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PMCPatients_common3783
[ { "from": "human", "value": "As a physician engaged in 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 female presented to our department with matting of the hair for the past 2 days. Two weeks after receiving the first cycle of chemotherapy, patient noticed sudden onset of hair loss from the scalp, especially from the front and the sides. This was accompanied with hair entanglement which led to difficulty in combing hair. As the hair loss and difficulty in combing increased over the next 2 days, the anxious patient purchased and used a new shampoo. Following this, the hair got severely matted together. There was no associated itching, pain, or foul odor. Her regular hair cleansing agent for more than the past 10 years was fuller's earth (“multani mitti”) and there is no history of any kind of chemical treatment of hair such as dying or straightening.\\nOn examination of the scalp, there was diffuse nonscarring alopecia in the frontal and bilateral temporal areas along with a firm to hard mass of matted hair over the vertex and occiput and extending down for a length of 20 cm [Figures and ]. Separation of hair strands was not possible. There were no signs of inflammation or infestation. Rest of the dermatological and systemic examination including psychiatric assessment was normal. Dermoscopy of the matted hair revealed irregular arrangement of intertwining hair shafts resembling a bird's nest []. Intact follicular ostia were visible on dermoscopy of the temporal and frontal areas []. The potassium hydroxide preparation was negative for fungal elements.\\nHer routine investigations showed anemia (hemoglobin 8.8), normal total (4200) and differential leukocyte count, and decreased platelet count (88,000). Cutting of the matted hair was advised and counseling regarding chemotherapy-associated hair loss and proper hair care measure was done.\nOUTPUT:" }, { "from": "agent", "value": "Plica Polonica, Lung Adenocarcinoma, Anagen Effluvium" } ]
As a physician engaged 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 female presented to our department with matting of the hair for the past 2 days. Two weeks after receiving the first cycle of chemotherapy, patient noticed sudden onset of hair loss from the scalp, especially from the front and the sides. This was accompanied with hair entanglement which led to difficulty in combing hair. As the hair loss and difficulty in combing increased over the next 2 days, the anxious patient purchased and used a new shampoo. Following this, the hair got severely matted together. There was no associated itching, pain, or foul odor. Her regular hair cleansing agent for more than the past 10 years was fuller's earth (“multani mitti”) and there is no history of any kind of chemical treatment of hair such as dying or straightening.\nOn examination of the scalp, there was diffuse nonscarring alopecia in the frontal and bilateral temporal areas along with a firm to hard mass of matted hair over the vertex and occiput and extending down for a length of 20 cm [Figures and ]. Separation of hair strands was not possible. There were no signs of inflammation or infestation. Rest of the dermatological and systemic examination including psychiatric assessment was normal. Dermoscopy of the matted hair revealed irregular arrangement of intertwining hair shafts resembling a bird's nest []. Intact follicular ostia were visible on dermoscopy of the temporal and frontal areas []. The potassium hydroxide preparation was negative for fungal elements.\nHer routine investigations showed anemia (hemoglobin 8.8), normal total (4200) and differential leukocyte count, and decreased platelet count (88,000). Cutting of the matted hair was advised and counseling regarding chemotherapy-associated hair loss and proper hair care measure was done. OUTPUT:
PMCPatients_common2308
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A previously healthy 23-year-old man presented with ten days of sore throat, myalgias, and night sweats. On admission, the patient was febrile and tachycardic. Physical examination revealed posterior oropharyngeal erythema and shotty cervical lymphadenopathy. Chest radiograph revealed multiple patchy diffuse infiltrates (). Ultrasound of the neck showed nonocclusive thrombus of the left internal jugular vein extending into the proximal subclavian vein. Computed tomography (CT) of the chest confirmed the presence of patchy bilateral cavitary lung nodules and pleural effusions.\\nBlood cultures later were positive for Fusobacterium necrophorum and confirmed the diagnosis. The patient's respiratory status rapidly decompensated five days into the patient's hospital course despite supportive care and prompt initiation of antimicrobial therapy. Repeat chest radiograph demonstrated worsening bilateral pulmonary infiltrates and pleural effusions (). Radiographic evidence, PaO2/FiO2 ratio of 88 mmHg, and the timeline of decompensation were consistent with diagnosis of severe ARDS. The patient was intubated and remained on mechanical ventilation for eight days after a seven-day weaning period (). The highest positive end-expiratory pressure (PEEP) and FiO2 required to maintain oxygenation were 5 cmH2O and 40% respectively, and albuterol/ipratropium bromide was given throughout ventilation. In addition, the patient required chest tube drainage of bilateral empyemas. The patient was started on unfractioned heparin to treat the internal jugular vein thrombus. However, he later developed an acute anemia requiring premature discontinuation of anticoagulation.\\nThe patient's hospital course was further complicated by the development of pyomyositis of the right deltoid requiring surgical debridement and drainage. Abdominal imaging revealed a splenic infarct and transthoracic echocardiogram demonstrated a tricuspid valve vegetation consistent with endocarditis. The patient was discharged 23 days after admission and completed four weeks of outpatient treatment with metronidazole and aztreonam.\nOUTPUT:" }, { "from": "agent", "value": "Acute Respiratory Distress Syndrome, 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: A previously healthy 23-year-old man presented with ten days of sore throat, myalgias, and night sweats. On admission, the patient was febrile and tachycardic. Physical examination revealed posterior oropharyngeal erythema and shotty cervical lymphadenopathy. Chest radiograph revealed multiple patchy diffuse infiltrates (). Ultrasound of the neck showed nonocclusive thrombus of the left internal jugular vein extending into the proximal subclavian vein. Computed tomography (CT) of the chest confirmed the presence of patchy bilateral cavitary lung nodules and pleural effusions.\nBlood cultures later were positive for Fusobacterium necrophorum and confirmed the diagnosis. The patient's respiratory status rapidly decompensated five days into the patient's hospital course despite supportive care and prompt initiation of antimicrobial therapy. Repeat chest radiograph demonstrated worsening bilateral pulmonary infiltrates and pleural effusions (). Radiographic evidence, PaO2/FiO2 ratio of 88 mmHg, and the timeline of decompensation were consistent with diagnosis of severe ARDS. The patient was intubated and remained on mechanical ventilation for eight days after a seven-day weaning period (). The highest positive end-expiratory pressure (PEEP) and FiO2 required to maintain oxygenation were 5 cmH2O and 40% respectively, and albuterol/ipratropium bromide was given throughout ventilation. In addition, the patient required chest tube drainage of bilateral empyemas. The patient was started on unfractioned heparin to treat the internal jugular vein thrombus. However, he later developed an acute anemia requiring premature discontinuation of anticoagulation.\nThe patient's hospital course was further complicated by the development of pyomyositis of the right deltoid requiring surgical debridement and drainage. Abdominal imaging revealed a splenic infarct and transthoracic echocardiogram demonstrated a tricuspid valve vegetation consistent with endocarditis. The patient was discharged 23 days after admission and completed four weeks of outpatient treatment with metronidazole and aztreonam. OUTPUT:
PMCPatients_common2793
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: In February 2006, a 57-year-old man presented with vague right upper quadrant discomfort. He had no surgical history and was on antihypertensive (perindopril) and antidiabetic (metformin) medication. He had a history of acute myocardial infarction 5 years earlier and was suffering from hypertensive cardiomyopathy. He was subjected to abdominal ultrasound which revealed bilateral renal tumors, and cholelithiasis which was probably the cause of his right upper quadrant discomfort.\\nIn order to investigate the finding of bilateral renal tumors, a contrast CT scan was performed which showed two round hyperdense masses, one in each kidney, with homogeneous contrast uptake and well defined margins, arising from the renal cortex. The differential diagnosis included lymphoma, atypical cysts, metastases and RCC.\\nSubsequent magnetic resonance imaging (MRI) confirmed an enhancing, exophytic, well circumscribed solid tumor, arising from the middle of the right kidney (3.7cm). On the anterior surface of the left kidney, an enhancing, exophytic, well circumscribed solid tumor was described (Figures and ) and no abnormally enlarged retroperitoneal lymph nodes were detected. Bone scan with 99mTc-MDP did not show evidence of bone metastases.\\nIn April 2006, the patient was subjected to open partial nephrectomy on the left kidney, which revealed a 4 cm chromophobe renal cell carcinoma (Fuhrman II), with clear surgical margins.\\nIn May 2006, a second open partial nephrectomy was performed on the right kidney, revealing a 3.5 cm chromophobe renal cell carcinoma (Fuhrman II), with clear surgical margins. A surgical collagen sponge with fibrinogen and thrombin was used to aid in hemostasis in both kidneys.\\nThe patient did well postoperatively. Follow-up MRI at 14 months showed no evidence of recurrence (Figure ).\nOUTPUT:" }, { "from": "agent", "value": "Bilateral synchronous occurrence of three different histological types of renal tumor: chromophobe renal cell carcinoma, oncocytoma, angiomyolipoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: In February 2006, a 57-year-old man presented with vague right upper quadrant discomfort. He had no surgical history and was on antihypertensive (perindopril) and antidiabetic (metformin) medication. He had a history of acute myocardial infarction 5 years earlier and was suffering from hypertensive cardiomyopathy. He was subjected to abdominal ultrasound which revealed bilateral renal tumors, and cholelithiasis which was probably the cause of his right upper quadrant discomfort.\nIn order to investigate the finding of bilateral renal tumors, a contrast CT scan was performed which showed two round hyperdense masses, one in each kidney, with homogeneous contrast uptake and well defined margins, arising from the renal cortex. The differential diagnosis included lymphoma, atypical cysts, metastases and RCC.\nSubsequent magnetic resonance imaging (MRI) confirmed an enhancing, exophytic, well circumscribed solid tumor, arising from the middle of the right kidney (3.7cm). On the anterior surface of the left kidney, an enhancing, exophytic, well circumscribed solid tumor was described (Figures and ) and no abnormally enlarged retroperitoneal lymph nodes were detected. Bone scan with 99mTc-MDP did not show evidence of bone metastases.\nIn April 2006, the patient was subjected to open partial nephrectomy on the left kidney, which revealed a 4 cm chromophobe renal cell carcinoma (Fuhrman II), with clear surgical margins.\nIn May 2006, a second open partial nephrectomy was performed on the right kidney, revealing a 3.5 cm chromophobe renal cell carcinoma (Fuhrman II), with clear surgical margins. A surgical collagen sponge with fibrinogen and thrombin was used to aid in hemostasis in both kidneys.\nThe patient did well postoperatively. Follow-up MRI at 14 months showed no evidence of recurrence (Figure ). OUTPUT:
PMCPatients_common1515
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A right-handed 9-year-old boy fell on an outstretched hand two weeks before admitted to the hospital. The patient presented with a right wrist-drop and right elbow flexion stiffness. On the physical examination, the patient cannot extend his right wrist and thumb. The distal pulsation is solid and regular. The right elbow joint was stiff with a limited flexion-extension range of motion (60–90°). Radiographs showed a displaced SCF classified as Gartland type III. The parents first sought treatment from a traditional bonesetter before came to the hospital (, , ).\\nSurgical management is preferred for this case, and we decided to explore the nerve while simultaneously reduce and stabilize the fracture. The scar and fibrous tissue were carefully resected, leaving a 2 cm gap in the nerve. We approximate the nerve with end-to-end neurorrhaphy after the fracture was reduced and stabilized with 3-Kirschner wire. Postoperatively, the elbow was kept in long-arm cast with elbow flexed 90° to avoid nerve stretching for six weeks. The distal vascular status is good after the operation and cast application (, , , ).\\nAt the 4-month follow-up, the fracture was united. The elbow range of motion has improved; 20° to 115° elbow flexion is seen. The neurological status showed an improvement. The patient could extend his right thumb and wrist but developed a tingling sensation in the posterior forearm, extending to the dorsum of the hand and lateral three and a half fingers; the tingling was triggered by full extension of the elbow. At 1-year follow-up, the motor and sensory function fully recovered (, , ).\nOUTPUT:" }, { "from": "agent", "value": "Supracondylar humerus fracture, Radial nerve injury, Ulnar nerve injury" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A right-handed 9-year-old boy fell on an outstretched hand two weeks before admitted to the hospital. The patient presented with a right wrist-drop and right elbow flexion stiffness. On the physical examination, the patient cannot extend his right wrist and thumb. The distal pulsation is solid and regular. The right elbow joint was stiff with a limited flexion-extension range of motion (60–90°). Radiographs showed a displaced SCF classified as Gartland type III. The parents first sought treatment from a traditional bonesetter before came to the hospital (, , ).\nSurgical management is preferred for this case, and we decided to explore the nerve while simultaneously reduce and stabilize the fracture. The scar and fibrous tissue were carefully resected, leaving a 2 cm gap in the nerve. We approximate the nerve with end-to-end neurorrhaphy after the fracture was reduced and stabilized with 3-Kirschner wire. Postoperatively, the elbow was kept in long-arm cast with elbow flexed 90° to avoid nerve stretching for six weeks. The distal vascular status is good after the operation and cast application (, , , ).\nAt the 4-month follow-up, the fracture was united. The elbow range of motion has improved; 20° to 115° elbow flexion is seen. The neurological status showed an improvement. The patient could extend his right thumb and wrist but developed a tingling sensation in the posterior forearm, extending to the dorsum of the hand and lateral three and a half fingers; the tingling was triggered by full extension of the elbow. At 1-year follow-up, the motor and sensory function fully recovered (, , ). OUTPUT:
PMCPatients_common2810
[ { "from": "human", "value": "As a physician engaged in 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 Caucasian male presented with complaints of malaise, fatigue and 20 pound weight loss within one month. He also complained of anxiety, palpitation and tremor. He had a two month history of moderate pain and decreased range of motion in the left elbow. He was taking naproxen with no relief. He had no significant past medical history. Physical examination revealed an ill appearing male who was nonfebrile with a heart rate of 110 beats per minute. The thyroid gland was soft, non tender, not enlarged and without nodules. Heart auscultation revealed irregular rhythm but no murmurs. Left elbow was enlarged, warm and slightly tender with limited extension and flexion, but no clear evidence of effusion. The deep tendon reflexes of his extremities were hyperactive. Laboratory evaluation was significant for low TSH: <0.01 mcIU/ml (0.45-6.2), and high free T4: 3.27 ng/dl (0.54-1.24). The titers of thyroglobulin and thyroid peroxidase antibodies were increased: 999 IU/ml (<20), 41 IU/ml (<35) respectively. ESR was normal: 12 mm/hr (0-15). EKG demonstrated atrial fibrillation with rapid ventricular response. Left elbow x-ray showed degenerative spurring. Thyroid uptake scan (RAIU) showed a reduced twenty four hour uptake of 2.6% and little uptake throughout the thyroid gland (). Treatment with metoprolol was initiated. On the second visit three weeks later his heart rhythm was regular. He complained of morning stiffness and bilateral ankle pain. He had lost five additional pounds. His ankles were swollen, warm and tender with limited extension. He was started on methotrexate (MTX) and prednisone for newly diagnosed RA. Five months from initial presentation, laboratory evaluation revealed normal TSH: 1.79 and free T4:0.88. He remains in euthyroid state on subsequent follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Transient thyrotoxicosis, Rheumatoid arthritis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 41-year-old Caucasian male presented with complaints of malaise, fatigue and 20 pound weight loss within one month. He also complained of anxiety, palpitation and tremor. He had a two month history of moderate pain and decreased range of motion in the left elbow. He was taking naproxen with no relief. He had no significant past medical history. Physical examination revealed an ill appearing male who was nonfebrile with a heart rate of 110 beats per minute. The thyroid gland was soft, non tender, not enlarged and without nodules. Heart auscultation revealed irregular rhythm but no murmurs. Left elbow was enlarged, warm and slightly tender with limited extension and flexion, but no clear evidence of effusion. The deep tendon reflexes of his extremities were hyperactive. Laboratory evaluation was significant for low TSH: <0.01 mcIU/ml (0.45-6.2), and high free T4: 3.27 ng/dl (0.54-1.24). The titers of thyroglobulin and thyroid peroxidase antibodies were increased: 999 IU/ml (<20), 41 IU/ml (<35) respectively. ESR was normal: 12 mm/hr (0-15). EKG demonstrated atrial fibrillation with rapid ventricular response. Left elbow x-ray showed degenerative spurring. Thyroid uptake scan (RAIU) showed a reduced twenty four hour uptake of 2.6% and little uptake throughout the thyroid gland (). Treatment with metoprolol was initiated. On the second visit three weeks later his heart rhythm was regular. He complained of morning stiffness and bilateral ankle pain. He had lost five additional pounds. His ankles were swollen, warm and tender with limited extension. He was started on methotrexate (MTX) and prednisone for newly diagnosed RA. Five months from initial presentation, laboratory evaluation revealed normal TSH: 1.79 and free T4:0.88. He remains in euthyroid state on subsequent follow-up. OUTPUT:
PMCPatients_common4587
[ { "from": "human", "value": "As a physician engaged in 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 man, non-hypertensive and non-diabetic, presented with chest pain and dyspnea at rest for the last one week prior to admission. His hemodynamic status was stable. Blood pressure was 126/80 mmHg. Clinically, there were no signs of overt heart failure and DVT. ECG showed sinus rhythm with T-wave inversion in V1-4. Lab investigation showed D-dimer 5 µg/mL. CTPA showed extensive thrombi in both left and right PAs (, Pre-procedure, Case 2) and dilatation of RV. Percutaneous catheter-based intervention was performed via right femoral vein access with 8Fr vascular sheath. GC 6Fr MPA-2 was advanced to main PA and showed PA pressure of 121/50 mmHg. Initial diagnostic runs were performed using a 6Fr pigtail catheter in the main PA with the help of injector, contrast volume 30 mL/s, in anteroposterior projections and left anterior oblique projections, which demonstrated large thrombi in both left and right PAs ( and ). GC MPA-1/8Fr and JR 3.5/8Fr were used for thrombus fragmentation and aspiration in left () and right PAs (), respectively.\\nFollowing aspiration, a significant amount of thrombus material was collected and patient's PA pressure significantly reduced to 66/10 mmHg. Subsequently, a bolus of 250,000 units of Streptokinase was given in each right and left PAs over 10 min, and then followed by a maintenance dose of 100,000 units per hour for the next 10 h through pigtail catheter kept in main PA. Repeat CTPA was performed 48 h after the procedure that still showed thrombus in both PAs but much less compared with pre procedure (, post-procedure 48 h, Case 2). Hospital stay was uneventful and the patient was successfully discharged with dual antiplatelet therapy for eight weeks. Follow up CTPA at three months showed complete resolution of thrombus in both PAs (). There was also T-wave resolution in precordial leads in ECG at 3 months ().\nOUTPUT:" }, { "from": "agent", "value": "Pulmonary thromboembolism" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 37-year-old man, non-hypertensive and non-diabetic, presented with chest pain and dyspnea at rest for the last one week prior to admission. His hemodynamic status was stable. Blood pressure was 126/80 mmHg. Clinically, there were no signs of overt heart failure and DVT. ECG showed sinus rhythm with T-wave inversion in V1-4. Lab investigation showed D-dimer 5 µg/mL. CTPA showed extensive thrombi in both left and right PAs (, Pre-procedure, Case 2) and dilatation of RV. Percutaneous catheter-based intervention was performed via right femoral vein access with 8Fr vascular sheath. GC 6Fr MPA-2 was advanced to main PA and showed PA pressure of 121/50 mmHg. Initial diagnostic runs were performed using a 6Fr pigtail catheter in the main PA with the help of injector, contrast volume 30 mL/s, in anteroposterior projections and left anterior oblique projections, which demonstrated large thrombi in both left and right PAs ( and ). GC MPA-1/8Fr and JR 3.5/8Fr were used for thrombus fragmentation and aspiration in left () and right PAs (), respectively.\nFollowing aspiration, a significant amount of thrombus material was collected and patient's PA pressure significantly reduced to 66/10 mmHg. Subsequently, a bolus of 250,000 units of Streptokinase was given in each right and left PAs over 10 min, and then followed by a maintenance dose of 100,000 units per hour for the next 10 h through pigtail catheter kept in main PA. Repeat CTPA was performed 48 h after the procedure that still showed thrombus in both PAs but much less compared with pre procedure (, post-procedure 48 h, Case 2). Hospital stay was uneventful and the patient was successfully discharged with dual antiplatelet therapy for eight weeks. Follow up CTPA at three months showed complete resolution of thrombus in both PAs (). There was also T-wave resolution in precordial leads in ECG at 3 months (). OUTPUT:
PMCPatients_common2509
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 79-year-old woman presented to another hospital for evaluation of abdominal pain after a meal. She was taking a proton pump inhibitor by oral administration. She was a housewife and had no family history. On physical examination, she was 141 cm tall, weighed 55 kg, and had a body mass index (BMI) of 27.7 kg/m2. Her abdomen was soft and slightly distended. The patient also had grade M reflux esophagitis according to the Los Angeles classification. Esophagography showed retention of contrast material in the intramediastinal stomach. However, no obstruction was present. ), a stone within the gall bladder (Fig. ). Colonoscopy revealed no diverticulosis. The postoperative course was uneventful, and the patient was discharged 13 days after the operation. She was still in good health 5 months after the operation.\nOUTPUT:" }, { "from": "agent", "value": "Umbilical hernia, Cholelithiasis, Hiatal 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 79-year-old woman presented to another hospital for evaluation of abdominal pain after a meal. She was taking a proton pump inhibitor by oral administration. She was a housewife and had no family history. On physical examination, she was 141 cm tall, weighed 55 kg, and had a body mass index (BMI) of 27.7 kg/m2. Her abdomen was soft and slightly distended. The patient also had grade M reflux esophagitis according to the Los Angeles classification. Esophagography showed retention of contrast material in the intramediastinal stomach. However, no obstruction was present. ), a stone within the gall bladder (Fig. ). Colonoscopy revealed no diverticulosis. The postoperative course was uneventful, and the patient was discharged 13 days after the operation. She was still in good health 5 months after the operation. OUTPUT:
PMCPatients_common3796
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 16-year-old female was admitted in the internal medicine ward with severe and sudden onset pain of the right femoropubic region radiating down to the knee. Her pain began 3 days prior to admission and was exacerbated with movement or light touch. At the onset of pain the affected region was cold and cyanotic. There was oedema of the entire right lower limb. The patient was afebrile, and her left lower limb demonstrated no pathology. The patient reported a preceding soft tissue injury of the right lower limb ten days prior to admission.\\nPreceding the rheumatology consultation, the patient was assessed by internists, neurosurgeons, orthopaedic surgeons, neurologists, vascular surgeons, and psychiatrists. Collectively, they ordered a number of investigations including an MRI of the lumbar spine, MRI and MRA of the thighs and pelvis, radiographs of the affected joints, MRI of the brain, CT of the brain, ultrasound Doppler of lower limb, electromyography, and electroencephalography. None of the above clinical assessments and investigations revealed any pathology indicative of a diagnosis.\\nRheumatological assessment revealed severe hyperalgesia in the right lower limb in conjunction with cyanosis and reduced temperature. The left lower limb was well perfused and warm. There were no findings suggestive of arthritis. Upon further questioning, the patient reported having had a similar event two years prior to the current complaint. All investigations and clinical assessments from the previous episode revealed no pathology either and were treated with physiotherapy alone.\\nA Tc-99m-MDP bone scintigraphy scan was requested by her rheumatologist. The first and second phases of the scan revealed mildly reduced uptake in the right lower limb as compared to the left. The third phase of the scan revealed increased uptake in the area of the right ankle, indicative of increased bone metabolism. Patient refused further drug therapy. Intensive physiotherapy was initiated with improvement of her symptoms after 2 months. The patient was followed-up monthly for 6 months and the current plan is to review biannually.\nOUTPUT:" }, { "from": "agent", "value": "Complex Regional Pain 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 16-year-old female was admitted in the internal medicine ward with severe and sudden onset pain of the right femoropubic region radiating down to the knee. Her pain began 3 days prior to admission and was exacerbated with movement or light touch. At the onset of pain the affected region was cold and cyanotic. There was oedema of the entire right lower limb. The patient was afebrile, and her left lower limb demonstrated no pathology. The patient reported a preceding soft tissue injury of the right lower limb ten days prior to admission.\nPreceding the rheumatology consultation, the patient was assessed by internists, neurosurgeons, orthopaedic surgeons, neurologists, vascular surgeons, and psychiatrists. Collectively, they ordered a number of investigations including an MRI of the lumbar spine, MRI and MRA of the thighs and pelvis, radiographs of the affected joints, MRI of the brain, CT of the brain, ultrasound Doppler of lower limb, electromyography, and electroencephalography. None of the above clinical assessments and investigations revealed any pathology indicative of a diagnosis.\nRheumatological assessment revealed severe hyperalgesia in the right lower limb in conjunction with cyanosis and reduced temperature. The left lower limb was well perfused and warm. There were no findings suggestive of arthritis. Upon further questioning, the patient reported having had a similar event two years prior to the current complaint. All investigations and clinical assessments from the previous episode revealed no pathology either and were treated with physiotherapy alone.\nA Tc-99m-MDP bone scintigraphy scan was requested by her rheumatologist. The first and second phases of the scan revealed mildly reduced uptake in the right lower limb as compared to the left. The third phase of the scan revealed increased uptake in the area of the right ankle, indicative of increased bone metabolism. Patient refused further drug therapy. Intensive physiotherapy was initiated with improvement of her symptoms after 2 months. The patient was followed-up monthly for 6 months and the current plan is to review biannually. OUTPUT:
PMCPatients_common2557
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: We report the case of a 58-year-old female patient with a history of acute pancreatitis with conservative treatment 2 years ago, chronic alcohol consumption with affirmative abandoning in the last 12 months, and an admission for a left pleural effusion one month ago, with resolution under antibiotic treatment. Due to the persistent abdominal pain, the patient underwent an abdominal ultrasound and CT scan which showed biliary lithiasis and the presence of 3 distinct large cystic masses in the pancreas and spleen (Figures and ). Surgery was proposed but the patient refused it.\\nThe patient was subsequently admitted for intense abdominal pain with altered general status (blood pressure 90/60, pulse 110) and a drop of the hemoglobin level to 8.2 g/dL. At 2-year follow-up the patient presents with no abdominal complaints and no recurrence.\nOUTPUT:" }, { "from": "agent", "value": "Pancreatic Pseudocyst, Splenic Artery Erosion, Retroperitoneal Hematoma, Splenic 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: We report the case of a 58-year-old female patient with a history of acute pancreatitis with conservative treatment 2 years ago, chronic alcohol consumption with affirmative abandoning in the last 12 months, and an admission for a left pleural effusion one month ago, with resolution under antibiotic treatment. Due to the persistent abdominal pain, the patient underwent an abdominal ultrasound and CT scan which showed biliary lithiasis and the presence of 3 distinct large cystic masses in the pancreas and spleen (Figures and ). Surgery was proposed but the patient refused it.\nThe patient was subsequently admitted for intense abdominal pain with altered general status (blood pressure 90/60, pulse 110) and a drop of the hemoglobin level to 8.2 g/dL. At 2-year follow-up the patient presents with no abdominal complaints and no recurrence. OUTPUT:
PMCPatients_common2875
[ { "from": "human", "value": "As a physician engaged in 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 man with nausea and vomiting of two days duration was found to be hypotensive and in acute hypoxic respiratory failure requiring mechanical ventilation. Hypotension persisted in spite of aggressive initial fluid resuscitation. The electrolytes, renal function, white blood count and hemoglobin were all within normal limits. The Chest x-ray revealed normal heart size with pulmonary congestion. The EKG revealed a heart rate of 96/min with normal axis and rhythm and without ischemic changes. Patient remained hypotensive in spite of initiation of dopamine infusion. A bed side echocardiography revealed a left ventricular ejection fraction (LVEF) of 30% with global hypokinesia. The isovolumetric contraction time and isovolumetric relaxation time were prolonged with increased myocardial performance index (MPI) of (0.56) indicating that there was both systolic and diastolic dysfunction. An echocardiogram done six month ago showed a normal LVEF and normal MPI.\\nHypotension persisted in spite of high dose dopamine infusion. Intravenous thyroxin at a dose of 0.050 mg was administered and the dose increased to 0.075 mg in the next 48 hours resulting in stabilization of the blood pressure and weaning off the dopamine and subsequently weaned off ventilator during the next 72 hours. A repeat echocardiography done in one month revealed normal LV function with LVEF of 60% with normal MPI of 0.35.\nOUTPUT:" }, { "from": "agent", "value": "Cardiogenic shock, Hypothyroid myopathy" } ]
As a physician engaged 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 man with nausea and vomiting of two days duration was found to be hypotensive and in acute hypoxic respiratory failure requiring mechanical ventilation. Hypotension persisted in spite of aggressive initial fluid resuscitation. The electrolytes, renal function, white blood count and hemoglobin were all within normal limits. The Chest x-ray revealed normal heart size with pulmonary congestion. The EKG revealed a heart rate of 96/min with normal axis and rhythm and without ischemic changes. Patient remained hypotensive in spite of initiation of dopamine infusion. A bed side echocardiography revealed a left ventricular ejection fraction (LVEF) of 30% with global hypokinesia. The isovolumetric contraction time and isovolumetric relaxation time were prolonged with increased myocardial performance index (MPI) of (0.56) indicating that there was both systolic and diastolic dysfunction. An echocardiogram done six month ago showed a normal LVEF and normal MPI.\nHypotension persisted in spite of high dose dopamine infusion. Intravenous thyroxin at a dose of 0.050 mg was administered and the dose increased to 0.075 mg in the next 48 hours resulting in stabilization of the blood pressure and weaning off the dopamine and subsequently weaned off ventilator during the next 72 hours. A repeat echocardiography done in one month revealed normal LV function with LVEF of 60% with normal MPI of 0.35. OUTPUT:
PMCPatients_common2643
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 21-year-old male patient was admitted to our center with acute headache and loss of consciousness in 2009. Intraventricular haematoma was confirmed by computed tomography (CT) scan (Fig. A-a, b). The patient recovered consciousness after ventricular drainage and the removal of intraventricular haematoma (Fig. A-c–f). One week after the haemorrhage, the patient was diagnosed with digital subtraction angiography (DSA) for the causes of haemorrhage, but no positive results were obtained (Fig. A-a). DSA was repeated 1 month later with a micro-catheter to obtain super-selective angiograpy of micro cerebral arteries, including posterior choroidal arteries. However, no cerebrovascular disease was identified (Fig. A-b; Additional file ). The patient was discharged 1 month after his haemorrhage without any measurable neurological deficit.\\nIn 2015, the patient was hospitalized in our center again for haemorrhage in splenium corporis callosi (Fig. B). He had headache, lost consciousness, and experienced plegia and aphasia. DSA was performed 3 days after haemorrhage. No sign of abnormal cerebral angioarchitecture was observed (Fig. A-c). A micro AVM with two non-compact niduses in different parts of the brain was identified. One of the niduses was supplied by an arteriole of the left callosomarginal artery and the other by a branch of the left anterior choroidal artery. These two micro niduses were drained via the same veinlet, one of the thalamic veins, to the great cerebral vein (Fig. B-a, b). The feeding arteries of these two niduses were embolised with 0.5 ml Onyx (Covidien, Irvine, CA, USA; Fig. B-c). In the end, the patient was discharged without any neurological deficit.\nOUTPUT:" }, { "from": "agent", "value": "Dormant micro arteriovenous malformations, Recurrent cerebral haemorrhage" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 21-year-old male patient was admitted to our center with acute headache and loss of consciousness in 2009. Intraventricular haematoma was confirmed by computed tomography (CT) scan (Fig. A-a, b). The patient recovered consciousness after ventricular drainage and the removal of intraventricular haematoma (Fig. A-c–f). One week after the haemorrhage, the patient was diagnosed with digital subtraction angiography (DSA) for the causes of haemorrhage, but no positive results were obtained (Fig. A-a). DSA was repeated 1 month later with a micro-catheter to obtain super-selective angiograpy of micro cerebral arteries, including posterior choroidal arteries. However, no cerebrovascular disease was identified (Fig. A-b; Additional file ). The patient was discharged 1 month after his haemorrhage without any measurable neurological deficit.\nIn 2015, the patient was hospitalized in our center again for haemorrhage in splenium corporis callosi (Fig. B). He had headache, lost consciousness, and experienced plegia and aphasia. DSA was performed 3 days after haemorrhage. No sign of abnormal cerebral angioarchitecture was observed (Fig. A-c). A micro AVM with two non-compact niduses in different parts of the brain was identified. One of the niduses was supplied by an arteriole of the left callosomarginal artery and the other by a branch of the left anterior choroidal artery. These two micro niduses were drained via the same veinlet, one of the thalamic veins, to the great cerebral vein (Fig. B-a, b). The feeding arteries of these two niduses were embolised with 0.5 ml Onyx (Covidien, Irvine, CA, USA; Fig. B-c). In the end, the patient was discharged without any neurological deficit. OUTPUT:
PMCPatients_common2256
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 28-year-old woman gave birth to a healthy male infant following a normal, uneventful vaginal delivery (gravida 10, para 8). The patient was admitted to the emergency department six days postpartum with the acute onset, two hours prior, of substernal chest pain radiating to the left arm and interscapular region. The patient had no coronary risk factors such as hypertension, diabetes, or dyslipidemia, had no family history of heart disease, and did not have a history of oral contraceptive use. She did not smoke and did not use alcohol or drugs.\\nOn physical examination, her blood pressure was 110/65 mmHg and her heart rate 89 beats/min, temperature of 37.2°C, and oxygen saturation of 94%. Auscultation of heart and lung fields was normal. Physical examination revealed no signs of heart failure. Chest X-ray was normal. Electrocardiography demonstrated the presence of ST-segment elevation in leads I, aVL (both 1 mm) and V1–V5 (all 3 mm), along with reciprocal ST segment depression in leads II, III, and aVF (all 2 mm). There was a 80% stenosis of the true lumen of the mid-LAD caused by external compression by the hematoma in the false lumen. The patient underwent percutaneous transluminal coronary angioplasty with bare-metal stent (3.0 × 18 mm) placed in the LAD (). We continued with low-molecular-weight heparin, clopidogrel, ramipril, metoprolol, and aspirin. The patient was discharged with good hemodynamic balance on the fourth day after admittance. One month after the control examination, the patient had no chest pain at all. Follow-up echocardiography revealed normal left ventricular function.\nOUTPUT:" }, { "from": "agent", "value": "Spontaneous Coronary Artery Dissection" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 28-year-old woman gave birth to a healthy male infant following a normal, uneventful vaginal delivery (gravida 10, para 8). The patient was admitted to the emergency department six days postpartum with the acute onset, two hours prior, of substernal chest pain radiating to the left arm and interscapular region. The patient had no coronary risk factors such as hypertension, diabetes, or dyslipidemia, had no family history of heart disease, and did not have a history of oral contraceptive use. She did not smoke and did not use alcohol or drugs.\nOn physical examination, her blood pressure was 110/65 mmHg and her heart rate 89 beats/min, temperature of 37.2°C, and oxygen saturation of 94%. Auscultation of heart and lung fields was normal. Physical examination revealed no signs of heart failure. Chest X-ray was normal. Electrocardiography demonstrated the presence of ST-segment elevation in leads I, aVL (both 1 mm) and V1–V5 (all 3 mm), along with reciprocal ST segment depression in leads II, III, and aVF (all 2 mm). There was a 80% stenosis of the true lumen of the mid-LAD caused by external compression by the hematoma in the false lumen. The patient underwent percutaneous transluminal coronary angioplasty with bare-metal stent (3.0 × 18 mm) placed in the LAD (). We continued with low-molecular-weight heparin, clopidogrel, ramipril, metoprolol, and aspirin. The patient was discharged with good hemodynamic balance on the fourth day after admittance. One month after the control examination, the patient had no chest pain at all. Follow-up echocardiography revealed normal left ventricular function. OUTPUT:
PMCPatients_common3150
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Five years earlier, he began treatment with entecavir. In the past 9 mo, he experienced unexplained weight loss (approximately 10 kg).\\nHis physical examination did not reveal any abnormalities, except for liver palmar and spider nevus.\\nPlasma tumor marker levels, including alpha-fetoprotein (AFP), and liver function appeared normal.\\nAbdominal ultrasound revealed a solid tumor, which was considered to be an HCC (38 mm × 35 mm), occupying the segments 4/8 of the liver. Abdominal dynamic contrast-enhanced magnetic resonance imaging (MRI) revealed a lesion in the segments 4/5/8 (45 mm × 41 mm) of the liver, with multiple satellite nodules. The lesions invaded the middle hepatic vein (Figure ). No extrahepatic metastasis was observed on positron emission tomography-computed tomography (PET-CT).\\nThe patient had a history of smoking for over 20 years.\\nFollowing a preoperative examination, the patient underwent resection of the liver segments 4/5/8. Postoperative pathological results revealed an SHC with satellite nodules, neurologic invasion, and no definite intravascular thrombus formation (Figure ). The patient recovered well after surgery.\nOUTPUT:" }, { "from": "agent", "value": "Sarcomatoid hepatocellular carcinoma, Hepatitis B cirrhosis, Portal hypertension, Type 2 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: Five years earlier, he began treatment with entecavir. In the past 9 mo, he experienced unexplained weight loss (approximately 10 kg).\nHis physical examination did not reveal any abnormalities, except for liver palmar and spider nevus.\nPlasma tumor marker levels, including alpha-fetoprotein (AFP), and liver function appeared normal.\nAbdominal ultrasound revealed a solid tumor, which was considered to be an HCC (38 mm × 35 mm), occupying the segments 4/8 of the liver. Abdominal dynamic contrast-enhanced magnetic resonance imaging (MRI) revealed a lesion in the segments 4/5/8 (45 mm × 41 mm) of the liver, with multiple satellite nodules. The lesions invaded the middle hepatic vein (Figure ). No extrahepatic metastasis was observed on positron emission tomography-computed tomography (PET-CT).\nThe patient had a history of smoking for over 20 years.\nFollowing a preoperative examination, the patient underwent resection of the liver segments 4/5/8. Postoperative pathological results revealed an SHC with satellite nodules, neurologic invasion, and no definite intravascular thrombus formation (Figure ). The patient recovered well after surgery. OUTPUT:
PMCPatients_common4212
[ { "from": "human", "value": "As a physician engaged in 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 man visited our hospital with abdominal pain and vomiting. He had type 2 diabetes mellitus and no history of surgery. His physical examination revealed a body temperature of 36.3°C, blood pressure of 126/90 mmHg and pulse rate of 90 bpm. He showed slight tenderness to palpation in the lower right abdomen. His laboratory findings were unremarkable. Plain X-ray imaging of the abdomen revealed dilated loops of the small intestine. Enhanced computed tomography showed the evidence of an intestinal obstruction in the pelvic area, with dilatation of the small intestine at the proximal side []. A 5-cm stone was detected in the small intestine, and pneumobilia was observed in the gallbladder. The site of obstruction was identified by locating the terminal ileum and tracing it proximally. The patient had no post-operative complications and was discharged after 7 days. Examination of the right upper abdomen revealed adhesions in the second portion of the duodenum to a chronically inflamed gallbladder. Finally, laparoscopic cholecystectomy was performed. The post-operative course was uneventful, and the patient was discharged on the 6th post-operative day.\nOUTPUT:" }, { "from": "agent", "value": "Gallstone ileus, Cholecystoduodenal fistula" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 65-year-old man visited our hospital with abdominal pain and vomiting. He had type 2 diabetes mellitus and no history of surgery. His physical examination revealed a body temperature of 36.3°C, blood pressure of 126/90 mmHg and pulse rate of 90 bpm. He showed slight tenderness to palpation in the lower right abdomen. His laboratory findings were unremarkable. Plain X-ray imaging of the abdomen revealed dilated loops of the small intestine. Enhanced computed tomography showed the evidence of an intestinal obstruction in the pelvic area, with dilatation of the small intestine at the proximal side []. A 5-cm stone was detected in the small intestine, and pneumobilia was observed in the gallbladder. The site of obstruction was identified by locating the terminal ileum and tracing it proximally. The patient had no post-operative complications and was discharged after 7 days. Examination of the right upper abdomen revealed adhesions in the second portion of the duodenum to a chronically inflamed gallbladder. Finally, laparoscopic cholecystectomy was performed. The post-operative course was uneventful, and the patient was discharged on the 6th post-operative day. OUTPUT:
PMCPatients_common3970
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A previously healthy 35-year-old man visited our hospital with a 1-month history of short-term memory difficulties and disorientation. The patient had a history of alcohol abuse for one year and tobacco abuse for ten years. A general physical examination identified whitish patches and a fissured ulcer on the left lateral side of the patient's tongue. A punch biopsy was performed. In addition, a Mini-Mental State Examination score was 26/30 due to deficits in orientation, calculation and recall. A neurological examination revealed otherwise unremarkable findings. A lumbar puncture performed on the first day revealed 48 WBCs·mm-3 (92% lymphocytes) and elevated protein levels (88 mg·dL-1). Gram stain, KOH mount, India ink method and AFB stain did not reveal any organisms.\\nHowever, a brain MRI performed upon admission showed high signal changes in the bilateral mesial temporal lobes including both hippocampi and amygdalae on a spin echo (T2) and fluid-attenuated inversion recovery (FLAIR) sequences (). Diffusion weighted image (DWI) sequences revealed no definite abnormalities. In addition, no enhancement, evidence of areas of petechial hemorrhages or mass effect was noted. The patient was suspected of having herpes encephalitis, and was thus placed on acyclovir empirically. However, the cerebrospinal fluid (CSF) results of IgG, IgM and polymerase chain reaction (PCR) for herpes simplex virus were all negative. The CSF bacterial, fungal and AFB cultures revealed no growth. Subsequently, the results of the quantitative serum venereal disease research laboratory (VDRL) were 16.3 RU and found to be reactive. Further CSF analyses yielded repeated positive results for the CSF VDRL test (titer, 1:8) and the fluorescent treponemal antibody absorption (FTA-ABS) test. On the 7th day after admission, the result of the punch biopsy on the tongue was diagnosed as a syphilitic chancre, a characteristic skin lesion of primary syphilis. One month after the discharge, the patient returned for a follow-up evaluation and was found to have improved cognitive function.\nOUTPUT:" }, { "from": "agent", "value": "Neurosyphilis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A previously healthy 35-year-old man visited our hospital with a 1-month history of short-term memory difficulties and disorientation. The patient had a history of alcohol abuse for one year and tobacco abuse for ten years. A general physical examination identified whitish patches and a fissured ulcer on the left lateral side of the patient's tongue. A punch biopsy was performed. In addition, a Mini-Mental State Examination score was 26/30 due to deficits in orientation, calculation and recall. A neurological examination revealed otherwise unremarkable findings. A lumbar puncture performed on the first day revealed 48 WBCs·mm-3 (92% lymphocytes) and elevated protein levels (88 mg·dL-1). Gram stain, KOH mount, India ink method and AFB stain did not reveal any organisms.\nHowever, a brain MRI performed upon admission showed high signal changes in the bilateral mesial temporal lobes including both hippocampi and amygdalae on a spin echo (T2) and fluid-attenuated inversion recovery (FLAIR) sequences (). Diffusion weighted image (DWI) sequences revealed no definite abnormalities. In addition, no enhancement, evidence of areas of petechial hemorrhages or mass effect was noted. The patient was suspected of having herpes encephalitis, and was thus placed on acyclovir empirically. However, the cerebrospinal fluid (CSF) results of IgG, IgM and polymerase chain reaction (PCR) for herpes simplex virus were all negative. The CSF bacterial, fungal and AFB cultures revealed no growth. Subsequently, the results of the quantitative serum venereal disease research laboratory (VDRL) were 16.3 RU and found to be reactive. Further CSF analyses yielded repeated positive results for the CSF VDRL test (titer, 1:8) and the fluorescent treponemal antibody absorption (FTA-ABS) test. On the 7th day after admission, the result of the punch biopsy on the tongue was diagnosed as a syphilitic chancre, a characteristic skin lesion of primary syphilis. One month after the discharge, the patient returned for a follow-up evaluation and was found to have improved cognitive function. OUTPUT:
PMCPatients_common5084
[ { "from": "human", "value": "As a physician engaged in 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 male child, who was a product of nonconsanguineous marriage, presented in our pediatric emergency with generalized tonic colonic seizures. History revealed that he had a first episode of right-sided focal convulsion at the age of 9 months, and since then, he had been on an anticonvulsant therapy. Developmental history suggested delayed milestones. Physical examination revealed that there was extensive port-wine staining over both sides of his face, extending to both lower eyelids and cheeks, with an area of bluish gray pigmentation of the episclera [Figures –]. The nevus flammeus descended on to the neck, chest and both the legs (from thighs to soles). His right lower limb showed a relative hypertrophy []. There was a difference of 2 cm in length (right:left 39:37 cm) and 4.5 cm in circumference of both lower limbs (right:left 29.5:25 cm). Dilated superficial veins were noted over medial aspect of the foot as well as lateral aspect of the lower limb on the right side.\\nThe hematologic, biochemical, and urinary laboratory tests were normal. Abdominal ultrasonography revealed no abnormality. Doppler USG of vessels of the lower extremities showed narrowing with less blood flow on right-sided venous system compared to the left. Ophthalmoscopy showed glaucomatous cupping of the disc with tortuous retinal blood vessels, more on the left side compared to right. On cranial computed tomography (CT) scan, there was atrophy in both the hemispheres along with gyral calcification on the left side. Ground glass appearance of skull bones with mild cortical thickening was also noted []. Contrast magnetic resonance imaging (MRI) revealed evidence of leptomeningeal angiomatosis in the left fronto-parieto-temporal region and enlarged ipsilateral choroid plexus []. MRI angiography of cerebral vessels did not demonstrate any arteriovenous communications. Electroencephalography (EEG) showed multiple epileptiform foci on both sides and voltage suppression on the left hemisphere. The patient was diagnosed to have SWS in association with KTS, according to the results of physical examination and neuroimaging.\nOUTPUT:" }, { "from": "agent", "value": "Sturge–Weber Syndrome, Klippel–Trenaunay Syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 3-year-old male child, who was a product of nonconsanguineous marriage, presented in our pediatric emergency with generalized tonic colonic seizures. History revealed that he had a first episode of right-sided focal convulsion at the age of 9 months, and since then, he had been on an anticonvulsant therapy. Developmental history suggested delayed milestones. Physical examination revealed that there was extensive port-wine staining over both sides of his face, extending to both lower eyelids and cheeks, with an area of bluish gray pigmentation of the episclera [Figures –]. The nevus flammeus descended on to the neck, chest and both the legs (from thighs to soles). His right lower limb showed a relative hypertrophy []. There was a difference of 2 cm in length (right:left 39:37 cm) and 4.5 cm in circumference of both lower limbs (right:left 29.5:25 cm). Dilated superficial veins were noted over medial aspect of the foot as well as lateral aspect of the lower limb on the right side.\nThe hematologic, biochemical, and urinary laboratory tests were normal. Abdominal ultrasonography revealed no abnormality. Doppler USG of vessels of the lower extremities showed narrowing with less blood flow on right-sided venous system compared to the left. Ophthalmoscopy showed glaucomatous cupping of the disc with tortuous retinal blood vessels, more on the left side compared to right. On cranial computed tomography (CT) scan, there was atrophy in both the hemispheres along with gyral calcification on the left side. Ground glass appearance of skull bones with mild cortical thickening was also noted []. Contrast magnetic resonance imaging (MRI) revealed evidence of leptomeningeal angiomatosis in the left fronto-parieto-temporal region and enlarged ipsilateral choroid plexus []. MRI angiography of cerebral vessels did not demonstrate any arteriovenous communications. Electroencephalography (EEG) showed multiple epileptiform foci on both sides and voltage suppression on the left hemisphere. The patient was diagnosed to have SWS in association with KTS, according to the results of physical examination and neuroimaging. OUTPUT:
PMCPatients_common3891
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 68-year-old female was referred to our breast clinic by her primary care physician after undergoing screening mammography. Upon mammography, a breast mass was visualized in the left upper quadrant, measuring 13 mm × 8 mm. Patient was planned for wide local excision and axillary clearance under general anaesthesia. Patient was discussed postoperatively in the multidisciplinary breast cancer meeting and adjuvant Tamoxifen and breast radiotherapy were instituted (16 fractions in a total dose of 42.56 Gy).\\nOne month after surgery patient presented to our breast clinic with a fever and swelling and redness of the skin in the left axilla. Antibiotic treatment was instituted for one week and she remained free of symptoms for a couple of months.\\nOne year after surgery and radiotherapy, our patient was seen in the breast clinic for follow up. Mammography was unremarkable. ). Her arm and shoulder function were impaired. The dead space was closed with a latissimus dorsi skin and muscle flap. Low suction drains were left in place. The drains were removed on the second day post-surgery.\\nSix weeks after surgery patient was evaluated in the outpatient clinic. Movement of her shoulder had improved greatly and abduction of the right arm was now possible up to 160° (Fig. ).\nOUTPUT:" }, { "from": "agent", "value": "Hormone positive ductal breast carcinoma, Lymph node metastasis, Infected seroma, Fibrotic seroma pocket, Radiation dermatitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 68-year-old female was referred to our breast clinic by her primary care physician after undergoing screening mammography. Upon mammography, a breast mass was visualized in the left upper quadrant, measuring 13 mm × 8 mm. Patient was planned for wide local excision and axillary clearance under general anaesthesia. Patient was discussed postoperatively in the multidisciplinary breast cancer meeting and adjuvant Tamoxifen and breast radiotherapy were instituted (16 fractions in a total dose of 42.56 Gy).\nOne month after surgery patient presented to our breast clinic with a fever and swelling and redness of the skin in the left axilla. Antibiotic treatment was instituted for one week and she remained free of symptoms for a couple of months.\nOne year after surgery and radiotherapy, our patient was seen in the breast clinic for follow up. Mammography was unremarkable. ). Her arm and shoulder function were impaired. The dead space was closed with a latissimus dorsi skin and muscle flap. Low suction drains were left in place. The drains were removed on the second day post-surgery.\nSix weeks after surgery patient was evaluated in the outpatient clinic. Movement of her shoulder had improved greatly and abduction of the right arm was now possible up to 160° (Fig. ). OUTPUT:
PMCPatients_common3672
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 58-year old female was referred for evaluation due to persistent exophytic tumor of external genitalia shaped like cauliflower with propagation to legs and behind persisting for more than 10 years (). Examination of the vulvar skin revealed a 15 x 20 cm fleshy, vascular mass. Vaginal mucosa and cervix appeared normal. PAP smear of cervix and vulva revealed no abnormality. Vulvar smear was screened to detect HPV DNA.\\nWe used polymerase chain reaction (PCR). HPV types of high risk and low risk groups were detected. Colposcopy did not detect any HPV lesion. Proctoscopy was refused. Inguinal lymph nodes were enlarged both sides and fine needle aspiration cytology was done, but cytologic examination identified no malignant cells. Routine laboratory tests, including a complete blood count, blood chemistry, urinalysis, immunological, and serological investigations like The Venereal Disease Research Laboratory (VDRL) and Human Immunodeficiency Virus (HIV), hepatitis A, B and C were negative. Electrophoresis of serum proteins and immunoelectrophoresis revealed no abnormality. Tumor markers were normal. Chest X-ray investigation, electrocardiography, abdominal and pelvic ultrasound and computed tomography (CT), as well as cystoscopy were unremarkable. After we detected a wide base of condylomas predominantly in vulvar region, we performed multiple biopsies to detect potential malignancy.\\nHowever, malignancy was not confirmed histologically. The diagnosis of large benign condyloma acuminatum was made (). The patient was initially treated by the loop electrosurgical excision procedure (LEEP) and podophilin solution on the rest of the condyloma (). Later, we performed a wide surgical excision of the rest of the condylomas. Condyloma acuminatum, WSCC and ISCC were confirmed histologically (Figs. , ). Radical vulvectomy and inguinal lymphadenctomy was performed. The patient was advised to remain under close follow- up. Reccurence of condylomas was confirmed several times during follow –up (Fig. 6). A ll were removed surgically and confirmed pathohistologically.\nOUTPUT:" }, { "from": "agent", "value": "Condylomata Acuminata, Warty Squamous Cell Carcinoma, 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 58-year old female was referred for evaluation due to persistent exophytic tumor of external genitalia shaped like cauliflower with propagation to legs and behind persisting for more than 10 years (). Examination of the vulvar skin revealed a 15 x 20 cm fleshy, vascular mass. Vaginal mucosa and cervix appeared normal. PAP smear of cervix and vulva revealed no abnormality. Vulvar smear was screened to detect HPV DNA.\nWe used polymerase chain reaction (PCR). HPV types of high risk and low risk groups were detected. Colposcopy did not detect any HPV lesion. Proctoscopy was refused. Inguinal lymph nodes were enlarged both sides and fine needle aspiration cytology was done, but cytologic examination identified no malignant cells. Routine laboratory tests, including a complete blood count, blood chemistry, urinalysis, immunological, and serological investigations like The Venereal Disease Research Laboratory (VDRL) and Human Immunodeficiency Virus (HIV), hepatitis A, B and C were negative. Electrophoresis of serum proteins and immunoelectrophoresis revealed no abnormality. Tumor markers were normal. Chest X-ray investigation, electrocardiography, abdominal and pelvic ultrasound and computed tomography (CT), as well as cystoscopy were unremarkable. After we detected a wide base of condylomas predominantly in vulvar region, we performed multiple biopsies to detect potential malignancy.\nHowever, malignancy was not confirmed histologically. The diagnosis of large benign condyloma acuminatum was made (). The patient was initially treated by the loop electrosurgical excision procedure (LEEP) and podophilin solution on the rest of the condyloma (). Later, we performed a wide surgical excision of the rest of the condylomas. Condyloma acuminatum, WSCC and ISCC were confirmed histologically (Figs. , ). Radical vulvectomy and inguinal lymphadenctomy was performed. The patient was advised to remain under close follow- up. Reccurence of condylomas was confirmed several times during follow –up (Fig. 6). A ll were removed surgically and confirmed pathohistologically. OUTPUT:
PMCPatients_common5329
[ { "from": "human", "value": "As a physician engaged 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 last intake of rivaroxaban was 21 h before symptom onset.\\nOn admission, blood pressure was 114/76 mm Hg and the NIHSS score equaled 9. Blood tests showed an increased partial thromboplastin time (41.9 s; normal 23-36), a normal thrombin time (18.9 s; normal 14-21) and a slightly elevated international normalized ratio (INR: 1.41; normal 0.85-1.18). Rivaroxaban plasma concentration was below the detection limit, and anti-factor Xa activity (COATEST®; Chromogenix, Lexington, Mass., USA) was absent. Platelet count was normal, whereas renal function was impaired (creatinine 132 μmol/l, normal <103; creatinine clearance according to the Cockcroft-Gault formula 28.2 ml/min). Cranial CT and CT-angiography revealed no early signs of cerebral ischemia or ICH, and the large brain vessels were patent. Shortly afterwards, the neurological status rapidly improved. On a follow-up blood examination, partial thromboplastin time (52.5 s) and INR (1.33) continued to be slightly elevated, while renal function was still impaired (creatinine clearance 27.8 ml/min). ICH could be ruled out by a follow-up cranial CT. Ultrasound examination of the cerebral vasculature was normal, as was echocardiography. Twenty-four hours after thrombolysis, creatinine clearance had increased above 30.0 ml/min, and treatment with dabigatran 110 mg twice daily was initiated. The NIHSS score at discharge was 1.\nOUTPUT:" }, { "from": "agent", "value": "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: The last intake of rivaroxaban was 21 h before symptom onset.\nOn admission, blood pressure was 114/76 mm Hg and the NIHSS score equaled 9. Blood tests showed an increased partial thromboplastin time (41.9 s; normal 23-36), a normal thrombin time (18.9 s; normal 14-21) and a slightly elevated international normalized ratio (INR: 1.41; normal 0.85-1.18). Rivaroxaban plasma concentration was below the detection limit, and anti-factor Xa activity (COATEST®; Chromogenix, Lexington, Mass., USA) was absent. Platelet count was normal, whereas renal function was impaired (creatinine 132 μmol/l, normal <103; creatinine clearance according to the Cockcroft-Gault formula 28.2 ml/min). Cranial CT and CT-angiography revealed no early signs of cerebral ischemia or ICH, and the large brain vessels were patent. Shortly afterwards, the neurological status rapidly improved. On a follow-up blood examination, partial thromboplastin time (52.5 s) and INR (1.33) continued to be slightly elevated, while renal function was still impaired (creatinine clearance 27.8 ml/min). ICH could be ruled out by a follow-up cranial CT. Ultrasound examination of the cerebral vasculature was normal, as was echocardiography. Twenty-four hours after thrombolysis, creatinine clearance had increased above 30.0 ml/min, and treatment with dabigatran 110 mg twice daily was initiated. The NIHSS score at discharge was 1. OUTPUT:
PMCPatients_common252
[ { "from": "human", "value": "As a physician engaged in 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 male with known history of hypertension and hypothyroidism presented to the emergency department (ED) with sudden, painless loss of vision in his left eye of two hours duration. The patient reported that he had sneezed four times in rapid succession and then stated he lost vision in his left eye, but experienced no eye pain. The patient then drove himself to the ED. He denied any other accompanying symptoms on extensive review of systems. Examination revealed 20/30 vision in his right eye with corrective lenses (eyeglasses), but no light perception in his left. The left pupil did not have any direct light response but had preserved consensual response. Consensual light response was absent in the right pupil, but direct response was preserved. Point-of-care ocular ultrasound was performed but did not reveal any apparent abnormality. The patient had no other focal neurological deficits and was found to be in normal sinus rhythm on electrocardiogram. Tonometry was not available at this facility nor were ophthalmologic services. A head computed tomography (CT) without contrast showed no acute hemorrhage or apparent infarct and he was sent emergently to the ophthalmology clinic at the tertiary care hospital several miles away in consultation with the receiving ophthalmologist.\\nIn the ophthalmology clinic, the patient was confirmed to have multiple arterial thrombi with characteristic cherry-red spot on exam consistent with CRAO. He was then transferred directly from the ophthalmology clinic to the hyperbaric chamber for hyperbaric oxygen therapy. Upon the initial dive at 33 feet of therapy he began seeing letters and his vision continued to improve after one hour at 60 feet. Vision in the affected eye improved from solely light perception to 20/50 at 24 hours, with subsequent resolution of symptoms.\nOUTPUT:" }, { "from": "agent", "value": "Central Retinal Artery Occlusion, Carotid Artery Occlusion" } ]
As a physician engaged 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 male with known history of hypertension and hypothyroidism presented to the emergency department (ED) with sudden, painless loss of vision in his left eye of two hours duration. The patient reported that he had sneezed four times in rapid succession and then stated he lost vision in his left eye, but experienced no eye pain. The patient then drove himself to the ED. He denied any other accompanying symptoms on extensive review of systems. Examination revealed 20/30 vision in his right eye with corrective lenses (eyeglasses), but no light perception in his left. The left pupil did not have any direct light response but had preserved consensual response. Consensual light response was absent in the right pupil, but direct response was preserved. Point-of-care ocular ultrasound was performed but did not reveal any apparent abnormality. The patient had no other focal neurological deficits and was found to be in normal sinus rhythm on electrocardiogram. Tonometry was not available at this facility nor were ophthalmologic services. A head computed tomography (CT) without contrast showed no acute hemorrhage or apparent infarct and he was sent emergently to the ophthalmology clinic at the tertiary care hospital several miles away in consultation with the receiving ophthalmologist.\nIn the ophthalmology clinic, the patient was confirmed to have multiple arterial thrombi with characteristic cherry-red spot on exam consistent with CRAO. He was then transferred directly from the ophthalmology clinic to the hyperbaric chamber for hyperbaric oxygen therapy. Upon the initial dive at 33 feet of therapy he began seeing letters and his vision continued to improve after one hour at 60 feet. Vision in the affected eye improved from solely light perception to 20/50 at 24 hours, with subsequent resolution of symptoms. OUTPUT:
PMCPatients_common2483
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: We report a 28-year-old Caucasian male who was in his usual state of excellent health until 2 months before presentation. He presented with progressive weakness, flu-like symptoms, and recurrent fevers. He had an enlarged and painless lymph node in the posterior part of his left neck. Core needle biopsy revealed that the lymph node was benign. Home medications included ibuprofen and acetaminophen as needed for fever. Review of systems was positive for hip pain bilaterally and negative for cough, diarrhea, weight loss, and night sweats. He denied any recent travel or exposure to animals. Vital signs were within normal limits except for temperature of 100.3°F. His exam was unremarkable except for a left cervical scar from the aforementioned lymph node biopsy and malar rash that started 4 days before presentation. His laboratory workup showed pancytopenia with neutropenia, abnormal liver function tests, hypertriglyceridemia, fibrinogen level of 126 mg/dL, and a ferritin level of more than 40,000 ng/mL. Bone marrow (BM) biopsy showed hemophagocytosis. Infectious workup was negative. A tentative diagnosis of HLH was made based on clinical presentation and the laboratory data, which satisfied the HLH-2008 diagnostic criteria []. The patient was transferred to a regional quaternary medical center and treated with an HLH protocol using etoposide and dexamethasone. Later, it was determined that his HLH was actually secondary to a primary diagnosis of SLE after a workup of his malar rash. The diagnosis of SLE was made with clinical/laboratory findings of malar rash, arthritis, pancytopenia, positive antinuclear antibody (ANA) test, positive antidouble stranded DNA (dsDNA) test, and low complement levels (C3, C4, and CH50). The patient was treated for SLE with an immunosuppressive regimen of cyclosporine and dexamethasone, and he improved dramatically.\nOUTPUT:" }, { "from": "agent", "value": "Systemic Lupus Erythematosus, Hemophagocytic Lymphohistiocytosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: We report a 28-year-old Caucasian male who was in his usual state of excellent health until 2 months before presentation. He presented with progressive weakness, flu-like symptoms, and recurrent fevers. He had an enlarged and painless lymph node in the posterior part of his left neck. Core needle biopsy revealed that the lymph node was benign. Home medications included ibuprofen and acetaminophen as needed for fever. Review of systems was positive for hip pain bilaterally and negative for cough, diarrhea, weight loss, and night sweats. He denied any recent travel or exposure to animals. Vital signs were within normal limits except for temperature of 100.3°F. His exam was unremarkable except for a left cervical scar from the aforementioned lymph node biopsy and malar rash that started 4 days before presentation. His laboratory workup showed pancytopenia with neutropenia, abnormal liver function tests, hypertriglyceridemia, fibrinogen level of 126 mg/dL, and a ferritin level of more than 40,000 ng/mL. Bone marrow (BM) biopsy showed hemophagocytosis. Infectious workup was negative. A tentative diagnosis of HLH was made based on clinical presentation and the laboratory data, which satisfied the HLH-2008 diagnostic criteria []. The patient was transferred to a regional quaternary medical center and treated with an HLH protocol using etoposide and dexamethasone. Later, it was determined that his HLH was actually secondary to a primary diagnosis of SLE after a workup of his malar rash. The diagnosis of SLE was made with clinical/laboratory findings of malar rash, arthritis, pancytopenia, positive antinuclear antibody (ANA) test, positive antidouble stranded DNA (dsDNA) test, and low complement levels (C3, C4, and CH50). The patient was treated for SLE with an immunosuppressive regimen of cyclosporine and dexamethasone, and he improved dramatically. OUTPUT:
PMCPatients_common5106
[ { "from": "human", "value": "As a physician engaged in 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 male patient presented with a severe form of HCM involving both the ventricles. At Mayo Clinic, he underwent extended septal wall myomectomy that involved surgical excision of tissue from both right and left ventricles. The result was a dramatic improvement in symptoms.\\nMaintenance drug is Tenormin (50 mg in the morning and 25 mg at night). The family has been against the placement of an implantable cardioverter-defibrillator (ICD), and at 22 years of age, additional testing was performed to help with risk stratification. The Holter revealed ventricular ectopy but no runs of ventricular tachycardia. His stress test confirmed the presence of an abnormal fall in BP with exercise. There was a 2–3/6 systolic ejection murmur present at the base with radiation to the back, head and neck.\\nThe electrocardiogram showed voltage criteria for biventricular hypertrophy.\\nThe echocardiogram confirmed the presence of a significant dilatation of inferior-anterior portion of the right ventricle. There was mid-cavity obliteration in systole in the right ventricle. There was no significant left ventricular outflow tract (LVOT) obstruction. The sites of the previous myectomy were well visualized. There was minor mitral and tricuspid valve insufficiency.\nOUTPUT:" }, { "from": "agent", "value": "Hypertrophic Cardiomyopathy, RV 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 22-year-old male patient presented with a severe form of HCM involving both the ventricles. At Mayo Clinic, he underwent extended septal wall myomectomy that involved surgical excision of tissue from both right and left ventricles. The result was a dramatic improvement in symptoms.\nMaintenance drug is Tenormin (50 mg in the morning and 25 mg at night). The family has been against the placement of an implantable cardioverter-defibrillator (ICD), and at 22 years of age, additional testing was performed to help with risk stratification. The Holter revealed ventricular ectopy but no runs of ventricular tachycardia. His stress test confirmed the presence of an abnormal fall in BP with exercise. There was a 2–3/6 systolic ejection murmur present at the base with radiation to the back, head and neck.\nThe electrocardiogram showed voltage criteria for biventricular hypertrophy.\nThe echocardiogram confirmed the presence of a significant dilatation of inferior-anterior portion of the right ventricle. There was mid-cavity obliteration in systole in the right ventricle. There was no significant left ventricular outflow tract (LVOT) obstruction. The sites of the previous myectomy were well visualized. There was minor mitral and tricuspid valve insufficiency. OUTPUT:
PMCPatients_common128
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: In February 2018, the best corrected visual acuity (BCVA) of her right eye had decreased from 0.4 to 0.2, and the optical coherence tomography (OCT) revealed recurrence of macular exudation (Fig. ). The patient was treated with an IVI of aflibercept. At the 72 h post-IVI control visit, the patient was symptomless. The BCVA of her right eye had improved to 0.3 and no macular fluid was present. However, the LFP flare had increased from 8.6 ph/ms pre-injection to 664 ph/ms. Clinical examination revealed discreet conjunctival hyperemia, clear cornea, 3+ cells in the anterior chamber, and no hypopyon. On fundoscopy, the vitreous was slightly cloudy. After 2 h, before vitrectomy was performed, the BCVA was counting fingers, biomicroscopy showed a fine hypopyon in the anterior chamber, and the retina could not be visualized on fundoscopy. A diagnostic vitrectomy was performed followed by IVI of 0.1 ml vancomycin and 0.1 ml ceftazidime. At the same time, systemic moxifloxacin (400 mg/day) was started with daily parabulbar injections of betamethasone for 7 days. Microbiological analysis identified Staphylococcus epidermidis. The treatment response was satisfactory with gradual flare regression (Fig. ). At the last follow-up visit 4 months later, the patient had a BCVA of 0.3, a flare of 17.9 ph/ms, and OCT showed a dry macula (Fig. ).\nOUTPUT:" }, { "from": "agent", "value": "Endophthalmitis, Bilateral exudative age-related macular degeneration" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: In February 2018, the best corrected visual acuity (BCVA) of her right eye had decreased from 0.4 to 0.2, and the optical coherence tomography (OCT) revealed recurrence of macular exudation (Fig. ). The patient was treated with an IVI of aflibercept. At the 72 h post-IVI control visit, the patient was symptomless. The BCVA of her right eye had improved to 0.3 and no macular fluid was present. However, the LFP flare had increased from 8.6 ph/ms pre-injection to 664 ph/ms. Clinical examination revealed discreet conjunctival hyperemia, clear cornea, 3+ cells in the anterior chamber, and no hypopyon. On fundoscopy, the vitreous was slightly cloudy. After 2 h, before vitrectomy was performed, the BCVA was counting fingers, biomicroscopy showed a fine hypopyon in the anterior chamber, and the retina could not be visualized on fundoscopy. A diagnostic vitrectomy was performed followed by IVI of 0.1 ml vancomycin and 0.1 ml ceftazidime. At the same time, systemic moxifloxacin (400 mg/day) was started with daily parabulbar injections of betamethasone for 7 days. Microbiological analysis identified Staphylococcus epidermidis. The treatment response was satisfactory with gradual flare regression (Fig. ). At the last follow-up visit 4 months later, the patient had a BCVA of 0.3, a flare of 17.9 ph/ms, and OCT showed a dry macula (Fig. ). OUTPUT:
PMCPatients_common5119
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: In May 2010, a 20-month-old boy presented with seizure and left hemiparesis; he was admitted to the pediatric department at our hospital. He appeared irritable and had an abnormal pattern of sleep; no other neurological deficits were noted. Laboratory finding were negative for hemato-oncological abnormality. Based on these radiological findings, the initial diagnosis was an intra-axial tumor, such as pilocytic astrocytoma or dysembryoplastic neuroepithelial tumor. He was transferred to the neurosurgery unit for brain tumor surgery. Because of the peritumoral edema, the steroid (dexamethasone) was administered before the surgery.\\nThe patient underwent a major surgery with frontal craniotomy. The dura mater was tense. After the dura mater was opened, the tumor was seen to be partially adhered to the surrounding brain tissue but it had no dural attachment. Since the tumor originated from the parenchyme, it was designated as an intra-axial tumor. The intraparenchymal tumor located in right frontoparietal area was removed. The patient showed remnant neurological deficit, the left hemiparesis. But, no seizure attack was noted. Anticonvulsant therapy was maintained. During the follow-up 9 months after the surgery, he appeared well and did not experience seizure and recovered the full motor power. The brain MRI showed no recurrence of the tumor, porencephaly in a site where the tumor has been resected ().\nOUTPUT:" }, { "from": "agent", "value": "WHO grade I meningioma, transitional type" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: In May 2010, a 20-month-old boy presented with seizure and left hemiparesis; he was admitted to the pediatric department at our hospital. He appeared irritable and had an abnormal pattern of sleep; no other neurological deficits were noted. Laboratory finding were negative for hemato-oncological abnormality. Based on these radiological findings, the initial diagnosis was an intra-axial tumor, such as pilocytic astrocytoma or dysembryoplastic neuroepithelial tumor. He was transferred to the neurosurgery unit for brain tumor surgery. Because of the peritumoral edema, the steroid (dexamethasone) was administered before the surgery.\nThe patient underwent a major surgery with frontal craniotomy. The dura mater was tense. After the dura mater was opened, the tumor was seen to be partially adhered to the surrounding brain tissue but it had no dural attachment. Since the tumor originated from the parenchyme, it was designated as an intra-axial tumor. The intraparenchymal tumor located in right frontoparietal area was removed. The patient showed remnant neurological deficit, the left hemiparesis. But, no seizure attack was noted. Anticonvulsant therapy was maintained. During the follow-up 9 months after the surgery, he appeared well and did not experience seizure and recovered the full motor power. The brain MRI showed no recurrence of the tumor, porencephaly in a site where the tumor has been resected (). OUTPUT:
PMCPatients_common4969
[ { "from": "human", "value": "As a physician engaged in 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 man was referred to the Emergency Department for loss of consciousness and shortness of breath which had developed one and a half hours after intake of an evacuant solution (PEG-3350, Colyte®, Taejoon pharma Co., Ltd., Seoul, Korea) during preparation of colonoscopy in 2013. He was diagnosed with mild atopic dermatitis, but he did not have any other allergic diseases to any drug or food. Ten years ago, he had colonoscopy safely with Colyte®. Intramuscular administration of epinephrine (epinephrine injection solution, Daihan Pharm Co., Ltd., Seoul, Korea) 0.3 mg rapidly restored blood pressure and alleviated respiratory symptoms. Fortunately, his clinical conditions fully improved without sequelae. In laboratory test, serum total IgE level was not increased (69 KU/L) and skin prick test revealed strong positive only to house dust mites. However, the initial serum tryptase level was significantly increased to 91.9 mg/L (0.00-11.40 mg/L).\\nWe performed skin prick and intradermal tests with different concentrations of Colyte® solutions, histamine as a positive control, and normal saline as a negative control 2 months after the event in 2013. As shown in , all skin prick test results were negative, but the intradermal test with 10 mg/mL Colyte® showed a 5 × 5 mm sized wheal. Next, basophil activation and histamine releasability tests were conducted to evaluate the non-IgE mediated mechanism of Colyte®; however, both tests gave negative results. Finally, oral provocation tests with cefixime were performed to evaluate drug allergy, but the result was also negative.\nOUTPUT:" }, { "from": "agent", "value": "Anaphylaxis to Polyethylene Glycol (Colyte®), Diverticulitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 39-year-old man was referred to the Emergency Department for loss of consciousness and shortness of breath which had developed one and a half hours after intake of an evacuant solution (PEG-3350, Colyte®, Taejoon pharma Co., Ltd., Seoul, Korea) during preparation of colonoscopy in 2013. He was diagnosed with mild atopic dermatitis, but he did not have any other allergic diseases to any drug or food. Ten years ago, he had colonoscopy safely with Colyte®. Intramuscular administration of epinephrine (epinephrine injection solution, Daihan Pharm Co., Ltd., Seoul, Korea) 0.3 mg rapidly restored blood pressure and alleviated respiratory symptoms. Fortunately, his clinical conditions fully improved without sequelae. In laboratory test, serum total IgE level was not increased (69 KU/L) and skin prick test revealed strong positive only to house dust mites. However, the initial serum tryptase level was significantly increased to 91.9 mg/L (0.00-11.40 mg/L).\nWe performed skin prick and intradermal tests with different concentrations of Colyte® solutions, histamine as a positive control, and normal saline as a negative control 2 months after the event in 2013. As shown in , all skin prick test results were negative, but the intradermal test with 10 mg/mL Colyte® showed a 5 × 5 mm sized wheal. Next, basophil activation and histamine releasability tests were conducted to evaluate the non-IgE mediated mechanism of Colyte®; however, both tests gave negative results. Finally, oral provocation tests with cefixime were performed to evaluate drug allergy, but the result was also negative. OUTPUT:
PMCPatients_common3594
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 78-year-old woman visited our hospital in May 2013 complaining of epigastric pain and indigestion. To evaluate these problems, a biopsy was conducted by gastroduodenoscopy and colonoscopy, and colon cancer was diagnosed with no metastasis (cT2N1M0). The final pathological findings revealed no residual tumor cells in the colon and no metastasis in the lymph nodes (0/19).\\nThe patient received postoperative adjuvant chemotherapy with 5-fluorouracil plus leucovorin for 12 cycles. At the same time, the patient complained about visual disturbances and multiple flesh-colored palpable masses on her scalp (Figure ). Adenocarcinoma was confirmed by skin biopsy (Figure ). After 8 mo, the level of serum carcinoembryonic antigen was elevated from 2.83 ng/mL to 4.61 ng/mL. All the masses had increased in size, and disease progression was confirmed. Although second-line chemotherapy was administered, the disease was worsening. The patient consequently died.\nOUTPUT:" }, { "from": "agent", "value": "Stage IV colon cancer with multiple metastases (scalp, right choroid, and lung)" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 78-year-old woman visited our hospital in May 2013 complaining of epigastric pain and indigestion. To evaluate these problems, a biopsy was conducted by gastroduodenoscopy and colonoscopy, and colon cancer was diagnosed with no metastasis (cT2N1M0). The final pathological findings revealed no residual tumor cells in the colon and no metastasis in the lymph nodes (0/19).\nThe patient received postoperative adjuvant chemotherapy with 5-fluorouracil plus leucovorin for 12 cycles. At the same time, the patient complained about visual disturbances and multiple flesh-colored palpable masses on her scalp (Figure ). Adenocarcinoma was confirmed by skin biopsy (Figure ). After 8 mo, the level of serum carcinoembryonic antigen was elevated from 2.83 ng/mL to 4.61 ng/mL. All the masses had increased in size, and disease progression was confirmed. Although second-line chemotherapy was administered, the disease was worsening. The patient consequently died. OUTPUT:
PMCPatients_common651
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 73-year-old male with a past medical history of RCC, which was treated with right-sided radical nephrectomy 33 years prior, presented with abrupt onset moderate to severe right upper quadrant abdominal pain, radiating to the back. Associated symptoms included nausea and nonbloody vomiting. The patient denied any exposure to contaminated food, sick contacts, pharmacological agents like nonsteroidal anti-inflammatory drugs, corticosteroids, toxins, or alcohol. A review of systems revealed minor unintentional weight loss. Physical examination revealed a blood pressure of 208/95 mmHg, otherwise normal vital signs and epigastric tenderness. Laboratory evaluation was remarkable for microcytic anemia (hemoglobin 7.2 g/dL, mean corpuscular volume 72.2 fl). Iron studies showed low serum iron levels (15 ug/dL), low transferrin saturation (3%), and an elevated total iron-binding capacity (TIBC) (515 ug/dL). Stool guaiac was negative. CT scan of the abdomen and pelvis revealed several enlarged lymph nodes (LNs) in pancreaticoduodenal, para-aortic, and pre-caval regions, without the involvement of liver, pancreas, duodenum, or kidney (Figures -). Considering the possibility of occult gastrointestinal bleeding, esophagogastroduodenoscopy (EGD) was performed, which revealed two deep, friable, malignant appearing ulcers in major duodenal papilla and a normal-appearing second portion of the duodenum (Figure ). Biopsy from the ulcer margins showed small intestinal mucosa with scattered deposits of metastatic tumor cells with abundant pale cytoplasm, prominent cell borders, round nuclei, and prominent nucleoli (Figure ). Immunohistochemistry showed strong positivity for PAX-8 and cytokeratin 7 and was negative for CD 10 and vimentin (Figure ). This was consistent with a metastatic chromophobe RCC. Follow-up staging included a whole-body bone scan and MRI of the brain, which were negative for metastatic disease. The patient received supportive management for acute pain and iron deficiency anemia with outpatient follow-up care established with oncology. Due to extensive LN involvement, the patient was deemed to be a poor surgical candidate and was commenced on a combination of immune checkpoint inhibitors.\nOUTPUT:" }, { "from": "agent", "value": "Chromophobe Renal Cell Carcinoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 73-year-old male with a past medical history of RCC, which was treated with right-sided radical nephrectomy 33 years prior, presented with abrupt onset moderate to severe right upper quadrant abdominal pain, radiating to the back. Associated symptoms included nausea and nonbloody vomiting. The patient denied any exposure to contaminated food, sick contacts, pharmacological agents like nonsteroidal anti-inflammatory drugs, corticosteroids, toxins, or alcohol. A review of systems revealed minor unintentional weight loss. Physical examination revealed a blood pressure of 208/95 mmHg, otherwise normal vital signs and epigastric tenderness. Laboratory evaluation was remarkable for microcytic anemia (hemoglobin 7.2 g/dL, mean corpuscular volume 72.2 fl). Iron studies showed low serum iron levels (15 ug/dL), low transferrin saturation (3%), and an elevated total iron-binding capacity (TIBC) (515 ug/dL). Stool guaiac was negative. CT scan of the abdomen and pelvis revealed several enlarged lymph nodes (LNs) in pancreaticoduodenal, para-aortic, and pre-caval regions, without the involvement of liver, pancreas, duodenum, or kidney (Figures -). Considering the possibility of occult gastrointestinal bleeding, esophagogastroduodenoscopy (EGD) was performed, which revealed two deep, friable, malignant appearing ulcers in major duodenal papilla and a normal-appearing second portion of the duodenum (Figure ). Biopsy from the ulcer margins showed small intestinal mucosa with scattered deposits of metastatic tumor cells with abundant pale cytoplasm, prominent cell borders, round nuclei, and prominent nucleoli (Figure ). Immunohistochemistry showed strong positivity for PAX-8 and cytokeratin 7 and was negative for CD 10 and vimentin (Figure ). This was consistent with a metastatic chromophobe RCC. Follow-up staging included a whole-body bone scan and MRI of the brain, which were negative for metastatic disease. The patient received supportive management for acute pain and iron deficiency anemia with outpatient follow-up care established with oncology. Due to extensive LN involvement, the patient was deemed to be a poor surgical candidate and was commenced on a combination of immune checkpoint inhibitors. OUTPUT:
PMCPatients_common5379
[ { "from": "human", "value": "As a physician engaged in 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 patient who had undergone two lower back surgeries, a left partial laminectomy for disc herniation at the L4/5 and L5/S1 levels 4 years prior, and a discectomy at the L4/5 level 1 year and 5 months after the first operation was referred to our unit. Lower back pain and numbness in the left calf had developed about 6 months after the second operation and had gradually worsened. Her VAS score was 7 out of 10 and her Oswestry Disability Index was 48%. Examination revealed normal motor power and sensation in the lower extremities, and normal pulsation of the dorsalis pedis and tibial arteries. The straight leg raise test of her left leg was positive at 70 degrees. She complained of severe numbness and a pulling pain in her left leg after walking for more than 20 minutes. She had received various medications and treatments including transdermal fentanyl patch (12 µg/hr), Celecoxib 200 mg/day (Celebrex®, Pfizer, Inc., New York, NY, USA), repeated epidural steroid injections, and percutaneous epidural adhesiolysis using a Navigation catheter. Despite these interventions, she complained of persistent symptoms and only demonstrated a 20% improvement for 3 weeks after treatment; further, there were no improvements in her functional status or walking distance. We therefore decided to perform transforaminal balloon adhesiolysis. A filling defect in the medial side of her left L5 pedicle was confirmed by fluoroscopy using a contrast medium. A 3-Fr Fogarty catheter was introduced into the epidural space of her left L5 intervertebral foramen, followed by serial balloon decompression. After removal of the Fogarty balloon catheter, she was administered 3 ml of a mixture of 0.8% lidocaine, 20 mg triamcinolone, and 1500 IU hyaluronidase. There were no complications throughout the procedure. For the next 17 weeks, the patient reported reduced leg pain (VAS 2 of 10), an improved functional status (28%), and increased walking time (60 minutes). Eighteen weeks after treatment, her symptoms reoccurred but were more tolerable (VAS 4 of 10) than prior to treatment.\nOUTPUT:" }, { "from": "agent", "value": "Failed back surgery 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 76-year-old female patient who had undergone two lower back surgeries, a left partial laminectomy for disc herniation at the L4/5 and L5/S1 levels 4 years prior, and a discectomy at the L4/5 level 1 year and 5 months after the first operation was referred to our unit. Lower back pain and numbness in the left calf had developed about 6 months after the second operation and had gradually worsened. Her VAS score was 7 out of 10 and her Oswestry Disability Index was 48%. Examination revealed normal motor power and sensation in the lower extremities, and normal pulsation of the dorsalis pedis and tibial arteries. The straight leg raise test of her left leg was positive at 70 degrees. She complained of severe numbness and a pulling pain in her left leg after walking for more than 20 minutes. She had received various medications and treatments including transdermal fentanyl patch (12 µg/hr), Celecoxib 200 mg/day (Celebrex®, Pfizer, Inc., New York, NY, USA), repeated epidural steroid injections, and percutaneous epidural adhesiolysis using a Navigation catheter. Despite these interventions, she complained of persistent symptoms and only demonstrated a 20% improvement for 3 weeks after treatment; further, there were no improvements in her functional status or walking distance. We therefore decided to perform transforaminal balloon adhesiolysis. A filling defect in the medial side of her left L5 pedicle was confirmed by fluoroscopy using a contrast medium. A 3-Fr Fogarty catheter was introduced into the epidural space of her left L5 intervertebral foramen, followed by serial balloon decompression. After removal of the Fogarty balloon catheter, she was administered 3 ml of a mixture of 0.8% lidocaine, 20 mg triamcinolone, and 1500 IU hyaluronidase. There were no complications throughout the procedure. For the next 17 weeks, the patient reported reduced leg pain (VAS 2 of 10), an improved functional status (28%), and increased walking time (60 minutes). Eighteen weeks after treatment, her symptoms reoccurred but were more tolerable (VAS 4 of 10) than prior to treatment. OUTPUT:
PMCPatients_common1388
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 15-month-old Caucasian girl presented with a 3-month history of regression in motor milestones. She had been previously fit and well, and had been cruising around furniture at 11 months of age. At 12 months she had a bout of chickenpox, and subsequently became lethargic and weak. She gradually lost gross motor skills, becoming unable to walk, stand, or even sit unsupported. Her mother described a persistent low grade fever, and noticed that her eyes appeared puffy. On examination there was marked proximal muscle weakness and hypotonia. She was not able to sit without support, could not roll over, and there was marked head lag when she was pulled to sit from the supine position. She exhibited little spontaneous movement, but when propped up in a sitting position she could play with toys placed in front of her. Her deep tendon reflexes were difficult to elicit. She had periorbital oedema and erythema, but there were no other cutaneous signs. She was miserable. The diagnosis of JDM was suspected, even though her age was young and initial investigations were inconclusive: laboratory investigations revealed only mildly elevated muscle enzymes (creatine phosphokinase 303U/L, alanine transaminase 104U/L, aspartate transaminase 93U/L, lactate dehydrogenase 461U/L), normal inflammatory markers, and normal/negative complement C3 and C4, rheumatoid factor, anti-neutrophil cytoplasmic antibody and anti-nuclear antibody nerve conduction studies and electromyography were within normal limits; varicella zoster serology was positive. A magnetic resonance imaging (MRI) scan of her thigh muscles was performed, along with imaging of her brain and spine, and further neurometabolic investigations were planned. However, these were not required because the MRI showed marked muscle and subcutaneous oedema, supporting the diagnosis of myositis (Figure ). Treatment with methylprednisolone was initiated, followed with long-term methotrexate and prednisolone. Subsequently the diagnosis of JDM was confirmed as her heliotrope rash became more pronounced, and she developed Gottron’s papules and nail fold telangiectasia. She made a gradual improvement, and at 9 months post-diagnosis is able to crawl, pull herself to stand and walk independently.\nOUTPUT:" }, { "from": "agent", "value": "Juvenile dermatomyositis" } ]
As a physician engaged 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 15-month-old Caucasian girl presented with a 3-month history of regression in motor milestones. She had been previously fit and well, and had been cruising around furniture at 11 months of age. At 12 months she had a bout of chickenpox, and subsequently became lethargic and weak. She gradually lost gross motor skills, becoming unable to walk, stand, or even sit unsupported. Her mother described a persistent low grade fever, and noticed that her eyes appeared puffy. On examination there was marked proximal muscle weakness and hypotonia. She was not able to sit without support, could not roll over, and there was marked head lag when she was pulled to sit from the supine position. She exhibited little spontaneous movement, but when propped up in a sitting position she could play with toys placed in front of her. Her deep tendon reflexes were difficult to elicit. She had periorbital oedema and erythema, but there were no other cutaneous signs. She was miserable. The diagnosis of JDM was suspected, even though her age was young and initial investigations were inconclusive: laboratory investigations revealed only mildly elevated muscle enzymes (creatine phosphokinase 303U/L, alanine transaminase 104U/L, aspartate transaminase 93U/L, lactate dehydrogenase 461U/L), normal inflammatory markers, and normal/negative complement C3 and C4, rheumatoid factor, anti-neutrophil cytoplasmic antibody and anti-nuclear antibody nerve conduction studies and electromyography were within normal limits; varicella zoster serology was positive. A magnetic resonance imaging (MRI) scan of her thigh muscles was performed, along with imaging of her brain and spine, and further neurometabolic investigations were planned. However, these were not required because the MRI showed marked muscle and subcutaneous oedema, supporting the diagnosis of myositis (Figure ). Treatment with methylprednisolone was initiated, followed with long-term methotrexate and prednisolone. Subsequently the diagnosis of JDM was confirmed as her heliotrope rash became more pronounced, and she developed Gottron’s papules and nail fold telangiectasia. She made a gradual improvement, and at 9 months post-diagnosis is able to crawl, pull herself to stand and walk independently. OUTPUT:
PMCPatients_common3091
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 28-year-old female presented with a 2-month history of pain and enlargement of the mandible. The patient had no known comorbidities. Clinically, the patient displayed frontal bossing, hypertelorism, and bony enlargement of the mandible. Intraorally, the mandibular bony enlargement was noted bilaterally with a soft region palpable on the right corpus suggestive of cortical bone perforation. The radiographic examination included a panoramic radiograph that revealed multiple radiolucent, well-circumscribed, cystic lesions present throughout the mandible; one lesion was associated with an impacted tooth 48 []. A facial posteroanterior radiograph and a computed tomography scan confirmed calcifications of the falx cerebri and displayed a thickened outer table of the frontal sinus, whereas chest radiographs confirmed multiple bifid ribs [Figures and ]. Biopsies were performed on the right mandibular corpus, and histological examination confirmed the diagnosis of OKC. Due to the clinical presentation, BCNS was diagnosed clinically. The extensive nature of the mandibular cavitation resulted in a treatment plan that involved a combination of enucleation and marsupialization of the cystic lesions. After removal of the tooth 48, the posterior cavities of the mandibular ramus were enucleated bilaterally, followed by the application of nonmodified Carnoy's solution in three cycles of 3 min. The corpal cavities were marsupialized, with Bismuth Iodoform Paraffin Paste (BIPP) ribbon placement. The BIPP ribbon was subsequently gradually removed by 10 cm on either side every fortnight, followed by cystectomy. Two years postoperatively, a decrease in the size and radiolucency of the cystic cavities were noted radiographically []. The posterior lesions (treated by enucleation and irrigation with nonmodified Carnoy's solution) displayed greater resolution than the anterior lesions (treated by marsupialization). Recurrence involving the right mandibular ramus was noted 32 months postoperatively []. At the time of writing, irrigation with nonmodified Carnoy's solution and enucleation of the lesion is planned.\nOUTPUT:" }, { "from": "agent", "value": "Mandibular Odontogenic Keratocysts, Basal Cell Nevus 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 28-year-old female presented with a 2-month history of pain and enlargement of the mandible. The patient had no known comorbidities. Clinically, the patient displayed frontal bossing, hypertelorism, and bony enlargement of the mandible. Intraorally, the mandibular bony enlargement was noted bilaterally with a soft region palpable on the right corpus suggestive of cortical bone perforation. The radiographic examination included a panoramic radiograph that revealed multiple radiolucent, well-circumscribed, cystic lesions present throughout the mandible; one lesion was associated with an impacted tooth 48 []. A facial posteroanterior radiograph and a computed tomography scan confirmed calcifications of the falx cerebri and displayed a thickened outer table of the frontal sinus, whereas chest radiographs confirmed multiple bifid ribs [Figures and ]. Biopsies were performed on the right mandibular corpus, and histological examination confirmed the diagnosis of OKC. Due to the clinical presentation, BCNS was diagnosed clinically. The extensive nature of the mandibular cavitation resulted in a treatment plan that involved a combination of enucleation and marsupialization of the cystic lesions. After removal of the tooth 48, the posterior cavities of the mandibular ramus were enucleated bilaterally, followed by the application of nonmodified Carnoy's solution in three cycles of 3 min. The corpal cavities were marsupialized, with Bismuth Iodoform Paraffin Paste (BIPP) ribbon placement. The BIPP ribbon was subsequently gradually removed by 10 cm on either side every fortnight, followed by cystectomy. Two years postoperatively, a decrease in the size and radiolucency of the cystic cavities were noted radiographically []. The posterior lesions (treated by enucleation and irrigation with nonmodified Carnoy's solution) displayed greater resolution than the anterior lesions (treated by marsupialization). Recurrence involving the right mandibular ramus was noted 32 months postoperatively []. At the time of writing, irrigation with nonmodified Carnoy's solution and enucleation of the lesion is planned. OUTPUT:
PMCPatients_common4159
[ { "from": "human", "value": "As a physician engaged 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 study was performed according to the tenets of the Declaration of Helsinki and was approved by the University Ethics Committee. The patient was fully informed about the possible consequences of the present study, and he filled in an informed consent form to participate.\\nHis vital signs were normal. Physical examination demonstrated a systolic ejection murmur attributed to the mitral and tricuspid valves. Laboratory data and arterial blood gas analyses were within limits. Electrocardiogram revealed sinus rhythm of 70bpm, with right bundle branch block. Chest X-ray was normal. Transesophageal echocardiography revealed a dilated coronary sinus of 2.2cm (Fig. ). ). Saline contrast echocardiography and multislice computed tomography confirmed the presence of PLSVC, draining into dilated coronary sinus (Fig. ). Jugular internal, subclavian and innominate veins were normal. On appropriate antiarrythmic medication, the course was uneventful. The patient was discharged home, with the recommendation of annual clinical follow up.\nOUTPUT:" }, { "from": "agent", "value": "Cardiac Arrhythmias, Persistent Left Superior Vena Cava" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The study was performed according to the tenets of the Declaration of Helsinki and was approved by the University Ethics Committee. The patient was fully informed about the possible consequences of the present study, and he filled in an informed consent form to participate.\nHis vital signs were normal. Physical examination demonstrated a systolic ejection murmur attributed to the mitral and tricuspid valves. Laboratory data and arterial blood gas analyses were within limits. Electrocardiogram revealed sinus rhythm of 70bpm, with right bundle branch block. Chest X-ray was normal. Transesophageal echocardiography revealed a dilated coronary sinus of 2.2cm (Fig. ). ). Saline contrast echocardiography and multislice computed tomography confirmed the presence of PLSVC, draining into dilated coronary sinus (Fig. ). Jugular internal, subclavian and innominate veins were normal. On appropriate antiarrythmic medication, the course was uneventful. The patient was discharged home, with the recommendation of annual clinical follow up. OUTPUT:
PMCPatients_common2073
[ { "from": "human", "value": "As a physician engaged 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 first symptom of PD was right upper extremity stiffness and tremor. He takes carbidopa/levodopa 25/100 mg three times daily (TID), carbidopa/levodopa extended-release 25/100 mg at night, rasagiline 1 mg once in the morning, and amantadine 100 mg twice daily (BID). He sustained no head trauma and briefly lost consciousness and awakened startled but not confused. He was immediately taken to the hospital emergency room where an electrocardiogram showed normal sinus rhythm and heart rate (HR) of 75 beats per minute (bpm). Blood tests were reportedly normal and he was sent home with instructions to follow-up with his neurologist.\\nUpon visiting his neurologist a few days later, Mr. B’s blood pressure (BP) was 158/84 mmHg with a HR of 72 bpm while supine, and 102/70 mmHg with a HR of 105 bpm immediately after standing. Due to the elevated standing HR, the neurologist rechecked standing BP and HR 2 min later and found that they were 88/60 mmHg and 107 bpm, respectively. The patient looked pale and felt unsteady. A complete blood count and basic metabolic panel were requested. Blood urea nitrogen and creatinine were elevated and consistent with dehydration. Hematocrit was 32% and hemoglobin was 10 gm/dL. Ferritin was low and red blood cells were microcytic. Review of the patient’s records showed that, 4 months prior, his hematocrit was 37% and his hemoglobin was 12 gm/dL. A few weeks later, the patient reported no further symptoms of OH and no additional syncopal events.\nOUTPUT:" }, { "from": "agent", "value": "Neurogenic Orthostatic Hypotension, Parkinson Disease, Microcytic Ferropenic Anemia" } ]
As a physician engaged 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 first symptom of PD was right upper extremity stiffness and tremor. He takes carbidopa/levodopa 25/100 mg three times daily (TID), carbidopa/levodopa extended-release 25/100 mg at night, rasagiline 1 mg once in the morning, and amantadine 100 mg twice daily (BID). He sustained no head trauma and briefly lost consciousness and awakened startled but not confused. He was immediately taken to the hospital emergency room where an electrocardiogram showed normal sinus rhythm and heart rate (HR) of 75 beats per minute (bpm). Blood tests were reportedly normal and he was sent home with instructions to follow-up with his neurologist.\nUpon visiting his neurologist a few days later, Mr. B’s blood pressure (BP) was 158/84 mmHg with a HR of 72 bpm while supine, and 102/70 mmHg with a HR of 105 bpm immediately after standing. Due to the elevated standing HR, the neurologist rechecked standing BP and HR 2 min later and found that they were 88/60 mmHg and 107 bpm, respectively. The patient looked pale and felt unsteady. A complete blood count and basic metabolic panel were requested. Blood urea nitrogen and creatinine were elevated and consistent with dehydration. Hematocrit was 32% and hemoglobin was 10 gm/dL. Ferritin was low and red blood cells were microcytic. Review of the patient’s records showed that, 4 months prior, his hematocrit was 37% and his hemoglobin was 12 gm/dL. A few weeks later, the patient reported no further symptoms of OH and no additional syncopal events. OUTPUT:
PMCPatients_common3009
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 34-year-old female with an unremarkable past medical history presented with symptoms of general weakness, sweating, tremors and visual changes 2 days postpartum; the pregnancy was uncomplicated and she gave birth to a female baby in good health at full term. Blood analysis revealed severe hypoglycemia (36 mg/dL), while a cerebral computed tomography (CT) scan excluded neurological disorders. Tests for anti-insulin antibodies were negative. Calcium, phosphorus and potassium levels were normal, which excluded hyperparathyroidism. Together with the absence of a family history of endocrinopathies, these findings made the diagnosis of multiple endocrine neoplasia type 1 (MEN 1) highly unlikely. Abdominal ultrasound was normal, while magnetic resonance imaging (MRI) showed an isolated enhancing lesion measuring 10×8 mm localized in the head of the pancreas. She was discharged with a planned clinical and imaging follow-up, of abdominal ultrasound and CT. Twelve months after surgery, the patient currently remains euglycemic, with no signs of relapse or other complaints.\nOUTPUT:" }, { "from": "agent", "value": "Insulinoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 34-year-old female with an unremarkable past medical history presented with symptoms of general weakness, sweating, tremors and visual changes 2 days postpartum; the pregnancy was uncomplicated and she gave birth to a female baby in good health at full term. Blood analysis revealed severe hypoglycemia (36 mg/dL), while a cerebral computed tomography (CT) scan excluded neurological disorders. Tests for anti-insulin antibodies were negative. Calcium, phosphorus and potassium levels were normal, which excluded hyperparathyroidism. Together with the absence of a family history of endocrinopathies, these findings made the diagnosis of multiple endocrine neoplasia type 1 (MEN 1) highly unlikely. Abdominal ultrasound was normal, while magnetic resonance imaging (MRI) showed an isolated enhancing lesion measuring 10×8 mm localized in the head of the pancreas. She was discharged with a planned clinical and imaging follow-up, of abdominal ultrasound and CT. Twelve months after surgery, the patient currently remains euglycemic, with no signs of relapse or other complaints. OUTPUT:
PMCPatients_common86
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 60-year-old male presented with growth over the glans penis for two months associated with pain. There was no history of contact bleeding. The patient was not circumcised. He had noticed a swelling on the scrotum for the past six months. On examination, there was a 2 x 3 cm ulceroproliferative growth over the glans extending over the corona onto the shaft of penis. The ulcer was fixed to the ventral aspect of glans penis with induration proximally extending up to mid shaft of penis (Figure ).\\nBilateral inguinal lymph nodes were palpable, 3-4 on each side, 0.5 cm in size, firm and mobile in nature. The patient also had a right-sided primary vaginal hydrocele. A clinical diagnosis of SCC of penis was made and a wedge biopsy done. Histopathological analysis revealed an ulcerated stratified squamous epithelial lining with underlying lesion composed of fascicles of spindle cells with moderate pleomorphism. These were very few in number to proceed with IHC stains. A possibility of a primary sarcoma of penis was suggested.\\nFine needle aspiration cytology (FNAC) was done from bilateral inguinal nodes which revealed reactive hyperplasia. All blood parameters, liver and renal function tests were normal. The chest X-ray and ultrasound abdomen were unremarkable.\\nTotal penectomy with perineal urethrostomy was performed. The hydrocele was aspirated under aseptic precautions, three days before surgery. Post-operative course was uneventful. The patient was discharged on the eighth post-operative day and was advised to follow up with the regional cancer center for further management.\\nThe final histopathological examination revealed moderate pleomorphic spindle cells arranged in sheets of fascicles, the overlying squamous epithelium was dysplastic. Focal areas of necrosis were seen. The urethra, proximal resected skin and shaft were free of tumor.\nOUTPUT:" }, { "from": "agent", "value": "Sarcomatoid carcinoma (spindle cell carcinoma) of penis" } ]
As a physician engaged 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 male presented with growth over the glans penis for two months associated with pain. There was no history of contact bleeding. The patient was not circumcised. He had noticed a swelling on the scrotum for the past six months. On examination, there was a 2 x 3 cm ulceroproliferative growth over the glans extending over the corona onto the shaft of penis. The ulcer was fixed to the ventral aspect of glans penis with induration proximally extending up to mid shaft of penis (Figure ).\nBilateral inguinal lymph nodes were palpable, 3-4 on each side, 0.5 cm in size, firm and mobile in nature. The patient also had a right-sided primary vaginal hydrocele. A clinical diagnosis of SCC of penis was made and a wedge biopsy done. Histopathological analysis revealed an ulcerated stratified squamous epithelial lining with underlying lesion composed of fascicles of spindle cells with moderate pleomorphism. These were very few in number to proceed with IHC stains. A possibility of a primary sarcoma of penis was suggested.\nFine needle aspiration cytology (FNAC) was done from bilateral inguinal nodes which revealed reactive hyperplasia. All blood parameters, liver and renal function tests were normal. The chest X-ray and ultrasound abdomen were unremarkable.\nTotal penectomy with perineal urethrostomy was performed. The hydrocele was aspirated under aseptic precautions, three days before surgery. Post-operative course was uneventful. The patient was discharged on the eighth post-operative day and was advised to follow up with the regional cancer center for further management.\nThe final histopathological examination revealed moderate pleomorphic spindle cells arranged in sheets of fascicles, the overlying squamous epithelium was dysplastic. Focal areas of necrosis were seen. The urethra, proximal resected skin and shaft were free of tumor. OUTPUT:
PMCPatients_common1463
[ { "from": "human", "value": "As a physician engaged in 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 obese female with a BMI of 41 presented to the emergency room with slurred speech, dizziness, and left-sided weakness which started about two hours before presentation. The patient did not report any cough, fever, shortness of breath, loss of smell, or body aches. She had no pre-existing medical conditions and was not taking any medications. She was a non-smoker. There were no sick contacts at home. On examination, she was hemodynamically stable alert, awake, and oriented with oxygen saturation of 98% in room air. Her pulse rate was 85/minute, her blood pressure 130/85 mmHg, and her Glasgow Coma Score was 15/15. In neurological examination, she had slurred speech and 3/5 weakness in the left upper and lower extremity but normal sensations with no neck stiffness. The rest of the neurological examination as well as chest, cardiovascular, abdominal, and musculoskeletal examination was normal.\\nThe laboratory investigations showed hemoglobin of 12.4 gram/L, white blood cells (WBC) 7.2x109, lymphocytes 17% and C-reactive protein 8.7 mg/L (normal value 0.1-4.9 mg/L). Blood culture done on admission was negative for any bacterial growth. All other investigations, including urea and electrolytes, liver function test, D dimer, and coagulation profile were within normal limits. Her chest x-ray was normal without evidence of consolidation or infiltration (Figure ).\\nThe patient was within the window of tissue plasminogen activator (TPA) for acute stroke and underwent an emergent brain CT scan without contrast which showed no evidence of recent major territorial infarction, intracranial hemorrhage, or focal mass lesions with the normal appearance of the ventricular system and posterior fossa structures (Figures , ).\\nShe was treated with intravenous TPA and was admitted to the intensive care unit (ICU) for monitoring. She did not have any abnormal electrocardiogram (EKG) rhythm while in ICU and had full recovery of her neurological symptoms within few hours without any bleeding complications. She was screened for COVID-19 on admission as per hospital protocol and the result came back later as positive. She was subsequently discharged in good health and advised home isolation.\nOUTPUT:" }, { "from": "agent", "value": "Neurological Manifestations of 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 42-year-old obese female with a BMI of 41 presented to the emergency room with slurred speech, dizziness, and left-sided weakness which started about two hours before presentation. The patient did not report any cough, fever, shortness of breath, loss of smell, or body aches. She had no pre-existing medical conditions and was not taking any medications. She was a non-smoker. There were no sick contacts at home. On examination, she was hemodynamically stable alert, awake, and oriented with oxygen saturation of 98% in room air. Her pulse rate was 85/minute, her blood pressure 130/85 mmHg, and her Glasgow Coma Score was 15/15. In neurological examination, she had slurred speech and 3/5 weakness in the left upper and lower extremity but normal sensations with no neck stiffness. The rest of the neurological examination as well as chest, cardiovascular, abdominal, and musculoskeletal examination was normal.\nThe laboratory investigations showed hemoglobin of 12.4 gram/L, white blood cells (WBC) 7.2x109, lymphocytes 17% and C-reactive protein 8.7 mg/L (normal value 0.1-4.9 mg/L). Blood culture done on admission was negative for any bacterial growth. All other investigations, including urea and electrolytes, liver function test, D dimer, and coagulation profile were within normal limits. Her chest x-ray was normal without evidence of consolidation or infiltration (Figure ).\nThe patient was within the window of tissue plasminogen activator (TPA) for acute stroke and underwent an emergent brain CT scan without contrast which showed no evidence of recent major territorial infarction, intracranial hemorrhage, or focal mass lesions with the normal appearance of the ventricular system and posterior fossa structures (Figures , ).\nShe was treated with intravenous TPA and was admitted to the intensive care unit (ICU) for monitoring. She did not have any abnormal electrocardiogram (EKG) rhythm while in ICU and had full recovery of her neurological symptoms within few hours without any bleeding complications. She was screened for COVID-19 on admission as per hospital protocol and the result came back later as positive. She was subsequently discharged in good health and advised home isolation. OUTPUT:
PMCPatients_common603
[ { "from": "human", "value": "As a physician engaged in 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 woman with RA (onset age: 53 years) was treated with MTX 6 mg/wk and PSL 7 mg/d preoperatively for RA management. She reported numbness and clumsiness in both hands and a gait disturbance. Her walking ability had gradually declined, and she required a wheelchair 3 months after symptom onset. Radiographs showed irreducible AAS and deformation at the mid and lower cervical spine, including spondylolisthesis at C3–4 and C6–7 levels (Fig. A). MRI revealed compression of the spinal cord at C1–2, C3–4, and C6–7 levels (Fig. B). Occipito-C2 posterior fusion (using an occipital plate, C2 laminar screw on the right side, C2 pedicle screw on the left side, and iliac bone graft), double door laminoplasty using hydroxyapatite spacers at the C3–4 levels, and open door laminoplasty at the C5–7 levels were performed (Fig. C).\\nAt 3 weeks postoperative, spontaneous dehiscence of the surgical wound and purulent exudate from the opened portion of the wound were observed, and she developed persistent neck pain. MRI revealed abscess formation around the deep subfascial space (Fig. D). A microbiological culture was taken from the discharged fluid. The Gram staining procedure revealed gram-positive cocci.\\nSurgical treatment using ALBC was performed (Figs. E, F, G). Specimens for microbiological culture were taken intraoperatively from the subfascial infected tissues. The Gram staining procedure identified gram-positive cocci. The microbiological culture revealed the same strain of methicillin-resistant coagulase negative staphylococci from the preoperative and intraoperative specimens. Two weeks after the second operation, the patient could walk without aid and she maintained a good clinical outcome of the index surgery without recurrence of SSI up to the final follow-up at postoperative 11 months, when she died from hemorrhagic cerebral infarction.\nOUTPUT:" }, { "from": "agent", "value": "Deep surgical site infection, Rheumatoid upper cervical subluxation" } ]
As a physician engaged 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 woman with RA (onset age: 53 years) was treated with MTX 6 mg/wk and PSL 7 mg/d preoperatively for RA management. She reported numbness and clumsiness in both hands and a gait disturbance. Her walking ability had gradually declined, and she required a wheelchair 3 months after symptom onset. Radiographs showed irreducible AAS and deformation at the mid and lower cervical spine, including spondylolisthesis at C3–4 and C6–7 levels (Fig. A). MRI revealed compression of the spinal cord at C1–2, C3–4, and C6–7 levels (Fig. B). Occipito-C2 posterior fusion (using an occipital plate, C2 laminar screw on the right side, C2 pedicle screw on the left side, and iliac bone graft), double door laminoplasty using hydroxyapatite spacers at the C3–4 levels, and open door laminoplasty at the C5–7 levels were performed (Fig. C).\nAt 3 weeks postoperative, spontaneous dehiscence of the surgical wound and purulent exudate from the opened portion of the wound were observed, and she developed persistent neck pain. MRI revealed abscess formation around the deep subfascial space (Fig. D). A microbiological culture was taken from the discharged fluid. The Gram staining procedure revealed gram-positive cocci.\nSurgical treatment using ALBC was performed (Figs. E, F, G). Specimens for microbiological culture were taken intraoperatively from the subfascial infected tissues. The Gram staining procedure identified gram-positive cocci. The microbiological culture revealed the same strain of methicillin-resistant coagulase negative staphylococci from the preoperative and intraoperative specimens. Two weeks after the second operation, the patient could walk without aid and she maintained a good clinical outcome of the index surgery without recurrence of SSI up to the final follow-up at postoperative 11 months, when she died from hemorrhagic cerebral infarction. OUTPUT:
PMCPatients_common1007
[ { "from": "human", "value": "As a physician engaged 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 65-year-old man underwent hemicolectomy and partial ileal resection for a gastrointestinal stromal tumour (GIST). Afterwards he began oral adjuvant therapy with Imatinib (400 mg/day), a tyrosine kinase inhibitor (TKI) and the first drug used as targeted therapy. Few days after the first administrations, he developed neck muscle weakness, chewing and swallowing difficulties, so Imatinib treatment was temporary stopped for 2 days, with symptoms improvement. Subsequently, Imatinib was restarted, and 2 days later, the previous symptoms appeared again, associated with the onset of right eye ptosis. The neurological examination showed fluctuating and fatigable right eye ptosis, marked neck extensor weakness with head drop, dysphagia, dysphonia and masticatory weakness. Limb weakness was absent, and sensory examination was normal. Brain CT and Chest Radiograph did not show significant abnormalities. Blood test revealed CPK level slightly elevated (462 U/L). Because of the strong suspicion of myasthenic syndrome, we administered symptomatic therapy (pyridostigmine 60 mg, four times a day), and we planned five sections of plasma exchange. Despite these treatments, the patient rapidly worsened, and, after the second plasma exchange session, he developed acute respiratory failure. He was transferred to the Intensive Care Unit, and mechanical ventilation was supplied. In addition, steroid therapy was administered (methylprednisolone 120 mg/day). Anti-titin antibodies also resulted positive, while anti-MusK antibodies were negative. Total body CT excluded thymic disease and GIST metastases. After a course of intravenous immunoglobulins (IVIg) cycle (2 g/kg), the patient recovered. After hospital discharge, the patient performed 1 month of intensive rehabilitation, and his neurological examination returned completely normal. However, because of anti-AChR antibodies still show high titre positivity, steroid therapy was maintained over the following months even if gradually tapered.\nOUTPUT:" }, { "from": "agent", "value": "Myasthenia Gravis" } ]
As a physician engaged 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 65-year-old man underwent hemicolectomy and partial ileal resection for a gastrointestinal stromal tumour (GIST). Afterwards he began oral adjuvant therapy with Imatinib (400 mg/day), a tyrosine kinase inhibitor (TKI) and the first drug used as targeted therapy. Few days after the first administrations, he developed neck muscle weakness, chewing and swallowing difficulties, so Imatinib treatment was temporary stopped for 2 days, with symptoms improvement. Subsequently, Imatinib was restarted, and 2 days later, the previous symptoms appeared again, associated with the onset of right eye ptosis. The neurological examination showed fluctuating and fatigable right eye ptosis, marked neck extensor weakness with head drop, dysphagia, dysphonia and masticatory weakness. Limb weakness was absent, and sensory examination was normal. Brain CT and Chest Radiograph did not show significant abnormalities. Blood test revealed CPK level slightly elevated (462 U/L). Because of the strong suspicion of myasthenic syndrome, we administered symptomatic therapy (pyridostigmine 60 mg, four times a day), and we planned five sections of plasma exchange. Despite these treatments, the patient rapidly worsened, and, after the second plasma exchange session, he developed acute respiratory failure. He was transferred to the Intensive Care Unit, and mechanical ventilation was supplied. In addition, steroid therapy was administered (methylprednisolone 120 mg/day). Anti-titin antibodies also resulted positive, while anti-MusK antibodies were negative. Total body CT excluded thymic disease and GIST metastases. After a course of intravenous immunoglobulins (IVIg) cycle (2 g/kg), the patient recovered. After hospital discharge, the patient performed 1 month of intensive rehabilitation, and his neurological examination returned completely normal. However, because of anti-AChR antibodies still show high titre positivity, steroid therapy was maintained over the following months even if gradually tapered. OUTPUT:
PMCPatients_common34
[ { "from": "human", "value": "As a physician engaged in 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 Caucasian male with a medical history significant for intravenous (IV) drug use presented to the emergency department with restlessness, agitation, and profuse sweating. He reported no pain in the chest, neck, back, or abdomen. He denied a history of diabetes mellitus, hypertension, coronary artery disease, or connective tissue disease and was not taking any medication. He reported smoking one pack per day for the last 20 years. On presentation, he had a blood pressure of 120/32 mmHg; pulse of 90 beats per min; temperature of 100.1 F, and respiratory rate of 24 breaths/min. His oxygen saturation was 95% on two-liter of oxygen. He was fully oriented but found to be agitated and restless. A cardiovascular examination revealed grade 3/6 decrescendo diastolic murmur heard best on the left parasternal border on expiration. There were clear breath sounds bilaterally with no audible wheezes or crackles. The abdominal and neurological exams were benign.\\nHis electrocardiogram showed nonspecific T wave changes in V1-V2 with sinus rhythm. His chest X-ray was unremarkable as well. The laboratory reports were normal except for creatinine of 2.5 mg/dl. Blood cultures were drawn and empiric broad-spectrum antibiotics were started. A transthoracic echocardiogram (TTE) was ordered to look for possible valvular pathology/vegetation. Emergent aortic root replacement along with ascending aorta and hemi-arch replacement were performed. The postoperative course was uneventful and he was discharged in a stable condition.\nOUTPUT:" }, { "from": "agent", "value": "Painless Aortic Dissection, Infective Endocarditis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 43-year-old Caucasian male with a medical history significant for intravenous (IV) drug use presented to the emergency department with restlessness, agitation, and profuse sweating. He reported no pain in the chest, neck, back, or abdomen. He denied a history of diabetes mellitus, hypertension, coronary artery disease, or connective tissue disease and was not taking any medication. He reported smoking one pack per day for the last 20 years. On presentation, he had a blood pressure of 120/32 mmHg; pulse of 90 beats per min; temperature of 100.1 F, and respiratory rate of 24 breaths/min. His oxygen saturation was 95% on two-liter of oxygen. He was fully oriented but found to be agitated and restless. A cardiovascular examination revealed grade 3/6 decrescendo diastolic murmur heard best on the left parasternal border on expiration. There were clear breath sounds bilaterally with no audible wheezes or crackles. The abdominal and neurological exams were benign.\nHis electrocardiogram showed nonspecific T wave changes in V1-V2 with sinus rhythm. His chest X-ray was unremarkable as well. The laboratory reports were normal except for creatinine of 2.5 mg/dl. Blood cultures were drawn and empiric broad-spectrum antibiotics were started. A transthoracic echocardiogram (TTE) was ordered to look for possible valvular pathology/vegetation. Emergent aortic root replacement along with ascending aorta and hemi-arch replacement were performed. The postoperative course was uneventful and he was discharged in a stable condition. OUTPUT:
PMCPatients_common584
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The first case was an 8-month-old spayed female referred in 2011 due to seizures of suspected idiopathic origin that were poorly controlled with phenobarbital (Gardenal®, 2.5 mg/kg, orally q12h; Safoni, Brazil). The dog was evaluated by the referring veterinarian 2 months after the onset of tonic–clonic seizures, which had progressed over the last 2 weeks to 2–3 seizures per week. In our service, the owner reported that the dog experienced cluster seizures that occurred over 48 h and were treated with diazepam and thiopental. On presentation, neurological examination was performed 1 week after cluster seizures and was unremarkable. Based on a history of seizures, the lesion was localized to the forebrain. Physical examination findings, biochemical profile, and complete blood count (CBC) were normal; polymerase chain reaction (PCR) for canine distemper virus in urine and indirect immunofluorescent antibody tests (IFAT) for antibodies against Toxoplasma gondii and Neospora caninum were negative.\\nMRI showed mixed parieto-occipital agyria and pachygyria of the frontal and parietal lobes (Fig. ). Temporal and occipital regions lacked gyri and sulci. ). Treatment with phenobarbital (Gardenal®, 3 mg/kg, orally q12h; Safoni, Brazil) and levetiracetam as an adjunct (Keppra®, 20 mg/kg, orally q8h; UCB Biopharma, Brazil) effectively controlled cluster seizures after presentation. Levetiracetam was discontinued after 4 weeks. It was not possible to obtain information regarding survival for this dog.\nOUTPUT:" }, { "from": "agent", "value": "Lissencephaly" } ]
As a physician engaged 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 first case was an 8-month-old spayed female referred in 2011 due to seizures of suspected idiopathic origin that were poorly controlled with phenobarbital (Gardenal®, 2.5 mg/kg, orally q12h; Safoni, Brazil). The dog was evaluated by the referring veterinarian 2 months after the onset of tonic–clonic seizures, which had progressed over the last 2 weeks to 2–3 seizures per week. In our service, the owner reported that the dog experienced cluster seizures that occurred over 48 h and were treated with diazepam and thiopental. On presentation, neurological examination was performed 1 week after cluster seizures and was unremarkable. Based on a history of seizures, the lesion was localized to the forebrain. Physical examination findings, biochemical profile, and complete blood count (CBC) were normal; polymerase chain reaction (PCR) for canine distemper virus in urine and indirect immunofluorescent antibody tests (IFAT) for antibodies against Toxoplasma gondii and Neospora caninum were negative.\nMRI showed mixed parieto-occipital agyria and pachygyria of the frontal and parietal lobes (Fig. ). Temporal and occipital regions lacked gyri and sulci. ). Treatment with phenobarbital (Gardenal®, 3 mg/kg, orally q12h; Safoni, Brazil) and levetiracetam as an adjunct (Keppra®, 20 mg/kg, orally q8h; UCB Biopharma, Brazil) effectively controlled cluster seizures after presentation. Levetiracetam was discontinued after 4 weeks. It was not possible to obtain information regarding survival for this dog. OUTPUT:
PMCPatients_common3444
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 19-year-old woman with a nodular sclerosis cHL stage II-B refractory to\\nadriamycin, bleomycin, vinblastine, dacarbazine (ABVD) achieved complete\\nresponse (CR) after a second line with ifosfamide, carboplatin, etoposide (ICE)\\nregimen and ASCT. Unfortunately, she relapsed after nine doses of BV maintenance\\nafter ASCT at 1.8 mg/kg every 3 weeks; it was well tolerated without relevant\\ntoxicity and dose reduction. Third line was initiated with nivolumab 3 mg/kg\\nevery 2 weeks when she was 20 years old. After six cycles, positron emission\\ntomography/computed tomography (PET/CT) scan showed an undetermined response and\\nshe continued with additional cycles. After the ninth cycle, she developed\\npruritus. At that point, a combined strategy was initiated adding bendamustine\\nat a dose of 90 mg/m2 on days 1 and 2 of 21-day cycle. After two\\ndoses of nivolumab-bendamustine, she achieved partial response (PR), and the\\nfinal PET/CT evaluation after six cycles was CR with resolution of the pruritus.\\nNo toxicities were seen. She underwent bone marrow reduced intensity allo-SCT\\nfrom her haploidentical mother, conditioned with busulfan, fludarabine, and\\ncyclophosphamide, using post-transplant cyclophosphamide (PTCY) in combination\\nwith sirolimus and mycophenolate mofetil as graft-versus-host\\ndisease (GVHD) prophylaxis. One month after allo-SCT, she developed acute\\ngraft-versus-host disease (aGVHD) global grade II (skin 1,\\ngastrointestinal 1, liver 0) that completely resolved with oral steroids.\\nFurthermore, during post-transplant recovery she presented a noninfectious\\nfebrile episode. No chronic GVHD (cGVHD) was observed. The patient is still\\nalive in CR at 27 months after allo-SCT.\nOUTPUT:" }, { "from": "agent", "value": "Classical Hodgkin’s lymphoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 19-year-old woman with a nodular sclerosis cHL stage II-B refractory to\nadriamycin, bleomycin, vinblastine, dacarbazine (ABVD) achieved complete\nresponse (CR) after a second line with ifosfamide, carboplatin, etoposide (ICE)\nregimen and ASCT. Unfortunately, she relapsed after nine doses of BV maintenance\nafter ASCT at 1.8 mg/kg every 3 weeks; it was well tolerated without relevant\ntoxicity and dose reduction. Third line was initiated with nivolumab 3 mg/kg\nevery 2 weeks when she was 20 years old. After six cycles, positron emission\ntomography/computed tomography (PET/CT) scan showed an undetermined response and\nshe continued with additional cycles. After the ninth cycle, she developed\npruritus. At that point, a combined strategy was initiated adding bendamustine\nat a dose of 90 mg/m2 on days 1 and 2 of 21-day cycle. After two\ndoses of nivolumab-bendamustine, she achieved partial response (PR), and the\nfinal PET/CT evaluation after six cycles was CR with resolution of the pruritus.\nNo toxicities were seen. She underwent bone marrow reduced intensity allo-SCT\nfrom her haploidentical mother, conditioned with busulfan, fludarabine, and\ncyclophosphamide, using post-transplant cyclophosphamide (PTCY) in combination\nwith sirolimus and mycophenolate mofetil as graft-versus-host\ndisease (GVHD) prophylaxis. One month after allo-SCT, she developed acute\ngraft-versus-host disease (aGVHD) global grade II (skin 1,\ngastrointestinal 1, liver 0) that completely resolved with oral steroids.\nFurthermore, during post-transplant recovery she presented a noninfectious\nfebrile episode. No chronic GVHD (cGVHD) was observed. The patient is still\nalive in CR at 27 months after allo-SCT. OUTPUT:
PMCPatients_common2352
[ { "from": "human", "value": "As a physician engaged in 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 Indo-Caribbean man with three-vessel coronary artery disease underwent elective coronary artery bypass surgery on the beating heart with left internal mammary to the left anterior descending coronary artery and a saphenous vein graft to the posterior descending coronary artery.\\nSurgery was uneventful and the patient returned to the intensive care unit in stable condition. Two hours later, however, due to sudden bleeding and cardiac arrest, he required resuscitation and re-exploration. In order to control massive bleeding from a tear of the aorta at the proximal venous anastomosis and the persistent depressed cardiac function, it became necessary to establish cardiopulmonary bypass. The hemoglobin (Hb) before re-exploration was 4.5 mg/dl. The tear in the aorta was repaired, and the venous graft re-implanted higher in the Ascending Aorta. Transfusion of 6 Units of packed red cells (PRC) and 3 Units of fresh frozen plasma (FFP) was required to achieve Hb of 8.8 mg/dl at the end of surgery. Weaning from cardiopulmonary bypass was achieved with no inotropic support; however, it was difficult to ventilate the patient. The lungs were very stiff and distended. Despite of high positive pressure and % FiO2 the blood saturation remained very low. This was soon followed by copious pulmonary secretion requiring bronchial suction (around 100 ml of fluid collected each time), every 5 to 10 minutes. The fluid was clear, yellowish, and not frothy. The total amount of collected bronchial fluid before transfer to ICU was over 1700 ml. An IABP was inserted, but any attempt to close the chest resulted in significant decrease in the systemic arterial pressure. The patient was therefore return to the intensive care unit with the chest open.\\nRepeated bronchial suctions were required for about five hours before improvement in oxygen saturation. Bronchial secretion reduced and then suddenly stopped two hours after transfer to the ICU. Oxygenation improved and it was possible to close the chest the following day. Respiratory distress remained and the patient was extubated on day 5 postoperatively. He made a slow but uneventful recovery and was discharge home on day 20.\nOUTPUT:" }, { "from": "agent", "value": "Transfusion related acute lung injury" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 72 year-old Indo-Caribbean man with three-vessel coronary artery disease underwent elective coronary artery bypass surgery on the beating heart with left internal mammary to the left anterior descending coronary artery and a saphenous vein graft to the posterior descending coronary artery.\nSurgery was uneventful and the patient returned to the intensive care unit in stable condition. Two hours later, however, due to sudden bleeding and cardiac arrest, he required resuscitation and re-exploration. In order to control massive bleeding from a tear of the aorta at the proximal venous anastomosis and the persistent depressed cardiac function, it became necessary to establish cardiopulmonary bypass. The hemoglobin (Hb) before re-exploration was 4.5 mg/dl. The tear in the aorta was repaired, and the venous graft re-implanted higher in the Ascending Aorta. Transfusion of 6 Units of packed red cells (PRC) and 3 Units of fresh frozen plasma (FFP) was required to achieve Hb of 8.8 mg/dl at the end of surgery. Weaning from cardiopulmonary bypass was achieved with no inotropic support; however, it was difficult to ventilate the patient. The lungs were very stiff and distended. Despite of high positive pressure and % FiO2 the blood saturation remained very low. This was soon followed by copious pulmonary secretion requiring bronchial suction (around 100 ml of fluid collected each time), every 5 to 10 minutes. The fluid was clear, yellowish, and not frothy. The total amount of collected bronchial fluid before transfer to ICU was over 1700 ml. An IABP was inserted, but any attempt to close the chest resulted in significant decrease in the systemic arterial pressure. The patient was therefore return to the intensive care unit with the chest open.\nRepeated bronchial suctions were required for about five hours before improvement in oxygen saturation. Bronchial secretion reduced and then suddenly stopped two hours after transfer to the ICU. Oxygenation improved and it was possible to close the chest the following day. Respiratory distress remained and the patient was extubated on day 5 postoperatively. He made a slow but uneventful recovery and was discharge home on day 20. OUTPUT:
PMCPatients_common3581
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An 11-year-old, intact male, Brittany Spaniel Mix weighing 26.6 kg (58.6 lb) was presented to a private veterinary hospital in Waco, Texas with a 2-week history of inappetence and lethargy. The dog was mildly febrile (39.6°C [103.2°F]) and had mild nasal discharge, which was chronic according to the owner. No external parasites were noted on physical exam or in the dog's history. There was a marked neutrophilia (50,950/μL; RI: 3,000–12,000/μL) and thrombocytopenia (5,000/μL; RI: 200,000–500,000/μL), which was confirmed by blood smear examination. In addition, numerous spirochetes were observed throughout the blood smear. Indirect fluorescent antibody serology was positive for R. rickettsii (sample screened at ≥1 : 16), and Lyme borreliosis (B31 strain, sample screened at ≥1 : 60). The dog was administered minocycline (3.5 mg/kg [1.6 mg/lb] PO, q12h) for 28 days, and carprofen (2 mg/kg [0.9 mg/lb] PO, q24 h) for fever and inflammation. The dog recovered uneventfully; however, died 8 months later secondary to a hemoabdomen from a presumed liver mass. The decreased albumin and increase in ALKP activity were attributed to liver disease and hemorrhage; however, vector-borne disease might have contributed to these abnormalities.\nOUTPUT:" }, { "from": "agent", "value": "Tick-Borne Relapsing Fever" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 11-year-old, intact male, Brittany Spaniel Mix weighing 26.6 kg (58.6 lb) was presented to a private veterinary hospital in Waco, Texas with a 2-week history of inappetence and lethargy. The dog was mildly febrile (39.6°C [103.2°F]) and had mild nasal discharge, which was chronic according to the owner. No external parasites were noted on physical exam or in the dog's history. There was a marked neutrophilia (50,950/μL; RI: 3,000–12,000/μL) and thrombocytopenia (5,000/μL; RI: 200,000–500,000/μL), which was confirmed by blood smear examination. In addition, numerous spirochetes were observed throughout the blood smear. Indirect fluorescent antibody serology was positive for R. rickettsii (sample screened at ≥1 : 16), and Lyme borreliosis (B31 strain, sample screened at ≥1 : 60). The dog was administered minocycline (3.5 mg/kg [1.6 mg/lb] PO, q12h) for 28 days, and carprofen (2 mg/kg [0.9 mg/lb] PO, q24 h) for fever and inflammation. The dog recovered uneventfully; however, died 8 months later secondary to a hemoabdomen from a presumed liver mass. The decreased albumin and increase in ALKP activity were attributed to liver disease and hemorrhage; however, vector-borne disease might have contributed to these abnormalities. OUTPUT:
PMCPatients_common4911
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Despite locally advanced tumor, we decided to perform resection.\\nDuring laparotomy, we identified that the left portal vein and left hepatic artery were encased as well as the second-order branches of the right hepatic ducts were deeply involved by the tumor. Thus, we abandoned curative resection and decided to perform palliative BDR with cluster HJ.\\nThe patient had total destruction of hilar bile duct structures, hence the tumor over the right hepatic artery was removed (). Four intrahepatic bile duct openings (3 from the right liver and 1 from the left liver) were identified and their edges were repaired to prepare them for anastomosis; subsequently, four size-matched silastic stents were temporarily inserted (). The caudate ducts were not markedly dilated, thus small coronary dilators were inserted to identify their course. The anterior wall of the bile duct opening was anchored with multiple 5-0 Prolene sutures (). The posterior wall of the bile duct opening was continuously sutured with 5-0 Prolene sutures after dividing into 3 segments with 2 internal intervening sutures (). The corner stitches were retracted with rubber vessel loops to make the operative field wide. Four silastic stents and one additional stent were firmly inserted into each beaked bile duct opening after forceful mechanical dilatation, and then transfixed with 5-0 Prolene suture (). The anterior wall was finally closed by using interrupted sutures that were previously anchored (). After these surgical procedures, a leak test was performed with injection of methylene blue solution through the pre-existing PTBD tube.\\nThe patient recovered uneventfully without any noticeable complication, and is currently undergoing adjuvant chemoradiation therapy.\nOUTPUT:" }, { "from": "agent", "value": "Perihilar cholangiocarcinoma of Bismuth-Corlette type IV, 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: Despite locally advanced tumor, we decided to perform resection.\nDuring laparotomy, we identified that the left portal vein and left hepatic artery were encased as well as the second-order branches of the right hepatic ducts were deeply involved by the tumor. Thus, we abandoned curative resection and decided to perform palliative BDR with cluster HJ.\nThe patient had total destruction of hilar bile duct structures, hence the tumor over the right hepatic artery was removed (). Four intrahepatic bile duct openings (3 from the right liver and 1 from the left liver) were identified and their edges were repaired to prepare them for anastomosis; subsequently, four size-matched silastic stents were temporarily inserted (). The caudate ducts were not markedly dilated, thus small coronary dilators were inserted to identify their course. The anterior wall of the bile duct opening was anchored with multiple 5-0 Prolene sutures (). The posterior wall of the bile duct opening was continuously sutured with 5-0 Prolene sutures after dividing into 3 segments with 2 internal intervening sutures (). The corner stitches were retracted with rubber vessel loops to make the operative field wide. Four silastic stents and one additional stent were firmly inserted into each beaked bile duct opening after forceful mechanical dilatation, and then transfixed with 5-0 Prolene suture (). The anterior wall was finally closed by using interrupted sutures that were previously anchored (). After these surgical procedures, a leak test was performed with injection of methylene blue solution through the pre-existing PTBD tube.\nThe patient recovered uneventfully without any noticeable complication, and is currently undergoing adjuvant chemoradiation therapy. OUTPUT:
PMCPatients_common236
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A healthy 13 month-old boy was receiving oral propranolol hydrochloride for a large IH. The initial dose of propranolol hydrochloride was 0,5 mg/kg/day and over several weeks was titrated to 1mg/kg/d. He received the treatment for about 9 months and had a significant reduction in the size of IH. The night prior to hospitalization, the child looked tired, drowsy and had a very poor oral intake. Due to his sleepiness, he didn’t receive the evening dose of propranolol. With the child's poor feeding, it was important to skip the propranolol dose and hold it temporarily. Since his mother had no clear information about the importance of taking propranolol with food, as well as when to stop temporarily the propranolol, she gave him the missed dose during the night, without food (about six hours before hospital admission). In the morning the child was unresponsive, unarousable, with a grey pallor. The mother didn’t inform us at the first moment that the child was taking propranolol for IH. The child was given initially 30 ml of 10% dextrose solution intravenously, which resulted in stabilization of his glucose level. We continued the treatment with 7.5% dextrose for a few hours after. Clinical condition was completely normalized.\nOUTPUT:" }, { "from": "agent", "value": "Deep coma, Severe hypoglycemia, Infantile hemangioma" } ]
As a physician engaged 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 healthy 13 month-old boy was receiving oral propranolol hydrochloride for a large IH. The initial dose of propranolol hydrochloride was 0,5 mg/kg/day and over several weeks was titrated to 1mg/kg/d. He received the treatment for about 9 months and had a significant reduction in the size of IH. The night prior to hospitalization, the child looked tired, drowsy and had a very poor oral intake. Due to his sleepiness, he didn’t receive the evening dose of propranolol. With the child's poor feeding, it was important to skip the propranolol dose and hold it temporarily. Since his mother had no clear information about the importance of taking propranolol with food, as well as when to stop temporarily the propranolol, she gave him the missed dose during the night, without food (about six hours before hospital admission). In the morning the child was unresponsive, unarousable, with a grey pallor. The mother didn’t inform us at the first moment that the child was taking propranolol for IH. The child was given initially 30 ml of 10% dextrose solution intravenously, which resulted in stabilization of his glucose level. We continued the treatment with 7.5% dextrose for a few hours after. Clinical condition was completely normalized. OUTPUT:
PMCPatients_common430
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 58-year-old female presented with a 3 cm mass in the lower inner quadrant of the left breast. Ultrasound and mammography revealed a Breast Imaging Reporting and Data System [] (BI-RADS) 4 lesion. The patient subsequently refused adjuvant radiation and chemotherapy.\\nFive years after her surgery, the patient presented with a painless, mobile, 15 cm mass involving the upper and lower outer quadrants of the left breast. No evidence of nipple retraction or discharge was observed. Mammography revealed a BI-RADS 5 lesion. A core biopsy showed breast tissue containing areas of bone formation with partially calcified osteoid material surrounded by stellate and spindle-shaped stromal cells. There was also osteoclast-like giant cells present.\\nContrast-enhanced computed tomography (CT) of the chest and abdomen revealed a large lobulated left breast mass with cystic and calcific foci, measuring 7.1 × 10.7 × 11.6 cm with no evidence of invasion into the chest wall or skin. No pulmonary, hepatic, or bony lesions were identified.\\nThe patient refused mastectomy and chose to have a wide local excision of the breast mass (see ).\\nPathologic examination of the mass showed osteogenic sarcoma with malignant cells admixed with neoplastic woven bone and frequent mitotic figures (see ). The tumour was noted to involve all margins.\nOUTPUT:" }, { "from": "agent", "value": "Primary Osteosarcoma of the Breast, Invasive Ductal 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 58-year-old female presented with a 3 cm mass in the lower inner quadrant of the left breast. Ultrasound and mammography revealed a Breast Imaging Reporting and Data System [] (BI-RADS) 4 lesion. The patient subsequently refused adjuvant radiation and chemotherapy.\nFive years after her surgery, the patient presented with a painless, mobile, 15 cm mass involving the upper and lower outer quadrants of the left breast. No evidence of nipple retraction or discharge was observed. Mammography revealed a BI-RADS 5 lesion. A core biopsy showed breast tissue containing areas of bone formation with partially calcified osteoid material surrounded by stellate and spindle-shaped stromal cells. There was also osteoclast-like giant cells present.\nContrast-enhanced computed tomography (CT) of the chest and abdomen revealed a large lobulated left breast mass with cystic and calcific foci, measuring 7.1 × 10.7 × 11.6 cm with no evidence of invasion into the chest wall or skin. No pulmonary, hepatic, or bony lesions were identified.\nThe patient refused mastectomy and chose to have a wide local excision of the breast mass (see ).\nPathologic examination of the mass showed osteogenic sarcoma with malignant cells admixed with neoplastic woven bone and frequent mitotic figures (see ). The tumour was noted to involve all margins. OUTPUT:
PMCPatients_common974
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 17-year-old girl was referred to our care due to periorbital and lower limb oedema, high fever and asthenia that had been persisting for over a week. The urine dipstick tested positive for proteins (4+). Over the following weeks not only no significant improvement was observed but the patient also developed long-lasting fever (15 days) and arthralgia.\\nIn view of the age of onset, the atypical course of the disease and the symptoms developed while on immune-suppressive therapy a workup for secondary glomerulopathies was repeated: blood tests, blood cultures, viral markers, chest x-ray and abdominal ultrasound were all normal except for increased CRP levels (21.1 mg/dL) and erythrocyte sedimentation rate (ESR) (56 mm/h). Due to the persistence of the fever and the increased inflammatory parameters in a patient with otherwise normal laboratory tests, ultrasonography and x-ray investigations, a total body magnetic resonance imaging (MRI) was performed to further investigate (Fig. ).\nOUTPUT:" }, { "from": "agent", "value": "Nephrotic syndrome, Focal segmental glomerulosclerosis (FSGS)" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 17-year-old girl was referred to our care due to periorbital and lower limb oedema, high fever and asthenia that had been persisting for over a week. The urine dipstick tested positive for proteins (4+). Over the following weeks not only no significant improvement was observed but the patient also developed long-lasting fever (15 days) and arthralgia.\nIn view of the age of onset, the atypical course of the disease and the symptoms developed while on immune-suppressive therapy a workup for secondary glomerulopathies was repeated: blood tests, blood cultures, viral markers, chest x-ray and abdominal ultrasound were all normal except for increased CRP levels (21.1 mg/dL) and erythrocyte sedimentation rate (ESR) (56 mm/h). Due to the persistence of the fever and the increased inflammatory parameters in a patient with otherwise normal laboratory tests, ultrasonography and x-ray investigations, a total body magnetic resonance imaging (MRI) was performed to further investigate (Fig. ). OUTPUT:
PMCPatients_common2780
[ { "from": "human", "value": "As a physician engaged 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 initial postoperative period was uneventful with 0 to 100 degrees of knee flexion. The X-ray (Figure ) showed good knee alignment with a slight tibial overhang. An untrimmed osteophyte was identified at the postero-medial femoral condyle. In the first follow-up at 6 weeks, the patient complained of minimal pain and swelling at the anteromedial aspect of the knee. His symptoms progressed and, at 6 months, the patient underwent an arthroscopic exploration with washout and samples were sent for culture & sensitivity. All samples were negative for any microorganisms. C-reactive protein, white-cell count and erythrocyte sedimentation rate remained stable and the pain appeared to settle. At 1-year follow up, the patient had some medial knee pain which was controllable. At this stage, he seemed pleased with the outcome of the surgery. At 3 years, he presented at the clinic again due to recurrence of medial knee pain. X-rays showed no changes. Technetium 99 m diphosphonate bone scintigraphy showed increased uptake on the delayed phase mainly in the medial femoral and tibial condyle, which was inconclusive. Inflammatory markers were again stable. The pain disappeared shortly after the scan. The pain recurred once again 5 years after surgery and examination revealed a tender point at the medial joint line with a palpable lump and good range of flexion. No changes were observed on a repeat X-ray (Figure ). At this stage, the medial joint line was explored which showed a small osteophyte at the postero-medial border of the femur, causing a localised polyethylene rim wear (non-articulating part) and localised medial synovial reaction. The osteophyte was excised. Tibial and femoral components were stable and hence not revised. At 2 years post-osteophyte excision (Figure ), the patient was pain-free and asymptomatic. Throughout this period, the patient had good knee alignment with 0 to 100 degrees of flexion.\nOUTPUT:" }, { "from": "agent", "value": "Osteoarthritis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The initial postoperative period was uneventful with 0 to 100 degrees of knee flexion. The X-ray (Figure ) showed good knee alignment with a slight tibial overhang. An untrimmed osteophyte was identified at the postero-medial femoral condyle. In the first follow-up at 6 weeks, the patient complained of minimal pain and swelling at the anteromedial aspect of the knee. His symptoms progressed and, at 6 months, the patient underwent an arthroscopic exploration with washout and samples were sent for culture & sensitivity. All samples were negative for any microorganisms. C-reactive protein, white-cell count and erythrocyte sedimentation rate remained stable and the pain appeared to settle. At 1-year follow up, the patient had some medial knee pain which was controllable. At this stage, he seemed pleased with the outcome of the surgery. At 3 years, he presented at the clinic again due to recurrence of medial knee pain. X-rays showed no changes. Technetium 99 m diphosphonate bone scintigraphy showed increased uptake on the delayed phase mainly in the medial femoral and tibial condyle, which was inconclusive. Inflammatory markers were again stable. The pain disappeared shortly after the scan. The pain recurred once again 5 years after surgery and examination revealed a tender point at the medial joint line with a palpable lump and good range of flexion. No changes were observed on a repeat X-ray (Figure ). At this stage, the medial joint line was explored which showed a small osteophyte at the postero-medial border of the femur, causing a localised polyethylene rim wear (non-articulating part) and localised medial synovial reaction. The osteophyte was excised. Tibial and femoral components were stable and hence not revised. At 2 years post-osteophyte excision (Figure ), the patient was pain-free and asymptomatic. Throughout this period, the patient had good knee alignment with 0 to 100 degrees of flexion. OUTPUT:
PMCPatients_common4958
[ { "from": "human", "value": "As a physician engaged 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 boy, born of a nonconsanguineous marriage, presented to the hospital emergency with a three-day history of dysphagia. The patient gave a history of two similar episodes of dysphagia that were relievedon treatment. He was under the care of a gastroenterologist who performed an endoscopy and a barium swallow that revealed a very tight stricture at the upper end of esophagus []. He was referred to dermatology departmentfor pigmentation of skin and nail dystrophy. A detailed history revealed that the patient developed splitting and dystrophy of his fingernails and toenails at 5 years of age. This was followed by pigmentation of the skin within a year. Pigmentation first appeared on the neck and lower limbs, followed by the extensive involvement of the entire body with sparing of the face. Around this time he started developing oral ulcers that were recurrent despite treatment. He gave no history of eye complaints, loss of hair, dental caries, or difficulty in keeping up with studies. Except dysphagia, patient gave no history of systemic symptoms. The patient's maternal uncle had a history of similar type of skin pigmentation and nail dystrophy, and died of unknown causes at 55 years of age.\\nA thorough examination of the patient revealed generalized fine, lacy, reticulated, greyish-brown pattern of hyperpigmentation with areas of epidermal atrophy (poikiloderma), sparing the face [Figure and ]. Examination of the genitals revealed no signs of testicular atrophy. Splitting of nails with pterygium formation and dystrophy was present, more over the fingers than the toes []. Examination of the oral mucosa revealed the presence of a whitish, well-defined leukoplakic plaque on the dorsal surface of the tongue, interrupted by lingual ulcers []. Buccal and labial mucosa were spared. There were no significant systemic findings. Routine investigations along with skin biopsy were done. Histopathological examination of skin sample revealed melanophages in the upper dermis and vacuolization of basal cells. Routine investigations of the patient were normal. Bone marrow biopsy and lingual biopsy were refused by the patient. The classic clinical findings, family history and consistent histopathology enabled us to make a diagnosis of DKC.\nOUTPUT:" }, { "from": "agent", "value": "Dyskeratosis congenita" } ]
As a physician engaged 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 boy, born of a nonconsanguineous marriage, presented to the hospital emergency with a three-day history of dysphagia. The patient gave a history of two similar episodes of dysphagia that were relievedon treatment. He was under the care of a gastroenterologist who performed an endoscopy and a barium swallow that revealed a very tight stricture at the upper end of esophagus []. He was referred to dermatology departmentfor pigmentation of skin and nail dystrophy. A detailed history revealed that the patient developed splitting and dystrophy of his fingernails and toenails at 5 years of age. This was followed by pigmentation of the skin within a year. Pigmentation first appeared on the neck and lower limbs, followed by the extensive involvement of the entire body with sparing of the face. Around this time he started developing oral ulcers that were recurrent despite treatment. He gave no history of eye complaints, loss of hair, dental caries, or difficulty in keeping up with studies. Except dysphagia, patient gave no history of systemic symptoms. The patient's maternal uncle had a history of similar type of skin pigmentation and nail dystrophy, and died of unknown causes at 55 years of age.\nA thorough examination of the patient revealed generalized fine, lacy, reticulated, greyish-brown pattern of hyperpigmentation with areas of epidermal atrophy (poikiloderma), sparing the face [Figure and ]. Examination of the genitals revealed no signs of testicular atrophy. Splitting of nails with pterygium formation and dystrophy was present, more over the fingers than the toes []. Examination of the oral mucosa revealed the presence of a whitish, well-defined leukoplakic plaque on the dorsal surface of the tongue, interrupted by lingual ulcers []. Buccal and labial mucosa were spared. There were no significant systemic findings. Routine investigations along with skin biopsy were done. Histopathological examination of skin sample revealed melanophages in the upper dermis and vacuolization of basal cells. Routine investigations of the patient were normal. Bone marrow biopsy and lingual biopsy were refused by the patient. The classic clinical findings, family history and consistent histopathology enabled us to make a diagnosis of DKC. OUTPUT:
PMCPatients_common502
[ { "from": "human", "value": "As a physician engaged 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 seen three years following his hemorrhage for a routine examination. Our expectation was that HG would be capable of detecting unilateral stimuli in both hemifields, but would eventually fail to report the left stimulus when a competitive item appeared simultaneously on the right (which would correspond to an extinction phenomenon). Preliminary testing showed that the patient always saw a stimulus presented in the right hemifield, but also reported an additional stimulus at the mirror position in his left hemifield.\nOUTPUT:" }, { "from": "agent", "value": "Right parietal hemorrhage, partial sensory loss of the left arm, left inferior quadrantanopia, moderate spatial neglect, visual-constructive deficits, partial epileptic seizures, spatial neglect in activities of daily living, illusory perception" } ]
As a physician engaged 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 seen three years following his hemorrhage for a routine examination. Our expectation was that HG would be capable of detecting unilateral stimuli in both hemifields, but would eventually fail to report the left stimulus when a competitive item appeared simultaneously on the right (which would correspond to an extinction phenomenon). Preliminary testing showed that the patient always saw a stimulus presented in the right hemifield, but also reported an additional stimulus at the mirror position in his left hemifield. OUTPUT:
PMCPatients_common2632
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 26-year-old female with an uneventful antenatal period delivered a full-term baby by normal vaginal delivery. She developed persistent fever 1 month after delivery. Chest X-ray and computed tomography (CT) showed right pleural effusion and homonymous lung infiltration (Fig. and ), which was not observed before delivery. Patient was initially treated as a case of bacterial pleuropneumonia with parenteral antibiotics during 3 weeks of hospitalization with decline of fever; pleural effusion decreased gradually for 3 months.\\nHowever, fever recurred 4 months after the delivery with gradually worsening abdominal distention, and she was admitted to our department. Chest X-ray and CT showed residual lung infiltrations without cavity and effusion (Fig. and ). Abdominal CT revealed moderate ascites, intraabdominal mass lesions and lymph nodes swelling, and bilateral adnexal masses (Fig. and ). Diagnostic puncture yielded clear yellow fluid, which was consistent with exudates. The sputum and ascites acid-fast bacillus smear were negative, and both cultures isolated no common bacteria. Although the CA125 serum level was high (247 IU/ml), ascitic cytology did not reveal malignant cells. Further serology tests were negative for antinuclear antibody and HIV-Ab. One week after the chemotherapy was started, worsening of the pre-existing lung infiltrations with new contralateral effusion was noted, and continued for 3 weeks (Fig. and ). Improvement of abdominal findings was not observed in this period. Then, the lung infiltrations and effusion were gradually improved by continuation of chemotherapy (Fig. and ). The sputum acid-fast bacilli cultures became negative and ascites disappeared. The CA125 serum level was reduced to the normal range after chemotherapy.\nOUTPUT:" }, { "from": "agent", "value": "Disseminated tuberculosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 26-year-old female with an uneventful antenatal period delivered a full-term baby by normal vaginal delivery. She developed persistent fever 1 month after delivery. Chest X-ray and computed tomography (CT) showed right pleural effusion and homonymous lung infiltration (Fig. and ), which was not observed before delivery. Patient was initially treated as a case of bacterial pleuropneumonia with parenteral antibiotics during 3 weeks of hospitalization with decline of fever; pleural effusion decreased gradually for 3 months.\nHowever, fever recurred 4 months after the delivery with gradually worsening abdominal distention, and she was admitted to our department. Chest X-ray and CT showed residual lung infiltrations without cavity and effusion (Fig. and ). Abdominal CT revealed moderate ascites, intraabdominal mass lesions and lymph nodes swelling, and bilateral adnexal masses (Fig. and ). Diagnostic puncture yielded clear yellow fluid, which was consistent with exudates. The sputum and ascites acid-fast bacillus smear were negative, and both cultures isolated no common bacteria. Although the CA125 serum level was high (247 IU/ml), ascitic cytology did not reveal malignant cells. Further serology tests were negative for antinuclear antibody and HIV-Ab. One week after the chemotherapy was started, worsening of the pre-existing lung infiltrations with new contralateral effusion was noted, and continued for 3 weeks (Fig. and ). Improvement of abdominal findings was not observed in this period. Then, the lung infiltrations and effusion were gradually improved by continuation of chemotherapy (Fig. and ). The sputum acid-fast bacilli cultures became negative and ascites disappeared. The CA125 serum level was reduced to the normal range after chemotherapy. OUTPUT:
PMCPatients_common3084
[ { "from": "human", "value": "As a physician engaged in 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 with a twin pregnancy at 36 wk and one day gestation (gravida 1, 0 abortions) was referred to our emergency unit.\\nThe patient presented with malaise, fever, and a non-productive cough for 6 d prior to admission.\\nNo remarkable past medical history.\\nNo remarkable personal and family medical history.\\nOn physical examination, she was febrile, tachycardic, hypoxic with O2 saturation of 92%, and diffuse rhonchi on auscultation.\\nThe most significant laboratory finding was an increased erythrocyte sedimentation rate. Both infants were in a good condition with a first minute APGAR score of 9/10. They were isolated from their mother and transferred to the Neonatal Intensive Care Unit for close observation. Meropenem, azithromycin, and hydroxychloroquine as well as supplemental oxygen were started after delivery. Favipiravir was added to her medications. Her clinical course during hospitalization improved, particularly during the second week.\\nAfter twelve days, another CT scan was performed, and the results showed only very faint residual ground-glass opacities. Therefore, the dramatic response to this therapeutic regimen was notable (Figure ).\nOUTPUT:" }, { "from": "agent", "value": "COVID-19 pneumonia" } ]
As a physician engaged 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 with a twin pregnancy at 36 wk and one day gestation (gravida 1, 0 abortions) was referred to our emergency unit.\nThe patient presented with malaise, fever, and a non-productive cough for 6 d prior to admission.\nNo remarkable past medical history.\nNo remarkable personal and family medical history.\nOn physical examination, she was febrile, tachycardic, hypoxic with O2 saturation of 92%, and diffuse rhonchi on auscultation.\nThe most significant laboratory finding was an increased erythrocyte sedimentation rate. Both infants were in a good condition with a first minute APGAR score of 9/10. They were isolated from their mother and transferred to the Neonatal Intensive Care Unit for close observation. Meropenem, azithromycin, and hydroxychloroquine as well as supplemental oxygen were started after delivery. Favipiravir was added to her medications. Her clinical course during hospitalization improved, particularly during the second week.\nAfter twelve days, another CT scan was performed, and the results showed only very faint residual ground-glass opacities. Therefore, the dramatic response to this therapeutic regimen was notable (Figure ). OUTPUT:
PMCPatients_common3902
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: There was serous discharge that did not smell foul. He sought treatment at private clinics twice and was given multiple courses of broad-spectrum antibiotics including oral augmentin, but no improvement was seen. However, the lesion persisted by becoming enlarged and reaching the interphalangeal joint area. The patient felt pain in that area.\\nOn examination, his vital signs were within the normal range and his capillary blood glucose was 7.9 mmol/L. The skin surrounding the lesion looked normal with no signs of inflammation (). There were no palpable nodules over the dorsum of the left hand or the left forearm and no palpable lymph nodes.\\nA full blood panel revealed a hemoglobin level of 13.0 g/dL, white blood count of 6.0×109/L and platelet count of 165×109/L. His baseline liver function and renal function test results were in the normal range. His latest hemoglobin A1c result was 7.9%. A skin biopsy taken from the lesion showed irregular epidermal hyperplasia with hyperkeratosis and parakeratosis. Inflammatory cell infiltration was seen within the epidermis. The dermal layers showed marked acute and chronic inflammatory cell infiltration with histiocytes. The culture media showed growth of S. schenckii. Culture and sensitivity tests for Mycobacterium tuberculosis were negative.\\nOral itraconazole 200 mg twice daily was prescribed for 4 months; after 2 months, the lesion showed marked improvement.\nOUTPUT:" }, { "from": "agent", "value": "Diabetes Mellitus, Finger Ulcer" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: There was serous discharge that did not smell foul. He sought treatment at private clinics twice and was given multiple courses of broad-spectrum antibiotics including oral augmentin, but no improvement was seen. However, the lesion persisted by becoming enlarged and reaching the interphalangeal joint area. The patient felt pain in that area.\nOn examination, his vital signs were within the normal range and his capillary blood glucose was 7.9 mmol/L. The skin surrounding the lesion looked normal with no signs of inflammation (). There were no palpable nodules over the dorsum of the left hand or the left forearm and no palpable lymph nodes.\nA full blood panel revealed a hemoglobin level of 13.0 g/dL, white blood count of 6.0×109/L and platelet count of 165×109/L. His baseline liver function and renal function test results were in the normal range. His latest hemoglobin A1c result was 7.9%. A skin biopsy taken from the lesion showed irregular epidermal hyperplasia with hyperkeratosis and parakeratosis. Inflammatory cell infiltration was seen within the epidermis. The dermal layers showed marked acute and chronic inflammatory cell infiltration with histiocytes. The culture media showed growth of S. schenckii. Culture and sensitivity tests for Mycobacterium tuberculosis were negative.\nOral itraconazole 200 mg twice daily was prescribed for 4 months; after 2 months, the lesion showed marked improvement. OUTPUT:
PMCPatients_common4968
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Male patient, 48 years old, from the metropolitan area of Porto Alegre (RS), sought\\nmedical attention due to disseminated erythematous lesions and fever for the past\\nfour days.\\nHe reported a spider bite in the right buttock region. The spider was not found and\\nthe patient reported pain in the area while sleeping in his beach house. In 48 hours\\na violaceous spot appeared on the site.\\nOn the third day he presented an erythematous eruption accompanied by several\\ndisseminated small non-follicular pustules, fever over 38ºC and pruritus ().\\nThe gluteal lesion evolved, in four days, with the onset of a necrotic plaque, dry\\nand well delimited. The edema and erythema adjacent to the lesion increased (). The patient denied use of painkillers\\nor other drugs. Since infection was suspected, cephalexin was prescribed.\\nHe presented leukocytosis (27,260 leukocytes, with predominance of neutrophils) and\\nincreased transaminases (ALT 268; AST 56), GGT (366) and bilirubin (TB 2.5, IB 1.7,\\nDB 0.8). As viral serology was negative and the diagnosis was AGEP, treatment was\\nbegun with prednisone (80 mg / day).\\nThe clinical picture progressed with diffuse desquamation and periorbital edema\\n(), as well as of hands and feet.\\nOn palms and plants, there was the onset of blisters with later desquamation. There\\nwas clinical and laboratorial improvement, which prompted gradual decrease of\\nprednisone until its suspension. The buttock lesion evolved with detachment of the\\nnecrotic plaque and local ulcer.\\nHistopathology showed pustular dermatitis with neutrophilic vasculitis, focally\\npurpuric, discrete edema in the dermal papillae and absence of leukocytoclasia\\n( and ).\nOUTPUT:" }, { "from": "agent", "value": "Acute generalized exanthematous pustulosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Male patient, 48 years old, from the metropolitan area of Porto Alegre (RS), sought\nmedical attention due to disseminated erythematous lesions and fever for the past\nfour days.\nHe reported a spider bite in the right buttock region. The spider was not found and\nthe patient reported pain in the area while sleeping in his beach house. In 48 hours\na violaceous spot appeared on the site.\nOn the third day he presented an erythematous eruption accompanied by several\ndisseminated small non-follicular pustules, fever over 38ºC and pruritus ().\nThe gluteal lesion evolved, in four days, with the onset of a necrotic plaque, dry\nand well delimited. The edema and erythema adjacent to the lesion increased (). The patient denied use of painkillers\nor other drugs. Since infection was suspected, cephalexin was prescribed.\nHe presented leukocytosis (27,260 leukocytes, with predominance of neutrophils) and\nincreased transaminases (ALT 268; AST 56), GGT (366) and bilirubin (TB 2.5, IB 1.7,\nDB 0.8). As viral serology was negative and the diagnosis was AGEP, treatment was\nbegun with prednisone (80 mg / day).\nThe clinical picture progressed with diffuse desquamation and periorbital edema\n(), as well as of hands and feet.\nOn palms and plants, there was the onset of blisters with later desquamation. There\nwas clinical and laboratorial improvement, which prompted gradual decrease of\nprednisone until its suspension. The buttock lesion evolved with detachment of the\nnecrotic plaque and local ulcer.\nHistopathology showed pustular dermatitis with neutrophilic vasculitis, focally\npurpuric, discrete edema in the dermal papillae and absence of leukocytoclasia\n( and ). OUTPUT:
PMCPatients_common789
[ { "from": "human", "value": "As a physician engaged in 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 woman was admitted into our department complaining about perineal abscess for 2 days (No 12 in Table ). Skin necrosis was seen in abdomen and perineum. The swelling and inflammation involved abdomen and perineum (Fig. a, b), with a tendency of progressing to right buttock. Crepitus was heard in the abdomen. The body temperature was 38.3 ℃, the blood pressure (BP) was 88/54 mmHg, the heart rate (HR) was 103 beats/min. In addition, the lactate level was 2.9 mmol/L, and WBC was 19.0 × 109/L. In terms of treatment, Ceftriaxone (2 g/time, 1 time/day, Shanghai Roche Pharmaceuticals Co., Ltd) and ornidazole (0.5 g/time, 2 times/day, Sichuan Kelun Pharmaceuticals Co., Ltd) were applied empirically. An emergency operation was performed at 6 h after admission under general anesthesia. Intraoperatively, a widespread infection progressing along the deep fascial plane was observed, which showed the manifestations of tawny pus, putrid odor, vascular thrombosis and skin necrosis (Fig. c–e). Bacteria culture revealed the presence of Escherichia coli infection in both the wound bed and blood, and the original empirical antibiotic treatment regimen was maintained. At the same time, an insulin pump was applied to control the blood glucose at about 8–10 mmol/L. Emergency operation was carried out to control the infection, while the other two operations were performed on the following 5th and 11th days to remove the residual necrotic tissue and to culture the wound bed (Fig. f, g). Other treatments included parenteral nutrition support (25–30 kcal/kg/day) and blood transfusion. Moreover, granulation tissue was raised with a fixation of NPWT (Fig. h). For wound closure, the wounds in perineum, right buttock and partial abdomen were sutured, while skin graft was used to cover the residual defect in abdomen (Fig. i, j). The patient was discharged on the 29th day after admission and no relapse was observed.\nOUTPUT:" }, { "from": "agent", "value": "Fournier’s gangrene" } ]
As a physician engaged 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 woman was admitted into our department complaining about perineal abscess for 2 days (No 12 in Table ). Skin necrosis was seen in abdomen and perineum. The swelling and inflammation involved abdomen and perineum (Fig. a, b), with a tendency of progressing to right buttock. Crepitus was heard in the abdomen. The body temperature was 38.3 ℃, the blood pressure (BP) was 88/54 mmHg, the heart rate (HR) was 103 beats/min. In addition, the lactate level was 2.9 mmol/L, and WBC was 19.0 × 109/L. In terms of treatment, Ceftriaxone (2 g/time, 1 time/day, Shanghai Roche Pharmaceuticals Co., Ltd) and ornidazole (0.5 g/time, 2 times/day, Sichuan Kelun Pharmaceuticals Co., Ltd) were applied empirically. An emergency operation was performed at 6 h after admission under general anesthesia. Intraoperatively, a widespread infection progressing along the deep fascial plane was observed, which showed the manifestations of tawny pus, putrid odor, vascular thrombosis and skin necrosis (Fig. c–e). Bacteria culture revealed the presence of Escherichia coli infection in both the wound bed and blood, and the original empirical antibiotic treatment regimen was maintained. At the same time, an insulin pump was applied to control the blood glucose at about 8–10 mmol/L. Emergency operation was carried out to control the infection, while the other two operations were performed on the following 5th and 11th days to remove the residual necrotic tissue and to culture the wound bed (Fig. f, g). Other treatments included parenteral nutrition support (25–30 kcal/kg/day) and blood transfusion. Moreover, granulation tissue was raised with a fixation of NPWT (Fig. h). For wound closure, the wounds in perineum, right buttock and partial abdomen were sutured, while skin graft was used to cover the residual defect in abdomen (Fig. i, j). The patient was discharged on the 29th day after admission and no relapse was observed. OUTPUT:
PMCPatients_common1204
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 48-year-old woman was referred to the hepatologist in order to investigate elevated levels of liver enzymes. Except for a treated systemic hypertension, mild obesity and a ten-year irregular use of amfepramone, she had no remarkable medical history. She also had no familiar history of liver disease or alcohol consumption. Physical examination revealed only mild hepatomegaly.\\nLaboratory tests are summarized in . She presented a positive antinuclear antibody (ANA) test (titer > 1/640) with a rim-like membranous and cytoplasmic speckled pattern, suggestive of anti-mitochondrial positivity (). These ANA patterns are known to be associated to antibodies to gp210 and mitocondrial antigens, respectively. Indirect immunofluorescence (IIF) tests for anti-smooth muscle antibodies (SMA), anti-liver/kidney microsome 1 (LKM-1), and neutrophil cytoplasm antigens (ANCA) were negative. IIF-AMA on in-house rodent tissue preparations was performed as previously described [] and was positive at 1/160. Anti-pyruvate dehydrogenase antibodies (anti-M2 fraction) were positive and detected by enzyme immunosorbent assay (ELISA-Orgentec, Mainz, Germany). There was also reactivity for anti-M2-E3 BPO, anti-gp210 and anti-Sp-100 (Euroline profile, Euroimmun, Lubeck, Germany).\\nLiver biopsy revealed bridging portal fibrosis, lymphomononuclear infiltrate with lymphocytic interface hepatitis and marginal ductular reaction. Surprisingly, some of the portal tracts revealed small biliary ducts with concentric fibrosis (“onion skin” type) with duct obliteration (, ). Magnetic resonance cholangiography was then performed, with normal findings. Diagnosis of small duct PSC was done, and she was treated with ursodeoxycholic acid (UDCA) with progressive normalization of liver enzymes within 4 months.\nOUTPUT:" }, { "from": "agent", "value": "Primary Biliary Cirrhosis, Small Duct Primary Sclerosing Cholangitis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 48-year-old woman was referred to the hepatologist in order to investigate elevated levels of liver enzymes. Except for a treated systemic hypertension, mild obesity and a ten-year irregular use of amfepramone, she had no remarkable medical history. She also had no familiar history of liver disease or alcohol consumption. Physical examination revealed only mild hepatomegaly.\nLaboratory tests are summarized in . She presented a positive antinuclear antibody (ANA) test (titer > 1/640) with a rim-like membranous and cytoplasmic speckled pattern, suggestive of anti-mitochondrial positivity (). These ANA patterns are known to be associated to antibodies to gp210 and mitocondrial antigens, respectively. Indirect immunofluorescence (IIF) tests for anti-smooth muscle antibodies (SMA), anti-liver/kidney microsome 1 (LKM-1), and neutrophil cytoplasm antigens (ANCA) were negative. IIF-AMA on in-house rodent tissue preparations was performed as previously described [] and was positive at 1/160. Anti-pyruvate dehydrogenase antibodies (anti-M2 fraction) were positive and detected by enzyme immunosorbent assay (ELISA-Orgentec, Mainz, Germany). There was also reactivity for anti-M2-E3 BPO, anti-gp210 and anti-Sp-100 (Euroline profile, Euroimmun, Lubeck, Germany).\nLiver biopsy revealed bridging portal fibrosis, lymphomononuclear infiltrate with lymphocytic interface hepatitis and marginal ductular reaction. Surprisingly, some of the portal tracts revealed small biliary ducts with concentric fibrosis (“onion skin” type) with duct obliteration (, ). Magnetic resonance cholangiography was then performed, with normal findings. Diagnosis of small duct PSC was done, and she was treated with ursodeoxycholic acid (UDCA) with progressive normalization of liver enzymes within 4 months. OUTPUT:
PMCPatients_common4616
[ { "from": "human", "value": "As a physician engaged in 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 patient presented with a history of shortness of breath and multiple episodes of seizure of one week duration. On evaluation, he was diagnosed with right lung non-small cell lung cancer (squamous cell carcinoma) with metastasis to brain and superior vena caval syndrome (stage IV). He was started on tab phenytoin 300 mg at bedtime and anti-edema measures with steroids (tab dexamethasone 8 mg 3 times daily during RT and tapered over 2 weeks post RT). He received palliative RT to the mediastinum and whole brain with a total dose of 20 Gray in 5 fractions over one week with Co-60 gamma rays. Two weeks post radiotherapy, his general condition improved and he received one cycle of palliative chemotherapy with paclitaxel-carboplatin combination. Nearly 3 weeks after completing the RT, he presented with painful, erythematous lesions in the scalp, which subsequently generalized. During examination, he was afebrile with pulse rate 98/min, respiratory rate 28/min, blood pressure 109/83 mm Hg, and features of mild dehydration. Examination of the skin revealed erythematous, tender macules over the scalp, face, trunk, and limbs with areas of confluent epidermal detachment and blistering involving almost 30% of his body surface area (). Conjunctivitis, hemorrhagic crusting on lips, erosions over buccal and nasal mucosa and over the glans penis were noted, strongly suggesting TEN caused by phenytoin. Hemogram and biochemical parameters were normal except for hyponatremia. Phenytoin was immediately discontinued, and he was managed with intravenous fluid replacement, electrolyte correction, systemic antibiotics, steroids (dexamethasone 16 mg/day tapered at 2 mg/day over one week), and local skin care with antibiotic and antifungal dressings. After primary supportive care, his condition worsened and he died due to septicemia on the seventh day of hospital admission.\nOUTPUT:" }, { "from": "agent", "value": "Toxic epidermal necrolysis" } ]
As a physician engaged 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 patient presented with a history of shortness of breath and multiple episodes of seizure of one week duration. On evaluation, he was diagnosed with right lung non-small cell lung cancer (squamous cell carcinoma) with metastasis to brain and superior vena caval syndrome (stage IV). He was started on tab phenytoin 300 mg at bedtime and anti-edema measures with steroids (tab dexamethasone 8 mg 3 times daily during RT and tapered over 2 weeks post RT). He received palliative RT to the mediastinum and whole brain with a total dose of 20 Gray in 5 fractions over one week with Co-60 gamma rays. Two weeks post radiotherapy, his general condition improved and he received one cycle of palliative chemotherapy with paclitaxel-carboplatin combination. Nearly 3 weeks after completing the RT, he presented with painful, erythematous lesions in the scalp, which subsequently generalized. During examination, he was afebrile with pulse rate 98/min, respiratory rate 28/min, blood pressure 109/83 mm Hg, and features of mild dehydration. Examination of the skin revealed erythematous, tender macules over the scalp, face, trunk, and limbs with areas of confluent epidermal detachment and blistering involving almost 30% of his body surface area (). Conjunctivitis, hemorrhagic crusting on lips, erosions over buccal and nasal mucosa and over the glans penis were noted, strongly suggesting TEN caused by phenytoin. Hemogram and biochemical parameters were normal except for hyponatremia. Phenytoin was immediately discontinued, and he was managed with intravenous fluid replacement, electrolyte correction, systemic antibiotics, steroids (dexamethasone 16 mg/day tapered at 2 mg/day over one week), and local skin care with antibiotic and antifungal dressings. After primary supportive care, his condition worsened and he died due to septicemia on the seventh day of hospital admission. OUTPUT:
PMCPatients_common4877
[ { "from": "human", "value": "As a physician engaged in 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 gentleman, a non-smoker, presented with persistent productive cough with mucoid sputum of 16 years duration. He had no associated symptoms of dyspnoea, fever, chest pain or haemoptysis. He had noticed progressive symmetric, swelling of both his lower limbs and discolouration of the nails for the past 6 years. He did not have any family history of RA or YNS. On examination, his vitals were stable, and physical examination revealed bilaterally symmetric non-pitting pedal oedema extending to the lower one-third of the thigh (Fig. ). ). Musculoskeletal system examination revealed the presence of tenderness and limitation of movement of the bilateral metacarpophalangeal, elbow and knee joints. The rest of the systemic examination including respiratory system examination was within normal limits. Routine blood and urine investigations were normal. Sputum examination for acid fast bacilli was negative. Imaging of the thorax revealed multilobar peribronchial thickening with cylindrical and cystic bronchiectasis with no evidence of pleural effusion (Fig. ). His spirometry showed obstructive airway disease. An echocardiogram ruled out cardiac impairment and pulmonary hypertension. A diagnosis of YNS with treatment-naive RA was made. Further investigations including HIV, HBsAg, anti-nuclear antibody, and anti-neutrophil cytoplasmic antibody done to rule out other associations were non-contributory. He was started on hydroxychloroquine, sulfasalazine and oral steroids for his RA. He was initiated on tiotropium and deriphyllin along with bronchial hygiene and pulmonary rehabilitation. He was advised compression stockings, manual lymphatic drainage measures and leg end elevation for his lymphoedema.\nOUTPUT:" }, { "from": "agent", "value": "Yellow nail syndrome, Rheumatoid arthritis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 57-year-old gentleman, a non-smoker, presented with persistent productive cough with mucoid sputum of 16 years duration. He had no associated symptoms of dyspnoea, fever, chest pain or haemoptysis. He had noticed progressive symmetric, swelling of both his lower limbs and discolouration of the nails for the past 6 years. He did not have any family history of RA or YNS. On examination, his vitals were stable, and physical examination revealed bilaterally symmetric non-pitting pedal oedema extending to the lower one-third of the thigh (Fig. ). ). Musculoskeletal system examination revealed the presence of tenderness and limitation of movement of the bilateral metacarpophalangeal, elbow and knee joints. The rest of the systemic examination including respiratory system examination was within normal limits. Routine blood and urine investigations were normal. Sputum examination for acid fast bacilli was negative. Imaging of the thorax revealed multilobar peribronchial thickening with cylindrical and cystic bronchiectasis with no evidence of pleural effusion (Fig. ). His spirometry showed obstructive airway disease. An echocardiogram ruled out cardiac impairment and pulmonary hypertension. A diagnosis of YNS with treatment-naive RA was made. Further investigations including HIV, HBsAg, anti-nuclear antibody, and anti-neutrophil cytoplasmic antibody done to rule out other associations were non-contributory. He was started on hydroxychloroquine, sulfasalazine and oral steroids for his RA. He was initiated on tiotropium and deriphyllin along with bronchial hygiene and pulmonary rehabilitation. He was advised compression stockings, manual lymphatic drainage measures and leg end elevation for his lymphoedema. OUTPUT:
PMCPatients_common2262
[ { "from": "human", "value": "As a physician engaged 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 29 year old Asian woman from\\nIran who was referred to the Women’s Hospital in\\nFebruary 2007 due to a missed period (gestational\\nage: eight weeks) and elevated human chorionic\\ngonadotropin β (β-hCG) titer (15000 units/ml). Her\\ngynecologic history was unremarkable except for\\nprimary infertility of one year’s duration due to polycyctic\\novary syndrome. She was having vaginal\\nbleeding since six days prior to admission with\\nthe passage of a clot and associated pelvic pain. Her\\npast medical and surgical histories were unremarkable.\\nShe was a nonsmoker and had no allergies.\\nThe patient underwent a physical examination;\\nblood pressure was 90/60, pulse 110 and a temperature\\nof 37°C. The chest was clear and the electrocardiography\\n(ECG) was normal. The patient had\\nleft lower quadrant (LLQ) tenderness by abdominal\\npalpation . There was brown blood in the vagina.\\nInternal examination revealed a retroverted uterus\\nwith left adnexal masse. Tenderness in the left adnexa\\nand cervical motion tenderness were present.\\nThe patient underwent ultrasonography. There was\\nno gestational sac in the uterus; the endometrial\\nthickness was 9 mm, a left adenexal mass that consisted\\nof a suspicious echofree area gestational sac\\n(GS) of 18×28 mm and free fluid in the cul-de-sac\\nwere noted (Figs , ).\\nThe patient underwent laparotomy. The fallopian\\ntube was resected due to a rupture that extended to\\nthe subserosal surface.\nOUTPUT:" }, { "from": "agent", "value": "Molar Pregnancy, Tubal Ectopic Pregnancy" } ]
As a physician engaged 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 29 year old Asian woman from\nIran who was referred to the Women’s Hospital in\nFebruary 2007 due to a missed period (gestational\nage: eight weeks) and elevated human chorionic\ngonadotropin β (β-hCG) titer (15000 units/ml). Her\ngynecologic history was unremarkable except for\nprimary infertility of one year’s duration due to polycyctic\novary syndrome. She was having vaginal\nbleeding since six days prior to admission with\nthe passage of a clot and associated pelvic pain. Her\npast medical and surgical histories were unremarkable.\nShe was a nonsmoker and had no allergies.\nThe patient underwent a physical examination;\nblood pressure was 90/60, pulse 110 and a temperature\nof 37°C. The chest was clear and the electrocardiography\n(ECG) was normal. The patient had\nleft lower quadrant (LLQ) tenderness by abdominal\npalpation . There was brown blood in the vagina.\nInternal examination revealed a retroverted uterus\nwith left adnexal masse. Tenderness in the left adnexa\nand cervical motion tenderness were present.\nThe patient underwent ultrasonography. There was\nno gestational sac in the uterus; the endometrial\nthickness was 9 mm, a left adenexal mass that consisted\nof a suspicious echofree area gestational sac\n(GS) of 18×28 mm and free fluid in the cul-de-sac\nwere noted (Figs , ).\nThe patient underwent laparotomy. The fallopian\ntube was resected due to a rupture that extended to\nthe subserosal surface. OUTPUT:
PMCPatients_common1455
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 19-year-old male basic military trainee reported chronic, intermittent bilateral hip and groin pain since childhood, which acutely worsened over the past two weeks related to increased physical training. He reported mild discomfort associated with long periods of walking which increased with running, left greater than right. Pain decreased but persisted at rest. The patient’s pain resulted in walking with a limp. Physical examination was notable for joint pain in both hips with active and passive motion, which worsened with weightbearing. The patient appeared younger than his stated age. Bilateral hip radiographs were obtained with frog leg views (Figure ). Findings were concerning for left SCFE, possible right SCFE, and abnormal delayed skeletal maturation without significant closure of the femoral physes or apophyses.\\nThe radiologist recommended orthopedic referral and obtaining a bone age assessment to estimate the amount of delay in skeletal maturation. He was subsequently admitted by the orthopedic department for treatment with bilateral surgical pinning. Initial follow-up bone age studies demonstrated mild progression of physeal closure (not shown).\nOUTPUT:" }, { "from": "agent", "value": "Slipped Capital Femoral Epiphysis, Pseudohypoparathyroidism, Juvenile Hypothyroidism, Hashimoto thyroiditis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 19-year-old male basic military trainee reported chronic, intermittent bilateral hip and groin pain since childhood, which acutely worsened over the past two weeks related to increased physical training. He reported mild discomfort associated with long periods of walking which increased with running, left greater than right. Pain decreased but persisted at rest. The patient’s pain resulted in walking with a limp. Physical examination was notable for joint pain in both hips with active and passive motion, which worsened with weightbearing. The patient appeared younger than his stated age. Bilateral hip radiographs were obtained with frog leg views (Figure ). Findings were concerning for left SCFE, possible right SCFE, and abnormal delayed skeletal maturation without significant closure of the femoral physes or apophyses.\nThe radiologist recommended orthopedic referral and obtaining a bone age assessment to estimate the amount of delay in skeletal maturation. He was subsequently admitted by the orthopedic department for treatment with bilateral surgical pinning. Initial follow-up bone age studies demonstrated mild progression of physeal closure (not shown). OUTPUT:
PMCPatients_common4884
[ { "from": "human", "value": "As a physician engaged in 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 presented with abdominal pain, non-bloody diarrhea for two months and 15-pound weight loss. Her frequency of bowel movements was 10-12 times a day with occasional nocturnal bowel movements. Her past history was significant for follicular lymphoma since 2009, treated with rituximab with remission until recurrence in 2012 when she was treated with R-CHOP and R-ICE regimens. Her disease continued to progress and she was started on oral idelalisib 10 months prior to this admission. Physical exam showed stable vital signs, non-tender abdomen without guarding. Initial lab findings showed potassium 2.8 mEq/L (normal: 3.5-5.0 mEq/L), chloride 98 mEq/L (normal 101-111 mEq/L), WBC 9.9, hemoglobin 12.5, TSH 2.56 mIU/L, morning cortisol 18 μg/dL and negative tissue IgA transglutaminase with normal immunoglobulin level. The patient was started on IV hydration with potassium supplementation. Stool studies were positive for occult blood, but negative for infectious organisms such as Salmonella, Shigella, Campylobacter, Cyclospora, Microspora, and Clostridium difficile PCR. CT abdomen and pelvis with and without contrast, mainly to rule out lymphadenopathy with her history of lymphoma, was normal. Upper endoscopy and duodenal biopsy were negative for celiac disease. Subsequent colonoscopy revealed ileitis () and mild colitis. Random biopsies showed focal inflammation, crypt drop out cryptitis, increased lymphocytes, plasma cells and eosinophils in lamina propria in ileum (), and mild cryptitis () in colon. Review of her medications revealed use of idelalisib, a known cause of chronic diarrhea and entero-colitis. The medication was discontinued and patient was started on prednisone 40 mg q.d. with slow tapering over 8 weeks leading to a significant improvement in patient’s condition; idelalisib was then re-started with close monitoring of patient’s symptoms.\nOUTPUT:" }, { "from": "agent", "value": "Enterocolitis" } ]
As a physician engaged 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 presented with abdominal pain, non-bloody diarrhea for two months and 15-pound weight loss. Her frequency of bowel movements was 10-12 times a day with occasional nocturnal bowel movements. Her past history was significant for follicular lymphoma since 2009, treated with rituximab with remission until recurrence in 2012 when she was treated with R-CHOP and R-ICE regimens. Her disease continued to progress and she was started on oral idelalisib 10 months prior to this admission. Physical exam showed stable vital signs, non-tender abdomen without guarding. Initial lab findings showed potassium 2.8 mEq/L (normal: 3.5-5.0 mEq/L), chloride 98 mEq/L (normal 101-111 mEq/L), WBC 9.9, hemoglobin 12.5, TSH 2.56 mIU/L, morning cortisol 18 μg/dL and negative tissue IgA transglutaminase with normal immunoglobulin level. The patient was started on IV hydration with potassium supplementation. Stool studies were positive for occult blood, but negative for infectious organisms such as Salmonella, Shigella, Campylobacter, Cyclospora, Microspora, and Clostridium difficile PCR. CT abdomen and pelvis with and without contrast, mainly to rule out lymphadenopathy with her history of lymphoma, was normal. Upper endoscopy and duodenal biopsy were negative for celiac disease. Subsequent colonoscopy revealed ileitis () and mild colitis. Random biopsies showed focal inflammation, crypt drop out cryptitis, increased lymphocytes, plasma cells and eosinophils in lamina propria in ileum (), and mild cryptitis () in colon. Review of her medications revealed use of idelalisib, a known cause of chronic diarrhea and entero-colitis. The medication was discontinued and patient was started on prednisone 40 mg q.d. with slow tapering over 8 weeks leading to a significant improvement in patient’s condition; idelalisib was then re-started with close monitoring of patient’s symptoms. OUTPUT:
PMCPatients_common2560
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 55-year-old male presented to the emergency department with left lower limb painless swelling and redness which started gradually over two weeks prior to presentation. He stated that he usually does not stay immobilized for a long period of time and there was no recent history of immobilization or surgeries. He denies any trauma to his left lower limb. His medical background includes obstructive sleep apnea. He has never been a smoker and his family history was negative for thromboembolic events or other hematological disorders. On physical examination, there were swelling and redness in his left lower limb extending from the foot to the upper thigh. Warmth was also noted compared to the right lower limb. The rest of the physical exam was unremarkable, there was no evidence of injury or venous stasis.\\nBiochemical and haematological investigations were normal. CT revealed absent infrarenal IVC () associated with multiple para-aortic collaterals and tortuous dilatation of the inferior mesenteric vein. After that, he was started on Warfarin and required life-long anticoagulation. Following daily measurement of the calf and thigh circumference, his DVT had resolved. After discharge, life-long Warfarin was continued and he was advised to use elastic stocking. No recurrence of DVT has occurred at three and six months of follow-up. Thrombophilia studies, including lupus anticoagulant, cardiolipin antibody, antithrombin III, antinuclear antibody, factor V Leiden, and prothrombin gene mutation, were normal. However, his proteins C and S activity was low. As thrombophilia studies were done after initiating treatment, low activity level of anticoagulant proteins (proteins C and S) could be attributed to treatment with Warfarin [].\nOUTPUT:" }, { "from": "agent", "value": "Deep Vein Thrombosis, Inferior Vena Cava Agenesis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 55-year-old male presented to the emergency department with left lower limb painless swelling and redness which started gradually over two weeks prior to presentation. He stated that he usually does not stay immobilized for a long period of time and there was no recent history of immobilization or surgeries. He denies any trauma to his left lower limb. His medical background includes obstructive sleep apnea. He has never been a smoker and his family history was negative for thromboembolic events or other hematological disorders. On physical examination, there were swelling and redness in his left lower limb extending from the foot to the upper thigh. Warmth was also noted compared to the right lower limb. The rest of the physical exam was unremarkable, there was no evidence of injury or venous stasis.\nBiochemical and haematological investigations were normal. CT revealed absent infrarenal IVC () associated with multiple para-aortic collaterals and tortuous dilatation of the inferior mesenteric vein. After that, he was started on Warfarin and required life-long anticoagulation. Following daily measurement of the calf and thigh circumference, his DVT had resolved. After discharge, life-long Warfarin was continued and he was advised to use elastic stocking. No recurrence of DVT has occurred at three and six months of follow-up. Thrombophilia studies, including lupus anticoagulant, cardiolipin antibody, antithrombin III, antinuclear antibody, factor V Leiden, and prothrombin gene mutation, were normal. However, his proteins C and S activity was low. As thrombophilia studies were done after initiating treatment, low activity level of anticoagulant proteins (proteins C and S) could be attributed to treatment with Warfarin []. OUTPUT:
PMCPatients_common3725
[ { "from": "human", "value": "As a physician engaged in 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 woman who had been diagnosed with CML 3 months prior to this encounter was treated initially with imatinib but, because of nausea and edema, had to stop therapy and was switched to nilotinib. After a few days of being on nilotinib, she presented to the emergency department at Mount Carmel West Hospital with severe, acute abdominal pain and inability to tolerate oral intake. Her vital signs on presentation showed a temperature of 99.5°F, a heart rate of 86 bpm, a respiratory rate of 20 BRPM, and a blood pressure of 147/60 mm Hg. The remainder of her physical examination revealed a soft abdomen with moderate midepigastric tenderness to palpation. Serum lipase was elevated at 81 U/L (normal 18–58). BUN (blood urea nitrogen) was elevated at 19 mg/dL. A CT scan of the abdomen with contrast showed stranding around the head of the pancreas in addition to splenic granulomata and enlarged retroperitoneal lymph nodes (Fig. ). Her lipid panel was unremarkable, with normal triglyceride levels at 60 mg/dL. She did not have any acute biliary abnormalities on magnetic resonance cholangiopancreatography. The patient was admitted and treated supportively with IV fluids and pain management. Nilotinib was discontinued after a discussion with her oncologist. The patient felt better within 3 days. The lipase level went down to 19 U/L and BUN down to 4 mg/dL. She was eventually discharged home in a stable condition. Her oncologist switched her to bosutinib (Bosulif), which has not been shown to be associated with pancreatitis.\nOUTPUT:" }, { "from": "agent", "value": "Nilotinib-Induced Acute Pancreatitis, 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 66-year-old woman who had been diagnosed with CML 3 months prior to this encounter was treated initially with imatinib but, because of nausea and edema, had to stop therapy and was switched to nilotinib. After a few days of being on nilotinib, she presented to the emergency department at Mount Carmel West Hospital with severe, acute abdominal pain and inability to tolerate oral intake. Her vital signs on presentation showed a temperature of 99.5°F, a heart rate of 86 bpm, a respiratory rate of 20 BRPM, and a blood pressure of 147/60 mm Hg. The remainder of her physical examination revealed a soft abdomen with moderate midepigastric tenderness to palpation. Serum lipase was elevated at 81 U/L (normal 18–58). BUN (blood urea nitrogen) was elevated at 19 mg/dL. A CT scan of the abdomen with contrast showed stranding around the head of the pancreas in addition to splenic granulomata and enlarged retroperitoneal lymph nodes (Fig. ). Her lipid panel was unremarkable, with normal triglyceride levels at 60 mg/dL. She did not have any acute biliary abnormalities on magnetic resonance cholangiopancreatography. The patient was admitted and treated supportively with IV fluids and pain management. Nilotinib was discontinued after a discussion with her oncologist. The patient felt better within 3 days. The lipase level went down to 19 U/L and BUN down to 4 mg/dL. She was eventually discharged home in a stable condition. Her oncologist switched her to bosutinib (Bosulif), which has not been shown to be associated with pancreatitis. OUTPUT:
PMCPatients_common3017
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 55-year-old woman with weakness, fatigue and anemia requiring transfusion monthly was referred to our hematology department for further investigation. Her hematologic parameters were as follows: white blood cell (WBC) count of 4,940/mm3, neutrophil count of 890/mm3, hemoglobin (Hb) level of 8.1 g/dL, mean corpuscular volume (MCV) of 116 fL, and platelet count of 343,000/mm3. Because her nutritional and hemolysis parameters were normal, bone marrow biopsy was performed with the provisional diagnosis of MDS. Her bone marrow aspiration showed elevated blast ratio of 10% with dismegakaryopoietic signs. Bone marrow biopsy revealed increase in the number of megakaryocytes, signs of dismegakaryopoiesis. Decitabine was started at a daily dose of 20 mg/m2 1 - 5 days and lenalidomide was started at daily doses of 10 mg 6 - 20 days in a month. After two cycles, her hemoglobin value increased and transfusion dependency ceased. After four cycles, her hematologic parameters were as follows: WBC of 5,860/mm3, neutrophil count of 1,430/mm3, Hb level of 10.5 g/dL and platelet count of 201,000/mm3. Bone marrow aspiration showed blast ratio of < 5%. Decitabine and lenalidomide were applied for three more cycles. Hemogram values after seven cycles were as follows: WBC count of 7,150/mm3, neutrophil count of 2,780/mm3, Hb level of 12.1 g/dL and platelet count of 168,000/mm3. Decitabine was terminated after seven cycles and lenalidomide has been continued for 12 months. Most recent blood values (February 2020) were as follows: WBC of 8,670/mm3, neutrophil count of 3,470/mm3, Hb level of 11.7 g/dL and platelet count of 203,000/mm3, and the patient continues to follow-up without treatment (-).\nOUTPUT:" }, { "from": "agent", "value": "Myelodysplastic Syndrome, 5q-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 55-year-old woman with weakness, fatigue and anemia requiring transfusion monthly was referred to our hematology department for further investigation. Her hematologic parameters were as follows: white blood cell (WBC) count of 4,940/mm3, neutrophil count of 890/mm3, hemoglobin (Hb) level of 8.1 g/dL, mean corpuscular volume (MCV) of 116 fL, and platelet count of 343,000/mm3. Because her nutritional and hemolysis parameters were normal, bone marrow biopsy was performed with the provisional diagnosis of MDS. Her bone marrow aspiration showed elevated blast ratio of 10% with dismegakaryopoietic signs. Bone marrow biopsy revealed increase in the number of megakaryocytes, signs of dismegakaryopoiesis. Decitabine was started at a daily dose of 20 mg/m2 1 - 5 days and lenalidomide was started at daily doses of 10 mg 6 - 20 days in a month. After two cycles, her hemoglobin value increased and transfusion dependency ceased. After four cycles, her hematologic parameters were as follows: WBC of 5,860/mm3, neutrophil count of 1,430/mm3, Hb level of 10.5 g/dL and platelet count of 201,000/mm3. Bone marrow aspiration showed blast ratio of < 5%. Decitabine and lenalidomide were applied for three more cycles. Hemogram values after seven cycles were as follows: WBC count of 7,150/mm3, neutrophil count of 2,780/mm3, Hb level of 12.1 g/dL and platelet count of 168,000/mm3. Decitabine was terminated after seven cycles and lenalidomide has been continued for 12 months. Most recent blood values (February 2020) were as follows: WBC of 8,670/mm3, neutrophil count of 3,470/mm3, Hb level of 11.7 g/dL and platelet count of 203,000/mm3, and the patient continues to follow-up without treatment (-). OUTPUT:
PMCPatients_common398
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: An 80-year-old woman was evaluated in ED for syncope that occurred while she was trying to stand up from sitting position. She denied chest pain, palpitation, headache, convulsion or incontinence. Her medical history was suggestive of hypertension, diabetes mellitus type 2, asthma and obesity grade 3. On examination, she had tachycardia 140/min, tachypnea 22/min and a normal blood pressure of 134/78 mmHg. Physical examination showed mildly tender and swollen left leg compared to the right. ECG was suggestive of sinus tachycardia with a new-onset right bundle branch block (Figure ). The patient was advised urgent coronary angiogram but she refused and declined any other invasive intervention.\\nThe Wells score was 7.5 (high-risk group; 40.6% chance of PE), the PERC rule score was 3 (cannot rule out PE). CT pulmonary angiogram was deferred in lieu of the elevated creatinine. Instead, a bedside TTE was done. It showed normal ejection fraction (EF > 55%), mildly dilated RV with reduced RVEF, elevated RV systolic pressure (>60 mmHg) and moderate tricuspid regurgitation. Hyperkinesis of the RV apex and hypokinesis of the RV free wall were also noted (McConnell's sign) (Video ).\\nWith a high suspicion of PE and McConnell’s sign on echocardiogram, she was started on heparin infusion and later shifted to oral anticoagulation. After a week, the patient was stable to be discharged. Repeat ECG before discharge was normal (Figure ).\\nMcConnell's sign along with the high Wells score justified starting and continuing anticoagulation to complete six months of therapy.\nOUTPUT:" }, { "from": "agent", "value": "Acute deep vein thrombosis, PE (Pulmonary Embolism)" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 80-year-old woman was evaluated in ED for syncope that occurred while she was trying to stand up from sitting position. She denied chest pain, palpitation, headache, convulsion or incontinence. Her medical history was suggestive of hypertension, diabetes mellitus type 2, asthma and obesity grade 3. On examination, she had tachycardia 140/min, tachypnea 22/min and a normal blood pressure of 134/78 mmHg. Physical examination showed mildly tender and swollen left leg compared to the right. ECG was suggestive of sinus tachycardia with a new-onset right bundle branch block (Figure ). The patient was advised urgent coronary angiogram but she refused and declined any other invasive intervention.\nThe Wells score was 7.5 (high-risk group; 40.6% chance of PE), the PERC rule score was 3 (cannot rule out PE). CT pulmonary angiogram was deferred in lieu of the elevated creatinine. Instead, a bedside TTE was done. It showed normal ejection fraction (EF > 55%), mildly dilated RV with reduced RVEF, elevated RV systolic pressure (>60 mmHg) and moderate tricuspid regurgitation. Hyperkinesis of the RV apex and hypokinesis of the RV free wall were also noted (McConnell's sign) (Video ).\nWith a high suspicion of PE and McConnell’s sign on echocardiogram, she was started on heparin infusion and later shifted to oral anticoagulation. After a week, the patient was stable to be discharged. Repeat ECG before discharge was normal (Figure ).\nMcConnell's sign along with the high Wells score justified starting and continuing anticoagulation to complete six months of therapy. OUTPUT:
PMCPatients_common2995
[ { "from": "human", "value": "As a physician engaged in 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 non-Hispanic white Caucasian female went for a consultation after treatment of a ductal carcinoma in situ of the breast that was positive for the estrogen and progesterone receptors. A clinical geneticist analyzed her pedigree to discover that the patient is a single child. Her daughter and son are in their twenties and are healthy. Using next generation sequencing, her genome indicated the presence of a pathogenic deletion between exons 62–63 in the ATM gene and a variant of unknown significance (c.2840T>C [p.Leu947Ser]) in the PALB2 gene. A pelvic examination including palpation revealed an adnexal mass. Diagnostic workup including computed tomography showed a complex adnexal mass that was 8 cm long () and elevated circulating levels of CA-125 (134 U/mL with a reference range of 0–35 U/mL). Differential diagnosis included endometrioma and an ovarian malignancy. Subsequently, the patient underwent complete cytoreductive surgery along with bilateral salpingo-oophorectomy, lymph node dissection, and omentectomy. The pathological results showed a stage IC clear cell carcinoma of the left ovary. Endometriosis was identified in the fallopian tubes and right ovary. Following this diagnosis, the patient received 6 cycles of adjuvant chemotherapy using a combination of carboplatin and paclitaxel. During a follow-up appointment after 32 months of treatment, the patient exhibited no symptoms of disease.\nOUTPUT:" }, { "from": "agent", "value": "Breast and Ovarian 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 50-year-old non-Hispanic white Caucasian female went for a consultation after treatment of a ductal carcinoma in situ of the breast that was positive for the estrogen and progesterone receptors. A clinical geneticist analyzed her pedigree to discover that the patient is a single child. Her daughter and son are in their twenties and are healthy. Using next generation sequencing, her genome indicated the presence of a pathogenic deletion between exons 62–63 in the ATM gene and a variant of unknown significance (c.2840T>C [p.Leu947Ser]) in the PALB2 gene. A pelvic examination including palpation revealed an adnexal mass. Diagnostic workup including computed tomography showed a complex adnexal mass that was 8 cm long () and elevated circulating levels of CA-125 (134 U/mL with a reference range of 0–35 U/mL). Differential diagnosis included endometrioma and an ovarian malignancy. Subsequently, the patient underwent complete cytoreductive surgery along with bilateral salpingo-oophorectomy, lymph node dissection, and omentectomy. The pathological results showed a stage IC clear cell carcinoma of the left ovary. Endometriosis was identified in the fallopian tubes and right ovary. Following this diagnosis, the patient received 6 cycles of adjuvant chemotherapy using a combination of carboplatin and paclitaxel. During a follow-up appointment after 32 months of treatment, the patient exhibited no symptoms of disease. OUTPUT:
PMCPatients_common3589
[ { "from": "human", "value": "As a physician engaged in 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 complained of paresthesia of both thighs for 1 year. He received transforaminal epidural steroid injection (TFESI) around/into bilateral L5 and S1 nerve roots under the impression of bilateral lumbosacral radiculopathies at his community hospital on January 10, 2015. At each site, a 5-mL mixture of dexamethasone (1.25 mg), lidocaine, bupivacaine, and normal saline was injected. On the next day (January 11, 2015), SDAVFs were revealed by magnetic resonance imaging (MRI) (). Because his symptoms persisted after intravenous steroid therapy, he was transferred to our hospital on January 12, 2015. On physical examination performed in the emergency room, the strength of both lower extremities was 0/5 in the manual muscle test. During sensory evaluation, decreased light touch and pain sensations were identified below the bilateral T11 level. He experienced urinary and fecal incontinence. Contraction of the anal sphincter was absent. Careful history taking revealed a history of voiding difficulty (need for abdominal straining during voiding) for more than one year. While reviewing his initial MRI taken before TFESI (January 9, 2015), tortuous fluid void structures, which were missed before ESI, were noted above the L1 vertebral level (). On spinal angiography, SDAVFs supplied by the right T6 intercostal artery were noted (). After glue embolization of SDAVFs at the right T6 level, motor and sensory functions started to improve. On the day of discharge (February 24, 2015), the strength of both lower extremities was improved to 4/5–5/5. However, he was on intermittent catheterization as he could not self-void till that time. When he was followed up after 1 year, it was observed that gait disturbance and failure to void persisted.\nOUTPUT:" }, { "from": "agent", "value": "Spinal Dural Arteriovenous Fistulas, Acute Paraplegia" } ]
As a physician engaged 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 complained of paresthesia of both thighs for 1 year. He received transforaminal epidural steroid injection (TFESI) around/into bilateral L5 and S1 nerve roots under the impression of bilateral lumbosacral radiculopathies at his community hospital on January 10, 2015. At each site, a 5-mL mixture of dexamethasone (1.25 mg), lidocaine, bupivacaine, and normal saline was injected. On the next day (January 11, 2015), SDAVFs were revealed by magnetic resonance imaging (MRI) (). Because his symptoms persisted after intravenous steroid therapy, he was transferred to our hospital on January 12, 2015. On physical examination performed in the emergency room, the strength of both lower extremities was 0/5 in the manual muscle test. During sensory evaluation, decreased light touch and pain sensations were identified below the bilateral T11 level. He experienced urinary and fecal incontinence. Contraction of the anal sphincter was absent. Careful history taking revealed a history of voiding difficulty (need for abdominal straining during voiding) for more than one year. While reviewing his initial MRI taken before TFESI (January 9, 2015), tortuous fluid void structures, which were missed before ESI, were noted above the L1 vertebral level (). On spinal angiography, SDAVFs supplied by the right T6 intercostal artery were noted (). After glue embolization of SDAVFs at the right T6 level, motor and sensory functions started to improve. On the day of discharge (February 24, 2015), the strength of both lower extremities was improved to 4/5–5/5. However, he was on intermittent catheterization as he could not self-void till that time. When he was followed up after 1 year, it was observed that gait disturbance and failure to void persisted. OUTPUT:
PMCPatients_common2890
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 59-year-old woman was admitted to her reference hospital for dyspnea. Chest radiography showed a severe right pleural effusion. The patient did not have other diseases or congenital malformations and had not required previous abdominal or thoracic surgeries. The last normal follow-up was 2 months prior to her admission for the dyspnea. A thoracic tube was inserted, and 1,000 cc of pleural fluid was drained. After cytology revealed the presence of malignant breast cells, right-sided talc pleurodesis was performed. The patient had a good postoperative evolution, without fever or pain, and was discharged four days after the talc pleurodesis.\\nThe patient came to our center for oncological treatment. ). The patient was asymptomatic, without fever, abdominal pain or abnormal laboratory tests. Hormonal treatment (exemestane) was started. A new CT scan was performed one month later. without any tumor progression at distal sites. Laboratory analysis yielded the following values: bilirubin 1.66 mg/dL; GOT 146 UI/L; GPT 112 UI/L; LDH 2,934 UI/L; GGT 1,405 UI/L; and alkaline phosphatase 1,383 UI/L. An initial cycle of 50 mg/m2 doxorubicin hydrochloride and 500 mg/m2 cyclophosphamide was administered.\nOUTPUT:" }, { "from": "agent", "value": "Hepatic breast cancer dissemination, Metastatic breast cancer, Hepatic 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 59-year-old woman was admitted to her reference hospital for dyspnea. Chest radiography showed a severe right pleural effusion. The patient did not have other diseases or congenital malformations and had not required previous abdominal or thoracic surgeries. The last normal follow-up was 2 months prior to her admission for the dyspnea. A thoracic tube was inserted, and 1,000 cc of pleural fluid was drained. After cytology revealed the presence of malignant breast cells, right-sided talc pleurodesis was performed. The patient had a good postoperative evolution, without fever or pain, and was discharged four days after the talc pleurodesis.\nThe patient came to our center for oncological treatment. ). The patient was asymptomatic, without fever, abdominal pain or abnormal laboratory tests. Hormonal treatment (exemestane) was started. A new CT scan was performed one month later. without any tumor progression at distal sites. Laboratory analysis yielded the following values: bilirubin 1.66 mg/dL; GOT 146 UI/L; GPT 112 UI/L; LDH 2,934 UI/L; GGT 1,405 UI/L; and alkaline phosphatase 1,383 UI/L. An initial cycle of 50 mg/m2 doxorubicin hydrochloride and 500 mg/m2 cyclophosphamide was administered. OUTPUT:
PMCPatients_common4234
[ { "from": "human", "value": "As a physician engaged 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 favorable mitral valve anatomy []. This was confirmed on three-dimensional (3-D) imaging and color-flow Doppler revealed the absence of an interatrial shunt []. It was recognized that the standard transseptal puncture for MitraClip in the superior aspect of the septum would be challenging in the presence of a closure device, and evidence of thrombus would be a contraindication to MitraClip procedure. The decision was made to proceed with MitraClip placement.\\nLA catheterization under general anesthesia was performed by a careful posterior-inferior transseptal puncture using a BRK-1 Transseptal Needle (St. Jude Medical, Inc., St. Paul, Minnesota, USA) under TEE guidance, entering the LA inferior to the interatrial mass. Despite a lower entry point on the interatrial septum, there was ~4 cm of height above the mitral annulus as the LA chamber was severely enlarged. The 22F MitraClip sheath and the delivery system were then advanced into the LA [Figures and ]. The MitraClip was successfully placed with mild residual MR and a normal gradient across mitral valve [].\nOUTPUT:" }, { "from": "agent", "value": "Severe primary MR, Pulmonary hypertension, Excess atrial septal tissue in the region of foramen ovale" } ]
As a physician engaged 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 favorable mitral valve anatomy []. This was confirmed on three-dimensional (3-D) imaging and color-flow Doppler revealed the absence of an interatrial shunt []. It was recognized that the standard transseptal puncture for MitraClip in the superior aspect of the septum would be challenging in the presence of a closure device, and evidence of thrombus would be a contraindication to MitraClip procedure. The decision was made to proceed with MitraClip placement.\nLA catheterization under general anesthesia was performed by a careful posterior-inferior transseptal puncture using a BRK-1 Transseptal Needle (St. Jude Medical, Inc., St. Paul, Minnesota, USA) under TEE guidance, entering the LA inferior to the interatrial mass. Despite a lower entry point on the interatrial septum, there was ~4 cm of height above the mitral annulus as the LA chamber was severely enlarged. The 22F MitraClip sheath and the delivery system were then advanced into the LA [Figures and ]. The MitraClip was successfully placed with mild residual MR and a normal gradient across mitral valve []. OUTPUT:
PMCPatients_common321
[ { "from": "human", "value": "As a physician engaged 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 admission, chest X-ray, esophagogram and direct laryngoscopy were performed with negative results. Despite antibiotic therapy (amoxicillin + clavulanic acid) fever developed after 6 days with elevated C-reactive protein (CRP) (38 mg/L), and chest radiography showed atelectasis with pneumonia of the right lower lobe. During bronchoscopy no sign of a foreign body was found, and according to bacteriological culturing of bronchial lavage, antibiotic therapy was completed with netilmycin. Physiotherapy, bronchodilators, expectorants, and inhalation were applied with switching of antibiotic therapy (to trimethoprim/sulfamethoxazole and cefuroxime). One month after the incident the patient was discharged with normal blood work, and chest radiography showing decreased signs of pleuropneumonia. During the next 5 months applied conservative treatment proved ineffective for recurring symptoms. Nine months after the accident, control bronchoscopy revealed signs of inflammation in the right lower bronchi with huge amounts of secretion. Due to recurrent symptoms and confirmation of chronic pneumonia, surgery was decided. After posterolateral thoracotomy, severe adhesions were found between the chest wall and the right lower- and middle lobe, with inflamed hilar lymph nodes. After an uneventful postoperative period, the asymptomatic patient was discharged on the 13th postoperative day.\nOUTPUT:" }, { "from": "agent", "value": "Awn aspiration, Bronchopleural fistula, Bronchiectasis" } ]
As a physician engaged 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 admission, chest X-ray, esophagogram and direct laryngoscopy were performed with negative results. Despite antibiotic therapy (amoxicillin + clavulanic acid) fever developed after 6 days with elevated C-reactive protein (CRP) (38 mg/L), and chest radiography showed atelectasis with pneumonia of the right lower lobe. During bronchoscopy no sign of a foreign body was found, and according to bacteriological culturing of bronchial lavage, antibiotic therapy was completed with netilmycin. Physiotherapy, bronchodilators, expectorants, and inhalation were applied with switching of antibiotic therapy (to trimethoprim/sulfamethoxazole and cefuroxime). One month after the incident the patient was discharged with normal blood work, and chest radiography showing decreased signs of pleuropneumonia. During the next 5 months applied conservative treatment proved ineffective for recurring symptoms. Nine months after the accident, control bronchoscopy revealed signs of inflammation in the right lower bronchi with huge amounts of secretion. Due to recurrent symptoms and confirmation of chronic pneumonia, surgery was decided. After posterolateral thoracotomy, severe adhesions were found between the chest wall and the right lower- and middle lobe, with inflamed hilar lymph nodes. After an uneventful postoperative period, the asymptomatic patient was discharged on the 13th postoperative day. OUTPUT:
PMCPatients_common2666
[ { "from": "human", "value": "As a physician engaged in 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 presented with a non tender hard atrophic left testicle. The rest of the examination was normal. There had been no previous scrotal surgery or trauma.\\nTumour markers including lactate dehydrogenase (LDH), human chorionic gonadotrophin (HCG), alpha fetoprotein (AFP) and prostate specific antigen (PSA) were normal. His total white cell count was normal. An ultrasound of the scrotum demonstrated a localised tumour of the testis. Chest x-ray was normal. A standard left radical orchidectomy was performed by the inguinal approach. The tumour appeared to be confined to the upper pole of the testis and was clinically described as T1 or T2. Macroscopic histological examination suggested no involvement of the tunica albuginea, epididymis or spermatic cord. Tumour involved the tunica albuginea but did not extend through it. There was no vascular invasion. (Fig ). Other structures in the spermatic cord were not involved.\\nA post operative CT scan demonstrated two separate masses. A 2.8 cm by 2.3 cm central abdominal mesenteric mass and a 7.6 cm by 5.4 cm irregular heterogeneous lobulated soft tissue mass within the pelvis arising from the prostate and extending into the mesorectal fascia. There were no enlarged retroperitoneal, pelvic, inguinal or thoracic lymph nodes. (Fig and ). The chest CT scan was normal. The patient has received chemotherapy and is currently under follow up according to standard EUA guidelines. There is no evidence of residual or recurrent disease. The CT scan performed after completion of the course of chemotherapy demonstrated complete resolution of the two metastatic masses. (Fig and ).\nOUTPUT:" }, { "from": "agent", "value": "Testicular seminoma" } ]
As a physician engaged 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 presented with a non tender hard atrophic left testicle. The rest of the examination was normal. There had been no previous scrotal surgery or trauma.\nTumour markers including lactate dehydrogenase (LDH), human chorionic gonadotrophin (HCG), alpha fetoprotein (AFP) and prostate specific antigen (PSA) were normal. His total white cell count was normal. An ultrasound of the scrotum demonstrated a localised tumour of the testis. Chest x-ray was normal. A standard left radical orchidectomy was performed by the inguinal approach. The tumour appeared to be confined to the upper pole of the testis and was clinically described as T1 or T2. Macroscopic histological examination suggested no involvement of the tunica albuginea, epididymis or spermatic cord. Tumour involved the tunica albuginea but did not extend through it. There was no vascular invasion. (Fig ). Other structures in the spermatic cord were not involved.\nA post operative CT scan demonstrated two separate masses. A 2.8 cm by 2.3 cm central abdominal mesenteric mass and a 7.6 cm by 5.4 cm irregular heterogeneous lobulated soft tissue mass within the pelvis arising from the prostate and extending into the mesorectal fascia. There were no enlarged retroperitoneal, pelvic, inguinal or thoracic lymph nodes. (Fig and ). The chest CT scan was normal. The patient has received chemotherapy and is currently under follow up according to standard EUA guidelines. There is no evidence of residual or recurrent disease. The CT scan performed after completion of the course of chemotherapy demonstrated complete resolution of the two metastatic masses. (Fig and ). OUTPUT:
PMCPatients_common3032
[ { "from": "human", "value": "As a physician engaged 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 March 19 (at 9 p.m.) upon arrival, he was fully conscious but complained of severe RLQ pain and tenderness. He had no respiratory symptoms or fever.\\nHe had hypertension, diabetes mellitus, hyperlipidemia, and chronic kidney disease.\\nThe patient’s wife had been diagnosed with COVID-19 10 d earlier, and the patient was in close contact with her. The patient tested negative twice (10 and 8 d earlier) in upper respiratory COVID-19 RT-PCR screens performed at the public health center.\\nHe had localized tenderness in the RLQ.\\nHis vital signs were as follows: Blood pressure, 150/80 mmHg; heart rate, 80 beats/min; respiratory rate, 20/min; and body temperature, 37.2 °C. Laboratory data showed a significant white blood cell count of 8.8 × 109 cells/L, containing 72.7% neutrophils. Both the C-reactive protein level and erythrocyte sedimentation rates were elevated: 6.5 mg/L (reference: < 0.5 mg/dL) and 48 mm/h (reference: 0–10 mm/h), respectively. The coagulation test results were normal.\\nThe patient had no respiratory symptoms, but COVID-19 RT-PCR screening and radiography of the chest were performed outside the ER according to the ER policy. The chest radiograph showed ground-glass opacity in the right upper lobe; therefore, the patient was immediately moved to an isolation room (Figure ). Contrast-enhanced chest computed tomography (CT) revealed patchy ground-glass opacity in both upper lobes (Figure ).\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: On March 19 (at 9 p.m.) upon arrival, he was fully conscious but complained of severe RLQ pain and tenderness. He had no respiratory symptoms or fever.\nHe had hypertension, diabetes mellitus, hyperlipidemia, and chronic kidney disease.\nThe patient’s wife had been diagnosed with COVID-19 10 d earlier, and the patient was in close contact with her. The patient tested negative twice (10 and 8 d earlier) in upper respiratory COVID-19 RT-PCR screens performed at the public health center.\nHe had localized tenderness in the RLQ.\nHis vital signs were as follows: Blood pressure, 150/80 mmHg; heart rate, 80 beats/min; respiratory rate, 20/min; and body temperature, 37.2 °C. Laboratory data showed a significant white blood cell count of 8.8 × 109 cells/L, containing 72.7% neutrophils. Both the C-reactive protein level and erythrocyte sedimentation rates were elevated: 6.5 mg/L (reference: < 0.5 mg/dL) and 48 mm/h (reference: 0–10 mm/h), respectively. The coagulation test results were normal.\nThe patient had no respiratory symptoms, but COVID-19 RT-PCR screening and radiography of the chest were performed outside the ER according to the ER policy. The chest radiograph showed ground-glass opacity in the right upper lobe; therefore, the patient was immediately moved to an isolation room (Figure ). Contrast-enhanced chest computed tomography (CT) revealed patchy ground-glass opacity in both upper lobes (Figure ). OUTPUT:
PMCPatients_common3280
[ { "from": "human", "value": "As a physician engaged 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 continued the treatment for 1½ year. After that, planned for a baby and stopped the medication with the advice of the therapist. She would remain to preoccupy that “how she will cope with labor and childbirth” and would have “baichani” and palpitation which would persist most of the day. She consulted an obstetrician, clinical examination and blood investigations, including thyroid profile, ultrasound, electrocardiogramand vitals, including blood pressure, were within normal limit. Following which, visited psychiatry outpatient department. Pharmacological and nonpharmacological therapy were offered and explained the pros and cons of the drugs.\\nPatient and family member opted for the Biofeedback therapy and breathing exercise. Biofeedback therapy sessions were started with regular monitoring of severity of symptoms on GAD-7 and clinically. Initially, 2–3 session/week, 30–45 min, were given for 3 weeks and had 60%–70% (GAD-7 score came down from 13 to 7) improvement. Gradually, frequency of session reduced to 1/week and had complete improvement in 2 months (GAD Score was 3). Thereafter, she would visit 1–2 times/month and delivered a normal baby at the full term by normal vaginal delivery without any adverse consequences.\nOUTPUT:" }, { "from": "agent", "value": "Panic disorder, Anxiety disorder" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: She continued the treatment for 1½ year. After that, planned for a baby and stopped the medication with the advice of the therapist. She would remain to preoccupy that “how she will cope with labor and childbirth” and would have “baichani” and palpitation which would persist most of the day. She consulted an obstetrician, clinical examination and blood investigations, including thyroid profile, ultrasound, electrocardiogramand vitals, including blood pressure, were within normal limit. Following which, visited psychiatry outpatient department. Pharmacological and nonpharmacological therapy were offered and explained the pros and cons of the drugs.\nPatient and family member opted for the Biofeedback therapy and breathing exercise. Biofeedback therapy sessions were started with regular monitoring of severity of symptoms on GAD-7 and clinically. Initially, 2–3 session/week, 30–45 min, were given for 3 weeks and had 60%–70% (GAD-7 score came down from 13 to 7) improvement. Gradually, frequency of session reduced to 1/week and had complete improvement in 2 months (GAD Score was 3). Thereafter, she would visit 1–2 times/month and delivered a normal baby at the full term by normal vaginal delivery without any adverse consequences. OUTPUT:
PMCPatients_common3892
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 19-year-old male was admitted to the ICU about 24 h after having ingested 30 tablets each of amlodipine 5 mg and atenolol 25 mg. He was resuscitated in another hospital before the transfer.\\nOn arrival to the ICU, he was on high dose of multiple vasopressors (noradrenaline, adrenaline, dopamine, and vasopressin) and had a temporary transvenous pacer in situ. His HR was 78/min, in sinus rhythm and well above the pacing rate; BP was 90/50 mmHg; SpO2 98% on 40% FiO2; and central venous pressure was 24 mmHg with cold peripheries. Echocardiogram showed normal LV function. Baseline ABG showed metabolic acidosis with a pH of 7.16 and lactate level of 4.59 mmol/dL. He was resuscitated with standard doses of IV calcium gluconate, intralipid insulin, glucagon, and sodium bicarbonate []. Despite 14 h of aggressive resuscitation, his vasopressor requirements increased and his shock worsened leading to initiation of a peripheral VA ECMO. The cannulation technique was similar to that used for case 1 and the ECMO flow was set at 4 L/min. Over the next 24 h, his vasopressor requirements reduced significantly [] and he was completely weaned off vasopressor support. Urine output and lactate levels improved immediately. By the 4th day, the calcium, insulin, and glucagon infusions were sequentially stopped. ECMO was decannulated on the 5th day, and he was extubated on the 6th day. However, on the 7th day, he developed swelling and tenderness in the left lower limb over the arterial cannulation site, requiring fasciotomy for impending compartment syndrome. He responded well to treatment and was moved out of ICU on the 13th day.\nOUTPUT:" }, { "from": "agent", "value": "Drug Overdose" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 19-year-old male was admitted to the ICU about 24 h after having ingested 30 tablets each of amlodipine 5 mg and atenolol 25 mg. He was resuscitated in another hospital before the transfer.\nOn arrival to the ICU, he was on high dose of multiple vasopressors (noradrenaline, adrenaline, dopamine, and vasopressin) and had a temporary transvenous pacer in situ. His HR was 78/min, in sinus rhythm and well above the pacing rate; BP was 90/50 mmHg; SpO2 98% on 40% FiO2; and central venous pressure was 24 mmHg with cold peripheries. Echocardiogram showed normal LV function. Baseline ABG showed metabolic acidosis with a pH of 7.16 and lactate level of 4.59 mmol/dL. He was resuscitated with standard doses of IV calcium gluconate, intralipid insulin, glucagon, and sodium bicarbonate []. Despite 14 h of aggressive resuscitation, his vasopressor requirements increased and his shock worsened leading to initiation of a peripheral VA ECMO. The cannulation technique was similar to that used for case 1 and the ECMO flow was set at 4 L/min. Over the next 24 h, his vasopressor requirements reduced significantly [] and he was completely weaned off vasopressor support. Urine output and lactate levels improved immediately. By the 4th day, the calcium, insulin, and glucagon infusions were sequentially stopped. ECMO was decannulated on the 5th day, and he was extubated on the 6th day. However, on the 7th day, he developed swelling and tenderness in the left lower limb over the arterial cannulation site, requiring fasciotomy for impending compartment syndrome. He responded well to treatment and was moved out of ICU on the 13th day. OUTPUT:
PMCPatients_common2398
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 53-year-old woman presented with an open wound on the left lower leg. It was a de-epithelized abrasion and its size was about 3.5 × 1.5 cm2 (Figure A). The patient had no notable medical history. She works as a janitor, and was cleaning the floor of the building, when she spilled undiluted cleansing solution that consisted of sodium hypochlorite (NaClO) on her left lower leg. After the accident, an abrasion was noted on that area and she visited her local dermatologic clinic for treatment on the very next day. At the clinic, she received HeNe laser therapy directly to the wound daily for 10 days. The treatment continued for 8 to 9 minutes on each occasion. However, we were unable to determine the details of laser therapy, such as power, wavelength, and so on. The treatment was not beneficial and the wound size was constant. The patient visited our clinic three weeks after the injury and we planned an excision of the unhealed area under the local anesthesia.\\nDuring the first operation, the open wound was excised and primary repair was done (Figure B). We planned a second operation and evaluated positron emission tomography–computed tomography for metastatic lesions before the second operation. After confirming that there was no metastasis, the patient received a second operation 3 weeks from the first. Wide excision was done with a 2 to 3 cm safe margin (Figure A). During the operation, the resection margin including the tumor base was free from tumors, as demonstrated by a frozen study. The total defect size of the left lower leg measured 9 × 7 cm2 and the defect was successfully reconstructed with a thoracodorsal artery perforator free flap transfer (Figure B,C). Microanastomosis was achieved, using the anterior tibial artery and its accompanying vein as recipient vessels. The patient recovered without complication. After 3 months, the transferred flap was well taken with a good contour (Figure ).\nOUTPUT:" }, { "from": "agent", "value": "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 53-year-old woman presented with an open wound on the left lower leg. It was a de-epithelized abrasion and its size was about 3.5 × 1.5 cm2 (Figure A). The patient had no notable medical history. She works as a janitor, and was cleaning the floor of the building, when she spilled undiluted cleansing solution that consisted of sodium hypochlorite (NaClO) on her left lower leg. After the accident, an abrasion was noted on that area and she visited her local dermatologic clinic for treatment on the very next day. At the clinic, she received HeNe laser therapy directly to the wound daily for 10 days. The treatment continued for 8 to 9 minutes on each occasion. However, we were unable to determine the details of laser therapy, such as power, wavelength, and so on. The treatment was not beneficial and the wound size was constant. The patient visited our clinic three weeks after the injury and we planned an excision of the unhealed area under the local anesthesia.\nDuring the first operation, the open wound was excised and primary repair was done (Figure B). We planned a second operation and evaluated positron emission tomography–computed tomography for metastatic lesions before the second operation. After confirming that there was no metastasis, the patient received a second operation 3 weeks from the first. Wide excision was done with a 2 to 3 cm safe margin (Figure A). During the operation, the resection margin including the tumor base was free from tumors, as demonstrated by a frozen study. The total defect size of the left lower leg measured 9 × 7 cm2 and the defect was successfully reconstructed with a thoracodorsal artery perforator free flap transfer (Figure B,C). Microanastomosis was achieved, using the anterior tibial artery and its accompanying vein as recipient vessels. The patient recovered without complication. After 3 months, the transferred flap was well taken with a good contour (Figure ). OUTPUT:
PMCPatients_common2909
[ { "from": "human", "value": "As a physician engaged in 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 woman presented with a slowly growing vulvar mass with pruritus. Two years prior to presentation, she noted a painless red firm nodule on her vulva. Subsequently, erythema around the nodule appeared. The nodule and erythema had gradually enlarged during the 2-year period. Physical examination revealed a 2 cm × 2 cm × 2 cm slightly erosive, nodular red firm mass on the centre of 5 cm × 7 cm area of irregular eczematoid erythema covering her mons pubis (Fig.). There was no swelling of lymph nodes in bilateral groins. Biopsy of inguinal lymph node was negative. The complete mass and part of the erythema were excised for histological evaluation. The patient's medical history was unremarkable. Metastasis from other cancers was excluded by routine blood tests, cystoscopy, oesophagogastroduodenoscopy, colonoscopy, abdominopelvic computed tomography (CT), chest radiography and positron emission tomography-CT. All these examinations were normal. At 3-month follow-up, the patient had local mass recurrence and non-palpable inguinal lymph nodes.\\nHematoxylin and Eosin staining of the biopsy from the lesion showed large round cells with ample pale-staining cytoplasm, pleomorphic nuclei, and occasional prominent nucleoli infiltrating throughout the epidermis, indicative of Paget cells (Fig. ). This carcinoma spread dermal, and a poorly differentiated adenocarcinoma was present in the dermis.(Fig. ). Immunohistochemical stainings for gross cystic disease fluid protein-15 (GCDFP-15) (Fig. ), cytokeratin7(CK7) (Fig. ), cytokeratin 19 (CK19) and carcinoembryonic antigen (CEA) were strongly positive. Epithelial membrane antigen (EMA) was positive, while S-100 protein, bcl-2 and CK20 (Fig. ) were all negative. Neoplastic cells were positive for periodic acid-Schiff (PAS). Moreover, the Paget cells and low-differentiated adenocarcinoma shared common immunohistological features. These immunohistochemical appearances supported the diagnosis of EMPD.\nOUTPUT:" }, { "from": "agent", "value": "Extramammary Paget'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 66-year-old Chinese woman presented with a slowly growing vulvar mass with pruritus. Two years prior to presentation, she noted a painless red firm nodule on her vulva. Subsequently, erythema around the nodule appeared. The nodule and erythema had gradually enlarged during the 2-year period. Physical examination revealed a 2 cm × 2 cm × 2 cm slightly erosive, nodular red firm mass on the centre of 5 cm × 7 cm area of irregular eczematoid erythema covering her mons pubis (Fig.). There was no swelling of lymph nodes in bilateral groins. Biopsy of inguinal lymph node was negative. The complete mass and part of the erythema were excised for histological evaluation. The patient's medical history was unremarkable. Metastasis from other cancers was excluded by routine blood tests, cystoscopy, oesophagogastroduodenoscopy, colonoscopy, abdominopelvic computed tomography (CT), chest radiography and positron emission tomography-CT. All these examinations were normal. At 3-month follow-up, the patient had local mass recurrence and non-palpable inguinal lymph nodes.\nHematoxylin and Eosin staining of the biopsy from the lesion showed large round cells with ample pale-staining cytoplasm, pleomorphic nuclei, and occasional prominent nucleoli infiltrating throughout the epidermis, indicative of Paget cells (Fig. ). This carcinoma spread dermal, and a poorly differentiated adenocarcinoma was present in the dermis.(Fig. ). Immunohistochemical stainings for gross cystic disease fluid protein-15 (GCDFP-15) (Fig. ), cytokeratin7(CK7) (Fig. ), cytokeratin 19 (CK19) and carcinoembryonic antigen (CEA) were strongly positive. Epithelial membrane antigen (EMA) was positive, while S-100 protein, bcl-2 and CK20 (Fig. ) were all negative. Neoplastic cells were positive for periodic acid-Schiff (PAS). Moreover, the Paget cells and low-differentiated adenocarcinoma shared common immunohistological features. These immunohistochemical appearances supported the diagnosis of EMPD. OUTPUT:
PMCPatients_common3204
[ { "from": "human", "value": "As a physician engaged 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 exam the patient was noted to be pulseless and apneic. After resuscitation, initiation of a mass transfusion protocol and return of spontaneous circulation, the patient was GCS 11 (E4V1TM6) and was noted to have no movement in any extremities. The patient was noted to have serosanginous drainage from the neck wound consistent with a CSF leak. After an unsuccessful trail of conservative management, a lumbar drain was placed and confirmed with fluoroscopic guidance without CSF egress. A magnetic resonance imaging (MRI) scan of the cervical spine was obtained which demonstrated a pronounced CSF fistula and a complete obstruction of the CSF space at the C3–6 levels ().\\nAn EVD was placed in the intensive care unit after informed consent was obtained. The EVD was placed under sterile conditions using local anesthesia consisting of lidocaine with 1% epinepherine and mild conscious sedation consisting of 5 mg of diazepam, and 2 mg of morphine. Ten milliliter of CSF was drained every hour. The EVD was exchanged on Day 14 as customary at our institution due minimal but persistent CSF leak. CSF diversion was continued for a total of 25 days due to the large size of the wound and the initial partial closure. The external drain was removed after a successful 48-hour clamp trial. There were no complications associated with the csf diversion. The patient remained free of CSF leak at 1 year follow-up. Dynamic cervical films revealed no gross instability and the patient remained ASIA A on ventilatory support.\nOUTPUT:" }, { "from": "agent", "value": "Cerebrospinal fluid leak, gunshot wound through the left face and neck, left C2–3 facet fracture, left vertebral artery dissection, left internal and external carotid artery transections." } ]
As a physician engaged 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 exam the patient was noted to be pulseless and apneic. After resuscitation, initiation of a mass transfusion protocol and return of spontaneous circulation, the patient was GCS 11 (E4V1TM6) and was noted to have no movement in any extremities. The patient was noted to have serosanginous drainage from the neck wound consistent with a CSF leak. After an unsuccessful trail of conservative management, a lumbar drain was placed and confirmed with fluoroscopic guidance without CSF egress. A magnetic resonance imaging (MRI) scan of the cervical spine was obtained which demonstrated a pronounced CSF fistula and a complete obstruction of the CSF space at the C3–6 levels ().\nAn EVD was placed in the intensive care unit after informed consent was obtained. The EVD was placed under sterile conditions using local anesthesia consisting of lidocaine with 1% epinepherine and mild conscious sedation consisting of 5 mg of diazepam, and 2 mg of morphine. Ten milliliter of CSF was drained every hour. The EVD was exchanged on Day 14 as customary at our institution due minimal but persistent CSF leak. CSF diversion was continued for a total of 25 days due to the large size of the wound and the initial partial closure. The external drain was removed after a successful 48-hour clamp trial. There were no complications associated with the csf diversion. The patient remained free of CSF leak at 1 year follow-up. Dynamic cervical films revealed no gross instability and the patient remained ASIA A on ventilatory support. OUTPUT:
PMCPatients_common2480
[ { "from": "human", "value": "As a physician engaged 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 presented to our trauma center with tetraparesis, with upper extremity weakness predominating. He had significant hyperpathia with associated severe neck and back pain, in addition to urinary retention. Significant sensory deficits were present from his upper torso to the plantar regions of his feet bilaterally. Bilateral Hoffman’s sign was present, in addition to brisk lower extremity reflexes. A concerning lucency through a syndesmophyte at C6-7 was present (Figure ).\\nMRI of the cervical spine revealed an acute spinal cord injury at C3-4, which was the level of the large posterior osteophyte complex (Figure ).\\nNo thoracic or lumbar spine fractures were noted. Upon admission to the surgical intensive care unit, he was started on a methylprednisolone drip. The patient’s upper extremity function continued to decline, and we opted to intervene with surgical intervention. We performed a C3-6 decompressive laminectomy, with C2 pars screws, and C3-7 lateral mass screws. Intraoperatively, there was evident hypermobility between C3 and C4. Obvious distraction was visualized between the right C3 inferior articulating process and C4 superior articulating process. Postoperative CT and MRI scans showed adequate hardware placement (Figure ).\\nSince surgery, the patient has had a steady progressive improvement in neurological function and is currently ambulating with good functional use of his upper extremities.\nOUTPUT:" }, { "from": "agent", "value": "Central Cord Syndrome, Diffuse Idiopathic Skeletal Hyperostosis, Ossification of the Posterior Longitudinal Ligament" } ]
As a physician engaged 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 presented to our trauma center with tetraparesis, with upper extremity weakness predominating. He had significant hyperpathia with associated severe neck and back pain, in addition to urinary retention. Significant sensory deficits were present from his upper torso to the plantar regions of his feet bilaterally. Bilateral Hoffman’s sign was present, in addition to brisk lower extremity reflexes. A concerning lucency through a syndesmophyte at C6-7 was present (Figure ).\nMRI of the cervical spine revealed an acute spinal cord injury at C3-4, which was the level of the large posterior osteophyte complex (Figure ).\nNo thoracic or lumbar spine fractures were noted. Upon admission to the surgical intensive care unit, he was started on a methylprednisolone drip. The patient’s upper extremity function continued to decline, and we opted to intervene with surgical intervention. We performed a C3-6 decompressive laminectomy, with C2 pars screws, and C3-7 lateral mass screws. Intraoperatively, there was evident hypermobility between C3 and C4. Obvious distraction was visualized between the right C3 inferior articulating process and C4 superior articulating process. Postoperative CT and MRI scans showed adequate hardware placement (Figure ).\nSince surgery, the patient has had a steady progressive improvement in neurological function and is currently ambulating with good functional use of his upper extremities. OUTPUT:
PMCPatients_common968
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 73-year-old Caucasian male was admitted to our hospital with acute intestinal obstruction. Computed tomography (CT) of the abdomen showed left-sided obstructive colon tumor, retroperitoneal nodes, liver metastases, and inferior vena cava thrombosis. The tumor marker carcinoembryonic antigen was elevated (308 µg/L); other tumor markers were normal. An urgent colonoscopy was rendered. Colonoscopy reported an occlusive lesion at 30 cm from the anal verge. It was biopsied and a self-expandable metal stent was placed. The biopsy reported an adenocarcinoma. No RAS gene mutation or BRAF (v-raf murine sarcoma viral oncogene homolog B1) mutation was found.\\nDuring the hospital stay, the patient also complained of a painless purple-shiny bump, located in his left leg. It appeared six months ago and had been growing larger. The biopsy confirmed the diagnosis of MCC. The administration frequency was every two weeks.\\nAfter six cycles, body CT showed a partial response of the colon, liver, and retroperitoneal lesions. Besides, it was remarkable that the MCC was significantly reduced in size and it had changed colour (from purple to light pink).\\nThe following reviews of CT described stable disease. A progression-free survival of >one year has been achieved. On the other hand, the MCC lesion continues to get smaller and flattened and it has practically disappeared (Figure ).\nOUTPUT:" }, { "from": "agent", "value": "Merkel Cell Carcinoma, Colorectal 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 73-year-old Caucasian male was admitted to our hospital with acute intestinal obstruction. Computed tomography (CT) of the abdomen showed left-sided obstructive colon tumor, retroperitoneal nodes, liver metastases, and inferior vena cava thrombosis. The tumor marker carcinoembryonic antigen was elevated (308 µg/L); other tumor markers were normal. An urgent colonoscopy was rendered. Colonoscopy reported an occlusive lesion at 30 cm from the anal verge. It was biopsied and a self-expandable metal stent was placed. The biopsy reported an adenocarcinoma. No RAS gene mutation or BRAF (v-raf murine sarcoma viral oncogene homolog B1) mutation was found.\nDuring the hospital stay, the patient also complained of a painless purple-shiny bump, located in his left leg. It appeared six months ago and had been growing larger. The biopsy confirmed the diagnosis of MCC. The administration frequency was every two weeks.\nAfter six cycles, body CT showed a partial response of the colon, liver, and retroperitoneal lesions. Besides, it was remarkable that the MCC was significantly reduced in size and it had changed colour (from purple to light pink).\nThe following reviews of CT described stable disease. A progression-free survival of >one year has been achieved. On the other hand, the MCC lesion continues to get smaller and flattened and it has practically disappeared (Figure ). OUTPUT:
PMCPatients_common133
[ { "from": "human", "value": "As a physician engaged 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 past medical history included chronic obstructive airways disease, hypertension, and diabetes mellitus. The patient is a current smoker, with a history of 20 pack-years. Preoperative chest radiography, electrocardiogram, full blood count, and serum biochemistry were within the normal range. After being diagnosed with SCC as a result of incisional biopsy, the patient underwent the resection of SCC on the right buccal mucosa of the mandible, modified radical neck dissection, and primary reconstruction with a fibula-free flap. Tourniquet pressure was 300 mm/Hg, and its application time was 60 min. Total on-table time was approximately 7 h. Upon admission to the SICU after the 7-h operation, hypothermia and hypotension were noted. On the first postoperative day, the patient exhibited oliguria and proteinuria and elevation of CK, AST, ALT, and LDH. Together with the nephrology and neurology staff, we tried to figure out our patient’s symptoms and clinical findings. Thus, she was managed with high-dose loop diuretic therapy. Additionally, we gave her hepatotonic to recover her liver function. The patient was supplemented with 150 to 250 mL/h of lactated Ringer’s solution and 0.9% NaCl. When the volume was full, urine output of above 100 mL/h was maintained by 20 mg intravenous injection with furosemide.\\nHer urine output for the first hour is at 20 mL/hour, but after the medication, her urine output began to improve on day 4 with a corresponding reversal in the serum creatinine. After postoperative day 4, the muscular enzyme showed a downward trend. We treated the patient with medication and hydration, and then the result became favorable. In the end, she was able to recover fully from the symptoms. Figures and show the change in serum enzyme levels during hospitalization (Figs. and ).\nOUTPUT:" }, { "from": "agent", "value": "Rhabdomyolysis, 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: Her past medical history included chronic obstructive airways disease, hypertension, and diabetes mellitus. The patient is a current smoker, with a history of 20 pack-years. Preoperative chest radiography, electrocardiogram, full blood count, and serum biochemistry were within the normal range. After being diagnosed with SCC as a result of incisional biopsy, the patient underwent the resection of SCC on the right buccal mucosa of the mandible, modified radical neck dissection, and primary reconstruction with a fibula-free flap. Tourniquet pressure was 300 mm/Hg, and its application time was 60 min. Total on-table time was approximately 7 h. Upon admission to the SICU after the 7-h operation, hypothermia and hypotension were noted. On the first postoperative day, the patient exhibited oliguria and proteinuria and elevation of CK, AST, ALT, and LDH. Together with the nephrology and neurology staff, we tried to figure out our patient’s symptoms and clinical findings. Thus, she was managed with high-dose loop diuretic therapy. Additionally, we gave her hepatotonic to recover her liver function. The patient was supplemented with 150 to 250 mL/h of lactated Ringer’s solution and 0.9% NaCl. When the volume was full, urine output of above 100 mL/h was maintained by 20 mg intravenous injection with furosemide.\nHer urine output for the first hour is at 20 mL/hour, but after the medication, her urine output began to improve on day 4 with a corresponding reversal in the serum creatinine. After postoperative day 4, the muscular enzyme showed a downward trend. We treated the patient with medication and hydration, and then the result became favorable. In the end, she was able to recover fully from the symptoms. Figures and show the change in serum enzyme levels during hospitalization (Figs. and ). OUTPUT:
PMCPatients_common4694
[ { "from": "human", "value": "As a physician engaged in 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 female harboring EML4/ALK rearranged advanced NSCLC with liver and bone metastases presented with visual disturbance with a left ocular black spot, within a year of undergoing chemotherapy at our institution (). She underwent first-line crizotinib for 6 months with partial response (PR), followed by four cycles of cisplatin/pemetrexed for 4 months with PR. At diagnosis, 70% EML-4/ALK rearrangement via fluorescent in situ hybridization was revealed in the primary pulmonary site. However, hepatic biopsy at progression before third-line treatment revealed a decline of EML-4/ALK rearrangement to 20%. An exudative fluid was seen under the retina representing a retinal detachment. Two weeks later, systemic symptoms, including fever, bone pains, arthralgia, and visual disturbance were exacerbated. Multiple liver metastatic sites also decreased in size and were assessed as showing PR according to the response evaluation criteria in solid tumors (RECIST version 1.1) (). At the second week, her vision was completely recovered, however, she temporarily discontinued alectinib after 2 weeks because of skin rash due to alectinib and concurrently resumed alectinib and antihistamine. Her skin rash did not reappear and she sustained PR with improved eye sight for more than 5 months.\nOUTPUT:" }, { "from": "agent", "value": "Choroidal metastasis, Crizotinib-resistant ALK rearranged positive non-small cell lung cancer" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 30-year-old female harboring EML4/ALK rearranged advanced NSCLC with liver and bone metastases presented with visual disturbance with a left ocular black spot, within a year of undergoing chemotherapy at our institution (). She underwent first-line crizotinib for 6 months with partial response (PR), followed by four cycles of cisplatin/pemetrexed for 4 months with PR. At diagnosis, 70% EML-4/ALK rearrangement via fluorescent in situ hybridization was revealed in the primary pulmonary site. However, hepatic biopsy at progression before third-line treatment revealed a decline of EML-4/ALK rearrangement to 20%. An exudative fluid was seen under the retina representing a retinal detachment. Two weeks later, systemic symptoms, including fever, bone pains, arthralgia, and visual disturbance were exacerbated. Multiple liver metastatic sites also decreased in size and were assessed as showing PR according to the response evaluation criteria in solid tumors (RECIST version 1.1) (). At the second week, her vision was completely recovered, however, she temporarily discontinued alectinib after 2 weeks because of skin rash due to alectinib and concurrently resumed alectinib and antihistamine. Her skin rash did not reappear and she sustained PR with improved eye sight for more than 5 months. OUTPUT:
PMCPatients_common3297
[ { "from": "human", "value": "As a physician engaged in 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-y-old right-handed man was admitted to the Emergency Department with a bilateral headache, accompanied by numbness, weakness, and clumsiness in the limbs during the past week. He reported a severe headache worse before sleep and when waking in the morning. He always felt numbness in the arms and legs, concomitant with weakness and clumsiness in his hands. Physical examination revealed left pronator drift, bilateral Hoffmann’s sign (+), decreased muscle strength, and increased reflexes in upper and lower extremities both sides (left > right). There was mild numbness in both upper and lower limbs bilaterally. He noted similar symptoms 3 mo ago, which resolved spontaneously after a few days. The medical history of the patient and his family were unremarkable. Laboratory tests, including complete blood count, liver function, kidney function, erythrocyte sedimentation rate, vitamin B12 level, and metabolic profile were within normal limits. Brain MRI showed 3 well-circumscribed concentric lamellar lesions in the bilateral frontal and the right parietal-temporal with slight perilesional edema and no mass effect. The lesions demonstrated alternate bands of hypointense to isointense on T1-weighted (T1W) image, isointense to hyperintense on T2-weighted (T2W), and fluid attenuated inversion recovery (FLAIR) images. The lesions were unrestricted diffuse on diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) images. The lesions showed striking but incomplete ring enhancement after contrast administration (). Magnetic resonance spectroscopy (MRS) revealed characteristic spectra of BCS with choline peak increased and N-acetylaspartate peak decreased (). The typical concentric pattern detected on MRI was consistent with a diagnosis of BCS. The patient was treated with intravenous (IV) methylprednisolone acetate at a dose of 1200 mg/d for 3 d, then 600 mg/d for the next 6 d, and then tapered with oral prednisone over 4 wk, starting at 60 mg. His symptoms improved significantly after the first 3 d of treatment. His neurologic examination returned to almost normal after 2 wk. On a 6-mo follow-up examination, patient was doing well with no evidence of dissemination of the disease.\nOUTPUT:" }, { "from": "agent", "value": "Balo’s Concentric Sclerosis" } ]
As a physician engaged 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-y-old right-handed man was admitted to the Emergency Department with a bilateral headache, accompanied by numbness, weakness, and clumsiness in the limbs during the past week. He reported a severe headache worse before sleep and when waking in the morning. He always felt numbness in the arms and legs, concomitant with weakness and clumsiness in his hands. Physical examination revealed left pronator drift, bilateral Hoffmann’s sign (+), decreased muscle strength, and increased reflexes in upper and lower extremities both sides (left > right). There was mild numbness in both upper and lower limbs bilaterally. He noted similar symptoms 3 mo ago, which resolved spontaneously after a few days. The medical history of the patient and his family were unremarkable. Laboratory tests, including complete blood count, liver function, kidney function, erythrocyte sedimentation rate, vitamin B12 level, and metabolic profile were within normal limits. Brain MRI showed 3 well-circumscribed concentric lamellar lesions in the bilateral frontal and the right parietal-temporal with slight perilesional edema and no mass effect. The lesions demonstrated alternate bands of hypointense to isointense on T1-weighted (T1W) image, isointense to hyperintense on T2-weighted (T2W), and fluid attenuated inversion recovery (FLAIR) images. The lesions were unrestricted diffuse on diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) images. The lesions showed striking but incomplete ring enhancement after contrast administration (). Magnetic resonance spectroscopy (MRS) revealed characteristic spectra of BCS with choline peak increased and N-acetylaspartate peak decreased (). The typical concentric pattern detected on MRI was consistent with a diagnosis of BCS. The patient was treated with intravenous (IV) methylprednisolone acetate at a dose of 1200 mg/d for 3 d, then 600 mg/d for the next 6 d, and then tapered with oral prednisone over 4 wk, starting at 60 mg. His symptoms improved significantly after the first 3 d of treatment. His neurologic examination returned to almost normal after 2 wk. On a 6-mo follow-up examination, patient was doing well with no evidence of dissemination of the disease. OUTPUT:
PMCPatients_common3005
[ { "from": "human", "value": "As a physician engaged in 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 man was diagnosed with nodular sclerosing cluster of differentiation (CD) 30+, CD15+ HL almost a year prior. He was found to have stage IV disease with diffuse involvement of the lymph nodes, bone marrow and liver. A power-injectable port was inserted and six cycles of ABVD chemotherapy (adriamycin, bleomycin, vinblastine, dacarbazine) was initiated achieving only partial response. He underwent two other lines of chemotherapy, with poor clinical response. He was being evaluated for autologous hematopoietic stem cell transplant (HSCT) when the pretransplant transthoracic echocardiogram (TTE) revealed a 2.2 × 1.8 cm RA mass with normal cardiac function (). He was then sent to the emergency room for further evaluation.\\nOn arrival, he was hemodynamically stable and asymptomatic. Physical examination was unremarkable. His laboratory findings showed leukocytosis of 15,000 cells/mm3, hemoglobin of 7.5 mg/dL, and a normal platelet count. Computed tomography (CT) imaging showed the RA mass with unclear etiology and other extra-cardiac findings consistent with diffuse HL. Patient was started on heparin for anticoagulation and cardiac thoracic surgery was consulted for possible thrombectomy. During his hospital stay, he developed fever, hypotension and pancytopenia. He was managed in the intensive care unit with broad spectrum antibiotics and vasopressors. Despite aggressive treatment, he rapidly deteriorated and succumbed to the disease.\nOUTPUT:" }, { "from": "agent", "value": "Hodgkin Lymphoma, Right Atrial Mass, CRAT" } ]
As a physician engaged 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 man was diagnosed with nodular sclerosing cluster of differentiation (CD) 30+, CD15+ HL almost a year prior. He was found to have stage IV disease with diffuse involvement of the lymph nodes, bone marrow and liver. A power-injectable port was inserted and six cycles of ABVD chemotherapy (adriamycin, bleomycin, vinblastine, dacarbazine) was initiated achieving only partial response. He underwent two other lines of chemotherapy, with poor clinical response. He was being evaluated for autologous hematopoietic stem cell transplant (HSCT) when the pretransplant transthoracic echocardiogram (TTE) revealed a 2.2 × 1.8 cm RA mass with normal cardiac function (). He was then sent to the emergency room for further evaluation.\nOn arrival, he was hemodynamically stable and asymptomatic. Physical examination was unremarkable. His laboratory findings showed leukocytosis of 15,000 cells/mm3, hemoglobin of 7.5 mg/dL, and a normal platelet count. Computed tomography (CT) imaging showed the RA mass with unclear etiology and other extra-cardiac findings consistent with diffuse HL. Patient was started on heparin for anticoagulation and cardiac thoracic surgery was consulted for possible thrombectomy. During his hospital stay, he developed fever, hypotension and pancytopenia. He was managed in the intensive care unit with broad spectrum antibiotics and vasopressors. Despite aggressive treatment, he rapidly deteriorated and succumbed to the disease. OUTPUT:
PMCPatients_common3106
[ { "from": "human", "value": "As a physician engaged in 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 male, average built, attended our hospital with an ulcer on the floor of the oral cavity for 3 months and 6 × 5 cm swelling over the right side of the neck for 8 days. It was associated with painful swallowing and voice changes. On the sixth day at the hospital, the patient became tachypneic and developed desaturation (SpO2 up to 70%), which improved with O2 supplementation, and slow breathing in forward bending position. He was unable to breathe in the supine position. Hence, an emergency tracheostomy under general anesthesia was planned.\\nOn presentation, he was drowsy but arousable, was on 5 L/min O2 supplement, maintaining normal saturation. His mouth opening was 2 cm, neck movement was restricted with modified Mallampati class 4 view. The cervical X-ray showed tracheal deviation towards left — his heart rate 130/min, blood pressure 180/100 mmHg, and using accessory muscles of respiration. Inspiratory suprasternal and the intercostal indrawing feature was prominent in lying down position.\\nIn view of the difficult airway, risk explained and consent was obtained for fiberoptic intubation. The airway was prepared with 4 mL of 4% lignocaine nebulization, two puffs of 10% lignocaine spray over the posterior pharyngeal wall, 2% lignocaine jelly for nostril, and spray as you go method was applied in propped-up position. With difficulty, the endoscope was introduced from the posterior part of the opening during expiration, and the airway was secured with a 7 mm cuffed flexo metallic tube. In the postoperative period, the patient was still irritable and confused and therefore, was shifted to the intensive care unit for further evaluation in context to preoperative hypoxic insult, if any.\nOUTPUT:" }, { "from": "agent", "value": "Floppy epiglottis, extra-laryngeal mass, inducible laryngeal obstruction, hypoxemic event, 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 40-year-old male, average built, attended our hospital with an ulcer on the floor of the oral cavity for 3 months and 6 × 5 cm swelling over the right side of the neck for 8 days. It was associated with painful swallowing and voice changes. On the sixth day at the hospital, the patient became tachypneic and developed desaturation (SpO2 up to 70%), which improved with O2 supplementation, and slow breathing in forward bending position. He was unable to breathe in the supine position. Hence, an emergency tracheostomy under general anesthesia was planned.\nOn presentation, he was drowsy but arousable, was on 5 L/min O2 supplement, maintaining normal saturation. His mouth opening was 2 cm, neck movement was restricted with modified Mallampati class 4 view. The cervical X-ray showed tracheal deviation towards left — his heart rate 130/min, blood pressure 180/100 mmHg, and using accessory muscles of respiration. Inspiratory suprasternal and the intercostal indrawing feature was prominent in lying down position.\nIn view of the difficult airway, risk explained and consent was obtained for fiberoptic intubation. The airway was prepared with 4 mL of 4% lignocaine nebulization, two puffs of 10% lignocaine spray over the posterior pharyngeal wall, 2% lignocaine jelly for nostril, and spray as you go method was applied in propped-up position. With difficulty, the endoscope was introduced from the posterior part of the opening during expiration, and the airway was secured with a 7 mm cuffed flexo metallic tube. In the postoperative period, the patient was still irritable and confused and therefore, was shifted to the intensive care unit for further evaluation in context to preoperative hypoxic insult, if any. OUTPUT:
PMCPatients_common4187
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 48-year-old man presenting with a progressive cough was admitted to our department. A flexible bronchoscopy exam revealed a tracheal neoplasm in the lower membranous trachea, which was approximately 1 cm in length and nearly obstructed the orifice of the left main bronchus (Fig a). The pathologic biopsy revealed that the tumor originated from smooth muscle. Chest computed tomography revealed a 4 × 3 cm extra-luminal mass above the carina.\\nWe performed a completely portal robotic approach using the da Vinci Surgical System (Intuitive Surgical, Sunnyvale, CA, USA). The patient was induced by general anesthesia with single-lumen endotracheal intubation. An artificial pneumothorax was applied to allow sufficient access for surgery before transecting the trachea. The surgical steps taken were as follows (Fig ). The robotic surgical system docked to the patient with four arms. Appropriate and circumferential tracheal rings with the tumor were resected, and the assistant inserted an endobronchial tube into the left main bronchus to keep single lung ventilation by creating an additional port in the third intercostal space at the midaxillary line. With single lung ventilation by transthoracic tube, the anastomosis began from the midpoint of cartilaginous trachea, using one 2-0 polypropylene suture in a continuous fashion. Because of the dilated terminal of the trachea, the mismatched calibers were anastomosed and modulated by pulling the proximal smaller lumen into the distal larger lumen like a telescope. After changing back to an oral approach endotracheal tube, the membranous trachea was anastomosed.\\nPericardial fat pad was harvested to cover the anastomosis. The patient recovered uneventfully. The postoperative bronchoscopy exam taken the first month after discharge showed the reconstructed trachea without stenosis or recurrence (Fig b).\nOUTPUT:" }, { "from": "agent", "value": "Leiomyosarcoma" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 48-year-old man presenting with a progressive cough was admitted to our department. A flexible bronchoscopy exam revealed a tracheal neoplasm in the lower membranous trachea, which was approximately 1 cm in length and nearly obstructed the orifice of the left main bronchus (Fig a). The pathologic biopsy revealed that the tumor originated from smooth muscle. Chest computed tomography revealed a 4 × 3 cm extra-luminal mass above the carina.\nWe performed a completely portal robotic approach using the da Vinci Surgical System (Intuitive Surgical, Sunnyvale, CA, USA). The patient was induced by general anesthesia with single-lumen endotracheal intubation. An artificial pneumothorax was applied to allow sufficient access for surgery before transecting the trachea. The surgical steps taken were as follows (Fig ). The robotic surgical system docked to the patient with four arms. Appropriate and circumferential tracheal rings with the tumor were resected, and the assistant inserted an endobronchial tube into the left main bronchus to keep single lung ventilation by creating an additional port in the third intercostal space at the midaxillary line. With single lung ventilation by transthoracic tube, the anastomosis began from the midpoint of cartilaginous trachea, using one 2-0 polypropylene suture in a continuous fashion. Because of the dilated terminal of the trachea, the mismatched calibers were anastomosed and modulated by pulling the proximal smaller lumen into the distal larger lumen like a telescope. After changing back to an oral approach endotracheal tube, the membranous trachea was anastomosed.\nPericardial fat pad was harvested to cover the anastomosis. The patient recovered uneventfully. The postoperative bronchoscopy exam taken the first month after discharge showed the reconstructed trachea without stenosis or recurrence (Fig b). OUTPUT:
PMCPatients_common59
[ { "from": "human", "value": "As a physician engaged in 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 woman with reduced vision in her left eye was examined in the Tokyo Medical and Dental University Hospital on June 27, 2015. Her best-corrected visual acuity (BCVA) in her left eye was 20/50, and both eyes were pseudophakic. The refractive error of the left eye was − 1.75 diopters, and the axial length was 25.89 mm. Although we intended to inject silicone oil into the vitreous cavity, a sufficient amount could not be injected because of an obstruction at the trocar insertion site. During the surgery, a reduction of choroidal elevation was observed. ). However, the RRD on the inferior quadrant remained, and a scleral encircling procedure was performed on day 63, and silicone oil was reinjected to tamponade the retina. A future surgery is planned to remove the silicone oil.\nOUTPUT:" }, { "from": "agent", "value": "Suprachoroidal hemorrhage, Rhegmatogenous 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 66-year-old woman with reduced vision in her left eye was examined in the Tokyo Medical and Dental University Hospital on June 27, 2015. Her best-corrected visual acuity (BCVA) in her left eye was 20/50, and both eyes were pseudophakic. The refractive error of the left eye was − 1.75 diopters, and the axial length was 25.89 mm. Although we intended to inject silicone oil into the vitreous cavity, a sufficient amount could not be injected because of an obstruction at the trocar insertion site. During the surgery, a reduction of choroidal elevation was observed. ). However, the RRD on the inferior quadrant remained, and a scleral encircling procedure was performed on day 63, and silicone oil was reinjected to tamponade the retina. A future surgery is planned to remove the silicone oil. OUTPUT:
PMCPatients_common4932
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 78-year-old man who had CABG operation 6 years ago admitted to our outpatient clinic with stable angina pectoris. In his history, he has had hypertension for 20 years, and abdominal aortic aneurysm (AAA) was diagnosed 4 years ago. During examination, chest radiography of the patient revealed an anterior mediastinal mass (, A and B). Inferolateral wall hypokinesia with ejection fraction 45% and mild aortic insuffıciency were seen by transthoracic echocardiography. The newly occurred flow into aneurysmal dilatation at the distal edge of the covered stent was confirmed with coronary angiography (, A). The MPS revealed ischemic perfusion defects on inferolateral wall. Because of the high mortality rate and Society of Thoracic Surgery score (20), treatment with the implementation of a PTFE-covered stent by percutaneous intervention again was decided. CT was repeated for surveillance 6 months after the intervention. There was no more flow into the aneurysm or progressive aneurysmal dilatation, and the PTFE-covered stent was patent (, C).\nOUTPUT:" }, { "from": "agent", "value": "Saphenous vein graft 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 78-year-old man who had CABG operation 6 years ago admitted to our outpatient clinic with stable angina pectoris. In his history, he has had hypertension for 20 years, and abdominal aortic aneurysm (AAA) was diagnosed 4 years ago. During examination, chest radiography of the patient revealed an anterior mediastinal mass (, A and B). Inferolateral wall hypokinesia with ejection fraction 45% and mild aortic insuffıciency were seen by transthoracic echocardiography. The newly occurred flow into aneurysmal dilatation at the distal edge of the covered stent was confirmed with coronary angiography (, A). The MPS revealed ischemic perfusion defects on inferolateral wall. Because of the high mortality rate and Society of Thoracic Surgery score (20), treatment with the implementation of a PTFE-covered stent by percutaneous intervention again was decided. CT was repeated for surveillance 6 months after the intervention. There was no more flow into the aneurysm or progressive aneurysmal dilatation, and the PTFE-covered stent was patent (, C). OUTPUT:
PMCPatients_common2219
[ { "from": "human", "value": "As a physician engaged 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 15. Two additional cases were found, both family members: SF (case 16), a 38 year old woman (M’s mother) and RV (case 17), a 12 year old student (M’s sister).\nOUTPUT:" }, { "from": "agent", "value": "Plasmodium knowlesi, P. falciparum, P. malariae" } ]
As a physician engaged 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 15. Two additional cases were found, both family members: SF (case 16), a 38 year old woman (M’s mother) and RV (case 17), a 12 year old student (M’s sister). OUTPUT:
PMCPatients_common2889
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 30-year-old man, a nonsmoker, presented to the hospital casualty ward with complaints of acute-onset breathlessness since early morning. He had been cleaning a nitric acid container the previous evening in the chemical and fertilizer unit where he was employed.\\nHe was working with two co-workers when the incident occurred, and none of them was wearing any protective devices. They were exposed to fumes of nitric acid during cleaning. The duration of exposure was around 10 minutes, following which, immediately, he had some dry cough and a feeling of suffocation for a very short period. There was no eye, nasal, or skin irritation at that time. After around six hours, he developed progressive dyspnea, and he reported to the casualty ward in the morning with severe dyspnea. On arrival at the casualty ward, he had an SpO2 of 88%; pulse-112/min; B.P.-110/70 mmHg; RR-44/min; X-ray chest- bilateral upper, mid, and lower acinar opacities with right upper lobe consolidation [].\\nHe was admitted to the ICU and was given high-flow oxygen with nasal mask and rebreathing bag. However, he continued to worsen, with RR- 70/min and SpO2-91%. His arterial blood gases showed significant hypoxia, with pH-7.45, pO2-60 mmHg, and pCO2-28 mmHg. His complete blood counts, renal and hepatic parameters were normal.\\nHis CT scan revealed bilateral interstitial opacities with air trapping and with right upper lobe consolidation [].\\nA decision was made to intubate and initiate ventilatory support.\\nHe was treated with methylprednisolone 125 mg and antibiotics and nebulized with bronchodilators and N-acetylcysteine (NAC).\\nThe patient showed good clinical and radiological improvement. He was weaned off from the ventilator on day 4 and discharged after a week. Findings from his X-ray chest and pulmonary function test after one month were normal.\nOUTPUT:" }, { "from": "agent", "value": "Acute lung injury" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 30-year-old man, a nonsmoker, presented to the hospital casualty ward with complaints of acute-onset breathlessness since early morning. He had been cleaning a nitric acid container the previous evening in the chemical and fertilizer unit where he was employed.\nHe was working with two co-workers when the incident occurred, and none of them was wearing any protective devices. They were exposed to fumes of nitric acid during cleaning. The duration of exposure was around 10 minutes, following which, immediately, he had some dry cough and a feeling of suffocation for a very short period. There was no eye, nasal, or skin irritation at that time. After around six hours, he developed progressive dyspnea, and he reported to the casualty ward in the morning with severe dyspnea. On arrival at the casualty ward, he had an SpO2 of 88%; pulse-112/min; B.P.-110/70 mmHg; RR-44/min; X-ray chest- bilateral upper, mid, and lower acinar opacities with right upper lobe consolidation [].\nHe was admitted to the ICU and was given high-flow oxygen with nasal mask and rebreathing bag. However, he continued to worsen, with RR- 70/min and SpO2-91%. His arterial blood gases showed significant hypoxia, with pH-7.45, pO2-60 mmHg, and pCO2-28 mmHg. His complete blood counts, renal and hepatic parameters were normal.\nHis CT scan revealed bilateral interstitial opacities with air trapping and with right upper lobe consolidation [].\nA decision was made to intubate and initiate ventilatory support.\nHe was treated with methylprednisolone 125 mg and antibiotics and nebulized with bronchodilators and N-acetylcysteine (NAC).\nThe patient showed good clinical and radiological improvement. He was weaned off from the ventilator on day 4 and discharged after a week. Findings from his X-ray chest and pulmonary function test after one month were normal. OUTPUT:
PMCPatients_common2511
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 13 years old male child reported to the department of pedodontics, PGIDS, Rohtak with chief complaint of difficulty in drinking water and change in voice since 1 month. Patient gave history of traumatic removal of his right upper back tooth (due to caries) 1 month back following which these problems started. On examination, his right maxillary permanent first molar was missing, there was slight opening on the buccal side of the alveolar process. There was nasal discharge of oral fluids along with nasal twang. Diagnosis of OAF was made ( and ). Patient was then referred to department of oral and maxillofacial surgery for further management.\\nManagement: His maxillary antrum was irrigated with normal saline three times within a week. After taking informed written consent for the surgery and getting necessary blood investigations, closure with BFP under local anesthesia was planned. Right posterior superior alveolar nerve block and greater palatine nerve block was given with 2% lignocaine with 1:200000 adrenaline along with the right buccal vestibule infiltration. The mucoperiosteal flap was raised from mesial to 15 to distal to 17 with molt’s periosteal elevator after giving incision with no. 15 blade. The defect () was curetted with the help of Lucas curette. A incision was given over the periosteum on the undersurface of the flap and with pressure applied to the zygomatic arch region, the BFP easily extruded into the operative side. Dissection with a Metzenbaum scissors helped to mobilize as much BFP () as needed to obtain a tension-free closure across the communication. The palatal mucosa margin was freshened. The fat pad was then sutured with resorbable suture to palatal mucosa. The buccal flap was then positioned over the BFP and was sutured to palatal mucosa with 3-0 silk suture (). Antibiotics and analgesics were prescribed for 5 days. Patient was advised soft diet and to maintain oral hygiene. Sutures were removed after 2 weeks. The postoperative period was uneventful ().\nOUTPUT:" }, { "from": "agent", "value": "Oroantral Fistula" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: A 13 years old male child reported to the department of pedodontics, PGIDS, Rohtak with chief complaint of difficulty in drinking water and change in voice since 1 month. Patient gave history of traumatic removal of his right upper back tooth (due to caries) 1 month back following which these problems started. On examination, his right maxillary permanent first molar was missing, there was slight opening on the buccal side of the alveolar process. There was nasal discharge of oral fluids along with nasal twang. Diagnosis of OAF was made ( and ). Patient was then referred to department of oral and maxillofacial surgery for further management.\nManagement: His maxillary antrum was irrigated with normal saline three times within a week. After taking informed written consent for the surgery and getting necessary blood investigations, closure with BFP under local anesthesia was planned. Right posterior superior alveolar nerve block and greater palatine nerve block was given with 2% lignocaine with 1:200000 adrenaline along with the right buccal vestibule infiltration. The mucoperiosteal flap was raised from mesial to 15 to distal to 17 with molt’s periosteal elevator after giving incision with no. 15 blade. The defect () was curetted with the help of Lucas curette. A incision was given over the periosteum on the undersurface of the flap and with pressure applied to the zygomatic arch region, the BFP easily extruded into the operative side. Dissection with a Metzenbaum scissors helped to mobilize as much BFP () as needed to obtain a tension-free closure across the communication. The palatal mucosa margin was freshened. The fat pad was then sutured with resorbable suture to palatal mucosa. The buccal flap was then positioned over the BFP and was sutured to palatal mucosa with 3-0 silk suture (). Antibiotics and analgesics were prescribed for 5 days. Patient was advised soft diet and to maintain oral hygiene. Sutures were removed after 2 weeks. The postoperative period was uneventful (). OUTPUT:
PMCPatients_common1997
[ { "from": "human", "value": "As a physician engaged in 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 female office administrator was admitted with a 6-month history of increasing left knee pain. In 1990 and 1995, she underwent surgery for removal of a haemangioma located near the medial border of the patella. Examination of the knee showed no abnormalities, and angulation was possible without any significant limitation in the range of motion. On physical examination, she had spontaneous pain in the anterior region of the knee, with a maximum point of tenderness just near the surgical scar, at the superomedial corner of the patella. In addition, pressure on the patella itself was painful. Magnetic resonance imaging (MRI) was performed for further evaluation (3T Skyra, Siemens, Erlangen, Germany). The protocol consisted of T1- and T2-weighted images as well as fluid-sensitive short tau inversion recovery (STIR) sequences and contrast enhanced T1-weighted images. MRI revealed two different angiomatous masses that were the most likely cause of the patient’s pain. The bigger one with a maximum extension of almost 7 cm and a fusiform shape with partial intraosseous extension were located on the medial edge of femoral diaphysis and arising from the upper part of the medial aspect of the intercondyloid fossa. The smaller mass was located on the medial upper border of the patella, with a maximum diameter of 2 cm. ). The doubled PT was additionally confirmed on a subsequent grey-scale sonography (Fig. ).\nOUTPUT:" }, { "from": "agent", "value": "Crossed-doubled patellar tendon, Hemangiomas" } ]
As a physician engaged 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 female office administrator was admitted with a 6-month history of increasing left knee pain. In 1990 and 1995, she underwent surgery for removal of a haemangioma located near the medial border of the patella. Examination of the knee showed no abnormalities, and angulation was possible without any significant limitation in the range of motion. On physical examination, she had spontaneous pain in the anterior region of the knee, with a maximum point of tenderness just near the surgical scar, at the superomedial corner of the patella. In addition, pressure on the patella itself was painful. Magnetic resonance imaging (MRI) was performed for further evaluation (3T Skyra, Siemens, Erlangen, Germany). The protocol consisted of T1- and T2-weighted images as well as fluid-sensitive short tau inversion recovery (STIR) sequences and contrast enhanced T1-weighted images. MRI revealed two different angiomatous masses that were the most likely cause of the patient’s pain. The bigger one with a maximum extension of almost 7 cm and a fusiform shape with partial intraosseous extension were located on the medial edge of femoral diaphysis and arising from the upper part of the medial aspect of the intercondyloid fossa. The smaller mass was located on the medial upper border of the patella, with a maximum diameter of 2 cm. ). The doubled PT was additionally confirmed on a subsequent grey-scale sonography (Fig. ). OUTPUT:
PMCPatients_common913
[ { "from": "human", "value": "As a physician engaged in 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 patient with chronic hepatitis C virus-induced liver cirrhosis was diagnosed with HCC for which he received a liver transplantation in 2018. As transplantation indication he initially had one lesion <5 cm with adequate liver function but with vascular invasion (tumor thrombus), which was first treated with transarterial radioembolization after which there was complete resolvement of the thrombus (BCLC-score C and MELD-score was 6 at time of transplantation). His hepatitis C was treated with peginterferon and ribavirin in 2003, after which there was complete remission. At start of the study and during hospital admissions patient used clopidogrel, temazepam, pravastatin, oxycodon, ursodeoxycholicacid and pantoprazole as concomitant medication. Immunosuppressive treatment consisted of mycophenolate mofetil (MMF) 1000 mg b.i.d. and tacrolimus (4 mg b.i.d., which was later reduced to 4 mg q.d.). Later, the patient switched from MMF to sirolimus (2 mg q.d.) due to livertoxicity. In April 2019, the patient had a recurrence of disease after which sorafenib was started in a dose of 200 mg b.i.d. Both tacrolimus and sirolimus concentrations were adequate at baseline (Ctrough = 4.7 μg/L and Ctrough = 8.0 μg/L, respectively). At day eight of sorafenib treatment, tacrolimus was stopped by the gastroenterologist according to physician’s choice and the patient continued with sirolimus monotherapy. After cessation of tacrolimus, the sorafenib concentration initially decreased and remained relatively stable until disease progression, which was also the case for sirolimus concentration (). AUC0–7.5h and Cmax of sorafenib decreased with 40.0% and 37.3% respectively at day 14 compared to day 7 (). After just 2 months of treatment, this patient had disease progression after which sorafenib treatment was stopped and best supportive care was started. After stopping sorafenib therapy, the sirolimus plasma levels further decreased with 42.6% compared to the latest Ctrough with the combination therapy.\nOUTPUT:" }, { "from": "agent", "value": "Hepatocellular 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 65-year old male patient with chronic hepatitis C virus-induced liver cirrhosis was diagnosed with HCC for which he received a liver transplantation in 2018. As transplantation indication he initially had one lesion <5 cm with adequate liver function but with vascular invasion (tumor thrombus), which was first treated with transarterial radioembolization after which there was complete resolvement of the thrombus (BCLC-score C and MELD-score was 6 at time of transplantation). His hepatitis C was treated with peginterferon and ribavirin in 2003, after which there was complete remission. At start of the study and during hospital admissions patient used clopidogrel, temazepam, pravastatin, oxycodon, ursodeoxycholicacid and pantoprazole as concomitant medication. Immunosuppressive treatment consisted of mycophenolate mofetil (MMF) 1000 mg b.i.d. and tacrolimus (4 mg b.i.d., which was later reduced to 4 mg q.d.). Later, the patient switched from MMF to sirolimus (2 mg q.d.) due to livertoxicity. In April 2019, the patient had a recurrence of disease after which sorafenib was started in a dose of 200 mg b.i.d. Both tacrolimus and sirolimus concentrations were adequate at baseline (Ctrough = 4.7 μg/L and Ctrough = 8.0 μg/L, respectively). At day eight of sorafenib treatment, tacrolimus was stopped by the gastroenterologist according to physician’s choice and the patient continued with sirolimus monotherapy. After cessation of tacrolimus, the sorafenib concentration initially decreased and remained relatively stable until disease progression, which was also the case for sirolimus concentration (). AUC0–7.5h and Cmax of sorafenib decreased with 40.0% and 37.3% respectively at day 14 compared to day 7 (). After just 2 months of treatment, this patient had disease progression after which sorafenib treatment was stopped and best supportive care was started. After stopping sorafenib therapy, the sirolimus plasma levels further decreased with 42.6% compared to the latest Ctrough with the combination therapy. OUTPUT:
PMCPatients_common2168
[ { "from": "human", "value": "As a physician engaged in 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 was admitted to Peking Union Medical College Hospital, Beijing, China, on 13 May 2015 because he had been experiencing intermittent fever with chills and fatigue for six months. Antibiotic therapy (lack of detailed information) prescribed by the community hospital was completed before he came to our hospital, but the symptoms persisted. On physical examinations, the patient was revealed to be healthy except for an unstable temperature with intermittent fever, hypotension [103/38 mmHg] and weight loss of 15 kg during the course of illness. Laboratory tests revealed that the patient had an increased erythrocyte sedimentation rate (ESR) of >140 mm/h and suspected anemia with Hb of 57 g/L. His symptoms were slightly alleviated after a blood transfusion with 2 units of condensed erythrocytes. Cardiac auscultation revealed consecutive murmurs in the second aortic valve area. Echocardiography was prescribed to determine the cause of the murmurs. Based on the above evidence and the current physical condition, the patient was hospitalized in the cardiac surgery department on 26 May, and a cardiac surgical operation was performed to rectify the CHD and IE condition on 1 June 2015. A peripheral blood sample was sent to microbiology laboratory for blood culture testing on 26 May and was positive; the pathogen from the blood culture was revealed to be a novel species of the family Flavobacteriaceae on 6 June. Empirical treatment with ceftriaxone (IV, 2 g, qd) for 2 weeks during his hospitalization was prescribed. The patient recovered well after the operation and was discharged on 10 June 2015 with prolonged antibiotic treatment with ceftriaxone for 5 weeks. Since he was discharged, no significant clinical events have occurred during follow-up.\nOUTPUT:" }, { "from": "agent", "value": "Infectious endocarditis, Congenital heart disease of patent ductus arteriosus" } ]
As a physician engaged 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 was admitted to Peking Union Medical College Hospital, Beijing, China, on 13 May 2015 because he had been experiencing intermittent fever with chills and fatigue for six months. Antibiotic therapy (lack of detailed information) prescribed by the community hospital was completed before he came to our hospital, but the symptoms persisted. On physical examinations, the patient was revealed to be healthy except for an unstable temperature with intermittent fever, hypotension [103/38 mmHg] and weight loss of 15 kg during the course of illness. Laboratory tests revealed that the patient had an increased erythrocyte sedimentation rate (ESR) of >140 mm/h and suspected anemia with Hb of 57 g/L. His symptoms were slightly alleviated after a blood transfusion with 2 units of condensed erythrocytes. Cardiac auscultation revealed consecutive murmurs in the second aortic valve area. Echocardiography was prescribed to determine the cause of the murmurs. Based on the above evidence and the current physical condition, the patient was hospitalized in the cardiac surgery department on 26 May, and a cardiac surgical operation was performed to rectify the CHD and IE condition on 1 June 2015. A peripheral blood sample was sent to microbiology laboratory for blood culture testing on 26 May and was positive; the pathogen from the blood culture was revealed to be a novel species of the family Flavobacteriaceae on 6 June. Empirical treatment with ceftriaxone (IV, 2 g, qd) for 2 weeks during his hospitalization was prescribed. The patient recovered well after the operation and was discharged on 10 June 2015 with prolonged antibiotic treatment with ceftriaxone for 5 weeks. Since he was discharged, no significant clinical events have occurred during follow-up. OUTPUT:
PMCPatients_common4717
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: We report a 68-year old right handed Hispanic woman with a history of diabetes mellitus type II, hypertension, hyperlipidemia, and two prior strokes with residual right hemiparesis, who presented with sudden onset vertigo, slurred speech, and blurred vision. The second stroke was a cryptogenic stroke that occurred around 5 years prior to admission for which she was outside the time window of thrombolytic therapy and was maintained on aspirin 81 mg daily. Her initial exam showed dysarthria, left sided sensory loss, skew deviation with upgaze vertical nystagmus, mild right hemiparesis, and an NIHSS score of 4. Since she had a new fixed and potentially disabling neurological deficit and she was within the 4.5 h window, decision was made to administer thrombolytic therapy. She received IV tPA 2.5 h from symptom onset. An hour after the IV tPA infusion was complete, she complained of an acute severe headache without a change in neurological exam and repeat CT head showed right temporal ICH with a subdural component (). She received 20 units of cryoprecipitate and 6 units of platelets within 60 min.\\nTwo hours after the completion of this treatment, she became somnolent and had new left hemiparesis. In the next 3 h, her exam continued to deteriorate, became stuporous and stopped following commands. The decision was made to administer recombinant factor VIIa (50 mcg/kg) and she was subsequently taken to the operating room with successful clot evacuation. Postoperatively, her exam slowly improved and she was back to her baseline neurological exam on post-operative day 3 ().\nOUTPUT:" }, { "from": "agent", "value": "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: We report a 68-year old right handed Hispanic woman with a history of diabetes mellitus type II, hypertension, hyperlipidemia, and two prior strokes with residual right hemiparesis, who presented with sudden onset vertigo, slurred speech, and blurred vision. The second stroke was a cryptogenic stroke that occurred around 5 years prior to admission for which she was outside the time window of thrombolytic therapy and was maintained on aspirin 81 mg daily. Her initial exam showed dysarthria, left sided sensory loss, skew deviation with upgaze vertical nystagmus, mild right hemiparesis, and an NIHSS score of 4. Since she had a new fixed and potentially disabling neurological deficit and she was within the 4.5 h window, decision was made to administer thrombolytic therapy. She received IV tPA 2.5 h from symptom onset. An hour after the IV tPA infusion was complete, she complained of an acute severe headache without a change in neurological exam and repeat CT head showed right temporal ICH with a subdural component (). She received 20 units of cryoprecipitate and 6 units of platelets within 60 min.\nTwo hours after the completion of this treatment, she became somnolent and had new left hemiparesis. In the next 3 h, her exam continued to deteriorate, became stuporous and stopped following commands. The decision was made to administer recombinant factor VIIa (50 mcg/kg) and she was subsequently taken to the operating room with successful clot evacuation. Postoperatively, her exam slowly improved and she was back to her baseline neurological exam on post-operative day 3 (). OUTPUT:
PMCPatients_common3694
[ { "from": "human", "value": "As a physician engaged 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 female patient with good performance status and without signs of senility was admitted as a result of an abnormal chest X-ray, which showed a mass over 7 cm in diameter in the left lower field (Fig a). Chest computed tomography (CT) indicated swelling in multiple lymph nodes and 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET) displayed high standard uptake values (Fig a,b). Because of the multiple lymph node metastases (numbers 7, 10, and 11) and severe obstructive pulmonary function (vital capacity 1.69L [74.1%], forced expiratory volume in 1 second [FEV 1] 870 mL, FEV 1/forced vital capacity [FVC] 55.4%), four cycles of chemotherapy (carboplatin AUC 5, 290 mg/body day 1, tegafur-gimeracil-oteracil potassium [S-1], 80 mg/body days 1–14) were performed each month and no side effects over grade 3 were observed. After chemotherapy, the main tumor had shrunk to 4.7 × 2.6 cm and the size and shape of the lymph nodes had decreased to within normal range. FDG-PET showed diminished standard uptake values, resulting in stage ycT2aN0M0-IB (Figs b, c,d). Good physical capacity was maintained and respiratory function was improved with a bronchodilating preparation (vital capacity 2.37L [106.8%], FEV 1 1220 mL, FEV1/FVC 56.0%); therefore, a left lower lobectomy, and a lymphadenectomy were performed uneventfully. Pathological findings revealed that the viable tumor was 1.4 cm in diameter (Ef2), staged as ypT1aN0M0-IA (Fig b–d). Although the ambulatory patient was discharged 39 days after surgery because of rehabilitation and therapy for allergic bronchopulmonary aspergillosis, she was good in health with the same pretreatment and preoperative performance status, and did not experience recurrence from initial therapy for over a year.\nOUTPUT:" }, { "from": "agent", "value": "Primary squamous cell lung cancer" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: An 81-year-old female patient with good performance status and without signs of senility was admitted as a result of an abnormal chest X-ray, which showed a mass over 7 cm in diameter in the left lower field (Fig a). Chest computed tomography (CT) indicated swelling in multiple lymph nodes and 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET) displayed high standard uptake values (Fig a,b). Because of the multiple lymph node metastases (numbers 7, 10, and 11) and severe obstructive pulmonary function (vital capacity 1.69L [74.1%], forced expiratory volume in 1 second [FEV 1] 870 mL, FEV 1/forced vital capacity [FVC] 55.4%), four cycles of chemotherapy (carboplatin AUC 5, 290 mg/body day 1, tegafur-gimeracil-oteracil potassium [S-1], 80 mg/body days 1–14) were performed each month and no side effects over grade 3 were observed. After chemotherapy, the main tumor had shrunk to 4.7 × 2.6 cm and the size and shape of the lymph nodes had decreased to within normal range. FDG-PET showed diminished standard uptake values, resulting in stage ycT2aN0M0-IB (Figs b, c,d). Good physical capacity was maintained and respiratory function was improved with a bronchodilating preparation (vital capacity 2.37L [106.8%], FEV 1 1220 mL, FEV1/FVC 56.0%); therefore, a left lower lobectomy, and a lymphadenectomy were performed uneventfully. Pathological findings revealed that the viable tumor was 1.4 cm in diameter (Ef2), staged as ypT1aN0M0-IA (Fig b–d). Although the ambulatory patient was discharged 39 days after surgery because of rehabilitation and therapy for allergic bronchopulmonary aspergillosis, she was good in health with the same pretreatment and preoperative performance status, and did not experience recurrence from initial therapy for over a year. OUTPUT:
PMCPatients_common545
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: We report a case of a 65-year-old woman affected by a severe form of CD, diagnosed in 1991. From the beginning, the disease had an ileocolonic localization with a stricturing-fistulizing phenotype. Because of the extensive and aggressive disease, together with the lack of response to conventional and biological treatments (i.e. Infliximab, Adalimumab, salazopyrine, multiple cycles of systemic steroids and antibiotics), the patient underwent multiple abdominal surgical resections, the last one in 2010, with a final ileo-colonic anastomosis. Overall, the remaining gut was of about 110 cm in length. Thus, the patient developed a SBS, although she did not required parenteral nutrition.\\nIn November 2015, while she was under treatment with Adalimumab, she reported from 20 to 40 bowel movements per day with watery stools and progressive loss weight with a body mass index of 17 kg/m2. Due to significant electrolyte losses and recurrent metabolic acidosis, the patient underwent biweekly infusions of magnesium, potassium, and bicarbonate in addition to oral supplementation. Moreover, she was supplied with enteral nutrition, since oral nutrition resulted in worsening of the diarrhea.\\nIn March 2016, after an ineffective attempt with octreotide, the patient was treated with TED 0.05 mg/kg daily, although the drug was approved only for patients with SBS on parenteral nutrition. However, after 24 weeks of treatment with TED, enteral nutrition was reduced by at least 50% and, after 72 weeks, it was suspended permanently. Moreover, intravenous infusions of magnesium and potassium were nearly abolished (i.e. once every 3 months). The patient, currently under treatment, is on oral feeding and is reporting four evacuations/day with formed stools. During treatment, the patient did not develop mild side effects, except for a diffuse abdominal pain and nausea, occurring only during the first week of treatment. No serious side effects were recorded during the whole period. Of note, the therapy markedly improved the quality of life of the patient, resulting in a normal social and private life.\nOUTPUT:" }, { "from": "agent", "value": "Crohn’s disease, short bowel syndrome" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: We report a case of a 65-year-old woman affected by a severe form of CD, diagnosed in 1991. From the beginning, the disease had an ileocolonic localization with a stricturing-fistulizing phenotype. Because of the extensive and aggressive disease, together with the lack of response to conventional and biological treatments (i.e. Infliximab, Adalimumab, salazopyrine, multiple cycles of systemic steroids and antibiotics), the patient underwent multiple abdominal surgical resections, the last one in 2010, with a final ileo-colonic anastomosis. Overall, the remaining gut was of about 110 cm in length. Thus, the patient developed a SBS, although she did not required parenteral nutrition.\nIn November 2015, while she was under treatment with Adalimumab, she reported from 20 to 40 bowel movements per day with watery stools and progressive loss weight with a body mass index of 17 kg/m2. Due to significant electrolyte losses and recurrent metabolic acidosis, the patient underwent biweekly infusions of magnesium, potassium, and bicarbonate in addition to oral supplementation. Moreover, she was supplied with enteral nutrition, since oral nutrition resulted in worsening of the diarrhea.\nIn March 2016, after an ineffective attempt with octreotide, the patient was treated with TED 0.05 mg/kg daily, although the drug was approved only for patients with SBS on parenteral nutrition. However, after 24 weeks of treatment with TED, enteral nutrition was reduced by at least 50% and, after 72 weeks, it was suspended permanently. Moreover, intravenous infusions of magnesium and potassium were nearly abolished (i.e. once every 3 months). The patient, currently under treatment, is on oral feeding and is reporting four evacuations/day with formed stools. During treatment, the patient did not develop mild side effects, except for a diffuse abdominal pain and nausea, occurring only during the first week of treatment. No serious side effects were recorded during the whole period. Of note, the therapy markedly improved the quality of life of the patient, resulting in a normal social and private life. OUTPUT:
PMCPatients_common245
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Patient 2 is a 66-year-old woman who suffered two falls with secondary brief loss of consciousness in 2009 and 2014 and was diagnosed with concussion at those times. She presented to the W-TBI clinic in May 2016 after having trouble reading for many months in addition to episodes of double vision which subsided with naps since 1997. Review of systems was positive for constipation, dysautonomias (including trouble urinating and sexual dysfunction), muscle twitching and gait problems, stuttering, hyperthyroidism, chronic respiratory problems, poor memory, large changes in blood pressure, and PTSD. The patient demonstrated hypermobile joints (Beighton score 5/9) and confirmed that she was “double jointed”. Her past medical history was significant for syncope and GERD. Patient 2 was found to have convergence insufficiency, deficiency of smooth pursuit movements, diplopia, eye pain, suspected postconcussion syndrome, and dysautonomia. An MRI of the brain and orbits was ordered and the patient was provided orthoptic exercises and asked to use a walking stick for balance with re-evaluation in three months. The MRI indicated mild anterolisthesis and possible impingement upon the spinal cord. Patient 2 returned in August 2016 and reported decreased eye pain and diplopia. Review of systems was unchanged except for a new complaint of back and hip pain. The patient returned to the W-TBI clinic in August 2017 and reported improved vision, although infrequent blurred vision and/or orbital discomfort still occurred. Review of systems was newly positive for GERD and possible gastroparesis, dysautonomia, pain hypersensitivity, fibromyalgia, and balance problems. The vision improvement with orthoptic therapy supported the diagnosis that the visual symptoms were secondary to concussion.\nOUTPUT:" }, { "from": "agent", "value": "Ehlers Danlos syndrome, hypermobility type III" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Patient 2 is a 66-year-old woman who suffered two falls with secondary brief loss of consciousness in 2009 and 2014 and was diagnosed with concussion at those times. She presented to the W-TBI clinic in May 2016 after having trouble reading for many months in addition to episodes of double vision which subsided with naps since 1997. Review of systems was positive for constipation, dysautonomias (including trouble urinating and sexual dysfunction), muscle twitching and gait problems, stuttering, hyperthyroidism, chronic respiratory problems, poor memory, large changes in blood pressure, and PTSD. The patient demonstrated hypermobile joints (Beighton score 5/9) and confirmed that she was “double jointed”. Her past medical history was significant for syncope and GERD. Patient 2 was found to have convergence insufficiency, deficiency of smooth pursuit movements, diplopia, eye pain, suspected postconcussion syndrome, and dysautonomia. An MRI of the brain and orbits was ordered and the patient was provided orthoptic exercises and asked to use a walking stick for balance with re-evaluation in three months. The MRI indicated mild anterolisthesis and possible impingement upon the spinal cord. Patient 2 returned in August 2016 and reported decreased eye pain and diplopia. Review of systems was unchanged except for a new complaint of back and hip pain. The patient returned to the W-TBI clinic in August 2017 and reported improved vision, although infrequent blurred vision and/or orbital discomfort still occurred. Review of systems was newly positive for GERD and possible gastroparesis, dysautonomia, pain hypersensitivity, fibromyalgia, and balance problems. The vision improvement with orthoptic therapy supported the diagnosis that the visual symptoms were secondary to concussion. OUTPUT:
PMCPatients_common1756
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: In 2012, a 7-year-old Japanese girl was referred to our hospital owing to difficulty opening her mouth following a facial bruise caused by a fall from a pull-up bar that occurred in August 2010. Initially, she underwent observation, and gradually her mouth-opening became more restricted. At her first visit, her maximum aperture was 13 mm and the movement of the right mandible was severely restricted (Fig. ). The opening mainly involved a rolling movement, and no gliding was observed. There were no special medical, family, or psychosocial histories related to this patient. Her panoramic radiography and computed tomography (CT) scans demonstrated left condyle deformation caused by bone addition as well as a severe loss of joint space (Fig. ). On magnetic resonance imaging, the joint cavity and articular disk were not visible. Based on these findings, we diagnosed left TMJa.\\nTaking the risk of jaw undergrowth into consideration while also taking care to avoid the risk of brain damage, we performed TMJ arthroplasty using a surgical navigation system (Figs. , ). First, a preauricular incision was made to reveal the TMJa region. Preoperative CT indicated that the skull width was only 0.7 mm at the thinnest point, and the error of the navigation system was confirmed to be 0.3 mm. Therefore, after confirming the position of the medial cranial fossa and the distance from the glenoid fossa to the skull base with the assistance of the Medtronic StealthStation S7 workstation with Synergy Fusion Cranial software (Medtronic Navigation, Louisville, CO), we performed a 10-mm-wide osteotomy and TMJ release. At that stage, the maximum aperture was 32 mm. Finally, the temporal muscle and fascia were inserted into the glenoid fossa created by the surgery. No complications occurred.\\nMouth-opening training was initiated the day after surgery. Six months after surgery, the maximum aperture was 38 mm and there were no longer any impediments to side mandibular movement (Fig. ). In addition, CT demonstrated a loss of bony adhesions in the condyle and glenoid, improvement of the condylar deformity, and the joint cavity intervention (Fig. ).\nOUTPUT:" }, { "from": "agent", "value": "Temporomandibular joint ankylosis" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: In 2012, a 7-year-old Japanese girl was referred to our hospital owing to difficulty opening her mouth following a facial bruise caused by a fall from a pull-up bar that occurred in August 2010. Initially, she underwent observation, and gradually her mouth-opening became more restricted. At her first visit, her maximum aperture was 13 mm and the movement of the right mandible was severely restricted (Fig. ). The opening mainly involved a rolling movement, and no gliding was observed. There were no special medical, family, or psychosocial histories related to this patient. Her panoramic radiography and computed tomography (CT) scans demonstrated left condyle deformation caused by bone addition as well as a severe loss of joint space (Fig. ). On magnetic resonance imaging, the joint cavity and articular disk were not visible. Based on these findings, we diagnosed left TMJa.\nTaking the risk of jaw undergrowth into consideration while also taking care to avoid the risk of brain damage, we performed TMJ arthroplasty using a surgical navigation system (Figs. , ). First, a preauricular incision was made to reveal the TMJa region. Preoperative CT indicated that the skull width was only 0.7 mm at the thinnest point, and the error of the navigation system was confirmed to be 0.3 mm. Therefore, after confirming the position of the medial cranial fossa and the distance from the glenoid fossa to the skull base with the assistance of the Medtronic StealthStation S7 workstation with Synergy Fusion Cranial software (Medtronic Navigation, Louisville, CO), we performed a 10-mm-wide osteotomy and TMJ release. At that stage, the maximum aperture was 32 mm. Finally, the temporal muscle and fascia were inserted into the glenoid fossa created by the surgery. No complications occurred.\nMouth-opening training was initiated the day after surgery. Six months after surgery, the maximum aperture was 38 mm and there were no longer any impediments to side mandibular movement (Fig. ). In addition, CT demonstrated a loss of bony adhesions in the condyle and glenoid, improvement of the condylar deformity, and the joint cavity intervention (Fig. ). OUTPUT:
PMCPatients_common1257
[ { "from": "human", "value": "As a physician engaged in 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 gentleman presented with a left shoulder skin lesion that was initially totally excised. He relapsed sometime after this initial resection and underwent a second surgery followed by several other relapses and re-resections and 2 courses of radiation therapy and ended up having multifocal disease sites on the upper torso, the shoulder and neck. Plastic surgeons exhausted all available skin that could be spared for flaps and reconstruction. After the third relapse and the first round of radiotherapy, he received Imatinib at 400 mg daily with a positive response lasting for about 2 years. Upon progression, he was offered Imatinib 800 mg daily with non negligible side effects and no response.\\nAll pathology readings of repeated excisions were reported as DFSP except for one time, where the presence of cellular pleomorphism and the lack of CD 34 expression raised the possibility of transformation into a fibrosarcoma. Margins following his third resection were always positive.\\nThere was no FISH analysis or RT-PCR or molecular studies ordered to detect the presence of the typical chromosomal translocation t(17;22)(q21;q13) in the tumor of this patient, resulting in the chimeric gene COL1A1-PDGFB.\\nThe patient ended up with left upper extremity amputation at the level of the shoulder and was referred to us.\\nHe presented with massive and bulky soft tissue lesions on his upper torso and in the neck. A contrast enhanced CT scan also revealed large mediastinal masses and post obstructive pneumopathy on the left.\\nHe was offered to start on Sorafenib as it was made available for us on compassionate use. A dramatic response was seen after only few days of treatment (Figures and ). The patient received Sorafenib 800 mg daily for 5 months without recurrence or progression of the tumor. There was no significant side effect reported beside moderate fatigue, and dehiscence of prior surgical wounds. However, he suffered from recurrent pulmonary infections despite decompression of his left main bronchus since attaining a very good partial response, and unfortunately passed away after an episode of septic shock. He remained progression free during the whole treatment time. Therapy was discontinued only one week prior to his death.\nOUTPUT:" }, { "from": "agent", "value": "Dermatofibrosarcoma Protuberans" } ]
As a physician engaged 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 gentleman presented with a left shoulder skin lesion that was initially totally excised. He relapsed sometime after this initial resection and underwent a second surgery followed by several other relapses and re-resections and 2 courses of radiation therapy and ended up having multifocal disease sites on the upper torso, the shoulder and neck. Plastic surgeons exhausted all available skin that could be spared for flaps and reconstruction. After the third relapse and the first round of radiotherapy, he received Imatinib at 400 mg daily with a positive response lasting for about 2 years. Upon progression, he was offered Imatinib 800 mg daily with non negligible side effects and no response.\nAll pathology readings of repeated excisions were reported as DFSP except for one time, where the presence of cellular pleomorphism and the lack of CD 34 expression raised the possibility of transformation into a fibrosarcoma. Margins following his third resection were always positive.\nThere was no FISH analysis or RT-PCR or molecular studies ordered to detect the presence of the typical chromosomal translocation t(17;22)(q21;q13) in the tumor of this patient, resulting in the chimeric gene COL1A1-PDGFB.\nThe patient ended up with left upper extremity amputation at the level of the shoulder and was referred to us.\nHe presented with massive and bulky soft tissue lesions on his upper torso and in the neck. A contrast enhanced CT scan also revealed large mediastinal masses and post obstructive pneumopathy on the left.\nHe was offered to start on Sorafenib as it was made available for us on compassionate use. A dramatic response was seen after only few days of treatment (Figures and ). The patient received Sorafenib 800 mg daily for 5 months without recurrence or progression of the tumor. There was no significant side effect reported beside moderate fatigue, and dehiscence of prior surgical wounds. However, he suffered from recurrent pulmonary infections despite decompression of his left main bronchus since attaining a very good partial response, and unfortunately passed away after an episode of septic shock. He remained progression free during the whole treatment time. Therapy was discontinued only one week prior to his death. OUTPUT:
PMCPatients_common2044
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The case pertains to a man in his thirties with mental deficiency. He had an elder sister who had malignant colonic tumor (details unknown); however, she died a year ago. ). He underwent upper gastrointestinal series at our department, which revealed esophageal dilatation with a maximum transverse diameter of 55 mm, along with delayed esophageal clearance of barium, leading to the suspicion of achalasia (Fig. ). ). A relatively well-defined, contrast-enhanced tumor with a maximal diameter of approximately 50 mm was observed in the lesser curvature of the upper gastric corpus by abdominal computed tomography (CT). Serum ACTH and cortisol were within normal ranges, and alacrima, muscular atrophy, and muscle weakness were not observed. Intraoperatively, an exophytic tumor was identified in the lesser curvature of the upper gastric corpus of the stomach, with multiple peritoneal metastatic nodules on the jejunal serosa. Despite non-curative, total gastrectomy with Roux-en-Y reconstruction was carried out to improve dysphagia and to avoid complications such as bleeding from the tumor (Fig. ). A postoperative contrast study using gastrografin was carried out 4 days following surgery, in which passage from the esophagus to the jejunum was good without anastomotic leakage. The patient was discharged from the hospital on postoperative day 9 and is currently undergoing follow-up as an outpatient, with no dysphagia.\nOUTPUT:" }, { "from": "agent", "value": "Type 2 Achalasia, Gastrointestinal Stromal Tumor (GIST)" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: The case pertains to a man in his thirties with mental deficiency. He had an elder sister who had malignant colonic tumor (details unknown); however, she died a year ago. ). He underwent upper gastrointestinal series at our department, which revealed esophageal dilatation with a maximum transverse diameter of 55 mm, along with delayed esophageal clearance of barium, leading to the suspicion of achalasia (Fig. ). ). A relatively well-defined, contrast-enhanced tumor with a maximal diameter of approximately 50 mm was observed in the lesser curvature of the upper gastric corpus by abdominal computed tomography (CT). Serum ACTH and cortisol were within normal ranges, and alacrima, muscular atrophy, and muscle weakness were not observed. Intraoperatively, an exophytic tumor was identified in the lesser curvature of the upper gastric corpus of the stomach, with multiple peritoneal metastatic nodules on the jejunal serosa. Despite non-curative, total gastrectomy with Roux-en-Y reconstruction was carried out to improve dysphagia and to avoid complications such as bleeding from the tumor (Fig. ). A postoperative contrast study using gastrografin was carried out 4 days following surgery, in which passage from the esophagus to the jejunum was good without anastomotic leakage. The patient was discharged from the hospital on postoperative day 9 and is currently undergoing follow-up as an outpatient, with no dysphagia. OUTPUT:
PMCPatients_common1139
[ { "from": "human", "value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Baseline rhythm was atrial fibrillation with slow ventricular response. He was on amiodarone, beta-blocker and angiotensin receptor blocker at the time of implantation, without heart failure symptoms.\\nThe patient continued to have symptomatic VT episodes with appropriate ICD discharges. Amiodarone was increased, but it was discontinued due to severe hypothyroidism. He was placed on sotalol 80 mg twice a day, but soon stopped after patient developed QT prolongation and asthenia. Patient was switched to propafenone 300 mg 3 times daily, but again side effects (diarrhea, nausea-vomiting) led to therapy discontinuation. Symptomatic VT episodes with multiple morphologies requiring ICD discharges and/or emergency room visits continued, despite optimization of ATP therapy.\\nProcainamide was initiated with better tolerance, although patient continued to be symptomatic with frequent VT episodes. Of note, cardiac function in consecutive echocardiograms had initially remained stable after ICD implantation. The rest of pharmacological agents had not been modified. After myocardial ischemia was ruled out, a catheter ablation procedure was planned, but patient refused invasive procedures. Trying dronedarone was offered, with clear understanding of its off-label and compassionate use. After informed consent, patient was switched to droneradone 400 mg twice daily. On follow-up, patient reported significant improvement of his symptoms, with just one episode of VT successfully treated with ATP therapy over the next 12 months, and systolic function recovery to prior 30% coinciding with the decrease of arrhythmic burden. Significant reduction of ICD shocks before and after droneradone initiation is shown in .\nOUTPUT:" }, { "from": "agent", "value": "Recurrent Ventricular Tachycardia, Non-ischemic dilated cardiomyopathy, Severe ventricular systolic dysfunction" } ]
As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it. INPUT: Baseline rhythm was atrial fibrillation with slow ventricular response. He was on amiodarone, beta-blocker and angiotensin receptor blocker at the time of implantation, without heart failure symptoms.\nThe patient continued to have symptomatic VT episodes with appropriate ICD discharges. Amiodarone was increased, but it was discontinued due to severe hypothyroidism. He was placed on sotalol 80 mg twice a day, but soon stopped after patient developed QT prolongation and asthenia. Patient was switched to propafenone 300 mg 3 times daily, but again side effects (diarrhea, nausea-vomiting) led to therapy discontinuation. Symptomatic VT episodes with multiple morphologies requiring ICD discharges and/or emergency room visits continued, despite optimization of ATP therapy.\nProcainamide was initiated with better tolerance, although patient continued to be symptomatic with frequent VT episodes. Of note, cardiac function in consecutive echocardiograms had initially remained stable after ICD implantation. The rest of pharmacological agents had not been modified. After myocardial ischemia was ruled out, a catheter ablation procedure was planned, but patient refused invasive procedures. Trying dronedarone was offered, with clear understanding of its off-label and compassionate use. After informed consent, patient was switched to droneradone 400 mg twice daily. On follow-up, patient reported significant improvement of his symptoms, with just one episode of VT successfully treated with ATP therapy over the next 12 months, and systolic function recovery to prior 30% coinciding with the decrease of arrhythmic burden. Significant reduction of ICD shocks before and after droneradone initiation is shown in . OUTPUT: