration and mild scrotal hyperpigmentation were present. Laboratory results were as follows: Serum Na: 95 mEq/L (N: 135-143 mEq/L), K: 6.9 mEq/L (N: 3.5-5.5 mEq/L ), blood pH: 7.3, HCO3: 11.7 mmol/L, BUN: 26 mg/dL (0-10 mg/dL), creatinine: 0.47 mg/dL (0.3-1.2 mg/dL). Urinalysis was positive for nitrite and leukocytes and there was a growth of 100 000 colonies of Klebsiella on urine culture. Fludrocortisone and antibiotics were started together with intravenous fluid treatment. Renal ultrasonographic investigation for UTI showed prominent collective structures in the left kidney and grade 2 VUR on the voiding cystogram. Antibiotic prophylaxis was started. Hormonal evaluation revealed basal cortisol of 18 mug/dL, ACTH 89.5 pg/mL (N: 3-46 pg/mL), renin: 186 pg/mL (N: 2.4-37 pg/mL), and aldosterone level of 2 000 pg/mL (N:20-700 pg/mL). The preliminary diagnosis was PHA. The patient benefited from fludrocortisone treatment. Taking into account the high serum ACTH level, an ACTH stimulation test was performed to rule out CAH and the 17-OHP response was as follows: 27.6 ng/mL at 0 time, 44.1 ng/mL at 30 minutes and 41.2 ng/mL at 60 minutes. Hydrocortisone was added to the fludrocortisone and salt treatment. Genetic analysis revealed a large deletion of the 21-OH gene. The patient is currently 1 year old and is being followed-up without any problems on hydrocortisone, fludrocortisone and oral 1 g/day salt treatment. Age at presentation and laboratory findings of the patients are given in Table 1.\nOUTPUT:" }, { "from": "agent", "value": "Pseudohypoaldosteronism, Congenital Adrenal Hyperplasia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: indicating a weight loss of 8% since birth. The patient's general condition was poor. Marked dehydration and mild scrotal hyperpigmentation were present. Laboratory results were as follows: Serum Na: 95 mEq/L (N: 135-143 mEq/L), K: 6.9 mEq/L (N: 3.5-5.5 mEq/L ), blood pH: 7.3, HCO3: 11.7 mmol/L, BUN: 26 mg/dL (0-10 mg/dL), creatinine: 0.47 mg/dL (0.3-1.2 mg/dL). Urinalysis was positive for nitrite and leukocytes and there was a growth of 100 000 colonies of Klebsiella on urine culture. Fludrocortisone and antibiotics were started together with intravenous fluid treatment. Renal ultrasonographic investigation for UTI showed prominent collective structures in the left kidney and grade 2 VUR on the voiding cystogram. Antibiotic prophylaxis was started. Hormonal evaluation revealed basal cortisol of 18 mug/dL, ACTH 89.5 pg/mL (N: 3-46 pg/mL), renin: 186 pg/mL (N: 2.4-37 pg/mL), and aldosterone level of 2 000 pg/mL (N:20-700 pg/mL). The preliminary diagnosis was PHA. The patient benefited from fludrocortisone treatment. Taking into account the high serum ACTH level, an ACTH stimulation test was performed to rule out CAH and the 17-OHP response was as follows: 27.6 ng/mL at 0 time, 44.1 ng/mL at 30 minutes and 41.2 ng/mL at 60 minutes. Hydrocortisone was added to the fludrocortisone and salt treatment. Genetic analysis revealed a large deletion of the 21-OH gene. The patient is currently 1 year old and is being followed-up without any problems on hydrocortisone, fludrocortisone and oral 1 g/day salt treatment. Age at presentation and laboratory findings of the patients are given in Table 1. OUTPUT:
Multicare_common882
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: On examination, green nasal discharge was seen in the right nasal cavity. The patient had a history of DM, HTN and post percutaneous transluminal coronary angioplasty. He was treated with corticosteroids in his weeklong hospitalization and was prescribed Dexamethasone in tapering doses over a period of 6 days. CE- MRI brain [Figure 4] was suggestive of a target-shaped lesion signal alteration in the right frontal lobe, inferomedially in paramedian location, with peripheral enhancement and non-enhancing center. The lesion was contiguous with ethmoidal air cells on the right. Major flow voids along with chronic ischemic changes in bilateral subcortical and deep periventricular white matter were seen. Neurosurgical and ENT surgeons teamed up to take up the surgical challenge. Abscess excision with FESS and orbital decompression was done in a single sitting. Right Frontal craniotomy was performed and abscess cavity was accessed via sub-frontal approach. After the evacuation of greenis pus [Figure 5], the abscess wall was cauterized and excised. It was seen that the cribriform plate, ethmoidal sinus, and falx were eroded, therefore, the base of the skull was repaired with a peri-cranium patch and glue. A lumbar drain was also put to prevent cerebrospinal fluid leakage and swift healing of the skull base. The patient gradually improved post-operatively with no new-onset neurological deficit. On his 2nd Postoperative day, lumbar drain was removed. Postoperatively, the patient was started on amphotericin B and meropenem intravenously. However, on the 9th postoperative day, he had an episode of GTCS, therefore, dual antiepileptics (which antiepileptics? Please mention) were started. Subsequent, contrast MRI brain, did not show any significant residual mass lesion, and the patient was shifted to the surgery ward after 10 days of ICU monitoring. Culture-appropriate antibiotics were started, and the patient responded positively to the treatment. (Refer to [Table 1] for relevant blood investigation reports).\nOUTPUT:" }, { "from": "agent", "value": "Rhino-orbital-cerebral mucormycosis, COVID-19 pneumonia, Klebsiella pneumoniae infection" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: On examination, green nasal discharge was seen in the right nasal cavity. The patient had a history of DM, HTN and post percutaneous transluminal coronary angioplasty. He was treated with corticosteroids in his weeklong hospitalization and was prescribed Dexamethasone in tapering doses over a period of 6 days. CE- MRI brain [Figure 4] was suggestive of a target-shaped lesion signal alteration in the right frontal lobe, inferomedially in paramedian location, with peripheral enhancement and non-enhancing center. The lesion was contiguous with ethmoidal air cells on the right. Major flow voids along with chronic ischemic changes in bilateral subcortical and deep periventricular white matter were seen. Neurosurgical and ENT surgeons teamed up to take up the surgical challenge. Abscess excision with FESS and orbital decompression was done in a single sitting. Right Frontal craniotomy was performed and abscess cavity was accessed via sub-frontal approach. After the evacuation of greenis pus [Figure 5], the abscess wall was cauterized and excised. It was seen that the cribriform plate, ethmoidal sinus, and falx were eroded, therefore, the base of the skull was repaired with a peri-cranium patch and glue. A lumbar drain was also put to prevent cerebrospinal fluid leakage and swift healing of the skull base. The patient gradually improved post-operatively with no new-onset neurological deficit. On his 2nd Postoperative day, lumbar drain was removed. Postoperatively, the patient was started on amphotericin B and meropenem intravenously. However, on the 9th postoperative day, he had an episode of GTCS, therefore, dual antiepileptics (which antiepileptics? Please mention) were started. Subsequent, contrast MRI brain, did not show any significant residual mass lesion, and the patient was shifted to the surgery ward after 10 days of ICU monitoring. Culture-appropriate antibiotics were started, and the patient responded positively to the treatment. (Refer to [Table 1] for relevant blood investigation reports). OUTPUT:
Multicare_common4130
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Exercise-stress cardiac scintigraphy showed significant myocardial ischemia with a total perfusion defect of 19 % in the anteroseptal left ventricle (Fig. 2A-B). Because of the patient's metal allergy concerns based on her history of contact dermatitis to metal, we performed patch tests for various metal alloys, which showed mercury, zinc, and nickel allergies (Fig. 2C). Thereafter, CAG showed the proximal LAD stenosis. Because of the patient's strong willingness to undergo stentless PCI and her refusal to undergo CABG, an additional IVUS examination for preoperatively evaluating plaque morphology revealed a soft plaque with mild superficial calcification, which was expectedly suitable for DCA (Fig. 3A-D). Based on these findings, the heart team elected to perform stentless PCI with DCA/DCB angioplasty as a revascularization strategy. DCA was performed using Atherocut L in six sessions with 30 total cuts (maximum cutting pressure: 4 atm), which enabled the optimal reduction in plaque volume from preoperatively 78 % to postoperatively 45 % on IVUS images (Fig. 3E). Balloon angioplasty with a 3.5/13-mm scoring balloon and 4.0/20-mm PCB was performed. Then, using a 2.25/10-mm cutting balloon and subsequent 2.5/30-mm PCB for the diagonal branch, the final CAG showed optimal results with TIMI grade 3. The patient had an uneventful clinical course after stentless PCI, and CAG, 9 months later, showed no restenosis (Fig. 3F-H).\nOUTPUT:" }, { "from": "agent", "value": "Worsening angina" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Exercise-stress cardiac scintigraphy showed significant myocardial ischemia with a total perfusion defect of 19 % in the anteroseptal left ventricle (Fig. 2A-B). Because of the patient's metal allergy concerns based on her history of contact dermatitis to metal, we performed patch tests for various metal alloys, which showed mercury, zinc, and nickel allergies (Fig. 2C). Thereafter, CAG showed the proximal LAD stenosis. Because of the patient's strong willingness to undergo stentless PCI and her refusal to undergo CABG, an additional IVUS examination for preoperatively evaluating plaque morphology revealed a soft plaque with mild superficial calcification, which was expectedly suitable for DCA (Fig. 3A-D). Based on these findings, the heart team elected to perform stentless PCI with DCA/DCB angioplasty as a revascularization strategy. DCA was performed using Atherocut L in six sessions with 30 total cuts (maximum cutting pressure: 4 atm), which enabled the optimal reduction in plaque volume from preoperatively 78 % to postoperatively 45 % on IVUS images (Fig. 3E). Balloon angioplasty with a 3.5/13-mm scoring balloon and 4.0/20-mm PCB was performed. Then, using a 2.25/10-mm cutting balloon and subsequent 2.5/30-mm PCB for the diagonal branch, the final CAG showed optimal results with TIMI grade 3. The patient had an uneventful clinical course after stentless PCI, and CAG, 9 months later, showed no restenosis (Fig. 3F-H). OUTPUT:
Multicare_common6851
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: We report a case of 68 year-old-man who was admitted to our hospital with a complaint of bulge and pain in the right groin area from 2 weeks before. Physical examination showed a right groin bulge and non-palpable testis in the scrotum. 1, Fig. 2). With the patient in the spine position after induction of general anesthesia, three trocars were placed through the abdominal wall. The first trocar was placed into the umbilicus for the laparoscope. After making a pneumoperitoneum, the next two trocars were placed into the right and left middle abdomen for the operator. 3). Pulling the hernial sac back to the abdominal cavity, we could find out the intracanalicular testis along with a spermatic cord and a testicular vessels, then they were cut and ligated (Fig. 4). The testis was extracted through the umbilical port site, after the incision was extended to 2 cm. The operation time was 81 min and little blood loss was observed. Postoperative period was uneventful and the patient was discharged home on the 1st postoperative day. Pathological examination of the specimen was reported as atrophic testis with no malignancy. There has been no recurrence during a follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Right inguinal hernia, Cryptorchidism" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: We report a case of 68 year-old-man who was admitted to our hospital with a complaint of bulge and pain in the right groin area from 2 weeks before. Physical examination showed a right groin bulge and non-palpable testis in the scrotum. 1, Fig. 2). With the patient in the spine position after induction of general anesthesia, three trocars were placed through the abdominal wall. The first trocar was placed into the umbilicus for the laparoscope. After making a pneumoperitoneum, the next two trocars were placed into the right and left middle abdomen for the operator. 3). Pulling the hernial sac back to the abdominal cavity, we could find out the intracanalicular testis along with a spermatic cord and a testicular vessels, then they were cut and ligated (Fig. 4). The testis was extracted through the umbilical port site, after the incision was extended to 2 cm. The operation time was 81 min and little blood loss was observed. Postoperative period was uneventful and the patient was discharged home on the 1st postoperative day. Pathological examination of the specimen was reported as atrophic testis with no malignancy. There has been no recurrence during a follow-up. OUTPUT:
Multicare_common6918
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 71 years-old female with a medical history of pelvic and lowerback pain for about six months was admitted to our hospital. She didn't report history of dysuria or tenesmus. Abdominal Ultrasound (US) and digital rectal examination were found not diagnostic. contrast enhanced computed tomography (CECT) of abdomen and pelvis showed an oval-shaped hypodense solid mass of 27 x 38 x 19 mm (CC x AP x LL), close to the rectum. 1). The patient also underwent a contrast magnetic resonance imaging (MRI) of abdomen and pelvis which revealed a well-defined lesion in the presacral space with doubt comunication with the rectum which was displaced laterally. (Fig. 2). In accord with literature a CT-guided fine needle aspiration wasn't performed in order to avoid the risk of tumor seeding. The surgical procedure was performed also to provide a definitive diagnosis. The tumor was below the coccygeal level, so we opted for a posterior approach. The patient was placed in prone position (jackknife-position) and operated under general anesthesia. The gluteal region were pulled laterally with adesive draps and pre-operative incisional planning was performed (Fig. 3a). Afterwards a right longitudinal incision was made above the sacrococcygeal midline and the exploration of the presacral space confirmed the presence of the mass (Fig. 3b). It was located anterior to S4 and completely removed (Fig. 3c). The communication between the mass and the anal canal or the rectal wall was excluded by the injection of hydrogen peroxide and methylene blue and through a frequent intraoperative digital rectal examination. Post-operative days were uneventful and the drain was removed in second post-operative day. The patient was discharged on 4th day after surgery. A digital rectal examination and a CT scan of abdomen and pelvis performed after one year from surgery have excluded a local recurrence and at the moment the patient doesn't refer symptoms.\nOUTPUT:" }, { "from": "agent", "value": "Epidermoid cyst" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 71 years-old female with a medical history of pelvic and lowerback pain for about six months was admitted to our hospital. She didn't report history of dysuria or tenesmus. Abdominal Ultrasound (US) and digital rectal examination were found not diagnostic. contrast enhanced computed tomography (CECT) of abdomen and pelvis showed an oval-shaped hypodense solid mass of 27 x 38 x 19 mm (CC x AP x LL), close to the rectum. 1). The patient also underwent a contrast magnetic resonance imaging (MRI) of abdomen and pelvis which revealed a well-defined lesion in the presacral space with doubt comunication with the rectum which was displaced laterally. (Fig. 2). In accord with literature a CT-guided fine needle aspiration wasn't performed in order to avoid the risk of tumor seeding. The surgical procedure was performed also to provide a definitive diagnosis. The tumor was below the coccygeal level, so we opted for a posterior approach. The patient was placed in prone position (jackknife-position) and operated under general anesthesia. The gluteal region were pulled laterally with adesive draps and pre-operative incisional planning was performed (Fig. 3a). Afterwards a right longitudinal incision was made above the sacrococcygeal midline and the exploration of the presacral space confirmed the presence of the mass (Fig. 3b). It was located anterior to S4 and completely removed (Fig. 3c). The communication between the mass and the anal canal or the rectal wall was excluded by the injection of hydrogen peroxide and methylene blue and through a frequent intraoperative digital rectal examination. Post-operative days were uneventful and the drain was removed in second post-operative day. The patient was discharged on 4th day after surgery. A digital rectal examination and a CT scan of abdomen and pelvis performed after one year from surgery have excluded a local recurrence and at the moment the patient doesn't refer symptoms. OUTPUT:
Multicare_common10466
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Regarding the safety of the drug, we observed side effects in three of seven patients. One patient reported mouth ulcers; since he was not treated with mTOR, it was attributed to leflunomide. Oral ulcers are reported in 3%-5% of leflunomide-medicated patients with rheumatoid arthritis who develop adverse events; withdrawal of leflunomide for a month results in <50% healing. For another patient, leflunomide was suspected to cause hemolytic anemia. The dosage of the drug was reduced by 50%. However, secondary increase in the dose did not cause anemia. Finally, a 16-year-old female patient experienced biological pancreatitis after 11 months of leflunomide therapy. Leflunomide was indeed reported to be associated with pancreas toxicity. In our patient, the average leflunomide concentration was as high as 53 mg/L, even though the dose administered in this patient was only 20 mg, which illustrated the interindividual variability of the exposure and supports routine TDM for this drug. According to Kiely, et al, there is no relationship between the plasma concentration of teriflunomide and adverse events. In our patients, leflunomide concentrations were not significantly different when an adverse event occurred. However, this series included a CF patient. After exclusion of CF patient from the analysis, the mean leflunomide concentration was significantly higher when an adverse event occurred (53.3+-14.8 ng/mL vs. 33.7+-15.5 ng/mL, p<0.0001). Immunosuppression was reduced by an average 92% cut in dosage in mycophenolate and 48% in tacrolimus, without any impacts on the graft loss. Of note, leflunomide concentrations were significantly higher when viremia was controlled. This study evidenced the wide interindividual variability of the exposure and supported the routine practice of TDM with a suggested target level of 30-40 mg/L in pediatric kidney transplanted patients. However, because of the very limited number of patients included in this study, further investigations are needed to validate this suggestion.\nOUTPUT:" }, { "from": "agent", "value": "BK virus" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Regarding the safety of the drug, we observed side effects in three of seven patients. One patient reported mouth ulcers; since he was not treated with mTOR, it was attributed to leflunomide. Oral ulcers are reported in 3%-5% of leflunomide-medicated patients with rheumatoid arthritis who develop adverse events; withdrawal of leflunomide for a month results in <50% healing. For another patient, leflunomide was suspected to cause hemolytic anemia. The dosage of the drug was reduced by 50%. However, secondary increase in the dose did not cause anemia. Finally, a 16-year-old female patient experienced biological pancreatitis after 11 months of leflunomide therapy. Leflunomide was indeed reported to be associated with pancreas toxicity. In our patient, the average leflunomide concentration was as high as 53 mg/L, even though the dose administered in this patient was only 20 mg, which illustrated the interindividual variability of the exposure and supports routine TDM for this drug. According to Kiely, et al, there is no relationship between the plasma concentration of teriflunomide and adverse events. In our patients, leflunomide concentrations were not significantly different when an adverse event occurred. However, this series included a CF patient. After exclusion of CF patient from the analysis, the mean leflunomide concentration was significantly higher when an adverse event occurred (53.3+-14.8 ng/mL vs. 33.7+-15.5 ng/mL, p<0.0001). Immunosuppression was reduced by an average 92% cut in dosage in mycophenolate and 48% in tacrolimus, without any impacts on the graft loss. Of note, leflunomide concentrations were significantly higher when viremia was controlled. This study evidenced the wide interindividual variability of the exposure and supported the routine practice of TDM with a suggested target level of 30-40 mg/L in pediatric kidney transplanted patients. However, because of the very limited number of patients included in this study, further investigations are needed to validate this suggestion. OUTPUT:
Multicare_common9900
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 3-mo-old male infant was initially referred to our hospital with micropenis. His growth was normal. His penile length was 1.0 cm and the bilateral testes were palpable in the scrotum with volumes of 1 mL. There were no other abnormal findings, such as cryptorchidism or hypospadias. The laboratory findings are presented in Table 1. A chromosomal analysis revealed a 46,XY karyotype. Serum LH and testosterone levels were undetectable, and serum FSH level was low for his age. Minipuberty occurs in the first 3-6 mo of life, and serum LH and testosterone levels peak at 2.5-3 mo of age. The fact that serum LH and testosterone levels were undetectable at 3 mo of age in this patient suggested a gonadotropin deficiency. Thyroid function plasma IGF-1 and serum dehydroepiandrosterone sulfate levels were normal. At five months of age, a GnRH stimulation test was performed. The basal serum LH and FSH levels were low for his age but increased in response to GnRH (Table 2). Reference values for the GnRH stimulation test in infants could not be found. Since serum gonadotropin levels decrease to the prepubertal range by 4-6 mo of age in boys, GnRH stimulation test results at 5 mo of age may vary among individuals. Therefore, it was impossible to estimate the status of gonadotropin secretory capacity from LH and FSH responses to GnRH stimulation. Magnetic resonance imaging (MRI) revealed a normal pituitary gland and olfactory bulb. Since serum LH, FSH, and testosterone levels were low at 3 mo of age and MRI showed normal olfactory bulbs, normosmic CHH was suspected.\nOUTPUT:" }, { "from": "agent", "value": "Congenital hypogonadotropic hypogonadism, Neuroblastoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 3-mo-old male infant was initially referred to our hospital with micropenis. His growth was normal. His penile length was 1.0 cm and the bilateral testes were palpable in the scrotum with volumes of 1 mL. There were no other abnormal findings, such as cryptorchidism or hypospadias. The laboratory findings are presented in Table 1. A chromosomal analysis revealed a 46,XY karyotype. Serum LH and testosterone levels were undetectable, and serum FSH level was low for his age. Minipuberty occurs in the first 3-6 mo of life, and serum LH and testosterone levels peak at 2.5-3 mo of age. The fact that serum LH and testosterone levels were undetectable at 3 mo of age in this patient suggested a gonadotropin deficiency. Thyroid function plasma IGF-1 and serum dehydroepiandrosterone sulfate levels were normal. At five months of age, a GnRH stimulation test was performed. The basal serum LH and FSH levels were low for his age but increased in response to GnRH (Table 2). Reference values for the GnRH stimulation test in infants could not be found. Since serum gonadotropin levels decrease to the prepubertal range by 4-6 mo of age in boys, GnRH stimulation test results at 5 mo of age may vary among individuals. Therefore, it was impossible to estimate the status of gonadotropin secretory capacity from LH and FSH responses to GnRH stimulation. Magnetic resonance imaging (MRI) revealed a normal pituitary gland and olfactory bulb. Since serum LH, FSH, and testosterone levels were low at 3 mo of age and MRI showed normal olfactory bulbs, normosmic CHH was suspected. OUTPUT:
Multicare_common7462
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Her uncorrected distance visual acuity (VA) improved from 20/200 (manifest refraction: +2.75-0.25 x 10; corrected distance VA: 20/40) to 20/20 (manifest refraction: -0.25-0.25 x 5) at 1 week postoperatively. Uncorrected near VA was J2 using Birkhauser reading chart at a distance of 40 cm. She visited our clinic 2 months later with complaints of visual glare and decreased visual acuity. The corrected distance VA decreased to 20/63 with a manifest refraction of -0.75-7.00 x 35 and uncorrected near VA decreased to J5. An Nd:YAG laser posterior capsulotomy was performed at the area of posterior capsule striae [Figure 1b]. However, corrected distance VA only mildly increased (20/40) and -4.5 D lenticular astigmatism was remained (manifest refraction: -0.75-4.50 x 25). Then, the optic segment was removed and haptics were left in the capsular bag. At 1 month, postoperatively, the uncorrected distance VA and corrected distance VA were returned to 20/20 with manifest refraction of -0.5-0.5 x 15.\nOUTPUT:" }, { "from": "agent", "value": "Posterior subcapsular cataract, IOL tilting" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Her uncorrected distance visual acuity (VA) improved from 20/200 (manifest refraction: +2.75-0.25 x 10; corrected distance VA: 20/40) to 20/20 (manifest refraction: -0.25-0.25 x 5) at 1 week postoperatively. Uncorrected near VA was J2 using Birkhauser reading chart at a distance of 40 cm. She visited our clinic 2 months later with complaints of visual glare and decreased visual acuity. The corrected distance VA decreased to 20/63 with a manifest refraction of -0.75-7.00 x 35 and uncorrected near VA decreased to J5. An Nd:YAG laser posterior capsulotomy was performed at the area of posterior capsule striae [Figure 1b]. However, corrected distance VA only mildly increased (20/40) and -4.5 D lenticular astigmatism was remained (manifest refraction: -0.75-4.50 x 25). Then, the optic segment was removed and haptics were left in the capsular bag. At 1 month, postoperatively, the uncorrected distance VA and corrected distance VA were returned to 20/20 with manifest refraction of -0.5-0.5 x 15. OUTPUT:
Multicare_common5141
[ { "from": "human", "value": "As a physician engaged 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 man presented with a 1-month history of weakness and numbness in both his legs. At his first visit, neurological examination revealed normal muscle strength with a muscle stretch reflex indicating hyperreflexia in the lower limbs. In addition, pain radiating to the back was induced by back flexion or extension and jumping. He was ambulatory, although a spastic gait was evident. Magnetic resonance imaging (MRI) showed an intradural extramedullary lesion with hypointense changes on T1 and isointense changes on T2 as well as heterogeneous gadolinium enhancement at the T10 and T11 levels (Figure 1). Although MRI findings appeared circumscribed, the mass was large and was located on the ventrolateral side. An accurate preoperative diagnosis was considered important; thus, we performed myelography to obtain more detailed information. Injection of iohexol was performed following puncture at the L4 and L5 levels, and 1 ml of cerebrospinal fluid (CSF) was collected for a CSF analysis. He reported back and lower limb pain after the injection of 2 ml of iohexol. As he reported severe pain just after the injection of 5 ml of iohexol, 3 ml of CSF was drained, and the pain improved immediately. Computed tomography (CT) after myelography revealed a rostrally migrated intradural mass with an approximately 10 mm discrepancy in the exact location compared to MRI findings (Figure 2). A second lumbar puncture was performed, and 10 ml of CSF was drained. After CSF drainage, the symptoms:including weakness and sensory disturbance:immediately improved. Surgical treatment the day after myelography achieved complete resection of the intradural extramedullary tumor, and a histological examination confirmed the diagnosis of schwannoma (Figure 3). At 12 months after surgery (Figure 4), he was working as a physical education teacher despite having hyperreflexia in his lower limbs.\nOUTPUT:" }, { "from": "agent", "value": "Paraplegia, Thoracic Mobile Schwannoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 25-year-old man presented with a 1-month history of weakness and numbness in both his legs. At his first visit, neurological examination revealed normal muscle strength with a muscle stretch reflex indicating hyperreflexia in the lower limbs. In addition, pain radiating to the back was induced by back flexion or extension and jumping. He was ambulatory, although a spastic gait was evident. Magnetic resonance imaging (MRI) showed an intradural extramedullary lesion with hypointense changes on T1 and isointense changes on T2 as well as heterogeneous gadolinium enhancement at the T10 and T11 levels (Figure 1). Although MRI findings appeared circumscribed, the mass was large and was located on the ventrolateral side. An accurate preoperative diagnosis was considered important; thus, we performed myelography to obtain more detailed information. Injection of iohexol was performed following puncture at the L4 and L5 levels, and 1 ml of cerebrospinal fluid (CSF) was collected for a CSF analysis. He reported back and lower limb pain after the injection of 2 ml of iohexol. As he reported severe pain just after the injection of 5 ml of iohexol, 3 ml of CSF was drained, and the pain improved immediately. Computed tomography (CT) after myelography revealed a rostrally migrated intradural mass with an approximately 10 mm discrepancy in the exact location compared to MRI findings (Figure 2). A second lumbar puncture was performed, and 10 ml of CSF was drained. After CSF drainage, the symptoms:including weakness and sensory disturbance:immediately improved. Surgical treatment the day after myelography achieved complete resection of the intradural extramedullary tumor, and a histological examination confirmed the diagnosis of schwannoma (Figure 3). At 12 months after surgery (Figure 4), he was working as a physical education teacher despite having hyperreflexia in his lower limbs. OUTPUT:
Multicare_common848
[ { "from": "human", "value": "As a physician engaged 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 male was 42 years old with a two month period of sobriety. The subject was recruited from G & G Holistic Addition Center alumni group. He was currently employed but complained about anxiety and a continuation of craving, \"white knuckle\" sobriety. The study was approved by the PATH Foundation NY Institutional Review Board as part of an approved research project related to genetic testing and novel approaches to SUD treatment (RB NIH registration is # (IRB00002334). The patient signed a consent statement prior to the experiment. The patient was not taking any psychoactive medication at the time of the evaluation. He was drug free as assessed by urine testing. A qEEG analysis obtained one-day prior to NEAT-12 treatments was considered as the pretest. At the exact same time only one day later the patient utilized the NEAT 12 for a one-hour period. Immediately after this treatment the subject was re-evaluated by qEEG analysis. The NEAT 12 has twelve independent programs associated to patient's condition whether it is acute, sub-acute or chronic. The program used in this case study was for post chronic conditions. The current characteristics were 25 uA, at a frequency of 0.44 Hz, polarity change 2.25 seconds every 17 pulses with a modulated pulse. The electric parameters for the NEAT-12 device are shown in Table 1 and Figure 1. The memory of the NEAT-12 device stores data for 12 different therapeutic waveforms and pulse sequences, each of which is described in Table 2. In a current search of the existing devices approved for market by the FDA for Cranial Electrical Stimulation no device was found to have any similar waveform characteristics. Many claimed to have waveform harmonics which are trade secrets but from our research the duration, polarity and modulation of our waveform has very little resemblance of any other device on the market today. Nineteen electrodes using an electro-cap consistent with the International 10/20 systems were placed. Routine EEG was recorded on a Cadwell Easy II using a linked ear montage and with electrodes digitally referenced to the Cz electrode allowing for retrospective montage analysis of all data. Using data gathered under technical conditions as listed above, 59.99 seconds of EEG were selected and subjected to quantitative analysis of absolute power, relative power, power asymmetry and coherence. These measurements are logarithmically transformed and referenced to age-adjusted population norms.\nOUTPUT:" }, { "from": "agent", "value": "Alcoholism" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The male was 42 years old with a two month period of sobriety. The subject was recruited from G & G Holistic Addition Center alumni group. He was currently employed but complained about anxiety and a continuation of craving, "white knuckle" sobriety. The study was approved by the PATH Foundation NY Institutional Review Board as part of an approved research project related to genetic testing and novel approaches to SUD treatment (RB NIH registration is # (IRB00002334). The patient signed a consent statement prior to the experiment. The patient was not taking any psychoactive medication at the time of the evaluation. He was drug free as assessed by urine testing. A qEEG analysis obtained one-day prior to NEAT-12 treatments was considered as the pretest. At the exact same time only one day later the patient utilized the NEAT 12 for a one-hour period. Immediately after this treatment the subject was re-evaluated by qEEG analysis. The NEAT 12 has twelve independent programs associated to patient's condition whether it is acute, sub-acute or chronic. The program used in this case study was for post chronic conditions. The current characteristics were 25 uA, at a frequency of 0.44 Hz, polarity change 2.25 seconds every 17 pulses with a modulated pulse. The electric parameters for the NEAT-12 device are shown in Table 1 and Figure 1. The memory of the NEAT-12 device stores data for 12 different therapeutic waveforms and pulse sequences, each of which is described in Table 2. In a current search of the existing devices approved for market by the FDA for Cranial Electrical Stimulation no device was found to have any similar waveform characteristics. Many claimed to have waveform harmonics which are trade secrets but from our research the duration, polarity and modulation of our waveform has very little resemblance of any other device on the market today. Nineteen electrodes using an electro-cap consistent with the International 10/20 systems were placed. Routine EEG was recorded on a Cadwell Easy II using a linked ear montage and with electrodes digitally referenced to the Cz electrode allowing for retrospective montage analysis of all data. Using data gathered under technical conditions as listed above, 59.99 seconds of EEG were selected and subjected to quantitative analysis of absolute power, relative power, power asymmetry and coherence. These measurements are logarithmically transformed and referenced to age-adjusted population norms. OUTPUT:
Multicare_common8687
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 43-yr-old female presented with a 2-day history of increasing swelling of the face and right upper extremity. In addition, she had one week history of fever, progressive shortness of breath, and cough with yellow sputum production. An unsuccessful attempt was made to lyse the thrombus with urokinase. She had been an active smoker of one pack of cigarettes a day for 20 years. She did not own a pet and denied any contact with animals but she had a history of cat scratch disease. Laboratory results revealed an elevated WBC count of 21 cells/ml. Sputum culture obtained at admission produced moderate growth (2+) of B. bronchiseptica and C. albicans. In vitro testing indicated sensitivity to amikacin, gentamicin, tobramycin and piperacillin. Blood and urine cultures were negative. Chest X-ray demonstrated bilateral pleural effusions and lower lung infiltrates. Intravenous cefotaxime 1gm thrice daily was begun empirically along with 1 dose of intravenous tobramycin 90 mg. On the fourth day of hospitalization, the dyspnea worsened. Chest x-ray demonstrated a left greater than right pleural effusion. One week after admission, the patient developed severe respiratory distress. Cefotaxime was changed to intravenous piperacillin 3g every four hours and tobramycin 100mg every eight hours. Sputum cultures again grew C. albicans as well as 4+ B. bronchiseptica sensitive to amikacin, ceftazidime, gentamicin, tobramycin and piperacillin. On day 9 of admission, the patient developed fever of 39.5 C, septic shock and multi-organ system failure. Sputum culture grew 2+ C. albicans and 1+ B. bronchiseptica again sensitive to the same antibiotics tested previously. Blood culture grew S. epidermidis. She expired the following day.\nOUTPUT:" }, { "from": "agent", "value": "Bordetella bronchiseptica infection, Superior vena cava syndrome, Malignant thymoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 43-yr-old female presented with a 2-day history of increasing swelling of the face and right upper extremity. In addition, she had one week history of fever, progressive shortness of breath, and cough with yellow sputum production. An unsuccessful attempt was made to lyse the thrombus with urokinase. She had been an active smoker of one pack of cigarettes a day for 20 years. She did not own a pet and denied any contact with animals but she had a history of cat scratch disease. Laboratory results revealed an elevated WBC count of 21 cells/ml. Sputum culture obtained at admission produced moderate growth (2+) of B. bronchiseptica and C. albicans. In vitro testing indicated sensitivity to amikacin, gentamicin, tobramycin and piperacillin. Blood and urine cultures were negative. Chest X-ray demonstrated bilateral pleural effusions and lower lung infiltrates. Intravenous cefotaxime 1gm thrice daily was begun empirically along with 1 dose of intravenous tobramycin 90 mg. On the fourth day of hospitalization, the dyspnea worsened. Chest x-ray demonstrated a left greater than right pleural effusion. One week after admission, the patient developed severe respiratory distress. Cefotaxime was changed to intravenous piperacillin 3g every four hours and tobramycin 100mg every eight hours. Sputum cultures again grew C. albicans as well as 4+ B. bronchiseptica sensitive to amikacin, ceftazidime, gentamicin, tobramycin and piperacillin. On day 9 of admission, the patient developed fever of 39.5 C, septic shock and multi-organ system failure. Sputum culture grew 2+ C. albicans and 1+ B. bronchiseptica again sensitive to the same antibiotics tested previously. Blood culture grew S. epidermidis. She expired the following day. OUTPUT:
Multicare_common2545
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 17-year-old boy diagnosed with early precursor T-cell, ALL and no other medical comorbidities completed his induction phase with vincristine, cytarabine, and cyclophosphamide in July 2015. In the beginning of August 2015, he was started on consolidation phase of chemotherapy with vincristine, daunorubicin, polyethylene glycol daunorubicin asparaginase, and prednisolone. Midway through the consolidation (after 2 cycles) phase, he developed tingling sensation in the plantar aspect and toes of his feet, which progressed to \"pins and needles\" sensation in 1 week. They started him on ultracet (tramadol 37.5 mg + paracetamol 325 mg) 4 times a day for pain. However, the boy did not have adequate pain control. He was referred to the department of pain and palliative medicine for pain management. The patient spent most time in bed and used a wheel chair to go to the toilet. On examination, the pain score was 7/10 (on Edmonton Symptom Assessment Scale). He had developed Grade III neuropathy (Cancer Therapy Evaluation Program, Common Terminology Criteria for Adverse Events, Version 3.0). He was started on tablet pregabalin 75 mg at night and escalated his dose every 3rd day by 75 mg until pain was controlled. Ultracet was stopped. The boy had good pain control (Edmonton Symptom Assessment Scale - 1/10) on day 15 with no side effects. There was complete resolution of his neuropathy. He was able to walk to the bathroom without support and do his routine activities without any discomfort. There was complete resolution of the tingling sensation in the fingers. He was discharged with a plan of restarting his chemotherapy.\nOUTPUT:" }, { "from": "agent", "value": "Chemotherapy Induced Neuropathic Pain" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 17-year-old boy diagnosed with early precursor T-cell, ALL and no other medical comorbidities completed his induction phase with vincristine, cytarabine, and cyclophosphamide in July 2015. In the beginning of August 2015, he was started on consolidation phase of chemotherapy with vincristine, daunorubicin, polyethylene glycol daunorubicin asparaginase, and prednisolone. Midway through the consolidation (after 2 cycles) phase, he developed tingling sensation in the plantar aspect and toes of his feet, which progressed to "pins and needles" sensation in 1 week. They started him on ultracet (tramadol 37.5 mg + paracetamol 325 mg) 4 times a day for pain. However, the boy did not have adequate pain control. He was referred to the department of pain and palliative medicine for pain management. The patient spent most time in bed and used a wheel chair to go to the toilet. On examination, the pain score was 7/10 (on Edmonton Symptom Assessment Scale). He had developed Grade III neuropathy (Cancer Therapy Evaluation Program, Common Terminology Criteria for Adverse Events, Version 3.0). He was started on tablet pregabalin 75 mg at night and escalated his dose every 3rd day by 75 mg until pain was controlled. Ultracet was stopped. The boy had good pain control (Edmonton Symptom Assessment Scale - 1/10) on day 15 with no side effects. There was complete resolution of his neuropathy. He was able to walk to the bathroom without support and do his routine activities without any discomfort. There was complete resolution of the tingling sensation in the fingers. He was discharged with a plan of restarting his chemotherapy. OUTPUT:
Multicare_common10292
[ { "from": "human", "value": "As a physician engaged 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 man with end-stage idiopathic pulmonary fibrosis underwent bilateral sequential LT. Antimicrobial coverage was broadened to include levofloxacin, metronidazole, and micafungin. Baseline lab (Table 2) and computed tomography of the head, chest, and abdomen were unrevealing. Electroencephalogram was negative for seizures. Serum ammonia (NH3) level on post-op day six was 245 mumol/L, which was elevated from the immediate post-transplant level of 55 mumol/L (normal <60 mumol/L). A comprehensive workup for an infection that included blood cultures for urea-splitting organisms, bacteria, and fungi was negative. Serum ammonia continued to rise despite the implementation of RRT and aggressive bowel decontamination with lactulose and metronidazole. With the above therapies, the patient's serum ammonia returned to normal over the next 3 days. This coincided with the normalization of his hemodynamics, serum lactate level, and resolution of his altered mental status. At this point, the patient's family withdrew care.\nOUTPUT:" }, { "from": "agent", "value": "Hyperammonemia, Severe encephalopathy, Distributive shock, Urea cycle disorder, Septic shock from a perforated cecum, Hemorrhagic shock" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 68-year-old man with end-stage idiopathic pulmonary fibrosis underwent bilateral sequential LT. Antimicrobial coverage was broadened to include levofloxacin, metronidazole, and micafungin. Baseline lab (Table 2) and computed tomography of the head, chest, and abdomen were unrevealing. Electroencephalogram was negative for seizures. Serum ammonia (NH3) level on post-op day six was 245 mumol/L, which was elevated from the immediate post-transplant level of 55 mumol/L (normal <60 mumol/L). A comprehensive workup for an infection that included blood cultures for urea-splitting organisms, bacteria, and fungi was negative. Serum ammonia continued to rise despite the implementation of RRT and aggressive bowel decontamination with lactulose and metronidazole. With the above therapies, the patient's serum ammonia returned to normal over the next 3 days. This coincided with the normalization of his hemodynamics, serum lactate level, and resolution of his altered mental status. At this point, the patient's family withdrew care. OUTPUT:
Multicare_common1848
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Patient A is a 22-year-old male who developed hematochezia at the age of 16. Colonoscopy by his pediatrician revealed diffuse inflammation of the large intestine with more intense inflammation in the distal colon He responded promptly to corticosteroid therapy, but his remission was not durable despite therapy with oral and topical mesalamine. MP (50 mg) was initiated to enable steroid withdrawal after normal TPMT enzyme activity (23.0 U/ml RBC, normal >21 U/ml RBC) was demonstrated (Table 1). However, during attempts to increase the dose of MP, levels of alanine aminotransferase (ALT) reached a maximum of 114 U/l (normal <35), without clinical signs of adverse effects. Subsequent measurement of thiopurine metabolites revealed high levels of 6-MMP of 13,477 pmol/8 x 108 RBC, whereas 6-TGN remained at subtherapeutic levels (<235 pmol/8 x 108 RBC). Reduction of the MP dose to 75 mg resulted in normalization of liver tests and lower levels of thiopurine metabolites (6-TGN 137 and 6-MMP 3,700 pmol/8 x 108). In the next year, the patient was not able to achieve steroid-free remission with MP and oral and topical mesalamine. Allopurinol 100 mg was introduced to skew the MP metabolism toward higher 6-TGN levels and lower 6-MMP levels. The dose of MP was reduced to 25 mg to prevent a disproportionate increase in 6-TGN levels that could potentially cause myelotoxicity. He responded well to this strategy over the course of the following months. He achieved full clinical remission in the absence of hepatotoxicity or myelotoxicity and was able to discontinue corticosteroids. The dose of MP was increased to 50 mg daily to obtain optimum levels of 6-TGN, on the basis of MP metabolites. Recent measurement of thiopurine metabolites showed a 6-TGN level of 422 pmol/8 x 108 RBC and 6-MMP was not quantifiable (lower detection level 255 pmol/8 x 108 RBC). On follow-up 14 months after initiation of the combination therapy, he remains in stable, steroid-free remission on allopurinol 100 mg and MP 50 mg.\nOUTPUT:" }, { "from": "agent", "value": "Ulcerative colitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Patient A is a 22-year-old male who developed hematochezia at the age of 16. Colonoscopy by his pediatrician revealed diffuse inflammation of the large intestine with more intense inflammation in the distal colon He responded promptly to corticosteroid therapy, but his remission was not durable despite therapy with oral and topical mesalamine. MP (50 mg) was initiated to enable steroid withdrawal after normal TPMT enzyme activity (23.0 U/ml RBC, normal >21 U/ml RBC) was demonstrated (Table 1). However, during attempts to increase the dose of MP, levels of alanine aminotransferase (ALT) reached a maximum of 114 U/l (normal <35), without clinical signs of adverse effects. Subsequent measurement of thiopurine metabolites revealed high levels of 6-MMP of 13,477 pmol/8 x 108 RBC, whereas 6-TGN remained at subtherapeutic levels (<235 pmol/8 x 108 RBC). Reduction of the MP dose to 75 mg resulted in normalization of liver tests and lower levels of thiopurine metabolites (6-TGN 137 and 6-MMP 3,700 pmol/8 x 108). In the next year, the patient was not able to achieve steroid-free remission with MP and oral and topical mesalamine. Allopurinol 100 mg was introduced to skew the MP metabolism toward higher 6-TGN levels and lower 6-MMP levels. The dose of MP was reduced to 25 mg to prevent a disproportionate increase in 6-TGN levels that could potentially cause myelotoxicity. He responded well to this strategy over the course of the following months. He achieved full clinical remission in the absence of hepatotoxicity or myelotoxicity and was able to discontinue corticosteroids. The dose of MP was increased to 50 mg daily to obtain optimum levels of 6-TGN, on the basis of MP metabolites. Recent measurement of thiopurine metabolites showed a 6-TGN level of 422 pmol/8 x 108 RBC and 6-MMP was not quantifiable (lower detection level 255 pmol/8 x 108 RBC). On follow-up 14 months after initiation of the combination therapy, he remains in stable, steroid-free remission on allopurinol 100 mg and MP 50 mg. OUTPUT:
Multicare_common5485
[ { "from": "human", "value": "As a physician engaged 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 man, reformed smoker and occasional consumer of alcohol, presented with scanty hemoptysis and breathlessness on exertion of 3 months duration. There was no previous history of genital ulcer or skin rash. Patient gave history of multiple unprotected extramarital sexual exposures, the last episode being 8 years prior to onset of present complaints. He had two healthy children and his wife was also in good health. Examination revealed a normal heart rate with feeble left radial, brachial and carotid pulses. Rest of the general and systemic examination was within normal limits. Ocular examination was normal. Investigations revealed normal hematological and biochemical parameters. Bronchoscopy confirmed extrinsic compression of left side mid-trachea. Spirometry was suggestive of severe obstruction. Electrocardiogram and two-dimensional echocardiography studies were normal. Serum Venereal Disease Research Laboratory (VDRL) was found to be positive in titers of 1:32. Treponema pallidum hemagglutination (TPHA) done for confirmation was also found to be positive in titers of 1:64. Enzyme linked immunosorbent assay for human immunodeficiency virus, hepatitis B surface antigen and anti-hepatitis C virus were negative. It revealed: 02 white blood cells/mm3, protein of 21 mg % and sugar of 53 mg %. CSF VDRL was negative, CSF TPHA was positive with a TPHA index of 23.5.\nOUTPUT:" }, { "from": "agent", "value": "Tertiary syphilis, Aortic aneurysm" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 35-year-old man, reformed smoker and occasional consumer of alcohol, presented with scanty hemoptysis and breathlessness on exertion of 3 months duration. There was no previous history of genital ulcer or skin rash. Patient gave history of multiple unprotected extramarital sexual exposures, the last episode being 8 years prior to onset of present complaints. He had two healthy children and his wife was also in good health. Examination revealed a normal heart rate with feeble left radial, brachial and carotid pulses. Rest of the general and systemic examination was within normal limits. Ocular examination was normal. Investigations revealed normal hematological and biochemical parameters. Bronchoscopy confirmed extrinsic compression of left side mid-trachea. Spirometry was suggestive of severe obstruction. Electrocardiogram and two-dimensional echocardiography studies were normal. Serum Venereal Disease Research Laboratory (VDRL) was found to be positive in titers of 1:32. Treponema pallidum hemagglutination (TPHA) done for confirmation was also found to be positive in titers of 1:64. Enzyme linked immunosorbent assay for human immunodeficiency virus, hepatitis B surface antigen and anti-hepatitis C virus were negative. It revealed: 02 white blood cells/mm3, protein of 21 mg % and sugar of 53 mg %. CSF VDRL was negative, CSF TPHA was positive with a TPHA index of 23.5. OUTPUT:
Multicare_common6850
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 53-year-old male with a posttraumatic incomplete spinal cord injury (AIS D, sub C4) was examined during his neurological rehabilitation at the Spinal Cord Injury Center at Balgrist University Hospital, Switzerland. The study was approved by the \"Kantonale Ethikkommission Zurich\" (EK-04/2006 / PB_2016-02051, clinicaltrial.gov number: NCT02138344) and written informed consent for publication was obtained from the patient. Light touch was normal within the cervical segments, and sharp dull discrimination was preserved while the intensity of the pinprick stimulus was only mildly attenuated. The upper extremity motor score (left: 11/25, right: 11/25) showed a profound weakness of elbow extensors, and no voluntary muscle activity in the finger flexors and abductors bilaterally. The lower extremity motor score was normal (left: 25/25, right: 25/25). Biceps and brachioradialis reflexes, as well as knee-jerk and ankle-jerk reflexes were bilaterally exaggerated. The Babinski sign was negative. Muscle tone was normal without signs of spasticity. Coordination and gait showed discrete signs of ataxia. Ulnar somatosensory evoked potentials (SEPs) and sensory nerve conduction studies were normal (Figure 1D). The CHEP recording was performed according to an established protocol. Stimulus application was performed in a slow fashion in order to favor recruitment of A-delta fibers. The skin was stimulated 20 times from a distance of 1 cm within 1 s. The experimenter was trained prior to the experiment to guarantee the stimuli are uniformly applied. CHEPs were normal at C4 and T4 with high pain ratings to the heat stimulation, but almost complete loss of painful heat sensation and absent CHEPs at the level of C6 (Figure 1B). In contrast, PEPs remained preserved at all segments (Figure 1C).\nOUTPUT:" }, { "from": "agent", "value": "Snake Eye Appearance Myelopathy, Central Cord Syndrome, Mechanical Allodynia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 53-year-old male with a posttraumatic incomplete spinal cord injury (AIS D, sub C4) was examined during his neurological rehabilitation at the Spinal Cord Injury Center at Balgrist University Hospital, Switzerland. The study was approved by the "Kantonale Ethikkommission Zurich" (EK-04/2006 / PB_2016-02051, clinicaltrial.gov number: NCT02138344) and written informed consent for publication was obtained from the patient. Light touch was normal within the cervical segments, and sharp dull discrimination was preserved while the intensity of the pinprick stimulus was only mildly attenuated. The upper extremity motor score (left: 11/25, right: 11/25) showed a profound weakness of elbow extensors, and no voluntary muscle activity in the finger flexors and abductors bilaterally. The lower extremity motor score was normal (left: 25/25, right: 25/25). Biceps and brachioradialis reflexes, as well as knee-jerk and ankle-jerk reflexes were bilaterally exaggerated. The Babinski sign was negative. Muscle tone was normal without signs of spasticity. Coordination and gait showed discrete signs of ataxia. Ulnar somatosensory evoked potentials (SEPs) and sensory nerve conduction studies were normal (Figure 1D). The CHEP recording was performed according to an established protocol. Stimulus application was performed in a slow fashion in order to favor recruitment of A-delta fibers. The skin was stimulated 20 times from a distance of 1 cm within 1 s. The experimenter was trained prior to the experiment to guarantee the stimuli are uniformly applied. CHEPs were normal at C4 and T4 with high pain ratings to the heat stimulation, but almost complete loss of painful heat sensation and absent CHEPs at the level of C6 (Figure 1B). In contrast, PEPs remained preserved at all segments (Figure 1C). OUTPUT:
Multicare_common971
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 64-year-old woman with severe back pain was admitted to the primary hospital. Six months ago, she underwent cardiac stent implantation for myocardial infarction and was prescribed oral aspirin (100 mg/daily) and clopidogrel (75 mg/daily). The prothrombin time (PT) and activated partial thromboplastin time (APTT) were within the normal range on preoperative laboratory examination. The lumbar magnetic resonance imaging (MRI) showed a L1 and L2 compression fracture; the high signal of the short time inversion recovery (STIR) sequence was seen in the L1 vertebral body (Figure 1A and B). She had no neurological symptoms, and she underwent the L1 PKP. The puncture, balloon dilatation, and cement injection were performed using intraoperative fluoroscopy (Figure 2A-F). Immediately after the operation, the back pain improved significantly without neurological deficit. However, 12 hours later, she developed progressive weakness of bilateral lower limbs. No intraspinal cement leakage was obvious on the postoperative lumbar radiograph (Figure 3) and computed tomography (CT) (Figure 4). The patient was transferred to our hospital and underwent an emergency MRI examination, which revealed a high signal aggregation in front of the spinal cord from T12 to L1, indicating spinal cord compression (Figure 1C and D). Physical examination revealed grade III strength in the bilateral iliopsoas, quadriceps femoris, and tibialis anterior muscles. We suspected postoperative SEH and performed laminectomy and decompression from T12-L1. Following excision of SEH and decompression of the spinal cord, the neurological deficit of the lower limbs improved. On follow-up after 6 months, the muscle strength of the bilateral lower limbs had returned to normal.\nOUTPUT:" }, { "from": "agent", "value": "Spinal Epidural Hematoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 64-year-old woman with severe back pain was admitted to the primary hospital. Six months ago, she underwent cardiac stent implantation for myocardial infarction and was prescribed oral aspirin (100 mg/daily) and clopidogrel (75 mg/daily). The prothrombin time (PT) and activated partial thromboplastin time (APTT) were within the normal range on preoperative laboratory examination. The lumbar magnetic resonance imaging (MRI) showed a L1 and L2 compression fracture; the high signal of the short time inversion recovery (STIR) sequence was seen in the L1 vertebral body (Figure 1A and B). She had no neurological symptoms, and she underwent the L1 PKP. The puncture, balloon dilatation, and cement injection were performed using intraoperative fluoroscopy (Figure 2A-F). Immediately after the operation, the back pain improved significantly without neurological deficit. However, 12 hours later, she developed progressive weakness of bilateral lower limbs. No intraspinal cement leakage was obvious on the postoperative lumbar radiograph (Figure 3) and computed tomography (CT) (Figure 4). The patient was transferred to our hospital and underwent an emergency MRI examination, which revealed a high signal aggregation in front of the spinal cord from T12 to L1, indicating spinal cord compression (Figure 1C and D). Physical examination revealed grade III strength in the bilateral iliopsoas, quadriceps femoris, and tibialis anterior muscles. We suspected postoperative SEH and performed laminectomy and decompression from T12-L1. Following excision of SEH and decompression of the spinal cord, the neurological deficit of the lower limbs improved. On follow-up after 6 months, the muscle strength of the bilateral lower limbs had returned to normal. OUTPUT:
Multicare_common6273
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 63-year-old male was referred to our tertiary hospital with recurrent Dt-GCT of his left knee. Two years prior to referral, Dt-GCT was diagnosed and (partial) arthroscopically removed elsewhere. MRI showed a diffuse-TGCT growth-pattern involving all compartments of the entire knee joint, including a Bakers cyst (Figures 2(a) and 2(b)). Consequently, a two-staged anterior and posterior synovectomy in two tempi was performed; macroscopically all pathological tissue was removed. A transarticular distal femoral resection and resection of all Dt-GCT tissue was performed. The knee joint was reconstructed using an endoprosthetic-reconstruction (EPR). Thereafter patient's knee function seemed to improve. However, several months later, swelling and increasing knee pain developed. C-reactive protein (CRP) and erythrocyte sedimentation rate were elevated; nevertheless cultures of aspirated knee fluid were negative. Along with general deterioration of the patient, wound debridement, antibiotics, irrigation, and retention (DAIR) was performed. Two out of six cultures, showed coagulase negative staphylococci without a sign of recurrent TGCT. Despite the DAIR procedure, his EPR had to be replaced with a gentamicin loaded spacer. The EPR was reimplanted. After two additional DAIR procedures the patient preferred an above-knee amputation over another DAIR procedure, life-long antibiotics, or a third 2-stage revision. At present he is pain-free and ambulatory with an above-knee prosthetic leg.\nOUTPUT:" }, { "from": "agent", "value": "Tenosynovial Giant Cell Tumour, Chondromalacia grades 3-4, Progressive osteoarthritis, Low-grade infection" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 63-year-old male was referred to our tertiary hospital with recurrent Dt-GCT of his left knee. Two years prior to referral, Dt-GCT was diagnosed and (partial) arthroscopically removed elsewhere. MRI showed a diffuse-TGCT growth-pattern involving all compartments of the entire knee joint, including a Bakers cyst (Figures 2(a) and 2(b)). Consequently, a two-staged anterior and posterior synovectomy in two tempi was performed; macroscopically all pathological tissue was removed. A transarticular distal femoral resection and resection of all Dt-GCT tissue was performed. The knee joint was reconstructed using an endoprosthetic-reconstruction (EPR). Thereafter patient's knee function seemed to improve. However, several months later, swelling and increasing knee pain developed. C-reactive protein (CRP) and erythrocyte sedimentation rate were elevated; nevertheless cultures of aspirated knee fluid were negative. Along with general deterioration of the patient, wound debridement, antibiotics, irrigation, and retention (DAIR) was performed. Two out of six cultures, showed coagulase negative staphylococci without a sign of recurrent TGCT. Despite the DAIR procedure, his EPR had to be replaced with a gentamicin loaded spacer. The EPR was reimplanted. After two additional DAIR procedures the patient preferred an above-knee amputation over another DAIR procedure, life-long antibiotics, or a third 2-stage revision. At present he is pain-free and ambulatory with an above-knee prosthetic leg. OUTPUT:
Multicare_common7910
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: We present a case of a 69-year-old female with a past medical history of multiple myeloma followed by autologous peripheral stem cell transplant who was hospitalized after presenting with worsening dyspnea. Subsequent studies revealed no central nervous system (CNS) involvement, and flucytosine was discontinued. She was discharged from the hospital to complete two weeks of intravenous liposomal amphotericin B and a year of oral fluconazole. She was readmitted after two weeks due to constitutional symptoms of fever, loss of appetite, and fatigue in addition to dry cough. Cryptococcus serum titers were 1 : 640 during this time as compared to 1 : 2560 at diagnosis. Bacterial and fungal cultures taken from peripheral and central access sites revealed no growth and Aspergillus serum antigen was negative. In this setting, a bronchoscopy with bronchoalveolar lavage was recommended. Concurrently, due to the expected low likelihood of dual infection with Cryptococcus and Aspergillus, empiric treatment of immune reconstitution syndrome was considered but held until invasive fungal infection was definitively ruled out. Oral fluconazole was switched to oral voriconazole to provide additional coverage. Upon initiation of oral voriconazole, the patient defervesced and remained afebrile for the remainder of her nine-day hospital stay. Repeat chest CT at three months (Figure 2) and six months (Figure 3) from hospitalization shows significant interval improvement of both infiltrate and effusion and outpatient Cryptococcus serum antigen titers showed a continual decrease from discharge (Figure 4). The patient was continued on oral voriconazole treatment for the duration of a year and tolerated the treatment well.\nOUTPUT:" }, { "from": "agent", "value": "Pulmonary Aspergillosis, Pulmonary Cryptococcus Neoformans" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: We present a case of a 69-year-old female with a past medical history of multiple myeloma followed by autologous peripheral stem cell transplant who was hospitalized after presenting with worsening dyspnea. Subsequent studies revealed no central nervous system (CNS) involvement, and flucytosine was discontinued. She was discharged from the hospital to complete two weeks of intravenous liposomal amphotericin B and a year of oral fluconazole. She was readmitted after two weeks due to constitutional symptoms of fever, loss of appetite, and fatigue in addition to dry cough. Cryptococcus serum titers were 1 : 640 during this time as compared to 1 : 2560 at diagnosis. Bacterial and fungal cultures taken from peripheral and central access sites revealed no growth and Aspergillus serum antigen was negative. In this setting, a bronchoscopy with bronchoalveolar lavage was recommended. Concurrently, due to the expected low likelihood of dual infection with Cryptococcus and Aspergillus, empiric treatment of immune reconstitution syndrome was considered but held until invasive fungal infection was definitively ruled out. Oral fluconazole was switched to oral voriconazole to provide additional coverage. Upon initiation of oral voriconazole, the patient defervesced and remained afebrile for the remainder of her nine-day hospital stay. Repeat chest CT at three months (Figure 2) and six months (Figure 3) from hospitalization shows significant interval improvement of both infiltrate and effusion and outpatient Cryptococcus serum antigen titers showed a continual decrease from discharge (Figure 4). The patient was continued on oral voriconazole treatment for the duration of a year and tolerated the treatment well. OUTPUT:
Multicare_common6292
[ { "from": "human", "value": "As a physician engaged 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 female presented with a constant, throbbing and worsening headache over the past three days. The headache was generalized in nature, associated vomiting, photophobia, dizziness and diplopia. There was no history convulsion, limb weakness or parasthesia. She denied any history of trauma, fever or any loss of consciousness. She was on Zidovudine, Lamivudine and Nevirapine treatment, and her last CD4 count was 293 cell/microl two months ago. She did not smoke cigarettes and had never used contraceptive pills. There was no family history of strokes, sudden deaths or clotting disorders. On examination, the patient was teary, in obvious discomfort, afebrile and with normal vital signs. Her Glasgow coma scale was GCS 15/15 with normal pupils and extra-ocular muscle movement. There were signs of meningism without any neurological deficits. Examinations of other systems were unremarkable and she had normal baseline blood tests. Lumbar puncture had an opening pressure of 23 cm H2O with a closing pressure of 10 cmH2O and normal laboratory cerebrospinal fluid results. The patient was admitted for observation in the ward and discharged three days later when her CSF culture results were negative. Two days after discharge, she was readmitted with worsening headache, photophobia and diplopia. On examination she had normal vital signs, neck stiffness and bilateral lateral rectus muscle weakness. A repeat lumbar puncture showed opening and closing pressures of 30cm and 15cm of H2O respectively. The headache improved after lumbar puncture, and her cerebrospinal fluid microscopy and culture results were once more negative. A non-contrast computed tomography showed ill-defined sulci and hyper-density along the sagittal, right transverse and sigmoid sinuses. There were no obvious haemorrhages, infarcts or mass effect noted. The patient was started on low molecular weight heparin and subsequently continued on oral warfarin. Few days later, she had five episodes of generalised seizures without any residual neurological deficits. Fundoscopy revealed papilloedema that subsequently improved with intravenous Manitol. Similarly, her seizures were controlled by phenytoin and she was discharged about three weeks later without any neurologic deficit.\nOUTPUT:" }, { "from": "agent", "value": "Cerebral venous sinus thrombosis, HIV disease" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 44-year old female presented with a constant, throbbing and worsening headache over the past three days. The headache was generalized in nature, associated vomiting, photophobia, dizziness and diplopia. There was no history convulsion, limb weakness or parasthesia. She denied any history of trauma, fever or any loss of consciousness. She was on Zidovudine, Lamivudine and Nevirapine treatment, and her last CD4 count was 293 cell/microl two months ago. She did not smoke cigarettes and had never used contraceptive pills. There was no family history of strokes, sudden deaths or clotting disorders. On examination, the patient was teary, in obvious discomfort, afebrile and with normal vital signs. Her Glasgow coma scale was GCS 15/15 with normal pupils and extra-ocular muscle movement. There were signs of meningism without any neurological deficits. Examinations of other systems were unremarkable and she had normal baseline blood tests. Lumbar puncture had an opening pressure of 23 cm H2O with a closing pressure of 10 cmH2O and normal laboratory cerebrospinal fluid results. The patient was admitted for observation in the ward and discharged three days later when her CSF culture results were negative. Two days after discharge, she was readmitted with worsening headache, photophobia and diplopia. On examination she had normal vital signs, neck stiffness and bilateral lateral rectus muscle weakness. A repeat lumbar puncture showed opening and closing pressures of 30cm and 15cm of H2O respectively. The headache improved after lumbar puncture, and her cerebrospinal fluid microscopy and culture results were once more negative. A non-contrast computed tomography showed ill-defined sulci and hyper-density along the sagittal, right transverse and sigmoid sinuses. There were no obvious haemorrhages, infarcts or mass effect noted. The patient was started on low molecular weight heparin and subsequently continued on oral warfarin. Few days later, she had five episodes of generalised seizures without any residual neurological deficits. Fundoscopy revealed papilloedema that subsequently improved with intravenous Manitol. Similarly, her seizures were controlled by phenytoin and she was discharged about three weeks later without any neurologic deficit. OUTPUT:
Multicare_common9762
[ { "from": "human", "value": "As a physician engaged 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 23-year-old male patient came to the Emergency Department of Ariana Medical Complex, a private hospital in Kabul, Afghanistan, with dry cough, fever, muscle pain and diffuse palpable purpura on the skin of his left leg and lower part of abdomen (Figure 1). The patient had started feeling unwell 15 days before, followed by fatigue, muscle pain, mild fever, dry cough and skin rash over the last five days. On the last day, the symptoms were accompanied by dry cough and difficulty breathing, which caused him to be referred to the hospital. On physical examination, the patient had high fever (38.4 C), low oxygen saturation (SpO2=77%), and dyspnea with wet rales in both lungs. Other systems were normal. He had no history of medication and underlying comorbidities. Warm O2-therapy started immediately in the emergency ward. Real-Time Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) advised to confirm the initial diagnosis. Bilateral ground glass opacities were noted on Chest Computed Tomography (CT) (Figure 2). The patient was admitted to the isolation ward. Dexamethasone 6 Milli grams (mg) once daily for 10 days with invasive mechanical ventilation was considered standard general management. Prophylactic anticoagulation was implemented to maintain the prothrombotic state and prevent cloth formation. Infusion of Paracetamol 1.5 grams daily used to control fever and empirical usage of antibiotics, ie 625 mg Co-Amoxiclav and Clavulanate twice a day for 10 days, was advised to prevent secondary bacterial infection. Meanwhile, chest physiotherapy and nutritional support were also considered to accelerate the course of improvement. During the treatment, the patient's symptoms, including skin rash and lung problems, were improved, and he was discharged on day 19th of admission. Five days later, the patient was re-examined for follow-up investigation. Chest CT scan showed improvement of the lung lesions (Figure 3).\nOUTPUT:" }, { "from": "agent", "value": "COVID-19" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 23-year-old male patient came to the Emergency Department of Ariana Medical Complex, a private hospital in Kabul, Afghanistan, with dry cough, fever, muscle pain and diffuse palpable purpura on the skin of his left leg and lower part of abdomen (Figure 1). The patient had started feeling unwell 15 days before, followed by fatigue, muscle pain, mild fever, dry cough and skin rash over the last five days. On the last day, the symptoms were accompanied by dry cough and difficulty breathing, which caused him to be referred to the hospital. On physical examination, the patient had high fever (38.4 C), low oxygen saturation (SpO2=77%), and dyspnea with wet rales in both lungs. Other systems were normal. He had no history of medication and underlying comorbidities. Warm O2-therapy started immediately in the emergency ward. Real-Time Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) advised to confirm the initial diagnosis. Bilateral ground glass opacities were noted on Chest Computed Tomography (CT) (Figure 2). The patient was admitted to the isolation ward. Dexamethasone 6 Milli grams (mg) once daily for 10 days with invasive mechanical ventilation was considered standard general management. Prophylactic anticoagulation was implemented to maintain the prothrombotic state and prevent cloth formation. Infusion of Paracetamol 1.5 grams daily used to control fever and empirical usage of antibiotics, ie 625 mg Co-Amoxiclav and Clavulanate twice a day for 10 days, was advised to prevent secondary bacterial infection. Meanwhile, chest physiotherapy and nutritional support were also considered to accelerate the course of improvement. During the treatment, the patient's symptoms, including skin rash and lung problems, were improved, and he was discharged on day 19th of admission. Five days later, the patient was re-examined for follow-up investigation. Chest CT scan showed improvement of the lung lesions (Figure 3). OUTPUT:
Multicare_common7802
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: HPeV is subdivided into 16 different genotypes. The prototypes of HPeVs, including HPeV-1 and HPeV-2, were originally classified as echo-22 and echo-23, in enterovirus but were regrouped as a separate genus according to their genome organization and biological properties. Among these HPeV genotypes, some were associated with certain specific diseases. Recombination analysis was also performed based on these genomes and one putative recombinant was found.\nOUTPUT:" }, { "from": "agent", "value": "Diarrhea, Gastroenteritis, Sepsis syndromes, Aseptic meningitis/Meningoencephalitis, Lymphadenitis, Neonatal sepsis, Reye syndrome, Non-polio acute flaccid paralysis, Enteritis, Paralysis, Fever" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: HPeV is subdivided into 16 different genotypes. The prototypes of HPeVs, including HPeV-1 and HPeV-2, were originally classified as echo-22 and echo-23, in enterovirus but were regrouped as a separate genus according to their genome organization and biological properties. Among these HPeV genotypes, some were associated with certain specific diseases. Recombination analysis was also performed based on these genomes and one putative recombinant was found. OUTPUT:
Multicare_common3054
[ { "from": "human", "value": "As a physician engaged 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 condition preceded by gastrointestinal manifestations in 7 of them with vomiting, diarrhea with high grade fever. The other 4 had fever with cough preceding the weakness. All of them received IVIG with good response. The collected data was reviewed for completeness and logical consistency. Pre-coded data will be entered on the computer using Microsoft Office Excel software program for Windows 2019.Data was transferred to the Statistical Package for the Social Sciences (SPSS version 26) (IBM Corp., Armonk, NY, USA) to be statistically analyzed. Quantitative variables were described as mean, standard deviation, median, IQR. They were compared using Mann-Whitney U test, where p-value is significant if less than 0.05.Qualitative variables were described as frequency and percentage. They were compared using Chi-square test or Fisher's exact test accordingly where p-value is significant if less than 0.05. Exact test was used instead when the expected frequency is less than 5\nThe datasets generated and/or analyzed during the current study are not publicly available due to the current Cairo University regulations and Egyptian legislation but are available from the corresponding author on reasonable request and after institutional approval. An informed written consent was taken from each patient. All data obtained from every patient were confidential and were not used outside the study. The patients have rights to withdraw from the study at any time without giving any reason. All the cost of the investigations was afforded by the researcher. Our study was approved by ethical committee of the Department of Neurology, Faculty of Medicine, Cairo University on 12/7/2021. Not applicable.\nOUTPUT:" }, { "from": "agent", "value": "COVID and post COVID polyneuropathies, acute inflammatory demyelinating polyneuropathy (AIDP)" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The condition preceded by gastrointestinal manifestations in 7 of them with vomiting, diarrhea with high grade fever. The other 4 had fever with cough preceding the weakness. All of them received IVIG with good response. The collected data was reviewed for completeness and logical consistency. Pre-coded data will be entered on the computer using Microsoft Office Excel software program for Windows 2019.Data was transferred to the Statistical Package for the Social Sciences (SPSS version 26) (IBM Corp., Armonk, NY, USA) to be statistically analyzed. Quantitative variables were described as mean, standard deviation, median, IQR. They were compared using Mann-Whitney U test, where p-value is significant if less than 0.05.Qualitative variables were described as frequency and percentage. They were compared using Chi-square test or Fisher's exact test accordingly where p-value is significant if less than 0.05. Exact test was used instead when the expected frequency is less than 5 The datasets generated and/or analyzed during the current study are not publicly available due to the current Cairo University regulations and Egyptian legislation but are available from the corresponding author on reasonable request and after institutional approval. An informed written consent was taken from each patient. All data obtained from every patient were confidential and were not used outside the study. The patients have rights to withdraw from the study at any time without giving any reason. All the cost of the investigations was afforded by the researcher. Our study was approved by ethical committee of the Department of Neurology, Faculty of Medicine, Cairo University on 12/7/2021. Not applicable. OUTPUT:
Multicare_common2428
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Our patient is a 26-year-old male who presented with a left tentorial SDH following blunt trauma to the head. The patient was brought to our Emergency department alert and oriented to person, place, and date and had no focal neurologic deficits. Noncontrast computed tomography (CT) imaging of the head revealed a 4 mm left tentorial SDH and 2 mm of pneumocephalus [Figure 1]. The patient was discharged on postadmission day 2 following an uncomplicated hospital course. At the time of discharge patient did not exhibit any lower extremity symptoms. The patient returned on postinjury day 8 for follow up and discontinuation of his antiseizure prophylaxis. The patient noted that he was experiencing progressively worsening lower back pain that radiated into both lower extremities and had started one day after discharge. He also reported occasional ataxia and dizziness. He denied any changes in bowel or bladder function. The patient had 5/5 strength on confrontational motor testing in all lower extremity muscle groups. Imaging of the cervical and thoracic spine revealed no abnormal enhancement and showed normal alignment. No cord deformity, compression, or edema was seen. There was a signal difference in the fluid of the thecal sac and moderate facet hypertrophy was observed at L4-L5 and L5-S1 [Figure 2]. Follow up MR angiography was negative for vascular malformations or spinal dural arteriovenous (AV) fistulas. Given that the patient had no focal neurologic deficits, the decision was made to manage the patient conservatively.\nOUTPUT:" }, { "from": "agent", "value": "Traumatic intracranial subdural hematoma, Lumbar radiculopathy" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Our patient is a 26-year-old male who presented with a left tentorial SDH following blunt trauma to the head. The patient was brought to our Emergency department alert and oriented to person, place, and date and had no focal neurologic deficits. Noncontrast computed tomography (CT) imaging of the head revealed a 4 mm left tentorial SDH and 2 mm of pneumocephalus [Figure 1]. The patient was discharged on postadmission day 2 following an uncomplicated hospital course. At the time of discharge patient did not exhibit any lower extremity symptoms. The patient returned on postinjury day 8 for follow up and discontinuation of his antiseizure prophylaxis. The patient noted that he was experiencing progressively worsening lower back pain that radiated into both lower extremities and had started one day after discharge. He also reported occasional ataxia and dizziness. He denied any changes in bowel or bladder function. The patient had 5/5 strength on confrontational motor testing in all lower extremity muscle groups. Imaging of the cervical and thoracic spine revealed no abnormal enhancement and showed normal alignment. No cord deformity, compression, or edema was seen. There was a signal difference in the fluid of the thecal sac and moderate facet hypertrophy was observed at L4-L5 and L5-S1 [Figure 2]. Follow up MR angiography was negative for vascular malformations or spinal dural arteriovenous (AV) fistulas. Given that the patient had no focal neurologic deficits, the decision was made to manage the patient conservatively. OUTPUT:
Multicare_common9843
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 6-month-old male infant was admitted in our clinic for fever (38.3 Celsius), rhinorrhea and diarrhea. The onset of the symptoms was ~24 h before admission. We must mention that both parents presented respiratory symptoms. The patient's history revealed that he was obtained by in vitro fertilization, fully vaccinated according to the national recommendations, with appropriate development for his age, and no pathologies up to this age. The clinical exam revealed influenced general status, serous rhinorrhea, pharyngeal erythema and diarrhea (~5 stools/day). The patient weighed 7,700 g.\nThe laboratory tests performed on the day of admission pointed out microcytic anemia (hemoglobin 10.7 g/dL, medium erythrocyte volume 75.9 fL), low erythrocyte count (3.99 x 106/muL), neutropenia (1,070/muL), a normal count of leukocytes (8,250/muL) and lymphocytes (2,540/muL), and a C-reactive protein (CRP) of 2.2 mg/L. The tests for other viral infections (Influenza A and B, Syncytial virus) were negative. Taking into account the epidemiological context, nasopharyngeal/oropharyngeal swab-based polymerase chain reaction tests for SARS-CoV-2 infection were performed for the infant and his parents. The test was positive for both parents, but in the infant the result was inconclusive. Thus, we repeated the test and the second test confirmed the infection in our patient too. No signs of pediatric multisystem inflammatory syndrome (PIMS-TS) or organ failure were identified during the clinical course of this case. After the admission we initiated symptomatic treatment with antipyretics in case of fever and anti-diarrheic drugs (diosmectite and racecadotril). The fever persisted only for 1 day as well as diarrhea. Thus, when the second test for SARS-CoV-2 infection came back positive, the infant was asymptomatic, and the chest radiography revealed no pathological findings. After ~4 days of hospitalization in our clinic, the patient was transferred to the infectious diseases clinic taking into account that his mother was admitted there, but he was asymptomatic and his clinical course was outstandingly favorable. No sequelae or unanticipated events as a part of the patient's follow-up.\nOUTPUT:" }, { "from": "agent", "value": "COVID-19" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 6-month-old male infant was admitted in our clinic for fever (38.3 Celsius), rhinorrhea and diarrhea. The onset of the symptoms was ~24 h before admission. We must mention that both parents presented respiratory symptoms. The patient's history revealed that he was obtained by in vitro fertilization, fully vaccinated according to the national recommendations, with appropriate development for his age, and no pathologies up to this age. The clinical exam revealed influenced general status, serous rhinorrhea, pharyngeal erythema and diarrhea (~5 stools/day). The patient weighed 7,700 g. The laboratory tests performed on the day of admission pointed out microcytic anemia (hemoglobin 10.7 g/dL, medium erythrocyte volume 75.9 fL), low erythrocyte count (3.99 x 106/muL), neutropenia (1,070/muL), a normal count of leukocytes (8,250/muL) and lymphocytes (2,540/muL), and a C-reactive protein (CRP) of 2.2 mg/L. The tests for other viral infections (Influenza A and B, Syncytial virus) were negative. Taking into account the epidemiological context, nasopharyngeal/oropharyngeal swab-based polymerase chain reaction tests for SARS-CoV-2 infection were performed for the infant and his parents. The test was positive for both parents, but in the infant the result was inconclusive. Thus, we repeated the test and the second test confirmed the infection in our patient too. No signs of pediatric multisystem inflammatory syndrome (PIMS-TS) or organ failure were identified during the clinical course of this case. After the admission we initiated symptomatic treatment with antipyretics in case of fever and anti-diarrheic drugs (diosmectite and racecadotril). The fever persisted only for 1 day as well as diarrhea. Thus, when the second test for SARS-CoV-2 infection came back positive, the infant was asymptomatic, and the chest radiography revealed no pathological findings. After ~4 days of hospitalization in our clinic, the patient was transferred to the infectious diseases clinic taking into account that his mother was admitted there, but he was asymptomatic and his clinical course was outstandingly favorable. No sequelae or unanticipated events as a part of the patient's follow-up. OUTPUT:
Multicare_common2823
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 40-year-old woman presented to the emergency department with fever, cough, diarrhea and vomiting 4 days prior to the admission. The patient did not have a significant past medical history. Her children also had sore throat and fever 2 days before the onset of her symptoms. On examination, her temperature was 39.6 C, blood pressure was 90/60 mmHg, pulse rate was 116 beats/min, respiratory rate was 30 breaths/min, and oxygen saturation was 95% (40% fraction of inspired oxygen, 9 L/min). A chest X-ray and computed tomography revealed infiltration with air bronchogram in the right lower lobe and bilateral pleural effusions. When the blood and sputum cultures grew S. pyogenes, this regimen was simplified to penicillin G (3 million units every 4 h) and clindamycin (600 mg every 8 h). Since renal function was exacerbated and pleural effusion increased, she also required hemodialysis and chest tube placement. Her condition was subsequently complicated by a drug-induced fever, skin eruption, and pneumonia. Therefore, the combination changed just to CTRX (2 g every 24 h) on day 14 and then to LVFX (500 mg every 24 h) on day 20. The patient completed a course for 24 days and was then discharged.\nOUTPUT:" }, { "from": "agent", "value": "Mucoid Streptococcus pyogenes pneumonia, Septic shock, Toxic shock syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 40-year-old woman presented to the emergency department with fever, cough, diarrhea and vomiting 4 days prior to the admission. The patient did not have a significant past medical history. Her children also had sore throat and fever 2 days before the onset of her symptoms. On examination, her temperature was 39.6 C, blood pressure was 90/60 mmHg, pulse rate was 116 beats/min, respiratory rate was 30 breaths/min, and oxygen saturation was 95% (40% fraction of inspired oxygen, 9 L/min). A chest X-ray and computed tomography revealed infiltration with air bronchogram in the right lower lobe and bilateral pleural effusions. When the blood and sputum cultures grew S. pyogenes, this regimen was simplified to penicillin G (3 million units every 4 h) and clindamycin (600 mg every 8 h). Since renal function was exacerbated and pleural effusion increased, she also required hemodialysis and chest tube placement. Her condition was subsequently complicated by a drug-induced fever, skin eruption, and pneumonia. Therefore, the combination changed just to CTRX (2 g every 24 h) on day 14 and then to LVFX (500 mg every 24 h) on day 20. The patient completed a course for 24 days and was then discharged. OUTPUT:
Multicare_common6961
[ { "from": "human", "value": "As a physician engaged 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 non-smoking man presented at our outpatient department with painless swelling of the right anterobasal chest wall noticed for 2 months while taking a shower. There was no history of weight loss or trauma. His hemogram and liver function tests were within normal limits. A thorax-abdomen-brain computed tomography (CT) scan revealed homogenous solid tissue (dense mass of 80 mm x 62 mm), in the anterobasal region of the right hemothorax involving the anterior arch of the seventh, eighth, and ninth ribs and their cartilages (Figure 1). The mass had polycyclic contours, projecting into the chest wall touching the liver with no infiltration. The patient underwent right anterolateral thoracotomy at the seventh intercostal space which, confirmed the CT scan findings and revealed infiltration of the serratus muscle and the medial portion of the diaphragm. The tumor was resected with a wide full-thickness chest wall resection of the affected ribs (7th, 8th, 9th, and 10th), diaphragm, and serratus muscle. The resected diaphragm and chest wall were reconstructed using two separate biological patches of a porcine dermal collagen implant (Permacol Surgical Implant) (Limura and Giordano,). The resected specimen was 130 mm x 120 mm x 60 mm (with a mass of 90 mm). Postoperative X-ray was unremarkable, and the patient had an uneventful recovery and was discharged 6 days after surgery. Written informed consent was obtained from the patient for the publication of this case report.\nOUTPUT:" }, { "from": "agent", "value": "Extra-Abdominal Desmoid Tumor" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 68-year-old non-smoking man presented at our outpatient department with painless swelling of the right anterobasal chest wall noticed for 2 months while taking a shower. There was no history of weight loss or trauma. His hemogram and liver function tests were within normal limits. A thorax-abdomen-brain computed tomography (CT) scan revealed homogenous solid tissue (dense mass of 80 mm x 62 mm), in the anterobasal region of the right hemothorax involving the anterior arch of the seventh, eighth, and ninth ribs and their cartilages (Figure 1). The mass had polycyclic contours, projecting into the chest wall touching the liver with no infiltration. The patient underwent right anterolateral thoracotomy at the seventh intercostal space which, confirmed the CT scan findings and revealed infiltration of the serratus muscle and the medial portion of the diaphragm. The tumor was resected with a wide full-thickness chest wall resection of the affected ribs (7th, 8th, 9th, and 10th), diaphragm, and serratus muscle. The resected diaphragm and chest wall were reconstructed using two separate biological patches of a porcine dermal collagen implant (Permacol Surgical Implant) (Limura and Giordano,). The resected specimen was 130 mm x 120 mm x 60 mm (with a mass of 90 mm). Postoperative X-ray was unremarkable, and the patient had an uneventful recovery and was discharged 6 days after surgery. Written informed consent was obtained from the patient for the publication of this case report. OUTPUT:
Multicare_common13
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 57-year-old man had noticed a right chest wall mass lesion for 15 years, but had ignored the lesion in the 5 years before presentation. He was admitted to our hospital without significant symptoms and with no history of tuberculosis. Magnetic resonance imaging (MRI) was performed, and a 5-cm-diameter lesion was found. The signal was isointense on T1-weighted imaging (T1WI) and hyperintense on T2-weighted imaging (T2WI) (Fig. 1). Needle biopsy was performed, and histopathology showed lymphocyte infiltration with no evidence of malignancy. The patient was followed up for the next 7 years, and during that interval he had no significant symptoms. On MRI after 7 years of follow-up, the primary chest wall mass lesion was without any significant change, but a small subcutaneous mass lesion was found nearby. The MRI signal of this subcutaneous mass was almost identical with the original mass (Fig. 2). Diffusion-weighted imaging (DWI) was performed and both lesions exhibited high signal on DWI and a low apparent diffusion coefficient (ADC) (about 0.5) on the ADC map (Fig. 3). In light of the MRI findings, hypercellular malignant tumors (including melanoma and lymphoma), atheroma, and nodular fasciitis were suspected. Excisional biopsy was not performed since that would make definitive re-excision more extensive due to the contamination of surrounding tissue planes. Therefore an open biopsy of both lesions was performed. 4). In this case, no other tumors were found, so radiation therapy only (36 Gy/20 French) was given. The patient was discharged, and follow-up found the patient in good condition with no apparent signs of recurrence after 2 years.\nOUTPUT:" }, { "from": "agent", "value": "Primary marginal zone B-cell lymphoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 57-year-old man had noticed a right chest wall mass lesion for 15 years, but had ignored the lesion in the 5 years before presentation. He was admitted to our hospital without significant symptoms and with no history of tuberculosis. Magnetic resonance imaging (MRI) was performed, and a 5-cm-diameter lesion was found. The signal was isointense on T1-weighted imaging (T1WI) and hyperintense on T2-weighted imaging (T2WI) (Fig. 1). Needle biopsy was performed, and histopathology showed lymphocyte infiltration with no evidence of malignancy. The patient was followed up for the next 7 years, and during that interval he had no significant symptoms. On MRI after 7 years of follow-up, the primary chest wall mass lesion was without any significant change, but a small subcutaneous mass lesion was found nearby. The MRI signal of this subcutaneous mass was almost identical with the original mass (Fig. 2). Diffusion-weighted imaging (DWI) was performed and both lesions exhibited high signal on DWI and a low apparent diffusion coefficient (ADC) (about 0.5) on the ADC map (Fig. 3). In light of the MRI findings, hypercellular malignant tumors (including melanoma and lymphoma), atheroma, and nodular fasciitis were suspected. Excisional biopsy was not performed since that would make definitive re-excision more extensive due to the contamination of surrounding tissue planes. Therefore an open biopsy of both lesions was performed. 4). In this case, no other tumors were found, so radiation therapy only (36 Gy/20 French) was given. The patient was discharged, and follow-up found the patient in good condition with no apparent signs of recurrence after 2 years. OUTPUT:
Multicare_common7523
[ { "from": "human", "value": "As a physician engaged 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 man in his 40s presented with persistent periorbital swelling for 7 months. The swelling first appeared 2 days after stripping floors during his work. He denied any associated pruritus, oral symptoms, facial pain, dyspnea, fever, weight changes, myalgias, arthralgias, weakness, or fatigue. He also denied coming into contact with any new products on his face or any new medications. He had a history of asthma but no history of allergies or photosensitivity. He also had eczema, hypertension, and depression well controlled with triamcinolone cream, amlodipine, and doxepin, respectively. He used ibuprofen about 4 times a week for tension headaches for several years without any adverse reactions, but he stopped using it within days of noticing the periorbital swelling. However, the swelling did not improve. A few months after, at an outside hospital, he was given a diagnosis of sinusitis and treated with amoxicillin/clavulanate and systemic steroids. Symptoms initially improved but relapsed when prednisone was tapered to less than 20 mg.\nAfter 7 months of having the above symptoms and lack of improvement of the swelling, he presented to our service. Review of systems yielded normal results other than the indicated above. Physical examination found edema and erythema of the right lower and upper eyelids and on the left upper eyelid (Fig 1). The following laboratory investigations were within normal limits: complete blood count, complete metabolic profile, C-reactive protein, creatine kinase, IgE levels, C4, C1-INH, C1q, and total hemolytic complement. Results for antinuclear antibody (ANA), anti-Sjogren's syndrome-related antigen A and antigen B, antineutrophil cytoplasmic antibody, antimicrosomal antibody, antihistone antibody, aldolase, anti-Jo1, and anti-Mi2 antibody were normal. Anti-dsDNA level was quantified at 45 IU/mL (nl < 4 IU/mL), and anti-Smith level was 1 AI (nl < 1 AI). Angiotensin-converting enzyme levels, chest radiograph, and urinalysis were normal. A maxillofacial computed tomography scan found soft tissue swelling in the right lacrimal fossa with no focal abscess. Biopsy results of the right lower eyelid are shown in Fig 2.\nOUTPUT:" }, { "from": "agent", "value": "Cutaneous lupus erythematosus" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A man in his 40s presented with persistent periorbital swelling for 7 months. The swelling first appeared 2 days after stripping floors during his work. He denied any associated pruritus, oral symptoms, facial pain, dyspnea, fever, weight changes, myalgias, arthralgias, weakness, or fatigue. He also denied coming into contact with any new products on his face or any new medications. He had a history of asthma but no history of allergies or photosensitivity. He also had eczema, hypertension, and depression well controlled with triamcinolone cream, amlodipine, and doxepin, respectively. He used ibuprofen about 4 times a week for tension headaches for several years without any adverse reactions, but he stopped using it within days of noticing the periorbital swelling. However, the swelling did not improve. A few months after, at an outside hospital, he was given a diagnosis of sinusitis and treated with amoxicillin/clavulanate and systemic steroids. Symptoms initially improved but relapsed when prednisone was tapered to less than 20 mg. After 7 months of having the above symptoms and lack of improvement of the swelling, he presented to our service. Review of systems yielded normal results other than the indicated above. Physical examination found edema and erythema of the right lower and upper eyelids and on the left upper eyelid (Fig 1). The following laboratory investigations were within normal limits: complete blood count, complete metabolic profile, C-reactive protein, creatine kinase, IgE levels, C4, C1-INH, C1q, and total hemolytic complement. Results for antinuclear antibody (ANA), anti-Sjogren's syndrome-related antigen A and antigen B, antineutrophil cytoplasmic antibody, antimicrosomal antibody, antihistone antibody, aldolase, anti-Jo1, and anti-Mi2 antibody were normal. Anti-dsDNA level was quantified at 45 IU/mL (nl < 4 IU/mL), and anti-Smith level was 1 AI (nl < 1 AI). Angiotensin-converting enzyme levels, chest radiograph, and urinalysis were normal. A maxillofacial computed tomography scan found soft tissue swelling in the right lacrimal fossa with no focal abscess. Biopsy results of the right lower eyelid are shown in Fig 2. OUTPUT:
Multicare_common201
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Histopathology of the resected tissue showed extensive ulceration of the jejunum and the ascending colon, chronic crypt architectural distortion, and crypt abscesses. Two months later, he re-presented with abdominal pain and was found to have narrowing at the anastomotic site on coloscopy. The biopsy of the anastomotic site revealed severe inflammation and ulceration and therefore started on steroids and azathioprine. Azathioprine was later substituted with methotrexate due to gastrointestinal intolerance and leucopenia. In October 2020, he was admitted to our department with a one-month history of fever, fatigue, and productive cough with yellowish sputum. He was febrile with a temperature of 39 C, and a chest examination revealed bilateral coarse crackles over mid-lower lung zones. He had no pets and no known contact with birds. His laboratory investigations are summarized in (Table 1). A Chest x-ray showed a right-sided ill-defined nodular infiltrate (Fig. 1A). He was initially treated as a community-acquired chest infection with ceftriaxone and azithromycin. A computerized tomography (CT) chest was requested as there was an inadequate clinical response to treatment. The CT scan revealed scattered nodules and patchy ground-glass opacities in the right lower lobe (Fig. 1B,C,D). Subsequently, bronchoscopy with transbronchial biopsies from the right lower zone was performed. Bronchoalveolar lavage showed 55% lymphocytes and a positive culture for cryptococcus neoformans. Histopathology was noticeable for non-necrotizing granulomatous inflammation, and Grocott stain identified rounded organisms with a thick capsule consistent with cryptococcus neoformans (Fig. 2). Based on the absence of neurological symptoms, lumbar puncture was not carried out. He was started on a 6- month course of daily oral fluconazole. At one month's follow-up, he reported total resolution of his symptoms with a chest X-ray showing mild regression of the right-sided infiltrates.\nOUTPUT:" }, { "from": "agent", "value": "Isolated pulmonary cryptococcosis, Crohn's disease" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Histopathology of the resected tissue showed extensive ulceration of the jejunum and the ascending colon, chronic crypt architectural distortion, and crypt abscesses. Two months later, he re-presented with abdominal pain and was found to have narrowing at the anastomotic site on coloscopy. The biopsy of the anastomotic site revealed severe inflammation and ulceration and therefore started on steroids and azathioprine. Azathioprine was later substituted with methotrexate due to gastrointestinal intolerance and leucopenia. In October 2020, he was admitted to our department with a one-month history of fever, fatigue, and productive cough with yellowish sputum. He was febrile with a temperature of 39 C, and a chest examination revealed bilateral coarse crackles over mid-lower lung zones. He had no pets and no known contact with birds. His laboratory investigations are summarized in (Table 1). A Chest x-ray showed a right-sided ill-defined nodular infiltrate (Fig. 1A). He was initially treated as a community-acquired chest infection with ceftriaxone and azithromycin. A computerized tomography (CT) chest was requested as there was an inadequate clinical response to treatment. The CT scan revealed scattered nodules and patchy ground-glass opacities in the right lower lobe (Fig. 1B,C,D). Subsequently, bronchoscopy with transbronchial biopsies from the right lower zone was performed. Bronchoalveolar lavage showed 55% lymphocytes and a positive culture for cryptococcus neoformans. Histopathology was noticeable for non-necrotizing granulomatous inflammation, and Grocott stain identified rounded organisms with a thick capsule consistent with cryptococcus neoformans (Fig. 2). Based on the absence of neurological symptoms, lumbar puncture was not carried out. He was started on a 6- month course of daily oral fluconazole. At one month's follow-up, he reported total resolution of his symptoms with a chest X-ray showing mild regression of the right-sided infiltrates. OUTPUT:
Multicare_common3102
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 21-year-old woman pregnant with twins at 29 weeks of gestation was admitted to the previous hospital for preterm labor. After one week of tocolysis with intravenous ritodrine, she developed acute dyspnea and was referred to our hospital. On admission, she also presented with hypertension (152/112 mmHg) and proteinuria (3.8 g/day). After starting magnesium sulfate, her systolic blood pressure did not exceed 140 mmHg, and no further antihypertensive agent was necessary. On day 3 of admission, her SpO2 fell to 95% with 5 liters of supplemental oxygen, and NPPV was initiated. After implementation of NPPV, her subjective dyspnea improved, and her SpO2 rose to 99% on room air. However, her serum creatinine level was increased to 1.0 mg/dl at 33 weeks of gestation, indicating reduced kidney function. Other symptoms, such as increase in liver enzymes, platelet reduction, and gastrointestinal or neurological symptoms, were not detected. Fetal conditions in utero were favorable. She underwent a cesarean section at 33 weeks and 1 day of gestation due to initiation of labor. The patient delivered healthy male twin infants weighing 1496 g and 1876 g. NPPV was continued intermittently after delivery until she was successfully weaned off of it.\nOUTPUT:" }, { "from": "agent", "value": "Severe preeclampsia, Pulmonary edema" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 21-year-old woman pregnant with twins at 29 weeks of gestation was admitted to the previous hospital for preterm labor. After one week of tocolysis with intravenous ritodrine, she developed acute dyspnea and was referred to our hospital. On admission, she also presented with hypertension (152/112 mmHg) and proteinuria (3.8 g/day). After starting magnesium sulfate, her systolic blood pressure did not exceed 140 mmHg, and no further antihypertensive agent was necessary. On day 3 of admission, her SpO2 fell to 95% with 5 liters of supplemental oxygen, and NPPV was initiated. After implementation of NPPV, her subjective dyspnea improved, and her SpO2 rose to 99% on room air. However, her serum creatinine level was increased to 1.0 mg/dl at 33 weeks of gestation, indicating reduced kidney function. Other symptoms, such as increase in liver enzymes, platelet reduction, and gastrointestinal or neurological symptoms, were not detected. Fetal conditions in utero were favorable. She underwent a cesarean section at 33 weeks and 1 day of gestation due to initiation of labor. The patient delivered healthy male twin infants weighing 1496 g and 1876 g. NPPV was continued intermittently after delivery until she was successfully weaned off of it. OUTPUT:
Multicare_common9662
[ { "from": "human", "value": "As a physician engaged 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 right-handed former high school mathematics teacher was referred for evaluation of PD. He was being treated with long-acting ropinirole 8 mg/day and was obviously undertreated with significant bradykinesia, rest tremor, and rigidity, all of which were more marked on the right than the left. Carbidopa/levo-dopa 25/100 1 tablet b.i.d was started. Over the next 6 months this was increased to 1.5 tabs b.i.d, and then 2 tablets b.i.d., in addition to an unchanged dose of long-acting ropinirole, with a significant reduction in bradykinesia and improvement in functioning. (He preferred this dosing schedule for convenience.) The patient had previously reported an interest in drawing, but had never pursued this, despite his wife providing materials for him. He had never engaged in any other creative activity, such as creative writing or music. His wife urged him to join her at a regular art class where students copied a work presented by the class instructor. His wife reported a progressive increase over time in the level of detail and similarity to the copied work (Fig. 1). Interestingly, in the 3rd image in the series (row C), the patient painted a mirror image of the model painting. He did not produce art outside the classes, and there were no signs of any compulsive behaviors or other neuropsychiatric complaints. The patient's wife also noted that when he was initially diagnosed with PD he was not able to perform simple arithmetic or solve mathematical word problems. These functions improved as his dopaminergic therapy was increased, also suggesting that he had improved ability with tasks requiring attention, as discussed below. The patient has given his consent for this case report to be published.\nOUTPUT:" }, { "from": "agent", "value": "PD (Parkinson's Disease)" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 68-year old right-handed former high school mathematics teacher was referred for evaluation of PD. He was being treated with long-acting ropinirole 8 mg/day and was obviously undertreated with significant bradykinesia, rest tremor, and rigidity, all of which were more marked on the right than the left. Carbidopa/levo-dopa 25/100 1 tablet b.i.d was started. Over the next 6 months this was increased to 1.5 tabs b.i.d, and then 2 tablets b.i.d., in addition to an unchanged dose of long-acting ropinirole, with a significant reduction in bradykinesia and improvement in functioning. (He preferred this dosing schedule for convenience.) The patient had previously reported an interest in drawing, but had never pursued this, despite his wife providing materials for him. He had never engaged in any other creative activity, such as creative writing or music. His wife urged him to join her at a regular art class where students copied a work presented by the class instructor. His wife reported a progressive increase over time in the level of detail and similarity to the copied work (Fig. 1). Interestingly, in the 3rd image in the series (row C), the patient painted a mirror image of the model painting. He did not produce art outside the classes, and there were no signs of any compulsive behaviors or other neuropsychiatric complaints. The patient's wife also noted that when he was initially diagnosed with PD he was not able to perform simple arithmetic or solve mathematical word problems. These functions improved as his dopaminergic therapy was increased, also suggesting that he had improved ability with tasks requiring attention, as discussed below. The patient has given his consent for this case report to be published. OUTPUT:
Multicare_common5597
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 53-year-old male was referred to our institution complaining of pain during swallowing. Esophagogastroduodenoscopy showed a distorted protruding lesion on the left arytenoid (shown in Fig. 5a), and the biopsy specimen revealed a well-differentiated SCC. 5b). A well-experienced therapeutic radiologist (N.F.) opined that chemoradiotherapy alone would not suffice for such a large-volume protruding cancer. It took approximately 140 min to remove the primary lesion by ELPS combined with ESD with a negative vertical margin during a 19-day hospitalization (shown in Fig. 5c). Pathologic evaluation of the resected specimen confirmed that a well-differentiated SCC invaded subepithelial layer (invasion depth 10,000 mum) with negative vertical resection margins. The lateral margin was difficult to determine because of the effect of burning during resection. However, the final pathology diagnosis was positive because of the presence of tumor at the margins (shown in Fig. 6). Lymphatic and venous invasions were negative which assessed by D2-40 staining and Elastica van Gieson staining, respectively. The mucosal defect was completely covered by normal mucosa 2 months after resection (shown in Fig. 5d). Thirty-nine months after the treatment, the patient was recurrence-free and survived without any additional treatment.\nOUTPUT:" }, { "from": "agent", "value": "Superficial Hypopharyngeal Cancer, Synchronous Lymph Node Metastasis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 53-year-old male was referred to our institution complaining of pain during swallowing. Esophagogastroduodenoscopy showed a distorted protruding lesion on the left arytenoid (shown in Fig. 5a), and the biopsy specimen revealed a well-differentiated SCC. 5b). A well-experienced therapeutic radiologist (N.F.) opined that chemoradiotherapy alone would not suffice for such a large-volume protruding cancer. It took approximately 140 min to remove the primary lesion by ELPS combined with ESD with a negative vertical margin during a 19-day hospitalization (shown in Fig. 5c). Pathologic evaluation of the resected specimen confirmed that a well-differentiated SCC invaded subepithelial layer (invasion depth 10,000 mum) with negative vertical resection margins. The lateral margin was difficult to determine because of the effect of burning during resection. However, the final pathology diagnosis was positive because of the presence of tumor at the margins (shown in Fig. 6). Lymphatic and venous invasions were negative which assessed by D2-40 staining and Elastica van Gieson staining, respectively. The mucosal defect was completely covered by normal mucosa 2 months after resection (shown in Fig. 5d). Thirty-nine months after the treatment, the patient was recurrence-free and survived without any additional treatment. OUTPUT:
Multicare_common2943
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Six patients (1.6% of total patients; mean age, 75 years; range, 61-82 years; 50% males, 50% females) were enrolled in the study. One patient had low blood pressure (SBP <=100 mmHg). Five patients had altered mentation (GCS <15), and one patient complain of abdominal pain. All patients had abdominal distension and tenderness. All patients had a high respiratory rate (>=22 breaths/min). C-reactive protein (CRP) and lactate levels were high (mean, 21.6 mg/L and 2.4 mmol/L, respectively). All patients were diagnosed by the presence of ischemic bowel signs (portal venous gas, pneumatosis intestinalis, and absence of bowel wall enhancement) without occlusion or thrombus of the mesenteric arteries in the CT scan findings (Fig. 1). All patients underwent emergency abdominal operations. Five patients underwent intestinal resection; one patient could not undergo intestinal resection because the extent of necrosis was too great. Pathological findings in the resected intestines showed nonocclusive and segmental enterointestinal damage with ulcer and necrosis on the membrane (Fig. 2). These were characteristic pathological findings. Four patients were discharged with mRS scores >=4, and two patients died during the postoperative period in the hospital. The results are summarized in Table 1.\nOUTPUT:" }, { "from": "agent", "value": "Nonocclusive Mesenteric Ischemia, Stroke, Subarachnoid Hemorrhage, Cerebral Infarction, Intracerebral Hemorrhage" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Six patients (1.6% of total patients; mean age, 75 years; range, 61-82 years; 50% males, 50% females) were enrolled in the study. One patient had low blood pressure (SBP <=100 mmHg). Five patients had altered mentation (GCS <15), and one patient complain of abdominal pain. All patients had abdominal distension and tenderness. All patients had a high respiratory rate (>=22 breaths/min). C-reactive protein (CRP) and lactate levels were high (mean, 21.6 mg/L and 2.4 mmol/L, respectively). All patients were diagnosed by the presence of ischemic bowel signs (portal venous gas, pneumatosis intestinalis, and absence of bowel wall enhancement) without occlusion or thrombus of the mesenteric arteries in the CT scan findings (Fig. 1). All patients underwent emergency abdominal operations. Five patients underwent intestinal resection; one patient could not undergo intestinal resection because the extent of necrosis was too great. Pathological findings in the resected intestines showed nonocclusive and segmental enterointestinal damage with ulcer and necrosis on the membrane (Fig. 2). These were characteristic pathological findings. Four patients were discharged with mRS scores >=4, and two patients died during the postoperative period in the hospital. The results are summarized in Table 1. OUTPUT:
Multicare_common1348
[ { "from": "human", "value": "As a physician engaged 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 did well as an infant and remained healthy throughout childhood. Mother recalls she was social, talkative and engaged. At age 25 yo, her father died unexpectedly, after which she began to regress with a decline in speech, activity level and social interactions. Her family was led to believe this was a typical course for DS. She also developed periods of incontinence, loss of daily living skills like showering, and developed compulsive moving of objects from room to room. Subsequent to lorazepam administration, she seemed more engaged and interactive and started to read again. Despite increasing lorazepam gradually to 15 mg/day, improvement was not sustained. Trials of minocycline, memantine and N-acetyl cysteine did not stimulate improvement. Sertraline caused significant side effects (sleep, dizziness, anorexia) and was discontinued when pharmacogenomic testing revealed reduced CYP2C19 enzyme function, which decreases the rate of clearance of sertraline thereby causing side effects. Lorazepam was continued at 15 mg/day in 3 doses. BC received 17 ECT treatments from 8/8/16 through 10/12/16, resulting in significant improvement. Over the next 6 months, symptoms gradually reoccurred. Treatment was augmented with dextromethorphan/quinidine two tablets/day and a second course of 16 ECT treatments. She responded well and her mother estimated that she was back to 85% of baseline functioning. Dextromethorphan/quinidine 20/10 was continued; remission lasted approximately 8 months. In August 2018 she received a third course of 14 ECT treatments. She continues on monthly maintenance ECT, lorazepam and dextromethorphan/quinidine. She is considered almost at baseline with BFCRS scores of 2 and 3 (1-17-19).\nOUTPUT:" }, { "from": "agent", "value": "Down syndrome, unspecified catatonia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: She did well as an infant and remained healthy throughout childhood. Mother recalls she was social, talkative and engaged. At age 25 yo, her father died unexpectedly, after which she began to regress with a decline in speech, activity level and social interactions. Her family was led to believe this was a typical course for DS. She also developed periods of incontinence, loss of daily living skills like showering, and developed compulsive moving of objects from room to room. Subsequent to lorazepam administration, she seemed more engaged and interactive and started to read again. Despite increasing lorazepam gradually to 15 mg/day, improvement was not sustained. Trials of minocycline, memantine and N-acetyl cysteine did not stimulate improvement. Sertraline caused significant side effects (sleep, dizziness, anorexia) and was discontinued when pharmacogenomic testing revealed reduced CYP2C19 enzyme function, which decreases the rate of clearance of sertraline thereby causing side effects. Lorazepam was continued at 15 mg/day in 3 doses. BC received 17 ECT treatments from 8/8/16 through 10/12/16, resulting in significant improvement. Over the next 6 months, symptoms gradually reoccurred. Treatment was augmented with dextromethorphan/quinidine two tablets/day and a second course of 16 ECT treatments. She responded well and her mother estimated that she was back to 85% of baseline functioning. Dextromethorphan/quinidine 20/10 was continued; remission lasted approximately 8 months. In August 2018 she received a third course of 14 ECT treatments. She continues on monthly maintenance ECT, lorazepam and dextromethorphan/quinidine. She is considered almost at baseline with BFCRS scores of 2 and 3 (1-17-19). OUTPUT:
Multicare_common7913
[ { "from": "human", "value": "As a physician engaged 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 eight-month-old male child presented with fever, diarrhoea, and difficulty in breathing was admitted to the paediatric ward of the Amirou Boubacar Diallo national hospital (HNABD) of Niamey. The mother of the child had fever and shortness of breath approximately four weeks prior to admission and subsequently died. Upon clinical examination, the child was lethargic with dehydration but without shock or cyanosis, and he weighed 5 kg and was 78 cm in height. He had tachypnoea with a respiratory rate of 56 cycles/min, tachycardia at 148 heartbeats per minute, and temperature of 38.5 C. Oxygen saturation, measured with a pulse oximeter (SpO2), was 90% in ambient air. The pulmonary examination revealed moderate respiratory distress with chest indrawing. Auscultation showed bronchial rales in the right pulmonary system, and the abdomen was flexible with moderate hepatomegaly. Virological analysis was conducted using real-time reverse transcriptase polymerase chain reaction (rRT-PCR). The blood count was normal, the plasma test was negative, and blood glucose was 1.42 g/L. The renal function and blood ion gram were normal. The chest X-ray showed features of pneumonic consolidation in the right lung (Figure 1). Treatment started immediately with oxygen therapy at 1 l/min, and a combination of ceftriaxone (75 mg/kg/day) and gentamycin (3 mg/kg/day) was instituted. Finally, dietary support was provided with therapeutic milk using a feeding tube. The clinical course was marked by severe respiratory distress and the gradual decrease of SpO2, despite oxygen therapy. Unfortunately, the child died 48 hours following admission. The laboratory diagnosis confirmed an infection by SARS-CoV-2 a few hours after the child's death.\nOUTPUT:" }, { "from": "agent", "value": "COVID-19, Severe Acute Malnutrition" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An eight-month-old male child presented with fever, diarrhoea, and difficulty in breathing was admitted to the paediatric ward of the Amirou Boubacar Diallo national hospital (HNABD) of Niamey. The mother of the child had fever and shortness of breath approximately four weeks prior to admission and subsequently died. Upon clinical examination, the child was lethargic with dehydration but without shock or cyanosis, and he weighed 5 kg and was 78 cm in height. He had tachypnoea with a respiratory rate of 56 cycles/min, tachycardia at 148 heartbeats per minute, and temperature of 38.5 C. Oxygen saturation, measured with a pulse oximeter (SpO2), was 90% in ambient air. The pulmonary examination revealed moderate respiratory distress with chest indrawing. Auscultation showed bronchial rales in the right pulmonary system, and the abdomen was flexible with moderate hepatomegaly. Virological analysis was conducted using real-time reverse transcriptase polymerase chain reaction (rRT-PCR). The blood count was normal, the plasma test was negative, and blood glucose was 1.42 g/L. The renal function and blood ion gram were normal. The chest X-ray showed features of pneumonic consolidation in the right lung (Figure 1). Treatment started immediately with oxygen therapy at 1 l/min, and a combination of ceftriaxone (75 mg/kg/day) and gentamycin (3 mg/kg/day) was instituted. Finally, dietary support was provided with therapeutic milk using a feeding tube. The clinical course was marked by severe respiratory distress and the gradual decrease of SpO2, despite oxygen therapy. Unfortunately, the child died 48 hours following admission. The laboratory diagnosis confirmed an infection by SARS-CoV-2 a few hours after the child's death. OUTPUT:
Multicare_common583
[ { "from": "human", "value": "As a physician engaged 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 right optic disc was already deeply excavated when the diagnosis of primary open angle glaucoma was first made. He was a non-smoker and there was no significant past medical or family history. One year after raised intraocular pressures were first recorded, the patient reported painless visual loss in his right eye over a one-month period down to 3/60 ( Figure 3 ). A peripapillary haemorrhage was present at the superotemporal disc margin and the rapid visual deterioration was ascribed to end-stage glaucomatous damage in an already severely compromised optic nerve. Nine months later, the patient experienced rapid visual loss in his left eye with an expanding dense central scotoma. At the nadir, the patient's best-corrected visual acuities were 3/60 bilaterally. MRI of the brain and orbit with gadolinium contrast enhancement was normal. A neuro-ophthalmological second opinion was sought and the patient was found to harbour a homoplasmic m.11778G>A LHON mutation during his investigative work-up. He self-initiated treatment with idebenone (300 milligrams, three times a day) shortly after the molecular diagnosis was made ( Table 1 ). The visual acuity in his right eye gradually improved to 6/9 over the following two-year period and the patient has opted to remain on long-term idebenone treatment. This study had the relevant institutional ethical approval (County Durham & Tees Valley 1 Research Ethics Committee, 08/H0905/106) and it was carried out in compliance with the Declaration of Helsinki. Participants provided their written consent for genetic testing and participation into this study.\nOUTPUT:" }, { "from": "agent", "value": "Leber Hereditary Optic Neuropathy, Right-sided advanced glaucoma, Left-sided ocular hypertension" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The right optic disc was already deeply excavated when the diagnosis of primary open angle glaucoma was first made. He was a non-smoker and there was no significant past medical or family history. One year after raised intraocular pressures were first recorded, the patient reported painless visual loss in his right eye over a one-month period down to 3/60 ( Figure 3 ). A peripapillary haemorrhage was present at the superotemporal disc margin and the rapid visual deterioration was ascribed to end-stage glaucomatous damage in an already severely compromised optic nerve. Nine months later, the patient experienced rapid visual loss in his left eye with an expanding dense central scotoma. At the nadir, the patient's best-corrected visual acuities were 3/60 bilaterally. MRI of the brain and orbit with gadolinium contrast enhancement was normal. A neuro-ophthalmological second opinion was sought and the patient was found to harbour a homoplasmic m.11778G>A LHON mutation during his investigative work-up. He self-initiated treatment with idebenone (300 milligrams, three times a day) shortly after the molecular diagnosis was made ( Table 1 ). The visual acuity in his right eye gradually improved to 6/9 over the following two-year period and the patient has opted to remain on long-term idebenone treatment. This study had the relevant institutional ethical approval (County Durham & Tees Valley 1 Research Ethics Committee, 08/H0905/106) and it was carried out in compliance with the Declaration of Helsinki. Participants provided their written consent for genetic testing and participation into this study. OUTPUT:
Multicare_common5094
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 27-year-old male patient reported to the Department of Orthodontics, BBDCODS, Lucknow with the chief complaint of forwardly placed lower front teeth and impaired speech that has led to low confidence levels in him. Clinical frontal examination revealed a grossly symmetrical face with mesoprosopic facial form, no incisal show at rest and half of the incisors could be seen on smiling. The profile assessment revealed concave profile with anterior facial divergence, deficient midface, flat cheekbone contour, orthognathic maxilla, and prognathic mandible with protrusive lower lip and low mandibular plane angle. Figure 1 shows extraoral pretreatment photographs whereas Figure 2 shows intraoral photographs. The mandibular midline was shifted to right by 1 mm and reverse overjet of 3 mm and an overbite of 4 mm were recorded. Scissors bite was observed with respect to 24, 35. Temporomandibular joint examination did not reveal any discrepancy between centric relation and/centric occlusion and patient did not complain of pain or clicking in the joint. Cephalometric examination revealed retrognathic maxilla, prognathic mandible, with horizontal growth pattern and proclined maxillary incisors and retroclined mandibular incisors. Table 1 gives details of cephalometeric examination. Mild vertical deficiency was evident. Soft tissue examination on lateral cephalogram revealed concave profile, increased nasal prominence, normal nasolabial angle, increased upper lip thickness, and protrusive lower lip. Good soft tissue thickness camouflaged the retrognathic maxilla. Figure 3 shows pretreatment radiographs of the patient. A panoramic radiograph showed that all teeth were present including the third molars. There were no supernumerary teeth. The crown-root ratios were normal with good alveolar bone levels, no bone pathology, mandibular condyles, nasal floor, and maxillary sinuses appeared normal.\nOUTPUT:" }, { "from": "agent", "value": "Skeletal Class III malocclusion" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 27-year-old male patient reported to the Department of Orthodontics, BBDCODS, Lucknow with the chief complaint of forwardly placed lower front teeth and impaired speech that has led to low confidence levels in him. Clinical frontal examination revealed a grossly symmetrical face with mesoprosopic facial form, no incisal show at rest and half of the incisors could be seen on smiling. The profile assessment revealed concave profile with anterior facial divergence, deficient midface, flat cheekbone contour, orthognathic maxilla, and prognathic mandible with protrusive lower lip and low mandibular plane angle. Figure 1 shows extraoral pretreatment photographs whereas Figure 2 shows intraoral photographs. The mandibular midline was shifted to right by 1 mm and reverse overjet of 3 mm and an overbite of 4 mm were recorded. Scissors bite was observed with respect to 24, 35. Temporomandibular joint examination did not reveal any discrepancy between centric relation and/centric occlusion and patient did not complain of pain or clicking in the joint. Cephalometric examination revealed retrognathic maxilla, prognathic mandible, with horizontal growth pattern and proclined maxillary incisors and retroclined mandibular incisors. Table 1 gives details of cephalometeric examination. Mild vertical deficiency was evident. Soft tissue examination on lateral cephalogram revealed concave profile, increased nasal prominence, normal nasolabial angle, increased upper lip thickness, and protrusive lower lip. Good soft tissue thickness camouflaged the retrognathic maxilla. Figure 3 shows pretreatment radiographs of the patient. A panoramic radiograph showed that all teeth were present including the third molars. There were no supernumerary teeth. The crown-root ratios were normal with good alveolar bone levels, no bone pathology, mandibular condyles, nasal floor, and maxillary sinuses appeared normal. OUTPUT:
Multicare_common500
[ { "from": "human", "value": "As a physician engaged 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 89-year-old female nursing home resident was feeling generally unwell for 8 days and attended the ED following a temperature spike (38 C) on 22nd March. In the ambulance to ED, she desaturated to 80%. Heart rate at that time was 60 beats/minute, respiratory rate (RR) was 22/minute and blood pressure (BP) 112/70 mmHg. She denied any chest pain, dyspnoea, or palpitations. Her white cell count (WCC) was 22x109/L with neutrophilia, and C Reactive Protein (CRP) was 126 mg/L. Her lymphocyte count was normal and her chest x-ray (CXR) was reported as demonstrating no focal infiltrates. Prothrombin Time (PT) was prolonged at 13 seconds and Activated Partial Thromboplastin Time (APTT) was reduced at 21.8 seconds and fibrinogen level was raised at 5.4 g/L. She was treated with IV antibiotics but, despite resolution of pyrexia, reduction of WCC and CRP, she continued to complain of lassitude, weakness and tiredness. A D-dimer initially performed in her CBB was 2655 microg/1. In view of this and lack of clinical progress, a CTPA was performed which showed significant bilateral pulmonary emboli with a right sided infarct and reversal of blood flow noted in the hepatic inferior vena cava (IVC) indicative of right heart strain. If calculated in ED, her WS was estimated as 0. Echocardiogram revealed raised Pulmonary Arterial Pressure (PAP) at 48 mmHg. Her Charlson Comorbidity Index(CCI) score was 6 points and Clinical Frailty Scale (CFS) score was 7.\nOUTPUT:" }, { "from": "agent", "value": "Extensive Pulmonary Embolus" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 89-year-old female nursing home resident was feeling generally unwell for 8 days and attended the ED following a temperature spike (38 C) on 22nd March. In the ambulance to ED, she desaturated to 80%. Heart rate at that time was 60 beats/minute, respiratory rate (RR) was 22/minute and blood pressure (BP) 112/70 mmHg. She denied any chest pain, dyspnoea, or palpitations. Her white cell count (WCC) was 22x109/L with neutrophilia, and C Reactive Protein (CRP) was 126 mg/L. Her lymphocyte count was normal and her chest x-ray (CXR) was reported as demonstrating no focal infiltrates. Prothrombin Time (PT) was prolonged at 13 seconds and Activated Partial Thromboplastin Time (APTT) was reduced at 21.8 seconds and fibrinogen level was raised at 5.4 g/L. She was treated with IV antibiotics but, despite resolution of pyrexia, reduction of WCC and CRP, she continued to complain of lassitude, weakness and tiredness. A D-dimer initially performed in her CBB was 2655 microg/1. In view of this and lack of clinical progress, a CTPA was performed which showed significant bilateral pulmonary emboli with a right sided infarct and reversal of blood flow noted in the hepatic inferior vena cava (IVC) indicative of right heart strain. If calculated in ED, her WS was estimated as 0. Echocardiogram revealed raised Pulmonary Arterial Pressure (PAP) at 48 mmHg. Her Charlson Comorbidity Index(CCI) score was 6 points and Clinical Frailty Scale (CFS) score was 7. OUTPUT:
Multicare_common2558
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Upon investigation, he appeared to have chills and night sweats but denied having coughs, myalgias, bowel movement abnormalities, headaches, or any burning sensation with urination. On physical examination, he had a fever of 39 C, a 1 cm large, not painful, cervical lymph node, a stooped over posture, and a totally rigid spine. He had a blood pressure of 120/60 mmHg, and on cardiovascular examination, he had no murmur. Laboratory tests demonstrated a normal blood count, an elevated CRP of 244 mg/L, an accelerated erythrocyte rate of 37 mmH1, an inflammatory pattern on serum protein electrophoresis, and slightly elevated liver enzymes (AST = 46 UI/L and ALT = 36 UI/L) while liver and renal functions were normal. Blood cultures were negative and serologic tests for EBV, CMV, Brucella, HSV, HIV, and HCV were negative. Transthoracic cardiac ultrasound showed no signs of endocarditis. Antinuclear antibodies were positive (1:100), but anti-ENA antibodies were negative and without other signs of systemic lupus erythematosus. C3 and C4 complement fractions were normal. A computed tomography scan of the neck, chest, and abdomen showed a lymph node of the 4th cervical chain but no abscesses or internal lymphadenopathy. PCR for C. burnetii DNA was not performed. Treatment with etanercept was thus placed on hold and doxycycline 200 mg per day was prescribed for two weeks. Liver enzymes were progressively back to normal as well as CRP levels that were negative during his last medical visit.\nOUTPUT:" }, { "from": "agent", "value": "Acute Q Fever, Ankylosing Spondyloarthritis, Chronic Hepatitis B" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Upon investigation, he appeared to have chills and night sweats but denied having coughs, myalgias, bowel movement abnormalities, headaches, or any burning sensation with urination. On physical examination, he had a fever of 39 C, a 1 cm large, not painful, cervical lymph node, a stooped over posture, and a totally rigid spine. He had a blood pressure of 120/60 mmHg, and on cardiovascular examination, he had no murmur. Laboratory tests demonstrated a normal blood count, an elevated CRP of 244 mg/L, an accelerated erythrocyte rate of 37 mmH1, an inflammatory pattern on serum protein electrophoresis, and slightly elevated liver enzymes (AST = 46 UI/L and ALT = 36 UI/L) while liver and renal functions were normal. Blood cultures were negative and serologic tests for EBV, CMV, Brucella, HSV, HIV, and HCV were negative. Transthoracic cardiac ultrasound showed no signs of endocarditis. Antinuclear antibodies were positive (1:100), but anti-ENA antibodies were negative and without other signs of systemic lupus erythematosus. C3 and C4 complement fractions were normal. A computed tomography scan of the neck, chest, and abdomen showed a lymph node of the 4th cervical chain but no abscesses or internal lymphadenopathy. PCR for C. burnetii DNA was not performed. Treatment with etanercept was thus placed on hold and doxycycline 200 mg per day was prescribed for two weeks. Liver enzymes were progressively back to normal as well as CRP levels that were negative during his last medical visit. OUTPUT:
Multicare_common1831
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Attempt to assess the patient's body weight with ICU bed equipped with weight scales resulted in alarm that 250 kg is exceeded, while no other equipment for precise measurements of that range of weight was available. Taking his height of 178 cm, his body mass index is >85 kg/m2. Enterobacter aerogenes (ESBL negative; Ampc-positive; MIC 0,064 mg/L) was cultivated from tracheal aspirate and treatment was started with ertapenem 1,5 g per day. The dose of 1,5 g was chosen empirically. SPC recommends 1 g daily; we increased the dose arbitrarily with the assumption to somewhat increased volume distribution in this particular patient. The albumin levels and renal function were close to normal through the entire treatment period (Figure 1). Thanks to a research program we had the possibility of measuring ertapenem concentrations in the blood with validated ultrahigh performance liquid chromatography tandem mass spectrometry method. The results became available with delay, and thus the data did not influence our treatment. The measured maximum total concentration (Cmax) of ertapenem at steady state was 106.66 mg/L and through concentration (Cmin) 3.38 mg/L. According to the product information, the average Cmax and Cmin of ertapenem following a single 1 g intravenous dose in healthy young adults were 155 mg/L and 1 mg/L, respectively. Pneumonia responded well to the treatment. After 10 days the inflammatory markers were markedly decreased (CRP 13 mg/L, procalcitonin 0,12 mcg/L) and clinical symptoms resolved.\nOUTPUT:" }, { "from": "agent", "value": "Bilateral bacterial pneumonia, Acute respiratory failure, Sepsis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Attempt to assess the patient's body weight with ICU bed equipped with weight scales resulted in alarm that 250 kg is exceeded, while no other equipment for precise measurements of that range of weight was available. Taking his height of 178 cm, his body mass index is >85 kg/m2. Enterobacter aerogenes (ESBL negative; Ampc-positive; MIC 0,064 mg/L) was cultivated from tracheal aspirate and treatment was started with ertapenem 1,5 g per day. The dose of 1,5 g was chosen empirically. SPC recommends 1 g daily; we increased the dose arbitrarily with the assumption to somewhat increased volume distribution in this particular patient. The albumin levels and renal function were close to normal through the entire treatment period (Figure 1). Thanks to a research program we had the possibility of measuring ertapenem concentrations in the blood with validated ultrahigh performance liquid chromatography tandem mass spectrometry method. The results became available with delay, and thus the data did not influence our treatment. The measured maximum total concentration (Cmax) of ertapenem at steady state was 106.66 mg/L and through concentration (Cmin) 3.38 mg/L. According to the product information, the average Cmax and Cmin of ertapenem following a single 1 g intravenous dose in healthy young adults were 155 mg/L and 1 mg/L, respectively. Pneumonia responded well to the treatment. After 10 days the inflammatory markers were markedly decreased (CRP 13 mg/L, procalcitonin 0,12 mcg/L) and clinical symptoms resolved. OUTPUT:
Multicare_common102
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Beginning in October 2021, he suffered from recurrent paroxysms of palpitation, accompanied by occasional shocks. In November 2021, he was admitted to a small hospital due to syncope. At arrival to the hospital, the patient was hemodynamically stable (arterial blood pressure of 100/47 mmHg). A physical examination and an electrocardiogram (baseline rhythm: sinus rhythm/DDD pacing mode, 74 beats/min) did not provide evidence of acute decompensation of heart failure or acute coronary syndrome. Laboratory examinations found the level of hemoglobin was decreased (110 g/L) and the brain natriuretic peptide level was slightly increased (1,786.58 pg/ml). Electrolyte abnormalities and hyperthyroidism were excluded. Because of the lack of qualification to reprogram a CRTD, the local medical staff contacted the device specialist from the author's hospital for emergent technical assistance. The maximum frequency of VF episodes was 45 times within 26 h. Antitachycardia pacing (ATP) terminated 54 of the 64 episodes of VF. Ten episodes of VF were unaffected by ATP and required a shock for termination. The shocks were ineffective in 2 episodes of VF, with successful termination by a subsequent shock.\nOUTPUT:" }, { "from": "agent", "value": "Dilated cardiomyopathy, Complete left bundle branch block, Dukes D stage rectal cancer, Ventricular fibrillation" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Beginning in October 2021, he suffered from recurrent paroxysms of palpitation, accompanied by occasional shocks. In November 2021, he was admitted to a small hospital due to syncope. At arrival to the hospital, the patient was hemodynamically stable (arterial blood pressure of 100/47 mmHg). A physical examination and an electrocardiogram (baseline rhythm: sinus rhythm/DDD pacing mode, 74 beats/min) did not provide evidence of acute decompensation of heart failure or acute coronary syndrome. Laboratory examinations found the level of hemoglobin was decreased (110 g/L) and the brain natriuretic peptide level was slightly increased (1,786.58 pg/ml). Electrolyte abnormalities and hyperthyroidism were excluded. Because of the lack of qualification to reprogram a CRTD, the local medical staff contacted the device specialist from the author's hospital for emergent technical assistance. The maximum frequency of VF episodes was 45 times within 26 h. Antitachycardia pacing (ATP) terminated 54 of the 64 episodes of VF. Ten episodes of VF were unaffected by ATP and required a shock for termination. The shocks were ineffective in 2 episodes of VF, with successful termination by a subsequent shock. OUTPUT:
Multicare_common3153
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 35 year-old male presented with a right-sided, scrotal swelling of three days' duration associated with acute scrotal pain of increasing severity. His past medical history was not significant and there was no history of trauma. Clinical examination revealed an enlarged, firm, tender nodule, three cm in diameter, while the contralateral testis was normal. A clinical diagnosis of torsion testis/testicular neoplasm was made. All routine investigations gave normal results. An emergency scrotal ultrasonography (USG) revealed a 2.5 cm, single, ovoid, well-defined, hypoechoic, solitary mass in the right testis. Guided aspiration was done under local anesthesia using a 10 mL syringe and a 24 gauge needle to obtain a scanty, grey-white aspirate. The smears were stained with hematoxylin-eosin (H and E), Papanicolaou, and May-Grunwald-Giemsa (MGG) stains. The cells were round to oval, having eccentric, vesicular nuclei with a fine granular chromatin along with a pale/vacuolated cytoplasm [Figure 1]. The patient underwent orchidectomy as the mass was firmly adherent to the tunica albugenia making conservative surgery unfeasible. The specimen showed the testis with a well circumscribed, encapsulated mass measuring 2.5 x 2 cm [Figure 2] and its cut section was gray white. Histopathological examination (HPE) showed cuboidal to flat epithelial cells in solid cords, some lining the cystic spaces. Some of these epithelial cells showed prominent cytoplasmic vacuolation. Intervening stroma showed fibrocollagenous tissue with sparse lymphocytic infiltrates [Figure 3].\nOUTPUT:" }, { "from": "agent", "value": "Adenomatoid tumor" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 35 year-old male presented with a right-sided, scrotal swelling of three days' duration associated with acute scrotal pain of increasing severity. His past medical history was not significant and there was no history of trauma. Clinical examination revealed an enlarged, firm, tender nodule, three cm in diameter, while the contralateral testis was normal. A clinical diagnosis of torsion testis/testicular neoplasm was made. All routine investigations gave normal results. An emergency scrotal ultrasonography (USG) revealed a 2.5 cm, single, ovoid, well-defined, hypoechoic, solitary mass in the right testis. Guided aspiration was done under local anesthesia using a 10 mL syringe and a 24 gauge needle to obtain a scanty, grey-white aspirate. The smears were stained with hematoxylin-eosin (H and E), Papanicolaou, and May-Grunwald-Giemsa (MGG) stains. The cells were round to oval, having eccentric, vesicular nuclei with a fine granular chromatin along with a pale/vacuolated cytoplasm [Figure 1]. The patient underwent orchidectomy as the mass was firmly adherent to the tunica albugenia making conservative surgery unfeasible. The specimen showed the testis with a well circumscribed, encapsulated mass measuring 2.5 x 2 cm [Figure 2] and its cut section was gray white. Histopathological examination (HPE) showed cuboidal to flat epithelial cells in solid cords, some lining the cystic spaces. Some of these epithelial cells showed prominent cytoplasmic vacuolation. Intervening stroma showed fibrocollagenous tissue with sparse lymphocytic infiltrates [Figure 3]. OUTPUT:
Multicare_common3663
[ { "from": "human", "value": "As a physician engaged 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 was associated with left-sided neck pain with swallowing, choking on food, and shortness of breath. She denied fever, chills, or excessive sweats. Also, her CT abdominal scan with intravenous contrast showed a 3.6 cm lesion of the medial right hepatic lobe (segment 8) concerning for metastases. A few days later, the patient experienced respiratory distress and failure secondary to mechanical airway obstruction that required urgent intubation and mechanical ventilation. The discussion among different specialties, including general surgery, concluded that the patient was not a candidate for surgical intervention or tracheostomy, and recommendations were to proceed to palliative chemotherapy. Her condition dramatically improved, and she was extubated after 5 days of receiving the first cycle of R-CHOP therapy.\nOUTPUT:" }, { "from": "agent", "value": "Thyroid Lymphoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: It was associated with left-sided neck pain with swallowing, choking on food, and shortness of breath. She denied fever, chills, or excessive sweats. Also, her CT abdominal scan with intravenous contrast showed a 3.6 cm lesion of the medial right hepatic lobe (segment 8) concerning for metastases. A few days later, the patient experienced respiratory distress and failure secondary to mechanical airway obstruction that required urgent intubation and mechanical ventilation. The discussion among different specialties, including general surgery, concluded that the patient was not a candidate for surgical intervention or tracheostomy, and recommendations were to proceed to palliative chemotherapy. Her condition dramatically improved, and she was extubated after 5 days of receiving the first cycle of R-CHOP therapy. OUTPUT:
Multicare_common1204
[ { "from": "human", "value": "As a physician engaged 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 kidney biopsy was performed in a 37-year-old man with proteinuria of 2.1 g/day, serum creatinine of 2.48 mg/dl and a glomerular filtration rate of 44 ml/min (table 1). 1). The patient was started on meprednisone 40 mg/day, valsartan 320 mg/day and a gradual increase in aliskiren dose until 300 mg/day were reached. Low-sodium diet compliance was followed with urinary sodium excretion. One month later, serum creatinine increased to 2.7 mg/dl and proteinuria decreased to 0.8 g/day. Three months later, the steroid dose was tapered and the creatinine clearance improved to 54 ml/min and proteinuria remained steady for the following months (0.6-1 g/day). Twenty months later, while on dual blockade (valsartan had been lowered to 160 mg/day due to hypotension) and meprednisone 4 mg/day, proteinuria increased to 1.9 g/day. Steroids were restarted but proteinuria worsened to 6.8 g/day and creatinine clearance increased to 56 ml/min. A new kidney biopsy was performed and a test for alpha-galactosidase levels displayed low levels (0.7 ng/ml). A mutation [c.98A>G (D33G)] was identified in the gene of alpha-galactosidase A, diagnosed by sequential analysis. 2). Electron microscopy and genetic studies confirmed the diagnosis (fig. 3). The patient was started on agalsidase beta (Fabrazyme, Genzyme Corp., Cambridge, Mass., USA) intravenously at 1 mg/kg body weight every fortnight and steroids gradually decreased, while the dual blockade was unchanged. Two months after diagnosis, his proteinuria decreased to 2.7 g/day, his creatinine clearance was 46 ml/min and steroids were discontinued. One month later, his proteinuria increased to 3 g/day and the creatinine clearance was 40 ml/min. As adjuvant therapy, meprednisone 10 mg was restarted and added to the regime. Proteinuria decreased to 2 g/day and creatinine clearance was 37 ml/min.\nOUTPUT:" }, { "from": "agent", "value": "Fabry's Disease, Focal and Segmental Glomerulosclerosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A kidney biopsy was performed in a 37-year-old man with proteinuria of 2.1 g/day, serum creatinine of 2.48 mg/dl and a glomerular filtration rate of 44 ml/min (table 1). 1). The patient was started on meprednisone 40 mg/day, valsartan 320 mg/day and a gradual increase in aliskiren dose until 300 mg/day were reached. Low-sodium diet compliance was followed with urinary sodium excretion. One month later, serum creatinine increased to 2.7 mg/dl and proteinuria decreased to 0.8 g/day. Three months later, the steroid dose was tapered and the creatinine clearance improved to 54 ml/min and proteinuria remained steady for the following months (0.6-1 g/day). Twenty months later, while on dual blockade (valsartan had been lowered to 160 mg/day due to hypotension) and meprednisone 4 mg/day, proteinuria increased to 1.9 g/day. Steroids were restarted but proteinuria worsened to 6.8 g/day and creatinine clearance increased to 56 ml/min. A new kidney biopsy was performed and a test for alpha-galactosidase levels displayed low levels (0.7 ng/ml). A mutation [c.98A>G (D33G)] was identified in the gene of alpha-galactosidase A, diagnosed by sequential analysis. 2). Electron microscopy and genetic studies confirmed the diagnosis (fig. 3). The patient was started on agalsidase beta (Fabrazyme, Genzyme Corp., Cambridge, Mass., USA) intravenously at 1 mg/kg body weight every fortnight and steroids gradually decreased, while the dual blockade was unchanged. Two months after diagnosis, his proteinuria decreased to 2.7 g/day, his creatinine clearance was 46 ml/min and steroids were discontinued. One month later, his proteinuria increased to 3 g/day and the creatinine clearance was 40 ml/min. As adjuvant therapy, meprednisone 10 mg was restarted and added to the regime. Proteinuria decreased to 2 g/day and creatinine clearance was 37 ml/min. OUTPUT:
Multicare_common3757
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Computed tomography was ordered in February 2019 showing diminution of lymph node size around 60 %, and appearance of new, rapidly growing lung nodules in the right middle and lower lobes (Fig. 1A-B). No respiratory symptoms, fever or further weight loss were present. Computed tomography-guided transthoracic needle biopsy of pulmonary nodules was performed and histopathology revealed a chronic granulomatous inflammatory infiltrate with Langhans giant cells and presence of multibudding yeast cell in periodic acid-Schiff (PAS) stain, compatible with Paracoccidioides sp. (Fig. 2). Immunodiffusion test for Histoplasma spp. and Paracoccidioides spp. were negative. Cryptococcal antigen (CrAg) in serum was negative. The fungal cultures of the biopsy specimen were negative. Erythrocyte sedimentation rate (ESR) was 113 mm/h. It was found that the patient had lived in Pucallpa approximately 35 years before (low jungle of Peru) in his youth. Treatment was started with itraconazole 200 mg QID for 4 months with an improvement of ESR (12 mm/h) and tomographic resolution of lung lesions (Fig. 1C). A total gastrectomy with D2 lymphadenectomy was performed (June 2019). The biopsies performed showed a single lymph node group positive to neoplasm. No fungal involvement in lymph nodes or stomach was observed. During the perioperative period he received treatment with amphotericin B deoxycholate and at discharge antifungal maintenance with trimethoprim/sulfamethoxazole (TMP-SMX 160/800 mg BID) for additional 8 months. Tolerance to therapy was good. No evidence of reactivation of fungal infection occurred. The patient was treated with radiotherapy and chemotherapy with capecitabine during this period. However, developed bone metastases, confirmed by histopathology, with clinical deterioration causing finally his death.\nOUTPUT:" }, { "from": "agent", "value": "Paracoccidiodomycosis lung reactivation, Signet-ring cell gastric adenocarcinoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Computed tomography was ordered in February 2019 showing diminution of lymph node size around 60 %, and appearance of new, rapidly growing lung nodules in the right middle and lower lobes (Fig. 1A-B). No respiratory symptoms, fever or further weight loss were present. Computed tomography-guided transthoracic needle biopsy of pulmonary nodules was performed and histopathology revealed a chronic granulomatous inflammatory infiltrate with Langhans giant cells and presence of multibudding yeast cell in periodic acid-Schiff (PAS) stain, compatible with Paracoccidioides sp. (Fig. 2). Immunodiffusion test for Histoplasma spp. and Paracoccidioides spp. were negative. Cryptococcal antigen (CrAg) in serum was negative. The fungal cultures of the biopsy specimen were negative. Erythrocyte sedimentation rate (ESR) was 113 mm/h. It was found that the patient had lived in Pucallpa approximately 35 years before (low jungle of Peru) in his youth. Treatment was started with itraconazole 200 mg QID for 4 months with an improvement of ESR (12 mm/h) and tomographic resolution of lung lesions (Fig. 1C). A total gastrectomy with D2 lymphadenectomy was performed (June 2019). The biopsies performed showed a single lymph node group positive to neoplasm. No fungal involvement in lymph nodes or stomach was observed. During the perioperative period he received treatment with amphotericin B deoxycholate and at discharge antifungal maintenance with trimethoprim/sulfamethoxazole (TMP-SMX 160/800 mg BID) for additional 8 months. Tolerance to therapy was good. No evidence of reactivation of fungal infection occurred. The patient was treated with radiotherapy and chemotherapy with capecitabine during this period. However, developed bone metastases, confirmed by histopathology, with clinical deterioration causing finally his death. OUTPUT:
Multicare_common3182
[ { "from": "human", "value": "As a physician engaged 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 22-year-old man complained of dyspnea and recurrent epistaxis. He had a history of bronchial asthma, attention deficit hyperactivity disorder, learning disabilities and dysgraphia. He had telangiectasias in his fingers and lips, clubbing, and expiratory wheezing. A vascular murmur (bruit) was auscultated in his right lower back. Arterial blood gas showed a partial pressure of arterial oxygen (PaO2) of 51.4 mmHg and arterial oxygen saturation (SpO2) of 83% on room air. Blood testing revealed a hemoglobin level of 20 g/dl. Chest radiograph showed a large nodule in the right lower lung field with enlarged vessels. Chest CT revealed a PAVM located in the right segment (S) 10, which was 60 mm in diameter (Fig. 3). The PAVM was characterized as a simple type with a feeding artery of 10 mm and a draining vein of 13 mm in diameter. Perfusion scintigraphy showed a right-to-left shunt fraction of 29.7%. Brain magnetic resonance imaging (MRI) and abdominal CT were normal. A gastrointestinal endoscopy did not show any vascular lesions. Surgical treatment was indicated because the PAVM was unilateral and peripherally located. Transcatheter embolization of the feeding artery was thought to be difficult because the PAVM was very large and both the feeding artery and the draining vein were thick. There was a higher risk of paradoxical embolization such as migration of occlusive devices or blood clots. Therefore, we treated the PAVM by segmentectomy with video-assisted thoracoscopic surgery (VATS). After the surgery, the shunt fraction decreased to 14.2% and SpO2 rose to 94% on room air. Chest CT taken 16 months post-operatively revealed a new asymptomatic small PAVM, 3 mm in diameter, in the right upper lobe. As the feeding artery was less than 3 mm in diameter and the patient had no symptoms, we recommended careful observation.\nOUTPUT:" }, { "from": "agent", "value": "Hereditary hemorrhagic telangiectasia and pulmonary arteriovenous malformations" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 22-year-old man complained of dyspnea and recurrent epistaxis. He had a history of bronchial asthma, attention deficit hyperactivity disorder, learning disabilities and dysgraphia. He had telangiectasias in his fingers and lips, clubbing, and expiratory wheezing. A vascular murmur (bruit) was auscultated in his right lower back. Arterial blood gas showed a partial pressure of arterial oxygen (PaO2) of 51.4 mmHg and arterial oxygen saturation (SpO2) of 83% on room air. Blood testing revealed a hemoglobin level of 20 g/dl. Chest radiograph showed a large nodule in the right lower lung field with enlarged vessels. Chest CT revealed a PAVM located in the right segment (S) 10, which was 60 mm in diameter (Fig. 3). The PAVM was characterized as a simple type with a feeding artery of 10 mm and a draining vein of 13 mm in diameter. Perfusion scintigraphy showed a right-to-left shunt fraction of 29.7%. Brain magnetic resonance imaging (MRI) and abdominal CT were normal. A gastrointestinal endoscopy did not show any vascular lesions. Surgical treatment was indicated because the PAVM was unilateral and peripherally located. Transcatheter embolization of the feeding artery was thought to be difficult because the PAVM was very large and both the feeding artery and the draining vein were thick. There was a higher risk of paradoxical embolization such as migration of occlusive devices or blood clots. Therefore, we treated the PAVM by segmentectomy with video-assisted thoracoscopic surgery (VATS). After the surgery, the shunt fraction decreased to 14.2% and SpO2 rose to 94% on room air. Chest CT taken 16 months post-operatively revealed a new asymptomatic small PAVM, 3 mm in diameter, in the right upper lobe. As the feeding artery was less than 3 mm in diameter and the patient had no symptoms, we recommended careful observation. OUTPUT:
Multicare_common280
[ { "from": "human", "value": "As a physician engaged 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 senior author (R.J.S.) All players were male, and the average age of the player was 27 years (range, 18-32 years). There were 11 midfielders, 2 forwards, and 8 defenders. They had been playing soccer an average of 14 years prior to their inciting injury. Two players had concomitant ACL injuries and required ACL reconstruction. Three players had medial femoral condyle lesions, 7 had lateral femoral condyle lesions, 1 had a lateral tibial plateau lesion, and 1 had a patella lesion. The remaining 9 players had combined lesions. Two patients had a medial femoral condyle lesion and a lateral femoral condyle lesion, 2 had medial femoral condyle and trochlear groove lesions, 2 had lateral femoral condyle and patella lesions, 1 had lateral femoral condyle and trochlear groove lesions, and 2 had kissing lesions in the lateral compartment. The one player who did not return was the oldest player of the cohort at age 32 years. He had been playing soccer for 25 years prior to his most recent inciting injury. The players who did return to professional soccer continued to play an average of 5 years (range, 1-13 years) (Fig. 1). Years of continued play negatively correlated with years of age (r = -0.41).\nOUTPUT:" }, { "from": "agent", "value": "Microfracture" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The senior author (R.J.S.) All players were male, and the average age of the player was 27 years (range, 18-32 years). There were 11 midfielders, 2 forwards, and 8 defenders. They had been playing soccer an average of 14 years prior to their inciting injury. Two players had concomitant ACL injuries and required ACL reconstruction. Three players had medial femoral condyle lesions, 7 had lateral femoral condyle lesions, 1 had a lateral tibial plateau lesion, and 1 had a patella lesion. The remaining 9 players had combined lesions. Two patients had a medial femoral condyle lesion and a lateral femoral condyle lesion, 2 had medial femoral condyle and trochlear groove lesions, 2 had lateral femoral condyle and patella lesions, 1 had lateral femoral condyle and trochlear groove lesions, and 2 had kissing lesions in the lateral compartment. The one player who did not return was the oldest player of the cohort at age 32 years. He had been playing soccer for 25 years prior to his most recent inciting injury. The players who did return to professional soccer continued to play an average of 5 years (range, 1-13 years) (Fig. 1). Years of continued play negatively correlated with years of age (r = -0.41). OUTPUT:
Multicare_common10390
[ { "from": "human", "value": "As a physician engaged 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 case of 58-year-old grand multiparous, 3-years postmenopausal woman, who presented with a one-month history of moderate to severe lower abdominal pain of sudden onset, continuous, crushing in character, worse with urge to defecate and micturate, relieved by intake of analgesic and not related to position. However, there was no abdominal mass or swelling, no change in bowel habit and there was no preceding trauma. There was associated urinary frequency, urgency, urge incontinence, dysuria and occasional passage of purulent fluid and blood in urine but no fever. There was no history of bleeding per vaginam, post coital bleeding and vaginal discharge; no chronic cough, bone pain but weight loss. She had total abdominal hysterectomy 5 years prior to the onset of symptoms in a private hospital due to suspected endometrial hyperplasia. However, there was no evidence of histological analysis of the tissue removed. On examination, her vital signs were stable, there was no palpable abdominal mass. Examination of the urogenital system revealed a gauze partially extruded from the urethral meatus with purulent discharge as shown in Fig. 1. The pelvic examination was unremarkable. CT urography result revealed presence of foreign body in the bladder with pelvic abscess collection. Other investigations showed normal laboratory findings. Intraoperative findings revealed: presence of gauze shown in Fig. 1, protruding from the urethra on vaginal examination as shown in Fig. 1; dense peritoneal adhesion involving the gut, omentum and bladder, all adherent to the anterior abdominal wall; erosion of the posterior wall of the bladder with a gauze inside the bladder and purulent urine exiting from the bladder. Adhesiolysis was performed, the gauze in the bladder was removed and fistula in the posterior wall of the bladder repaired. Injury to the gut (ileum) in the course of adhesiolysis was promptly repaired. She remained stable throughout the post-operative days and was discharged on the 13th day post operatively. She has been seen in the Gynaecology clinic on two occasions after surgery and still remained stable.\nOUTPUT:" }, { "from": "agent", "value": "Gossypiboma, Cystitis secondary to foreign body in the bladder complicated by fistulous formation" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A case of 58-year-old grand multiparous, 3-years postmenopausal woman, who presented with a one-month history of moderate to severe lower abdominal pain of sudden onset, continuous, crushing in character, worse with urge to defecate and micturate, relieved by intake of analgesic and not related to position. However, there was no abdominal mass or swelling, no change in bowel habit and there was no preceding trauma. There was associated urinary frequency, urgency, urge incontinence, dysuria and occasional passage of purulent fluid and blood in urine but no fever. There was no history of bleeding per vaginam, post coital bleeding and vaginal discharge; no chronic cough, bone pain but weight loss. She had total abdominal hysterectomy 5 years prior to the onset of symptoms in a private hospital due to suspected endometrial hyperplasia. However, there was no evidence of histological analysis of the tissue removed. On examination, her vital signs were stable, there was no palpable abdominal mass. Examination of the urogenital system revealed a gauze partially extruded from the urethral meatus with purulent discharge as shown in Fig. 1. The pelvic examination was unremarkable. CT urography result revealed presence of foreign body in the bladder with pelvic abscess collection. Other investigations showed normal laboratory findings. Intraoperative findings revealed: presence of gauze shown in Fig. 1, protruding from the urethra on vaginal examination as shown in Fig. 1; dense peritoneal adhesion involving the gut, omentum and bladder, all adherent to the anterior abdominal wall; erosion of the posterior wall of the bladder with a gauze inside the bladder and purulent urine exiting from the bladder. Adhesiolysis was performed, the gauze in the bladder was removed and fistula in the posterior wall of the bladder repaired. Injury to the gut (ileum) in the course of adhesiolysis was promptly repaired. She remained stable throughout the post-operative days and was discharged on the 13th day post operatively. She has been seen in the Gynaecology clinic on two occasions after surgery and still remained stable. OUTPUT:
Multicare_common4828
[ { "from": "human", "value": "As a physician engaged 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 background history of hypertension and anaemia. She had no significant family history, psychosocial history, or previous surgical history. She was on an antihypertensive medication for her hypertension. She progressed as expected post operatively with no immediate intra operative complications with jejunostomy feeds commenced the following day. On day 2, a routine post-operative contrast CT scan to interrogate the anastomosis did not demonstrate a leak, but bilateral pleural effusions were present. On day 4, she had multiple vomits and had not opened her bowels since the procedure. Examination revealed she was tachycardic (Heart rate 140bpm), febrile (Temperature 39.4 degrees Celsius) and dyspnoeic (Respiratory rate 27, sp02 96% 6 L 02). Her abdomen was mildly tender and her peripheries were cool. Her biochemical markers revealed pH 7.45, Lactate 4.2 mmol/L, white cell count 1.9 x 109/L, C-reactive protein 456 mg/L. A septic workup and repeat CT chest abdomen pelvis followed. She was commenced on broad spectrum antibiotics for a suspected aspiration pneumonia. 1]. A right hemicolectomy was performed and the jejunostomy was un-kinked from its obstructive point with subsequent clinical confirmation of small bowel viability. The feeding tube was removed and the small bowel defect repaired primarily. She subsequently developed bacteraemia which required further intravenous antibiotics and a prolonged admission in intensive care for a tracheostomy, ARDS, and pericardial effusion and pleural effusions, but eventually made a full recovery.\nOUTPUT:" }, { "from": "agent", "value": "Caecal volvulus, Gastric carcinoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: She had a background history of hypertension and anaemia. She had no significant family history, psychosocial history, or previous surgical history. She was on an antihypertensive medication for her hypertension. She progressed as expected post operatively with no immediate intra operative complications with jejunostomy feeds commenced the following day. On day 2, a routine post-operative contrast CT scan to interrogate the anastomosis did not demonstrate a leak, but bilateral pleural effusions were present. On day 4, she had multiple vomits and had not opened her bowels since the procedure. Examination revealed she was tachycardic (Heart rate 140bpm), febrile (Temperature 39.4 degrees Celsius) and dyspnoeic (Respiratory rate 27, sp02 96% 6 L 02). Her abdomen was mildly tender and her peripheries were cool. Her biochemical markers revealed pH 7.45, Lactate 4.2 mmol/L, white cell count 1.9 x 109/L, C-reactive protein 456 mg/L. A septic workup and repeat CT chest abdomen pelvis followed. She was commenced on broad spectrum antibiotics for a suspected aspiration pneumonia. 1]. A right hemicolectomy was performed and the jejunostomy was un-kinked from its obstructive point with subsequent clinical confirmation of small bowel viability. The feeding tube was removed and the small bowel defect repaired primarily. She subsequently developed bacteraemia which required further intravenous antibiotics and a prolonged admission in intensive care for a tracheostomy, ARDS, and pericardial effusion and pleural effusions, but eventually made a full recovery. OUTPUT:
Multicare_common7457
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 32-year-old woman and her 35-year-old husband presented in 2016 with a 5-year history of primary infertility and two failed attempts of conventional in vitro fertilization (IVF)/ICSI. The findings of hysteroscopy were normal and the hormonal parameters were as expected (follicle-stimulating hormone [FSH]: 7.40 mIU/ml, luteinizing hormone: 9.89 mIU/ml, and prolactin: 15.84 ng/ml). The semen analysis showed normal semen parameters. The chromosomal analysis showed normal male and female karyotypes. The female started an IVF program in which she was given clomiphene tablets orally for the first 5 days, and from day 7 to 13, 150 IU of recombinant FSH was administered subcutaneously. From day 8 to 14, 150 IU of menotropin and from day 10 to 14, 0.25 mg of cetrorelix were administered subcutaneously. The patient was evaluated continuously, and when leading follicle of 20 mm (only follicle) on day 15 was observed, 250 mug recombinant human chorionic gonadotropin-alpha was administered subcutaneously for triggering. After 36 h, one oocyte was collected which was found to be immature [Figure 1] (germinal vesicle stage) when denuded. The denuded oocyte was subjected to rescue IVM for 25 h (until the extrusion of the first polar body) in culture medium (Vitrolife , Goteborg, Sweden). The matured oocyte [Figure 2] (metaphase II) was injected with the husband sperm after processing the semen by swim-up method. Two pronuclei [Figure 3] were seen 18 h post-ICSI and a grade 1 embryo [Figure 4] was generated on day 3. A successful pregnancy was achieved. Fetal cardiac activity was noted from 6 weeks' gestational age. The patient developed gestational hypertension which along with the diabetes was managed optimally with antihypertensives and insulin, respectively. As the patient developed preeclampsia at 32 weeks, pregnancy was terminated by a safe cesarean section and a healthy male infant (birth weight 2200 mg) was delivered.\nOUTPUT:" }, { "from": "agent", "value": "Type 1 Diabetes, Polycystic Ovary Syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 32-year-old woman and her 35-year-old husband presented in 2016 with a 5-year history of primary infertility and two failed attempts of conventional in vitro fertilization (IVF)/ICSI. The findings of hysteroscopy were normal and the hormonal parameters were as expected (follicle-stimulating hormone [FSH]: 7.40 mIU/ml, luteinizing hormone: 9.89 mIU/ml, and prolactin: 15.84 ng/ml). The semen analysis showed normal semen parameters. The chromosomal analysis showed normal male and female karyotypes. The female started an IVF program in which she was given clomiphene tablets orally for the first 5 days, and from day 7 to 13, 150 IU of recombinant FSH was administered subcutaneously. From day 8 to 14, 150 IU of menotropin and from day 10 to 14, 0.25 mg of cetrorelix were administered subcutaneously. The patient was evaluated continuously, and when leading follicle of 20 mm (only follicle) on day 15 was observed, 250 mug recombinant human chorionic gonadotropin-alpha was administered subcutaneously for triggering. After 36 h, one oocyte was collected which was found to be immature [Figure 1] (germinal vesicle stage) when denuded. The denuded oocyte was subjected to rescue IVM for 25 h (until the extrusion of the first polar body) in culture medium (Vitrolife , Goteborg, Sweden). The matured oocyte [Figure 2] (metaphase II) was injected with the husband sperm after processing the semen by swim-up method. Two pronuclei [Figure 3] were seen 18 h post-ICSI and a grade 1 embryo [Figure 4] was generated on day 3. A successful pregnancy was achieved. Fetal cardiac activity was noted from 6 weeks' gestational age. The patient developed gestational hypertension which along with the diabetes was managed optimally with antihypertensives and insulin, respectively. As the patient developed preeclampsia at 32 weeks, pregnancy was terminated by a safe cesarean section and a healthy male infant (birth weight 2200 mg) was delivered. OUTPUT:
Multicare_common8998
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 27-year-old female, who is medically free with no past ocular history, presented with vision loss in the left eye after being involved in a motor vehicle accident. The patient reported wearing a seat belt and driving at a speed of 80/km/hour when she hit another vehicle. The airbag system immediately deployed, and she had no extraocular trauma. Initial examination revealed visual acuity of 20/30 in the right eye and hand motion in the left eye with no relative afferent pupillary defect. Periocular examination revealed mild periorbital swelling in the left eye. The anterior segment examination demonstrated a central corneal epithelial defect with marked corneal stromal edema and descemet folds (Figure 1A). The remaining ocular examination was unremarkable, including the right eye. Anterior segment optical coherence tomography (AS-OCT) demonstrated profound corneal stromal edema with descemet folds and a thickness of 999 microm (Figure 1B). The patient was started on topical prednisolone acetate 1% Q6H, moxifloxacin 0.5% Q6H, and cyclopentolate 1% Q8H. Topical prednisolone acetate 1% was tapered over 3 weeks, and the other treatments were discontinued. and the visual acuity has recovered to 20/30.\nOUTPUT:" }, { "from": "agent", "value": "Corneal Endothelial Cell Loss" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 27-year-old female, who is medically free with no past ocular history, presented with vision loss in the left eye after being involved in a motor vehicle accident. The patient reported wearing a seat belt and driving at a speed of 80/km/hour when she hit another vehicle. The airbag system immediately deployed, and she had no extraocular trauma. Initial examination revealed visual acuity of 20/30 in the right eye and hand motion in the left eye with no relative afferent pupillary defect. Periocular examination revealed mild periorbital swelling in the left eye. The anterior segment examination demonstrated a central corneal epithelial defect with marked corneal stromal edema and descemet folds (Figure 1A). The remaining ocular examination was unremarkable, including the right eye. Anterior segment optical coherence tomography (AS-OCT) demonstrated profound corneal stromal edema with descemet folds and a thickness of 999 microm (Figure 1B). The patient was started on topical prednisolone acetate 1% Q6H, moxifloxacin 0.5% Q6H, and cyclopentolate 1% Q8H. Topical prednisolone acetate 1% was tapered over 3 weeks, and the other treatments were discontinued. and the visual acuity has recovered to 20/30. OUTPUT:
Multicare_common6399
[ { "from": "human", "value": "As a physician engaged 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 and continued to take oral diabetes medications, Metformin 1000 mg twice daily, Glipizide 10 mg daily, Actos (pioglitazone) 45 mg daily, and Januvia (sitagliptan) 100 mg daily. During the treatment period, the patient did not markedly vary in weight and had no remarkable change in diet or exercise. No routine medications were either started or discontinued, and compliance with medication regimen was determined by patient interview. Oral treatment of omeprazole, 40 mg, twice daily, was added to his daily regimen to obtain sustained reduction in gastric acidity and sustained elevation in serum gastrin. He continued to record fasting AM blood glucose throughout the test period and continued on all other medications. HgbA1c, fasting glucose, gastrin, insulin, and C-peptide levels were obtained in a fasting state prior to starting the omeprazole treatment and at 1 and 2 hours following a standard glucose tolerance test (GTT). All laboratory measurements were performed by a commercial laboratory (Quest Diagnostics), and samples were collected by a professional phlebotomist employed by Quest Diagnostics in their standardized fashion. Daily fasting glucose measurements were obtained with a commercial glucometer by the patient and recorded. After 2 and 4 months the patient returned to the clinic, in a fasting state, having taken no medications on the morning of testing for repeat measurements of HgbA1c, gastrin, and a 2-hour GTT measuring glucose, insulin, and C-peptide. Statistical analysis was performed with commercial statistical software, \"Analyse-It for Microsoft Excel v2.20\". Calculation of pancreatic beta-cell mass by HOMA was performed by the method of Matthews et al., and an alternative calculation of beta-cell area was performed using 2-hour glucose after GTT by the method described by Meier et al..\nOUTPUT:" }, { "from": "agent", "value": "Type 2 diabetes, Dyslipidemia, Hypertension" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: He had been taking and continued to take oral diabetes medications, Metformin 1000 mg twice daily, Glipizide 10 mg daily, Actos (pioglitazone) 45 mg daily, and Januvia (sitagliptan) 100 mg daily. During the treatment period, the patient did not markedly vary in weight and had no remarkable change in diet or exercise. No routine medications were either started or discontinued, and compliance with medication regimen was determined by patient interview. Oral treatment of omeprazole, 40 mg, twice daily, was added to his daily regimen to obtain sustained reduction in gastric acidity and sustained elevation in serum gastrin. He continued to record fasting AM blood glucose throughout the test period and continued on all other medications. HgbA1c, fasting glucose, gastrin, insulin, and C-peptide levels were obtained in a fasting state prior to starting the omeprazole treatment and at 1 and 2 hours following a standard glucose tolerance test (GTT). All laboratory measurements were performed by a commercial laboratory (Quest Diagnostics), and samples were collected by a professional phlebotomist employed by Quest Diagnostics in their standardized fashion. Daily fasting glucose measurements were obtained with a commercial glucometer by the patient and recorded. After 2 and 4 months the patient returned to the clinic, in a fasting state, having taken no medications on the morning of testing for repeat measurements of HgbA1c, gastrin, and a 2-hour GTT measuring glucose, insulin, and C-peptide. Statistical analysis was performed with commercial statistical software, "Analyse-It for Microsoft Excel v2.20". Calculation of pancreatic beta-cell mass by HOMA was performed by the method of Matthews et al., and an alternative calculation of beta-cell area was performed using 2-hour glucose after GTT by the method described by Meier et al.. OUTPUT:
Multicare_common2263
[ { "from": "human", "value": "As a physician engaged 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 successful macular hole surgery on his right eye, and had normal-appearing macula on his asymptomatic left eye. However, a perifoveal PVD was detected in the SD-OCT images of the left eye (Figure 1A). The SD-OCT B-scan images showed that the fovea appeared flatter than that before the macular PVD. The macular thickness maps and surface maps clearly showed changes in the foveal shape, namely, a widening and deepening of the foveal floor (Figures 1C-F and 2A-D). This flat foveal contour in the left eye remained for 2 years in the SD-OCT images recorded every 6 months. The left eye was asymptomatic and its BCVA remained at 20/20 for the 2 years after the macular PVD in the left eye. At 1 year after the development of macular PVD, the central foveal thickness decreased by 16.7%, the pit depth deepened by 20.5%, the foveola diameter enlarged by 14.7%, and the pit volume increased by 19.4%, as compared to the values before the macular PVD (initial visit, Table 1). At the same visit, the average regional retinal thickness in the ETDRS chart (Figure 1G and H) was decreased by 1.4% to 13.0% (Table 1). The percentage reduction was highest in the central subfield (-13.0%). Comparable changes were found in the inner ring subfields (3.9% to 6.6%) and in the outer subfield (1.4% to 5.5%). The values of foveal shape parameters did not change significantly during the 2-year follow-up after the development of the macular PVD. The pit depth was 149, 155, 147, 159, and 153 mum, pit volume was 0.145, 0.149, 0.148, 0.160, and 0.151 mm3, and central foveal thickness was 179, 179, 178, 176, and 172 mum at 0, 6, 12, 18, and 24 months, respectively, after the visit when the macular PVD was detected.\nOUTPUT:" }, { "from": "agent", "value": "Macular Posterior Vitreous Detachment" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 66-year-old man underwent successful macular hole surgery on his right eye, and had normal-appearing macula on his asymptomatic left eye. However, a perifoveal PVD was detected in the SD-OCT images of the left eye (Figure 1A). The SD-OCT B-scan images showed that the fovea appeared flatter than that before the macular PVD. The macular thickness maps and surface maps clearly showed changes in the foveal shape, namely, a widening and deepening of the foveal floor (Figures 1C-F and 2A-D). This flat foveal contour in the left eye remained for 2 years in the SD-OCT images recorded every 6 months. The left eye was asymptomatic and its BCVA remained at 20/20 for the 2 years after the macular PVD in the left eye. At 1 year after the development of macular PVD, the central foveal thickness decreased by 16.7%, the pit depth deepened by 20.5%, the foveola diameter enlarged by 14.7%, and the pit volume increased by 19.4%, as compared to the values before the macular PVD (initial visit, Table 1). At the same visit, the average regional retinal thickness in the ETDRS chart (Figure 1G and H) was decreased by 1.4% to 13.0% (Table 1). The percentage reduction was highest in the central subfield (-13.0%). Comparable changes were found in the inner ring subfields (3.9% to 6.6%) and in the outer subfield (1.4% to 5.5%). The values of foveal shape parameters did not change significantly during the 2-year follow-up after the development of the macular PVD. The pit depth was 149, 155, 147, 159, and 153 mum, pit volume was 0.145, 0.149, 0.148, 0.160, and 0.151 mm3, and central foveal thickness was 179, 179, 178, 176, and 172 mum at 0, 6, 12, 18, and 24 months, respectively, after the visit when the macular PVD was detected. OUTPUT:
Multicare_common4129
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Her medical history included rheumatoid arthritis since the age of 60 years and diabetes mellitus diagnosed at the age of 83 years that was being treated using voglibose. She noticed thigh pain 36 months after the operation, which worsened 2 months later without any episode of injury. According to her, she felt pain at first and then fell because of the pain. Internal fixation with a locking plate was performed at the hospital (Figure 4). The remaining gap between the fragments was evident. To promote fracture healing, low-intensity pulsed ultrasound and teriparatide administration were started six days and two months after the surgery, respectively. Despite these treatments, the fracture did not heal in nine months; she was therefore referred to our department. The retrospective radiographic analysis revealed that a periosteal thickening of the lateral cortex at the stem tip level had existed at least two months before the fracture (Figure 5). On admission to our hospital, she could hardly walk due to the left thigh pain. Radiographs of her contralateral femur showed lateral bowing but no features of AFF (Figure 7). The implant was replaced with a longer stem (Exeter; Stryker, Tokyo, Japan) using the cemented technique. The implant of bipolar arthroplasty was not loosened. Osteosynthesis was performed with a locking plate for the distal femur (NCB Periprosthetic Femur Plate; Zimmer Biomet, Tokyo, Japan) and a cable system (Figure 8). She regained the ability to stand up and walk without either a cane or a walker for short distances with no pain, as seen on the latest follow-up performed two years after the last surgery. Bony union was successfully achieved, and no issues were seen with the hemiarthroplasty (Figure 9).\nOUTPUT:" }, { "from": "agent", "value": "Periprosthetic Femoral Fracture, Atypical Femoral Fracture" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Her medical history included rheumatoid arthritis since the age of 60 years and diabetes mellitus diagnosed at the age of 83 years that was being treated using voglibose. She noticed thigh pain 36 months after the operation, which worsened 2 months later without any episode of injury. According to her, she felt pain at first and then fell because of the pain. Internal fixation with a locking plate was performed at the hospital (Figure 4). The remaining gap between the fragments was evident. To promote fracture healing, low-intensity pulsed ultrasound and teriparatide administration were started six days and two months after the surgery, respectively. Despite these treatments, the fracture did not heal in nine months; she was therefore referred to our department. The retrospective radiographic analysis revealed that a periosteal thickening of the lateral cortex at the stem tip level had existed at least two months before the fracture (Figure 5). On admission to our hospital, she could hardly walk due to the left thigh pain. Radiographs of her contralateral femur showed lateral bowing but no features of AFF (Figure 7). The implant was replaced with a longer stem (Exeter; Stryker, Tokyo, Japan) using the cemented technique. The implant of bipolar arthroplasty was not loosened. Osteosynthesis was performed with a locking plate for the distal femur (NCB Periprosthetic Femur Plate; Zimmer Biomet, Tokyo, Japan) and a cable system (Figure 8). She regained the ability to stand up and walk without either a cane or a walker for short distances with no pain, as seen on the latest follow-up performed two years after the last surgery. Bony union was successfully achieved, and no issues were seen with the hemiarthroplasty (Figure 9). OUTPUT:
Multicare_common3237
[ { "from": "human", "value": "As a physician engaged 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 with past medical history significant only for hypothyroidism presented to the ED with hematochezia and diarrhea of unknown etiology. Her last colonoscopy, three years prior, was unremarkable. On colonoscopy, a mass-like lesion was identified at the ileocecal valve (Figure 1(a)). Notably, on previous imaging studies, from three months prior, during a workup for painless jaundice, no mass was detected within the abdomen. Biopsies were taken of the mass-like lesion, as well as throughout the colon. The biopsies demonstrated hyalinized lamina propria, atrophic crypts, ulceration, and active inflammation, indicative of IC (Figure 1(b)). Three months prior to this ED visit she was treated with steroids for presumed autoimmune hepatitis following a workup and admission for painless jaundice, decreased appetite, right upper quadrant pain, \"mustard yellow\" urine and pale stools, elevated transaminases, and hyperbilirubinemia. An ultrasound was unrevealing, and CT showed no intrahepatic or extrahepatic bile duct dilatation, with a contracted gallbladder with pericholecystic edema of uncertain etiology. There was a nonspecific periportal edema extending towards the porta hepatis and a short segment jejunojejunal intussusception. Pathology of her liver biopsy showed an acute hepatitis pattern of injury with mild lobular cholestasis. The precise etiology was not readily apparent with the differential diagnosis including acute viral hepatitis and drug-induced liver injury. Plasma cells were inconspicuous, and the patient reportedly had negative F-actin serology; as a result, autoimmune hepatitis was not favored, though it could not be completely ruled out. The patient underwent a repeat colonoscopy two months later, following supportive treatment for her symptoms, although she endorsed additional episodes of diarrhea. After three months a CT angiogram was obtained which showed mild to moderate calcific atherosclerotic changes and mild tortuosity of the abdominal aorta without evidence of aneurysm or dissection. The celiac, superior, and inferior mesenteric arteries were widely patent without evidence of significant stenosis.\nOUTPUT:" }, { "from": "agent", "value": "Ischemic Colitis, Lymphocytic Colitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 55-year-old female with past medical history significant only for hypothyroidism presented to the ED with hematochezia and diarrhea of unknown etiology. Her last colonoscopy, three years prior, was unremarkable. On colonoscopy, a mass-like lesion was identified at the ileocecal valve (Figure 1(a)). Notably, on previous imaging studies, from three months prior, during a workup for painless jaundice, no mass was detected within the abdomen. Biopsies were taken of the mass-like lesion, as well as throughout the colon. The biopsies demonstrated hyalinized lamina propria, atrophic crypts, ulceration, and active inflammation, indicative of IC (Figure 1(b)). Three months prior to this ED visit she was treated with steroids for presumed autoimmune hepatitis following a workup and admission for painless jaundice, decreased appetite, right upper quadrant pain, "mustard yellow" urine and pale stools, elevated transaminases, and hyperbilirubinemia. An ultrasound was unrevealing, and CT showed no intrahepatic or extrahepatic bile duct dilatation, with a contracted gallbladder with pericholecystic edema of uncertain etiology. There was a nonspecific periportal edema extending towards the porta hepatis and a short segment jejunojejunal intussusception. Pathology of her liver biopsy showed an acute hepatitis pattern of injury with mild lobular cholestasis. The precise etiology was not readily apparent with the differential diagnosis including acute viral hepatitis and drug-induced liver injury. Plasma cells were inconspicuous, and the patient reportedly had negative F-actin serology; as a result, autoimmune hepatitis was not favored, though it could not be completely ruled out. The patient underwent a repeat colonoscopy two months later, following supportive treatment for her symptoms, although she endorsed additional episodes of diarrhea. After three months a CT angiogram was obtained which showed mild to moderate calcific atherosclerotic changes and mild tortuosity of the abdominal aorta without evidence of aneurysm or dissection. The celiac, superior, and inferior mesenteric arteries were widely patent without evidence of significant stenosis. OUTPUT:
Multicare_common7864
[ { "from": "human", "value": "As a physician engaged 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 19-year-old male patient, with body mass index (BMI) of 8.45 kg/m and previous diagnosis of cerebral palsy, was admitted due to upper gastrointestinal bleeding Blatchford score of 10. Upon initial assessment, the patient required a blood transfusion due to hemoglobin level of 5.48 g/dl. The upper gastrointestinal endoscopy reported an esophageal ulcer Forrest IIC and esophagitis. Given the symptoms associated with chronic malnutrition and severe deconditioning, a gastrostomy was recommended. Initially an endoscopic gastrostomy was decided as the ideal approach, which was unsuccessful due to suboptimal translumination. Despite considering a new attempt to perform endoscopic gastrostomy at a later date, the patient s nutritional and metabolic condition could worsen in case it failed a second time. Thus, an open gastrostomy was considered by the gastroenterology department to ensure an early start of the enteral nutritional route. The institutional anesthesiologist considered the patient's high risk would be reduced once he was in adequate nutritional and metabolic so the surgery was performed without any initial complications. An upper gastrointestinal endoscopy on the third postoperative day revealed adequate positioning of the gastrostomy and enteral nutrition was initiated and well tolerated. Ten days after surgery, patient in-hospital presented diffuse abdominal pain and multiple diarrheic episodes, of insidious origin, referring it began two days after surgical procedure and gradually increased its intensity. 1, Fig. 2). The CT scan showed no evidence of an intra-abdominal collection or abscess that could otherwise explain the findings, as there was also no clinical or laboratory signs of systemic inflammatory response syndrome or infection. Patient showed improved outcome regarding symptomatology 24 h later. One month after the surgery, the patient was discharged in good conditions, with nutritional supplement via gastrostomy and integral rehabilitation.\nOUTPUT:" }, { "from": "agent", "value": "Pneumoperitoneum, Pneumatosis intestinalis, Portal venous gas" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 19-year-old male patient, with body mass index (BMI) of 8.45 kg/m and previous diagnosis of cerebral palsy, was admitted due to upper gastrointestinal bleeding Blatchford score of 10. Upon initial assessment, the patient required a blood transfusion due to hemoglobin level of 5.48 g/dl. The upper gastrointestinal endoscopy reported an esophageal ulcer Forrest IIC and esophagitis. Given the symptoms associated with chronic malnutrition and severe deconditioning, a gastrostomy was recommended. Initially an endoscopic gastrostomy was decided as the ideal approach, which was unsuccessful due to suboptimal translumination. Despite considering a new attempt to perform endoscopic gastrostomy at a later date, the patient s nutritional and metabolic condition could worsen in case it failed a second time. Thus, an open gastrostomy was considered by the gastroenterology department to ensure an early start of the enteral nutritional route. The institutional anesthesiologist considered the patient's high risk would be reduced once he was in adequate nutritional and metabolic so the surgery was performed without any initial complications. An upper gastrointestinal endoscopy on the third postoperative day revealed adequate positioning of the gastrostomy and enteral nutrition was initiated and well tolerated. Ten days after surgery, patient in-hospital presented diffuse abdominal pain and multiple diarrheic episodes, of insidious origin, referring it began two days after surgical procedure and gradually increased its intensity. 1, Fig. 2). The CT scan showed no evidence of an intra-abdominal collection or abscess that could otherwise explain the findings, as there was also no clinical or laboratory signs of systemic inflammatory response syndrome or infection. Patient showed improved outcome regarding symptomatology 24 h later. One month after the surgery, the patient was discharged in good conditions, with nutritional supplement via gastrostomy and integral rehabilitation. OUTPUT:
Multicare_common2081
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 56-year-old Caucasian woman was referred to for a 1-month history of an enlarging nodule beneath her right upper eyelid. She denied any visual changes. She admitted to feeling pressure and a \"twitching\" feeling around the nodule. She has no significant past ocular history. Her medical history was significant for removal of a brain aneurysm several years prior and hand reconstructive surgery. Examination showed that her best-corrected visual acuity (BCVA) was 20/20 in OU. Pupils were equal, round, and reactive to light. There was no relative afferent pupillary defect. Hertel measurements at a base of 90 were 16.5 and 15.0 in the OD and OS, respectively. The intraocular pressure (IOP) was 20 mm Hg OU. Slit lamp biomicroscopy showed mild nuclear sclerotic cataracts in OU. There was a palpable mass in the lacrimal fossa along the right upper eyelid with overlying periocular inflammation. A CT scan of the orbits and sella demonstrated an asymmetric prominence of the right lacrimal gland without bony changes (Fig. 1). The patient underwent a right orbitotomy and incisional biopsy without complication. Gross examination of the biopsy specimen revealed a piece of tan tissue measuring 7 x 2 x 2 mm. Microscopic examination showed a mass composed of numerous histiocytes with ground glass cytoplasm (Fig. 2). There were occasional giant cells present, and some of the histiocytes contained vacuolated cytoplasm. Rare lymphocytes were present. Immunohistochemical stains were positive for CD68 and vimentin and negative for CD1a and S100 in the histiocytes. The lymphocytes immunostained for CD3. This study was Health Insurance Portability and Accountability Act compliant at this institution.\nOUTPUT:" }, { "from": "agent", "value": "Reticulohistiocytoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 56-year-old Caucasian woman was referred to for a 1-month history of an enlarging nodule beneath her right upper eyelid. She denied any visual changes. She admitted to feeling pressure and a "twitching" feeling around the nodule. She has no significant past ocular history. Her medical history was significant for removal of a brain aneurysm several years prior and hand reconstructive surgery. Examination showed that her best-corrected visual acuity (BCVA) was 20/20 in OU. Pupils were equal, round, and reactive to light. There was no relative afferent pupillary defect. Hertel measurements at a base of 90 were 16.5 and 15.0 in the OD and OS, respectively. The intraocular pressure (IOP) was 20 mm Hg OU. Slit lamp biomicroscopy showed mild nuclear sclerotic cataracts in OU. There was a palpable mass in the lacrimal fossa along the right upper eyelid with overlying periocular inflammation. A CT scan of the orbits and sella demonstrated an asymmetric prominence of the right lacrimal gland without bony changes (Fig. 1). The patient underwent a right orbitotomy and incisional biopsy without complication. Gross examination of the biopsy specimen revealed a piece of tan tissue measuring 7 x 2 x 2 mm. Microscopic examination showed a mass composed of numerous histiocytes with ground glass cytoplasm (Fig. 2). There were occasional giant cells present, and some of the histiocytes contained vacuolated cytoplasm. Rare lymphocytes were present. Immunohistochemical stains were positive for CD68 and vimentin and negative for CD1a and S100 in the histiocytes. The lymphocytes immunostained for CD3. This study was Health Insurance Portability and Accountability Act compliant at this institution. OUTPUT:
Multicare_common7803
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 53-year-old woman presented to hospital reporting diffuse abdominal pain and abnormal vaginal bleeding. The clinical examination revealed a painful abdominal mass, as well as metrorrhagia. The abdominal echography revealed the presence of ascites and a large mass of the uterus with ill-defined, irregular borders. Thoracic computed tomography showed multiple round solid masses in the lungs and mediastinum. A paracentesis was performed and 5 ml of abdominal fluid was sent for pathological examination. The cytological evaluation identified isolated or clustered malignant cells, round or spindle-shaped, highly suggestive for sarcoma (Figure 1b). The patient underwent total hysterectomy and bilateral adnexectomy. After interdisciplinary consultations, the oncologist contraindicated cytoreductive therapy due to the presence of distant metastases. The patient died a few months after the last hospitalization. The uterus weighed 10 kg and it was deformed by a giant tumor measuring 28/27/24 cm with polycyclic contour. On cut surface, this was fleshy, fasciculated, with cystic spaces, necrosis and hemorrhage (Figure 1a). The omentum showed white-gray multiple nodules. Microscopically, the tumor was composed of a dense malignant cell population with fusiform appearance, moderate to severe cytological pleomorphism and an important mitotic activity (12 mitoses/10 high power fields) (Figure 1c). Areas of tumor necrosis were identified, as well as angio-lymphatic invasion. The immunohistochemical tests revealed a positive immunostaining for p16, Ki67 and also the overexpression of p53. Negative immunoexpression for Estrogen (ER) and Progesteron receptor (PR) was noticed, as well as weak focal reaction for Smooth Muscle Actin (SMA) and Desmin (Figure 2).\nOUTPUT:" }, { "from": "agent", "value": "Uterine Leiomyosarcoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 53-year-old woman presented to hospital reporting diffuse abdominal pain and abnormal vaginal bleeding. The clinical examination revealed a painful abdominal mass, as well as metrorrhagia. The abdominal echography revealed the presence of ascites and a large mass of the uterus with ill-defined, irregular borders. Thoracic computed tomography showed multiple round solid masses in the lungs and mediastinum. A paracentesis was performed and 5 ml of abdominal fluid was sent for pathological examination. The cytological evaluation identified isolated or clustered malignant cells, round or spindle-shaped, highly suggestive for sarcoma (Figure 1b). The patient underwent total hysterectomy and bilateral adnexectomy. After interdisciplinary consultations, the oncologist contraindicated cytoreductive therapy due to the presence of distant metastases. The patient died a few months after the last hospitalization. The uterus weighed 10 kg and it was deformed by a giant tumor measuring 28/27/24 cm with polycyclic contour. On cut surface, this was fleshy, fasciculated, with cystic spaces, necrosis and hemorrhage (Figure 1a). The omentum showed white-gray multiple nodules. Microscopically, the tumor was composed of a dense malignant cell population with fusiform appearance, moderate to severe cytological pleomorphism and an important mitotic activity (12 mitoses/10 high power fields) (Figure 1c). Areas of tumor necrosis were identified, as well as angio-lymphatic invasion. The immunohistochemical tests revealed a positive immunostaining for p16, Ki67 and also the overexpression of p53. Negative immunoexpression for Estrogen (ER) and Progesteron receptor (PR) was noticed, as well as weak focal reaction for Smooth Muscle Actin (SMA) and Desmin (Figure 2). OUTPUT:
Multicare_common676
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 31-year-old woman with a gestational age of 12-13 weeks was admitted to the emergency department with severe abdominal pain as a major complaint. The pain got worse 24 hours before hospital admission and made her unable to walk. She felt the pain since 2 weeks, and it increased gradually, interfering her daily routine. She also suffered nausea, vomiting, dizziness and weakness. She has a history of vacuum delivery for her first pregnancy, suffered miscarriage in the second pregnancy, and an ectopic pregnancy located at the left fallopian tube in her third pregnancy 5 years ago. Left salpingectomy was performed to remove the previous tubal pregnancy. The patient has no ultrasonography examination in her first trimester because she was reluctant to go to the medical care centre amid the Covid-19 pandemic situation. Laboratory examination showed her haemoglobin was 8.4 g/dL, haematocrit was 25% and leukocytes count was 21.870/mm3, indicating a bleeding process. Ultrasonography examination revealed the presence of an extra-uterine pregnancy. She had haemoperitoneum with a total blood volume of 2600 mL, and clots were evident inside. The placenta surrounded the posterior corpus uteri and omentum (Figure 1). Some part of placenta was located in the right cornu of the uterus and intestines. The dead foetus was taken out from the right side of flank. The cord was identified, ligated and cut (Figure 2). After removing the foetus from the abdominal cavity, placenta was removed as much as possible, and the insertion was sutured (Figure 3). There was no active bleeding after the foetus was extracted and the surrounding tissue was cleaned. Bilateral ovaries were normal. Mild erosion and congestion were present over a part of the colon and caecum. Placenta and dissected tissue of posterior uterus with the remaining placenta were sent for histopathological examination. After the surgery, the patient was then shifted to the inpatient ward in satisfactory condition. A total of four units of whole blood were transfused postoperatively. She was discharged from hospital after full recovery.\nOUTPUT:" }, { "from": "agent", "value": "Right abdominal pregnancy, Hemorrhagic shock" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 31-year-old woman with a gestational age of 12-13 weeks was admitted to the emergency department with severe abdominal pain as a major complaint. The pain got worse 24 hours before hospital admission and made her unable to walk. She felt the pain since 2 weeks, and it increased gradually, interfering her daily routine. She also suffered nausea, vomiting, dizziness and weakness. She has a history of vacuum delivery for her first pregnancy, suffered miscarriage in the second pregnancy, and an ectopic pregnancy located at the left fallopian tube in her third pregnancy 5 years ago. Left salpingectomy was performed to remove the previous tubal pregnancy. The patient has no ultrasonography examination in her first trimester because she was reluctant to go to the medical care centre amid the Covid-19 pandemic situation. Laboratory examination showed her haemoglobin was 8.4 g/dL, haematocrit was 25% and leukocytes count was 21.870/mm3, indicating a bleeding process. Ultrasonography examination revealed the presence of an extra-uterine pregnancy. She had haemoperitoneum with a total blood volume of 2600 mL, and clots were evident inside. The placenta surrounded the posterior corpus uteri and omentum (Figure 1). Some part of placenta was located in the right cornu of the uterus and intestines. The dead foetus was taken out from the right side of flank. The cord was identified, ligated and cut (Figure 2). After removing the foetus from the abdominal cavity, placenta was removed as much as possible, and the insertion was sutured (Figure 3). There was no active bleeding after the foetus was extracted and the surrounding tissue was cleaned. Bilateral ovaries were normal. Mild erosion and congestion were present over a part of the colon and caecum. Placenta and dissected tissue of posterior uterus with the remaining placenta were sent for histopathological examination. After the surgery, the patient was then shifted to the inpatient ward in satisfactory condition. A total of four units of whole blood were transfused postoperatively. She was discharged from hospital after full recovery. OUTPUT:
Multicare_common10209
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 43 year-old male was admitted to the rheumatology clinic with the complaints of long-standing neck and low back pain and left lower extremity paresthesia. Neck pain was neuropathic character while low back pain was fulfilling the criteria for inflammatory back pain. Inflammatory back pain is typically characterized by following features: age of onset <40 years, insidious onset, improvement with exercise (no improvement with rest), and pain at the second half of night. His past medical history included NF1 (Figure 1). Sensorimotor polyneuropathy (SM-PNP) accompanied by mixed type axonal degeneration and demyelination in the lower extremities had been detected in electromyographic examination (EMG). Then, metabolic and paraneoplastic causes of PNP had been ruled out. SM-PNP was partially controlled by gabapentin treatment. Because of the prior diagnosis of NF1, brain magnetic resonance imaging (MRI) had been taken. Neurofibromas on the scalp (Figure 2(a)) and 30 x 14 mm in size arachnoid cyst in the right anterior temporal lobe (Figure 2(b)) had been detected on MRI. In addition, extruded disc herniation and myelopathy due to cord compression at C4-C5 level, syringohydromyelia cavity at T12-L1 level, and biforaminal disc protrusion at L3-L4 level had been identified by MRI. Partial relief in painful SM-PNP was provided through 6-day methylprednisolone treatment at dose of 80 mg/day with gabapentin 600 mg twice a day. On physical examination, lumbar spinal motion in sagittal and frontal planes was limited. Sacroiliac joint provocation tests were positive. Neurologically, the patient exhibited mild unsteadiness during the performance of tandem gait and Rhomberg's test. Upper and lower extremity motor strengths and deep tendon reflexes appeared to be decreased slightly. On admission, hemogram, urinalysis, erythrocyte sedimentation rate, and C-reactive protein tests were within normal limits. Initial investigations also revealed normal renal and liver function. However, human leukocyte antigen B27 test was positive. Radiograph of sacroiliac joints depicted bilateral grade III-IV sacroiliitis (Figure 3). Therefore, the patient was diagnosed as AS. Meloxicam at the dose of 15 mg/day was added to patient's current treatment and the patient's symptoms abated. The patient who had stable vital signs was discharged after 3 days.\nOUTPUT:" }, { "from": "agent", "value": "Ankylosing Spondylitis, Neurofibromatosis Type 1" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 43 year-old male was admitted to the rheumatology clinic with the complaints of long-standing neck and low back pain and left lower extremity paresthesia. Neck pain was neuropathic character while low back pain was fulfilling the criteria for inflammatory back pain. Inflammatory back pain is typically characterized by following features: age of onset <40 years, insidious onset, improvement with exercise (no improvement with rest), and pain at the second half of night. His past medical history included NF1 (Figure 1). Sensorimotor polyneuropathy (SM-PNP) accompanied by mixed type axonal degeneration and demyelination in the lower extremities had been detected in electromyographic examination (EMG). Then, metabolic and paraneoplastic causes of PNP had been ruled out. SM-PNP was partially controlled by gabapentin treatment. Because of the prior diagnosis of NF1, brain magnetic resonance imaging (MRI) had been taken. Neurofibromas on the scalp (Figure 2(a)) and 30 x 14 mm in size arachnoid cyst in the right anterior temporal lobe (Figure 2(b)) had been detected on MRI. In addition, extruded disc herniation and myelopathy due to cord compression at C4-C5 level, syringohydromyelia cavity at T12-L1 level, and biforaminal disc protrusion at L3-L4 level had been identified by MRI. Partial relief in painful SM-PNP was provided through 6-day methylprednisolone treatment at dose of 80 mg/day with gabapentin 600 mg twice a day. On physical examination, lumbar spinal motion in sagittal and frontal planes was limited. Sacroiliac joint provocation tests were positive. Neurologically, the patient exhibited mild unsteadiness during the performance of tandem gait and Rhomberg's test. Upper and lower extremity motor strengths and deep tendon reflexes appeared to be decreased slightly. On admission, hemogram, urinalysis, erythrocyte sedimentation rate, and C-reactive protein tests were within normal limits. Initial investigations also revealed normal renal and liver function. However, human leukocyte antigen B27 test was positive. Radiograph of sacroiliac joints depicted bilateral grade III-IV sacroiliitis (Figure 3). Therefore, the patient was diagnosed as AS. Meloxicam at the dose of 15 mg/day was added to patient's current treatment and the patient's symptoms abated. The patient who had stable vital signs was discharged after 3 days. OUTPUT:
Multicare_common10485
[ { "from": "human", "value": "As a physician engaged 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-ml specimen of the morning fasting venous blood was obtained from the patient at different phases of disease (at 8, 10, 23 and 32 days after admission) to allow comparison with two healthy volunteers. These two healthy volunteers (a 33-year-old male and a 35-year-old male) were persons who received physical examination in January 2016 in the outpatient clinic of China-Japan Union Hospital of Jilin University. The volunteers signed informed consent regarding participation in this study. Blood was taken in EDTA tubes and centrifuged at 1,500 x g, 4 C for 20 min. Supernatant plasma was collected and stored at -20 C prior to measurement of vWF and vWF-cp concentrations. Measurements were performed using a double antibody sandwich ELISA kit (CSB-E08437h; Cusabio Biotech Co., Ltd., Wuhan, China) according to the manufacturer's protocols. Following PE, hematologic and biochemical parameters (analyzed using an automatic biochemical analyzer) began to gradually improve over the 32 days after admission; PLT, SCr and serum lactate dehydrogenase concentration returned to their normal ranges. Furthermore, plasma vWF concentrations decreased and vWF-cp activity increased (Table I). On day 8 after admission, the patient's vWF concentration was increased compared with the normal control, then gradually decreased, and was close to normal level at discharge. On day 8 after admission, the patient's vWF-cp activity was markedly increased compared with the normal control, maintained at a very high level, and it did not recover to the normal level at discharge. Once PLT had returned to the normal range (193x109 cells/l) at 32 days after admission, the patient's plasma vWF concentration was broadly comparable with that of healthy volunteers. Additionally, plasma vWF-cp activity had markedly increased compared with that of healthy volunteers controls (Table I). Plasma vWF concentration decreased to normal levels over the 32 days after admission, and vWF-cp activity remained very high and did not recover to normal level at discharge (Table I).\nOUTPUT:" }, { "from": "agent", "value": "Thrombotic Thrombocytopenic Purpura" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 4-ml specimen of the morning fasting venous blood was obtained from the patient at different phases of disease (at 8, 10, 23 and 32 days after admission) to allow comparison with two healthy volunteers. These two healthy volunteers (a 33-year-old male and a 35-year-old male) were persons who received physical examination in January 2016 in the outpatient clinic of China-Japan Union Hospital of Jilin University. The volunteers signed informed consent regarding participation in this study. Blood was taken in EDTA tubes and centrifuged at 1,500 x g, 4 C for 20 min. Supernatant plasma was collected and stored at -20 C prior to measurement of vWF and vWF-cp concentrations. Measurements were performed using a double antibody sandwich ELISA kit (CSB-E08437h; Cusabio Biotech Co., Ltd., Wuhan, China) according to the manufacturer's protocols. Following PE, hematologic and biochemical parameters (analyzed using an automatic biochemical analyzer) began to gradually improve over the 32 days after admission; PLT, SCr and serum lactate dehydrogenase concentration returned to their normal ranges. Furthermore, plasma vWF concentrations decreased and vWF-cp activity increased (Table I). On day 8 after admission, the patient's vWF concentration was increased compared with the normal control, then gradually decreased, and was close to normal level at discharge. On day 8 after admission, the patient's vWF-cp activity was markedly increased compared with the normal control, maintained at a very high level, and it did not recover to the normal level at discharge. Once PLT had returned to the normal range (193x109 cells/l) at 32 days after admission, the patient's plasma vWF concentration was broadly comparable with that of healthy volunteers. Additionally, plasma vWF-cp activity had markedly increased compared with that of healthy volunteers controls (Table I). Plasma vWF concentration decreased to normal levels over the 32 days after admission, and vWF-cp activity remained very high and did not recover to normal level at discharge (Table I). OUTPUT:
Multicare_common9911
[ { "from": "human", "value": "As a physician engaged 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, gravida 6, para 4 woman received a Mirena IUD 8 weeks after elective repeat cesarean delivery. No complication or difficulty was encountered upon placement of the device. One year later, the patient became pregnant with the IUD in situ and aborted spontaneously. Her physician attempted to remove the IUD at her follow-up visit, resulting in avulsion of the strings from the IUD. Operative hysteroscopy revealed the body of the device protruding into the uterine cavity from the anterior uterine wall. Cystoscopy was normal, and attempts to remove the device, both under direct hysteroscopic vision and blindly using polyp forceps were unsuccessful. We received the patient in consultation and obtained a pelvic magnetic resonance imaging (MRI). This confirmed the moderate uterine retroflexion appreciated upon physical examination, and showed the IUD deeply embedded within the anterior myometrium at the level of the flexure. Again, the patient was taken to surgery and diagnostic hysteroscopy performed. This time, no portion of the IUD was visible within the uterine cavity, and hysteroscopic dissection using a resectoscope under fluoroscopic guidance was unsuccessful in locating the device. Diagnostic laparoscopy was performed and the uterus seen to be grossly normal. Fluoroscopy was then used, and the IUD was located within the myometrium. A 1-cm incision was made in the anterior uterine wall just above it, exposing the IUD, which was then easily withdrawn from the surrounding tissue, and the operative site laparoscopically sutured to close the wound in 2 layers. The patient recovered without incident and was discharged home on the day of her surgery.\nOUTPUT:" }, { "from": "agent", "value": "Perforated intrauterine device" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 28-year-old, gravida 6, para 4 woman received a Mirena IUD 8 weeks after elective repeat cesarean delivery. No complication or difficulty was encountered upon placement of the device. One year later, the patient became pregnant with the IUD in situ and aborted spontaneously. Her physician attempted to remove the IUD at her follow-up visit, resulting in avulsion of the strings from the IUD. Operative hysteroscopy revealed the body of the device protruding into the uterine cavity from the anterior uterine wall. Cystoscopy was normal, and attempts to remove the device, both under direct hysteroscopic vision and blindly using polyp forceps were unsuccessful. We received the patient in consultation and obtained a pelvic magnetic resonance imaging (MRI). This confirmed the moderate uterine retroflexion appreciated upon physical examination, and showed the IUD deeply embedded within the anterior myometrium at the level of the flexure. Again, the patient was taken to surgery and diagnostic hysteroscopy performed. This time, no portion of the IUD was visible within the uterine cavity, and hysteroscopic dissection using a resectoscope under fluoroscopic guidance was unsuccessful in locating the device. Diagnostic laparoscopy was performed and the uterus seen to be grossly normal. Fluoroscopy was then used, and the IUD was located within the myometrium. A 1-cm incision was made in the anterior uterine wall just above it, exposing the IUD, which was then easily withdrawn from the surrounding tissue, and the operative site laparoscopically sutured to close the wound in 2 layers. The patient recovered without incident and was discharged home on the day of her surgery. OUTPUT:
Multicare_common4714
[ { "from": "human", "value": "As a physician engaged 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 underwent a right occipital lobectomy to resect cancer that had metastasized to the brain. She had remained in complete remission for more than 5 years, but follow-up laboratory examination showed increased serum tumor marker levels, and whole-body computed tomography (CT) scan revealed a brain mass. She was admitted to our hospital, and brain magnetic resonance imaging (MRI) revealed a right occipital metastatic tumor (Fig. 1). She received postoperative radiotherapy. Two years later, the patient presented with headache and gait disturbance. 2). Left homonymous hemianopsia had already been noted, and an occipital lobectomy was performed in the prone position. The deep venous system and sinus vessels around the tumor were not injured during the operation. The ventricle was not breached during surgery. The patient regained consciousness soon after surgery. Three hours later, the patient complained of a progressive headache and developed consciousness disturbance. Follow-up CT showed a left frontal intracranial hemorrhage (ICH) away from the operation site (Fig. 3). Immediate revision surgery was performed to evacuate the hematoma, and intraoperative findings did not reveal injury or apparent dissemination on the surface of the brain. Postoperative MRI revealed a decrease in the degree of brain edema and an improvement in the midline shift (Fig. 4). The patient had no history of arterial hypertension, and her blood pressure was stable during the perioperative period. She was not treated with anticoagulants, and her laboratory findings including the coagulation parameters were normal. Preoperative MRI revealed no frontal lobe abnormalities and preoperative MR venography (MRV) revealed no sinus vessel obstruction. However, postoperative MRV revealed the left frontal cortical veins were poorly depicted (Fig. 5). The patient gradually recovered but remained severely disabled; she was discharged with total aphasia and right hemiparesis.\nOUTPUT:" }, { "from": "agent", "value": "Remote Supratentorial Hemorrhage, Lung Adenocarcinoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 62-year-old woman underwent a right occipital lobectomy to resect cancer that had metastasized to the brain. She had remained in complete remission for more than 5 years, but follow-up laboratory examination showed increased serum tumor marker levels, and whole-body computed tomography (CT) scan revealed a brain mass. She was admitted to our hospital, and brain magnetic resonance imaging (MRI) revealed a right occipital metastatic tumor (Fig. 1). She received postoperative radiotherapy. Two years later, the patient presented with headache and gait disturbance. 2). Left homonymous hemianopsia had already been noted, and an occipital lobectomy was performed in the prone position. The deep venous system and sinus vessels around the tumor were not injured during the operation. The ventricle was not breached during surgery. The patient regained consciousness soon after surgery. Three hours later, the patient complained of a progressive headache and developed consciousness disturbance. Follow-up CT showed a left frontal intracranial hemorrhage (ICH) away from the operation site (Fig. 3). Immediate revision surgery was performed to evacuate the hematoma, and intraoperative findings did not reveal injury or apparent dissemination on the surface of the brain. Postoperative MRI revealed a decrease in the degree of brain edema and an improvement in the midline shift (Fig. 4). The patient had no history of arterial hypertension, and her blood pressure was stable during the perioperative period. She was not treated with anticoagulants, and her laboratory findings including the coagulation parameters were normal. Preoperative MRI revealed no frontal lobe abnormalities and preoperative MR venography (MRV) revealed no sinus vessel obstruction. However, postoperative MRV revealed the left frontal cortical veins were poorly depicted (Fig. 5). The patient gradually recovered but remained severely disabled; she was discharged with total aphasia and right hemiparesis. OUTPUT:
Multicare_common640
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A previously healthy 72-year-old woman presented with 6 days of left lower quadrant abdominal pain and constipation. There were no report of fever, melena, hematochezia or change in appetite. The physical exam demonstrated a distended abdomen with palpable left lower quadrant pain, without guarding. The blood work revealed a normal white blood cell count but an increased C-reactive protein (110 mg/L). The patient was treated with IV antibiotics (Ceftriaxone 2 g daily and Metronidazole 500 mg three times daily), with an adequate resolution of her signs and symptoms. The patient subsequently confessed to have eaten shellfish in paella the week prior to admission. Diverticulosis is a common illness in developed countries where it is present in 50% of people over the age of 60. In 88% of cases the patients are unconscious about the ingested foreign body; furthermore, in 76% of cases the foreign body passes spontaneously without complication. The predisposing risk factor for ingestion is the use of dentures which reduces the sensibility of the palate (72%); however, this was not the case for our patient . About 10%-20% of all ingested foreign bodies must be removed endoscopically and 1%-14% need operative removal . The patient left hospital after completing antibiotic treatment without complication. She remained asymptomatic three months after discharge.\nOUTPUT:" }, { "from": "agent", "value": "Calcifying bowel inflammation, Sigmoid diverticulitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A previously healthy 72-year-old woman presented with 6 days of left lower quadrant abdominal pain and constipation. There were no report of fever, melena, hematochezia or change in appetite. The physical exam demonstrated a distended abdomen with palpable left lower quadrant pain, without guarding. The blood work revealed a normal white blood cell count but an increased C-reactive protein (110 mg/L). The patient was treated with IV antibiotics (Ceftriaxone 2 g daily and Metronidazole 500 mg three times daily), with an adequate resolution of her signs and symptoms. The patient subsequently confessed to have eaten shellfish in paella the week prior to admission. Diverticulosis is a common illness in developed countries where it is present in 50% of people over the age of 60. In 88% of cases the patients are unconscious about the ingested foreign body; furthermore, in 76% of cases the foreign body passes spontaneously without complication. The predisposing risk factor for ingestion is the use of dentures which reduces the sensibility of the palate (72%); however, this was not the case for our patient . About 10%-20% of all ingested foreign bodies must be removed endoscopically and 1%-14% need operative removal . The patient left hospital after completing antibiotic treatment without complication. She remained asymptomatic three months after discharge. OUTPUT:
Multicare_common2529
[ { "from": "human", "value": "As a physician engaged 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 male Saudi patient, 50 years old was admitted to the Plastic Surgery Unit at Dammam Central Hospital (DCH), complaining of a swelling in the plantar aspect of the left foot near the heads of the metatarsals. The swelling was of about 2 years duration gradually increasing in size. It was a firm brownish swelling measuring 2 cm x 1.5 cm, with no bleeding or ulceration. He was treated at health centers and clinics by chemical cauterization for what was diagnosed as a corn but with no improvement. History revealed that he was a diabetic controlled on treatment for non-insulin dependent diabetes mellitus (NIDDM). General examination showed normal systems and at left lower limb no enlarged lymph nodes at the popliteal area or groin. His investigation showed ESR 70 mm/hour and other blood investigations were within normal limits. His chest X-ray was normal and his left foot X-ray showed no bony abnormality. In view of the history and previous treatments, a plan of excision and histopathology examination was made. The tumor was made up of epithiloid and spindle cells arranged in diffuse sheets and nests (Fig. 1). Two to three mitoses were seen per high power field. The cells were large with pleomorphic, hyperchromatic nuclei with prominent nucleoli and moderate amount of cytoplasm. Intracellular melanin pigment was seen in large areas (Fig. 2). The epidermal component was seen in focal areas. The tumor infiltrated the subcutaneous fat (Clark's Level V) and showed features of Breslow's high-risk category (thickness 14 mm). A second surgery of wide excision under general anesthesia was carried out and the defect was covered by split thickness skin graft. The patient's recovery was uneventful and the graft took successfully (Fig. 3). The patient was referred to the oncologist for further treatment.\nOUTPUT:" }, { "from": "agent", "value": "Malignant melanoma of the skin" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A male Saudi patient, 50 years old was admitted to the Plastic Surgery Unit at Dammam Central Hospital (DCH), complaining of a swelling in the plantar aspect of the left foot near the heads of the metatarsals. The swelling was of about 2 years duration gradually increasing in size. It was a firm brownish swelling measuring 2 cm x 1.5 cm, with no bleeding or ulceration. He was treated at health centers and clinics by chemical cauterization for what was diagnosed as a corn but with no improvement. History revealed that he was a diabetic controlled on treatment for non-insulin dependent diabetes mellitus (NIDDM). General examination showed normal systems and at left lower limb no enlarged lymph nodes at the popliteal area or groin. His investigation showed ESR 70 mm/hour and other blood investigations were within normal limits. His chest X-ray was normal and his left foot X-ray showed no bony abnormality. In view of the history and previous treatments, a plan of excision and histopathology examination was made. The tumor was made up of epithiloid and spindle cells arranged in diffuse sheets and nests (Fig. 1). Two to three mitoses were seen per high power field. The cells were large with pleomorphic, hyperchromatic nuclei with prominent nucleoli and moderate amount of cytoplasm. Intracellular melanin pigment was seen in large areas (Fig. 2). The epidermal component was seen in focal areas. The tumor infiltrated the subcutaneous fat (Clark's Level V) and showed features of Breslow's high-risk category (thickness 14 mm). A second surgery of wide excision under general anesthesia was carried out and the defect was covered by split thickness skin graft. The patient's recovery was uneventful and the graft took successfully (Fig. 3). The patient was referred to the oncologist for further treatment. OUTPUT:
Multicare_common7212
[ { "from": "human", "value": "As a physician engaged 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 1996, a 60-year-old female patient presented with redness and decreased sweating over the left half of the face, which slowly progressed to all other parts of the body throughout 23 years and only left a patchy area with increased sweating on the left lower quadrant of her trunk. The patient had not applied topical medication to any part of the body. There was no history of joint or muscular pains, but she complained of a prickly sensation anywhere in the skin. The patient presented by inspection with dry and scaly skin. Upon physical examination, we found redness and moisture corresponding to a 20 x 30 cm, band-shaped segmental area on the left lower of the trunk (corresponding to the 6th-8th dermatomes). There was also an altered/decreased sense of touch in the area of anhidrosis. Deep tendon reflexes were absent both in the upper and lower limbs. Pupillary examination showed a tonic pupil on the right side and anisocoria with the right pupil smaller than the left (Fig. 1). There were no tremor, bradykinesia, dysarthria, or incoordination of the limbs or postural instability. There was neither motor weakness nor any wasting. Twenty-four-hour ambulatory blood pressure monitoring was normal. A minor test (starch-iodine test) was performed to confirm hyperhidrosis (Fig. 2). Histopathological examination from the anhidrotic area showed atrophic epidermis but basally located small eccrine sweat glands, excluding a primary sweat gland disorder. Nerve conduction studies revealed evidence of a mild distal sensory polyneuropathy of the axonal type. Magnetic resonance imaging (MRI) of the brain and the spinal canal was unremarkable. Antinuclear antibodies andSjogren'sautoantibodies were within normal limits. Tilt-table testing showed signs of orthostatic hypotension with evidence of reduced sympathetic function.\nOUTPUT:" }, { "from": "agent", "value": "Ross Syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: In 1996, a 60-year-old female patient presented with redness and decreased sweating over the left half of the face, which slowly progressed to all other parts of the body throughout 23 years and only left a patchy area with increased sweating on the left lower quadrant of her trunk. The patient had not applied topical medication to any part of the body. There was no history of joint or muscular pains, but she complained of a prickly sensation anywhere in the skin. The patient presented by inspection with dry and scaly skin. Upon physical examination, we found redness and moisture corresponding to a 20 x 30 cm, band-shaped segmental area on the left lower of the trunk (corresponding to the 6th-8th dermatomes). There was also an altered/decreased sense of touch in the area of anhidrosis. Deep tendon reflexes were absent both in the upper and lower limbs. Pupillary examination showed a tonic pupil on the right side and anisocoria with the right pupil smaller than the left (Fig. 1). There were no tremor, bradykinesia, dysarthria, or incoordination of the limbs or postural instability. There was neither motor weakness nor any wasting. Twenty-four-hour ambulatory blood pressure monitoring was normal. A minor test (starch-iodine test) was performed to confirm hyperhidrosis (Fig. 2). Histopathological examination from the anhidrotic area showed atrophic epidermis but basally located small eccrine sweat glands, excluding a primary sweat gland disorder. Nerve conduction studies revealed evidence of a mild distal sensory polyneuropathy of the axonal type. Magnetic resonance imaging (MRI) of the brain and the spinal canal was unremarkable. Antinuclear antibodies andSjogren'sautoantibodies were within normal limits. Tilt-table testing showed signs of orthostatic hypotension with evidence of reduced sympathetic function. OUTPUT:
Multicare_common9024
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 53-year-old woman presented to her primary care physician complaining of feeling anxious, with panic at times. She was having difficulty finding words and had bilateral hand and wrist pain, which had largely improved although there was still some lack of coordination. She also had trouble getting out of the bed and getting dressed. However, she denied headache, nausea or vomiting. The patient described her anxiety symptoms as insomnia, shortness of breath and feeling 'closed in'. She had experienced these symptoms for a few years but they had got worse over the past month. She denied suicidal and homicidal ideation. The patient felt more comfortable sleeping during the day, but this caused her to stay up late at night. She had a past medical history of allergic rhinitis, asthma, hyperglycaemia and hyperlipidaemia. She had a positive family history of anxiety. Physical examination showed normal vital signs, mild nasal congestion, quiet and clear speech, possible mild bilateral thenar atrophy, a mildly positive Phalen's test, and a negative Tinel sign. Mild left facial asymmetry was also noted. Electromyography was normal. Two days later, the patient presented to the emergency department complaining of progressive left-sided weakness and difficulty in speech. A CT scan of the head to rule out stroke surprisingly showed a mass in the right frontal lobe. MRI confirmed the presence of this mass which extended to the corpus callosum. The mass measured 5.7 cm by 3.8 cm (Fig. 1). CT scans of the chest, abdomen and pelvis were negative for any metastases. A right frontal stereotactic craniotomy revealed a multicystic, vascular, necrotic mass which was soft in many areas. Frozen sections and biopsy slides (Fig. 2) showed an infiltrating astrocytic tumour with necrosis, microvascular proliferation, and brisk mitotic activity. The tumour cells were strongly immunoreactive to GFAP, and negative for Cam 5.2 and IDH1 R132H mutant antibody. Neurofilament immunostaining highlighted the infiltrating nature of this tumour. P53 immunostaining showed nuclear expression in a minor subset of the tumour cells. All immunostaining was performed with appropriate controls on separate slides. The final diagnosis was GBM of the brain.\nOUTPUT:" }, { "from": "agent", "value": "Glioblastoma Multiforme of the brain" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 53-year-old woman presented to her primary care physician complaining of feeling anxious, with panic at times. She was having difficulty finding words and had bilateral hand and wrist pain, which had largely improved although there was still some lack of coordination. She also had trouble getting out of the bed and getting dressed. However, she denied headache, nausea or vomiting. The patient described her anxiety symptoms as insomnia, shortness of breath and feeling 'closed in'. She had experienced these symptoms for a few years but they had got worse over the past month. She denied suicidal and homicidal ideation. The patient felt more comfortable sleeping during the day, but this caused her to stay up late at night. She had a past medical history of allergic rhinitis, asthma, hyperglycaemia and hyperlipidaemia. She had a positive family history of anxiety. Physical examination showed normal vital signs, mild nasal congestion, quiet and clear speech, possible mild bilateral thenar atrophy, a mildly positive Phalen's test, and a negative Tinel sign. Mild left facial asymmetry was also noted. Electromyography was normal. Two days later, the patient presented to the emergency department complaining of progressive left-sided weakness and difficulty in speech. A CT scan of the head to rule out stroke surprisingly showed a mass in the right frontal lobe. MRI confirmed the presence of this mass which extended to the corpus callosum. The mass measured 5.7 cm by 3.8 cm (Fig. 1). CT scans of the chest, abdomen and pelvis were negative for any metastases. A right frontal stereotactic craniotomy revealed a multicystic, vascular, necrotic mass which was soft in many areas. Frozen sections and biopsy slides (Fig. 2) showed an infiltrating astrocytic tumour with necrosis, microvascular proliferation, and brisk mitotic activity. The tumour cells were strongly immunoreactive to GFAP, and negative for Cam 5.2 and IDH1 R132H mutant antibody. Neurofilament immunostaining highlighted the infiltrating nature of this tumour. P53 immunostaining showed nuclear expression in a minor subset of the tumour cells. All immunostaining was performed with appropriate controls on separate slides. The final diagnosis was GBM of the brain. OUTPUT:
Multicare_common8935
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 32-year-old woman, gravida 5 para 2, had no regular prenatal care before 24 weeks of gestation. During pregnancy, the mother was smoking 15 cigarettes per day. An unfavorable prognosis to the fetus was predicted and conservative management of prenatal care had been chosen. The woman was admitted to the tertiary level obstetrics and gynecology clinic during active stage of labor, at gestational age of 42 weeks. Despite unfavorable prognosis to the fetus, mother had chosen intrapartum fetal heart monitoring. Due to fetal distress at a cervical dilation of 6 cm, cesarean section was performed. The newborn was a female of 3300 g weight and 44 cm height who scored 8 (1 min) and 8 (5 min) on Apgar scale (Figure 3, Supporting Information Video 1 in Supplementary Material available online at http://dx.doi.org/10.1155/2016/5097059). At birth, the infant had hypotonia, weak cry, and generalized facial cyanosis. Ectopic heart with partial absence of the pericardium was beating outside the thoracic cavity, at a rate of 130/min with remittent bradycardia. After birth, the infant's heart was covered with warm saline-soaked sterile dressing. The newborn girl was transferred to the specialized cardiac surgery centre, children's intensive care unit. She died within 24 hours. The parents declined postmortem newborn's autopsy.\nOUTPUT:" }, { "from": "agent", "value": "Thoracic Ectopia Cordis, Septal Ventricular Defect, Anterior Abdominal Wall Defect, Supraumbilical Omphalocele" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 32-year-old woman, gravida 5 para 2, had no regular prenatal care before 24 weeks of gestation. During pregnancy, the mother was smoking 15 cigarettes per day. An unfavorable prognosis to the fetus was predicted and conservative management of prenatal care had been chosen. The woman was admitted to the tertiary level obstetrics and gynecology clinic during active stage of labor, at gestational age of 42 weeks. Despite unfavorable prognosis to the fetus, mother had chosen intrapartum fetal heart monitoring. Due to fetal distress at a cervical dilation of 6 cm, cesarean section was performed. The newborn was a female of 3300 g weight and 44 cm height who scored 8 (1 min) and 8 (5 min) on Apgar scale (Figure 3, Supporting Information Video 1 in Supplementary Material available online at http://dx.doi.org/10.1155/2016/5097059). At birth, the infant had hypotonia, weak cry, and generalized facial cyanosis. Ectopic heart with partial absence of the pericardium was beating outside the thoracic cavity, at a rate of 130/min with remittent bradycardia. After birth, the infant's heart was covered with warm saline-soaked sterile dressing. The newborn girl was transferred to the specialized cardiac surgery centre, children's intensive care unit. She died within 24 hours. The parents declined postmortem newborn's autopsy. OUTPUT:
Multicare_common5061
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: During mother's fifth pregnancy, polyhydramnios at 30 weeks gestation led to a diagnosis of dextrocardia, single atrioventricular valve, and unobstructed double-outlet right ventricle in the fetus. Prenatal MRI at 34 weeks gestation demonstrated a left frontal hemorrhagic infarction. This boy was born at 36 weeks 5 days gestation following induction with a birthweight of 2770 grams (80th percentile), head circumference of 32.5 cm (50th percentile), and Apgar scores of 8 at one and five minutes. Placental pathology demonstrated a small intervillous hematoma, and the feto : placental weight ratio was low at 6 : 3, but there was no histological evidence for chorioamnionitis. Chromosomal analysis and testing for a 22q11 deletion were normal. An MRI at 10 days of age showed multiple subacute and chronic areas of parenchymal hemorrhagic infarction within the frontal lobes, left occipital lobe, and left cerebellum as well as a right porencephalic cyst, hypoplastic corpus callosum, and delay in myelination. In addition, the child had a seizure disorder, cortical visual impairment, microcephaly, and severe language impairment. During the mother's sixth and last pregnancy, she noticed weakness of her right arm and face with slight right leg weakness and slurred speech at 23 weeks 3 days gestation. Initial investigation and management were done at another site. An MRI and magnetic resonance angiogram demonstrated a left frontal lobe hemorrhagic infarction as well as confluent signal abnormalities in the periventricular white matter and posterior limb of the internal capsule. While carotid ultrasounds were normal, a transesophageal echocardiogram showed a patent foramen ovale. Heparin was initiated and used for two weeks. There has been no recurrence of stroke symptoms, but significant short-term memory loss and migraine headaches persist.\nOUTPUT:" }, { "from": "agent", "value": "Spastic quadriplegic cerebral palsy, Complex congenital heart disease" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: During mother's fifth pregnancy, polyhydramnios at 30 weeks gestation led to a diagnosis of dextrocardia, single atrioventricular valve, and unobstructed double-outlet right ventricle in the fetus. Prenatal MRI at 34 weeks gestation demonstrated a left frontal hemorrhagic infarction. This boy was born at 36 weeks 5 days gestation following induction with a birthweight of 2770 grams (80th percentile), head circumference of 32.5 cm (50th percentile), and Apgar scores of 8 at one and five minutes. Placental pathology demonstrated a small intervillous hematoma, and the feto : placental weight ratio was low at 6 : 3, but there was no histological evidence for chorioamnionitis. Chromosomal analysis and testing for a 22q11 deletion were normal. An MRI at 10 days of age showed multiple subacute and chronic areas of parenchymal hemorrhagic infarction within the frontal lobes, left occipital lobe, and left cerebellum as well as a right porencephalic cyst, hypoplastic corpus callosum, and delay in myelination. In addition, the child had a seizure disorder, cortical visual impairment, microcephaly, and severe language impairment. During the mother's sixth and last pregnancy, she noticed weakness of her right arm and face with slight right leg weakness and slurred speech at 23 weeks 3 days gestation. Initial investigation and management were done at another site. An MRI and magnetic resonance angiogram demonstrated a left frontal lobe hemorrhagic infarction as well as confluent signal abnormalities in the periventricular white matter and posterior limb of the internal capsule. While carotid ultrasounds were normal, a transesophageal echocardiogram showed a patent foramen ovale. Heparin was initiated and used for two weeks. There has been no recurrence of stroke symptoms, but significant short-term memory loss and migraine headaches persist. OUTPUT:
Multicare_common6657
[ { "from": "human", "value": "As a physician engaged 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 8-year old female patient presented in the pediatric unit with abdominal discomfort, nausea and bitter vomitus. Physical examination revealed a mass in the abdomen. Abdominal ultrasound sonography revealed a 3 cm large mass in the head of the pancreas. Endoscopic sonography confirmed a cystic tumor of the pancreatic caput and fine needle biopsies were taken for histopathology, Fig. 1a & b. Blood chemistry revealed elevated c-reactive protein (CRP: 7.2 mg/dl; normal range <0.5 mg/dl) and high white blood count (WBC: 16.2/nl; normal range: 4-10/nl). Serum lipase was mildly elevated (179 U/l; normal range: < 60 U/l). All liver enzymes including bilirubin were within normal range. Equally, the tumor markers carbohydrate antigen 19-9 (CA 19-9), carcinoembryonic antigen (CEA) and chromogranin A were within normal limits. Magnet resonance imaging (MRI) of the abdomen showed a thick-walled, cystic mass in the head of the pancreas with compression of the duodenum, Fig. 2a-c. Histopathology from the fine needle biopsies was inconclusive. The case was discussed at the interdisciplinary board and surgical exploration was recommended. A well capsulated mass of the pancreatic head without macroscopic signs of malignancy was found and completely enucleated during laparotomy, Fig. 3. Surgery and recovery were uneventful and the patient was discharged 7 days later with normal pancreatic function. Histopathology confirmed the diagnosis of SPN following positive stains on immunohistochemistry with antitrypsin, vimentin, beta-catenin, CD 56 and CD 10, Fig. 4a-f.\nOUTPUT:" }, { "from": "agent", "value": "Gastric outlet obstruction, Solid-pseudopapillary neoplasm of the pancreas" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 8-year old female patient presented in the pediatric unit with abdominal discomfort, nausea and bitter vomitus. Physical examination revealed a mass in the abdomen. Abdominal ultrasound sonography revealed a 3 cm large mass in the head of the pancreas. Endoscopic sonography confirmed a cystic tumor of the pancreatic caput and fine needle biopsies were taken for histopathology, Fig. 1a & b. Blood chemistry revealed elevated c-reactive protein (CRP: 7.2 mg/dl; normal range <0.5 mg/dl) and high white blood count (WBC: 16.2/nl; normal range: 4-10/nl). Serum lipase was mildly elevated (179 U/l; normal range: < 60 U/l). All liver enzymes including bilirubin were within normal range. Equally, the tumor markers carbohydrate antigen 19-9 (CA 19-9), carcinoembryonic antigen (CEA) and chromogranin A were within normal limits. Magnet resonance imaging (MRI) of the abdomen showed a thick-walled, cystic mass in the head of the pancreas with compression of the duodenum, Fig. 2a-c. Histopathology from the fine needle biopsies was inconclusive. The case was discussed at the interdisciplinary board and surgical exploration was recommended. A well capsulated mass of the pancreatic head without macroscopic signs of malignancy was found and completely enucleated during laparotomy, Fig. 3. Surgery and recovery were uneventful and the patient was discharged 7 days later with normal pancreatic function. Histopathology confirmed the diagnosis of SPN following positive stains on immunohistochemistry with antitrypsin, vimentin, beta-catenin, CD 56 and CD 10, Fig. 4a-f. OUTPUT:
Multicare_common1799
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: When she was 13 years old, she had a 48-hour ambulatory EEG, which was normal. She had multiple events that were associated with muscle artifact but no epileptiform discharges. She returned to our facility a few months later, at which time she was taking valproic acid, levetiracetam, and clorazepate. She continued to have multiple eyelid fluttering episodes daily. She was again evaluated in the epilepsy monitoring unit. At that time, she had multiple push-button events for eyelid fluttering with a normal EEG. She was weaned off of valproic acid during that hospitalization and has remained off of this medication. She had a brain magnetic resonance imaging during that hospitalization that showed T1-hyperintense signal and decreased susceptibility signal within the globi pallidi bilaterally in a symmetric pattern and a head CT that showed moderate progression of calcifications in the bilateral globi pallidi and the subcortical white matter of both frontal lobes when compared with the prior CT done at age 5 years (Figures 3 and 4). Two months after her hospitalization, she was reevaluated in clinic and was weaned off of clorazepate. Three months later, she had a 24-hour ambulatory EEG, which was normal, and she was weaned off of levetiracetam. She had a repeat EEG 4 months after coming off of all medications, which showed generalized epileptiform discharges; a photoparoxysmal response which did not change even after using a blue filter; and 2 episodes of eyelid flutter associated with generalized epileptiform discharges suspicious for generalized nonconvulsive seizures. She was restarted on levetiracetam and remains on this medication. Most recently, an EEG was repeated after reinitiating levetiracetam and continues to show generalized epileptiform discharges, some of which were induced by eye closure and a generalized photoparoxysmal response.\nOUTPUT:" }, { "from": "agent", "value": "Intractable Generalized Epilepsy, Autosomal Dominant Hypocalcemia, Intellectual Disability, Impulse Control Disorder" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: When she was 13 years old, she had a 48-hour ambulatory EEG, which was normal. She had multiple events that were associated with muscle artifact but no epileptiform discharges. She returned to our facility a few months later, at which time she was taking valproic acid, levetiracetam, and clorazepate. She continued to have multiple eyelid fluttering episodes daily. She was again evaluated in the epilepsy monitoring unit. At that time, she had multiple push-button events for eyelid fluttering with a normal EEG. She was weaned off of valproic acid during that hospitalization and has remained off of this medication. She had a brain magnetic resonance imaging during that hospitalization that showed T1-hyperintense signal and decreased susceptibility signal within the globi pallidi bilaterally in a symmetric pattern and a head CT that showed moderate progression of calcifications in the bilateral globi pallidi and the subcortical white matter of both frontal lobes when compared with the prior CT done at age 5 years (Figures 3 and 4). Two months after her hospitalization, she was reevaluated in clinic and was weaned off of clorazepate. Three months later, she had a 24-hour ambulatory EEG, which was normal, and she was weaned off of levetiracetam. She had a repeat EEG 4 months after coming off of all medications, which showed generalized epileptiform discharges; a photoparoxysmal response which did not change even after using a blue filter; and 2 episodes of eyelid flutter associated with generalized epileptiform discharges suspicious for generalized nonconvulsive seizures. She was restarted on levetiracetam and remains on this medication. Most recently, an EEG was repeated after reinitiating levetiracetam and continues to show generalized epileptiform discharges, some of which were induced by eye closure and a generalized photoparoxysmal response. OUTPUT:
Multicare_common8668
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 48-year-old man was referred by an orthopedic surgeon due to suspicious generalized osteoporosis and multiple long bone fractures. He had two long bone fractures in his right extreme upper and lower points occurred during last six months, with negative history of the major traumatic events. The patient fractures were managed by open reduction and internal fixation surgery, respectively (Figure 1). On the first visit, he was complaining from generalized bone pain and muscle weakness. He also showed a history of polyuria and polydipsia with a clear history of severe renal colic with the passage of large stones. Laboratory data obtained are summarized in Table 1. Ultrasonographic examination of kidneys and thyroid gland revealed multiple kidney stones in both side and a well-defined hypoechoic mass measuring 12 x 13 x 11 mm in the right inferior thyroid lobe. A generalized osteoporotic feature was obvious in extremities, thoracic and lumbosacral vertebrae, and iliac bones. A classic neck exploration with a horizontal thyroid incision was performed. All other three glands were examined grossly during surgery and no abnormality was found. Serum calcium level returned to normal level (9.7 mg/dl) in 24-hour postoperatively. PTH level on 3rd postoperative day was in the normal range. Patient complaint of muscle weakness and bone pain disappeared during the first week postoperatively.\nOUTPUT:" }, { "from": "agent", "value": "Parathyroid adenoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 48-year-old man was referred by an orthopedic surgeon due to suspicious generalized osteoporosis and multiple long bone fractures. He had two long bone fractures in his right extreme upper and lower points occurred during last six months, with negative history of the major traumatic events. The patient fractures were managed by open reduction and internal fixation surgery, respectively (Figure 1). On the first visit, he was complaining from generalized bone pain and muscle weakness. He also showed a history of polyuria and polydipsia with a clear history of severe renal colic with the passage of large stones. Laboratory data obtained are summarized in Table 1. Ultrasonographic examination of kidneys and thyroid gland revealed multiple kidney stones in both side and a well-defined hypoechoic mass measuring 12 x 13 x 11 mm in the right inferior thyroid lobe. A generalized osteoporotic feature was obvious in extremities, thoracic and lumbosacral vertebrae, and iliac bones. A classic neck exploration with a horizontal thyroid incision was performed. All other three glands were examined grossly during surgery and no abnormality was found. Serum calcium level returned to normal level (9.7 mg/dl) in 24-hour postoperatively. PTH level on 3rd postoperative day was in the normal range. Patient complaint of muscle weakness and bone pain disappeared during the first week postoperatively. OUTPUT:
Multicare_common2411
[ { "from": "human", "value": "As a physician engaged 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 with a long history of arterial hypertension under ACEI, complicated by end-stage kidney disease was placed on automated peritoneal dialysis (APD) for 21 months with a KT/V urea at 1,69. The patient was also under calcium carbonate for secondary hyperparathyroidism diagnosed during her follow-up (a PTH at 780 pg/ml). The patient was consulted for erythematous, necrotic, and painful skin lesions of her right leg (Figure 3.1). The clinical examination found inflammatory signs with redness and pain around these lesions. Peripheral pulses were present and symmetrical. Her body mass index was at 28,3 kg/m2. The lesions worsened and spread to the contralateral leg within 5 days (Figure 3.2). CT angiography did not indicate stenosis of the vascular axes but showed diffuse calcifications that extended to the lower limbs. The initial treatment consisted of the correction of anemia with erythropoietin to optimize the tissue perfusion as well as analgesics to manage the pain. Parathyroidectomy was performed as soon to control the disturbances of the phosphocalcic balance and the PTH levels decreased to 417 pg/ml the 2nd day after parathyroidectomy. Necrosectomy with local care and optimization of dialysis parameters were also implemented. A treatment based on sodium thiosulfate and hyperbaric oxygen was proposed to our patient but was not performed due to a lack of her financial resources. Fortunately, the complete healing of the lesions was obtained by 4 months (Figure 5).\nOUTPUT:" }, { "from": "agent", "value": "Calciphylaxis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 69-year-old woman with a long history of arterial hypertension under ACEI, complicated by end-stage kidney disease was placed on automated peritoneal dialysis (APD) for 21 months with a KT/V urea at 1,69. The patient was also under calcium carbonate for secondary hyperparathyroidism diagnosed during her follow-up (a PTH at 780 pg/ml). The patient was consulted for erythematous, necrotic, and painful skin lesions of her right leg (Figure 3.1). The clinical examination found inflammatory signs with redness and pain around these lesions. Peripheral pulses were present and symmetrical. Her body mass index was at 28,3 kg/m2. The lesions worsened and spread to the contralateral leg within 5 days (Figure 3.2). CT angiography did not indicate stenosis of the vascular axes but showed diffuse calcifications that extended to the lower limbs. The initial treatment consisted of the correction of anemia with erythropoietin to optimize the tissue perfusion as well as analgesics to manage the pain. Parathyroidectomy was performed as soon to control the disturbances of the phosphocalcic balance and the PTH levels decreased to 417 pg/ml the 2nd day after parathyroidectomy. Necrosectomy with local care and optimization of dialysis parameters were also implemented. A treatment based on sodium thiosulfate and hyperbaric oxygen was proposed to our patient but was not performed due to a lack of her financial resources. Fortunately, the complete healing of the lesions was obtained by 4 months (Figure 5). OUTPUT:
Multicare_common926
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 50-year-old female patient was admitted with chest tightness and shortness of breath after activities. The patient denied previous cardiovascular antecedents and family history. She reported a history of right radical mastectomy performed 10 years ago. She did not receive radiotherapy, chemotherapy, or endocrine treatment after the operation. On admission, the patient's body temperature was normal (36.5 C) with a blood pressure of 139/70 mmHg, and a heart rate of 84 bpm. The patient was 158 cm tall and weighed 61.3 kg. Physical examination revealed a grade III/VI systolic murmur at the left sternal margin. Jugular venous distention, generalized edema, and shifting dullness indicated severe right heart failure. The liver was enlarged, exceeding one transverse finger below the costal margin. By palpation, the liver edge felt slightly firm. There was no tenderness or rebound pain in the abdomen. The patient did not complain of other symptoms. The physical examination showed no positive signs of other systems. Electrocardiography showed sinus rhythm, right axis deviation, and incomplete right bundle branch block (Supplementary Figure 1). Routine blood examination: Hemoglobin level was 147 g/L; hematocrit level was 43.3%; and serum leukocyte and platelet levels were 3.93 x 109/L and 175 x 109/L, respectively. The biochemical investigation showed no alteration in the following serum levels: liver enzymes, albumin, urea, creatinine, potassium, glucose, and sodium. Direct and indirect bilirubin levels were elevated (20.89 and 33.88 mumol/L, respectively). Myocardial enzymes and myocardial markers including creatine kinase (CK), creatine kinase isoenzyme mass (CK-MB), myoglobin (MYO), and high-sensitivity troponin T (HS-TnT) were normal. B-type natriuretic peptide (BNP) level was 3,732.00 pg/mL. The blood tests for tumor markers were not evident except for an elevated CA125 level of 240 U/mL.\nOUTPUT:" }, { "from": "agent", "value": "Cardiac venous malformation, Multiple hepatic venous malformations" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 50-year-old female patient was admitted with chest tightness and shortness of breath after activities. The patient denied previous cardiovascular antecedents and family history. She reported a history of right radical mastectomy performed 10 years ago. She did not receive radiotherapy, chemotherapy, or endocrine treatment after the operation. On admission, the patient's body temperature was normal (36.5 C) with a blood pressure of 139/70 mmHg, and a heart rate of 84 bpm. The patient was 158 cm tall and weighed 61.3 kg. Physical examination revealed a grade III/VI systolic murmur at the left sternal margin. Jugular venous distention, generalized edema, and shifting dullness indicated severe right heart failure. The liver was enlarged, exceeding one transverse finger below the costal margin. By palpation, the liver edge felt slightly firm. There was no tenderness or rebound pain in the abdomen. The patient did not complain of other symptoms. The physical examination showed no positive signs of other systems. Electrocardiography showed sinus rhythm, right axis deviation, and incomplete right bundle branch block (Supplementary Figure 1). Routine blood examination: Hemoglobin level was 147 g/L; hematocrit level was 43.3%; and serum leukocyte and platelet levels were 3.93 x 109/L and 175 x 109/L, respectively. The biochemical investigation showed no alteration in the following serum levels: liver enzymes, albumin, urea, creatinine, potassium, glucose, and sodium. Direct and indirect bilirubin levels were elevated (20.89 and 33.88 mumol/L, respectively). Myocardial enzymes and myocardial markers including creatine kinase (CK), creatine kinase isoenzyme mass (CK-MB), myoglobin (MYO), and high-sensitivity troponin T (HS-TnT) were normal. B-type natriuretic peptide (BNP) level was 3,732.00 pg/mL. The blood tests for tumor markers were not evident except for an elevated CA125 level of 240 U/mL. OUTPUT:
Multicare_common6910
[ { "from": "human", "value": "As a physician engaged 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 could not identify any specific cause and received new-generation antihistamines and systemic corticosteroids several times a month to manage his symptoms. See Table 1 for the test results obtained during the first visit. According to the manufacturer's instructions, total IgE levels, sIgE and serum Tryptase were measured using the ImmunoCAP system (Thermo-Fisher, Uppsala, Sweden). However, 2 months ago, while commuting to work, she experienced an episode of itching, restlessness, and loss of consciousness. She was immediately taken to the emergency room, received first aid, and was discharged after 12 h of observation. According to the patient, before leaving home, she had breakfast, which included bread and other wheat products. During this period, she did not take non-steroidal anti-inflammatory drugs, had no signs of infection, and had no menstrual period. Following the episode, the patient underwent a diagnostic study called multiplex component-based allergen microarray test (MADx), which revealed a positive analysis for omega-5-gliadin (Table 2). The highest measured IgE concentration per allergen group is as follows: <0.3 kUA/L (negative or uncertain), 0.3-1 kUA/L (low IgE level), 1-5 kUA/L (moderate IgE level), 5-15 kUA/L (high IgE level), and >15 kUA/L (very-high IgE level). There is no clinical relevance for other positive allergens. Based on these findings, the patient has been diagnosed with WDEIA. After the mentioned episode, the patient is on a gluten-free diet, during which no episode of anaphylaxis occurred.\nOUTPUT:" }, { "from": "agent", "value": "Wheat-dependent exercise-induced anaphylaxis, Chronic spontaneous urticaria" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: He could not identify any specific cause and received new-generation antihistamines and systemic corticosteroids several times a month to manage his symptoms. See Table 1 for the test results obtained during the first visit. According to the manufacturer's instructions, total IgE levels, sIgE and serum Tryptase were measured using the ImmunoCAP system (Thermo-Fisher, Uppsala, Sweden). However, 2 months ago, while commuting to work, she experienced an episode of itching, restlessness, and loss of consciousness. She was immediately taken to the emergency room, received first aid, and was discharged after 12 h of observation. According to the patient, before leaving home, she had breakfast, which included bread and other wheat products. During this period, she did not take non-steroidal anti-inflammatory drugs, had no signs of infection, and had no menstrual period. Following the episode, the patient underwent a diagnostic study called multiplex component-based allergen microarray test (MADx), which revealed a positive analysis for omega-5-gliadin (Table 2). The highest measured IgE concentration per allergen group is as follows: <0.3 kUA/L (negative or uncertain), 0.3-1 kUA/L (low IgE level), 1-5 kUA/L (moderate IgE level), 5-15 kUA/L (high IgE level), and >15 kUA/L (very-high IgE level). There is no clinical relevance for other positive allergens. Based on these findings, the patient has been diagnosed with WDEIA. After the mentioned episode, the patient is on a gluten-free diet, during which no episode of anaphylaxis occurred. OUTPUT:
Multicare_common1011
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Mr. L. S. was a 67-year-old gent who presented to the emergency department of a large regional hospital with a one-day history of lower abdominal pain, nausea, and vomiting. He had been discharged two days previously after a three-day admission under a general medical team with vomiting and diarrhoea, presumed to be secondary to gastroenteritis. The examination revealed a moderately obese gent with a distended abdomen and generalised abdominal tenderness. The patient was haemodynamically stable with no signs of peritonism. A small reducible umbilical hernia was present. On complete blood count, the patient was shown to have a leukocytosis of 20.1 x 109/L, with a neutrophilia of 16.76 x 109/L. His electrolytes were unremarkable; however, evidence of acute renal failure was apparent with a high creatinine of 236 umol/L and an eGFR of 24. Given the above findings, a CT scan was performed (Figure 1). The large bowel was completely collapsed. The lesion was reported as a possible foreign body or gallstone ileus. Mr. L. S. was taken to the operating theatre for a laparoscopy. This revealed a transition point in the distal ileum; however, the obstructing lesion was not identified. The operation was converted to an open laparotomy. The foreign body was discovered close to the ileocaecal junction and milked proximally. Enterotomy was performed, and a nectarine pit was retrieved. The enterotomy was closed primarily. A short segment of ileum was resected, and a side-side anastomosis was performed with a linear stapler. After a 24-hour stay in ICU, the patient was discharged to the ward. The rest of his stay was unremarkable, and he was discharged on postoperative day 5. On later questioning, Mr. L. S. was unable to recall eating a nectarine in the days leading up to his admission; however, his wife stated that they had been eating nectarines over the last week.\nOUTPUT:" }, { "from": "agent", "value": "Small bowel obstruction and perforation" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Mr. L. S. was a 67-year-old gent who presented to the emergency department of a large regional hospital with a one-day history of lower abdominal pain, nausea, and vomiting. He had been discharged two days previously after a three-day admission under a general medical team with vomiting and diarrhoea, presumed to be secondary to gastroenteritis. The examination revealed a moderately obese gent with a distended abdomen and generalised abdominal tenderness. The patient was haemodynamically stable with no signs of peritonism. A small reducible umbilical hernia was present. On complete blood count, the patient was shown to have a leukocytosis of 20.1 x 109/L, with a neutrophilia of 16.76 x 109/L. His electrolytes were unremarkable; however, evidence of acute renal failure was apparent with a high creatinine of 236 umol/L and an eGFR of 24. Given the above findings, a CT scan was performed (Figure 1). The large bowel was completely collapsed. The lesion was reported as a possible foreign body or gallstone ileus. Mr. L. S. was taken to the operating theatre for a laparoscopy. This revealed a transition point in the distal ileum; however, the obstructing lesion was not identified. The operation was converted to an open laparotomy. The foreign body was discovered close to the ileocaecal junction and milked proximally. Enterotomy was performed, and a nectarine pit was retrieved. The enterotomy was closed primarily. A short segment of ileum was resected, and a side-side anastomosis was performed with a linear stapler. After a 24-hour stay in ICU, the patient was discharged to the ward. The rest of his stay was unremarkable, and he was discharged on postoperative day 5. On later questioning, Mr. L. S. was unable to recall eating a nectarine in the days leading up to his admission; however, his wife stated that they had been eating nectarines over the last week. OUTPUT:
Multicare_common3529
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 51-year-old hypertensive Pakistani male patient was admitted in the cardiac intensive care unit in King Fahd University Hospital on 30 July 2017 complaining of chest and back pain for two weeks prior to the presentation; he took nonsteroidal anti-inflammatory drugs but were not effective. Physical examination was done in the emergency department and revealed stable vital signs; the patient was conscious, moving all his limbs; there were warm palpable pulses of the upper arms. There was no other evidence of vascular dissection or occlusion below the level of the renal arteries (Figures 1 and 2). The patient underwent general anesthesia for thoracic endovascular repair (TEVAR) two days after his first day of admission; the procedure was done through the right femoral approach; an angiogram was performed intraoperatively (Figure 3). Stent graft with a size of 34 mm x 15 cm was used and deployed into the descending thoracic aorta; the intimal entry tear was completely covered by the stent, and the false lumen was obliterated. The patient was postoperatively moving all his limbs, and the peripheral pulses were intact. He got discharged one day after the surgery and was doing well afterward. We evaluated patient's prognosis by following up for 3 to 6 months for a chest X-ray, CTA, and CT aorta 3D reconstruction (Figures 4 and 5) which confirmed no endovascular leak as well as no ischemic or stroke signs in the clinical follow-up; we assessed the patency of the subclavian arteries by examining the bilateral upper arms' blood supply in addition to radial arteries by evaluating the pulses with no evidence of morbidity.\nOUTPUT:" }, { "from": "agent", "value": "Right Aberrant Subclavian Artery, Kommerell's Diverticulum, Isolated Left Vertebral Artery, Type B Aortic Dissection" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 51-year-old hypertensive Pakistani male patient was admitted in the cardiac intensive care unit in King Fahd University Hospital on 30 July 2017 complaining of chest and back pain for two weeks prior to the presentation; he took nonsteroidal anti-inflammatory drugs but were not effective. Physical examination was done in the emergency department and revealed stable vital signs; the patient was conscious, moving all his limbs; there were warm palpable pulses of the upper arms. There was no other evidence of vascular dissection or occlusion below the level of the renal arteries (Figures 1 and 2). The patient underwent general anesthesia for thoracic endovascular repair (TEVAR) two days after his first day of admission; the procedure was done through the right femoral approach; an angiogram was performed intraoperatively (Figure 3). Stent graft with a size of 34 mm x 15 cm was used and deployed into the descending thoracic aorta; the intimal entry tear was completely covered by the stent, and the false lumen was obliterated. The patient was postoperatively moving all his limbs, and the peripheral pulses were intact. He got discharged one day after the surgery and was doing well afterward. We evaluated patient's prognosis by following up for 3 to 6 months for a chest X-ray, CTA, and CT aorta 3D reconstruction (Figures 4 and 5) which confirmed no endovascular leak as well as no ischemic or stroke signs in the clinical follow-up; we assessed the patency of the subclavian arteries by examining the bilateral upper arms' blood supply in addition to radial arteries by evaluating the pulses with no evidence of morbidity. OUTPUT:
Multicare_common3089
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 60-year old woman known to have diabetes, hypertension, dyslipidemia, morbid obesity and chronic obstructive pulmonary disease presented to the emergency department (ED) with a 3- week history of vague abdominal pain on the right side of the abdomen. The severity of abdominal pain had increased over 3 days prior to the index admission, and was associated with fever. There was no past history of surgical intervention. The initial physical examination revealed high body temperature of 38.5 C, diffuse abdominal tenderness on the right side of the abdomen extending from right inguinal region up to the right flank along with erythema and fluctuation. Laboratory findings showed elevated blood sugar of 17.5 mmol/L. white cell count (13.8 x 109/L), low hemoglobin (10.7 g/L), and normal platelet count (235 109/L), urea (6.05 mmol/L) and bilirubin (16.1 mumol/L). Fig. 1(A&B) shows ultrasound findings. The patient was taken to the operating room. There was a considerable amount of pus but the cavity was seen communicating with the inguinal canal forming an inguinal abscess. The incision was extended towards the inguinal canal for proper exposure and drainage. On opening the inguinal canal, there was small bowel along with cecum, and severely inflamed appendix with obvious perforation. The inguinal canal was completely opened and the abdominal cavity in the right iliac fossa was explored through it. Fig. 2(A&B) shows the intraoperative findings. A standard open appendectomy was done. The peritoneum and inguinal canal were closed, we used proline suture without mesh. Due to the multiple co-morbid conditions, the patient was shifted to surgical intensive care unit for monitoring and kept on regular intravenous antibiotics. She was kept on daily wash of the abscess cavity. Over a period of 3 weeks there was good granulation tissue. Later on, the patient was discharged in a stable condition and followed up in outpatient clinic.\nOUTPUT:" }, { "from": "agent", "value": "Acute appendicitis, Abdominal wall abscess" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 60-year old woman known to have diabetes, hypertension, dyslipidemia, morbid obesity and chronic obstructive pulmonary disease presented to the emergency department (ED) with a 3- week history of vague abdominal pain on the right side of the abdomen. The severity of abdominal pain had increased over 3 days prior to the index admission, and was associated with fever. There was no past history of surgical intervention. The initial physical examination revealed high body temperature of 38.5 C, diffuse abdominal tenderness on the right side of the abdomen extending from right inguinal region up to the right flank along with erythema and fluctuation. Laboratory findings showed elevated blood sugar of 17.5 mmol/L. white cell count (13.8 x 109/L), low hemoglobin (10.7 g/L), and normal platelet count (235 109/L), urea (6.05 mmol/L) and bilirubin (16.1 mumol/L). Fig. 1(A&B) shows ultrasound findings. The patient was taken to the operating room. There was a considerable amount of pus but the cavity was seen communicating with the inguinal canal forming an inguinal abscess. The incision was extended towards the inguinal canal for proper exposure and drainage. On opening the inguinal canal, there was small bowel along with cecum, and severely inflamed appendix with obvious perforation. The inguinal canal was completely opened and the abdominal cavity in the right iliac fossa was explored through it. Fig. 2(A&B) shows the intraoperative findings. A standard open appendectomy was done. The peritoneum and inguinal canal were closed, we used proline suture without mesh. Due to the multiple co-morbid conditions, the patient was shifted to surgical intensive care unit for monitoring and kept on regular intravenous antibiotics. She was kept on daily wash of the abscess cavity. Over a period of 3 weeks there was good granulation tissue. Later on, the patient was discharged in a stable condition and followed up in outpatient clinic. OUTPUT:
Multicare_common5089
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Timeline: the patient was born to normal parents with consanguineous marriage, and no other family member had a similar syndrome. She was diagnosed with XP when she was 2 months old, and she had no specific neurodegenerative condition at the time of consultation. Diagnostic assessment: a panoramic radiograph was performed as the limited mouth opening did not allow the use of retro alveolar radiographs (Figure 1D). A periodontal probing was performed and revealed the presence of periodontal pockets, localized to the lower incisors. The dermatologist was contacted to seek other medical information about the patient and to discuss the treatment approaches. Therapeutic intervention: the first appointment was short and dedicated to emergency care. Before the oral examination, the UV at the office was assessed with a UV-meter (Figure 1E), and UV exposure was checked for a safe environment. At first, patient care included protection against UV rays. Indeed, the patient was equipped with her sunscreen that she renewed every hour, and the appointment was given at the end of the afternoon. The light was kept off at the perioperative area and a UV filter was used over the surgical light while the patient kept her sunglasses on her eyes. Periodontal treatment included hygiene motivation and teaching of proper brushing methods followed by ultrasonic scaling. Decay removal was carried out by using an electrical handpiece ball burr on low speed, the filling was done using a self-curing glass ionomer restorative material (RIVA SELF CURE*). The patient was seen one week after the elimination of etiological factors and root planning was realized. Follow-up and outcomes: after 2 months, a re-evaluation was performed, the pain had disappeared, the bleeding had stopped, and the depth of the pockets had decreased. A maintenance phase was initiated, to see the patient twice a year. The sessions include hygiene motivation and plaque control. Patient perspective: the patient expressed her gratitude for the care she received and expressed optimism about her condition's progress. Informed consent: because her condition was unusual, the patient agreed to the publication of a case incorporating her clinical data because she wished to aid in the treatment of similar cases in the future.\nOUTPUT:" }, { "from": "agent", "value": "Xeroderma pigmentosum, moderate localized periodontitis, dental crowding, inflammation of the gum, several caries" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Timeline: the patient was born to normal parents with consanguineous marriage, and no other family member had a similar syndrome. She was diagnosed with XP when she was 2 months old, and she had no specific neurodegenerative condition at the time of consultation. Diagnostic assessment: a panoramic radiograph was performed as the limited mouth opening did not allow the use of retro alveolar radiographs (Figure 1D). A periodontal probing was performed and revealed the presence of periodontal pockets, localized to the lower incisors. The dermatologist was contacted to seek other medical information about the patient and to discuss the treatment approaches. Therapeutic intervention: the first appointment was short and dedicated to emergency care. Before the oral examination, the UV at the office was assessed with a UV-meter (Figure 1E), and UV exposure was checked for a safe environment. At first, patient care included protection against UV rays. Indeed, the patient was equipped with her sunscreen that she renewed every hour, and the appointment was given at the end of the afternoon. The light was kept off at the perioperative area and a UV filter was used over the surgical light while the patient kept her sunglasses on her eyes. Periodontal treatment included hygiene motivation and teaching of proper brushing methods followed by ultrasonic scaling. Decay removal was carried out by using an electrical handpiece ball burr on low speed, the filling was done using a self-curing glass ionomer restorative material (RIVA SELF CURE*). The patient was seen one week after the elimination of etiological factors and root planning was realized. Follow-up and outcomes: after 2 months, a re-evaluation was performed, the pain had disappeared, the bleeding had stopped, and the depth of the pockets had decreased. A maintenance phase was initiated, to see the patient twice a year. The sessions include hygiene motivation and plaque control. Patient perspective: the patient expressed her gratitude for the care she received and expressed optimism about her condition's progress. Informed consent: because her condition was unusual, the patient agreed to the publication of a case incorporating her clinical data because she wished to aid in the treatment of similar cases in the future. OUTPUT:
Multicare_common6965
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: On examination, BP: 115/70, PR: 76/min, T: 37.2 oral, RR: 16/min. Subungual hemorrhage was seen in nearly all fingers plus a purple patch on the left sole. Muscle force, DTR and the remainder of examinations were normal. TTE was done before admission and was normal. A complete blood count and results of liver function tests were normal as were plasma levels of electrolytes, ESR and CRP. Serum Creatinin level was 1.6mg/dl and urine analysis revealed proteinuria and hematuria (Table 1). Chest CT scan was done and right sided pleural effusion with multiple small nodules in right lung parenchyma was seen (Figure 2). Pleural fluid analysis was exudative (Table 2), so imipenem and ciprofloxacin were started and because of the possibility of underlying malignancy, cytologic analysis of pleural fluid was requested. On the fourth day of admission, he suddenly experiences a very severe right flank pain. Transthorasic echocardiography was repeated and this time a large size mass (12*5 mm) was seen on aortic valve that was suggestive for vegetation, so antibiotics were changed to cefazoline, ampicillin and gentamycin. During the next days Hemoglobin level dropped to 11.3gr/dl and due to thrombocytopenia and abnormal coagulation tests and fragmented RBCs in peripheral blood smear, subclinical DIC was suggested and FFP and packed cell were transfused and renal biopsy was canceled. Two days later right hemi paresis was evolved and on examination right hemiparesia without any sphinctral dysfunction or sensory abnormality was detected. This time Brain MRI revealed evidence of one hyper signal lesion in left hemisphere of cerebellum (Figure 4).\nOUTPUT:" }, { "from": "agent", "value": "Systemic Vasculitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: On examination, BP: 115/70, PR: 76/min, T: 37.2 oral, RR: 16/min. Subungual hemorrhage was seen in nearly all fingers plus a purple patch on the left sole. Muscle force, DTR and the remainder of examinations were normal. TTE was done before admission and was normal. A complete blood count and results of liver function tests were normal as were plasma levels of electrolytes, ESR and CRP. Serum Creatinin level was 1.6mg/dl and urine analysis revealed proteinuria and hematuria (Table 1). Chest CT scan was done and right sided pleural effusion with multiple small nodules in right lung parenchyma was seen (Figure 2). Pleural fluid analysis was exudative (Table 2), so imipenem and ciprofloxacin were started and because of the possibility of underlying malignancy, cytologic analysis of pleural fluid was requested. On the fourth day of admission, he suddenly experiences a very severe right flank pain. Transthorasic echocardiography was repeated and this time a large size mass (12*5 mm) was seen on aortic valve that was suggestive for vegetation, so antibiotics were changed to cefazoline, ampicillin and gentamycin. During the next days Hemoglobin level dropped to 11.3gr/dl and due to thrombocytopenia and abnormal coagulation tests and fragmented RBCs in peripheral blood smear, subclinical DIC was suggested and FFP and packed cell were transfused and renal biopsy was canceled. Two days later right hemi paresis was evolved and on examination right hemiparesia without any sphinctral dysfunction or sensory abnormality was detected. This time Brain MRI revealed evidence of one hyper signal lesion in left hemisphere of cerebellum (Figure 4). OUTPUT:
Multicare_common9267
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: CPI mainly acts via T-lymphocytes. However, recent literature suggests also a role for B cells modulating its efficacy and tolerability of CPI. In the absence of the mutation of the proto-oncogene b-raf, treatment with the PD-1 inhibitor nivolumab was initiated. This therapy was well tolerated and resulted in a deep partial response, which is ongoing for 14+ months. Flow cytometric analysis of peripheral blood mononuclear cells revealed 15% IL-10 producing and 14% CD24 and CD38 double positive regulatory B cells. Obviously, B cells were not required for the efficacy of CPI in our patient. Moreover, the depletion of regulatory B cells may have improved efficacy of CPI. Excisional surgery and sentinel lymph-node extirpation was performed: TNM classification 8th Edition (American Joint Classification of Cancer, AJCC): pT4a pN0 (sentinel lymph node negative) cM0 (no metastasis in clinical and radiologic examinations). Proto-oncogenes B-RAF, NRAS and cKIT were not mutated. In May 2019, she suffered from progressive disease with asymptomatic metastases in brain, lungs, lymph nodes and skin (stage IV M1d, AJCC). Serum levels of lactate dehydrogenase and S100 were within normal limits.\nOUTPUT:" }, { "from": "agent", "value": "Metastatic Melanoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: CPI mainly acts via T-lymphocytes. However, recent literature suggests also a role for B cells modulating its efficacy and tolerability of CPI. In the absence of the mutation of the proto-oncogene b-raf, treatment with the PD-1 inhibitor nivolumab was initiated. This therapy was well tolerated and resulted in a deep partial response, which is ongoing for 14+ months. Flow cytometric analysis of peripheral blood mononuclear cells revealed 15% IL-10 producing and 14% CD24 and CD38 double positive regulatory B cells. Obviously, B cells were not required for the efficacy of CPI in our patient. Moreover, the depletion of regulatory B cells may have improved efficacy of CPI. Excisional surgery and sentinel lymph-node extirpation was performed: TNM classification 8th Edition (American Joint Classification of Cancer, AJCC): pT4a pN0 (sentinel lymph node negative) cM0 (no metastasis in clinical and radiologic examinations). Proto-oncogenes B-RAF, NRAS and cKIT were not mutated. In May 2019, she suffered from progressive disease with asymptomatic metastases in brain, lungs, lymph nodes and skin (stage IV M1d, AJCC). Serum levels of lactate dehydrogenase and S100 were within normal limits. OUTPUT:
Multicare_common1057
[ { "from": "human", "value": "As a physician engaged 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 febrile, tachycardic, tachypneic, and hypoxemic upon arrival. The chest X-ray showed bilateral lung infiltrates for which she was treated with azithromycin, ceftriaxone, and hydroxychloroquine. At 2 weeks into her course, the patient remained obtunded off of sedation. The head CT obtained on days 16 and 25 after admission demonstrated decreased attenuation in the left subinsular cortex and the thalamic region. EEG on day 17 showed severe generalized slowing. On day 26, portable 0.06-T MRI (Hyperfine) of the brain without contrast was performed, showing areas of T2 and FLAIR hyperintensity in the left thalamus and lentiform nuclei, though technically limited (Figure 3). By day 27, she was extubated but remained confused, with the psychomotor slowed, and unable to follow commands. Clinical improvement was noted on the following day after the administration of IV lorazepam, levetiracetam, and lacosamide, with EEG transitioning to moderate background, slowing with intermittent left temporal sharp waves. A follow-up 3-T contrast-enhanced brain MRI on day 39 showed T2, FLAIR, and diffusion-weighted imaging (DWI) hyperintensity without restricted diffusion along the bilateral olfactory tracts, caudate heads, posterior commissural fibers of the fornices, hippocampal tails, and right temporal lobe (Figure 3). By day 49, the patient was discharged to rehabilitation, alert and capable of conversation, though with moderate persistent cognitive and bilateral proximal weakness. Summaries of the pertinent clinical details of each case are presented in Table 1.\nOUTPUT:" }, { "from": "agent", "value": "Acute Seizures, SARS-CoV-2, COVID-19, Acute respiratory distress syndrome, Non-convulsive status epilepticus" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: She was febrile, tachycardic, tachypneic, and hypoxemic upon arrival. The chest X-ray showed bilateral lung infiltrates for which she was treated with azithromycin, ceftriaxone, and hydroxychloroquine. At 2 weeks into her course, the patient remained obtunded off of sedation. The head CT obtained on days 16 and 25 after admission demonstrated decreased attenuation in the left subinsular cortex and the thalamic region. EEG on day 17 showed severe generalized slowing. On day 26, portable 0.06-T MRI (Hyperfine) of the brain without contrast was performed, showing areas of T2 and FLAIR hyperintensity in the left thalamus and lentiform nuclei, though technically limited (Figure 3). By day 27, she was extubated but remained confused, with the psychomotor slowed, and unable to follow commands. Clinical improvement was noted on the following day after the administration of IV lorazepam, levetiracetam, and lacosamide, with EEG transitioning to moderate background, slowing with intermittent left temporal sharp waves. A follow-up 3-T contrast-enhanced brain MRI on day 39 showed T2, FLAIR, and diffusion-weighted imaging (DWI) hyperintensity without restricted diffusion along the bilateral olfactory tracts, caudate heads, posterior commissural fibers of the fornices, hippocampal tails, and right temporal lobe (Figure 3). By day 49, the patient was discharged to rehabilitation, alert and capable of conversation, though with moderate persistent cognitive and bilateral proximal weakness. Summaries of the pertinent clinical details of each case are presented in Table 1. OUTPUT:
Multicare_common9758
[ { "from": "human", "value": "As a physician engaged 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 64-year-old female patient was initially transferred to our hospital by a smaller district clinic for further treatment after a CT-scan revealed a large left-sided kidney-stone (2 cm) accompanied by an obstructive pyelonephritis. A Double-J-Stent was placed and after successful antibiotic therapy of the pyelonephritis the patient was released from the hospitalization in order to perform a ureterorenoscopic lithotripsy and stone-extraction in an outpatient setting 3 weeks later. Due to the stone's size a complete stone-extraction was not possible in one instance which led us to a second ureterorenoscopy 5 weeks after the initial consultation. This second procedure started uneventfully with the cystoscopic removal of the Double-J-Stent and the insertion of a guide-wire. Following this the cystoscope was removed in order to insert a standard silicone Ch 12 Foley-Catheter (Nelaton-Tip) blocked with 2.5ml NaCl as it is custom for semirigid ureterorenoscopy in our clinic. Upon entering the bladder with the semirigid instrument, the position of the Foley-Catheter seemed suspicious. Further inspection revealed that the recently placed bladder-catheter led directly into the left-sided ureter. The balloon block was deflated immediately and the catheter was repositioned correctly into the bladder. We therefore decided to reinsert a Double-J-Stent and end the procedure. The already established antibiotic therapy with Ciprofloxacin due to the initial obstructive pyelonephritis preoperatively was continued for another week. 6 weeks later the patient was readmitted for control and in order to complete the stone-extraction. The stone-extraction was thus finished without any further intraoperative complications. During that hospitalization the Double-J-Stent which was exchanged during the last ureterorenoscopy was also removed. Blood-tests showed unsuspicious renal function and further sonographic controls proved normal renal drainage.\nOUTPUT:" }, { "from": "agent", "value": "Ureteral Rupture" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The 64-year-old female patient was initially transferred to our hospital by a smaller district clinic for further treatment after a CT-scan revealed a large left-sided kidney-stone (2 cm) accompanied by an obstructive pyelonephritis. A Double-J-Stent was placed and after successful antibiotic therapy of the pyelonephritis the patient was released from the hospitalization in order to perform a ureterorenoscopic lithotripsy and stone-extraction in an outpatient setting 3 weeks later. Due to the stone's size a complete stone-extraction was not possible in one instance which led us to a second ureterorenoscopy 5 weeks after the initial consultation. This second procedure started uneventfully with the cystoscopic removal of the Double-J-Stent and the insertion of a guide-wire. Following this the cystoscope was removed in order to insert a standard silicone Ch 12 Foley-Catheter (Nelaton-Tip) blocked with 2.5ml NaCl as it is custom for semirigid ureterorenoscopy in our clinic. Upon entering the bladder with the semirigid instrument, the position of the Foley-Catheter seemed suspicious. Further inspection revealed that the recently placed bladder-catheter led directly into the left-sided ureter. The balloon block was deflated immediately and the catheter was repositioned correctly into the bladder. We therefore decided to reinsert a Double-J-Stent and end the procedure. The already established antibiotic therapy with Ciprofloxacin due to the initial obstructive pyelonephritis preoperatively was continued for another week. 6 weeks later the patient was readmitted for control and in order to complete the stone-extraction. The stone-extraction was thus finished without any further intraoperative complications. During that hospitalization the Double-J-Stent which was exchanged during the last ureterorenoscopy was also removed. Blood-tests showed unsuspicious renal function and further sonographic controls proved normal renal drainage. OUTPUT:
Multicare_common1242
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Part of this case has already been reported previously. Afterwards, he became poor at ordinary conversation with his wife. Therefore, she took him to the local hospital. Because a cerebrovascular disease was suspected in the institute and the patient was recommended to consult neurosurgery, he came to our hospital on the same day as onset of the symptoms. On admission, the patient exhibited acalculia, finger agnosia, right-left disorientation, agraphia, and hemispatial agnosia. A CT scan was obtained immediately. Multiple high density spots were evident in a wide area of the left temporal, parietal, and occipital lobes on plain CT scan. They were thought to be dilated draining cortical veins. The left transverse-sigmoid sinus corresponding to the draining sinus also became larger than the right side on the CT scan. A cerebral angiography was subsequently performed. A DAVF in the left transverse-sigmoid sinus with cortical vein reflux in the left temporal, parietal, and occipital lobes was demonstrated on the left common carotid artery angiogram. Its feeding arteries were the left occipital artery, posterior auricular artery, middle meningeal artery, and superficial temporal artery (Figure 1). After the examinations, the patient was admitted to the intensive care unit. In a former axial image of 3D-CT angiography arterial phase obtained after admission, abnormal vessels appeared in the left cerebral hemisphere including the left dorsolateral prefrontal cortex (DLPFC) (Figure 2). After the three endovascular surgeries, the DAVF including the cortical vein reflux disappeared on the angiogram (Figure 3). The quantity of the antidepressants for the patient decreased after the treatment, and the patient returned to work without any antidepressant two years after the treatment.\nOUTPUT:" }, { "from": "agent", "value": "Depression, Dural arteriovenous fistula, Gerstmann's syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Part of this case has already been reported previously. Afterwards, he became poor at ordinary conversation with his wife. Therefore, she took him to the local hospital. Because a cerebrovascular disease was suspected in the institute and the patient was recommended to consult neurosurgery, he came to our hospital on the same day as onset of the symptoms. On admission, the patient exhibited acalculia, finger agnosia, right-left disorientation, agraphia, and hemispatial agnosia. A CT scan was obtained immediately. Multiple high density spots were evident in a wide area of the left temporal, parietal, and occipital lobes on plain CT scan. They were thought to be dilated draining cortical veins. The left transverse-sigmoid sinus corresponding to the draining sinus also became larger than the right side on the CT scan. A cerebral angiography was subsequently performed. A DAVF in the left transverse-sigmoid sinus with cortical vein reflux in the left temporal, parietal, and occipital lobes was demonstrated on the left common carotid artery angiogram. Its feeding arteries were the left occipital artery, posterior auricular artery, middle meningeal artery, and superficial temporal artery (Figure 1). After the examinations, the patient was admitted to the intensive care unit. In a former axial image of 3D-CT angiography arterial phase obtained after admission, abnormal vessels appeared in the left cerebral hemisphere including the left dorsolateral prefrontal cortex (DLPFC) (Figure 2). After the three endovascular surgeries, the DAVF including the cortical vein reflux disappeared on the angiogram (Figure 3). The quantity of the antidepressants for the patient decreased after the treatment, and the patient returned to work without any antidepressant two years after the treatment. OUTPUT:
Multicare_common8962
[ { "from": "human", "value": "As a physician engaged 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 histologic diagnosis prompted definitive radiotherapy (RT) to the involved whole breast to 40 Gy in 20 daily fractions (representing the standard of care at the time; RT doses in this setting have since decreased). The patient's family history was notable for prostatic and lung adenocarcinomas in first-degree relatives, and her social history was negative for tobacco or alcohol usage. Biopsy of the right orbital mass revealed recurrent extranodal marginal zone lymphoma, and for this she was treated with rituximab monotherapy for 9 months; this resulted in a metabolic complete response in the orbit and the patient has remained disease-free from her marginal zone lymphoma since that time (8 years ago) until her most recent follow-up. While the patient was receiving rituximab for her recurrent lymphoma, she underwent abdominopelvic mass excision which revealed a GIST of the small intestinal serosa measuring 21x18 cm with four mitotic figures per 50 HPF, negative margins, and positive tumor staining CD117 and CD34 (Figure 3). She received adjuvant imatinib for 12 months. She went on to have four local (abdominopelvic) recurrences of her GIST, all managed with a combination of surgical resection and (neo)adjuvant imatinib over the subsequent 7 years to the time of last follow-up. Pathology from subsequent resections revealed exon 11 c-KIT mutation. At the time of last follow-up, the patient was alive with recurrent disease (representing her fifth recurrence), with plans for neoadjuvant sorafenib and surgical resection.\nOUTPUT:" }, { "from": "agent", "value": "Primary breast lymphoma, Gastrointestinal stromal tumor" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: This histologic diagnosis prompted definitive radiotherapy (RT) to the involved whole breast to 40 Gy in 20 daily fractions (representing the standard of care at the time; RT doses in this setting have since decreased). The patient's family history was notable for prostatic and lung adenocarcinomas in first-degree relatives, and her social history was negative for tobacco or alcohol usage. Biopsy of the right orbital mass revealed recurrent extranodal marginal zone lymphoma, and for this she was treated with rituximab monotherapy for 9 months; this resulted in a metabolic complete response in the orbit and the patient has remained disease-free from her marginal zone lymphoma since that time (8 years ago) until her most recent follow-up. While the patient was receiving rituximab for her recurrent lymphoma, she underwent abdominopelvic mass excision which revealed a GIST of the small intestinal serosa measuring 21x18 cm with four mitotic figures per 50 HPF, negative margins, and positive tumor staining CD117 and CD34 (Figure 3). She received adjuvant imatinib for 12 months. She went on to have four local (abdominopelvic) recurrences of her GIST, all managed with a combination of surgical resection and (neo)adjuvant imatinib over the subsequent 7 years to the time of last follow-up. Pathology from subsequent resections revealed exon 11 c-KIT mutation. At the time of last follow-up, the patient was alive with recurrent disease (representing her fifth recurrence), with plans for neoadjuvant sorafenib and surgical resection. OUTPUT:
Multicare_common1177
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: His past medical history included three gunshot wounds on separate occasions, the last one over 10 years ago with a bullet lodged in the left kidney. His past surgical history included a right pulmonary lobectomy and multiple bowel surgeries with mesh placement from a prior gunshot wound that resulted in injury of the right kidney. After partial right nephrectomy, the patient showed renal insufficiency with a creatinine of 2.6 mg/dL. After the latest gunshot wound, no attempt at removal of the left sided bullet was performed due to risk of injury to the solitary functioning left kidney. Physical examination findings were unremarkable. The CT scan revealed hydronephrosis of the left kidney and a 15 mm calcification in the left UPJ and an atrophic right kidney (Fig. 1a, b). The patient then underwent urgent cystoscopy with bilateral retrograde pyelograms showing a filling defect consistent of a calculus in the left UPJ causing hydronephrosis. The patient underwent left ureteral stent placement with plans for either ureteroscopic laser lithotripsy or extracorporeal shockwave lithotripsy (SWL). Upon planning the elective procedure, review of the films with radiologist in context of the patient's prior history of a left gunshot wound indicated the high possibility that the calcification in the left UPJ was actually the bullet possibly surrounded by stone formation (Fig. 2). Therefore, ureteroscopic laser lithotripsy by a retrograde approach and SWL were contraindicated. The patient then underwent left percutaneous ultrasonic lithotripsy of the calcified stone formation over the bullet and endoscopic removal of the bullet shell. The ultrasonic probe was used to chip off stone fragment surrounding the gun shell. Several large stone chunks were removed. Using a 100 W holmium laser, the final remaining stone fragments were removed from around the bullet. Due to the inability of the laser to fragment the metal, the gun shell shard was grasped, pulled into the sheath, and the sheath and fragment were removed together (Fig. 3). The patient had an unremarkable recovery and was discharged 2 days after the procedure.\nOUTPUT:" }, { "from": "agent", "value": "Acute Renal Failure" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: His past medical history included three gunshot wounds on separate occasions, the last one over 10 years ago with a bullet lodged in the left kidney. His past surgical history included a right pulmonary lobectomy and multiple bowel surgeries with mesh placement from a prior gunshot wound that resulted in injury of the right kidney. After partial right nephrectomy, the patient showed renal insufficiency with a creatinine of 2.6 mg/dL. After the latest gunshot wound, no attempt at removal of the left sided bullet was performed due to risk of injury to the solitary functioning left kidney. Physical examination findings were unremarkable. The CT scan revealed hydronephrosis of the left kidney and a 15 mm calcification in the left UPJ and an atrophic right kidney (Fig. 1a, b). The patient then underwent urgent cystoscopy with bilateral retrograde pyelograms showing a filling defect consistent of a calculus in the left UPJ causing hydronephrosis. The patient underwent left ureteral stent placement with plans for either ureteroscopic laser lithotripsy or extracorporeal shockwave lithotripsy (SWL). Upon planning the elective procedure, review of the films with radiologist in context of the patient's prior history of a left gunshot wound indicated the high possibility that the calcification in the left UPJ was actually the bullet possibly surrounded by stone formation (Fig. 2). Therefore, ureteroscopic laser lithotripsy by a retrograde approach and SWL were contraindicated. The patient then underwent left percutaneous ultrasonic lithotripsy of the calcified stone formation over the bullet and endoscopic removal of the bullet shell. The ultrasonic probe was used to chip off stone fragment surrounding the gun shell. Several large stone chunks were removed. Using a 100 W holmium laser, the final remaining stone fragments were removed from around the bullet. Due to the inability of the laser to fragment the metal, the gun shell shard was grasped, pulled into the sheath, and the sheath and fragment were removed together (Fig. 3). The patient had an unremarkable recovery and was discharged 2 days after the procedure. OUTPUT:
Multicare_common6262
[ { "from": "human", "value": "As a physician engaged 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 subject was a 33-year-old massively obese female who was brought to our hospital by the Emergency Medical Service after experiencing a collapse at home. Four years prior to this event, she had been seen in the Emergency Department of our hospital with complaints of shortness of breath and heavy menstrual bleeding. Vital signs included blood pressure recordings in the range of 160-167/67-80 mmHg. Blood hemoglobin and hematocrit were 5.9 grams per deciliter (g/dl) and 21.3 percent (%), respectively. The woman was given a bolus of medroxyprogesterone and transfused with 2 units of packed erythrocytes which resulted in a rise of the hemoglobin to 7.5g/dl. She was started on oral iron medication and discharged. She was not seen again in our health care system until she was brought to our Emergency Medical Department in extremis. A history given by the woman's mother revealed that the woman had been complaining of shortness of breath for the past 3 weeks. The mother reported that subsequently the woman became acutely distressed one morning and complained that she was \"hurting all over\". She was on her way to her primary care physician when she was found unresponsive and pulseless. Cardiopulmonary resuscitation (CPR) was initiated by bystanders, Emergency Assistance was not called until 10 minutes after. When the emergency medical service (EMS) arrived, she was found to have a \"non-shockable rhythm.\" Thirteen rounds of cardiopulmonary resuscitation (CPR) were performed, and 8 doses of epinephrine were given. The EMS was unable to intubate her given her clinched jaw, so a nasopharyngeal airway was placed instead. On arrival at the emergency room, CPR had been performed for approximately an hour. CPR was continued. The clinical team was unable to intubate her given her body habitus; however, laryngeal mask airway (LMA) was placed successfully. Despite ongoing CPR, the woman exhibited pulseless electrical activity (PEA), which was resistant to resuscitative efforts. She was pronounced dead in the Emergency Room. Permission for an unrestricted autopsy was obtained.\nOUTPUT:" }, { "from": "agent", "value": "Extreme obesity, Anemia, Asthma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The subject was a 33-year-old massively obese female who was brought to our hospital by the Emergency Medical Service after experiencing a collapse at home. Four years prior to this event, she had been seen in the Emergency Department of our hospital with complaints of shortness of breath and heavy menstrual bleeding. Vital signs included blood pressure recordings in the range of 160-167/67-80 mmHg. Blood hemoglobin and hematocrit were 5.9 grams per deciliter (g/dl) and 21.3 percent (%), respectively. The woman was given a bolus of medroxyprogesterone and transfused with 2 units of packed erythrocytes which resulted in a rise of the hemoglobin to 7.5g/dl. She was started on oral iron medication and discharged. She was not seen again in our health care system until she was brought to our Emergency Medical Department in extremis. A history given by the woman's mother revealed that the woman had been complaining of shortness of breath for the past 3 weeks. The mother reported that subsequently the woman became acutely distressed one morning and complained that she was "hurting all over". She was on her way to her primary care physician when she was found unresponsive and pulseless. Cardiopulmonary resuscitation (CPR) was initiated by bystanders, Emergency Assistance was not called until 10 minutes after. When the emergency medical service (EMS) arrived, she was found to have a "non-shockable rhythm." Thirteen rounds of cardiopulmonary resuscitation (CPR) were performed, and 8 doses of epinephrine were given. The EMS was unable to intubate her given her clinched jaw, so a nasopharyngeal airway was placed instead. On arrival at the emergency room, CPR had been performed for approximately an hour. CPR was continued. The clinical team was unable to intubate her given her body habitus; however, laryngeal mask airway (LMA) was placed successfully. Despite ongoing CPR, the woman exhibited pulseless electrical activity (PEA), which was resistant to resuscitative efforts. She was pronounced dead in the Emergency Room. Permission for an unrestricted autopsy was obtained. OUTPUT:
Multicare_common10124
[ { "from": "human", "value": "As a physician engaged 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 has no complaints. In our hospital, laboratory data on the liver, pancreas were within normal ranges. It was suggested renal dysfunction that GFR was 59 mL/min. The serum CEA and CA19-9 levels were 3.7 ng/mL and 42.8U/mL, respectively. 1). The size of the tumor of pancreas was 3 cm x 4 cm. There was septum in the cystic tumor of pancreas. Magnetic resonance cholangiopancreatography showed the cystic tumor of pancreas and dilatation of main pancreatic duct. Gastrointestinal fiber showed mucinous discharge oozing from the ampulla of Vater. FDG-PET CT showed FDG uptake in the tumor of pancreas. It has not showed metastasis in the other organs. Then, we diagnosed that the tumor of pancreas was IPMC. Laboratory data showed antiplatelet antibody. The level of the antibody was 79 ng/107ce. The patient was not diagnosed with the dysfunction of valve of heart or intracranial aneurysm. We performed distal pancreatectomy (Fig. 2). Pathological examination of the resected specimens revealed dilatation of main and branched pancreatic duct involving papillary proliferation. The ducts were filled with mucin (Fig. 3a, b). The tumor cells invaded not only in these ducts but also the pancreatic parenchyma (Fig. 3c). The patient had no recurrence after the operation for 5 years.\nOUTPUT:" }, { "from": "agent", "value": "Intraductal Papillary Mucinous Neoplasm of the Pancreas, Polycystic Liver and Kidney Disease, Thrombocytopenia, Hypertension, Diabetes Mellitus, Duodenitis, Gastritis, Helicobacter Pylori Infection, Invasive Intraductal Mucinous Carcinoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: He has no complaints. In our hospital, laboratory data on the liver, pancreas were within normal ranges. It was suggested renal dysfunction that GFR was 59 mL/min. The serum CEA and CA19-9 levels were 3.7 ng/mL and 42.8U/mL, respectively. 1). The size of the tumor of pancreas was 3 cm x 4 cm. There was septum in the cystic tumor of pancreas. Magnetic resonance cholangiopancreatography showed the cystic tumor of pancreas and dilatation of main pancreatic duct. Gastrointestinal fiber showed mucinous discharge oozing from the ampulla of Vater. FDG-PET CT showed FDG uptake in the tumor of pancreas. It has not showed metastasis in the other organs. Then, we diagnosed that the tumor of pancreas was IPMC. Laboratory data showed antiplatelet antibody. The level of the antibody was 79 ng/107ce. The patient was not diagnosed with the dysfunction of valve of heart or intracranial aneurysm. We performed distal pancreatectomy (Fig. 2). Pathological examination of the resected specimens revealed dilatation of main and branched pancreatic duct involving papillary proliferation. The ducts were filled with mucin (Fig. 3a, b). The tumor cells invaded not only in these ducts but also the pancreatic parenchyma (Fig. 3c). The patient had no recurrence after the operation for 5 years. OUTPUT:
Multicare_common3113
[ { "from": "human", "value": "As a physician engaged 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 hair pull test was strongly positive in the perilesional skin. Trichoscopy revealed numerous exclamation mark hairs and confirmed the clinical diagnosis of AA [Figure 2]. At the edges of AA area white, short vellus hairs, and dystrophic hairs were noticed together with black and yellow dots. The hair pull test was negative in the perilesional skin. On trichoscopy, a number of broken hairs were observed. Direct mycological examination of the hairs from the lesional skin did not show any fungal elements. There were no other signs or symptoms of dermatological disorders either in the skin or nails or hair. The child had a positive family history of atopy. Extensive laboratory investigations such as complete blood cell count, serum chemistry, and thyroid function tests were all found to be within normal limits. Only slight anemia was proved. Because of the suspicion of TT, an interview with the child's parents was asked and they approved that the child was hyperactive, and he was seen several times pulling out the hair. The patient demonstrated the self-injurious behavior on clinical examination which confirmed the clinical suspicion even at that point. Treatment for iron deficiency anemia was started with Sorbifer accordingly to the age and recommendation of topical potent steroids for AA was prescribed. A psychiatric evaluation was asked, psychological counseling and therapy were recommended for the child and parents. The patient was seen again in consultation 8 months later, and positive results were remarked.\nOUTPUT:" }, { "from": "agent", "value": "Alopecia Areata, Trichotillomania" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The hair pull test was strongly positive in the perilesional skin. Trichoscopy revealed numerous exclamation mark hairs and confirmed the clinical diagnosis of AA [Figure 2]. At the edges of AA area white, short vellus hairs, and dystrophic hairs were noticed together with black and yellow dots. The hair pull test was negative in the perilesional skin. On trichoscopy, a number of broken hairs were observed. Direct mycological examination of the hairs from the lesional skin did not show any fungal elements. There were no other signs or symptoms of dermatological disorders either in the skin or nails or hair. The child had a positive family history of atopy. Extensive laboratory investigations such as complete blood cell count, serum chemistry, and thyroid function tests were all found to be within normal limits. Only slight anemia was proved. Because of the suspicion of TT, an interview with the child's parents was asked and they approved that the child was hyperactive, and he was seen several times pulling out the hair. The patient demonstrated the self-injurious behavior on clinical examination which confirmed the clinical suspicion even at that point. Treatment for iron deficiency anemia was started with Sorbifer accordingly to the age and recommendation of topical potent steroids for AA was prescribed. A psychiatric evaluation was asked, psychological counseling and therapy were recommended for the child and parents. The patient was seen again in consultation 8 months later, and positive results were remarked. OUTPUT:
Multicare_common1705
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 30-year-old G4P3003 at 26 weeks pregnant presented to urgent care with nonspecific symptoms and fatigue. Laboratory evaluation revealed pancytopenia. She established prenatal care and repeat labs showed persistent pancytopenia, raising concern for a haematologic malignancy. She was admitted to the hospital and started on induction chemotherapy, 7 + 3 (cytarabine 100 mg/m2/day continuous infusion for 7 days + daunorubicin 90 mg/m2/day intravenous days 1-3). Maternal fetal medicine was also consulted on admission. She was counseled on the risks and her pregnancy was followed with serial growth ultrasounds and weekly Doppler ultrasounds (see Figure 2) to monitor for fetal growth restriction and fetal anemia. She tolerated the chemotherapy well and subsequently received high-dose cytarabine for consolidation therapy (cytarabine 3 g/m2/day continuous infusion for 6 days). At 34 2/7 weeks, she was admitted for neutropenic fever (cycle 1, day 19). Fetal monitoring was nonreactive but with moderate variability, occasional variable decelerations. The patient's hemoglobin was 5.8 with platelet count of 39 K/UL. She received platelet and blood transfusions with subsequent improvement in fetal tracing. At 34 5/7 weeks, the fetal MCA PSV was noted to have risen to a borderline value, at 1.48 MoM (previously always within normal limits). Fetal growth was normal at the 33rd percentile. At 34 6/7 weeks, the fetal MCA PSV improved (1.28 MoM) but the fetal tracing worsened with decreased variability and increase in the number of variable decelerations. At 35 0/7 weeks, the MCA PI was now centralized with a MCA PSV of 1.38 MoM; a biophysical profile was found to be 6/10, and with continued worsening in the fetal tracing, the decision was made to proceed with delivery. She underwent an uncomplicated repeat cesarean section with no bleeding complications. Her postoperative course was unremarkable. The infant was born with anemia (hematocrit 30%) but did not require any blood transfusions. The platelet count (274 K/UL) and white blood cell count (7.7 K/UL) were normal at birth. The infant was discharged on hospital day 7. The patient is currently undergoing work-up for a bone marrow transplant.\nOUTPUT:" }, { "from": "agent", "value": "Acute Myelogenous Leukemia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 30-year-old G4P3003 at 26 weeks pregnant presented to urgent care with nonspecific symptoms and fatigue. Laboratory evaluation revealed pancytopenia. She established prenatal care and repeat labs showed persistent pancytopenia, raising concern for a haematologic malignancy. She was admitted to the hospital and started on induction chemotherapy, 7 + 3 (cytarabine 100 mg/m2/day continuous infusion for 7 days + daunorubicin 90 mg/m2/day intravenous days 1-3). Maternal fetal medicine was also consulted on admission. She was counseled on the risks and her pregnancy was followed with serial growth ultrasounds and weekly Doppler ultrasounds (see Figure 2) to monitor for fetal growth restriction and fetal anemia. She tolerated the chemotherapy well and subsequently received high-dose cytarabine for consolidation therapy (cytarabine 3 g/m2/day continuous infusion for 6 days). At 34 2/7 weeks, she was admitted for neutropenic fever (cycle 1, day 19). Fetal monitoring was nonreactive but with moderate variability, occasional variable decelerations. The patient's hemoglobin was 5.8 with platelet count of 39 K/UL. She received platelet and blood transfusions with subsequent improvement in fetal tracing. At 34 5/7 weeks, the fetal MCA PSV was noted to have risen to a borderline value, at 1.48 MoM (previously always within normal limits). Fetal growth was normal at the 33rd percentile. At 34 6/7 weeks, the fetal MCA PSV improved (1.28 MoM) but the fetal tracing worsened with decreased variability and increase in the number of variable decelerations. At 35 0/7 weeks, the MCA PI was now centralized with a MCA PSV of 1.38 MoM; a biophysical profile was found to be 6/10, and with continued worsening in the fetal tracing, the decision was made to proceed with delivery. She underwent an uncomplicated repeat cesarean section with no bleeding complications. Her postoperative course was unremarkable. The infant was born with anemia (hematocrit 30%) but did not require any blood transfusions. The platelet count (274 K/UL) and white blood cell count (7.7 K/UL) were normal at birth. The infant was discharged on hospital day 7. The patient is currently undergoing work-up for a bone marrow transplant. OUTPUT:
Multicare_common3588
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 38-year-old Malay female presented with complaints of bilateral ocular irritation of a few months duration. Hertel exophthalmometer readings were 23 mm bilaterally, which is significant for proptosis in an East-Asian population. There was no previous documentation of proptosis and the remainder of the ophthalmic exam was normal with no evidence of orbital inflammation. An orbital computed tomography (CT) scan showed normal extraocular muscle dimensions, increased orbital fat with prolapse, and thick lateral orbital wall and marrow space with globe prolapse [Figure 2]. The patient underwent lateral wall bone decompression with fat decompression. Using a high-speed neurosurgical drill, cortical bone was removed from the lacrimal gland fossa, the marrow space of the sphenoid between the superior and inferior orbital fissure, and the zygomatic marrow space on the anterior rim of the inferior orbital fissure. The intraconal fat, located between the lateral and inferior rectus muscles, was bluntly dissected out of the muscle cone and excised (2CC from the right side and 1CC from the left).\nOUTPUT:" }, { "from": "agent", "value": "Acquired Epiblepharon, Primary Hypothyroidism, Ventricular Septal Defect, Morbid Obesity" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 38-year-old Malay female presented with complaints of bilateral ocular irritation of a few months duration. Hertel exophthalmometer readings were 23 mm bilaterally, which is significant for proptosis in an East-Asian population. There was no previous documentation of proptosis and the remainder of the ophthalmic exam was normal with no evidence of orbital inflammation. An orbital computed tomography (CT) scan showed normal extraocular muscle dimensions, increased orbital fat with prolapse, and thick lateral orbital wall and marrow space with globe prolapse [Figure 2]. The patient underwent lateral wall bone decompression with fat decompression. Using a high-speed neurosurgical drill, cortical bone was removed from the lacrimal gland fossa, the marrow space of the sphenoid between the superior and inferior orbital fissure, and the zygomatic marrow space on the anterior rim of the inferior orbital fissure. The intraconal fat, located between the lateral and inferior rectus muscles, was bluntly dissected out of the muscle cone and excised (2CC from the right side and 1CC from the left). OUTPUT:
Multicare_common9201
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The patient had no complaint. On clinical exam, the child was in excellent condition. The femoral pulses were not palpable, the child was hypertensive on the upper extremities with a significant differential blood pressure between the upper and lower limbs (Table 1). The electrocardiogram showed sinus rhythm with signs of left auricular hypertrophy, but no ventricular hypertrophy. CMR with angiography showed absence of continuity between the ascending aorta distal to the left subclavian artery (Type 1) and the descending aorta, extending over 5 mm. There was no patent ductus arteriosus (PDA), no associated endofibroelastosis and the descending aorta was fed exclusively by massive systemic collateral circulation (Figures 4-6).\nOUTPUT:" }, { "from": "agent", "value": "Atresia of the aortic arch, aortic coarctation, bicuspid aortic valve" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The patient had no complaint. On clinical exam, the child was in excellent condition. The femoral pulses were not palpable, the child was hypertensive on the upper extremities with a significant differential blood pressure between the upper and lower limbs (Table 1). The electrocardiogram showed sinus rhythm with signs of left auricular hypertrophy, but no ventricular hypertrophy. CMR with angiography showed absence of continuity between the ascending aorta distal to the left subclavian artery (Type 1) and the descending aorta, extending over 5 mm. There was no patent ductus arteriosus (PDA), no associated endofibroelastosis and the descending aorta was fed exclusively by massive systemic collateral circulation (Figures 4-6). OUTPUT:
Multicare_common8602
[ { "from": "human", "value": "As a physician engaged 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 22-year-old woman (patient 5.1, Table 1) manifested a rash at birth and later developed a dermatitis associated with S aureus superinfection. She had asthma and multiple food and environmental allergies. As a teenager, her dermatitis was controlled for several years with topical steroid therapy, use of chlorinated pools, Dakin solution, chlorhexadine washes, and intermittent linezolid therapy for chronic methicillin-resistant S aureus. At the of age 17 years, she developed linezolid-resistant S aureus infection and was placed on a prophylactic regimen of doxycycline and rifampin. Her dermatitis flared after she ingested peanut oil, requiring treatment with prednisone for the next 2 years. She had numerous respiratory tract infections, including miliary Histoplasma capsulatum pneumonia. She had severe primary varicella at the age of 6 years, followed by multiple episodes of herpes zoster. When she was 19 years old, she developed confluent verrucae on the distal aspect of her fingers (Figure 3A). She had molluscum contagiosum, which formed plaques on her face, neck (Figure 3B), chest, abdomen, and periaxillary and pubic areas. The verrucae were refractory to cryotherapy, salicyclic acid, cimetidine, and topical imiquimod under occlusion. Interferon alfa therapy exacerbated her eczema. A trial of oral cidofovir was limited by the elevation of transaminase levels. Intravenous cidofovir was later used, with significant improvement of the verrucae but not of the molluscum. The patient and her affected sister (patient 5.2) were found to have compound heterozygous deletions within DOCK8, resulting in the complete absence of protein. At the age of 21 years, the patient underwent umbilical cord blood hematopoietic stem cell transplantation (HSCT) but developed human herpesvirus 6 encephalitis and died without engraftment 3 months later.\nOUTPUT:" }, { "from": "agent", "value": "DOCK8 deficiency syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 22-year-old woman (patient 5.1, Table 1) manifested a rash at birth and later developed a dermatitis associated with S aureus superinfection. She had asthma and multiple food and environmental allergies. As a teenager, her dermatitis was controlled for several years with topical steroid therapy, use of chlorinated pools, Dakin solution, chlorhexadine washes, and intermittent linezolid therapy for chronic methicillin-resistant S aureus. At the of age 17 years, she developed linezolid-resistant S aureus infection and was placed on a prophylactic regimen of doxycycline and rifampin. Her dermatitis flared after she ingested peanut oil, requiring treatment with prednisone for the next 2 years. She had numerous respiratory tract infections, including miliary Histoplasma capsulatum pneumonia. She had severe primary varicella at the age of 6 years, followed by multiple episodes of herpes zoster. When she was 19 years old, she developed confluent verrucae on the distal aspect of her fingers (Figure 3A). She had molluscum contagiosum, which formed plaques on her face, neck (Figure 3B), chest, abdomen, and periaxillary and pubic areas. The verrucae were refractory to cryotherapy, salicyclic acid, cimetidine, and topical imiquimod under occlusion. Interferon alfa therapy exacerbated her eczema. A trial of oral cidofovir was limited by the elevation of transaminase levels. Intravenous cidofovir was later used, with significant improvement of the verrucae but not of the molluscum. The patient and her affected sister (patient 5.2) were found to have compound heterozygous deletions within DOCK8, resulting in the complete absence of protein. At the age of 21 years, the patient underwent umbilical cord blood hematopoietic stem cell transplantation (HSCT) but developed human herpesvirus 6 encephalitis and died without engraftment 3 months later. OUTPUT: