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PMCPatients_common2783 | [
{
"from": "human",
"value": "As a physician engaged in 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 presented with rapidly deteriorating left-sided hearing loss, vertigo and mild intermittent dull ache in her left ear of 2 months' duration, followed by a left-sided lower motor neurone facial nerve weakness. She recalled 2 or 3 similar episodes of vertigo 2 years previously that resolved spontaneously. Thirteen years before, she had been diagnosed with invasive lobular adenocarcinoma of her right breast, treated by simple mastectomy and 5 years of adjuvant tamoxifen. 2 years later, she underwent prophylactic contralateral mastectomy. Regular follow-up had shown no evidence of disease recurrence. On present admission, physical examination revealed absent left corneal reflex and ipsilateral lower motor neurone facial nerve dysfunction (House Brackmann grade 6). The Unterberger's stepping test was to the left, Romberg was unsteady and Hitzelberger sign was positive. Pure tone audiometry showed left-sided high frequency sensorineural hearing loss. The lesion was excised via a translabyrinthine approach. Intra-operatively, it resembled a vestibular schwannoma, albeit unusually vascular. Temporal bone and adjacent structures were uninvolved. No schwannoma was demonstrated. Immunohistochemistry was consistent with a breast primary with oestrogen receptor (Figure ), pan-cytokeratin (Figure ), cytokeratin 7, epithelial membrane antigen and E-cadherin positivity. CK20 was negative. There was no evidence of intracranial tumor recurrence on repeat MRI 6 months after surgery.\nOUTPUT:"
},
{
"from": "agent",
"value": "Internal auditory canal metastasis, Metastatic adenocarcinoma infiltrating the nerve sheath, Multiple bone metastases"
}
] | As a physician engaged 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 presented with rapidly deteriorating left-sided hearing loss, vertigo and mild intermittent dull ache in her left ear of 2 months' duration, followed by a left-sided lower motor neurone facial nerve weakness. She recalled 2 or 3 similar episodes of vertigo 2 years previously that resolved spontaneously. Thirteen years before, she had been diagnosed with invasive lobular adenocarcinoma of her right breast, treated by simple mastectomy and 5 years of adjuvant tamoxifen. 2 years later, she underwent prophylactic contralateral mastectomy. Regular follow-up had shown no evidence of disease recurrence. On present admission, physical examination revealed absent left corneal reflex and ipsilateral lower motor neurone facial nerve dysfunction (House Brackmann grade 6). The Unterberger's stepping test was to the left, Romberg was unsteady and Hitzelberger sign was positive. Pure tone audiometry showed left-sided high frequency sensorineural hearing loss. The lesion was excised via a translabyrinthine approach. Intra-operatively, it resembled a vestibular schwannoma, albeit unusually vascular. Temporal bone and adjacent structures were uninvolved. No schwannoma was demonstrated. Immunohistochemistry was consistent with a breast primary with oestrogen receptor (Figure ), pan-cytokeratin (Figure ), cytokeratin 7, epithelial membrane antigen and E-cadherin positivity. CK20 was negative. There was no evidence of intracranial tumor recurrence on repeat MRI 6 months after surgery.
OUTPUT: |
PMCPatients_common2761 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 44 year old male, presented to the ER with complaints of bleeding per rectum for 1 day. His complaints started with 4 episodes of watery diarrhea with dark blood. He denied any fever, abdominal pain, weight loss, and change in bowel pattern, hematemesis or jaundice. The patient had immigrated to USA 18 months prior from India where he was found to be anemic requiring two blood transfusions over the last four years. Past medical history was significant for anemia only and his home medication was an iron and folate supplement. His anemia was investigated with an esophagogastroduodenoscopy (EGD) and colonoscopy 6 months prior in India, both of which were normal. In the emergency room his vital signs revealed: temperature 98.6°F, pulse 115/min, BP 80/55 mmHg, respiratory rate 32/min and O2 saturation 100% on room air. He was not in acute distress, abdomen was soft, non-tender, non-distended, no masses or organomegaly and normal bowel sounds. Rectal exam revealed frank blood. Significant initial lab findings included a hemoglobin level of 8.1 gm/dl and hematocrit of 25.1%. Aggressive fluid replacement via two wide bore IV lines was instituted accompanied by two units of PRBC and he was admitted to the intensive care unit. After stabilization, an EGD did not show any bleeding source. Colonoscopy showed a bleeding mass [Figure ] in the ileum 20 cm from the ileocecal valve. Emergent laparotomy and excision of the mass was done. Numerous smaller intraluminal nodules were scattered throughout the small bowel. CT scan of thorax, abdomen and pelvis suggested probable metastasis to lymph nodes [Table ] without liver involvement. The patient's 24 hr urine 5-HIAA level was 13.1 which is insignificant considering the fact that the patient was getting lorazepam, β-blocker and fruits in his diet, all of which can contribute to a slightly increased level.\nOUTPUT:"
},
{
"from": "agent",
"value": "Carcinoid tumor"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 44 year old male, presented to the ER with complaints of bleeding per rectum for 1 day. His complaints started with 4 episodes of watery diarrhea with dark blood. He denied any fever, abdominal pain, weight loss, and change in bowel pattern, hematemesis or jaundice. The patient had immigrated to USA 18 months prior from India where he was found to be anemic requiring two blood transfusions over the last four years. Past medical history was significant for anemia only and his home medication was an iron and folate supplement. His anemia was investigated with an esophagogastroduodenoscopy (EGD) and colonoscopy 6 months prior in India, both of which were normal. In the emergency room his vital signs revealed: temperature 98.6°F, pulse 115/min, BP 80/55 mmHg, respiratory rate 32/min and O2 saturation 100% on room air. He was not in acute distress, abdomen was soft, non-tender, non-distended, no masses or organomegaly and normal bowel sounds. Rectal exam revealed frank blood. Significant initial lab findings included a hemoglobin level of 8.1 gm/dl and hematocrit of 25.1%. Aggressive fluid replacement via two wide bore IV lines was instituted accompanied by two units of PRBC and he was admitted to the intensive care unit. After stabilization, an EGD did not show any bleeding source. Colonoscopy showed a bleeding mass [Figure ] in the ileum 20 cm from the ileocecal valve. Emergent laparotomy and excision of the mass was done. Numerous smaller intraluminal nodules were scattered throughout the small bowel. CT scan of thorax, abdomen and pelvis suggested probable metastasis to lymph nodes [Table ] without liver involvement. The patient's 24 hr urine 5-HIAA level was 13.1 which is insignificant considering the fact that the patient was getting lorazepam, β-blocker and fruits in his diet, all of which can contribute to a slightly increased level.
OUTPUT: |
PMCPatients_common1288 | [
{
"from": "human",
"value": "As a physician engaged in 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 female with no relevant medical history was referred to our unit with clinical symptoms consisting in abdominal discomfort and distension, nauseas, vomiting, and weight loss. On physical exploration, there was a palpable mass in the hypogastrium with high volume of ascites. Laboratory tests showed a high serum AFP level (397.0 ng/mL, normal, 0–5) and high serum CA125 level (1247 U/mL, normal, 0–35). One gastroscopy and colonoscopy were normal. A complete cytoreduction surgery included pelvic peritonectomy with total hysterectomy and bilateral salpingo-oophorectomy including Douglas pouch, complete omentectomy, right diaphragmatic peritonectomy, and appendectomy. The patient was discharged on the sixth postoperative day without any adverse event. Adjuvant treatment was completed with a combination of 6 cycles of systemic chemotherapy with carboplatin (AUC × 6) and paclitaxel (175 mg/m2).\nOUTPUT:"
},
{
"from": "agent",
"value": "Hepatoid Carcinoma of the Ovary, Peritoneal Dissemination"
}
] | As a physician engaged 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 female with no relevant medical history was referred to our unit with clinical symptoms consisting in abdominal discomfort and distension, nauseas, vomiting, and weight loss. On physical exploration, there was a palpable mass in the hypogastrium with high volume of ascites. Laboratory tests showed a high serum AFP level (397.0 ng/mL, normal, 0–5) and high serum CA125 level (1247 U/mL, normal, 0–35). One gastroscopy and colonoscopy were normal. A complete cytoreduction surgery included pelvic peritonectomy with total hysterectomy and bilateral salpingo-oophorectomy including Douglas pouch, complete omentectomy, right diaphragmatic peritonectomy, and appendectomy. The patient was discharged on the sixth postoperative day without any adverse event. Adjuvant treatment was completed with a combination of 6 cycles of systemic chemotherapy with carboplatin (AUC × 6) and paclitaxel (175 mg/m2).
OUTPUT: |
PMCPatients_common2119 | [
{
"from": "human",
"value": "As a physician engaged 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 never received bisphosphonate. The left lower limb was in an external mal-rotation of 600 and LLD of 7cm. Radiographs showed a mal-united, mal-rotated right femur with NSA of 870 and obvious mal-rotation. We used similar surgical procedure as described below in October, 2013. A Rush rod sized 1F (6.5mm) and two Kirschner wires sized 1.6mm were used to fix the osteotomy. One year after the surgery, the patient ambulated more easily with walking frame. The NSA was maintained at 1100, LLD was improved to 4cm and rotation was corrected. The ability to ambulate has remained good until the most recent phone conversation in May 2017.\\nWe performed the procedure in both patients in the supine position with standard lateral exposure. Transverse osteotomy was carried out at the subtrochanteric level. The proximal segment was reamed retrograde from the osteotomy site using cannulated drill to ensure it started at the lateral most and exited at the greater trochanter. Next, a few Kirschner wires sized 1.6mm were inserted from the lateral femur at subtrochanteric level to the neck. These wires acted as joy-sticks during manipulation of the proximal femur to the required neck-shaft angle (NSA). The distal segment was also reamed using cannulated drill bit to ensure no penetration of the cortex. In the first patient, a Rush rod of selected length and diameter was inserted antegrade from the greater trochanter to the osteotomy site. The Rush rod was then passed through the osteotomy side to distal femur while the NSA was maintained by the Kirschner wires (). In the second patient, the Rush rod was inserted retrograde from the knee joint to greater trochanter while the NSA was maintained by the Kirschner wires. The wires were bent flush on the lateral side of the femur and held with cerclage wires to maintain the NSA and avoid rotation ().\nOUTPUT:"
},
{
"from": "agent",
"value": "Osteogenesis Imperfecta"
}
] | As a physician engaged 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 never received bisphosphonate. The left lower limb was in an external mal-rotation of 600 and LLD of 7cm. Radiographs showed a mal-united, mal-rotated right femur with NSA of 870 and obvious mal-rotation. We used similar surgical procedure as described below in October, 2013. A Rush rod sized 1F (6.5mm) and two Kirschner wires sized 1.6mm were used to fix the osteotomy. One year after the surgery, the patient ambulated more easily with walking frame. The NSA was maintained at 1100, LLD was improved to 4cm and rotation was corrected. The ability to ambulate has remained good until the most recent phone conversation in May 2017.\nWe performed the procedure in both patients in the supine position with standard lateral exposure. Transverse osteotomy was carried out at the subtrochanteric level. The proximal segment was reamed retrograde from the osteotomy site using cannulated drill to ensure it started at the lateral most and exited at the greater trochanter. Next, a few Kirschner wires sized 1.6mm were inserted from the lateral femur at subtrochanteric level to the neck. These wires acted as joy-sticks during manipulation of the proximal femur to the required neck-shaft angle (NSA). The distal segment was also reamed using cannulated drill bit to ensure no penetration of the cortex. In the first patient, a Rush rod of selected length and diameter was inserted antegrade from the greater trochanter to the osteotomy site. The Rush rod was then passed through the osteotomy side to distal femur while the NSA was maintained by the Kirschner wires (). In the second patient, the Rush rod was inserted retrograde from the knee joint to greater trochanter while the NSA was maintained by the Kirschner wires. The wires were bent flush on the lateral side of the femur and held with cerclage wires to maintain the NSA and avoid rotation ().
OUTPUT: |
PMCPatients_common1864 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: At the age of 56 years, he was admitted for another stroke-like episode. He presented to the emergency department with vertigo, confusion, speech disturbance, difficulties in finding words, impaired concentration, and ataxic gait. Clinical exam revealed weak head anteflexion, cerebellar speech, visual impairment with only light/dark discrimination, hypoacusis, mild ptosis bilaterally, diffuse wasting of the upper limbs, bradydiadochokinesia bilaterally, wasting of the thighs, lower limb ataxia, and reduced Achilles tendon reflexes. There was ataxic stance and gait requiring a walker. Cerebral MRI showed a typical acute, stroke-like lesion (SLL) in an occipito-temporal distribution. Revision of imaging studies from a previous hospitalisation revealed that the pre-epiglottic cyst with 1 cm in diameter and protein-rich content had been first detected accidentally on ultrasound and later by MRI already at the age of 50 years (Figure ). Since then the cyst had remained unchanged regarding morphology and extension. He denied speech disturbance or dysphagia. A branchiogenic cyst was excluded due to the atypical location. Zenker’s diverticulum was excluded due to the location and morphology. The previous history was negative for previous trauma, chronic infection, or surgery at the site of the cyst. There was no indication for parasitosis.\nOUTPUT:"
},
{
"from": "agent",
"value": "Tongue Root Cyst, Mitochondrial Encephalopathy, Lactic Acidosis, Stroke-like Episodes (MELAS) 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: At the age of 56 years, he was admitted for another stroke-like episode. He presented to the emergency department with vertigo, confusion, speech disturbance, difficulties in finding words, impaired concentration, and ataxic gait. Clinical exam revealed weak head anteflexion, cerebellar speech, visual impairment with only light/dark discrimination, hypoacusis, mild ptosis bilaterally, diffuse wasting of the upper limbs, bradydiadochokinesia bilaterally, wasting of the thighs, lower limb ataxia, and reduced Achilles tendon reflexes. There was ataxic stance and gait requiring a walker. Cerebral MRI showed a typical acute, stroke-like lesion (SLL) in an occipito-temporal distribution. Revision of imaging studies from a previous hospitalisation revealed that the pre-epiglottic cyst with 1 cm in diameter and protein-rich content had been first detected accidentally on ultrasound and later by MRI already at the age of 50 years (Figure ). Since then the cyst had remained unchanged regarding morphology and extension. He denied speech disturbance or dysphagia. A branchiogenic cyst was excluded due to the atypical location. Zenker’s diverticulum was excluded due to the location and morphology. The previous history was negative for previous trauma, chronic infection, or surgery at the site of the cyst. There was no indication for parasitosis.
OUTPUT: |
PMCPatients_common3475 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 33-year-old female Chinese patient was admitted to our hospital with intermittent fever and weakness for 3 mo.\\nAbout 2 mo previously, this patient was admitted to a local hospital due to fever and decreased appetite. The laboratory examination showed leukopenia and liver function damage. EBV-DNA was 6.09 × 105 IU/mL in September 2017. Fever was not effectively improved with cephalosporin and ganciclovir. Interferon was given; EBV-DNA decreased slightly, but fever persisted. The fever had lasted 3 mo when she was admitted to our hospital in December 2017.\\nThe patient had no other previous medical history.\\nThe patient had no personal or family history of similar illnesses.\\nPhysical examination revealed enlargement of multiple superficial lymph nodes and splenomegaly. Abdominal ultrasonography showed that the spleen was 15.7 cm in diameter.\\nComplete blood count revealed bicytopenia with a white blood cell count of 1.39 × 109/L, hemoglobin 14.2 gm/dL, and platelet count of 89 × 109/L. ALT and AST were elevated to 95 U/L and 173.2 U/L, respectively. EBV-DNA (whole blood) was 5.1 × 104 copies/mL and EBV-DNA (plasma) was 5.60 × 104 copies/mL in December 2017. Natural killer cell was mainly involved in lymphocyte subsets of EBV infection, despite the accumulation of all lymphocyte subsets. Flow cytometry of the bone marrow revealed about 2.26% abnormal phenotype natural killer (NK) cells, expressing CD56bri, CD2, CD7, CD94bri, CD161, and CD159a. Biopsy was taken from the swollen left inguinal lymph node and bone marrow. However, no tumor was detected, and EBV-encoded small RNA (EBER) was not found by in situ hybridization of two biopsies. The tests of hepatitis virus, human immunodeficiency virus, antinuclear antibody, and rheumatoid antibody were all negative.\nOUTPUT:"
},
{
"from": "agent",
"value": "Chronic active Epstein-Barr virus infection"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 33-year-old female Chinese patient was admitted to our hospital with intermittent fever and weakness for 3 mo.\nAbout 2 mo previously, this patient was admitted to a local hospital due to fever and decreased appetite. The laboratory examination showed leukopenia and liver function damage. EBV-DNA was 6.09 × 105 IU/mL in September 2017. Fever was not effectively improved with cephalosporin and ganciclovir. Interferon was given; EBV-DNA decreased slightly, but fever persisted. The fever had lasted 3 mo when she was admitted to our hospital in December 2017.\nThe patient had no other previous medical history.\nThe patient had no personal or family history of similar illnesses.\nPhysical examination revealed enlargement of multiple superficial lymph nodes and splenomegaly. Abdominal ultrasonography showed that the spleen was 15.7 cm in diameter.\nComplete blood count revealed bicytopenia with a white blood cell count of 1.39 × 109/L, hemoglobin 14.2 gm/dL, and platelet count of 89 × 109/L. ALT and AST were elevated to 95 U/L and 173.2 U/L, respectively. EBV-DNA (whole blood) was 5.1 × 104 copies/mL and EBV-DNA (plasma) was 5.60 × 104 copies/mL in December 2017. Natural killer cell was mainly involved in lymphocyte subsets of EBV infection, despite the accumulation of all lymphocyte subsets. Flow cytometry of the bone marrow revealed about 2.26% abnormal phenotype natural killer (NK) cells, expressing CD56bri, CD2, CD7, CD94bri, CD161, and CD159a. Biopsy was taken from the swollen left inguinal lymph node and bone marrow. However, no tumor was detected, and EBV-encoded small RNA (EBER) was not found by in situ hybridization of two biopsies. The tests of hepatitis virus, human immunodeficiency virus, antinuclear antibody, and rheumatoid antibody were all negative.
OUTPUT: |
PMCPatients_common15 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A three-year-old girl was referred to the Reference Centre of Rare Diseases in Paris. Her medical history was noncontributory. According to her mother, she complained with pain while eating, moderate sensitivity during tooth brushing and above all poor aesthetic aspect of her teeth. Intraoral examination revealed a hypoplastic AIH with yellow teeth and rough surfaces (Fig. ). Brown extrinsic discoloration was seen in the hypoplastic area. Enamel was reduced in thickness and severely hypoplastic, giving the idea of a false microdontia with multiple diastemas. Molars were the most affected teeth showing reduced crown height. In addition, anterior open bite was noted without thumb sucking. Treatment was planned following 3 objectives at this age:Pain prevention and treatment Protection of dental tissue integrity in order to maintain occlusal function and limit dental biofilm retention Restoration of smile aesthetics.\\nOn primary molars, the choice of treatment was stainless steel crowns (3 M™ ESPE™) because the occlusal morphology was lost (Fig. ). This way, vertical dimension was slightly increased and maintained. The incisors and canines were isolated with a rubber dam and direct dental composite restorations were placed (Herculite, Kerr [, ] with ER2 adhesives Optibond SL). Teeth were not prepared; we etched with 35% Phosphatidic acid for 30 s, rinsed for 30 s with air and water. Then teeth were air dried, adhesive was applied with an applicator tip, excesses were removed with air before polymerization for 45 s. Affected enamel was not removed but bonding was directly applied to it. As enamel surface appeared rough, a flow composite (Tetric Evoflow, Ivoclar) was applied and served as intermediate material. Its higher fluidity and wettability would allow penetrating enamel roughness (Fig. ). Because tooth morphology of anterior teeth was not severely altered, “Odus” molds were not useful to offer a correct restoration. Composite resins were applied in one layer. Finishing and polishing were achieved with abrasive discs (Sof-lex/3 M ESPE). Patient follow-ups were done 6 months and 1 year after treatment. Composite sealing and oral hygiene were controlled.\nOUTPUT:"
},
{
"from": "agent",
"value": "Amelogenesis imperfecta"
}
] | As a physician engaged 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 three-year-old girl was referred to the Reference Centre of Rare Diseases in Paris. Her medical history was noncontributory. According to her mother, she complained with pain while eating, moderate sensitivity during tooth brushing and above all poor aesthetic aspect of her teeth. Intraoral examination revealed a hypoplastic AIH with yellow teeth and rough surfaces (Fig. ). Brown extrinsic discoloration was seen in the hypoplastic area. Enamel was reduced in thickness and severely hypoplastic, giving the idea of a false microdontia with multiple diastemas. Molars were the most affected teeth showing reduced crown height. In addition, anterior open bite was noted without thumb sucking. Treatment was planned following 3 objectives at this age:Pain prevention and treatment Protection of dental tissue integrity in order to maintain occlusal function and limit dental biofilm retention Restoration of smile aesthetics.\nOn primary molars, the choice of treatment was stainless steel crowns (3 M™ ESPE™) because the occlusal morphology was lost (Fig. ). This way, vertical dimension was slightly increased and maintained. The incisors and canines were isolated with a rubber dam and direct dental composite restorations were placed (Herculite, Kerr [, ] with ER2 adhesives Optibond SL). Teeth were not prepared; we etched with 35% Phosphatidic acid for 30 s, rinsed for 30 s with air and water. Then teeth were air dried, adhesive was applied with an applicator tip, excesses were removed with air before polymerization for 45 s. Affected enamel was not removed but bonding was directly applied to it. As enamel surface appeared rough, a flow composite (Tetric Evoflow, Ivoclar) was applied and served as intermediate material. Its higher fluidity and wettability would allow penetrating enamel roughness (Fig. ). Because tooth morphology of anterior teeth was not severely altered, “Odus” molds were not useful to offer a correct restoration. Composite resins were applied in one layer. Finishing and polishing were achieved with abrasive discs (Sof-lex/3 M ESPE). Patient follow-ups were done 6 months and 1 year after treatment. Composite sealing and oral hygiene were controlled.
OUTPUT: |
PMCPatients_common1473 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 4 days old baby girl, presented with respiratory difficulty to a missionary hospital, was diagnosed clinically as early onset sepsis case. Despite antibiotic therapy, she remained in cardiorespiratory distress. Hence, she was referred to a tertiary hospital with chest X-ray evidence of cardiomegaly. The neonate was born from nonconsangeous marriage.\\nThe patient weight, Height and Head circumference was 2,920gm, 47cm, and 34cm standardized to (25th–50th) (5th–10th) and (25th–50th) centile, respectively. RR-70/minute and AHR132bpm, BP-88/51mmHg, T-36.7oC and O2 sat 92% and 74% with and without oxygen respectively. Neonate had pink conjunctiva and the lung fields were clear. There was grade 3/6 holo-systolic murmur at tricuspid area, and liver age was tipped. There were four hypomelanotic macules over the buttock, legs and the trunk, the largest measuring 5 X 10mm in size.\\nChest X-ray showed an enlarged heart shadow compressing the lung fields bilaterally (). 2D-echocardiography showed multiple, large echogenic masses in the right and left ventricular cavity, embedding the septum, left ventricular posterior wall and left atrium. The mass compressed the atrio-ventricular valves causing mitral and tricuspid regurgitation (). Similarly, brain magnetic resonance imaging showed brain surface, sub-ependymal nodules and cortical tubers (). Nevertheless, the EKG read as normal for age, trans-fontanel, and renal ultrasound studies were reported normal. Finally, the patient improved, the heart rate decreased from 160 to 104 bpm, RR decreased from 90 to 60/minute, and O2 sat increased from 74% to 98% at 3 litter oxygen. It was reported that the repeat echocardiography before discharge showed decrease in tumor size. The patient was discharged in a stable condition. The parents were counseled on future risks of epilepsy and accompanying cognitive abnormalities. Currently, the patient is 3 years and 6 months old, well thriving having follow-up at a missionary hospital in her locality.\nOUTPUT:"
},
{
"from": "agent",
"value": "Cardiac Rhabdomyoma, Tuberous Sclerosis Complex"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 4 days old baby girl, presented with respiratory difficulty to a missionary hospital, was diagnosed clinically as early onset sepsis case. Despite antibiotic therapy, she remained in cardiorespiratory distress. Hence, she was referred to a tertiary hospital with chest X-ray evidence of cardiomegaly. The neonate was born from nonconsangeous marriage.\nThe patient weight, Height and Head circumference was 2,920gm, 47cm, and 34cm standardized to (25th–50th) (5th–10th) and (25th–50th) centile, respectively. RR-70/minute and AHR132bpm, BP-88/51mmHg, T-36.7oC and O2 sat 92% and 74% with and without oxygen respectively. Neonate had pink conjunctiva and the lung fields were clear. There was grade 3/6 holo-systolic murmur at tricuspid area, and liver age was tipped. There were four hypomelanotic macules over the buttock, legs and the trunk, the largest measuring 5 X 10mm in size.\nChest X-ray showed an enlarged heart shadow compressing the lung fields bilaterally (). 2D-echocardiography showed multiple, large echogenic masses in the right and left ventricular cavity, embedding the septum, left ventricular posterior wall and left atrium. The mass compressed the atrio-ventricular valves causing mitral and tricuspid regurgitation (). Similarly, brain magnetic resonance imaging showed brain surface, sub-ependymal nodules and cortical tubers (). Nevertheless, the EKG read as normal for age, trans-fontanel, and renal ultrasound studies were reported normal. Finally, the patient improved, the heart rate decreased from 160 to 104 bpm, RR decreased from 90 to 60/minute, and O2 sat increased from 74% to 98% at 3 litter oxygen. It was reported that the repeat echocardiography before discharge showed decrease in tumor size. The patient was discharged in a stable condition. The parents were counseled on future risks of epilepsy and accompanying cognitive abnormalities. Currently, the patient is 3 years and 6 months old, well thriving having follow-up at a missionary hospital in her locality.
OUTPUT: |
PMCPatients_common4578 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Ms A, 62-year-old homemaker has been suffering from bipolar affective disorder for 35 years. She presented to us with a relapse which started about 7-8 months ago characterized by symptoms of depressed mood, anxiety, decreased socialization, loss of appetite and subsequent weight loss, decreased interest in household, poor self-care, ideas of worthlessness, pessimistic views of future, forgetfulness and psychomotor retardation. Later on she developed nihilistic delusions in which she negated the existence of her body parts and existence of her family members. Negation of existence of family members was not accompanied by any persecutory delusion or misidentification delusions. She also believed that she has been rendered very poor. She would say that their house may collapse any day and the occupants will die. Over the period she started refusing food as she considered herself to be dead. Her illness further progressed and about 4 weeks prior to admission to inpatient unit she developed mutism, refusal to eat, rigidity in all the limbs and fecal and urinary incontinence. She was brought to the emergency room of our institute with aforementioned symptoms. Her physical examination revealed mild pallor, dehydration, bilateral pitting edema and she was emaciated. On mental state examination she had sad affect, mutism, rigidity in all the four limbs and negativism. Her investigation showed hemoglobin of 10 gm/dl, hypoproteinemia and hypoalbuminemia. Further investigation revealed low vitamin D₃ levels and the magnetic resonance imaging of brain showed cerebral atrophy with mild subdural effusion. She was given a trial of intravenous lorazepam but to no relief. Therefore, decision to start ECT was taken. She was given bilateral modified ECT using thiopentone for induction and succinlycholine for muscle relaxation. Her catatonic and depressive symptoms melted away with a course of 8 ECTs and her score on Bush Francis Catatonia Rating Scale score reduced from 14 to 0 at end of 8 ECTs. Her nutritional deficiencies were addressed appropriately. Later on she was started on mood stabilizers, olanzapine and fluoxetine.\nOUTPUT:"
},
{
"from": "agent",
"value": "Cotard's syndrome, Bipolar affective disorder current episode severe depression with psychotic symptoms, Malnutrition, 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: Ms A, 62-year-old homemaker has been suffering from bipolar affective disorder for 35 years. She presented to us with a relapse which started about 7-8 months ago characterized by symptoms of depressed mood, anxiety, decreased socialization, loss of appetite and subsequent weight loss, decreased interest in household, poor self-care, ideas of worthlessness, pessimistic views of future, forgetfulness and psychomotor retardation. Later on she developed nihilistic delusions in which she negated the existence of her body parts and existence of her family members. Negation of existence of family members was not accompanied by any persecutory delusion or misidentification delusions. She also believed that she has been rendered very poor. She would say that their house may collapse any day and the occupants will die. Over the period she started refusing food as she considered herself to be dead. Her illness further progressed and about 4 weeks prior to admission to inpatient unit she developed mutism, refusal to eat, rigidity in all the limbs and fecal and urinary incontinence. She was brought to the emergency room of our institute with aforementioned symptoms. Her physical examination revealed mild pallor, dehydration, bilateral pitting edema and she was emaciated. On mental state examination she had sad affect, mutism, rigidity in all the four limbs and negativism. Her investigation showed hemoglobin of 10 gm/dl, hypoproteinemia and hypoalbuminemia. Further investigation revealed low vitamin D₃ levels and the magnetic resonance imaging of brain showed cerebral atrophy with mild subdural effusion. She was given a trial of intravenous lorazepam but to no relief. Therefore, decision to start ECT was taken. She was given bilateral modified ECT using thiopentone for induction and succinlycholine for muscle relaxation. Her catatonic and depressive symptoms melted away with a course of 8 ECTs and her score on Bush Francis Catatonia Rating Scale score reduced from 14 to 0 at end of 8 ECTs. Her nutritional deficiencies were addressed appropriately. Later on she was started on mood stabilizers, olanzapine and fluoxetine.
OUTPUT: |
PMCPatients_common4372 | [
{
"from": "human",
"value": "As a physician engaged in 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 postmenopausal woman who was 160 cm in height and weighed 67.1 kg (body mass index 26.2) came to our institute with a 1-mo history of vaginal bleeding with no associated abdominal pain.\\nThe patient has been treated for diabetes mellitus for the past 8 years. She had no history of hypertension and reported did not use tobacco or alcohol. She had no history of exposure to oral estrogen, and her family history was unremarkable.\\nGynecologic examination revealed an enlarged smooth-faced cervix and decreased mobility of the uterus, but no gross lesion.\\nSerum carbohydrate antigen (CA)-199 was 85 U/mL (normal range 0-35 U/mL), and carcinoembryonic antigen (CEA), CA-125, and CA-724 were normal. Human papillomavirus (HPV) DNA testing was negative.\\nBiopsy of fractional curettage resulted in the diagnosis of endocervical poorly differentiated adenocarcinoma, and endometrial endometrioid adenocarcinoma, in conjunction with atypical hyperplasia. Further esophagogastroduodenoscopy examination revealed multiple ulcerative lesions in the gastric angle and antrum. Biopsy results revealed gastric intraepithelial neoplasia with focal intramucosal cancerization.\nOUTPUT:"
},
{
"from": "agent",
"value": "Synchronous quadruple primary malignancies of the cervix, endometrium, ovary, and stomach"
}
] | As a physician engaged 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 postmenopausal woman who was 160 cm in height and weighed 67.1 kg (body mass index 26.2) came to our institute with a 1-mo history of vaginal bleeding with no associated abdominal pain.\nThe patient has been treated for diabetes mellitus for the past 8 years. She had no history of hypertension and reported did not use tobacco or alcohol. She had no history of exposure to oral estrogen, and her family history was unremarkable.\nGynecologic examination revealed an enlarged smooth-faced cervix and decreased mobility of the uterus, but no gross lesion.\nSerum carbohydrate antigen (CA)-199 was 85 U/mL (normal range 0-35 U/mL), and carcinoembryonic antigen (CEA), CA-125, and CA-724 were normal. Human papillomavirus (HPV) DNA testing was negative.\nBiopsy of fractional curettage resulted in the diagnosis of endocervical poorly differentiated adenocarcinoma, and endometrial endometrioid adenocarcinoma, in conjunction with atypical hyperplasia. Further esophagogastroduodenoscopy examination revealed multiple ulcerative lesions in the gastric angle and antrum. Biopsy results revealed gastric intraepithelial neoplasia with focal intramucosal cancerization.
OUTPUT: |
PMCPatients_common538 | [
{
"from": "human",
"value": "As a physician engaged in 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 female patient with a history of radical hysterectomy for endometrioid carcinoma (FIGO II) presented with a tumor in the tail of the pancreas during her follow-up and she was referred to our hospital for additional work up. MRI scan showed a pancreatic tumor that measured 8.6 cm x 7 cm x 9 cm infiltrating the surrounding tissues (spleen, left kidney, and left adrenal gland) and a metastatic lesion (segment IV) in the liver as can be seen in Figure .\\nTumor markers carcinoembryonic antigen, carbohydrate antigen 19-9, and serum chromogranin-A were within the normal range. An endoscopic ultrasound (EUS) and fine needle aspiration (FNA) of the tumor were performed and the cytology described the lesion as clear cell carcinoma of the kidney. The patient was referred to the medical oncology department with a provisional diagnosis of renal cell tumor and a multi-targeted receptor tyrosine kinase inhibitor (sunitinib) 50 mg/day was initiated. After four cycles of sunitinib, a follow-up CT scan demonstrated a decrease in the size of the tumor (6.3 cm x 4.3 cm x 3 cm) (Figure ).\\nNext, following the decision of multidisciplinary meeting, the patient underwent exploratory laparotomy. A distal pancreatectomy en bloc with the spleen and left kidney was performed in addition to liver metastasectomy. No signs of other metastases were recognized during surgery. The kidney was in close proximity with the tumor without being infiltrated. The neoplastic cells were with clear cytoplasm and glycogen rich by periodic acid-Schiff stain (Figure ). No adjuvant chemotherapy was administered and at last follow-up three years post-operatively, the patient was asymptomatic without clinical or radiographic evidence of recurrent disease.\nOUTPUT:"
},
{
"from": "agent",
"value": "Serous Microcystic Cystadenocarcinoma of the Pancreas, Synchronous Liver Metastases"
}
] | As a physician engaged 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 female patient with a history of radical hysterectomy for endometrioid carcinoma (FIGO II) presented with a tumor in the tail of the pancreas during her follow-up and she was referred to our hospital for additional work up. MRI scan showed a pancreatic tumor that measured 8.6 cm x 7 cm x 9 cm infiltrating the surrounding tissues (spleen, left kidney, and left adrenal gland) and a metastatic lesion (segment IV) in the liver as can be seen in Figure .\nTumor markers carcinoembryonic antigen, carbohydrate antigen 19-9, and serum chromogranin-A were within the normal range. An endoscopic ultrasound (EUS) and fine needle aspiration (FNA) of the tumor were performed and the cytology described the lesion as clear cell carcinoma of the kidney. The patient was referred to the medical oncology department with a provisional diagnosis of renal cell tumor and a multi-targeted receptor tyrosine kinase inhibitor (sunitinib) 50 mg/day was initiated. After four cycles of sunitinib, a follow-up CT scan demonstrated a decrease in the size of the tumor (6.3 cm x 4.3 cm x 3 cm) (Figure ).\nNext, following the decision of multidisciplinary meeting, the patient underwent exploratory laparotomy. A distal pancreatectomy en bloc with the spleen and left kidney was performed in addition to liver metastasectomy. No signs of other metastases were recognized during surgery. The kidney was in close proximity with the tumor without being infiltrated. The neoplastic cells were with clear cytoplasm and glycogen rich by periodic acid-Schiff stain (Figure ). No adjuvant chemotherapy was administered and at last follow-up three years post-operatively, the patient was asymptomatic without clinical or radiographic evidence of recurrent disease.
OUTPUT: |
PMCPatients_common1765 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She also complained of involuntary leakage of urine for the last 7 years. The incontinence was throughout both day and night. She did not have an urge to pass urine. The urinary flow was intermittent. There was no fecal incontinence. Sexual activity was also compromised due to coital incontinence.\\nOver the last 7 years, she had been admitted on three occasions for urinary tract infections to a gynecology ward at a tertiary hospital. The reason for pyelonephritis on the last admission was attributed to hydronephrosis. She had also been on clinic follow-up for urinary incontinence and had been treated with antimuscarinics and lifestyle modifications. She had not undergone any surgery for urinary incontinence. As there had not been any improvement, she had later defaulted follow-up.\\nOn abdominal examination, a distended bladder was found. Neurological examination revealed a saddle sensory loss of S2–S4 dermatomes. There was no sensory loss over the lower limbs. Bladder sensation was absent, but there was some degree (reduced) of anal sphincter tone. Motor functions and reflexes were normal in the limbs.\\nMagnetic resonance imaging (MRI) revealed L5–S1 spondylolisthesis (Fig. ). Computerized tomography (CT) of the brain was normal. Despite bladder decompression, serum creatinine remained elevated with persistent bilateral hydronephrosis indicative of secondary bilateral vesicoureteric junctional obstruction due to a grossly thickened bladder wall. Thus, bilateral ureteric stents were placed. Subsequently the serum creatinine improved from 6.54 to 2.57 mg/dL, and upper tract dilation reduced significantly.\nOUTPUT:"
},
{
"from": "agent",
"value": "Cauda equina lesion, Vulval abscess"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: She also complained of involuntary leakage of urine for the last 7 years. The incontinence was throughout both day and night. She did not have an urge to pass urine. The urinary flow was intermittent. There was no fecal incontinence. Sexual activity was also compromised due to coital incontinence.\nOver the last 7 years, she had been admitted on three occasions for urinary tract infections to a gynecology ward at a tertiary hospital. The reason for pyelonephritis on the last admission was attributed to hydronephrosis. She had also been on clinic follow-up for urinary incontinence and had been treated with antimuscarinics and lifestyle modifications. She had not undergone any surgery for urinary incontinence. As there had not been any improvement, she had later defaulted follow-up.\nOn abdominal examination, a distended bladder was found. Neurological examination revealed a saddle sensory loss of S2–S4 dermatomes. There was no sensory loss over the lower limbs. Bladder sensation was absent, but there was some degree (reduced) of anal sphincter tone. Motor functions and reflexes were normal in the limbs.\nMagnetic resonance imaging (MRI) revealed L5–S1 spondylolisthesis (Fig. ). Computerized tomography (CT) of the brain was normal. Despite bladder decompression, serum creatinine remained elevated with persistent bilateral hydronephrosis indicative of secondary bilateral vesicoureteric junctional obstruction due to a grossly thickened bladder wall. Thus, bilateral ureteric stents were placed. Subsequently the serum creatinine improved from 6.54 to 2.57 mg/dL, and upper tract dilation reduced significantly.
OUTPUT: |
PMCPatients_common666 | [
{
"from": "human",
"value": "As a physician engaged 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 suffered from throbbing and pulsating headaches at bilateral temporal area, accompanied by nausea and vomiting. The headache occurred 2 to 3 times in a month and the duration of pain was 48 to 72 hours. The patient felt neck stiffness, fatigue, and depression 2 days before the onset of headache. She was managed with a combination of drugs, including acetaminophen 325 mg, dichloralphenazone 100 mg, and isometheptene 65 mg 3 times a day, as well as dexibuprofen 300 mg 3 times a day and metoclopramide 10 mg 3 times a day prescribed by a neurologist. Despite these medications, pain intensity was 7 using VAS, while the MIDAS score was 32 (Table ). After informed consent was obtained, ultrasonography-guided SGB was performed by injecting 5 mL of 1.5% lidocaine at the anterior aspect of the right 6th cervical spine transverse process. Thirty minutes after the right SGB, the left SGB was performed. During the intervention, the patient was monitored with noninvasive blood pressure, heart rate, and pulse oxygenation, and no complications associated with SGB were observed. The patient received bilateral SGB every 2 weeks for a month. Pain severity was 4 on the VAS score, which lasted 24 hours. In addition, premonitory symptoms such as fatigue and mood change disappeared and the pain occurred 1 day before menstruation cycle. Therefore, bilateral SGB was performed once a month. Four months after bilateral SGB, the MIDAS score was 6 and pain was 3 on VAS, respectively (Table ). The pain was treated with oral acetaminophen 600 mg 3 times a day. Therefore, patient is still receiving bilateral SGB and oral acetaminophen 1200 mg once a month.\nOUTPUT:"
},
{
"from": "agent",
"value": "Migraine"
}
] | As a physician engaged 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 suffered from throbbing and pulsating headaches at bilateral temporal area, accompanied by nausea and vomiting. The headache occurred 2 to 3 times in a month and the duration of pain was 48 to 72 hours. The patient felt neck stiffness, fatigue, and depression 2 days before the onset of headache. She was managed with a combination of drugs, including acetaminophen 325 mg, dichloralphenazone 100 mg, and isometheptene 65 mg 3 times a day, as well as dexibuprofen 300 mg 3 times a day and metoclopramide 10 mg 3 times a day prescribed by a neurologist. Despite these medications, pain intensity was 7 using VAS, while the MIDAS score was 32 (Table ). After informed consent was obtained, ultrasonography-guided SGB was performed by injecting 5 mL of 1.5% lidocaine at the anterior aspect of the right 6th cervical spine transverse process. Thirty minutes after the right SGB, the left SGB was performed. During the intervention, the patient was monitored with noninvasive blood pressure, heart rate, and pulse oxygenation, and no complications associated with SGB were observed. The patient received bilateral SGB every 2 weeks for a month. Pain severity was 4 on the VAS score, which lasted 24 hours. In addition, premonitory symptoms such as fatigue and mood change disappeared and the pain occurred 1 day before menstruation cycle. Therefore, bilateral SGB was performed once a month. Four months after bilateral SGB, the MIDAS score was 6 and pain was 3 on VAS, respectively (Table ). The pain was treated with oral acetaminophen 600 mg 3 times a day. Therefore, patient is still receiving bilateral SGB and oral acetaminophen 1200 mg once a month.
OUTPUT: |
PMCPatients_common201 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 21-year old male conscript presented to his unit’s medical center with headache, tiredness and fever at midnight in June, 2014. He was given 1000 mg of Amoxicillin, 1000 mg of Paracetamol and an IV dose of Ringer’s lactate solution. Besides DuyDNT, only two other isolates of ST 13074 have been found, both were carrier strains identified in Vietnam in 2017 (submitted to PubMLST by our group from unpublished data). ST 13074 shared ≥ 5 identical alleles at seven typed loci with three other STs (1576, 11013 and 13455), thus making it the central ST of this group by PubMLST group’s definition (Table ). Except for isolate M3369 (ST 1576) that was identified in Italy from an invasive case, all other isolates of this group have only been detected in Vietnam, during the period from 1986 to 2017. This group do not form any clonal complex with any known isolates to date.\nOUTPUT:"
},
{
"from": "agent",
"value": "Neisseria meningitidis B, meningitis, sepsis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 21-year old male conscript presented to his unit’s medical center with headache, tiredness and fever at midnight in June, 2014. He was given 1000 mg of Amoxicillin, 1000 mg of Paracetamol and an IV dose of Ringer’s lactate solution. Besides DuyDNT, only two other isolates of ST 13074 have been found, both were carrier strains identified in Vietnam in 2017 (submitted to PubMLST by our group from unpublished data). ST 13074 shared ≥ 5 identical alleles at seven typed loci with three other STs (1576, 11013 and 13455), thus making it the central ST of this group by PubMLST group’s definition (Table ). Except for isolate M3369 (ST 1576) that was identified in Italy from an invasive case, all other isolates of this group have only been detected in Vietnam, during the period from 1986 to 2017. This group do not form any clonal complex with any known isolates to date.
OUTPUT: |
PMCPatients_common3344 | [
{
"from": "human",
"value": "As a physician engaged 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 taking warfarin (international normalised ratio (INR) 3.2) due to a history of subclavian vein thrombosis in the symptomatic limb. No other relevant medical history was noted. She described symptoms of pain and paraesthesiae along the distribution of the median nerve. Direct needle infiltration can involve pain and with the high INR, there was also an associated risk of bleeding. This manoeuvre allows the median nerve to be identified by rolling it in an ulnar to radial direction. A small blister of local anaesthetic was infiltrated into the volar aspect of the wrist over the proximal wrist crease (; ). The cannula is passed at a 45° angle underneath the TCL and then the angle is further reduced to prevent contact with the median nerve as the cannula is fed distally (). Therefore, blunt piercing of the TCL does not take place but rather the antebrachial fascia of the forearm. Prior to infiltration, the cannula tip should be at its most distal position (). The steroid is slowly infiltrated (10 mg of triamcinolone) into the tunnel and the cannula is withdrawn proximally while infiltrating. The technique is approachable, even with a slight learning curve to it. It can be taught to trainees and most importantly it is comfortable for the patient. The trajectory and length of the cannula is illustrated in .\nOUTPUT:"
},
{
"from": "agent",
"value": "Severe carpal tunnel syndrome"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: The patient was taking warfarin (international normalised ratio (INR) 3.2) due to a history of subclavian vein thrombosis in the symptomatic limb. No other relevant medical history was noted. She described symptoms of pain and paraesthesiae along the distribution of the median nerve. Direct needle infiltration can involve pain and with the high INR, there was also an associated risk of bleeding. This manoeuvre allows the median nerve to be identified by rolling it in an ulnar to radial direction. A small blister of local anaesthetic was infiltrated into the volar aspect of the wrist over the proximal wrist crease (; ). The cannula is passed at a 45° angle underneath the TCL and then the angle is further reduced to prevent contact with the median nerve as the cannula is fed distally (). Therefore, blunt piercing of the TCL does not take place but rather the antebrachial fascia of the forearm. Prior to infiltration, the cannula tip should be at its most distal position (). The steroid is slowly infiltrated (10 mg of triamcinolone) into the tunnel and the cannula is withdrawn proximally while infiltrating. The technique is approachable, even with a slight learning curve to it. It can be taught to trainees and most importantly it is comfortable for the patient. The trajectory and length of the cannula is illustrated in .
OUTPUT: |
PMCPatients_common929 | [
{
"from": "human",
"value": "As a physician engaged in 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 Asian primigravida was referred to our department in the 21st week of gestation. She complained of tachycardia, palpitations, sleeplessness and loss of weight since 4 weeks and had been started on metoprolol (47.5 mg/day) for symptom control. Thyroid function tests had been within normal range on several occasions (see Table ). She had conceived after ovarian stimulation and insemination. ). Tumor markers (CA125, Inhibin B) and beta-HCG were within normal range. Ovarian size was stable. She now complained of deepening and hoarseness of her voice; when asked, she confirmed worsening seborrhea and hypertrophy of the clitoris. Hormone analysis revealed excessively elevated androgen levels (see Table ). A provisional diagnosis of HL was established. The patient was reluctant to undergo any further diagnostic tests. A conservative approach with close clinical and laboratory controls was agreed upon. Further complications did not occur. Induction of labor was performed at 37 weeks of gestation with the aim to reduce prolonged maternal and fetal exposure to high circulating testosterone levels. She delivered a healthy male baby without signs of hyperandrogenism (weight 2920 g, Apgar 9/10/10, umbilical artery pH 7.22).\\nBreastfeeding was initiated successfully without delay. Two days after delivery, magnetic resonance imaging (MRI) was performed to rule out adrenal or ovarian malignancy (see Fig. ). During the subsequent weeks, serial ultrasound examinations showed a progressive decline of the ovarian volume; serum androgen levels normalized within 20 days. The vocal changes improved gradually; however, 1 year after delivery, a full recovery has not occurred.\nOUTPUT:"
},
{
"from": "agent",
"value": "Hyperreactio luteinalis, Gestational diabetes, Hyperthyroidism"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 34-year-old Asian primigravida was referred to our department in the 21st week of gestation. She complained of tachycardia, palpitations, sleeplessness and loss of weight since 4 weeks and had been started on metoprolol (47.5 mg/day) for symptom control. Thyroid function tests had been within normal range on several occasions (see Table ). She had conceived after ovarian stimulation and insemination. ). Tumor markers (CA125, Inhibin B) and beta-HCG were within normal range. Ovarian size was stable. She now complained of deepening and hoarseness of her voice; when asked, she confirmed worsening seborrhea and hypertrophy of the clitoris. Hormone analysis revealed excessively elevated androgen levels (see Table ). A provisional diagnosis of HL was established. The patient was reluctant to undergo any further diagnostic tests. A conservative approach with close clinical and laboratory controls was agreed upon. Further complications did not occur. Induction of labor was performed at 37 weeks of gestation with the aim to reduce prolonged maternal and fetal exposure to high circulating testosterone levels. She delivered a healthy male baby without signs of hyperandrogenism (weight 2920 g, Apgar 9/10/10, umbilical artery pH 7.22).\nBreastfeeding was initiated successfully without delay. Two days after delivery, magnetic resonance imaging (MRI) was performed to rule out adrenal or ovarian malignancy (see Fig. ). During the subsequent weeks, serial ultrasound examinations showed a progressive decline of the ovarian volume; serum androgen levels normalized within 20 days. The vocal changes improved gradually; however, 1 year after delivery, a full recovery has not occurred.
OUTPUT: |
PMCPatients_common3215 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 36-year-old male patient with an electrical injury sustained at the workplace and without any protective equipment at the time of injury was referred to our hospital. A current of 1,200 V passed through his right arm and exited from his right lower extremity. The patient lost his consciousness at the site of the accident and fell. He was admitted to the intensive care unit. He suffered third-degree burns all over his extremities.\\nOnce the patient had resumed consciousness 2 days later, he was starting to complain from a painless decrease in vision in both eyes. His best corrected visual acuity was 20/100 in the right eye and 20/200 in the left eye. The intraocular pressure (IOP) was 13 mm Hg in both eyes, and pupil examination showed a round, regular and reactive pupil without relative afferent pupillary defect. Second-degree burns were also noticed on the lids and face. Anterior segment examination showed conjunctival chemosis, mild corneal edema, diffuse superficial punctuate keratitis and a quiet anterior chamber bilaterally. ). A Watzke-Allen test was negative. ).\\nTwo weeks later, the patient started to complain from severe pain and photophobia in the right eye. Iridocyclitis with fibrin covering the pupil margin was found with an increase in IOP to 30 mm Hg. Proper treatment with topical prednisone as well as mydriatic and antiglaucoma medication was given to the patient. ).\nOUTPUT:"
},
{
"from": "agent",
"value": "Bilateral Impending Macular Hole, Cataract, Uveitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 36-year-old male patient with an electrical injury sustained at the workplace and without any protective equipment at the time of injury was referred to our hospital. A current of 1,200 V passed through his right arm and exited from his right lower extremity. The patient lost his consciousness at the site of the accident and fell. He was admitted to the intensive care unit. He suffered third-degree burns all over his extremities.\nOnce the patient had resumed consciousness 2 days later, he was starting to complain from a painless decrease in vision in both eyes. His best corrected visual acuity was 20/100 in the right eye and 20/200 in the left eye. The intraocular pressure (IOP) was 13 mm Hg in both eyes, and pupil examination showed a round, regular and reactive pupil without relative afferent pupillary defect. Second-degree burns were also noticed on the lids and face. Anterior segment examination showed conjunctival chemosis, mild corneal edema, diffuse superficial punctuate keratitis and a quiet anterior chamber bilaterally. ). A Watzke-Allen test was negative. ).\nTwo weeks later, the patient started to complain from severe pain and photophobia in the right eye. Iridocyclitis with fibrin covering the pupil margin was found with an increase in IOP to 30 mm Hg. Proper treatment with topical prednisone as well as mydriatic and antiglaucoma medication was given to the patient. ).
OUTPUT: |
PMCPatients_common410 | [
{
"from": "human",
"value": "As a physician engaged 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 attack reoccurred 1 to 2 times/year. He reported long-term use of amlodipine (5 mg/day), smoking 400 cigarettes/year for 30 years, and denied any history of alcohol abuse. A physical examination showed a BP of 134/80 mmHg, clear consciousness, verbal communication, bilateral pupil diameters of 2.0 mm, sensitivity to light reflection, normal eye movements, normal limb muscle strength and tension, bilateral sacral reflex symmetry, and no signs of meningeal irritation; no bilateral pathology was identified.\\nAfter admission, the ophthalmology consultation examination showed no abnormalities in the eyeballs, fundus, or visual field. No notable abnormalities were observed on a head MRI. ). Digital subtraction angiography (DSA) showed that the right ICA was absent, the ipsilateral MCA emerged from the contralateral carotid siphon, and the ipsilateral ACA was compensated by the contralateral ICA (Figs. –). No symptom onset was observed during follow-up.\nOUTPUT:"
},
{
"from": "agent",
"value": "Right eye amaurosis, Congenital absence of the right internal carotid artery, Hypertension"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: The attack reoccurred 1 to 2 times/year. He reported long-term use of amlodipine (5 mg/day), smoking 400 cigarettes/year for 30 years, and denied any history of alcohol abuse. A physical examination showed a BP of 134/80 mmHg, clear consciousness, verbal communication, bilateral pupil diameters of 2.0 mm, sensitivity to light reflection, normal eye movements, normal limb muscle strength and tension, bilateral sacral reflex symmetry, and no signs of meningeal irritation; no bilateral pathology was identified.\nAfter admission, the ophthalmology consultation examination showed no abnormalities in the eyeballs, fundus, or visual field. No notable abnormalities were observed on a head MRI. ). Digital subtraction angiography (DSA) showed that the right ICA was absent, the ipsilateral MCA emerged from the contralateral carotid siphon, and the ipsilateral ACA was compensated by the contralateral ICA (Figs. –). No symptom onset was observed during follow-up.
OUTPUT: |
PMCPatients_common1680 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 29-year-old man presented with abdominal distension, which had lasted for more than 2 months, accompanied by a weight loss of 10 kg. No complaints of chills and fever, nausea, vomiting, abdominal pain, or diarrhea were reported by this patient. Physical examination revealed a swollen abdomen with a mass of 10 cm in diameter in the upper abdomen and multiple swollen lymph nodes in the neck. Laboratory tests revealed that he had anemia and leukopenia, in addition to elevated erythrocyte sedimentation rate, C-reactive protein and procalcitonin levels (Table ). Abdominal computed tomography (CT) scan showed a giant mass in the upper abdomen (Fig. a). Based on the clinical and imaging findings, lymphoma was suspected. ). ). When the diagnosis of T. marneffei was confirmed by NGS, the current treatment was continued. After 2 weeks, oral itraconazole for consolidation therapy along with antiretroviral therapy was started, resulting in a favorable clinical response in 1 month and shrinkage of the abdominal mass (Fig. b). The patient was discharged from the hospital in a stable condition.\nOUTPUT:"
},
{
"from": "agent",
"value": "Talaromyces marneffei infected lymphadenopathy, HIV-1 infection"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 29-year-old man presented with abdominal distension, which had lasted for more than 2 months, accompanied by a weight loss of 10 kg. No complaints of chills and fever, nausea, vomiting, abdominal pain, or diarrhea were reported by this patient. Physical examination revealed a swollen abdomen with a mass of 10 cm in diameter in the upper abdomen and multiple swollen lymph nodes in the neck. Laboratory tests revealed that he had anemia and leukopenia, in addition to elevated erythrocyte sedimentation rate, C-reactive protein and procalcitonin levels (Table ). Abdominal computed tomography (CT) scan showed a giant mass in the upper abdomen (Fig. a). Based on the clinical and imaging findings, lymphoma was suspected. ). ). When the diagnosis of T. marneffei was confirmed by NGS, the current treatment was continued. After 2 weeks, oral itraconazole for consolidation therapy along with antiretroviral therapy was started, resulting in a favorable clinical response in 1 month and shrinkage of the abdominal mass (Fig. b). The patient was discharged from the hospital in a stable condition.
OUTPUT: |
PMCPatients_common2322 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: He had no ocular complaints. Visual acuity was 20/20 uncorrected in both eyes. There was no afferent pupillary defect in either eye and intraocular pressure was 16 mmHg bilaterally. Anterior segment exam was significant only for mild nuclear sclerosis in each eye. Posterior segment exam revealed sea-fan neovascularization peripherally in both eyes in areas of vascular occlusion. High-performance liquid chromatography revealed 64.1% hemoglobin S, 34.7% hemoglobin E, and 1.2% hemoglobin F. Hemoglobin A1C value was 5.1%, indicating good diabetic control. The neovascularization regressed over the next 6 months with the preservation of 20/20 vision in both eyes without complications. Mitochondrial DNA point mutation analysis for maternal haplogroups revealed haplogroup L2a1, consistent with maternal origin in Sub-Saharan Africa. Y chromosome analysis revealed haplogroup E1b1a8a, indicating paternal origin in Western Africa. Overall, less than 0.5% of the patient's DNA was traced to Asian origins.\nOUTPUT:"
},
{
"from": "agent",
"value": "Proliferative Retinopathy, Hemoglobin SE 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: He had no ocular complaints. Visual acuity was 20/20 uncorrected in both eyes. There was no afferent pupillary defect in either eye and intraocular pressure was 16 mmHg bilaterally. Anterior segment exam was significant only for mild nuclear sclerosis in each eye. Posterior segment exam revealed sea-fan neovascularization peripherally in both eyes in areas of vascular occlusion. High-performance liquid chromatography revealed 64.1% hemoglobin S, 34.7% hemoglobin E, and 1.2% hemoglobin F. Hemoglobin A1C value was 5.1%, indicating good diabetic control. The neovascularization regressed over the next 6 months with the preservation of 20/20 vision in both eyes without complications. Mitochondrial DNA point mutation analysis for maternal haplogroups revealed haplogroup L2a1, consistent with maternal origin in Sub-Saharan Africa. Y chromosome analysis revealed haplogroup E1b1a8a, indicating paternal origin in Western Africa. Overall, less than 0.5% of the patient's DNA was traced to Asian origins.
OUTPUT: |
PMCPatients_common745 | [
{
"from": "human",
"value": "As a physician engaged 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 was an 80-year-old male farmer from Beijing. He had been experiencing cough, expectoration, fatigue, and anorexia for 2 months. The abnormal laboratory test results included the following: white blood cell count, 1.08 × 109 cells/L; monocyte percentage, 13.9%; hemoglobin content, 107 g/L; aspartate aminotransferase, 52 U/L, γ-glutamyl transpeptidase, 103 U/L; alkaline phosphatase, 207 U/L; creatine kinase, 26 U/L; total protein, 94.8 g/L; albumin, 30 g/L; albumin/globulin, 0.46; immunoglobulin G, 47.3 g/L; immunoglobulin M, 6.22 g/L; complement C3, 0.427 g/L; complement C4, 0.114 g/L; rheumatoid factor, 1,990 IU/mL; and serum ferritin, 1,335.21 ng/mL. The patient had previously been diagnosed with hypertension and diabetes. At the local hospital, the patient was diagnosed with bronchitis and treated using levofloxacin, azithromycin, ambroxol, vitamin B4, and recombinant human granulocyte colony stimulating factor for 2 months, but his condition did not improve and he was transferred to our hospital. In our hospital, the results of bone marrow mNGS tests showed that almost all non-human sequences (18,070/18,150) belonged to Leishmania ( and ), and further analysis revealed that they were L. infantum sequences. Nevertheless, no pathogen sequences were detected by plasma mNGS. The bone marrow contained a small number of nucleated cells, and Leishmania amastigotes were found (). Sodium antimonate gluconate was injected for 13 days. The treatment was interrupted due to nose bleeding, and the patient was discharged from hospital with recommendations to repeat the treatment in 1 month.\nOUTPUT:"
},
{
"from": "agent",
"value": "Leishmaniasis"
}
] | As a physician engaged 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 was an 80-year-old male farmer from Beijing. He had been experiencing cough, expectoration, fatigue, and anorexia for 2 months. The abnormal laboratory test results included the following: white blood cell count, 1.08 × 109 cells/L; monocyte percentage, 13.9%; hemoglobin content, 107 g/L; aspartate aminotransferase, 52 U/L, γ-glutamyl transpeptidase, 103 U/L; alkaline phosphatase, 207 U/L; creatine kinase, 26 U/L; total protein, 94.8 g/L; albumin, 30 g/L; albumin/globulin, 0.46; immunoglobulin G, 47.3 g/L; immunoglobulin M, 6.22 g/L; complement C3, 0.427 g/L; complement C4, 0.114 g/L; rheumatoid factor, 1,990 IU/mL; and serum ferritin, 1,335.21 ng/mL. The patient had previously been diagnosed with hypertension and diabetes. At the local hospital, the patient was diagnosed with bronchitis and treated using levofloxacin, azithromycin, ambroxol, vitamin B4, and recombinant human granulocyte colony stimulating factor for 2 months, but his condition did not improve and he was transferred to our hospital. In our hospital, the results of bone marrow mNGS tests showed that almost all non-human sequences (18,070/18,150) belonged to Leishmania ( and ), and further analysis revealed that they were L. infantum sequences. Nevertheless, no pathogen sequences were detected by plasma mNGS. The bone marrow contained a small number of nucleated cells, and Leishmania amastigotes were found (). Sodium antimonate gluconate was injected for 13 days. The treatment was interrupted due to nose bleeding, and the patient was discharged from hospital with recommendations to repeat the treatment in 1 month.
OUTPUT: |
PMCPatients_common5068 | [
{
"from": "human",
"value": "As a physician engaged 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 vital signs at admission were normal and laboratory results were WBC 4,290/mm3, hemoglobin 12.5 g/dL, hematocrit 37.2%, platelet 172 k/mm3, ESR 7 mm/h, and CEA (carcinoembryonic antigen) 0.86 ng/mL. A serology test and culture for mycoplasma, chlamydia, and tuberculosis were all negative. Chest computed tomography and PET-CT showed a 1.9×1.7 cm mass in the left upper lobe and suspicious metastatic lymph nodes in multiple bilateral mediastinal lymph nodes (2R, 3a, 4R, 4L, 5, 6, 7, 8R) (). Bronchoscopic findings were non-specific and PCNA (percutaneous needle aspiration) of the mass under chest CT revealed adenocarcinoma. We biopsied the right paratracheal lymph nodes (2R, 4R) under mediastinoscopy and the pathology reports showed that they were benign and non-caseous granuloma. We chose to operate and performed a thoracotomy for a left upper lobectomy and mediastinal lymph node dissection. The tuberculosis polymerase chain reaction (Tb-PCR) test from the specimens was negative. The stage was estimated to be IB (T2N0M0). The patient was discharged on the sixth postoperative day without any complications.\nOUTPUT:"
},
{
"from": "agent",
"value": "Lung Cancer, Sarcoidosis"
}
] | As a physician engaged 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 vital signs at admission were normal and laboratory results were WBC 4,290/mm3, hemoglobin 12.5 g/dL, hematocrit 37.2%, platelet 172 k/mm3, ESR 7 mm/h, and CEA (carcinoembryonic antigen) 0.86 ng/mL. A serology test and culture for mycoplasma, chlamydia, and tuberculosis were all negative. Chest computed tomography and PET-CT showed a 1.9×1.7 cm mass in the left upper lobe and suspicious metastatic lymph nodes in multiple bilateral mediastinal lymph nodes (2R, 3a, 4R, 4L, 5, 6, 7, 8R) (). Bronchoscopic findings were non-specific and PCNA (percutaneous needle aspiration) of the mass under chest CT revealed adenocarcinoma. We biopsied the right paratracheal lymph nodes (2R, 4R) under mediastinoscopy and the pathology reports showed that they were benign and non-caseous granuloma. We chose to operate and performed a thoracotomy for a left upper lobectomy and mediastinal lymph node dissection. The tuberculosis polymerase chain reaction (Tb-PCR) test from the specimens was negative. The stage was estimated to be IB (T2N0M0). The patient was discharged on the sixth postoperative day without any complications.
OUTPUT: |
PMCPatients_common1890 | [
{
"from": "human",
"value": "As a physician engaged in 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, Hispanic male with no known past medical history presented to the emergency room with a chief complaint of sudden-onset right-sided weakness over the past 24 hours. The patient denied any associated dizziness, visual disturbance, or reduced level of consciousness. He had not seen a physician in over 20 years. His social history was significant for chronic alcohol abuse with consumption of at least one pint of tequila or beer per day for at least 35 years. The patient was tachycardic to 101/min with a physical exam that was remarkable for right-sided facial droop as well as 1/5 strength in the right upper and lower extremities. He was noted to have a National Institutes of Health stroke scale of 17.\\nA stat computed tomography (CT) of the head without contrast as well as magnetic resonance imaging (MRI) without contrast were negative for acute stroke. The patient's urine drug screen and alcohol level was unremarkable. His labs were significant for an ALT of 70, AST 251, direct bilirubin 0.4, INR 1.1, platelets 79 x 10^3 (Table ). All of his other labs were normal. Computed tomography of the abdomen and pelvis revealed a micronodular appearance of the liver with numerous scattered hypodensities (Figure ). A hepatitis A, B, C panel, autoimmune panel, alpha-1 antitrypsin deficiency panel and iron panel were all negative. Once an ammonia level was found to be 140 micro mol/L, the patient was started on lactulose and rifaximin. The patient opted out of physical therapy the first two days of admission; however, his neurological symptoms resolved without residual neurological deficits about 36 hours after treatment of lactulose and rifaximin. We discharged our patient with close follow-up at a GI clinic and repeat labs one month after discharge (Table ).\nOUTPUT:"
},
{
"from": "agent",
"value": "Cirrhosis"
}
] | As a physician engaged 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, Hispanic male with no known past medical history presented to the emergency room with a chief complaint of sudden-onset right-sided weakness over the past 24 hours. The patient denied any associated dizziness, visual disturbance, or reduced level of consciousness. He had not seen a physician in over 20 years. His social history was significant for chronic alcohol abuse with consumption of at least one pint of tequila or beer per day for at least 35 years. The patient was tachycardic to 101/min with a physical exam that was remarkable for right-sided facial droop as well as 1/5 strength in the right upper and lower extremities. He was noted to have a National Institutes of Health stroke scale of 17.\nA stat computed tomography (CT) of the head without contrast as well as magnetic resonance imaging (MRI) without contrast were negative for acute stroke. The patient's urine drug screen and alcohol level was unremarkable. His labs were significant for an ALT of 70, AST 251, direct bilirubin 0.4, INR 1.1, platelets 79 x 10^3 (Table ). All of his other labs were normal. Computed tomography of the abdomen and pelvis revealed a micronodular appearance of the liver with numerous scattered hypodensities (Figure ). A hepatitis A, B, C panel, autoimmune panel, alpha-1 antitrypsin deficiency panel and iron panel were all negative. Once an ammonia level was found to be 140 micro mol/L, the patient was started on lactulose and rifaximin. The patient opted out of physical therapy the first two days of admission; however, his neurological symptoms resolved without residual neurological deficits about 36 hours after treatment of lactulose and rifaximin. We discharged our patient with close follow-up at a GI clinic and repeat labs one month after discharge (Table ).
OUTPUT: |
PMCPatients_common1062 | [
{
"from": "human",
"value": "As a physician engaged in 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 previously healthy female presented to the emergency department in the early morning hours with a feeling that her heart was racing. Her symptoms had been ongoing for several hours with accompanying shortness of breath, lightheadedness, nausea, and vomiting. She had experienced recurrent palpitations that usually spontaneously resolved within 20 min over the past year. On the evening prior to presentation, she had drunk multiple cans of caffeinated soda and was up most of the night. She denied drug and alcohol use, fever, recent illness, or any other significant past medical history.\\nAt presentation, her heart rate was 220 beats per minute. The electrocardiogram (ECG) revealed a wide complex tachycardia with left bundle branch morphology, a superior axis, an rS in lead III, an R wave in V1, and late QRS transition (after V5) (Figure ). She was treated with 6 mg rapid-infusion adenosine intravenously, which reduced her heart rate to 78 beats per minute. The repeat ECG showed a sinus rhythm with premature ventricular complexes and left bundle branch block morphology (Figure ).\\nUrine toxicology screen, complete blood count, complete metabolic panel, thyroid function tests, and beta-HCG laboratory work all came back within normal limits.\\nThe patient was hospitalized for additional monitoring and remained stable on Metoprolol. Just prior to discharge she developed another episode of sustained tachycardia of the same character, which reverted back to sinus rhythm after the administration of adenosine. She was then discharged on extended release Metoprolol, 25 mg PO daily. A cardiac catheterization with an electrophysiologic study was scheduled to be performed on an outpatient basis.\\nElectrophysiology showed normal baseline conduction intervals. However, on rapid atrial pacing she demonstrated the same widened QRS complexes with left bundle branch pattern and axis of about 0 degrees on the frontal plane without PR shortening.\nOUTPUT:"
},
{
"from": "agent",
"value": "Mahaim fiber accessory pathway"
}
] | As a physician engaged 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 previously healthy female presented to the emergency department in the early morning hours with a feeling that her heart was racing. Her symptoms had been ongoing for several hours with accompanying shortness of breath, lightheadedness, nausea, and vomiting. She had experienced recurrent palpitations that usually spontaneously resolved within 20 min over the past year. On the evening prior to presentation, she had drunk multiple cans of caffeinated soda and was up most of the night. She denied drug and alcohol use, fever, recent illness, or any other significant past medical history.\nAt presentation, her heart rate was 220 beats per minute. The electrocardiogram (ECG) revealed a wide complex tachycardia with left bundle branch morphology, a superior axis, an rS in lead III, an R wave in V1, and late QRS transition (after V5) (Figure ). She was treated with 6 mg rapid-infusion adenosine intravenously, which reduced her heart rate to 78 beats per minute. The repeat ECG showed a sinus rhythm with premature ventricular complexes and left bundle branch block morphology (Figure ).\nUrine toxicology screen, complete blood count, complete metabolic panel, thyroid function tests, and beta-HCG laboratory work all came back within normal limits.\nThe patient was hospitalized for additional monitoring and remained stable on Metoprolol. Just prior to discharge she developed another episode of sustained tachycardia of the same character, which reverted back to sinus rhythm after the administration of adenosine. She was then discharged on extended release Metoprolol, 25 mg PO daily. A cardiac catheterization with an electrophysiologic study was scheduled to be performed on an outpatient basis.\nElectrophysiology showed normal baseline conduction intervals. However, on rapid atrial pacing she demonstrated the same widened QRS complexes with left bundle branch pattern and axis of about 0 degrees on the frontal plane without PR shortening.
OUTPUT: |
PMCPatients_common2313 | [
{
"from": "human",
"value": "As a physician engaged in 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 woman (gravida, 2; para, 2) presented to our outpatient department with macrohematuria during her menstrual period. She had not received any hormonal treatment. No abnormal findings were noted on physical examination. Transvaginal ultrasonography indicated the presence of an unclear mass surrounding the left adnexa. The serum CA-125 level was high (251.6 IU/mL). We considered conditions such as ureteral cancer, ovarian cancer, and other benign diseases in the differential diagnosis, which was explained to the patient, along with the treatment options, risks, and benefits. No other lesions were noted.\nOUTPUT:"
},
{
"from": "agent",
"value": "Endometriosis in the left ureter, ovary, and internal iliac lymph node"
}
] | As a physician engaged 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 woman (gravida, 2; para, 2) presented to our outpatient department with macrohematuria during her menstrual period. She had not received any hormonal treatment. No abnormal findings were noted on physical examination. Transvaginal ultrasonography indicated the presence of an unclear mass surrounding the left adnexa. The serum CA-125 level was high (251.6 IU/mL). We considered conditions such as ureteral cancer, ovarian cancer, and other benign diseases in the differential diagnosis, which was explained to the patient, along with the treatment options, risks, and benefits. No other lesions were noted.
OUTPUT: |
PMCPatients_common3898 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: This is the case of a 53-year-old non-smoking male with history of anemia, blood transfusions and recurrent episodes of epistaxis who was presented to the emergency room with cough of ~2 weeks. Cough was mostly dry initially then became productive with evidence of blood in the sputum, to the amount of three cups daily. Other symptoms were minimal dyspnea and generalized weakness. The patient was born in the Caribbean, denied recent travel, exposure to sick contacts, weight loss and night sweats. Furthermore, a recent PPD was negative. He had neither previous episodes of hemoptysis nor any family history of hematologic or cutaneous problems. On physical examination, the patient was coughing up fresh bright red blood. Additionally, mucocutaneous telangiectasias were identified on the lips and tongue (Fig. ). Lungs were essentially clear to auscultation. Hemoglobin was 5.4 g/dl, MCV of 69 fl, MCH of 19.8 pg and platelets level of 304 000. Metabolic and coagulation profiles were grossly unremarkable. Chest computed tomography scan was remarkable for a 2.5 × 3.7 × 4.0 cm smooth oval circumscribed anterior left lower lobe mass associated with bronchovascular structures, suggestive of a large arteriovenous malformation (AVM) (Fig. ). No evidence of lung parenchymal infiltrates or lesions was identified. Patient was admitted to the intensive care unit for volume resuscitation with blood products. After resuscitation, the patient was transferred to the interventional radiology suite for a pulmonary angiogram with embolization of a large left lung AVM, which proved to be successful in controlling the bleeding (Figs –). After immediate response following the procedure, patient was discharged 3 days later. We followed up the patient up to 3 months and he remained asymptomatic without associated complications or further episodes of hemoptysis. Follow-up brain magnetic resonance imaging, endoscopy and colonoscopy were negative for others AVMs.\nOUTPUT:"
},
{
"from": "agent",
"value": "Osler–Weber–Rendu 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: This is the case of a 53-year-old non-smoking male with history of anemia, blood transfusions and recurrent episodes of epistaxis who was presented to the emergency room with cough of ~2 weeks. Cough was mostly dry initially then became productive with evidence of blood in the sputum, to the amount of three cups daily. Other symptoms were minimal dyspnea and generalized weakness. The patient was born in the Caribbean, denied recent travel, exposure to sick contacts, weight loss and night sweats. Furthermore, a recent PPD was negative. He had neither previous episodes of hemoptysis nor any family history of hematologic or cutaneous problems. On physical examination, the patient was coughing up fresh bright red blood. Additionally, mucocutaneous telangiectasias were identified on the lips and tongue (Fig. ). Lungs were essentially clear to auscultation. Hemoglobin was 5.4 g/dl, MCV of 69 fl, MCH of 19.8 pg and platelets level of 304 000. Metabolic and coagulation profiles were grossly unremarkable. Chest computed tomography scan was remarkable for a 2.5 × 3.7 × 4.0 cm smooth oval circumscribed anterior left lower lobe mass associated with bronchovascular structures, suggestive of a large arteriovenous malformation (AVM) (Fig. ). No evidence of lung parenchymal infiltrates or lesions was identified. Patient was admitted to the intensive care unit for volume resuscitation with blood products. After resuscitation, the patient was transferred to the interventional radiology suite for a pulmonary angiogram with embolization of a large left lung AVM, which proved to be successful in controlling the bleeding (Figs –). After immediate response following the procedure, patient was discharged 3 days later. We followed up the patient up to 3 months and he remained asymptomatic without associated complications or further episodes of hemoptysis. Follow-up brain magnetic resonance imaging, endoscopy and colonoscopy were negative for others AVMs.
OUTPUT: |
PMCPatients_common3956 | [
{
"from": "human",
"value": "As a physician engaged 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 83-year-old woman presented with a dry cough and dyspnea for 2 months duration. She had an 8-kg weight loss over that period, but had not experienced night sweats or fever. Her medical, smoking, and family histories were all noncontributory.\\nOn admission, her physical examination, including ear, nose, and throat was unremarkable. No abnormal laboratory findings were detected. Chest CT showed diffuse narrowing of the tracheobronchial tree with endobronchial nodularities, resulting in the collapse of the right middle lobe (RML) and small peripheral nodules in both lungs (). At bronchoscopy, multiple, variable-sized nodules causing bronchial narrowing were seen from the proximal trachea to bronchi of both lungs, including the carina (). Specimens obtained from the right-second carina revealed small monophasic lymphoid tumor cells, diffusely infiltrating the bronchial mucosa, and characteristic lymphoepithelial lesions (). Immunohistochemical analysis of these lesions indicated uniform presence of B-cell markers CD20 and CD 79a, the absence of CD3, CD5, CD23, and CD45RO, and positive staining for anti-kappa light chain. Therefore, the lesion was compatible with an EMZL of mucosa-associated lymphoid tissue.\\nWe performed CT of the abdomen and neck, gastrofiberscopy, and a bone marrow biopsy to establish the stage. The bone marrow biopsy and gastrofiberscopy indicated no lymphoma involvement. In contrast, CT of the neck and abdomen showed multiple, variable-sized lymphadenopathies in the cervical area and left pelvic cavity. Ann Arbor stage IIIE was diagnosed, and 6 cycles of CVP (cyclophosphamide, vincristine, and prednisolone) chemotherapy were administered. After the treatment, follow-up CT of the chest and abdomen showed improvement of the diffuse bronchial narrowing and multiple lymphadenopathies. At that time, bronchoscopy was performed to evaluate pneumonia. However, we found no abnormal mucosal lesion in the tracheobronchial tree or evidence of lymphoma recurrence in a bronchial biopsy.\nOUTPUT:"
},
{
"from": "agent",
"value": "Extranodal Marginal Zone 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: An 83-year-old woman presented with a dry cough and dyspnea for 2 months duration. She had an 8-kg weight loss over that period, but had not experienced night sweats or fever. Her medical, smoking, and family histories were all noncontributory.\nOn admission, her physical examination, including ear, nose, and throat was unremarkable. No abnormal laboratory findings were detected. Chest CT showed diffuse narrowing of the tracheobronchial tree with endobronchial nodularities, resulting in the collapse of the right middle lobe (RML) and small peripheral nodules in both lungs (). At bronchoscopy, multiple, variable-sized nodules causing bronchial narrowing were seen from the proximal trachea to bronchi of both lungs, including the carina (). Specimens obtained from the right-second carina revealed small monophasic lymphoid tumor cells, diffusely infiltrating the bronchial mucosa, and characteristic lymphoepithelial lesions (). Immunohistochemical analysis of these lesions indicated uniform presence of B-cell markers CD20 and CD 79a, the absence of CD3, CD5, CD23, and CD45RO, and positive staining for anti-kappa light chain. Therefore, the lesion was compatible with an EMZL of mucosa-associated lymphoid tissue.\nWe performed CT of the abdomen and neck, gastrofiberscopy, and a bone marrow biopsy to establish the stage. The bone marrow biopsy and gastrofiberscopy indicated no lymphoma involvement. In contrast, CT of the neck and abdomen showed multiple, variable-sized lymphadenopathies in the cervical area and left pelvic cavity. Ann Arbor stage IIIE was diagnosed, and 6 cycles of CVP (cyclophosphamide, vincristine, and prednisolone) chemotherapy were administered. After the treatment, follow-up CT of the chest and abdomen showed improvement of the diffuse bronchial narrowing and multiple lymphadenopathies. At that time, bronchoscopy was performed to evaluate pneumonia. However, we found no abnormal mucosal lesion in the tracheobronchial tree or evidence of lymphoma recurrence in a bronchial biopsy.
OUTPUT: |
PMCPatients_common2668 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: He was readmitted 4 months later with fever, intermittently painful and pulsatile swelling over the upper third of the sternum that appeared over a period of 15 days and had gradually increased in size to attain its present size of 6 × 4 cm (Fig. ). The chest was opened through the previous scar reducing the CPB flows and obtaining digital control over the defect on the aorta. Subsequently a vent cannula has been placed in the right superior pulmonary vein to decompress the left side of the heart. The extrathoracic component of the pseudoaneurysm was opened and the clots evacuated. Adhesions over the right ventricle were taken down, and both pleura were opened. ). The bioprosthesis was explored through the defect and was found to be normal. The defect was closed using 3 × 3 cm polytetrafluoroethylene patch.\\nAfter deairing the patient was rewarmed and the heart picked up after single electric shock in sinus rhythm.\nOUTPUT:"
},
{
"from": "agent",
"value": "Ascending aorta pseudoaneurysm, Infection at the previous aortotomy site, Staphylococcus aureus infection"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: He was readmitted 4 months later with fever, intermittently painful and pulsatile swelling over the upper third of the sternum that appeared over a period of 15 days and had gradually increased in size to attain its present size of 6 × 4 cm (Fig. ). The chest was opened through the previous scar reducing the CPB flows and obtaining digital control over the defect on the aorta. Subsequently a vent cannula has been placed in the right superior pulmonary vein to decompress the left side of the heart. The extrathoracic component of the pseudoaneurysm was opened and the clots evacuated. Adhesions over the right ventricle were taken down, and both pleura were opened. ). The bioprosthesis was explored through the defect and was found to be normal. The defect was closed using 3 × 3 cm polytetrafluoroethylene patch.\nAfter deairing the patient was rewarmed and the heart picked up after single electric shock in sinus rhythm.
OUTPUT: |
PMCPatients_common1664 | [
{
"from": "human",
"value": "As a physician engaged in 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 Taiwanese male patient without any family history of hyperthyroidism presented to the emergency room of our institution with an initial symptom of acute limb weakness (level of muscle power is 2-3). Other abnormal findings were observed: a thyroid function test (TFT) revealed hyperthyroidism with serum free thyroxine (fT4) level >6.60 ng/dL and a thyroid-stimulating hormone (TSH) level 0.06 mU/L. These showed profound electrolyte abnormalities such as hypokalemia. Due to the findings of severe hyperthyroidism and hypokalemia, he was admitted to the ICU for further care and he then received potassium replacement (potassium 10 mEq) acutely. He was administered 15 mg of methimazole and 30 mg of propranolol per day for complications due to hyperthyroidism. Following the treatment, the potassium level improved to 3.7 mEq/L. One month after treatment, a follow-up TFT revealed a near-normal fT4 (1.38 ng/dL) without rebound hyperkalemia. No paralysis occurred, and the hyperthyroidism was well controlled with continued anti-thyroid drugs and β-blockers prescribed in the outpatient department.\nOUTPUT:"
},
{
"from": "agent",
"value": "Thyrotoxic Periodic Paralysis, Graves' Disease, Chronic Alcohol Abuse-Induced Hypokalemia"
}
] | As a physician engaged 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 Taiwanese male patient without any family history of hyperthyroidism presented to the emergency room of our institution with an initial symptom of acute limb weakness (level of muscle power is 2-3). Other abnormal findings were observed: a thyroid function test (TFT) revealed hyperthyroidism with serum free thyroxine (fT4) level >6.60 ng/dL and a thyroid-stimulating hormone (TSH) level 0.06 mU/L. These showed profound electrolyte abnormalities such as hypokalemia. Due to the findings of severe hyperthyroidism and hypokalemia, he was admitted to the ICU for further care and he then received potassium replacement (potassium 10 mEq) acutely. He was administered 15 mg of methimazole and 30 mg of propranolol per day for complications due to hyperthyroidism. Following the treatment, the potassium level improved to 3.7 mEq/L. One month after treatment, a follow-up TFT revealed a near-normal fT4 (1.38 ng/dL) without rebound hyperkalemia. No paralysis occurred, and the hyperthyroidism was well controlled with continued anti-thyroid drugs and β-blockers prescribed in the outpatient department.
OUTPUT: |
PMCPatients_common2963 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She was referred for ophthalmologic evaluation for visual turbidity complaint. The patient had visual acuity of 20/80 in the right eye and 20/50 in the left eye.\\nThe funduscopy showed bilateral pale papilla, with physiological digging, vessels with reduced caliber and some phantom vessels, macula with decreased foveal brightness, pale retina, RPE hyperplasia in the middle periphery (see and ). The macular optical coherence tomography (StratusOCT) showed retinal thickening and cysts formation (see ). The improvement of macular edema with the use of intravitreal injection of anti-VEGF as observed was not permanent and did not have a determined number of intravitreal procedures necessary to stabilize the macular condition. Continuous treatment is necessary to maintain acuity improvement. Intravitreal Dexamethasone treatment was not performed due to pallor of the optic nerve and ischemic neuropathy of increased intraocular pressure risk of further injury.–\nOUTPUT:"
},
{
"from": "agent",
"value": "Radiation Retinopathy, Myelodysplasia"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: She was referred for ophthalmologic evaluation for visual turbidity complaint. The patient had visual acuity of 20/80 in the right eye and 20/50 in the left eye.\nThe funduscopy showed bilateral pale papilla, with physiological digging, vessels with reduced caliber and some phantom vessels, macula with decreased foveal brightness, pale retina, RPE hyperplasia in the middle periphery (see and ). The macular optical coherence tomography (StratusOCT) showed retinal thickening and cysts formation (see ). The improvement of macular edema with the use of intravitreal injection of anti-VEGF as observed was not permanent and did not have a determined number of intravitreal procedures necessary to stabilize the macular condition. Continuous treatment is necessary to maintain acuity improvement. Intravitreal Dexamethasone treatment was not performed due to pallor of the optic nerve and ischemic neuropathy of increased intraocular pressure risk of further injury.–
OUTPUT: |
PMCPatients_common102 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: He underwent right-lobe hepatectomy in 2009. However, the cancer recurred, and he underwent transarterial chemoembolization seven times. In February 2017, he underwent radiofrequency ablation for the recurrent hepatoma. Three weeks after the treatment, he presented with the concern about intractable cough with yellowish sputum. Chest film examination indicated right lower lung consolidation; moreover, computed tomography demonstrated right middle lobe consolidation with pleural effusion and right subphrenic fluid collection (Fig. A and B). The laboratory findings also show abnormality (CRP 28.5 mg/dL, ALP 121 U/L, r-GT 111 U/L, Bil T/D 3.18/1.79 mg/dL, AST 16 U/L, ALT 17 U/L). Percutaneous echo-guided transhepatic cholangiography demonstrated an abnormal tract from the liver to the lung. C).\\nSurgical intervention was not considered because the patient’s general condition was not adequate for surgery. We decided to perform percutaneous drainage. The patient’s biliptysis was considerably alleviated after the procedure. However, the amount of fluid drained did not decrease in 2 weeks, and we observed that occluding the drainage tube would lead to biliptysis recurrence. We decided to perform endoscopic retrograde biliary drainage combined with percutaneous drainage (Fig. D) because we assumed that a biliary tract stricture might occur after radiofrequency ablation and lead to inadequate bile drainage. Follow-up computed tomography conducted five months after the episode demonstrated satisfactory recovery of the liver and lung parenchyma.\nOUTPUT:"
},
{
"from": "agent",
"value": "Bronchobiliary fistula, Hepatocellular carcinoma, Right-side subphrenic abscess with empyema thoracis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: He underwent right-lobe hepatectomy in 2009. However, the cancer recurred, and he underwent transarterial chemoembolization seven times. In February 2017, he underwent radiofrequency ablation for the recurrent hepatoma. Three weeks after the treatment, he presented with the concern about intractable cough with yellowish sputum. Chest film examination indicated right lower lung consolidation; moreover, computed tomography demonstrated right middle lobe consolidation with pleural effusion and right subphrenic fluid collection (Fig. A and B). The laboratory findings also show abnormality (CRP 28.5 mg/dL, ALP 121 U/L, r-GT 111 U/L, Bil T/D 3.18/1.79 mg/dL, AST 16 U/L, ALT 17 U/L). Percutaneous echo-guided transhepatic cholangiography demonstrated an abnormal tract from the liver to the lung. C).\nSurgical intervention was not considered because the patient’s general condition was not adequate for surgery. We decided to perform percutaneous drainage. The patient’s biliptysis was considerably alleviated after the procedure. However, the amount of fluid drained did not decrease in 2 weeks, and we observed that occluding the drainage tube would lead to biliptysis recurrence. We decided to perform endoscopic retrograde biliary drainage combined with percutaneous drainage (Fig. D) because we assumed that a biliary tract stricture might occur after radiofrequency ablation and lead to inadequate bile drainage. Follow-up computed tomography conducted five months after the episode demonstrated satisfactory recovery of the liver and lung parenchyma.
OUTPUT: |
PMCPatients_common4880 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The patient had three centimeter shortening along with fixed flexion and adduction deformity. Preoperative radiograph showed presence of a large osteophyte at the floor of the acetabulum []. Intraoperatively, a 3.2 mm drill was used to identify the floor of the acetabulum and the depth of reaming. The procedure was uneventful with around 300 ml of intraoperative blood loss. Two hours later, the patient developed unexplained hypotension with tachycardia, which was treated with colloids and 2 units of blood. After next 2 h, he complained of lower abdominal pain. An interventional radiologist treated the pseudoaneurysm with coil embolization []. On 19th day, the patient was discharged from the hospital with complete recovery and full weight bearing. A total of 16 units of blood, 4 units of FFP and 6 units of platelets were required for the treatment during his hospital stay. At 6 years followup, there were no symptoms related to the hip replacement. Similarly, no evidence of pseudoaneurysm was detected on repeat computed tomography (CT) angiography []. Blood ion levels and MRI scans also did not show any adverse metal reaction. Patient consent has been taken to report this case.\nOUTPUT:"
},
{
"from": "agent",
"value": "Internal iliac artery pseudoaneurysm, Severe arthritis of left hip, Avascular necrosis of the femoral head, Retroperitoneal hematoma, Acute renal failure"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: The patient had three centimeter shortening along with fixed flexion and adduction deformity. Preoperative radiograph showed presence of a large osteophyte at the floor of the acetabulum []. Intraoperatively, a 3.2 mm drill was used to identify the floor of the acetabulum and the depth of reaming. The procedure was uneventful with around 300 ml of intraoperative blood loss. Two hours later, the patient developed unexplained hypotension with tachycardia, which was treated with colloids and 2 units of blood. After next 2 h, he complained of lower abdominal pain. An interventional radiologist treated the pseudoaneurysm with coil embolization []. On 19th day, the patient was discharged from the hospital with complete recovery and full weight bearing. A total of 16 units of blood, 4 units of FFP and 6 units of platelets were required for the treatment during his hospital stay. At 6 years followup, there were no symptoms related to the hip replacement. Similarly, no evidence of pseudoaneurysm was detected on repeat computed tomography (CT) angiography []. Blood ion levels and MRI scans also did not show any adverse metal reaction. Patient consent has been taken to report this case.
OUTPUT: |
PMCPatients_common830 | [
{
"from": "human",
"value": "As a physician engaged 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 77-year-old man who fell from the loading platform of a truck (height 1.5 m) and landed on the back of his head. He could initially walk without weakness or other symptoms. However, he gradually developed dyspnea and right hemiplegia and presented to the emergency department of another hospital. The physician found it difficult to diagnose and treat the patient, and he was immediately transferred to our emergency department by ambulance.\\nOn arrival, his consciousness was alert and his vital signs were stable. He felt occipital and posterior cervical pain. There was no dyspnea or right hemiplegia. His medical history included paroxysmal atrial fibrillation, for which warfarin was prescribed. On physical examination, there was no external wound, with only spontaneous pain and tenderness at the back of his head and neck. A motor and sensory examination of the extremities and trunk was normal. ). The patient’s activity level was gradually increased. On hospital day 4, CT was reperformed, revealing the complete disappearance of air in the veins. We therefore administered adrenocortical steroids and the patient gradually recovered from hyponatremia. A long period was required to treat hyponatremia. He was discharged on hospital day 34 without sequelae.\nOUTPUT:"
},
{
"from": "agent",
"value": "Basilar skull fracture, Traumatic subarachnoid hemorrhage, Pneumocephalus, Vascular air embolism, Cerebral salt wasting syndrome"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: The patient was a 77-year-old man who fell from the loading platform of a truck (height 1.5 m) and landed on the back of his head. He could initially walk without weakness or other symptoms. However, he gradually developed dyspnea and right hemiplegia and presented to the emergency department of another hospital. The physician found it difficult to diagnose and treat the patient, and he was immediately transferred to our emergency department by ambulance.\nOn arrival, his consciousness was alert and his vital signs were stable. He felt occipital and posterior cervical pain. There was no dyspnea or right hemiplegia. His medical history included paroxysmal atrial fibrillation, for which warfarin was prescribed. On physical examination, there was no external wound, with only spontaneous pain and tenderness at the back of his head and neck. A motor and sensory examination of the extremities and trunk was normal. ). The patient’s activity level was gradually increased. On hospital day 4, CT was reperformed, revealing the complete disappearance of air in the veins. We therefore administered adrenocortical steroids and the patient gradually recovered from hyponatremia. A long period was required to treat hyponatremia. He was discharged on hospital day 34 without sequelae.
OUTPUT: |
PMCPatients_common3880 | [
{
"from": "human",
"value": "As a physician engaged in 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 grand multiparous woman gravida 9 para 8 was referred to our hospital at 24 weeks of gestation for a detailed anatomy scan because of a foetus with bilateral enlarged cystic kidneys, oligohydramnios, and microcephaly. She has history of a first degree consanguineous marriage. Our antenatal ultrasonographic scan revealed multicystic dysplastic kidneys (Fig. The patient was counselled in detail regarding the poor foetal prognosis. A termination of the pregnancy was not offered as an option because of cultural and religious constraints.\\nAt 30.2 weeks of gestation, she experienced labour pains. Five hours after admission, she had a spontaneous vaginal delivery of a male foetus with an Apgar score of 1 in 1 min and 1 in 5 min and a weight of 2.4 kg. with head circumference 25.5 cm, occipital encephalocele (Fig. ), cleft lip and cleft palate (Fig. ), upper slanting of eyes (Fig. ), low set ears, huge distended abdomen due to bilateral renal mass (Fig. ), flexion of both wrist joint and post-axial hexadactyly on both feet. We kept the new-born under human care after counselling the parents. Approximately 1 h after delivery, the baby expired.\\nA diagnosis of MGS was suggested, based on the presence of the classical features. The patient denied consent for a genetic analysis and autopsy of the infant.\nOUTPUT:"
},
{
"from": "agent",
"value": "Meckel Gruber syndrome, anencephaly"
}
] | As a physician engaged 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 grand multiparous woman gravida 9 para 8 was referred to our hospital at 24 weeks of gestation for a detailed anatomy scan because of a foetus with bilateral enlarged cystic kidneys, oligohydramnios, and microcephaly. She has history of a first degree consanguineous marriage. Our antenatal ultrasonographic scan revealed multicystic dysplastic kidneys (Fig. The patient was counselled in detail regarding the poor foetal prognosis. A termination of the pregnancy was not offered as an option because of cultural and religious constraints.\nAt 30.2 weeks of gestation, she experienced labour pains. Five hours after admission, she had a spontaneous vaginal delivery of a male foetus with an Apgar score of 1 in 1 min and 1 in 5 min and a weight of 2.4 kg. with head circumference 25.5 cm, occipital encephalocele (Fig. ), cleft lip and cleft palate (Fig. ), upper slanting of eyes (Fig. ), low set ears, huge distended abdomen due to bilateral renal mass (Fig. ), flexion of both wrist joint and post-axial hexadactyly on both feet. We kept the new-born under human care after counselling the parents. Approximately 1 h after delivery, the baby expired.\nA diagnosis of MGS was suggested, based on the presence of the classical features. The patient denied consent for a genetic analysis and autopsy of the infant.
OUTPUT: |
PMCPatients_common2351 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 35-year-old male patient presented to our urology department with a severe (>5 cm), tortuous stricture of the penile urethra, previously diagnosed by descending cystourethrogram (). A suprapubic catheter was in place. Via suprapubic cystostomy, the urinary bladder was filled with 300 millilitres of diluted iodinated contrast (contrast/normal saline: 1/3). A 0035′′ J-tip standard angiographic guide-wire was inserted into the urinary bladder through the suprapubic catheter. The latter was removed and exchanged with a short (11 cm), 5-French angiographic sheath. The angiographic guidewire was subsequently withdrawn and an angiographic catheter loaded with a hydrophilic, J-tip guidewire was inserted into the bladder. The angiographic catheter was subsequently advanced through the stenosis, over the guidewire (). The hub of the catheter was cut off and the vascular sheath as well as the guidewire was removed. The posterior part of the catheter was stabilized on the abdominal wall with a suture. The patient was then taken to the operating room and he was placed in lithotomy position under spinal anaesthesia. The guidewire was now placed antegrade through the angiographic catheter in order to facilitate the passage of the angiographic catheter through the working channel of the rigid urethrotome. By keeping the angiographic catheter stretched, the instrument was inserted and guided to the face of the stricture. The stricture was cut at the 12 o'clock location along the entire stenosis (). Upon completion of the internal incision(s), the instrument was withdrawn and an appropriately sized Foley catheter was inserted through the repair into the urinary bladder. Hospitalization lasted 2 days and the patient kept the catheter a few days.\nOUTPUT:"
},
{
"from": "agent",
"value": "Urethral Strictures"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 35-year-old male patient presented to our urology department with a severe (>5 cm), tortuous stricture of the penile urethra, previously diagnosed by descending cystourethrogram (). A suprapubic catheter was in place. Via suprapubic cystostomy, the urinary bladder was filled with 300 millilitres of diluted iodinated contrast (contrast/normal saline: 1/3). A 0035′′ J-tip standard angiographic guide-wire was inserted into the urinary bladder through the suprapubic catheter. The latter was removed and exchanged with a short (11 cm), 5-French angiographic sheath. The angiographic guidewire was subsequently withdrawn and an angiographic catheter loaded with a hydrophilic, J-tip guidewire was inserted into the bladder. The angiographic catheter was subsequently advanced through the stenosis, over the guidewire (). The hub of the catheter was cut off and the vascular sheath as well as the guidewire was removed. The posterior part of the catheter was stabilized on the abdominal wall with a suture. The patient was then taken to the operating room and he was placed in lithotomy position under spinal anaesthesia. The guidewire was now placed antegrade through the angiographic catheter in order to facilitate the passage of the angiographic catheter through the working channel of the rigid urethrotome. By keeping the angiographic catheter stretched, the instrument was inserted and guided to the face of the stricture. The stricture was cut at the 12 o'clock location along the entire stenosis (). Upon completion of the internal incision(s), the instrument was withdrawn and an appropriately sized Foley catheter was inserted through the repair into the urinary bladder. Hospitalization lasted 2 days and the patient kept the catheter a few days.
OUTPUT: |
PMCPatients_common3388 | [
{
"from": "human",
"value": "As a physician engaged in 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 man was referred to the Emergency Department of our hospital with severe hematuria and a massive bladder clot.\\nThe patient had a history of bilateral cryptorchidism since childhood and was untreated and had hepatitis B-associated cirrhosis for 16 years. He underwent splenectomy with devascularization surgery of the lower esophagus and proximal stomach 10 years ago due to hematemesis and melena.\\nThe physical examination revealed uplift of the suprapubic region and dullness percussion. His pubic hair was sparsely distributed, the penis and scrotum were underdeveloped, and the testis was impalpable in the scrotum (Figure ).\\nBlood analysis revealed an abnormal hemogram, including 3.09 × 109/L red blood cells (normal range: 3.5-5.5 × 109/L) with 9.0 g/dL hemoglobin (normal range: 12.0-15.5 g/dL) and normal leukocytic and platelet counts. Prothrombin and partial thromboplastin times were normal, and D-dimer level was slightly increased at 0.85 mg/L. The results of liver and kidney function were normal. Serological assays for markers of hepatitis B were positive. Color Doppler flow imaging showed a color flow signal inside the tube-like echoes (Figure ). Computed tomography (CT) revealed multiple tortuous and thickened veins on the anterior and both sidewalls of the bladder and enlargement of the inferior mesenteric veins (Figures and ). Three-dimensional (3D) visualization technology clearly revealed many abnormally dilated blood vessels surrounding the bladder in the pelvis. In this patient, the dilated vesical varices on the right side drained into the internal iliac vein, and those on the left side were connected with the inferior mesenteric vein and finally entered the splenic vein (Figure ).\nOUTPUT:"
},
{
"from": "agent",
"value": "Severe hematuria due to vesical varices, Portal hypertension"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 53-year-old man was referred to the Emergency Department of our hospital with severe hematuria and a massive bladder clot.\nThe patient had a history of bilateral cryptorchidism since childhood and was untreated and had hepatitis B-associated cirrhosis for 16 years. He underwent splenectomy with devascularization surgery of the lower esophagus and proximal stomach 10 years ago due to hematemesis and melena.\nThe physical examination revealed uplift of the suprapubic region and dullness percussion. His pubic hair was sparsely distributed, the penis and scrotum were underdeveloped, and the testis was impalpable in the scrotum (Figure ).\nBlood analysis revealed an abnormal hemogram, including 3.09 × 109/L red blood cells (normal range: 3.5-5.5 × 109/L) with 9.0 g/dL hemoglobin (normal range: 12.0-15.5 g/dL) and normal leukocytic and platelet counts. Prothrombin and partial thromboplastin times were normal, and D-dimer level was slightly increased at 0.85 mg/L. The results of liver and kidney function were normal. Serological assays for markers of hepatitis B were positive. Color Doppler flow imaging showed a color flow signal inside the tube-like echoes (Figure ). Computed tomography (CT) revealed multiple tortuous and thickened veins on the anterior and both sidewalls of the bladder and enlargement of the inferior mesenteric veins (Figures and ). Three-dimensional (3D) visualization technology clearly revealed many abnormally dilated blood vessels surrounding the bladder in the pelvis. In this patient, the dilated vesical varices on the right side drained into the internal iliac vein, and those on the left side were connected with the inferior mesenteric vein and finally entered the splenic vein (Figure ).
OUTPUT: |
PMCPatients_common1270 | [
{
"from": "human",
"value": "As a physician engaged in 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 was admitted to the surgical department of our hospital for abdominal and chest pain associated with vomiting. A physical examination revealed palpation pain in the left epigastrium. Physical examination also revealed weakness of abduction and external rotation of the left upper extremity. The patient reported suffering from deep and diffused, poorly localized pain of the left shoulder for 5 months, and further examination revealed atrophy of the left supraspinatus muscle. However, he denied even a slight trauma of this region. The patient denied pain or weakness of the right shoulder. The right infraspinatus muscle was normal. The width of the bridge in the proximal, middle and distal aspects was 7.2, 5.8 and 8.8 mm, respectively. The IrP was 37.4 %.\nOUTPUT:"
},
{
"from": "agent",
"value": "Stomach ulcer, Suprascapular neuropathy, Coexistence of a suprascapular notch and a suprascapular foramen"
}
] | As a physician engaged 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 was admitted to the surgical department of our hospital for abdominal and chest pain associated with vomiting. A physical examination revealed palpation pain in the left epigastrium. Physical examination also revealed weakness of abduction and external rotation of the left upper extremity. The patient reported suffering from deep and diffused, poorly localized pain of the left shoulder for 5 months, and further examination revealed atrophy of the left supraspinatus muscle. However, he denied even a slight trauma of this region. The patient denied pain or weakness of the right shoulder. The right infraspinatus muscle was normal. The width of the bridge in the proximal, middle and distal aspects was 7.2, 5.8 and 8.8 mm, respectively. The IrP was 37.4 %.
OUTPUT: |
PMCPatients_common1778 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 38-year-old woman with HCS presented with severe cervical and upper thoracic back pain that had significantly worsened over the past six months. She previously tried physical therapy and other conservative measures with no significant improvement. Flexion-extension plain films demonstrated a fixed deformity. A review of prior imaging revealed continued progression of her deformity over the past several years.\\nGiven these findings, a staged correction was recommended. The first stage of surgery included posterior facetectomies at C4/5, C5/6, and C6/7 with subsequent anterior C5 and C6 corpectomies and C4 to C7 anterior fusion with expandable cage placement and plating. After anterior deformity correction, posterior instrumentation was completed from C4 to C7, intentionally placing her in greater coronal malalignment to allow for global correction with the second stage of surgery. The second stage of surgery was posterior C4-T11 deformity correction and fusion. Bilateral facetectomies were performed from T5 to T8.\\nHer hospital course was uneventful and she was discharged home on postoperative day six. One month after surgery, she was very happy with her progress; she denied any significant pain and felt that her function was returning appropriately. Plain films showed excellent spinal alignment with no evidence of complications (Figure ). At six months, she continued to improve with CT imaging demonstrating excellent bony fusion and no fractures. She reported minimal lumbar paraspinal muscle tenderness but was otherwise asymptomatic, with complete resolution of her presenting concerns. Her neurological exam remained normal throughout her perioperative course and follow-up.\nOUTPUT:"
},
{
"from": "agent",
"value": "Hajdu-Cheney Syndrome, cervicothoracic scoliosis, osteoporosis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 38-year-old woman with HCS presented with severe cervical and upper thoracic back pain that had significantly worsened over the past six months. She previously tried physical therapy and other conservative measures with no significant improvement. Flexion-extension plain films demonstrated a fixed deformity. A review of prior imaging revealed continued progression of her deformity over the past several years.\nGiven these findings, a staged correction was recommended. The first stage of surgery included posterior facetectomies at C4/5, C5/6, and C6/7 with subsequent anterior C5 and C6 corpectomies and C4 to C7 anterior fusion with expandable cage placement and plating. After anterior deformity correction, posterior instrumentation was completed from C4 to C7, intentionally placing her in greater coronal malalignment to allow for global correction with the second stage of surgery. The second stage of surgery was posterior C4-T11 deformity correction and fusion. Bilateral facetectomies were performed from T5 to T8.\nHer hospital course was uneventful and she was discharged home on postoperative day six. One month after surgery, she was very happy with her progress; she denied any significant pain and felt that her function was returning appropriately. Plain films showed excellent spinal alignment with no evidence of complications (Figure ). At six months, she continued to improve with CT imaging demonstrating excellent bony fusion and no fractures. She reported minimal lumbar paraspinal muscle tenderness but was otherwise asymptomatic, with complete resolution of her presenting concerns. Her neurological exam remained normal throughout her perioperative course and follow-up.
OUTPUT: |
PMCPatients_common1320 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 62 year-old man presented with 3–4 months history of two pink-papules on the scalp, and a pink crusted plaque on the left neck. His lymphoma was under control after the chemotherapy, but he did had bone marrow extension at the time of diagnosis. A hematopoietic allogeneic transplant was done after his original diagnosis of acute myeloid leukemia. Two punch biopsies were obtained. The biopsy from the left neck (Figure \\n) showed a mixed dermal inflammatory infiltrate with scattered atypical large multinucleated and mononuclear cells, intermixed with aggregates of neutrophils, small lymphocytes and histiocytes. The mononuclear cells had hyperchromatic nuclei with vesicular smudged chromatin and prominent cherry red nucleoli, resembling Reed-Sternberg cells. By immunohistochemistry (Figure \\n), the atypical cells were positive for CD30, CD20, CD79a, and had dim CD15 and PAX5 staining. They were negative for CD45. A CD3 and CD43 highlighted the abundant intermixed T-cells, but were negative among the atypical large cells. CD68 stained a rich histiocytic background. A Melan-A and S100 stains were also negative. There were large nests of atypical melanocytes with light eosinophilic cytoplasm, hyperchromatic and vesicular nuclei with variable prominent nucleoli. Scattered mitotic figures were seen, including in the deeper portion of the lesion. No maturation towards the base of the lesion was seen. An intraepidermal melanocytic component was present in one of the biopsies. No perineural or lymphovascular space invasion was identified. Immunohistochemistry for Melan-A and HMB-45 confirmed the melanocytic origin of the tumor cells.\nOUTPUT:"
},
{
"from": "agent",
"value": "Malignant Melanoma, Classical Hodgkin 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 62 year-old man presented with 3–4 months history of two pink-papules on the scalp, and a pink crusted plaque on the left neck. His lymphoma was under control after the chemotherapy, but he did had bone marrow extension at the time of diagnosis. A hematopoietic allogeneic transplant was done after his original diagnosis of acute myeloid leukemia. Two punch biopsies were obtained. The biopsy from the left neck (Figure \n) showed a mixed dermal inflammatory infiltrate with scattered atypical large multinucleated and mononuclear cells, intermixed with aggregates of neutrophils, small lymphocytes and histiocytes. The mononuclear cells had hyperchromatic nuclei with vesicular smudged chromatin and prominent cherry red nucleoli, resembling Reed-Sternberg cells. By immunohistochemistry (Figure \n), the atypical cells were positive for CD30, CD20, CD79a, and had dim CD15 and PAX5 staining. They were negative for CD45. A CD3 and CD43 highlighted the abundant intermixed T-cells, but were negative among the atypical large cells. CD68 stained a rich histiocytic background. A Melan-A and S100 stains were also negative. There were large nests of atypical melanocytes with light eosinophilic cytoplasm, hyperchromatic and vesicular nuclei with variable prominent nucleoli. Scattered mitotic figures were seen, including in the deeper portion of the lesion. No maturation towards the base of the lesion was seen. An intraepidermal melanocytic component was present in one of the biopsies. No perineural or lymphovascular space invasion was identified. Immunohistochemistry for Melan-A and HMB-45 confirmed the melanocytic origin of the tumor cells.
OUTPUT: |
PMCPatients_common25 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 70-year-old woman was diagnosed with DLBCL (Ann Arbor Stage: IIIA) and received chemotherapy but relapsed. She was admitted to our hospital in 2017 to undergo auto-PBSCT after salvage chemotherapy. She suddenly developed grade 3 haematuria on the day of transplantation. Although she received immunoglobulin and adenine arabinoside, the HC symptoms did not improve. Although we administered cidofovir (1 mg/kg, three times a week) from days 8 to 26 post-auto-PBSCT, the HC symptoms persisted. Chest computed tomography (CT) showed ground-glass opacity (GGO) in the bilateral upper lobe, and we performed BAL at day 34. Although BAL fluid (BALF) was not macroscopically reddish, BAL slightly detected red blood cells on cytology. After re-administering cidofovir, respiratory symptoms and GGO in CT abated, although HC symptoms persisted (Fig. ).\nOUTPUT:"
},
{
"from": "agent",
"value": "BK virus pneumonia, Diffuse large B-cell lymphoma, Haemorrhagic cystitis, BK viraemia"
}
] | As a physician engaged 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 70-year-old woman was diagnosed with DLBCL (Ann Arbor Stage: IIIA) and received chemotherapy but relapsed. She was admitted to our hospital in 2017 to undergo auto-PBSCT after salvage chemotherapy. She suddenly developed grade 3 haematuria on the day of transplantation. Although she received immunoglobulin and adenine arabinoside, the HC symptoms did not improve. Although we administered cidofovir (1 mg/kg, three times a week) from days 8 to 26 post-auto-PBSCT, the HC symptoms persisted. Chest computed tomography (CT) showed ground-glass opacity (GGO) in the bilateral upper lobe, and we performed BAL at day 34. Although BAL fluid (BALF) was not macroscopically reddish, BAL slightly detected red blood cells on cytology. After re-administering cidofovir, respiratory symptoms and GGO in CT abated, although HC symptoms persisted (Fig. ).
OUTPUT: |
PMCPatients_common5386 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 17-year-old boy presented with fever, progressive swelling and erythema of the right upper and lower lids and periorbital soft tissues of 5 days’ duration (A). He had received intramuscular gentamicin and oral ciprofloxacin over the last 5 days. He had no history of trauma, systemic disease or insect bites. No abnormal findings such as lymphadenopathy or hepatosplenomegaly were noted on systemic physical examination. He was ill and had high grade fever. Visual acuity was 8/10 in both eyes and relative afferent pupillary defect was negative. Ocular motility was normal but painful in the affected eye. Slit lamp examination and funduscopy were unremarkable and intraocular pressure was within normal limits. The patient had no evidence of dental infections or dacryocystitis. A complete blood count (CBC), blood culture, and other laboratory tests were requested.\\nThe patient was admitted with a clinical impression of preseptal cellulitis and impending orbital involvement; intravenous ceftriaxone 1 gm every 12 hours was initiated empirically. The swelling and erythema progressed throughout the right facial and left periorbital area, and some blisters appeared on the right upper eyelid the day after admission (B). Orbital and paranasal sinus computed tomography (CT) images showed right periorbital soft tissue swelling without sinus involvement (). Chemotherapy including cytarabine 100 mg/m2 and idarubicin 12 mg/m2 together with broad spectrum antibiotics including vancomycin 1 gm every 12 hours, ceftazidime 1 gm every 8 hours and imipenem 500 mg every 6 hours were initiated. Signs and symptoms regressed after two courses of chemotherapy over 2 months and he was relapse free for 2 years (C).\nOUTPUT:"
},
{
"from": "agent",
"value": "Acute Myelogenous Leukemia"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 17-year-old boy presented with fever, progressive swelling and erythema of the right upper and lower lids and periorbital soft tissues of 5 days’ duration (A). He had received intramuscular gentamicin and oral ciprofloxacin over the last 5 days. He had no history of trauma, systemic disease or insect bites. No abnormal findings such as lymphadenopathy or hepatosplenomegaly were noted on systemic physical examination. He was ill and had high grade fever. Visual acuity was 8/10 in both eyes and relative afferent pupillary defect was negative. Ocular motility was normal but painful in the affected eye. Slit lamp examination and funduscopy were unremarkable and intraocular pressure was within normal limits. The patient had no evidence of dental infections or dacryocystitis. A complete blood count (CBC), blood culture, and other laboratory tests were requested.\nThe patient was admitted with a clinical impression of preseptal cellulitis and impending orbital involvement; intravenous ceftriaxone 1 gm every 12 hours was initiated empirically. The swelling and erythema progressed throughout the right facial and left periorbital area, and some blisters appeared on the right upper eyelid the day after admission (B). Orbital and paranasal sinus computed tomography (CT) images showed right periorbital soft tissue swelling without sinus involvement (). Chemotherapy including cytarabine 100 mg/m2 and idarubicin 12 mg/m2 together with broad spectrum antibiotics including vancomycin 1 gm every 12 hours, ceftazidime 1 gm every 8 hours and imipenem 500 mg every 6 hours were initiated. Signs and symptoms regressed after two courses of chemotherapy over 2 months and he was relapse free for 2 years (C).
OUTPUT: |
PMCPatients_common804 | [
{
"from": "human",
"value": "As a physician engaged in 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 years old female, primigravida with a normal first antenatal visit at 7 weeks period of gestation (POG) presented with vomiting on and off in outpatient clinic. The transabdominal obstetric scan was done on first antenatal check-up elsewhere showed crown-rump length (CRL) 10.7mm (7 weeks 1 day) with a fetal heart rate of 110bpm (). She denied of pain abdomen, per vaginal bleeding, or fever. Her vital parameters were stables. Transabdominal obstetric scan at 12 weeks POG was done for regular normal nuchal translucency measurement. It revealed a large irregular gestational sac with the disproportionately small embryo (CRL 8.8 mm, corresponding to 6 weeks 6 days) with no cardiac activity. Additionally, there was markedly thickened placenta measuring of 30mm in thickness. However, no cystic spaces noted within the placenta ( and ). The lab investigation report showed remarkable raised B-hCG level of 76,670 mIU/ ml. Other routine investigations were within normal limit including normal thyroid function test. Subsequently, the suction evacuation was performed and the sample was sent for histopathology. She was kept on regular follow up with serial (B-hCG) level which revealed progressively declined on post suction evacuation days; 3 days (14,480 mIU/ml), 10 days (1880 mIU/ ml), 22 days (84 mIU/ml), 37 days (17.1 mIU/ml), and normal in 2 months. She is under a regular follow up with B-hCG monitoring.\nOUTPUT:"
},
{
"from": "agent",
"value": "Partial Hydatidiform Mole"
}
] | As a physician engaged 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 years old female, primigravida with a normal first antenatal visit at 7 weeks period of gestation (POG) presented with vomiting on and off in outpatient clinic. The transabdominal obstetric scan was done on first antenatal check-up elsewhere showed crown-rump length (CRL) 10.7mm (7 weeks 1 day) with a fetal heart rate of 110bpm (). She denied of pain abdomen, per vaginal bleeding, or fever. Her vital parameters were stables. Transabdominal obstetric scan at 12 weeks POG was done for regular normal nuchal translucency measurement. It revealed a large irregular gestational sac with the disproportionately small embryo (CRL 8.8 mm, corresponding to 6 weeks 6 days) with no cardiac activity. Additionally, there was markedly thickened placenta measuring of 30mm in thickness. However, no cystic spaces noted within the placenta ( and ). The lab investigation report showed remarkable raised B-hCG level of 76,670 mIU/ ml. Other routine investigations were within normal limit including normal thyroid function test. Subsequently, the suction evacuation was performed and the sample was sent for histopathology. She was kept on regular follow up with serial (B-hCG) level which revealed progressively declined on post suction evacuation days; 3 days (14,480 mIU/ml), 10 days (1880 mIU/ ml), 22 days (84 mIU/ml), 37 days (17.1 mIU/ml), and normal in 2 months. She is under a regular follow up with B-hCG monitoring.
OUTPUT: |
PMCPatients_common145 | [
{
"from": "human",
"value": "As a physician engaged 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 LCA was extending to the\\n6th rib and making anastomoses with intercostal arteries. First,\\nballoon angioplasty was performed in the left SCA. After that, the LCA was\\nobliterated via coil embolization. Finally, the left SCA was stented. Stent placed\\nin the SCA also occluded the LITA ostium inadvertently. The patient, being\\nhemodynamically stable, was discharged from the hospital a week after admission with\\na medical treatment comprising of acetylsalicylic acid mg and metoprolol 100 mg. In\\nfollow-up visits, cardiac parameters have been found to be normal.\\nIn our institution, LITA flow measurement is done by intraoperative free-bleeding\\ntechnique. LITA is harvested and explored using electrocautery and metallic clips.\\nTopical application of 0.2% papaverin solution at 37ºC is routinely done to prevent\\nLITA spams. In the free-bleeding technique, the harvested LITA graft, before any\\nballoon dilatation or topical papaverin application, is let to freely bleed from the\\ndistal end to a measuring cylinder for a minute while the heart rate and arterial\\ntension are within normal limits. After measuring the total volume of blood in the\\ncylinder, LITA graft with flow of 30 ml/min or more is considered to be proper for\\nbypass grafting ().\nOUTPUT:"
},
{
"from": "agent",
"value": "Unstable angina pectoris, ST segment elevation, Left subclavian artery occlusion, Left anterior descending artery stenosis"
}
] | As a physician engaged 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 LCA was extending to the\n6th rib and making anastomoses with intercostal arteries. First,\nballoon angioplasty was performed in the left SCA. After that, the LCA was\nobliterated via coil embolization. Finally, the left SCA was stented. Stent placed\nin the SCA also occluded the LITA ostium inadvertently. The patient, being\nhemodynamically stable, was discharged from the hospital a week after admission with\na medical treatment comprising of acetylsalicylic acid mg and metoprolol 100 mg. In\nfollow-up visits, cardiac parameters have been found to be normal.\nIn our institution, LITA flow measurement is done by intraoperative free-bleeding\ntechnique. LITA is harvested and explored using electrocautery and metallic clips.\nTopical application of 0.2% papaverin solution at 37ºC is routinely done to prevent\nLITA spams. In the free-bleeding technique, the harvested LITA graft, before any\nballoon dilatation or topical papaverin application, is let to freely bleed from the\ndistal end to a measuring cylinder for a minute while the heart rate and arterial\ntension are within normal limits. After measuring the total volume of blood in the\ncylinder, LITA graft with flow of 30 ml/min or more is considered to be proper for\nbypass grafting ().
OUTPUT: |
PMCPatients_common1733 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 61-year-old gentleman presented to the emergency department with a 3-day history of bilateral upper limb weakness, more distally, involving the hands and described as an inability to perform fine hand movements such as buttoning his shirt and holding the pen properly when writing. He denied having any numbness or pain. There were no other neurological deficits. There was no antecedent history of respiratory tract or gastrointestinal tract infection. He had no record of a previous similar attack. His symptoms started four days after receiving the second dose of the COVID-19 vaccine (Moderna).\\nOn examination, the patient had normal vital signs. Neurological examination was remarkable for decreased power in the distal muscle group with a power of 4/5. Both upper limbs showed no fasciculation, no abnormal movements, and normal tone. He had normal deep tendon reflexes all over. The sensory and cerebellar examinations were normal. Neurological examination of the lower limbs was normal. Cardiac, respiratory, and abdominal examinations were normal. Complete blood count, urea, creatinine, electrolytes, C-reactive protein, procalcitonin, vitamin B12, folic acid, and thyroid function tests were normal, which excluded an infectious or nutritional deficiency as a cause of his symptoms (Table ). Lumbar puncture was performed, CSF analysis revealed pink fluid, RBC 3000/ul, WBC 4/ul, Glucose 4.27 mmol/L, protein 0.5 gm/L [normal range 0.15–0.45 gm/L] indicating albumin-cytologic dissociation (Table ).\\nNerve conduction studies showed electrophysiological evidence of pure motor neuropathy with primary demyelinating features suggestive of demyelinating polyneuropathy (Figure ). The patient received IV immunoglobulin therapy total of 2 gm/kg; IVIG 0.4 gm/kg per day for five days. His power improved throughout his hospital stay, and he was discharged home. Upon follow-up in the outpatient department, he had recovered entirely with full power upon examination.\nOUTPUT:"
},
{
"from": "agent",
"value": "Guillain-Barre 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 61-year-old gentleman presented to the emergency department with a 3-day history of bilateral upper limb weakness, more distally, involving the hands and described as an inability to perform fine hand movements such as buttoning his shirt and holding the pen properly when writing. He denied having any numbness or pain. There were no other neurological deficits. There was no antecedent history of respiratory tract or gastrointestinal tract infection. He had no record of a previous similar attack. His symptoms started four days after receiving the second dose of the COVID-19 vaccine (Moderna).\nOn examination, the patient had normal vital signs. Neurological examination was remarkable for decreased power in the distal muscle group with a power of 4/5. Both upper limbs showed no fasciculation, no abnormal movements, and normal tone. He had normal deep tendon reflexes all over. The sensory and cerebellar examinations were normal. Neurological examination of the lower limbs was normal. Cardiac, respiratory, and abdominal examinations were normal. Complete blood count, urea, creatinine, electrolytes, C-reactive protein, procalcitonin, vitamin B12, folic acid, and thyroid function tests were normal, which excluded an infectious or nutritional deficiency as a cause of his symptoms (Table ). Lumbar puncture was performed, CSF analysis revealed pink fluid, RBC 3000/ul, WBC 4/ul, Glucose 4.27 mmol/L, protein 0.5 gm/L [normal range 0.15–0.45 gm/L] indicating albumin-cytologic dissociation (Table ).\nNerve conduction studies showed electrophysiological evidence of pure motor neuropathy with primary demyelinating features suggestive of demyelinating polyneuropathy (Figure ). The patient received IV immunoglobulin therapy total of 2 gm/kg; IVIG 0.4 gm/kg per day for five days. His power improved throughout his hospital stay, and he was discharged home. Upon follow-up in the outpatient department, he had recovered entirely with full power upon examination.
OUTPUT: |
PMCPatients_common2170 | [
{
"from": "human",
"value": "As a physician engaged 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 no complaints of difficulty with urination, except that it took a long time to urinate. She denied pain while urinating and urinary frequency. A urine analysis did not reveal hematuria or bacteriuria. She had two vaginal deliveries and no history of major trauma in external genitalia at birth. She denied past history of pelvic trauma or infectious disease in the external genitalia. She was menopausal at 40 years of age, and had never undergone a Papanicolaou (Pap) smear for cervical cancer screening.\\nInspection of her external genitalia showed that her clitoris was normal in size, and the labia majora and anus were visualized (Fig. ); however, the urethral meatus and vagina orifice were not seen on careful inspection of her vulva (Fig. ). On palpation of her external genitalia, there was a pinhole opening at the midpoint between her clitoris and anus. A transrectal ultrasound revealed an atrophic uterus (Fig. ) and large amount of fluid retention in her vagina (Fig. ). A cystoscopic examination was performed in an effort to define the anatomic structures in the closed vaginal cavity before an invasive procedure was undertaken (Additional file : Video 1). The pinhole was dilated and a fiber was inserted into the hole. The tip of the fiber reached her bladder, and we confirmed that the urethra, cervix, and urethral meatus within her vagina were filled with urine. Thus, surgical intervention was recommended. ). A Pap smear showed no cervical abnormalities. We gave our patient local hygiene recommendations and applied an estrogen ointment to prevent reformation of adhesions. She is currently healthy and has had no recurrence 3 months after surgery.\nOUTPUT:"
},
{
"from": "agent",
"value": "Labial fusion, Stage IV esophageal 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: ). She had no complaints of difficulty with urination, except that it took a long time to urinate. She denied pain while urinating and urinary frequency. A urine analysis did not reveal hematuria or bacteriuria. She had two vaginal deliveries and no history of major trauma in external genitalia at birth. She denied past history of pelvic trauma or infectious disease in the external genitalia. She was menopausal at 40 years of age, and had never undergone a Papanicolaou (Pap) smear for cervical cancer screening.\nInspection of her external genitalia showed that her clitoris was normal in size, and the labia majora and anus were visualized (Fig. ); however, the urethral meatus and vagina orifice were not seen on careful inspection of her vulva (Fig. ). On palpation of her external genitalia, there was a pinhole opening at the midpoint between her clitoris and anus. A transrectal ultrasound revealed an atrophic uterus (Fig. ) and large amount of fluid retention in her vagina (Fig. ). A cystoscopic examination was performed in an effort to define the anatomic structures in the closed vaginal cavity before an invasive procedure was undertaken (Additional file : Video 1). The pinhole was dilated and a fiber was inserted into the hole. The tip of the fiber reached her bladder, and we confirmed that the urethra, cervix, and urethral meatus within her vagina were filled with urine. Thus, surgical intervention was recommended. ). A Pap smear showed no cervical abnormalities. We gave our patient local hygiene recommendations and applied an estrogen ointment to prevent reformation of adhesions. She is currently healthy and has had no recurrence 3 months after surgery.
OUTPUT: |
PMCPatients_common2460 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 63-year-old woman who had never smoked and previously was preparing to run a 5 km race presented with dyspnea on exertion, chest tightness, palpitations, and productive cough. She denied hemoptysis, weight loss, fever, chills, or night sweats. Nine years earlier, she underwent RAE and right nephrectomy for a 10.5 cm clear cell RCC. Preembolization imaging showed a large strikingly hypervascular right renal mass, with many contributing arteries. There was no evidence of arteriovenous malformation. The embolization procedure with 700–900-micron spherical particles resulted in extensive devascularization of the tumor. The primary tumor had been staged at stage T3a on the basis of invasion of perirenal adipose tissue. A chest radiograph showed a mass-like density in the left lower lobe with bulky, large mediastinal and left hilar lymphadenopathy and multiple nodules not present on previous imaging. Computed tomography of the chest with contrast medium was notable for a density in the left lower lobe, mediastinal and hilar lymphadenopathy, and multiple nodules (). Bronchoscopy showed a partially obstructive lesion in the left mainstem bronchus that bled with suctioning; bronchoalveolar lavage was negative and endoscopic ultrasonographic biopsy of the lymph nodes was nondiagnostic.\\nThe patient underwent wedge resections of the lingula and left lower lobe and biopsy of a hilar lymph node. Sections of the hilar lymph node showed metastatic RCC.\nOUTPUT:"
},
{
"from": "agent",
"value": "Trisacryl Gelatin Microembolism, Metastases in the Lung, 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 63-year-old woman who had never smoked and previously was preparing to run a 5 km race presented with dyspnea on exertion, chest tightness, palpitations, and productive cough. She denied hemoptysis, weight loss, fever, chills, or night sweats. Nine years earlier, she underwent RAE and right nephrectomy for a 10.5 cm clear cell RCC. Preembolization imaging showed a large strikingly hypervascular right renal mass, with many contributing arteries. There was no evidence of arteriovenous malformation. The embolization procedure with 700–900-micron spherical particles resulted in extensive devascularization of the tumor. The primary tumor had been staged at stage T3a on the basis of invasion of perirenal adipose tissue. A chest radiograph showed a mass-like density in the left lower lobe with bulky, large mediastinal and left hilar lymphadenopathy and multiple nodules not present on previous imaging. Computed tomography of the chest with contrast medium was notable for a density in the left lower lobe, mediastinal and hilar lymphadenopathy, and multiple nodules (). Bronchoscopy showed a partially obstructive lesion in the left mainstem bronchus that bled with suctioning; bronchoalveolar lavage was negative and endoscopic ultrasonographic biopsy of the lymph nodes was nondiagnostic.\nThe patient underwent wedge resections of the lingula and left lower lobe and biopsy of a hilar lymph node. Sections of the hilar lymph node showed metastatic RCC.
OUTPUT: |
PMCPatients_common1689 | [
{
"from": "human",
"value": "As a physician engaged 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 tremors lasted minutes, and on several occasions, terminated with non-stimulated ejaculation. He had no fever, seizure-like activity, or changes in appetite, diet, bowel habits, or level of activity. During the same period, he had profuse perspiration during sleep. The parents sensed anger and possible pain from his change in behavior when having tremors. After one week of symptoms, he was evaluated by his primary care provider and was prescribed hydroxyzine hydrochloride for five days without improvement. Three months prior to this admission, he was admitted with GI symptoms. He was observed for multisystem inflammatory syndrome in children (MIS-C) after testing SARS-CoV-2 positive. Since his initial hospitalization, he became withdrawn and was requesting more hugs from his mother. The facies were not dysmorphic and the thyroid was not enlarged. The heart and lung examinations were normal. There was right upper quadrant tenderness on palpation of the abdomen. Tremors of extremities appeared uncontrolled, coarse, at rest, increased with pain, and decreased with relaxation. A finger-to-nose test was performed without shaking fingers. There were no focal sensory or motor deficits on neurological examination.\\nElectroencephalogram showed normal brain wave activity. MRI without contrast revealed a tiny focus of increased diffusion-weighted imaging (DWI) signal in the left anterolateral aspect of the proximal cervical spinal cord at C1 level, no hemorrhage, edema, or focal lesion in brain parenchyma. ECG tracing showed sinus tachycardia and nonspecific T-wave abnormality. The radiograph of the chest was normal. Laboratory tests are shown in Table .\nOUTPUT:"
},
{
"from": "agent",
"value": "Post Severe Acute Respiratory Syndrome Coronavirus 2 Infection Tremors, Nonverbal Autism, Obesity Class II, Hepatomegaly, Hepatic Steatosis"
}
] | As a physician engaged 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 tremors lasted minutes, and on several occasions, terminated with non-stimulated ejaculation. He had no fever, seizure-like activity, or changes in appetite, diet, bowel habits, or level of activity. During the same period, he had profuse perspiration during sleep. The parents sensed anger and possible pain from his change in behavior when having tremors. After one week of symptoms, he was evaluated by his primary care provider and was prescribed hydroxyzine hydrochloride for five days without improvement. Three months prior to this admission, he was admitted with GI symptoms. He was observed for multisystem inflammatory syndrome in children (MIS-C) after testing SARS-CoV-2 positive. Since his initial hospitalization, he became withdrawn and was requesting more hugs from his mother. The facies were not dysmorphic and the thyroid was not enlarged. The heart and lung examinations were normal. There was right upper quadrant tenderness on palpation of the abdomen. Tremors of extremities appeared uncontrolled, coarse, at rest, increased with pain, and decreased with relaxation. A finger-to-nose test was performed without shaking fingers. There were no focal sensory or motor deficits on neurological examination.\nElectroencephalogram showed normal brain wave activity. MRI without contrast revealed a tiny focus of increased diffusion-weighted imaging (DWI) signal in the left anterolateral aspect of the proximal cervical spinal cord at C1 level, no hemorrhage, edema, or focal lesion in brain parenchyma. ECG tracing showed sinus tachycardia and nonspecific T-wave abnormality. The radiograph of the chest was normal. Laboratory tests are shown in Table .
OUTPUT: |
PMCPatients_common1416 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 33-year-old healthy Caucasian male skier was transferred to our institution 48 hours after a ski accident. His left leg had been temporarily fixed with a plaster cast. The wound had been debrided, irrigated, and closed at a local ski resort hospital. A Gustilo grade II open left tibial fracture (42-A2.2 according to the Orthopaedic Trauma Association)\\n[,] was diagnosed (Figure \\n). Reevaluation of the patient showed a Glasgow Coma Scale of 15, an Injury Severity Score (ISS)\\n[] of 9, a New Injury Severity Score (NISS)\\n[] of 9, and unremarkable chest radiography (Figure \\n). No other sites of injury were identified.\\nStandard reamed antegrade tibial nailing was performed 6 hours later (Figure \\n) with fluted, flexible, intramedullary reamers to insert a 12-mm T2 nail (Stryker/Howmedica, Rutherford, NJ, USA) with proximal and distal locking screws. Just after introduction of the nail, the overall state of the patient started to deteriorate, with decreased oxygen saturation and a confusional state. When the surgical procedure had been completed, the patient was transferred to the intensive care unit (ICU), where he presented with dyspnea, hypoxemia (blood gas analysis revealed the PO2 to be < 60 mmHg), and fever (38.5°C). Twenty-four hours later, petechiae appeared on the lateral chest and abdomen and on the right axilla (Figure \\n). Chest radiography and contrast-enhanced computed tomography (CT) showed diffuse bilateral pulmonary infiltrates (snow-storm appearance) (Figures \\n and\\n).\\nDuring his 5-day stay in the ICU, the patient did not require intubation, although supplemental oxygen was provided (initially, 4 liters/min via nasal cannulae) under continuous pulse oximetry monitoring and repeated blood gas analyses until complete resolution of his symptoms. After 1 week the patient was asymptomatic, and his chest radiograph was normal. Outpatient follow-up was performed until the fracture healed completely and uneventfully.\nOUTPUT:"
},
{
"from": "agent",
"value": "Fat embolism 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 33-year-old healthy Caucasian male skier was transferred to our institution 48 hours after a ski accident. His left leg had been temporarily fixed with a plaster cast. The wound had been debrided, irrigated, and closed at a local ski resort hospital. A Gustilo grade II open left tibial fracture (42-A2.2 according to the Orthopaedic Trauma Association)\n[,] was diagnosed (Figure \n). Reevaluation of the patient showed a Glasgow Coma Scale of 15, an Injury Severity Score (ISS)\n[] of 9, a New Injury Severity Score (NISS)\n[] of 9, and unremarkable chest radiography (Figure \n). No other sites of injury were identified.\nStandard reamed antegrade tibial nailing was performed 6 hours later (Figure \n) with fluted, flexible, intramedullary reamers to insert a 12-mm T2 nail (Stryker/Howmedica, Rutherford, NJ, USA) with proximal and distal locking screws. Just after introduction of the nail, the overall state of the patient started to deteriorate, with decreased oxygen saturation and a confusional state. When the surgical procedure had been completed, the patient was transferred to the intensive care unit (ICU), where he presented with dyspnea, hypoxemia (blood gas analysis revealed the PO2 to be < 60 mmHg), and fever (38.5°C). Twenty-four hours later, petechiae appeared on the lateral chest and abdomen and on the right axilla (Figure \n). Chest radiography and contrast-enhanced computed tomography (CT) showed diffuse bilateral pulmonary infiltrates (snow-storm appearance) (Figures \n and\n).\nDuring his 5-day stay in the ICU, the patient did not require intubation, although supplemental oxygen was provided (initially, 4 liters/min via nasal cannulae) under continuous pulse oximetry monitoring and repeated blood gas analyses until complete resolution of his symptoms. After 1 week the patient was asymptomatic, and his chest radiograph was normal. Outpatient follow-up was performed until the fracture healed completely and uneventfully.
OUTPUT: |
PMCPatients_common347 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 63-year-old male patient was referred with lower urinary tract symptoms, who never had haematuria but suffered from episodic right flank pains that he described as pressure like pains. There was no previous history of renal trauma, renal biopsy or renal surgery. Physical examination was unremarkable. Ultrasound study outlined a large, high-output AVM at the upper pole of right kidney (). Computed tomography angiography demonstrated enlargement of the right main renal artery, its anterior branch and the upper pole segmental artery of the anterior branch. An arteriovenous fistula was noted between a branch of upper pole segmental artery and a single draining vein. No nidus was seen. Ectasia of the feeding arterial segment and aneurysmal dilatation of the draining vein was seen at the site of the AVM ().\\nEndovascular management was the best option after weighing the risk versus benefit of a more invasive surgical option. Renal angiography was performed with a 5F C2 (cobra) catheter and angle tip 0.035” hydrophilic guide wire (Merit). A high-output AVM was outlined (). A 0.018” guide wire and 2.8F micro-catheter were passed through a C2 catheter and positioned in the ectatic feeding artery of the AVM. The first micro coil slipped to the venous side because of high flow, but it did not migrate proximally and stayed close to the arterial feeder. Two micro coils were placed in the arterial feeder. The ectatic segment of the feeding artery was packed with two coils. However, the fistula was still filling due to high flow () and the procedure was abandoned because of incomplete embolisation with plans made for a second intervention.\\nAt the second intervention, the empty spaces between the previously deployed coils in the feeding artery were packed with seven coils of different sizes. One small coil slipped into one of the branches of the upper pole segmental artery. Complete occlusion of the feeding artery was noted on the final angiograms. No filling of the venous channel was seen ().\\nFollowing coil embolisation, no obvious post-embolisation syndrome (fever, nausea, vomiting and pains) was noted 48 h after the procedure. At the 2-week follow-up, renal Doppler demonstrated satisfactory occlusion of the AVM. The findings remained unchanged 4 weeks later ().\nOUTPUT:"
},
{
"from": "agent",
"value": "Renal arteriovenous malformation"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 63-year-old male patient was referred with lower urinary tract symptoms, who never had haematuria but suffered from episodic right flank pains that he described as pressure like pains. There was no previous history of renal trauma, renal biopsy or renal surgery. Physical examination was unremarkable. Ultrasound study outlined a large, high-output AVM at the upper pole of right kidney (). Computed tomography angiography demonstrated enlargement of the right main renal artery, its anterior branch and the upper pole segmental artery of the anterior branch. An arteriovenous fistula was noted between a branch of upper pole segmental artery and a single draining vein. No nidus was seen. Ectasia of the feeding arterial segment and aneurysmal dilatation of the draining vein was seen at the site of the AVM ().\nEndovascular management was the best option after weighing the risk versus benefit of a more invasive surgical option. Renal angiography was performed with a 5F C2 (cobra) catheter and angle tip 0.035” hydrophilic guide wire (Merit). A high-output AVM was outlined (). A 0.018” guide wire and 2.8F micro-catheter were passed through a C2 catheter and positioned in the ectatic feeding artery of the AVM. The first micro coil slipped to the venous side because of high flow, but it did not migrate proximally and stayed close to the arterial feeder. Two micro coils were placed in the arterial feeder. The ectatic segment of the feeding artery was packed with two coils. However, the fistula was still filling due to high flow () and the procedure was abandoned because of incomplete embolisation with plans made for a second intervention.\nAt the second intervention, the empty spaces between the previously deployed coils in the feeding artery were packed with seven coils of different sizes. One small coil slipped into one of the branches of the upper pole segmental artery. Complete occlusion of the feeding artery was noted on the final angiograms. No filling of the venous channel was seen ().\nFollowing coil embolisation, no obvious post-embolisation syndrome (fever, nausea, vomiting and pains) was noted 48 h after the procedure. At the 2-week follow-up, renal Doppler demonstrated satisfactory occlusion of the AVM. The findings remained unchanged 4 weeks later ().
OUTPUT: |
PMCPatients_common5349 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Due to the severity of the symptoms and condition, he was started on systemic ciclosporin (3.0 mg/kg, twice daily). His ultimate ciclosporin dose was 4.0 mg/kg which was gradually increased from the initial dose of 3.0 mg/kg. The patient’s baseline findings are presented in Table . Good clinical response was achieved whilst on ciclosporin and he was maintained on it for 4 months (the later 3 months on the maximum dose) with stable serial blood tests.\\nDuring routine follow-up, he was found to be in acute renal impairment with urea of 17 μmol/L, creatinine of 266 μmol/L and deranged liver function tests with bilirubin 37 μmol/L, alanine transaminase 304 U/L and aspartate transaminase 48 IU/L. Investigations included a urine dipstick and renal ultrasound which were both normal. The ciclosporin level during routine follow-up was elevated (trough level 622 μmol/L) despite consistency with the dose over 3 months and two stable previous blood tests.\\nOn direct questioning, the patient admitted that he had been recently taking a “supplement”. The patient had purchased this over the Internet from an online shop and this was dispatched along with some written information. Subsequently, the “supplement” was found to be oral methyl-1-testosterone (systematic name: 17 alpha methyl-17beta-hydroxy-androst-1-ene-3-one). The patient discontinued both ciclosporin and methyl-1-testosterone and his renal function and liver function tests returned to normal within 1 week. The patient had been administered irregular amounts of methyl-1-testosterone with no regular pattern. This article does not contain any studies with human subjects performed by any of the authors.\nOUTPUT:"
},
{
"from": "agent",
"value": "Acute Kidney Injury, Severe Atopic 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: Due to the severity of the symptoms and condition, he was started on systemic ciclosporin (3.0 mg/kg, twice daily). His ultimate ciclosporin dose was 4.0 mg/kg which was gradually increased from the initial dose of 3.0 mg/kg. The patient’s baseline findings are presented in Table . Good clinical response was achieved whilst on ciclosporin and he was maintained on it for 4 months (the later 3 months on the maximum dose) with stable serial blood tests.\nDuring routine follow-up, he was found to be in acute renal impairment with urea of 17 μmol/L, creatinine of 266 μmol/L and deranged liver function tests with bilirubin 37 μmol/L, alanine transaminase 304 U/L and aspartate transaminase 48 IU/L. Investigations included a urine dipstick and renal ultrasound which were both normal. The ciclosporin level during routine follow-up was elevated (trough level 622 μmol/L) despite consistency with the dose over 3 months and two stable previous blood tests.\nOn direct questioning, the patient admitted that he had been recently taking a “supplement”. The patient had purchased this over the Internet from an online shop and this was dispatched along with some written information. Subsequently, the “supplement” was found to be oral methyl-1-testosterone (systematic name: 17 alpha methyl-17beta-hydroxy-androst-1-ene-3-one). The patient discontinued both ciclosporin and methyl-1-testosterone and his renal function and liver function tests returned to normal within 1 week. The patient had been administered irregular amounts of methyl-1-testosterone with no regular pattern. This article does not contain any studies with human subjects performed by any of the authors.
OUTPUT: |
PMCPatients_common1126 | [
{
"from": "human",
"value": "As a physician engaged 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 84-year-old woman was admitted to our hospital due to fever, abdominal pain and nausea, in May, 2011. At the age of 81 she has been diagnosed as Churg-Strauss syndrome and has been treated by prednisolone (7.5 - 10 mg/day). On the admission, her body temperature was 37.9 oC and blood pressure was 154/95 mmHg. Physical examination revealed pain and muscular defense in her abdomen. Her body weight was 43 kg and height 148 cm (BMI 19.6 kg/m2). Fasting plasma glucose level (150 mg/dl) and hemoglobin A1C level (6.8%; normal range, 4.3 - 5.8%) were elevated. Laboratory data showed increased leukocyte counts (23,600/μl). Serum levels of asparatate aminotransferase (73 U/l; normal range, 10 - 40 U/l), alkaline phosphatase (374 U/L; normal range, 115 - 359 U/L), γ-glutamyl transpeptidase (61 U/L; normal range, < 30 U/L) and C-reactive protein (15.1 mg/dl; normal range, 0 - 0.3 mg/dl) were significantly elevated. Abdominal ultrasound showed enlarged and distended gallbladder containing debris, and thickness of the wall of gallbladder (). Abdominal enhanced computed tomography (CT) also revealed enlarged gallbladder and thickness of the gallbladder wall, and ascites around gallbladder, however, CT did not show a conical structure connecting the gallbladder to the liver (). Abdominal operation revealed the necrosis of gallbladder by torsion due to a floating gallbladder (). The perforation of gallbladder wall was not detected.\nOUTPUT:"
},
{
"from": "agent",
"value": "Acute Cholecystitis, Steroid-induced 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: An 84-year-old woman was admitted to our hospital due to fever, abdominal pain and nausea, in May, 2011. At the age of 81 she has been diagnosed as Churg-Strauss syndrome and has been treated by prednisolone (7.5 - 10 mg/day). On the admission, her body temperature was 37.9 oC and blood pressure was 154/95 mmHg. Physical examination revealed pain and muscular defense in her abdomen. Her body weight was 43 kg and height 148 cm (BMI 19.6 kg/m2). Fasting plasma glucose level (150 mg/dl) and hemoglobin A1C level (6.8%; normal range, 4.3 - 5.8%) were elevated. Laboratory data showed increased leukocyte counts (23,600/μl). Serum levels of asparatate aminotransferase (73 U/l; normal range, 10 - 40 U/l), alkaline phosphatase (374 U/L; normal range, 115 - 359 U/L), γ-glutamyl transpeptidase (61 U/L; normal range, < 30 U/L) and C-reactive protein (15.1 mg/dl; normal range, 0 - 0.3 mg/dl) were significantly elevated. Abdominal ultrasound showed enlarged and distended gallbladder containing debris, and thickness of the wall of gallbladder (). Abdominal enhanced computed tomography (CT) also revealed enlarged gallbladder and thickness of the gallbladder wall, and ascites around gallbladder, however, CT did not show a conical structure connecting the gallbladder to the liver (). Abdominal operation revealed the necrosis of gallbladder by torsion due to a floating gallbladder (). The perforation of gallbladder wall was not detected.
OUTPUT: |
PMCPatients_common3079 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She was deemed a satisfactory candidate and placed on the lung transplant waitlist. Her arterial blood gas analysis revealed worsening hypercapnia and hypoxemia with a PaCO2 of 68 and PaO2/FiO2 ratio of 153. Concerns about the potential adverse impact of prolonged invasive mechanical ventilatory support on patient’s transplant candidacy prompted the medical team to explore the option of negative pressure ventilation (NPV) with BPCV. She was initiated on a control mode with an initial setting of −15 cm H2O synchronized to patient’s inspiration and + 5 cm H2O synchronized for expiration. Frequency as well as inspiratory-to-expiratory ratio was adjusted to synchronize patient efforts. Patient demonstrated easy tolerance for BPCV. Follow-up arterial blood gas after the first 60 min session of BPCV revealed significant improvement in hypercapnia (). Over the next few days, patient was able to maintain acceptable PaCO2 levels with BPCV. She was discharged home with the device with recommendations to use BPCV with sleep as well as on an as needed basis in the day. The patient reported excellent compliance with the device. She also utilized vibration and cough modes of this device on a routine basis to assist with clearance of secretions. Patient underwent successful bilateral sequential lung transplantation approximately 4 months after initiation of BPCV.\nOUTPUT:"
},
{
"from": "agent",
"value": "End-stage lung disease secondary to immotile cilia syndrome with bronchiectasis, Bronchiectasis exacerbation, Respiratory failure"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: She was deemed a satisfactory candidate and placed on the lung transplant waitlist. Her arterial blood gas analysis revealed worsening hypercapnia and hypoxemia with a PaCO2 of 68 and PaO2/FiO2 ratio of 153. Concerns about the potential adverse impact of prolonged invasive mechanical ventilatory support on patient’s transplant candidacy prompted the medical team to explore the option of negative pressure ventilation (NPV) with BPCV. She was initiated on a control mode with an initial setting of −15 cm H2O synchronized to patient’s inspiration and + 5 cm H2O synchronized for expiration. Frequency as well as inspiratory-to-expiratory ratio was adjusted to synchronize patient efforts. Patient demonstrated easy tolerance for BPCV. Follow-up arterial blood gas after the first 60 min session of BPCV revealed significant improvement in hypercapnia (). Over the next few days, patient was able to maintain acceptable PaCO2 levels with BPCV. She was discharged home with the device with recommendations to use BPCV with sleep as well as on an as needed basis in the day. The patient reported excellent compliance with the device. She also utilized vibration and cough modes of this device on a routine basis to assist with clearance of secretions. Patient underwent successful bilateral sequential lung transplantation approximately 4 months after initiation of BPCV.
OUTPUT: |
PMCPatients_common4506 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: PUVA, methotrexate, cyclosporine and acitretin\\nhad to be discontinued because of inefficacy, intolerance or toxicity. He had a\\nhistory of pulmonary tuberculosis, which was duly treated 29 years ago. The viral load was undetectable for HBV. Anti-HCV and anti-HIV\\nwere also negative. There were no respiratory symptoms, while the chest X-ray and\\nMantoux test were normal.\\nThe patient was prophylactically treated with isoniazid for 6 months before starting\\nthe biologic treatment, and vaccinated against HBV, achieving anti-HBs positivity.\\nLamivudine (75mg per day) was started on the same day as the ustekinumab induction\\ndose (45mg), lasting throughout the whole treatment period.\\nLesions improved significantly 3 weeks after the first dose of ustekinumab (PASI 18 /\\nBSA 47%). The patient responded excellently, maintaining PASI 3.8 / BSA 13%, normal\\nliver tests, with no adverse effects in a three-year follow-up ().\nOUTPUT:"
},
{
"from": "agent",
"value": "Severe psoriasis, Positive HBV serology"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: PUVA, methotrexate, cyclosporine and acitretin\nhad to be discontinued because of inefficacy, intolerance or toxicity. He had a\nhistory of pulmonary tuberculosis, which was duly treated 29 years ago. The viral load was undetectable for HBV. Anti-HCV and anti-HIV\nwere also negative. There were no respiratory symptoms, while the chest X-ray and\nMantoux test were normal.\nThe patient was prophylactically treated with isoniazid for 6 months before starting\nthe biologic treatment, and vaccinated against HBV, achieving anti-HBs positivity.\nLamivudine (75mg per day) was started on the same day as the ustekinumab induction\ndose (45mg), lasting throughout the whole treatment period.\nLesions improved significantly 3 weeks after the first dose of ustekinumab (PASI 18 /\nBSA 47%). The patient responded excellently, maintaining PASI 3.8 / BSA 13%, normal\nliver tests, with no adverse effects in a three-year follow-up ().
OUTPUT: |
PMCPatients_common3998 | [
{
"from": "human",
"value": "As a physician engaged in 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 man visited us with a chief complaint of intermittent intractable pain occurring in the right chest. On past history, the patient sustained a fracture of the left femur. At department of orthopedic surgery of our medical institution, the patient was hospitalized to take the surgery. At the time of admission, due to the presentation of varicella zoster and its resulting pain extensivly occurring along the right 6-8th dermatomes, the patient received drug treatments at department of dermatology. During the hospitalization treatments, the symptoms were improved. Two months following the discharge, the patient complained of severe pain occurring in the corresponding dermatomes. Then, the patient visited department of dermatology and was referred to a pain clinic. On physical examination, the patient complained of allodynia, hyperesthesia and hyperalgesia where there was a concurrent presence of the scar tissue formed in the right 6th, 7th and 8th dermatomes. Besides, the patient also complained of sleep disturbance. At the time of admission, VAS was 8/10 points. On routine lab test, there were no notable findings that impede the treatments for diabetes mellitus, blood coaguation disorder and hemostasis abnormality. For the treatment, a needle was placed in the thoracic 8th and 9th multifidus muscle and thoracic 7th and 8th, 8th and 9th and 9th and 10th tissue around the vertebral facet. Four weeks following the treatment, VAS was decreased from 8 points at the time of admission to 2 points. An examination was performed two weeks later, and this showed that VAS was maintained at 2 points and this led to a closure of the treatment.\\nIn the above patients, the treatment period and frequency were four weeks and a total of six times. Based on the characteristics of patients, the age, sex, disease duration, the pattern of pain and the affected dermatomes showed the different characteristics (). Following the treatment, VAS improvement rate (VAS improvement rate (%)= VAS prior to treatment - VAS during evaluation × 100 ) was almost consistent ().\nOUTPUT:"
},
{
"from": "agent",
"value": "Postherpetic neuralgia"
}
] | As a physician engaged 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 man visited us with a chief complaint of intermittent intractable pain occurring in the right chest. On past history, the patient sustained a fracture of the left femur. At department of orthopedic surgery of our medical institution, the patient was hospitalized to take the surgery. At the time of admission, due to the presentation of varicella zoster and its resulting pain extensivly occurring along the right 6-8th dermatomes, the patient received drug treatments at department of dermatology. During the hospitalization treatments, the symptoms were improved. Two months following the discharge, the patient complained of severe pain occurring in the corresponding dermatomes. Then, the patient visited department of dermatology and was referred to a pain clinic. On physical examination, the patient complained of allodynia, hyperesthesia and hyperalgesia where there was a concurrent presence of the scar tissue formed in the right 6th, 7th and 8th dermatomes. Besides, the patient also complained of sleep disturbance. At the time of admission, VAS was 8/10 points. On routine lab test, there were no notable findings that impede the treatments for diabetes mellitus, blood coaguation disorder and hemostasis abnormality. For the treatment, a needle was placed in the thoracic 8th and 9th multifidus muscle and thoracic 7th and 8th, 8th and 9th and 9th and 10th tissue around the vertebral facet. Four weeks following the treatment, VAS was decreased from 8 points at the time of admission to 2 points. An examination was performed two weeks later, and this showed that VAS was maintained at 2 points and this led to a closure of the treatment.\nIn the above patients, the treatment period and frequency were four weeks and a total of six times. Based on the characteristics of patients, the age, sex, disease duration, the pattern of pain and the affected dermatomes showed the different characteristics (). Following the treatment, VAS improvement rate (VAS improvement rate (%)= VAS prior to treatment - VAS during evaluation × 100 ) was almost consistent ().
OUTPUT: |
PMCPatients_common2348 | [
{
"from": "human",
"value": "As a physician engaged in 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 Afro-Caribbean man presented with a 12-month history of change in bowel habit with alternating constipation and diarrhea. He complained of excessive mucus discharge, abdominal distension, and pain particularly in the left iliac fossa. Notably, he maintained a good appetite and stable weight and denied any rectal bleeding. His only comorbidity was vitiligo, not taking any regular medications, and had no known allergies. There was no family history of colorectal cancer or inflammatory bowel disease.\\nMonths prior to being referred to our colorectal team, he underwent a colonoscopy privately, which showed multiple small polyps in the sigmoid colon. Histopathological results showed “likely hyperplastic polyps with no evidence of dysplasia.”\\nOn review in the outpatient clinic, abdominal and rectal examinations were unremarkable. The blood results were normal including no anaemia. Histology showed “features most in keeping with inflammatory polyps.”\\nThe case was discussed at the lower gastrointestinal cancer multidisciplinary team (MDT) meeting where it was felt that, despite the histological findings, there was sufficient concern endoscopically to merit proceeding to a sigmoid colectomy for definitive diagnosis.\\nThe patient underwent an elective laparoscopic anterior resection and loop ileostomy. The procedure was uneventful. The resection was sent for histopathological examination. Macroscopically, the bowel wall showed numerous air-filled cystic spaces varying in size from a few millimeters to more than a centimeter (). On microscopy, the cyst-like spaces were situated predominantly in the submucosa and were lined by endothelial cells, macrophages, and multinucleate giant cells. The stroma between the cysts showed patchy chronic inflammatory cell infiltrate rich in eosinophils. The overlying mucosa showed focal hyperplastic changes and patchy nonspecific chronic active inflammation. There was no dysplasia or malignancy.\nOUTPUT:"
},
{
"from": "agent",
"value": "Pneumatosis Coli"
}
] | As a physician engaged 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 Afro-Caribbean man presented with a 12-month history of change in bowel habit with alternating constipation and diarrhea. He complained of excessive mucus discharge, abdominal distension, and pain particularly in the left iliac fossa. Notably, he maintained a good appetite and stable weight and denied any rectal bleeding. His only comorbidity was vitiligo, not taking any regular medications, and had no known allergies. There was no family history of colorectal cancer or inflammatory bowel disease.\nMonths prior to being referred to our colorectal team, he underwent a colonoscopy privately, which showed multiple small polyps in the sigmoid colon. Histopathological results showed “likely hyperplastic polyps with no evidence of dysplasia.”\nOn review in the outpatient clinic, abdominal and rectal examinations were unremarkable. The blood results were normal including no anaemia. Histology showed “features most in keeping with inflammatory polyps.”\nThe case was discussed at the lower gastrointestinal cancer multidisciplinary team (MDT) meeting where it was felt that, despite the histological findings, there was sufficient concern endoscopically to merit proceeding to a sigmoid colectomy for definitive diagnosis.\nThe patient underwent an elective laparoscopic anterior resection and loop ileostomy. The procedure was uneventful. The resection was sent for histopathological examination. Macroscopically, the bowel wall showed numerous air-filled cystic spaces varying in size from a few millimeters to more than a centimeter (). On microscopy, the cyst-like spaces were situated predominantly in the submucosa and were lined by endothelial cells, macrophages, and multinucleate giant cells. The stroma between the cysts showed patchy chronic inflammatory cell infiltrate rich in eosinophils. The overlying mucosa showed focal hyperplastic changes and patchy nonspecific chronic active inflammation. There was no dysplasia or malignancy.
OUTPUT: |
PMCPatients_common910 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Under sedation with midazolam, access was established via the right femoral vein. We were unable to place the coronary sinus (CS) catheter in place due to an enlarged right atrium (RA) and possible rotation. We placed the CS catheter on the posterior septal region. Ablation of the CTI was done with conventional mapping only. An 8mm Blazer™ Catheter (Boston Scientific, Marlborough, USA) was used as well as RAMP™ sheath (Abbott, Chicago, USA). This was true in the reverse fashion as well. The procedure was completed without any complications, and the patient was discharged on the second day postoperatively. The patient was followed up serially for two years and showed no recurrence of arrhythmias until his death at the end of the second year.\nOUTPUT:"
},
{
"from": "agent",
"value": "Ebstein’s Anomaly, Atrial Flutter, Reduced left ventricular systolic function"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Under sedation with midazolam, access was established via the right femoral vein. We were unable to place the coronary sinus (CS) catheter in place due to an enlarged right atrium (RA) and possible rotation. We placed the CS catheter on the posterior septal region. Ablation of the CTI was done with conventional mapping only. An 8mm Blazer™ Catheter (Boston Scientific, Marlborough, USA) was used as well as RAMP™ sheath (Abbott, Chicago, USA). This was true in the reverse fashion as well. The procedure was completed without any complications, and the patient was discharged on the second day postoperatively. The patient was followed up serially for two years and showed no recurrence of arrhythmias until his death at the end of the second year.
OUTPUT: |
PMCPatients_common478 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 44-year-old gentleman was referred to the vascular surgery team by his GP with a several month history of a lump on the volar aspect of his right hand. He did not recall any significant or repetitive trauma. His past medical history includes only well-controlled asthma and primary Raynaud Syndrome. Of note, he is a musician and has played multiple instruments, including saxophone, clarinet, piano and guitar, for most of his life. He is also a regular golfer. He has no family history of aneurysms and is a lifelong non-smoker.\\nAn initial ultrasound scan showed a pulsatile, anechoic sac measuring 18.9 × 9.3 mm in size, consistent with an aneurysm. The dynamic contrast study showed good collateral supply to the right middle and ring fingers. The patient was referred to the plastic surgery hand team due to concerns with the potential complexity of surgical management.\\nAfter discussion with the team, the patient opted to proceed with surgical excision and understood that a vein graft may be required if blood supply to the fingers was affected by removal of the aneurysm.\\nPreoperative modified Allen test was normal and the patient underwent excision of the lesion as a day case procedure under a general anaesthetic with brachial plexus block supplementation and arm tourniquet. The aneurysm was clamped both proximally and distally and good distal perfusion was confirmed (). The aneurysm was excised and sent for histology, both ends were tied off and the skin closed. Perfusion of the fingers was confirmed after application of dressings. Histology confirmed the diagnosis of true aneurysm. At one-month follow-up the patient had no ongoing sequelae.\nOUTPUT:"
},
{
"from": "agent",
"value": "Digital artery aneurysm"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 44-year-old gentleman was referred to the vascular surgery team by his GP with a several month history of a lump on the volar aspect of his right hand. He did not recall any significant or repetitive trauma. His past medical history includes only well-controlled asthma and primary Raynaud Syndrome. Of note, he is a musician and has played multiple instruments, including saxophone, clarinet, piano and guitar, for most of his life. He is also a regular golfer. He has no family history of aneurysms and is a lifelong non-smoker.\nAn initial ultrasound scan showed a pulsatile, anechoic sac measuring 18.9 × 9.3 mm in size, consistent with an aneurysm. The dynamic contrast study showed good collateral supply to the right middle and ring fingers. The patient was referred to the plastic surgery hand team due to concerns with the potential complexity of surgical management.\nAfter discussion with the team, the patient opted to proceed with surgical excision and understood that a vein graft may be required if blood supply to the fingers was affected by removal of the aneurysm.\nPreoperative modified Allen test was normal and the patient underwent excision of the lesion as a day case procedure under a general anaesthetic with brachial plexus block supplementation and arm tourniquet. The aneurysm was clamped both proximally and distally and good distal perfusion was confirmed (). The aneurysm was excised and sent for histology, both ends were tied off and the skin closed. Perfusion of the fingers was confirmed after application of dressings. Histology confirmed the diagnosis of true aneurysm. At one-month follow-up the patient had no ongoing sequelae.
OUTPUT: |
PMCPatients_common2558 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A complete remission has been kept after surgical resection of ovarian metastasis since in November 2013. She met the eligibility criteria for the DC vaccination therapy as HLA-DNA typing demonstrated a HLA-A*24:02 type compatible with WT1-235 (class I) and HLA-DPB1*05:01 type with WT1-332 (class II) peptides. DC vaccination containing WT1-235 and 332 peptides (a total of 7.34 × 107 DCs; mean, 1.05 × 107 DCs per session) was administered in one course (seven sessions, biweekly) together with oral low-dose chemotherapeutic agents (daily 50 mg/day of cyclophosphamide) from February to May 2014. No grade 3 or higher National Cancer Institute Common Toxicity Criteria toxicities were associated with vaccination or low-dose chemotherapy. Skin reactions defined as erythema ≥3 cm with induration at intradermal injection sites after 48 h were measured. Grade 1 fever within 48 h of DC vaccination was tolerable. No recurrences of disease or new lesions were noted on CT without the need for additional chemotherapy.\nOUTPUT:"
},
{
"from": "agent",
"value": "Advanced Colorectal Cancer, Left Ovarian Metastasis due to Rectal Cancer, Mucinous Adenocarcinoma"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A complete remission has been kept after surgical resection of ovarian metastasis since in November 2013. She met the eligibility criteria for the DC vaccination therapy as HLA-DNA typing demonstrated a HLA-A*24:02 type compatible with WT1-235 (class I) and HLA-DPB1*05:01 type with WT1-332 (class II) peptides. DC vaccination containing WT1-235 and 332 peptides (a total of 7.34 × 107 DCs; mean, 1.05 × 107 DCs per session) was administered in one course (seven sessions, biweekly) together with oral low-dose chemotherapeutic agents (daily 50 mg/day of cyclophosphamide) from February to May 2014. No grade 3 or higher National Cancer Institute Common Toxicity Criteria toxicities were associated with vaccination or low-dose chemotherapy. Skin reactions defined as erythema ≥3 cm with induration at intradermal injection sites after 48 h were measured. Grade 1 fever within 48 h of DC vaccination was tolerable. No recurrences of disease or new lesions were noted on CT without the need for additional chemotherapy.
OUTPUT: |
PMCPatients_common3211 | [
{
"from": "human",
"value": "As a physician engaged in 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 diagnosed with idiopathic DCM in 2013 following resuscitation from an out-of-hospital cardiac arrest caused by ventricular fibrillation. At that time, we did not have any histologic proof of the aetiology of his cardiomyopathy. The patient was treated with a dual chamber implantable cardioverter-defibrillator (ICD) and usual medications with a good response for three years. He developed ventricular tachycardia (VT) in 2016, and conduction disturbances with complete atrioventricular block. Genetic testing for DCM was negative, as was the standard exhaustive aetiological assessment including infectious diseases. Despite optimal medical treatment and upgrade of his ICD with resynchronization, he had two acute HF decompensations in late 2019 and in February 2020.\\nHe was admitted to the ICU in April 2020 for cardiogenic shock. His COVID-19 polymerase chain reaction (PCR) was negative. Cardiac evaluation revealed severe left ventricular hypokinesis, low CO, and good RV function. Despite inotropic support, the patient’s liver enzymes and creatinin increased greatly, requiring higher dose of inotropes. In order to achieve haemodynamic stability, a decision was made to give LVAD support as a bridge to transplantation. On Day 9, he was taken to the operating room (OR) for implantation of a HeartMate 3TM LVAD. Over the next 2 days, dobutamin was weaned and the patient was discharged to the cardiac rehabilitation centre on post-operative day 22. The patient is currently well at home and is awaiting a transplant.\nOUTPUT:"
},
{
"from": "agent",
"value": "End-stage heart failure, Idiopathic dilated cardiomyopathy, Giant cell myocarditis"
}
] | As a physician engaged 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 diagnosed with idiopathic DCM in 2013 following resuscitation from an out-of-hospital cardiac arrest caused by ventricular fibrillation. At that time, we did not have any histologic proof of the aetiology of his cardiomyopathy. The patient was treated with a dual chamber implantable cardioverter-defibrillator (ICD) and usual medications with a good response for three years. He developed ventricular tachycardia (VT) in 2016, and conduction disturbances with complete atrioventricular block. Genetic testing for DCM was negative, as was the standard exhaustive aetiological assessment including infectious diseases. Despite optimal medical treatment and upgrade of his ICD with resynchronization, he had two acute HF decompensations in late 2019 and in February 2020.\nHe was admitted to the ICU in April 2020 for cardiogenic shock. His COVID-19 polymerase chain reaction (PCR) was negative. Cardiac evaluation revealed severe left ventricular hypokinesis, low CO, and good RV function. Despite inotropic support, the patient’s liver enzymes and creatinin increased greatly, requiring higher dose of inotropes. In order to achieve haemodynamic stability, a decision was made to give LVAD support as a bridge to transplantation. On Day 9, he was taken to the operating room (OR) for implantation of a HeartMate 3TM LVAD. Over the next 2 days, dobutamin was weaned and the patient was discharged to the cardiac rehabilitation centre on post-operative day 22. The patient is currently well at home and is awaiting a transplant.
OUTPUT: |
PMCPatients_common4648 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 44-year-old man was admitted with severe posterior neck pain radiating to both shoulder of 13 days duration, and which had aggravated 4 days before admission. He had been transferred from other hospital. He developed high-grade fever on the day of hospitalization. On examination, he was febrile (38℃), with a pulse rate of 110/min and blood pressure of 120/60mmHg. Chest auscultation revealed coarse crepitations in the left infrascapular area. Neurological examination revealed no motor weakness or sensory loss. Investigations showed a total leukocyte count of 12,860/µl, ESR 23mm/hr, and CRP 24.96mg/dl. Renal and liver function tests were normal. Chest X-ray showed no active lesion in either lung or heart enlargement. He was already treated by the triple antibiotics (ceftriaxone, vancomycin, rifampin) before admission. The patient had a previous history of heart disease some 10 years before admission. And we decided to continue the intravenous antibiotics for 8 weeks when his pain improved within 2 weeks of admission. And follow-up echocardiography at four weeks showed no change in the vegetation. The patient was well at his 6-month follow-up, and symptoms almost completely subsided.\nOUTPUT:"
},
{
"from": "agent",
"value": "Cervical Epidural Abscess, Bacterial Endocarditis with Streptococcus Viridans, Discitis, Osteomyelitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 44-year-old man was admitted with severe posterior neck pain radiating to both shoulder of 13 days duration, and which had aggravated 4 days before admission. He had been transferred from other hospital. He developed high-grade fever on the day of hospitalization. On examination, he was febrile (38℃), with a pulse rate of 110/min and blood pressure of 120/60mmHg. Chest auscultation revealed coarse crepitations in the left infrascapular area. Neurological examination revealed no motor weakness or sensory loss. Investigations showed a total leukocyte count of 12,860/µl, ESR 23mm/hr, and CRP 24.96mg/dl. Renal and liver function tests were normal. Chest X-ray showed no active lesion in either lung or heart enlargement. He was already treated by the triple antibiotics (ceftriaxone, vancomycin, rifampin) before admission. The patient had a previous history of heart disease some 10 years before admission. And we decided to continue the intravenous antibiotics for 8 weeks when his pain improved within 2 weeks of admission. And follow-up echocardiography at four weeks showed no change in the vegetation. The patient was well at his 6-month follow-up, and symptoms almost completely subsided.
OUTPUT: |
PMCPatients_common4964 | [
{
"from": "human",
"value": "As a physician engaged in 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 white male presented with a 10-year history of bilateral yellow swelling of the upper and lower eyelids (Fig. , A1). Surgical reduction was attempted twice at 5-year intervals, but was always followed by relapse. Cervical adenopathy and a soft tissue mass of the left cheek were found on examination. He had a history of elevated IgE.\\nAt presentation, laboratory tests were normal except for an eosinophil blood cell count of 920/mm3 and for polyclonal hypergammaglobulinemia with a total IgG level of 17 g/L. Immunophenotyping of blood lymphocytes and T cell clonality did not reveal any sign of lymphoproliferative syndrome. Serum IgG4 level, assessed retrospectively, was 1 g/L. An orbital MRI confirmed bilateral preseptal and anterior orbital infiltration, and lacrimal gland hypertrophy (Fig. , A2). The palpebral biopsy revealed fibrous septa infiltrated by numerous foamy histiocytes, characteristic Touton giant cells as well as IgG4 + plasma cells after immunostaining (Fig. , A1 and B1). A subcutaneous tissue biopsy of the left cheek showed both xanthogranulomatous reaction with Touton giant cells and benign lymphoid hyperplasia organized in follicular germinal centers (Fig. , A1). B- and T-cell clonality on the left cheek tissue sample was negative by polymerase chain reaction analysis for clonal rearrangement of the T-cell receptor gamma chain gene or clonal immunoglobulin rearrangement. Reexamination of the cheek biopsy demonstrated a significant IgG4 + plasma cell infiltrate (Fig. , B1). Oral prednisone, initiated at 1 mg/kg daily, led to a dramatic decrease of the eyelid swelling and of the size of the soft tissue mass in the left cheek. Asthma resolved after the patient started the corticosteroid treatment. Corticosteroids were then tapered to 5 mg daily without any relapse of ocular or systemic manifestations after 72 months of follow-up.\nOUTPUT:"
},
{
"from": "agent",
"value": "Adult Onset Asthma and Periocular Xanthogranuloma (AAPOX), IgG4-Related 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 65-year-old white male presented with a 10-year history of bilateral yellow swelling of the upper and lower eyelids (Fig. , A1). Surgical reduction was attempted twice at 5-year intervals, but was always followed by relapse. Cervical adenopathy and a soft tissue mass of the left cheek were found on examination. He had a history of elevated IgE.\nAt presentation, laboratory tests were normal except for an eosinophil blood cell count of 920/mm3 and for polyclonal hypergammaglobulinemia with a total IgG level of 17 g/L. Immunophenotyping of blood lymphocytes and T cell clonality did not reveal any sign of lymphoproliferative syndrome. Serum IgG4 level, assessed retrospectively, was 1 g/L. An orbital MRI confirmed bilateral preseptal and anterior orbital infiltration, and lacrimal gland hypertrophy (Fig. , A2). The palpebral biopsy revealed fibrous septa infiltrated by numerous foamy histiocytes, characteristic Touton giant cells as well as IgG4 + plasma cells after immunostaining (Fig. , A1 and B1). A subcutaneous tissue biopsy of the left cheek showed both xanthogranulomatous reaction with Touton giant cells and benign lymphoid hyperplasia organized in follicular germinal centers (Fig. , A1). B- and T-cell clonality on the left cheek tissue sample was negative by polymerase chain reaction analysis for clonal rearrangement of the T-cell receptor gamma chain gene or clonal immunoglobulin rearrangement. Reexamination of the cheek biopsy demonstrated a significant IgG4 + plasma cell infiltrate (Fig. , B1). Oral prednisone, initiated at 1 mg/kg daily, led to a dramatic decrease of the eyelid swelling and of the size of the soft tissue mass in the left cheek. Asthma resolved after the patient started the corticosteroid treatment. Corticosteroids were then tapered to 5 mg daily without any relapse of ocular or systemic manifestations after 72 months of follow-up.
OUTPUT: |
PMCPatients_common1316 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 12-month old male infant, with weight 4.8 kg, height 68.9 cm (weight-for-height z-score −6.21, weight-for-age z-score −5.61, length-for-age z-score −2.88) was admitted to icddr,b's, Dhaka Hospital. He had a history of watery stool for five days and high-grade intermittent fever with cough for four days. On admission, physical examination revealed a temperature of 38.7 ºC, heart rate 120/min with normal rhythm, and respiration rate 48/min. On auscultation of the chest, coarse crackles were found in both lungs, and the heart sounds were normal. The abdomen was soft and non-tender. On admission, biochemical data showed Na 139.1 mmol/L, K 1.82 mmol/L, and P 2.4 mg/dL. The chest x-ray showed bilateral hilar consolidation. Initial treatment was given with intravenous antibiotics and fluid therapy. On the second day, tetanic spasm was developed as secondary complication due to hypocalcaemia (Ca 1.68 mmol/L). The tetanic spasm was treated with intravenous calcium gluconate and vitamin D. By the 6th day, the patient recovered from fever and was discharged on the 9th day with normal plasma electrolyte levels (Na 136.8 mmol/L, K 4.30 mmol/L, Ca 2.35 mmol/L, P 5.2 mg/dL).\nOUTPUT:"
},
{
"from": "agent",
"value": "Pneumonia complicated by sepsis, severe malnutrition, hypokalaemia, and hypophosphataemia."
}
] | As a physician engaged 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 12-month old male infant, with weight 4.8 kg, height 68.9 cm (weight-for-height z-score −6.21, weight-for-age z-score −5.61, length-for-age z-score −2.88) was admitted to icddr,b's, Dhaka Hospital. He had a history of watery stool for five days and high-grade intermittent fever with cough for four days. On admission, physical examination revealed a temperature of 38.7 ºC, heart rate 120/min with normal rhythm, and respiration rate 48/min. On auscultation of the chest, coarse crackles were found in both lungs, and the heart sounds were normal. The abdomen was soft and non-tender. On admission, biochemical data showed Na 139.1 mmol/L, K 1.82 mmol/L, and P 2.4 mg/dL. The chest x-ray showed bilateral hilar consolidation. Initial treatment was given with intravenous antibiotics and fluid therapy. On the second day, tetanic spasm was developed as secondary complication due to hypocalcaemia (Ca 1.68 mmol/L). The tetanic spasm was treated with intravenous calcium gluconate and vitamin D. By the 6th day, the patient recovered from fever and was discharged on the 9th day with normal plasma electrolyte levels (Na 136.8 mmol/L, K 4.30 mmol/L, Ca 2.35 mmol/L, P 5.2 mg/dL).
OUTPUT: |
PMCPatients_common4492 | [
{
"from": "human",
"value": "As a physician engaged in 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 was transferred to our emergency room (ER) with epigastric pain. One month previously, he had been diagnosed with ITP. The patient had taken oral steroids for ITP (prednisolone 55 mg/day), which had increased the platelet count from 8000 to 73000/uL. At ER admission, his platelet count was 80000/uL. Electrocardiography (ECG) showed ST segment elevation in leads V 1-3, which was consistent with an anterior wall acute myocardial infarction. Cardiac enzyme (troponin I) was elevated (7.61 ng/mL, normal range: 0.0-0.1 ng/mL). Blood coagulation tests showed a prothrombin time (PT) of 13.4 seconds {international normalized ratio (INR) 1.15} and an activated partial thromboplastin time (aPTT) of 35.1 seconds. Primary percutaneous coronary intervention (PCI) with loading dose clopidogrel 300 mg and aspirin (ASA) 500 mg was performed. After balloon angioplasty, one drug eluting stent (DES, 3.0×28 mm, Coroflex® please; B. Braun Melsungen AG, Germany) was implanted in the proximal LAD, and achieved an optimal angiographic result and TIMI grade 3 flow in the LAD (). After removing the sheath introducer, careful manual compression of the femoral puncture site was performed and no bleeding complication occurred. ECG after PCI showed complete resolution of ST segment elevation without chest pain. Daily treatment with ASA 100 mg and Clopidogrel 75 mg was continued and no symptoms or bleeding complication were noted after discharge.\nOUTPUT:"
},
{
"from": "agent",
"value": "Idiopathic Thrombocytopenic Purpura, Coronary Artery Disease"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 65-year-old man was transferred to our emergency room (ER) with epigastric pain. One month previously, he had been diagnosed with ITP. The patient had taken oral steroids for ITP (prednisolone 55 mg/day), which had increased the platelet count from 8000 to 73000/uL. At ER admission, his platelet count was 80000/uL. Electrocardiography (ECG) showed ST segment elevation in leads V 1-3, which was consistent with an anterior wall acute myocardial infarction. Cardiac enzyme (troponin I) was elevated (7.61 ng/mL, normal range: 0.0-0.1 ng/mL). Blood coagulation tests showed a prothrombin time (PT) of 13.4 seconds {international normalized ratio (INR) 1.15} and an activated partial thromboplastin time (aPTT) of 35.1 seconds. Primary percutaneous coronary intervention (PCI) with loading dose clopidogrel 300 mg and aspirin (ASA) 500 mg was performed. After balloon angioplasty, one drug eluting stent (DES, 3.0×28 mm, Coroflex® please; B. Braun Melsungen AG, Germany) was implanted in the proximal LAD, and achieved an optimal angiographic result and TIMI grade 3 flow in the LAD (). After removing the sheath introducer, careful manual compression of the femoral puncture site was performed and no bleeding complication occurred. ECG after PCI showed complete resolution of ST segment elevation without chest pain. Daily treatment with ASA 100 mg and Clopidogrel 75 mg was continued and no symptoms or bleeding complication were noted after discharge.
OUTPUT: |
PMCPatients_common1210 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 9-year-old boy was referred to the Department of Pediatric Dentistry, Mashhad University of Medical Sciences, Mashhad, Iran. At the same time his parents requested to treat his gingival pigmentation. His oral examination revealed that his gingiva is deeply pigmented from the right second primary molar to the left second primary molar (). He had been checked by a physician previously and there were no pathologic disorders (e.g. Albright syndrome, trauma, hemachromatosis and racial pigmentation) in this case. Therefore, we started depigmentation therapy by cryosurgery technique.\\nLiquid nitrogen was provided in the morning of treatment day by a consumer gas factory and was transferred to the dental facility. In order to transfer the liquid nitrogen, it had been saved in a two-layer flask (metallic inner layer and glassy outer layer).\\nIn the first step isolation was instated by suction and cotton rolls; then hyperpigmentation areas were dried byair spray and 10% topical lidocaine gel was used to achieve anesthesia. During treatment, liquid nitrogen was poured into the glass mug and was rolled on the pigmentation area by cotton swabs (). After the gingiva blanched, the operation was started in another area; after 20 seconds this process was repeated. It is possible repeat this process three or four times for each area. The total time needed for this operation was 30 minutes. In order to record and analyze the results, five standard photos were taken in different positions. Standard high-quality images were taken at baseline and after one, three, six and twelve months (). All the photos were taken by a Canon digital camera (Ixus 800IS, Japan) in the same position, while the patient was sitting upright, and the distance between patient and camera was fixed to about 30 centimeters.\\nMinimal reddish erythema was observed after cryosurgery. After one month the gingival color was ideal. No complications were observed during the follow-up. No recurrent lesions were observed in 12-month follow-up ().\nOUTPUT:"
},
{
"from": "agent",
"value": "Physiological Hyperpigmentation of Oral Mucosa, Amelogenesis Imperfecta"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 9-year-old boy was referred to the Department of Pediatric Dentistry, Mashhad University of Medical Sciences, Mashhad, Iran. At the same time his parents requested to treat his gingival pigmentation. His oral examination revealed that his gingiva is deeply pigmented from the right second primary molar to the left second primary molar (). He had been checked by a physician previously and there were no pathologic disorders (e.g. Albright syndrome, trauma, hemachromatosis and racial pigmentation) in this case. Therefore, we started depigmentation therapy by cryosurgery technique.\nLiquid nitrogen was provided in the morning of treatment day by a consumer gas factory and was transferred to the dental facility. In order to transfer the liquid nitrogen, it had been saved in a two-layer flask (metallic inner layer and glassy outer layer).\nIn the first step isolation was instated by suction and cotton rolls; then hyperpigmentation areas were dried byair spray and 10% topical lidocaine gel was used to achieve anesthesia. During treatment, liquid nitrogen was poured into the glass mug and was rolled on the pigmentation area by cotton swabs (). After the gingiva blanched, the operation was started in another area; after 20 seconds this process was repeated. It is possible repeat this process three or four times for each area. The total time needed for this operation was 30 minutes. In order to record and analyze the results, five standard photos were taken in different positions. Standard high-quality images were taken at baseline and after one, three, six and twelve months (). All the photos were taken by a Canon digital camera (Ixus 800IS, Japan) in the same position, while the patient was sitting upright, and the distance between patient and camera was fixed to about 30 centimeters.\nMinimal reddish erythema was observed after cryosurgery. After one month the gingival color was ideal. No complications were observed during the follow-up. No recurrent lesions were observed in 12-month follow-up ().
OUTPUT: |
PMCPatients_common1931 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: No evidence of pulmonary, cerebral, or hepatic vascular shunts, including AVMs, was demonstrated on prior follow-up contrast-enhanced CT scans. One month before admission, the patient's hemoglobin level was 4.8 g/dL (MCV 75.6.2 fL, MCH 18.5 pg), WBC count was 1.970/mm3, and platelets were 103.000/mm3. At admission, the patient was still pancytopenic (Hb 3.9 g/dL, WBC 2.810/mm3, and PLT 131.000/mm3). The remaining of the chemical workup was normal. Contrast-enhanced CT of the abdomen revealed a markedly enlarged spleen (17,5 cm), a splenic artery saccular aneurysm with calcified walls (28 mm) (), and a grossly dilated portal vein (26 mm) with an increased splenoportal axis calibre. No evidence of hepatic AVMs was found, although the liver was mildly enlarged and accessory right dorsal hepatic veins were detected. Multiple vascular variants were also found, including the left hepatic artery originating from the left gastric artery and the right hepatic artery from the superior mesenteric artery. The patient underwent coil embolization of the splenic artery aneurysm, followed by rapid increase of white blood cell and platelet count. During the hospital stay, single-balloon push-and-pull enteroscopy was also performed, and multiple bleeding duodenal and jejunal angiodysplasias were controlled by Argon-plasma coagulation. After six days, hemoglobin level rose to 8.2 g/dL, WBC count was 13.540/mm3, and platelets were 321.000/mm3. The patient was finally discharged and addressed to our outpatient follow-up.\nOUTPUT:"
},
{
"from": "agent",
"value": "Rendu-Osler-Weber Syndrome, Pancytopenia, Uncommon Vascular Abnormalities, Hypersplenism"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: No evidence of pulmonary, cerebral, or hepatic vascular shunts, including AVMs, was demonstrated on prior follow-up contrast-enhanced CT scans. One month before admission, the patient's hemoglobin level was 4.8 g/dL (MCV 75.6.2 fL, MCH 18.5 pg), WBC count was 1.970/mm3, and platelets were 103.000/mm3. At admission, the patient was still pancytopenic (Hb 3.9 g/dL, WBC 2.810/mm3, and PLT 131.000/mm3). The remaining of the chemical workup was normal. Contrast-enhanced CT of the abdomen revealed a markedly enlarged spleen (17,5 cm), a splenic artery saccular aneurysm with calcified walls (28 mm) (), and a grossly dilated portal vein (26 mm) with an increased splenoportal axis calibre. No evidence of hepatic AVMs was found, although the liver was mildly enlarged and accessory right dorsal hepatic veins were detected. Multiple vascular variants were also found, including the left hepatic artery originating from the left gastric artery and the right hepatic artery from the superior mesenteric artery. The patient underwent coil embolization of the splenic artery aneurysm, followed by rapid increase of white blood cell and platelet count. During the hospital stay, single-balloon push-and-pull enteroscopy was also performed, and multiple bleeding duodenal and jejunal angiodysplasias were controlled by Argon-plasma coagulation. After six days, hemoglobin level rose to 8.2 g/dL, WBC count was 13.540/mm3, and platelets were 321.000/mm3. The patient was finally discharged and addressed to our outpatient follow-up.
OUTPUT: |
PMCPatients_common3330 | [
{
"from": "human",
"value": "As a physician engaged 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 index patient was a 15-year-old male who presented at the children emergency room with a 3-week history of recurrent colicky epigastric abdominal pain. The pain progressively increased in intensity and frequency. The pain was usually associated with epigastric abdominal swelling which disappeared once the pain subsided. There was associated projectile vomiting which was most times bilious. There were weight loss and anorexia, no abdominal distension, constipation, nor fever. He was not a known peptic ulcer disease patient.\\nOn examination, he was acutely ill-looking with intermittent painful distress, not pale, but mildly dehydrated. His pulse rate was 80 beats per minute and respiratory rate was 22 cycles per minute. Chest and cardiovascular examinations were not remarkable.\\nThe examination of the abdomen revealed fullness in the epigastrium with visible peristaltic waves in the epigastrium during episodes of colics. There was mild tenderness in the epigastric region with hyperactive bowel sounds. Rectal examination was not remarkable. Serum electrolytes were within normal limits. Plain abdominal radiograph showed a paucity of bowel gases []. Abdominal ultrasound scan suggested jejunojejunal intussusception. Barium meal and follow through showed grossly dilated stomach and duodenal C-loop with duodenojejunal loop on the right side of the midline [].\\nThe patient had exploratory laparotomy done via upper midline incision. The congenital bands were divided, twisted bowel was derotated and appendicectomy was done.\\nHe had an uneventful post-operative care and was discharged home to the paediatric surgical outpatient clinic for follow-up.\nOUTPUT:"
},
{
"from": "agent",
"value": "Malrotation of the Midgut, Horseshoe Kidney, Gastric Outlet Obstruction"
}
] | As a physician engaged 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 index patient was a 15-year-old male who presented at the children emergency room with a 3-week history of recurrent colicky epigastric abdominal pain. The pain progressively increased in intensity and frequency. The pain was usually associated with epigastric abdominal swelling which disappeared once the pain subsided. There was associated projectile vomiting which was most times bilious. There were weight loss and anorexia, no abdominal distension, constipation, nor fever. He was not a known peptic ulcer disease patient.\nOn examination, he was acutely ill-looking with intermittent painful distress, not pale, but mildly dehydrated. His pulse rate was 80 beats per minute and respiratory rate was 22 cycles per minute. Chest and cardiovascular examinations were not remarkable.\nThe examination of the abdomen revealed fullness in the epigastrium with visible peristaltic waves in the epigastrium during episodes of colics. There was mild tenderness in the epigastric region with hyperactive bowel sounds. Rectal examination was not remarkable. Serum electrolytes were within normal limits. Plain abdominal radiograph showed a paucity of bowel gases []. Abdominal ultrasound scan suggested jejunojejunal intussusception. Barium meal and follow through showed grossly dilated stomach and duodenal C-loop with duodenojejunal loop on the right side of the midline [].\nThe patient had exploratory laparotomy done via upper midline incision. The congenital bands were divided, twisted bowel was derotated and appendicectomy was done.\nHe had an uneventful post-operative care and was discharged home to the paediatric surgical outpatient clinic for follow-up.
OUTPUT: |
PMCPatients_common5249 | [
{
"from": "human",
"value": "As a physician engaged 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 EEG and brain CT were both normal. He was started on valproic acid 900 mg and was shifted to lamotrigine 200 mg daily 3 years later. After a 5-year period without seizures, lamotrigine was slowly tapered off and the patient completely stopped the intake 1 month before the present admission. He had no neurological or other complaints up to the seizure. Brain CT was normal, but an MRI scan showed an infarct in the left cerebellar hemisphere (fig. ) and a left-sided pontine infarction (fig. ). Subsequent MR angiography showed a right VAD (fig. ).\\nIn addition, the blood samples for kidney and liver function, haemoglobin and coagulation factors were all in the normal range of reference. However, there was a high leucocyte count with an overabundance of neutrophils. Moreover, the patient's blood pressure at the time of admission was normal (127/87 mm Hg), and he was afebrile. The patient was started on heparin and the oral anticoagulant warfarin, which he continued for 6 months (from January 10 until June 21). The treatment with lamotrigine was also resumed. Recovery of neurologic function was excellent, and he was discharged after 14 days. ). The patient still continued treatment with aspirin and dipyridamole.\nOUTPUT:"
},
{
"from": "agent",
"value": "Vertebral Artery Dissection, Generalized Convulsive Seizures, Juvenile Myoclonic Epilepsy"
}
] | As a physician engaged 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 EEG and brain CT were both normal. He was started on valproic acid 900 mg and was shifted to lamotrigine 200 mg daily 3 years later. After a 5-year period without seizures, lamotrigine was slowly tapered off and the patient completely stopped the intake 1 month before the present admission. He had no neurological or other complaints up to the seizure. Brain CT was normal, but an MRI scan showed an infarct in the left cerebellar hemisphere (fig. ) and a left-sided pontine infarction (fig. ). Subsequent MR angiography showed a right VAD (fig. ).\nIn addition, the blood samples for kidney and liver function, haemoglobin and coagulation factors were all in the normal range of reference. However, there was a high leucocyte count with an overabundance of neutrophils. Moreover, the patient's blood pressure at the time of admission was normal (127/87 mm Hg), and he was afebrile. The patient was started on heparin and the oral anticoagulant warfarin, which he continued for 6 months (from January 10 until June 21). The treatment with lamotrigine was also resumed. Recovery of neurologic function was excellent, and he was discharged after 14 days. ). The patient still continued treatment with aspirin and dipyridamole.
OUTPUT: |
PMCPatients_common4615 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: As minimal invasive surgery was planned, epidural was not attempted, and patient was administered general anaesthesia. Intra-operatively due to surgical reasons, open laparotomy had to be done. Rest of the intraoperative course was uneventful with blood loss of around a litre. In view of the midline incision extending from a point 3 cm above pubic symphysis right up to xiphisternum, adequate post-operative pain relief was essential. After wound closure, under anaesthesia and with adequate asepsis, a 16 gauge Touhy's epidural needle was inserted in the RS space, lateral to the upper end of the incision, under ultrasound guidance. After confirmation of the RS space using saline, epidural catheter was threaded in the space around 5–7 cm of length. The same procedure was repeated on the opposite side. The catheters were fixed with steristrips and tegaderm to prevent accidental dislodgement []. A volume of 20 cc of 0.25% bupivacaine was administered through each RS catheter after insertion and repeated 6–8 hourly. For the next 24 h, the patient received concomitant analgesia in the form of intermittent doses of diclofenac 50 mg, paracetamol 1 g, and tramadol 50 mg by the intravenous (IV) route. From the 2nd day onward, only paracetamol was continued, and the opioid was administered as a rescue, along with the 20 cc of 0.25% bupivacaine 8 hourly through each RS catheter. The patient was encouraged to ambulate right from the first postoperative day, and the RS catheters were removed after 72 h. The worst pain score recorded by acute pain service team using the numeric rating scale in the first 72 h was 3/10.\nOUTPUT:"
},
{
"from": "agent",
"value": "Carcinoma colon, Gastrointestinal stromal tumour of the stomach"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: As minimal invasive surgery was planned, epidural was not attempted, and patient was administered general anaesthesia. Intra-operatively due to surgical reasons, open laparotomy had to be done. Rest of the intraoperative course was uneventful with blood loss of around a litre. In view of the midline incision extending from a point 3 cm above pubic symphysis right up to xiphisternum, adequate post-operative pain relief was essential. After wound closure, under anaesthesia and with adequate asepsis, a 16 gauge Touhy's epidural needle was inserted in the RS space, lateral to the upper end of the incision, under ultrasound guidance. After confirmation of the RS space using saline, epidural catheter was threaded in the space around 5–7 cm of length. The same procedure was repeated on the opposite side. The catheters were fixed with steristrips and tegaderm to prevent accidental dislodgement []. A volume of 20 cc of 0.25% bupivacaine was administered through each RS catheter after insertion and repeated 6–8 hourly. For the next 24 h, the patient received concomitant analgesia in the form of intermittent doses of diclofenac 50 mg, paracetamol 1 g, and tramadol 50 mg by the intravenous (IV) route. From the 2nd day onward, only paracetamol was continued, and the opioid was administered as a rescue, along with the 20 cc of 0.25% bupivacaine 8 hourly through each RS catheter. The patient was encouraged to ambulate right from the first postoperative day, and the RS catheters were removed after 72 h. The worst pain score recorded by acute pain service team using the numeric rating scale in the first 72 h was 3/10.
OUTPUT: |
PMCPatients_common2152 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: No family history of neurological or psychological illness was identified. Despite taking neuroleptics, in the course of the disease, the patient experienced 4 episodes (for several weeks) with paranoid-hallucinatory exacerbation. In these episodes, the patient suffered from formal thought disorders, fear, and delusions of persecution; auditory hallucinations with commenting, discussing, and commanding voices; visual hallucinations involving seeing persons in his room; and tactile hallucinations with the feeling of being touched from behind. Neurological and medical examinations showed no further clinical disorders. The patient had been treated with amisulpride, benperidol, chlorprothixene, levomepromazine, olanzapine, and clozapine at standard doses and for an adequate period of time. Because he did not properly response to any of these medications, we diagnosed him as having TRS and initiated an individual treatment regime with M-ECT. In total, 24 ECT treatments were administered over a 1-year period, and the treatment success was evaluated by the Psychotic Symptom Rating Scales (PSYRATS), (Table ). [ Before beginning ECT treatment, the patient showed clear deficits in almost every PSYRATS subscale; however, after 24 ECT treatment sessions, the symptom severity was much weaker and limited to only some of the PSYRATS subscales (see tables). His neuroleptic medication, olanzapine (10 mg given morning and night), remained stable during the treatment course. Moreover, there was no need for add-on psychiatric in-house treatment during the whole M-ECT treatment course (Table ).\nOUTPUT:"
},
{
"from": "agent",
"value": "Treatment-resistant schizophrenia"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: No family history of neurological or psychological illness was identified. Despite taking neuroleptics, in the course of the disease, the patient experienced 4 episodes (for several weeks) with paranoid-hallucinatory exacerbation. In these episodes, the patient suffered from formal thought disorders, fear, and delusions of persecution; auditory hallucinations with commenting, discussing, and commanding voices; visual hallucinations involving seeing persons in his room; and tactile hallucinations with the feeling of being touched from behind. Neurological and medical examinations showed no further clinical disorders. The patient had been treated with amisulpride, benperidol, chlorprothixene, levomepromazine, olanzapine, and clozapine at standard doses and for an adequate period of time. Because he did not properly response to any of these medications, we diagnosed him as having TRS and initiated an individual treatment regime with M-ECT. In total, 24 ECT treatments were administered over a 1-year period, and the treatment success was evaluated by the Psychotic Symptom Rating Scales (PSYRATS), (Table ). [ Before beginning ECT treatment, the patient showed clear deficits in almost every PSYRATS subscale; however, after 24 ECT treatment sessions, the symptom severity was much weaker and limited to only some of the PSYRATS subscales (see tables). His neuroleptic medication, olanzapine (10 mg given morning and night), remained stable during the treatment course. Moreover, there was no need for add-on psychiatric in-house treatment during the whole M-ECT treatment course (Table ).
OUTPUT: |
PMCPatients_common10 | [
{
"from": "human",
"value": "As a physician engaged in 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 Asian man with a 55-year history of type 2 diabetes mellitus was referred to our hospital for right intermittent claudication of 3 years. He had diabetic retinopathy and had been treated with insulin for 3 years. Vascular examination revealed right femoral bruit and diminished right popliteal pulse, suggesting the presence of a right femoral lesion. However, the right ABI measured by a volume plethysmograph (Form PWV/ABI; Omron Health Care Co., Kyoto, Japan) was 1.28, within the normal range (1.00–1.40) (Fig. ). On the other hand, the left ABI was elevated to 1.55 (> 1.40), suggesting that the infrapopliteal arteries at the left ankle were incompressible. Upstroke time, the transit time from the nadir to the peak of the pulse volume waveform recording, of the right ankle was prolonged to 201 milliseconds (≥ 180 milliseconds), whereas upstroke time of the left ankle was within the normal range (130 milliseconds) (Fig. ). These findings suggest that the right ABI was falsely normalized due to incompressible infrapopliteal arteries at the right ankle despite the presence of PAD in the right extremity. Indeed, intra-arterial angiography revealed the presence of a severe stenotic lesion at the origin of the right superficial femoral artery (SFA) (Fig. A), whereas there was no occlusive arterial disease in the left extremity. Fluoroscopic images showed severe calcification of infrapopliteal arteries at the right ankle (Fig. B). Computed tomography also revealed severe calcification of the bilateral infrapopliteal arteries (Fig. ). Revascularization was not performed, and supervised exercise training was initiated. After completion of the 6-month supervised exercise training program, he continued to spend 2 hours a day walking. Five years from the initial assessment, the right ABI had decreased to 0.83, with upstroke time at the right ankle of 242 milliseconds, indicating the progression of the right lower extremity PAD (Fig. ). However, there was no deterioration in his symptoms, and he had no difficulty in performing daily activities.\nOUTPUT:"
},
{
"from": "agent",
"value": "Lower-extremity peripheral artery disease"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 76-year-old Asian man with a 55-year history of type 2 diabetes mellitus was referred to our hospital for right intermittent claudication of 3 years. He had diabetic retinopathy and had been treated with insulin for 3 years. Vascular examination revealed right femoral bruit and diminished right popliteal pulse, suggesting the presence of a right femoral lesion. However, the right ABI measured by a volume plethysmograph (Form PWV/ABI; Omron Health Care Co., Kyoto, Japan) was 1.28, within the normal range (1.00–1.40) (Fig. ). On the other hand, the left ABI was elevated to 1.55 (> 1.40), suggesting that the infrapopliteal arteries at the left ankle were incompressible. Upstroke time, the transit time from the nadir to the peak of the pulse volume waveform recording, of the right ankle was prolonged to 201 milliseconds (≥ 180 milliseconds), whereas upstroke time of the left ankle was within the normal range (130 milliseconds) (Fig. ). These findings suggest that the right ABI was falsely normalized due to incompressible infrapopliteal arteries at the right ankle despite the presence of PAD in the right extremity. Indeed, intra-arterial angiography revealed the presence of a severe stenotic lesion at the origin of the right superficial femoral artery (SFA) (Fig. A), whereas there was no occlusive arterial disease in the left extremity. Fluoroscopic images showed severe calcification of infrapopliteal arteries at the right ankle (Fig. B). Computed tomography also revealed severe calcification of the bilateral infrapopliteal arteries (Fig. ). Revascularization was not performed, and supervised exercise training was initiated. After completion of the 6-month supervised exercise training program, he continued to spend 2 hours a day walking. Five years from the initial assessment, the right ABI had decreased to 0.83, with upstroke time at the right ankle of 242 milliseconds, indicating the progression of the right lower extremity PAD (Fig. ). However, there was no deterioration in his symptoms, and he had no difficulty in performing daily activities.
OUTPUT: |
PMCPatients_common4545 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: As well, labs at this time did not show any eosinophilia.\nOUTPUT:"
},
{
"from": "agent",
"value": "Erythema Annulare Centrifugum-Like Eruption, Hepatitis C"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: As well, labs at this time did not show any eosinophilia.
OUTPUT: |
PMCPatients_common3152 | [
{
"from": "human",
"value": "As a physician engaged in 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 50-year-old man experienced black widow spider (BWS) envenomation. After the bite, he manifested sweating, wrist paraesthesia, and pain at the initial bite site with inoculum spreading to the upper arms. Laboratory tests revealed leukocytosis and increased plasma levels of C-reactive protein, cardiac troponin-I, and brain natriuretic peptide (Table ). Arterial blood gas analysis, chest X-rays, and echocardiographic examinations were normal at admission; electrocardiogram (ECG) showed diphasic T waves in lateral leads (Fig. a) which were not present in previous outpatient ECGs.\\nDue to the lack of available antidotes, the patient was empirically treated with intravenous fluids for hydration, analgesics for the relief of pain, benzodiazepines for agitation, antibiotics to prevent infection, steroids, and anti-histamines for periorbital edema. On day 1 of hospitalization, the ECG showed negative T waves in lateral and inferior leads (Fig. b), abnormalities in the wall motion of the left ventricle (LV) in association with moderate systolic dysfunction (hypokinesia of the LV middle/basal segments of the inferior, lateral and inferior-lateral walls); and LV ejection fraction (LVEF) of 48%. The decrease in LVEF was confirmed by speckle tracking analysis: global longitudinal strain (GLS) showed a reduced LV contractile performance (− 14%). Angiotensin-converting enzyme inhibitors, beta-blockers, and diuretics were administered. A minimal area of focal fibrosis was detected at the junction between the left atrium and ventricle, although this finding was not specific (Fig. ). Coronary angiography excluded coronary stenosis (Fig. ).\\nOn day 11, the echocardiographic findings (LVEF 55%, GLS − 19%) and cardiac enzymes were normal and the patient was discharged with medical therapy for heart failure.\nOUTPUT:"
},
{
"from": "agent",
"value": "Acute Myocarditis"
}
] | As a physician engaged 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 50-year-old man experienced black widow spider (BWS) envenomation. After the bite, he manifested sweating, wrist paraesthesia, and pain at the initial bite site with inoculum spreading to the upper arms. Laboratory tests revealed leukocytosis and increased plasma levels of C-reactive protein, cardiac troponin-I, and brain natriuretic peptide (Table ). Arterial blood gas analysis, chest X-rays, and echocardiographic examinations were normal at admission; electrocardiogram (ECG) showed diphasic T waves in lateral leads (Fig. a) which were not present in previous outpatient ECGs.\nDue to the lack of available antidotes, the patient was empirically treated with intravenous fluids for hydration, analgesics for the relief of pain, benzodiazepines for agitation, antibiotics to prevent infection, steroids, and anti-histamines for periorbital edema. On day 1 of hospitalization, the ECG showed negative T waves in lateral and inferior leads (Fig. b), abnormalities in the wall motion of the left ventricle (LV) in association with moderate systolic dysfunction (hypokinesia of the LV middle/basal segments of the inferior, lateral and inferior-lateral walls); and LV ejection fraction (LVEF) of 48%. The decrease in LVEF was confirmed by speckle tracking analysis: global longitudinal strain (GLS) showed a reduced LV contractile performance (− 14%). Angiotensin-converting enzyme inhibitors, beta-blockers, and diuretics were administered. A minimal area of focal fibrosis was detected at the junction between the left atrium and ventricle, although this finding was not specific (Fig. ). Coronary angiography excluded coronary stenosis (Fig. ).\nOn day 11, the echocardiographic findings (LVEF 55%, GLS − 19%) and cardiac enzymes were normal and the patient was discharged with medical therapy for heart failure.
OUTPUT: |
PMCPatients_common3437 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 50-year-old woman presented to our hospital with ventricular tachycardia and loss of consciousness. She received an electric shock and returned to sinus rhythm. She had no past medical history. Herat rate was 89 beats/min (regular rhythm); blood pressure was 98/56 mmHg. No heart murmur was heard at presentation. We performed coronary angiography, which revealed an occluded lesion in the distal right coronary artery (). After crossing of a 0.014-inch guidewire (SION-blue), IVUS (Eagle-Eye Platinum) showed an extensive IMH. Because of unstable haemodynamics, we switched to PCI with a 2.0 × 10 mm CB that was gently inflated to generate re-entry on the IMH. The CB angioplasty successfully relieved the compression of the true lumen by the IMH, which promptly improved the coronary flow (). Although the coronary dissection remained, no additional treatment was performed because the dissection did not impair coronary flow and IVUS showed that the IMH was fenestrated and reduced (). After PCI, heparin was administered at a dose of 12 000 units/day for 24-h in the CCU. Consciousness was restored on the second day. Dual antiplatelet therapy was given immediately before PCI and continued for 3 months, followed by aspirin alone. She spent days without chest pain and underwent contrast-enhanced computed tomography coronary angiography 6, 12, and 36 months after PCI. The coronary dissection formed after PCI was observed for up to 12 months. However, it healed spontaneously by 36 months (). Based on this finding, the aspirin could be discontinued.\\nIn both cases, we did not perform a ‘re-look’ because there was no recurrence of chest pain after PCI, and because repeat coronary angiography may cause dissection progression.\nOUTPUT:"
},
{
"from": "agent",
"value": "Acute ST-elevation myocardial infarction, Type-2 SCAD"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 50-year-old woman presented to our hospital with ventricular tachycardia and loss of consciousness. She received an electric shock and returned to sinus rhythm. She had no past medical history. Herat rate was 89 beats/min (regular rhythm); blood pressure was 98/56 mmHg. No heart murmur was heard at presentation. We performed coronary angiography, which revealed an occluded lesion in the distal right coronary artery (). After crossing of a 0.014-inch guidewire (SION-blue), IVUS (Eagle-Eye Platinum) showed an extensive IMH. Because of unstable haemodynamics, we switched to PCI with a 2.0 × 10 mm CB that was gently inflated to generate re-entry on the IMH. The CB angioplasty successfully relieved the compression of the true lumen by the IMH, which promptly improved the coronary flow (). Although the coronary dissection remained, no additional treatment was performed because the dissection did not impair coronary flow and IVUS showed that the IMH was fenestrated and reduced (). After PCI, heparin was administered at a dose of 12 000 units/day for 24-h in the CCU. Consciousness was restored on the second day. Dual antiplatelet therapy was given immediately before PCI and continued for 3 months, followed by aspirin alone. She spent days without chest pain and underwent contrast-enhanced computed tomography coronary angiography 6, 12, and 36 months after PCI. The coronary dissection formed after PCI was observed for up to 12 months. However, it healed spontaneously by 36 months (). Based on this finding, the aspirin could be discontinued.\nIn both cases, we did not perform a ‘re-look’ because there was no recurrence of chest pain after PCI, and because repeat coronary angiography may cause dissection progression.
OUTPUT: |
PMCPatients_common4489 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 49 year-old man who presented with recurrent upper\\nabdominal pain of 9 years, and 6 months history of\\nright hypochondrial swelling and weight loss. He also\\nhad history of early satiety and vomiting. No history\\nsuggestive of upper gastrointestinal bleeding. Clinical\\nexamination revealed wasting, pallor and ankle oedema.\\nHe had hepatomegaly which was firm, irregular and\\ntender. Succussion splash was positive. An impression\\nof gastric outlet obstruction secondary to antral\\ncarcinoma to rule out carcinoma head of pancreas\\nwith hepatic metastasis was made.\\nAbdominal ultrasound scan revealed hepatomegaly\\nand a mass distal to the stomach.\\nPeripheral blood film examination revealed iron\\ndeficiency anaemia and thrombocytosis, while serum\\nchemistry showed hypoalbuminaemia.\\nAn upper gastrointestinal endoscopy revealed a mass\\nin the second part of the duodenum which was\\nulcerating and vascular. Multiple biopsies were taken\\nfor histopathology. The tissue was sectioned and stained\\nwith haematoxylin and eosin. It showed spindle shaped\\ncells containing large nuclei with blunt edges and were\\nsurrounded with mild to moderate cytoplasm. There\\nis loss of overlying mucosa . There were metastases to the liver and\\nparaaortic lymph nodes. He is presently stable\\nand on follow up .He has been commenced on cyclical\\ncytotoxic chemotherapy using 5- fluorouracil.\nOUTPUT:"
},
{
"from": "agent",
"value": "Gastrointestinal Stromal Tumour"
}
] | As a physician engaged 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 49 year-old man who presented with recurrent upper\nabdominal pain of 9 years, and 6 months history of\nright hypochondrial swelling and weight loss. He also\nhad history of early satiety and vomiting. No history\nsuggestive of upper gastrointestinal bleeding. Clinical\nexamination revealed wasting, pallor and ankle oedema.\nHe had hepatomegaly which was firm, irregular and\ntender. Succussion splash was positive. An impression\nof gastric outlet obstruction secondary to antral\ncarcinoma to rule out carcinoma head of pancreas\nwith hepatic metastasis was made.\nAbdominal ultrasound scan revealed hepatomegaly\nand a mass distal to the stomach.\nPeripheral blood film examination revealed iron\ndeficiency anaemia and thrombocytosis, while serum\nchemistry showed hypoalbuminaemia.\nAn upper gastrointestinal endoscopy revealed a mass\nin the second part of the duodenum which was\nulcerating and vascular. Multiple biopsies were taken\nfor histopathology. The tissue was sectioned and stained\nwith haematoxylin and eosin. It showed spindle shaped\ncells containing large nuclei with blunt edges and were\nsurrounded with mild to moderate cytoplasm. There\nis loss of overlying mucosa . There were metastases to the liver and\nparaaortic lymph nodes. He is presently stable\nand on follow up .He has been commenced on cyclical\ncytotoxic chemotherapy using 5- fluorouracil.
OUTPUT: |
PMCPatients_common3992 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: The patient had syncopal episodes while drinking fluids starting seven years ago. He reported the feeling of a foreign body sensation at his mid sternal area after drinking a cold beverage, and then suddenly lost consciousness. The duration of unconsciousness was a few seconds. There were no seizure-like movements or incontinence during the attack, and he felt no numbness or motor weakness before or after the events. He was also diagnosed with diabetes mellitus three years ago. His echocardiography did not show any significant abnormality of the heart except bilateral atrial enlargement. On the second day of admission, he felt a globulous sensation at the mid esophagus after drinking a cold beverage in the sitting position, and then lost consciousness. On the treadmill test, his heart rate and blood pressure increased to 176/min and 218/83 mmHg, respectively. The head-up tilt test three months before admission was negative; the head-up tilt test was repeated.\nOUTPUT:"
},
{
"from": "agent",
"value": "Deglutition Syncope, Ventricular Asystole, Permanent Atrial Fibrillation"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: The patient had syncopal episodes while drinking fluids starting seven years ago. He reported the feeling of a foreign body sensation at his mid sternal area after drinking a cold beverage, and then suddenly lost consciousness. The duration of unconsciousness was a few seconds. There were no seizure-like movements or incontinence during the attack, and he felt no numbness or motor weakness before or after the events. He was also diagnosed with diabetes mellitus three years ago. His echocardiography did not show any significant abnormality of the heart except bilateral atrial enlargement. On the second day of admission, he felt a globulous sensation at the mid esophagus after drinking a cold beverage in the sitting position, and then lost consciousness. On the treadmill test, his heart rate and blood pressure increased to 176/min and 218/83 mmHg, respectively. The head-up tilt test three months before admission was negative; the head-up tilt test was repeated.
OUTPUT: |
PMCPatients_common2935 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 31-year-old Arab male presented with two days history of diffuse colicky abdominal pain along with guarding and spleno-megaly. He was on prophylactic aspirin and regular phlebotomy every 2-3 months.\\nLaboratory studies showed hemoglobin of 14g/dL, hematocrit of 49% with normal white cell and platelet counts. He underwent emergency small bowel resection with end to end anastomosis. On the second post operative day, he developed intermittent narrow QRS atrial tachycardia and became hypoxic and hypotensive with new right bundle branch block on ECG. There was severe tricuspid regurgitation with RV systolic pressure of 70 mmHg. Ultrasound Doppler of inferior vena cava and lower limb veins did not show any thrombi. He also developed intermittent melena and gastroscopy showed Grade I esophageal varices. He was stabilized with blood transfusion and inotropes. He was advised surgical removal of the RA thrombus but he declined. Thrombolysis was contraindicated and hence, he was continued on heparin with overlap warfarin. He improved hemodynamically with no recurrence of atrial tachycardia. A repeat TTE after two weeks showed complete resolution of RA thrombus () with RV systolic pressure of 45mmHg.\nOUTPUT:"
},
{
"from": "agent",
"value": "Mobile Right Heart Thrombus, Pulmonary Embolism, Polycythemia Rubra Vera, Splanchnic Vein Thrombosis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 31-year-old Arab male presented with two days history of diffuse colicky abdominal pain along with guarding and spleno-megaly. He was on prophylactic aspirin and regular phlebotomy every 2-3 months.\nLaboratory studies showed hemoglobin of 14g/dL, hematocrit of 49% with normal white cell and platelet counts. He underwent emergency small bowel resection with end to end anastomosis. On the second post operative day, he developed intermittent narrow QRS atrial tachycardia and became hypoxic and hypotensive with new right bundle branch block on ECG. There was severe tricuspid regurgitation with RV systolic pressure of 70 mmHg. Ultrasound Doppler of inferior vena cava and lower limb veins did not show any thrombi. He also developed intermittent melena and gastroscopy showed Grade I esophageal varices. He was stabilized with blood transfusion and inotropes. He was advised surgical removal of the RA thrombus but he declined. Thrombolysis was contraindicated and hence, he was continued on heparin with overlap warfarin. He improved hemodynamically with no recurrence of atrial tachycardia. A repeat TTE after two weeks showed complete resolution of RA thrombus () with RV systolic pressure of 45mmHg.
OUTPUT: |
PMCPatients_common3736 | [
{
"from": "human",
"value": "As a physician engaged 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 August 2012, a 64-year-old, male smoker presented with chest pain. A computed tomography (CT) scan showed a right lung nodule with rib metastasis (stage IV). His carcinoembryonic antigen (CEA) serum level was 12.5 ng/mL, while his neuron specific enolase (NSE) level was unremarkable. A multiplex analysis by MALDI-TOF with LungCarta Panel (Agena Bioscience, Mountain View, CA, USA) yielded no mutations in EGFR, K-RAS, BRAF and in the other tested genes (AKT1, ALK, BRAF, DDR2, EGFR, EPHA3, EPHA5, ERBB2, FGFR4, JAK2, KRAS, MAP2K1 , MET , NOTCH1 , NRAS, NRF2, NTRK1, NTRK2, NTRK3, PIK3CA, PTCH1, PTEN, PTPN11, PTPRD, STK11, TP53). ALK and ROS-1 rearrangement by immunohistochemistry (IHC) and fluorescence in-situ hybridization (FISH) were negative. The patient received cisplatin/pemetrexed chemotherapy for four cycles and achieved a partial response (PR). Afterward, the patient underwent an atypical lung resection with a concomitant biopsy of the rib lesion. The original histology was confirmed. Because the bone lesion was not radically resected, radiotherapy to the rib (45 Gy) was performed. Radiological follow-up showed no clear signs of disease progression during the subsequent three years. In February 2015, a CT scan showed a significant increase in the lung lesion with concomitant enlargement of mediastinal lymph nodes. While CEA levels ranged from 2.5 to 5.6 ng/mL, a rapid increase of NSE (25.6 μg/L) was observed. Based on this data, the patient was treated with four cycles of carboplatin/etoposide and once again achieved PR (Fig ). The patient is still alive after 44 months of follow-up.\nOUTPUT:"
},
{
"from": "agent",
"value": "Adenocarcinoma, 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: In August 2012, a 64-year-old, male smoker presented with chest pain. A computed tomography (CT) scan showed a right lung nodule with rib metastasis (stage IV). His carcinoembryonic antigen (CEA) serum level was 12.5 ng/mL, while his neuron specific enolase (NSE) level was unremarkable. A multiplex analysis by MALDI-TOF with LungCarta Panel (Agena Bioscience, Mountain View, CA, USA) yielded no mutations in EGFR, K-RAS, BRAF and in the other tested genes (AKT1, ALK, BRAF, DDR2, EGFR, EPHA3, EPHA5, ERBB2, FGFR4, JAK2, KRAS, MAP2K1 , MET , NOTCH1 , NRAS, NRF2, NTRK1, NTRK2, NTRK3, PIK3CA, PTCH1, PTEN, PTPN11, PTPRD, STK11, TP53). ALK and ROS-1 rearrangement by immunohistochemistry (IHC) and fluorescence in-situ hybridization (FISH) were negative. The patient received cisplatin/pemetrexed chemotherapy for four cycles and achieved a partial response (PR). Afterward, the patient underwent an atypical lung resection with a concomitant biopsy of the rib lesion. The original histology was confirmed. Because the bone lesion was not radically resected, radiotherapy to the rib (45 Gy) was performed. Radiological follow-up showed no clear signs of disease progression during the subsequent three years. In February 2015, a CT scan showed a significant increase in the lung lesion with concomitant enlargement of mediastinal lymph nodes. While CEA levels ranged from 2.5 to 5.6 ng/mL, a rapid increase of NSE (25.6 μg/L) was observed. Based on this data, the patient was treated with four cycles of carboplatin/etoposide and once again achieved PR (Fig ). The patient is still alive after 44 months of follow-up.
OUTPUT: |
PMCPatients_common4809 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 10-year-old boy presented with a history of diminution of vision left face turn, nystagmus and photophobia of both eyes for the last 7 years. There were no similar complaints in the family members and no history of any trauma or any systemic disease. He had a visual acuity of 20/100 in right eye (RE) and 20/80 in left eye (LE) (Snellen visual acuity chart) and was not improving with correction. His near vision was N6 in both eyes (Times new roman chart). Cycloplegic refraction showed a refractive error of + 1.0 Dioptre Sphere (DS) −1.5 Dioptre cylinder (DC) at 180° in the RE and + 0.5 DS − 1.0 DC at 160° in the LE.\\nThe child adopted a left face turn for both distance and near. Cover test for distance and near, showing a left hypertropia in the forced primary position. A Prism Bar Cover test showed 20 prism diopters (PD) of left hypertropia for distance and 15 PD of left hypertropia for near. He was orthophoric in the preferred head posture. Elevation was normal in abduction []. Worth Four Dot Test revealed the fusion for near and distance with the preferred head posture. Stereoacuity with Randot showed a stereopsis of 600 s of arc. A horizontal jerk nystagmus with null point in the right gaze was seen. On slit lamp examination, iris hypopigmentation with transillumination defects was seen with normal pupillary reaction. Indirect ophthalmoscopic examination showed an albinotic fundus with foveal hypoplasia [Figures and , and ]. The foveal hypoplasia was confirmed on optical coherence tomography (Cirrus; Carl Zeiss Meditec, Dublin, CA) []. However a 3-lead visual evoked potentials was not performed.\nOUTPUT:"
},
{
"from": "agent",
"value": "Brown's syndrome, Ocular albinism"
}
] | As a physician engaged 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 10-year-old boy presented with a history of diminution of vision left face turn, nystagmus and photophobia of both eyes for the last 7 years. There were no similar complaints in the family members and no history of any trauma or any systemic disease. He had a visual acuity of 20/100 in right eye (RE) and 20/80 in left eye (LE) (Snellen visual acuity chart) and was not improving with correction. His near vision was N6 in both eyes (Times new roman chart). Cycloplegic refraction showed a refractive error of + 1.0 Dioptre Sphere (DS) −1.5 Dioptre cylinder (DC) at 180° in the RE and + 0.5 DS − 1.0 DC at 160° in the LE.\nThe child adopted a left face turn for both distance and near. Cover test for distance and near, showing a left hypertropia in the forced primary position. A Prism Bar Cover test showed 20 prism diopters (PD) of left hypertropia for distance and 15 PD of left hypertropia for near. He was orthophoric in the preferred head posture. Elevation was normal in abduction []. Worth Four Dot Test revealed the fusion for near and distance with the preferred head posture. Stereoacuity with Randot showed a stereopsis of 600 s of arc. A horizontal jerk nystagmus with null point in the right gaze was seen. On slit lamp examination, iris hypopigmentation with transillumination defects was seen with normal pupillary reaction. Indirect ophthalmoscopic examination showed an albinotic fundus with foveal hypoplasia [Figures and , and ]. The foveal hypoplasia was confirmed on optical coherence tomography (Cirrus; Carl Zeiss Meditec, Dublin, CA) []. However a 3-lead visual evoked potentials was not performed.
OUTPUT: |
PMCPatients_common1442 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: After retrobulbar anesthesia, a vision system was used to view the surgical field, and an inferotemporal sclerotomy was created using a 25G+ trocar. The trocar obliquely punctured the bulbar conjunctiva and sclera at an angle of 45° (sclerotomy), approximately 4 mm from the limbus and parallel to it. The trocar was twisted into the eyeball, and its orientation was gradually changed perpendicular to the limbus. After confirming that the cannula was inside the eye, we pulled out the trocar and inserted an infusion cannula into the port. Two more sclerotomies were created in the superotemporal and superonasal quadrants. However, when we pulled out the superonasal trocar, the collar of the cannula fell off and the cannula tube was missing (Fig. a). Therefore, a bulbar conjunctival incision was placed to search for the missing cannula. No cannula was found in the subconjunctival space. We used a scleral depressor to look for the missing cannula tube along the peripheral retina and found the broken cannula tip in the ciliary body corresponding to the superonasal sclerotomy site. We created a new sclerotomy 2 mm above the original incision and 4 mm from the limbus and subsequently performed vitrectomy around the broken cannula to mobilize it for extraction. The new scleral incision was extended to 3 mm parallel to the limbus and allowed entry of a foreign body forceps (Fig. b). The broken tip of the cannula was brought into view by indenting the sclera adjacent to the original sclerotomy. We used the foreign body forceps to clamp and pull the fractured cannula toward the central vitreous body (Fig. c). With the help of the light probe, the longitudinal length of the cannula was aligned with the foreign body forceps and retrieved through the enlarged incision (Fig. d). No leakage occurred from the original sutureless scleral incision. The extended scleral incision was sutured with 7-0 polyglactin 910 suture.\nOUTPUT:"
},
{
"from": "agent",
"value": "Proliferative Diabetic Retinopathy"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: After retrobulbar anesthesia, a vision system was used to view the surgical field, and an inferotemporal sclerotomy was created using a 25G+ trocar. The trocar obliquely punctured the bulbar conjunctiva and sclera at an angle of 45° (sclerotomy), approximately 4 mm from the limbus and parallel to it. The trocar was twisted into the eyeball, and its orientation was gradually changed perpendicular to the limbus. After confirming that the cannula was inside the eye, we pulled out the trocar and inserted an infusion cannula into the port. Two more sclerotomies were created in the superotemporal and superonasal quadrants. However, when we pulled out the superonasal trocar, the collar of the cannula fell off and the cannula tube was missing (Fig. a). Therefore, a bulbar conjunctival incision was placed to search for the missing cannula. No cannula was found in the subconjunctival space. We used a scleral depressor to look for the missing cannula tube along the peripheral retina and found the broken cannula tip in the ciliary body corresponding to the superonasal sclerotomy site. We created a new sclerotomy 2 mm above the original incision and 4 mm from the limbus and subsequently performed vitrectomy around the broken cannula to mobilize it for extraction. The new scleral incision was extended to 3 mm parallel to the limbus and allowed entry of a foreign body forceps (Fig. b). The broken tip of the cannula was brought into view by indenting the sclera adjacent to the original sclerotomy. We used the foreign body forceps to clamp and pull the fractured cannula toward the central vitreous body (Fig. c). With the help of the light probe, the longitudinal length of the cannula was aligned with the foreign body forceps and retrieved through the enlarged incision (Fig. d). No leakage occurred from the original sutureless scleral incision. The extended scleral incision was sutured with 7-0 polyglactin 910 suture.
OUTPUT: |
PMCPatients_common5384 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 67-year-old woman was treated for a pertrochanteric fracture (AO classification 31-A1.2) following a low-energy fall at home with closed reduction and internal fixation with a locked IMN (Bi-Nail, Gruppo Bioimpianti, Peschiera Borromeo, Italy). At three weeks, she was walking with full weight bearing without support, and bony union had occurred by 12 weeks. Eighteen months after surgery, the fracture had clinical and radiographical signs of complete healing. Twenty months after the operation, the patient complained of continuous discomfort over the great trochanter; anteroposterior view documented the apex of the implant protruding proximally and the lag screw that was set in the center of the neck [].\\nDue to this discomfort, the need for IMN removal was felt. The day after the removal of the hardware, the patient complained of a left inguinal pain that increased during weight bearing. No traumatic events occurred postoperatively. Standard X-rays were taken and no fracture signs were present. In view of the minimally displaced impacted fracture and the rapid reduction of the symptoms at rest, conservative management with medication and close X-ray monitoring was conducted. The patient was allowed to walk with bilateral crutches with no weight bearing on the left limb, and was discharged after 10 days. Antiosteoporotic therapy was started with calcium and vitamin D supplementation in addition to antiresorptive drugs. At the radiographic follow-up at 30 days, no displacement was detected and the fracture line was not visible any more. Six months postoperatively, radiographs showed complete healing of the fracture []. At the clinical follow-up at six months, the patient had returned to previous daily activities, and clinical assessment showed a satisfactory range of motion with no pain on walking.\nOUTPUT:"
},
{
"from": "agent",
"value": "Femoral neck fracture"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 67-year-old woman was treated for a pertrochanteric fracture (AO classification 31-A1.2) following a low-energy fall at home with closed reduction and internal fixation with a locked IMN (Bi-Nail, Gruppo Bioimpianti, Peschiera Borromeo, Italy). At three weeks, she was walking with full weight bearing without support, and bony union had occurred by 12 weeks. Eighteen months after surgery, the fracture had clinical and radiographical signs of complete healing. Twenty months after the operation, the patient complained of continuous discomfort over the great trochanter; anteroposterior view documented the apex of the implant protruding proximally and the lag screw that was set in the center of the neck [].\nDue to this discomfort, the need for IMN removal was felt. The day after the removal of the hardware, the patient complained of a left inguinal pain that increased during weight bearing. No traumatic events occurred postoperatively. Standard X-rays were taken and no fracture signs were present. In view of the minimally displaced impacted fracture and the rapid reduction of the symptoms at rest, conservative management with medication and close X-ray monitoring was conducted. The patient was allowed to walk with bilateral crutches with no weight bearing on the left limb, and was discharged after 10 days. Antiosteoporotic therapy was started with calcium and vitamin D supplementation in addition to antiresorptive drugs. At the radiographic follow-up at 30 days, no displacement was detected and the fracture line was not visible any more. Six months postoperatively, radiographs showed complete healing of the fracture []. At the clinical follow-up at six months, the patient had returned to previous daily activities, and clinical assessment showed a satisfactory range of motion with no pain on walking.
OUTPUT: |
PMCPatients_common4715 | [
{
"from": "human",
"value": "As a physician engaged in 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 woman presented to the emergency room with cough, anorexia, and general weakness, symptoms that had been present over a period of 2 months. The only disease found in her medical history was ischemic heart disease, which was diagnosed 4 years previously. Her vital sign and physical examinations were normal, although she presented with low-grade fever and fine inspiratory crackle in the right middle lung fields on auscultation.\\nRoutine laboratory values were within normal limits, although the patient was anemic, with hemoglobin levels of 10.7 g/dL, and presented with hyponatremia (126 mEq/L), hypoalbuminemia (3.0 g/dL), and elevated C-reactive protein levels (12.26 mg/dL). Three acid-fast bacilli tests of sputum were negative. A chest radiograph showed an ill-defined consolidation in the right lower lung fields and fibrotic change in the right upper lung fields (). Computed tomography (CT) scans of the chest showed multiple, ill-defined nodules in the right middle lung and multiple variable-sized mediastinal lymph nodes (). Bacteria, fungal culture, and malignant cells were not observed in washing fluids or biopsy.\nOUTPUT:"
},
{
"from": "agent",
"value": "Fistula Formation between Right Upper Bronchus and Bronchus Intermedius, Endobronchial 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 73-year-old woman presented to the emergency room with cough, anorexia, and general weakness, symptoms that had been present over a period of 2 months. The only disease found in her medical history was ischemic heart disease, which was diagnosed 4 years previously. Her vital sign and physical examinations were normal, although she presented with low-grade fever and fine inspiratory crackle in the right middle lung fields on auscultation.\nRoutine laboratory values were within normal limits, although the patient was anemic, with hemoglobin levels of 10.7 g/dL, and presented with hyponatremia (126 mEq/L), hypoalbuminemia (3.0 g/dL), and elevated C-reactive protein levels (12.26 mg/dL). Three acid-fast bacilli tests of sputum were negative. A chest radiograph showed an ill-defined consolidation in the right lower lung fields and fibrotic change in the right upper lung fields (). Computed tomography (CT) scans of the chest showed multiple, ill-defined nodules in the right middle lung and multiple variable-sized mediastinal lymph nodes (). Bacteria, fungal culture, and malignant cells were not observed in washing fluids or biopsy.
OUTPUT: |
PMCPatients_common4125 | [
{
"from": "human",
"value": "As a physician engaged 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 2010, a 68-year-old man presented with the slowness in his right leg and resting tremor in his left hand. At that time, the early (1.48) and delayed H/M ratios (1.41) on myocardial 123I-MIBG uptake testing was decreased. In 2012, he consulted our hospital, and parkinsonian features such as bradykinesia, left-dominant rigidity and left-hand resting tremor were evident. These features responded to levodopa (300 mg/d) and trihexyphenidyl (2 mg/d). Schellong test did not show a drop in systolic and diastolic blood pressures of >20 and >10 mmHg, respectively, with change in position from sitting to standing. By 2016, the severity of PD had slowly progressed to Hoehn–Yahr stage 4, and trunk flexion was also evident. In early February 2017, bradykinesia developed over the course of 1 week, and the patient required considerable assistance to perform activities of daily living. Finally, he was admitted to our hospital because of impaired consciousness, severe bradykinesia, and coldness of the body. On the day of admission, his consciousness was mildly impaired, the body temperature was 33°C, and rigidity in all four limbs had markedly increased. Motor paresis was absent. Cranial CT was normal. Electrocardiography showed bradycardia without Osborn waves. WBC (2900/μL) and the serum CRP (0.2 mg/dL) were not elevated, and the thyroid function was normal. On Day 2, brain MRI showed an acute cerebral lacunar infarction in the right corona radiate. On Day 5, the patient resumed an alert level of consciousness. One month after admission, the patient had regained his former clinical state.\nOUTPUT:"
},
{
"from": "agent",
"value": "Accidental hypothermia, Parkinson’s disease"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: In 2010, a 68-year-old man presented with the slowness in his right leg and resting tremor in his left hand. At that time, the early (1.48) and delayed H/M ratios (1.41) on myocardial 123I-MIBG uptake testing was decreased. In 2012, he consulted our hospital, and parkinsonian features such as bradykinesia, left-dominant rigidity and left-hand resting tremor were evident. These features responded to levodopa (300 mg/d) and trihexyphenidyl (2 mg/d). Schellong test did not show a drop in systolic and diastolic blood pressures of >20 and >10 mmHg, respectively, with change in position from sitting to standing. By 2016, the severity of PD had slowly progressed to Hoehn–Yahr stage 4, and trunk flexion was also evident. In early February 2017, bradykinesia developed over the course of 1 week, and the patient required considerable assistance to perform activities of daily living. Finally, he was admitted to our hospital because of impaired consciousness, severe bradykinesia, and coldness of the body. On the day of admission, his consciousness was mildly impaired, the body temperature was 33°C, and rigidity in all four limbs had markedly increased. Motor paresis was absent. Cranial CT was normal. Electrocardiography showed bradycardia without Osborn waves. WBC (2900/μL) and the serum CRP (0.2 mg/dL) were not elevated, and the thyroid function was normal. On Day 2, brain MRI showed an acute cerebral lacunar infarction in the right corona radiate. On Day 5, the patient resumed an alert level of consciousness. One month after admission, the patient had regained his former clinical state.
OUTPUT: |
PMCPatients_common3730 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 75-year-old woman with a known intracranial mass referred to our outpatient clinic. The lesion was incidentally discovered after a head computed tomography (CT) scan that she had in the past for the evaluation of a confusion episode secondary to hypoglycemia (diabetes mellitus being the only comorbidity in this patient). Magnetic resonance imaging (MRI) of her brain revealed a cystic sellar mass with mass effect on the right lateral ventricle []. The patient had ophthalmologic and endocrinologic evaluations that demonstrated a left temporal, a right superior temporal visual field deficit, and panhypopituitarism. She was then placed on steroid therapy as well as hormone replacement therapy, and surgical resection was planned. In the interim, she began developing severe lower extremity weakness that delayed surgery. Her Glasgow Coma Scale (GCS) score on initial presentation was 10. Noncontrast head CT imaging demonstrated changes in the density of the cyst and the density of the ventricular cerebrospinal fluid (CSF) []. Subsequent MRI of the brain was strongly suggestive of intraventricular rupture of the cyst []. Intraventricular cyst rupture was confirmed by a lumbar puncture that demonstrated marked pleocytosis with elevated levels of cholesterol and lactate dehydrogenase identified by CSF analysis. Once her clinical condition was medically optimized, the patient was taken to the operating room for endoscopic-assisted intracystic placement of an Ommaya reservoir []. Cytopathologic analysis of the aspirate revealed proteinaceous material, blood, and histiocytes, some with hemosiderin. She underwent shunt placement for continued ventriculomegaly 5 days after Ommaya reservoir placement. Her condition improved, and she was discharged from the Intensive Care Unit within 2 weeks from her admission.\nOUTPUT:"
},
{
"from": "agent",
"value": "Craniopharyngioma, Steroid-induced myopathy, Chemical ventriculitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 75-year-old woman with a known intracranial mass referred to our outpatient clinic. The lesion was incidentally discovered after a head computed tomography (CT) scan that she had in the past for the evaluation of a confusion episode secondary to hypoglycemia (diabetes mellitus being the only comorbidity in this patient). Magnetic resonance imaging (MRI) of her brain revealed a cystic sellar mass with mass effect on the right lateral ventricle []. The patient had ophthalmologic and endocrinologic evaluations that demonstrated a left temporal, a right superior temporal visual field deficit, and panhypopituitarism. She was then placed on steroid therapy as well as hormone replacement therapy, and surgical resection was planned. In the interim, she began developing severe lower extremity weakness that delayed surgery. Her Glasgow Coma Scale (GCS) score on initial presentation was 10. Noncontrast head CT imaging demonstrated changes in the density of the cyst and the density of the ventricular cerebrospinal fluid (CSF) []. Subsequent MRI of the brain was strongly suggestive of intraventricular rupture of the cyst []. Intraventricular cyst rupture was confirmed by a lumbar puncture that demonstrated marked pleocytosis with elevated levels of cholesterol and lactate dehydrogenase identified by CSF analysis. Once her clinical condition was medically optimized, the patient was taken to the operating room for endoscopic-assisted intracystic placement of an Ommaya reservoir []. Cytopathologic analysis of the aspirate revealed proteinaceous material, blood, and histiocytes, some with hemosiderin. She underwent shunt placement for continued ventriculomegaly 5 days after Ommaya reservoir placement. Her condition improved, and she was discharged from the Intensive Care Unit within 2 weeks from her admission.
OUTPUT: |
PMCPatients_common2250 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Initial workup revealed anemia (hemoglobin level, 9.9 g/dL [normal: 13 to 17 g/dL]) with low normal reticulocyte (0.6%, [normal: 0.5 to 2%]), thrombocytopenia (platelet level 101 × 103/microL [normal: 140-400 × 103/microL]), hypertriglyceridemia (triglycerides level, 309 mg/dL [normal: 0–149 mg/dL]), and marked elevation in ferritin (> 40,000.00 ng/mL [normal: 30–400 ng/mL]) and lactate dehydrogenase (2762 U/L [normal: 140–480 U/L]). Computed tomography depicted the size of spleen in upper normal (13 cm). Extensive lab and radiologic work up to identify any infectious agents was unremarkable. Study of natural killer (NK) cells showed decreased NK cell function. Soluble CD163 (sCD163) level was 6384 ng/mL (Reference range: 387–1785 ng/mL) (Table ).\\nPatient was treated with high-dose glucocorticoids (oral prednisone administered at 1 mg per kilogram per day) within 24 h after admission. Rapid resolution of fever, nausea and gradual improvement in his arthralgia were noted. Patient’s anemia and thrombocytopenia improved after administration of glucocorticoids, therefore, we did not perform bone marrow biopsy. After 5 weeks of high-dose glucocorticoids, steroid dose was tapered over 7 weeks without recurring symptoms. Pembrolizumab was permanently discontinued.\nOUTPUT:"
},
{
"from": "agent",
"value": "Hemophagocytic lymphohistiocytosis, Metastatic melanoma"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Initial workup revealed anemia (hemoglobin level, 9.9 g/dL [normal: 13 to 17 g/dL]) with low normal reticulocyte (0.6%, [normal: 0.5 to 2%]), thrombocytopenia (platelet level 101 × 103/microL [normal: 140-400 × 103/microL]), hypertriglyceridemia (triglycerides level, 309 mg/dL [normal: 0–149 mg/dL]), and marked elevation in ferritin (> 40,000.00 ng/mL [normal: 30–400 ng/mL]) and lactate dehydrogenase (2762 U/L [normal: 140–480 U/L]). Computed tomography depicted the size of spleen in upper normal (13 cm). Extensive lab and radiologic work up to identify any infectious agents was unremarkable. Study of natural killer (NK) cells showed decreased NK cell function. Soluble CD163 (sCD163) level was 6384 ng/mL (Reference range: 387–1785 ng/mL) (Table ).\nPatient was treated with high-dose glucocorticoids (oral prednisone administered at 1 mg per kilogram per day) within 24 h after admission. Rapid resolution of fever, nausea and gradual improvement in his arthralgia were noted. Patient’s anemia and thrombocytopenia improved after administration of glucocorticoids, therefore, we did not perform bone marrow biopsy. After 5 weeks of high-dose glucocorticoids, steroid dose was tapered over 7 weeks without recurring symptoms. Pembrolizumab was permanently discontinued.
OUTPUT: |
PMCPatients_common2540 | [
{
"from": "human",
"value": "As a physician engaged 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 girl accompanied by her mother was reported to the Department of Pediatric and Preventive Dentistry, Navodaya Dental College and Hospital. An appropriate habit history and clinical evaluation was done along with the patient pretreatment record including radiographs, study models, and photographs.\\nIt revealed that she was the 3rd child to her parents who belongs to a middle class family. The other two elder siblings also had the habit. Her relationship with her peers was good but she was subjected to being cursed upon practicing the habit. Psychological evaluation revealed positive attitude towards discontinuing the habit practice.\\nExtraorally, it revealed depression just above the corner of the mouth, and the lips were slightly inwards at the corner of the mouth. Patient responded positively and was motivated to stop practicing the habit. Parents were also counseled to motivate and support her in discontinuing the habit.\\nShe was started on the modified quadhelix appliance with a roller (). During this she showed positive attitude and was willing to try the appliance as an aid to stop the habit. She was on a passive appliance initially followed by activation of the appliance to correct the deformities for a total period of 9 months. At the end of the treatment, she intercepted the habit practice and the deformities were refrained and transformed to a proper relationship (Figures , , and ).\nOUTPUT:"
},
{
"from": "agent",
"value": "Thumb sucking habit, Anterior open bite, Proclined upper/lower incisors, Unilateral posterior crossbite, Compensatory tongue thrust, Mild lisping in speech"
}
] | As a physician engaged 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 girl accompanied by her mother was reported to the Department of Pediatric and Preventive Dentistry, Navodaya Dental College and Hospital. An appropriate habit history and clinical evaluation was done along with the patient pretreatment record including radiographs, study models, and photographs.\nIt revealed that she was the 3rd child to her parents who belongs to a middle class family. The other two elder siblings also had the habit. Her relationship with her peers was good but she was subjected to being cursed upon practicing the habit. Psychological evaluation revealed positive attitude towards discontinuing the habit practice.\nExtraorally, it revealed depression just above the corner of the mouth, and the lips were slightly inwards at the corner of the mouth. Patient responded positively and was motivated to stop practicing the habit. Parents were also counseled to motivate and support her in discontinuing the habit.\nShe was started on the modified quadhelix appliance with a roller (). During this she showed positive attitude and was willing to try the appliance as an aid to stop the habit. She was on a passive appliance initially followed by activation of the appliance to correct the deformities for a total period of 9 months. At the end of the treatment, she intercepted the habit practice and the deformities were refrained and transformed to a proper relationship (Figures , , and ).
OUTPUT: |
PMCPatients_common2052 | [
{
"from": "human",
"value": "As a physician engaged 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 clinical case of a 48-year-old female runner with complaints of mechanical pain in the right calcaneal and pre-tibial regions, lasting for about 7 weeks and without any traumatic episode. The patient was trying to manage the pain with self-medicated analgesics and non-medical prescribed physiotherapy. Clinical examination revealed slight lateral-side edema, without any other signs of inflammation. There was pain at the distal peroneus and extensor retinaculum, upon palpation. ). Ultrasonography confirmed the existence of a fibular fracture and excluded lesions in the adjacent soft tissues (Fig. ). Upon exploring the previous medical history, the patient reported irregularities in her menstrual cycle in relation to a hormonal imbalance, which was already being addressed by a rheumatology assistant. The patient was discharged home and maintained a non-weight bearing regimen for the right limb for 2 weeks. Hormonal tests revealed the following: TSH 0.473 mUI/L (0.550–4.780 mUI/L), T3 0.87 ng/mL (0.60–1.81 ng/mL), free T3 2.79 pg/mL (2.3–4.2 pg/mL), T4 9.2 μg/dL (4.5–10.9 μg/dL), free T4 1.15 ng/dL (0.89–1.76 ng/dL), FSH 6.9 UI/L, progesterone 0.71 ng/mL, ACTH 14.6 pg/mL (<46.0 pg/mL); bone densitometry (Fig. ): L2L4 T-score −1.4 (osteopenic), femoral neck T-score -0.8 (normal). At twelve weeks post-injury, the patient was, against medical opinion, running 7 km a day and reporting only light pain. Radiographic evaluation showed a hypertrophic callus, with no misalignment.\\nFollow-up at 6 months indicated a pain free athlete, capable of performing base training without symptoms. Radiography documented callus reabsorption and bone remodeling, with fracture consolidation (Fig. ).\nOUTPUT:"
},
{
"from": "agent",
"value": "Stress fractures"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: We report a clinical case of a 48-year-old female runner with complaints of mechanical pain in the right calcaneal and pre-tibial regions, lasting for about 7 weeks and without any traumatic episode. The patient was trying to manage the pain with self-medicated analgesics and non-medical prescribed physiotherapy. Clinical examination revealed slight lateral-side edema, without any other signs of inflammation. There was pain at the distal peroneus and extensor retinaculum, upon palpation. ). Ultrasonography confirmed the existence of a fibular fracture and excluded lesions in the adjacent soft tissues (Fig. ). Upon exploring the previous medical history, the patient reported irregularities in her menstrual cycle in relation to a hormonal imbalance, which was already being addressed by a rheumatology assistant. The patient was discharged home and maintained a non-weight bearing regimen for the right limb for 2 weeks. Hormonal tests revealed the following: TSH 0.473 mUI/L (0.550–4.780 mUI/L), T3 0.87 ng/mL (0.60–1.81 ng/mL), free T3 2.79 pg/mL (2.3–4.2 pg/mL), T4 9.2 μg/dL (4.5–10.9 μg/dL), free T4 1.15 ng/dL (0.89–1.76 ng/dL), FSH 6.9 UI/L, progesterone 0.71 ng/mL, ACTH 14.6 pg/mL (<46.0 pg/mL); bone densitometry (Fig. ): L2L4 T-score −1.4 (osteopenic), femoral neck T-score -0.8 (normal). At twelve weeks post-injury, the patient was, against medical opinion, running 7 km a day and reporting only light pain. Radiographic evaluation showed a hypertrophic callus, with no misalignment.\nFollow-up at 6 months indicated a pain free athlete, capable of performing base training without symptoms. Radiography documented callus reabsorption and bone remodeling, with fracture consolidation (Fig. ).
OUTPUT: |
PMCPatients_common1249 | [
{
"from": "human",
"value": "As a physician engaged 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 brought in by an ambulance with complaints of acute left flank pain with radiation to the scrotum, nausea, and macroscopic hematuria. Slight rebound tenderness to the left lower quadrant suspicious for peritoneal irritation was disclosed on examination; body temperature was 38°C.\\nLaboratory investigation showed leukocytosis and pyuria. Computed tomography (CT) with contrast enhancement was performed 2 hours later and showed distribution of the contrast around the left kidney ().\\nAlso lower third ureter scanning was performed showing a 4-millimeter obstructive stone at the left ureterovesical junction ().\\nA double-J ureteric stent was placed immediately after tomography without technical problems. On the next day, the patient did not have any discomfort and was discharged from the hospital with the prescriptions for peroral tamsulosin and diclofenac.\\nThree weeks later, he had no complaints as well. Discharge of stone has not been observed during this period. The red blood cell count, serum creatinine, and urea were normal, and ultrasound of the upper urinary tract was unremarkable.\\nControl CT showed a partial distal migration of the ureteric stent (), which was removed with following CT urography showing no extravasation of the contrast out of the upper urinary tract (). On the CT images, there was no evidence of the stone in the urinary tract ().\\nThe patient was discharged from the hospital with recommendations (high fluid intake, reduced physical activity, and follow-up examination 3–6 months later).\nOUTPUT:"
},
{
"from": "agent",
"value": "Spontaneous Pelvic Rupture, Renal Colic, Klinefelter Syndrome, Nephrolithiasis"
}
] | As a physician engaged 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 brought in by an ambulance with complaints of acute left flank pain with radiation to the scrotum, nausea, and macroscopic hematuria. Slight rebound tenderness to the left lower quadrant suspicious for peritoneal irritation was disclosed on examination; body temperature was 38°C.\nLaboratory investigation showed leukocytosis and pyuria. Computed tomography (CT) with contrast enhancement was performed 2 hours later and showed distribution of the contrast around the left kidney ().\nAlso lower third ureter scanning was performed showing a 4-millimeter obstructive stone at the left ureterovesical junction ().\nA double-J ureteric stent was placed immediately after tomography without technical problems. On the next day, the patient did not have any discomfort and was discharged from the hospital with the prescriptions for peroral tamsulosin and diclofenac.\nThree weeks later, he had no complaints as well. Discharge of stone has not been observed during this period. The red blood cell count, serum creatinine, and urea were normal, and ultrasound of the upper urinary tract was unremarkable.\nControl CT showed a partial distal migration of the ureteric stent (), which was removed with following CT urography showing no extravasation of the contrast out of the upper urinary tract (). On the CT images, there was no evidence of the stone in the urinary tract ().\nThe patient was discharged from the hospital with recommendations (high fluid intake, reduced physical activity, and follow-up examination 3–6 months later).
OUTPUT: |
PMCPatients_common4895 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 31-year-old female (gravida 2 para 1) at 18 weeks gestation presented to the Emergency Department with sudden onset right iliac fossa pain of <12 hours duration. She had associated nausea but no vomiting, fevers, urinary symptoms or per vaginal discharge. The patient had no history of dysmenorrhoea, dyspareunia, subfertility or other gynaecological concerns.\\nOn examination, the patient was afebrile and haemodynamically stable. Abdominal palpation revealed tenderness in the right iliac fossa with voluntary guarding, percussion and rebound tenderness. Neither bimanual nor speculum examination was performed. Blood tests demonstrated leukocytosis (11.6 × 109/L), neutrophilia (8.63 × 109/L; 75%) and mildly elevated C-reactive protein (9.6 mg/L). Beta-human chorionic gonadotropin was appropriate for gestational age (23 000 IU/L). Urine analysis was unremarkable. Ultrasound confirmed a viable intrauterine pregnancy, an inflamed appendix and surrounding free fluid. ).\\nDuring laparoscopic appendectomy, an enlarged appendiceal tip with fibrinous adhesions and haemoserous pericaecal free fluid was seen (Fig. ). The gross appearance of the appendix was suspicious for appendiceal malignancy (Fig. ). The appendix was mobilized and transected using endoloops. No other peritoneal or pelvic pathology was identified intraoperatively.\\nSurprisingly, histopathological examination demonstrated a constricted appendiceal lumen engulfed by decidualized endometriosis (Fig. ). She went on to deliver a live infant via elective repeat lower section caesarean section at 39 weeks gestation.\nOUTPUT:"
},
{
"from": "agent",
"value": "Endometrial decidualization, Acute appendicitis"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 31-year-old female (gravida 2 para 1) at 18 weeks gestation presented to the Emergency Department with sudden onset right iliac fossa pain of <12 hours duration. She had associated nausea but no vomiting, fevers, urinary symptoms or per vaginal discharge. The patient had no history of dysmenorrhoea, dyspareunia, subfertility or other gynaecological concerns.\nOn examination, the patient was afebrile and haemodynamically stable. Abdominal palpation revealed tenderness in the right iliac fossa with voluntary guarding, percussion and rebound tenderness. Neither bimanual nor speculum examination was performed. Blood tests demonstrated leukocytosis (11.6 × 109/L), neutrophilia (8.63 × 109/L; 75%) and mildly elevated C-reactive protein (9.6 mg/L). Beta-human chorionic gonadotropin was appropriate for gestational age (23 000 IU/L). Urine analysis was unremarkable. Ultrasound confirmed a viable intrauterine pregnancy, an inflamed appendix and surrounding free fluid. ).\nDuring laparoscopic appendectomy, an enlarged appendiceal tip with fibrinous adhesions and haemoserous pericaecal free fluid was seen (Fig. ). The gross appearance of the appendix was suspicious for appendiceal malignancy (Fig. ). The appendix was mobilized and transected using endoloops. No other peritoneal or pelvic pathology was identified intraoperatively.\nSurprisingly, histopathological examination demonstrated a constricted appendiceal lumen engulfed by decidualized endometriosis (Fig. ). She went on to deliver a live infant via elective repeat lower section caesarean section at 39 weeks gestation.
OUTPUT: |
PMCPatients_common1874 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 35-year-old patient at Gravida 2, Para 1 was admitted to our Department at 21 wks because of an ache in the lower abdomen for 2 days. The previous CS was performed at a different hospital and we had no information about the used operation technique at 40 wks, as a consequence of the threatened asphyxia of the fetus, in 2010.\\nThe first scan she had after the CS was when she missed menstruation. No “niche” was mentioned. The patient had a First Trimester Screening Program for chromosomal abnormalities at 12 wks, performed by a Fetal Medicine Foundation licensed obstetrician. No abnormalities were found. When she came for the second scan in this Program, she complained about cramps. In the scan, the LUS had thinned to 3.4 mm with dehiscence of the myometrium ().\\nThe patient was admitted to our Department for observation and spent 5 weeks there (from 21 wks to 25 wks). After prophylactic steroid treatment for lung maturation, the patient departed the hospital on her own request. The area of the scar (2.6 mm) was only covered by a thin layer of peritonea with a total dehiscence of the myometrium. The placenta was on the posterior wall of the corpus of the uterus. The uterus was sutured typically (double-layer continuous), and the patient came through the postoperative period well.\nOUTPUT:"
},
{
"from": "agent",
"value": "Scar Tissue after a Cesarean Section"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 35-year-old patient at Gravida 2, Para 1 was admitted to our Department at 21 wks because of an ache in the lower abdomen for 2 days. The previous CS was performed at a different hospital and we had no information about the used operation technique at 40 wks, as a consequence of the threatened asphyxia of the fetus, in 2010.\nThe first scan she had after the CS was when she missed menstruation. No “niche” was mentioned. The patient had a First Trimester Screening Program for chromosomal abnormalities at 12 wks, performed by a Fetal Medicine Foundation licensed obstetrician. No abnormalities were found. When she came for the second scan in this Program, she complained about cramps. In the scan, the LUS had thinned to 3.4 mm with dehiscence of the myometrium ().\nThe patient was admitted to our Department for observation and spent 5 weeks there (from 21 wks to 25 wks). After prophylactic steroid treatment for lung maturation, the patient departed the hospital on her own request. The area of the scar (2.6 mm) was only covered by a thin layer of peritonea with a total dehiscence of the myometrium. The placenta was on the posterior wall of the corpus of the uterus. The uterus was sutured typically (double-layer continuous), and the patient came through the postoperative period well.
OUTPUT: |
PMCPatients_common294 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A forty-seven-year-old man was diagnosed with a preoperatively ruptured large right-sided temporal AVM (diameter 80 mm, SMG 5). The AVM was first diagnosed and embolized after bleeding at the age of 20. Further treatment included embolization and proton therapy. After the patient started to suffer from severe headache, hallucinations and vertigo, CT-scan was performed showing a small intraventricular hemorrhage.\\nThe surgery was done via right-sided temporal craniotomy. The AVM was attached to the dura at multiple sites. Multiple temporary clips were placed on the feeding arteries during the operation. Intraoperative angiography showed filling also from the posterior circulation. The AVM started filling quickly from deep basal arteries after it was thought to be dissected successfully. These were coagulated and the nidus removed. Some occipital residual AVM was visualized and removed. There was some hemorrhage during clip removal which was coagulated. Blood loss during surgery was 300 ml.\\nThe postoperative SBP target was 100–130 mmHg. CT-scan and DSA showed no complications at 1st POD. On the 3rd POD, CT-scan showed blood in subdural space, resection cavity and subcutaneously. Cerebrospinal fluid (CSF) analysis on the 3rd POD showed potential infection and vancomycin and ceftazidime were started. The patient was extubated on the 4th POD, but reintubated due to worsening general status on the 5th POD. The SBP target was set to normotension on the 5th POD. The patient was extubated on the 7th POD. The patient was transferred to city hospital on the 29th POD. GOS at the first follow-up was 3. The patient initially developed right-sided ptosis which resolved by itself but was blind in his right eye at first follow-up visit due to uncertain etiology. The patient was deemed receptive for occupational and physiotherapy.\nOUTPUT:"
},
{
"from": "agent",
"value": "Brain Arteriovenous Malformations"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A forty-seven-year-old man was diagnosed with a preoperatively ruptured large right-sided temporal AVM (diameter 80 mm, SMG 5). The AVM was first diagnosed and embolized after bleeding at the age of 20. Further treatment included embolization and proton therapy. After the patient started to suffer from severe headache, hallucinations and vertigo, CT-scan was performed showing a small intraventricular hemorrhage.\nThe surgery was done via right-sided temporal craniotomy. The AVM was attached to the dura at multiple sites. Multiple temporary clips were placed on the feeding arteries during the operation. Intraoperative angiography showed filling also from the posterior circulation. The AVM started filling quickly from deep basal arteries after it was thought to be dissected successfully. These were coagulated and the nidus removed. Some occipital residual AVM was visualized and removed. There was some hemorrhage during clip removal which was coagulated. Blood loss during surgery was 300 ml.\nThe postoperative SBP target was 100–130 mmHg. CT-scan and DSA showed no complications at 1st POD. On the 3rd POD, CT-scan showed blood in subdural space, resection cavity and subcutaneously. Cerebrospinal fluid (CSF) analysis on the 3rd POD showed potential infection and vancomycin and ceftazidime were started. The patient was extubated on the 4th POD, but reintubated due to worsening general status on the 5th POD. The SBP target was set to normotension on the 5th POD. The patient was extubated on the 7th POD. The patient was transferred to city hospital on the 29th POD. GOS at the first follow-up was 3. The patient initially developed right-sided ptosis which resolved by itself but was blind in his right eye at first follow-up visit due to uncertain etiology. The patient was deemed receptive for occupational and physiotherapy.
OUTPUT: |
PMCPatients_common1290 | [
{
"from": "human",
"value": "As a physician engaged 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 subsequently received six cycles of neoadjuvant chemotherapy. A follow-up mammectomy was performed in November 2009. In June 2012, the patient presented with palpable masses on the right thyroid, isthmus and lateral neck. Subsequently, the patient underwent a bilateral subtotal thyroidectomy and lymphadenectomy. Histological assessment of the surgical thyroid specimens and the neck lymph nodes revealed multiple carcinoma foci. The metastases excised from the right and left thyroid three years later were 30×20×15 and 20×15×12 mm in size, respectively, and the lymph nodes contained sheets of metastatic carcinoma (4/9). The diagnosis of metastatic carcinoma was made based on immunostaining data for the estrogen receptor (ER), progesterone receptor (PR) and CerbB-2 in neoplastic cells. Tumor cells in metastatic foci exhibited negative staining for the ER and PR and strong positive staining for CerbB-2, similar to the staining pattern of the primary breast lesion. The adjacent normal thyroid tissue was positive for TTF-1 (, lower panel, region IV) and TG (, lower panel, region II); however, the metastatic tumor cells were negative for both markers (, lower panel, regions III and I). These two markers indicate that the cancer lesions did not originate from the thyroid component.\nOUTPUT:"
},
{
"from": "agent",
"value": "Thyroid gland metastasis arising from breast cancer, Infiltrating ductal carcinoma in the right breast"
}
] | As a physician engaged 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 subsequently received six cycles of neoadjuvant chemotherapy. A follow-up mammectomy was performed in November 2009. In June 2012, the patient presented with palpable masses on the right thyroid, isthmus and lateral neck. Subsequently, the patient underwent a bilateral subtotal thyroidectomy and lymphadenectomy. Histological assessment of the surgical thyroid specimens and the neck lymph nodes revealed multiple carcinoma foci. The metastases excised from the right and left thyroid three years later were 30×20×15 and 20×15×12 mm in size, respectively, and the lymph nodes contained sheets of metastatic carcinoma (4/9). The diagnosis of metastatic carcinoma was made based on immunostaining data for the estrogen receptor (ER), progesterone receptor (PR) and CerbB-2 in neoplastic cells. Tumor cells in metastatic foci exhibited negative staining for the ER and PR and strong positive staining for CerbB-2, similar to the staining pattern of the primary breast lesion. The adjacent normal thyroid tissue was positive for TTF-1 (, lower panel, region IV) and TG (, lower panel, region II); however, the metastatic tumor cells were negative for both markers (, lower panel, regions III and I). These two markers indicate that the cancer lesions did not originate from the thyroid component.
OUTPUT: |
PMCPatients_common3151 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 14-month-old girl, who had neuroblastoma with bone metastasis, had been treated with neoadjuvant chemotherapy with the Vincristine, Prednisolone, Etoposide and Chlorambucil (OPEC) protocol for two courses. She then underwent complete excision of an abdominal mass and left kidney surgery. Then chemotherapy followed (Topotecan/Endoxan) for 5 cycles. Because iodine-131-meta-iodobenzylguanidine (MIBG) was normal, she was candidate for haematopoietic stem cell transplantation (HSCT) at the age of 24 months. In 2017, she underwent autologous stem cell transplantation. Having good conditions, she was discharged on day 13. On day 28, the patient returned to hospital with symptoms of abdominal distention () and pain, malaise, fever, weight gain, vomiting and low urine output. During the examination, she had abdominal ascites and tender hepatomegaly. She was admitted to the hospital with a possible diagnosis of VOD. Laboratory studies indicated that she had high serum aminotransferases, bilirubin and thrombocytopenia (). Abdominal sonography showed marked hepatomegaly and mild to moderate ascites. Serologic analyses for hepatitis and cytomegalovirus (CMV) yielded negative results. During hospitalization on day 29, the patient developed respiratory distress, low oxygen saturation, tachypnea, and tachycardia. She was transferred to the intensive care unit. She was treated with antibiotics, heparin, Nacetylcysteine, low dose dopamine, albumin and a diuretic. According to serial laboratory tests, the patient's bilirubin was rising. On day 31, because of the severe VOD, treatment with Defibrotide (25mg/kg/day) was commenced. Defibrotide treatment for 21 days was administered. She responded well to treatment and was discharged in a good general condition.\nOUTPUT:"
},
{
"from": "agent",
"value": "Severe veno-occlusive 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 14-month-old girl, who had neuroblastoma with bone metastasis, had been treated with neoadjuvant chemotherapy with the Vincristine, Prednisolone, Etoposide and Chlorambucil (OPEC) protocol for two courses. She then underwent complete excision of an abdominal mass and left kidney surgery. Then chemotherapy followed (Topotecan/Endoxan) for 5 cycles. Because iodine-131-meta-iodobenzylguanidine (MIBG) was normal, she was candidate for haematopoietic stem cell transplantation (HSCT) at the age of 24 months. In 2017, she underwent autologous stem cell transplantation. Having good conditions, she was discharged on day 13. On day 28, the patient returned to hospital with symptoms of abdominal distention () and pain, malaise, fever, weight gain, vomiting and low urine output. During the examination, she had abdominal ascites and tender hepatomegaly. She was admitted to the hospital with a possible diagnosis of VOD. Laboratory studies indicated that she had high serum aminotransferases, bilirubin and thrombocytopenia (). Abdominal sonography showed marked hepatomegaly and mild to moderate ascites. Serologic analyses for hepatitis and cytomegalovirus (CMV) yielded negative results. During hospitalization on day 29, the patient developed respiratory distress, low oxygen saturation, tachypnea, and tachycardia. She was transferred to the intensive care unit. She was treated with antibiotics, heparin, Nacetylcysteine, low dose dopamine, albumin and a diuretic. According to serial laboratory tests, the patient's bilirubin was rising. On day 31, because of the severe VOD, treatment with Defibrotide (25mg/kg/day) was commenced. Defibrotide treatment for 21 days was administered. She responded well to treatment and was discharged in a good general condition.
OUTPUT: |
PMCPatients_common2562 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 35-year-old female was transferred to the emergency department (ED) of our hospital from a drug rehabilitation center for necrotic skin lesions. Two days before this presentation, the patient had noticed an itching sensation in her left ear. Later a reddish black rash appeared on the left ear. The rash was painful and progressively got worse, involving the right ear, hands, and lower back.\\nShe denied fever, arthralgia, insect bite, or recent travel. Her medical history was significant for seizure disorder, asthma, bipolar disorder, and polysubstance abuse. She denied any recent use of recreational drugs and attested that she last used cocaine 8 months prior to being incarcerated.\\nOn examination patient was afebrile. Vital signs were noted as blood pressure 135/73 mm of hg, pulse rate of 95/min, and respiratory rate of 17/min, saturating 98% on room air. She was alert and oriented to time, place, and self. Precordial examination revealed normal heart sounds without any murmur or gallops. Auscultation of lungs revealed bilateral air entry without any adventitious sounds. There were multiple necrotic purple lesions on arms () bilateral pinnae, buttocks, and finger. All lesions had erythematous base, clear margins, no pus, or discharge.\\nThe patient had a similar rash two years before this presentation and was diagnosed with levamisole-induced purpura as the workup to elucidate other etiologies that could have explained that the rash was unremarkable ().\nOUTPUT:"
},
{
"from": "agent",
"value": "Recurrent Thrombotic Vasculopathy"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 35-year-old female was transferred to the emergency department (ED) of our hospital from a drug rehabilitation center for necrotic skin lesions. Two days before this presentation, the patient had noticed an itching sensation in her left ear. Later a reddish black rash appeared on the left ear. The rash was painful and progressively got worse, involving the right ear, hands, and lower back.\nShe denied fever, arthralgia, insect bite, or recent travel. Her medical history was significant for seizure disorder, asthma, bipolar disorder, and polysubstance abuse. She denied any recent use of recreational drugs and attested that she last used cocaine 8 months prior to being incarcerated.\nOn examination patient was afebrile. Vital signs were noted as blood pressure 135/73 mm of hg, pulse rate of 95/min, and respiratory rate of 17/min, saturating 98% on room air. She was alert and oriented to time, place, and self. Precordial examination revealed normal heart sounds without any murmur or gallops. Auscultation of lungs revealed bilateral air entry without any adventitious sounds. There were multiple necrotic purple lesions on arms () bilateral pinnae, buttocks, and finger. All lesions had erythematous base, clear margins, no pus, or discharge.\nThe patient had a similar rash two years before this presentation and was diagnosed with levamisole-induced purpura as the workup to elucidate other etiologies that could have explained that the rash was unremarkable ().
OUTPUT: |
PMCPatients_common786 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: She denied any personal or family history of previous skin cancers or other malignancies. An increased egress of fluid or increased bleeding was not noted during the operation. Representative histological slides can be seen in . The tumor showed absence of staining for MSH-2 and MSH-6 with preserved staining for MLH-1 and PMS-2. The adipocytes also appeared to encroach into the dermis, but were of normal size. There was an impression of mucin deposition between adipocytes; no significant inflammation was noted.\\nBecause of the immunohistochemical loss of mismatch repair proteins, the patient was referred for genetic testing. She subsequently underwent a colonoscopy that was found to be normal. Her post-operative course was uneventful and she did not have any issues post-operatively with wound healing and did not have any issues with local alopecia.\nOUTPUT:"
},
{
"from": "agent",
"value": "Muir-Torre Syndrome, Sebaceous Carcinoma, Lipedematous Scalp"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: She denied any personal or family history of previous skin cancers or other malignancies. An increased egress of fluid or increased bleeding was not noted during the operation. Representative histological slides can be seen in . The tumor showed absence of staining for MSH-2 and MSH-6 with preserved staining for MLH-1 and PMS-2. The adipocytes also appeared to encroach into the dermis, but were of normal size. There was an impression of mucin deposition between adipocytes; no significant inflammation was noted.\nBecause of the immunohistochemical loss of mismatch repair proteins, the patient was referred for genetic testing. She subsequently underwent a colonoscopy that was found to be normal. Her post-operative course was uneventful and she did not have any issues post-operatively with wound healing and did not have any issues with local alopecia.
OUTPUT: |
PMCPatients_common4277 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: A 57-year-old man with stage IVA2 SS presented with erythroderma in 2010, with onset over the past 6 months. A skin biopsy showed MF. CD4:CD8 ratio was 20:1, and a TCR clone was identified. The patient complained of severe itch at various visits (VAS, 5–10) and had prior treatment with topical steroids, gabapentin, doxepin, mirtazapine, extracorporeal photopheresis, interferon-alpha, and bexarotene. Treatment with vorinostat resulted in significant improvement in itch (VAS decreased from 9 to 5), but was discontinued due to significant diarrhea. One month after discontinuation off all therapy, he had worsening itch (VAS, 7) and a high CD4:CD8 ratio of >10:1 by flow cytometry.\\nTwo years after his initial diagnosis, the patient was started on romidepsin 14 mg/m2 qw 3/4 for worsening of disease and pruritus. He had dramatic reduction of CD4:CD8 to 2:1 at 6 months, improvement in itch (VAS, 3), and resolution of erythroderma (Figure ). Because of significant nausea, vomiting, and severe dysgeusia often lasting 3 or 4 days after infusion, romidepsin was reduced to 10 mg/m2. At 12 months, the CD4:CD8 ratio was 2:1, no TCR clone was observed in the blood, and VAS was 1. Romidepsin was changed to 10 mg/m2 every other week and occasionally once monthly. Blood was TCR negative at 18 months, and itch was reported to have been gone “for the past year.” Romidepsin was discontinued at month 19 due to ongoing nausea and dysgeusia. He remained disease free for 12 months afterward. At month 14, a skin biopsy showed MF. Romidepsin was restarted at 14 mg/m2 qw 3/4. Over 2 months, there was a partial response in the blood and itch did not recur. The patient underwent a bone marrow transplant and romidepsin was discontinued.\nOUTPUT:"
},
{
"from": "agent",
"value": "Cutaneous T-cell lymphoma"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 57-year-old man with stage IVA2 SS presented with erythroderma in 2010, with onset over the past 6 months. A skin biopsy showed MF. CD4:CD8 ratio was 20:1, and a TCR clone was identified. The patient complained of severe itch at various visits (VAS, 5–10) and had prior treatment with topical steroids, gabapentin, doxepin, mirtazapine, extracorporeal photopheresis, interferon-alpha, and bexarotene. Treatment with vorinostat resulted in significant improvement in itch (VAS decreased from 9 to 5), but was discontinued due to significant diarrhea. One month after discontinuation off all therapy, he had worsening itch (VAS, 7) and a high CD4:CD8 ratio of >10:1 by flow cytometry.\nTwo years after his initial diagnosis, the patient was started on romidepsin 14 mg/m2 qw 3/4 for worsening of disease and pruritus. He had dramatic reduction of CD4:CD8 to 2:1 at 6 months, improvement in itch (VAS, 3), and resolution of erythroderma (Figure ). Because of significant nausea, vomiting, and severe dysgeusia often lasting 3 or 4 days after infusion, romidepsin was reduced to 10 mg/m2. At 12 months, the CD4:CD8 ratio was 2:1, no TCR clone was observed in the blood, and VAS was 1. Romidepsin was changed to 10 mg/m2 every other week and occasionally once monthly. Blood was TCR negative at 18 months, and itch was reported to have been gone “for the past year.” Romidepsin was discontinued at month 19 due to ongoing nausea and dysgeusia. He remained disease free for 12 months afterward. At month 14, a skin biopsy showed MF. Romidepsin was restarted at 14 mg/m2 qw 3/4. Over 2 months, there was a partial response in the blood and itch did not recur. The patient underwent a bone marrow transplant and romidepsin was discontinued.
OUTPUT: |
PMCPatients_common535 | [
{
"from": "human",
"value": "As a physician engaged 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 83-year-old woman presented with dyspnoea. Her chest X-ray showed a right-sided pleural effusion (Fig. ). A thoracic drain was inserted, and the pleural effusion was drained because she had a peripheral capillary oxygen saturation (SpO2) of 93%. A nodular shadow was also visualized in the anterior chest on computed tomography (CT) scans (Fig. ). However, the pleural cell block was insufficient for CGP testing. Hence, pleuroscopy under local anaesthesia was performed to gather sufficient tissue for CGP testing.\\nFlex-rigid pleuroscopy was performed using an LTF-240 (Olympus, Japan). Pleuroscopy showed the mass in the anterior chest (Fig. ). The mass was biopsied by conventional biopsy forceps (FB-231D; Olympus), but the mass was solid, and the tissue samples obtained were insufficient (Fig. ). Therefore, the mass was biopsied with a cryoprobe (2.0 mm probe; Erbe Elektromedizin, GmbH, Germany). The tip of the probe was attached to the mass, and it was cooled once with carbon dioxide for 5 sec and then for 7 sec in the same place (Fig. ). The frozen tissue sample was extracted by pulling and released from the probe by thawing with normal saline. Slight bleeding was seen in one biopsied part, but it was stanched spontaneously. The tissue size obtained was 2 mm by conventional biopsy forceps, and 5 mm at 5 sec and 12 mm at 7 sec by cryobiopsy (Fig. ). Histological analysis of the conventional biopsy forceps specimen showed cancer cells in the glandular cavity, but it was insufficient for CGP testing. The cryobiopsy specimens showed cancer cells, and there was sufficient tissue for CGP testing (Fig. ). On CGP, EGFR exon 19 deletion was positive, and the patient was started on osimertinib.\nOUTPUT:"
},
{
"from": "agent",
"value": "Adenocarcinoma"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: An 83-year-old woman presented with dyspnoea. Her chest X-ray showed a right-sided pleural effusion (Fig. ). A thoracic drain was inserted, and the pleural effusion was drained because she had a peripheral capillary oxygen saturation (SpO2) of 93%. A nodular shadow was also visualized in the anterior chest on computed tomography (CT) scans (Fig. ). However, the pleural cell block was insufficient for CGP testing. Hence, pleuroscopy under local anaesthesia was performed to gather sufficient tissue for CGP testing.\nFlex-rigid pleuroscopy was performed using an LTF-240 (Olympus, Japan). Pleuroscopy showed the mass in the anterior chest (Fig. ). The mass was biopsied by conventional biopsy forceps (FB-231D; Olympus), but the mass was solid, and the tissue samples obtained were insufficient (Fig. ). Therefore, the mass was biopsied with a cryoprobe (2.0 mm probe; Erbe Elektromedizin, GmbH, Germany). The tip of the probe was attached to the mass, and it was cooled once with carbon dioxide for 5 sec and then for 7 sec in the same place (Fig. ). The frozen tissue sample was extracted by pulling and released from the probe by thawing with normal saline. Slight bleeding was seen in one biopsied part, but it was stanched spontaneously. The tissue size obtained was 2 mm by conventional biopsy forceps, and 5 mm at 5 sec and 12 mm at 7 sec by cryobiopsy (Fig. ). Histological analysis of the conventional biopsy forceps specimen showed cancer cells in the glandular cavity, but it was insufficient for CGP testing. The cryobiopsy specimens showed cancer cells, and there was sufficient tissue for CGP testing (Fig. ). On CGP, EGFR exon 19 deletion was positive, and the patient was started on osimertinib.
OUTPUT: |
PMCPatients_common4402 | [
{
"from": "human",
"value": "As a physician engaged in 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 was primarily presented with a simple spontaneous swelling and pain on the dorsum of the foot. Initially, the internist treated the problem as gout. However, the problem persisted and thus radiography and magnetic resonance imaging (MRI) evaluations were carried out. A unicameral bone cyst (talocalcaneal and talonavicular joints) was suggested () and the patient underwent surgical curettage followed by harvesting autologous bone graft from the iliac crest. As the surgery was carried out at another center, we had no information on the surgical setting, preoperative planning, or the surgeon’s decision on the differential diagnoses of the disease. At this stage, knee amputation was suggested. However, the patient rejected this option and requested another tumor excision attempt. We accepted the request conditioned to amputation if a margin-free tumor excision was not possible. Two weeks later, regretfully, we had to perform another operation for a below-the-knee amputation. After 9 months, during a follow-up visit, a bulge in the pelvis around the previous site of donor graft was observed. Sonography, MRI, and CT-scan evaluations revealed a mass on the ilium at the graft harvesting site of the first surgery (). Another surgery was performed and the mass was excised. Spindle cells had distinct lobulation and were arranged in fascicles.\\nBased on the above course of events, we deduced the implantation of the primary tumor cells of the foot to the graft harvesting site. We believe that the first surgeon did not consider the possibility of a malignant tumor and used the same surgical devices for both the tumor excision and the graft harvesting. Written informed consent was obtained from the patient for the publication of this case report, including accompanying images.\nOUTPUT:"
},
{
"from": "agent",
"value": "Synovial Cell Sarcoma"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: A 30-year-old man was primarily presented with a simple spontaneous swelling and pain on the dorsum of the foot. Initially, the internist treated the problem as gout. However, the problem persisted and thus radiography and magnetic resonance imaging (MRI) evaluations were carried out. A unicameral bone cyst (talocalcaneal and talonavicular joints) was suggested () and the patient underwent surgical curettage followed by harvesting autologous bone graft from the iliac crest. As the surgery was carried out at another center, we had no information on the surgical setting, preoperative planning, or the surgeon’s decision on the differential diagnoses of the disease. At this stage, knee amputation was suggested. However, the patient rejected this option and requested another tumor excision attempt. We accepted the request conditioned to amputation if a margin-free tumor excision was not possible. Two weeks later, regretfully, we had to perform another operation for a below-the-knee amputation. After 9 months, during a follow-up visit, a bulge in the pelvis around the previous site of donor graft was observed. Sonography, MRI, and CT-scan evaluations revealed a mass on the ilium at the graft harvesting site of the first surgery (). Another surgery was performed and the mass was excised. Spindle cells had distinct lobulation and were arranged in fascicles.\nBased on the above course of events, we deduced the implantation of the primary tumor cells of the foot to the graft harvesting site. We believe that the first surgeon did not consider the possibility of a malignant tumor and used the same surgical devices for both the tumor excision and the graft harvesting. Written informed consent was obtained from the patient for the publication of this case report, including accompanying images.
OUTPUT: |
PMCPatients_common4605 | [
{
"from": "human",
"value": "As a physician engaged in 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 male developed an ulcer over his chronic scalp scar, which he developed due to bear mauling about 50 years back. The lesion developed following a minor trauma to the scar tissue and went through a cycle of apparent healing and deterioration. The ulcer continued to increase in size, and a cauliflower-like granulomatous mass appeared in the center with repeated episodes of foul smelling serosanguinous discharge and contact bleeding.\\nOn examination, he was conscious, with stable vital signs. A fungating growth of size 12×10×5 cm with irregular and indurated margin was found over the scar on his occipital area. The surface was covered with pale granulation tissue with intervening hemorrhage and necrosis []. Fine-needle aspiration cytology of the enlarged right occipital and posterior triangle lymph nodes showed features of inflammation and reactive hyperplasia. Computed tomography scan showed a right occipital extra-calvarial isodense lesion with underlying bone erosion and meningeal thickening [].\\nDefinitive surgery was planned based on prior discussion with the plastic surgeons. The patency of scalp vasculature was confirmed and marked over skin by Doppler ultrasound to plan rotational flap. With the patient in prone position, wide excision of the lesion was carried out with a 2 cm margin of normal skin. The underlying bone was found to be eroded with the dura infiltrated and adherent to the brain tissue below it. The unhealthy bone margins were nibbled away. The involved dura and an area of abnormal cortical brain tissue were excised and the dural defect was repaired using a G-dura patch []. The scalp defect was closed with local rotation flap based on left occipital artery in the same sitting. The secondary defect was grafted with split thickness skin graft. One hundred percentages flap survival was achieved post-operatively with uneventful wound healing and acceptable cosmetic outcome []. On the 8th day, he was discharged with advice to attend radiotherapy department for possible radiotherapy.\nOUTPUT:"
},
{
"from": "agent",
"value": "Penetrating Marjolin's ulcer of scalp with intracranial extension, 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 male developed an ulcer over his chronic scalp scar, which he developed due to bear mauling about 50 years back. The lesion developed following a minor trauma to the scar tissue and went through a cycle of apparent healing and deterioration. The ulcer continued to increase in size, and a cauliflower-like granulomatous mass appeared in the center with repeated episodes of foul smelling serosanguinous discharge and contact bleeding.\nOn examination, he was conscious, with stable vital signs. A fungating growth of size 12×10×5 cm with irregular and indurated margin was found over the scar on his occipital area. The surface was covered with pale granulation tissue with intervening hemorrhage and necrosis []. Fine-needle aspiration cytology of the enlarged right occipital and posterior triangle lymph nodes showed features of inflammation and reactive hyperplasia. Computed tomography scan showed a right occipital extra-calvarial isodense lesion with underlying bone erosion and meningeal thickening [].\nDefinitive surgery was planned based on prior discussion with the plastic surgeons. The patency of scalp vasculature was confirmed and marked over skin by Doppler ultrasound to plan rotational flap. With the patient in prone position, wide excision of the lesion was carried out with a 2 cm margin of normal skin. The underlying bone was found to be eroded with the dura infiltrated and adherent to the brain tissue below it. The unhealthy bone margins were nibbled away. The involved dura and an area of abnormal cortical brain tissue were excised and the dural defect was repaired using a G-dura patch []. The scalp defect was closed with local rotation flap based on left occipital artery in the same sitting. The secondary defect was grafted with split thickness skin graft. One hundred percentages flap survival was achieved post-operatively with uneventful wound healing and acceptable cosmetic outcome []. On the 8th day, he was discharged with advice to attend radiotherapy department for possible radiotherapy.
OUTPUT: |
PMCPatients_common3099 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: Initial clinical presentation, MRI, and [ A 69-year-old Caucasian woman presented to an outside Emergency Department (ED) with confusion and fever and was found to be septic with pneumonia and treated with antibiotics. At the time of transfer to our institution, the patient was intact neurologically, but MRI demonstrated multiple contrast enhancing lesions in the left hemisphere (thalamus, temporal lobe, and peri-trigonal white matter). The largest of these was a heterogeneous 4.4 cm mass in the left thalamus. Increased rCBV and MRS abnormalities were consistent with a high-grade glial neoplasm. Additionally, a right thalamic mass of 3.2 cm, which was non-enhancing and without rCBV or MRS abnormalities, was also visualized. [11C]-AMT-PET demonstrated severely increased radiotracer uptake in the left posterior thalamus (SUV ratio = 3.96), with additional uptake extending into the adjacent white matter. Molecular analysis demonstrated wild-type isocitrate dehydrogenase 1 and 2 (IDH1 and 2), and O6-methylguanine-DNA-methyltransferase (MGMT) promoter methylation of 15%.\\nClinical course and follow-up MRI: The patient could not complete the prescribed full courses of CRT due to the development of bilateral pulmonary emboli. Within the next six weeks, the patient received partial brain radiotherapy to 60 Gy and TMZ doses off and on at the reduced dosage of 140 mg/day for a total of three weeks.\\nSeven months after the initial diagnosis, MRI demonstrated new nodular enhancement in the left posterolateral thalamus and left external capsule but remained inconclusive whether this was due to radiation injury or infiltrating tumor. The final MRI one month later, after clinical worsening, demonstrated extensive FLAIR hyperintensities throughout both hemispheres and a 6-mm rightward midline shift, although the two thalamic lesions remained stable. She died shortly thereafter at 18 months after the original diagnosis.\nOUTPUT:"
},
{
"from": "agent",
"value": "Gliomatosis cerebri, WHO grade III anaplastic astrocytic diffusely infiltrative glioma"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Initial clinical presentation, MRI, and [ A 69-year-old Caucasian woman presented to an outside Emergency Department (ED) with confusion and fever and was found to be septic with pneumonia and treated with antibiotics. At the time of transfer to our institution, the patient was intact neurologically, but MRI demonstrated multiple contrast enhancing lesions in the left hemisphere (thalamus, temporal lobe, and peri-trigonal white matter). The largest of these was a heterogeneous 4.4 cm mass in the left thalamus. Increased rCBV and MRS abnormalities were consistent with a high-grade glial neoplasm. Additionally, a right thalamic mass of 3.2 cm, which was non-enhancing and without rCBV or MRS abnormalities, was also visualized. [11C]-AMT-PET demonstrated severely increased radiotracer uptake in the left posterior thalamus (SUV ratio = 3.96), with additional uptake extending into the adjacent white matter. Molecular analysis demonstrated wild-type isocitrate dehydrogenase 1 and 2 (IDH1 and 2), and O6-methylguanine-DNA-methyltransferase (MGMT) promoter methylation of 15%.\nClinical course and follow-up MRI: The patient could not complete the prescribed full courses of CRT due to the development of bilateral pulmonary emboli. Within the next six weeks, the patient received partial brain radiotherapy to 60 Gy and TMZ doses off and on at the reduced dosage of 140 mg/day for a total of three weeks.\nSeven months after the initial diagnosis, MRI demonstrated new nodular enhancement in the left posterolateral thalamus and left external capsule but remained inconclusive whether this was due to radiation injury or infiltrating tumor. The final MRI one month later, after clinical worsening, demonstrated extensive FLAIR hyperintensities throughout both hemispheres and a 6-mm rightward midline shift, although the two thalamic lesions remained stable. She died shortly thereafter at 18 months after the original diagnosis.
OUTPUT: |
PMCPatients_common1546 | [
{
"from": "human",
"value": "As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.\nINPUT: He was asymptomatic and denied any respiratory complaints. At the time of presentation, he was being treated with leflunomide, hydroxychloroquine and sulfasalazine. Pt is a Navy veteran with exposure to asbestos while he was in the Navy. Following his discharge from the Navy, he worked 10 years overseeing production of plastic and metal parts for guided radar systems. He then transitioned to working in residential construction, hanging, siding and replacing windows. The biopsies were negative for malignancy. There was no evidence of infection on bronchoalveolar lavage. His AFB and fungal cultures were also negative.\\nThree years following his biopsy, the patient presented with lower extremity edema and dyspnea on exertion. The staining was negative for amyloid and no silica deposits were identified. CT chest did not show worsening or progression of the nodule\nOUTPUT:"
},
{
"from": "agent",
"value": "Caplan’s Syndrome, Silico-anthracotic nodules, Minimal Change Disease, Focal Segmental Glomerulosclerosis, Mild Pulmonary Hypertension"
}
] | As a physician engaged in clinical diagnostic reasoning, here is a case report from Pubmed, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: He was asymptomatic and denied any respiratory complaints. At the time of presentation, he was being treated with leflunomide, hydroxychloroquine and sulfasalazine. Pt is a Navy veteran with exposure to asbestos while he was in the Navy. Following his discharge from the Navy, he worked 10 years overseeing production of plastic and metal parts for guided radar systems. He then transitioned to working in residential construction, hanging, siding and replacing windows. The biopsies were negative for malignancy. There was no evidence of infection on bronchoalveolar lavage. His AFB and fungal cultures were also negative.\nThree years following his biopsy, the patient presented with lower extremity edema and dyspnea on exertion. The staining was negative for amyloid and no silica deposits were identified. CT chest did not show worsening or progression of the nodule
OUTPUT: |