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PMCPatients_common4279
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 41-year-old male patient presented with a history of swelling in the neck for 5 years, palpitation, tremor, weight loss, and generalized body ache. On evaluation, the thyroid function test shows raised free triiodothyronine >20 pg/mL (normal range 2.3–4.2 pg/mL), raised free thyroxine >12.0 ng/mL (normal range 0.89–1.76 ng/mL), and suppressed thyroid-stimulating hormone <0.01 mIU/L (normal range 0.34–5.5 mIU/L). Ultrasonography neck was suggestive of enlarged thyroid gland with features of thyroiditis. Planar image of the neck and upper chest acquired in anterior view 20 min after intravenous injection with 5 mCi of Tc-99m sodium pertechnetate showed homogeneously increased tracer uptake in the enlarged thyroid gland with suppression of salivary glands tracer uptake []. The tracer uptake at 20 min was 22.3% (normal range 0.4%–4.0%). However, there was an additional focus of tracer uptake in the upper chest on the right side, separate from the thyroid gland [ arrow], which persisted on additional planar image acquired after drinking of water.\\nSPECT-CT images with low-dose, noncontrast CT of the chest were acquired to characterize the abnormal focus of tracer uptake in the chest []. However, due to ethical reasons, the biopsy from this lesion was not obtained. This may be due to its small size or its presence behind the manubrium.\nOUTPUT:" }, { "from": "agent", "value": "Graves’ Disease, Ectopic Mediastinal Thyroid Tissue, Diffuse Toxic Goiter" } ]
As a physician 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 41-year-old male patient presented with a history of swelling in the neck for 5 years, palpitation, tremor, weight loss, and generalized body ache. On evaluation, the thyroid function test shows raised free triiodothyronine >20 pg/mL (normal range 2.3–4.2 pg/mL), raised free thyroxine >12.0 ng/mL (normal range 0.89–1.76 ng/mL), and suppressed thyroid-stimulating hormone <0.01 mIU/L (normal range 0.34–5.5 mIU/L). Ultrasonography neck was suggestive of enlarged thyroid gland with features of thyroiditis. Planar image of the neck and upper chest acquired in anterior view 20 min after intravenous injection with 5 mCi of Tc-99m sodium pertechnetate showed homogeneously increased tracer uptake in the enlarged thyroid gland with suppression of salivary glands tracer uptake []. The tracer uptake at 20 min was 22.3% (normal range 0.4%–4.0%). However, there was an additional focus of tracer uptake in the upper chest on the right side, separate from the thyroid gland [ arrow], which persisted on additional planar image acquired after drinking of water.\nSPECT-CT images with low-dose, noncontrast CT of the chest were acquired to characterize the abnormal focus of tracer uptake in the chest []. However, due to ethical reasons, the biopsy from this lesion was not obtained. This may be due to its small size or its presence behind the manubrium. OUTPUT:
PMCPatients_common3655
[ { "from": "human", "value": "As a physician engaged 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 second and third right foot digits have already been amputated because of subsequent ulceration, infection, and necrosis. He had pale, cold legs with ulceration of right toe. Periphery pulses of both legs were absent. He was a heavy cigarette smoker using 2 packs a year for 30 years. Color Doppler ultrasound showed occlusion of both popliteal arteries. Diagnostic angiography revealed occlusion of both popliteal arteries. There were typical “corkscrew” collaterals around knees at the level of occlusions (–, ).\\nPercutaneous transluminal angioplasty was planned and a 6F vascular sheath (Medtronic Corp, Minneapolis, MN) was inserted to right femoral artery via antegrade femoral puncture and 10000 IU unfractionated heparin was administered and added according to the result of activated clothing time during procedure. The occluded part of the popliteal artery was successfully passed with 0.014 guidewire (Abbott Laboratories, Abbott Park, Illonis) via the support catheter (Quick-Cross, The Spectranetics Corporation Colorado Springs) () demonstrated by micro-injection via support catheter (). The first angioplasty was performed with 2.5x80 mm balloon (Medtronic Corp, Minneapolis, MN) to the popliteal artery (). The sequential drug coated balloon angioplasties were then performed on the posterior tibial artery (), anterior tibial artery (), and dorsalis pedis artery (). Final angioplasty was performed to popliteal artery with 4.0x100 mm balloon () and complete blood flow of the foot was restored (–, Video –). The pain resolved and the patient was mobile the following morning. The ulcer healed within the following three weeks. The patient was recommended to quit smoking cigarette. A daily dose of 100 mg acetylsalicylic acid and 75 mg clopidogrel was recommended for the following 12 months although there is no consensus regarding treatment duration. The fifth month visit was uneventful with an increased capacity of ambulation.\nOUTPUT:" }, { "from": "agent", "value": "Thromboangitis obliterans (Buerger'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: His second and third right foot digits have already been amputated because of subsequent ulceration, infection, and necrosis. He had pale, cold legs with ulceration of right toe. Periphery pulses of both legs were absent. He was a heavy cigarette smoker using 2 packs a year for 30 years. Color Doppler ultrasound showed occlusion of both popliteal arteries. Diagnostic angiography revealed occlusion of both popliteal arteries. There were typical “corkscrew” collaterals around knees at the level of occlusions (–, ).\nPercutaneous transluminal angioplasty was planned and a 6F vascular sheath (Medtronic Corp, Minneapolis, MN) was inserted to right femoral artery via antegrade femoral puncture and 10000 IU unfractionated heparin was administered and added according to the result of activated clothing time during procedure. The occluded part of the popliteal artery was successfully passed with 0.014 guidewire (Abbott Laboratories, Abbott Park, Illonis) via the support catheter (Quick-Cross, The Spectranetics Corporation Colorado Springs) () demonstrated by micro-injection via support catheter (). The first angioplasty was performed with 2.5x80 mm balloon (Medtronic Corp, Minneapolis, MN) to the popliteal artery (). The sequential drug coated balloon angioplasties were then performed on the posterior tibial artery (), anterior tibial artery (), and dorsalis pedis artery (). Final angioplasty was performed to popliteal artery with 4.0x100 mm balloon () and complete blood flow of the foot was restored (–, Video –). The pain resolved and the patient was mobile the following morning. The ulcer healed within the following three weeks. The patient was recommended to quit smoking cigarette. A daily dose of 100 mg acetylsalicylic acid and 75 mg clopidogrel was recommended for the following 12 months although there is no consensus regarding treatment duration. The fifth month visit was uneventful with an increased capacity of ambulation. OUTPUT:
PMCPatients_common208
[ { "from": "human", "value": "As a physician engaged in 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 female presented to the emergency department with a two-day history of recurrent, severe, thunderclap headaches. Headaches were associated with focal motor seizures with secondary generalization. She also reported a blockage of the urinary catheter and experienced recurrent headaches when she attempted to flush the catheter. On our initial assessment, there was no change in the neurological examination from her baseline. Computed tomography (CT) head revealed a subarachnoid hemorrhage as shown in Figure . The CT angiogram of the head, as shown in Figure , was remarkable for multifocal narrowing of the anterior cerebral artery, bilateral middle cerebral arteries (MCA), right posterior cerebral artery, and pericallosal artery.\\nMagnetic resonance imaging (MRI) of the brain, as shown in Figure , revealed T2 fluid attenuated inversion recovery (FLAIR) hyperintensity in the bilateral frontal lobes and petechial hemorrhage in susceptibility weighted imaging (SWI). Initial workup, consisting of routine blood tests, erythrocyte sedimentation rate (ESR), comprehensive drug screening, antinuclear antibodies, anti-neutrophil cytoplasmic antibody (ANCA) panel, and angiotensin-converting enzyme, were within normal limits.\\nThe diagnostic cerebral angiogram was remarkable for stenosis of the bilateral posterior cerebral arteries, callosal and pericallosal branches of the right anterior cerebral artery, and right middle cerebral artery as shown in Figure and Figure . During her hospital stay, her headaches recurred, which were associated with episodes of flushing, sweating, and elevated blood pressure. These events were precipitated by unclogging or flushing her foley catheter. Midodrine was discontinued and her headaches improved significantly at the time of discharge. Three months after discharge from the hospital, she underwent repeat diagnostic cerebral angiogram, which was unremarkable as shown in Figure and Figure . The patient denied a recurrence of symptoms during the subsequent follow-up visit.\nOUTPUT:" }, { "from": "agent", "value": "Reversible Cerebral Vasoconstriction Syndrome, Autonomic Dysreflexia" } ]
As a physician 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 female presented to the emergency department with a two-day history of recurrent, severe, thunderclap headaches. Headaches were associated with focal motor seizures with secondary generalization. She also reported a blockage of the urinary catheter and experienced recurrent headaches when she attempted to flush the catheter. On our initial assessment, there was no change in the neurological examination from her baseline. Computed tomography (CT) head revealed a subarachnoid hemorrhage as shown in Figure . The CT angiogram of the head, as shown in Figure , was remarkable for multifocal narrowing of the anterior cerebral artery, bilateral middle cerebral arteries (MCA), right posterior cerebral artery, and pericallosal artery.\nMagnetic resonance imaging (MRI) of the brain, as shown in Figure , revealed T2 fluid attenuated inversion recovery (FLAIR) hyperintensity in the bilateral frontal lobes and petechial hemorrhage in susceptibility weighted imaging (SWI). Initial workup, consisting of routine blood tests, erythrocyte sedimentation rate (ESR), comprehensive drug screening, antinuclear antibodies, anti-neutrophil cytoplasmic antibody (ANCA) panel, and angiotensin-converting enzyme, were within normal limits.\nThe diagnostic cerebral angiogram was remarkable for stenosis of the bilateral posterior cerebral arteries, callosal and pericallosal branches of the right anterior cerebral artery, and right middle cerebral artery as shown in Figure and Figure . During her hospital stay, her headaches recurred, which were associated with episodes of flushing, sweating, and elevated blood pressure. These events were precipitated by unclogging or flushing her foley catheter. Midodrine was discontinued and her headaches improved significantly at the time of discharge. Three months after discharge from the hospital, she underwent repeat diagnostic cerebral angiogram, which was unremarkable as shown in Figure and Figure . The patient denied a recurrence of symptoms during the subsequent follow-up visit. OUTPUT:
PMCPatients_common2394
[ { "from": "human", "value": "As a physician engaged in 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 Chinese male presented to the Deaprtment of Pathology, The Third Affiliated Hospital of Soochow University (Changzhou, China) in May 2009 with complaints of a 2-cm asymptomatic, smooth and firm nodule in the left inguinal region. There was no discoloration or other visible abnormality of the overlying skin. Surgical excision of the lesion was performed and a diagnosis of malignant lymphoma was formed at the Changzhou No.2 People’s Hospital (Changzhou, China). The patient’s medical history revealed a previous resection of a similar painless nodule in the subcutaneous region of the left knee 6 months previously, but a pathological examination had not been performed. The nodule in the left groin was suspected to be a metastatic lesion.\\nUpon review of 4-μm sections of the lesion by light microscopy, the entire thickness of the dermis was observed to be widely infiltrated by small round monomorphic cells, with minimal cytoplasm, hyperchromatic nuclei and small nucleoli (). Apparent nuclear atypia and multiple mitotic figures were observed. These neoplastic cells showed diffuse distribution and infiltrated into the deep mesenchyme, where blood vessels were plentiful (). Immunohistochemical staining was performed on 4-μm thick, formalin-fixed, paraffin-embedded tissue sections provided by the external hospital. The results demonstrated that the tumor cells were strongly positive for neuroendocrine markers, including chromogranin A (CgA) and synaptophysin (Syn), and epithelial markers cytokeratin (CK) 20, CK8/18 and epithelial membrane antigen (EMA) (), but negative for leukocyte common antigens (LCA), thyroid transcription factor-1 (TTF-1), Melan-A, human melanoma black 45 (HMB45), vimentin (Vim), S-100, cluster of differentiation (CD)34, CD57 and CD99. These histopathological and immunohistochemical features were consistent with a diagnosis of MCC. Therefore, a corrected diagnosis of MCC was made for this patient.\nOUTPUT:" }, { "from": "agent", "value": "Merkel cell carcinoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 66-year-old Chinese male presented to the Deaprtment of Pathology, The Third Affiliated Hospital of Soochow University (Changzhou, China) in May 2009 with complaints of a 2-cm asymptomatic, smooth and firm nodule in the left inguinal region. There was no discoloration or other visible abnormality of the overlying skin. Surgical excision of the lesion was performed and a diagnosis of malignant lymphoma was formed at the Changzhou No.2 People’s Hospital (Changzhou, China). The patient’s medical history revealed a previous resection of a similar painless nodule in the subcutaneous region of the left knee 6 months previously, but a pathological examination had not been performed. The nodule in the left groin was suspected to be a metastatic lesion.\nUpon review of 4-μm sections of the lesion by light microscopy, the entire thickness of the dermis was observed to be widely infiltrated by small round monomorphic cells, with minimal cytoplasm, hyperchromatic nuclei and small nucleoli (). Apparent nuclear atypia and multiple mitotic figures were observed. These neoplastic cells showed diffuse distribution and infiltrated into the deep mesenchyme, where blood vessels were plentiful (). Immunohistochemical staining was performed on 4-μm thick, formalin-fixed, paraffin-embedded tissue sections provided by the external hospital. The results demonstrated that the tumor cells were strongly positive for neuroendocrine markers, including chromogranin A (CgA) and synaptophysin (Syn), and epithelial markers cytokeratin (CK) 20, CK8/18 and epithelial membrane antigen (EMA) (), but negative for leukocyte common antigens (LCA), thyroid transcription factor-1 (TTF-1), Melan-A, human melanoma black 45 (HMB45), vimentin (Vim), S-100, cluster of differentiation (CD)34, CD57 and CD99. These histopathological and immunohistochemical features were consistent with a diagnosis of MCC. Therefore, a corrected diagnosis of MCC was made for this patient. OUTPUT:
PMCPatients_common1321
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 57-year-old male was diagnosed as suffering from pPCL. Hepatosplenomegaly, anemia, thrombocytopenia, fever, fatigue, and weight loss were the indicative symptoms. The serum creatinine was 1.07 mg/100 ml (normal level up to 1.5 mg/100 ml); calcium, 8.5 mg/100 ml (normal level up to 10.2 mg/100 ml); serum lactate dehydrogenase (LDH) level was 662 U/l (normal level up to 480 U/l); serum aspartate aminotrasferase (AST) level was 42 U/l (normal up to 40 U/l); and serum ß2-microglobulin level was 4.12 mg/l (normal level up to 2.3 mg/l). Total serum protein was within normal range at 7.3 gm/dl (normal value 6-8.5 gm/dl) but serum albumin was 3.4 gm/dl (normal value 3.8-5 gm/dl); serum IgG level was 812 mg/dl (700-1600 mg/dl); serum IgA level was 140 gm/dl (70-400 mg/dl); and serum IgD level was 48.9 mg/dl (40-230 mg/dl). No treatment had been administered prior to the test.\\nAll human studies have been approved by the ethics committee of the Atomic Energy Commission, Damascus, Syria and have therefore been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments. The patient gave his informed consent prior to its inclusion in this study.\nOUTPUT:" }, { "from": "agent", "value": "Primary Plasma Cell 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 57-year-old male was diagnosed as suffering from pPCL. Hepatosplenomegaly, anemia, thrombocytopenia, fever, fatigue, and weight loss were the indicative symptoms. The serum creatinine was 1.07 mg/100 ml (normal level up to 1.5 mg/100 ml); calcium, 8.5 mg/100 ml (normal level up to 10.2 mg/100 ml); serum lactate dehydrogenase (LDH) level was 662 U/l (normal level up to 480 U/l); serum aspartate aminotrasferase (AST) level was 42 U/l (normal up to 40 U/l); and serum ß2-microglobulin level was 4.12 mg/l (normal level up to 2.3 mg/l). Total serum protein was within normal range at 7.3 gm/dl (normal value 6-8.5 gm/dl) but serum albumin was 3.4 gm/dl (normal value 3.8-5 gm/dl); serum IgG level was 812 mg/dl (700-1600 mg/dl); serum IgA level was 140 gm/dl (70-400 mg/dl); and serum IgD level was 48.9 mg/dl (40-230 mg/dl). No treatment had been administered prior to the test.\nAll human studies have been approved by the ethics committee of the Atomic Energy Commission, Damascus, Syria and have therefore been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments. The patient gave his informed consent prior to its inclusion in this study. OUTPUT:
PMCPatients_common1359
[ { "from": "human", "value": "As a physician engaged in 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 woman had suffered from amenorrhea for 12 years and presented with deteriorated visual function and mild diabetes insipidus. She underwent transsphenoidal biopsy for suprasellar tumor. She received systemic chemotherapy with bleomycin, etoposide, and cis-diamminedichloroplatinum, and irradiation to the tumor bed (20 Gy). After completion of the initial treatment, MR imaging revealed complete resolution of the tumor. She had remained in good condition with hormonal replacement therapy, including dexamethasone, levothyroxine, and desmopressin acetate daily. No abnormal findings were seen at follow-up MR imaging examinations, which were performed every 6 months thereafter. Six years after the first therapy, she suffered headache and easy fatigability. Intraoperative rapid diagnosis suggested inflammatory disorder with massive infiltration of lymphocytes in the pituitary tissue, dura mater, and extradural sphenoidal mucosa, so surgery was limited to biopsy. Pulse dose hydrocortisone treatment was started from the day of the surgery using intravenous 200 mg hydrocortisone initially and tapered gradually. Histological examination of the biopsy specimen showed massive infiltration of inflammatory cells including lymphocytes in both the internal and external tissue of the dura mater. Staining for IgG4 was positive in the cytoplasm of approximately 40% of invaded plasma cells (Figure \\n).\nOUTPUT:" }, { "from": "agent", "value": "Autoimmune hypophysitis, Germinoma, Panhypopituitarism, Hypothyroidism, Granulomatous hypophysitis" } ]
As a physician 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 woman had suffered from amenorrhea for 12 years and presented with deteriorated visual function and mild diabetes insipidus. She underwent transsphenoidal biopsy for suprasellar tumor. She received systemic chemotherapy with bleomycin, etoposide, and cis-diamminedichloroplatinum, and irradiation to the tumor bed (20 Gy). After completion of the initial treatment, MR imaging revealed complete resolution of the tumor. She had remained in good condition with hormonal replacement therapy, including dexamethasone, levothyroxine, and desmopressin acetate daily. No abnormal findings were seen at follow-up MR imaging examinations, which were performed every 6 months thereafter. Six years after the first therapy, she suffered headache and easy fatigability. Intraoperative rapid diagnosis suggested inflammatory disorder with massive infiltration of lymphocytes in the pituitary tissue, dura mater, and extradural sphenoidal mucosa, so surgery was limited to biopsy. Pulse dose hydrocortisone treatment was started from the day of the surgery using intravenous 200 mg hydrocortisone initially and tapered gradually. Histological examination of the biopsy specimen showed massive infiltration of inflammatory cells including lymphocytes in both the internal and external tissue of the dura mater. Staining for IgG4 was positive in the cytoplasm of approximately 40% of invaded plasma cells (Figure \n). OUTPUT:
PMCPatients_common2367
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 26-year-old man who presented with abdominal pain and vomiting was transferred to our hospital seven days after the onset of the symptoms. The patient had no history of abdominal surgery. On arrival, his vital signs were normal. Abdominal findings revealed distension and tenderness in the entire abdomen without any muscular defense signs. Laboratory examinations showed a white blood cell count of 7420/mm3, a C-reactive protein level of 0.3 mg/dL, and all other measured values within their normal limits.\\nAn abdominal X-ray examination showed a dilatation and an air-fluid level of the small bowel. Abdominal computed tomography revealed an extensively dilated small bowel and a closed loop of small bowel in the mesosigmoid (). There was no blood flow obstruction at the closed loop of the small bowel. An ileus tube was inserted to decompress the small bowel prior to an elective single-incision laparoscopic surgery that was performed six days after admission.\\nThe operation was performed using a 2.0 cm transumbilical vertical incision. The fascia and peritoneum were then vertically opened, and three 5 mm trocars were inserted into the abdomen to introduce endoscopic instruments. Carbon dioxide was used to inflate the abdomen at 8 mmHg pressure. The operator used two 5 mm forceps, and the first assistant handled a 30 degree 5 mm laparoscope (Karl Storz, Tuttlingen, Germany). The incarcerated small bowel was reduced after adhesiolysis. The defect in the mesosigmoid was approximately 3 cm, and the length of the incarcerated small bowel was approximately 10 cm. We confirmed that incarcerated small bowel was viable (). The patient had an uneventful recovery and was discharged on postoperative day five.\nOUTPUT:" }, { "from": "agent", "value": "Intersigmoid Hernia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 26-year-old man who presented with abdominal pain and vomiting was transferred to our hospital seven days after the onset of the symptoms. The patient had no history of abdominal surgery. On arrival, his vital signs were normal. Abdominal findings revealed distension and tenderness in the entire abdomen without any muscular defense signs. Laboratory examinations showed a white blood cell count of 7420/mm3, a C-reactive protein level of 0.3 mg/dL, and all other measured values within their normal limits.\nAn abdominal X-ray examination showed a dilatation and an air-fluid level of the small bowel. Abdominal computed tomography revealed an extensively dilated small bowel and a closed loop of small bowel in the mesosigmoid (). There was no blood flow obstruction at the closed loop of the small bowel. An ileus tube was inserted to decompress the small bowel prior to an elective single-incision laparoscopic surgery that was performed six days after admission.\nThe operation was performed using a 2.0 cm transumbilical vertical incision. The fascia and peritoneum were then vertically opened, and three 5 mm trocars were inserted into the abdomen to introduce endoscopic instruments. Carbon dioxide was used to inflate the abdomen at 8 mmHg pressure. The operator used two 5 mm forceps, and the first assistant handled a 30 degree 5 mm laparoscope (Karl Storz, Tuttlingen, Germany). The incarcerated small bowel was reduced after adhesiolysis. The defect in the mesosigmoid was approximately 3 cm, and the length of the incarcerated small bowel was approximately 10 cm. We confirmed that incarcerated small bowel was viable (). The patient had an uneventful recovery and was discharged on postoperative day five. OUTPUT:
PMCPatients_common1178
[ { "from": "human", "value": "As a physician engaged 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 test revealed severe flow impairment in the left IJV, while the right IJV presented with normal outflow. Sonographic findings were confirmed by catheter venography. Venography of the right IJV, both brachiocephalic veins and the azygous vein, did not demonstrate lesions. Consequently, the patient underwent balloon angioplasty of the left IJV at the level of jugular valve (). Postprocedural venography demonstrated an improved, still not perfect, outflow from the vein (). The patient was followed up 10 months after the endovascular procedure. Her neurological status remained unchanged: EDSS was 5.5 and MSIS-29 was 103 points. Yet, control Doppler sonography revealed totally collapsed middle part of the left IJV in the supine position, with no flow through the vein detected (Figures and ). Anatomical and flow parameters in the right IJV were normal. Of note, left IJV widened and the flow was restored with the patient's mouth opened (). Thus, the compression seemed to be caused by aberrant OH. According to the above-described sonographic findings, patient qualified for surgical decompression of the vein. Surgical exploration revealed atypical OH, which was obviously squeezing the vein (). Transection of pathological muscle—performed in general anesthesia—resulted in widening of the vein () and normal blood flow was restored. Perioperative course, except for some nausea, probably due to anesthesia, was uneventful. Color Doppler sonography performed during followup 3 weeks after the surgical procedure demonstrated physiological flow in a fully decompressed vein (). Still, neurological assessment performed 2 months after the operation has shown a slight deterioration of clinical status: EDSS was 6.5 and MSIS-29 was 110 points.\nOUTPUT:" }, { "from": "agent", "value": "Multiple Sclerosis, Internal Jugular Vein Entrapment, CCSVI" } ]
As a physician 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 test revealed severe flow impairment in the left IJV, while the right IJV presented with normal outflow. Sonographic findings were confirmed by catheter venography. Venography of the right IJV, both brachiocephalic veins and the azygous vein, did not demonstrate lesions. Consequently, the patient underwent balloon angioplasty of the left IJV at the level of jugular valve (). Postprocedural venography demonstrated an improved, still not perfect, outflow from the vein (). The patient was followed up 10 months after the endovascular procedure. Her neurological status remained unchanged: EDSS was 5.5 and MSIS-29 was 103 points. Yet, control Doppler sonography revealed totally collapsed middle part of the left IJV in the supine position, with no flow through the vein detected (Figures and ). Anatomical and flow parameters in the right IJV were normal. Of note, left IJV widened and the flow was restored with the patient's mouth opened (). Thus, the compression seemed to be caused by aberrant OH. According to the above-described sonographic findings, patient qualified for surgical decompression of the vein. Surgical exploration revealed atypical OH, which was obviously squeezing the vein (). Transection of pathological muscle—performed in general anesthesia—resulted in widening of the vein () and normal blood flow was restored. Perioperative course, except for some nausea, probably due to anesthesia, was uneventful. Color Doppler sonography performed during followup 3 weeks after the surgical procedure demonstrated physiological flow in a fully decompressed vein (). Still, neurological assessment performed 2 months after the operation has shown a slight deterioration of clinical status: EDSS was 6.5 and MSIS-29 was 110 points. OUTPUT:
PMCPatients_common168
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The patient was a 34-year-old Japanese man, whose family history included a father with hypertension, and a mother that suffered a subarachnoid hemorrhage, but which did not include either a consanguineous marriage or any incidence of renal cysts. At the age of 31, the patient presented with mild albuminuria, and a serum creatinine (Cr) level of 2.98 mg/dL. At the age of 34, the patient was admitted to hospital with a creatinine level of 8.2 mg/dL.\\nUpon admission, the patient's height, weight, and blood pressure were 179 cm, 58 kg, and 126/80 mm Hg, respectively. An abdominal ultrasonography revealed that, although the size of both kidneys appeared to be normal, the patient's renal parenchyma showed increased brightness. We performed targeted sequencing using a next-generation sequencer, with the approval by the research ethics committee of Tokyo Medical and Dental University in accordance with the Declaration of Helsinki and the patient's written informed consent.\nOUTPUT:" }, { "from": "agent", "value": "ESRD, NPHP" } ]
As a physician 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 was a 34-year-old Japanese man, whose family history included a father with hypertension, and a mother that suffered a subarachnoid hemorrhage, but which did not include either a consanguineous marriage or any incidence of renal cysts. At the age of 31, the patient presented with mild albuminuria, and a serum creatinine (Cr) level of 2.98 mg/dL. At the age of 34, the patient was admitted to hospital with a creatinine level of 8.2 mg/dL.\nUpon admission, the patient's height, weight, and blood pressure were 179 cm, 58 kg, and 126/80 mm Hg, respectively. An abdominal ultrasonography revealed that, although the size of both kidneys appeared to be normal, the patient's renal parenchyma showed increased brightness. We performed targeted sequencing using a next-generation sequencer, with the approval by the research ethics committee of Tokyo Medical and Dental University in accordance with the Declaration of Helsinki and the patient's written informed consent. OUTPUT:
PMCPatients_common4728
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 75-year-old man presented with progressive left eyelid swelling that started four weeks previously. The tumor cells expressed cytoplasmic cytokeratin- 7 (CK7) but not cytokeratin-20 (CK20). The eyelid swelling improved with prednisone administration. However, leg weakness and swelling developed one week prior, and the patient was consequently transferred to the oncology department of our hospital with a suspected spinal or vertebral metastasis. Orbital magnetic resonance imaging (MRI) revealed exophthalmos and a T2-weighted high-signal-intensity lesion accompanying fatty stranding on the preseptal and septal areas. The lesion was mostly enhanced and spread to the extraconal area; the inferior rectus muscle was also thickened without any definite mass. There was no specific finding showing an acute infarct on brain MRI. The overall imaging findings were suggestive of preseptal and septal cellulitis. Therefore, teicoplanin and ceftriaxone were administered because of concern about the potential for clinical complications of orbital cellulitis including visual disturbances and central nervous system manifestations.\\nUpon physical examination at our clinic, the patient presented with localized relatively ill-demarcated erythematous swelling and indurations at the left upper and lower eyelid (). Histopathological examination revealed diffuse infiltration with tumor cells that formed strands or clusters between the collagen bundles throughout the upper dermis (). The infiltrating tumor cells were round and polygonal and of variable size. Cytoplasm was eosinophilic, while the nuclei of the tumor cells were pleomorphic with conspicuous nucleoli with mitotic figures. Signet ring cells with intracytoplasmic mucinous vacuoles that exhibited nuclei laterally were also observed. Immunohistochemical staining showed the tumor cells expressed cytoplasmic epithelial membrane antigen (EMA) () and CK7 () but neither CK20 nor carcinoembryonic antigen (CEA). The patient's condition deteriorated rapidly, and he died two weeks later.\nOUTPUT:" }, { "from": "agent", "value": "Metastatic 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: A 75-year-old man presented with progressive left eyelid swelling that started four weeks previously. The tumor cells expressed cytoplasmic cytokeratin- 7 (CK7) but not cytokeratin-20 (CK20). The eyelid swelling improved with prednisone administration. However, leg weakness and swelling developed one week prior, and the patient was consequently transferred to the oncology department of our hospital with a suspected spinal or vertebral metastasis. Orbital magnetic resonance imaging (MRI) revealed exophthalmos and a T2-weighted high-signal-intensity lesion accompanying fatty stranding on the preseptal and septal areas. The lesion was mostly enhanced and spread to the extraconal area; the inferior rectus muscle was also thickened without any definite mass. There was no specific finding showing an acute infarct on brain MRI. The overall imaging findings were suggestive of preseptal and septal cellulitis. Therefore, teicoplanin and ceftriaxone were administered because of concern about the potential for clinical complications of orbital cellulitis including visual disturbances and central nervous system manifestations.\nUpon physical examination at our clinic, the patient presented with localized relatively ill-demarcated erythematous swelling and indurations at the left upper and lower eyelid (). Histopathological examination revealed diffuse infiltration with tumor cells that formed strands or clusters between the collagen bundles throughout the upper dermis (). The infiltrating tumor cells were round and polygonal and of variable size. Cytoplasm was eosinophilic, while the nuclei of the tumor cells were pleomorphic with conspicuous nucleoli with mitotic figures. Signet ring cells with intracytoplasmic mucinous vacuoles that exhibited nuclei laterally were also observed. Immunohistochemical staining showed the tumor cells expressed cytoplasmic epithelial membrane antigen (EMA) () and CK7 () but neither CK20 nor carcinoembryonic antigen (CEA). The patient's condition deteriorated rapidly, and he died two weeks later. OUTPUT:
PMCPatients_common5392
[ { "from": "human", "value": "As a physician engaged 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 male child presented with a history of facial puffiness and edema of one year duration. He was diagnosed to have nephrotic syndrome and was treated by a local physician with steroids. He did not improve, however, and was referred to this hospital for further management.\\nThere was no family history of kidney disease. He is the first child of non-consanguineous marriage. There was no history of drug ingestion including exposure to mycotoxins or other herbal medicines. No history of recurrent respiratory symptoms. On examination, patient had stunted growth with moon facies, secondary to steroids and had clinical features of rickets.\\nHis investigations revealed hemoglobin of 10 g/dl, blood urea 33 mg/dl and serum creatinine 0.7 mg/dl. His liver functions revealed hypoalbuminemia of 2.6 g/dl. His liver enzymes were within normal limits. He was human immunodeficiency virus non-reactive and hepatitis B surface antigen and hepatitis C virus and 24 h urine protein was 3565 mg/dl. Complete urine examination showed 2+ albumin, 4-6 red blood cells and granular casts. Ultrasound revealed normal sized kidneys with normal echotexture.\\nHe was started on cyclophosphamide. However, there was no response even after 6 months. Hence a kidney biopsy was done. Biopsy showed 23 glomeruli, four of whom showed segmental sclerosis []. Basement membrane and cellularity were normal in the uninvolved glomeruli. Tubular epithelial cells revealed changes diffusely. The lining cells in many cells revealed enlarged nuclei with lobulated appearance. These cells are larger than the normal tubular epithelial cells []. There was chromatin clumping giving a hyperchromatic appearance. Mitoses were sparse. There is atrophy of the tubules with thickening of tubular basement membrane. There is interstitial fibrosis and interstitial mild lymphomononuclear infiltration [].\\nImmunohistochemical stains for BK virus and cytomegalovirus were negative. Ki-67 index was low. Immunofluorescence did not reveal any significant immune deposits.\\nHe is under regular follow-up and his last creatinine has increased to 1.2 mg/dl.\nOUTPUT:" }, { "from": "agent", "value": "Karyomegalic interstitial nephritis, Focal 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: An 8-year-old male child presented with a history of facial puffiness and edema of one year duration. He was diagnosed to have nephrotic syndrome and was treated by a local physician with steroids. He did not improve, however, and was referred to this hospital for further management.\nThere was no family history of kidney disease. He is the first child of non-consanguineous marriage. There was no history of drug ingestion including exposure to mycotoxins or other herbal medicines. No history of recurrent respiratory symptoms. On examination, patient had stunted growth with moon facies, secondary to steroids and had clinical features of rickets.\nHis investigations revealed hemoglobin of 10 g/dl, blood urea 33 mg/dl and serum creatinine 0.7 mg/dl. His liver functions revealed hypoalbuminemia of 2.6 g/dl. His liver enzymes were within normal limits. He was human immunodeficiency virus non-reactive and hepatitis B surface antigen and hepatitis C virus and 24 h urine protein was 3565 mg/dl. Complete urine examination showed 2+ albumin, 4-6 red blood cells and granular casts. Ultrasound revealed normal sized kidneys with normal echotexture.\nHe was started on cyclophosphamide. However, there was no response even after 6 months. Hence a kidney biopsy was done. Biopsy showed 23 glomeruli, four of whom showed segmental sclerosis []. Basement membrane and cellularity were normal in the uninvolved glomeruli. Tubular epithelial cells revealed changes diffusely. The lining cells in many cells revealed enlarged nuclei with lobulated appearance. These cells are larger than the normal tubular epithelial cells []. There was chromatin clumping giving a hyperchromatic appearance. Mitoses were sparse. There is atrophy of the tubules with thickening of tubular basement membrane. There is interstitial fibrosis and interstitial mild lymphomononuclear infiltration [].\nImmunohistochemical stains for BK virus and cytomegalovirus were negative. Ki-67 index was low. Immunofluorescence did not reveal any significant immune deposits.\nHe is under regular follow-up and his last creatinine has increased to 1.2 mg/dl. OUTPUT:
PMCPatients_common4957
[ { "from": "human", "value": "As a physician engaged in 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 lady presented to our unit with a history of progressive ipsilateral left upper and lower limb weakness on exertion for over four years. This was associated with intermittent aches in affected limbs which worsened on exertion. She occasionally experienced shortness of breath but no orthopnoea, chest pain, cough nor leg swelling. She consulted at several primary care hospitals with no amelioration of symptoms.\\nOn examination, she was stable and not in any distress, apyretic with absent pulses on left upper limb. There was no blood pressure reading on affected limb but the right arm had a blood pressure of 169/79 mmHg and pulse of 69 beats per minute. There was a right carotid bruit and very faint left carotid pulse. The rest of the peripheral pulses were normally palpable. Heart, neurological and the rest of the examination was unremarkable. Investigations included: a normal full blood count; raised erythrocyte sedimentation rate: 25 mm at first hour (normal ≤ 10 mm) and 59 mm at second hour (normal ≤ 25 mm); normal C-reactive protein: 0.29 mg/L (normal ≤ 5 mg/L); normal serum creatinine: 7 mg/L; negative hepatitis B and C serological tests; normal thyroid function tests; negative anti-nuclear antibody test; and negative Veneral Disease Research Laboratory and Treponema pallidum hemagluttin antigen tests . Chest X-ray, electrocardiography and cardiac echography were normal. Doppler vascular assessment revealed significant reduction of abdominal aortic lumen from inflammation, occlusion of left carotid, subclavian, axillary and vertebral arteries. There was also involvement of the brachial, ophthalmic and radial arteries. A reverse flow pattern was observed in the left common carotid, with perfusion of left upper limb from brain ( to ). She was placed on steroids and at two months follow-up, reported marked amelioration of symptoms, but was later lost to follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Takayasu’s arteritis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 30-year-old lady presented to our unit with a history of progressive ipsilateral left upper and lower limb weakness on exertion for over four years. This was associated with intermittent aches in affected limbs which worsened on exertion. She occasionally experienced shortness of breath but no orthopnoea, chest pain, cough nor leg swelling. She consulted at several primary care hospitals with no amelioration of symptoms.\nOn examination, she was stable and not in any distress, apyretic with absent pulses on left upper limb. There was no blood pressure reading on affected limb but the right arm had a blood pressure of 169/79 mmHg and pulse of 69 beats per minute. There was a right carotid bruit and very faint left carotid pulse. The rest of the peripheral pulses were normally palpable. Heart, neurological and the rest of the examination was unremarkable. Investigations included: a normal full blood count; raised erythrocyte sedimentation rate: 25 mm at first hour (normal ≤ 10 mm) and 59 mm at second hour (normal ≤ 25 mm); normal C-reactive protein: 0.29 mg/L (normal ≤ 5 mg/L); normal serum creatinine: 7 mg/L; negative hepatitis B and C serological tests; normal thyroid function tests; negative anti-nuclear antibody test; and negative Veneral Disease Research Laboratory and Treponema pallidum hemagluttin antigen tests . Chest X-ray, electrocardiography and cardiac echography were normal. Doppler vascular assessment revealed significant reduction of abdominal aortic lumen from inflammation, occlusion of left carotid, subclavian, axillary and vertebral arteries. There was also involvement of the brachial, ophthalmic and radial arteries. A reverse flow pattern was observed in the left common carotid, with perfusion of left upper limb from brain ( to ). She was placed on steroids and at two months follow-up, reported marked amelioration of symptoms, but was later lost to follow-up. OUTPUT:
PMCPatients_common2881
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 65 year old male presented to our ENT clinic as an outpatient for a routine yearly check up. He had a history of chronic otitis media with subtotal ear drum perforation in both ears. Left myringoplasty was performed thirty years ago. Otoscopic examination revealed stenosis of the right EEC due to the presence of a mass occupying the superior-posterior part of the canal, which prevented visualization of almost half of the perforated tympanic membrane (Figure ). The middle ear had no signs of infection. Audiometry showed a moderate conductive hearing loss. The patient didn't detect any changes in his ear condition.\\nTemporal bone CT (Figure and ) showed a soft tissue mass in the right EEC. The posterior-superior bony wall of the EEC was eroded; the mass expanded into the mastoid antrum and was separated from the middle cranial fossa by a thin bony plate. Erosion of the ossicles of the right ear was also present. At MRI the mass appeared homogeneous with increased signal intensity relatively to the brain on both T1- and T2- weighted images (Figure and ). Inner ear formations were normal in both ears and pneumatization of both temporal bones was poor. The diagnosis of CG was supposed.\\nBlood work was normal. The cyst was drained and the brownish semi-liquid material was cultivated; no microorganisms where found. The mastoid antrum was entered and the cyst was excised along its direction to the EEC. The posterior canal wall was reconstructed with a piece of auricular cartilage. Then a type III tympanoplasty was performed. The postoperative course was uneventful. The histopathologic report confirmed the diagnosis of CG.\nOUTPUT:" }, { "from": "agent", "value": "Cholesterol granuloma" } ]
As a physician 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 65 year old male presented to our ENT clinic as an outpatient for a routine yearly check up. He had a history of chronic otitis media with subtotal ear drum perforation in both ears. Left myringoplasty was performed thirty years ago. Otoscopic examination revealed stenosis of the right EEC due to the presence of a mass occupying the superior-posterior part of the canal, which prevented visualization of almost half of the perforated tympanic membrane (Figure ). The middle ear had no signs of infection. Audiometry showed a moderate conductive hearing loss. The patient didn't detect any changes in his ear condition.\nTemporal bone CT (Figure and ) showed a soft tissue mass in the right EEC. The posterior-superior bony wall of the EEC was eroded; the mass expanded into the mastoid antrum and was separated from the middle cranial fossa by a thin bony plate. Erosion of the ossicles of the right ear was also present. At MRI the mass appeared homogeneous with increased signal intensity relatively to the brain on both T1- and T2- weighted images (Figure and ). Inner ear formations were normal in both ears and pneumatization of both temporal bones was poor. The diagnosis of CG was supposed.\nBlood work was normal. The cyst was drained and the brownish semi-liquid material was cultivated; no microorganisms where found. The mastoid antrum was entered and the cyst was excised along its direction to the EEC. The posterior canal wall was reconstructed with a piece of auricular cartilage. Then a type III tympanoplasty was performed. The postoperative course was uneventful. The histopathologic report confirmed the diagnosis of CG. OUTPUT:
PMCPatients_common4536
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Relatives noted she was discussing her family matters with her own image. While seeing her children directly, she declared that they were trying to cheat her by putting on the appearance of her children but could recognize them when they spoke to her from the next room or when their reflected images where shown. When she was told the images of her children and the people in front belonged to each other, she insisted that ‘those people’ did not carry the emotions and the mannerisms that were so familiar to her. She vehemently denied that the people in her front were her own children rather became quite defensive and said that “I am sure that they are not my children at all”. (The patient identified the reflected images of her children and by their voice and did not recognize when they came in front of them. The children were seated parallel to the patient in front of the mirror and only the same mirror (45 cm × 45 cm) was used. The patient did feel her old friend next to the image of the children. We did not make her speak to the children in this context when she was asked to identify the reflected image. She felt that the reflected image had all the characteristics of her children. When the children were in the different room, her ability to recognize was inferred by the way she responded to their oral communication from the next room. They were enquiring about general matters such as “How she's doing? What about her food? and their personal matters with reference to routine agricultural activities in the house. To these questions, she relied quite coherently and relevantly without showing any features of disinterest or suspicion but with a sense of authority and experience, which was reconfirmed by her relatives who were quite familiar with her similar premorbid conversational manner.\nOUTPUT:" }, { "from": "agent", "value": "Neurodegeneration, Mirror Image Agnosia, Alzheimer's disease, Coronary artery disease" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Relatives noted she was discussing her family matters with her own image. While seeing her children directly, she declared that they were trying to cheat her by putting on the appearance of her children but could recognize them when they spoke to her from the next room or when their reflected images where shown. When she was told the images of her children and the people in front belonged to each other, she insisted that ‘those people’ did not carry the emotions and the mannerisms that were so familiar to her. She vehemently denied that the people in her front were her own children rather became quite defensive and said that “I am sure that they are not my children at all”. (The patient identified the reflected images of her children and by their voice and did not recognize when they came in front of them. The children were seated parallel to the patient in front of the mirror and only the same mirror (45 cm × 45 cm) was used. The patient did feel her old friend next to the image of the children. We did not make her speak to the children in this context when she was asked to identify the reflected image. She felt that the reflected image had all the characteristics of her children. When the children were in the different room, her ability to recognize was inferred by the way she responded to their oral communication from the next room. They were enquiring about general matters such as “How she's doing? What about her food? and their personal matters with reference to routine agricultural activities in the house. To these questions, she relied quite coherently and relevantly without showing any features of disinterest or suspicion but with a sense of authority and experience, which was reconfirmed by her relatives who were quite familiar with her similar premorbid conversational manner. OUTPUT:
PMCPatients_common605
[ { "from": "human", "value": "As a physician engaged in 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 female with HPV-related OPC was referred to our hospital in December 2016. She had had no recurrence. She was neither a smoker nor a drinker. Fiberoptic laryngoscopy revealed a tumor extending from the tonsil to the soft palate on the right (Figure ). Biopsy of the oropharyngeal lesion confirmed well-differentiated squamous cell carcinoma of the right soft palate. Their maximum diameter was approximately 2 cm. There was no evidence of extranodal infiltration (Figure ). Computed tomography (CT) of the chest, abdomen, and pelvis revealed no abnormalities.\\nShe was staged as clinical T2N2cM0 (stage IVA, AJCC 7th edition 2010, Stage II, AJCC 8th edition 2018, HPV IHC[+], p16/INK4a gene expression [++], type 16 positive and type 18 positive). At the tumor board meeting, it was decided that she should receive cisplatin (CDDP)-based chemoradiotherapy (CRT). Following the placement of percutaneous endoscopic gastrostomy (PEG), CRT (intensity-modulated radiation therapy (IMRT) 70 Gy/35 fractions and CDDP 80 mg/m2 for two cycles) were initiated in February 2017. As she developed Grade 3 neutropenia and leukopenia, chemotherapy was delayed, but she was able to complete radiation therapy without radiation interruption. Radiation dermatitis was Grade 2 and mucositis was Grade 3. After the treatment was completed, she required tube feeding via PEG. Following rehabilitation, she could eat orally after two months. She achieved a complete response and has remained alive since then.\nOUTPUT:" }, { "from": "agent", "value": "Human Papillomavirus-Related Oropharyngeal Cancer, Cervical Cancer" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 69-year-old female with HPV-related OPC was referred to our hospital in December 2016. She had had no recurrence. She was neither a smoker nor a drinker. Fiberoptic laryngoscopy revealed a tumor extending from the tonsil to the soft palate on the right (Figure ). Biopsy of the oropharyngeal lesion confirmed well-differentiated squamous cell carcinoma of the right soft palate. Their maximum diameter was approximately 2 cm. There was no evidence of extranodal infiltration (Figure ). Computed tomography (CT) of the chest, abdomen, and pelvis revealed no abnormalities.\nShe was staged as clinical T2N2cM0 (stage IVA, AJCC 7th edition 2010, Stage II, AJCC 8th edition 2018, HPV IHC[+], p16/INK4a gene expression [++], type 16 positive and type 18 positive). At the tumor board meeting, it was decided that she should receive cisplatin (CDDP)-based chemoradiotherapy (CRT). Following the placement of percutaneous endoscopic gastrostomy (PEG), CRT (intensity-modulated radiation therapy (IMRT) 70 Gy/35 fractions and CDDP 80 mg/m2 for two cycles) were initiated in February 2017. As she developed Grade 3 neutropenia and leukopenia, chemotherapy was delayed, but she was able to complete radiation therapy without radiation interruption. Radiation dermatitis was Grade 2 and mucositis was Grade 3. After the treatment was completed, she required tube feeding via PEG. Following rehabilitation, she could eat orally after two months. She achieved a complete response and has remained alive since then. OUTPUT:
PMCPatients_common2176
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The second patient was an 87-year-old female with a height of 135 cm and body weight of 37 kg. Palliative BAV had not dramatically reduced the severity of the AS, although the valve parameters were slightly improved (AVA 0.61 cm2, Vmax 4.01 m/s, peak PG 64 mmHg, mean PG 38 mmHg by TTE). The anesthesia was induced and maintained using the same drugs as in the first case. Before the incision, PECS II block was performed under ultrasound guidance. The procedure of the block was the same as in the first case except for using a Tuohy needle (Arrow Epidural Needle; Teleflex, USA) for a bolus injection of 20 mL 0.375% ropivacaine and not for inserting a catheter.\\nThe thoracotomy and the insertion of the chest drainage tube were performed at the same intercostal levels as in case 1. After the implantation of the valve (3 h after the previous block), the PECS II block was repeated with a bolus injection of 20 mL 0.2% ropivacaine, and subsequently, a catheter was inserted for postoperative pain management (Contiplex C needle, B. Braun, Melsungen, Germany) (Fig. ). Thereafter, continuous infusion was started as in case 1 before the patient was extubated and transferred to the ICU, where high-quality pain control was obtained without need for additional analgesia, although the patient had nausea, which was treated by intravenous injections of 10 mg metoclopramide. She was transferred from the ICU to the ward on POD 2.\nOUTPUT:" }, { "from": "agent", "value": "Severe AS, Alzheimer’s dementia" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The second patient was an 87-year-old female with a height of 135 cm and body weight of 37 kg. Palliative BAV had not dramatically reduced the severity of the AS, although the valve parameters were slightly improved (AVA 0.61 cm2, Vmax 4.01 m/s, peak PG 64 mmHg, mean PG 38 mmHg by TTE). The anesthesia was induced and maintained using the same drugs as in the first case. Before the incision, PECS II block was performed under ultrasound guidance. The procedure of the block was the same as in the first case except for using a Tuohy needle (Arrow Epidural Needle; Teleflex, USA) for a bolus injection of 20 mL 0.375% ropivacaine and not for inserting a catheter.\nThe thoracotomy and the insertion of the chest drainage tube were performed at the same intercostal levels as in case 1. After the implantation of the valve (3 h after the previous block), the PECS II block was repeated with a bolus injection of 20 mL 0.2% ropivacaine, and subsequently, a catheter was inserted for postoperative pain management (Contiplex C needle, B. Braun, Melsungen, Germany) (Fig. ). Thereafter, continuous infusion was started as in case 1 before the patient was extubated and transferred to the ICU, where high-quality pain control was obtained without need for additional analgesia, although the patient had nausea, which was treated by intravenous injections of 10 mg metoclopramide. She was transferred from the ICU to the ward on POD 2. OUTPUT:
PMCPatients_common111
[ { "from": "human", "value": "As a physician engaged in 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 brought into the emergency department (ED) after being found unresponsive. Paramedics in the field noted that the patient was obtunded, with a Glasgow Coma Score of 3 and a blood sugar of 33 milligrams per deciliter (mg/dL). After multiple unsuccessful attempts were made to gain intravenous (IV) access, paramedics used the EZ-IO® to place a 45 mm IO needle into the left proximal tibia()and administered dextrose at a concentration of 50% (D50). Upon arrival to the ED, the patient remained hypoglycemic and unresponsive. He was intubated, and two 50 mL doses of D50 were administered through the IO needle. Nurses noted resistance upon subsequent administration of medications.\\nPOCUS was performed to evaluate the functionality of the IO needle. A high-frequency linear probe (5–10 MHz; SonoSite® M-turbo) with color Doppler was used to evaluate the area proximal and distal to the IO access in transverse (short) plane of the tibial bone. Color Doppler showed absence of flow in the IO space during injection of a small amount of normal saline, concerning for inappropriate IO needle placement (). Subsequently, the tibial IO needle was removed and a second, 45 mm IO needle was placed into the right humerus (). The patient was resuscitated and stabilized, receiving medications without complication through the humeral IO infusion.\\nFifteen minutes after arrival to the ED, the patient’s left lower extremity was noted to be cool and mottled. A radiograph showed that the IO needle had punctured both the anterior and posterior cortex of the tibia, extending 2 mm beyond the posterior cortex ().\nOUTPUT:" }, { "from": "agent", "value": "Compartment 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 63-year-old male was brought into the emergency department (ED) after being found unresponsive. Paramedics in the field noted that the patient was obtunded, with a Glasgow Coma Score of 3 and a blood sugar of 33 milligrams per deciliter (mg/dL). After multiple unsuccessful attempts were made to gain intravenous (IV) access, paramedics used the EZ-IO® to place a 45 mm IO needle into the left proximal tibia()and administered dextrose at a concentration of 50% (D50). Upon arrival to the ED, the patient remained hypoglycemic and unresponsive. He was intubated, and two 50 mL doses of D50 were administered through the IO needle. Nurses noted resistance upon subsequent administration of medications.\nPOCUS was performed to evaluate the functionality of the IO needle. A high-frequency linear probe (5–10 MHz; SonoSite® M-turbo) with color Doppler was used to evaluate the area proximal and distal to the IO access in transverse (short) plane of the tibial bone. Color Doppler showed absence of flow in the IO space during injection of a small amount of normal saline, concerning for inappropriate IO needle placement (). Subsequently, the tibial IO needle was removed and a second, 45 mm IO needle was placed into the right humerus (). The patient was resuscitated and stabilized, receiving medications without complication through the humeral IO infusion.\nFifteen minutes after arrival to the ED, the patient’s left lower extremity was noted to be cool and mottled. A radiograph showed that the IO needle had punctured both the anterior and posterior cortex of the tibia, extending 2 mm beyond the posterior cortex (). OUTPUT:
PMCPatients_common2239
[ { "from": "human", "value": "As a physician engaged in 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 presented to the gastroenterology clinic complaining of a two-year history of bloating and early satiety. He had a past medical history of diabetes mellitus, coronary artery disease status post stent placement, hypertension, and stage I left palpebral marginal zone lymphoma status post radiation. He denied any prior history of smoking, dysphagia, hematemesis, melena, hematochezia, rectal bleeding, or unintentional weight loss.Due to the reported symptoms, an esophagogastroduodenoscopy (EGD) was performed, showing a normal esophagus (Figure ) and a 2.5 cm polypoid lesion with a wide base at the proximal corpus toward the lesser curvature and distant to the gastric cardia (Figure ). Histopathology elucidated tumor cells positive for cytokeratin 5/6 (CK 5/6) and p63 and negative for CK7, CK20 (Figure , panels A-D).\\nBased on the histopathology results, the patient underwent an endoscopic ultrasound (EUS) and attempted endoscopic mucosal resection (EMR). The EUS showed evidence of a hypoechoic irregular mass at the body of the stomach with sonographic evidence suggesting invasion into the submucosa (layer three of five) and abutting the muscularis propria. Per sonographic criteria, this malignancy was categorized as T2 N0 Mx. An EMR was attempted for a snare mucosal resection and was unsuccessful to obtain tissue for staining.\\nA positron emission tomography (PET) scan demonstrated a 24-mm markedly hypermetabolic lesion in the gastric body, less curvature, and no other lesions in the body. The patient was referred to surgical oncology and underwent a proximal gastrectomy. Referral to medical oncology was also arranged for initiating 5-fluorouracil chemotherapy.\nOUTPUT:" }, { "from": "agent", "value": "Primary Gastric Squamous Cell Carcinoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 66-year-old man presented to the gastroenterology clinic complaining of a two-year history of bloating and early satiety. He had a past medical history of diabetes mellitus, coronary artery disease status post stent placement, hypertension, and stage I left palpebral marginal zone lymphoma status post radiation. He denied any prior history of smoking, dysphagia, hematemesis, melena, hematochezia, rectal bleeding, or unintentional weight loss.Due to the reported symptoms, an esophagogastroduodenoscopy (EGD) was performed, showing a normal esophagus (Figure ) and a 2.5 cm polypoid lesion with a wide base at the proximal corpus toward the lesser curvature and distant to the gastric cardia (Figure ). Histopathology elucidated tumor cells positive for cytokeratin 5/6 (CK 5/6) and p63 and negative for CK7, CK20 (Figure , panels A-D).\nBased on the histopathology results, the patient underwent an endoscopic ultrasound (EUS) and attempted endoscopic mucosal resection (EMR). The EUS showed evidence of a hypoechoic irregular mass at the body of the stomach with sonographic evidence suggesting invasion into the submucosa (layer three of five) and abutting the muscularis propria. Per sonographic criteria, this malignancy was categorized as T2 N0 Mx. An EMR was attempted for a snare mucosal resection and was unsuccessful to obtain tissue for staining.\nA positron emission tomography (PET) scan demonstrated a 24-mm markedly hypermetabolic lesion in the gastric body, less curvature, and no other lesions in the body. The patient was referred to surgical oncology and underwent a proximal gastrectomy. Referral to medical oncology was also arranged for initiating 5-fluorouracil chemotherapy. OUTPUT:
PMCPatients_common4493
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An 81-year-old woman underwent laparoscopic resection rectopexy because of rectal prolapse. The initial hospitalization was uneventful and during the operation no epidural analgesy was applied. Three weeks later, she presented with increasing back pain without neurological signs and symptoms or fever. Due to elevated C-reactive protein (CRP), a deep-seated surgical site infection was suspected. Computed tomography (CT) scan and magnetic resonance imaging (MRI) of the pelvis were normal besides presacral seroma. However, one of four blood culture bottles was positive with Pseudomonas aeruginosa and the patient was treated with Piperacillin/Tazobactam for 14 days. Pain improved transiently but returned shortly after cessation of antibiotics. Subsequent symptomatic therapy was without benefit.\\nThree months after the initial operation, the patient presented with severe back pain radiating to both legs. The lower lumbar spine was highly tender on percussion, but the neurologic examination revealed only a slight loss of muscle strength in the big right toe. Vascular diseases of the lower extremities were excluded. The patient did not have fever at any time. Leucocytes were normal and CRP was moderately elevated to 42 mg/l. ). A barium enema excluded fistulas to the rectum (Fig. ). Culture of CT-guided needle biopsy was positive with P. aeruginosa and antibiotic therapy with 6× 1 g Ceftazidime i.v. per day was started. The pain slowly improved and CRP values declined. After 20 days, the patient developed β-lactam-associated neutropenia. Therefore, treatment was changed to oral ciprofloxacin and continued for another 9 weeks. Pain was managed with fentanyl skin patch, paracetamol, metamizol and pregabalin. The patient fully recovered from the lower back pain. The loss of muscle strength in the big right toe persisted and was interpreted as stenosis of right S5 foramina due to infective destruction which did not require neurosurgical decompression.\nOUTPUT:" }, { "from": "agent", "value": "Vertebral discitis" } ]
As a physician 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 81-year-old woman underwent laparoscopic resection rectopexy because of rectal prolapse. The initial hospitalization was uneventful and during the operation no epidural analgesy was applied. Three weeks later, she presented with increasing back pain without neurological signs and symptoms or fever. Due to elevated C-reactive protein (CRP), a deep-seated surgical site infection was suspected. Computed tomography (CT) scan and magnetic resonance imaging (MRI) of the pelvis were normal besides presacral seroma. However, one of four blood culture bottles was positive with Pseudomonas aeruginosa and the patient was treated with Piperacillin/Tazobactam for 14 days. Pain improved transiently but returned shortly after cessation of antibiotics. Subsequent symptomatic therapy was without benefit.\nThree months after the initial operation, the patient presented with severe back pain radiating to both legs. The lower lumbar spine was highly tender on percussion, but the neurologic examination revealed only a slight loss of muscle strength in the big right toe. Vascular diseases of the lower extremities were excluded. The patient did not have fever at any time. Leucocytes were normal and CRP was moderately elevated to 42 mg/l. ). A barium enema excluded fistulas to the rectum (Fig. ). Culture of CT-guided needle biopsy was positive with P. aeruginosa and antibiotic therapy with 6× 1 g Ceftazidime i.v. per day was started. The pain slowly improved and CRP values declined. After 20 days, the patient developed β-lactam-associated neutropenia. Therefore, treatment was changed to oral ciprofloxacin and continued for another 9 weeks. Pain was managed with fentanyl skin patch, paracetamol, metamizol and pregabalin. The patient fully recovered from the lower back pain. The loss of muscle strength in the big right toe persisted and was interpreted as stenosis of right S5 foramina due to infective destruction which did not require neurosurgical decompression. OUTPUT:
PMCPatients_common4540
[ { "from": "human", "value": "As a physician engaged in 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 girl admitted with abdominal distention, vomiting, constipation and hyperventilation episodes lasting for 1 week. Seizure disorders, constipation and air swallowing were the major symptoms obtained from the medical history. Also it was learned from the family that the patient had difficulty in evacuation of stool from the rectum for a long time. The family was using rectal enema during constipation or rectal digitation for defecation. It was learned that there had been no stool discharge for 4 days. In her physical examination, abdominal distension, abdominal tenderness, rebound, septic appearance were revealed. Bloody discharge was observed in rectal examination. Increased sphincter tonus was palpated in rectal examination. Turgol-tonus was decreased. Abdominal X-ray showed dilated bowel segments with air-fluid levels. Preoperative laboratory evaluation including coagulation function and liver function were normal. Blood Urea Nitrogen, creatinine, white blood cell count, serum sodium, blood glucose, and plasma CRP levels were increased. Blood gases showed acute metabolic acidosis. Electrocardiography showed sinus tachycardia with 500 ms QT interval. In the abdominal exploration, there were several hard nodular lesions in the liver. Hartman procedure and liver biopsy were performed. In the postoperative period, the patient was followed with septic shock. Although intensive care management was given, pulmonary and cardiac functions deteriorated and the patient suddenly died on the second postoperative day. Although permission is taken from the relatives for the study, no further genetic analysis was performed because of the refusal of the relatives.\nOUTPUT:" }, { "from": "agent", "value": "Rett syndrome, Colon cancer, Sigmoid volvulus, Musinous adenocarcinoma, Adenocarcinoma 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 22-year-old girl admitted with abdominal distention, vomiting, constipation and hyperventilation episodes lasting for 1 week. Seizure disorders, constipation and air swallowing were the major symptoms obtained from the medical history. Also it was learned from the family that the patient had difficulty in evacuation of stool from the rectum for a long time. The family was using rectal enema during constipation or rectal digitation for defecation. It was learned that there had been no stool discharge for 4 days. In her physical examination, abdominal distension, abdominal tenderness, rebound, septic appearance were revealed. Bloody discharge was observed in rectal examination. Increased sphincter tonus was palpated in rectal examination. Turgol-tonus was decreased. Abdominal X-ray showed dilated bowel segments with air-fluid levels. Preoperative laboratory evaluation including coagulation function and liver function were normal. Blood Urea Nitrogen, creatinine, white blood cell count, serum sodium, blood glucose, and plasma CRP levels were increased. Blood gases showed acute metabolic acidosis. Electrocardiography showed sinus tachycardia with 500 ms QT interval. In the abdominal exploration, there were several hard nodular lesions in the liver. Hartman procedure and liver biopsy were performed. In the postoperative period, the patient was followed with septic shock. Although intensive care management was given, pulmonary and cardiac functions deteriorated and the patient suddenly died on the second postoperative day. Although permission is taken from the relatives for the study, no further genetic analysis was performed because of the refusal of the relatives. OUTPUT:
PMCPatients_common1698
[ { "from": "human", "value": "As a physician engaged in 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 Caucasian man presented to the emergency department (ED) with pain in the lower abdomen for the previous 48 hours, and associated nausea and decreased appetite. The patient reported that this was the first time that he had this episode; he denied any similar episode in the past, as well as any bowel movement or flatus passed in the last 24 hours. Laboratory investigations showed hemoglobin of 15 gram/dl, white blood count of 16,800 x 103 mm3, the calcium of 9.2 mg/dL, aspartate aminotransferase of 14 U/l, alanine aminotransferase of 19 U/l, alkaline phosphatase of 81 U/l, amylase of 19 U/l, lipase of 25 U/l and triglycerides of 76 mg/dL. Based on the laboratory investigations, an ultrasound of the abdomen was ordered, the results of which were unremarkable. CT scan of the abdomen with contrast was planned to determine the cause of non-specified pain.\\nThe patient was started on Ringer’s lactate at a rate of 250cc/hr, morphine for pain management, and ondansetron for nausea. A CT scan was planned during his follow-up visit in two weeks, which the patient did not attend.\nOUTPUT:" }, { "from": "agent", "value": "Acute Interstitial Pancreatitis, Ulcerative Colitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 44-year-old Caucasian man presented to the emergency department (ED) with pain in the lower abdomen for the previous 48 hours, and associated nausea and decreased appetite. The patient reported that this was the first time that he had this episode; he denied any similar episode in the past, as well as any bowel movement or flatus passed in the last 24 hours. Laboratory investigations showed hemoglobin of 15 gram/dl, white blood count of 16,800 x 103 mm3, the calcium of 9.2 mg/dL, aspartate aminotransferase of 14 U/l, alanine aminotransferase of 19 U/l, alkaline phosphatase of 81 U/l, amylase of 19 U/l, lipase of 25 U/l and triglycerides of 76 mg/dL. Based on the laboratory investigations, an ultrasound of the abdomen was ordered, the results of which were unremarkable. CT scan of the abdomen with contrast was planned to determine the cause of non-specified pain.\nThe patient was started on Ringer’s lactate at a rate of 250cc/hr, morphine for pain management, and ondansetron for nausea. A CT scan was planned during his follow-up visit in two weeks, which the patient did not attend. OUTPUT:
PMCPatients_common165
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Case 2: A 24-year-old previously healthy gravida 3 para 0200 arrived in the U.S. at 11 weeks of gestation, after emigrating from Cuba through Central America and Mexico. She and her husband denied any symptoms consistent with a flavivirus infection; they had unprotected intercourse through the first and early second trimester. She was seen for her initial prenatal visit at 15 weeks’ gestation, and testing for ZIKV by serum and urine NAT and IgM were initially and persistently negative. A fetal ultrasound with neurosonography performed at 23 weeks showed no microcephaly but was significant for borderline asymmetric ventriculomegaly, with a thin cortex and dolichocephaly, but absence of microcephaly; amniocentesis was declined. Serial fetal ultrasound imaging throughout pregnancy was performed secondary to initial 23-week ultrasound findings. At 37 weeks, induction of labor was undertaken for intrahepatic cholestasis of pregnancy and a cesarean delivery was performed for fetal intolerance of labor. Neonatal findings were significant for craniofacial dimorphism with a cleft palate, microopthalmia, and hypertonia with asymmetric EEG findings consistent with abnormalities in the right hemisphere. She developed neonatal seizures and failed her newborn hearing screen. Representative neonatal and infant brain imaging are shown in , and include callosal dysgenesis with asymmetric ventriculomegaly, a thin cortex, and dolichocephaly with bilateral optic nerve hypoplasia. There were no patellar nor limb abnormalities. Neonatal and infant ZIKV and TORCH laboratory testing was negative. No evidence of small nor large structural chromosomal variations by CMA was found, and whole exome sequencing (WES) failed to reveal neither pathogenic nor likely pathogenic variants in disease genes related to the clinical phenotype. A novel de novo heterozygous c.3667G>C (p.V1223L) variant in the MED12 gene (located on ChrX:70349255) of unknown clinical significance (VUS) was found. This female infant has clinically persistent neurologic disease and early developmental delay.\nOUTPUT:" }, { "from": "agent", "value": "Congenital Zika 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: Case 2: A 24-year-old previously healthy gravida 3 para 0200 arrived in the U.S. at 11 weeks of gestation, after emigrating from Cuba through Central America and Mexico. She and her husband denied any symptoms consistent with a flavivirus infection; they had unprotected intercourse through the first and early second trimester. She was seen for her initial prenatal visit at 15 weeks’ gestation, and testing for ZIKV by serum and urine NAT and IgM were initially and persistently negative. A fetal ultrasound with neurosonography performed at 23 weeks showed no microcephaly but was significant for borderline asymmetric ventriculomegaly, with a thin cortex and dolichocephaly, but absence of microcephaly; amniocentesis was declined. Serial fetal ultrasound imaging throughout pregnancy was performed secondary to initial 23-week ultrasound findings. At 37 weeks, induction of labor was undertaken for intrahepatic cholestasis of pregnancy and a cesarean delivery was performed for fetal intolerance of labor. Neonatal findings were significant for craniofacial dimorphism with a cleft palate, microopthalmia, and hypertonia with asymmetric EEG findings consistent with abnormalities in the right hemisphere. She developed neonatal seizures and failed her newborn hearing screen. Representative neonatal and infant brain imaging are shown in , and include callosal dysgenesis with asymmetric ventriculomegaly, a thin cortex, and dolichocephaly with bilateral optic nerve hypoplasia. There were no patellar nor limb abnormalities. Neonatal and infant ZIKV and TORCH laboratory testing was negative. No evidence of small nor large structural chromosomal variations by CMA was found, and whole exome sequencing (WES) failed to reveal neither pathogenic nor likely pathogenic variants in disease genes related to the clinical phenotype. A novel de novo heterozygous c.3667G>C (p.V1223L) variant in the MED12 gene (located on ChrX:70349255) of unknown clinical significance (VUS) was found. This female infant has clinically persistent neurologic disease and early developmental delay. OUTPUT:
PMCPatients_common2037
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Psychiatric symptoms developed in a previously healthy 46-year-old woman, and she received prolonged ventilatory support because of central hypoventilation, seizures, involuntary movements, and autonomic instability (see [ for details). In brief, in late March 2008, she presented with distortion of visual perception and unusual behavior. In early April, she was entered to our hospital because of generalized seizures and delusional thinking. Brain MRI on day 1 was normal (Fig. A). Twelve days after admission, involuntary movements and frequent seizures developed. She required ventilatory support and intravenous sedative drugs. On day 19 and day 42 after admission, brain MRI showed that DCA was progressing without abnormal intensity (Fig. B, C). The disease course is shown in a previously published figure (Supplemental Figure 1 see [ for details). Autonomic instability also occurred. The involuntary movements and seizures were unresponsive to antiepileptic drugs. High doses of intravenous propofol (4 mg/kg/h) and midazolam (3.75 mg/kg/h) werr needed while she received mechanical ventilation from April 2008 through February 2011. She repeatedly received intravenous steroids (500 mg/day, 3 days, 2 times), plasmapheresis (4 times, alternating days), and intravenous immunoglobulin (0.4 g/kg/day, 5 days). A teratoma or other type of tumor was not found. Frequencies of seizures and involuntary movements were decreased in November 2009, and the dose of intravenous propofol was slowly tapered. She was free of ventilatory support in February 2011. Brain MRI in December 2011 showed the further progression of DCA (Fig. D). In April 2012, she required constant nursing care, and she was bedridden and incontinent. Anti-NMDAR antibody titers in serum and cerebrospinal fluid (CSF) samples were 1:1600 and 1:320, respectively, at the first sampling and 1:200 and 1:80 4 years after the onset of disease.\nOUTPUT:" }, { "from": "agent", "value": "Anti-N-methyl-D-aspartate receptor encephalitis" } ]
As a physician 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: Psychiatric symptoms developed in a previously healthy 46-year-old woman, and she received prolonged ventilatory support because of central hypoventilation, seizures, involuntary movements, and autonomic instability (see [ for details). In brief, in late March 2008, she presented with distortion of visual perception and unusual behavior. In early April, she was entered to our hospital because of generalized seizures and delusional thinking. Brain MRI on day 1 was normal (Fig. A). Twelve days after admission, involuntary movements and frequent seizures developed. She required ventilatory support and intravenous sedative drugs. On day 19 and day 42 after admission, brain MRI showed that DCA was progressing without abnormal intensity (Fig. B, C). The disease course is shown in a previously published figure (Supplemental Figure 1 see [ for details). Autonomic instability also occurred. The involuntary movements and seizures were unresponsive to antiepileptic drugs. High doses of intravenous propofol (4 mg/kg/h) and midazolam (3.75 mg/kg/h) werr needed while she received mechanical ventilation from April 2008 through February 2011. She repeatedly received intravenous steroids (500 mg/day, 3 days, 2 times), plasmapheresis (4 times, alternating days), and intravenous immunoglobulin (0.4 g/kg/day, 5 days). A teratoma or other type of tumor was not found. Frequencies of seizures and involuntary movements were decreased in November 2009, and the dose of intravenous propofol was slowly tapered. She was free of ventilatory support in February 2011. Brain MRI in December 2011 showed the further progression of DCA (Fig. D). In April 2012, she required constant nursing care, and she was bedridden and incontinent. Anti-NMDAR antibody titers in serum and cerebrospinal fluid (CSF) samples were 1:1600 and 1:320, respectively, at the first sampling and 1:200 and 1:80 4 years after the onset of disease. OUTPUT:
PMCPatients_common2315
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 76-year-old woman complained of left inferior limb pain and intermittent claudication. She was diagnosed with ASO in another clinic about 10 years ago. While the prolonged conservative medical treatment was undergone, the condition got worse. Then, she consulted a vascular surgeon in another hospital and the angiographic examination was undergone. The complete obstruction of left femoral artery was observed. Percutaneous transluminal angiography (PTA) was performed and stent was detained at the left femoral artery (). Revascularization was achieved and she could walk about 300 meters postoperatively. However, the left inferior limb pain still remained. Since the limb pain got worse, she was not able to walk five months after detaining stent. She was diagnosed with rapidly destructive coxarthrosis by plain radiography in an orthopaedic clinic and admitted to our hospital for the purpose of total hip arthroplasty (THA). Terminal stage of coxarthrosis was diagnosed from these findings. Angiography taken just before THA at our hospital showed increasing of blood vessel around left hip joint (). These findings suggested compensation of the ischemia. Six months after detaining stent, THA was performed with noncemented cup and cemented stem. From microscopic findings in high magnification field (×100), empty lacuna and addition of newly formed bones adjacent to those necrotic bone areas were observed (). These histological findings indicated that bone necrosis occurred firstly and osteoarthritic change progressed secondarily.\nOUTPUT:" }, { "from": "agent", "value": "Osteonecrosis of Femoral Head" } ]
As a physician 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 76-year-old woman complained of left inferior limb pain and intermittent claudication. She was diagnosed with ASO in another clinic about 10 years ago. While the prolonged conservative medical treatment was undergone, the condition got worse. Then, she consulted a vascular surgeon in another hospital and the angiographic examination was undergone. The complete obstruction of left femoral artery was observed. Percutaneous transluminal angiography (PTA) was performed and stent was detained at the left femoral artery (). Revascularization was achieved and she could walk about 300 meters postoperatively. However, the left inferior limb pain still remained. Since the limb pain got worse, she was not able to walk five months after detaining stent. She was diagnosed with rapidly destructive coxarthrosis by plain radiography in an orthopaedic clinic and admitted to our hospital for the purpose of total hip arthroplasty (THA). Terminal stage of coxarthrosis was diagnosed from these findings. Angiography taken just before THA at our hospital showed increasing of blood vessel around left hip joint (). These findings suggested compensation of the ischemia. Six months after detaining stent, THA was performed with noncemented cup and cemented stem. From microscopic findings in high magnification field (×100), empty lacuna and addition of newly formed bones adjacent to those necrotic bone areas were observed (). These histological findings indicated that bone necrosis occurred firstly and osteoarthritic change progressed secondarily. OUTPUT:
PMCPatients_common692
[ { "from": "human", "value": "As a physician engaged in 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 unmarried man was referred to the men’s health clinic of our hospital due to flu-like symptoms that developed after ejaculation by masturbation and that persisted for about 2 days. He had his first masturbation with hand thrust at the age of 19 years. Since then, he experienced general fatigue, chills, headache, nasal congestion, and muscle pain almost every after ejaculation. The symptoms lasted for about 2 days and spontaneously disappeared. Moreover, the frequency of his morning erection significantly decreased. The patient’s symptoms met the POIS criteria; therefore, he was diagnosed with POIS.\\nThe growth of his pubic hair and penis was normal (each with a Tanner’s grade of 5). On physical examination, his testicular volume was a little atrophic on the left side (12 mL).\\nHis total testosterone level (4.75 ng/mL), gonadotropic level (luteinizing hormone: 3.5 mIU/mL and follicle stimulating hormone: 8.7 mIU/mL) was normal, and free testosterone level (10.3 pg/mL) was mildly low.\\nThe patient’s AMS score was 45 (psychological: 10, somatic: 19, and sexual: 16), and his SHIM score was 3.\\nAntihistamine drugs were administered for allergic symptoms. However, the treatment was not effective. For headache and muscle pain, celecoxib 200 mg, which is an NSAID, was administered daily just after ejaculation. Immediately after the intake of the drug, headache and muscle pain were relieved, and the patient was able to ejaculate 3 days per week. However, general fatigue did not improve.\\nThereafter, in addition to NSAIDs, 250 mg of testosterone enanthate was administered as a TRT every 2 weeks because the patient’s serum free testosterone level was lower than 70% of the average value in young adult men. His general fatigue significantly improved, and morning erection has been achieved every day. Therefore, he can ejaculate everyday by masturbation. The patient’s AMS score decreased to 21 and SHIM score increased to 7. The interval of drug administration was changed from 2 to 4 weeks. However, no recurrence of symptoms was observed.\\nTRT was switched to testosterone ointment (Glowmin®; Daito Pharma, Tokyo, Japan), and his symptoms continually improved.\nOUTPUT:" }, { "from": "agent", "value": "Post-orgasmic illness syndrome, Hypogonadism" } ]
As a physician 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 unmarried man was referred to the men’s health clinic of our hospital due to flu-like symptoms that developed after ejaculation by masturbation and that persisted for about 2 days. He had his first masturbation with hand thrust at the age of 19 years. Since then, he experienced general fatigue, chills, headache, nasal congestion, and muscle pain almost every after ejaculation. The symptoms lasted for about 2 days and spontaneously disappeared. Moreover, the frequency of his morning erection significantly decreased. The patient’s symptoms met the POIS criteria; therefore, he was diagnosed with POIS.\nThe growth of his pubic hair and penis was normal (each with a Tanner’s grade of 5). On physical examination, his testicular volume was a little atrophic on the left side (12 mL).\nHis total testosterone level (4.75 ng/mL), gonadotropic level (luteinizing hormone: 3.5 mIU/mL and follicle stimulating hormone: 8.7 mIU/mL) was normal, and free testosterone level (10.3 pg/mL) was mildly low.\nThe patient’s AMS score was 45 (psychological: 10, somatic: 19, and sexual: 16), and his SHIM score was 3.\nAntihistamine drugs were administered for allergic symptoms. However, the treatment was not effective. For headache and muscle pain, celecoxib 200 mg, which is an NSAID, was administered daily just after ejaculation. Immediately after the intake of the drug, headache and muscle pain were relieved, and the patient was able to ejaculate 3 days per week. However, general fatigue did not improve.\nThereafter, in addition to NSAIDs, 250 mg of testosterone enanthate was administered as a TRT every 2 weeks because the patient’s serum free testosterone level was lower than 70% of the average value in young adult men. His general fatigue significantly improved, and morning erection has been achieved every day. Therefore, he can ejaculate everyday by masturbation. The patient’s AMS score decreased to 21 and SHIM score increased to 7. The interval of drug administration was changed from 2 to 4 weeks. However, no recurrence of symptoms was observed.\nTRT was switched to testosterone ointment (Glowmin®; Daito Pharma, Tokyo, Japan), and his symptoms continually improved. OUTPUT:
PMCPatients_common1440
[ { "from": "human", "value": "As a physician engaged 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 morbidly obese 17-year-old Hispanic man who arrived at the emergency department with a three-day of worsening epigastric and right upper quadrant abdominal pain associated with emesis. On arrival, he had a temperature of 99.8 °F, blood pressure of 140/57 mmHg, heart rate of 121 beats per minute, respiratory rate of 20, oxygen saturation of 94% at room air, and body mass index (BMI) of 40.37 kg/m2. He was obese on physical examination, with hyperpigmentation, velvety skin, and multiple skin tags around the neck area, significant central adiposity, and mild epigastric tenderness. Labs were notable for lipase of 458 mg/dl and blood glucose (BG) of 350 mg/dl. He had a milky blood sample prompting triglyceride (TG) level check, which was greater than 4000 mg/dl (Table ).\\nOn further investigation it was found that he had a hemoglobin A1C of 10.3%. Serum alcohol level was normal and CT abdomen did not show any gallbladder pathology, also he has denied any trauma to the abdomen. Due to hemodynamic stability, insulin drip with a goal of TG less than 500 mg/dl and BG of 250 mg/dl was recommended instead of immediate plasmapheresis by nephrology services. While on insulin drip blood glucose was closely monitored to prevent hypoglycemia (Table ).\\nLater, he got transferred to the intensive care unit (ICU) and evaluated by an endocrinology service for subcutaneous insulin transition. TG levels significantly improved within 12 hours (4000→1,482) as shown in the table above and transitioned to subcutaneous insulin at a 548 mg/dl TG level.\\nAfter three days, he was successfully discharged home from ICU with subcutaneous insulin and fenofibrate prescriptions. He was extensively counseled regarding life style modifications, together with weight reduction, healthy dietary habits and medication compliance.\nOUTPUT:" }, { "from": "agent", "value": "New Onset Diabetes Mellitus, Hypertriglyceridemia-Induced Pancreatitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: We present a case of a morbidly obese 17-year-old Hispanic man who arrived at the emergency department with a three-day of worsening epigastric and right upper quadrant abdominal pain associated with emesis. On arrival, he had a temperature of 99.8 °F, blood pressure of 140/57 mmHg, heart rate of 121 beats per minute, respiratory rate of 20, oxygen saturation of 94% at room air, and body mass index (BMI) of 40.37 kg/m2. He was obese on physical examination, with hyperpigmentation, velvety skin, and multiple skin tags around the neck area, significant central adiposity, and mild epigastric tenderness. Labs were notable for lipase of 458 mg/dl and blood glucose (BG) of 350 mg/dl. He had a milky blood sample prompting triglyceride (TG) level check, which was greater than 4000 mg/dl (Table ).\nOn further investigation it was found that he had a hemoglobin A1C of 10.3%. Serum alcohol level was normal and CT abdomen did not show any gallbladder pathology, also he has denied any trauma to the abdomen. Due to hemodynamic stability, insulin drip with a goal of TG less than 500 mg/dl and BG of 250 mg/dl was recommended instead of immediate plasmapheresis by nephrology services. While on insulin drip blood glucose was closely monitored to prevent hypoglycemia (Table ).\nLater, he got transferred to the intensive care unit (ICU) and evaluated by an endocrinology service for subcutaneous insulin transition. TG levels significantly improved within 12 hours (4000→1,482) as shown in the table above and transitioned to subcutaneous insulin at a 548 mg/dl TG level.\nAfter three days, he was successfully discharged home from ICU with subcutaneous insulin and fenofibrate prescriptions. He was extensively counseled regarding life style modifications, together with weight reduction, healthy dietary habits and medication compliance. OUTPUT:
PMCPatients_common3238
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 26-year-old woman was referred to Madani Heart Hospital, affiliated with Tabriz University of Medical Sciences, Tabriz, Iran, due to palpitation and exertional dyspnea, which had been intensified in the preceding 5 months. The patient had no remarkable medical history, and her ECG illustrated a sinus rhythm. In the physical examination, there was a 2/6 systolic murmur at the left sternal border, a 3/6 mid-diastolic murmur, and a mitral opening snap at the apex area. Additionally, pulmonary artery pressure and the Wilkins score were calculated to be 38 mmHg and 8, respectively. The patient was, therefore, candidated for PBMV ().\\nThe patient underwent PBMV using the Inoue-Balloon Catheter with a 28-mm balloon. These findings were subsequently confirmed by TEE ( & ).\\nConsequently, the patient received 1 mg/kg (60 mg) of enoxaparin through the subcutaneous route twice a day plus 5 mg of warfarin daily through the oral route. The subsequent TTE examinations revealed a decrease in the size of clot 48 hours after the treatment and no mass 4 days after the treatment.\nOUTPUT:" }, { "from": "agent", "value": "Severe rheumatic mitral stenosis, (2+) mitral regurgitation, Right atrial clot 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 26-year-old woman was referred to Madani Heart Hospital, affiliated with Tabriz University of Medical Sciences, Tabriz, Iran, due to palpitation and exertional dyspnea, which had been intensified in the preceding 5 months. The patient had no remarkable medical history, and her ECG illustrated a sinus rhythm. In the physical examination, there was a 2/6 systolic murmur at the left sternal border, a 3/6 mid-diastolic murmur, and a mitral opening snap at the apex area. Additionally, pulmonary artery pressure and the Wilkins score were calculated to be 38 mmHg and 8, respectively. The patient was, therefore, candidated for PBMV ().\nThe patient underwent PBMV using the Inoue-Balloon Catheter with a 28-mm balloon. These findings were subsequently confirmed by TEE ( & ).\nConsequently, the patient received 1 mg/kg (60 mg) of enoxaparin through the subcutaneous route twice a day plus 5 mg of warfarin daily through the oral route. The subsequent TTE examinations revealed a decrease in the size of clot 48 hours after the treatment and no mass 4 days after the treatment. OUTPUT:
PMCPatients_common770
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 37-year-old Nepalese man, with hypertension that was controlled by medications, presented with a two-day history of fever and myalgia. There was no history of any recent travel or contact with an ill person.\\nOn the initial presentation, his clinical examination was remarkable, with a high-grade temperature of 39°C. He was breathing comfortably in room air, and a respiratory system examination indicated that he was normal. The test was negative for the SARS-CoV-2 virus, and thus, he was discharged home with symptomatic treatment, and no further investigations were performed.\\nTen days later, he presented with a five-day history of fever, cough, and generalized body aches. This time, the patient’s breathing rate increased to 24 breaths per minute, with tachycardia of 100-110 beats per minute, oxygen saturation of 94%-95% in room air, and bilateral basal crackles on chest auscultation.\\nHis chest X-ray (CXR; Figure ) showed bilateral middle and lower zone opacities, and treatment was initiated with ceftriaxone and azithromycin for community-acquired pneumonia. However, his condition did not improve. Septic workup, including blood and sputum culture, tuberculosis (TB) workup including sputum smear, and urine culture were negative. Laboratory investigations were remarkable for lymphopenia, high D-dimer, C-reactive protein (CRP), and ferritin. He improved during his hospital stay with no further clinical deterioration and was discharged home with follow-up in the outpatient department.\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 37-year-old Nepalese man, with hypertension that was controlled by medications, presented with a two-day history of fever and myalgia. There was no history of any recent travel or contact with an ill person.\nOn the initial presentation, his clinical examination was remarkable, with a high-grade temperature of 39°C. He was breathing comfortably in room air, and a respiratory system examination indicated that he was normal. The test was negative for the SARS-CoV-2 virus, and thus, he was discharged home with symptomatic treatment, and no further investigations were performed.\nTen days later, he presented with a five-day history of fever, cough, and generalized body aches. This time, the patient’s breathing rate increased to 24 breaths per minute, with tachycardia of 100-110 beats per minute, oxygen saturation of 94%-95% in room air, and bilateral basal crackles on chest auscultation.\nHis chest X-ray (CXR; Figure ) showed bilateral middle and lower zone opacities, and treatment was initiated with ceftriaxone and azithromycin for community-acquired pneumonia. However, his condition did not improve. Septic workup, including blood and sputum culture, tuberculosis (TB) workup including sputum smear, and urine culture were negative. Laboratory investigations were remarkable for lymphopenia, high D-dimer, C-reactive protein (CRP), and ferritin. He improved during his hospital stay with no further clinical deterioration and was discharged home with follow-up in the outpatient department. OUTPUT:
PMCPatients_common1421
[ { "from": "human", "value": "As a physician engaged in 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 gentleman, a known case of rheumatic heart disease with mitral valve regurgitation and bicuspid aortic valve, presented to the emergency department complaining of pain in the left upper abdomen for two days. The pain was sudden in onset, progressive, not responding to analgesics, and associated with abdominal distension. There was no history of nausea, vomiting, fever, and constipation. Additionally, there was no history of trauma or any surgery. On presentation, he was conscious and oriented, with tachycardia (120 beats/minutes) and hypotension (90/60 mmHg). On examination, his abdomen was distended with tenderness in the left hypochondriac region.\\nBlood investigation showed normocytic normochromic anemia (hemoglobin 6.5 g/dL) and a total leucocyte count of 1.94 lakhs/dL. Ultrasonography of the abdomen revealed free fluid abdomen, splenomegaly, and a subcapsular splenic hematoma. Contrast-enhanced computed tomography (CECT) confirmed splenomegaly (19 cm) with a grade three splenic laceration (3.3 × 2.6 cm) in the lower pole with a subcapsular hematoma (>50% of surface area) with hemoperitoneum (Figure ).\\nBecause of hemodynamic instability, despite resuscitation, he underwent emergency splenectomy. Intraoperatively, 1,200 mL of hemoperitoneum was observed. Spleen was enlarged (18 cm) with a 3 cm laceration in the lower pole and a ruptured subcapsular hematoma (Figure ).\\nIntraoperatively, he was transfused with four units of packed cells, fresh frozen plasma, and platelets. The postoperative period was uneventful. He was further evaluated for CML with bone marrow biopsy, which revealed CML in the chronic phase with World Health Organization grade I reticulin fibrosis. Histopathological examination of the spleen revealed features consistent with CML in the chronic phase (Figure ).\\nHe was started on hydroxyurea and discharged for further follow-up with medical oncology.\nOUTPUT:" }, { "from": "agent", "value": "Spontaneous Splenic Rupture, Chronic Myeloid 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 48-year-old gentleman, a known case of rheumatic heart disease with mitral valve regurgitation and bicuspid aortic valve, presented to the emergency department complaining of pain in the left upper abdomen for two days. The pain was sudden in onset, progressive, not responding to analgesics, and associated with abdominal distension. There was no history of nausea, vomiting, fever, and constipation. Additionally, there was no history of trauma or any surgery. On presentation, he was conscious and oriented, with tachycardia (120 beats/minutes) and hypotension (90/60 mmHg). On examination, his abdomen was distended with tenderness in the left hypochondriac region.\nBlood investigation showed normocytic normochromic anemia (hemoglobin 6.5 g/dL) and a total leucocyte count of 1.94 lakhs/dL. Ultrasonography of the abdomen revealed free fluid abdomen, splenomegaly, and a subcapsular splenic hematoma. Contrast-enhanced computed tomography (CECT) confirmed splenomegaly (19 cm) with a grade three splenic laceration (3.3 × 2.6 cm) in the lower pole with a subcapsular hematoma (>50% of surface area) with hemoperitoneum (Figure ).\nBecause of hemodynamic instability, despite resuscitation, he underwent emergency splenectomy. Intraoperatively, 1,200 mL of hemoperitoneum was observed. Spleen was enlarged (18 cm) with a 3 cm laceration in the lower pole and a ruptured subcapsular hematoma (Figure ).\nIntraoperatively, he was transfused with four units of packed cells, fresh frozen plasma, and platelets. The postoperative period was uneventful. He was further evaluated for CML with bone marrow biopsy, which revealed CML in the chronic phase with World Health Organization grade I reticulin fibrosis. Histopathological examination of the spleen revealed features consistent with CML in the chronic phase (Figure ).\nHe was started on hydroxyurea and discharged for further follow-up with medical oncology. OUTPUT:
PMCPatients_common1219
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The second patient was a 56-year-old Caucasian woman who underwent a mastectomy for a relapse after a first breast cancer treated by tumorectomy followed by radiotherapy. Despite the possibilities of immediate breast reconstruction, she refused to undergo such a procedure. Ten months later, she was motivated for a delayed procedure. Because we were not used to performing deep inferior epigastric perforator flaps at that time, she had a breast reconstruction using a pedicled TRAM flap.\\nDespite the absence of intraoperative complications and patient-related risk factors, the flap presented an early venous congestion that was treated from the second to the fifth postoperative day by leeching and heparin-moist gauzes. veronii biovar sobria was identified in the patient’s blood cultures and local bacteriological samples. An antibiogram showed resistance to amoxicillin/clavulanic acid, which was stopped at day 10 and replaced by cefotaxime (6g/day) for 10 days followed by oral ofloxacin (400mg/day) for eight days. The fever ceased on the eleventh postoperative day after four days of antibiotic treatment. She left the hospital at day 20.\\nFor our two patients, the sample was plated to blood agar, Drigalski agar and a brain-heart infusion. The isolate was identified by using a Vitek 2 Gram-negative card (bioMérieux Inc., Marcy L’étoile, France). Antimicrobial susceptibility was tested by using a 24-hour disk-diffusion method on Mueller-Hinton agar plates incubated at 37°C in an ambient air incubator.\nOUTPUT:" }, { "from": "agent", "value": "Septicemia, Partial necrosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The second patient was a 56-year-old Caucasian woman who underwent a mastectomy for a relapse after a first breast cancer treated by tumorectomy followed by radiotherapy. Despite the possibilities of immediate breast reconstruction, she refused to undergo such a procedure. Ten months later, she was motivated for a delayed procedure. Because we were not used to performing deep inferior epigastric perforator flaps at that time, she had a breast reconstruction using a pedicled TRAM flap.\nDespite the absence of intraoperative complications and patient-related risk factors, the flap presented an early venous congestion that was treated from the second to the fifth postoperative day by leeching and heparin-moist gauzes. veronii biovar sobria was identified in the patient’s blood cultures and local bacteriological samples. An antibiogram showed resistance to amoxicillin/clavulanic acid, which was stopped at day 10 and replaced by cefotaxime (6g/day) for 10 days followed by oral ofloxacin (400mg/day) for eight days. The fever ceased on the eleventh postoperative day after four days of antibiotic treatment. She left the hospital at day 20.\nFor our two patients, the sample was plated to blood agar, Drigalski agar and a brain-heart infusion. The isolate was identified by using a Vitek 2 Gram-negative card (bioMérieux Inc., Marcy L’étoile, France). Antimicrobial susceptibility was tested by using a 24-hour disk-diffusion method on Mueller-Hinton agar plates incubated at 37°C in an ambient air incubator. OUTPUT:
PMCPatients_common4697
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 9-year-old right-handed girl with a history of hemolytic anemia, status post-splenectomy, and previously identified right frontal encephalomalacia presented with a 1-month history of episodic right upper extremity weakness and ‘garbled’ speech.\\nHer neurological examination was notable for episodes of nonfluent speech and dysarthria, some right-left confusion, and episodic distal right arm weakness and paresthesias. Her laboratory studies were notable for a macrocytic hemolytic anemia and thrombocytosis, but negative for hypercoagulable, inflammatory, cardiac, infectious, and autoimmune markers. Extensive hematological testing performed for anemia 3 years earlier had revealed an Hb Casper mutation. However, she never returned for follow-up until her current presentation. There was no known family history of strokes, cardiac issues or hematologic abnormalities.\\nAn initial MRI showed multiple foci of impeded diffusion in the left frontal lobe (fig. ). Fluid-attenuated inversion-recovery (FLAIR) imaging showed an increased T2 signal involving the left hemispheric leptomeninges and perivascular spaces (fig. ) and chronic right frontal encephalomalacia (not shown). Subsequent conventional angiography showed an occlusion of the petrous right internal carotid artery (ICA) with distal reconstitution of the right middle cerebral artery (MCA) and A1 segments through prominent vascular collaterals (not shown), and an occlusion of the proximal supraclinoid left ICA (fig. arrow) with skull base collateral reconstitution of the left anterior cerebral artery (ACA) (fig. ). Left vertebral angiography (fig. ) showed extensive pial-collateral flow over the cerebral convexities from the distal posterior cerebral artery branches with reconstitution of distal MCA territories bilaterally. The patient ultimately underwent bilateral pial synangiosis surgery 2 months later, with no subsequent neurological deficits. More surgically relevant aspects of this patient's treatment have been recently described elsewhere [].\nOUTPUT:" }, { "from": "agent", "value": "Hemoglobin Casper/Southampton, Moyamoya 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 9-year-old right-handed girl with a history of hemolytic anemia, status post-splenectomy, and previously identified right frontal encephalomalacia presented with a 1-month history of episodic right upper extremity weakness and ‘garbled’ speech.\nHer neurological examination was notable for episodes of nonfluent speech and dysarthria, some right-left confusion, and episodic distal right arm weakness and paresthesias. Her laboratory studies were notable for a macrocytic hemolytic anemia and thrombocytosis, but negative for hypercoagulable, inflammatory, cardiac, infectious, and autoimmune markers. Extensive hematological testing performed for anemia 3 years earlier had revealed an Hb Casper mutation. However, she never returned for follow-up until her current presentation. There was no known family history of strokes, cardiac issues or hematologic abnormalities.\nAn initial MRI showed multiple foci of impeded diffusion in the left frontal lobe (fig. ). Fluid-attenuated inversion-recovery (FLAIR) imaging showed an increased T2 signal involving the left hemispheric leptomeninges and perivascular spaces (fig. ) and chronic right frontal encephalomalacia (not shown). Subsequent conventional angiography showed an occlusion of the petrous right internal carotid artery (ICA) with distal reconstitution of the right middle cerebral artery (MCA) and A1 segments through prominent vascular collaterals (not shown), and an occlusion of the proximal supraclinoid left ICA (fig. arrow) with skull base collateral reconstitution of the left anterior cerebral artery (ACA) (fig. ). Left vertebral angiography (fig. ) showed extensive pial-collateral flow over the cerebral convexities from the distal posterior cerebral artery branches with reconstitution of distal MCA territories bilaterally. The patient ultimately underwent bilateral pial synangiosis surgery 2 months later, with no subsequent neurological deficits. More surgically relevant aspects of this patient's treatment have been recently described elsewhere []. OUTPUT:
PMCPatients_common3262
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A.T.P, male, 69 years old, in June 2018, reported a tumor associated with pain in the soft-tissue region of the left forearm. Imaging examinations and a biopsy of the lesion were performed, and a high-grade malignant ESFT was identified. The patient was then submitted to neoadjuvant chemotherapy associated with local radiotherapy and later to marginal resection of the lesion with free margins in the pathological examination.\\nSix months later, during routine follow-up with his urologist, the patient presented a prostate-specific antigen value of 9.04 ng/mL. He underwent a multiparametric magnetic resonance imaging of the prostate, which demonstrated a highly suspected peripheral prostatic abnormality for clinically significant neoplasia (Prostate Imaging-Reporting and Data System 4). A biopsy of the prostate was then performed by transrectal ultrasound, and the anatomopathological study was compatible with prostate adenocarcinoma, Gleason 9 (4 + 5) in one fragment in the left apex and in two fragments in the left middle third and Gleason 7 (3 + 4) in a fragment at the apex on the right.\\nIn order to complete the PC staging, a PET/CT using a 68Ga-PSMA study was requested. The study demonstrated multiple focal areas of abnormal uptake in the prostate with standard uptake value maximum (SUVmax) up to 5.0 and also a single diffuse intramedullary lesion in the right humerus with SUVmax = 10.8 [Figures -]. The radical prostatectomy was contraindicated, which was the initially planned procedure.\nOUTPUT:" }, { "from": "agent", "value": "Extrapleural solitary fibrous tumor, High-risk prostate cancer" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A.T.P, male, 69 years old, in June 2018, reported a tumor associated with pain in the soft-tissue region of the left forearm. Imaging examinations and a biopsy of the lesion were performed, and a high-grade malignant ESFT was identified. The patient was then submitted to neoadjuvant chemotherapy associated with local radiotherapy and later to marginal resection of the lesion with free margins in the pathological examination.\nSix months later, during routine follow-up with his urologist, the patient presented a prostate-specific antigen value of 9.04 ng/mL. He underwent a multiparametric magnetic resonance imaging of the prostate, which demonstrated a highly suspected peripheral prostatic abnormality for clinically significant neoplasia (Prostate Imaging-Reporting and Data System 4). A biopsy of the prostate was then performed by transrectal ultrasound, and the anatomopathological study was compatible with prostate adenocarcinoma, Gleason 9 (4 + 5) in one fragment in the left apex and in two fragments in the left middle third and Gleason 7 (3 + 4) in a fragment at the apex on the right.\nIn order to complete the PC staging, a PET/CT using a 68Ga-PSMA study was requested. The study demonstrated multiple focal areas of abnormal uptake in the prostate with standard uptake value maximum (SUVmax) up to 5.0 and also a single diffuse intramedullary lesion in the right humerus with SUVmax = 10.8 [Figures -]. The radical prostatectomy was contraindicated, which was the initially planned procedure. OUTPUT:
PMCPatients_common3299
[ { "from": "human", "value": "As a physician engaged 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 Caucasian boy was admitted to the emergency department reporting a progressive bilateral visual loss. One month before, the patient had started to exhibit a decrease in vision initially in the left eye and latterly in the right eye. He also complained of intermittent headaches, which varied in severity, taking 8 months to evolve, eventually occurring as frequently as on a daily basis, and most frequently in the month prior to admittance. The patient had a normal Body Mass Index. There was no family history of visual loss nor substance abuse.\\nNeuro-ophthalmological examination revealed best correct visual acuity (BCVA) of 1/10 in the right eye and counting fingers in the left eye, pupils with few reactions to light but with relative afferent pupillary defect in the left eye. Slit-lamp examination and intraocular pressure were normal. Fundus examination demonstrated bilateral moderate optic disc elevation, suggesting papilledema ( and ). Brain and orbits Magnetic Resonance Imaging (MRI) showed T2 hyperintensity in the posterior region of the left optic nerve and the optic chiasm (). The result of an extensive workup for inflammatory, infectious and auto-immune conditions was negative. The headaches improved but the loss of visual acuity remained. Targeted mutation analysis for LHON was performed, yielding homoplasmy for MTND4* LHON11778A mutation. After 1 year of clinical follow-up, his best visual acuity was counting fingers and presented pallor optic discs in both eyes. Currently, he is 17 years old and shows the same visual outcome.\nOUTPUT:" }, { "from": "agent", "value": "Childhood-Onset Leber Hereditary Optic Neuropathy, Idiopathic Intracranial 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: An 8-year-old Caucasian boy was admitted to the emergency department reporting a progressive bilateral visual loss. One month before, the patient had started to exhibit a decrease in vision initially in the left eye and latterly in the right eye. He also complained of intermittent headaches, which varied in severity, taking 8 months to evolve, eventually occurring as frequently as on a daily basis, and most frequently in the month prior to admittance. The patient had a normal Body Mass Index. There was no family history of visual loss nor substance abuse.\nNeuro-ophthalmological examination revealed best correct visual acuity (BCVA) of 1/10 in the right eye and counting fingers in the left eye, pupils with few reactions to light but with relative afferent pupillary defect in the left eye. Slit-lamp examination and intraocular pressure were normal. Fundus examination demonstrated bilateral moderate optic disc elevation, suggesting papilledema ( and ). Brain and orbits Magnetic Resonance Imaging (MRI) showed T2 hyperintensity in the posterior region of the left optic nerve and the optic chiasm (). The result of an extensive workup for inflammatory, infectious and auto-immune conditions was negative. The headaches improved but the loss of visual acuity remained. Targeted mutation analysis for LHON was performed, yielding homoplasmy for MTND4* LHON11778A mutation. After 1 year of clinical follow-up, his best visual acuity was counting fingers and presented pallor optic discs in both eyes. Currently, he is 17 years old and shows the same visual outcome. OUTPUT:
PMCPatients_common2986
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: This is a case of a 20-year-old female who presented to her physician with complaints of continuous and heavy vaginal bleeding despite being on oral contraceptive pills. After a syncopal episode, the patient was found to be acutely anemic, requiring blood transfusion. On physical exam, she was found to have a “small mass protruding from the cervix.” Pelvic Doppler Ultrasound (U/S) revealed a 3.5 cm x 3.5 cm x 2.5 cm oval echogenic mass with prominent vessels located within the cervix and extending from the fundus, compatible with a lower uterine segment polyp ().\\nShe further underwent D&C with polypectomy and specimen was sent for pathological examination. Grossly, the polyp had a tan-pink friable cut surface. Microscopic examination revealed an epithelioid neoplasm arranged in a nested pattern present within a highly vascular, edematous and fibrous stroma. The neoplastic cells displayed an abundant granular eosinophilic cytoplasm with prominent enlarged round nucleoli ( and ()). Immunohistochemistry (IHC) was performed showing strong nuclear positivity for TFE-3. The cells also expressed p53, INI-1, SMA (rare), and cathepsin-K ( and ()). Periodic acid–Schiff stain (PAS) highlighted intracellular crystalline material with the cytoplasm ( and ()). Fluorescence in-situ hybridization (FISH) studies showed evidence of TFE-3 and ASPSCR1 gene rearrangements. The tumor cells were negative for epithelial markers, melanocytic markers, Oct 3/4 and SALL4. Given the overall morphology along with the immunophenotype and FISH results, the overall findings were consistent with the diagnosis of ASPS.\\nAfter exhaustive physical examination and imagining studies, clinical suspicious for metastatic disease by the surgical team was low. Patient underwent hysterectomy with lymph node sparing and her clinical status at the time of this publication has been uneventful. Currently, she follows up with her surgeon and has no new complains. No new masses or compromise of her health has been reported.\nOUTPUT:" }, { "from": "agent", "value": "Alveolar soft part sarcoma" } ]
As a physician 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 is a case of a 20-year-old female who presented to her physician with complaints of continuous and heavy vaginal bleeding despite being on oral contraceptive pills. After a syncopal episode, the patient was found to be acutely anemic, requiring blood transfusion. On physical exam, she was found to have a “small mass protruding from the cervix.” Pelvic Doppler Ultrasound (U/S) revealed a 3.5 cm x 3.5 cm x 2.5 cm oval echogenic mass with prominent vessels located within the cervix and extending from the fundus, compatible with a lower uterine segment polyp ().\nShe further underwent D&C with polypectomy and specimen was sent for pathological examination. Grossly, the polyp had a tan-pink friable cut surface. Microscopic examination revealed an epithelioid neoplasm arranged in a nested pattern present within a highly vascular, edematous and fibrous stroma. The neoplastic cells displayed an abundant granular eosinophilic cytoplasm with prominent enlarged round nucleoli ( and ()). Immunohistochemistry (IHC) was performed showing strong nuclear positivity for TFE-3. The cells also expressed p53, INI-1, SMA (rare), and cathepsin-K ( and ()). Periodic acid–Schiff stain (PAS) highlighted intracellular crystalline material with the cytoplasm ( and ()). Fluorescence in-situ hybridization (FISH) studies showed evidence of TFE-3 and ASPSCR1 gene rearrangements. The tumor cells were negative for epithelial markers, melanocytic markers, Oct 3/4 and SALL4. Given the overall morphology along with the immunophenotype and FISH results, the overall findings were consistent with the diagnosis of ASPS.\nAfter exhaustive physical examination and imagining studies, clinical suspicious for metastatic disease by the surgical team was low. Patient underwent hysterectomy with lymph node sparing and her clinical status at the time of this publication has been uneventful. Currently, she follows up with her surgeon and has no new complains. No new masses or compromise of her health has been reported. OUTPUT:
PMCPatients_common5079
[ { "from": "human", "value": "As a physician engaged 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 did not have a medical history such as bleeding disorder or coagulopathies. The patient was not taking any antiplatelet drug. Initial laboratory data yielded creatinine: 2.1 mg/dl, hemoglobin: 12.9 g/dL, hematocrit: 39.6%, platelets: 252×109/L, prothrombin time: 11 seconds, activated-partial thromboplastin time (aPTT): 29 seconds. In the second day of admission, the patient had an episode of abdominal and back pain. The aPTT result was found to be prolonged. Also, hemoglobin level was found to be 10.4 g/dL significantly decreased compared to the admission value of 12.9 g/dL. Further decrease of the blood pressure occurred (100/60 mmHg). Enoxaparin treatment was then stopped. Then the patient was transfused 5 units of packed red cells and 16 units of frozen fresh plasma, given intravenous infusion of saline and lactated Ringers solution. So blood pressure increased to 110/70 mmHg. The supportive treatment was continued and the patient's clinical condition was stable. In the following days, hemoglobin levels and blood pressure stabilized and at day 21 returned to normal. The patient was followed with medical supportive treatment.\nOUTPUT:" }, { "from": "agent", "value": "Pulmonary embolism, Retroperitoneal 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: The patient did not have a medical history such as bleeding disorder or coagulopathies. The patient was not taking any antiplatelet drug. Initial laboratory data yielded creatinine: 2.1 mg/dl, hemoglobin: 12.9 g/dL, hematocrit: 39.6%, platelets: 252×109/L, prothrombin time: 11 seconds, activated-partial thromboplastin time (aPTT): 29 seconds. In the second day of admission, the patient had an episode of abdominal and back pain. The aPTT result was found to be prolonged. Also, hemoglobin level was found to be 10.4 g/dL significantly decreased compared to the admission value of 12.9 g/dL. Further decrease of the blood pressure occurred (100/60 mmHg). Enoxaparin treatment was then stopped. Then the patient was transfused 5 units of packed red cells and 16 units of frozen fresh plasma, given intravenous infusion of saline and lactated Ringers solution. So blood pressure increased to 110/70 mmHg. The supportive treatment was continued and the patient's clinical condition was stable. In the following days, hemoglobin levels and blood pressure stabilized and at day 21 returned to normal. The patient was followed with medical supportive treatment. OUTPUT:
PMCPatients_common1956
[ { "from": "human", "value": "As a physician engaged in 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 years old man presented with symptoms of dysphagia of 5 years duration to solids which was insidious in onset and persistent. His appetite was normal but had weight loss secondary to decreased intake. His bowel habits were normal. He underwent 4 sessions of esophageal dilations by surgeons under general anaesthesia, but the webs recurred and he was referred to gastroenterology services.\\nOn evaluation he was thin built and pale. General physical examination was unremarkable except for pallor. Barium swallow showed multiple esophageal webs in the post cricoid region (). He had microcytic and hypochromic anemia with a hemoglobin of 8.2g%. Stool for occult blood was negative and iron studies showed severe iron deficiency state with serum iron of 13 micrograms/dl and percent transferrin saturation of 2.7%. Upper gastro-intestinal endoscopy showed multiple cervical webs and scalloping and grooving of the proximal duodenum (). He was advised gluten free diet and iron supplementation. On this treatment his dysphagia was resolved, and there was no recurrence of webs. He gained 6 kilograms of weight, and his anemia and serum iron profile also started showing improvement (hemoglobin 12g%, serum iron 53 mg/dl, and percent transferring saturation 9.8%) within six weeks of treatment. He developed a pruritic papular skin rash over extensor aspects of limbs suggestive of dermatitis herpertiformis which responded to Dapsone therapy. He has been doing well since then and is asymptomatic on 7 years of follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Celiac 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 35 years old man presented with symptoms of dysphagia of 5 years duration to solids which was insidious in onset and persistent. His appetite was normal but had weight loss secondary to decreased intake. His bowel habits were normal. He underwent 4 sessions of esophageal dilations by surgeons under general anaesthesia, but the webs recurred and he was referred to gastroenterology services.\nOn evaluation he was thin built and pale. General physical examination was unremarkable except for pallor. Barium swallow showed multiple esophageal webs in the post cricoid region (). He had microcytic and hypochromic anemia with a hemoglobin of 8.2g%. Stool for occult blood was negative and iron studies showed severe iron deficiency state with serum iron of 13 micrograms/dl and percent transferrin saturation of 2.7%. Upper gastro-intestinal endoscopy showed multiple cervical webs and scalloping and grooving of the proximal duodenum (). He was advised gluten free diet and iron supplementation. On this treatment his dysphagia was resolved, and there was no recurrence of webs. He gained 6 kilograms of weight, and his anemia and serum iron profile also started showing improvement (hemoglobin 12g%, serum iron 53 mg/dl, and percent transferring saturation 9.8%) within six weeks of treatment. He developed a pruritic papular skin rash over extensor aspects of limbs suggestive of dermatitis herpertiformis which responded to Dapsone therapy. He has been doing well since then and is asymptomatic on 7 years of follow-up. OUTPUT:
PMCPatients_common4899
[ { "from": "human", "value": "As a physician engaged in 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 Indian lady presented with itchy rash with distinct indurated margins extending across her anterior chest, abdomen and parts of her neck. The affected skin was teetered to the underlying structures with some crusting over both breasts (Fig. ). The rash had started from the right infra-mammary region and had gradually spread to this entire area over a period of ∼2 years. There was no history of weight loss, fever or breast lump. She did not have diabetes mellitus or immunodeficiency. She was treated by general practitioners and dermatologists over this period with multiple oral and topical antibiotics and steroids, with no relief. Even topical antifungals and unknown indigenous emollients had been applied to her skin (which is quite a common practice in rural India) over this time. She also gave history of progressive spreading of erythema along with change of color and oozing for last 3–4 months. No definite mass was palpable in her breasts, but axillary lymph nodes were palpable on the right side. General and systemic examination showed evidence of pleural effusion on the right side. Her routine blood examinations were normal. We advised punch skin biopsies, which proved inconclusive.\\nFull-thickness skin biopsies from multiple sites were taken for histological exam and reviewed at multiple centers (Fig. ). They showed clusters of pleomorphic malignant cells invading the papillary dermis, lymphatic channels and spreading in-between the collagen bundles with positive immunostaining for cytokeratin 7, estrogen receptor (ER), gross cystic disease fluid protein 15 (GCDFP-15) and AE1/AE3 (Figs –). Contrast enhanced CT scan (CECT) chest and abdomen showed moderate right-sided pleural effusion and suspicious mass in the right breast with multiple bony metastases (Figs and ). Examination of the pleural fluid showed a hemorrhagic effusion with plenty of pleomorphic cells suggestive of adenocarcinoma. Chemotherapy with Danorubicin and Etopocide along with supportive therapy including Zolundronic acid was started as palliative treatment after oncology revision. Unfortunately, she expired after her third chemotherapy cycle.\nOUTPUT:" }, { "from": "agent", "value": "Breast Cancer with 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 43-year-old Indian lady presented with itchy rash with distinct indurated margins extending across her anterior chest, abdomen and parts of her neck. The affected skin was teetered to the underlying structures with some crusting over both breasts (Fig. ). The rash had started from the right infra-mammary region and had gradually spread to this entire area over a period of ∼2 years. There was no history of weight loss, fever or breast lump. She did not have diabetes mellitus or immunodeficiency. She was treated by general practitioners and dermatologists over this period with multiple oral and topical antibiotics and steroids, with no relief. Even topical antifungals and unknown indigenous emollients had been applied to her skin (which is quite a common practice in rural India) over this time. She also gave history of progressive spreading of erythema along with change of color and oozing for last 3–4 months. No definite mass was palpable in her breasts, but axillary lymph nodes were palpable on the right side. General and systemic examination showed evidence of pleural effusion on the right side. Her routine blood examinations were normal. We advised punch skin biopsies, which proved inconclusive.\nFull-thickness skin biopsies from multiple sites were taken for histological exam and reviewed at multiple centers (Fig. ). They showed clusters of pleomorphic malignant cells invading the papillary dermis, lymphatic channels and spreading in-between the collagen bundles with positive immunostaining for cytokeratin 7, estrogen receptor (ER), gross cystic disease fluid protein 15 (GCDFP-15) and AE1/AE3 (Figs –). Contrast enhanced CT scan (CECT) chest and abdomen showed moderate right-sided pleural effusion and suspicious mass in the right breast with multiple bony metastases (Figs and ). Examination of the pleural fluid showed a hemorrhagic effusion with plenty of pleomorphic cells suggestive of adenocarcinoma. Chemotherapy with Danorubicin and Etopocide along with supportive therapy including Zolundronic acid was started as palliative treatment after oncology revision. Unfortunately, she expired after her third chemotherapy cycle. OUTPUT:
PMCPatients_common5054
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Bullae and erosions were also observed on the trunk, both arms, both thighs, and both feet. The lesions on the scalp had been present for about 20 years, with a variable course and recurrent superinfections. The patient was prescribed medications by his prior physician for suspected seborrheic dermatitis; however, the scalp lesions did not resolve. Subsequently, multiple bullae appeared on the trunk, arms, legs, and feet 5 days before visiting our department. No additional dermatological or medical history was present.\\nThe physical examination revealed multiple irregular erosions accompanied by crusts and hair loss on the scalp; clusters of hair appeared to emerge from single follicular openings in the area with the crust (). In addition, flaccid bullae and vesicles were observed on the abdomen, back, both arms, both thighs, and the feet. Some bullae were ruptured and had formed erosions. No other skin or mucous membrane manifestations were present. The complete blood count showed leukocytosis; other routine blood tests were normal. Fungal cultures from the affected area of the scalp were negative, but bacterial cultures grew Staphylococcus epidermidis.\\nThe histological evaluation of lesions on the scalp showed acantholysis with formation of intra-epidermal blisters and separation of the epidermis. Clustering of several adjacent hair follicles with perifollicular inflammatory cell infiltration was observed. A perivascular infiltrate with many lymphocytes and relatively few eosinophils was observed in the dermis (). Another specimen obtained from the scalp showed suprabasal acantholytic cleft formation and a row of tombstone patterned cells (). No spores or hyphae were noted on periodic acid Schiff staining. A direct immunofluorescence test was positive for C3 on the cell surface of keratinocytes. Additional blood samples to determine anti-dsg-1 and anti-dsg-3 antibodies were not available due to refusal by the patient. With this treatment, the lesion responded slowly and improved by the follow-up evaluation.\nOUTPUT:" }, { "from": "agent", "value": "Pemphigus Vulgaris, Tufted Hair Folliculitis" } ]
As a physician 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: Bullae and erosions were also observed on the trunk, both arms, both thighs, and both feet. The lesions on the scalp had been present for about 20 years, with a variable course and recurrent superinfections. The patient was prescribed medications by his prior physician for suspected seborrheic dermatitis; however, the scalp lesions did not resolve. Subsequently, multiple bullae appeared on the trunk, arms, legs, and feet 5 days before visiting our department. No additional dermatological or medical history was present.\nThe physical examination revealed multiple irregular erosions accompanied by crusts and hair loss on the scalp; clusters of hair appeared to emerge from single follicular openings in the area with the crust (). In addition, flaccid bullae and vesicles were observed on the abdomen, back, both arms, both thighs, and the feet. Some bullae were ruptured and had formed erosions. No other skin or mucous membrane manifestations were present. The complete blood count showed leukocytosis; other routine blood tests were normal. Fungal cultures from the affected area of the scalp were negative, but bacterial cultures grew Staphylococcus epidermidis.\nThe histological evaluation of lesions on the scalp showed acantholysis with formation of intra-epidermal blisters and separation of the epidermis. Clustering of several adjacent hair follicles with perifollicular inflammatory cell infiltration was observed. A perivascular infiltrate with many lymphocytes and relatively few eosinophils was observed in the dermis (). Another specimen obtained from the scalp showed suprabasal acantholytic cleft formation and a row of tombstone patterned cells (). No spores or hyphae were noted on periodic acid Schiff staining. A direct immunofluorescence test was positive for C3 on the cell surface of keratinocytes. Additional blood samples to determine anti-dsg-1 and anti-dsg-3 antibodies were not available due to refusal by the patient. With this treatment, the lesion responded slowly and improved by the follow-up evaluation. OUTPUT:
PMCPatients_common1268
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 46 year old man, father of three children, without significant previous medical history, consulted for the gradual emergence of an isolated left supraclavicular mass. On physical examination, the patient was afebrile, in good general condition, pleuropulmonary and abdominal examination was normal. The genital examination found an empty right purse, the left testicle was normal. The inguinal examination found no palpable mass but a suspect induration was reported. The ORL examination revealed no abnormalities. Chest radiography showed a normal pulmonary transparency. On ultrasonographic scanning of supraclavicular fossa and whole abdomen showed a supraclavicular lymphadenopathy measuring 31 × 23 mm and an heterogeneous mass in the right iliac fossa with irregular contours. The laboratory investigations were all normal; apart from a slightly elevated serum beta- human chorionic gonadotropin (β-HCG) 428 mmol/L. The serum alpha- fetoprotein (α-FP) was within normal limits, and lactate dehydrogenase (LDH) at 308 U/l. The thoracoabdominopelvien computed tomography (CT) scan revealed a right pelvic mass measuring 100 × 80 mm (Figure ), and mediastinal lymph nodes (Figure ). No intraperitoneal or retroperitoneal abnormalities were noted. The resection was performed without complications. The patient was referred to receive adjuvant chemotherapy consisting of a combination of cisplatinum 20 mg/m2, etoposide 100 mg/m2 given on five consecutive days and bleomycin 30 mg on days one, eight, and 15. There was no clinical evidence of local recurrence or distant metastasis after 18-months follow up after discharge.\nOUTPUT:" }, { "from": "agent", "value": "Tumor in undescended intrapelvic testis, Metastatic lymphadenopathy of an embryonal carcinoma, Non-seminomatous 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 46 year old man, father of three children, without significant previous medical history, consulted for the gradual emergence of an isolated left supraclavicular mass. On physical examination, the patient was afebrile, in good general condition, pleuropulmonary and abdominal examination was normal. The genital examination found an empty right purse, the left testicle was normal. The inguinal examination found no palpable mass but a suspect induration was reported. The ORL examination revealed no abnormalities. Chest radiography showed a normal pulmonary transparency. On ultrasonographic scanning of supraclavicular fossa and whole abdomen showed a supraclavicular lymphadenopathy measuring 31 × 23 mm and an heterogeneous mass in the right iliac fossa with irregular contours. The laboratory investigations were all normal; apart from a slightly elevated serum beta- human chorionic gonadotropin (β-HCG) 428 mmol/L. The serum alpha- fetoprotein (α-FP) was within normal limits, and lactate dehydrogenase (LDH) at 308 U/l. The thoracoabdominopelvien computed tomography (CT) scan revealed a right pelvic mass measuring 100 × 80 mm (Figure ), and mediastinal lymph nodes (Figure ). No intraperitoneal or retroperitoneal abnormalities were noted. The resection was performed without complications. The patient was referred to receive adjuvant chemotherapy consisting of a combination of cisplatinum 20 mg/m2, etoposide 100 mg/m2 given on five consecutive days and bleomycin 30 mg on days one, eight, and 15. There was no clinical evidence of local recurrence or distant metastasis after 18-months follow up after discharge. OUTPUT:
PMCPatients_common812
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 72-year-old female with a past medical history of hypertension, hyperlipidemia, and type 2 diabetes was admitted to our department with the chief complaint of shortness of breath since a week. Symptoms were present at rest as well as with exertion. The patient also complained of increase in abdominal girth and bloating over the last two months. One month prior to presentation, she was seen by a gynecologist for vaginal bleeding. Ultrasonography of the abdomen and pelvis was performed, which showed a pelvic mass. The patient missed the follow-up appointment with the gynecologist. The patient denied any joint pain, peripheral edema, or history of liver or cardiovascular disease. On respiratory examination, there was right-sided dullness with absent breath sounds, and abdominal examination revealed shifting dullness on percussion. Chest X-ray (Figure ) on admission showed a large right-sided pleural effusion.\\nPulmonology service was consulted, and thoracentesis was performed, during which 1,500 cc of amber color fluid was obtained. A right PleurX® catheter (Becton, Dickinson and Company, Franklin Lakes, NJ, USA) was placed on pulmonology recommendations. However, on day 3 of admission, the patient’s cancer antigen 125 (CA 125) level was 3,653. The postoperative course was uneventful, and the PleurX® catheter was removed on the third postoperative day. The patient is scheduled to receive six courses of carboplatin and taxols.\nOUTPUT:" }, { "from": "agent", "value": "Pseudo-Meigs' Syndrome, Ovarian Metastasis, Ovarian Malignancy, Secondary Malignancy of the Omentum, Pelvic Peritoneum and Pelvic 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: A 72-year-old female with a past medical history of hypertension, hyperlipidemia, and type 2 diabetes was admitted to our department with the chief complaint of shortness of breath since a week. Symptoms were present at rest as well as with exertion. The patient also complained of increase in abdominal girth and bloating over the last two months. One month prior to presentation, she was seen by a gynecologist for vaginal bleeding. Ultrasonography of the abdomen and pelvis was performed, which showed a pelvic mass. The patient missed the follow-up appointment with the gynecologist. The patient denied any joint pain, peripheral edema, or history of liver or cardiovascular disease. On respiratory examination, there was right-sided dullness with absent breath sounds, and abdominal examination revealed shifting dullness on percussion. Chest X-ray (Figure ) on admission showed a large right-sided pleural effusion.\nPulmonology service was consulted, and thoracentesis was performed, during which 1,500 cc of amber color fluid was obtained. A right PleurX® catheter (Becton, Dickinson and Company, Franklin Lakes, NJ, USA) was placed on pulmonology recommendations. However, on day 3 of admission, the patient’s cancer antigen 125 (CA 125) level was 3,653. The postoperative course was uneventful, and the PleurX® catheter was removed on the third postoperative day. The patient is scheduled to receive six courses of carboplatin and taxols. OUTPUT:
PMCPatients_common2379
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 43-year-old woman was admitted to the Ophthalmology Department because of vision loss in her left eye for 20 days after single sudden syncope (lasting for about ten seconds; Overlooked by an ophthalmologist at a local hospital). Before admission, she had received treatment by the ophthalmologist at the local hospital, however without improvement. On admission, she was found with visual acuities of 20/25 OD and fingers OS. Intraocular pressure was 16 mmHg OD and 13 mmHg OS. The visual field of the left eye was defected with poor pupillary light reflex. Fundus examination of the left eye showed obscure boundary of optic disc with reflective dispersion of the retina and poor light reflex of central fovea. She had no prior history of cardiac disease. No ischemic infarct, vertebrobasilar artery insufficiency or other diseases were found after examination. The patient was transferred to the Cardiac Surgical ward for surgery. The physical examination was normal with a blood pressure of 124/70 mmHg and heart rate 57 bpm. Electrocardiogram showed sinus bradycardia, and chest-X-ray showed a normal cardiac silhouette. Bilateral carotid and vertebral artery ultrasound showed no abnormalities. Cerebral MRI revealed no abnormalities. The postoperative course was uneventful and the patient was discharged one week after surgery. She was stable at 12-month follow-up, and her visual acuities improved to 20/400 OS.\nOUTPUT:" }, { "from": "agent", "value": "Retinal artery occlusion, Left atrial myxoma" } ]
As a physician 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 woman was admitted to the Ophthalmology Department because of vision loss in her left eye for 20 days after single sudden syncope (lasting for about ten seconds; Overlooked by an ophthalmologist at a local hospital). Before admission, she had received treatment by the ophthalmologist at the local hospital, however without improvement. On admission, she was found with visual acuities of 20/25 OD and fingers OS. Intraocular pressure was 16 mmHg OD and 13 mmHg OS. The visual field of the left eye was defected with poor pupillary light reflex. Fundus examination of the left eye showed obscure boundary of optic disc with reflective dispersion of the retina and poor light reflex of central fovea. She had no prior history of cardiac disease. No ischemic infarct, vertebrobasilar artery insufficiency or other diseases were found after examination. The patient was transferred to the Cardiac Surgical ward for surgery. The physical examination was normal with a blood pressure of 124/70 mmHg and heart rate 57 bpm. Electrocardiogram showed sinus bradycardia, and chest-X-ray showed a normal cardiac silhouette. Bilateral carotid and vertebral artery ultrasound showed no abnormalities. Cerebral MRI revealed no abnormalities. The postoperative course was uneventful and the patient was discharged one week after surgery. She was stable at 12-month follow-up, and her visual acuities improved to 20/400 OS. OUTPUT:
PMCPatients_common9
[ { "from": "human", "value": "As a physician engaged 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 the operation, a saline-soaked absorbent cotton was placed at the subglottis to protect the trachea. Repeat direct rigid laryngoscopy showed no abnormalities. This patient is considered to be a common throat in TML and discharged from the hospital. At 23 h after initial surgery, she returned to emergency room presenting subcutaneous emphysema and cough. Re-evaluation with a head, neck, and chest CT was done, which showed mediastinal emphysema and extensive subcutaneous emphysema from the base of the skull to the chest. A suspected tear on the membranous trachea located 4.5 cm under the glottis, extending to ∼8.5 cm under the glottis was noted (Fig. A–D). ).\nOUTPUT:" }, { "from": "agent", "value": "Tracheal rupture, Bilateral vocal cord polyps" } ]
As a physician 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 the operation, a saline-soaked absorbent cotton was placed at the subglottis to protect the trachea. Repeat direct rigid laryngoscopy showed no abnormalities. This patient is considered to be a common throat in TML and discharged from the hospital. At 23 h after initial surgery, she returned to emergency room presenting subcutaneous emphysema and cough. Re-evaluation with a head, neck, and chest CT was done, which showed mediastinal emphysema and extensive subcutaneous emphysema from the base of the skull to the chest. A suspected tear on the membranous trachea located 4.5 cm under the glottis, extending to ∼8.5 cm under the glottis was noted (Fig. A–D). ). OUTPUT:
PMCPatients_common3895
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 75-year-old man was referred to Kyung-Hee Dental Hospital from a local clinic for evaluation of paresthesia of the left lower lip and a firm mass on the left buccal side. He had a slight swelling localized in the area of the body of the left mandible. On palpation, the swelling was hard, attached to the body of the mandible, and slightly tender. Paresthesia was present on the left lower lip. An intraoral examination revealed a large erythematous mass in the lingual vestibular area (). The regional lymph nodes could not be detected by palpation. His medical history was unremarkable. According to his dental history, the patient had experienced dull pain in his left lower molar region 7 months earlier and underwent extraction of the left lower first molars because of a periapical abscess (). The patient underwent implant surgery approximately 4 months after the tooth extraction (). Two months later, explantation for peri-implantitis was performed. Since then, he had experienced continuous dull pain and swelling in the body of the left mandible and reported numbness of the left lower lip. The panoramic radiograph showed ill-defined, permeative bone destruction from the left lower premolar area to the second molar area. Comparison of this panoramic image with the one obtained from the local clinic on his first visit () showed that the lesion had expanded into the mandibular canal (). On the periapical view, there was infiltrative bone destruction and an enlarged soft tissue shadow (). Cone-beam computed tomography was performed to obtain more detailed information about the lesions. The sagittal images showed osteolytic destruction in the left mandibular body area and loss of cortication in the mandibular canal (). On the cross-sectional view, there was partial perforation and erosion of the buccal and lingual cortical plates (). An initial biopsy was performed under local anesthesia. A histopathologic examination revealed sheets of atypical plasmacytoid cells (). On immunohistochemistry, the tumor cells were negative for CD20, a B-cell marker (), but positive for CD138, a plasma cell marker (). While the kappa light chain was expressed in all of the tumor cells (), the lambda light chain was negative, indicating that the tumor cell population was monoclonal. The patient is currently receiving radiotherapy.\nOUTPUT:" }, { "from": "agent", "value": "Solitary plasmacytoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 75-year-old man was referred to Kyung-Hee Dental Hospital from a local clinic for evaluation of paresthesia of the left lower lip and a firm mass on the left buccal side. He had a slight swelling localized in the area of the body of the left mandible. On palpation, the swelling was hard, attached to the body of the mandible, and slightly tender. Paresthesia was present on the left lower lip. An intraoral examination revealed a large erythematous mass in the lingual vestibular area (). The regional lymph nodes could not be detected by palpation. His medical history was unremarkable. According to his dental history, the patient had experienced dull pain in his left lower molar region 7 months earlier and underwent extraction of the left lower first molars because of a periapical abscess (). The patient underwent implant surgery approximately 4 months after the tooth extraction (). Two months later, explantation for peri-implantitis was performed. Since then, he had experienced continuous dull pain and swelling in the body of the left mandible and reported numbness of the left lower lip. The panoramic radiograph showed ill-defined, permeative bone destruction from the left lower premolar area to the second molar area. Comparison of this panoramic image with the one obtained from the local clinic on his first visit () showed that the lesion had expanded into the mandibular canal (). On the periapical view, there was infiltrative bone destruction and an enlarged soft tissue shadow (). Cone-beam computed tomography was performed to obtain more detailed information about the lesions. The sagittal images showed osteolytic destruction in the left mandibular body area and loss of cortication in the mandibular canal (). On the cross-sectional view, there was partial perforation and erosion of the buccal and lingual cortical plates (). An initial biopsy was performed under local anesthesia. A histopathologic examination revealed sheets of atypical plasmacytoid cells (). On immunohistochemistry, the tumor cells were negative for CD20, a B-cell marker (), but positive for CD138, a plasma cell marker (). While the kappa light chain was expressed in all of the tumor cells (), the lambda light chain was negative, indicating that the tumor cell population was monoclonal. The patient is currently receiving radiotherapy. OUTPUT:
PMCPatients_common3509
[ { "from": "human", "value": "As a physician engaged 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 child's mother revealed that he was unable to stop the habit even after repeated motivation from them. Lips were competent both at rest and during swallowing. Intraoral examination revealed normal shape and size of the tongue. Mesial step molar relationship was present and interdental and primate spaces were absent. The parents were explained about various appliances for interception of the habit but they were not willing for any intraoral appliance. Hence, with mutual understanding, we came to the conclusion for RURS elbow guard as an alternative for an extraoral appliance. Modified RURS elbow guard was fabricated by the technique given by Anand et al. in 2017.\\nStep 1—The patient's elbow impression was made using a double layer of the modeling wax at 45 to 60° angulations or at rest position which served as a spacer to make a negative replica of the elbow ().\\nStep 2—A sheet of modeling wax was added vertically to both ends and the dental stone was poured to make a positive replica of the elbow.\\nStep 3—Self-cure acrylic was used to fabricate an acrylic elbow guard skeleton.\\nStep 4—Dewaxing was done in a hot water bathtub for 10 minutes, trimming and polishing of acrylic was done.\\nStep 5—A layer of sponge for cushioning was placed to allow limited movement of the elbow.\\nStep 6—A blue color velvet cloth was stitched over the acrylic elbow guard with four velcro straps for better retention ().\\nThe appliance was then delivered to the patient (). The child was happy and contented with the modified RURS elbow guard appliance. The patient was asked to wear the appliance during sleeping hours. Regular follow-up was done every month till the habit was terminated. The habit of the child was ceased in 6 months including 2 months of the retention period.\nOUTPUT:" }, { "from": "agent", "value": "Thumb Sucking" } ]
As a physician 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 child's mother revealed that he was unable to stop the habit even after repeated motivation from them. Lips were competent both at rest and during swallowing. Intraoral examination revealed normal shape and size of the tongue. Mesial step molar relationship was present and interdental and primate spaces were absent. The parents were explained about various appliances for interception of the habit but they were not willing for any intraoral appliance. Hence, with mutual understanding, we came to the conclusion for RURS elbow guard as an alternative for an extraoral appliance. Modified RURS elbow guard was fabricated by the technique given by Anand et al. in 2017.\nStep 1—The patient's elbow impression was made using a double layer of the modeling wax at 45 to 60° angulations or at rest position which served as a spacer to make a negative replica of the elbow ().\nStep 2—A sheet of modeling wax was added vertically to both ends and the dental stone was poured to make a positive replica of the elbow.\nStep 3—Self-cure acrylic was used to fabricate an acrylic elbow guard skeleton.\nStep 4—Dewaxing was done in a hot water bathtub for 10 minutes, trimming and polishing of acrylic was done.\nStep 5—A layer of sponge for cushioning was placed to allow limited movement of the elbow.\nStep 6—A blue color velvet cloth was stitched over the acrylic elbow guard with four velcro straps for better retention ().\nThe appliance was then delivered to the patient (). The child was happy and contented with the modified RURS elbow guard appliance. The patient was asked to wear the appliance during sleeping hours. Regular follow-up was done every month till the habit was terminated. The habit of the child was ceased in 6 months including 2 months of the retention period. OUTPUT:
PMCPatients_common2836
[ { "from": "human", "value": "As a physician engaged in 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 Caucasian Turkish male was admitted to ER with right lower quadrant pain, and accompanying fever, sweating, constipation and significant weight loss (>10%) during the last two months. Physical examination revealed normal findings apart from painful right lower quadrant palpable mass. Routine biochemical analysis and CBC were unremarkable. CT examination revealed a 3 × 2 × 2 cm size conglomerated solid mass with no contrast localization. The patient improved and passed flatus after five days of supportive therapy with IV fluid replacement and antibiotic therapy and discharged from hospital. However, the USG two weeks after CT scan, revealed a 5 × 3 cm size irregular contoured, heterogenous caecal mass that was neighboring with the urinary bladder. We also proved the increase in size of the mass by physical examination. This finding has led us to the primary diagnosis of a colonic malignancy.\\nIn an attempt to rule out a colonic malignancy, an urgent colonoscopy was performed, which was unyielding due to inability to pass beyond the hepatic flexure. Therefore, we performed an FDG PET/CT study to aid in the differential diagnosis, which showed markedly increased glucose metabolism in two masses localized in the right lower quadrant which were 2 cm in diameter (,).\\nThe high SUV values (early: 10.8, late: 14.7) suggested that these masses were most likely related with malignant tissue (). Later in several days, the size of mass has decreased on physical and USG examinations, therefore we decided to follow-up conservatively. In two months, the mass has reduced to nearly an unpalpable size. Surgical exploration revealed a peri-appendicular mass consisting mainly of the omentum at the tip of the appendix. Patient underwent appendectomy and resection of neighboring mass. He had an uneventful postoperative period and discharged from the hospital at the end of the first week.\nOUTPUT:" }, { "from": "agent", "value": "Appendicitis" } ]
As a physician 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 Caucasian Turkish male was admitted to ER with right lower quadrant pain, and accompanying fever, sweating, constipation and significant weight loss (>10%) during the last two months. Physical examination revealed normal findings apart from painful right lower quadrant palpable mass. Routine biochemical analysis and CBC were unremarkable. CT examination revealed a 3 × 2 × 2 cm size conglomerated solid mass with no contrast localization. The patient improved and passed flatus after five days of supportive therapy with IV fluid replacement and antibiotic therapy and discharged from hospital. However, the USG two weeks after CT scan, revealed a 5 × 3 cm size irregular contoured, heterogenous caecal mass that was neighboring with the urinary bladder. We also proved the increase in size of the mass by physical examination. This finding has led us to the primary diagnosis of a colonic malignancy.\nIn an attempt to rule out a colonic malignancy, an urgent colonoscopy was performed, which was unyielding due to inability to pass beyond the hepatic flexure. Therefore, we performed an FDG PET/CT study to aid in the differential diagnosis, which showed markedly increased glucose metabolism in two masses localized in the right lower quadrant which were 2 cm in diameter (,).\nThe high SUV values (early: 10.8, late: 14.7) suggested that these masses were most likely related with malignant tissue (). Later in several days, the size of mass has decreased on physical and USG examinations, therefore we decided to follow-up conservatively. In two months, the mass has reduced to nearly an unpalpable size. Surgical exploration revealed a peri-appendicular mass consisting mainly of the omentum at the tip of the appendix. Patient underwent appendectomy and resection of neighboring mass. He had an uneventful postoperative period and discharged from the hospital at the end of the first week. OUTPUT:
PMCPatients_common2645
[ { "from": "human", "value": "As a physician engaged 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 bilateral brisk patellar reflexes and a left four beat ankle clonus. The patient reported shooting pain into her legs on deep forward bending. Preoperative MRI and CT scans revealed a flattened cord at the apex of the kyphosis with a penetrating left 6th RH adjacent to the cord without compression (Figures –).\\nA combined fusion and posterior RH excision were planned with the aid of multimodal spinal cord monitoring. During the T4–T9 discectomies a transient loss of Motor Evoked Potentials (MEPs) occurred bilaterally in lower limbs, which responded to an increase in the mean arterial blood pressure. Somatosensory Evoked Potentials (SSEPs) remained normal.\\nNormal reference traces were present at the beginning of the second stage: posterior instrumented spinal fusion. After completion of the instrumentation and prior to correction manoeuvres all MEPs and SSEPs were lost completely. Following a laminectomy, the dislocated RH, which was not adherent to the dura but was impinging on the cord, was excised. Wake-up test showed no spontaneous movement in the lower limbs with good upper limbs movement.\\nPostoperative neurological examination showed grade 3 muscle power (MRC grading) in all muscle groups of the left lower limb. Right lower limb was normal. Fine touch and proprioception remained intact bilaterally. 48 h postop MRI scan showed no evidence of cord signal changes. 72 h postop the patient regained normal muscle power and urinary continence.\\nFifteen days postoperatively the patient underwent posterior correction of the deformity. The MEPs remained stable during the procedure. Postoperative radiographs evidenced a main thoracic curve of 45° (51% correction). Lateral radiographs and CT scan confirmed a correction of the thoracic kyphosis to 48° (36% correction). At 2-year follow-up () there has been no significant loss of correction and the patient remains asymptomatic.\nOUTPUT:" }, { "from": "agent", "value": "Intracanal Rib Head Dislocation, Neurofibromatosis Type 1, Dystrophic Kyphoscoliosis" } ]
As a physician 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 bilateral brisk patellar reflexes and a left four beat ankle clonus. The patient reported shooting pain into her legs on deep forward bending. Preoperative MRI and CT scans revealed a flattened cord at the apex of the kyphosis with a penetrating left 6th RH adjacent to the cord without compression (Figures –).\nA combined fusion and posterior RH excision were planned with the aid of multimodal spinal cord monitoring. During the T4–T9 discectomies a transient loss of Motor Evoked Potentials (MEPs) occurred bilaterally in lower limbs, which responded to an increase in the mean arterial blood pressure. Somatosensory Evoked Potentials (SSEPs) remained normal.\nNormal reference traces were present at the beginning of the second stage: posterior instrumented spinal fusion. After completion of the instrumentation and prior to correction manoeuvres all MEPs and SSEPs were lost completely. Following a laminectomy, the dislocated RH, which was not adherent to the dura but was impinging on the cord, was excised. Wake-up test showed no spontaneous movement in the lower limbs with good upper limbs movement.\nPostoperative neurological examination showed grade 3 muscle power (MRC grading) in all muscle groups of the left lower limb. Right lower limb was normal. Fine touch and proprioception remained intact bilaterally. 48 h postop MRI scan showed no evidence of cord signal changes. 72 h postop the patient regained normal muscle power and urinary continence.\nFifteen days postoperatively the patient underwent posterior correction of the deformity. The MEPs remained stable during the procedure. Postoperative radiographs evidenced a main thoracic curve of 45° (51% correction). Lateral radiographs and CT scan confirmed a correction of the thoracic kyphosis to 48° (36% correction). At 2-year follow-up () there has been no significant loss of correction and the patient remains asymptomatic. OUTPUT:
PMCPatients_common4429
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 77-year-old woman presented to our clinic with a mass on her left flank that had grown rapidly over 3 months. The patient had been diagnosed with NF-1 45 years ago. She also had asthma, hypertension, and atrial fibrillation, and had undergone percutaneous nephrostomy insertion in her left kidney to treat a urethral obstruction.\\nClinical examination revealed a protruding firm nodule arising from a dermal neurofibroma in the patient’s left flank (). An ulcerated lesion with bloody discharge was present in the most prominent area, and the patient reported experiencing pain and tenderness. Magnetic resonance imaging revealed a well-enhancing mass (3.9×2.5×3.4 cm) with a broad base along the dermis, with a round bulging contour on the lateral side. The mass showed intermediate-to-high T1 signals with relatively homogeneous enhancement (). Histological examination showed infiltration of tumor tissue into the dermis, which was consistent with the appearance of interlacing bundles of neoplastic spindle cells with marked pleomorphism. The hypercellular areas consisted of clusters and sheets of epithelioid round cells admixed with fascicles of hyperchromatic spindled cells. No lymphatic or vascular invasion was identified (). Immunohistochemical staining was positive for S-100 protein in the tumor cell cytoplasm ().\\nAfter diagnosis of the mass as a cutaneous epithelioid MPNST (CE-MPNST), complete surgical excision was planned. With the patient under general anesthesia, the grossly visible tumor was completely excised with lateral and deep resection margins of 30 mm and 15 mm, respectively (). After frozen biopsy to confirm the absence of malignancy, additional undermining was performed to elevate the surrounding subcutaneous tissue. A bilateral fasciocutaneous flap was elevated and advanced and was then closed layer by layer. The wound healed well after surgery, and no signs of local recurrence or metastasis were observed 15 months later ().\\nThis study was approved by the Institutional Review Board of Kyung Hee University Medical Center on October 4, 2019 (IRB No. 2019-09-041) and was performed in accordance with the principles of the Declaration of Helsinki. Informed consent was obtained from the patient.\nOUTPUT:" }, { "from": "agent", "value": "Soft tissue sarcoma, Neurofibromatosis type 1, Malignant peripheral nerve sheath tumor 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 77-year-old woman presented to our clinic with a mass on her left flank that had grown rapidly over 3 months. The patient had been diagnosed with NF-1 45 years ago. She also had asthma, hypertension, and atrial fibrillation, and had undergone percutaneous nephrostomy insertion in her left kidney to treat a urethral obstruction.\nClinical examination revealed a protruding firm nodule arising from a dermal neurofibroma in the patient’s left flank (). An ulcerated lesion with bloody discharge was present in the most prominent area, and the patient reported experiencing pain and tenderness. Magnetic resonance imaging revealed a well-enhancing mass (3.9×2.5×3.4 cm) with a broad base along the dermis, with a round bulging contour on the lateral side. The mass showed intermediate-to-high T1 signals with relatively homogeneous enhancement (). Histological examination showed infiltration of tumor tissue into the dermis, which was consistent with the appearance of interlacing bundles of neoplastic spindle cells with marked pleomorphism. The hypercellular areas consisted of clusters and sheets of epithelioid round cells admixed with fascicles of hyperchromatic spindled cells. No lymphatic or vascular invasion was identified (). Immunohistochemical staining was positive for S-100 protein in the tumor cell cytoplasm ().\nAfter diagnosis of the mass as a cutaneous epithelioid MPNST (CE-MPNST), complete surgical excision was planned. With the patient under general anesthesia, the grossly visible tumor was completely excised with lateral and deep resection margins of 30 mm and 15 mm, respectively (). After frozen biopsy to confirm the absence of malignancy, additional undermining was performed to elevate the surrounding subcutaneous tissue. A bilateral fasciocutaneous flap was elevated and advanced and was then closed layer by layer. The wound healed well after surgery, and no signs of local recurrence or metastasis were observed 15 months later ().\nThis study was approved by the Institutional Review Board of Kyung Hee University Medical Center on October 4, 2019 (IRB No. 2019-09-041) and was performed in accordance with the principles of the Declaration of Helsinki. Informed consent was obtained from the patient. OUTPUT:
PMCPatients_common349
[ { "from": "human", "value": "As a physician engaged 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 woman have had two fetuses with congenital heart disease and terminated pregnancies at 29 and 31 years old in 2012 and 2014, respectively. The karyotype of the woman was 46, XX, t (1;17)(q42;q21) (Fig. ), and that of her husband was 46, XY.\\nIn 2015, the patient underwent in vitro fertilization (IVF) followed by PGT-SR to assist in pregnancy. Eighteen eggs were acquired, and 5 were fertilized by intracytoplasmic sperm injection (ICSI). Blastocyst biopsy was performed on day 6 embryos for microarray-based comparative genomic hybridization (array-CGH) for PGT-SR. Two embryos were balanced, and 3 embryos were unbalanced (Table ). One balanced embryo was implanted during the thawing cycle, and the patient successfully achieved pregnancy. Amniocentesis was performed at the 19th week of gestation for karyotype analysis. To detect whether there were microdeletion/microduplication that can’t be detected by PGT-SR, single nucleotide polymorphism (SNP)-array was undertaken []. ). Peripheral blood from both parents was extracted for SNP-array analysis, and SNP loci analysis and comparison were performed then. After full genetic counseling, the couple decided to continue pregnancy. The patient gave birth to a healthy boy by cesarean section at 38 weeks, with a body length of 49 cm and a weight of 3250 g. Apgar score was 10. Phenylketonuria (PKU) and thyroid function screening of the neonate were normal. The newborn is now 3.5 years old and developed normally.\nOUTPUT:" }, { "from": "agent", "value": "Mosaic 47, XXY, Paternal iUPD (9)" } ]
As a physician 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 woman have had two fetuses with congenital heart disease and terminated pregnancies at 29 and 31 years old in 2012 and 2014, respectively. The karyotype of the woman was 46, XX, t (1;17)(q42;q21) (Fig. ), and that of her husband was 46, XY.\nIn 2015, the patient underwent in vitro fertilization (IVF) followed by PGT-SR to assist in pregnancy. Eighteen eggs were acquired, and 5 were fertilized by intracytoplasmic sperm injection (ICSI). Blastocyst biopsy was performed on day 6 embryos for microarray-based comparative genomic hybridization (array-CGH) for PGT-SR. Two embryos were balanced, and 3 embryos were unbalanced (Table ). One balanced embryo was implanted during the thawing cycle, and the patient successfully achieved pregnancy. Amniocentesis was performed at the 19th week of gestation for karyotype analysis. To detect whether there were microdeletion/microduplication that can’t be detected by PGT-SR, single nucleotide polymorphism (SNP)-array was undertaken []. ). Peripheral blood from both parents was extracted for SNP-array analysis, and SNP loci analysis and comparison were performed then. After full genetic counseling, the couple decided to continue pregnancy. The patient gave birth to a healthy boy by cesarean section at 38 weeks, with a body length of 49 cm and a weight of 3250 g. Apgar score was 10. Phenylketonuria (PKU) and thyroid function screening of the neonate were normal. The newborn is now 3.5 years old and developed normally. OUTPUT:
PMCPatients_common1607
[ { "from": "human", "value": "As a physician engaged 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 denied fever and abdominal pain. She was never an alcohol consumer and denied intake of any other medications recently. Systemic examination was unremarkable except for icterus. Investigation showed hyperbilirubinemia (total bilirubin of 208 µmol/L, conjugated 124 µmol/L) and elevated liver enzymes (alanine aminotransferase [ALT] of 224 U/L, aspartate aminotransferase [AST] of 163 U/L, and alkaline phosphatase [ALP] of 347 U/L) (Table ).\\nOther causes of hepatitis and cholestasis were excluded (viral profile and autoimmune serology were normal). Obstructive causes were excluded by ultrasound and MRI imaging. She was continued on propranolol. Attempts to arrange radioactive iodine treatment or treat the patient surgically were not successful due to technical and logistical reasons. Her thyroid function tests (TFTs) continued to worsen and she started to have recurrence of symptoms of hyperthyroidism, while the liver function tests (LFTs) slowly started trending down (Table ). Hence, we started her on steroids and PTU on day 12. Her LFTs continued to improve gradually, and the symptoms of hyperthyroidism began to resolve. She was discharged after three weeks, and upon discharge her LFTs were as follows: ALT of 84 U/L, AST of 62 U/L, ALP of 117 U/L, total bilirubin of 87 µmol/L, and direct bilirubin of 44 µmol/L. The patient was followed up for six months after discharge and was doing well clinically on follow-up; her repeat TFT and LFT were completely normal.\nOUTPUT:" }, { "from": "agent", "value": "Carbimazole-Induced Jaundice, Thyrotoxicosis" } ]
As a physician 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 denied fever and abdominal pain. She was never an alcohol consumer and denied intake of any other medications recently. Systemic examination was unremarkable except for icterus. Investigation showed hyperbilirubinemia (total bilirubin of 208 µmol/L, conjugated 124 µmol/L) and elevated liver enzymes (alanine aminotransferase [ALT] of 224 U/L, aspartate aminotransferase [AST] of 163 U/L, and alkaline phosphatase [ALP] of 347 U/L) (Table ).\nOther causes of hepatitis and cholestasis were excluded (viral profile and autoimmune serology were normal). Obstructive causes were excluded by ultrasound and MRI imaging. She was continued on propranolol. Attempts to arrange radioactive iodine treatment or treat the patient surgically were not successful due to technical and logistical reasons. Her thyroid function tests (TFTs) continued to worsen and she started to have recurrence of symptoms of hyperthyroidism, while the liver function tests (LFTs) slowly started trending down (Table ). Hence, we started her on steroids and PTU on day 12. Her LFTs continued to improve gradually, and the symptoms of hyperthyroidism began to resolve. She was discharged after three weeks, and upon discharge her LFTs were as follows: ALT of 84 U/L, AST of 62 U/L, ALP of 117 U/L, total bilirubin of 87 µmol/L, and direct bilirubin of 44 µmol/L. The patient was followed up for six months after discharge and was doing well clinically on follow-up; her repeat TFT and LFT were completely normal. OUTPUT:
PMCPatients_common4134
[ { "from": "human", "value": "As a physician engaged 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 child was unable to retain a COP in the eye socket. He underwent a Fornix formation suture (FFS) with mucus membrane grafting to deepen the fornix after 6 weeks. Over a follow-up period of 12 months, no complications were noted.\\nThe baseline demographics, pre- and postoperative socket findings, and the results of surgery are as described in . None of the six patients developed complications of the spherical or PSI over a mean of 21-month follow-up. Three patients underwent a simultaneous inferior fornix formation suture for a shelved inferior fornix. Two patients underwent subsequent fornix formation suture and mucus membrane graft for grade 1 contracted socket with shallow inferior fornix. One patient required a levator reattachment for anophthalmic ptosis and one patient had persistent severe SSD for which hyaluronic acid gel filler was injected into the brow fat. The mean pre- and postoperative enophthalmos was 2.33 ± 0.81 and 0.5 ± 0.83 mm, respectively (P = 0.14). The mean preoperative SSD was grade 2 and postoperatively grade 0 (P = 0.1). The mean pre- and postoperative COP weights were 2.7 ± 1.25 and 2.2 ± 0.88 g, respectively (P = 0.37). The mean pre- and postoperative COP thickness was 7.16 ± 2.99 and 6.33 ± 1.21, respectively (P = 0.47). The mean PSI implant weight was 2.66 ± 0.53 g. There was no reduction in ocular motility post surgery with PSI []. The average patient score of satisfaction with the final prosthetic outcome was 9 on 10.\nOUTPUT:" }, { "from": "agent", "value": "Retinoblastoma, Spherical Orbital Implant Migration" } ]
As a physician 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 child was unable to retain a COP in the eye socket. He underwent a Fornix formation suture (FFS) with mucus membrane grafting to deepen the fornix after 6 weeks. Over a follow-up period of 12 months, no complications were noted.\nThe baseline demographics, pre- and postoperative socket findings, and the results of surgery are as described in . None of the six patients developed complications of the spherical or PSI over a mean of 21-month follow-up. Three patients underwent a simultaneous inferior fornix formation suture for a shelved inferior fornix. Two patients underwent subsequent fornix formation suture and mucus membrane graft for grade 1 contracted socket with shallow inferior fornix. One patient required a levator reattachment for anophthalmic ptosis and one patient had persistent severe SSD for which hyaluronic acid gel filler was injected into the brow fat. The mean pre- and postoperative enophthalmos was 2.33 ± 0.81 and 0.5 ± 0.83 mm, respectively (P = 0.14). The mean preoperative SSD was grade 2 and postoperatively grade 0 (P = 0.1). The mean pre- and postoperative COP weights were 2.7 ± 1.25 and 2.2 ± 0.88 g, respectively (P = 0.37). The mean pre- and postoperative COP thickness was 7.16 ± 2.99 and 6.33 ± 1.21, respectively (P = 0.47). The mean PSI implant weight was 2.66 ± 0.53 g. There was no reduction in ocular motility post surgery with PSI []. The average patient score of satisfaction with the final prosthetic outcome was 9 on 10. OUTPUT:
PMCPatients_common1936
[ { "from": "human", "value": "As a physician engaged in 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 was brought to the hospital when she collapsed during her first marathon, an hour into the run. Her friends threw some water on her face to no avail. Emergency medical service was called and patient was immediately brought to the hospital. At presentation, she was severely encephalopathic. Her vitals were pertinent for a temperature of 40.2°C, blood pressure of 82/54 mmHg, and a heart rate of 125 bmp. Her BMI was around 23.29. Laboratory work-up revealed a creatinine of 1.6 mg/dL, potassium of 5.6 mg/dL, lactate of 2.5 mmol/L, and creatine kinase (CK) of 1825 U/L. A computed tomography (CT) scan of the head was negative for any acute disease. She was treated with intravenous (IV) infusion of cold normal saline, cooling blankets, and ice packs with improvement in her mental status. The next day, patient developed abdominal pain and bloody diarrhea with a lactate of 3.6 mmol/L. She did report general intermittent use of ibuprofen but not recently. CT scan of the abdomen revealed ascending colon wall thickening signifying ischemic colitis (). Further work-up revealed acute liver injury with elevated transaminases (ALT of 1484 U/L and AST of 1217 U/L) and worsening of rhabdomyolysis with further elevation of CK (2213 U/L). Patient's course was further complicated by disseminated intravascular coagulation (DIC) evident from a platelet count of 92000/μL, d-dimer of 4.2 mcg/mL, fibrinogen of 98 mg/d, prothrombin time of 21 seconds, and partial thromboplastin time of 48 seconds. She was managed with aggressive IV fluid resuscitation for 3 days with normalization of creatinine and lactate and significant improvement in her liver function tests and coagulation parameters. She was discharged after a 4-day hospital course and seen in clinic after 2 weeks with normalization of the rest of her lab abnormalities.\nOUTPUT:" }, { "from": "agent", "value": "Bowel Ischemia, Heat Stroke" } ]
As a physician 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 was brought to the hospital when she collapsed during her first marathon, an hour into the run. Her friends threw some water on her face to no avail. Emergency medical service was called and patient was immediately brought to the hospital. At presentation, she was severely encephalopathic. Her vitals were pertinent for a temperature of 40.2°C, blood pressure of 82/54 mmHg, and a heart rate of 125 bmp. Her BMI was around 23.29. Laboratory work-up revealed a creatinine of 1.6 mg/dL, potassium of 5.6 mg/dL, lactate of 2.5 mmol/L, and creatine kinase (CK) of 1825 U/L. A computed tomography (CT) scan of the head was negative for any acute disease. She was treated with intravenous (IV) infusion of cold normal saline, cooling blankets, and ice packs with improvement in her mental status. The next day, patient developed abdominal pain and bloody diarrhea with a lactate of 3.6 mmol/L. She did report general intermittent use of ibuprofen but not recently. CT scan of the abdomen revealed ascending colon wall thickening signifying ischemic colitis (). Further work-up revealed acute liver injury with elevated transaminases (ALT of 1484 U/L and AST of 1217 U/L) and worsening of rhabdomyolysis with further elevation of CK (2213 U/L). Patient's course was further complicated by disseminated intravascular coagulation (DIC) evident from a platelet count of 92000/μL, d-dimer of 4.2 mcg/mL, fibrinogen of 98 mg/d, prothrombin time of 21 seconds, and partial thromboplastin time of 48 seconds. She was managed with aggressive IV fluid resuscitation for 3 days with normalization of creatinine and lactate and significant improvement in her liver function tests and coagulation parameters. She was discharged after a 4-day hospital course and seen in clinic after 2 weeks with normalization of the rest of her lab abnormalities. OUTPUT:
PMCPatients_common206
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: S.B. reported regularly to the anticoagulation clinic for international normalized ratio (INR) monitoring, generally with 5- to 8-week follow-up intervals. Most of the time, she remained within her prescribed therapeutic range (INR goal of 2–3). As she suffered from numerous sequelae related to CVA, she decided to pursue HBOT as a means to improve her clinical status and quality of life. The week prior to her HBOT, she arrived at the anticoagulation clinic for her regular follow-up, and it was determined that her INR was elevated at 3.5. During the ensuing discussion, her son, who was also her caregiver, mentioned that she would be undergoing HBOT for 1-hour sessions, five times a week, for 6 weeks of total duration of treatment. Due to the extended course of treatment and the fact that they would be devoting their resources to travel the long distance to the HBOT treatment site, the patient and her son were resistant to alter the warfarin dose at that time. Concerns for increased risk of bleeding events were discussed and the patient was scheduled for return monitoring. Her next INR continued slightly out of range at 3.2, and no dose change was made. At that time, she was 3 weeks into her HBOT treatment plan without any bleeding complications noted. Her INR 4 days after her last HBOT was within target range at 2.7, and again it was recorded that there had been no complication of bleeding during the treatments and no adjustment to warfarin dose.\nOUTPUT:" }, { "from": "agent", "value": "Atrial Fibrillation, Ischemic Cerebral Vascular Accident, Hemorrhagic Stroke, Left Hemiplegia" } ]
As a physician 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: S.B. reported regularly to the anticoagulation clinic for international normalized ratio (INR) monitoring, generally with 5- to 8-week follow-up intervals. Most of the time, she remained within her prescribed therapeutic range (INR goal of 2–3). As she suffered from numerous sequelae related to CVA, she decided to pursue HBOT as a means to improve her clinical status and quality of life. The week prior to her HBOT, she arrived at the anticoagulation clinic for her regular follow-up, and it was determined that her INR was elevated at 3.5. During the ensuing discussion, her son, who was also her caregiver, mentioned that she would be undergoing HBOT for 1-hour sessions, five times a week, for 6 weeks of total duration of treatment. Due to the extended course of treatment and the fact that they would be devoting their resources to travel the long distance to the HBOT treatment site, the patient and her son were resistant to alter the warfarin dose at that time. Concerns for increased risk of bleeding events were discussed and the patient was scheduled for return monitoring. Her next INR continued slightly out of range at 3.2, and no dose change was made. At that time, she was 3 weeks into her HBOT treatment plan without any bleeding complications noted. Her INR 4 days after her last HBOT was within target range at 2.7, and again it was recorded that there had been no complication of bleeding during the treatments and no adjustment to warfarin dose. OUTPUT:
PMCPatients_common2980
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 24-year-old male presented with diminished vision in the left eye (OS) for 5 years. He gave a history of trauma around OS 10 years ago. Visual acuity in the right eye (OD) was 20/20 and in OS was 20/200. Ocular examination revealed clear cornea and lens in both eyes. Intraocular pressure measured by applanation tonometry was 14 mm Hg in both eyes. Examination of the fundus revealed normal disc, vessels, and macula in OD. In OS, macula showed an ERM with concomitant dragging of retinal vessels. The fovea appeared to protrude into the vitreous through a defect in the ERM. There was no clinical evidence of uveitis, peripheral vascular lesions, or retinal breaks. OD was clinically normal. Spectral-domain optical coherence tomography (SD-OCT) using the Spectralis (Heidelberg Engineering, Heidelberg, Germany) through the macula in OS showed a taut ERM with the thickened inner retina. A central defect measuring 1018 μ was noted in the ERM. The outer retinal layers presented a normal configuration without ragged borders [].\\nThe patient underwent 25-G pars plana vitrectomy. The posterior vitreous was detached with the aid of triamcinolone acetonide. After using trypan blue, the ERM was peeled. Visual acuity had improved to 20/60 [].\nOUTPUT:" }, { "from": "agent", "value": "Foveal herniation, Epiretinal membrane" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 24-year-old male presented with diminished vision in the left eye (OS) for 5 years. He gave a history of trauma around OS 10 years ago. Visual acuity in the right eye (OD) was 20/20 and in OS was 20/200. Ocular examination revealed clear cornea and lens in both eyes. Intraocular pressure measured by applanation tonometry was 14 mm Hg in both eyes. Examination of the fundus revealed normal disc, vessels, and macula in OD. In OS, macula showed an ERM with concomitant dragging of retinal vessels. The fovea appeared to protrude into the vitreous through a defect in the ERM. There was no clinical evidence of uveitis, peripheral vascular lesions, or retinal breaks. OD was clinically normal. Spectral-domain optical coherence tomography (SD-OCT) using the Spectralis (Heidelberg Engineering, Heidelberg, Germany) through the macula in OS showed a taut ERM with the thickened inner retina. A central defect measuring 1018 μ was noted in the ERM. The outer retinal layers presented a normal configuration without ragged borders [].\nThe patient underwent 25-G pars plana vitrectomy. The posterior vitreous was detached with the aid of triamcinolone acetonide. After using trypan blue, the ERM was peeled. Visual acuity had improved to 20/60 []. OUTPUT:
PMCPatients_common2861
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 67 years old Caucasian woman gravida 3, para 1 presented with three days history of right flank pain and difficulty in urination. Her medical history was significant for obesity, hypertension and previous salpingectomy due to ectopic pregnancy. 15 years previously a cervical cautery was performed due to cervical ectropion.\\nOn admission her vital signs were stable. Physical examination revealed tenderness in both costovertebral angles and fullness in the lower abdomen. In gynecologic exam a huge soft cystic mass was bulging in the vagina to the level of the hymen. It was suspected to be a distended cervix. The external cervical os was not identified.\\nComputed tomography of the abdomen revealed a distended urinary bladder with bilateral hydronephrosis and hydroureter. Adjacent to the bladder was a cystic mass of 10 cm in the pelvis that was suspected to be a dilated cervix (figure ). The uterus was extra pelvic on top of the mass and was of normal size with dilated cavity up to 2.5 cm (figure ). No ascites or pelvic lymphadenopathy were noticed. Urethral catheterization drained 2000 ml of clear urine. Blood and chemistry profile were normal.\\nAn explorative laparatomy was performed; the uterine cervix was found to be distended with very thin walls and when was incised proved to be a large hematocervix and about 700 ml of old blood was drained. Due to cervical distention and difficulty differentiating the margins of the cervix from the vagina a modified radical hysterectomy was performed. Due to suspected malignancy, surgical staging was completed by omentectomy and lymph node dissection.\\nHistological examination of the specimens revealed grade I adenocarcinoma of the uterus located in the fundus with more than two thirds myometrial invasion. There was no lymph-vascular space involvement. The lower uterine segment, cervix and omentum were free of disease. Two of the pelvic lymph nodes were positive for metastases; stage IIIC according to the International Federation of Gynecologists and Obstetricians staging system. Following surgery the patient was treated by pelvic radiation and was doing well one year after surgery with no signs of disease recurrence.\nOUTPUT:" }, { "from": "agent", "value": "Endometrial Cancer" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 67 years old Caucasian woman gravida 3, para 1 presented with three days history of right flank pain and difficulty in urination. Her medical history was significant for obesity, hypertension and previous salpingectomy due to ectopic pregnancy. 15 years previously a cervical cautery was performed due to cervical ectropion.\nOn admission her vital signs were stable. Physical examination revealed tenderness in both costovertebral angles and fullness in the lower abdomen. In gynecologic exam a huge soft cystic mass was bulging in the vagina to the level of the hymen. It was suspected to be a distended cervix. The external cervical os was not identified.\nComputed tomography of the abdomen revealed a distended urinary bladder with bilateral hydronephrosis and hydroureter. Adjacent to the bladder was a cystic mass of 10 cm in the pelvis that was suspected to be a dilated cervix (figure ). The uterus was extra pelvic on top of the mass and was of normal size with dilated cavity up to 2.5 cm (figure ). No ascites or pelvic lymphadenopathy were noticed. Urethral catheterization drained 2000 ml of clear urine. Blood and chemistry profile were normal.\nAn explorative laparatomy was performed; the uterine cervix was found to be distended with very thin walls and when was incised proved to be a large hematocervix and about 700 ml of old blood was drained. Due to cervical distention and difficulty differentiating the margins of the cervix from the vagina a modified radical hysterectomy was performed. Due to suspected malignancy, surgical staging was completed by omentectomy and lymph node dissection.\nHistological examination of the specimens revealed grade I adenocarcinoma of the uterus located in the fundus with more than two thirds myometrial invasion. There was no lymph-vascular space involvement. The lower uterine segment, cervix and omentum were free of disease. Two of the pelvic lymph nodes were positive for metastases; stage IIIC according to the International Federation of Gynecologists and Obstetricians staging system. Following surgery the patient was treated by pelvic radiation and was doing well one year after surgery with no signs of disease recurrence. OUTPUT:
PMCPatients_common2845
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 3-year-old Caucasian girl accompanied by her mother was referred by her pediatric dentist to the outpatient stomatology clinic at the São José dos Campos Dental School, UNESP, because of the lack of eruption of some teeth and marked atrophy of the left posterior inferior alveolar border (Figure ). During investigation of her medical, dental and familial history, the mother reported the presence of maculae in various regions of the child's body. This was confirmed by physical examination, with the observation of bilateral, slate-brown maculae in the axillary region (Figure ), on the back, and in the hypochondrium and groin. With respect to clinical history, the mother reported that her daughter had suffered some episodes of seizures when she was approximately one month old, and that at that time small blisters had appeared that followed the same trajectory as the current maculae. During that time, the reported blisters were diagnosed as herpes zoster and treated with topical acyclovir, but the outcome was unsatisfactory. After a period of approximately one month, the mother noted remission of the bullous lesions; however, maculae started to develop in these regions and persisted until the time of the visit.\\nThe physical and intellectual development of the girl was considered to be normal by pediatricians despite the presence of discrete strabismus. After extra- and intraoral examination, a panoramic X-ray was requested to evaluate tooth germ development (Figure ) and to determine the reason for the lack of some teeth in the region of the third quadrant and the presence of conoid teeth 71 and 82. The X-ray revealed the absence of some deciduous and permanent tooth germs in the third quadrant (74, 75, 34, 35), as well as the lack of tooth 62 and of various permanent tooth germs at other sites. The mother was asked about the existence of family members with similar signs, which she denied. Hematologic tests showed no alterations.\\nBased on the clinical history and clinical and radiographic findings, the final diagnosis was IP []. At present, the girl is under complete medical follow-up, mainly taking into account alterations in the skin, eyes, CNS and mouth.\nOUTPUT:" }, { "from": "agent", "value": "Incontinentia pigmenti" } ]
As a physician 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-year-old Caucasian girl accompanied by her mother was referred by her pediatric dentist to the outpatient stomatology clinic at the São José dos Campos Dental School, UNESP, because of the lack of eruption of some teeth and marked atrophy of the left posterior inferior alveolar border (Figure ). During investigation of her medical, dental and familial history, the mother reported the presence of maculae in various regions of the child's body. This was confirmed by physical examination, with the observation of bilateral, slate-brown maculae in the axillary region (Figure ), on the back, and in the hypochondrium and groin. With respect to clinical history, the mother reported that her daughter had suffered some episodes of seizures when she was approximately one month old, and that at that time small blisters had appeared that followed the same trajectory as the current maculae. During that time, the reported blisters were diagnosed as herpes zoster and treated with topical acyclovir, but the outcome was unsatisfactory. After a period of approximately one month, the mother noted remission of the bullous lesions; however, maculae started to develop in these regions and persisted until the time of the visit.\nThe physical and intellectual development of the girl was considered to be normal by pediatricians despite the presence of discrete strabismus. After extra- and intraoral examination, a panoramic X-ray was requested to evaluate tooth germ development (Figure ) and to determine the reason for the lack of some teeth in the region of the third quadrant and the presence of conoid teeth 71 and 82. The X-ray revealed the absence of some deciduous and permanent tooth germs in the third quadrant (74, 75, 34, 35), as well as the lack of tooth 62 and of various permanent tooth germs at other sites. The mother was asked about the existence of family members with similar signs, which she denied. Hematologic tests showed no alterations.\nBased on the clinical history and clinical and radiographic findings, the final diagnosis was IP []. At present, the girl is under complete medical follow-up, mainly taking into account alterations in the skin, eyes, CNS and mouth. OUTPUT:
PMCPatients_common3621
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 42-year-old man presented with sudden onset right flank pain which started one week ago. The pain resolved by itself but presented again with the same right flank pain of approximately 24-hour duration. There was also associated lower back pain, nausea, vomiting, chilling sense and generalized myalgia. The pain was dull and constant in nature. He denied any urinary symptoms. He had started taking an antihypertensive agent one month ago and the blood pressure was well controlled. He denied any trauma or sudden changes in position.\\nHis BMI was 25.88 kg/m2. Right lower quadrant tenderness and right costovertebral angle tenderness were positive. His initial blood pressure was 160/103 mmHg and the temperature was 36.3°C (97.34°F). The laboratory value was significant for WBC 15,400 cells/mm3, with 85.9% neutrophils. However, C-reactive protein (CRP) level was normal. His serum creatinine level was 1.02 mg/dL urinalysis was negative. Plain X-ray of the KUB was normal. At the same time, antihypertensive therapy was started with amlodipine besylate 5 mg every 12 hours and analgesics were given. The pain was settled within 4 days. A follow-up CT was conducted on hospital day 7. He was discharged with antiplatelet and antihypertensive medication on hospital day 11. He was advised to continue the prescribed medications and visit the hospital every 6 months with CT.\nOUTPUT:" }, { "from": "agent", "value": "Spontaneous Renal Artery Dissection, Renal Infarction" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 42-year-old man presented with sudden onset right flank pain which started one week ago. The pain resolved by itself but presented again with the same right flank pain of approximately 24-hour duration. There was also associated lower back pain, nausea, vomiting, chilling sense and generalized myalgia. The pain was dull and constant in nature. He denied any urinary symptoms. He had started taking an antihypertensive agent one month ago and the blood pressure was well controlled. He denied any trauma or sudden changes in position.\nHis BMI was 25.88 kg/m2. Right lower quadrant tenderness and right costovertebral angle tenderness were positive. His initial blood pressure was 160/103 mmHg and the temperature was 36.3°C (97.34°F). The laboratory value was significant for WBC 15,400 cells/mm3, with 85.9% neutrophils. However, C-reactive protein (CRP) level was normal. His serum creatinine level was 1.02 mg/dL urinalysis was negative. Plain X-ray of the KUB was normal. At the same time, antihypertensive therapy was started with amlodipine besylate 5 mg every 12 hours and analgesics were given. The pain was settled within 4 days. A follow-up CT was conducted on hospital day 7. He was discharged with antiplatelet and antihypertensive medication on hospital day 11. He was advised to continue the prescribed medications and visit the hospital every 6 months with CT. OUTPUT:
PMCPatients_common4043
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Recently, she had undergone cardiac surgery due to heart valve malformation (mechanical heart valve replacement) performed approximately 2 months earlier, when full coumarin anticoagulation (sodium warfarin 5 mg/day) was introduced. 1). Therapeutic endoscopy was not indicated (Fig. 2).\\nConsidering the endoscopic findings of prominent vascularization in the small bowel, the patient underwent a diagnostic laparoscopy, which allowed the identification of aberrant vascularization at the jejunoileal junction. An enterectomy with 60-cm resection of the small bowel loops was performed (Fig. 3).\nOUTPUT:" }, { "from": "agent", "value": "Gastrointestinal Bleeding, Turner 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: Recently, she had undergone cardiac surgery due to heart valve malformation (mechanical heart valve replacement) performed approximately 2 months earlier, when full coumarin anticoagulation (sodium warfarin 5 mg/day) was introduced. 1). Therapeutic endoscopy was not indicated (Fig. 2).\nConsidering the endoscopic findings of prominent vascularization in the small bowel, the patient underwent a diagnostic laparoscopy, which allowed the identification of aberrant vascularization at the jejunoileal junction. An enterectomy with 60-cm resection of the small bowel loops was performed (Fig. 3). OUTPUT:
PMCPatients_common4752
[ { "from": "human", "value": "As a physician engaged 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 operation time was 99 minutes, and the amount of intraoperative bleeding was 224 mL. Postoperative radiographs are shown in . The amount of postoperative bleeding was 614 mL.\nOUTPUT:" }, { "from": "agent", "value": "Severe Hemophilia A, Hepatitis C, HIV, Early deep infection following Total Knee Arthroplasty" } ]
As a physician 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 operation time was 99 minutes, and the amount of intraoperative bleeding was 224 mL. Postoperative radiographs are shown in . The amount of postoperative bleeding was 614 mL. OUTPUT:
PMCPatients_common4057
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An 18-year-old male was sleeping on the floor after taking dinner woke up at 4:00 am with pain abdomen, vomiting, and weakness. He was taken to a hospital in the comatose state where he was intubated and referred to our hospital with a provisional diagnosis of unknown poisoning. At admission, he was atonic with the Glasgow coma scale (GCS) of E1VTM1, areflexia, pupils were dilated and fixed with absent doll's eye reflex and no respiratory efforts. He was immediately shifted to the Intensive Care Unit (ICU). His pulse rate was 120/min and blood pressure was 120/60 SpO2 98% with no respiratory efforts. His first arterial blood gas was suggestive of respiratory acidosis. He was ventilated on synchronized intermittent mandatory ventilation with volume control mode of ventilation. His initial investigation were all within the normal limit with normal computed tomography (CT) brain and ultrasound abdomen except total leukocyte count (TLC) count of 28.96 thou/cumm S. K-5.18 mmol/L and aspartate aminotransferase/alanine aminotransferase (U/L)-138/100. Fundus examination showed normal disc. He was managed with broad-spectrum antibiotics, antacids, and mechanical ventilation. After 8 h, he started slight flickering in fingers and eyes and started having some respiratory efforts. The same dose of ASV dose was repeated after 12 h. The paralysis improved and was extubated on the 4th day of ventilation. TLC, liver enzymes and S. Potassium came in normal range. Antibiotics were stepped down. When he was shifted out of ICU on the 4th day, he has Grade 4 power in upper and lower limb and breathing well but had truncal muscle weakness. Pupils were mid-dilated sluggishly reacting and otherwise stable.\nOUTPUT:" }, { "from": "agent", "value": "Severe envenomation from snake bite" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 18-year-old male was sleeping on the floor after taking dinner woke up at 4:00 am with pain abdomen, vomiting, and weakness. He was taken to a hospital in the comatose state where he was intubated and referred to our hospital with a provisional diagnosis of unknown poisoning. At admission, he was atonic with the Glasgow coma scale (GCS) of E1VTM1, areflexia, pupils were dilated and fixed with absent doll's eye reflex and no respiratory efforts. He was immediately shifted to the Intensive Care Unit (ICU). His pulse rate was 120/min and blood pressure was 120/60 SpO2 98% with no respiratory efforts. His first arterial blood gas was suggestive of respiratory acidosis. He was ventilated on synchronized intermittent mandatory ventilation with volume control mode of ventilation. His initial investigation were all within the normal limit with normal computed tomography (CT) brain and ultrasound abdomen except total leukocyte count (TLC) count of 28.96 thou/cumm S. K-5.18 mmol/L and aspartate aminotransferase/alanine aminotransferase (U/L)-138/100. Fundus examination showed normal disc. He was managed with broad-spectrum antibiotics, antacids, and mechanical ventilation. After 8 h, he started slight flickering in fingers and eyes and started having some respiratory efforts. The same dose of ASV dose was repeated after 12 h. The paralysis improved and was extubated on the 4th day of ventilation. TLC, liver enzymes and S. Potassium came in normal range. Antibiotics were stepped down. When he was shifted out of ICU on the 4th day, he has Grade 4 power in upper and lower limb and breathing well but had truncal muscle weakness. Pupils were mid-dilated sluggishly reacting and otherwise stable. OUTPUT:
PMCPatients_common1283
[ { "from": "human", "value": "As a physician engaged 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 developed nephrotic syndrome. Serum creatinine level was 1.1 mg/dL, eGFR (CKD-EPI) 62.7 mL/min/1.73 m2, urine protein excretion 13.52 g/d, total cholesterol 324 mg/dL, HDL-chol 35 mg/dL, LDL-chol 289 mg/dL, and albumin 24.44 g/L. Physical examination showed no edema. The kidney biopsy generated 14 glomeruli, one with global sclerosis. Glomerular basement membrane thickening of the capillary wall and increase in mesangial matrix as well as spikes in some glomeruli were shown on light microscopy suggesting a membranous nephropathy. Other images like “railroad tracks” with silver stains, low tubulointerstitial fibrosis with tubular atrophy, and chronic inflammation were also seen (Figures and ). Immunofluorescence () showed diffuse patchy granular and mesangial IgG, C3, and κ deposits. Electron microscopy showed extensive glomerular deposition of electron-dense fibrils in the mesangium and glomerular basement membrane: fibril ranging from 15 to 20 nm (). Congo red stains were negative and a diagnosis of FGN was made. The patient was treated with dual RAS blockers, statins, omega 3 fatty acids, and depletive therapy with torasemide, amiloride, and hydrochlorothiazide. Three months later, due to unremitting nephrotic syndrome, we offered the patient to add prednisone 20 mg/d and cyclophosphamide 2 mg/kg/d for 6 months, with no response. Despite persistent nephrotic syndrome, renal function (Ccr and eGFR) did not change.\nOUTPUT:" }, { "from": "agent", "value": "Fibrillary Glomerulonephritis, Diabetes Mellitus" } ]
As a physician 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 developed nephrotic syndrome. Serum creatinine level was 1.1 mg/dL, eGFR (CKD-EPI) 62.7 mL/min/1.73 m2, urine protein excretion 13.52 g/d, total cholesterol 324 mg/dL, HDL-chol 35 mg/dL, LDL-chol 289 mg/dL, and albumin 24.44 g/L. Physical examination showed no edema. The kidney biopsy generated 14 glomeruli, one with global sclerosis. Glomerular basement membrane thickening of the capillary wall and increase in mesangial matrix as well as spikes in some glomeruli were shown on light microscopy suggesting a membranous nephropathy. Other images like “railroad tracks” with silver stains, low tubulointerstitial fibrosis with tubular atrophy, and chronic inflammation were also seen (Figures and ). Immunofluorescence () showed diffuse patchy granular and mesangial IgG, C3, and κ deposits. Electron microscopy showed extensive glomerular deposition of electron-dense fibrils in the mesangium and glomerular basement membrane: fibril ranging from 15 to 20 nm (). Congo red stains were negative and a diagnosis of FGN was made. The patient was treated with dual RAS blockers, statins, omega 3 fatty acids, and depletive therapy with torasemide, amiloride, and hydrochlorothiazide. Three months later, due to unremitting nephrotic syndrome, we offered the patient to add prednisone 20 mg/d and cyclophosphamide 2 mg/kg/d for 6 months, with no response. Despite persistent nephrotic syndrome, renal function (Ccr and eGFR) did not change. OUTPUT:
PMCPatients_common4474
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: One day before admission, she experienced an abrupt blurred vision in the left eye, lightheadedness and mild headache while driving. This blurred vision continued for 5 to 10 min. Her height was 147 cm and she weighted 46 kg. She did not have findings associated with Horner’s syndrome or any cervical bruits. Initial routine laboratory examinations were unremarkable. Diffusion-weighted and T2-weighted magnetic resonance imaging (MRI) of the brain showed a hyperintense lesion in the genu of the left internal capsule and globus pallidus (). She was lying back during the first day of admission. The coefficient of variation of the RR intervals (CVRR) was decreased.\nOUTPUT:" }, { "from": "agent", "value": "Severe Orthostatic Hypotension, Unilateral Carotid Artery Dissection, Cerebral Infarction" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: One day before admission, she experienced an abrupt blurred vision in the left eye, lightheadedness and mild headache while driving. This blurred vision continued for 5 to 10 min. Her height was 147 cm and she weighted 46 kg. She did not have findings associated with Horner’s syndrome or any cervical bruits. Initial routine laboratory examinations were unremarkable. Diffusion-weighted and T2-weighted magnetic resonance imaging (MRI) of the brain showed a hyperintense lesion in the genu of the left internal capsule and globus pallidus (). She was lying back during the first day of admission. The coefficient of variation of the RR intervals (CVRR) was decreased. OUTPUT:
PMCPatients_common1872
[ { "from": "human", "value": "As a physician engaged 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 systemic diseases and no signs of temporomandibular joint dysfunction. Cephalometric analysis showed a concave facial profile and hyperdivergent growth pattern. Considering the patient’s age and growth patterns, treatment with customized BAMP miniplates was considered as the most optimal therapy.\\nFor the left maxilla, a ‘Y’ shaped plate was used and fixed at the zygomatic process to avoid possible disruption of the molar roots. An ‘L’ shaped plate was designed for the mandible and fixed at the symphysis of mandible. After preoperative simulation and fabrication, BAMP plates were used for the individualized rapid prototyping model (). Under local anesthesia, customized BAMP plates were installed at the simulated location using the transfer jig as a guide. The jig was precisely matched with the reference point for accurate installation of the miniplates (). The mean surgical time from incision to suture was 6.4 min for each side.\\nThe patient was advised to maintain good oral hygiene after the operation. The force of elastics (left: 5/16 3.50 oz; right: 3/16 3.50 oz) was increased to 150 g after 1 month of traction and again increased to 250 g after 3 months. The patient was instructed to wear the elastics full-time, except during meals and brushing. The patient also had to replace the elastics daily, with regular follow-up (). During the follow-up, the customized miniplates showed no loosening or inflammation. The miniplates were well-retained for over two years, showing sufficient retention force, and maintained good oral hygiene in the surrounding tissue. Superimposition of lateral cephalograms indicated that BAMP therapy successfully protracted the maxilla and prevented mandibular growth and hyperdivergent vertical growth ().\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: The patient had no systemic diseases and no signs of temporomandibular joint dysfunction. Cephalometric analysis showed a concave facial profile and hyperdivergent growth pattern. Considering the patient’s age and growth patterns, treatment with customized BAMP miniplates was considered as the most optimal therapy.\nFor the left maxilla, a ‘Y’ shaped plate was used and fixed at the zygomatic process to avoid possible disruption of the molar roots. An ‘L’ shaped plate was designed for the mandible and fixed at the symphysis of mandible. After preoperative simulation and fabrication, BAMP plates were used for the individualized rapid prototyping model (). Under local anesthesia, customized BAMP plates were installed at the simulated location using the transfer jig as a guide. The jig was precisely matched with the reference point for accurate installation of the miniplates (). The mean surgical time from incision to suture was 6.4 min for each side.\nThe patient was advised to maintain good oral hygiene after the operation. The force of elastics (left: 5/16 3.50 oz; right: 3/16 3.50 oz) was increased to 150 g after 1 month of traction and again increased to 250 g after 3 months. The patient was instructed to wear the elastics full-time, except during meals and brushing. The patient also had to replace the elastics daily, with regular follow-up (). During the follow-up, the customized miniplates showed no loosening or inflammation. The miniplates were well-retained for over two years, showing sufficient retention force, and maintained good oral hygiene in the surrounding tissue. Superimposition of lateral cephalograms indicated that BAMP therapy successfully protracted the maxilla and prevented mandibular growth and hyperdivergent vertical growth (). OUTPUT:
PMCPatients_common1984
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 54-year-old Chinese male visited our department with complaint of gradual bilateral vision loss during the past more than 1 year. He had been irregularly treated for uveitis with steroid and cyclosporine A without significant efficacy. All blood tests were negative except for the slight increase of lambda light chain and kappa light chain. Pathogenic examinations were also negative with regard to Treponema pallidum, human immunodeficiency virus, Mycobacterium tuberculosis, Cytomegalovirus, Epstein–Barr virus, and herpes virus. Serologic markers of autoimmune diseases, including antinuclear antibodies, rheumatoid factor, and anti-double-stranded deoxyribonucleic acid antibodies, were negative. The patient also underwent an enhanced brain magnetic resonance imaging, which revealed multiple gyriform enhancements of bilateral frontal, parietal, temporal, occipital lobes, and corpus callosum, suggesting inflammatory lesions. The cerebrospinal fluid analysis demonstrated a slight increase of protein content (50.40 mg/dL). Flow cytometry analysis and cytokine assay also presented negative results. The ocular examination revealed visual acuity of light perception for both eyes. For the right eye, slit-lamp examination detected cells in the anterior chamber and the keratic precipitates. Vitreous opacity, retinal hemorrhage, yellowish-white retinal, and subretinal infiltrations were also found at the posterior region. Based on these, BAG-PPV was performed for the purpose of diagnosis and therapy.\\nThe patient was fully informed of the potential risks and all possible postoperative consequences before the surgery. The written informed consents were obtained from the patient's family member after the discussion of the procedure. This study was consistent with the Declaration of Helsinki and was approved by the ethics committee of Zhejiang Provincial People's Hospital before applying this surgical procedure clinically.\nOUTPUT:" }, { "from": "agent", "value": "Masquerade 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 54-year-old Chinese male visited our department with complaint of gradual bilateral vision loss during the past more than 1 year. He had been irregularly treated for uveitis with steroid and cyclosporine A without significant efficacy. All blood tests were negative except for the slight increase of lambda light chain and kappa light chain. Pathogenic examinations were also negative with regard to Treponema pallidum, human immunodeficiency virus, Mycobacterium tuberculosis, Cytomegalovirus, Epstein–Barr virus, and herpes virus. Serologic markers of autoimmune diseases, including antinuclear antibodies, rheumatoid factor, and anti-double-stranded deoxyribonucleic acid antibodies, were negative. The patient also underwent an enhanced brain magnetic resonance imaging, which revealed multiple gyriform enhancements of bilateral frontal, parietal, temporal, occipital lobes, and corpus callosum, suggesting inflammatory lesions. The cerebrospinal fluid analysis demonstrated a slight increase of protein content (50.40 mg/dL). Flow cytometry analysis and cytokine assay also presented negative results. The ocular examination revealed visual acuity of light perception for both eyes. For the right eye, slit-lamp examination detected cells in the anterior chamber and the keratic precipitates. Vitreous opacity, retinal hemorrhage, yellowish-white retinal, and subretinal infiltrations were also found at the posterior region. Based on these, BAG-PPV was performed for the purpose of diagnosis and therapy.\nThe patient was fully informed of the potential risks and all possible postoperative consequences before the surgery. The written informed consents were obtained from the patient's family member after the discussion of the procedure. This study was consistent with the Declaration of Helsinki and was approved by the ethics committee of Zhejiang Provincial People's Hospital before applying this surgical procedure clinically. OUTPUT:
PMCPatients_common2830
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 39-year-old Caucasian (British) non-pregnant lady (para 3 with caesarean section; in a stable relationship) was admitted to gynaecology ward with complain of pelvic pain and temperature of 37.3°C. She was discharged from emergency department three days ago on antibiotics for urinary tract infection. There was no history of vomiting, diarrhoea or constipation. Also there was no past history of pelvic inflammatory disease. The laboratory findings were CRP 443 mg/L; Hb 111 g/L; WBCs 11.9 × 109 /L with 83% neutrophilia and Platelets were 386 × 109 /L. Urine dip stick revealed no infection. Her cervical smears were up to date and there was no family history of ovarian, cervical or endometrial carcinoma. Her CA-125 was also within normal limits.\\nThe ultrasound transvaginal () and ultrasound abdomino-pelvis () revealed right adnexal lesion measuring 9.3 × 8.3 × 6.6 cm with mixed echogenicity with small fluid areas as well as some focal echogenic areas consistent with some air or gas. There was some peripheral vascularity but no central vascularity on dopplers. No free fluid in pouch of Douglas noted and no abnormality seen in right iliac fossa. The appearances were most likely to represent a right tubo-ovarian abscess. The radiologist recommended no further investigations. Approximately 200 ml pus was drained from the area between posterior of uterine fundus and inflamed bowels. The gynaecology team performed right salpingo-oophorectomy while appendicectomy with right hemicolectomy was performed by surgeons. The patient made un-remarkable recovery.\nOUTPUT:" }, { "from": "agent", "value": "Appendicular mass" } ]
As a physician 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 39-year-old Caucasian (British) non-pregnant lady (para 3 with caesarean section; in a stable relationship) was admitted to gynaecology ward with complain of pelvic pain and temperature of 37.3°C. She was discharged from emergency department three days ago on antibiotics for urinary tract infection. There was no history of vomiting, diarrhoea or constipation. Also there was no past history of pelvic inflammatory disease. The laboratory findings were CRP 443 mg/L; Hb 111 g/L; WBCs 11.9 × 109 /L with 83% neutrophilia and Platelets were 386 × 109 /L. Urine dip stick revealed no infection. Her cervical smears were up to date and there was no family history of ovarian, cervical or endometrial carcinoma. Her CA-125 was also within normal limits.\nThe ultrasound transvaginal () and ultrasound abdomino-pelvis () revealed right adnexal lesion measuring 9.3 × 8.3 × 6.6 cm with mixed echogenicity with small fluid areas as well as some focal echogenic areas consistent with some air or gas. There was some peripheral vascularity but no central vascularity on dopplers. No free fluid in pouch of Douglas noted and no abnormality seen in right iliac fossa. The appearances were most likely to represent a right tubo-ovarian abscess. The radiologist recommended no further investigations. Approximately 200 ml pus was drained from the area between posterior of uterine fundus and inflamed bowels. The gynaecology team performed right salpingo-oophorectomy while appendicectomy with right hemicolectomy was performed by surgeons. The patient made un-remarkable recovery. OUTPUT:
PMCPatients_common397
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: He also complained of shortness of breath on exertion for three days. On examination, he had tachycardia 177/min, tachypnea 24/min, normal blood pressure and oxygen saturation. Distended neck veins were noted on examination. Basic laboratory investigations were significant only for mildly elevated creatinine of 1.4 mg/dl. Even though the Wells score was low, CT pulmonary angiogram was planned because of McConnell's sign on echocardiography. CT pulmonary angiogram was suggestive of a saddle pulmonary embolus within the main pulmonary artery (Figure ) extending into the right and left pulmonary arteries (Figure ). The HAS-BLED score was 0. He was anticoagulated with heparin and switched to oral anticoagulation.\nOUTPUT:" }, { "from": "agent", "value": "Paroxysmal atrial fibrillation, Submassive PE" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: He also complained of shortness of breath on exertion for three days. On examination, he had tachycardia 177/min, tachypnea 24/min, normal blood pressure and oxygen saturation. Distended neck veins were noted on examination. Basic laboratory investigations were significant only for mildly elevated creatinine of 1.4 mg/dl. Even though the Wells score was low, CT pulmonary angiogram was planned because of McConnell's sign on echocardiography. CT pulmonary angiogram was suggestive of a saddle pulmonary embolus within the main pulmonary artery (Figure ) extending into the right and left pulmonary arteries (Figure ). The HAS-BLED score was 0. He was anticoagulated with heparin and switched to oral anticoagulation. OUTPUT:
PMCPatients_common3829
[ { "from": "human", "value": "As a physician engaged in 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 otherwise healthy man presented to our department complaining of disturbing floaters in his right eye for more than 2 years. On examination, best corrected visual acuity (BCVA) was 20/20 in both eyes (OU) with myopic correction bilaterally of − 1 diopter. Anterior segment and fundus examination were unremarkable apart from some degree of vitreous degeneration more pronounced in the right than in the left. No PVD was detected in OU. After detailed explanation of the possible risks and benefits of vitrectomy a 6-month period of observation was advised, after which surgery was carried out because of persistence of symptoms. A 25-gauge transconjunctival sutureless pars plana vitrectomy (surgeon G.B.) was performed using the Alcon Constellation system (Alcon Laboratories Inc., Fort Worth, TX). After core vitrectomy, PVD was induced with aspiration from the cutter after injection of a small amount of triamcinolone acetonide to visualize the vitreous cortex. Careful peripheral vitrectomy with vitreous base shaving was achieved with scleral indentation. BCVA was diminished to 20/80 (Fig. ). The vitreous cavity was filled with a mixture of air and 20% sulfur hexafluoride. Postoperatively, the patient was asked to maintain a reading position for 6 h per day for 3 days and not to sleep on his back for a week. Consent for the publication for this case report and any additional related information was taken from the patient involved in the study.\nOUTPUT:" }, { "from": "agent", "value": "Macular Hole" } ]
As a physician 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 otherwise healthy man presented to our department complaining of disturbing floaters in his right eye for more than 2 years. On examination, best corrected visual acuity (BCVA) was 20/20 in both eyes (OU) with myopic correction bilaterally of − 1 diopter. Anterior segment and fundus examination were unremarkable apart from some degree of vitreous degeneration more pronounced in the right than in the left. No PVD was detected in OU. After detailed explanation of the possible risks and benefits of vitrectomy a 6-month period of observation was advised, after which surgery was carried out because of persistence of symptoms. A 25-gauge transconjunctival sutureless pars plana vitrectomy (surgeon G.B.) was performed using the Alcon Constellation system (Alcon Laboratories Inc., Fort Worth, TX). After core vitrectomy, PVD was induced with aspiration from the cutter after injection of a small amount of triamcinolone acetonide to visualize the vitreous cortex. Careful peripheral vitrectomy with vitreous base shaving was achieved with scleral indentation. BCVA was diminished to 20/80 (Fig. ). The vitreous cavity was filled with a mixture of air and 20% sulfur hexafluoride. Postoperatively, the patient was asked to maintain a reading position for 6 h per day for 3 days and not to sleep on his back for a week. Consent for the publication for this case report and any additional related information was taken from the patient involved in the study. OUTPUT:
PMCPatients_common5261
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 54-year-old male was admitted to our hospital with complaints of severe dyspnea, inability to lie in supine position, decrease in effort capacity, and pain in the left arm. Physical examination revealed tachycardia and 3/6 apical systolic murmur; bilateral rales in lower lung zones. Brachial, axillary, and radial pulses of the left arm were not palpable but were clearly palpated over the right arm. Lower extremity pulses were palpable. An echoacradiogram was performed which showed increased left ventricular diameter and left ventricular ejection fraction of 18% by the modified Simpson method. He was started on diuretic and vasodilator treatment with regression of failure symptoms. A differential diagnosis of CSSS was considered and patient underwent coronary angiography. It was observed on coronary angiography that point of origin of the left subclavian artery in the aorta was totally congested beginning from approximately 1 cm proximal []. A vertebral artery angiography was showed subclavian in bridge collaterals and flow to LIMA were observed in late period.\\nUsing a ringed polytetrafluoroethylene (PTFE) graft (Vascutek, Germany) with a diameter of 6 mm, a left carotid-subclavian bypass was performed on the patient in elective conditions. Carotid shunt was not used while systemic heparin (5000 units) was administered during the operation. Postoperatively, a good graft pulse was felt in addition to easily palpable left upper extremity pulses. There were no complications. Following the operation and in the postoperative period, the complaints of the patient related to chest pain, dyspnea, and left arm pain progressively decreased. The patient was discharged on the postoperative day 5. Control coronary-subclavian angiogram 1 month later revealed an intact PTFE graft between carotid and subclavian artery [].\nOUTPUT:" }, { "from": "agent", "value": "Ischemic Cardiomyopathy, Decompensated Heart Failure, 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: A 54-year-old male was admitted to our hospital with complaints of severe dyspnea, inability to lie in supine position, decrease in effort capacity, and pain in the left arm. Physical examination revealed tachycardia and 3/6 apical systolic murmur; bilateral rales in lower lung zones. Brachial, axillary, and radial pulses of the left arm were not palpable but were clearly palpated over the right arm. Lower extremity pulses were palpable. An echoacradiogram was performed which showed increased left ventricular diameter and left ventricular ejection fraction of 18% by the modified Simpson method. He was started on diuretic and vasodilator treatment with regression of failure symptoms. A differential diagnosis of CSSS was considered and patient underwent coronary angiography. It was observed on coronary angiography that point of origin of the left subclavian artery in the aorta was totally congested beginning from approximately 1 cm proximal []. A vertebral artery angiography was showed subclavian in bridge collaterals and flow to LIMA were observed in late period.\nUsing a ringed polytetrafluoroethylene (PTFE) graft (Vascutek, Germany) with a diameter of 6 mm, a left carotid-subclavian bypass was performed on the patient in elective conditions. Carotid shunt was not used while systemic heparin (5000 units) was administered during the operation. Postoperatively, a good graft pulse was felt in addition to easily palpable left upper extremity pulses. There were no complications. Following the operation and in the postoperative period, the complaints of the patient related to chest pain, dyspnea, and left arm pain progressively decreased. The patient was discharged on the postoperative day 5. Control coronary-subclavian angiogram 1 month later revealed an intact PTFE graft between carotid and subclavian artery []. OUTPUT:
PMCPatients_common1559
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Basic life support maneuvers were promptly started, but when paramedics arrived, he was asystolic at ECG. The victim played several competitive sports and had a syncope while playing football three years before. At external examination of the body no relevant sign was found. Both the lungs appeared swollen (weights: left—450 g, right—940 g), and multiorgan congestion was observed. Heart examination (weight: 530 g, longitudinal diameter: 11 cm, transverse diameter: 13 cm) presented no anomaly. Atria, valves, left ventricle (anterior wall thickness: 1.3 cm; lateral wall thickness: 1.4 cm; posterior wall thickness: 1.7 cm; interventricular septum thickness: 1.5 cm) and right ventricle (wall thickness: 0.5 cm) did not show any macroscopic relevant finding. Coronary circulation was right dominant. Left anterior descending coronary artery presented, at 2 cm from its beginning, a 0.3-cm-thick 5.5-cm-long myocardial bridging (). Other coronary arteries were macroscopically normal. The conduction system was carefully analyzed, and serial sectioning targeted blocks of areas of interest [,]. Histopathological examination of the myocardium () found wavering of myocardial fibers, fibrosis and disarray in the left ventricle myocardial area above the MB (); fibrosis in sino-atrial node area () and infiltration of fatty tissue (separated the myocardium) in the antero-lateral region of right ventricle free wall (). The atrio-ventricular node presented no microscopic anomalies. No signs of myocarditis were found.\nOUTPUT:" }, { "from": "agent", "value": "Sudden Death" } ]
As a physician 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: Basic life support maneuvers were promptly started, but when paramedics arrived, he was asystolic at ECG. The victim played several competitive sports and had a syncope while playing football three years before. At external examination of the body no relevant sign was found. Both the lungs appeared swollen (weights: left—450 g, right—940 g), and multiorgan congestion was observed. Heart examination (weight: 530 g, longitudinal diameter: 11 cm, transverse diameter: 13 cm) presented no anomaly. Atria, valves, left ventricle (anterior wall thickness: 1.3 cm; lateral wall thickness: 1.4 cm; posterior wall thickness: 1.7 cm; interventricular septum thickness: 1.5 cm) and right ventricle (wall thickness: 0.5 cm) did not show any macroscopic relevant finding. Coronary circulation was right dominant. Left anterior descending coronary artery presented, at 2 cm from its beginning, a 0.3-cm-thick 5.5-cm-long myocardial bridging (). Other coronary arteries were macroscopically normal. The conduction system was carefully analyzed, and serial sectioning targeted blocks of areas of interest [,]. Histopathological examination of the myocardium () found wavering of myocardial fibers, fibrosis and disarray in the left ventricle myocardial area above the MB (); fibrosis in sino-atrial node area () and infiltration of fatty tissue (separated the myocardium) in the antero-lateral region of right ventricle free wall (). The atrio-ventricular node presented no microscopic anomalies. No signs of myocarditis were found. OUTPUT:
PMCPatients_common305
[ { "from": "human", "value": "As a physician engaged in 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 woman underwent a cataract operation on her right eye in January 2019. She had diabetes but was well-controlled on oral hypoglycemic agents. Following successful surgery, a refractive correction was prescribed, and she was discharged from the cataract clinic after one month with a best-corrected visual acuity of 20/20. In late March 2019, the patient presented to the ED with pain, photophobia, and decreased vision. On examination, her visual acuity was 20/80, her intraocular pressure was normal, and dilated fundus examination showed a good fundal glow without any evidence of posterior segment pathology. The patient was immediately subjected to an anterior chamber wash. The lesion was gripped with tooth forceps, removed from the iris and plated onto sabouraud dextrose agar (SDA). An aqueous tap was also plated onto standard chocolate and blood agar. The patient was administered an intracameral injection of 0.1 mL containing 100 µg voriconazole using an insulin syringe.\\nThe examination the next day showed that the eye was mildly inflamed but less so than before the treatment. She was subsequently treated with topical steroids and topical 1% voriconazole drops, six times daily. (Figure ),\\nwhich was further confirmed on day 14 (Figure ).\\nAs her blood tests showed borderline increases in liver transaminases and an absence of any other risk factors for fungemia, she was not treated with any systemic antifungal agents. The patient was gradually tapered off both steroids and voriconazole over the next six to eight weeks. At three months, the patient had a best-corrected visual acuity of 20/20 and a noninflamed eye (Figure ).\nOUTPUT:" }, { "from": "agent", "value": "Postoperative Anterior Uveitis, Penicillium Spp. 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 50-year-old woman underwent a cataract operation on her right eye in January 2019. She had diabetes but was well-controlled on oral hypoglycemic agents. Following successful surgery, a refractive correction was prescribed, and she was discharged from the cataract clinic after one month with a best-corrected visual acuity of 20/20. In late March 2019, the patient presented to the ED with pain, photophobia, and decreased vision. On examination, her visual acuity was 20/80, her intraocular pressure was normal, and dilated fundus examination showed a good fundal glow without any evidence of posterior segment pathology. The patient was immediately subjected to an anterior chamber wash. The lesion was gripped with tooth forceps, removed from the iris and plated onto sabouraud dextrose agar (SDA). An aqueous tap was also plated onto standard chocolate and blood agar. The patient was administered an intracameral injection of 0.1 mL containing 100 µg voriconazole using an insulin syringe.\nThe examination the next day showed that the eye was mildly inflamed but less so than before the treatment. She was subsequently treated with topical steroids and topical 1% voriconazole drops, six times daily. (Figure ),\nwhich was further confirmed on day 14 (Figure ).\nAs her blood tests showed borderline increases in liver transaminases and an absence of any other risk factors for fungemia, she was not treated with any systemic antifungal agents. The patient was gradually tapered off both steroids and voriconazole over the next six to eight weeks. At three months, the patient had a best-corrected visual acuity of 20/20 and a noninflamed eye (Figure ). OUTPUT:
PMCPatients_common2649
[ { "from": "human", "value": "As a physician engaged in 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 was referred to our strabismus clinic with a complaint of double vision. She subsequently developed worsening diplopia and proptosis in her left eye 1 month prior to presentation. At the initial examination, her visual acuity was normal in both eyes (20/20), and 2 mm exophthalmos was noted in her left eye. She exhibited left hypotropia of 35 prism diopters (PD) in the primary position with marked limitation of left eye elevation (Fig. ). ). The forced duction test (FDT) revealed restriction in the upward direction in her left eye. She described a highly predictable fluctuating pattern of diplopia, that spontaneously switched at approximately 8 o’clock every night. To differentiate the causes of the fluctuating diplopia, such as myasthenia gravis, we performed laboratory tests, including a determination of acetylcholine receptor antibody titer; all results were normal. Based on her description, we recommended that she keep a diary to record her diplopia episodes and have her picture taken during episodes of both mild and severe diplopia. At the next visit, during which she exhibited relatively mild diplopia, cover testing revealed left hypotropia of 7 PD in the primary position with mild limitation of left eye elevation (Fig. ). Her diary clearly revealed the “every-other-day” pattern of diplopia. During the 6 months since the first visit, her thyroid function remained normal and the proptosis of her left eye decreased. A cycle involving diplopia-free days was gradually predominant. Finally, the left hypotropia of 7 PD remained, but without a cyclic pattern. Her diplopia was well compensated with mild chin elevation.\nOUTPUT:" }, { "from": "agent", "value": "Cyclic vertical deviation, Dysthyroid ophthalmopathy, Hyperthyroidism" } ]
As a physician 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 was referred to our strabismus clinic with a complaint of double vision. She subsequently developed worsening diplopia and proptosis in her left eye 1 month prior to presentation. At the initial examination, her visual acuity was normal in both eyes (20/20), and 2 mm exophthalmos was noted in her left eye. She exhibited left hypotropia of 35 prism diopters (PD) in the primary position with marked limitation of left eye elevation (Fig. ). ). The forced duction test (FDT) revealed restriction in the upward direction in her left eye. She described a highly predictable fluctuating pattern of diplopia, that spontaneously switched at approximately 8 o’clock every night. To differentiate the causes of the fluctuating diplopia, such as myasthenia gravis, we performed laboratory tests, including a determination of acetylcholine receptor antibody titer; all results were normal. Based on her description, we recommended that she keep a diary to record her diplopia episodes and have her picture taken during episodes of both mild and severe diplopia. At the next visit, during which she exhibited relatively mild diplopia, cover testing revealed left hypotropia of 7 PD in the primary position with mild limitation of left eye elevation (Fig. ). Her diary clearly revealed the “every-other-day” pattern of diplopia. During the 6 months since the first visit, her thyroid function remained normal and the proptosis of her left eye decreased. A cycle involving diplopia-free days was gradually predominant. Finally, the left hypotropia of 7 PD remained, but without a cyclic pattern. Her diplopia was well compensated with mild chin elevation. OUTPUT:
PMCPatients_common5023
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 41-year-old male, presented with history of fever, headache, and episodic seizures for one month. The neurological examination and routine investigations were normal, except for eosinophilia. A computed tomographic (CT) scan of the head showed numerous tiny hypodense foci scattered throughout the brain parenchyma. Cerebrospinal fluid serology was negative for antigens of herpes simplex, tubercular, and Japanese Encephalitis. Electroencephalography showed generalized slowing of the waves. The patient was managed with broad spectrum antibiotics and supportive treatments, but without any improvement. One week later magnetic resonance image (MRI), revealed numerous tiny lesions scattered throughout the brain parenchyma, with relative predilection for a gray-white junction and basal ganglia. The lesions were hyperintense on a T2-weighted image, without associated parenchymal edema. On contrast administration, none of these lesions showed enhancement. There was no intraventricular cyst or hydrocephalus []. Similar lesions were also noted on the scalp, tongue, extraocular muscles, muscles of the face, neck, trunk, and limbs. The diagnosis of cysticercosis was confirmed after a skin and muscle biopsy was taken, which showed cysticercus surrounded by an intense inflammatory infiltrate. The patient was treated with pyrantal pamoate, mannitol, steroids, and sodium valproate. However, the sensorium deteriorated with a Glasgow coma score (GCS) of E2V1M4. The trachea was intubated for ventilatory support, in the ICU. Two days later, the motor response deteriorated further (M2). Repeat MRI of the brain done two weeks later showed similar findings without any parenchymal edema. In view of the prolonged mechanical ventilation, percutaneous tracheostomy was done. He was gradually weaned off from the ventilator. In spite of continued supportive treatment, there was no neurological improvement. Oral albendazole was added to the treatment regimen. At present, after two months of treatment, the patient is on room air with a GCS of E4VTTM2.\nOUTPUT:" }, { "from": "agent", "value": "Neurocysticercosis" } ]
As a physician 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 41-year-old male, presented with history of fever, headache, and episodic seizures for one month. The neurological examination and routine investigations were normal, except for eosinophilia. A computed tomographic (CT) scan of the head showed numerous tiny hypodense foci scattered throughout the brain parenchyma. Cerebrospinal fluid serology was negative for antigens of herpes simplex, tubercular, and Japanese Encephalitis. Electroencephalography showed generalized slowing of the waves. The patient was managed with broad spectrum antibiotics and supportive treatments, but without any improvement. One week later magnetic resonance image (MRI), revealed numerous tiny lesions scattered throughout the brain parenchyma, with relative predilection for a gray-white junction and basal ganglia. The lesions were hyperintense on a T2-weighted image, without associated parenchymal edema. On contrast administration, none of these lesions showed enhancement. There was no intraventricular cyst or hydrocephalus []. Similar lesions were also noted on the scalp, tongue, extraocular muscles, muscles of the face, neck, trunk, and limbs. The diagnosis of cysticercosis was confirmed after a skin and muscle biopsy was taken, which showed cysticercus surrounded by an intense inflammatory infiltrate. The patient was treated with pyrantal pamoate, mannitol, steroids, and sodium valproate. However, the sensorium deteriorated with a Glasgow coma score (GCS) of E2V1M4. The trachea was intubated for ventilatory support, in the ICU. Two days later, the motor response deteriorated further (M2). Repeat MRI of the brain done two weeks later showed similar findings without any parenchymal edema. In view of the prolonged mechanical ventilation, percutaneous tracheostomy was done. He was gradually weaned off from the ventilator. In spite of continued supportive treatment, there was no neurological improvement. Oral albendazole was added to the treatment regimen. At present, after two months of treatment, the patient is on room air with a GCS of E4VTTM2. OUTPUT:
PMCPatients_common4840
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 60-year-old man presented with a headache suggestive of raised intracranial pressure for 2 months associated with vomiting and blurring of the vision at the peak of a headache. There was no past history suggestive of any primary malignancy in the body. There was no history suggestive of any genetic coagulopathy through detailed evaluation was not done. On examination, his blood pressure was 130/80 mmHg. He had bilateral papilledema and left side cerebellar signs; there were no other neurological deficits. Magnetic resonance imaging of the brain showed similar findings []. There was no imaging evidence of hemorrhage with either modality of imaging. Chest X-ray showed right lower zone ill-defined opacity. His preoperative platelet count was 2.48 lakhs/mm3. The patient underwent right frontal external ventricular drain (EVD) placement followed by left paramedian suboccipital craniectomy and excision of the cerebellar lesion. There was around 450 ml of blood loss during surgery, and no blood/blood product transfusion was given during the surgery. After surgery, the patient had delayed reversal from anesthesia. CT scan of head immediately after surgery showed multiple bleeds in supratentorial mass lesions []. There were no petechiae, ecchymosis, or other hemorrhagic manifestations. Postoperative coagulation profile was normal (international normalized ratio - 1.2, activated thromboplastin time - 35 s, and platelet count - 2.37 lakhs/mm3). The patient was managed aggressively in Intensive Care Unit for reduction of intracranial pressure. The patient improved gradually and discharged. Postoperative coagulation profile revealed normal platelet count, bleeding time and clotting time.\nOUTPUT:" }, { "from": "agent", "value": "Multiple intracranial hemorrhage, Multiple metastatic 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 60-year-old man presented with a headache suggestive of raised intracranial pressure for 2 months associated with vomiting and blurring of the vision at the peak of a headache. There was no past history suggestive of any primary malignancy in the body. There was no history suggestive of any genetic coagulopathy through detailed evaluation was not done. On examination, his blood pressure was 130/80 mmHg. He had bilateral papilledema and left side cerebellar signs; there were no other neurological deficits. Magnetic resonance imaging of the brain showed similar findings []. There was no imaging evidence of hemorrhage with either modality of imaging. Chest X-ray showed right lower zone ill-defined opacity. His preoperative platelet count was 2.48 lakhs/mm3. The patient underwent right frontal external ventricular drain (EVD) placement followed by left paramedian suboccipital craniectomy and excision of the cerebellar lesion. There was around 450 ml of blood loss during surgery, and no blood/blood product transfusion was given during the surgery. After surgery, the patient had delayed reversal from anesthesia. CT scan of head immediately after surgery showed multiple bleeds in supratentorial mass lesions []. There were no petechiae, ecchymosis, or other hemorrhagic manifestations. Postoperative coagulation profile was normal (international normalized ratio - 1.2, activated thromboplastin time - 35 s, and platelet count - 2.37 lakhs/mm3). The patient was managed aggressively in Intensive Care Unit for reduction of intracranial pressure. The patient improved gradually and discharged. Postoperative coagulation profile revealed normal platelet count, bleeding time and clotting time. OUTPUT:
PMCPatients_common3434
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 43-year-old woman with no significant medical, surgical or smoking history presented to the emergency department with 1-hour right-sided upper extremity weakness, slurred speech and difficulty with word finding. On examination in the emergency room, her vitals were as follows: heart rate 65 beats/min, blood pressure (BP) 120/73 mm Hg, respiration rate 20 breaths/min and oxygen saturation 100%. Tissue plasminogen activator (t-PA) was administered within 30 min of arrival as she presented within 4-hour window of symptom onset. She was subsequently admitted to the intensive care unit (ICU) in an isolation room. There was an associated arterial wall thickening around the thrombus, however, the clot did not appear to be adherent to the arterial wall.\nOUTPUT:" }, { "from": "agent", "value": "COVID-19, Ischaemic stroke, Carotid artery thrombosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 43-year-old woman with no significant medical, surgical or smoking history presented to the emergency department with 1-hour right-sided upper extremity weakness, slurred speech and difficulty with word finding. On examination in the emergency room, her vitals were as follows: heart rate 65 beats/min, blood pressure (BP) 120/73 mm Hg, respiration rate 20 breaths/min and oxygen saturation 100%. Tissue plasminogen activator (t-PA) was administered within 30 min of arrival as she presented within 4-hour window of symptom onset. She was subsequently admitted to the intensive care unit (ICU) in an isolation room. There was an associated arterial wall thickening around the thrombus, however, the clot did not appear to be adherent to the arterial wall. OUTPUT:
PMCPatients_common1253
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Figure shows the CGM summary graph of an 11-year-old female with T1D who had just started on SAP therapy. Her HbA1c was 7.4%. She was not aware of any particular problems in her blood sugar control, and download of her blood glucose meter showed most glucose readings were in her target range. Review of the CGM data summary for the few days prior to her appointment demonstrated stable overnight glucose levels (Figure , Summary Graph and Panel A), but examination of the CGM trend graphs revealed a pattern of post-prandial hyperglycemia (Figure , Panels B, C, and D). The data from CGM provided an opportunity for further improvement of glycemic control in this motivated, adherent patient and enabled her clinician to help her correlate the elevated post-prandial glucose levels with specific foods and timing of bolus insulin doses.\\nCan CGM use consistently improve HbA1c in children, particularly in patients, such as the one presented above, who already demonstrate good glycemic control? Meta-analyses of studies concluded prior to 2008 showed that CGM use was not superior to SMBG with regard to metabolic control among pediatric patients with T1D [,]. However, a subsequent sub-group analysis revealed that, for the 21% of children who used CGM 6+ days a week, HbA1c levels were lowered by 0.8% without an increase in hypoglycemia []. Subsequently, two multicenter, randomized controlled trials of adults and children with good control (HbA1c < 7.0% and 7.5%, respectively) demonstrated that RT-CGM use was associated with a mean improvement of −0.3% in HbA1c, suggesting CGM use could benefit patients whose HbA1c levels were already near their target range [,]. Other recent studies also support the effectiveness of frequent use of CGM in lowering HbA1c levels in children with T1D, and suggest SAP therapy may offer the most benefit to children [-].\nOUTPUT:" }, { "from": "agent", "value": "Type 1 Diabetes" } ]
As a physician 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: Figure shows the CGM summary graph of an 11-year-old female with T1D who had just started on SAP therapy. Her HbA1c was 7.4%. She was not aware of any particular problems in her blood sugar control, and download of her blood glucose meter showed most glucose readings were in her target range. Review of the CGM data summary for the few days prior to her appointment demonstrated stable overnight glucose levels (Figure , Summary Graph and Panel A), but examination of the CGM trend graphs revealed a pattern of post-prandial hyperglycemia (Figure , Panels B, C, and D). The data from CGM provided an opportunity for further improvement of glycemic control in this motivated, adherent patient and enabled her clinician to help her correlate the elevated post-prandial glucose levels with specific foods and timing of bolus insulin doses.\nCan CGM use consistently improve HbA1c in children, particularly in patients, such as the one presented above, who already demonstrate good glycemic control? Meta-analyses of studies concluded prior to 2008 showed that CGM use was not superior to SMBG with regard to metabolic control among pediatric patients with T1D [,]. However, a subsequent sub-group analysis revealed that, for the 21% of children who used CGM 6+ days a week, HbA1c levels were lowered by 0.8% without an increase in hypoglycemia []. Subsequently, two multicenter, randomized controlled trials of adults and children with good control (HbA1c < 7.0% and 7.5%, respectively) demonstrated that RT-CGM use was associated with a mean improvement of −0.3% in HbA1c, suggesting CGM use could benefit patients whose HbA1c levels were already near their target range [,]. Other recent studies also support the effectiveness of frequent use of CGM in lowering HbA1c levels in children with T1D, and suggest SAP therapy may offer the most benefit to children [-]. OUTPUT:
PMCPatients_common3517
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The patient is a 60-year-old female cafeteria worker who was originally diagnosed with stage II (cT1N1M0) ER-/PR+/HER2+ IDC of the right breast in 2004 and developed metastatic HER2+ recurrence involving bone and lymph nodes 4 years later. Initial treatment for stage II disease was right modified radical mastectomy followed by six cycles of adjuvant TAC (docetaxel, doxorubicin, and cyclophosphamide).\\nThe patient has received multiple lines of therapy for MBC, including vinorelbine plus trastuzumab at initial recurrence. After development of lung metastases, she was treated with T-DM1 on a clinical trial and experienced 6 years of disease control. She again experienced excellent disease control for 3 years with capecitabine plus lapatinib followed by slow progression of pulmonary metastases.\\nThe patient was reluctant to change to an intravenous regimen and remained asymptomatic from her disease. Upon FDA approval of neratinib in combination with capecitabine for HER2+ MBC, lapatinib was replaced with neratinib 240 mg qd with continuation of the same dose of capecitabine (1000 mg bid) based on prior tolerability. The patient received prophylactic loperamide 4 mg tid but paused the regimen after 4 days because of grade 2 nausea and grade 1 to 2 constipation. She then reinitiated neratinib with a DE schedule, starting at 120 mg/day with prophylactic loperamide 4 mg bid, with improved tolerability. She was able to titrate the neratinib dose to 160 mg/day after 1 week, to 200 mg/day after 2 additional weeks, and to 240 mg/day by week 5. The patient was able to continue on therapy with loperamide bid with regular bowel movements and no further nausea. Three months into treatment with neratinib plus capecitabine, the patient had a near-complete radiographic response, with residual scarring in the areas of prior pulmonary nodules. She remains free of recurrent diarrhea.\nOUTPUT:" }, { "from": "agent", "value": "HER2-Positive Breast Cancer" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The patient is a 60-year-old female cafeteria worker who was originally diagnosed with stage II (cT1N1M0) ER-/PR+/HER2+ IDC of the right breast in 2004 and developed metastatic HER2+ recurrence involving bone and lymph nodes 4 years later. Initial treatment for stage II disease was right modified radical mastectomy followed by six cycles of adjuvant TAC (docetaxel, doxorubicin, and cyclophosphamide).\nThe patient has received multiple lines of therapy for MBC, including vinorelbine plus trastuzumab at initial recurrence. After development of lung metastases, she was treated with T-DM1 on a clinical trial and experienced 6 years of disease control. She again experienced excellent disease control for 3 years with capecitabine plus lapatinib followed by slow progression of pulmonary metastases.\nThe patient was reluctant to change to an intravenous regimen and remained asymptomatic from her disease. Upon FDA approval of neratinib in combination with capecitabine for HER2+ MBC, lapatinib was replaced with neratinib 240 mg qd with continuation of the same dose of capecitabine (1000 mg bid) based on prior tolerability. The patient received prophylactic loperamide 4 mg tid but paused the regimen after 4 days because of grade 2 nausea and grade 1 to 2 constipation. She then reinitiated neratinib with a DE schedule, starting at 120 mg/day with prophylactic loperamide 4 mg bid, with improved tolerability. She was able to titrate the neratinib dose to 160 mg/day after 1 week, to 200 mg/day after 2 additional weeks, and to 240 mg/day by week 5. The patient was able to continue on therapy with loperamide bid with regular bowel movements and no further nausea. Three months into treatment with neratinib plus capecitabine, the patient had a near-complete radiographic response, with residual scarring in the areas of prior pulmonary nodules. She remains free of recurrent diarrhea. OUTPUT:
PMCPatients_common2068
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 36-year-old male patient was admitted to our clinic because of gait disorder, diplopia, and speech disorder. The patient experienced these symptoms for two weeks. The past medical history of the patient was unremarkable, and the family history was negative for neurological disorders. Oral aphthous ulcerations had been presented for approximately three months.\\nThe patient’s neurological examination revealed the presence of cerebellar-type dysarthria, truncal ataxia, wide-based ataxic gait, dysmetria, dysdiadochokinesia, and hyperreflexia in all his extremities. Body temperature was 36,0 °C. MR image showed mesencephalic lesion with oedemaas a hyperintense area (arrowheads) (). Contrast uptake was not seen in the MRI. Uveit was not found in the patient’s ophthalmic examination. Human leukocyte antigen B51 (HLADR B1) was found. The markers of collagen tissue disease were negative. Hematological markers, such as fibrinogen, antithrombin, and protein C and S were also in normal ranges, excluding ischemic stroke. Factor V Leiden, prothrombin G20210A gene mutations and MTHFR enzyme were not detected. Transthoracic and transesophageal echocardiography and carotidartery doppler were normal. The plasma Vit B (12), folic acid, and homocysteine levels were normal. Finally, the case was diagnosed as NBD.\\nAt the beginning of therapy, intravenous (IVP) methylprednisolone (1g/day) was administered for five days. The patient’s all neurological deficits improved within two weeks, and the patient was discharged.\\nThe follow up determined that genital aphthous ulcerations had developed within three months. A relapse of NBD was not seen in this patient, and recurrent corticosteroid and any drugs were not used. However, one year after NBD was diagnosed, the patient consulted an orthopedic surgeon for bilateral hip pain. The patient underwent surgery; there were no complications perioperatively, and the patient was discharged.\nOUTPUT:" }, { "from": "agent", "value": "Osteonecrosis in both femoral heads, Neuro-Behcet’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 36-year-old male patient was admitted to our clinic because of gait disorder, diplopia, and speech disorder. The patient experienced these symptoms for two weeks. The past medical history of the patient was unremarkable, and the family history was negative for neurological disorders. Oral aphthous ulcerations had been presented for approximately three months.\nThe patient’s neurological examination revealed the presence of cerebellar-type dysarthria, truncal ataxia, wide-based ataxic gait, dysmetria, dysdiadochokinesia, and hyperreflexia in all his extremities. Body temperature was 36,0 °C. MR image showed mesencephalic lesion with oedemaas a hyperintense area (arrowheads) (). Contrast uptake was not seen in the MRI. Uveit was not found in the patient’s ophthalmic examination. Human leukocyte antigen B51 (HLADR B1) was found. The markers of collagen tissue disease were negative. Hematological markers, such as fibrinogen, antithrombin, and protein C and S were also in normal ranges, excluding ischemic stroke. Factor V Leiden, prothrombin G20210A gene mutations and MTHFR enzyme were not detected. Transthoracic and transesophageal echocardiography and carotidartery doppler were normal. The plasma Vit B (12), folic acid, and homocysteine levels were normal. Finally, the case was diagnosed as NBD.\nAt the beginning of therapy, intravenous (IVP) methylprednisolone (1g/day) was administered for five days. The patient’s all neurological deficits improved within two weeks, and the patient was discharged.\nThe follow up determined that genital aphthous ulcerations had developed within three months. A relapse of NBD was not seen in this patient, and recurrent corticosteroid and any drugs were not used. However, one year after NBD was diagnosed, the patient consulted an orthopedic surgeon for bilateral hip pain. The patient underwent surgery; there were no complications perioperatively, and the patient was discharged. OUTPUT:
PMCPatients_common2240
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 54-year-old African American male with a past medical history of alcohol abuse with hepatic steatosis and recurrent pancreatitis presented to the emergency department at an outside hospital hypotensive and tachypneic. Prior to arrival, the patient had been found in a parking lot where he was experiencing multiple episodes of hematemesis and had subsequently become unresponsive. Soon after arrival at the emergency department, the patient suffered cardiac arrest. Return of spontaneous circulation (ROSC) was achieved, and the patient was treated with octreotide and PPI infusion as well as blood transfusion before being transferred to our tertiary care center for further management. Upon transfer, the patient was again found to be hypotensive with systolic pressures in the 50’s and tachypneic.\\nThe patient was resuscitated with blood transfusions, intravenous calcium, insulin, dextrose, and prothrombin complex concentrate and vasopressors were started. Laboratory work-up from post-resuscitation revealed hemoglobin of 15.1 g/dL, blood urea nitrogen (BUN) of 61 mg/dL, serum creatinine of 3.5 mg/dL, potassium of 8.2 mmol/L, lactate of 23 mmol/L, and an INR of 1.5. An emergent EGD revealed a black esophagus extending from the GEJ to the middle third of the esophagus with associated diffuse duodenal ulcer disease (Figure ). No esophagogastric varices were seen. Nil-per-os and high dose PPI therapy were continued and octreotide was stopped. Serum levels of common caustic substances including methanol, ethanol, isopropyl alcohol, acetone, ethylene glycol, and propylene glycol were negative. Despite initiation of hemodialysis for persistent hyperkalemia, the patient developed repeated episodes of cardiac arrest and was transitioned to comfort measures upon his family's request. He expired later in the evening.\nOUTPUT:" }, { "from": "agent", "value": "Acute Esophageal Necrosis, Severe acute pancreatitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 54-year-old African American male with a past medical history of alcohol abuse with hepatic steatosis and recurrent pancreatitis presented to the emergency department at an outside hospital hypotensive and tachypneic. Prior to arrival, the patient had been found in a parking lot where he was experiencing multiple episodes of hematemesis and had subsequently become unresponsive. Soon after arrival at the emergency department, the patient suffered cardiac arrest. Return of spontaneous circulation (ROSC) was achieved, and the patient was treated with octreotide and PPI infusion as well as blood transfusion before being transferred to our tertiary care center for further management. Upon transfer, the patient was again found to be hypotensive with systolic pressures in the 50’s and tachypneic.\nThe patient was resuscitated with blood transfusions, intravenous calcium, insulin, dextrose, and prothrombin complex concentrate and vasopressors were started. Laboratory work-up from post-resuscitation revealed hemoglobin of 15.1 g/dL, blood urea nitrogen (BUN) of 61 mg/dL, serum creatinine of 3.5 mg/dL, potassium of 8.2 mmol/L, lactate of 23 mmol/L, and an INR of 1.5. An emergent EGD revealed a black esophagus extending from the GEJ to the middle third of the esophagus with associated diffuse duodenal ulcer disease (Figure ). No esophagogastric varices were seen. Nil-per-os and high dose PPI therapy were continued and octreotide was stopped. Serum levels of common caustic substances including methanol, ethanol, isopropyl alcohol, acetone, ethylene glycol, and propylene glycol were negative. Despite initiation of hemodialysis for persistent hyperkalemia, the patient developed repeated episodes of cardiac arrest and was transitioned to comfort measures upon his family's request. He expired later in the evening. OUTPUT:
PMCPatients_common1172
[ { "from": "human", "value": "As a physician engaged in 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 with no systemic history was referred to the Department of Endodontics at Tabriz University of Medical Sciences.\\nThe chief complaint of the patient was pain in the lower left back teeth. Clinical examination revealed caries in teeth #20, 21. Vitality tests on both teeth showed painful response to cold, heat and electric pulpal test (EPT) and normal response to percussion. Nonsurgical endodontic treatment was planned in both #20 and #21 teeth in one visit. After the administration of the local anesthetic agent (2% lidocaine with 1: 100,000 epinephrine), under rubber dam isolation both #20 and #21 teeth were accessed.\\nIn both teeth two main canal orifices were found. After visualization under surgical operating microscope (OPMI pico Dental Microscope, Zeiss, Oberkochen, Germany) and staining with methylene blue presence of a third canal in #20 was detected.\\nWorking length was established with the use of an apex locator (Root ZX, J. Morita Inc., USA) and confirmed by a radiograph. The canals of teeth #20 were cleaned and shaped with hand K-files (Maillefer Dentsply, Baillaigues, Switzerland) and RaCe NiTi rotary file in a crown down manner up to final canal size of #0.06/30 in lingual canal and #0.06/25 in mesiobuccal and distobuccal canals. The canals were irrigated with 2.5% sodium hypochlorite during instrumentation and 17% EDTA at the end of instrumentation. After final rinse with normal saline, canals were dried and obturated with gutta-percha and AH26 sealer (Dentsply, De Trey, Konstanz, Germany) using the lateral compaction method ().\\nBoth teeth (#20,21) were asymptomatic and had normal periapical condition on radiographs in one-year follow-up ().\nOUTPUT:" }, { "from": "agent", "value": "Irreversible pulpitis" } ]
As a physician 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 with no systemic history was referred to the Department of Endodontics at Tabriz University of Medical Sciences.\nThe chief complaint of the patient was pain in the lower left back teeth. Clinical examination revealed caries in teeth #20, 21. Vitality tests on both teeth showed painful response to cold, heat and electric pulpal test (EPT) and normal response to percussion. Nonsurgical endodontic treatment was planned in both #20 and #21 teeth in one visit. After the administration of the local anesthetic agent (2% lidocaine with 1: 100,000 epinephrine), under rubber dam isolation both #20 and #21 teeth were accessed.\nIn both teeth two main canal orifices were found. After visualization under surgical operating microscope (OPMI pico Dental Microscope, Zeiss, Oberkochen, Germany) and staining with methylene blue presence of a third canal in #20 was detected.\nWorking length was established with the use of an apex locator (Root ZX, J. Morita Inc., USA) and confirmed by a radiograph. The canals of teeth #20 were cleaned and shaped with hand K-files (Maillefer Dentsply, Baillaigues, Switzerland) and RaCe NiTi rotary file in a crown down manner up to final canal size of #0.06/30 in lingual canal and #0.06/25 in mesiobuccal and distobuccal canals. The canals were irrigated with 2.5% sodium hypochlorite during instrumentation and 17% EDTA at the end of instrumentation. After final rinse with normal saline, canals were dried and obturated with gutta-percha and AH26 sealer (Dentsply, De Trey, Konstanz, Germany) using the lateral compaction method ().\nBoth teeth (#20,21) were asymptomatic and had normal periapical condition on radiographs in one-year follow-up (). OUTPUT:
PMCPatients_common4211
[ { "from": "human", "value": "As a physician engaged 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 circumference of the head was 18.0 cm (< 3rd percentile) [], and that of the abdomen was 14.4 cm (< 3rd percentile) []. Infantogram showed mildly hypoplastic thoracic cage (), and chest circumference was 14.6 cm (10th–25th percentile) []. Capillary vessel formation was also found in the peripheral region of the Wharton jelly (). Since only the pathology and autopsy findings of an already deceased fetus and only deidentified personal information of the mother and the fetus were used, the Institutional Review Board (IRB) of Asan Medical Center determined exemption (IRB number: 2017-1192).\nOUTPUT:" }, { "from": "agent", "value": "Umbilical Cord Stricture, Fetal Death" } ]
As a physician 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 circumference of the head was 18.0 cm (< 3rd percentile) [], and that of the abdomen was 14.4 cm (< 3rd percentile) []. Infantogram showed mildly hypoplastic thoracic cage (), and chest circumference was 14.6 cm (10th–25th percentile) []. Capillary vessel formation was also found in the peripheral region of the Wharton jelly (). Since only the pathology and autopsy findings of an already deceased fetus and only deidentified personal information of the mother and the fetus were used, the Institutional Review Board (IRB) of Asan Medical Center determined exemption (IRB number: 2017-1192). OUTPUT:
PMCPatients_common3217
[ { "from": "human", "value": "As a physician engaged in 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 gentleman presented with complaints of blurred vision in the right eye (RE) after a history of blunt trauma with a cricket ball seven days prior. He had been started on anti-glaucoma drops and topical steroids by a local physician. His corrected distance visual acuity (CDVA) was 20/800 in the RE and 20/20 in the left eye (LE). The intraocular pressure on applanation tonometry was 17 and 16 mm Hg in the RE and LE, respectively. On ocular examination, a resolving hyphema and anterior chamber reaction were noted in the RE. Funduscopy revealed a subretinal bleed at the posterior pole and inferiorly with a resolving vitreous hemorrhage []. There was no evidence of a rhegma or dialysis after a dilated indirect ophthalmoscopy with scleral indentation. The optical coherence scan (OCT) of the RE macula showed extensive subretinal scarring with gross disruption of the photoreceptor layer and decreased retinal thickness []. The LE examination was within normal limits.\\nThe patient was explained about the guarded vision prognosis and asked to review in a fortnight. An OCT scan revealed a thick preretinal membrane bridging the disc and macula with a pucker like concave configuration [, below]. A thorough fundus examination again did not reveal any breaks or dialysis.\\nIn view of the above development, a vitrectomy with membrane peeling and silicone oil infusion (for a longer tamponade) was done for the RE, following which the vision improved to 20/120 one-month post-surgery. There were poor outer retinal integrity and RPE clumping and scarring evident on both clinically and on the OCT scan []. An intraoperative peripheral retinal evaluation also did not reveal any predisposing breaks or dialysis.\\nSilicone oil removal was done 6 months later, following which the vision remained stable at 20/120 and the clinical findings remained status quo [].\nOUTPUT:" }, { "from": "agent", "value": "Macular tractional retinal detachment" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 25-year-old gentleman presented with complaints of blurred vision in the right eye (RE) after a history of blunt trauma with a cricket ball seven days prior. He had been started on anti-glaucoma drops and topical steroids by a local physician. His corrected distance visual acuity (CDVA) was 20/800 in the RE and 20/20 in the left eye (LE). The intraocular pressure on applanation tonometry was 17 and 16 mm Hg in the RE and LE, respectively. On ocular examination, a resolving hyphema and anterior chamber reaction were noted in the RE. Funduscopy revealed a subretinal bleed at the posterior pole and inferiorly with a resolving vitreous hemorrhage []. There was no evidence of a rhegma or dialysis after a dilated indirect ophthalmoscopy with scleral indentation. The optical coherence scan (OCT) of the RE macula showed extensive subretinal scarring with gross disruption of the photoreceptor layer and decreased retinal thickness []. The LE examination was within normal limits.\nThe patient was explained about the guarded vision prognosis and asked to review in a fortnight. An OCT scan revealed a thick preretinal membrane bridging the disc and macula with a pucker like concave configuration [, below]. A thorough fundus examination again did not reveal any breaks or dialysis.\nIn view of the above development, a vitrectomy with membrane peeling and silicone oil infusion (for a longer tamponade) was done for the RE, following which the vision improved to 20/120 one-month post-surgery. There were poor outer retinal integrity and RPE clumping and scarring evident on both clinically and on the OCT scan []. An intraoperative peripheral retinal evaluation also did not reveal any predisposing breaks or dialysis.\nSilicone oil removal was done 6 months later, following which the vision remained stable at 20/120 and the clinical findings remained status quo []. OUTPUT:
PMCPatients_common818
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She presented with a four-week history of productive cough. The cough was described as occurring intermittently throughout the day, productive of light-yellow colored sputum, and being associated with rhinorrhea and sinus congestion. She reported her uncle as a sick contact, who was being treated for an upper respiratory infection at the time she developed symptoms. The patient endorsed shortness of breath with mild exertion. The patient also complained of increased urinary frequency and dysuria that had started three days prior to admission; however, she denied any complaints of headaches, fever, chest pain, weakness, changes in vision, nausea, vomiting, or changes in bowel habits. The patient admitted to actively smoking tobacco and smokes approximately five cigarettes daily.\\nOn presentation to the emergency department, the patient was not in respiratory distress. Her vital signs showed a blood pressure of 148/77 mmHg, heart rate of 74 beats per minute, temperature of 98.3 degrees Fahrenheit, and oxygen saturation of 97% on room air. The patient’s physical examination was significant for absent breath sounds in the right basilar and anterior-mid lung field compared to the left with no wheezes or rales. Her examination was otherwise benign. Her laboratory studies are shown in Table .\\nShe was evaluated further with a chest X-ray (Figure ), computed tomography (CT) of the chest, abdomen, and pelvis (Figure ), which was compared to her CT chest from her visit three months prior to her current admission (Figure ), and magnetic resonance image (MRI) of the abdomen (Figure ). She received a dose of albuterol-ipratropium nebulizer therapy and a one-time 500 mg oral dose of levofloxacin followed by a chest tube placement. Upon removal of the chest tube three days later, the patient was discharged to her home in stable condition, with advice to follow-up regularly with the medical team in the outpatient clinic.\nOUTPUT:" }, { "from": "agent", "value": "Lymphangioleiomyomatosis, Recurrent Pneumothorax" } ]
As a physician 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 presented with a four-week history of productive cough. The cough was described as occurring intermittently throughout the day, productive of light-yellow colored sputum, and being associated with rhinorrhea and sinus congestion. She reported her uncle as a sick contact, who was being treated for an upper respiratory infection at the time she developed symptoms. The patient endorsed shortness of breath with mild exertion. The patient also complained of increased urinary frequency and dysuria that had started three days prior to admission; however, she denied any complaints of headaches, fever, chest pain, weakness, changes in vision, nausea, vomiting, or changes in bowel habits. The patient admitted to actively smoking tobacco and smokes approximately five cigarettes daily.\nOn presentation to the emergency department, the patient was not in respiratory distress. Her vital signs showed a blood pressure of 148/77 mmHg, heart rate of 74 beats per minute, temperature of 98.3 degrees Fahrenheit, and oxygen saturation of 97% on room air. The patient’s physical examination was significant for absent breath sounds in the right basilar and anterior-mid lung field compared to the left with no wheezes or rales. Her examination was otherwise benign. Her laboratory studies are shown in Table .\nShe was evaluated further with a chest X-ray (Figure ), computed tomography (CT) of the chest, abdomen, and pelvis (Figure ), which was compared to her CT chest from her visit three months prior to her current admission (Figure ), and magnetic resonance image (MRI) of the abdomen (Figure ). She received a dose of albuterol-ipratropium nebulizer therapy and a one-time 500 mg oral dose of levofloxacin followed by a chest tube placement. Upon removal of the chest tube three days later, the patient was discharged to her home in stable condition, with advice to follow-up regularly with the medical team in the outpatient clinic. OUTPUT:
PMCPatients_common1833
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 71-year-old man with no remarkable medical history experienced sudden lower abdominal pain. Computed tomography (CT) performed at a neighboring hospital revealed a right IIIAA (6.7 cm in diameter) with small volumes of contrast medium extravasation and hematoma (Fig. ). He was referred to our hospital due to a suspected ruptured right IIIAA. On emergency room arrival, the patient's general physical condition was stable (blood pressure, 120/70 mmHg; heart rate, 120 bpm). He complained of lower abdominal tenderness upon palpation and had bilateral lower limb cyanosis. Blood gas analysis showed lactic acidosis (pH, 7.258; lactate, 6.5 mmol/L). He was diagnosed with a ruptured right IIIAA complicated by peripheral circulatory failure. Considering his pre-shock status and probable time-consuming preparation for endovascular devices, emergency open surgical aneurysm repair was scheduled.\\nUnder general anesthesia, the abdominal cavity was entered through a lower midline skin incision. The intraperitoneal and retroperitoneal cavities were filled with large volumes of hematomas. After surgical hematoma evacuation, the large right IIIAA was easily identified in the pelvic cavity. The proximal neck of the right IIIAA was encircled carefully and ligated close to the right common iliac artery. Active bleeding from the aneurysmal surface was not observed. Encircling the distal IIA was considered difficult; therefore, we opened the aneurysm and removed a large mural thrombus and performed suture closure of distal IIA drainage sites (Fig. ). Circulatory status was stable throughout the operation. Perioperative hypotension was not observed.\\nThe patient was weaned from the ventilator immediately after the operation. However, he was found to have motor dysfunction from the bilateral thighs to the toes (Manual Muscle Testing of 1/1) and sensory disturbance below the L5 region. Spinal magnetic resonance imaging (MRI) confirmed presence of SCI at T12-L1 (Fig. ). The patient was treated with cerebrospinal fluid drainage and continuous intravenous infusion of naloxone. Although SCI was intensively managed, he could not stand independently, and neurogenic bladder and rectal disorder remained. Thereafter, after 51 postoperative days, he was transferred to the rehabilitation center.\nOUTPUT:" }, { "from": "agent", "value": "Spinal cord ischemia, Ruptured isolated internal iliac artery 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 71-year-old man with no remarkable medical history experienced sudden lower abdominal pain. Computed tomography (CT) performed at a neighboring hospital revealed a right IIIAA (6.7 cm in diameter) with small volumes of contrast medium extravasation and hematoma (Fig. ). He was referred to our hospital due to a suspected ruptured right IIIAA. On emergency room arrival, the patient's general physical condition was stable (blood pressure, 120/70 mmHg; heart rate, 120 bpm). He complained of lower abdominal tenderness upon palpation and had bilateral lower limb cyanosis. Blood gas analysis showed lactic acidosis (pH, 7.258; lactate, 6.5 mmol/L). He was diagnosed with a ruptured right IIIAA complicated by peripheral circulatory failure. Considering his pre-shock status and probable time-consuming preparation for endovascular devices, emergency open surgical aneurysm repair was scheduled.\nUnder general anesthesia, the abdominal cavity was entered through a lower midline skin incision. The intraperitoneal and retroperitoneal cavities were filled with large volumes of hematomas. After surgical hematoma evacuation, the large right IIIAA was easily identified in the pelvic cavity. The proximal neck of the right IIIAA was encircled carefully and ligated close to the right common iliac artery. Active bleeding from the aneurysmal surface was not observed. Encircling the distal IIA was considered difficult; therefore, we opened the aneurysm and removed a large mural thrombus and performed suture closure of distal IIA drainage sites (Fig. ). Circulatory status was stable throughout the operation. Perioperative hypotension was not observed.\nThe patient was weaned from the ventilator immediately after the operation. However, he was found to have motor dysfunction from the bilateral thighs to the toes (Manual Muscle Testing of 1/1) and sensory disturbance below the L5 region. Spinal magnetic resonance imaging (MRI) confirmed presence of SCI at T12-L1 (Fig. ). The patient was treated with cerebrospinal fluid drainage and continuous intravenous infusion of naloxone. Although SCI was intensively managed, he could not stand independently, and neurogenic bladder and rectal disorder remained. Thereafter, after 51 postoperative days, he was transferred to the rehabilitation center. OUTPUT:
PMCPatients_common1718
[ { "from": "human", "value": "As a physician engaged 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 other major comorbidity or systemic symptoms, no family history of SCA, and no social history of substance abuse. Baseline ECGs showed normal sinus rhythm with normal QRS, and QT intervals. He had undergone multiple appropriate ICD shocks for monomorphic VT (MMVT) after ICD implantation. The VT captured on 12 leads ECG was suggestive of the origin of arrhythmia from the inferolateral wall of the left ventricle. The patient could not undergo a cardiac MRI due to incompatibility with his ICD lead. He was referred for an electrophysiology study twice and ablations were performed targeting PVCs; however, he continued to have ICD shocks for VT. Ultimately, his ICD shocks decreased with mexiletine 200 mg TID.\nOUTPUT:" }, { "from": "agent", "value": "Mitral Valve Prolapse, Ventricular Tachycardia, Amiodarone-induced hypothyroidism, Mild Coronary Atherosclerosis" } ]
As a physician 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 other major comorbidity or systemic symptoms, no family history of SCA, and no social history of substance abuse. Baseline ECGs showed normal sinus rhythm with normal QRS, and QT intervals. He had undergone multiple appropriate ICD shocks for monomorphic VT (MMVT) after ICD implantation. The VT captured on 12 leads ECG was suggestive of the origin of arrhythmia from the inferolateral wall of the left ventricle. The patient could not undergo a cardiac MRI due to incompatibility with his ICD lead. He was referred for an electrophysiology study twice and ablations were performed targeting PVCs; however, he continued to have ICD shocks for VT. Ultimately, his ICD shocks decreased with mexiletine 200 mg TID. OUTPUT:
PMCPatients_common3927
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 7 year old boy who is a known cerebral palsy patient, mixed type (spastic and dystonic) was admitted to the pediatric ward with chief complaints of fever and difficulty in breathing for last 1 day. The child was a known case of bilirubin encephalopathy with involvement of bilateral basal ganglia region. Quadriplegic since birth, he also had a history of abnormal neck movements noticed by the parents for the last 4 months. Initially, the child was admitted and managed in general pediatric ward; however, due to progressively increasing distress and labored breathing, he was shifted to Pediatric Intensive Care Unit (PICU). Gradually, the acidosis was corrected, and the blood gas parameters improved. He was weaned off after 3 days but within a couple of hours following extubation, the child started hypoventilating and desaturating again. The ABG revealed profound respiratory acidosis. Thus, he was intubated. The Chest X-ray did not reveal any pulmonary pathology, and sepsis was also ruled out. He always needed minimum ventilator support. Surgical options with poor outcomes were discussed with the parents. Realizing a poor prognosis, the parents took the child to their hometown and he expired there after a couple of days.\nOUTPUT:" }, { "from": "agent", "value": "Cervical Myelopathy, Hypoventilation Syndrome, Type 2 Respiratory Failure" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 7 year old boy who is a known cerebral palsy patient, mixed type (spastic and dystonic) was admitted to the pediatric ward with chief complaints of fever and difficulty in breathing for last 1 day. The child was a known case of bilirubin encephalopathy with involvement of bilateral basal ganglia region. Quadriplegic since birth, he also had a history of abnormal neck movements noticed by the parents for the last 4 months. Initially, the child was admitted and managed in general pediatric ward; however, due to progressively increasing distress and labored breathing, he was shifted to Pediatric Intensive Care Unit (PICU). Gradually, the acidosis was corrected, and the blood gas parameters improved. He was weaned off after 3 days but within a couple of hours following extubation, the child started hypoventilating and desaturating again. The ABG revealed profound respiratory acidosis. Thus, he was intubated. The Chest X-ray did not reveal any pulmonary pathology, and sepsis was also ruled out. He always needed minimum ventilator support. Surgical options with poor outcomes were discussed with the parents. Realizing a poor prognosis, the parents took the child to their hometown and he expired there after a couple of days. OUTPUT:
PMCPatients_common1313
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 75-year-old man was admitted to our hospital with fever and general malaise.\\nA physical examination at the time of admission showed a body temperature of 38.9°C, blood pressure of 120/70 mmHg and a pulse rate of 80 beats/min. Laboratory findings showed a white blood cell count of 13,400/mm3 and C-reactive protein (CRP) of 23.7 mg/dL. A chest computed tomography (CT)-scan showed a ground-glass appearance in the right middle and lower lobes. His renal function was normal and the arterial blood gases analysis showed mild metabolic acidosis (Table ). The tubular reabsorption of phosphate (%TRP) was decreased, although the fractional excretion of uric acid (FEUA) was increased, indicating disturbed proximal tubular reabsorption. Despite the hypokalemia, his urinary potassium excretion was not suppressed. Elevations in urinary levels of β2-microglobulin (β2-MG) and N-acetyl-β-D-glucosaminidase (NAG), glycosuria and panaminoaciduria were also observed (Tables and ). There was no sign of extracellular fluid volume depletion. After treatment, his physical status recovered and his electrolyte abnormalities improved. Furthermore, his %TRP, FEUA, urinary β2-MG and NAG normalized, and the panaminoaciduria became undetectable (Figure A).\nOUTPUT:" }, { "from": "agent", "value": "Legionella pneumonia, Fanconi syndrome, Syndrome of inappropriate secretion of ADH (SIADH)" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 75-year-old man was admitted to our hospital with fever and general malaise.\nA physical examination at the time of admission showed a body temperature of 38.9°C, blood pressure of 120/70 mmHg and a pulse rate of 80 beats/min. Laboratory findings showed a white blood cell count of 13,400/mm3 and C-reactive protein (CRP) of 23.7 mg/dL. A chest computed tomography (CT)-scan showed a ground-glass appearance in the right middle and lower lobes. His renal function was normal and the arterial blood gases analysis showed mild metabolic acidosis (Table ). The tubular reabsorption of phosphate (%TRP) was decreased, although the fractional excretion of uric acid (FEUA) was increased, indicating disturbed proximal tubular reabsorption. Despite the hypokalemia, his urinary potassium excretion was not suppressed. Elevations in urinary levels of β2-microglobulin (β2-MG) and N-acetyl-β-D-glucosaminidase (NAG), glycosuria and panaminoaciduria were also observed (Tables and ). There was no sign of extracellular fluid volume depletion. After treatment, his physical status recovered and his electrolyte abnormalities improved. Furthermore, his %TRP, FEUA, urinary β2-MG and NAG normalized, and the panaminoaciduria became undetectable (Figure A). OUTPUT:
PMCPatients_common5389
[ { "from": "human", "value": "As a physician engaged 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 otherwise healthy 36-year-old male presented to our institute with a 4-day history of low-grade fever accompanied by sore throat, myalgia and nausea. Physical examination was remarkable for a temperature of 38.1°C and an injected pharynx without any neck tenderness or swelling. Complete blood cell count showed thrombocytopenia with platelet of 45,000/uL, hemoglobin of 14.8 g/dL and cell count of 8700 cells/uL (neutrophil of 85% and band form of 6%). Blood chemistry was remarkable for elevated creatinine of 2.1 mg/dL. He was diagnosed with viral upper respiratory tract infection and was admitted to general medicine service for rehydration. He received 2 L of intravenous normal saline over night; however, on the 2nd day of hospitalization, he developed high fever of 39.2°C along with pleuritic chest pain and low blood pressure of 80/50 mmHg. He was transferred to Intensive care unit and resuscitated with intravenous fluids. Blood cultures were obtained and empirical antibiotics (vancomycin and piperacillin/tazobactam) were initiated. Chest X-ray revealed bilateral patchy and irregular parenchymal opacities and subsequent chest computed tomography demonstrated right-sided pleural effusion and multiple thick-walled cavitary and nodular opacities consistent with septic emboli []. His blood cultures grew F. necrophorum on the following day and his antibiotic therapy was narrowed down to piperacillin/tazobactam. He responded well to intravenous fluids and antibiotics. His blood pressure was normalized without using any vasopressor or mechanical ventilation (he received 5 L of intravenous normal saline in total). Venous duplex ultrasonography was immediately obtained after the blood culture and demonstrated thrombus in the left IJV. His pleural effusion was managed conservatively. Piperacillin/tazobactam was continued for 7 days and he was discharged home with a 4-week course of intravenous ertapenem and recovered well from the infection. He did not receive any anticoagulation during the course of his treatment.\nOUTPUT:" }, { "from": "agent", "value": "Lemierre'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: An otherwise healthy 36-year-old male presented to our institute with a 4-day history of low-grade fever accompanied by sore throat, myalgia and nausea. Physical examination was remarkable for a temperature of 38.1°C and an injected pharynx without any neck tenderness or swelling. Complete blood cell count showed thrombocytopenia with platelet of 45,000/uL, hemoglobin of 14.8 g/dL and cell count of 8700 cells/uL (neutrophil of 85% and band form of 6%). Blood chemistry was remarkable for elevated creatinine of 2.1 mg/dL. He was diagnosed with viral upper respiratory tract infection and was admitted to general medicine service for rehydration. He received 2 L of intravenous normal saline over night; however, on the 2nd day of hospitalization, he developed high fever of 39.2°C along with pleuritic chest pain and low blood pressure of 80/50 mmHg. He was transferred to Intensive care unit and resuscitated with intravenous fluids. Blood cultures were obtained and empirical antibiotics (vancomycin and piperacillin/tazobactam) were initiated. Chest X-ray revealed bilateral patchy and irregular parenchymal opacities and subsequent chest computed tomography demonstrated right-sided pleural effusion and multiple thick-walled cavitary and nodular opacities consistent with septic emboli []. His blood cultures grew F. necrophorum on the following day and his antibiotic therapy was narrowed down to piperacillin/tazobactam. He responded well to intravenous fluids and antibiotics. His blood pressure was normalized without using any vasopressor or mechanical ventilation (he received 5 L of intravenous normal saline in total). Venous duplex ultrasonography was immediately obtained after the blood culture and demonstrated thrombus in the left IJV. His pleural effusion was managed conservatively. Piperacillin/tazobactam was continued for 7 days and he was discharged home with a 4-week course of intravenous ertapenem and recovered well from the infection. He did not receive any anticoagulation during the course of his treatment. OUTPUT:
PMCPatients_common1315
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A twenty-year-old 2nd gravida healthy mother delivered female twins per vaginum dated on 19-11-2012, following 36 weeks of uneventful gestation in a rural tertiary care—R L Jalappa Hospital, India. Amongst the twins, the first female twin baby was born by assisted breach delivery and cried soon after the birth with 1.84 kgs by weight, 47 cms in length, and 32 cms head circumference. On examination, the baby was referred as late-preterm baby with an uneventful neonatal period and normal examination. The second female twin baby born by vertex presentation and cried soon after birth; Apgar score at 1 minute was 8/10, weighing 1.94 kgs, 47 cms by length, and 30 cms head circumference. The placenta was completely expelled, monochorionic and diamniotic.\\nOn clinical examination, the 2nd twin baby showed the following abnormal features as shown in Figures and . Facial features: hypoplasia of the right malar region, micrognathia, and hypertelorism. Ears: bilateral accessory tags, right ear: external auditory canal stenosis. Oral cavity: right cleft lip (), bilateral complete cleft palate, and right facial cleft (macrostomia). Nose: normal external framework and cleft extending to bilateral nasal cavity. There were no skull, spinal, rib, or limb anomalies. Systemic examination did not reveal any cardiovascular or renal abnormality. Investigations revealed normal haemogram levels as follows: Hb 18.4%, WBC count 16800, neutrophils 68%, lymphocytes 20%, and Monocytes 2%, C-reactive proteins −ve, electrolytes: sodium 138 mEq/L, potassium 5.1 meq/L, blood urea −18 mg/dL, and serum creatinine-0.9%. Roentgenograms of the skull, spine, chest, and abdomen were normal. Abdominal ultrasound revealed sonologically normal kidneys.\nOUTPUT:" }, { "from": "agent", "value": "Goldenhar 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 twenty-year-old 2nd gravida healthy mother delivered female twins per vaginum dated on 19-11-2012, following 36 weeks of uneventful gestation in a rural tertiary care—R L Jalappa Hospital, India. Amongst the twins, the first female twin baby was born by assisted breach delivery and cried soon after the birth with 1.84 kgs by weight, 47 cms in length, and 32 cms head circumference. On examination, the baby was referred as late-preterm baby with an uneventful neonatal period and normal examination. The second female twin baby born by vertex presentation and cried soon after birth; Apgar score at 1 minute was 8/10, weighing 1.94 kgs, 47 cms by length, and 30 cms head circumference. The placenta was completely expelled, monochorionic and diamniotic.\nOn clinical examination, the 2nd twin baby showed the following abnormal features as shown in Figures and . Facial features: hypoplasia of the right malar region, micrognathia, and hypertelorism. Ears: bilateral accessory tags, right ear: external auditory canal stenosis. Oral cavity: right cleft lip (), bilateral complete cleft palate, and right facial cleft (macrostomia). Nose: normal external framework and cleft extending to bilateral nasal cavity. There were no skull, spinal, rib, or limb anomalies. Systemic examination did not reveal any cardiovascular or renal abnormality. Investigations revealed normal haemogram levels as follows: Hb 18.4%, WBC count 16800, neutrophils 68%, lymphocytes 20%, and Monocytes 2%, C-reactive proteins −ve, electrolytes: sodium 138 mEq/L, potassium 5.1 meq/L, blood urea −18 mg/dL, and serum creatinine-0.9%. Roentgenograms of the skull, spine, chest, and abdomen were normal. Abdominal ultrasound revealed sonologically normal kidneys. OUTPUT:
PMCPatients_common2431
[ { "from": "human", "value": "As a physician engaged in 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 female from a nursing home, with multiple comorbidities with a significant past medical history of renal transplant 2 months back and taking cellcept (myophenolate), prograft (tacrolimus) and prednisolone, comes to the ER with the shortness of breath and cough associated with green sputum for 1 day and rectal bleeding.\\nOn examination, the patient was moderately distressed and cachectic. She was hypotensive (85/50 mm Hg) with a pulse of 92 bpm. The patient was immediately resuscitated, appropriate labs were ordered and patient was started on empirical antibiotics, vancomycin and cefepime.\\nOn admission, CBC was significant for neutropenia with a total WBC count of 2.17, Hb of 8.2 and Hct of 27.2. A cell count 2 days prior to her admission was normal. Her fall in counts may be due to sepsis or side effect of cellcept.\\nChest X-ray showed right lower lobe consolidation. Chest CT reported bilateral basilar and lower lobe consolidation and small right apical pneumonia. CT of abdomen was suggestive of sigmoid colitis.\\nEcho showed possible tricuspid vegetation, which could be a source for the patient’s septicemia.\\nBronchoscopy was done the next day. BAL culture grew Pseudomonas aeruginosa.\\nA repeat CBC on the second day of admission revealed pancytopenia. Patient was treated with valgancyclovir, vancomycin, meropenem and neupogen. Her cellcept was put on hold, until the cell count stabilizes.\nOUTPUT:" }, { "from": "agent", "value": "Aspergillosis" } ]
As a physician 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 female from a nursing home, with multiple comorbidities with a significant past medical history of renal transplant 2 months back and taking cellcept (myophenolate), prograft (tacrolimus) and prednisolone, comes to the ER with the shortness of breath and cough associated with green sputum for 1 day and rectal bleeding.\nOn examination, the patient was moderately distressed and cachectic. She was hypotensive (85/50 mm Hg) with a pulse of 92 bpm. The patient was immediately resuscitated, appropriate labs were ordered and patient was started on empirical antibiotics, vancomycin and cefepime.\nOn admission, CBC was significant for neutropenia with a total WBC count of 2.17, Hb of 8.2 and Hct of 27.2. A cell count 2 days prior to her admission was normal. Her fall in counts may be due to sepsis or side effect of cellcept.\nChest X-ray showed right lower lobe consolidation. Chest CT reported bilateral basilar and lower lobe consolidation and small right apical pneumonia. CT of abdomen was suggestive of sigmoid colitis.\nEcho showed possible tricuspid vegetation, which could be a source for the patient’s septicemia.\nBronchoscopy was done the next day. BAL culture grew Pseudomonas aeruginosa.\nA repeat CBC on the second day of admission revealed pancytopenia. Patient was treated with valgancyclovir, vancomycin, meropenem and neupogen. Her cellcept was put on hold, until the cell count stabilizes. OUTPUT:
PMCPatients_common863
[ { "from": "human", "value": "As a physician engaged in 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 male with an unknown past medical history presented to the emergency department immediately following an unhelmeted motorcycle collision with a truck at highway speed. The patient was intubated at the scene, with the Glasgow Coma Scale calculated at 3T. Additional findings included a left flail chest with chest wall subcutaneous crepitus and diminished breath sounds. A bedside 36-French left chest tube immediately drained approximately 100 mL of blood. A 32-French thoracostomy tube was placed at the right fourth intercostal space. Upon entering the chest cavity, however, an audible gush of air was noted. The patient remained hemodynamically stable. Bronchoscopy and esophagogastroduodenoscopy (EGD) revealed no damage to the bronchial tree, esophagus, or stomach. The patient was then transferred to the intensive care unit (ICU) in stable condition, where he experienced an uneventful recovery. His chest tubes were removed 14 days post-admission, and he was subsequently discharged 19 days post-admission with the intent to follow up in one to two weeks in the clinic.\nOUTPUT:" }, { "from": "agent", "value": "Pneumopericardium, Bilateral pneumothoraxes, pneumomediastinum, pulmonary hemorrhage and contusions, closed left femur fracture, unstable pelvis, open left humerus fracture, left clavicle and scapula fracture, fractures of C7, T3, and the first rib." } ]
As a physician 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 male with an unknown past medical history presented to the emergency department immediately following an unhelmeted motorcycle collision with a truck at highway speed. The patient was intubated at the scene, with the Glasgow Coma Scale calculated at 3T. Additional findings included a left flail chest with chest wall subcutaneous crepitus and diminished breath sounds. A bedside 36-French left chest tube immediately drained approximately 100 mL of blood. A 32-French thoracostomy tube was placed at the right fourth intercostal space. Upon entering the chest cavity, however, an audible gush of air was noted. The patient remained hemodynamically stable. Bronchoscopy and esophagogastroduodenoscopy (EGD) revealed no damage to the bronchial tree, esophagus, or stomach. The patient was then transferred to the intensive care unit (ICU) in stable condition, where he experienced an uneventful recovery. His chest tubes were removed 14 days post-admission, and he was subsequently discharged 19 days post-admission with the intent to follow up in one to two weeks in the clinic. OUTPUT:
PMCPatients_common2024
[ { "from": "human", "value": "As a physician engaged in 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 male was admitted to hospital for liver transplantation. He had end-stage liver disease (MELD score 22) due to cirrhosis caused by hepatitis C virus infection and alcohol abuse. In addition, he had diabetes and was moderately overweight (body mass index of 32 kg/m2). He had no other risk factors for ischaemic heart disease and had normal renal function.\\nPre-transplant echocardiography revealed a left ventricular ejection fraction (LVEF) of 75% and moderate pulmonary hypertension with a systolic pulmonary artery pressure (PAP) of 41 mmHg. Cardiac catheterisation and coronary angiography prior to transplantation revealed normal coronary arteries and a mean PAP of 28 mmHg, falling to 23 mmHg after nitric oxide inhalation. His pulmonary vascular resistance was found to be 2.05 Wood units.\\nThe patient underwent an orthotopic liver transplantation. His ECG showed sinus tachycardia with no ischaemic changes. The hs-troponin T level was 0.154 ng/ml and pro-BNP concentration was also elevated to 22 842 ng/l. However, 72 hours later he showed no improvement in his left ventricular function and despite increasing doses of inotropic support, he remained hypotensive.\\nA decision was therefore made to insert the Tandem Heart left ventricular assist device (LVAD). The patient’s haemodynamics were stabilised with the LVAD and the inotropes were gently weaned. Therapy was commenced with carvedilol, enalapril and spironolactone. His left ventricular function gradually improved and he was weaned from the LVAD after nine days.\\nHe recovered well and at discharge 25 days post transplantation, his LVEF was 69%. At the four-month posttransplantation review he remained asymptomatic and his LVEF had improved to 75%.\nOUTPUT:" }, { "from": "agent", "value": "Takotsubo cardiomyopathy" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 56-year old male was admitted to hospital for liver transplantation. He had end-stage liver disease (MELD score 22) due to cirrhosis caused by hepatitis C virus infection and alcohol abuse. In addition, he had diabetes and was moderately overweight (body mass index of 32 kg/m2). He had no other risk factors for ischaemic heart disease and had normal renal function.\nPre-transplant echocardiography revealed a left ventricular ejection fraction (LVEF) of 75% and moderate pulmonary hypertension with a systolic pulmonary artery pressure (PAP) of 41 mmHg. Cardiac catheterisation and coronary angiography prior to transplantation revealed normal coronary arteries and a mean PAP of 28 mmHg, falling to 23 mmHg after nitric oxide inhalation. His pulmonary vascular resistance was found to be 2.05 Wood units.\nThe patient underwent an orthotopic liver transplantation. His ECG showed sinus tachycardia with no ischaemic changes. The hs-troponin T level was 0.154 ng/ml and pro-BNP concentration was also elevated to 22 842 ng/l. However, 72 hours later he showed no improvement in his left ventricular function and despite increasing doses of inotropic support, he remained hypotensive.\nA decision was therefore made to insert the Tandem Heart left ventricular assist device (LVAD). The patient’s haemodynamics were stabilised with the LVAD and the inotropes were gently weaned. Therapy was commenced with carvedilol, enalapril and spironolactone. His left ventricular function gradually improved and he was weaned from the LVAD after nine days.\nHe recovered well and at discharge 25 days post transplantation, his LVEF was 69%. At the four-month posttransplantation review he remained asymptomatic and his LVEF had improved to 75%. OUTPUT:
PMCPatients_common4295
[ { "from": "human", "value": "As a physician engaged 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 a routine laboratory workup of a 5-year-old girl status post repair of a tracheoesophageal fistula, the serum ammonia was found to be elevated to 71 mmol/L. Magnetic resonance imaging/magnetic resonance angiography (MRA) confirmed the shunt [Figure , ] and no significant intrahepatic portal veins. An ultrasound and fluoroscopy-guided right transjugular vein approach was utilized. 8 Fr sheath was placed. A 5 Fr Kumpe catheter and 0.035 in. wire were used to select the shunt. Selective portomesenteric venogram demonstrated a patent shunt from portal vein to IVC, enlarged superior mesenteric vein (SMV), and normal caliber splenic vein (SV) []. Pressures, both in the SMV and SV, were measured to be 7 mmHg. A 20 minute balloon occlusion test demonstrated a rise in pressure to 35 mmHg, and revealed the presence of a diminutive portal vein supplying the right lobe of the liver []. Following occlusion testing, a 12 × 8 mm Amplatzer plug (Abbott Medical, USA) was deployed into the portosystemic shunt [Figure , ]. Postprocedural ultrasound documented patency of SMV and SV with minimal flow to the IVC through the Amplatzer plug. The patient was observed in the ICU on a heparin drip for 3 days. Follow-up ultrasound revealed complete occlusion of the portosystemic shunt and patency of the superior mesenteric vein. There was normalization of serum ammonia levels on one-month follow- up, and no clinical or ultrasonological evidence of portal hypertension was found.\nOUTPUT:" }, { "from": "agent", "value": "Congenital extrahepatic portosystemic shunts, Abernethy Type 1 malformation, Focal nodular 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: During a routine laboratory workup of a 5-year-old girl status post repair of a tracheoesophageal fistula, the serum ammonia was found to be elevated to 71 mmol/L. Magnetic resonance imaging/magnetic resonance angiography (MRA) confirmed the shunt [Figure , ] and no significant intrahepatic portal veins. An ultrasound and fluoroscopy-guided right transjugular vein approach was utilized. 8 Fr sheath was placed. A 5 Fr Kumpe catheter and 0.035 in. wire were used to select the shunt. Selective portomesenteric venogram demonstrated a patent shunt from portal vein to IVC, enlarged superior mesenteric vein (SMV), and normal caliber splenic vein (SV) []. Pressures, both in the SMV and SV, were measured to be 7 mmHg. A 20 minute balloon occlusion test demonstrated a rise in pressure to 35 mmHg, and revealed the presence of a diminutive portal vein supplying the right lobe of the liver []. Following occlusion testing, a 12 × 8 mm Amplatzer plug (Abbott Medical, USA) was deployed into the portosystemic shunt [Figure , ]. Postprocedural ultrasound documented patency of SMV and SV with minimal flow to the IVC through the Amplatzer plug. The patient was observed in the ICU on a heparin drip for 3 days. Follow-up ultrasound revealed complete occlusion of the portosystemic shunt and patency of the superior mesenteric vein. There was normalization of serum ammonia levels on one-month follow- up, and no clinical or ultrasonological evidence of portal hypertension was found. OUTPUT:
PMCPatients_common1513
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A). Neuropsychological examination demonstrated no cognitive impairment. Due to volumetric expansion, surgery was proposed under awake condition to perform intraoperative multimodal mapping. Standard procedure was achieved to expose the left fronto-temporal region. The electrical stimulation was set at 60 Hz, 2.5 mA. A subpial dissection through the pars triangularis and the pars orbitalis was performed to reach the left insular lobe and remove the tumor.\\nTwo functional sites were identified at the subcortical level (see Fig. A,B). A schematic description of the intraoperative testing protocol is provided in Fig. C.\\nStimulation of the upper portion of the insula located under the superior limiting sulcus (S1) elicited a semantic paraphasia (the patient answered “fish” instead of “cat”) and an absence of response during 3 other items (≈12 s). At this time, the patient was unable to point out anything, with a facial expression of incomprehension. Stimulation located near the inferior limiting sulcus of the insula (S2) elicited semantic paraphasia with intense attempts of self-correction (the patient told “horse” then hesitated and finally found the right item “lion” spontaneously in a few second, suggesting that self-evaluative processes were not disrupted during this stimulation).\\nLater, a second stimulation at the S1 location was performed: the patient answered “star” instead of “hammer”, then stopped to produce responses. When she recovered all normal language abilities and a normal state of “consciousness”, she was asked if she was aware of her troubles and what she felt during the stimulation. She answered with surprise that she was strictly not aware of any troubles and that she did not remember any particular event.\nOUTPUT:" }, { "from": "agent", "value": "Low-grade glioma" } ]
As a physician 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). Neuropsychological examination demonstrated no cognitive impairment. Due to volumetric expansion, surgery was proposed under awake condition to perform intraoperative multimodal mapping. Standard procedure was achieved to expose the left fronto-temporal region. The electrical stimulation was set at 60 Hz, 2.5 mA. A subpial dissection through the pars triangularis and the pars orbitalis was performed to reach the left insular lobe and remove the tumor.\nTwo functional sites were identified at the subcortical level (see Fig. A,B). A schematic description of the intraoperative testing protocol is provided in Fig. C.\nStimulation of the upper portion of the insula located under the superior limiting sulcus (S1) elicited a semantic paraphasia (the patient answered “fish” instead of “cat”) and an absence of response during 3 other items (≈12 s). At this time, the patient was unable to point out anything, with a facial expression of incomprehension. Stimulation located near the inferior limiting sulcus of the insula (S2) elicited semantic paraphasia with intense attempts of self-correction (the patient told “horse” then hesitated and finally found the right item “lion” spontaneously in a few second, suggesting that self-evaluative processes were not disrupted during this stimulation).\nLater, a second stimulation at the S1 location was performed: the patient answered “star” instead of “hammer”, then stopped to produce responses. When she recovered all normal language abilities and a normal state of “consciousness”, she was asked if she was aware of her troubles and what she felt during the stimulation. She answered with surprise that she was strictly not aware of any troubles and that she did not remember any particular event. OUTPUT:
PMCPatients_common3251
[ { "from": "human", "value": "As a physician engaged in 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, Caucasian, right hand dominant male, otherwise healthy, was seen in the emergency department after a skateboard accident. He reported falling onto his dorsal left proximal forearm and experienced immediate pain in the area without other injuries. Physical examination was notable for tenderness over the proximal radius and ulna and limited pronosupination secondary to pain. Plain radiographs demonstrated non-displaced but slightly comminuted, short oblique fractures of the proximal third of the radius and ulna (, ). After discussion with the patient and his family, the decision was made to place the patient in a long arm cast (, ) and follow-up in the clinic in 1 week.\\nOn follow-up, the patient had satisfactory pain control, and the cast was appropriately in position. A hole was cut into the cast so that an ultrasound bone stimulator could be used to promote healing. The stimulator was positioned equidistant between the two fractures. The patient reported some mild increase in fracture site pain in the 1st week with the bone stimulator, but this abated after a few days. The next follow-up visit was 3 weeks later (4 weeks post-injury), and the patient reported significantly improved pain. The cast was removed, and his examination was significant for restoration of pronation and supination to 70 degrees each. Imaging demonstrated appropriate healing of the fracture with callus without displacement or malalignment (, ). Another long arm cast was placed for an additional month, at which time the fractures were completely clinically healed, so a removable splint was placed. With the cast off, the ultrasound stimulator could be placed directly over the fracture sites, one at a time.\\nOn his final follow-up visit, the patient was 3 months out from his injury. He had been continuing to use the bone stimulator and reported no pain. On examination, he had 90 degrees of pronation and supination; wrist extension was 60 degrees and wrist flexion was 80 degrees, all of which were similar to the opposite side. Imaging demonstrated healed radius and ulna fractures with no malalignment (, ). Given these findings, the patient was told to return to baseline activity with the exception of a custom forearm shell splint for skiing and to return to the clinic as needed.\nOUTPUT:" }, { "from": "agent", "value": "Both Bone Forearm Fractures" } ]
As a physician 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, Caucasian, right hand dominant male, otherwise healthy, was seen in the emergency department after a skateboard accident. He reported falling onto his dorsal left proximal forearm and experienced immediate pain in the area without other injuries. Physical examination was notable for tenderness over the proximal radius and ulna and limited pronosupination secondary to pain. Plain radiographs demonstrated non-displaced but slightly comminuted, short oblique fractures of the proximal third of the radius and ulna (, ). After discussion with the patient and his family, the decision was made to place the patient in a long arm cast (, ) and follow-up in the clinic in 1 week.\nOn follow-up, the patient had satisfactory pain control, and the cast was appropriately in position. A hole was cut into the cast so that an ultrasound bone stimulator could be used to promote healing. The stimulator was positioned equidistant between the two fractures. The patient reported some mild increase in fracture site pain in the 1st week with the bone stimulator, but this abated after a few days. The next follow-up visit was 3 weeks later (4 weeks post-injury), and the patient reported significantly improved pain. The cast was removed, and his examination was significant for restoration of pronation and supination to 70 degrees each. Imaging demonstrated appropriate healing of the fracture with callus without displacement or malalignment (, ). Another long arm cast was placed for an additional month, at which time the fractures were completely clinically healed, so a removable splint was placed. With the cast off, the ultrasound stimulator could be placed directly over the fracture sites, one at a time.\nOn his final follow-up visit, the patient was 3 months out from his injury. He had been continuing to use the bone stimulator and reported no pain. On examination, he had 90 degrees of pronation and supination; wrist extension was 60 degrees and wrist flexion was 80 degrees, all of which were similar to the opposite side. Imaging demonstrated healed radius and ulna fractures with no malalignment (, ). Given these findings, the patient was told to return to baseline activity with the exception of a custom forearm shell splint for skiing and to return to the clinic as needed. OUTPUT:
PMCPatients_common2406
[ { "from": "human", "value": "As a physician engaged 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\\narrival she was hypotensive, drowsy and irritable, and had a\\nGCS of 8/15. The right lower limb was externally rotated and\\nthere was a deformity of the right leg. Attempted movement\\naround the hips was painful. She was resuscitated and\\nintubated endotracheally at the Accident and Emergency\\ndepartment. Both lower limbs required splinting. The patient was admitted to\\nthe pediatric intensive care unit and was jointly managed by the general surgeon, neurosurgeon and the orthopedic team.\\nAbove knee skin traction were applied for both lower limb.\\nForty hours later, she underwent open reduction and fixation\\nof both femoral neck fractures, with two 4.0 mm partially\\nthreaded cancellous screws avoiding the femoral growth\\nplates. Physiotherapy was started for\\nmobilization of the joints and this was followed by axillary\\ncrutch gait training.\nOUTPUT:" }, { "from": "agent", "value": "Bilateral Traumatic Fracture of Neck of Femur, head injury, closed comminuted fracture of the proximal right tibia, fracture of the right pubic ramus, 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: On\narrival she was hypotensive, drowsy and irritable, and had a\nGCS of 8/15. The right lower limb was externally rotated and\nthere was a deformity of the right leg. Attempted movement\naround the hips was painful. She was resuscitated and\nintubated endotracheally at the Accident and Emergency\ndepartment. Both lower limbs required splinting. The patient was admitted to\nthe pediatric intensive care unit and was jointly managed by the general surgeon, neurosurgeon and the orthopedic team.\nAbove knee skin traction were applied for both lower limb.\nForty hours later, she underwent open reduction and fixation\nof both femoral neck fractures, with two 4.0 mm partially\nthreaded cancellous screws avoiding the femoral growth\nplates. Physiotherapy was started for\nmobilization of the joints and this was followed by axillary\ncrutch gait training. OUTPUT:
PMCPatients_common2172
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 20-year-old male presented in August 2016 with distal left thigh pain of a few months duration. A left lower extremity MRI revealed distal femoral metadiaphysis mass with surrounding periosteal reaction. A staging CT of his chest showed a 3 mm right upper lobe lung nodule. He underwent three cycles of neoadjuvant cisplatin (25 mg/m2, one to three days) and doxorubicin (25 mg/m2, one to three days). Two weeks after his first cycle, he developed a left pneumothorax, which recurred two weeks later. In December 2016, he underwent radical resection of the left distal femur with left total knee arthroplasty and distal femur replacement. The resected tumor showed 50% necrosis. Therefore, the decision was made to pursue three additional cycles of ifosfamide/doxorubicin alternating with ifosfamide/cisplatin. The cumulative doses of ifosfamide, cisplatin and doxorubicin were 27 g/m2, 80 mg/m2 and 150 mg/m2, respectively. Being hemodynamically stable, he was initially given his planned chemotherapy cycle of ifosfamide/cisplatin followed by chest imaging. A CT of his chest showed three bilateral subpleural cystic lesions which were not demonstrated on prior imaging. He underwent bilateral video-assisted thoracoscopy with lung nodule resection and pleurodesis.\nOUTPUT:" }, { "from": "agent", "value": "Osteoblastic osteosarcoma, Pneumothoraces, Hemothoraces" } ]
As a physician 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 20-year-old male presented in August 2016 with distal left thigh pain of a few months duration. A left lower extremity MRI revealed distal femoral metadiaphysis mass with surrounding periosteal reaction. A staging CT of his chest showed a 3 mm right upper lobe lung nodule. He underwent three cycles of neoadjuvant cisplatin (25 mg/m2, one to three days) and doxorubicin (25 mg/m2, one to three days). Two weeks after his first cycle, he developed a left pneumothorax, which recurred two weeks later. In December 2016, he underwent radical resection of the left distal femur with left total knee arthroplasty and distal femur replacement. The resected tumor showed 50% necrosis. Therefore, the decision was made to pursue three additional cycles of ifosfamide/doxorubicin alternating with ifosfamide/cisplatin. The cumulative doses of ifosfamide, cisplatin and doxorubicin were 27 g/m2, 80 mg/m2 and 150 mg/m2, respectively. Being hemodynamically stable, he was initially given his planned chemotherapy cycle of ifosfamide/cisplatin followed by chest imaging. A CT of his chest showed three bilateral subpleural cystic lesions which were not demonstrated on prior imaging. He underwent bilateral video-assisted thoracoscopy with lung nodule resection and pleurodesis. OUTPUT:
PMCPatients_common3794
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 7-year-old girl presented with progressive head enlargement since birth, features of raised intracranial pressure in the form of headache, vomiting, excessive crying and excessive drowsiness. Her visual acuity was reduced due to secondary optic atrophy. She had no history of any seizures since birth. All supratentorial ventricles were dilated and the mass was causing compression over adjoining midbrain (). A ventriculo-peritoneal shunt was placed for the drainage of excessively forming CSF 2 days prior to the surgery. A right temporal craniotomy was performed and the temporal horn was opened through mid temporal sulcus and the mass was reached. The tumor had its vascular supply from the anterior choroidal artery.\\nIntraoperative squash smear and tissue for frozen section were sent. Cellular cytosmears showing papillary structure with fibrovascular core lined by cuboidal cells having bland nuclei, scanty cytoplasm, present in hemorrhagic background. Flakes of calcification were also present.\\nComplete removal of the tumor mass was done after securing the vascular supply. There was no element of obstruction. The frozen section and histopathological findings of the excised tumor mass (Microsections showed fibrovascular fronds lined by cuboidal to low columnar cells with extreme area of calcification and focal areas of chondroid and osseous metaplasia in the stroma. No mitosis or necrosis was seen.) were diagnostic of CPP (WHO grade I) (). The immunohistochemistry study showed positivity for cytokeratin (CK7) () and S-100 (). The patient had an uneventful postoperative period. During the postoperative follow-up after 4 months, the patient was completely symptom free and her visual acuity had improved considerably.\nOUTPUT:" }, { "from": "agent", "value": "Choroid Plexus Papilloma, Bilateral Hypersecretory Hydrocephalus" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 7-year-old girl presented with progressive head enlargement since birth, features of raised intracranial pressure in the form of headache, vomiting, excessive crying and excessive drowsiness. Her visual acuity was reduced due to secondary optic atrophy. She had no history of any seizures since birth. All supratentorial ventricles were dilated and the mass was causing compression over adjoining midbrain (). A ventriculo-peritoneal shunt was placed for the drainage of excessively forming CSF 2 days prior to the surgery. A right temporal craniotomy was performed and the temporal horn was opened through mid temporal sulcus and the mass was reached. The tumor had its vascular supply from the anterior choroidal artery.\nIntraoperative squash smear and tissue for frozen section were sent. Cellular cytosmears showing papillary structure with fibrovascular core lined by cuboidal cells having bland nuclei, scanty cytoplasm, present in hemorrhagic background. Flakes of calcification were also present.\nComplete removal of the tumor mass was done after securing the vascular supply. There was no element of obstruction. The frozen section and histopathological findings of the excised tumor mass (Microsections showed fibrovascular fronds lined by cuboidal to low columnar cells with extreme area of calcification and focal areas of chondroid and osseous metaplasia in the stroma. No mitosis or necrosis was seen.) were diagnostic of CPP (WHO grade I) (). The immunohistochemistry study showed positivity for cytokeratin (CK7) () and S-100 (). The patient had an uneventful postoperative period. During the postoperative follow-up after 4 months, the patient was completely symptom free and her visual acuity had improved considerably. OUTPUT:
PMCPatients_common62
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 76-year-old female with past medical history of well-controlled hypertension, coronary artery disease presented with subacute progressive shortness of breath for two weeks. On presentation, blood pressure (BP) was 238/146 mm Hg, heart rate (HR) of 75 beats per minute (bpm), SaO2 (oxygen saturation) to 80% and was placed on 4 L nasal cannula (NC) with improvement in her oxygenation. Physical exam was remarkable for pulsus paradoxus, distant heart sounds without murmurs or gallops, marked jugular venous distension, diminished breath sounds at the bases and mild bilateral lower extremity pitting edema. She underwent pericardiocentesis with the removal of 1200 cc bloody fluid. There was a significant improvement in right-sided pressures following pericardial drainage, with a mean right atrial pressure of 10 mm Hg down from 21 mm Hg. Systemic blood pressure normalized after pericardiocentesis. Follow-up echocardiogram showed resolution of the pericardial effusion. Further workup was done to identify the etiology of the pericardial effusion, including fluid cytology, culture, lactate dehydrogenase (LDH), serum antinuclear antibodies (ANA), serum complement, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), anti-double-stranded DNA (dsDNA), and anti-Smith antibody. Analysis of the pericardial fluid showed exudative fluid and it was negative for malignant cells.\nOUTPUT:" }, { "from": "agent", "value": "Hypertensive Crisis, Cardiac Tamponade" } ]
As a physician 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 76-year-old female with past medical history of well-controlled hypertension, coronary artery disease presented with subacute progressive shortness of breath for two weeks. On presentation, blood pressure (BP) was 238/146 mm Hg, heart rate (HR) of 75 beats per minute (bpm), SaO2 (oxygen saturation) to 80% and was placed on 4 L nasal cannula (NC) with improvement in her oxygenation. Physical exam was remarkable for pulsus paradoxus, distant heart sounds without murmurs or gallops, marked jugular venous distension, diminished breath sounds at the bases and mild bilateral lower extremity pitting edema. She underwent pericardiocentesis with the removal of 1200 cc bloody fluid. There was a significant improvement in right-sided pressures following pericardial drainage, with a mean right atrial pressure of 10 mm Hg down from 21 mm Hg. Systemic blood pressure normalized after pericardiocentesis. Follow-up echocardiogram showed resolution of the pericardial effusion. Further workup was done to identify the etiology of the pericardial effusion, including fluid cytology, culture, lactate dehydrogenase (LDH), serum antinuclear antibodies (ANA), serum complement, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), anti-double-stranded DNA (dsDNA), and anti-Smith antibody. Analysis of the pericardial fluid showed exudative fluid and it was negative for malignant cells. OUTPUT:
PMCPatients_common628
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The patient was a 41-year-old Asian man, who suffered from diarrhea and skin itch 4 years ago and was diagnosed with HES. He received pharmacotherapy of methylprednisolone. The initial dosage was 40 mg per day and was gradually reduced to 28 mg per day. During the course of immunosuppression therapy, the patient received CMV-DNA test with a result of < 2000 copies/ml. This patient was transferred to our hospital due to an acute onset of abdominal pain for 3 h. He denied a history of parasite infection. Stool-rt was performed and ova weren’t found. There was no history of drug or food allergies or any other significant medical history. The physical examination found skin rashes over the entire body and typical signs of peritonitis. Laboratory examinations showed increased CRP levels of 102 mg/L. The complete blood cell count revealed a white blood cell count of 27.93*109/L with a differential of 60.0% eosinophils. The total level of IgE was greater than 2000 IU/ml. Abdominal contrast enhanced CT revealed that the descending colon wall was swollen and free air existed (Fig. a). The patient underwent an emergency operation of left hemicolectomy immediately. Swollen bowel wall, multiple deep ulcers and mucosal erosions were found in specimens (Fig. b). Pathological diagnosis revealed massive virus inclusion bodies (Fig. c) and infiltration of eosinophils, but without any evidence of thrombus, vasculitis or occlusion. Immunohistochemical staining confirmed CMV infection (Fig. d). CMV-DNA test was performed again postoperatively and the copy number of CMV in blood was 8.02*104/ml. The patient received Ganciclovir (5 mg/kg, twice daily for 21 days) therapy, and dexamethasone (5 mg per day) was also taken to control the symptoms of HES. Finally, the patient was discharged from our hospital 25 days after the operation. The CMV-PCR test results were lower than 2000 copies per milliliter, and the percentage of eosinophils decreased to the normal range.\nOUTPUT:" }, { "from": "agent", "value": "Colon perforation due to cytomegalovirus infection, Idiopathic hypereosinophilic syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The patient was a 41-year-old Asian man, who suffered from diarrhea and skin itch 4 years ago and was diagnosed with HES. He received pharmacotherapy of methylprednisolone. The initial dosage was 40 mg per day and was gradually reduced to 28 mg per day. During the course of immunosuppression therapy, the patient received CMV-DNA test with a result of < 2000 copies/ml. This patient was transferred to our hospital due to an acute onset of abdominal pain for 3 h. He denied a history of parasite infection. Stool-rt was performed and ova weren’t found. There was no history of drug or food allergies or any other significant medical history. The physical examination found skin rashes over the entire body and typical signs of peritonitis. Laboratory examinations showed increased CRP levels of 102 mg/L. The complete blood cell count revealed a white blood cell count of 27.93*109/L with a differential of 60.0% eosinophils. The total level of IgE was greater than 2000 IU/ml. Abdominal contrast enhanced CT revealed that the descending colon wall was swollen and free air existed (Fig. a). The patient underwent an emergency operation of left hemicolectomy immediately. Swollen bowel wall, multiple deep ulcers and mucosal erosions were found in specimens (Fig. b). Pathological diagnosis revealed massive virus inclusion bodies (Fig. c) and infiltration of eosinophils, but without any evidence of thrombus, vasculitis or occlusion. Immunohistochemical staining confirmed CMV infection (Fig. d). CMV-DNA test was performed again postoperatively and the copy number of CMV in blood was 8.02*104/ml. The patient received Ganciclovir (5 mg/kg, twice daily for 21 days) therapy, and dexamethasone (5 mg per day) was also taken to control the symptoms of HES. Finally, the patient was discharged from our hospital 25 days after the operation. The CMV-PCR test results were lower than 2000 copies per milliliter, and the percentage of eosinophils decreased to the normal range. OUTPUT:
PMCPatients_common1666
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 52-year-old Caucasian male presented to our hospital with complaints of ankle pain. He had a serpentine rash over his ankle which had been progressively worsening for the last several weeks with now, diffuse pruritus across his abdomen and chest, which he had been scratching for the aforementioned time period. He denied any insect bites or recent travel outside of the state of Florida but confessed to working outside - barefoot in an area where feral cats frequently defecate. The patient did not report any past medical history but did admit to a prior social history including both prior tobacco (30 pack year) and intravenous drug abuse (cocaine and amphetamine). The patient otherwise denied any active recreational drug use or alcohol intake. Upon arrival at the hospital, the patient's vital signs were temperature of 36.9°C, blood pressure of 121/70 mm Hg, pulse of 83 beats per minute, and oxygen saturation of 99% on room air. Multiple areas of serpentine tracks with erythema were noted on physical examination (Figures -).\\nCirculating eosinophils in peripheral laboratory studies were elevated at 2.1 x103/uL (24%) with a noted immunoglobulin E (IgE) of 1773 (normal <100). Human immunodeficiency virus (HIV) and stool parasites were negative. The patient fortunately continued to not have any respiratory complaints with oxygen saturations remaining stable on room air. He was ultimately discharged home with a course of oral doxycycline due to concerns of superimposed cellulitis with instructions to followup with an outpatient facility for routine surveillance of his serum eosinophilia and pulmonary infiltrates.\nOUTPUT:" }, { "from": "agent", "value": "Cutaneous Larva Migrans, Asymptomatic Löeffler’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: A 52-year-old Caucasian male presented to our hospital with complaints of ankle pain. He had a serpentine rash over his ankle which had been progressively worsening for the last several weeks with now, diffuse pruritus across his abdomen and chest, which he had been scratching for the aforementioned time period. He denied any insect bites or recent travel outside of the state of Florida but confessed to working outside - barefoot in an area where feral cats frequently defecate. The patient did not report any past medical history but did admit to a prior social history including both prior tobacco (30 pack year) and intravenous drug abuse (cocaine and amphetamine). The patient otherwise denied any active recreational drug use or alcohol intake. Upon arrival at the hospital, the patient's vital signs were temperature of 36.9°C, blood pressure of 121/70 mm Hg, pulse of 83 beats per minute, and oxygen saturation of 99% on room air. Multiple areas of serpentine tracks with erythema were noted on physical examination (Figures -).\nCirculating eosinophils in peripheral laboratory studies were elevated at 2.1 x103/uL (24%) with a noted immunoglobulin E (IgE) of 1773 (normal <100). Human immunodeficiency virus (HIV) and stool parasites were negative. The patient fortunately continued to not have any respiratory complaints with oxygen saturations remaining stable on room air. He was ultimately discharged home with a course of oral doxycycline due to concerns of superimposed cellulitis with instructions to followup with an outpatient facility for routine surveillance of his serum eosinophilia and pulmonary infiltrates. OUTPUT:
PMCPatients_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: Her right arm had a larger circumstance than her left arm, with circumferences of 7.7 cm and 6.5 cm at 5 cm above and below the elbow, respectively. In addition, Stemmer sign was observed, but peau d'orange change was not. A honeycomb pattern was observed in the right medial forearm and ventral side of the upper arm. The thickness of the skin and subcutaneous fat was increased on the right side (). The patient underwent ESWT with the same method as performed in case 1.\\nWhen comparing the CT scans () performed before and after treatment, the volume of the entire right upper extremity and the subcutaneous fat layers was reduced from 302,139.4 mm3 to 247,739.8 mm3 and from 187,719.4 mm3 to 147,184.6 mm3, respectively. The volume of the entire area and the subcutaneous fat layers at 5 cm above the elbow was reduced from 40,923.1 mm3 to 32,576.6 mm3 and from 26,096.8 mm3 to 19,882.9 mm3, respectively. The volume of the entire area and the subcutaneous fat layers at 5 cm below the elbow was reduced from 37,066.3 mm3 to 29,701.3 mm3 and from 21,505.2 mm3 to 14,500.9 mm3, respectively (). In addition, when the circumferences of both arms were compared, the difference was 5.0 cm and 4.8 cm at 5 cm above and below the elbow, respectively. These measurements were smaller than the initial measurements. However, the Stemmer sign observed in the right medial forearm persisted after treatment.\nOUTPUT:" }, { "from": "agent", "value": "Stage 3 Lymphedema" } ]
As a physician 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 right arm had a larger circumstance than her left arm, with circumferences of 7.7 cm and 6.5 cm at 5 cm above and below the elbow, respectively. In addition, Stemmer sign was observed, but peau d'orange change was not. A honeycomb pattern was observed in the right medial forearm and ventral side of the upper arm. The thickness of the skin and subcutaneous fat was increased on the right side (). The patient underwent ESWT with the same method as performed in case 1.\nWhen comparing the CT scans () performed before and after treatment, the volume of the entire right upper extremity and the subcutaneous fat layers was reduced from 302,139.4 mm3 to 247,739.8 mm3 and from 187,719.4 mm3 to 147,184.6 mm3, respectively. The volume of the entire area and the subcutaneous fat layers at 5 cm above the elbow was reduced from 40,923.1 mm3 to 32,576.6 mm3 and from 26,096.8 mm3 to 19,882.9 mm3, respectively. The volume of the entire area and the subcutaneous fat layers at 5 cm below the elbow was reduced from 37,066.3 mm3 to 29,701.3 mm3 and from 21,505.2 mm3 to 14,500.9 mm3, respectively (). In addition, when the circumferences of both arms were compared, the difference was 5.0 cm and 4.8 cm at 5 cm above and below the elbow, respectively. These measurements were smaller than the initial measurements. However, the Stemmer sign observed in the right medial forearm persisted after treatment. OUTPUT: