{"row_index": 0, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 35-year-old woman had a lump on the side of her face, on the left side, that grew over 2 years. At first, it looked like a harmless gland tumor, but later it got bigger and caused her face to droop. Doctors saw a hard, fixed lump that had spread into nearby muscles. An MRI showed the lump was growing inside the gland and had spread to muscles around it. She had surgery to remove the whole lump and nearby lymph nodes, and her facial nerve was kept safe. The test results showed this was a rare cancer called PNET, which starts in nerve tissue, and it had a special genetic change found in 60% of the cancer cells. After surgery, she got chemotherapy with four cycles of drugs (vincristine, doxorubicin, cyclophosphamide, ifosfamide, and etoposide), followed by radiation to the area. The treatment worked well, with only mild side effects like sore mouth and mild skin issues. She’s been checked every 3 months, and so far, no signs of cancer have come back.\"\n}"}
{"row_index": 1, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 35-year-old woman developed a tumor in her left parotid gland, a small gland near the jaw, two years prior. Initially, a small tumor was found, and a biopsy showed it was not cancerous. She had surgery to remove it, and the margins were clear, meaning no cancer was found at the edges. Six months later, a new, firm, painful lump appeared near the surgical site, and she began to lose movement on her left side—this is called facial paralysis. An MRI scan showed a larger tumor, measuring 42 mm, that had spread into nearby muscles and was not well-defined. The tumor was confirmed as a rare type of cancer called extra-skeletal Ewing’s sarcoma, a primary peripheral neuroectodermal tumor (PNET), which is known for spreading quickly. Pathology tests showed the tumor had a specific genetic change (EWING/PNET-type translocation) in 60% of its cells. She had surgery to remove the entire left parotid gland and nearby lymph nodes, with care taken to preserve the facial nerve. After surgery, she received chemotherapy with four cycles of vincristine, doxorubicin, cyclophosphamide, alternating with ifosfamide and etoposide, followed by external radiation therapy. The treatment was well-tolerated, with only mild side effects like mouth sores and mild skin irritation. She has been followed every three months with MRI scans, and at 10 months, there has been no sign of the cancer coming back locally or in distant parts of the body.\"\n}"}
{"row_index": 2, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 35-year-old female with no significant past medical history presented with a left parotid tumefaction that had been progressing over the previous two years. Initial biopsy revealed a mixed salivary gland tumor measuring 28 mm, which was histologically non-malignant, and she underwent a large resection with negative surgical margins. Six months later, she developed a new, firm, fixed, 6 cm nodule at the subangulomandibular level, palpable and painful, without signs of inflammation, accompanied by left peripheral facial paralysis. Lymph node examination was unremarkable. Magnetic resonance imaging (MRI) of the parotid region demonstrated an expansive, poorly defined process measuring 42 mm, showing moderate infiltration of the masseter and pterygoid muscles, heterogeneous spontaneous signal intensity, dynamic enhancement consistent with a type C curve, and a very low apparent diffusion coefficient (ADC), indicative of restricted water diffusion and high cellular density. Imaging studies of the thoraco-abdomino-pelvic region and bone scintigraphy, performed due to bone pain, were unremarkable. The patient underwent excision of the lesion, followed by a wide left parotidectomy with ipsilateral triangular lymph node dissection and preservation of the left facial nerve. Definitive pathological evaluation revealed an undifferentiated malignant tumor proliferation. Immunohistochemical staining demonstrated positive expression for cytokeratin (CK) and CD99, while synaptophysin, epithelial membrane antigen (EMA), neuronal-specific enolase (NSE), chromogranin, and vimentin were negative, supporting a diagnosis of a primary peripheral neuroectodermal tumor (PNET). Fluorescence in situ hybridization (FISH) analysis confirmed the presence of a specific EWING/PNET-type translocation in 60% of tumor cells, leading to the definitive diagnosis of extra-skeletal Ewing’s sarcoma. The patient received adjuvant chemotherapy with a VDC/IE regimen consisting of four cycles of vincristine, doxorubicin, and cyclophosphamide alternating with ifosfamide and etoposide. Following chemotherapy, she received external beam radiotherapy delivered at a total dose of 54 Gy using standard fractionation (1.8 Gy per session, five sessions per week) to the clinical target volume (CTV) with a 1.5 cm margin and planning target volume (PTV)"}
{"row_index": 3, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman who was pregnant for the first time had a serious blockage in both kidneys at 29 weeks. She had a surgery when she was 3 years old to fix a problem with her urine tubes (ureters), and it worked well back then. When she came in, she had back pain and her kidneys were swollen. Her body couldn’t filter waste properly, so she was admitted right away. Doctors placed small tubes (stents) into her urine tubes to unblock them. After that, she started urinating a lot, which helped her kidneys heal. A catheter was used to help her stay hydrated. After 7 days, the catheter was removed, but then she got a bad infection in her kidneys with fever and pain. Doctors treated it with antibiotics and put in a new catheter. When the infection went away, she was discharged at 33 weeks. She had no signs of early labor. At 39 weeks, she had high blood pressure and had her baby, a healthy boy, born naturally. After delivery, both stents moved into her urine opening (urethra) and caused pain and fever. Doctors put new stents in under anesthesia to fix the pain. Six months later, the stents were removed, but the right urine tube was still blocked. She will have another surgery to fix both tubes in the future.\"\n}"}
{"row_index": 4, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 24-year-old woman who was pregnant for the first time was referred to us at 29 weeks of gestation. She had a surgical procedure called bilateral Politano-Leadbetter ureteral reimplantation when she was 3 years old to fix a problem with urine flow from her kidneys. Since then, she had been doing well. But at this visit, she had back pain and an ultrasound showed severe swelling in both kidneys (hydronephrosis). Her kidney function was poor, so she was hospitalized right away. A stent was placed in each ureter to help drain urine and relieve pressure. After the stent was put in, her urine output increased greatly, and her kidney function improved quickly. A catheter was used to help prevent dehydration, and it was removed after 7 days. A week later, she developed a urinary tract infection, which was treated with antibiotics and a new catheter. Her symptoms went away, and she was discharged at 33 weeks. She did not have signs of preterm labor during her stay.\\n\\nAt 39 weeks, she was re-admitted due to high blood pressure. She delivered a healthy male baby weighing 3.14 kg, who had a good start at birth (Apgar scores of 9 and 10). After delivery, she started having back pain and fever. It was found that both stents had moved into her urethra. The stents were reinserted under spinal anesthesia, and her symptoms improved. She was discharged two weeks later. At 6 months post-delivery, the stents were removed, but a blockage was still present in the right ureter. A new stent was placed there, and she is now scheduled for a repeat surgery to fix both ureters.\"\n}"}
{"row_index": 5, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 24-year-old primigravida presented at 29 weeks of gestation with mild back pain and severe bilateral hydronephrosis, as detected by abdominal ultrasound. She had a history of bilateral Politano-Leadbetter ureteral reimplantation performed at age 3 years for vesicoureteral reflux (VUR), with an uneventful postoperative course. Her baseline blood pressure was 120/80 mmHg, but serum creatinine was elevated to 3.57 mg/dL, indicating acute postrenal failure due to obstructive uropathy. She was hospitalized immediately and underwent bilateral double-pigtail ureteral stenting (4.7 French) under ultrasound guidance without fluoroscopy. Post-stent placement, daily urine output exceeded 6 L, triggering post-obstructive diuresis; to prevent dehydration, an indwelling urethral catheter was inserted and intravenous saline infusion was initiated. Serum creatinine rapidly normalized to 1.1 mg/dL, and hydronephrosis significantly improved, allowing catheter removal after 7 days. However, within a week, the patient developed high fever and severe back pain, with laboratory findings consistent with pyelonephritis: white blood cell count of 13.1 × 10³/μL and C-reactive protein of 11.34 mg/dL. Urine culture isolated Streptococcus agalactiae, confirming bacterial infection. A second urethral catheter was placed and intravenous ceftriaxone sodium (2 g/day) was administered for 6 days, leading to clinical and laboratory resolution of infection. The catheter was removed when urine output declined, and she was discharged at 33 weeks of gestation without evidence of preterm labor (no cervical shortening or frequent uterine contractions). At 39 weeks, she was re-admitted for gestational hypertension, defined by persistently elevated systolic blood pressure (>140 mmHg) without proteinuria. She underwent labor induction and delivered a healthy male infant weighing 3140 g, with Apgar scores of 9 at 1 minute and 10 at 5 minutes. Postpartum, she developed acute back pain and fever on day 1 after delivery, which was attributed to spontaneous migration of both ureteral stents into the ure"}
{"row_index": 6, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 10-year-old girl from a Hindu family in Sindh, Pakistan, was healthy until she started having severe pain in her side, blood in her urine, vomiting, and fever for a week. She was very anxious and had high blood pressure. The doctor found her right kidney was swollen and painful, and a blood clot was blocking the blood vessel that supplies it — the right renal vein — and it went all the way into the main vein in her body. Tests showed no infections or other problems, but blood tests found she had a clotting issue linked to a condition called lupus. This is a known problem in people with lupus, called antiphospholipid syndrome.\\n\\nShe was given medicine to prevent clots — first enoxaparin, then warfarin — and later switched to rivaroxaban so she didn’t need frequent blood tests. Her high blood pressure was treated with medicine, and she started taking hydroxychloroquine to help with the lupus. Over time, her symptoms got better. Her blood pressure stayed normal, her kidneys kept working well, and she didn’t have any more clots or flare-ups of lupus.\\n\\nThe right kidney stopped working and was found to be non-functioning. Doctors said it might be removed, but her parents chose not to. Her kidney got smaller over time, and the left kidney grew bigger to help. She stayed healthy for 4 years, grew normally, and had no serious problems. She still takes medicine every day to prevent clots and protect her kidneys. Her mother later got lupus too. Her latest check-up showed normal blood pressure, normal kidney function, and no signs of active disease. She just has a bit of anemia from her periods, which is being managed.\"\n}"}
{"row_index": 7, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 10-year-old girl from a Hindu family in Sindh, Pakistan, who had been healthy until 2020, came in with a week-long history of severe abdominal pain, blood in her urine (gross hematuria), vomiting, and fever. She was anxious, had a high fever, and her blood pressure was very high. On exam, her right kidney was enlarged and tender. Other body systems were normal.\\n\\nLab tests showed low platelets, blood in the urine, and mild protein in the urine. Her kidney and liver functions were normal, and her blood clotting tests were normal. An ultrasound found that her right kidney was enlarged and had areas of abnormal tissue, and a color Doppler scan showed a large blood clot in the right renal vein that blocked blood flow and extended into the inferior vena cava. A CT scan confirmed the clot was fully blocking the vein.\\n\\nNo known risk factors for blood clots were found, and blood tests for inherited clotting disorders were negative. However, tests for lupus and antiphospholipid antibodies were positive, confirming a secondary antiphospholipid syndrome linked to lupus.\\n\\nShe was treated with anticoagulant medications (first enoxaparin, then warfarin), and her blood pressure was managed with captopril and later losartan. She improved over 10–12 days and was discharged. Her blood pressure and kidney function have remained stable over the next 4 years. The right kidney stopped working, and a scan showed it was nonfunctioning. Nephrectomy (removal of the kidney) was recommended, but her parents chose not to do it.\\n\\nHer anticoagulation was later switched to rivaroxaban to avoid frequent blood tests. She continues to take anticoagulants, antiplatelet medicine, blood pressure medication, and hydroxychloroquine to prevent flares and clots. Her growth and kidney function have been stable. Recent tests show normal kidney function, no protein in urine, and normal blood pressure (off blood pressure meds). She had a mild drop in red blood cells due to heavy periods, which was managed with medication. Her lupus markers are now normal, and there have been no new blood clots or flare-ups. Her mother later developed lupus as well.\\n\\nShe is still on long-term treatment and will likely need it for life,"}
{"row_index": 8, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 10-year-old female from a Hindu family in Sindh, Pakistan, with a low socioeconomic status, presented in 2020 with a 1-week history of severe right lumbar pain, gross hematuria, vomiting, and fever. The pain was refractory to analgesia and necessitated three emergency department visits prior to hospital admission. She denied dysuria, urinary retention, incontinence, or systemic manifestations such as joint pain, rash, mouth ulcers, or alopecia. Her medical history was unremarkable, including no prior renal disease, immunodeficiency, or family history of thrombotic or autoimmune disorders. She was born via cesarean section to unrelated parents, fully immunized, and developmentally normal, currently enrolled in the 8th grade.\\n\\nOn physical examination, she was febrile (101°F), hypertensive (systolic/diastolic blood pressure 130/96 mmHg, above the 95th percentile for age and height), anxious, and mildly anemic. Anthropometric parameters included weight 36.4 kg (50th percentile), height 141 cm (above 50th percentile), and body surface area (BSA) 1.2 m². No lymphadenopathy, jaundice, or skin rashes were observed. Abdominal examination revealed localized tenderness in the right lumbar region without splenomegaly. Systemic examinations of respiratory, cardiovascular, locomotor, and nervous systems were unremarkable.\\n\\nInitial laboratory investigations revealed a white blood cell count of 14.98 × 10⁹/L, platelet count of 75 × 10⁹/L (indicating thrombocytopenia), hemoglobin of 12.4 g/dL, and elevated C-reactive protein (48 mg/dL), lactate dehydrogenase (696 U/L), and D-dimer (19.8 mg/L), consistent with active inflammation and thrombotic processes. Urinalysis demonstrated hazy, reddish appearance with 3+ hematuria, 150 mg/dL proteinuria, numerous red blood cells (RBCs), and 15–20 white blood cells per high-power field (WBCs); leukocyte esterase and nitrites were negative. Spot"}
{"row_index": 9, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 61-year-old woman had a close call with her heart stopping suddenly. Doctors found a problem in her heart valve called mitral valve prolapse, where the valve leaks badly. This leak, along with other signs from heart tests, showed she was at risk for a sudden heart stop. To keep her safe, they put in a small device called an ICD that can shock her heart if it starts to beat wrong. They also plan to fix the leaking valve with a small surgery in three months. After the device was placed, she got better and was able to move around again. A few weeks later, her heart stayed stable, and after the surgery, a small fast heartbeat happened but was quickly fixed.\"\n}"}
{"row_index": 10, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 61-year-old woman had a near-fatal heart event and was saved with intensive care. She was found to have a condition called arrhythmogenic mitral valve prolapse, where the mitral valve in her heart doesn't close properly, leading to severe leakage. This condition, along with other signs seen on heart tests, increased her risk for sudden cardiac death. Tests showed abnormal electrical activity in her heart, including frequent ventricular arrhythmias and brief episodes of atrial fibrillation, which required anticoagulation therapy. An imaging test (CMR) revealed scar tissue in parts of the heart, which is a known risk factor for sudden cardiac death. The patient was given an internal automatic defibrillator (ICD) to monitor and prevent dangerous heart rhythms as a protective measure. She also underwent surgery three months later to repair the damaged mitral valve. After the procedure, she recovered well, regained mobility, and had no further serious heart rhythm issues during follow-up. The ICD successfully prevented any further life-threatening arrhythmias.\"\n}"}
{"row_index": 11, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 61-year-old female with a history of obesity (BMI 30.1 kg/m²) presented with an aborted sudden cardiac death. On admission, vital signs were stable: pulse 60/min, blood pressure 120/80 mmHg, temperature 36°C, and oxygen saturation 94% under mechanical ventilation. Physical examination revealed no abnormalities in heart, lungs, or abdomen. Laboratory studies were unremarkable, including complete blood count, coagulation profile (normal D-dimers), and clinical chemistry (C-reactive protein 6 mg/L, within normal limits of 5 mg/L). Electrocardiography (ECG) showed sinus rhythm with a heart rate of 60/min, no atrioventricular block, no QT interval prolongation, and inverted T-waves in inferior leads (III, aVF), suggestive of regional myocardial ischemia or early repolarization abnormalities. Fast echocardiography demonstrated preserved systolic function in both left and right ventricles, with severe mitral regurgitation and no pericardial effusion. Chest X-ray revealed normal cardiac size with pulmonary venous congestion, indicating left-sided volume overload.\\n\\nIntensive care management led to clinical stabilization; mechanical ventilation was discontinued on day 4. A hypoactive delirium was managed with neuroleptikum and resolved without persistent neurological deficits. The 12-lead ECG did not demonstrate typical electrocardiographic markers of channelopathies (e.g., Brugada syndrome, ARVC, long-QT or short-QT syndromes), ruling out common inherited arrhythmogenic disorders. However, recurrent ventricular arrhythmias (ventricular tachycardia, VT) were observed during continuous monitoring, and a transient atrial fibrillation with spontaneous termination was documented, prompting initiation of oral anticoagulation therapy.\\n\\nFollow-up echocardiography confirmed persistent severe mitral valve insufficiency with preserved left ventricular ejection fraction. The left ventricle exhibited mild end-systolic and end-diastolic dilation. A markedly enlarged left atrium (area 45 cm²) was identified, consistent with chronic volume overload. Doppler tissue imaging revealed a peak systolic lateral mitral annular velocity of 18 cm/s, indicating reduced annular contractility. Transesophageal echocardiography revealed a high-grade eccentric mitral"}
{"row_index": 12, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 45-year-old man working at a chemical plant got hurt on his right foot after stepping on a wet shoe that had ethylene oxide (EO) inside. He didn’t wear protective shoes or clothes and didn’t clean the shoe for 5 hours. The liquid soaked through his shoe and didn’t cause pain right away. It took more than 12 hours before he started feeling burning, redness, and oozing. When he finally went to the hospital, his foot was red, blistered, and had skin falling off. Doctors washed the area with salt water, covered it with a wet bandage, and applied medicine to prevent infection. He came back to the clinic every week for 4 weeks. After 9 months, his skin healed, but he still felt less sensation in his foot. He was checked by doctors for other problems, and everything was normal. No serious damage was found.\"\n}"}
{"row_index": 13, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 45-year-old man developed painful, red, oozing skin lesions on his right foot after working with ethylene oxide (EO) in a chemical plant. He was replacing a flowmeter connected to the EO tank and did not wear proper protective gear. A large amount of EO solution mixed with water spilled into his shoe, and he wore it for about 5 hours before showering. He didn’t feel any symptoms right away, but by the next morning, he had severe burning, pain, redness, and skin breakdown. The lesions were treated in the emergency department with saline irrigation, wet dressings, and topical antibiotics. He was followed up for 4 weeks at an outpatient clinic, and his skin healed completely with only slight darkening remaining. Nine months later, he reported reduced sensation in his foot, but tests showed no serious damage to his blood, lungs, or nerves. The case highlights the risk of delayed symptoms from chemical exposure and the importance of using proper protective equipment.\"\n}"}
{"row_index": 14, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 45-year-old male with no significant past medical history presented with painful, exudative lesions on the right foot following occupational exposure to ethylene oxide (EO). The patient worked in a chemical plant where he was responsible for replacing a worn-out flowmeter connected to the EO supply tank. He was not wearing personal protective equipment (PPE), including chemical-resistant clothing or footwear. EO is typically delivered via an automated isolation line, minimizing routine exposure; however, exposure can occur during maintenance procedures such as indicator system replacement, which involves manual handling of EO-containing lines.\\n\\nAt approximately 2:00 PM, a significant volume of EO solution mixed with water spilled onto the patient’s right shoe. The patient experienced no immediate symptoms and continued working with the contaminated footwear until approximately 5:30 PM, approximately 5 hours after initial exposure. He returned home and took a shower, which effectively decontaminated the affected area. Clinical symptoms, including a severe burning sensation, pain, erythema, and progressive desquamation, developed approximately 12–14 hours post-exposure, beginning with the dorsum of the right foot and extending to the proximal regions of the second and third digits and the hallux.\\n\\nOn presentation to the emergency department, the patient exhibited acute dermatological injury with subcutaneous tissue damage, characterized by severe erythema, dark pink dermal appearance, serosanguineous exudate, blister formation, and epidermal desquamation. The total burn surface area was assessed at 3.5% of the total body surface area (TBSA). Vital signs were stable, with normal hemodynamics and alert mental status. No respiratory distress or dyspnea was noted, and pulmonary examination revealed clear breath sounds.\\n\\nLaboratory investigations—including complete blood count (CBC), blood chemistry panel, urinalysis, and plain chest radiograph—were all within normal limits, indicating no systemic toxicity or organ involvement. The affected skin was irrigated with saline solution and treated with topical silver sulfadiazine to prevent infection in the open wounds. The patient was managed in an outpatient follow-up setting for a duration of 4 weeks, during which complete epidermal regeneration occurred without scarring or structural defects. At a 9-month follow-up, residual hyperpigmentation was observed, but no other abnormalities were detected.\\n\\nA comprehensive health assessment conducted 9 months post-exposure revealed reduced sensory"}
{"row_index": 15, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 69-year-old woman had a firm lump on her left thigh that grew over 6 years and caused pain. Doctors first removed the lump with surgery, and tests confirmed it was a type of cancer called soft tissue sarcoma. She had more surgeries and treatment with radioactive seeds, but the cancer came back. After that, she got a new treatment called HIFU — it uses focused sound waves to destroy the cancer. The treatment worked well, and the cancer was completely gone, with no major side effects except for some damage to the bone at the spot. About four months later, the lump came back again, but doctors found it was small and treated it with more surgery. Now she is stable, feels good, and lives a normal life.\"\n}"}
{"row_index": 16, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 69-year-old woman was diagnosed with an undifferentiated spindle cell soft tissue sarcoma on her left thigh. She first had surgery to remove the tumor, and the results confirmed the diagnosis. Over time, the cancer came back at the same site after multiple surgeries and treatments with radioactive particles. After 16 months, imaging showed the cancer had returned again, and she had three more surgeries and radioactive treatments. Despite this, the cancer still came back, so a new treatment called high-intensity focused ultrasound (HIFU) was used. HIFU is a non-invasive method that uses focused sound waves to destroy the tumor. The treatment was given over five sessions, and MRI scans showed the tumor was completely destroyed, with no signs of cancer cells left. The only side effect was minor bone damage at the treatment site. About four months later, the patient had a small break in the bone at the original tumor location, but further testing showed it was not cancer-related. She then had additional surgery to fix it and is now stable with a good quality of life.\"\n}"}
{"row_index": 17, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 69-year-old female patient presented with a 3-cm-diameter firm mass on the left thigh that had progressively increased over a 6-year period, accompanied by localized pain. Initial surgical management consisted of a lumpectomy performed at The Second Affiliated Hospital of Chongqing Medical University. Postoperative histopathological examination confirmed the lesion as an undifferentiated spindle cell soft tissue sarcoma. Immunohistochemical profiling revealed CK(-), EMA(-), Vim(+), S100(-), SMA(±), Act(-), CD34(+), BCL-2(-), CD9(±), Ki-67(+), 50% AB(+), MBP(-), NF(-), and CD68(+), consistent with a spindle cell sarcoma of undifferentiated phenotype, likely with features of sarcomatoid differentiation and active cell proliferation (Ki-67 >50%). The patient underwent an expanded resection to ensure clear margins.\\n\\nTwo years postoperatively, a firmer, tender mass was identified at the surgical site, prompting a second expanded resection followed by radioactive particle implantation (brachytherapy). Repeat immunohistochemistry demonstrated CK(-), EMA(±), DES(-), S100(-), SMA(-), CD34(+), SDX-10(-), CDK4(-), MDM2(-), CD68(-), CD99(±), BCL-2(+), Vim(+), and Ki-67(+) >50%, indicating persistent tumor cell proliferation and a shift in molecular profile, including upregulation of BCL-2, which may confer resistance to apoptosis and contribute to tumor recurrence.\\n\\nMagnetic resonance imaging (MRI) at 16 months post-second resection revealed local tumor relapse, leading to three additional lumpectomies and brachytherapy. Five months later, follow-up pathology confirmed a further relapse, indicating persistent disease progression despite multimodal local interventions.\\n\\nA novel treatment strategy was initiated involving five sessions of high-intensity focused ultrasound (HIFU), administered on March 5, June 11, August 20, October 13, and November 24, 2021, using an integrated circuit-type HIFU tumor treatment system (Chongqing Haifu Medical Technology Co., Ltd., China). The system comprises an ultrasonic generator"}
{"row_index": 18, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman in her 50s had been dealing with mood swings and crazy thoughts for 27 years. She was on many medicines, including lithium, which can hurt her kidneys. She came to the hospital because she was sad and had scary thoughts. She had a bladder infection, so she started antibiotics. After 5 days, she got fever and her body started to fail — her kidneys couldn’t work right. Her lithium level was too high (2.34), which damaged her kidneys. The doctors stopped the lithium and switched to safer antibiotics. They gave her fluids to help her kidneys recover. After a few days, she got better. But even after stopping the old medicines, she stayed sad and had worse scary thoughts. So they stopped all her old pills and started new ones: lamotrigine and aripiprazole. These helped a little, but didn’t fix it. Then they added quetiapine to help her sleep and calm down. But after giving her a high dose of quetiapine (400 mg a day), she got a serious problem called NMS — which means her body went into trouble. They gave her amantadine, lorazepam, and bromocriptine to fix it, and she got better. The doctors said the quetiapine was most likely to have caused the problem.\"\n}"}
{"row_index": 19, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 51-year-old woman with bipolar disorder, who had been managing her condition for 27 years, was admitted to the hospital because she was feeling very sad and had strange, persistent thoughts—like believing others were out to get her. She had been on several medications, including lithium, fluoxetine, olanzapine, gabapentine, perazine, and biperiden, to control her mood and symptoms. Before this hospital stay, she had a history of depression, mania, and one episode of psychosis in 1990. In the past, she had also had kidney problems from high lithium levels and was treated for hypothyroidism.\\n\\nShe was diagnosed with a urinary tract infection, and started on antibiotics. After five days, she began to feel worse—she developed a fever of 38.4°C and her lithium level became dangerously high at 2.34 mmol/l. This caused acute kidney failure, so her lithium was stopped and the antibiotics were changed to a less harmful type. She received fluids to help her body remove the excess lithium, and her kidney function slowly improved.\\n\\nOnce her body stabilized, her mental symptoms got worse—she became more depressed and her delusions returned. All her previous medications were stopped one by one. Instead, she started on lamotrigine and aripiprazole to help stabilize her mood and reduce the delusions. After six weeks, the aripiprazole wasn’t working well, and she started taking quetiapine to help with sleep and mood. However, increasing the quetiapine dose to 400 mg per day eventually led to a serious condition called neuroleptic malignant syndrome (NMS), which is a rare but dangerous reaction to certain psychiatric medications.\\n\\nTo treat NMS, she was given amantadine, lorazepam, and bromocriptine, and her condition improved. The doctors used a scoring system to evaluate how likely each drug was to have caused the NMS. Quetiapine was found to be the most likely contributor, followed by aripiprazole and lamotrigine.\\n\\nThis case shows that even with long-term treatment, changes in medications can lead to serious side effects, and close monitoring is essential, especially in people with a history of kidney issues or mental illness.\"\n}"}
{"row_index": 20, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 51-year-old female with a 27-year history of bipolar disorder was admitted to the psychiatric clinic in September 2017 presenting with depressed mood, ideas of reference, delusions of persecution, and anxiety. Her clinical course began with an acute paranoid psychotic episode in 1990, followed by recurrent hospitalizations for depressive and manic episodes, with a pattern of treatment shifts involving antidepressants (imipramine, venlafaxine), mood stabilizers (lithium, carbamazepine), and antipsychotics (perazine). Following outpatient management from 2000 to 2008, treatment was modified in 2015 due to lithium toxicity (>1.2 mmol/L), resulting in acute renal failure and extrapyramidal symptoms (EPS), necessitating withdrawal of lithium and initiation of gabapentine for EPS. Hypothyroidism was concurrently diagnosed and managed with levothyroxine until 2016. Between 2016 and 2017, the patient received fluoxetine (60 mg/d), perazine (150 mg/d), gabapentine (800 mg/d), and carbamazepine (200 mg/d, up to 800 mg/d), which was later discontinued due to worsening psychotic and depressive symptoms. Lithium was reintroduced at maximum dose (up to 1000 mg/d), along with olanzapine (5 mg/d) for psychosis and biperiden (4 mg/d) for muscle rigidity. No psychiatric comorbidities were identified throughout the disease course, with notable historical events including prior lithium intoxication and renal failure.\\n\\nAt admission, the patient was alert, oriented to person, place, and time, with stable vital signs: blood pressure 115/70 mmHg, pulse 72 bpm, respiratory rate 16/min, BMI 27.22. Physical examination revealed a regular systolic murmur, clear lung fields, symmetrical abdomen with normal bowel sounds, dry skin, and varicose veins of the lower extremities. Laboratory findings at admission included lithium level of 1.48 mmol/L, glomerular filtration rate (GFR) 35 ml/min, serum creatinine 1.56 mg/dL, and white blood cell count (WBC"}
{"row_index": 21, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old man in Iran found a lump on the back of his left hand and wrist. It had been there for about a month and got bigger over time. The doctor first thought it was a common bump called a ganglion cyst. He tried pain medicine for two months, but the lump kept growing. An MRI scan showed it was a rare type of tumor inside the hand, called synovial sarcoma. The doctor took a small sample of the tumor and tested it. The test showed it was cancer. The man didn’t come back for check-ups for two months. By then, the tumor had grown very large. This is a rare case because most people don’t get this kind of tumor in the hand and don’t follow up after the diagnosis. The doctor said he needed surgery, but the man refused and never came back for treatment.\"\n}"}
{"row_index": 22, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This study describes a rare case of metacarpal synovial sarcoma in a 32-year-old Iranian man. He first noticed a lump on the back of his left hand and wrist about one month before seeking medical help. The doctor initially thought it was a common ganglion cyst and treated it with pain relief medication for two months. During that time, the lump slowly grew larger. An MRI scan showed a soft tissue mass that was encasing part of the hand bone and pushing on tendons, which raised concern. A biopsy was done, and the results confirmed it was a synovial sarcoma — a rare type of cancer that starts in the connective tissue. The tumor was completely removed surgically. However, the patient had poor follow-up care and did not return to the clinic for two months after the surgery. When he finally came back, the tumor had grown significantly. Because of this late return, the cancer was no longer treatable, and the patient refused further treatment. This case is rare because synovial sarcoma in the hand or wrist is uncommon, and the delay in follow-up made it much harder to manage.\"\n}"}
{"row_index": 23, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old Iranian male with no significant past medical, family, or social history presented with a slowly progressive lump on the dorsal ulnar side of the right hand and wrist, first noted one month prior. The lesion had been increasing in size over the preceding month, with no history of trauma, constitutional symptoms (such as fever or chills), or systemic illness. Vital signs at admission were within normal limits: pulse rate 75 bpm, blood pressure 118/83 mmHg, temperature 36.7°C, and oxygen saturation 98%. Laboratory evaluations, excluding 25-hydroxyvitamin D3, were unremarkable; the patient was subsequently initiated on daily oral vitamin D3 supplementation (1000 mg) due to low serum 25-hydroxyvitamin D3 levels.\\n\\nStandard hand-wrist radiography was performed to exclude bony abnormalities or foreign bodies, and no evidence of fracture, cortical disruption, or bone invasion was observed. The initial clinical assessment by the primary care physician attributed the lesion to a ganglion cyst. The patient received conservative management including naproxen 500 mg as needed for pain for a duration of two months. During this period, the lesion progressively enlarged. On physical examination, a 30 × 20 mm mass was identified between the second and third metacarpal bones on the dorsal surface of the left hand, extending proximally toward the metacarpal heads and distally into the proximal aspect of the wrist joint. Neurovascular examination revealed no significant deficits: wrist flexion and extension were intact, deep tendon reflexes were normal, sensory function was preserved, and muscle strength was rated 5 out of 5, indicating full motor function.\\n\\nMagnetic Resonance Imaging (MRI) was subsequently performed and interpreted by a radiologist. The MRI demonstrated a T2-hypersignal lesion with iso-signal intensity on T1-weighted sequences in the deep soft tissue of the middle and medial regions of the hand, specifically involving the 3rd and 4th metacarpal web spaces. The lesion exhibited cystic characteristics with fine internal septations and heterogeneous signal intensity. Tendon displacement was observed: the flexor tendons were deviated due to mass effect, and the extensor tendons of the 3rd, 4th, and 5th fingers were displaced, indicating local"}
{"row_index": 24, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 56-year-old woman felt her heart was racing, so she went to the doctor. The doctor saw a small bump on her heart valve, about 8 millimeters big, and it was slightly leaking. At first, they thought it was a tumor, but after surgery, they found it was actually a weak, bulging part of the valve — like a small balloon that had stretched out. It wasn’t a cancer, but a sign of wear and tear from years of use. The doctors removed the bulge and fixed the valve with a ring to help it stay strong. After the surgery, she recovered well and has been feeling fine ever since. Ten months later, her heart valve is still healthy and not leaking at all. This kind of problem happens when the heart valve wears down over time, not because of disease or infection.\"\n}"}
{"row_index": 25, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 56-year-old woman was seen for palpitations. Her heart rhythm and sounds were normal, and initial tests showed no signs of infection or heart problems. An echo scan found an 8-mm mass on the anterior mitral leaflet with only slight valve leakage. Further testing confirmed the same finding. Surgery was planned to remove the mass and prevent a possible blood clot from forming. During surgery, it was discovered that the mass was not a tumor, but a bulge resembling an aneurysm, and there was no stretching of the supporting tissue. The surgeon removed the bulge and repaired the valve with a ring procedure. The patient recovered well and had no complications. Path tests showed signs of degenerative changes in the valve tissue, confirming that the issue was due to wear and tear over time. At 10 months after surgery, her heart function is stable with no further valve problems.\"\n}"}
{"row_index": 26, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 56-year-old woman with no history of infection presented for evaluation of palpitations. Her clinical examination revealed a regular sinus rhythm with no audible heart murmur. Standard electrocardiographic assessments, including resting ECG and Holter monitoring, as well as chest X-ray, were within normal limits. Transthoracic echocardiography identified an 8 × 8-mm mass localized to the posterior aspect of the anterior mitral leaflet, associated with minimal mitral valve insufficiency. Left ventricular systolic function, wall motion, and chamber dimensions were preserved, indicating no underlying systolic dysfunction. Transesophageal echocardiography confirmed the same lesion morphology, with no evidence of intracardiac thrombus or systemic embolic events. Computed tomography was negative for systemic emboli, further supporting the absence of a thrombotic source. Given the imaging findings and the clinical suspicion of a valvular tumor, surgical resection was performed with the primary goal of preventing potential embolic complications. Intraoperative inspection revealed that the lesion was not a neoplastic tumor, but rather an aneurysm-like bulge of the anterior mitral leaflet, characterized by absence of chordal elongation, which is a key histopathological and biomechanical feature distinguishing it from true neoplastic growths. The lesion was resected via a triangular resection technique, followed by ring annuloplasty to restore normal valve architecture and reduce the risk of residual regurgitation. Postoperative recovery was uneventful, with no complications reported. Histopathological analysis of the resected tissue demonstrated myxomatous degeneration, interstitial fibrosis, and hyalinization—pathological hallmarks of degenerative mitral valve disease. These findings are consistent with a chronic, progressive process involving extracellular matrix remodeling, likely driven by age-related changes in valve tissue elasticity and collagen turnover. At a 10-month follow-up, the patient remains asymptomatic, with no evidence of mitral regurgitation or valvular dysfunction, confirming successful surgical intervention and resolution of the structural abnormality. The case underscores the importance of accurate preoperative imaging and intraoperative differentiation between benign degenerative lesions and malignant tumors in the mitral valve, as misdiagnosis could lead to inappropriate resection or unnecessary intervention.\"\n}"}
{"row_index": 27, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 23-year-old man had a serious illness called Burkitt's lymphoma and was also dealing with a condition where his body attacked its own tissues (GVHD). He got very sick with confusion and trouble breathing, and when checked, had a bleed in his brain and a dead area in his brain from a stroke. Doctors found 12 weak spots in blood vessels in his brain — called aneurysms — that started showing up very fast, even though scans showed no sign of infection in his skull bones. The infection was caused by a rare fungus called Scedosporium. Even with strong medicine and surgery, the patient got worse, had infections in his lungs, and died 6 months later because his heart, lungs, and other organs stopped working. What made this case special was how fast the fungus spread through the blood vessels — new aneurysms appeared in just days, even when the brain scans looked clean.\"\n}"}
{"row_index": 28, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 23-year-old man with Burkitt's lymphoma and graft-versus-host disease was admitted to the hospital with confusion, sleepiness, and breathing problems. He had a bleeding stroke in his brain and signs of a prior brain injury. Imaging showed several aneurysms—bulges in blood vessels—that formed quickly, including 12 in the front part of the brain. These aneurysms were caused by a widespread infection from a fungus called Scedosporium, which spread rapidly through the blood vessels. Even though there was no clear sign of infection in the skull bones, new aneurysms appeared within days of imaging. The patient received antibiotics, antifungals, and surgery to remove the aneurysms. Despite these efforts, the infection spread and damaged multiple organs. He developed severe infections, including one caused by a drug-resistant bacteria in his lungs, and died six months later from multiorgan failure. This case shows how fast a fungal infection can spread through blood vessels in a patient with weakened immunity, leading to serious brain bleeding and organ damage.\"\n}"}
{"row_index": 29, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 23-year-old male with a history of Burkitt’s lymphoma and graft-versus-host disease (GVHD) requiring high-dose corticosteroid therapy was admitted to the Emergency Department with a two-day history of somnolence, confusion, and progressive respiratory distress necessitating endotracheal intubation. On admission, neurological examination revealed impaired eye opening to painful stimuli and intact command following. Initial non-contrast head CT demonstrated a flame-shaped intracerebral hemorrhage in the left gyrus rectus, suggestive of vascular origin, and a hypodense lesion in the left thalamus consistent with an established infarction. The next-day angiogram identified six fusiform aneurysms: three at the frontopolar branch of the left anterior cerebral artery (ACA), one at the orbitofrontal branch of the left ACA, one at the frontopolar branch of the right ACA, and one at the anterior temporal artery of the left middle cerebral artery (MCA). Body imaging revealed multiple cavitary lung lesions, consistent with pulmonary involvement by a systemic infection. Broad-spectrum antibiotics, antifungals, and antivirals were initiated empirically.\\n\\nThe hemorrhagic focus localized to the left ACA branch aneurysms, prompting surgical intervention to assess rupture status and obtain tissue for microbiological analysis. On postbleed day 2, a bicoronal craniotomy was performed with parent vessel sacrifice and excision of the three left ACA fusiform aneurysms. Intraoperatively, the aneurysms exhibited friable, thin-walled characteristics with high propensity for rupture. The right ACA aneurysm was managed conservatively. Microbiological analysis confirmed angioinvasive infection by Scedosporium apiospermum, leading to initiation of vericonazole, amphotericin B, and caspofungin, which were continued throughout the clinical course.\\n\\nOn postbleed day 4, a new left frontal intracerebral hemorrhage and intraventricular hemorrhage (IVH) were detected on CT, prompting placement of an emergency external ventricular drain. A follow-up angiogram revealed interval growth of the left orbitofrontal artery aneurysm. With definitive microbiological identification, endovascular parent vessel occlusion was recommended and successfully performed. A subsequent angiogram on postbleed day 7 demonstrated the emergence of three"}
{"row_index": 30, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman with a weak heart valve got very short of breath and sharp chest pain. Her heart valve was badly damaged and caused high pressure in her lungs. Doctors tried a simple balloon procedure to fix the valve, but it broke and caused the valve to leak badly, making lung pressure even higher. Because her heart was too weak to handle surgery, they used medicines and a machine (intra-aortic balloon pump) to help her heart pump better. They also used drugs to open her blood vessels and reduce pressure in her lungs. Even with all this, her body couldn’t keep up, so she and her family chose to focus on comfort and peace instead of more treatment.\"\n}"}
{"row_index": 31, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 64-year-old woman with a history of heart valve problems, high blood pressure, and previous stroke was admitted with sudden chest pain and shortness of breath. Tests showed severe narrowing of her mitral valve, which is a key heart valve that helps control blood flow. This narrowing was causing high pressure in her lungs (pulmonary hypertension), and her overall risk for surgery was high due to other health issues. Because of this, doctors decided against open heart surgery and instead performed a less invasive procedure called percutaneous mitral balloon valvuloplasty to open up the valve. However, during the procedure, a critical complication occurred: one of the supporting strings of the valve (chordae tendineae) ruptured, leading to severe leakage (mitral regurgitation) and a dramatic rise in lung pressure, now reaching levels above the systemic blood pressure (supra-systemic pulmonary hypertension). To manage this life-threatening situation, the patient received multiple medications, including vasopressors to support blood pressure, inodilators to reduce lung pressure, and an intra-aortic balloon pump to help improve heart function and reduce valve leakage. She also received lung vasodilators and other drugs to ease pressure in her lungs. Despite these efforts, her condition continued to worsen, and after failing to respond to full medical treatment, her family chose to focus on comfort care and hospice support. The main point is that this patient’s complex heart condition led to a serious complication during a planned valve procedure, and her care shifted from surgical to intensive medical management to stabilize her condition and ensure comfort.\"\n}"}
{"row_index": 32, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 64-year-old female presented to the emergency department with acute retrosternal chest pain and progressive dyspnea. She has a history of coronary artery disease, hypertension, atrial fibrillation, rheumatic mitral valve (MV) disease, and prior stroke with residual left-sided hemiplegia. Transesophageal echocardiography (TEE) demonstrated severe mitral stenosis (effective orifice area [EOA] 0.9 cm²; normal >1.0 cm²), mild mitral regurgitation (MR), minimal leaflet motion, pronounced valvular thickening, extensive calcification, and a Wilkins score of 14 indicating severe structural degeneration of the mitral valve apparatus. The sub-valvular apparatus showed minimal thickening, no vegetations, and no thrombus in the left atrial appendage. Left ventricular systolic function remained preserved.\\n\\nLeft heart catheterization confirmed non-obstructive coronary artery disease. Right heart catheterization (RHC) revealed a mean pulmonary artery pressure (PAP) of 71 mmHg and a pulmonary capillary wedge pressure (PCWP) of 15 mmHg, resulting in a transpulmonary pressure gradient (TPG) of 51 mmHg, consistent with severe pulmonary hypertension (PH) due to pulmonary venous hypertension. Her Society of Thoracic Surgeons (STS) surgical mortality risk was estimated at 31% due to the combination of severe PH and multiple comorbidities. A multidisciplinary team—including advanced heart failure, cardiac surgery, intensive care, and cardiac anesthesia—concluded that the patient was not a suitable candidate for surgical mitral valve replacement (MVR) due to the high risk of perioperative mortality and hemodynamic instability. Consequently, percutaneous mitral balloon valvuloplasty (PMBV) was performed under general anesthesia in the cardiac catheterization laboratory.\\n\\nPre-procedure, invasive lines (radial arterial line and right internal jugular vein catheter) were successfully placed. Induction of general anesthesia was achieved with endotracheal intubation. Repeat RHC showed a mean PAP of 61 mmHg and left atrial pressure of 30 mmHg. TEE confirmed a severely dilated right ventricle and a mitral EOA of 0.9 cm². Cardiac index"}
{"row_index": 33, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old Asian girl with leukemia had swelling in her gums and chin that got worse over time. Even with proper care, the infection didn’t go away and eventually caused a big hole in her face and jaw. Her teeth fell out on their own, and part of her jaw bone also came loose. Because of this, she couldn’t eat properly and kept drooling. After she got better, a simple surgery was done to fix her lips so she could eat again and stop drooling.\"\n}"}
{"row_index": 34, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 12-year-old Asian girl with acute myeloid leukemia (AML) developed worsening gingivitis, which started as swollen gums and chin. She had already received chemotherapy for her leukemia and was hospitalized for a high fever, which was treated with multiple antibiotics, antifungals, and antivirals. Her white blood cell count was very low, and her neutrophils were absent, making it hard to fight infections. Despite proper treatment, her oral condition got worse. Six days after the start, she had a cardiac arrest due to uncontrolled fever, but she recovered. Over time, the swelling turned into a full-thickness tissue loss in her mouth and face, causing the gums and underlying bone to separate and the teeth to fall out. After recovering from the illness, she had serious problems with her lips, making it hard to eat or control drooling. Because of her weakened blood counts, surgery was done simply to repair the lip and restore the ability to eat, using a local flap to reconnect the muscle that controls the lips.\"\n}"}
{"row_index": 35, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 12-year-old Asian female patient with acute myeloid leukemia (AML) was referred for evaluation and management of progressive gingival swelling and chin involvement. The patient had a history of patent ductus arteriosus (PDA) closure at age 6 and had undergone four cycles of induction chemotherapy for AML, diagnosed one year prior. She was admitted for neutropenic fever exceeding 39°C, managed with a broad-spectrum regimen including linezolid, meropenem, sulfamethoxazole, metronidazole, teicoplanin, cefpiramide, and amikacin, along with antifungals (fluconazole, nystatin, amphotericin B, voriconazole, caspofungin) and antiviral therapy (acyclovir), consistent with suspected vancomycin-resistant enterococci (VRE) sepsis. Laboratory findings revealed a white blood cell (WBC) count of 40/μL, platelet count of 8000/μL, and an absolute neutrophil count of 0/μL, confirming profound neutropenia and pancytopenia. Given the absence of viable neutrophils and the patient's unstable hematologic status, surgical intervention was contraindicated. Over the course of six days, the patient developed uncontrolled fever leading to cardiac arrest; return of spontaneous circulation (ROSC) was achieved through resuscitation, followed by gradual clinical improvement. The oral and facial lesions progressed to full-thickness necrotic gangrene, with complete separation of the necrotic alveolar bone from the surrounding mandibular bone. Teeth in the affected segment spontaneously exfoliated, and the necrotic bone segment also detached independently. Following resolution of fever and recovery of systemic stability, the patient faced persistent functional deficits, including lip incompetence and drooling due to loss of oral closure, rendering oral intake impossible. In the context of her pancytopenia and high surgical risk, a minimally invasive local flap procedure was performed to restore continuity of the orbicularis oris muscle, thereby achieving functional lip competency and enabling safe oral intake. The case illustrates the severe mucosal and skeletal complications of prolonged neutropenia in pediatric leukemia, particularly involving the maxillofacial region, with gingivitis progressing to full-thickness tissue and bone necrosis due to impaired host defense mechanisms, disrupted tissue perf"}
{"row_index": 36, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 48-year-old man had eye inflammation in his left eye that didn’t go away. His doctor tried a steroid called prednisolone, which helped a little, but when the dose was lowered, the eye swelling came back. He was referred to a better eye hospital because the problem kept returning. At first, his vision was okay, but his eye had signs of swelling and inflammation. Tests showed his eye had a type of blood vessel problem that matches a condition called Bechet’s disease. He also had mouth sores and red bumps on his legs, and a test showed a specific gene (HLA-A26) was present. He started a drug called adalimumab to reduce the need for steroids. It worked — his eye swelling got better and he could slowly cut down on the steroid. But after 8 months, he started feeling sick and tests found signs of tuberculosis (TB) in his lungs. He was diagnosed with miliary TB, a serious form of TB. His steroid and adalimumab were stopped right away, and he started TB treatment for 6 months. Even after that, the TB test stayed positive. During this time, his eye problem got worse, and his vision dropped. So, they restarted a different drug called infliximab, along with isoniazid to fight TB. After starting this, his eye swelling and vision improved again. No TB came back after 3 years of treatment. The key point: his eye problem needed special medicine, and TB was a serious side risk, but it was managed with the right steps.\"\n}"}
{"row_index": 37, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 48-year-old Japanese man was treated for eye inflammation (uveitis) in his left eye, which had developed into macula edema (swelling in the central part of the retina). His doctor first tried prednisolone, a steroid, which helped temporarily, but when the dose was reduced, the swelling returned. Because the condition didn't improve, he was referred to a specialized eye hospital in Tokyo. At the hospital, doctors found signs of Bechet’s disease — a rare condition that causes inflammation in blood vessels — through eye exams, blood tests, and imaging. Key signs included swollen blood vessels in the retina, recurring mouth sores, a rash on his legs, and a specific genetic marker (HLA-A26). He started treatment with adalimumab (ADA), a drug that reduces inflammation and helps lower steroid use. Over time, his eye swelling improved and he was able to reduce his steroid dose. However, eight months later, he developed symptoms of tuberculosis (TB), including fatigue and lung shadows on imaging. He was diagnosed with miliary TB, a serious form of TB. His steroid and ADA treatments were stopped immediately, and he began a six-month course of TB medication. Even after recovery, his TB test remained positive. During this time, his eye condition worsened, with increased swelling and vision loss. After stopping ADA, he used eye drops and injections to control the eye inflammation, but these only provided limited relief and caused some side effects like higher eye pressure. Eventually, he restarted treatment with infliximab (IFX), combined with isoniazid for TB prevention. After starting IFX, his eye swelling and vision improved, and his TB did not return during the next three years. This case shows that while treatments for Bechet’s disease can help control eye symptoms, patients need careful monitoring for infections like TB, especially when using anti-inflammatory drugs.\"\n}"}
{"row_index": 38, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 48-year-old Japanese male presented with uveitis of unknown origin in the left eye, initially managed at a general ophthalmology clinic. Macula oedema (ME) was identified, and prednisolone (PSL) 40 mg/day was initiated. Although ME showed transient improvement, tapering PSL to 20 mg/day resulted in relapse of ME, prompting referral to the Department of Ophthalmology, Tokyo Medical University Hospital due to persistent intraocular inflammation and worsening visual function. At presentation, best-corrected visual acuity (BCVA) was 20/12.5 in the right and 24/20 in the left eye, with normal intraocular pressure. Slit-lamp examination revealed 1+ anterior chamber cells; fundus photography demonstrated diffuse vitreous haze and mild peripheral retinal exudates; fluorescein angiography revealed diffuse retinal vasculitis involving the posterior pole and peripheral retina, consistent with Bechet’s disease (BD); optical coherence tomography (OCT) confirmed the presence of macula oedema. Peripheral blood tests showed elevated white blood cell count, increased neutrophil percentage, elevated lactate dehydrogenase (LDH), HLA-A26 positivity, negative HLA-B51, and negative results for both tuberculin skin test (TST) and T-SPOT.TB. Based on the clinical presentation—recurrent oral aphthous ulcers, erythema nodosum-like cutaneous rash, HLA-A26 positivity, and characteristic retinal vasculitis—the diagnosis of incomplete Bechet’s disease was established. Adalimumab (ADA), a tumor necrosis factor (TNF) inhibitor, was initiated as steroid-sparing therapy following screening for latent or active infection. Following ADA initiation, ME gradually improved, allowing successful tapering of PSL to 2 mg/day, resulting in sustained clinical remission of ocular inflammation.\\n\\nEight months after ADA initiation, the patient developed systemic symptoms of general malaise. Repeat peripheral blood testing revealed a positive T-SPOT.TB result. Chest X-ray and computed tomography (CT) demonstrated bilateral pulmonary granular shadows, leading to a diagnosis of miliary tuberculosis (TB). ADA and PSL were immediately discontinued due to the risk of exacerbating TB. A standard 4-drug regimen for miliary TB was commenced: isonia"}
{"row_index": 39, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 70-year-old Japanese woman had sudden, very bad neck pain that made her unable to move her neck at all. She had a fever of about 37.5°C and couldn’t turn her head. X-rays and scans showed a hard, yellow substance in her neck, like a small piece of old stone, between two bones (C5 and C6). The scan showed fluid inside this yellow part, and it looked like thick, yellow goo. Doctors found tiny crystals in the fluid that are linked to a condition called pseudogout, which affects the yellow ligament. This caused the pain and the swelling. She had surgery to remove the bad part and the fluid. After the surgery, her pain went away, and she never had another bad neck pain again. Now, 7 years later, she’s completely pain-free and has no nerve problems.\"\n}"}
{"row_index": 40, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 70-year-old Japanese woman developed sudden, severe neck pain that made it impossible for her to move her neck. She had a mild fever (37.5°C) and was experiencing intense pain, with her pain level rated at 100 out of 100. X-rays showed calcification between the C5 and C6 vertebrae, and MRI scans revealed a yellow fluid collection in the yellow ligament — a band of tissue in the neck. The fluid was cloudy and yellow, and under a microscope, it was found to contain calcium pyrophosphate dihydrate crystals, which are linked to a condition called pseudogout. This condition causes inflammation in the ligament, leading to severe pain and neck stiffness. The MRI also showed compression of the spinal cord, which is why surgery was needed. She underwent surgery to remove the affected yellow ligament and relieve pressure on the spinal cord. After the procedure, her pain improved, lab tests returned to normal, and she eventually had full relief of neck pain with no further issues, even 7 years later.\"\n}"}
{"row_index": 41, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 70-year-old Japanese woman presented with a 14-day history of progressive neck pain prior to hospital admission. She had no history of tuberculosis, recent head or neck trauma, or diabetes mellitus. Initial physical examination revealed mild limitation of neck motion without neurological deficits, including preserved motor strength, sensory function, and normal deep tendon reflexes. Plain lateral radiography demonstrated calcification within the interlaminar space at the C5-C6 level, consistent with yellow ligament calcification. Magnetic resonance imaging (MRI) revealed a low-signal lesion on both T1-weighted and T2-weighted sequences, with surrounding intermediate signal intensity on T1WI and high signal intensity on T2WI, accompanied by cord compression—findings suggestive of either a pseudogout attack or an epidural abscess. Her neck pain was initially managed with nonsteroidal anti-inflammatory drugs (NSAIDs), resulting in gradual improvement. However, two months later, her symptoms recurred with a moderately elevated fever (37.5 °C), severe neck pain preventing any range of motion, and a visual analog scale (VAS) pain score of 100 mm. Laboratory investigations showed a white blood cell count of 7800/mm³ (within normal range: 3500–9300/mm³) and markedly elevated C-reactive protein (5.13 mg/dL, normal: 0–0.3 mg/dL), indicating acute inflammation. Computed tomography (CT) confirmed a high-density area between the C5 and C6 laminae, consistent with calcification of the yellow ligament. Repeat MRI demonstrated persistent T1- and T2-low signal central region with surrounding intermediate and high signal intensity, confirming ongoing inflammatory or crystalline process with spinal cord compression. Despite continued NSAID therapy, pain remained uncontrolled. Surgical intervention was performed two weeks after the second admission, consisting of C6 laminectomy and resection of the C5-C6 yellow ligament. Intraoperative findings included a turbid, yellow fluid collection within the yellow ligament, visible calcifications, and dural adhesions to the ligament. Histopathological analysis of the fluid revealed calcium pyrophosphate dihydrate (CPPD) crystals, confirming the diagnosis of pseudogout (calcium pyrophosphate deposition disease) involving the yellow ligament. Postoperatively, her clinical course was uneventful; pain"}
{"row_index": 42, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 68-year-old woman had heart problems for a long time. Her heart couldn’t pump blood well, and doctors found a buildup of protein in her heart muscle called amyloidosis. After 3 years, she got a small device in her chest to help her heart beat better. For 7 years, she stayed quiet, but then at age 78, she started having shortness of breath and her heart was much bigger than normal. A scan showed a big lump in her liver and a tumor that had spread from the liver through blood vessels all the way to her heart’s upper chamber. This tumor was diagnosed as liver cancer (hepatocellular carcinoma). Her blood test showed very high levels of a cancer marker. Even though she was on medicine to prevent blood clots, her body still had clots for months. The cancer in her liver and the blood clot were likely what made her heart problems worse. Her symptoms got better with medicine that helps remove extra fluid from her body.\"\n}"}
{"row_index": 43, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old woman was first admitted to the hospital with heart failure caused by a type of protein buildup in her heart called AL type primary cardiac amyloidosis. After three years, she had a device implanted to help her heart beat more effectively — this is called cardiac resynchronization therapy (CRT). The device was used because her heart was not pumping well, with a left ventricular ejection fraction of only 34%, and she had severe heart failure symptoms (NYHA class III). She remained stable for seven years after the device was implanted. At age 78, she returned with worsening heart failure symptoms, including shortness of breath and an enlarged heart seen on chest X-ray. An ultrasound and CT scan revealed a large tumor in her liver — specifically, hepatocellular carcinoma (HCC) — and a tumor that had spread from the liver through blood vessels into her heart, filling the right atrium. The tumor was confirmed with a contrast CT, and her alpha-fetoprotein level was extremely high, which is a sign of liver cancer. Even though she was on blood-thinning medication, her blood had been abnormally clotting for more than six months before her symptoms returned. Her heart failure symptoms improved with standard diuretics. Doctors believe the tumor and its spread caused the heart problems in this case. The patient’s specialty care was in cardiology.\"\n}"}
{"row_index": 44, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old female was initially admitted to the hospital due to symptomatic heart failure, which was ultimately diagnosed as AL type primary cardiac amyloidosis, confirmed by endomyocardial biopsy. Following a 3-year period of clinical follow-up, she underwent implantation of a cardiac resynchronization therapy (CRT) device for biventricular pacing, due to recurrent heart failure episodes (New York Heart Association class III), a left ventricular ejection fraction of 34%, and a wide QRS complex of 143 ms indicative of complete left bundle branch block. She remained clinically stable for seven years post-implantation. At age 78, she presented with a recurrence of heart failure symptoms, including progressive shortness of breath, physical examination findings consistent with decompensated heart failure, and significant cardiomegaly evidenced by an extended cardiothoracic ratio of 74% on chest radiography. Echocardiographic evaluation revealed a large echogenic mass occupying the right atrium. Sixty-four multi-detector computed tomography (CT) imaging demonstrated a lobulated, heterogeneously enhancing mass in the right upper lobe of the liver, consistent with hepatocellular carcinoma (HCC), and a continuous tumor thrombus extending from the portal vein and hepatic vein through the inferior vena cava to the right atrium. Alpha-fetoprotein levels were markedly elevated at >20,000 ng/mL (reference range: 0.0–10.0 ng/mL), supporting the diagnosis of HCC. The presence of persistent hypercoagulability was documented for more than six months prior to the clinical deterioration, despite concomitant anticoagulant therapy, suggesting a prothrombotic state that likely contributed to the formation and propagation of the tumor thrombus. The extensive tumor thrombus was deemed the primary hemodynamic contributor to the decompensated heart failure, leading to impaired cardiac filling and outflow. The patient's symptoms were initially managed with standard diuretic therapy, which provided partial relief. This case illustrates a rare and severe complication in which advanced hepatocellular carcinoma with portal and hepatic venous invasion leads to systemic venous obstruction and right-sided heart dysfunction, likely mediated by both tumor-induced thrombosis and chronic hemodynamic stress in the context of pre-existing cardiac amyloidosis and CRT device use. The interplay between cardiac amyloidosis, chronic left"}
{"row_index": 45, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 80-year-old woman had a liver problem from hepatitis C, which caused scar tissue in her liver and a cancer in her liver (HCC). She had a small tumor treated with a procedure called RFA in two sessions, one 25 months ago and another 3 months later. A year before she got sick, a scan showed no signs of cancer or a hole in her diaphragm. Then, suddenly, she had a sharp pain in her belly. A chest X-ray showed part of her small intestine stuck in her chest. Doctors found that the intestine was trapped and not getting enough blood — this is called a strangulated diaphragmatic hernia. The hole where the intestine slipped through was about 2 cm wide. The doctors did emergency surgery to push the intestine back, cut out the damaged part, and fixed the hole with strong, dissolvable stitches. She recovered well and was out of the hospital in 10 days. Five months after surgery, no signs of the hole coming back were found.\"\n}"}
{"row_index": 46, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 80-year-old woman with liver damage from hepatitis C and a history of liver cancer (HCC) was admitted to the hospital with sudden, severe pain in her upper abdomen. She had previously received radiofrequency ablation (RFA) treatment for HCC in segments 6 and 7 of her liver, a procedure that uses heat to destroy cancer cells. Twenty-two months before her admission, she had a second RFA session. A follow-up CT scan done a month before admission showed no signs of cancer or a diaphragmatic hernia (DH). However, on the day of admission, she developed intense abdominal pain, and a chest X-ray showed gas in the chest area, suggesting the small intestine had pushed through the diaphragm into the chest. Emergency laparoscopic surgery was performed. The surgery found that the small intestine had herniated through a hole in the diaphragm, and part of it was damaged due to lack of blood supply (ischaemic). The damaged section was removed, and the hole was closed with absorbable stitches. The patient recovered well and was discharged on day 10. At her 15-month follow-up, no signs of hernia recurrence were found.\"\n}"}
{"row_index": 47, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 80-year-old woman with a history of hepatitis C-induced liver cirrhosis and hepatocellular carcinoma (HCC) involving segment 6 of the liver was admitted due to acute, sudden-onset epigastric pain. Prior to admission, she had undergone two ultrasonography-guided percutaneous radiofrequency ablation (RFA) procedures using the LeVeen Super Slim 3.0 device (Boston Scientific, Marlborough, Massachusetts, US). The first RFA session, performed 25 months earlier, targeted HCC in segment 6 and lasted 114 minutes, without the use of artificial pleural effusion or ascites. Three months later, a second RFA procedure was conducted for recurrent HCC in segment 6/7, again using the same device, this time with artificial pleural effusion, and lasted 125 minutes. A follow-up contrast-enhanced computed tomography (CT) scan performed one month prior to admission (21 months after the second RFA) showed no evidence of HCC recurrence or diaphragmatic hernia (DH). No history of trauma was present. On the day of presentation, she experienced acute, severe epigastric pain and was evaluated by her family physician. Chest radiography revealed a massive accumulation of intestinal gas above the right lobe of the liver, suggestive of intestinal herniation. She was transferred to our institution for further assessment. Vital signs at admission were stable: blood pressure 100/70 mmHg, pulse 80 beats per minute, and oxygen saturation 94% on room air. Physical examination revealed mild umbilical tenderness without signs of peritoneal irritation or trauma. Laboratory studies, including white blood cell count and C-reactive protein, were within normal limits. Hepatic function was impaired, with Child–Pugh Class B classification, mild hypoalbuminemia (3.2 g/dL), and a significantly prolonged prothrombin time (63% increase above baseline). Contrast-enhanced CT imaging demonstrated herniation of the small intestine into the right thoracic cavity, with congestion and haziness of the surrounding mesenteric fat, indicating ischemic changes; however, no evidence of bowel perforation was observed. Emergency laparoscopic surgery was performed under general anesthesia in the supine position using the open Hasson technique. A 12-mm port was placed above the umbilicus, followed"}
{"row_index": 48, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 41-year-old man had long-term joint pain from rheumatoid arthritis, which he didn’t properly treat for a year. His body started showing signs of damage — red, non-blanching rashes on his legs and fingers, swelling, and lots of protein in his urine. Doctors found a kidney problem called membranous nephropathy, where tiny blood clots formed in the kidney’s filters. Even after stopping pain medicines and arthritis drugs, the protein in his urine stayed high. He also developed blood vessel inflammation (vasculitis) and lung disease (sarcoidosis), both of which improved with steroids. But the kidney problem only got better a little, not fully. He tried a special medicine called Rituximab, which helped at first, but the protein in his urine slowly went back up. His skin and joint issues completely went away after starting strong steroids, but the kidney problem still isn’t fully fixed. His blood tests show he still has cryoglobulins, meaning the problem is ongoing.\"\n}"}
{"row_index": 49, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 41-year-old man with chronic rheumatoid arthritis had worsening symptoms, including skin rashes, swelling in his legs, and high protein in his urine, leading to a diagnosis of nephrotic syndrome. A kidney biopsy showed membranous nephropathy with blood clots inside the kidney's tiny blood vessels (intracapillary thrombi), which is linked to his autoimmune condition. Despite stopping his usual arthritis medications like NSAIDs and DMARDs, his proteinuria did not improve. He also developed cryoglobulinemic vasculitis and pulmonary sarcoidosis, both of which improved with high-dose steroids. Rituximab, a drug used to reduce immune system activity, helped reduce proteinuria initially, but only partially. After restarting the treatment, proteinuria gradually returned to higher levels, showing only partial response. His skin and joint symptoms fully resolved with treatment, but the underlying kidney issue remained difficult to fully control. His cryoglobulin levels stayed positive, suggesting ongoing immune system problems.\"\n}"}
{"row_index": 50, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 41-year-old Hispanic man with a 2-year history of rheumatoid arthritis (RA) and type 2 diabetes mellitus presented to the emergency department with newly developed bilateral lower extremity purpuric rash and edema following a 1-year period of lost follow-up. RA was initially diagnosed two years prior, characterized by polyarthritis and markedly elevated serum immunologic markers: rheumatoid factor titer of 1220 IU/ml (normal <20 IU/ml) and anti-cyclic citrullinated peptide (anti-CCP) titer of 240.05 U/ml (normal <20 U/ml; strongly positive >60 U/ml). Prior therapy with methotrexate, low-dose prednisone, and sulfasalazine achieved disease control, but the patient discontinued DMARDs and was intermittently managed with ibuprofen 800 mg every 8 hours for joint pain for approximately one month.\\n\\nOn admission (day 0), physical examination revealed non-tender, non-blanching purpuric macules coalescing into large patches on the left leg, with smaller lesions on the right, in a dependent, flexor-surface distribution. Polyarticular arthritis was present with pain and swelling in the right 2nd and 3rd metacarpophalangeal (MCP) joints and left 3rd MCP joint. Boutonniere deformities were observed bilaterally, with greater severity on the left. Subcutaneous nodules were present at the elbows. Significant pitting edema was noted in the lower extremities. Urinalysis showed 21 red blood cells/high power field (hpf) and 7 white blood cells/hpf. Creatinine was 0.9 mg/dL, with an estimated glomerular filtration rate (eGFR) of 93 mL/min by the MDRD equation. Nephrotic syndrome was diagnosed based on proteinuria of 11 g/gm, hypoalbuminemia (2.2 g/dL), and peripheral edema.\\n\\nSerologic evaluation revealed low complement levels: C3 (86, normal 88–201), C4 (24, normal 16–47), positive cryoglobulin qualitative test (<1% cryocrit), and negative c-ANCA, p-ANCA,"}
{"row_index": 51, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 79-year-old woman had a small hole in her heart’s left side that was still letting blood leak after surgery. Doctors used a tiny device (WATCHMAN) to close it. The device fit perfectly, stayed in place, and sealed the hole well. There was just 1.4 mm of tiny leak left, which is very small. After the procedure, she kept taking two pills: aspirin and apixaban. Six weeks later, the leak was still very small (1.49 mm) and there was no blood clot. So, her doctors stopped the apixaban pill and switched her to taking aspirin and another pill called clopidogrel. She hasn’t had any more bleeding, and they plan to stop the clopidogrel in 6 months, but she will keep taking aspirin forever.\"\n}"}
{"row_index": 52, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 79-year-old woman had a procedure to close off a small pocket in her left atrium (LAA) using a device called the WATCHMAN™. She had previously had surgery to fix her heart valves and had been on blood thinners because of a high risk of stroke, but she had trouble with bleeding in her stomach due to diverticulosis. Before the procedure, her heart was stable and her kidneys were working well, though she had mild anemia. During the procedure, imaging showed that the LAA was still open, with only 1.4 mm of leak (PDL), and the device was placed successfully, meeting all key safety and placement standards. After the procedure, she continued on apixaban and aspirin. At 6 weeks, a follow-up scan showed the leak had slightly increased to 1.49 mm but no blood clots were found. Her doctors decided to stop apixaban and switch her to aspirin and clopidogrel instead. She has not had any major bleeding since, and her team plans to stop clopidogrel after 6 months, while continuing aspirin forever.\"\n}"}
{"row_index": 53, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 79-year-old Black female with a history of mitral regurgitation, tricuspid regurgitation, and persistent atrial fibrillation complicated by recurrent significant gastrointestinal hemorrhage on anticoagulation due to diverticulosis was referred for percutaneous left atrial appendage occlusion (LAAO). Five months prior, she underwent surgical mitral and tricuspid valve repair, along with LAA ligation using a 35 mm AtriClip, driven by a high stroke risk (CHA2DS2-VASc score of 5) and intolerance to oral anticoagulation. Pre-procedural evaluation revealed a hemodynamically stable patient with regular heart rate and irregular rhythm, normal renal function (serum creatinine 0.81 mg/dL), and mild anemia (hemoglobin 10.8 g/dL, reference range 12.0–15.0 g/dL). Intra-procedural transesophageal echocardiography (TEE) confirmed complete closure of the left atrial appendage at the time of surgery. However, 40-day follow-up TEE and cardiac computed tomography (CT) demonstrated a persistent anatomic communication between the left atrium and the left atrial appendage, with no evidence of thrombus formation, indicating incomplete occlusion. Given this finding, a percutaneous LAAO device was considered to achieve definitive occlusion of the residual LAA pouch. Trans-septal puncture was performed under fluoroscopic and TEE guidance, with intracardiac ultrasound confirming mid-septal access. Intra-procedural TEE was utilized for precise LAA sizing, leading to the selection and deployment of a 27 mm WATCHMAN™ device. Deployment was successful, with all P.A.S.S. (Position, Anchor, Size, and Seal) criteria met. The residual patent left atrial appendage (PDL) measured 1.4 mm at the time of device placement. Post-procedural management included apixaban 5 mg twice daily and aspirin 81 mg daily. At 6-week follow-up TEE, a trivial PDL of 1.9 mm was identified along the posterior aspect of the appendage, with no detectable thrombus. The anticoagulation regimen was adjusted to"}
{"row_index": 54, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man in his 40s had a swollen belly and belly pain for months. His doctor couldn't find the cause at first, even after checking for cancer or liver problems. Tests showed no signs of infection or cancer, but later, his belly fluid had high levels of a substance linked to tuberculosis. When the doctor looked inside his belly with a small camera, they found a thick, fibrous layer wrapping around his small intestine, full of old infection signs. Biopsy samples proved it was tuberculosis, not cancer. After starting medicine to fight the TB, the swelling went down a lot and he started feeling better. He’s been back to normal for years with no more problems.\"\n}"}
{"row_index": 55, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 47-year-old man had a 3-month history of abdominal swelling, pain, and nausea. Even though he lost some weight, he didn’t have fever, cough, or night sweats. He had no history of liver disease or abdominal surgery, but had had tuberculous pleurisy about 20 years earlier. Tests showed no signs of cancer, infection, or liver problems, and imaging didn’t show obvious causes. His abdominal fluid was clear and contained no bacteria or cancer cells. After two months, his symptoms worsened, with more fatigue, weight loss, and increased abdominal swelling. New tests showed higher levels of markers linked to infection and inflammation. Imaging revealed a thick membrane covering his small intestine and small nodules in the abdominal lining, which raised concern for either cancer or tuberculosis. A laparoscopy was done and found a dense fibrous membrane wrapping the small bowel, with small nodules that tested positive for tuberculosis. Biopsies confirmed tuberculous infection. The surgery tried to remove the membrane and release the trapped bowel, but it was very difficult due to the thick, fibrous tissue. The patient was then treated with anti-tuberculosis medication for six months. After treatment, his abdominal fluid greatly decreased, his symptoms improved, and he returned to normal function. He has remained symptom-free for six years without needing further surgery.\"\n}"}
{"row_index": 56, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 47-year-old male presented with a three-month history of progressive abdominal distension, intermittent abdominal pain, and nausea, despite a 4 kg weight loss. He reported no fever, chronic cough, or night sweats, and had no prior history of abdominal surgery, liver cirrhosis, or chronic hepatitis virus infection. Notably, he had a history of tuberculous pleurisy approximately 20 years earlier. Physical examination revealed gross abdominal distension with ascitic fluid of unknown etiology, but no tenderness. Laboratory evaluation, including serum tumor markers, erythrocyte sedimentation rate (ESR), adenosine deaminase (ADA) activity, and anti-tuberculosis antibody (TB-Ab), was within normal limits. The tuberculin skin test was negative, and HIV serology was negative. Chest radiography showed no evidence of pulmonary tuberculosis. Plain upright abdominal X-ray demonstrated colonic air without air-fluid levels or free intraperitoneal gas, suggesting a non-obstructive fluid collection. Contrast-enhanced computed tomography (CT) of the abdomen revealed duodenal dilatation and congestion of small bowel loops trapped within a large volume of ascitic fluid, surrounded by a dense, fibrous membrane. Gastroscopy excluded gastrointestinal malignancy. Two paracenteses were performed, yielding blood-stained ascitic fluid without detection of malignant cells, acid-fast bacilli (AFB), or tuberculosis organisms. The ascitic fluid was classified as exudative, with ADA levels within the normal range (4–18 U/L), consistent with a non-infectious or non-tuberculous exudate. The patient declined laparoscopy and was discharged without a definitive diagnosis.\\n\\nTwo months later, the patient returned with worsening symptoms, including increased fatigue, emaciation, and a 10-kg weight loss over the prior two months. Repeat laboratory testing revealed elevated serum ADA (21 U/L, above the normal range of 4–18 U/L), elevated ESR (28 mm/h, normal 0–15 mm/h), and negative TB-Ab. Paracentesis fluid remained negative for bacteria, AFB, and malignant cells, but ascitic ADA increased significantly to 41 U/L, supporting an infectious etiology. Serum CA-125 was markedly elevated (97.39 U/mL, normal <35 U/mL), suggesting per"}
{"row_index": 57, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 45-year-old man had high blood sugar for six months and was hospitalized. Tests showed a big tumor in his abdomen, but his blood pressure was normal. Doctors found the tumor was benign (not cancer), and they removed it using a small surgery (laparoscopy) with no major problems. After surgery, his hormone levels (which were high before) went back to normal, but his blood sugar stayed high. Tests on the tumor’s genes showed no changes that would mean it was cancerous. He’s doing well now, but his sugar level still needs attention.\"\n}"}
{"row_index": 58, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 45-year-old man was hospitalized due to high blood sugar (hyperglycemia). He didn't have symptoms like headaches, high blood pressure, or heart palpitations. Tests showed his blood pressure was normal, but his serum and urine had high levels of catecholamines, which are chemicals linked to certain tumors. An abdominal CT scan found a 7.2 × 6.5 cm mass in the right area near the aorta, and the adrenal glands were normal. This led to a diagnosis of a large paraganglioma (PGL), a type of tumor that can cause high sugar levels. Because of financial reasons and lack of equipment, he didn't get a MIBG scan, which is often used to confirm such tumors. He was then treated with laparoscopic surgery — a minimally invasive procedure — where the tumor was safely removed. During surgery, his blood pressure stayed stable, and the procedure took 120 minutes with only about 50 mL of blood loss. He recovered well and was discharged on day 5. Pathology confirmed the tumor was benign, and DNA tests for SDHB and SDHD genes showed no mutations. Six months after surgery, his catecholamine levels returned to normal, but his blood sugar remained high, suggesting that the cause of his high sugar levels is still not fully explained.\"\n}"}
{"row_index": 59, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 45-year-old male presented with a six-month history of hyperglycemia. He denied symptoms of episodic headache, hypertension, palpitations, or diaphoresis. Initial evaluation included 24-hour electrocardiographic monitoring and serial blood pressure measurements, both of which remained within normal limits. Glycemic control was achieved with insulin therapy, with serum glucose levels returning to baseline. Laboratory investigations were otherwise unremarkable, except for elevated serum and urinary catecholamine levels, suggesting possible pheochromocytoma or paraganglioma (PGL). Abdominal-pelvic computed tomography (CT) with contrast revealed a 7.2 × 6.5 cm inhomogeneous mass in the right para-aortic region, at the level of the inferior mesenteric artery, with no evidence of adrenal parenchymal involvement. This finding supported a diagnosis of paraganglioma, specifically a large para-aortic paraganglioma (POZ). Despite the absence of hypertension or autonomic symptoms, the elevated catecholamines indicated a functional tumor. Preoperative management included intravascular volume expansion and alpha-adrenergic blockade with phenoxybenzamine for two weeks, even in the absence of elevated blood pressure, to mitigate potential intraoperative catecholamine surges. Given the tumor's size, location, and potential for vascular involvement, a comprehensive surgical strategy was implemented, with full contingency planning for conversion to open surgery in the event of acute hemorrhage, limited operative field, malignant tumor invasion, or vascular injury. A laparoscopic approach was adopted, with the patient positioned in 70° left lateral decubitus. Trocars were placed at the umbilicus (10 mm), right costal margin (10 mm), right anterior axillary line (10 mm), and subxiphoid (5 mm). A steep Trendelenburg position was utilized to displace the small bowel and omentum away from the mass. Dissection began with ultrasonic shearing of the hepatic triangular ligament and hepatocolic ligament to mobilize the liver and expose the upper pole of the right kidney. The ascending mesocolon was longitudinally incised and expanded to visualize the right kidney and renal vein, with the descending and horizontal duodenal segments separated to expose the tumor's vascular supply. The tumor was found to be well-encapsulated"}
{"row_index": 60, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old boy from Syria came to the hospital because he was bleeding from his nose, not eating, losing weight, and sweating at night. When doctors checked him, they found swollen lymph nodes in the neck and under the jaw. There was also a lump on the roof of his mouth that pushed his uvula to one side, making it hard for him to swallow and breathe. Blood tests showed high white blood cells and a very high inflammation level. An ultrasound showed a slightly enlarged spleen, and chest X-ray was normal. A CT scan found many swollen lymph nodes on the right side of his neck. A small piece of tissue from a neck lump was taken and tested. At first, doctors thought it was a type of cancer called Classical Hodgkin Lymphoma. But later, tests showed it was actually a different kind of cancer — ALK-negative Anaplastic Large Cell Lymphoma — because the cancer cells had certain markers that matched this type. The boy got chemotherapy, but after 5 months, his condition didn’t improve, so doctors retested. The new test confirmed the cancer type. He got 5 rounds of chemo, but sadly, he passed away six months later.\"\n}"}
{"row_index": 61, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 12-year-old Syrian boy was admitted to the hospital with bleeding from the nose (epistaxis), loss of appetite, weight loss, and night sweats. On exam, doctors found enlarged lymph nodes in the neck and under the jaw, with one node about 3 to 5 cm in size. A mass on the hard palate pushed the uvula to the right, causing trouble swallowing and breathing. Blood tests showed high white blood cells and elevated inflammation markers. An ultrasound showed a slightly enlarged spleen, and chest X-ray was normal. A CT scan found multiple enlarged lymph nodes on the right side of the neck. A biopsy of one of the lymph nodes showed abnormal cells that looked like Reed-Sternberg cells, leading to a preliminary diagnosis of Classical Hodgkin Lymphoma. However, because the lab tests needed to confirm the diagnosis were not available at the time, the exact type could not be confirmed. The boy started chemotherapy with the ABVD protocol, but after five months, there was no improvement, so the diagnosis was questioned. Later, immunohistochemistry tests confirmed the presence of CD30 and CD3 positive cells, but no ALK, CD15, or CD20, which led to the final diagnosis of ALK-negative Anaplastic Large Cell Lymphoma (ALCL). He received five cycles of chemotherapy, but unfortunately passed away six months after starting treatment.\"\n}"}
{"row_index": 62, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 12-year-old Syrian boy was admitted to our hospital with symptoms of epistaxis, anorexia, weight loss, and night sweats. Medical and family history were unremarkable. Physical examination revealed preauricular, postauricular, and submandibular lymphadenopathy, with the largest node measuring approximately 3 × 5 cm. A hard palate mass was identified, deviating the uvula to the right, resulting in dysphagia and dyspnea. Laboratory findings included a white blood cell count of 35,380/μL, hemoglobin of 10.1 g/dL, platelets of 641 × 10³/μL, and an erythrocyte sedimentation rate (ESR) of 124 mm/hr, indicating systemic inflammation. Abdominal ultrasound demonstrated mild splenomegaly without focal lesions. Chest radiography was normal, with no mediastinal widening. A computed tomography (CT) scan revealed multiple enlarged lymph nodes on the right side of the neck. An excisional biopsy of a cervical lymph node (3 × 4 cm) was performed. Histopathological examination showed complete effacement of lymph node architecture, with proliferation of medium to large-sized anaplastic cells resembling Reed-Sternberg cells located in the interfollicular zones and subcapsular sinuses, admixed with histiocytes, small lymphocytes, and sparse eosinophils. The neoplastic cells exhibited a cohesive growth pattern, abundant cytoplasm, wreath-like or multiple nuclei, multiple nucleoli, and occasional mitotic figures, consistent with a large B-cell lymphoma. Bone marrow aspiration revealed hypercellularity with reactive inflammatory changes, but no evidence of neoplastic infiltration was detected. Based on routine histological staining, the initial diagnosis was Classical Hodgkin Lymphoma (CHL), with a recommendation for immunohistochemical confirmation. At the time, immunohistochemistry was not available at our institution. The patient was initiated on ABVD chemotherapy (doxorubicin, bleomycin, vinblastine, and dacarbazine). Five months later, the patient presented with no clinical improvement, prompting a re-evaluation of the diagnosis. Immunohistochemical analysis confirmed strong CD30 positivity in large Reed-Sternberg-like cells and CD3 positivity, while ALK, CD15, and CD20"}
{"row_index": 63, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 6-year-old boy was brought to the emergency room because he suddenly couldn’t breathe after eating popcorn. At first, he was okay, but then he started coughing and had trouble breathing. He became very tired and hard to wake up. Doctors saw no blockage in his throat, but one side of his lung wasn’t working. A small bubble of air showed up under his skin on the right neck, which meant something was wrong with his breathing.\\n\\nHe was put to sleep with medicine to help him breathe, and a tube was put into his windpipe. A chest X-ray showed that air was trapped on the left side, and a small piece of popcorn was stuck in the main airway. Doctors knew it had to be removed right away.\\n\\nThey went into the operating room and used a special tool to look inside his airway. They found a piece of popcorn stuck in the trachea, right at the main split of the airway. They also saw a rare extra airway on the right side — it’s not normal, but it’s part of his body now.\\n\\nThe popcorn was safely taken out using a small tool. After that, the airway cleared up, and his breathing improved. He stayed in the hospital for a day, got medicine to help his airway heal, and was able to play and eat normally. He went home the next day feeling fine, with no more breathing problems.\"\n}"}
{"row_index": 64, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 6-year-old boy who had no prior medical or surgical issues was brought to the Emergency Department with severe shortness of breath after accidentally swallowing a piece of popcorn. At first, his oxygen levels were okay, but soon he became very distressed and could not breathe properly. He was quickly intubated (a tube placed into his airway) and taken to the operating room for a procedure called direct laryngobronchoscopy, which allows doctors to see the airway and remove a foreign object.\\n\\nDuring the procedure, the doctors found a piece of popcorn stuck in the trachea (the main airway), blocking airflow. They successfully removed it using special tools. While doing this, they also discovered that the boy had a rare condition called a tracheal bronchus — a small extra airway that connects the trachea to a bronchus, which can sometimes cause breathing problems.\\n\\nAfter the foreign body was removed, the boy’s breathing improved, and his oxygen levels stabilized. He was moved to the pediatric intensive care unit (PICU) and stayed there until he was fully awake and able to breathe on his own. He was given medicine to reduce airway swelling and was able to eat and play normally. He was discharged the next day in good health with no further treatment needed.\"\n}"}
{"row_index": 65, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 6-year-old male, medically and surgically free, with a body weight of 22 kg and height of 122 cm, was admitted to the emergency department (ED) by his teacher following sudden onset of severe shortness of breath after ingestion of popcorn. The clinical presentation began with acute respiratory distress, characterized by agitation, drowsiness, and semi-consciousness. Physical examination revealed no overt upper airway obstruction, but auscultation demonstrated absent air entry in the left lung, with subcutaneous emphysema noted on the right neck. Oxygen saturation remained stable with supplemental oxygen.\\n\\nShortly thereafter, the patient experienced a rapid deterioration in respiratory status and was intubated using a combination of midazolam, ketamine, and succinylcholine. Post-intubation chest radiography revealed proper endotracheal tube (ETT) placement, a hyperlucent left hemithorax, flattening of the left hemidiaphragm, rightward mediastinal shift, and a radiopaque lesion within the left main bronchus. Auscultation post-intubation showed minimal airflow in the left lung, with intermittent desaturation episodes.\\n\\nOtolaryngology–Head and Neck Surgery was consulted for urgent direct laryngoscopy and bronchoscopy (DLB). After stabilization, the patient was transferred to the operating room for DLB and foreign body removal, with informed consent obtained for potential complications including hemorrhage, infection, failure of foreign body extraction, pneumothorax, and dental injury.\\n\\nIn the operating room, the patient was intubated via bag-mask ventilation. Bilateral air entry was diminished, with scattered wheezing; significant chest wall expansion was observed on the left side, indicating impaired ventilation. Initial end-tidal CO₂ was 104 mm Hg. Arterial blood gas analysis revealed a pH of 6.87, PaCO₂ of 181 mm Hg (indicating severe respiratory acidosis), and PaO₂ of 231 mm Hg (mild hypoxemia).\\n\\nGeneral anesthesia was maintained with continuous propofol infusion at 250 mcg/kg/min and dexmedetomidine at 1 mcg/kg/hr. A single dose of dexamethasone (0.5 mg/kg"}
{"row_index": 66, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 37-year-old woman started feeling weak in her hands about 5 years ago, first in her left hand, then later in her right. The weakness got worse over time, making it hard to write, hold chopsticks, or make a fist. By the time she came to the hospital, her hands were very weak and had shriveled. She didn’t get proper care before this. Tests showed that her hands were weak, but her sense of touch and thinking were normal. The nerves in her arms were damaged, especially the ones that control hand movement, and the damage was seen in the median, ulnar, and radial nerves. There was no damage to her nerves that carry feeling. She also has a condition called Hashimoto’s thyroiditis, which means her body is attacking its own thyroid gland. Even though her thyroid hormones were normal, the antibodies were high, showing the immune system is active. She was treated with medicine that helps calm the immune system, and after a month, her hand strength improved a lot. She will keep coming back for check-ups.\"\n}"}
{"row_index": 67, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 37-year-old woman came to our hospital complaining of weakness in both hands. Five years ago, she first noticed mild weakness in her left hand, which slowly got worse. Two years later, her right hand also started to weaken. The weakness gradually progressed, making it hard for her to write, use chopsticks, or make a fist. She visited local clinics but wasn't properly evaluated. When she came to our hospital, her hands were severely weak and had noticeable muscle shrinkage, but she had no numbness or pain. Her mental abilities and brain function were normal, and there were no signs of problems in her face, eyes, or neck.\\n\\nNeurological tests showed severe weakness in the muscles of her hands, especially in the fingers and wrist areas, with poor muscle strength and visible muscle wasting. Her legs were not affected. Her reflexes in her arms were reduced, but her sense of touch and other sensory functions were normal.\\n\\nLab tests showed that her thyroid function (levels of hormones) was normal, but her immune system was active against the thyroid, which led to a diagnosis of Hashimoto's thyroiditis — a common autoimmune condition where the body attacks its own thyroid gland.\\n\\nElectrical tests of her nerves (nerve conduction studies) showed a specific pattern of weakness in the nerves that control hand movement, particularly in the median, ulnar, and radial nerves. This pattern is typical of a condition called Miller-Fisher-like neuropathy (MMN), which affects motor nerves without affecting sensation. Even though she didn’t have antibodies to certain nerve-related proteins, the clinical signs and test results clearly supported the diagnosis of MMN.\\n\\nA thyroid biopsy confirmed the presence of Hashimoto's thyroiditis. She was treated with high-dose intravenous immunoglobulin for five days, and one month later, her hand weakness and muscle deformities had improved significantly, with better nerve function. She is now being followed up regularly at our outpatient clinic.\"\n}"}
{"row_index": 68, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 37-year-old woman presented with progressive distal upper-limb weakness, initially noted in the left hand five years prior with insidious onset, followed by symmetric progression to the right hand two years later. The weakness evolved gradually, impairing fine motor functions such as writing, chopstick handling, and fist formation. Clinical evaluation revealed severe motor weakness in both hands, with Medical Research Council (MRC) grades ranging from 2/5 to 3/5 across multiple intrinsic hand muscles, including flexor digitorum profundus and sublimis, flexor pollicis longus, extensor digitorum communis, and abductor digiti minimi, with notable muscle atrophy and distal deformities. Motor function in the lower extremities was preserved, and deep tendon reflexes were reduced in the upper limbs. Sensory examination was intact, with normal cortical sensation, cranial nerve function, cerebellar signs, and no evidence of sensory neuropathy. Neurological examination confirmed alertness, intact orientation, and absence of cognitive impairment. No abnormal findings were observed in the cervical spine on magnetic resonance imaging (MRI), which showed only mild disc protrusions at C5-6 and C6-7 levels.\\n\\nLaboratory investigations revealed normal hemogram, electrolytes, renal function, cerebrospinal fluid, and autoimmune markers for systemic vasculitides including rheumatoid factor, anti-dsDNA, lupus anticoagulant, anticardiolipin, antithrombin III, ANCA, anti-SSA/SSB, complement 3/4, anti-Jo-1, cryoglobulin, immunofixation, and anti-GM1/GD1b antibodies. A mildly elevated fluorescent antinuclear antibody titer (1:40) was detected, but no evidence of systemic autoimmune disease was found. Tumor markers (alpha-fetoprotein, carcinoembryonic antigen, CA-19-9, CA-125) and enzymatic markers (hexosaminidases A and B, creatine kinase) were within normal limits. Notably, thyroid function tests showed normal levels of T3, free T4, and TSH, but significantly elevated antithyroglobulin antibody (794 U/mL; normal: 0–100 U/mL) and antimicrosomal antibody (26,030 U/mL"}
{"row_index": 69, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man in his 60s got serious burns over 35% of his body after setting himself on fire. The burns were on his chest, arms, neck, and face. He also had smoke in his nose and throat, which meant his airway was burned. He got a bad infection in his blood, called bacteremia, and needed antibiotics to fight it. While on antibiotics, a red rash started on his chest and arms and spread fast to his hands and legs. This rash wasn’t on the burned areas, which means it didn’t start where the burns were. Doctors thought it was a reaction to the medicine, called TEN. They stopped the antibiotics and gave him a strong steroid medicine for 3 days. The rash got better after that. After a few days, the redness faded and he started feeling better. He didn’t get any new infections and was finally able to go home after 41 days in the hospital.\"\n}"}
{"row_index": 70, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old man suffered severe burns covering 35% of his body after setting himself on fire while trying to commit suicide. He had second- and third-degree burns, and his burns were so severe that he needed hospitalization. During treatment, he developed a blood infection (bacteremia) caused by a resistant bacteria, leading to antibiotic use. However, after stopping the antibiotics, a rash appeared on his trunk and arms and quickly spread to his limbs. This rash was later diagnosed as TEN (toxic epidermal necrolysis), a serious skin reaction that usually occurs outside of burn areas. The rash improved after stopping the antibiotics and starting a short course of high-dose steroid medication (methylprednisolone, 1,000 mg per day for 3 days). The skin reaction was only on non-burned parts, which suggests that TEN did not start at the burn sites. After recovery, he received several skin grafts over time and was eventually discharged from the ICU on day 41. No specific cause for the TEN was found, but the treatment was successful and he fully recovered.\"\n}"}
{"row_index": 71, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old male presented with extensive thermal burns resulting from a self-inflicted fire incident involving the application of 10 liters of gasoline to his head and body, followed by ignition on a riverbed. He had a history of insomnia and anxiety but no known allergies or smoking history. On admission, his Glasgow Coma Scale was 15, body temperature 35.8°C, heart rate 98 bpm, blood pressure 170/85 mm Hg, respiratory rate 20 bpm, and oxygen saturation 100% on 10-liter mask. Clinical examination revealed erythema and bullae involving the auricular to mandibular neck, thorax, abdomen, occiput, right upper arm, right dorsal hand, and left forearm. The anterior chest and posterior neck were covered with soot, with corresponding grayish-white skin discoloration, indicating deep dermal and epidermal destruction. Soot was also present in the nasal cavity, pharynx, and larynx, confirming upper airway burn injury. Bronchoscopy demonstrated soot adhesion, peripheral edema, and mucosal erythema from the vocal cords to the pharynx, consistent with thermal injury to the upper respiratory tract. Total body surface area (TBSA) burned was 35%, comprising 20% second-degree and 15% third-degree burns, with a revised BAUX score of 120, indicating severe burn severity. Initial wound management included daily washing with warm water, application of dimethyl isopropylazulene and gentamicin sulfate ointment, and coverage with moist wound care pads. Due to lack of guarantor consent, aggressive initial interventions such as surgical debridement and skin grafting were withheld.\\n\\nOn day 8, the patient developed a high fever (38–40°C) with a marked systemic inflammatory response, and blood culture identified methicillin-resistant *Staphylococcus aureus* (MRSA). Empirical therapy with vancomycin and ampicillin/sulbactam was initiated to manage the burn-associated infection. Once infection control was achieved, first split-thickness skin grafts (STSG) were performed on day 17 using a 0.01-inch graft harvested from both thighs via electric dermatome, meshed at a 1:3 expansion ratio. Following this,"}
{"row_index": 72, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 50-year-old man had pain in his right eye, blurry vision, headaches, and trouble walking because he was unbalanced. Doctors found a fluid-filled sac inside his brain stem that was pressing on important parts of his brain. This sac was causing the symptoms. He had surgery to fix it. A small hole was made in his skull, and a tiny camera was used to drain the fluid from the sac and create a new path for brain fluid to flow. After the surgery, the fluid-filled sac got smaller, the brain’s fluid spaces shrank, and the fluid could now move freely through the brain’s tunnels. His walking, eye problems, and headaches all got better over time. Now he walks normally and feels much better.\"\n}"}
{"row_index": 73, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 50-year-old man came in with pain in his right eye, blurry vision, headaches, and trouble walking due to balance issues. He had no numbness or weakness in his arms or legs. He also had a history of diabetes, high blood pressure, and high cholesterol.\\n\\nOn exam, he was alert and his mental status was normal. His right eye had reduced vision and he had double vision when looking to the sides. He showed slight eye shaking (nystagmus) but other brain nerve functions were normal. His strength and sensation were normal, and although his gait was slightly unsteady, he didn’t have a Romberg sign, which means his balance wasn't due to loss of coordination.\\n\\nMRI scans showed three cysts in the right part of his midbrain, totaling about 2.2 cm in size, with one large cyst measuring up to 1.7 cm. This cyst was pressing on the narrow passage (aqueduct) that carries cerebrospinal fluid, causing mild buildup of fluid in the brain ventricles (hydrocephalus).\\n\\nHe had surgery to relieve the pressure. Under general anesthesia, two small holes (burr holes) were made in his skull. One was in the right front part of the skull to access the third ventricle and create a new opening (endoscopic third ventriculostomy or ETV) to let fluid flow properly. The second hole was used to reach the brainstem cyst. Using a small camera (endoscope), the surgeon opened the cyst (fenestration) and drained its fluid, which was found to be pure cerebrospinal fluid. An external drain was placed to monitor pressure after surgery.\\n\\nAfter the procedure, the patient recovered well. His intracranial pressure stayed normal, and the drain was removed the next day. He could walk without help and perform daily tasks independently. His thinking and memory were unchanged.\\n\\nFollow-up scans showed that the brain ventricles had shrunk and fluid was now flowing through the aqueduct and the new opening. The brainstem cysts also decreased in size. By one month, his balance and double vision had improved. By five months, his headaches and double vision had almost completely gone, and imaging showed the cysts and ventricles were well decompressed.\"\n}"}
{"row_index": 74, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 50-year-old male presented to the inpatient neurosurgical service with a progressive neurological syndrome characterized by right eye pain, blurred vision, occasional diplopia, headache, and gait imbalance with frequent falls. He denied peripheral sensory deficits or motor weakness. His medical history included type II diabetes mellitus, hypertension, and hyperlipidemia, all of which may contribute to cerebrovascular and neurodegenerative risk factors. On neurological examination, he was alert and oriented to person, place, and time. He exhibited decreased visual acuity in the right eye and diplopia on extreme lateral gaze, with subtle horizontal nystagmus. Cranial nerve examination beyond the ocular motor nerves was grossly intact, and all four extremities demonstrated normal strength and sensation. The Romberg sign was negative, though his gait was mildly ataxic, consistent with cerebellar or brainstem dysfunction.\\n\\nMagnetic resonance imaging (MRI) without contrast revealed a stable cluster of three cystic lesions localized within the tegmentum of the right midbrain, measuring 2.2 cm × 1.4 cm × 1.4 cm in aggregate. The largest cyst, located dorsomedially, reached a maximum dimension of 1.7 cm and demonstrated significant compression of the adjacent cerebral aqueduct. This compression was associated with mild hydrocephalus, evidenced by distention of both the lateral and third ventricles, indicating impaired cerebrospinal fluid (CSF) dynamics and impaired flow through the aqueduct.\\n\\nThe patient underwent an endoscopic third ventriculostomy (ETV) with cyst fenestration under general anesthesia. He was secured in a Mayfield head holder and stereotactic navigation was used to guide instrument placement. Two burr holes were created: a posterior burr hole in the right frontal region near the coronal suture for ETV access, and an anterior burr hole positioned anterior to the first to provide access to the brainstem cyst and posterior third ventricle. The endoscope was introduced via the posterior burr hole into the lateral ventricle and advanced through the foramen of Monro into the third ventricle. A conventional ETV was performed in the floor of the third ventricle, anterior to the mammillary bodies, establishing a new pathway for CSF flow.\\n\\nSubsequently, the endoscope was repositioned through the anterior burr hole and advanced posterior"}
{"row_index": 75, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 69-year-old man had cancer in his left breast back in the 1990s. The tumor was big, over 6 cm, and spread to nearby lymph nodes. He had surgery to remove the breast and the lymph nodes. After surgery, he got chemotherapy, but two months later, cancer spread to his lungs. He then started treatment for the breast cancer, including pills that stop estrogen. Two years later, he started having trouble going to the bathroom often. Tests found he also had prostate cancer — a cancer in the prostate gland — with a high PSA level of 40.5. He got radiation to the prostate, and later took a medicine called Estracyt® that stayed in the prostate and helped lower the PSA. The PSA went back to normal, and he kept taking it for three years. But after five years, he got a blood clot in his leg, which happened because of the cancer medicines. Later, when he stopped breast cancer treatment, the breast cancer came back and spread to his liver. Even though he tried other medicines for the prostate cancer, the breast cancer kept getting worse and he passed away five years after getting prostate cancer. This case shows that men can get breast cancer, and they need special care for both cancers at the same time.\"\n}"}
{"row_index": 76, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 69-year-old man was diagnosed with breast cancer in the 1990s. He had a large lump in his left breast, and tests showed it was a serious type of cancer (stage IIIC). He had a mastectomy and surgery to remove lymph nodes in his armpit. After surgery, he received chemotherapy, but two months later, the cancer spread to his lungs. He then started treatment for metastatic breast cancer using anti-estrogen therapy and 5-fluorouracil. Two years later, he started having trouble with urination, and tests found that he also had prostate cancer (stage III) with a high PSA level of 40.5 ng/mL. He received radiation therapy for the prostate cancer and later started using Estracyt® to control it. His PSA levels dropped and stayed normal for a few years. However, after five years, he developed a blood clot in his leg, which was linked to the hormone treatments. When he stopped breast cancer treatment, the breast cancer returned and spread to his liver. He continued prostate cancer treatment with other medications, but he eventually died from breast cancer progression five years after his prostate cancer diagnosis. This case shows that men can get breast cancer, and when they have both breast and prostate cancer, they need careful, ongoing care from a team of specialists.\"\n}"}
{"row_index": 77, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 69-year-old male presented to the Department of Breast Surgery at Shiga General Hospital (Moriyama, Shiga, Japan) in the 1990s with a palpable lump in the left breast. Physical examination revealed a mass exceeding 6 cm in the upper-lateral quadrant, without evidence of skin invasion, and associated axillary lymphadenopathy. The patient had a comorbid history of type 2 diabetes mellitus, hypertension, cerebral infarction, and a previously managed brain schwannoma, treated with oral glimepiride 0.5 mg, nifedipine 40 mg, and aspirin 100 mg. No significant family history of cancer was reported.\\n\\nUltrasonographic evaluation confirmed a solid breast mass and right-sided axillary lymph node enlargement. Core needle biopsy demonstrated a high histological grade invasive ductal carcinoma, characterized by estrogen receptor (ER)-positive, progesterone receptor (PgR)-negative, human epidermal growth factor receptor 2 (HER2)-negative, and androgen receptor (AR)-positive status (detected using anti-AR rabbit monoclonal antibody SP107; Roche Tissue Diagnostics, Ltd.), with a Ki-67 labeling index of 10%, indicating a moderately proliferative tumor. Based on the Union for International Cancer Control (UICC) 8th edition TNM classification, the tumor was staged as cT3N3M0, stage IIIC breast cancer.\\n\\nDue to the absence of preoperative systemic therapy, the patient underwent mastectomy with axillary lymph node dissection. Final pathological assessment confirmed pt3N3a (36/39) M0, consistent with stage IIIC disease. Postoperative adjuvant chemotherapy was administered with a CEF regimen: epirubicin 40 mg/m², 5-fluorouracil (5-FU) 500 mg/m² every 2 weeks, and oral cyclophosphamide 100 mg daily. Following two cycles of chemotherapy, a computed tomography (CT) scan revealed pleural metastasis in the right lung, indicating early dissemination. The patient was then initiated on first-line endocrine therapy with high-dose toremifene (TOR) 120 mg twice daily and oral 5-FU/5’DFUR (doxif"}
{"row_index": 78, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 45-year-old woman found a lump in her thyroid during a check-up and also had a blood clot in a vein near her thyroid. She didn’t feel sick or have any symptoms. The doctor saw nothing wrong during the exam. Tests showed her thyroid levels were normal. An ultrasound found a solid lump in her left thyroid and a clot in the middle thyroid vein. A small sample taken from the lump showed some cells that were growing, but it wasn’t clear if it was cancer. The doctor decided to remove part of her thyroid, the middle piece, and the lymph nodes near the neck to be safe. After surgery, the tissue test showed a very small type of thyroid cancer, and the clot was found to be part of the cancer spreading into the vein.\"\n}"}
{"row_index": 79, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 45-year-old woman was found to have a thyroid mass and a blood clot in the middle thyroid vein during a routine physical exam. She had no symptoms and the exam showed no signs of illness. An ultrasound revealed a solid nodule in her left thyroid and a clot in the middle thyroid vein. A biopsy of the nodule showed an atypical lesion with some cells that were growing (classified as TBSRTC III), and no BRAFV600E mutation was found. Because of these findings, she had surgery, including removal of the left thyroid, part of the middle thyroid (isthmus), and nearby lymph nodes. A procedure was also done to remove the blood clot. After surgery, the pathologist found a small papillary thyroid cancer (microcarcinoma) in the left thyroid, and the clot was confirmed to be a tumor thrombus, meaning it had spread from the thyroid cancer.\"\n}"}
{"row_index": 80, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 45-year-old woman presented with a thyroid mass and thrombosis in the middle thyroid vein identified during a routine physical examination. The thyroid mass was detected three months prior to presentation, with no associated symptoms. The patient reported undergoing surgery due to psychological stress related to the discovery, despite having no prior medical history of thyroid disease or familial predisposition to thyroid carcinoma. There was no history of childhood radiation exposure. Physical examination findings were unremarkable, with no signs of thyroid enlargement, neck tenderness, or other systemic abnormalities. Laboratory evaluation of thyroid function—specifically triiodothyronine (T3), free triiodothyronine (FT3), thyroxine (T4), thyroglobulin, and thyroid-stimulating hormone (TSH)—revealed normal values, indicating euthyroidism and ruling out overt thyroid dysfunction. Ultrasound imaging demonstrated a solid nodule in the left thyroid lobe, characterized by a medially echoic lesion, and concurrently revealed a thrombotic occlusion within the middle thyroid vein. Subsequent ultrasonography-guided fine-needle aspiration biopsy yielded a cytological diagnosis of an atypical lesion of ambiguous significance (TBSRTC III), exhibiting the presence of some actively proliferating cells, consistent with a biologically aggressive but non-malignant growth pattern. Notably, the BRAFV600E mutation, a well-established driver mutation commonly associated with papillary thyroid carcinoma, was not detected in the biopsy sample. The patient underwent a left thyroidectomy with isthmus lobectomy and prophylactic central neck lymph node dissection to ensure complete removal of potentially involved tissue. Additionally, thromboembolectomy was performed to remove the tumor thrombus from the middle thyroid vein. Final pathological examination confirmed the presence of a papillary microcarcinoma (pT1a) in the left thyroid, measuring less than 1 cm in greatest dimension, with no evidence of lymph node metastasis or extrathyroidal extension. The thrombus in the middle thyroid vein was histologically confirmed as a tumor-derived thrombus, consistent with extension of the papillary thyroid carcinoma into the venous system, a known phenomenon in certain subtypes of thyroid malignancy, particularly those with high vascularity or invasive growth patterns. This case illustrates the importance of imaging and biopsy in evaluating thyroid nodules with venous involvement, as well as the role of molecular testing in refining the biological characterization of thyroid lesions, even"}
{"row_index": 81, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 22-year-old woman went to the hospital after having diarrhea for 5 days. She started taking clindamycin to treat an infection from a tooth problem. After that, her diarrhea got worse and turned into a serious condition called toxic megacolon, where her colon became swollen and burst. This led to a dangerous infection in her blood, called sepsis. Doctors found a harmful bacteria in her stool, called C. difficile (type 087), and another bacteria, Klebsiella pneumoniae, in her blood. She was treated with antibiotics like metronidazole and ceftriaxone, but she still got worse. Even with treatment, she died 10 days after coming to the hospital. The doctors found yellow spots in her colon during autopsy, which is a sign of pseudomembranous colitis. This case shows that even young, healthy people can get very serious infections from antibiotics, especially if they don’t get the right treatment fast. The infection spread quickly because the bacteria made a lot of harmful toxins. This strain (087) is common in Hungary but rare elsewhere. The patient had no hospital visits before, but her college life was stopped by this illness. She needed surgery, but it wasn’t done in time. This case warns doctors: young people can get severe colitis, and fast action is key to saving lives.\"\n}"}
{"row_index": 82, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 22-year-old female university student was admitted to University Hospital of the West Indies, Jamaica with a 5-day history of diarrhea. The diarrhea started after she took clindamycin for a tooth infection. Despite stopping the antibiotic and starting other treatments, her condition worsened. She developed toxic megacolon, a severe swelling of the colon, which eventually led to a bowel perforation and blood infection (sepsis) caused by Gram-negative bacteria. Tests found that the diarrhea was due to Clostridium difficile (C. difficile) strain NAP1/ribotype 087, and blood cultures showed Klebsiella pneumoniae. She was treated with metronidazole and antibiotics to clear the bacteria, but her condition did not improve. She died 10 days after admission. An autopsy confirmed pseudomembranous colitis (PMC), a serious form of C. difficile infection, and found signs of severe inflammation in her large intestine. The case is unusual because it happened in a young person without prior hospital stays or health care exposure. While such severe complications are more common in older adults, this case shows that young people can also develop life-threatening forms of the infection. The doctors did not use recommended treatments like intracolonic vancomycin or surgery when needed, which may have contributed to the poor outcome. This highlights the importance of early recognition and proper treatment of C. difficile infections, even in younger patients.\"\n}"}
{"row_index": 83, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 22-year-old female university student was admitted to the University Hospital of the West Indies, Jamaica with a presumptive diagnosis of pseudomembranous colitis (PMC) following a 5-day history of diarrhoea and fever that began 5 days after initiation of clindamycin therapy for a dental abscess requiring tooth extraction. Despite discontinuation of clindamycin and initiation of empiric therapy with chloramphenicol and metronidazole, her diarrhoea and fever persisted. Physical examination revealed a febrile patient with severe cardiopulmonary distress, tachycardia (heart rate 150 beats/min), and hypertension (blood pressure 150/100 mmHg). Laboratory findings included haemoglobin 10.4 g/dL, leukopenia (white cell count 2.1 × 10⁹/L), and platelet count 182 × 10⁹/L. Clinical deterioration progressed to toxic megacolon, bowel perforation, and Gram-negative sepsis. Blood cultures collected in brain heart infusion and thioglycollate broths grown from all four bottles after 24-hour incubation at 37°C yielded Klebsiella pneumoniae. Stool specimens collected the day after admission tested positive for Clostridium difficile toxin A and B using ELISA (Alexon Inc., Sunnyvale, CA), and the organism was isolated on cycloserine, cefoxitin, fructose agar (CCFA).  \\n\\nSusceptibility testing of K. pneumoniae via Kirby Bauer disc diffusion demonstrated susceptibility to ceftriaxone, co-trimoxazole, ceporin, amikacin, gentamicin, ceftazidine, and augmentin, with resistance to chloramphenicol, piperacillin, and ampicillin. The patient received intravenous metronidazole, followed by ceftriaxone and gentamicin, which resulted in fever resolution and sterile blood cultures. However, persistent hypotension, pulmonary oedema, leucopenia, and thrombocytopenia required intensive care management, and the patient died 10 days after admission. Autopsy revealed florid pseudomembranous colitis with multiple discrete yellowish exudative plaques throughout the large bowel mucosa, confirming PMC. Additional pathologic findings included markedly"}
{"row_index": 84, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 58-year-old woman had a brain tumor before, called a meningioma, and had surgery for it when she was 31. She had more surgeries later, 16 and 26 years later. While treating a broken bone, doctors found a big lump in the back part of her pancreas. This lump looked scary, so they did scans and found it had blood vessels and was not normal. At first, they thought it might be a type of cancer or a rare tumor, but the test results showed it was actually a type of tumor called SFT, which started in her brain tumor. The doctors removed the pancreas part with the tumor safely, and she recovered well. Later, 4 years after surgery, the tumor came back in her brain, but no new tumors have come back in her belly. She is now being treated for the brain problem.\"\n}"}
{"row_index": 85, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 58-year-old woman with a history of brain tumors (diagnosed as meningioma) was seen for a cystic tumor in the tail of her pancreas. The tumor was found during a CT scan done for a bone fracture. Imaging showed a complex, blood-rich mass that could have been a type of pancreatic cancer or a rare tumor like a neuroendocrine neoplasm or solid pseudopapillary neoplasm. However, after surgery, the pathologist found it was a malignant hemangiopericytoma (SFT) of the pancreas, a type of tumor that originates from connective tissue. Importantly, the brain tumor she had before was found to be the same type as this pancreatic tumor, meaning the pancreatic tumor likely came from the brain lesion. The surgery was successful with no complications, and she recovered well. Four years after the surgery, she developed a recurrence of brain disease, but no new tumors have appeared in her abdomen. She is currently being treated for the brain recurrence.\"\n}"}
{"row_index": 86, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 58-year-old woman with a history of recurrent meningioma, initially resected at age 31 and subsequently reoperated at ages 16 and 26 years post-initial resection, was referred for evaluation of a cystic lesion in the pancreas tail. During admission for femoral fracture management, incidental detection via computed tomography (CT) revealed a 5.5-cm cystic mass in the pancreatic tail. Laboratory findings at presentation included a slightly elevated serum lipase (56 IU/L; normal range: 13–55 IU/L) and gamma-glutamyl transpeptidase (47 IU/L; normal range: 9–32 IU/L), with all tumor markers—carcinoembryonic antigen, carbohydrate antigen 19-9, and DUPAN-2—within normal limits. Endoscopic ultrasonography (EUS) demonstrated a well-encapsulated, circumscribed cystic mass with prominent intratumoral vascularity, including a hypervascular region resembling collateral vessels. Dynamic contrast-enhanced CT revealed a heterogeneously enhancing mass adjacent to the splenic hilum, characterized by strong arterial-to-portal phase enhancement of the solid components' rim and edge, with a large central non-enhancing area. During the portal to delayed phase, the solid components gradually isoattenuated relative to surrounding pancreatic parenchyma, with the non-enhancing region remaining distinct. Magnetic resonance imaging (MRI) confirmed low signal intensity on T1-weighted sequences and slightly higher signal intensity on T2-weighted sequences compared to normal pancreatic tissue, consistent with the presence of solid components. The large non-enhancing region on CT corresponded to a hyperintense signal on T2-weighted MRI, indicating cystic or necrotic transformation. Differential diagnoses included pancreatic neuroendocrine neoplasm, solid pseudopapillary neoplasm, hemangioma, and mucinous cystic neoplasm (due to patient sex and anatomical location), with invasive pancreatic carcinoma excluded based on imaging features. EUS-guided fine-needle aspiration was avoided due to the risk of cystic rupture and hemorrhage. The patient underwent distal pancreatectomy with regional lymph node dissection, with resection extending above the left edge of the superior mesenteric artery. The pancreatic stump was free of residual disease, with a margin of approximately 3 cm including stap"}
{"row_index": 87, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 70-year-old woman had trouble moving her right side, which started 4 months ago. Doctors used a brain scan and a blood vessel test to check her brain. They found a small, old damage in her brain that could explain the weakness. They also found a strange blood vessel problem under the brain’s cover, called a TDAVF. This problem was feeding from two small blood vessels on the back of the brain and was sending blood backward (like water going uphill), which is dangerous. To fix it, doctors used a special glue to block the main leaky spot. After that, a small new leak appeared — it wasn’t seen before and came from a hidden blood vessel. But one week later, this new leak went away on its own. The patient had no more problems, no more weakness, and no signs of the leak coming back. She’s back to normal and doing fine.\"\n}"}
{"row_index": 88, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 70-year-old woman had right-side weakness that had been present for 4 months. MRI showed a small area of damage (chronic infarction) in the left corona radiata, which likely caused her weakness. During the imaging, a vascular abnormality was found beneath the cerebellar tentorium. This abnormality was an arteriovenous fistula (TDAVF) supplied by the bilateral posterior meningeal arteries. It had a shunting point under the tentorium with blood flowing backward (retrograde flow), which is a type known as Borden III and Cognard III. This kind of abnormality can lead to bleeding, so it was treated with endovascular embolization using a special glue called n-butyl-2-cyanoacrylate (NBCA) to block the shunting point. After the procedure, the main shunt disappeared, but a small, new shunt was found that was not seen before. This new shunt was supplied by a blood vessel called the AWW, which was not visible on the preoperative scans. One week later, follow-up imaging showed that this residual shunt disappeared on its own. The patient had no further issues, no neurological problems, and no recurrence of the fistula after 6 months of follow-up. The treatment was successful in preventing complications.\"\n}"}
{"row_index": 89, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 70-year-old woman presented with a 4-month history of right hemispheric motor weakness, which was evaluated with magnetic resonance imaging (MRI). Fluid-attenuated inversion recovery (FLAIR) sequences revealed chronic lacunar infarction in the left corona radiata, consistent with a contributing pathophysiological mechanism for her right-sided motor deficit. No edema or acute infarct was observed in either supratentorial or infratentorial regions. MRI angiography (MRA) identified a vascular lesion located beneath the cerebellar tentorium on constructive interference in steady-state (CISS) images, suggesting an arteriovenous shunt. Cerebral angiography confirmed the presence of a dural arteriovenous fistula (TDAVF) supplied by the bilateral posterior meningeal arteries (PMAs), with no other identifiable feeders detected. The shunting point was situated on the inferior surface of the cerebellar tentorium, exhibiting retrograde venous flow into the tentorial sinus and ultimately the transverse sinus, consistent with Borden type III and Cognard type III classification. The left vertebral angiogram demonstrated venous congestion with no retrograde flow in the basal vein of Rosenthal, while the internal carotid and bilateral posterior cerebral arteries exhibited fetal-type vasculature. The straight sinus demonstrated anterograde flow, and no arterial feeders were observed in the internal carotid or vertebral systems. The arteriovenous shunt was primarily fed by the PMAs, with drainage via the superior vermian vein to the petrosal vein and superior petrosal sinus, and alternatively through the inferior hemispheric vein, inferior hemispheric vein, and tentorial sinus. A selective angiogram of the mastoid branch of the occipital artery confirmed the PMA as the primary arterial supply, with bilateral involvement observed in both left and right occipital territories. The shunting point was precisely localized beneath the cerebellar tentorium on maximum intensity projection (MIP) images, with venous drainage converging into the transverse sinus. Transarterial endovascular embolization was performed under general anesthesia using two Envoy 5F 90 cm microcatheters (MPD, Codman Neuro) introduced into the bilateral occipital arteries. A Masters HF 2.8-Fr/3.2-Fr 125 cm"}
{"row_index": 90, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 11-year-old girl had a serious bone cancer in her leg. Doctors removed the cancer and put in a fake joint (prosthesis) to replace the broken part. Six months later, the joint got infected, so they had to take it out and clean the area deeply. They used a temporary spacer with medicine to fight the infection. After healing, the girl broke a small bone in her thigh because she started walking too soon. This stopped her leg from growing longer. Her leg was now 5 cm shorter than the other. To fix this, they used a special growing prosthesis that can stretch over time. This device added 8 cm of bone length, helping her leg grow to the right size. The girl now walks without pain, carries her full weight, and plays sports again. There’s no sign of infection or cancer coming back. The leg is almost the same length now, and she’s doing well after all the surgeries.\"\n}"}
{"row_index": 91, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This report shares a case of a 11-year-old girl who had a serious bone cancer in her left leg, called high-grade osteosarcoma, which required surgery to remove the affected part of her femur. After the initial surgery, she developed a deep infection six months later, which required a two-stage revision. In the first stage, the infected implant was removed, the infection was treated with antibiotics, and the area was cleaned thoroughly. During recovery, she accidentally broke a bone in her tibia (the shin bone) because she started walking too early, which stopped her leg from growing properly. This caused a 5 cm difference in leg length.\\n\\nBecause the infection had already damaged the bone and growth plates, doctors chose a special bio-expandable prosthesis called MUTARS® BioXpand to fix the leg length. This device can grow longer over time by using a motorized nail that gently stretches the bone. It was designed to add 8 cm of bone length without needing to remove more bone or use a large implant. The prosthesis was placed, and the leg was gradually lengthened over several months. However, the family did not follow the required care schedule, which led to a small bony bridge forming at the break site. After adjusting the care plan, the lengthening was resumed safely.\\n\\nOnce the leg reached its full length, the temporary prosthesis was replaced with a permanent one. The new implant was stable and well-integrated. At the final follow-up, the girl was pain-free, walking without any support, and able to do all her normal activities, including sports. There was no sign of infection or cancer coming back. Although her knee joint is now slightly uneven due to the growth stoppage, she has excellent movement and function. Her outcomes were rated very well by medical scoring systems, showing a full return to daily life.\"\n}"}
{"row_index": 92, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 11-year-old female presented with high-grade osteosarcoma of the left distal femur, undergoing wide resection followed by initial prosthetic reconstruction with a conventional endoprosthesis. Six months postoperatively, during the final cycle of adjuvant chemotherapy, she developed septic shock secondary to acute deep infection characterized by extensive pus formation and skin necrosis on the anteromedial knee, exposing the implant. Microbiological analysis revealed polymicrobial flora including Staphylococcus epidermidis, Neisseria mucosa, Cutibacterium acnes, and Bacillus sp., with no detectable genetic markers of antibiotic resistance; sensitivity testing confirmed standard susceptibility to empiric agents.\\n\\nFirst-stage revision involved explantation of the infected endoprosthesis, followed by thorough debridement of soft tissues and intramedullary canals using high-pressure lavage irrigation. A reinforced temporary antibiotic cement spacer (containing Vancomycin-loaded calcium phosphate beads, STIMULAN®) was implanted to maintain joint space and deliver localized antimicrobial therapy. The surgical site was covered with a vacuum-assisted closure device. Empiric therapy with ciprofloxacin and metronidazole was initiated, subsequently switched to linezolid and cefixime upon culture confirmation. Clinical improvement was observed with wound healing and normalization of inflammatory markers.\\n\\nDespite infection control, the patient independently transitioned to full weight-bearing, resulting in a Salter-Harris type V-like fracture of the proximal tibia physis. This fracture formed a bony bridge across the lateral half of the physis, resulting in irreversible loss of growth potential in the proximal tibia. The combined resection of the distal femur and proximal tibia physeal structures resulted in a 5 cm leg length discrepancy at the time of planned second-stage reconstruction. The initial cement spacer measured 10 cm, which is insufficient for an expandable prosthesis due to the minimum required implant length of 18 cm for distal femoral endoprostheses.\\n\\nGiven the anticipated end-growth discrepancy of 10 cm, which would be unmanageable without a lengthening implant, and considering the prior deep infection and compromised bone quality, a bioexpandable MUTARS® BioXpand endoprosthesis (Implantcast, Germany) was selected. This system comprises a 10 cm-long femoral component"}
{"row_index": 93, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man in his 60s had trouble remembering things, had poor brain function, and had problems with his nerves and eyes. He had diabetes, but his blood sugar was well controlled. He also had trouble with his bladder, blood pressure, and hearing. Doctors thought it might be a rare nerve or brain problem, so they checked his genes. They found a gene mutation in WFS1 that has been seen before in a person with Wolfram syndrome — a rare condition that causes memory loss, eye problems, and nerve issues. The test also found missing pieces in his energy-producing parts of the cells, which supports this diagnosis. Even though he had a normal diet, he was missing thiamine (a vitamin), which likely hurt his brain and nerves. Treatment for the vitamin didn’t help much. The doctors now believe he has Wolfram syndrome, and this explains most of his problems.\"\n}"}
{"row_index": 94, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 61-year-old man with diabetes, memory problems, brain and nerve damage, and vision issues was initially diagnosed with a condition called multiple system atrophy. However, further testing showed that he had multiple problems in his mitochondria — the energy-producing parts of cells — and a severe lack of thiamine (a vitamin needed for brain function), even though he had a normal diet and no alcohol use. Tests found several mutations in his mitochondrial DNA, and while some genetic tests were negative, targeted exome sequencing revealed a specific mutation in the WFS1 gene. This mutation has been seen before in people with Wolfram syndrome, a rare disorder that affects the brain, eyes, pancreas, and nerves. The patient’s symptoms — including memory loss, vision problems, nerve damage, and diabetes — match what is seen in Wolfram syndrome. Although thiamine treatment had little effect, the genetic finding confirms the diagnosis. The patient now has a clear explanation for his condition and is being managed accordingly.\"\n}"}
{"row_index": 95, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 61-year-old man with a history of diabetes mellitus (DM), autonomic neuropathy, diffuse brain atrophy, optic nerve atrophy (OA), and severe amnestic syndrome was referred for neurologic evaluation. Initially diagnosed with multiple system atrophy-cerebellar type (MSAc) based on MRI findings of severe cerebellar and brainstem atrophy, the clinical picture raised significant diagnostic concerns due to the absence of cerebellar motor signs and the prominent, progressive anterograde amnesia. The patient's early history included childhood bedwetting and urinary urgency in early adulthood, followed by bladder dysfunction requiring intermittent catheterization and erectile dysfunction in his 20s. At age 33, he was diagnosed with type 1 diabetes, with a random C-peptide level of 0.6 ng/mL (reference range 0.9–4.3 ng/mL) at a blood glucose of 83 mg/dL, indicating significant insulin deficiency. Despite good long-term glycemic control (HbA1c 6.5–7.2%), he had no evidence of microvascular or macrovascular complications, and polyuria/polydipsia resolved with insulin therapy.\\n\\nIn his 30s, he began wearing unusual clothing, later diagnosed with color blindness. At age 53, ophthalmologic examination revealed bilateral optic atrophy with preserved vision, and brain MRI demonstrated severe atrophy of the cerebellar hemispheres, vermis, pons, and middle cerebellar peduncles, along with moderate cerebral atrophy—findings that worsened at age 61 with more pronounced cerebral atrophy. Notably, he reported no gait instability or upper extremity incoordination, which is inconsistent with typical cerebellar atrophy.\\n\\nNeuropsychological assessment revealed profound anterograde amnesia, with additional deficits in cognitive flexibility, executive function, naming, and high-order visual processing. Attention, mental tracking, verbal abstract reasoning, complex auditory instructions, and visual spatial functions remained intact. Psychiatric evaluation identified depression, which responded to sertraline. Concurrently, progressive autonomic neuropathy developed, manifesting as gastroparesis and severe postural hypotension—exceeding the expected severity given his well-controlled diabetes and absence of diabetic complications. Bladder dysfunction progressed to the need for suprapubic catheterization at age 6"}
{"row_index": 96, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 35-year-old housewife had sudden paralysis in her legs and trouble controlling her bladder after giving birth. She had back pain and couldn’t feel her legs properly, even though she was otherwise fine. Doctors found a growth outside her spine (in the middle back) that was pressing on her spinal cord. This growth, called an angiolipoma, was removed with surgery. The surgery worked well, and she recovered fully.\"\n}"}
{"row_index": 97, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 35-year-old housewife developed sudden paralysis in her lower limbs and loss of bladder control one month after giving birth. She also had back pain. Upon examination, she had no weakness or reflex issues in her upper body, but her lower limbs showed no muscle strength, stiff muscles, overactive reflexes, and a positive Babinski sign. Sensory tests showed she lost feeling below the umbilicus, and there was tenderness in the middle back. Blood tests were normal. An MRI scan revealed a tumor outside the spinal cord, between the fifth and eighth thoracic vertebrae (D5 to D8), pressing on the spinal cord. The tumor appeared similar to fat on imaging and showed signs of being made of blood vessels and fat (angiolipoma). It was surgically removed through a back approach with no major complications. The surgery was successful, and the patient recovered well. The diagnosis was confirmed through tissue testing after surgery.\"\n}"}
{"row_index": 98, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 35-year-old female presented to the emergency department with a sudden onset of bilateral lower limb paralysis lasting one month following vaginal delivery. The onset was acute and was accompanied by severe back pain and complete loss of sphincteric control, including urinary incontinence. On clinical examination, the patient was otherwise generally well with normal vital signs and a Glasgow Coma Scale (GCS) of 15/15. Cranial nerve function was intact, and upper limb motor strength, tone, and reflexes were normal, with preserved sensation to all modalities. In contrast, lower limb motor examination revealed complete paralysis (motor power grade 0), hypertonia, hyperreflexia (grade 4), and a positive Babinski sign, indicating upper motor neuron pathology. Sensory assessment demonstrated impaired vibration and position sense extending to the level of the umbilicus, consistent with a sensory level at T10. Mid-dorsal tenderness was noted, particularly at the D5–D8 region.\\n\\nHematological investigations were unremarkable, excluding hematologic causes of spinal cord compression. A dorsal lumbar MRI was performed, revealing a T1-weighted extradural hyperintense lesion extending from D5 to D8, posteriorly compressing the spinal cord. On T2-weighted imaging, the lesion exhibited hyperintensity relative to the spinal cord and was nearly isointense with normal adipose tissue, suggesting a lipid-rich composition. The lesion demonstrated characteristic myelopathic changes in the surrounding cord, consistent with acute compressive injury. Contrast-enhanced MRI showed focal, slightly inhomogeneous contrast uptake, indicating partial vascular permeability and possible active angiogenesis within the lesion.\\n\\nThe diagnosis was confirmed as a thoracic spinal extradural angiolipoma, a rare benign neoplasm composed of adipocytes and blood vessels, typically arising in the extradural space of the spinal column. Surgical intervention was performed via a posterior approach, involving dorsal decompressive laminectomy and complete resection of the lesion. The procedure was uncomplicated, with no intraoperative complications. The resected specimen was sent for histopathological analysis, which confirmed the presence of mature adipocytes, vascular channels, and a well-differentiated angiolipomatous tissue consistent with a benign angiolipoma. Postoperative recovery was excellent, with full restoration of motor and sensory function and resolution of sphincter dysfunction, indicating successful decompression and complete removal of the"}
{"row_index": 99, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 46-year-old man got very sick with fever, cough, and chest tightness. Doctors tested his lung fluid and did a lung scan to find out if it was COVID-19. The test came back positive. He got medicine to fight the virus, like interferon and ribavirin, and other medicines to calm his body, clear mucus, protect his liver, and stop his lungs from scarring. He used a machine that gives him extra oxygen through his nose and mouth to help breathe easier. His breathing got better over time, his lungs healed, and he was finally able to go home. He fully recovered.\"\n}"}
{"row_index": 100, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 46-year-old man was hospitalized with severe symptoms of fever, cough, and chest tightness that had lasted for about 11 days. He had recently traveled to several cities in China and had been in close contact with someone from Wuhan. Tests showed he had severe pneumonia, and although initial tests did not find the virus, a later test on his lung fluid (BALF) confirmed he had SARS-CoV-2 infection. To treat the virus, he received a combination of antiviral medications, including interferonalfa-1b and ribavirin, as well as lopinavir and ritonavir at different stages of his illness. He also got medicines to reduce inflammation, protect his liver, clear mucus, and support healthy gut bacteria. Because he was having trouble breathing, he was given oxygen through a BIPAP machine and later switched to high-flow humidified oxygen. His oxygen levels improved over time, and by early February, his symptoms had greatly improved. CT scans showed that the pneumonia was getting better. He was diagnosed with a mild liver issue possibly caused by the virus, and received treatment to protect his liver. To prevent long-term lung damage, he took a medication to support lung healing. By February 12, his lungs showed clear signs of recovery, and he was discharged from the hospital fully recovered.\"\n}"}
{"row_index": 101, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 46-year-old male from Yili Development Zone, Xinjiang, China, was admitted to the University of Hong Kong-Shenzhen Hospital on 19 January 2020 with an 11-day history of fever (38 °C), dry cough, muscle ache, and fatigue. He reported close contact with an individual from Wuhan on 10 January and traveled from Yili to Shanghai (16 January), Shanghai to Ningbo (17 January), and Ningbo to Shenzhen (19 January), with no exposure to Wuhan. On 18 January, symptoms progressed to chest tightness without chest pain or hemoptysis. Initial testing excluded influenza A/B, respiratory syncytial virus (RSV), Mycoplasma pneumoniae, Cryptococcus haemolyticus, Aspergillus, Epstein-Barr virus (EBV) IgM and DNA, and Cytomegalovirus (CMV) DNA/antigen. Blood gas analysis on admission revealed a pH of 7.445, PaCO₂ of 4.72 kPa, and PaO₂ of 7.82 kPa, indicating hypoxemia. The patient was isolated in a single ward and initially treated with levofloxacin for suspected bacterial pneumonia. On 22 January, BALF testing was negative for Aspergillus, Legionella, Pneumocystis carinii, acid-fast bacilli, and Mycobacterium tuberculosis, leading to a diagnosis of severe bilateral community-acquired pneumonia (not excluding COVID-19) with hypoxemia. Levofloxacin was discontinued and replaced with a combination of amoxicillin-clavulanate and doxycycline for broad-spectrum coverage. On 23 January, the patient was transferred to the Third People’s Hospital of Shenzhen for further management. He had no comorbidities, allergies, or gastrointestinal or renal abnormalities.\\n\\nDuring hospitalization, the patient received a multimodal therapeutic regimen. Interferon-alpha-1b (60 μg via inhalation, administered twice daily) was used for antiviral activity against RNA viruses. Bio-Three tablets (0.4 g orally, three times daily) and Bifid-triple viable capsules (420 mg, three times daily) were administered to modulate intestinal microbiota. Mucosolvan ("}
{"row_index": 102, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 60-year-old woman from Eritrea had a lump coming out of her left eye for 3 months, and her vision in that eye got worse. When doctors checked her, her left eye was bulging out a lot, her vision was very poor, and the back of her eye was swollen. Blood tests were normal, and a scan showed a fluid-filled cyst in her eye socket, which looked like a hydatid cyst. She took medicine for 2 weeks to help shrink it. Then, the doctors cut into her eye socket to remove the cyst. During surgery, the cyst broke and clear fluid came out, and the lining was taken out carefully. The tissue was tested and confirmed it was a hydatid cyst. After surgery, she had some swelling and trouble moving her eye slightly, but these improved over a week. Her vision and eye swelling got better. However, she moved back to Eritrea and we couldn’t check on her after that.\"\n}"}
{"row_index": 103, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 60-year-old Eritrean woman had a 3-month history of painless swelling in her left eye, along with slowly worsening vision. On exam, her left eye was noticeably bulging, her vision was very poor, and there was swelling in the back of the eye (papilledema). Blood tests were normal, and a CT scan showed a fluid-filled cyst in her orbital area, which is typical of a hydatid cyst. She was treated with two weeks of oral albendazole, a medication that helps fight the cyst. After that, she had surgery where the cyst was removed through an incision in the eye socket. During surgery, the cyst ruptured and was carefully removed, and the tissue was sent for testing. The biopsy confirmed it was a hydatid cyst. After surgery, she had mild swelling of the eyelid and some difficulty moving her eye inward (adduction), but these improved over time. Her vision and eye swelling also improved. However, she moved back to Eritrea and we were unable to monitor her condition further.\"\n}"}
{"row_index": 104, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 60-year-old female sheep herder from Eritrea presented to the St. Paul’s Hospital Millennium Medical College ophthalmology department with a three-month history of painless left eye proptosis accompanied by progressive decline in left eye visual acuity. Right eye visual acuity was 6/18, while left eye acuity was reduced to counting fingers at the front of the eye. Physical examination demonstrated a 4 mm exophthalmometric discrepancy between the eyes, with a proptosis measurement of 21 mm on the left side. Fundus examination revealed a tortuous temporal arcade and grade 4 papilledema in the left eye, indicating significant intracranial pressure due to optic nerve compression. Laboratory investigations, including a complete blood count, were within normal limits. A computed tomography (CT) scan of the brain and orbit demonstrated a well-defined, thin-walled, non-enhancing cystic lesion measuring 2.6 cm × 2.0 cm × 1.9 cm located in the left orbital cavity, exhibiting compression and lateral displacement of the globe and stretching of the optic nerve. The left medial rectus muscle was not distinctly delineated from the lesion, suggesting intimate adhesion. No osseous lytic or sclerotic changes were observed in the bony orbit, further supporting a non-invasive, soft-tissue origin. The imaging findings were consistent with a hydatid cyst of the orbit, a parasitic infection caused by *Echinococcus granulosus*. Abdominal ultrasound and chest X-ray were unremarkable, excluding extra-orbital hydatid disease or pulmonary involvement.\\n\\nThe patient was initiated on oral albendazole 400 mg twice daily for two weeks, a standard antihelminthic regimen targeting the larval stage of *Echinococcus*, with the goal of reducing cyst viability and preventing further growth. Following this medical phase, she underwent anterior medial orbitotomy for surgical excision of the cystic mass. Intraoperatively, a cystic lesion attached to the inferior aspect of the medial rectus muscle was identified. During manipulation, the cyst ruptured, releasing a clear fluid. The cyst wall, described as paper-white and laminated, was removed in piecemeal fashion, with careful preservation of the medial rectus muscle to avoid functional compromise. The external capsule was excised with meticulous dissection to prevent irreversible damage to the extraocular"}
{"row_index": 105, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 43-year-old man from Asia had cancer in his penis that had been growing for 3 years. The cancer spread to his right eye, where it damaged the inside of the eye and made him lose his vision. Doctors saw signs of cancer in the eye using scans — the cancer looked bright on one type of scan and dark on another. Because the eye pain was severe and vision couldn't be saved, they removed the entire right eye. After checking the tissue from the eye, they found it was cancer that started in the penis and had spread to the eye. This cancer was not very aggressive but still dangerous. The man got treatment with chemo and radiation, but later the cancer spread to his brain and he passed away.\"\n}"}
{"row_index": 106, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 43-year-old Asian man with a 3-year history of penile cancer developed cancer that spread to his right eye. He had been diagnosed with advanced cancer (stage T4N3M1) and had already lost vision in his right eye more than a month before. Imaging tests showed that the cancer had spread to the inside of his right eye, including the retina, optic nerve, and surrounding structures. On MRI, the tumor appeared bright on T1-weighted images and dark on T2-weighted images, which are signs of metastatic cancer. After removing the affected eye (enucleation) due to severe pain and no chance of recovery, pathologist tests confirmed it was metastatic, moderately differentiated penile squamous cell carcinoma. The cancer had spread into the eye's layers, including the sclera, choroid, and retina. He received chemotherapy and radiation for six months, but eventually died from brain metastasis.\"\n}"}
{"row_index": 107, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 43-year-old Asian male with a three-year history of progressively invasive penile carcinoma (PC) presented on January 31, 2015, with acute pain in the right eye and irreversible vision loss, with best-corrected visual acuity of no light perception in the right eye and 20/20 in the left eye. The patient was previously staged as T4N3M1 according to the TNM classification, indicating advanced local invasion (T4), regional lymph node involvement (N3), and distant metastasis (M1). Prior to ocular metastasis, he had developed bilateral inguinal lymph node and ipsilateral iliac node metastases, followed by systemic dissemination to the liver and lungs. His medical history included multiple prior surgical interventions, with no reported family history of hereditary disorders or psychiatric conditions.\\n\\nOphthalmological examination revealed mild proptosis and intact ocular motility in all directions. The right eye demonstrated a dilated pupil (5 mm) with absent pupillary reflex, and fundus examination showed post-equatorial retinal detachment with a black eminence and a pale optic disc. B-scan ultrasonography confirmed retinal detachment with intraretinal hemorrhage. Orbital magnetic resonance imaging (MRI) demonstrated thickening and structural strengthening of the right lateral orbital wall, consistent with metastatic tumor infiltration. The internal rectus and lateral rectus muscles were also thickened and hardened, with a 2-cm-long optic nerve exhibiting significant thickening and invasion at its stump. MRI sequences revealed hyperintensity on T1-weighted imaging and hypointensity on T2-weighted imaging, indicative of tumor-associated signal characteristics. Contrast-enhanced MRI showed inhomogeneous enhancement of the posterior orbital wall, supporting active tumor vascularity and cellular infiltration. Histopathological evidence confirmed invasion of the optic nerve, choroid, sclera, retina, and external intraocular structures by metastatic cells.\\n\\nIntraoperative evaluation of the enucleated right eye revealed complete tumor involvement of the globe. Histopathological analysis, performed using hematoxylin-and-eosin (H&E) staining, identified keratin pearls and sheets of keratinized squamous carcinoma cells with intercellular bridges, consistent with moderately differentiated penile squamous cell carcinoma. The tumor demonstrated infiltrative growth patterns, with extensive spread into the deep layers of the eye, including the choroid, which is a"}
{"row_index": 108, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 33-year-old man had belly pain and vomiting. Doctors found a 45-mm lump in his small intestine (ileum) that had some calcium inside it. The lump wasn’t blocking or twisting, so they didn’t think it was an emergency. After checking it with a scan, they knew it was a tumor. They did a small surgery through just one spot on his belly to remove part of the small intestine. The tumor looked like a soft, white growth with lots of thick, stiff tissue and tiny calcium spots. It had some immune cells inside. Tests showed that a certain protein (factor XIIIa) was present, but other tumor markers were missing. This pattern matched a type of rare tumor called CFT. The man got better after the surgery and hasn’t had any problems in 6 months. No signs of it coming back.\"\n}"}
{"row_index": 109, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 33-year-old man came in with abdominal pain and vomiting. His physical exam showed lower abdominal tenderness, but blood tests and imaging like ultrasound and X-ray were normal. A CT scan found a 45-mm mass in the ileum (a part of the small intestine) with some calcification, but no signs of blockage or twisting. The tumor was suspected, and after further testing with MRI, doctors considered several possibilities, including a gastrointestinal stromal tumor (GIST), a chronic hematoma, a leiomyoma, or a CFT (cystic fibrosis-related tumor — actually, in this case, a CFT refers to a specific type of tumor called IgG4-related fibrosis). The patient underwent laparoscopic surgery using a single small incision in the belly button. During the procedure, a white, pedunculated tumor was found in the ileum, and only that tumor was seen. A partial resection (removal) of the ileum was done, and the ends were reconnected. Pathology showed a tumor made up of spindle-shaped cells, dense collagen, and scattered calcifications, with some lymphoplasmacytic cells present. Key test results showed that factor XIIIa was positive, while other markers for common tumors were negative. Over 40% of the immune cells in the tumor were IgG4 positive, which is a key sign of CFT. Based on these findings, the tumor was finally diagnosed as a CFT. The patient recovered well, was discharged on day 7, and has had no signs of recurrence in the 6 months since surgery.\"\n}"}
{"row_index": 110, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 33-year-old man with no prior medical or surgical history presented with acute abdominal pain and vomiting. Physical examination revealed localized tenderness in the lower abdomen, while laboratory investigations were unremarkable: C-reactive protein at 0.16 mg/dL, white blood cell count of 9600 /μL, neutrophil percentage 91.3%, and lymphocyte count 5.4%. Initial imaging with ultrasonography and radiography failed to identify a source of pain. Contrast-enhanced computed tomography (CT) revealed a 45-mm-sized mass in the ileum with partial calcification, showing no signs of invagination, obstruction, or volvulus, and no other radiological findings suggestive of underlying pathology. The patient was clinically diagnosed with an ileal tumor, and his symptoms resolved spontaneously. Subsequently, magnetic resonance imaging (MRI) was performed to characterize the lesion, demonstrating hypointensity on both T1-weighted and T2-weighted images, with isointense enhancement on gadolinium-enhanced T1WI, which supported a differential diagnosis including gastrointestinal stromal tumor (GIST), chronic distending hematoma, leiomyoma, and carcinoid tumor of the gastrointestinal tract (CFT).\\n\\nLaparoscopic surgical intervention was performed for both diagnostic and therapeutic purposes using a single-port technique via a vertical 4-cm umbilical incision with EZ access and Lap Protector (Hakko Medical, Nagano, Japan), employing two 5-mm ports. Intraoperatively, a white-colored tumor was identified in the ileum at 100 cm from the terminal ileum. No additional tumors, lymph node metastases, or evidence of systemic dissemination were detected in the abdominal cavity. The tumor was extracorporeally retrieved and a partial resection of the ileum was carried out, followed by a functional end-to-end anastomosis. Macroscopically, the tumor was pedunculated and located on the antimesenteric side. Microscopically, it extended from the muscularis propria to the subserosa, exhibiting a hypocellular architecture composed of spindle cells embedded in dense hyalinized collagen with interspersed calcification and focal infiltration of lymphoplasmacytic cells. Immunohistochemical analysis showed negative or nearly negative staining for CD34, c-kit, DOG-1, desmin, S100"}
{"row_index": 111, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 24-year-old man from Somalia had a fever, headache, stomach pain, nausea, vomiting, and lost weight over two months. He had been treated before with medicine and a blood transfusion, but it didn’t help. When he came to the hospital, he looked very weak and pale, and his belly was swollen. His blood tests showed very low red blood cells, white blood cells, and platelets — this means his body wasn’t making enough blood cells. The test for malaria was positive, but after three days of anti-malarial medicine, his symptoms didn’t go away and his belly got worse. Other tests ruled out HIV, hepatitis, and infections like Brucella or Leishmania. Blood and bone marrow checks showed no infection or cancer. A small piece of the spleen was taken and tested — it confirmed the cause was visceral leishmaniasis. He was given a special medicine mix (sodium stibogluconate and paromomycin) for 17 days. After a few weeks, his symptoms got better, and by the end, he was fully back to normal. A second test of his spleen showed no more signs of the disease, and he was sent home.\"\n}"}
{"row_index": 112, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 24-year-old man from a rural area in Somalia, who recently moved from Yemen, came to the hospital with a two-month history of fever, headache, abdominal pain, nausea, vomiting, and weight loss. He had previously been treated at a local clinic with antibiotics, fever-reducers, and a blood transfusion, which gave only temporary relief. When he returned with worsening symptoms, he was found to be pale, weak, and had an enlarged spleen and liver. Blood tests showed low levels of red blood cells, white blood cells, and platelets (a condition called pancytopenia), and a rapid test for malaria was positive. However, after three days of anti-malarial treatment, his symptoms did not improve and his spleen continued to grow larger. Other tests for infections like HIV, hepatitis, and Brucella were negative, and blood and bone marrow exams showed no signs of infection or cancer. A biopsy of the spleen confirmed the diagnosis of visceral leishmaniasis, a serious parasitic infection. The patient was treated with a combination of sodium stibogluconate and paromomycin for 17 days. After four weeks, his symptoms improved significantly, and by the fifth week, he was fully recovered. A follow-up spleen biopsy showed normal results, and he was discharged.\"\n}"}
{"row_index": 113, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 24-year-old male patient from Sa’ada, northwest Yemen, recently relocated to Burhakaba, Somalia, was referred to our hospital with a complaint of a left upper hypochondrial mass. He presented with a two-month history of high-grade fever, headache, abdominal pain, nausea, vomiting, anorexia, and progressive weight loss. He reported a prior episode of similar symptoms three months earlier. Prior to hospital admission, he had been evaluated at a local health facility where he received symptomatic management with antipyretics, broad-spectrum antibiotics, and two units of whole blood transfusion, resulting in transient clinical improvement. However, symptoms recurred two months later, now accompanied by generalized weakness and further weight loss.\\n\\nOn presentation, the patient exhibited signs of chronic illness: pallor, fever (temperature 38.9°C), tachycardia (pulse 110 beats/minute), and splenomegaly. Vital signs included blood pressure 110/78 mmHg, respiratory rate 16 breaths/minute, blood glucose 110 mg/dL. Laboratory findings revealed profound pancytopenia: white blood cell count of 1.03 × 10⁹/L (normal 4.00–10.00 × 10⁹/L), hemoglobin 6.6 g/dL (normal 12.0–16.0 g/dL), hematocrit 0.203 (normal 0.400–0.540), and platelet count 70 × 10⁹/L (normal 100–300 × 10⁹/L). Inflammatory markers were elevated: C-reactive protein 45.73 mg/L (normal 2.5–10 mg/L), with significant hepatocellular enzyme elevation—ast 104.5 U/L (normal 6–38 U/L) and alt 112.5 U/L (normal 6–40 U/L). Renal function parameters were mildly impaired: serum creatinine 1.4 mg/dL (normal 0.4–1.4 mg/dL) and serum urea 54.3 mg/dL (normal 10–50 mg/dL).\\n\\nA rapid diagnostic"}
{"row_index": 114, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 34-year-old man felt short of breath when walking, had swelling in his legs, lost 50 pounds without trying, and was tired all the time. He had small spots in his lungs and fluid building up around his heart and lungs. Tests showed fluid pressing on his heart, which made it hard to pump blood. A drain was put in to remove the fluid, and after a while, the fluid came back and his heart stopped working properly. Doctors did an emergency surgery to open up the space around his heart to let the fluid go out. Later, scans showed the tissue around his heart was stiff and not moving right, which means his heart was being squeezed. Tests confirmed this was due to a disease called sarcoidosis, which causes small lumps in the lungs, lining of the lungs, and the sac around the heart. The surgery removed the stiff tissue, and the tissue tested showed small lumps, proving the disease was in the heart sac. Now he’s doing better, no more swelling, no shortness of breath, and he’s on medicine to keep it from coming back.\"\n}"}
{"row_index": 115, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 34-year-old man with a five-month history of shortness of breath when active, swelling in his legs, unexplained weight loss, and fatigue was evaluated. He had a cough and felt tired easily. Tests showed lung nodules, especially in the upper lungs, and fluid buildup in his lungs and around his heart. His heart was showing signs of pressure problems due to fluid around it, which led to a temporary drain being placed. After the drain was removed, the fluid returned and caused a serious heart condition called cardiogenic shock, requiring an emergency procedure to relieve the pressure. Imaging tests showed that the fluid around the heart was thickening and not moving normally, which is a sign of constrictive pericarditis. A procedure called pericardiectomy was done, and the tissue samples showed small, non-necrotizing granulomas, confirming that the condition was sarcoidosis affecting his lungs, pleura, and heart. He was started on steroids and later switched to a lower dose with methotrexate. Over time, his symptoms improved, his breathing got better, and his heart function returned to normal. Follow-up tests showed no ongoing issues and he was able to return to a stable condition.\"\n}"}
{"row_index": 116, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 34-year-old Caucasian male presented with a five-month history of progressive exertional dyspnea, productive cough, lower extremity edema, unintentional 50-pound weight loss, fatigue, and early satiety. His medical history included controlled hypertension managed with hydrochlorothiazide and carvedilol, with recent initiation of furosemide for peripheral edema. He was a non-smoker with no recent travel or environmental exposures. Physical examination revealed diaphoresis, pallor, diminished cardiac sounds, markedly reduced breath sounds in the right thorax, and 2+ pitting edema of the lower extremities. Vital signs showed oxygen saturation of 92% on 2 L/min supplemental oxygen and mild tachycardia.\\n\\nPulmonary function testing revealed an intrinsic restrictive ventilatory defect: forced vital capacity (FVC) of 4.03 L (59% of predicted) and diffusion capacity of the lung for carbon monoxide (DLCO) of 23.3 mL/min/mmHg (55% of predicted). Arterial blood gas analysis demonstrated hypoxemia with a partial pressure of oxygen (PaO₂) of 60 mmHg. High-resolution chest computed tomography (HRCT) showed diffuse pulmonary nodules with upper lobe predominance and perilymphatic distribution, diffuse partially calcified mediastinal and hilar lymphadenopathy, moderate to large right pleural effusion, and moderate to large pericardial effusion with pericardial thickening.\\n\\nTransthoracic echocardiography revealed preserved left ventricular systolic function, a large circumferential pericardial effusion, and evidence of respiratory variation in mitral and tricuspid inflow, along with paradoxical septal shift—findings consistent with early tamponade physiology. The patient was admitted and underwent urgent pericardiocentesis, during which 500 mL of serosanguinous fluid was removed, resulting in immediate clinical improvement. The fluid was monocyte-dominant, culture-negative, and showed no evidence of infection or malignancy. The pericardial drain was removed after several days of minimal output.\\n\\nDiagnostic workup included thoracentesis, fiberoptic bronchoscopy with bronchoalveolar lavage (BAL), transbronchial biopsy, and endobronchial ultrasound-guided"}
{"row_index": 117, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 62-year-old woman had high CA125 levels in her blood for a year. At first, doctors thought it was a harmless cyst called a chocolate cyst, but after checking with ultrasound and special imaging, they saw signs of a serious tumor. A test using contrast ultrasound showed the tumor had solid parts and blood flow, which made doctors think it might be cancer. The final test on the tumor tissue confirmed it was high-grade serous adenocarcinoma, a type of ovarian cancer. She had surgery to remove the tumor and then received chemotherapy, which worked well. Her CA125 levels went back to normal, and she is now doing well.\"\n}"}
{"row_index": 118, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 62-year-old woman had rising CA125 levels in her blood for one year, which raised concern for ovarian cancer. At a local hospital, her ultrasound showed a large mass in her pelvis, but the doctors initially thought it was a chocolate cyst—a common type of benign ovarian cyst. To get a clearer picture, she was referred to our hospital for further testing. Contrast CT and MRI scans showed a complex cystic mass in her right ovary, with features that could suggest either a benign or malignant condition. A transvaginal ultrasound combined with contrast-enhanced ultrasound (CEUS) revealed signs of a malignant tumor, leading doctors to suspect cystadenocarcinoma. After surgery, the tumor was found to be a high-grade serous adenocarcinoma, a type of aggressive ovarian cancer. Pathology confirmed the diagnosis, and the patient underwent chemotherapy with carboplatin and paclitaxel. Her CA125 levels dropped to normal after treatment, and she is now doing well with no signs of recurrence.\"\n}"}
{"row_index": 119, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 62-year-old woman presented with a progressively rising serum CA125 level, initially elevated to 50 U/ml (normal < 35 U/ml) in November 2018, which increased to 75 U/ml by November 2019. Her serum CEA and CA19-9 levels remained within normal limits, and initial transvaginal ultrasound (TUS) revealed no obvious abnormalities. Subsequent TUS at the local hospital demonstrated a large pelvic mass, prompting referral to our institution for further evaluation. Laboratory investigations, including tumor markers, reproductive hormone assays, and routine blood work, were within normal ranges. The patient was asymptomatic, with no palpable abdominal mass on physical examination. A positive family history was noted, as her mother had died of ovarian cancer.\\n\\nAbdominal computed tomography (CT) revealed a well-circumscribed, hypodense mass in the right adnexa. Contrast-enhanced CT demonstrated mild enhancement of the lesion and a fluid–fluid level sign. Magnetic resonance imaging (MRI) showed a well-defined, lobulated, cystic mass measuring 4.9 × 4.8 cm in the right pelvic cavity. On T2-weighted imaging (T2WI) and T1-weighted imaging (T1WI), the mass exhibited mixed signal intensity, with nodular hypointensity observed on both sequences. Diffusion-weighted imaging (DWI) revealed severe hyperintensity, consistent with restricted diffusion, and a fluid–fluid level sign was present. Based on these imaging features, the lesion was initially suspected to represent a chocolate cyst (endometriotic cyst), a benign condition commonly associated with endometriosis.\\n\\nPreoperative TUS revealed a right adnexal mass measuring approximately 5.6 × 4.4 × 5.5 cm, characterized by a well-defined cystic structure with mural and septal nodules. The largest internal papillary excrescences measured 3.0 × 1.4 × 1.7 cm. Doppler ultrasound detected blood flow within the internal septations, cystic wall, and papillary projections, with a resistive index of 0.9—indicative of vascular resistance consistent with a neoplastic process. Given the presence of papillary structures and abnormal vascularity, a primary diagnosis of malignant neoplasm was established.\\n\\nTo further characterize"}
{"row_index": 120, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 63-year-old woman had very bad kidney disease and couldn’t walk or move. She was confused for 5 days and had been on dialysis for months. She also had liver problems, high blood sugar, and a lung infection. A type of fungus called Candida guilliermondii was found in her blood and in the tube that goes into her vein. Even after changing her medicine, the fungus stayed in her blood. A small lump was found on her heart valve, but the family said no surgery because she had too many serious health problems. She was given medicine for the fungus, but it didn’t work. After 8 weeks, her condition got worse — the lump grew bigger and she had lung and spleen problems. She was given hospice care and sent home on a daily antifungal pill. She died a few weeks later from liver problems and being in a deep sleep.\"\n}"}
{"row_index": 121, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 63-year-old woman with end-stage kidney disease was admitted to the hospital after being confused for 5 days. She had been on dialysis since 2014 and had several serious health problems, including liver disease, tuberculosis-related lung issues, and an abnormal protein condition in her blood. She was permanently bedridden and did not use intravenous drugs. She was treated with dialysis through a catheter in her vein. Her first blood culture showed a type of fungus called Candida guilliermondii, and this fungus was found again in later blood tests and in the catheter tip, even after changing her antifungal medicine. A 1.2-cm mass was seen on her pulmonary valve, which is a sign of possible infection. Surgery was suggested, but the family refused due to her many health problems. She was given fluconazole as a long-term treatment, but she eventually died from liver-related confusion and coma.\"\n}"}
{"row_index": 122, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 63-year-old woman with end-stage renal disease (ESRD) was admitted to the hospital on June 3, 2015, following a 5-day course of disorientation. She had been undergoing maintenance hemodialysis (HD) since December 2014, initially initiated due to acute on chronic kidney disease secondary to pneumonia. The patient also had a history of hepatitis B-related liver cirrhosis (Child-Pugh class B with hepatic encephalopathy), Mycobacterium tuberculosis-related pleuritis, and an IgGλ monoclonal gammopathy, which remained untreated due to her permanent bedridden status. Hemodialysis was administered via a tunneled-cuffed catheter placed in the right subclavian vein, first inserted on December 8, 2014. She denied active intravenous drug use. On physical examination, she exhibited drowsy consciousness and splenomegaly; no lung crackles or skin track marks were observed. Laboratory findings included a white blood cell count of 2.86 × 10³/uL, absolute neutrophil count of 2116/mm³, platelet count of 14,000/uL, total bilirubin of 3.54 mg/dL, C-reactive protein of 2.31 mg/dL, and serum glucose of 992 mg/dL, without evidence of metabolic acidosis. Given the hyperglycemic hyperosmolar state, blood cultures were obtained and empiric therapy with vancomycin and cefuroxime was initiated. The initial blood culture yielded Candida guilliermondii without concomitant bacterial growth. Intravenous fluconazole 200 mg once daily was administered. The tunneled-cuffed catheter was removed on June 30 due to persistent fungemia, and subsequent catheter tip culture confirmed C. guilliermondii. Blood cultures drawn on July 14 and August 10 and 28 remained positive for C. guilliermondii, even after switching from caspofungin to fluconazole on July 28. No positive cultures were detected in sputum or urine during the 8-week hospitalization period. Transthoracic echocardiography performed on July 20 and August 21 showed no vegetations or congenital val"}
{"row_index": 123, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 46-year-old man with Malay background had pain in his belly and yellowing of his skin because of a tumor in his duodenum. The doctors found a big tumor and decided to remove it with surgery. Before surgery, he was at high risk because he had low blood, poor liver function, and blocked bile flow. During the surgery, a lot of bleeding happened, so they gave him many blood bags to stay alive. After surgery, he couldn’t make urine properly, which means his kidneys were not working well. So, they started a machine called CRRT right after the problem was found — within 24 hours — to help his kidneys. This machine ran for a few hours and helped his body start working again. His urine came back, his blood sugar went down, and the medicine for blood pressure was slowly stopped. By the sixth day after surgery, he was doing better and was able to leave the ICU. He was awake, breathing on his own, and no longer needed a tube in his nose or strong medicine to keep his blood pressure up.\"\n}"}
{"row_index": 124, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 46-year-old Malay man had abdominal pain and yellowing of the skin (jaundice) due to a tumor in the duodenum. Imaging showed large masses in the duodenum and near the bile duct, so surgery was planned. He was considered high risk before surgery because of anemia, jaundice, and poor liver function. During the operation, there was heavy bleeding (2500 cc) due to the size of the tumor, so he needed a large amount of blood transfusions.\\n\\nAfter surgery, he developed low urine output, which is a sign of acute kidney injury (AKI). To help his kidneys, we started early continuous renal replacement therapy (CRRT) within 24 hours of diagnosing AKI, using a method called continuous veno-venous hemofiltration (CVVH). This treatment helped remove waste and excess fluid from his blood. After just a few hours, his urine output improved, and his blood pressure and blood sugar levels stabilized. His inflammation markers also dropped over time, showing that his body was healing.\\n\\nThe infection signs that appeared after surgery were managed with a stronger antibiotic. By the fourth day after surgery, his condition had improved enough that he was awake, able to breathe on his own, and was taken off the ventilator. He was discharged from the intensive care unit on the sixth day after surgery.\"\n}"}
{"row_index": 125, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 46-year-old male of Malay ethnicity presented with persistent abdominal pain and obstructive jaundice, leading to referral to the digestive surgery service at Fatmawati Central General Hospital. Physical examination revealed abdominal distension and palpable hepatosplenomegaly. Abdominal contrast-enhanced computed tomography (CT) demonstrated lobulated masses involving the duodenum and ampulla of Vater, consistent with a stage IIIb duodenal neoplasm. Given the extent and location of the lesion, total pancreatectomy with splenectomy was performed, with the patient admitted to the intensive care unit (ICU) postoperatively.\\n\\nPreoperative assessment identified high surgical risk due to significant anemia, obstructive jaundice, and impaired liver function. Intraoperatively, extensive tumor resection resulted in massive hemorrhage of 2500 cc, necessitating substantial blood product transfusion. Upon ICU admission, the patient exhibited oliguria, prompting escalation of vasopressor support to 0.3 µg/kg/minute to maintain mean arterial pressure (MAP) above 65 mmHg and systolic blood pressure (SBP) above 95 mmHg. Laboratory findings included a lactate level of 5.8 mmol/L, C-reactive protein (CRP) of 30 mg/dL, white blood cell count of 26,700/μL, and procalcitonin >32 ng/mL, confirming the presence of systemic inflammatory response syndrome (SIRS) secondary to surgical trauma.\\n\\nTwelve hours postoperatively, the patient developed postoperative acute kidney injury (AKI), defined by urine output <0.3 cc/kg/hour, meeting KDIGO stage 2 criteria. Early continuous renal replacement therapy (CRRT) was initiated within 24 hours of AKI diagnosis. CRRT was performed via continuous veno-venous hemofiltration (CVVH) with an effluent dose of 27 cc/kg/hour and zero fluid removal. Within three hours of initiation, clinical improvement was observed, including an increase in urine output to 0.5–0.6 cc/kg/hour, allowing for rapid tapering of vasopressor support. Furosemide infusion was administered 18 hours after CVVH initiation, resulting in further improvement in urine output to 1–4 cc/kg"}
{"row_index": 126, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old man with AIDS had sudden belly pain for 4 days and fever for 2 days. He already had AIDS, pneumonia, and likely tuberculosis 2 months before. His immune system was very weak at first, with only 91 healthy immune cells in his blood. He got medicine for pneumonia and TB, and later started treatment for HIV. When doctors checked him, his belly hurt on the left side, but no skin rashes or other signs were seen. A scan showed a small spot on his spleen and swollen lymph nodes inside his belly. Tests found a fungus in his blood and bone marrow, which caused the infection. He got IV antifungal medicine first, but had kidney problems, so they switched to a safer version. After 21 days, he started taking itraconazole pills instead of IV medicine. He stayed in the hospital for 29 days and got better. After that, he went home and kept getting better at follow-up visits. No more symptoms or tests were needed.\"\n}"}
{"row_index": 127, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 27-year-old man with AIDS had sudden abdominal pain for 4 days and a fever for 2 days. He had been diagnosed with AIDS, pneumocystis pneumonia, and suspected tuberculosis two months earlier. His initial CD4 count was 91 cells/mm³. He received treatment for both infections and started anti-retroviral therapy later. On exam, he had tenderness in the left upper part of his abdomen but no skin rashes or other signs of illness. His CD4 count improved to 272 cells/mm³ (19%) during this visit. A CT scan showed a small lesion in the spleen and swollen lymph nodes in his abdomen. Tests showed a high level of a fungal marker (galactomannan), leading doctors to treat him with amphotericin B, which was later switched to a safer version due to kidney issues. Blood and bone marrow cultures confirmed the presence of T. marneffei, a rare fungus. After 21 days of IV treatment, he switched to oral itraconazole. He was discharged after 29 days and continued to improve at his follow-up visit. He remains healthy and symptom-free at 12 months after treatment.\"\n}"}
{"row_index": 128, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 27-year-old Thai male with AIDS, originally from Mukdahan Province in Northeastern Thailand and residing in Saraburi Province (200 km south of Bangkok), presented with acute onset of left upper quadrant abdominal pain lasting 4 days and a fever of 2 days' duration, peaking at 38.9 °C. He had been diagnosed with AIDS 2 months prior at another hospital, with an initial CD4 count of 91 cells/mm³ (percentage and viral load unknown), and no comprehensive immune status evaluation was conducted. At that time, he presented with respiratory distress subsequently identified as pneumocystis pneumonia and presumptive smear-negative pulmonary tuberculosis. He received a 3-week course of trimethoprim/sulfamethoxazole and a standard anti-tuberculosis regimen consisting of isoniazid, rifampicin, pyrazinamide, and ethambutol during hospitalization. Anti-retroviral therapy (ART) comprising tenofovir disoproxil fumarate, emtricitabine, and efavirenz was initiated 2 weeks later as an outpatient. The anti-tuberculosis regimen was subsequently modified to isoniazid, rifampicin, ethambutol, and levofloxacin after 4 days, and chest radiographic follow-up demonstrated complete resolution of prior pulmonary opacities after 50 days of therapy. The patient maintained 100% adherence to both anti-tuberculosis treatment and ART, with no additional concomitant medications. His CD4 count 8 weeks prior to admission remained at 91 cells/mm³ (unknown percentage).\\n\\nOn presentation, abdominal pain was localized to the left upper quadrant, described as a dull ache without radiation to the chest, abdomen, or extremities, and was not associated with meals, physical activity, or changes in position. No gastrointestinal symptoms such as diarrhea, nausea, or vomiting were reported. Two days later, a high-grade fever developed without chills. Emergency department evaluation revealed a blood pressure of 120/75 mmHg, heart rate of 110 beats/min, temperature of 38.7 °C, and respiratory rate of 20 breaths/min. Physical examination showed a soft abdomen with normal bowel sounds, but significant tenderness in the left upper quadrant; the spleen was not palpable. No cutaneous lesions were observed on"}
{"row_index": 129, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man with a fever got sick in November 2018. Doctors found a big lump on his right side of the chest, filling up the space where the lung should be. Tests showed the cancer was in the lining of the lung (pleura) and had spread there but not to other parts of the body. Because of this, they started treatment with three medicines: pembrolizumab, bevacizumab, and chemo. After 4 rounds, the cancer got a little smaller, and stayed under control for 5 months. But later, the man had a lung problem (pneumonia) that needed medicine to fix. When they tried the medicines again, the cancer came back and spread to many organs. He ended up getting very sick and passed away in October 2019.\"\n}"}
{"row_index": 130, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 51-year-old man with stage IIIB pleural mesothelioma received second-line treatment using pembrolizumab, bevacizumab, and chemotherapy after initially getting standard chemotherapy. His treatment was guided by genetic testing (second-generation sequencing) that showed specific mutations in his tumor. After four cycles, he had a partial response, meaning the cancer shrunk somewhat, and lived without disease progression for 5 months. Pembrolizumab was stopped because he developed grade 2 immune-related pneumonia, which improved with oral steroids. However, when immunotherapy was restarted and he was given anlotinib, the cancer progressed. He eventually developed multiorgan dysfunction and died suddenly in October 2019.\"\n}"}
{"row_index": 131, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 51-year-old Asian male presented with a three-day history of fever in November 2018, prompting hospital admission. No significant past medical history was identified, including asbestosis, and no notable family history of malignancy was reported. Physical examination revealed diminished breath sounds on the right side, suggesting pleural involvement. Whole blood was obtained for next-generation sequencing (NGS) using a targeted gene panel (Yucebio, Shenzhen, China), which identified a TP53 splicing variant in exon 4 at a frequency of 6.44%, consistent with aberrant mRNA splicing leading to loss of tumor suppressor function. The tumor was classified as microsatellite stable (MSS) and exhibited a moderate tumor mutational burden (TMB) of 2.70 mutations per megabase (Mut/Mb), indicating a relatively high mutational load that may influence immunotherapy response. Due to patient refusal, no repeat biopsy was performed, and PD-L1 expression analysis was not conducted. Chest computed tomography (CT) demonstrated right pleural occupation with pleural effusion, and whole-body CT revealed diffuse involvement of the ipsilateral pleural surfaces, confirming localized pleural dissemination without evidence of distant metastasis. Based on these findings, the patient was initiated on second-line therapy comprising pembrolizumab (a PD-1 inhibitor), bevacizumab (an anti-VEGF monoclonal antibody), and standard chemotherapy regimen. After four cycles, a partial response was observed, with a progression-free survival of 5 months. Pembrolizumab was subsequently discontinued due to the development of grade 2 immune-related pneumonia, which was clinically managed with oral glucocorticoids and resolved without long-term sequelae. However, upon rechallenge with immunotherapy, disease progression was observed, followed by subsequent treatment with anlotinib (a multi-kinase inhibitor targeting VEGFR, PDGFR, and c-KIT), which failed to halt disease advancement. The patient ultimately experienced multiorgan dysfunction syndrome and died suddenly in October 2019. The case underscores the complexity of immunotherapy in mesothelioma, particularly in the absence of PD-L1 expression and biopsy confirmation, and highlights the role of tumor genomic features such as TP53 splicing variants and moderate TMB in guiding therapeutic decisions. Additionally, the observed immune-related adverse events and subsequent progression post-rechallenge suggest potential immune exhaustion or"}
{"row_index": 132, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 43-year-old man got a deep cut on his left forehead and near his ear from a broken lawnmower blade. The cut was bleeding very badly and couldn't be stopped by pressure. His blood pressure was very low and his heart was racing. He lost consciousness quickly and needed a breathing tube. Doctors quickly started giving him blood. They cut open his neck to stop the bleeding by squeezing the outside neck artery (ECA) for 100 minutes. This stopped the massive bleeding. They also used a balloon to plug the wound. Later, a scan showed a metal piece from the blade stuck in his skull, and there were many broken bones on the left side. There was also bleeding inside his brain. The metal piece was removed. The maxillary artery was cut and tied off. After that, the neck artery was released and no more bleeding was seen. He got a lot of blood and plasma. He stayed in the hospital for 10 days. He woke up and could move his body, but his left face stayed paralyzed because the facial nerve was damaged. He also lost vision in his left eye because the optic nerve was badly hurt. The bleeding was stopped, but the damage to his face and eye is permanent.\"\n}"}
{"row_index": 133, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 43-year-old man suffered a severe injury to his left forehead and neck area when a broken grass-cutting blade pierced his skin. The wound caused a serious, non-compressible bleed from an artery, which is a life-threatening situation. His blood pressure was very low and his heart rate was extremely high, showing he was in serious danger. He quickly lost consciousness and needed emergency treatment, including intubation and blood transfusions.\\n\\nDoctors used a tourniquet to temporarily stop the bleeding by squeezing the external carotid artery (ECA), which took 8 minutes from the time the emergency team activated to the start of the procedure. This helped stabilize him. The bleeding was controlled, and the patient was then taken for a CT scan of his brain and neck, which showed a metal piece from the blade, multiple skull fractures, and bleeding in the brain (subarachnoid and subdural hemorrhage), but no direct injury to major brain arteries.\\n\\nAfter the scan, the patient returned to surgery. The metal object was removed, and the maxillary artery was completely cut and sealed. The ECA was then released and no active bleeding was found. The total time the tourniquet was applied was 100 minutes. The dura (the protective covering of the brain) was repaired, and a drain was placed.\\n\\nHe received several units of blood products, including red blood cells, plasma, and platelets. He stayed in the ICU for 10 days. After recovery, he had mild brain function issues, with good consciousness (GCS E4V5M6) and normal movement on one side, but he lost vision in his left eye due to damage to the optic nerve. He also has permanent facial paralysis on the left side because the facial nerve was damaged and reconnected to a nearby nerve. The injury was serious, but the team managed to save his life with timely intervention and staged surgery.\"\n}"}
{"row_index": 134, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 43-year-old male presented with a severe penetrating injury to the left frontotemporal and preauricular region caused by a broken grass-cutting blade, resulting in a noncompressible, pulsatile arterial hemorrhage. Upon arrival at the trauma center, his vital signs were critically unstable: systolic blood pressure of 60–70 mmHg, tachycardia at 140 beats per minute, and oxygen saturation of 80%. Physical examination identified active arterial bleeding originating from the maxillary artery anterior to the mandibular neck. His neurological status rapidly deteriorated to E1V1M5, prompting immediate endotracheal intubation and initiation of group O red blood cell transfusion.\\n\\nThe trauma plus protocol was activated, and the patient was rapidly transported to the operating room. A longitudinal incision was made along the anterior margin of the left sternocleidomastoid muscle, with the posterior belly of the digastric muscle dissected to expose the carotid bifurcation. The left common facial vein was divided, and the left common carotid, external carotid (ECA), and internal carotid arteries were exposed and secured with vascular slings. Transient occlusion of the ECA was achieved using a Rumel tourniquet, which successfully controlled the massive arterial bleed. The interval between trauma protocol activation and ECA occlusion was 8 minutes. The preauricular wound tract was tamponaded with a balloon to stabilize the bleeding site.\\n\\nThe patient was then transferred for computed tomographic angiography (CTA) of the brain and neck, which revealed a metallic foreign body embedded in the left skull with multiple comminuted fractures involving the zygomatic process of the left temporal bone, lateral wall of the left orbit, left orbit apex, left superior orbital fissure, left optic canal, squamous part of the left temporal bone, sphenoid and ethmoid sinus walls, and the greater and lesser wings of the sphenoid bone. Imaging also demonstrated acute subarachnoid hemorrhage along the left Sylvian fissure and acute subdural hemorrhage on the frontotemporal convexity with associated brain swelling. Notably, no intracranial arterial injury was identified.\\n\\nFollowing CTA, the patient returned to the operating room for foreign body removal. A complete transection of the maxillary artery was identified"}
{"row_index": 135, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 10-year-old boy from Ethiopia came to the hospital with sudden weakness in his legs and trouble controlling his bladder and bowels for 10 days. He had pain in his stomach area for a long time but no fever or injury. Tests showed his liver was damaged and had a very high level of a protein called AFP, which is a sign of liver cancer. A needle test from the liver and imaging showed tumors in his liver and that the cancer had spread to his spine. This means he had liver cancer with cancer in his spine. The doctors told his parents about the serious outcome, and they chose to go home and care for him at home instead of continuing treatment.\"\n}"}
{"row_index": 136, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 10-year-old Ethiopian boy arrived at a hospital in Addis Ababa with sudden weakness in his legs and loss of control over his bladder and bowels, which had been going on for 10 days. He also had long-standing pain in his upper abdomen. He did not have a fever, cough, or any recent injury. He had not been exposed to someone with a chronic cough. Because he was born before the national hepatitis B vaccine program started, he never received the hepatitis B vaccine. His temperature was slightly high, and his liver was enlarged and painful. Neurological tests showed that his spinal cord damage was at the level of T10, with no muscle strength in his legs and no reflexes. Blood tests showed elevated liver enzymes and a very high level of alpha-fetoprotein (AFP), which is a marker for liver cancer. Imaging scans showed multiple liver tumors and a collapsed vertebra with swelling around the spine, pressing on the spinal cord. The doctors suspected either tuberculosis or cancer spreading to the spine. Further tests found solid liver masses and involvement of the portal vein. The fine needle biopsy of the liver confirmed the presence of hepatocellular carcinoma (HCC) with spread to the spine. The family was given information about the serious prognosis and chose to stop treatment and go home for palliative care.\"\n}"}
{"row_index": 137, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 10-year-old Ethiopian male presented to Tikur Anbessa Specialized Hospital, Addis Ababa, with a sudden onset of lower extremity weakness beginning 10 days prior, associated with urinary and fecal incontinence. He had a history of chronic epigastric pain. No fever, diarrhea, cough, altered mental status, abnormal movements, or trauma was reported. No exposure to individuals with chronic cough was documented. He had received all routine childhood vaccinations, including four doses of oral polio vaccine, but was not vaccinated against hepatitis B due to the timing of his birth—prior to the implementation of a routine three-dose hepatitis B vaccination schedule in Ethiopia (which began in 2015), leading to a delayed exposure window. The patient presented in 2016.\\n\\nPhysical examination revealed an axillary temperature of 38.0 °C and tachycardia (115 beats per minute). Hepatomegaly was noted, measuring 16 cm in total span (10 cm below the right costal margin), described as hard and tender. Neurological assessment demonstrated a sensory level at T10, bilateral lower extremity muscle power of 0/5, areflexia, and hypotonic anal tone.\\n\\nLaboratory findings included a normal complete blood count and erythrocyte sedimentation rate (25 mm/hr). Liver function tests showed elevated alanine aminotransferase (160 U/L) and aspartate aminotransferase (136 U/L), with markedly elevated alkaline phosphatase (761 U/L) and low serum albumin (3.4 mg/dL). Coagulation profile, renal function, serum electrolytes, blood and urine cultures, human immunodeficiency virus (HIV), and hepatitis C virus (HCV) serologies were all negative. Hepatitis B surface antigen (HBsAg) was positive, confirming active hepatitis B infection. Further serologic characterization of the hepatitis B viral state (e.g., HBV DNA load, HBeAg status) was not available due to limited diagnostic access.\\n\\nThoracolumbar magnetic resonance imaging (MRI) revealed collapse of the T9 vertebral body with abnormal marrow signal characteristics: T1 isointensity and T2 heterogeneous hyperintensity, indicating intravertebral pathology. Extensive epidural and par"}
{"row_index": 138, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 28-year-old man with no prior health problems started having bad headaches and neck pain 2 months ago after lifting a heavy object. His symptoms got worse after a neck therapy session at a chiropractor he didn’t know was not trained properly. He began acting strangely and felt sick, with nausea and vomiting. When he finally went to the hospital, a brain scan showed blood buildup (SDH) on both sides of his brain. He had surgery to drain the blood, and right after, his headaches and neck pain went away. A follow-up scan 8 months later showed no blood left and no return of symptoms. He’s now fully better and back to normal.\"\n}"}
{"row_index": 139, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 28-year-old healthy man developed severe headaches and neck pain about 2 months ago after lifting a heavy object. His symptoms worsened after visiting a chiropractor for neck pain. He then started experiencing nausea, vomiting, and behavioral changes over the past two days. He went to the emergency department, where a brain CT scan showed bilateral subdural hematomas (SDHs) — collections of blood between the brain and the tissues covering it. He had no history of trauma, seizures, bleeding disorders, or drug use. After surgery, which involved small incisions in the skull to drain the blood, his symptoms improved quickly. The surgery was successful with no complications. A follow-up brain CT scan eight months later showed no remaining blood or signs of recurrence. He has been fully recovered and is back to normal without any ongoing symptoms.\"\n}"}
{"row_index": 140, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 28-year-old fit male soldier presented to the Emergency Department with a chronic history of severe headache, neck pain, nausea, and vomiting, accompanied by behavioral changes over the past two days. The headache and neck pain began two months prior following the lifting of a heavy object, with progressive worsening of symptoms. Prior to this episode, he had visited the ED twice, during which cervical spine X-rays were performed without brain imaging; he was discharged on analgesics and referred for outpatient follow-up, with no improvement in symptoms. Subsequently, he received a neck therapy session from an uncertified chiropractor, after which his headache and neurological symptoms significantly exacerbated. The headache became refractory and unbearable, prompting further evaluation with brain computerized tomography (CT), which revealed bilateral subdural hematomas (SDHs). There was no history of traumatic brain injury, loss of consciousness, seizures, or systemic conditions such as hematological disorders, coagulopathies, or bleeding tendencies. The patient denied smoking, alcohol, or illicit drug use, and had a negative family history of intracranial aneurysms or inherited bleeding disorders. Physical examination revealed stable vital signs, normal temperature, and alertness with orientation, though the patient exhibited signs of depression and agitation. A notable neurological finding was the onset of bilateral, involuntary, repetitive extension movements involving the little fingers, which began two days prior to presentation. The remainder of the neurological examination was unremarkable. All routine laboratory investigations, including complete blood count, coagulation profile (Factor VIII and XIII, vWF cofactor and antigen), and blood smear, were within normal limits. Advanced imaging studies—computed tomography angiography (CTA), magnetic resonance angiography (MRA), and whole-spine magnetic resonance imaging (MRI)—were performed to exclude underlying vascular pathology, arteriovenous malformations, or spinal cord compression, but no identifiable etiology was found. The patient underwent bilateral mini-craniotomies with placement of bilateral subdural drains for evacuation of the hematomas. Histopathological examination of the external membrane of the SDH demonstrated typical features consistent with subdural hematoma formation, including fibrin deposition, erythrocyte clots, and organized fibrous tissue, confirming the diagnosis. The surgical procedure was successful with no intraoperative complications or significant bleeding. Clinical symptoms improved immediately postoperatively. During hospitalization, additional hemostatic workup was completed and"}
{"row_index": 141, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 14-year-old boy got hurt when a baseball hit his right middle finger. At first, he wore a splint, but didn’t go back for check-ups. Five months later, his finger still hurt and couldn’t move well. Doctors saw that a piece of bone and cartilage was missing from the joint, and it was misaligned. They fixed it with surgery. A small hole was made in the finger’s joint, and a piece of bone and cartilage taken from the boy’s knee was put in the hole and pressed in place. The knee piece was taken from a part that doesn’t carry weight, so it didn’t hurt. After surgery, he started moving his finger right away and used a tape to help it heal. After 3 months, he stopped using the tape and went back to playing baseball. One year later, his finger no longer hurt, moved freely from straight to bent, and the joint looked smooth on a scan. The knee where the piece came from is still healthy, and the finger is back to normal.\"\n}"}
{"row_index": 142, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 14-year-old boy injured his right middle finger with a baseball hit. Initially, he was treated with a splint, but he didn’t follow up properly. Five months later, he still had pain and trouble moving his finger. X-rays and a CT scan showed a bony and cartilage defect in the joint of the finger, which meant the fracture had not healed properly. This condition was diagnosed as a malunited intra-articular fracture of the PIP joint. The boy had surgery to fix it. A small piece of bone and cartilage (osteochondral plug) was taken from his left knee, where the joint doesn’t bear much weight, and inserted into the damaged area of the finger. The plug was pressed into place using a drill hole. After surgery, he wore a splint for one day and then started gentle finger exercises. He continued buddy taping for three months and gradually returned to playing baseball. One year later, he has no pain, can fully bend and straighten his finger, and the joint looks healthy on MRI. The bone has healed well, and there is no damage to the knee donor site. A small amount of finger misalignment still remains, but it has improved significantly.\"\n}"}
{"row_index": 143, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 14-year-old right-handed male presented with persistent pain and restricted range of motion (ROM) in the right middle finger five months following a traumatic baseball impact. Initial management at the treating hospital included splint fixation for a fracture of the middle phalanx, but the patient discontinued follow-up care. Clinical examination at presentation revealed swelling and ulnar deviation of the proximal interphalangeal (PIP) joint at extension, with a limited ROM of 0° extension to 60° flexion. Radiographic evaluation—including posterior-anterior and lateral views—demonstrated a bony defect on the articular surface of the middle phalanx, with ulnar displacement of the digit. Lateral X-ray showed a depressed articular surface, and computed tomography (CT) confirmed a 5 × 6.5 × 2 mm bony defect localized to the PIP joint articular surface of the middle phalanx. Additional imaging revealed a 1 × 2 mm cartilage defect on the palmar aspect of the proximal phalanx articular surface. Based on these findings, a diagnosis of malunited intra-articular fracture of the PIP joint was established, prompting surgical intervention. A palmar incision was used to expose the PIP joint, and a columnar-shaped recipient hole was created at the site of the osteochondral lesion in the middle phalanx. A cylindrical autogenous osteochondral plug measuring 4.5 mm in diameter was harvested via the mosaicplasty autogenous osteochondral grafting system (Acufex, Smith & Nephew, Andover, MA, USA) from the upper lateral femoral condyle of the left knee—a non-weight-bearing site—using an obliquely angled cartilage surface aligned with the long axis to optimize insertion geometry. The osteochondral plug was press-fitted into the recipient site to achieve mechanical and biological integration. The proximal phalanx cartilage defect, measuring 1 × 2 mm, was left untreated due to its minimal size and lack of functional impact. Postoperatively, the patient underwent immediate splint fixation followed by early mobilization initiated the next day via buddy taping, which was maintained for up to three months. After removal of buddy taping, the patient gradually resumed athletic activity, including baseball. At one-year follow-up, the patient reported complete resolution of pain and restoration of PIP joint ROM to 0"}
{"row_index": 144, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old woman came to the emergency room with severe belly pain, nausea, and vomiting. She had a history of diabetes and prior belly problems. A scan showed a blockage in her small intestine, near the part called the jejunum, and enlarged lymph nodes in her pelvis. Doctors thought it could be cancer, scar tissue, or inflammation. Her condition got worse quickly, so they had to surgically remove part of her small intestine. After checking the tissue, doctors found cells that looked like cancer, especially T-cells that were growing fast and were all part of the same group. This matched a rare type of cancer called jejunal EATL. Five weeks later, she started having brain problems — her mind changed and she lost strength on her left face and arm. A brain scan showed a tumor in the right front part of her brain, with swelling around it. She had surgery to remove it, and the tissue tested confirmed the tumor was from the same type of cancer that had spread to her brain. This means the cancer started in her small intestine and spread to her brain.\"\n}"}
{"row_index": 145, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 65-year-old woman came to the emergency room with severe abdominal pain, nausea, and vomiting. She had a history of type 2 diabetes and previous intestinal problems. A CT scan showed a blockage in her small intestine, specifically in the jejunum, and enlarged lymph nodes in her pelvis. Doctors considered possible causes like a tumor, scar tissue, or inflammation.\\n\\nHer condition quickly got worse, so she needed emergency surgery to remove part of her small intestine. Examining the removed tissue showed signs of both benign T-cells (which can happen in celiac disease) and abnormal lymphocytes with unusual features. These abnormal cells were positive for CD-3, had a high rate of cell growth (90% stained positive for Ki-67), and showed a clonal pattern in T-cell gene testing — all signs of a rare type of lymphoma called jejunal extranodal T-cell lymphoma (EATL).\\n\\nFive weeks after diagnosis, she started having new neurological symptoms, including confusion and weakness on her left side. A brain MRI found a single abnormal area in the right front and parietal part of her brain, surrounded by swelling. She had surgery to remove this brain lesion, and the tissue sample confirmed it was metastatic EATL — meaning the cancer had spread from her intestine to her brain.\"\n}"}
{"row_index": 146, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 65-year-old female presented to the emergency room with uncontrolled abdominal pain, nausea, and vomiting. Her medical history included Type 2 diabetes mellitus, a prior history of intestinal intussusception, and chronic moderate abdominal pain. Initial abdominal computed tomography (CT) scan revealed a small bowel obstruction with a transition point localized in the jejunal region, accompanied by mildly enlarged lymph nodes in the right pelvic region. The differential diagnosis considered small bowel neoplasm, postoperative adhesions, or a reactive intestinal inflammatory process, such as celiac disease. Histological examination of the resected jejunal segments demonstrated small intestinal mucosa with intraepithelial and mucosal infiltrates of benign CD3-positive T-cells, consistent with celiac sprue, suggesting a prior immune-mediated enteropathy. In addition, the tissue showed medium-sized infiltrating lymphocytes exhibiting pleomorphic nuclei and prominent nucleoli, indicative of a proliferative lymphoid process. Immunohistochemical staining revealed tumor cells positive for CD-3, with weak positivity for BCL-2, and negative staining for CD5, CD20, CD10, and cyclin-D1—findings that exclude B-cell lymphoma and support a T-cell origin. Ki-67 immunoreactivity demonstrated a markedly elevated proliferative index, with 90% of the lymphocytes showing positive staining, reflecting a high rate of cell division and aggressive biological behavior. Polymerase chain reaction (PCR) analysis of the T-cell receptor-gamma (TCRγ) gene revealed clonal rearrangement, confirming the presence of a monoclonal population of T-cells, a hallmark of malignancy in T-cell lymphoproliferative disorders. The integrated morphological and immunophenotypic profile of the jejunal lesion is consistent with extranodal T-cell lymphoma, enteropathy type (EATL), specifically involving the small intestine. Systemic workup, including blood chemistry, imaging, and serologic markers, was non-contributory, supporting the localization of the primary disease to the gastrointestinal tract. The patient was discharged and initiated chemotherapy for the primary EATL. Three weeks after diagnosis, a whole-body positron emission tomography-CT (PET-CT) scan of the skull to mid-thigh demonstrated no hypermetabolic lesions suggestive of active malignancy in the cranial base or neck, indicating a clinically quiescent systemic disease at that time. However, five"}
{"row_index": 147, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 24-year-old woman has had muscle pain for many years, starting when she was 7. The pain comes and goes, used to happen every 1–2 years, but now happens up to four times a year. Each time, it starts with a sore throat, cough, or urinary tract infection. When the pain comes, her muscles hurt a lot, but it goes away quickly when she takes a medicine called prednisolone. She had her tonsils removed in 1992 because of frequent sore throats. No other health problems were found. This pattern — muscle pain starting with infections — has never been seen before in someone her age and with this frequency.\"\n}"}
{"row_index": 148, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 24-year-old Caucasian woman has had recurring muscle pain, especially in her legs, for over 18 years. The pain usually comes after infections like sore throats, coughs, or urinary tract infections, and has occurred up to four times a year in recent years. This pattern — frequent muscle inflammation triggered by infections — has not been seen before. When she had these episodes, her muscle enzymes (CK) were elevated, and the pain improved quickly with oral steroids. She had a tonsillectomy in 1992 due to repeated sore throats, but no other major health issues. Tests showed no evidence of common viruses like strep, flu, or EBV in active form, and no signs of immune deficiency. Muscle biopsies showed inflammation, especially from a type of white blood cell called CD4 lymphocytes, suggesting a specific immune reaction. Despite extensive testing, no clear cause was found, and the condition appears to be rare and unique to her case.\"\n}"}
{"row_index": 149, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 24-year-old Caucasian female presented with a 17-year history of recurrent lower limb myositis, initially occurring every 1–2 years since age seven, with a marked increase in frequency to four episodes annually starting in 2005. Each episode was preceded by upper respiratory tract infections (e.g., sore throat, cough) and, more recently, by urinary tract infections (dysuria). During active attacks, serum creatine kinase (CK) levels ranged from 89 to 700 U/litre (normal <175 U/litre), reflecting muscle damage, and normalized between episodes. Oral prednisolone provided rapid symptomatic relief, indicating a reversible inflammatory myopathy. A tonsillectomy was performed in 1992 based on a history of recurrent sore throats and elevated antistreptolysin O (ASOT) titre, with no other significant medical or drug history.\\n\\nDuring a detailed investigation in September 2005, a myositis episode was preceded by a productive cough with green sputum. Physical examination revealed mild pharyngeal injection and tenderness in the calves and anterior compartment muscles. Muscle biopsy of the right tibialis anterior demonstrated mild fiber atrophy of uncertain clinical significance. Laboratory findings included elevated erythrocyte sedimentation rate (ESR: 39 mm/hour), leukocytosis (16.6 × 10⁹/litre), with neutrophilia (13.6 × 10⁹/litre, 81.9%) and monocytosis (1.06 × 10⁹/litre, 6.4%). All other laboratory parameters—including lymphocyte, eosinophil, basophil counts, CK, renal, and hepatic function—were within normal limits.\\n\\nSerological testing was negative for influenza A/B, respiratory syncytial virus (RSV), Mycoplasma pneumoniae, Chlamydia, Q fever, adenovirus, enterovirus, and ASOT. Epstein-Barr virus (EBV) serology showed positive EBNA IgG, VCA IgG, and VCA IgM, which may reflect either a false-positive VCA IgM, a recent primary EBV infection (within 3–12 months), or EBV reactivation. Convalescent serology performed five months later revealed"}
{"row_index": 150, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 85-year-old woman who uses her left hand mostly had a lump on her thumb side of the hand that grew fast over six weeks. The lump was big, soft, and could move around — about 5 inches by 4 inches and covered the whole thumb area. Doctors first thought it might be cancer, but X-rays showed weak bones and damage near the thumb joint. A scan showed a fluid-filled sac near the joint. During surgery, they saw a lump with a neck that went into the thumb joint. Lab tests confirmed it was a ganglion cyst, a common type of fluid-filled bump. She recovered well and hasn’t had the lump come back.\"\n}"}
{"row_index": 151, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 85-year-old woman who uses her left hand mostly had a lump on the thumb side of her hand that grew quickly over six weeks. The lump was large, not painful, and could move around. It measured 5 by 4 centimeters and covered the entire thenar area. At first, doctors thought it might be a sarcoma, a type of cancer. X-rays showed weak bones and damage to the joint at the base of the thumb, along with a soft tissue swelling near a bone spur. MRI showed a cyst-like structure connected to the thumb joint, with signs of active joint inflammation. During surgery, the doctors saw a multilobulated lump that extended into the thumb joint. Lab tests confirmed it was a ganglion cyst, a common benign (non-cancerous) cyst that forms near joints. The patient recovered well after surgery and has not had any signs of the lump coming back.\"\n}"}
{"row_index": 152, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 85-year-old left hand-dominant female presented with a six-week history of a rapidly enlarging lump at the thenar eminence. Clinical examination identified a non-tender, large, lobulated, mobile swelling measuring 5 × 4 cm that involved the entire thenar region. Initial differential diagnosis included sarcoma due to the size, rapid growth, and location. Plain radiography demonstrated severe osteopenia with erosive changes at the first carpometacarpal (CMC) joint, along with a soft tissue mass adjacent to a detached osteophyte originating from the base of the first metacarpal. Magnetic resonance imaging (MRI) revealed a septate, thin-walled, cystic lesion extending from the first CMC joint space, occurring against a background of diffuse active synovitis, suggesting chronic joint inflammation and possible mechanical irritation. In the operating theater, a multilobulated lesion with a well-defined neck extending into the first CMC joint was observed, consistent with a complex cystic structure. Histological evaluation of a 3.4 g specimen previously excised confirmed a ganglion cyst, specifically a thenar ganglion arising from the synovial membrane of the first CMC joint, with characteristic features including a cystic lumen, fibrous septa, and associated synovial proliferation. The lesion was fully resected with clear margins. Post-operative course was uncomplicated, with no evidence of recurrence at follow-up. The pathogenesis is likely attributable to mechanical stress and joint instability, leading to synovial cyst formation via fluid accumulation in the joint capsule and surrounding connective tissue, a process amplified by age-related degenerative joint changes and osteopenia. The presence of active synovitis on MRI supports the inflammatory component of the cystic lesion, which may contribute to its growth and expansion over time.\"\n}"}
{"row_index": 153, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old woman had a lump in the area where the rectum and vagina meet for 9 years. It grew quickly in the last year, from 4 cm to 9.7 cm, and started causing problems like stool getting stuck. A doctor saw the lump with a special tube (endoscopy) and thought it might be a type of tumor or a fibroid. But when they tried to take a small piece of tissue from the lump with a needle (biopsy), they got too little tissue and also had bleeding from the vagina, so they couldn’t make a clear diagnosis. After talking with a team of doctors, they decided to try again using a better method: a needle guided by ultrasound to find the right spot. This time, they got enough tissue and found it was a rectal tumor called a GIST. The doctors recommended a drug called imatinib to shrink it first. After the tumor got smaller, they removed it through the back of the vagina. After surgery, they gave extra treatment to help prevent it from coming back. As of December 2019, the tumor hasn’t come back or spread anywhere.\"\n}"}
{"row_index": 154, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old woman had a mass in the area between her rectum and vagina for 9 years. It didn’t grow much until the past year, when it enlarged from 4.0 cm to 9.7 cm and started causing symptoms like difficulty passing stool due to pressure. An endoscopy showed a growth under the rectal lining, but repeated biopsies only found inflammation, not actual tumor tissue — which didn’t match her symptoms. She came to our hospital for a clearer diagnosis.\\n\\nInitial tests, including blood work and imaging, were normal. A CT scan and ultrasound showed a large, irregular mass in the rectovaginal space, which could be either a gastrointestinal stromal tumor (GIST) or an uterine fibroid growing outward.\\n\\nA first biopsy was done using a needle through the abdomen, but it failed because the tissue collected was too small and the procedure caused vaginal bleeding, which stopped the biopsy early. Pathologists could not make a definite diagnosis from that sample.\\n\\nAfter discussion among doctors from different specialties, a second biopsy was planned using a more precise method. This involved using ultrasound guidance — first with endoscopic ultrasound (ERUS) and then with contrast-enhanced ultrasound (CEUS) — to see exactly where the active, living parts of the tumor were, avoiding the dead (necrotic) areas. This helped ensure the needle would reach the right part of the tumor.\\n\\nThe second biopsy was done through the perineum (the area between the vagina and anus) under local anesthesia, with real-time ultrasound guidance. The doctors successfully collected tissue from the active part of the tumor. Pathology confirmed it was a rectal gastrointestinal stromal tumor (GIST).\\n\\nThe medical team recommended imatinib as the first-line treatment, which helped shrink the tumor. Once it was small enough, the tumor was removed through the back of the vagina. After surgery, additional treatment was given to reduce the risk of coming back. As of December 13, 2019, the patient has not had any recurrence or spread of the cancer.\"\n}"}
{"row_index": 155, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old female presented with a progressively enlarging mass in the rectovaginal space, initially detected during a routine examination 9 years prior. No significant growth was observed in annual follow-ups until a 12-month period of rapid expansion, during which the mass increased from a maximum diameter of 4.0 cm to 9.7 cm, resulting in symptomatic compression of the rectal lumen and the development of stool-related dents. Endoscopic evaluation at an external facility revealed a submucosal protrusion, yet repeated endoscopic biopsies over the preceding two years yielded only inflammatory findings—lacking definitive tumor tissue—contradicting the clinical suspicion of a neoplastic process. This discrepancy prompted referral to our institution for definitive diagnosis.\\n\\nThe patient had no significant comorbidities, no personal or familial history of malignancy, and preserved general health parameters, including normal mental status, appetite, sleep, weight, and absence of abdominal distension, tenesmus, rectal prolapse, diarrhea, or constipation. Digital rectal examination demonstrated a plump anterior rectal wall without tenderness or visible blood on the digit.\\n\\nLaboratory investigations, including complete blood count, coagulation profile, carcinoembryonic antigen (CEA), α-fetoprotein (AFP), carbohydrate antigen (CA) 19-9, and CA125, were within normal limits, excluding systemic malignancy or infection.\\n\\nContrast-enhanced computed tomography (CECT) revealed a heterogeneous mass within the rectovaginal space with central liquefaction necrosis (low-density region) and indistinct margins. Transabdominal ultrasound (US) identified a heterogeneous hypoechoic lesion measuring 9.7 cm in maximum diameter, consistent with either a rectal gastrointestinal stromal tumor (GIST) or an exophytic uterine fibroid.\\n\\nA transabdominal core needle biopsy (CNB) was performed using the MG1522 BARD MAGNUM Biopsy Instrument (16 G, 16 cm, disposable, Tempe, AZ, USA), with prior written informed consent obtained. Preoperative laboratory workup was unremarkable. However, spontaneous vaginal hemorrhage occurred during the procedure, terminating the biopsy prematurely. The retrieved tissue consisted of fragmented greyish material with a maximum diameter of less than 0.3 cm. Hist"}
{"row_index": 156, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 68-year-old woman had pain in her left leg for 3 weeks. At first, she went to urgent care for redness and swelling on her shin, and was given antibiotics for a possible infection, but it didn’t get better. When she came to the emergency room, she wasn’t feverish and was stable. Her leg was still red, swollen, and painful, especially when walking. Tests showed her body was fighting an infection. A scan (ultrasound) found a hole in her bone and fluid moving back and forth through it, which means the bone is infected. Doctors diagnosed it as bone infection (osteomyelitis) and treated her with strong antibiotics and surgery to drain the pus from the soft tissue. The surgery helped, and she’s now getting antibiotics for 6 weeks to make sure the infection is fully gone.\"\n}"}
{"row_index": 157, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old woman came to the emergency department with 3 weeks of increasing pain in her left lower leg. She first visited urgent care, where her left shin was red and swollen, and she was given antibiotics for a suspected skin infection (cellulitis) with ceftriaxone. The pain didn’t improve. At the emergency department, she was not feverish and her blood pressure was normal. Her left shin remained red, swollen, and tender, and the swelling stopped before reaching her knee. Blood tests showed high levels of inflammation. An ultrasound scan revealed a fluid collection near the bone, with a break in the bone surface and fluid flowing back and forth—this is a sign of bone infection. The imaging also showed a large fluid-filled area near the tibia, with connections to the inside of the bone. A CT scan confirmed a large abscess near the tibia, with signs of both skin and bone infection. She was diagnosed with osteomyelitis, an infection of the bone. She was started on strong antibiotics and had surgery to drain the abscess. No bacteria were found in the wound or blood samples. Her treatment continued with antibiotics for 6 weeks under the guidance of specialists.\"\n}"}
{"row_index": 158, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old female with a history of hypertension, hyperlipidemia, type 2 diabetes mellitus, gout, rheumatoid arthritis, and bilateral knee replacements—on clindamycin prophylaxis due to prior joint infections—presented to the emergency department with a three-week history of progressive left lower extremity pain. Initial evaluation at urgent care revealed erythema and swelling of the left shin, with plain radiographs showing no osseous abnormalities. She was empirically treated for cellulitis with intramuscular ceftriaxone for 10 days, but symptoms persisted without resolution. On presentation, she was afebrile and hemodynamically stable, with persistent erythema, swelling, and tenderness localized to the left pretibial soft tissues. The area of involvement extended distal to the knee joint, with no joint effusion or objective limitation in range of motion; pain was exacerbated by ambulation, though she maintained partial weight-bearing capacity. Repeat plain radiographs demonstrated focal soft tissue swelling overlying the anterior tibia. Point-of-care ultrasound, performed using orthogonal transverse and longitudinal scanning with a linear probe, revealed a large heterogeneous fluid collection adjacent to the tibial cortex. A focal defect in the cortical bone was identified, with pulsatile fluid communicating directly with the medullary cavity. Bidirectional flow of fluid was confirmed via color Doppler and pulsed-wave spectral Doppler, indicating active communication between the soft tissue collection and the intramedullary space. Laboratory findings included a normal white blood cell count (7.7 × 10³/μL), but markedly elevated systemic inflammatory markers: C-reactive protein (CRP) at 38 mg/dL and erythrocyte sedimentation rate (ESR) at 91 mm/hr. Computed tomography (CT) imaging revealed a 5.7 × 2.4 × 7.1 cm fluid collection adjacent to the tibial cortex, with well-defined sinus tracts extending into the medullary cavity, consistent with an abscess complicated by adjacent cellulitis and osteomyelitis. The patient was initiated on vancomycin and piperacillin/tazobactam, and orthopedic surgery was consulted. She was admitted to the internal medicine service and underwent incision and drainage of the left pretibial abscess. Neither wound nor blood cultures yielded growth. Infectious Diseases reviewed the"}
{"row_index": 159, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 71-year-old man had knee surgery 18 months ago and started having bad knee pain a few weeks after. The surgery went well, but the pain got worse over time. Doctors checked and found no problems with the knee or infection. The pain was sharp, spread to his ankle, and made his knee feel tingly. He had trouble with touch and pain in his knee, but his leg strength was normal. After trying medicine and other treatments, the pain didn’t go away. A short test with a nerve block helped a little, but only for about a month. Then he tried a pain device called a spinal cord stimulator, which works by sending gentle signals to his nerves. The device was placed successfully and worked great. Right after, his pain stopped completely. Six months later, he still has no pain and no longer needs pain pills.\"\n}"}
{"row_index": 160, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 71-year-old man who had knee surgery 18 months ago now suffers from chronic left knee pain that worsened over time. After the surgery, he did well initially, but started having increasing pain around the third week after surgery. His knee was working properly, and there was no sign of infection or hardware problems. The pain was sharp, rated 7 out of 10, and spread to his ankle, with numbness or tingling in the same area. He also had increased sensitivity to touch (allodynia) and sharp pain from light touch (hyperesthesia) on the front of his knee. His strength was normal, and his wound was healing well. After trying physical therapy and several pain medications with little success, he had a temporary improvement with a sympathetic nerve block, lasting about a month. He then had a trial of a spinal cord stimulator (SCS), which successfully reduced his pain. He received two 16-contact leads with a Boston Scientific SCS system, which delivers different types of electrical stimulation to block pain signals. After the first follow-up, he reported complete relief from pain. At his 6-month check-up, his pain was still fully gone, and he was able to stop using opioid pain medication entirely.\"\n}"}
{"row_index": 161, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 71-year-old Caucasian non-Hispanic male presented with chronic left knee pain persisting 18 months following total knee arthroplasty (TKA). His preoperative medical history included well-controlled hypertension, hyperlipidemia, and gastroesophageal reflux disease, with no significant comorbidities or prior surgical interventions. He measured 70 inches in height and weighed 215 lbs, with a normal body mass index (BMI) consistent with overweight status. He was retired, previously maintained an active lifestyle involving regular physical activity and daily functional mobility, and had no history of tobacco use; his social history included moderate social alcohol consumption. Post-TKA, he initially reported good recovery during the acute postoperative phase, but developed progressively worsening left knee pain beginning around the third postoperative week. The pain was described as sharp, with a visual analog scale (VAS) intensity of 7/10, poorly localized, radiating to the left ankle, and associated with paresthesias in a dermatomal distribution consistent with anterior lower extremity innervation. Physical examination revealed hyperesthesia and allodynia specifically along the anterior knee region, with intact motor function: lower left leg strength was 5/5 in both flexion and extension, and full strength (5/5) was observed in all lower extremity myotomes, including hip flexion, inversion, eversion, plantar flexion, and dorsiflexion. The surgical incision was well-healed, without signs of erythema, swelling, or tissue compromise. Orthopedic imaging and clinical assessment ruled out hardware loosening, infection, or mechanical joint pathology, supporting the exclusion of primary orthopedic causes of pain. Given the constellation of symptoms—including sensory hyperexcitability, allodynia, preserved motor function, and absence of structural or inflammatory joint pathology—a diagnosis of complex regional pain syndrome (CRPS) type I of the left lower extremity was established. Initial conservative management with physical therapy, non-steroidal anti-inflammatory drugs (NSAIDs), muscle relaxants, neuropathic agents (e.g., gabapentin, pregabalin), and low-dose opioids provided minimal to no symptomatic relief. A lumbar sympathetic block was performed, resulting in transient pain reduction to a VAS of 3/10, which lasted approximately one month, suggesting a sympathetic-mediated component to the pain pathway. This response prompted further intervention. The patient"}
{"row_index": 162, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 46-year-old woman had a long-term thyroid problem where her body wasn’t making enough thyroid hormone. She was taking a medicine called levothyroxine every day to fix it. For years, her thyroid tests looked normal, so her doctor kept the dose the same. Eight years later, her test showed very high levels of a hormone called FT4, but she had no signs of being overactive — like fast heartbeats or weight loss. This didn’t make sense. The lab checked again using a different testing method, and found the real level was actually low. The reason? Her body made antibodies that messed up the test. These antibodies thought the hormone was there when it wasn’t. This is called anti-T4 autoantibodies. The test that measures free T4 is not always accurate when these antibodies are present. After testing, her doctor gave her the original dose of medicine again, and her thyroid levels became normal. She doesn’t have any symptoms of overactive thyroid, and the problem was only caught because of the wrong test results.\"\n}"}
{"row_index": 163, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 46-year-old woman with long-term hypothyroidism, treated with levothyroxine, was seen eight years after her diagnosis. Her routine blood tests showed a high level of free thyroxine (FT4) and a slightly high TSH, but she had no symptoms of an overactive thyroid, like rapid heartbeat or weight loss. This was confusing because her thyroid function was stable for years, and she didn’t feel any different. Tests using two different lab methods showed a big difference: one method showed a very high FT4, while the other showed a low FT4. This inconsistency raised suspicion that her blood test was being affected by antibodies in her blood that react with thyroxine, specifically anti-T4 autoantibodies. These antibodies interfered with the test results, making the FT4 appear higher than it actually was. The problem was confirmed through special lab tests that showed the antibodies were causing the false high reading. The patient did not have symptoms of hyperthyroidism, and her other thyroid markers were normal. After confirming the interference, her levothyroxine dose was restored to the original level. This case shows that sometimes lab results can be misleading due to antibodies, and it’s important to use multiple testing methods when there’s a mismatch in results, especially in patients with long-standing thyroid conditions.\"\n}"}
{"row_index": 164, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"We report a case of a 46-year-old female with autoimmune hypothyroidism managed on chronic levothyroxine replacement, who presented eight years after diagnosis with a serum thyrotropin (TSH) of 7.393 µUI/mL (normal range: 0.5–5 µUI/mL) and a markedly elevated free thyroxine (FT4) level of 51.7 pg/mL (normal range: 8–18 pg/mL), alongside a normal free triiodothyronine (FT3) level of 2.8 pg/mL (normal range: 2.3–4.2 pg/mL). The patient exhibited no clinical signs of hyperthyroidism, including tremor, palpitations, sweating, insomnia, diarrhea, or visual disturbances, and had no family history of thyroid disease. Her body mass index was 35 kg/m², blood pressure was 129/88 mmHg, and heart rate was 98 bpm. She had recently gained 7 kg over six months, but denied symptoms consistent with hyperthyroidism. Given the absence of hyperthyroidism symptoms and the normal FT3 level in the context of high FT4, interference in FT4 quantification was suspected. The diagnosis of thyroid hormone resistance was ruled out due to normal FT3 levels and absence of familial thyroid disease.\\n\\nInitial testing was performed using the Siemens Healthcare Reagents Kit on the Advia Centaur platform, which reported a high FT4 value of 51.7 pg/mL. To evaluate potential assay interference, a parallel FT4 measurement was conducted in a second immunoassay platform, the Roche Cobas e 411, using a Roche Diagnostics reagent kit. The test was performed on serum collected 20 days after the initial sample, following overnight fasting and 24 hours post-levothyroxine administration. Serum samples were processed with 20-minute room temperature incubation, centrifuged at 3000g for 15 minutes, and either analyzed immediately or stored at −70°C for seven days. Quality control was maintained using freeze-dried human-based controls: Biorad Immunoassay Plus Control (Advia Centaur) and Roche Precinorm U (Cobas e 411), with intra- and inter-run coefficients of variation (CV) of <"}
{"row_index": 165, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 26-year-old man with no serious health problems before suddenly got weak in both legs after getting a shot of dexamethasone. He had muscle cramps earlier, which went away, but then woke up weak and couldn't stand. His legs were very weak, and he fell, hurting his arms. His blood showed very low potassium, which is a key mineral for muscles. Doctors gave him potassium shots, and within hours his legs started getting stronger. He could walk again after his potassium levels went back to normal. Tests showed he wasn’t losing potassium through his urine or stool, and no other medicines were causing it. The weak muscles came back fast when potassium was fixed, so doctors thought it was hypokalemic periodic paralysis. This condition is not hereditary in his family, and it was likely caused by the steroid shot. Later, he had another episode after eating a big meal with lots of carbs. Now he knows to avoid steroid shots and high-carb foods to stay safe.\"\n}"}
{"row_index": 166, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 26-year-old Asian man suddenly developed weakness in both legs after receiving an injection of dexamethasone, a steroid medication. He had no prior medical problems, except for a long-time history of aseptic meningitis that did not cause lasting issues. He worked as a construction worker and had been experiencing muscle cramps in his right shoulder and back for a week. He visited a traditional medicine practitioner who gave him anti-inflammatory drugs and another unknown injection. The cramps went away, but the next morning he woke up with sudden leg weakness, making it hard to stand and causing him to fall and get bruises on his arms.\\n\\nAt the emergency department, his temperature was slightly elevated, but his blood pressure and other vital signs were normal. His mental state was clear, and he was well-nourished. Examination showed that his leg muscles were weak, especially in the upper parts of the legs, with strength dropping from 2/5 to 1/5. His arms and reflexes were normal, and there was no sign of nerve damage. Blood tests showed low potassium levels (1.7 mEq/L), which is a key factor in muscle weakness. His ECG showed changes typical of low potassium, and after receiving potassium supplements, his muscle strength improved by the afternoon. His potassium levels returned to normal (4.0 mEq/L), and he was able to walk again.\\n\\nHis urine tests showed he wasn’t losing potassium through his urine, and he had not taken any medications known to cause potassium loss, such as diuretics or insulin. His hormone levels were mostly normal, except for a slightly high TSH, which may have played a role. The doctors believed the weakness was caused by hypokalemia (low potassium), and since it improved quickly after potassium was restored, they did not perform further tests like electromyography.\\n\\nIt was later found that the dexamethasone injection had triggered the condition. This type of hypokalemic periodic paralysis (HPP) is not inherited and is often triggered by certain medications or high-carbohydrate meals. The patient was advised to avoid corticosteroids and large meals high in carbohydrates to prevent future episodes. A year later, he had another episode after eating a large carbohydrate meal, confirming the pattern.\\n\\nThe final diagnosis was non-familial hypokalemic periodic paralysis, likely caused by the dexamethasone injection.\"\n}"}
{"row_index": 167, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 26-year-old Asian male presented to the emergency department with an acute onset of bilateral proximal lower limb weakness, initially manifesting as difficulty standing and subsequent falls resulting in upper limb contusions. The patient had no significant medical history beyond a prior episode of aseptic meningitis over a decade ago, which was asymptomatic. He was a construction worker engaged in heavy physical labor and reported intermittent muscle cramping in the right shoulder radiating to the back for one week. Prior to presentation, he received intramuscular injections of non-steroidal anti-inflammatory drugs (NSAIDs) and an unknown agent from a traditional medicine practitioner, after which the cramping resolved. However, upon waking in the morning, he developed acute, symmetric lower limb weakness, with initial muscle strength in both legs measured at 2/5, progressing to 1/5, while upper limb strength remained preserved. Neurological examination revealed intact deep tendon reflexes (knee jerks) and lower limb sensation, with no Babinski sign bilaterally, indicating no upper motor neuron involvement.\\n\\nVital signs were stable, with a tympanic temperature of 38.1°C, normotension, and no signs of systemic infection or shock. Laboratory investigations revealed a normal complete blood count, blood glucose, and urinalysis; however, serum potassium was markedly low at 1.7 mEq/L, with a mild elevation in creatine phosphokinase (178 U/L), consistent with myopathic changes. Electrocardiography demonstrated flattened T waves and prominent U waves in precordial leads V1–V3, which are characteristic of hypokalemia and reflect decreased cardiac membrane stability. Oral and intravenous potassium supplementation (initially 40 mEq) was administered, with serum potassium remaining at 2.0 mEq/L the following morning. A second bolus of 60 mEq was given, leading to a gradual improvement in lower limb muscle strength to 4/5 by afternoon. The patient was admitted and received an additional 20 mEq of intravenous potassium (total 120 mEq), resulting in normalization of serum potassium to 4.0 mEq/L and full recovery of ambulation.\\n\\nUrinary potassium excretion was low (urine potassium/creatinine ratio of 1.5 mmol/mmol), excluding significant renal potassium wasting. There was no evidence of gastrointestinal potassium loss, and"}
{"row_index": 168, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old man felt pain in his chest that spread to his back and left shoulder, like a heart attack, but tests showed no heart damage. His heart was sitting too far to the left, and X-rays showed lung tissue pushing between the aorta and the main lung artery. A special heart scan (MRI) found that the left layer of the heart's outer sac was missing — this is called left pericardial agenesis. The heart moves a lot and is twisted, which causes the lung tissue to push into places where it shouldn’t. He doesn’t need surgery right now and is just being watched closely. He should avoid lifting heavy things to prevent more pain.\"\n}"}
{"row_index": 169, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old man came in with chest pain that spread to his back and left shoulder, which reminded doctors of a heart attack. However, his ECG and heart enzymes were normal, and his overall exam was unremarkable. His heart rate was high (164 beats per minute), but his blood pressure and other tests were normal. A chest X-ray taken two days apart showed the heart shifted to the left side, with a bulging left border and a clear space between the aorta and pulmonary artery. This suggested something unusual about the heart's structure. A cardiac MRI confirmed that the patient had left pericardial agenesis — a rare condition where the protective sac around the left side of the heart is missing. This causes lung tissue to push between the aorta and pulmonary artery, and the heart rotates abnormally. The left atrial appendage also sticks out abnormally. There’s a small hole in the heart wall allowing blood to flow from the left side to the right side. The patient’s symptoms, especially during heavy lifting or exertion, are likely linked to this structural issue. He was treated with regular follow-up and advised not to lift heavy weights or do strenuous exercise.\"\n}"}
{"row_index": 170, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old male professional driver presented with episodic chest discomfort and radiating pain to the back and left shoulder, which exacerbated following four days of weight training. The symptoms began at age 10 and have recurred in association with physical exertion, including heavy lifting and uphill climbing. There is no history of comorbidities, surgical interventions, substance abuse, or familial history of ischemic heart disease. Clinical examination was unremarkable, with normal vital signs: heart rate of 164 bpm (indicating sinus tachycardia), blood pressure of 130/84 mmHg, respiratory rate of 24 breaths per minute (tachypnea), and normal blood glucose. Electrocardiography (ECG) was normal, and cardiac biomarkers (troponins, CK-MB) were within normal limits, ruling out acute myocardial infarction.\\n\\nInitial imaging via chest radiography revealed a normal cardiac apex and left heart border, but a lucent area—interpreted as lung tissue—was observed between the aorta and the pulmonary artery, as well as between the left hemidiaphragm and the base of the heart. The repeat chest X-ray, taken 24 hours later, demonstrated a leftward displacement of the cardiac apex (wandering cardiac apex), consistent with significant cardiac levorotation. Echocardiography confirmed marked levorotation of the heart, with normal left ventricular size, preserved systolic function (ejection fraction of 60%), and substantial cardiac mobility—defined as apex displacement exceeding 1.5–2 mm, indicating increased myocardial excursion. No pericardial or pleural effusion was detected, and ventricular wall motion was normal.\\n\\nCardiac MRI further delineated the anatomical abnormalities: significant anterior interposition of lung tissue between the main pulmonary artery and the descending aorta, and between the left ventricle and the diaphragm. The left atrial appendage was abnormally protruding along the lateral aspect of the aortic arch. A 6-mm defect in the middle atrial septum was identified, consistent with a secundum type of atrial septal defect (ASD), leading to left-to-right shunting. The left inferior pulmonary vein exhibited restricted caliber due to compression between the descending aorta and the left atrium, a consequence of the pronounced levorotation. Pulmonary vein diam"}
{"row_index": 171, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 71-year-old woman started feeling weak, lost weight, had diarrhea, and her skin turned yellow over two years. She had been checked regularly for liver problems, but nothing was clear. When she got really sick, she had very low blood pressure and her heart was barely working. She needed to be in the hospital’s intensive care unit because her body was failing. Tests showed damage in her liver, stomach, spleen, and brain. A second liver test finally found the cause: a rare condition that affects many parts of the body, called multisystem LCH, which caused her bile ducts to become scarred and blocked. This is known as secondary sclerosing cholangitis. She was given medicine to help her hormones and a special drug to stop the disease from getting worse. But she had many other health problems, like pancreatitis and diabetes, and after being in the hospital several times, she chose comfort care to focus on feeling better, not fighting the illness.\"\n}"}
{"row_index": 172, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 71-year-old woman came to the hospital with worsening weakness, weight loss, diarrhea, and yellowing of the skin (jaundice). She had been seeing her doctor for high liver enzymes over the past two years, but treatments like ursodiol and low-dose steroids didn’t help. When she arrived, she was very low on blood pressure and had a slow heart rate. Her blood tests showed high white blood cell counts, high liver enzymes, and signs of inflammation. Her thyroid function was also abnormal, with no active thyroid hormone levels.\\n\\nImaging scans showed damage in multiple organs, including the liver, gastrointestinal tract, spleen, and brain. The liver biopsy, which was previously inconclusive, now showed signs of a rare condition called multisystem Langerhans cell histiocytosis (LCH). This condition affects several organs and caused the liver disease in the form of secondary sclerosing cholangitis — a type of bile duct damage.\\n\\nShe needed intensive care because she developed severe shock, requiring medications to support her blood pressure and heart function. Brain imaging showed inflammation of the pituitary gland, which affects hormone production. She also had pancreatitis, blood sugar issues, and developed central diabetes insipidus.\\n\\nTreatment started with hormone replacement to fix her low hormone levels. After discussion with a team of specialists, she was given a drug called vemurafenib, which targets a specific mutation found in LCH cells. Despite treatment, she had repeated hospitalizations and eventually chose comfort care to focus on quality of life.\"\n}"}
{"row_index": 173, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 71-year-old female with a history of gastroesophageal reflux disease presented to the emergency department following a syncopal episode, accompanied by progressive diarrhea, unexplained weight loss, worsening jaundice, and fatigue. She had been undergoing outpatient evaluation for chronically elevated liver enzymes over the preceding two years. Prior therapeutic trials with ursodiol and low-dose prednisone were ineffective. On admission, her vital signs demonstrated hypotension (blood pressure 72/53 mm Hg) and a nadir heart rate of 62 beats per minute. Physical examination revealed jaundice and cachexia. Laboratory findings included leukocytosis (27.7 × 10⁹/L; normal 3.4–9.6 × 10⁹/L) with neutrophilic predominance. Hepatic function tests showed elevated aspartate aminotransferase (85 U/L; normal 8–43 U/L), alanine aminotransferase (85 U/L; normal 7–45 U/L), bilirubin (9.3 mg/dL; normal <1.2 mg/dL), and markedly elevated alkaline phosphatase (2262 U/L; normal 35–104 U/L) and gamma-glutamyl transferase (494 U/L; normal 5–36 U/L). C-reactive protein was elevated at 52 mg/L (normal <8 mg/L), and thyroid function tests revealed hyperthyroidism with elevated TSH (22.8 mIU/L; normal 0.3–4.2 mIU/L), undetectable free T3 and T4, consistent with panhypopituitarism. A prior 6-month liver biopsy demonstrated periportal fibrosis with lymphocytic and scattered neutrophilic infiltrates in portal tracts, but no evidence of histiocytic infiltration. Imaging studies included contrast-enhanced computed tomography (CT) of the abdomen and pelvis, which revealed diffusely heterogeneous liver parenchymal enhancement without ductal dilatation, duodenitis, and diffuse colonic thickening suggestive of pancolitis. CT chest showed bilateral centrilobular ground-glass opacities with mild pulmonary edema. Echocardiography was normal, excluding cardiac etiology. Brain magnetic resonance"}
{"row_index": 174, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 21-year-old woman from northern Tanzania, who had been breastfeeding for 8 months after having a baby by C-section, came in with belly pain, swelling, fever, and unusual discharge from her vagina. She had a hard lump in her lower belly that was tender and about the size of a 16-week pregnancy. A scan showed a possible infection in her pelvis, but after surgery, doctors found a large, swollen uterus with hair, oily stuff, and pus inside. They removed the whole uterus and tested the tissue. The test showed it was a type of growth called a mature teratoma, which is like a skin cyst that can grow and get infected. She recovered well, had no more symptoms, and has stayed healthy for 8 months after surgery.\"\n}"}
{"row_index": 175, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 21-year-old woman from the northern region of Tanzania, who is of Sukuma ethnicity, came to the hospital with abdominal pain, swelling, fever, and abnormal vaginal discharge that had lasted for three weeks. She had been breastfeeding for eight months after having a child via cesarean section. During her exam, doctors found a large, tender mass in her abdomen and signs of infection in her pelvic area. A pelvic ultrasound suggested a pelvic abscess, but after surgery, they found a different cause: a mature uterine teratoma, which is a type of benign tumor that contains skin-like tissue, hair, and sebaceous material. The tumor was infected and had pus inside. The surgery involved removing the entire uterus (total hysterectomy), and the tissue was tested under a microscope, confirming the diagnosis. The patient recovered well, received blood and antibiotics, and has not had any signs of the disease returning for eight months.\"\n}"}
{"row_index": 176, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 21-year-old female of Sukuma ethnicity from the northern region of Tanzania presented to the Bugando Medical Centre (BMC) outpatient clinic in Mwanza with a three-week history of abdominal pain, distension, fever (approximately 38.5 °C), and abnormal vaginal discharge. She was lactating for eight months following a previous cesarean section delivery. On physical examination, she exhibited signs of systemic illness, including weakness, fever, and a blood pressure of 110/70 mmHg. Her blood group was A, Rh-positive, with a hemoglobin level of 6.3 g/dL, indicating significant anemia. Abdominal examination revealed a sub-umbilical midline surgical scar and a palpable suprapubic mass corresponding to a uterus of approximately 16 weeks' gestational size, described as soft, tender, and mobile. Digital pelvic and vaginal examination demonstrated a closed cervix with tenderness on cervical mobility, tenderness in the posterior fornix, and gloved finger staining with pus-like discharge. Pelvic ultrasound imaging suggested the presence of a pelvic abscess.\\n\\nThe patient was referred for emergency laparotomy. Intraoperatively, the uterus was found to be markedly bulky with a discharging sinus located on the left fundal aspect. Both ovaries appeared normal in morphology and structure, with no evidence of adnexal pathology or fluid in the pouch of Douglas. A transverse incision was made at the level of the sinus tract. The uterine cavity contained yellowish, mucinous, tenacious material intermixed with hairy tissues and sebaceous debris. A decision was made to proceed with total hysterectomy, during which the excised uterus was observed to contain abundant hair and sticky sebaceous material within the uterine cavity.\\n\\nPostoperatively, the patient received one unit of packed red blood cells to correct her anemia and was administered intravenous antibiotics: ceftriaxone, gentamicin, and metronidazole, with concurrent prophylactic heparin therapy to prevent thromboembolic complications. The patient recovered uneventfully.\\n\\nHistopathological evaluation of the resected uterus, which measured 18 cm × 9 cm × 4 cm and contained no adnexal structures, revealed a cystic lesion measuring 10 cm in diameter located within the myometrium at the left fundal"}
{"row_index": 177, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 64-year-old woman had a filter put in her leg vein 3 months ago to stop a blood clot. The filter didn’t come out easily, and the doctor tried to pull it back but failed. Then, 3 months later, she got sudden, bad pain on her right side of the belly. Her urine was red, and she had swelling in her right leg. The filter’s hook went too far and cut into her right leg artery, causing a bulge (like a balloon) in the artery. This blocked her urine pipe, so her kidney swelled up. Both her leg veins and part of her main vein were completely blocked. The doctors did emergency surgery to remove the filter, the bulge, and the blocked parts. They fixed the artery and fixed her veins. The surgery found a bacteria called Staphylococcus aureus in the tissue, which was treated with antibiotics. After surgery, she stayed in the hospital for 12 days and started taking medicine to prevent clots and fight infection. Six months later, a scan showed the artery was open and her kidney swelling was only mild. She’s doing better now.\"\n}"}
{"row_index": 178, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 64-year-old woman was admitted with sudden, severe pain on the right side of her abdomen. She had previously had an IVC filter placed three months ago to prevent blood clots after a deep vein thrombosis in her left leg. The filter was placed through her right femoral vein and was meant to be removed later, but a previous attempt to retrieve it failed. Since then, imaging was stopped due to the pandemic.\\n\\nShe developed severe abdominal pain and noticed red urine, but no fever or other signs of infection. On exam, her abdomen was tender, her right leg was swollen, and her right femoral pulse was weak. Blood tests showed high white blood cells, indicating inflammation or infection.\\n\\nA CT scan revealed that the hook part of the filter had pierced into her right iliac artery, causing a bulge (pseudoaneurysm) in that artery. This also blocked her right ureter, leading to swelling of the kidney on that side. Both iliac veins and the lower part of her IVC were completely blocked, which affects blood flow.\\n\\nShe underwent emergency open surgery to remove the IVC filter, the pseudoaneurysm, and the damaged parts of the iliac veins and IVC. Her right iliac artery was reconstructed to restore blood flow. Bacteria (Staphylococcus aureus) were found in the tissue sample, and she was treated with antibiotics and anticoagulation therapy.\\n\\nShe was discharged on day 12. Six months later, a follow-up CT showed that her right iliac artery was open and flowing properly, and only mild kidney swelling remained. Her condition has improved, but ongoing care is needed.\"\n}"}
{"row_index": 179, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 64-year-old female presented to our institution with a 1-day history of severe right abdominal pain following a 3-month history of inferior vena cava (IVC) filter placement. The initial indication for IVC filter placement was deep venous thrombosis (DVT) of the left lower extremity, managed with anticoagulation. A double-basket retrievable IVC filter (Visee WXF-32, Shandong Visee Medical Devices Company Limited, China) was inserted infrarenally via the right femoral vein. Ten days later, endovascular retrieval of the filter using standard femoral venous access failed, and subsequent imaging follow-up was discontinued due to the COVID-19 pandemic. Three months later, the patient presented with acute right lower quadrant pain, no fever or chills, and reddish urine consistent with hematuria. She had a history of scoliosis, poorly controlled type 2 diabetes mellitus, and chronic substance use including tobacco and alcohol. On admission, vital signs were stable: heart rate 97 bpm, respiratory rate 23 breaths/min, blood pressure 126/73 mmHg. Physical examination revealed diffuse abdominal tenderness with rebound tenderness, mild right lower limb swelling, and a weak femoral artery pulse. Laboratory findings showed normal hepatic and renal function, hemoglobin 101 g/L, leukocyte count 14.74 × 10⁹/L, and neutrophilic granulocyte percentage of 91.0%, indicating a significant inflammatory response. During surgical intervention, a partial pseudoaneurysmal lesion was excised for tissue culture, yielding isolation of Staphylococcus aureus, which demonstrated sensitivity to moxifloxacin. Computed tomography angiography (CTA) revealed that the retrieval hook of the IVC filter had penetrated the right common iliac artery (CIA), resulting in a 52 mm × 48 mm × 55 mm pseudoaneurysm in the right iliac artery. This pseudoaneurysm was associated with complete right ureteral obstruction leading to ipsilateral hydronephrosis. Bilateral iliac veins and the distal segment of the IVC were completely occluded, with extensive pelvic varicosities observed. Emergency open surgical repair was performed, including complete removal of the IVC filter, the right"}
{"row_index": 180, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old woman felt越来越 short of breath, had no appetite, and woke up sweating every night for two weeks. Doctors found a big tumor in her left kidney that had grown into her main vein and reached her heart. The tumor was very large and pushed into her heart, which is a serious problem. She had surgery to remove the kidney and the tumor from her vein and heart. The tumor was found to be a rare cancer called Ewing's sarcoma, which started in the kidney and spread through the blood vessels. This cancer was confirmed by a test that looked for a specific gene change. After surgery, she started chemotherapy to kill any remaining cancer cells. She still takes blood thinners to prevent new clots because both the cancer and treatment can cause blood clots. Her scans show no more cancer, and she is doing well.\"\n}"}
{"row_index": 181, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old Iranian woman came in with worsening shortness of breath, loss of appetite, and night sweats over the past two weeks. Tests showed a tumor in her left kidney that had spread into the veins leading to her heart, including the inferior vena cava and into the right atrium. This was a rare and serious condition. She had surgery to remove the kidney and the tumor from the veins. During the surgery, the tumor was found extending into her right atrium and was diagnosed as Ewing's sarcoma, a type of cancer that starts in the kidneys and spreads. Pathology tests confirmed the presence of a genetic change (EWSR1 rearrangement) that is typical of this cancer. She started chemotherapy after surgery, with adjustments made to reduce side effects. Her follow-up scans showed no signs of cancer recurrence, and she is doing well with ongoing treatment and monitoring.\"\n}"}
{"row_index": 182, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old Iranian female presented with progressive dyspnea at rest, accompanied by anorexia, fever, chills, and night sweats over a two-week period prior to admission. Initial evaluation at Rajaei Hospital Cardiac Center included echocardiography and computed tomography (CT) angiography, which revealed pulmonary thromboembolism (PTE) consistent with a massive tumor thrombus. The diagnosis of PTE was confirmed, and she was initiated on heparin followed by transition to oral rivaroxaban for anticoagulation, with subsequent stable discharge under close follow-up.\\n\\nTwo weeks later, she returned with worsening dyspnea and systemic symptoms. Abdominal ultrasound and contrast-enhanced abdominopelvic CT demonstrated a solid, heterogeneously enhancing mass in the mid-to-lower pole of the left kidney measuring 70 mm × 75 mm × 105 mm, with tumor thrombus extending from the left renal vein through the inferior vena cava (IVC) to the right atrium over a craniocaudal length of approximately 23 cm. Mild hypodense fluid was noted in the pelvic cavity. CT findings also revealed filling defects in the right main pulmonary artery and its segmental branches, consistent with pulmonary thromboembolism, and a 7 mm ground-glass nodule in the left lower lobe superior segment. No signs of acute abdominal pathology, such as appendicitis, cholecystitis, pancreatitis, hydronephrosis, or free air, were identified.\\n\\nEchocardiography showed normal left ventricular systolic function (ejection fraction = 55%), with mild to moderate tricuspid regurgitation, mitral regurgitation, and pulmonary insufficiency. Mean pulmonary artery pressure was 27 mmHg, and peak instantaneous pressure gradient was 17 mmHg. A large, rope-like, hyperechoic mass was observed in the IVC measuring 14 cm × 2.7 cm, protruding into the right atrium, strongly suggestive of extensive intracardiac tumor thrombosis.\\n\\nGiven the clinical suspicion of a primary renal malignancy with extensive venous invasion, the patient underwent a combined surgical approach: open radical nephrectomy for the left kidney, followed by IVC thrombectomy under cardiopulmonary bypass. During surgery,"}
{"row_index": 183, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 53-year-old man had a broken hip and started having seizures after surgery. Doctors found a lump in his brain that was not in the normal brain area — it was on the outside of the brain, attached to the lining. This lump looked like a brain tumor, but it wasn’t a regular tumor. It was made of special cells that were not part of the brain. The doctors had to cut into the brain to remove it, and during the surgery, they had to cut some small blood vessels on the brain’s surface. Because of that, the man lost some movement on his left side. After surgery, a scan showed a bleed and a spot in his brain that was likely from those cut blood vessels. The doctors found this lump was not just in the brain — it was also in the nervous system, and it was the only place it was found. The man has not had seizures since, and his movement is slowly getting better. No other parts of his body showed signs of this condition.\"\n}"}
{"row_index": 184, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 53-year-old man with diabetes and a broken hip was admitted to the hospital. He had a seizure after surgery, and was referred for further evaluation. Brain imaging showed a mass on the right side of his brain, specifically in the parietal area, that was consistent with a type of tumor called meningioma en plaque. This tumor was attached tightly to the brain surface and had many small blood vessels running through it. To remove the tumor completely, these blood vessels had to be cut, which led to complications. The surgery was done through a frontotemporal craniotomy. After the procedure, the patient developed incomplete weakness on his left side and a bleeding area in the right frontal lobe, likely due to the damaged blood vessels. A biopsy showed unusual immune cells in the tumor, and the findings matched a rare condition called isolated central nervous system RDD (extranodal RDD), meaning the tumor started in the brain but is not spread to other parts of the body. The patient has been seizure-free since surgery and has slowly recovered from his weakness over six months. No signs of the disease spreading to other organs were found.\"\n}"}
{"row_index": 185, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 53-year-old homeless man was admitted for a right femoral neck fracture; his medical history included noninsulin-dependent diabetes mellitus. Physical examination at admission was unremarkable, with no fever, lymphadenopathy, or baseline neurological deficits. Laboratory findings showed white blood cell count of 4330 cells/mL, hemoglobin of 9.2 g/dL, and platelet count of 29,900 platelets/mL, consistent with normochromic-normocytic anemia; C-reactive protein was negative, indicating no active systemic inflammation. The orthopedic surgery for the fracture was successfully performed. However, during the postoperative course, the patient developed an episode of generalized seizures, for which phenytoin was administered. Subsequently, he was referred to our neurosurgical department for further evaluation.\\n\\nNon-contrast head computed tomography (CT) revealed a high-density, extraaxial mass in the right parietal convexity, with prominent peritumoral brain edema. Enhanced magnetic resonance imaging (MRI) demonstrated a dural-based, extraaxial, homogeneously enhancing lesion with well-defined borders, consistent with a meningioma en plaque. On T1-weighted imaging, the lesion was iso- to hyperintense; on fluid-attenuated inversion recovery (FLAIR) and T2-weighted sequences, it was iso- to hypointense. The imaging characteristics, combined with the dural attachment and vascular architecture, strongly supported the diagnosis of meningioma en plaque.\\n\\nThe tumor was resected via a right frontotemporal craniotomy. Microscopic examination revealed a firm, xanthochromic, nonaspiratable mass with high vascularity and dural origin. The tumor was tightly adherent to the adjacent cerebral cortex and was extensively infiltrated by pial arteries and veins of the brain surface. This intimate vascular integration rendered the preservation of these pial vessels during complete resection highly improbable, necessitating their sacrifice to achieve total tumor removal. Postoperatively, the patient developed incomplete left hemiparesis, likely secondary to ischemic injury from the disruption of pial arterial supply.\\n\\nA postoperative non-contrast brain CT demonstrated a hemorrhagic lesion and a low-density area in the right frontal lobe, which is believed to result from the surgical sacrifice of pial arteries at the tumor-brain interface. The"}
{"row_index": 186, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman in her 80s had a knee infection after a surgery she had seven years ago. Her knee was swollen, painful, and had pus coming out. Doctors found a type of yeast called Cy. fabianii in her knee during surgery. At first, they thought it was a different yeast called Candida utilis, but later testing proved it was really Cy. fabianii. This yeast can cause serious infections in joints, and the right treatment was needed to fix it. She got antibiotics to fight the infection and is now recovering at home.\"\n}"}
{"row_index": 187, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This study describes a case of infection in a prosthetic knee joint in an 85-year-old woman who had a total knee replacement seven years earlier. She developed pain, swelling, and pus in her right knee over three months. Tests showed signs of joint infection and bone infection (osteomyelitis). She received antibiotics initially, and the infected knee implant was removed. During surgery, fluid from the joint was tested and grew a type of yeast. At first, the yeast was wrongly identified as Candida utilis, but further testing using advanced lab methods correctly identified it as Cy. fabianii. This correct identification was confirmed through DNA analysis and comparison with known yeast samples in a database. The infection was treated with antifungal medications, and the patient recovered after completing a course of oral and intravenous antibiotics.\"\n}"}
{"row_index": 188, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 85-year-old Chinese woman with a history of hypertension, dyslipidemia, and a prior right total knee replacement seven years earlier presented with a three-month history of painful right knee swelling and purulent discharge, without recent trauma or surgical intervention. On admission, she was afebrile, with diffuse swelling, erythema, tenderness, and a sinus tract. Laboratory findings revealed a total white blood cell count of 7.8×10³ cells/µL, elevated C-reactive protein, and increased erythrocyte sedimentation rate, indicating active inflammation. Radiographic imaging demonstrated radiolucency in the distal femur and proximal tibia, consistent with osteomyelitis. The patient was diagnosed with prosthetic joint infection (PJI) of the right knee complicated by osteomyelitis, and empiric therapy with intravenous clindamycin and ciprofloxacin was initiated. Surgical intervention included removal of the prosthetic implant and arthrotomy with washout; intraoperative findings were consistent with osteomyelitic changes. Synovial fluid was inoculated into BD Bactec Plus Aerobic/F and BD Bactec Lytic/10 Anaerobic/F vials and incubated using BD BACTECTM FX. After 72 hours, the aerobic bottle yielded a positive culture. Gram staining revealed gram-positive ellipsoidal budding yeast cells. The isolate grew as cream-colored, smooth, glistening colonies on Sabouraud Dextrose Agar and as whitish colonies on CHROMagar. Corn meal agar culture showed only blastoconidia, with no germ tube formation or urease activity, supporting a non-germ tube-forming yeast phenotype. Bone marrow specimens also yielded identical growth. Initial phenotypic identification using the VITEK® 2 yeast identification system assigned the organism to *Candida utilis* with 95% probability. However, subsequent identification via matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF) by Bruker revealed the organism as *Candida fabianii*, a species frequently misidentified as *C. utilis* due to overlapping phenotypic characteristics. This finding was independently confirmed by molecular analysis: DNA was extracted using the Quick-DNA Fungal/Bacterial Miniprep Kit (Zymo Research), and the D1/D2 domain of the large subunit ("}
{"row_index": 189, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 56-year-old Moroccan woman had a big lump on one side of her face that grew over 4 months. It hurt a lot, made her mouth hard to open, blocked her nose, and she started bleeding from her nose. The lump was deep in her face and spread into her nose, eye area, and sinuses. Doctors saw it with scans and found it was a serious, fast-growing tumor. A small tissue sample showed it was a cancer called malignant schwannoma. Even though they gave her radiation to ease the pain, she passed away 10 days later because of breathing trouble.\"\n}"}
{"row_index": 190, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 56-year-old Moroccan woman was hospitalized in 2013 with a large swelling on one side of her face, on the right side, that had been growing over the previous 4 months. She first noticed sharp facial pain, which was initially thought to be a dental issue but didn’t improve. The swelling grew quickly, causing trouble opening her mouth, nasal blockage, and nosebleeds. She had a painful swelling on her right face, her eye appeared slightly bulging, and she had numbness in parts of her face controlled by the trigeminal nerve. A nasal exam found a tumor in her right nose that was fragile and bled easily. Her hard palate was eroded, and her mouth was so tight it was hard to examine. No lymph nodes or other parts of her throat showed signs of disease. Her hearing and ear exam were normal. She was given morphine for pain. CT and MRI scans showed a large, aggressive tumor in her right temple area, maxillary sinus, and around her eye, spreading into nearby structures like the sinuses and nasal passages. The tumor was invasive and had areas of dead tissue. A biopsy of the tumor confirmed it was a malignant schwannoma, a type of cancer that starts in nerve tissue. Tests showed no spread to other parts of her body. Because the cancer was advanced and not curable, the doctors chose palliative radiotherapy to relieve symptoms. The treatment helped a bit, but she passed away 10 days later due to severe breathing problems.\"\n}"}
{"row_index": 191, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 56-year-old Moroccan woman with a 38-year history of chronic cigarette smoking (approximately one pack per day) was hospitalized in 2013 presenting with a rapidly progressive right-sided hemifacial swelling that had evolved over four months. Initial symptoms included persistent, unilateral facial neuralgia localized to the trigeminal nerve distribution, initially misdiagnosed as dental in origin and managed without improvement. The pain progressively worsened to a disabling level, accompanied by a significant increase in right maxillary swelling, limitation of mouth opening (trismus), and recurrent nasal obstruction with epistaxis (nosebleeds). Clinical examination revealed a painful, inflammatory right hemifacial mass, right exophthalmos without evidence of visual acuity reduction, and hypoesthesia in the second and third divisions of the trigeminal nerve (V2 and V3), consistent with peripheral nerve involvement. Endonasal examination identified a friable, bleeding tumor mass within the right nasal cavity. Oral examination, severely limited by trismus, demonstrated erosion of the hard palate. Cervical lymphadenopathy was absent, and upper aerodigestive tract endoscopy showed no mucosal lesions. Otoscopy and audiometry were normal, excluding central nervous system or auditory pathway involvement. The patient was immediately initiated on intravenous morphine for pain control.\\n\\nImaging studies revealed a large, heterogeneous, infiltrative mass involving the right infratemporal fossa, masticator space, and right maxillary sinus. CT findings demonstrated lysis of the maxillary sinus walls, the ascending ramus of the mandible, and the orbital floor, with extension into the ethmoidal, parapharyngeal, and intraorbital compartments. MRI further characterized the lesion as aggressive and invasive, with irregular boundaries, heterogeneous signal intensity on both T1- and T2-weighted sequences, and heterogeneous contrast enhancement with areas of central necrosis. The tumor exhibited infiltrative growth into the jugular and temporozygomatic soft tissues, consistent with a highly destructive, locally advanced process. The radiological pattern supported extensive local invasion without evidence of distant spread.\\n\\nA nasal endoscopic biopsy was performed, and histopathological evaluation confirmed a poorly differentiated, invasive malignant process. Immunohistochemical analysis demonstrated strong, diffuse cytoplasmic positivity for anti-S100 protein, a hallmark marker of schwannoma lineage, leading to a definitive diagnosis of malignant schwann"}
{"row_index": 192, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 76-year-old man had been feeling numbness, pain, and weakness in his arms and legs for 7 years. He also had sweating, constipation, and lost weight without knowing why. In the past month, he started having shortness of breath, swelling in his feet and legs, and low blood pressure. His heart tests showed a strange sign: his heart looked bigger than it should, but the electrical signals were weak — this is a clue that his heart might be full of a harmful protein. Tests on his heart showed the same problem: the heart muscle wasn’t working well, and this matches what happens in a disease called cardiac amyloidosis. Blood tests ruled out a common type of amyloid disease (AL). A gene test found a mutation in the TTR gene — this is the same mutation found in people with a family disease called familial amyloid polyneuropathy (FAP) and heart disease from amyloid. This confirms he had hATTR Val30Met disease. His treatment with medicine didn’t work well. After 80 days, he died because his heart stopped working. His son later had the same symptoms and was found to have the same gene problem.\"\n}"}
{"row_index": 193, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 76-year-old man had been slowly getting worse over seven years, with numbness, pain, and weakness in his arms and legs, sweating, constipation, and unexplained weight loss. In the past month, he also developed shortness of breath, swelling in his body, and low blood pressure. Tests showed low electrical signals in his heart (low QRS voltage) that didn’t match his thickened heart muscle — this was a key sign pointing to cardiac amyloidosis (CA). Echocardiogram results, especially using advanced imaging, supported the diagnosis. Blood tests ruled out AL amyloidosis, a common type of amyloid disease, because his free light chain levels were normal. A genetic test found a specific mutation (c.148 G-A, Val30Met) in the TTR gene, which confirms the diagnosis of hereditary amyloidosis caused by a faulty protein called transthyretin. This condition is known as hATTR Val30Met, which leads to both nerve damage (familial amyloid polyneuropathy or FAP) and heart problems. His treatment with doxycycline, ursodeoxycholic acid, and tafamidis did not work well — he developed severe intestinal blockage and eventually died from heart failure. His son later developed similar symptoms and was found to have the same genetic mutation. No tissue biopsies were done after death due to family refusal.\"\n}"}
{"row_index": 194, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 76-year-old male presented with a seven-year history of progressive peripheral neuropathy characterized by limb numbness, pain, weakness, autonomic dysfunction including sweating and constipation, and unexplained weight loss. Over the preceding month, he developed systemic edema, hypotension, and shortness of breath. Physical examination revealed malnutrition, anemia, lethargy, generalized muscle weakness, decreased muscle tone, diminished tendon reflexes, sacroiliac decubitus necrosis, and severe edema. Laboratory findings included persistent elevation of high-sensitivity troponin I (hs-TnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), indicating myocardial injury; neutrophilic leukocytosis; moderate anemia with reduced erythrocyte count and hematocrit; and mild hypoxemia. Chest X-ray demonstrated bilateral pulmonary inflammation with pleural effusion. Electrocardiography (ECG) showed low QRS voltage in the limb leads, abnormal Q waves in leads II, III, and aVF, and a poor R-wave progression in V1–V6, which is inconsistent with left ventricular hypertrophy and suggestive of cardiac amyloidosis (CA). Echocardiography revealed left ventricular hypertrophy, diastolic dysfunction (grade II), and a small pericardial effusion, with a critical discordance between the low QRS voltage and the presence of hypertrophy—this discordance is a key pathological clue in the diagnosis of CA. Speckle tracking strain analysis demonstrated reduced global longitudinal strain (GLS) with apical sparing, an apical-to-basal strain ratio of 2.7, and an ejection fraction to GLS ratio (EFSR) of 4.4, findings that are consistent with the characteristic ultrasonic phenotype of cardiac amyloidosis. Chest CT scans revealed diffuse pulmonary interstitial changes, cystic lung lesions, and progressive subpleural calcifications, which are hallmark radiographic features of pulmonary amyloid deposition. The presence of pulmonary amyloidosis was further supported by the absence of evidence for active infection or inflammation, as confirmed by normal C-reactive protein and blood cell profile. Despite the critical clinical condition, cardiac magnetic resonance (CMR) and positron emission tomography with pyridyl-1,3-diamine (PYP) were not performed due to the patient's instability. To differentiate between"}
{"row_index": 195, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old boy had belly pain for four days, along with hard stools, watery poop, and a swollen belly. He was very sick, breathing fast, and his heart was beating too fast. When doctors looked with ultrasound, they saw the spleen had twisted like a corkscrew and was stuck in the lower belly, attached to the appendix and small intestine. Part of the spleen was dead because of the twist. The doctors did surgery to remove both the spleen and the appendix. The boy recovered well, stayed in hospital for 7 days, and then went home. He now takes medicine to prevent infections and will get vaccines for meningococcal and pneumococcal diseases to stay healthy.\"\n}"}
{"row_index": 196, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 12-year-old boy came in with crampy abdominal pain that had lasted for four days. He had a history of constipation, mucoid diarrhea, and a swollen belly. He was very sick-looking, with a fast heart rate and tender abdomen. On ultrasound, doctors saw a 'whirlpool sign' and found that his spleen was not in its normal place — it was located in the lower abdomen, twisted 720 degrees, and had areas of dead tissue (necrosis). The spleen was stuck to the appendix and the end of the small intestine. During surgery, they removed both the spleen and the appendix. The surgery went smoothly, and he recovered well. After recovery, he received vaccines to protect against meningococcal and pneumococcal infections, and started on antibiotics to prevent future infections.\"\n}"}
{"row_index": 197, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 12-year-old male presented with a four-day history of crampy, lower abdominal pain, accompanied by prior episodes of constipation, mucoid diarrhoea, and abdominal distension. He reported no vomiting, and there was no family history of similar gastrointestinal or systemic manifestations. The patient lived with his parents, three siblings, and grandparents, with no known congenital or inherited medical conditions in the family. On physical examination, he appeared acutely ill with marked distress; vital signs revealed tachycardia (heart rate 134 beats per minute), respiratory rate of 22 breaths per minute, normothermia (temperature 36.40°C), and normal blood pressure (110/75 mmHg). There was no sunken eye socket, and buccal mucosa was moist. Abdominal examination demonstrated generalized tenderness, distension that moved with respiration, and a firm, 8 cm × 5 cm mass in the left lower quadrant with its lower border inaccessible, consistent with a fixed, non-fluid-containing lesion. No free fluid was detected. Systemic examination was otherwise unremarkable.\\n\\nLaboratory findings included a white blood cell count of 10,300/μL with a neutrophilic predominance of 78.5%, moderate anemia (hemoglobin 8.6 g/dL, hematocrit 28%), mean corpuscular volume (MCV) of 86 fL, and platelet count of 775 × 10³/μL. Abdominal ultrasound revealed a 'whirlpool sign' at the splenic hilum, indicating vascular torsion, and demonstrated a wandering spleen located in the lower abdominal cavity, displaced below the level of the umbilicus. The spleen exhibited altered echogenicity, suggestive of focal infarction. The ultrasound diagnosis was confirmed as wandering spleen with multifocal infarction due to splenic volvulus.\\n\\nThe patient was managed with nil-by-mouth status, intravenous maintenance fluids, broad-spectrum antibiotic coverage, and analgesia. After stabilization, an emergency laparotomy was performed. Intraoperatively, a slightly enlarged spleen was identified within the peritoneal cavity, positioned below the umbilicus. The vascular pedicle was found to be torsioned 720°, with the torsion originating"}
{"row_index": 198, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 56-year-old man had a stroke that went away on its own. He didn’t have any major heart problems, but later started feeling tired, losing weight, and sweating at night. His body showed signs of inflammation — his blood tests showed high levels of markers that mean the body is fighting something. He had breathing problems and was diagnosed with a condition called ANCA-associated vasculitis, which means his body’s immune system attacked his lungs and heart. This condition made his breathing worse, and his heart wasn’t working well. Tests showed his heart was weak and had a leaking aortic valve, which let blood flow backward. The doctor replaced the faulty valve with a new one. After the surgery, his breathing got better. The tissue from the valve showed signs of swelling, inflammation, and thickening — proof that his immune system was causing damage. He’s now being watched closely by heart, lung, and immune specialists to keep his symptoms under control.\"\n}"}
{"row_index": 199, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 56-year-old man was diagnosed with ANCA-associated vasculitis, a type of autoimmune disease that causes inflammation in blood vessels. He first developed respiratory symptoms, including shortness of breath, which got worse over time. Initial tests showed signs of inflammation in his lungs and blood, and he was treated with steroids and methotrexate, which helped control the disease.\\n\\nAfter two years, his symptoms returned, especially shortness of breath, and his lung function declined. A heart exam revealed that his heart was not pumping effectively, with a low ejection fraction (30–35%), and he had severe aortic valve insufficiency — meaning the valve wasn't closing properly, allowing blood to leak back into the heart. This was confirmed by imaging and tissue analysis showing inflammation, thickening, and scarring in the aortic valve.\\n\\nHe had surgery to replace the damaged aortic valve with a bioprosthesis, which improved his symptoms. After surgery, his heart function and breathing stabilized. He also had a small heart rhythm issue, which was managed with medication. The condition of his lungs remained under close monitoring, and he continued treatment for his underlying vasculitis. This case shows how heart and lung problems can be linked in vasculitis, and why a full medical evaluation is needed when symptoms persist.\"\n}"}
{"row_index": 200, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 56-year-old male with a prior spontaneous cerebral stroke at age 49, which resolved without residual neurological deficit and was not evaluated with magnetic resonance imaging, presented at 56 years of age with evolving respiratory symptoms initially attributed to respiratory tract involvement. He had no traditional cardiovascular risk factors, aside from a family history of ischemic heart disease. Ten weeks after the stroke, he developed third-degree atrioventricular (AV) block, initially suspected to be due to acute Borrelia infection; however, the block persisted despite antibiotic therapy, necessitating dual-chamber pacemaker implantation.\\n\\nDuring hospitalization, he exhibited fatigue, unintentional weight loss, and night sweats. Laboratory findings revealed a sedimentation rate >100 mm/hr, hemoglobin of 5.0 g/mL (indicating severe anemia), thrombocytosis (615×10⁹/L), and C-reactive protein (CRP) of 95 mg/L, with no leukocytosis. Gastrointestinal bleeding was not suspected due to absence of gastrointestinal symptoms. At 4 months, he was diagnosed with ANCA-associated vasculitis, specifically MPO-ANCA-positive, characterized by systemic inflammation with malaise, low-grade fever, arthritis, sinusitis, interstitial lung disease (confirmed by ground-glass opacities on high-resolution computed tomography [HRCT] of both lungs, without biopsy), and absence of mononeuritis multiplex, asthma, skin, renal, cerebral, or gastrointestinal tract involvement. The Birmingham Vasculitis Activity Score (BVAS) was 15, indicating moderate disease activity.\\n\\nTreatment with high-dose corticosteroids for six months followed by methotrexate led to clinical remission, with normalization of MPO-ANCA titers. Methotrexate was discontinued after two years of sustained remission. One year later, he developed worsening respiratory symptoms, including dyspnea, with rising MPO-ANCA levels, prompting reinitiation of steroid and methotrexate therapy. Despite this, respiratory symptoms persisted, leading to multidisciplinary evaluation involving cardiology, pulmonology, and rheumatology.\\n\\nInitial cardiac evaluation via transthoracic echocardiography (TTE) showed preserved left ventricular (LV) function, no pulmonary hypertension, and mild-to-moderate aortic regurgitation. A treadmill exercise"}
{"row_index": 201, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A baby girl, 18 days old, was admitted to the hospital because her heart made a strange noise and her legs had weak pulses. Her blood pressure was much higher in her arms than in her legs. Doctors used an ultrasound to see her heart and found a narrow part in the main artery (aortic coarctation). They also saw that a blood vessel that feeds the heart (LCX) was not getting blood the normal way — it was flowing backward, through a small path from the lung artery instead of going into the heart. The heart was working fine, and the pressure in the lungs was normal. To fix this, doctors did surgery at day 23. They removed the narrow part of the artery and reconnected the heart's blood vessel back into the main artery. They also closed a small hole in the lung artery. After surgery, the baby had a fast heart rhythm that was treated with medicine. A follow-up check showed the heart blood vessel was now working properly. The baby recovered well and went home with normal heart tests.\"\n}"}
{"row_index": 202, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 18-day-old girl was admitted to the pediatric intensive care unit because of a heart murmur and weak pulses in her legs. She was otherwise healthy, breathing on her own and with normal blood pressure, except for a 30 mmHg difference in blood pressure between her arms and legs. An echocardiogram confirmed aortic coarctation — a narrowing of the aorta — and showed that the heart’s left coronary artery (LCA) was not flowing into the aorta as it should. Instead, it was being supplied by blood from a nearby artery (the right posterior descending artery) and flowed into the right pulmonary artery instead. A coronary angiogram revealed only one right coronary artery and no left main coronary artery. The left circumflex artery (LCX) was feeding through a bypass path, reaching the wall of the aorta without entering it. At 23 days old, she had surgery to remove the narrowed part of the aorta and reconnected the left coronary artery back into the aorta using a technique that kept the artery safe and intact. The defect in the pulmonary artery was closed with a patch. After surgery, she had a few episodes of fast heart rate, which were treated with medication. Follow-up tests showed normal blood flow in the left coronary artery. She recovered well and was discharged home with normal heart function and no signs of damage.\"\n}"}
{"row_index": 203, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 18-day-old female was admitted to the paediatric intensive care unit (PICU) due to a heart murmur and diminished femoral pulses. The patient was clinically stable, with spontaneous breathing on room air and normal vital signs, except for a significant blood pressure gradient of 30 mmHg between the upper and lower extremities, indicative of obstructive flow in the aortic arch. Transthoracic two-dimensional echocardiography confirmed the diagnosis of aortic coarctation, demonstrating a systolic pressure gradient of 30 mmHg and a closed arterial duct, consistent with a congenital narrowing of the aortic lumen proximal to the origin of the descending aorta. Additionally, the imaging revealed a total retrograde perfusion of the left circumflex coronary artery (LCX), with no visible ostial blood flow from the left aortic sinus, suggesting an abnormal coronary arterial supply pattern. The left ventricular function was preserved, with a normal ejection fraction, absent regional wall motion abnormalities, and no evidence of mitral valve regurgitation. Given the atypical coronary anatomy, coronary angiography was performed, which revealed the absence of a left main coronary artery and instead demonstrated a single right coronary artery (RCA) arising normally from the aortic wall. The LCX was perfused retrogradely via collateral vessels derived from the normal right posterior descending artery (RPD), coursing along the lateral wall of the ascending aorta without entering the aortic lumen, instead draining into the right pulmonary artery (RPA). Small, rudimentary branches of a left anterior descending (LAD) artery were observed arising from the LCX, indicating partial embryological persistence of coronary arterial development. Pulmonary artery pressure remained within normal limits, confirming no significant pulmonary hypertension. At 23 days of age, the patient underwent surgical correction involving resection of the aortic coarctation, end-to-end anastomosis of the aortic segments, and reimplantation of the left coronary artery (LCA) into the posterior aortic sinus using a button technique that avoided stretching or torsion of the coronary artery, thereby preserving coronary artery integrity and preventing ischemic injury. The defect in the right pulmonary artery was closed with a xenopericardial patch. Post-operatively, on day 4, the patient developed recurrent episodes of supraventricular tachycardia (SVT), which were effectively managed"}
{"row_index": 204, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old woman who was overweight since she was 6 years old had type 1 diabetes. She weighed 106.7 kg and was very heavy (BMI 42.2), needing 75 units of insulin every day. Her blood sugar was not well controlled, and her HbA1c was 9.0%. She had surgery called laparoscopic sleeve gastrectomy to lose weight. After the surgery, her weight went down to 81.0 kg (BMI 32.2), which is healthier. She now needs only 24 units of insulin a day, and her blood sugar improved to 7.7%. This means she’s doing better and her body fat, especially the dangerous belly fat, has gone down a lot. The surgery helped her lose weight and control her diabetes better.\"\n}"}
{"row_index": 205, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 36-year-old woman with severe obesity and type 1 diabetes mellitus (T1DM), diagnosed at age 6, was admitted for bariatric surgery. At her first visit, she weighed 106.7 kg and had a body mass index (BMI) of 42.2, which is very high. Her HbA1c was 9.0%, showing poor blood sugar control, and she needed 75 units of insulin daily. She had surgery called laparoscopic sleeve gastrectomy, which removes part of her stomach to help with weight loss. Before surgery, her blood sugar was carefully managed, and her weight was reduced to 101.1 kg. One year after surgery, her weight dropped to 81.0 kg, and her BMI improved to 32.2. Her insulin needs decreased to 24 units per day, and her HbA1c improved to 7.7%, meaning her blood sugar control got better. Her body fat, especially around the abdomen, also decreased significantly. There were no serious complications after the surgery.\"\n}"}
{"row_index": 206, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 36-year-old Japanese female with morbid obesity and type 1 diabetes mellitus (T1DM), diagnosed at age 6, was referred for bariatric surgery due to progressive weight gain and poor glycemic control. T1DM was managed with multiple daily insulin injections, with insulin requirements escalating in parallel with body weight. By age 20, her body weight was 70 kg, increasing to >100 kg by age 34. At initial assessment, she required 45 units of insulin aspart and 30 units of insulin glargine daily, reflecting a high insulin demand consistent with insulin-dependent diabetes. Preoperative laboratory evaluation revealed an HbA1c of 9.0%, indicating chronic hyperglycemia, and undetectable C-peptide levels (<0.01 ng/mL), confirming complete absence of endogenous insulin secretion, a hallmark of advanced T1DM. Her blood lipid profile remained within normal limits, suggesting no significant dyslipidemia. Abdominal computed tomography (CT) demonstrated a visceral fat area of 162.6 cm² and a subcutaneous fat area of 527.9 cm² at the umbilical level, reflecting substantial adiposity, particularly in the visceral compartment, which is strongly associated with insulin resistance and metabolic complications. Upper gastrointestinal endoscopy showed no structural abnormalities in the esophagus, stomach, or duodenum, ruling out gastrointestinal pathology as a contraindication to surgery. To mitigate the risk of postoperative hypoglycemia due to rapid insulin sensitivity improvement, she was admitted 2 weeks prior to surgery for intensive glycemic control, dietary restriction, and structured exercise therapy. This preoperative intervention achieved a reduction in HbA1c to 7.8% and a transient weight reduction to 101.1 kg. The procedure performed was a laparoscopic sleeve gastrectomy (LSG) using a five-port approach. The greater curvature of the stomach was resected from 4 cm proximal to the pylorus to the His angle, using a linear stapler, with the staple line reinforced by continuous seromuscular sutures with non-absorbable material to ensure anatomical integrity and reduce leakage risk. Postoperatively, insulin therapy was initiated with a sliding-scale regimen: a unit of insulin aspart was mixed with 5 g of glucose in the infusion solution,"}
{"row_index": 207, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"The patient had long-lasting pain in her knees and hips, plus bone weakness. Tests showed her phosphate levels were very low, and her bones were thin and damaged. A tumor was found in the left lower leg using a special scan, and the doctor removed it with surgery. The tumor was checked under a microscope and found to be a type called phosphaturia stromal tumor (PMT), which shows a certain protein (Vim) that helps confirm the type. After the surgery, her phosphate levels went back to normal fast, and her pain got much better. Now she walks easier and feels much better.\"\n}"}
{"row_index": 208, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"The patient had long-standing joint pain, especially in her knees, along with groin and back pain that worsened over time. She also had low bone density and very low phosphate levels in her blood, which are signs of a bone disorder. Tests showed increased activity of a protein called somatostatin receptors in her left tibia, leading doctors to suspect a rare condition called TIO (tumor-induced osteomalacia). A PET/CT scan successfully found a tumor in the left tibia, and the tumor was surgically removed. Pathology confirmed it was a phosphaturia stromal tumor (PMT), a type of tumor that causes the body to lose too much phosphate. The tumor showed positive staining for a protein called Vim, which helps confirm the diagnosis. After surgery, her phosphate levels quickly returned to normal, and her pain and symptoms greatly improved.\"\n}"}
{"row_index": 209, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 22-year-old female presented with a 10-year history of bilateral knee pain, progressively worsening over the past two months, accompanied by groin pain and right 12th rib pain following a fall. The pain was characterized by recurrent episodes without clear precipitating factors, including knee valgus and dislocation. Prior to the current exacerbation, she had developed low back pain two years earlier, which was transient and relieved with rest, but later progressed to severe pain and loss of mobility, requiring assistance with ambulation and stair climbing. Imaging revealed bone marrow edema in the right intertrochanteric region, femoral neck, lower left femur, and tibial intercondylar crest. Two weeks prior to admission, she experienced widespread joint pain, difficulty walking, and increased pain with weight bearing. Laboratory evaluation demonstrated hypophosphatemia (0.47 mmol/L), elevated serum alkaline phosphatase (257 IU/L), low 25-hydroxyvitamin D (41.1 nmol/L), and reduced bone mineral density as confirmed by dual-energy X-ray absorptiometry (DXA). Physical examination revealed scoliosis, unequal lower limb lengths (right 68 cm, left 67 cm; relative length ratio 77.5:76), reduced thigh and calf circumferences, bilateral knee pain, limited range of motion, left knee evagination, and an 'X'-shaped leg deformity. No joint swelling, tenderness, dislocation, or muscle atrophy was observed. Lower limb length discrepancy and skeletal deformities were consistent with chronic osteomalacia. Radiographic findings included multiple old rib fractures, bone islands in the left ilium and left sacrum, and an elliptical high-signal lesion (1.6 × 0.7 cm) at the posterior cortical edge of the left middle tibia, along with a small vertical nodular abnormal signal (1.5 cm) outside the bone. Quantitative T2-weighted MRI measurements showed T2 signal abnormalities at L1–L2, L1–L3, L1–L4, L2–L3, L2–L4, L3–L4, neck, Wards triangle, and great trochanter, with values ranging from −2.3 to −2.9, indicating generalized bone marrow edema and osteomalacic changes. Pathological evaluation"}
{"row_index": 210, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 55-year-old man had infections in his surgery scars for over a year. The scars were red, swollen, painful, and kept draining pus. Tests for common infections didn’t find anything wrong. A special test called mNGS found a tiny germ called M. senegalense in the scar tissue. This germ was confirmed with two other simple tests. The man took four antibiotics together for 60 days: clarithromycin, moxifloxacin, rifampicin, and oxycycline. After that, the scars healed and didn’t come back.\"\n}"}
{"row_index": 211, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 55-year-old man had repeated infections at surgical incision sites for over a year after having gallbladder surgery. The wounds were red, swollen, painful, and kept draining pus, but standard blood tests and bacterial cultures came back normal. Imaging showed a sinus tract under his chest bone, and surgery was done to remove the infected area and drain the abscess. He was treated with antibiotics, but the infection kept coming back. Tests for tuberculosis were negative, so doctors used a more advanced test called metagenomic next-generation sequencing (mNGS) to find the cause. This test found DNA from a rare bacterium called M. senegalense in the wound tissue. The result was confirmed using two other lab methods: PCR and capillary electrophoresis. The patient was then given a four-drug antibiotic therapy—clarithromycin, moxifloxacin, rifampicin, and oxycycline—for 60 days. After this treatment, his wounds healed completely and no new infections occurred.\"\n}"}
{"row_index": 212, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 55-year-old male patient presented to our hospital in August 2021 with recurrent surgical site infections at multiple incision sites, persisting for over 12 months following a laparoscopic cholecystectomy performed for gallstone disease complicated by cholangitis. Clinical examination revealed erythema, swelling, dehiscence, localized tenderness, hyperthermic skin, and minimal purulent exudation at the xiphoid process incisions. The patient experienced an average recurrence interval of approximately 25 days between infection episodes, with no abnormalities detected in routine complete blood count (CBC) parameters. B-mode ultrasonography suggested the presence of a subcutaneous sinus tract originating from the xiphoid region. In September 2021, the patient underwent laparoscopic reoperation and abdominal exploration, during which the sinus tract was excised and an abscess was drained. He was subsequently treated with piperacillin-tazobactam, a broad-spectrum beta-lactam/beta-lactamase inhibitor combination, but this regimen failed to achieve clinical resolution, with persistent wound dehiscence, surrounding skin erythema, swelling, pain, and purulent drainage continuing despite therapy.\\n\\nDespite normal body temperature and CBC results, conventional microbiological testing—including aerobic and anaerobic bacterial cultures, acid-fast bacilli (AFB) staining, and serological evaluation for tuberculous antigen (TB-Ab) antibodies—remained negative. Chest computed tomography (CT) and other tuberculosis-specific investigations were consistent with the absence of active tuberculosis, thereby excluding a tuberculous etiology. Given the persistent and refractory nature of the infections, and the absence of identifiable pathogens via standard diagnostic methods, metagenomic next-generation sequencing (mNGS) was employed to comprehensively detect microbial nucleic acids from tissue samples obtained from the infected incision sites. The mNGS analysis, conducted using the KingMed Diagnostics platform (Changsha, China), identified 53 out of 113 sequenced reads that mapped to *Mycobacterium senegalense*, representing a 0.09% coverage of the total sequencing depth and accounting for 58.76% of all detected microbial sequences, indicating a dominant pathogenic role.\\n\\nTo validate the mNGS findings, targeted polymerase chain reaction (PCR) assays were performed using two primer sets: ("}
{"row_index": 213, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 59-year-old woman who had cancer before, came back with pain and numbness in her left leg, numbness in her vulva, and trouble holding her urine. She had a tumor inside her spine, near the lower back, that was spreading. Doctors removed part of her spine to relieve her pain, but the cancer kept growing. After surgery, her leg symptoms got better, but soon she started having new problems — weakness on her right face, numbness, and blurry vision. Doctors found the cancer had spread to her brain and spinal lining, and she passed away two months later.\"\n}"}
{"row_index": 214, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 59-year-old woman with a history of recurring cancer of the uterus (endometrial carcinosarcoma) and previous treatments like chemotherapy and radiation now developed new pain, numbness in her left leg, and trouble with bladder control. She had a tumor found inside her spinal cord, just behind the L1 vertebra, that was growing and causing pressure on nerves. After surgery to remove part of the tumor and relieve pressure on her nerves, her leg symptoms improved. However, the cancer spread to the membranes surrounding her brain and spinal cord (leptomeningeal spread), leading to worsening symptoms including vision problems and facial numbness. Despite the surgery, she passed away within two months due to the advanced spread of her cancer.\"\n}"}
{"row_index": 215, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 59-year-old morbidly obese African-American female with a history of Stage IIIc recurrent endometrial carcinosarcoma and para-aortic and pelvic lymph node involvement presented with a 1-month history of left vulvar numbness, progressive left lower extremity pain and numbness, and episodic urinary incontinence. Imaging via thoracic-lumbar magnetic resonance (MR) demonstrated a 1.4 × 1.8 cm enhancing intradural extramedullary mass located inferior to the conus at the L1 and L4-L5 levels, accompanied by abnormal enhancement of the left-sided intradural nerve roots. Additional findings included bilateral perihilar lung metastases. The patient underwent a T12-L2 focal decompressive laminectomy with gross total resection of the L1 intradural/extramedullary lesion, performed primarily to achieve neurological symptom relief. Intraoperatively, diffuse carcinomatosis of the cauda equina was identified, with a large tumor mass located anteroinferior to the conus. The tumor exhibited a vascular architecture and involved multiple swollen, engorged nerve roots. Surgical dissection was discontinued when intraoperative electromyographic (EMG) monitoring indicated significant neural dysfunction, particularly in the gastrocnemius muscle, suggesting tumor infiltration and irreversible nerve root compromise. Permanent pathological examination confirmed a mesenchymal malignant Mullerian mixed tumor (carcinosarcoma) with no epithelial component, consistent with the original primary tumor's histological profile. Postoperatively, the patient showed improvement in left lower extremity pain and sensory deficits. However, two weeks later, she presented with worsening lower extremity symptoms, new-onset right-sided facial weakness, numbness, and blurred vision. Neuroimaging revealed leptomeningeal dissemination of disease, including hydrocephalus and multiple new intracranial metastases. Despite initial neurological stabilization, the patient died from progressive metastatic disease within two months of surgery, consistent with the aggressive biological behavior of carcinosarcoma and its propensity for early leptomeningeal spread, particularly in the context of recurrent, treatment-refractory disease and extensive pre-existing tumor burden.\"\n}"}
{"row_index": 216, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A four-year-old girl came in with a fever and pain in her left hip. She was walking with a limp, and moving her hip hurt, especially when turning it out. Her blood test showed she was anemic (low red blood cells) and had signs of inflammation. The doctors first thought it might be a common hip infection, but the X-ray and ultrasound didn’t show anything wrong. A CT scan of her belly found a tumor in her adrenal gland and swollen lymph nodes. Even though her bones didn’t seem damaged, the tumor was spreading to her bones. Tests showed this was a type of cancer called neuroblastoma. The cancer was spreading through her blood and bone marrow. She started chemotherapy, which helped a little, but the tumor didn’t go away. Because of side effects on her kidneys, they switched to a different drug combo. After 13 months, the tumor still wasn’t shrinking, so surgery wasn’t safe. Instead, she was given a treatment to replace her damaged bone marrow.\"\n}"}
{"row_index": 217, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A four-year-old girl came to the emergency room with a fever and a painful limp on her left hip. The pain was especially bad when moving her hip, especially turning it outward, but her range of motion was not severely limited. Blood tests showed anemia (low red blood cells) and signs of inflammation, which raised concerns that something was wrong with her hip. An X-ray of the pelvis didn't show any damage, and an ultrasound of the hip found fluid and swelling, suggesting possible infection or arthritis. A sample was taken and tested, but no bacteria were found. Because the symptoms were unusual, a CT scan of her abdomen and pelvis was done, which revealed a tumor in her left adrenal gland and swollen lymph nodes near major blood vessels. The scan also showed bone changes that suggested the tumor had spread. Further tests, including MRI and bone marrow biopsy, confirmed the presence of neuroblastoma — a type of cancer that starts in nerve cells. The tumor was found in the bone marrow and lymph nodes, and the biopsy showed it was spreading. The child started chemotherapy with a standard protocol, and after six months, the tumor hadn't gone away, though the spread had slightly decreased. Due to side effects from the initial treatment, a different chemotherapy plan (using irinotecan and temozolomide) was started. After 13 months, the tumor still hadn't shrunk enough to allow surgery, so the child was offered stem cell treatment instead. The initial signs of pain and anemia were key clues that something serious was going on, leading to the discovery of the tumor.\"\n}"}
{"row_index": 218, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A four-year-old girl presented to the emergency department with fever and a painful left hip, accompanied by a limp. There was no prior medical history, and no additional systemic or local symptoms were noted except for cervical lymphadenopathy. Physical examination revealed impaired left hip mobility with pain primarily on external rotation, although joint range of motion was not significantly restricted. Laboratory findings included anemia (hemoglobin 8.7 g/dL), normal white blood cell count, elevated erythrocyte sedimentation rate (ESBR 123 mm), and a reactive C-reactive protein level of 149.7 mg/L, suggesting acute inflammation. Initial pelvic X-ray was unremarkable. Ultrasound of the left hip demonstrated synovial inflammation and a small joint effusion. A guided joint aspiration was performed, and the effusion showed macroscopic features consistent with reactive arthritis; however, bacteriological cultures remained negative. Given the atypical presentation of hip pain and persistent inflammatory markers, a contrast-enhanced CT scan of the abdomen and pelvis was obtained, which revealed a left adrenal mass and retroperitoneal adenopathies involving the celiac trunk and superior mesenteric artery. Notably, the CT scan showed no evidence of bone or joint destruction, and thoracic imaging and peripheral blood smear evaluations were unremarkable. MRI was performed, and direct myelography demonstrated diffuse infiltration consistent with neuroblastoma. Histopathological analysis of cervical lymph node biopsy and bone marrow biopsy confirmed the diagnosis of neuroblastoma, not otherwise specified (NOS). Immunohistochemical staining revealed strong expression of synaptophysin and CD56 (NCAM), with absence of myogenin, supporting a neuronal origin and ruling out myogenic differentiation. Skeletal scintigraphy showed multiple osteoblastic foci, indicative of metastatic disease, and 123I-metaiodobenzylguanidine (MIBG) scintigraphy demonstrated low uptake in the adrenal mass (suggesting low noradrenergic transporter expression) and diffuse bone metastases with high noradrenergic transporter expression. Bone marrow biopsy confirmed extensive metastatic involvement. The patient initiated chemotherapy with eight cycles of the rapid COJEC protocol; after six months, the primary adrenal tumor remained unresectable, and metastatic burden showed partial reduction. Due to chemotherapy-induced renal toxicity, treatment was modified to irinotecan combined with temozolomide (TEMIRI)."}
{"row_index": 219, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A baby boy, seven months old, started having trouble eating, vomiting, and not moving his head or body right. Doctors thought it might be a brain problem called subacute rhombencephalitis, and gave him medicine that helped. After a few days, he got better and could eat again. Later, after a vaccine, he started getting worse — he became irritable, didn’t smile, and his muscles weakened. A new brain scan showed a serious brain condition called leukoencephalopathy with evanescent white matter, which is caused by a gene problem. The doctors found the gene fault in his body, and it was passed down from his parents. Even though his parents and brothers are healthy, they carry the gene. The baby had another fit at 15 months and couldn’t eat or respond to people. He needed help at home, and doctors gave him care for comfort. He passed away at 15 months because the disease kept getting worse. He died peacefully at home, with his family by his side.\"\n}"}
{"row_index": 220, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A seven-month-old baby boy was admitted to the hospital with severe vomiting, refusal to eat, and signs of neurological problems like weak muscle tone, poor head control, and lack of social interaction. His initial tests showed no serious issues, but a brain MRI revealed signs of subacute rhombencephalitis, a type of brain inflammation. He was treated with steroids and intravenous immune therapy, and his symptoms improved over time. By 10 months, he started showing a return of symptoms after receiving a vaccine — this is called a neurological regression. He became more irritable, lost his social smile, and his muscle weakness worsened. A new brain scan showed damage to the white matter of the brain, specifically in areas involved in movement and coordination, which led to a diagnosis of leukoencephalopathy with evanescent white matter. This is a rare genetic disorder that affects the brain's white matter and is inherited in an autosomal recessive pattern. The baby’s parents and two older brothers were found to be carriers but healthy. At 15 months, he had a seizure and needed further care. His condition continued to worsen, and he eventually stopped responding to stimuli and could no longer eat orally, requiring a feeding tube. He was cared for at home with palliative support and passed away at 15 months due to the progression of his disease.\"\n}"}
{"row_index": 221, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 7-month-old male infant presented with a severe, persistent vomiting syndrome, anorexia, and progressive neurological deterioration characterized by axial hypotonia, poor head control, impaired suck-swallow coordination, absence of social smiling, and abnormal oral-motor movements. Osteotendinous reflexes were preserved, and there was no perinatal, personal, or familial history of neurologic disorders or consanguinity. Initial evaluation included a comprehensive panel of laboratory, metabolic, autoimmune, neuroimaging, electroencephalographic, and auditory evoked potential studies, all of which yielded normal results except for the isolation of respiratory syncytial virus (RSV) in a nasopharyngeal aspirate and a brain magnetic resonance imaging (MRI) scan demonstrating bilateral, symmetric diffusion restriction in the anterior bulbo-protuberant junction, consistent with subacute rhombencephalitis. The patient was treated with two doses of intravenous immunoglobulin (2 g/kg total), leading to progressive clinical improvement and oral tolerance, followed by outpatient follow-up in a neuropediatric setting. During this period, the child exhibited modest clinical stabilization, including improved visual tracking, enhanced social contact, and brief periods of stable sitting without support, with intermittent masticatory movements observed only in supine position; osteotendinous reflexes remained intact.\\n\\nAt 10 months of age, the infant was readmitted following a post-vaccination episode of food rejection, which triggered a significant neurological regression. This included increased irritability, a flat affect, loss of social smiling, progressive worsening of axial hypotonia, proximal muscle weakness, and a striking transformation of the osteotendinous reflexes into hyperactive, equine-type reflexes. Neuroimaging was repeated, revealing generalized bilateral and symmetric abnormalities in the signal intensity of deep and subcortical white matter, involving the U-fibers and globus pallidus, consistent with a neurometabolic disorder suggestive of leukodystrophy. The MRI also showed a mild increase in choline concentration on spectroscopic analysis, with normal N-acetylmethionine (NAA) levels, indicating early disruption of myelin synthesis or integrity without overt neuronal loss. Given these findings, a clinical exome sequencing study targeting early-onset leukodystrophies was performed, which identified a pathogenic, homozygous mutation in the EIF2B5 gene. This mutation is associated with"}
{"row_index": 222, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man in his 60s went to the hospital feeling weak, having muscle aches, a fever, and belly pain. Doctors did a scan and found a blood clot in a vein called the SMV, which only affected that vein and didn’t spread to other important veins. He also had a fever and body aches that didn’t match the clot, so they tested for flu. The test came back positive for flu B. He didn’t need surgery or any other treatment — just medicine to thin his blood. After a few days, the scan showed the clot was getting better. He was sent home with pills to keep his blood thin and follow up with the doctor.\"\n}"}
{"row_index": 223, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 64-year-old man went to the hospital with weakness, muscle aches, fever, and abdominal pain that had started a week before. A CT scan showed a blood clot in the superior mesenteric vein (SMV), which supplies blood to the intestines. The clot was only in the SMV and did not spread to the portal or splenic veins, and the patient was stable overall. However, the fever and muscle pain didn't fit what was expected for SMV thrombosis, so the doctor tested for influenza. The test came back positive for influenza B. The patient was started on anticoagulation therapy (medication to prevent blood clots) without needing surgery. A follow-up CT scan showed the clot was improving, and the patient was discharged with ongoing oral anticoagulant treatment.\"\n}"}
{"row_index": 224, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 64-year-old male presented to a local medical center on March 4th with a one-week history of general weakness, myalgia, and abdominal pain. On presentation, his temperature was 37.9 °C, and he reported feeling hot, with associated headache; no cough, sputum, diarrhea, or vomiting were noted. Physical examination revealed mild tenderness in the right upper quadrant and hypoactive bowel sounds, with no rebound tenderness. Laboratory findings showed a white blood cell count of 16,160 /mL, erythrocyte sedimentation rate (ESR) of 86 mm/hr, and high-sensitivity C-reactive protein (HS-CRP) level of 16 mg/dL, indicating systemic inflammation. Abdominal computed tomography (CT) demonstrated a large, segmental thrombus extending from the superior mesenteric vein (SMV) gastrocolic trunk to its distal portion, resulting in complete obstruction of a segment of the SMV. The imaging also showed surrounding fat stranding and bowel wall edema consistent with ascending colon involvement, suggesting ischemic or inflammatory bowel changes secondary to venous obstruction. The patient was subsequently transferred to our hospital for further evaluation. Given the atypical presentation—particularly the presence of systemic fever and widespread myalgia not fully explained by the SMV thrombosis alone—a nasopharyngeal swab was collected for testing. An Influenza A/B rapid antigen test using the BD Veritor™ Plus System for Rapid Detection of Flu A+B was performed, with reported sensitivity of 81.3% (95% CI: 71.1–88.5%) and specificity of 98.2% (95% CI: 95.7–99.3%). The test returned a positive result for influenza B, which likely contributed to the patient’s fever and myalgia. Concurrently, a reverse transcription polymerase chain reaction (RT-PCR) test for SARS-CoV-2 (COVID-19) was performed in light of the ongoing pandemic context, though no positive result was reported. The thrombus was localized exclusively to the SMV, with no extension into the portal or splenic veins, confirming isolated venous occlusion. The patient was clinically stable and managed with anticoagulation therapy without surgical intervention. Follow-up CT imaging demonstrated resolution of the throm"}
{"row_index": 225, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 9-month-old girl had a bump in her eye socket on the right side, noticed by her mom three months before. Doctors first thought it was just a normal thing, but scans showed bone changes in the eye area, like a tumor was eating away at the bones. A scan of her chest and belly found a big tumor in her adrenal gland, along with swollen lymph nodes and spine changes. This matched a serious cancer called stage-4 neuroblastoma. She started chemo and surgery, and after 10 months, the cancer was gone and she hasn’t had any return.\"\n}"}
{"row_index": 226, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 9-month-old girl was diagnosed with isolated right-sided enophthalmos, which means her right eye appeared to be pulled back. Her mother noticed this three months before she visited the doctor, and several specialists initially thought it was just a normal variation. However, imaging tests showed bone changes in the orbit and surrounding areas, including osteolysis (bone loss) and thickening of the bone lining, which raised concern for a tumor. A CT scan of her chest and abdomen found a large mass in the left adrenal gland, along with swollen lymph nodes and bone changes, consistent with stage-4 neuroblastoma. This type of cancer is rare in young children and spreads beyond the original site. The child was referred to oncology, started on chemotherapy, and had surgery to remove remaining tissue. She achieved complete remission and has not had a recurrence at a 10-month follow-up.\"\n}"}
{"row_index": 227, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 9-month-old Caucasian female with no significant birth or past medical history presented with isolated right-sided enophthalmos, defined as a posterior displacement of the globe relative to the orbital cavity. The mother first noted the abnormality three months prior to presentation, describing a backward shift of the right eye. Initial evaluations by multiple specialists attributed the finding to a constitutional variant, with no evidence of systemic illness, neurological deficits, abdominal or skeletal abnormalities, or deterioration in general health. Ophthalmological examination confirmed mild right enophthalmos without associated facial flattening or structural deformity. All standard eye function tests—including pupillary size and reactivity to light, direct and consensual accommodation, fixation, following, binocular vision, and eye-hand coordination—were within normal limits. Slit lamp and fundus examinations revealed no signs of intraocular pathology. Prior to definitive imaging, routine laboratory assessments, including serum creatinine, were unremarkable, indicating preserved renal function and no evidence of systemic disease. Orbital computed tomography (CT) demonstrated irregular osteolysis with active periosteal reaction involving the right orbital walls, malar bones, and zygomatic arches, predominantly unilateral and asymmetric, which raised a high index of suspicion for an underlying orbital mass, likely neoplastic in origin. A subsequent thoracic-abdominal CT scan identified a retroperitoneal heterogeneous mass measuring 83 mm × 43 mm × 42 mm, located on the left adrenal gland, which encased adjacent vascular structures and was associated with enlarged left supraclavicular lymph nodes and vertebral body condensations. These imaging findings are characteristic of stage-4 neuroblastoma, a malignant peripheral nerve tumor of early childhood origin, typically arising from sympathoadrenal precursors. The diagnosis was confirmed through histopathological and molecular characterization. The patient was promptly referred to pediatric oncology for multimodal management, including induction chemotherapy and surgical evacuation of residual tumor burden. Treatment resulted in complete clinical remission, with no evidence of disease recurrence at a 10-month follow-up. The clinical course underscores the importance of imaging evaluation in the setting of isolated enophthalmos, particularly when orbital bony changes with periosteal reaction are present, as these findings may signal an occult neuroblastoma, even in the absence of other systemic symptoms or signs.\"\n}"}
{"row_index": 228, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 21-year-old girl started feeling short of breath and chest pain six months ago. She was diagnosed with heart failure, but had no history of heart problems. Doctors found a strange connection between a blood vessel in her arm (right subclavian artery) and a vein (superior vena cava) that was causing her heart to work harder. This connection, called a fistula, had a narrow part at the start, which made blood flow too fast. She had the fistula closed using a small device placed through a catheter in her vein. After the procedure, her symptoms got much better by the 3-month check-up.\"\n}"}
{"row_index": 229, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 21-year-old woman was diagnosed with new-onset heart failure after six months of worsening shortness of breath and chest pain. She had no prior heart problems, injuries, or surgeries. Examination found a continuous heart murmur heard in the right chest area, and imaging showed an enlarged heart and signs of right heart strain. Tests revealed a rare birth defect called a congenital arteriovenous fistula, where a blood vessel (the right subclavian artery) was abnormally connected to the superior vena cava, causing blood to flow directly from artery to vein without going through the heart. This connection was narrowed at its start, which increased pressure and worsened heart function. The fistula was successfully closed using a minimally invasive procedure called transcatheter occlusion, where a small device was guided through a blood vessel to seal the abnormal connection. After the procedure, the patient’s symptoms improved significantly by the three-month follow-up visit.\"\n}"}
{"row_index": 230, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 21-year-old female presented with a six-month history of progressive dyspnoea and chest pain, ultimately diagnosed with new-onset heart failure in the absence of any prior cardiovascular disease, trauma, or surgical history. Physical examination revealed a grade 3/6 continuous machinery murmur, most prominent between the right second and third intercostal spaces and radiating to the right infraclavicular fossa. Resting oxygen saturation was normal (SpO2 95%) with non-cyanotic skin colour, indicating adequate tissue oxygenation. Chest radiography demonstrated cardiomegaly, consistent with right-sided cardiac volume overload. Electrocardiography revealed sinus rhythm at 95 bpm, complete right bundle branch block, and right ventricular hypertrophy, reflecting chronic pressure overload on the right side of the heart. Pulmonary function tests were within normal limits, ruling out obstructive or restrictive lung disease as a contributing factor.\\n\\nTransthoracic echocardiography identified a dilated right subclavian artery (RSA) with an 8-mm arteriovenous fistula connecting to the superior vena cava (SVC), accompanied by significant stenosis at the proximal origin of the fistula. The right ventricle and right atrium were markedly dilated, consistent with chronic volume and pressure overload. Mild tricuspid regurgitation was observed. Continuous wave Doppler analysis demonstrated a sustained flow signal of 2.3 m/s from the RSA to the SVC with a pressure gradient of 22 mmHg, indicating a low-resistance shunt. At the site of stenosis, the peak flow velocity reached 3.9 m/s with a pressure gradient of 59 mmHg, reflecting a high-velocity, high-resistance flow pattern consistent with a critical stenotic lesion. Computed tomography angiography (CTA) provided detailed anatomical characterization of the arteriovenous fistula, confirming the direct connection between the RSA and SVC and the proximal stenosis, enabling precise procedural planning.\\n\\nThe patient underwent transcatheter occlusion of the arteriovenous fistula under local anaesthesia. A 10/12 mm Amplatzer ductal occluder was delivered via a 5-F H1 catheter and deployed from the SVC side using angiographic guidance. An 8F sheath was utilized to facilitate catheter advancement and occluder"}
{"row_index": 231, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 68-year-old woman came to the hospital because her legs were weak for more than 3 days. She also had neck pain, numbness in her hands and feet, trouble going to the bathroom, and couldn’t feel cold or heat well. She didn’t have fever, cough, or other common illness symptoms. She had high blood pressure but no diabetes or allergies. Tests showed her brain and blood were fine, but her spinal cord was inflamed — especially in the neck area. This is a rare case in China, and it’s different from usual cases of this illness. She was treated with strong medicine and immune therapy and got better. This kind of problem with anti-sulfatide antibodies usually affects nerves, but in her case, it hit the spinal cord, which is unusual.\"\n}"}
{"row_index": 232, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old woman was admitted to the hospital with weakness in her limbs that had lasted more than 3 days. She also had neck pain, numbness in her hands and feet, trouble controlling her bladder and bowels, and a reduced ability to feel temperature. She was diagnosed with a rare form of Guillain-Barré syndrome (GBS) that is positive for anti-sulfatide antibodies. This case was treated with methylprednisolone and intravenous immunoglobulin therapy. Unlike typical GBS cases, this patient showed signs of spinal cord involvement, which is not commonly seen. No other patients with this specific combination of symptoms have been reported in China before. The patient’s symptoms started gradually and were not linked to a recent infection or illness, and she had no history of diabetes or allergies.\"\n}"}
{"row_index": 233, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old female was admitted to the hospital with progressive limb weakness lasting over three days, accompanied by posterior neck pain, distal sensory disturbances, and a characteristic electric shock-like paresthesia upon tactile stimulation. Symptoms evolved to include impaired manual dexterity, bilateral lower extremity weakness, inability to ambulate, urinary and fecal retention, and heightened posterior neck pain. Notably, she reported cold-related pain in the upper extremities, which is atypical for common Guillain-Barré syndrome (GBS) presentations. Neurological examination revealed preserved consciousness, normal pupillary response, intact eye movements, and symmetrical frontal lines. Upper limb muscle strength was graded 4, lower limb strength was 3, with hypotonia and bilateral diminished tendon reflexes. The Babinski sign was positive bilaterally, indicating upper motor neuron involvement. Sensory examination demonstrated reduced perception of pain and temperature in the distal extremities, while vibration and joint position sensations remained intact. The two-handed finger-nose test was stable, suggesting preserved cerebellar function, whereas the heel-knee-shin test was unstable, indicating impaired proprioception. Meningeal signs were absent, and there was no evidence of autonomic dysfunction such as dysautonomia or respiratory compromise. Vital signs were stable: temperature 36.8 °C, pulse 76 beats/min, respiratory rate 20 breaths/min, blood pressure 145/78 mmHg. Physical examination revealed no signs of infection, cardiac abnormalities, or abdominal pathology; abdominal examination showed softness, no varices, no rebound or peritoneal tenderness, and only slightly reduced bowel sounds (2–3/min), without evidence of ascites. Laboratory studies, including complete blood count, liver and renal function, coagulation profile, and tumor markers, were within normal limits. Cranial CT and cranial MRI showed no evidence of hemorrhage, ischemia, or structural lesions. Lumbar puncture revealed elevated cerebrospinal fluid (CSF) pressure (116 mmH₂O) and cytoalbuminologic dissociation—characteristic of inflammatory demyelinating processes—without the presence of oligoclonal bands, aquaporin-4 antibodies, or anti-MOG antibodies, ruling out other central nervous system demyelinating disorders. Peripheral neuropathy immunoblotting demonstrated a positive IgG response to sulfatide"}
{"row_index": 234, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old man had trouble breathing and suddenly lost consciousness several times in one week. Each time, he would feel dizzy and lose awareness for 3 to 5 minutes, then wake up fine. The episodes happened when he was active or breathed cold air. He went to the hospital after the fourth episode. Tests showed blood clots in his heart and lungs. One clot was blocking a small hole in his heart (PFO), and clots were also in his lung blood vessels. Doctors placed a filter in his biggest vein to catch clots and used a medicine (alteplase) to break down the clots. Two days later, no clots were found in his heart. He was sent home on a blood thinner called warfarin and had no problems. This treatment helped stop the clots from coming back.\"\n}"}
{"row_index": 235, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old man had repeated episodes of sudden, brief loss of consciousness (syncope) and shortness of breath over a week. The episodes were triggered by physical activity or breathing cold air, and he had no warning signs before them. He went to the hospital after another episode on February 22, 2019. His initial tests showed high levels of a blood clot marker (D-dimer) and a protein linked to heart strain (NT-proBNP), while his blood pressure and other vital signs were normal. An electrocardiogram showed a fast heart rate, and ultrasound found a blood clot in his right leg vein. Echocardiography revealed a blood clot blocking a small hole between the upper chambers of the heart (patent foramen ovale), along with a large clot in the right atrium and a clot in the left atrium. CT scans confirmed blood clots in both pulmonary arteries, indicating pulmonary embolism. He received treatment with a filter placed in his inferior vena cava to prevent clots from traveling to the lungs and was given alteplase to dissolve the clots. Two days after treatment, follow-up echocardiography showed no clots in the heart chambers. He was discharged home two weeks later on warfarin, a blood thinner, without complications.\"\n}"}
{"row_index": 236, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old male presented to the emergency department with recurrent syncope and intermittent dyspnea over a 7-day period. The initial episode of chest distress occurred on February 15, 2019, followed by four episodes of transient, self-limited syncope each lasting 3–5 minutes with complete recovery between episodes. Triggers included physical exertion and inhalation of cold air; no prodromal symptoms or associated neurological features were reported. The patient sought medical evaluation on February 22, 2019, following a new episode of syncope. There was no personal or family history of thrombotic disorders, and the patient's sedentary lifestyle, due to employment as a news editor, contributed to reduced physical activity.\\n\\nVital signs at first presentation were stable: pulse rate 96 beats/min, respiratory rate 20 breaths/min, blood pressure 15.5/10.1 kPa, body mass index 23.1 kg/m². Physical examination revealed symmetric and light-responsive pupils, a prominent P2 component in the cardiac auscultation, symmetrical breath sounds without rales or wheezing, and warm extremities without edema. Neurological examination was unremarkable.\\n\\nInitial laboratory findings included markedly elevated serum D-dimer at 4150 ng/mL (normal <500 ng/mL), indicating active thrombin generation and fibrin formation. Arterial blood gas analysis under ambient air showed a PaO₂ of 79 mmHg, suggesting mild hypoxemia. N-terminal pro-B-type natriuretic peptide (NT-proBNP) was elevated at 4460 pg/mL (normal <450 pg/mL), reflecting right ventricular strain consistent with pulmonary hypertension. Cardiac enzyme levels were within normal limits, excluding acute myocardial injury.\\n\\nElectrocardiography demonstrated sinus tachycardia, likely secondary to hypoxemia and sympathetic activation. Transthoracic echocardiography revealed a deep venous thrombus in the right popliteal vein, a thrombus straddling a patent foramen ovale (PFO), a dilated right atrium, and moderate pulmonary hypertension. The thrombus dimensions were 3 mm × 20 mm in the left atrium and 8 mm × 25 mm in the right atrium. Computed tom"}
{"row_index": 237, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"We used two small cork-screws to safely remove a stuck hip implant when the hip kept slipping out because the socket was too far out of place. This worked well without hurting the patient, and by the second month, she could walk without help.\"\n}"}
{"row_index": 238, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A new method has been reported to remove a stable, cemented hip component that is causing recurrent dislocations due to improper positioning of the acetabular part. In this case, a 74-year-old woman had repeated hip dislocations (eight times) because the hip socket (acetabulum) was positioned incorrectly. Doctors used two cork-screws inserted into the rim of the hip socket to push out the plastic liner and create cracks in the cement. This allowed them to easily remove the damaged plastic cup. The cement was then carefully broken up and removed piece by piece. A new, reinforced ring and a new cemented hip socket were placed using standard techniques. The metal ball of the hip was replaced, but the stem was kept. There were no complications during or after the surgery. At two months after the procedure, the patient could walk without needing support.\"\n}"}
{"row_index": 239, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 74-year-old female underwent revision total hip arthroplasty for recurrent dislocation of a cemented total hip prosthesis, resulting from acetabular malposition, with a history of eight prior dislocations. The acetabular component was stable and cemented, necessitating a technique to remove the cemented acetabular cup without compromising the integrity of the underlying bone or the femoral stem. The all-polyethylene acetabular liner was drilled with a 4.5 mm drill to create a peripheral breach, followed by the insertion of two cork-screws into the rim of the acetabular component, advanced as far as anatomically feasible, to induce extrusion of the polyethylene liner from the cement mantle and to generate fissures within the cement layer. Application of manual torsional shear forces at the polyethylene-cement interface resulted in complete disruption of the polyethylene liner at the cement-polyethylene boundary, with no technical complications or resistance observed. This mechanical disruption enabled complete removal of the polyethylene cup with minimal effort. Subsequently, cement–splitting osteotomes were employed to remove the cement mantle in a piecemeal fashion, with meticulous curettage of residual cement plugs to ensure complete debridement. A roof reinforcement ring was implanted to stabilize the acetabular component, followed by placement of a cemented UHMW polyethylene cup using standard surgical techniques. The original metallic femoral head was replaced, while the cemented femoral stem was retained to preserve stability and biomechanical continuity. The perioperative course was uncomplicated, with no evidence of intraoperative or postoperative complications. At two months postoperatively, the patient achieved full weight-bearing ambulation without the need for external assistive devices, indicating successful restoration of hip joint stability and function. The described technique demonstrates a feasible, technically sound approach for the removal of a stable cemented acetabular component in the setting of recurrent dislocation due to malposition, leveraging mechanical disruption via cork-screw insertion and torsional shear forces to overcome the cement-liner interface without requiring additional instrumentation or surgical intervention.\"\n}"}
{"row_index": 240, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 25-year-old woman had a planned C-section at 39 weeks because she wanted to. After the surgery, she suddenly got a very high fever and her blood pressure dropped sharply. A few days later, doctors found a bad germ in her blood called Ralstonia mannitolilytica. This meant she had a serious infection that caused her body to go into shock. Doctors gave her lots of fluids, blood transfusions, medicines to raise her blood pressure, and strong antibiotics like imipenem and cefoperazone. She stayed in the hospital for a few days in a serious care unit, and after treatment, she got better. She was finally able to go home without any problems, and six months later, everything was normal.\"\n}"}
{"row_index": 241, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 25-year-old woman had a planned cesarean section at 39 weeks of pregnancy. After the surgery, she suddenly developed a high fever and low blood pressure, which are signs of a serious infection called sepsis. Five days later, a bacteria named Ralstonia mannitolilytica was found in her blood. This infection led to septic shock, so she received strong fluids, blood transfusions, and medicines to support her body. She was treated in the intensive care unit and recovered without major complications. She was discharged on day 15 and had no issues during a six-month follow-up.\"\n}"}
{"row_index": 242, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 25-year-old woman, gravida 1 para 0, with no history of chronic medical conditions, was admitted for an elective cesarean delivery at 39+1 weeks of gestation by maternal request. Combined spinal-epidural anesthesia was administered: 15 mg of 0.5% ropivacaine hydrochloride (AstraZeneca AB, Sweden) was injected into the subarachnoid space, and 5 mL of 2% lidocaine (Shanxi Shiyao Yinhu, China) was administered epidurally. Prophylactic intravenous cefathiamidine (1.0 g, Shandong Luoxin, China) was initiated preoperatively. During surgery, the patient developed shivering, but vital signs remained stable, and the procedure was completed successfully. Postoperatively, she was transferred to the anesthetic resuscitation room where she continued to shiver, reported generalized numbness and dyspnea, and developed a high fever of 40.7 °C. Her blood pressure dropped to 78/44 mmHg, with tachycardia reaching a maximum of 177 bpm, and intermittent vaginal bleeding was noted; oxygen saturation remained at 98%. Septic shock was clinically suspected, though anaphylactic shock could not be excluded. Immediate resuscitation was initiated with massive fluid resuscitation, intravenous dexamethasone (Sinopharm, China), and intramuscular carboprost tromethamine (250 μg, Pharmacia and Upjohn Company, USA) as a uterotonic agent. A Bakri postpartum balloon (Cook, USA) was placed to manage postpartum hemorrhage. Despite interventions, blood pressure remained critically low (<90/60 mmHg). Laboratory findings revealed severe metabolic acidosis (pH 7.252 [normal 7.35–7.45], serum lactate 6.52 mmol/L [normal 0.36–1.25]), markedly elevated procalcitonin (94.5 ng/mL [normal 0.0–0.5]), leukocytosis (WBC 15 × 10⁹/L [normal 4–10 × 10⁹/L]), neutrophilic predominance ("}
{"row_index": 243, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 71-year-old woman had early breast cancer in her right breast. She had surgery to remove the tumor, then took chemo, radiation, and hormone pills to fight it. She stayed healthy for years until 2015, when she started coughing. Doctors found the cancer had spread to her lungs and bones, like in the shoulder, hip, and back. She started taking two medicines to stop the cancer from growing — ribociclib and letrozole — which helped for a while. But she still had low blood cell counts, so her dose was cut in half. A few months later, she noticed white spots on her hands, feet, and face — like patches of skin losing color. These spots grew slowly and were not from an autoimmune problem. Her doctor tried creams, but they didn’t help much. This is a known side effect of the cancer medicines she’s taking.\"\n}"}
{"row_index": 244, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 71-year-old woman was first diagnosed with early-stage right breast cancer in 1999. The cancer was hormone-sensitive (HR+/HER2-) and small, less than 2 cm, with no spread to lymph nodes. She had breast-conserving surgery, followed by chemotherapy, radiation, and hormonal therapy with tamoxifen for 5 years. She stayed in good health and followed up regularly until 2015, when she started having a persistent cough. Imaging showed the cancer had spread to the lymph nodes near the lungs and to several bones, including the left shoulder, scapula, pelvis, and spine. A biopsy confirmed it was breast cancer that had spread. Her cancer remained hormone-sensitive, so she was treated with endocrine therapy, first with fulvestrant, then with exemestane and everolimus, but she had to stop due to lung and kidney side effects. She later joined a clinical trial testing a new drug class called CDK4/6 inhibitors, but stopped when her cancer progressed. After the FDA approved these drugs, she started taking ribociclib and letrozole, which worked well overall, though her blood counts were low, so her ribociclib dose was reduced. About 20 weeks into treatment, she noticed white, patchy spots on her hands, feet, and face that looked like vitiligo. These lesions spread slowly and were not linked to any family or personal history of autoimmune conditions. She saw a dermatologist, tried topical treatments, and was given steroids, but the spots did not improve significantly.\"\n}"}
{"row_index": 245, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 71-year-old female with a history of thalassemia minor and hypertension was diagnosed in 1999 with early-stage right breast cancer, specifically invasive ductal carcinoma measuring less than 2 cm, node-negative, with hormone receptor (HR) positivity (ER 90%, PR 30%) and HER2 negativity. She underwent breast-conserving surgery with axillary dissection, followed by adjuvant chemotherapy consisting of cyclophosphamide, methotrexate, and 5-fluorouracil (CMF), subsequent radiotherapy, and five years of tamoxifen therapy. The patient maintained excellent clinical and mammographic follow-up until 2015, when she presented with an intractable cough. Imaging revealed a left hilar lesion and multiple osteolytic bone metastases involving the left scapula, left shoulder, left iliac bone, and the fourth and seventh dorsal vertebrae. Fine needle aspiration via endobronchial ultrasound confirmed metastatic breast cancer with preservation of the same molecular phenotype: HR-positive, HER2-negative. Initial endocrine therapy with fulvestrant resulted in a progression-free survival of 2 years; she was subsequently switched to exemestane and everolimus, which was discontinued due to grade II pneumonitis and proteinuria consistent with prenephrotic range. During this period, she was enrolled in a double-blind, randomized clinical trial evaluating the addition of CDK4/6 inhibitors to aromatase inhibitor therapy. Due to disease progression, she was withdrawn from the trial and found to be on the placebo arm. Following FDA approval of CDK4/6 inhibitors, she was initiated on ribociclib and letrozole, which she tolerated with moderate neutropenia necessitating dose reduction to 400 mg daily on days 1–21 of a 28-day cycle. Approximately 20 weeks after starting this regimen, she developed small, rounded, well-demarcated hypopigmented lesions initially on both hands, which expanded to the midforearms. Three weeks later, similar lesions appeared on the face and feet. These lesions were clinically consistent with vitiligo-like depigmentation, and the patient had no personal or family history of autoimmune disorders. Dermatological evaluation was performed, and topical immunomodulators (calcineurin inhibitors) were offered but declined; she was managed with topical corticosteroids"}
{"row_index": 246, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 81-year-old woman came to the hospital because she was bleeding from her stomach and had black stools. She had a history of a cancer in her stomach area (GIST) that spread to her liver and belly, and she had been treated with medicine (sunitinib) for it. Four years earlier, she had surgery to fix her stomach and used a part of her small intestine (jejunum) to connect the stomach to the esophagus (Merendino procedure). During an emergency exam, doctors found a bleeding spot in the small intestine where the connection was made. They stopped the bleeding with medicine and a special powder, and gave her blood transfusions. But her blood count kept dropping, and they thought she had a reaction to the blood. She got fever, started passing blood in her urine, and her breathing got worse. Tests showed she had a serious infection caused by a type of bacteria called Clostridium perfringens, which spread to many of her organs. Even though the blood she got was checked, it wasn’t infected. She died three days after being admitted because of the severe infection. The infection had spread all over her body and damaged her tissues.\"\n}"}
{"row_index": 247, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 81-year-old woman was admitted to the hospital suddenly because she was bleeding from her stomach and had black, tarry stools (melena). She had a history of a cancer in the stomach area called a gastrointestinal stromal tumor (GIST), which had spread to her liver and abdomen. She had been treated with medication (sunitinib) for this advanced cancer and had undergone a surgery four years earlier called a Merendino procedure, where part of her small intestine was used to reconstruct her stomach and esophagus. During an emergency endoscopy, doctors found a bleeding ulcer in the reconstructed part of her small intestine. The bleeding was stopped right away, and she received blood transfusions. However, her blood levels continued to drop, and doctors suspected a reaction to the transfused blood. She was given treatment for a possible hemolytic transfusion reaction, but her condition worsened. Three days after admission, she died. Blood tests later showed that she had a severe infection caused by Clostridium perfringens, a type of bacteria that spreads widely in her organs. The autopsy confirmed that the bacteria had spread throughout her body, causing tissue damage and septic shock. The infection was not caused by contaminated blood products, and the bleeding ulcer was not the direct cause of death.\"\n}"}
{"row_index": 248, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 81-year-old female presented to the emergency department with acute hematemesis and melena, exhibiting poor general condition and hemodynamic instability. Initial laboratory findings showed a hemoglobin level of 7.7 mg/dL, with no leukocytosis or elevation in C-reactive protein (CRP), suggesting a non-infectious or non-inflammatory etiology at presentation. The patient had a history of a 6.5 cm gastrointestinal stromal tumor (GIST) originating in the cardia, initially treated with imatinib 400 mg/day for downsizing, followed by surgical resection of the gastroesophageal junction and reconstruction via a jejunal interposition (Merendino procedure) four years prior. Histopathological analysis of the primary tumor revealed a T3-stage lesion with a positive c-Kit mutation in exon 11 and a Ki-67 proliferation index of 15%, indicating a high proliferative activity. According to Miettinen's prognostic criteria, the tumor was classified as high-risk due to size (>5 cm) and mitotic rate (>5 mitoses per high-power field), leading to initiation of first-line adjuvant imatinib therapy at 400 mg/day. After two years of first-line therapy, the patient developed hepatic and peritoneal metastases, prompting transition to sunitinib as second-line therapy for metastatic disease. Proton pump inhibitor (PPI) use was discontinued for an unspecified duration prior to admission, which may have contributed to mucosal vulnerability and ulceration. Emergency gastroscopy revealed active bleeding from a vessel stump in the jejunal interposition, consistent with Forrest stage I b upper gastrointestinal bleeding. Endoscopic hemostasis was achieved through local adrenaline injection and polymer powder application. A thoracoabdominal CT scan demonstrated no active hemorrhage or free intraperitoneal fluid, with hepatic and peritoneal metastases remaining stable in size but increasingly necrotic compared to prior imaging. A subsequent decline in hemoglobin prompted repeat gastroscopy, which identified diffuse, non-localized bleeding, necessitating aggressive coagulopathy management. The patient received 9 units of packed red blood cells (pRBCs), 6 units of fresh frozen plasma (FFPs), 6 units of platelet concentrates, 3 g of fibrinogen, and 4000 IU of PPSB® (a prothrom"}
{"row_index": 249, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 67-year-old man started having problems with his legs, like numbness and pain, that went away on their own. Later, at age 73, he had eye problems and was told he had multiple sclerosis. His condition got worse over time, with more nerve issues in his spine and eyes. He tried medicines like interferon and steroids, but they didn’t help. He also tried natalizumab, but still had relapses — his eyes and legs got worse each time. After stopping natalizumab, he had plasma exchange treatments and started rituxan, which helped his symptoms stop worsening. But later, he had another serious back nerve attack. So, he started cyclophosphamide, and after that, he didn’t have any more attacks for 24 months. Tests later showed he had a specific antibody called anti-aquaporin-4, which explains his condition. This is a rare disease called neuromyelitis optica, not multiple sclerosis.\"\n}"}
{"row_index": 250, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 67-year-old man with no prior health issues first developed symptoms in his legs, including numbness and reduced pain sensation, which went away on their own. Later, at age 73, he had vision problems in both eyes (optic neuritis) and was initially diagnosed with multiple sclerosis (MS). His condition worsened over time, with MRI scans showing damage to his spinal cord and brain. He was treated with interferon and corticosteroids, but these did not stop the relapses. He then started natalizumab, which also failed—he had three more relapses, each affecting his vision and movement, leading to severe weakness and a significant drop in his disability score. After stopping natalizumab and undergoing repeated plasma exchanges, his symptoms began to stabilize. He started treatment with rituxan, which depleted his B cells, but later had another serious spinal relapse. This led to starting cyclophosphamide, an immune-suppressing drug, which successfully prevented any further relapses over the next 24 months. Testing later confirmed the presence of anti-aquaporin-4 antibodies, which are linked to neuromyelitis optica (NMO), a different condition from MS. This case shows that early diagnosis and appropriate treatment are key in managing such rare and serious autoimmune diseases.\"\n}"}
{"row_index": 251, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 67-year-old Caucasian male with no significant prior medical history presented with acute spinal symptoms characterized by transient hypesthesia and hypoalgesia in both lower extremities, which spontaneously resolved without a definitive diagnosis. At age 73, he developed bilateral optic neuritis, leading to a diagnosis of multiple sclerosis (MS) at an external healthcare facility. At that time, his expanded disability status scale (EDSS) score was 2.5. Magnetic resonance imaging (MRI) of the spinal cord revealed diffuse cord swelling and longitudinally extensive T2-hypertensive lesions spanning from C2 to T3, consistent with longitudinal myelitis. Cranial MRI demonstrated sparse periventricular and cerebellar lesions without contrast enhancement and did not meet the Barkhof criteria for MS. Cerebrospinal fluid (CSF) analysis revealed oligoclonal bands, a hallmark of MS, although anti-aquaporin-4 (AQP-4) antibody testing was not performed at the time. Initial therapy consisted of interferon beta-1a for six months, subsequently switched to interferon beta-1b by the treating neurologist. During this period, the patient experienced two additional spinal relapses, each managed with corticosteroid pulses without clinical benefit, resulting in a progressive worsening of disability, with EDSS increasing from 2.5 to 4.0. Subsequent initiation of natalizumab at an external clinic was associated with three relapses: the first occurring at four months, the second at six months, and the third at eight months post-initiation. Each relapse involved bilateral optic nerve involvement and spinal cord pathology, leading to progressive visual and motor deficits, culminating in high-grade spastic tetraparesis and bilateral visual acuity impairment, with EDSS progression to 8.0. Given the clinical pattern and persistence of relapses despite immunomodulatory therapy, neuromyelitis optica (NMO) was considered upon referral to our institution. Natalizumab was discontinued after nine courses. Following repeated cycles of plasma exchange, the disease course stabilized, and therapy with rituximab (anti-CD20 monoclonal antibody) was initiated. Despite complete B-cell depletion as confirmed by flow cytometry, a severe myelitis relapse occurred three months later. This prompted the initiation of additional immunosuppressive therapy with cyclophosphamide at a dose of"}
{"row_index": 252, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 22-year-old woman had a serious stomach problem called ulcerative colitis, which caused her to have diarrhea with blood, severe belly pain, vomiting, and a swollen belly. Tests found she had a harmful bacteria called C. difficile and her colon was too big and stretched (megacolon), which made things worse. She was given medicine by mouth to fight the bacteria and medicine by IV to calm down the inflammation, and her swollen belly went away. Even after that, her colitis kept getting bad, so she started a special medicine called infliximab, given by IV every few weeks. The doctors checked how much medicine was in her blood and how much inflammation was in her stool, and both showed the treatment was working. After 6 months, her symptoms got better, and she didn’t need surgery to remove her colon.\"\n}"}
{"row_index": 253, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 22-year-old woman was diagnosed with ulcerative colitis three months earlier, experiencing bloody diarrhea, abdominal pain, and weight loss. She stopped taking mesalamine because it caused stomach upset. Before hospitalization, her colonoscopy showed moderate inflammation. She was admitted due to worsening symptoms, including frequent bloody stools, severe abdominal pain, nausea, vomiting, and a 10-kilogram weight loss, with no improvement from previous antibiotics.\\n\\nAt admission, she was dehydrated, had a fast heart rate, low blood pressure, and a fever. Her abdomen was swollen and painful. Lab tests showed high inflammation and anemia. An X-ray showed her colon was dilated to 7 cm, indicating megacolon, a serious complication. Tests also found a toxin from Clostridium difficile, so she started oral vancomycin. However, her symptoms worsened, including more diarrhea, bleeding, and fever. A sigmoidoscopy revealed severe inflammation with bleeding in the lower colon, confirming active, severe ulcerative colitis.\\n\\nShe was treated with intravenous hydrocortisone for severe colitis, which helped reduce the swelling in her colon. After initial treatment, she started infliximab, a biologic medication, at a dose of 5 mg/kg. Her treatment was monitored through blood levels (trough level of 8.8 μg/mL) and a stool test (fecal calprotectin of 921 μg/g, which is above the normal limit of 30 μg/g). After one week, her drug level was too low, so she received a second infusion at week 1, following an accelerated treatment schedule (infusions at weeks 0, 1, 2, and 6). After six months of therapy, her symptoms improved both clinically and on endoscopy, and she did not need surgery (colectomy).\"\n}"}
{"row_index": 254, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 22-year-old female Caucasian patient with a three-month history of ulcerative colitis (UC) presented with progressive bloody diarrhea, abdominal pain, and significant weight loss (10 kg), leading to discontinuation of mesalamine therapy due to gastric intolerance. Colonoscopy performed two weeks prior to hospital admission demonstrated moderate endoscopic activity of UC, as evidenced by a Mayo endoscopic score of 2. Upon hospital admission, the patient exhibited severe clinical deterioration, including frequent liquid and bloody stools, intense abdominal pain, nausea, vomiting, dehydration, tachycardia (110 beats per minute), hypotension (100/60 mmHg), fever (>37.8 °C), and a diffusely painful, distended abdomen with rebound tenderness. Laboratory findings revealed signs of systemic inflammation (C-reactive protein 20.3 mg/dL) and severe anemia (hematocrit 25.8%, hemoglobin 8.1 g/dL). Abdominal X-ray confirmed colonic dilatation of 7 cm, consistent with megacolon, a complication of severe colonic inflammation and impaired motility. Stool testing for *Clostridium difficile* (C. difficile) revealed a positive toxin assay for both A and B toxins, indicating active pseudomembranous colitis. The patient was initiated on oral vancomycin 250 mg four times daily; however, within days, symptoms worsened, with increased diarrhea (>10 episodes/day), rectal bleeding, abdominal distension, and fever. A flexible sigmoidoscopy performed on day 4 of admission, conducted without insufflation and extended to 25 cm, revealed severe mucosal lesions including ulcers covered by fibrin, mucosal friability, edema, and intense enanthem with spontaneous bleeding in the sigmoid and rectum, consistent with severe UC activity (Mayo endoscopic score 3). Histopathological examination confirmed chronic active colitis with structural mucosal damage, crypt microabscesses, and plasmacytosis, supporting a diagnosis of severe inflammatory activity without evidence of *C. difficile* or cytomegalovirus infection. The patient was managed with intravenous hydrocortisone for severe colitis, which led to clinical and radiological improvement, including resolution of megacolon. Due to persistent severe colitis symptoms despite corticosteroid therapy"}
{"row_index": 255, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 34-year-old woman started having trouble walking and balance, and later had shaking in her hands and head, trouble speaking, and numbness. She also had dizziness, headaches, and lost weight. Tests showed damage to the parts of her brain that help with movement and balance. A gene test found two changes in a gene called POLR3A, which is linked to a rare brain disease called hypomyelinating leukodystrophy type 7. This disease affects how nerves grow and work in the brain. She was given medicines to help her nerves, like vitamin B12 and acetylglutamine, but after one month, her symptoms didn’t get better — she still had trouble walking and holding things. After leaving the hospital, she kept taking medicines, including herbs, and now she can walk slowly and climb stairs, her shaking is much better, and she can hold things and cook. But her speech is still slower and harder to understand than before.\"\n}"}
{"row_index": 256, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 34-year-old woman was seen because she had trouble with balance and coordination, a condition called ataxia. Over the past few years, she had developed walking problems, hand and head tremors, difficulty speaking, numbness in her limbs, and trouble swallowing. She also had dizziness, headaches, and nausea. Tests showed abnormal signals in the white matter of her brain, which are signs of damage to the myelin sheath—the protective covering around nerve fibers. This type of damage is known as demyelinating lesions. Genetic testing found two specific changes in the POLR3A gene: c.4044C > G and c.1186-2A > G. These mutations are linked to a rare disorder called hypomyelinating leukodystrophy type 7 (HLD7), which affects nerve development and function. The patient was treated with vitamin B12, acetylglutamine, and other supportive therapies, including traditional Chinese medicine. However, after one month, her symptoms did not improve and actually worsened. She needed help walking and could not hold objects. After discharge, she continued treatment and has shown some improvement—she can now walk slowly and climb stairs, her tremors have reduced, and she can hold objects and cook on her own. But her speech is still slower and less clear than before.\"\n}"}
{"row_index": 257, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 34-year-old Han female presented with progressive cerebellar ataxia, initially manifesting as a mild gait abnormality 7–8 years prior, which evolved into significant walking instability approximately one year before presentation. Postpartum, she developed worsening gait disturbance, static tremors involving the hands and head, dysarthria, occasional limb numbness, and a water-induced cough. Neurological examination revealed dysarthria, upbeating nystagmus with right gaze-evoked nystagmus, absent limb reflexes, impaired bilateral finger-nose test, instability on calcaneal-tibial testing, positive Romberg sign, and bilateral Babinski and Chaddock signs. The ataxia severity was quantified using a standardized ataxia assessment scale, yielding a total score of 24: gait (5), stance (4), sitting (2), speech (2), finger chase (2), nose–finger test (2), fast alternating hand movement (3), and heel–shin slide (4). Mini-Mental State Examination was within normal limits; Montreal Cognitive Scale was not completed due to severe hand and head tremors. Laboratory investigations, including tumor markers, ceruloplasmin, thyroid function (TSH, free T3, free T4, thyroglobulin antibody, thyroid peroxidase antibody), rheumatological markers (rheumatoid factor, anti-streptolysin O, hs-CRP), immunoglobulins (IgG, IgA, IgM), complement components (C3, C4), antinuclear antibody, anticardiolipin antibody, and anti-neutrophil cytoplasmic antibody (ANCA), were all within normal ranges. Lumbar puncture demonstrated no evidence of inflammatory or infectious pathology. Brain MRI revealed bilateral, speckled, and patchy hyperintense lesions in the corona radiata, paraventricular regions, frontal lobes, and left temporal lobe, appearing hypointense on T1-weighted images and hyperintense on T2 and FLAIR sequences, with no abnormal diffusion signals on DWI or ADC maps, consistent with multiple white matter demyelinating lesions. Color Doppler ultrasound of gynecological, abdominal, cardiac, carotid, and intracranial vessels showed no vascular abnormalities. Whole-exome sequencing identified two pathogenic variants in the POLR3A gene:"}
{"row_index": 258, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 23-year-old woman took a very large amount of metformin (about 30 grams) after a stressful event. Four hours later, she came to the hospital feeling tired but still alive. She had very low blood sugar several times (down to 6.3 mg/dL, then 38 mg/dL, and again 42 mg/dL), which made her feel weak and sick. Each time her blood sugar dropped, she also had a buildup of acid in her body (lactic acidosis), which made her blood too acidic. Her blood pressure dropped, so doctors gave her fluids and medicine to raise it. She needed a machine that filters her blood (CRRT) for 24 hours to help her body clear the poison and fix her blood. After 24 hours, her blood sugar and body started to get better. She was able to go home on day 5, but she didn’t follow up with her doctors for mental health, kidney, or general care.\"\n}"}
{"row_index": 259, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 23-year-old Arabic woman took 30 grams of metformin intentionally after a stressful event. Four hours later, she was brought to the emergency department. She was alert but feeling very tired. Her vital signs were normal at first, though she had low blood sugar and high lactate levels, which showed her body was under stress. She developed severe lactic acidosis and low blood pressure, which required fluid and medication (like norepinephrine) to stabilize. She had three episodes of very low blood sugar — 6.3 mg/dL, 38 mg/dL, and 42 mg/dL — each time requiring a 50% dextrose injection to raise her sugar levels. These low sugar episodes happened at the same time as her severe acidosis. She was treated with continuous renal replacement therapy (CRRT) for 24 hours, which helped her recover. After this, her blood pressure and blood sugar stabilized, and she improved. By day 3, she was able to eat normally and was transferred to a regular ward. A psychiatrist was involved to assess her mental health, and she was discharged on day 5. However, she did not attend any follow-up appointments for medicine, kidney, or mental health care.\"\n}"}
{"row_index": 260, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 23-year-old Arabic female with a body mass index of 28 was prescribed metformin for weight management in the context of polycystic ovary syndrome (PCOS). She intentionally ingested approximately 60 tablets of 500 mg metformin (totaling 30 g) following a stressful social event, which was initially recognized as a suicide attempt. Four years prior, she had undergone a living kidney donation to her brother, who had end-stage renal disease of unknown etiology; she has no known comorbidities, including psychiatric disorders, prior suicidal ideation, or substance use (no history of smoking or alcohol intake). She has no family history of diabetes mellitus or mental illness. On presentation to the emergency department (ED) approximately 4 hours after ingestion, she was alert, well-nourished, and generally fatigued, with no signs of pallor, jaundice, or cyanosis. Vital signs included blood pressure of 119/65 mmHg, heart rate of 122 beats/min, respiratory rate of 20 breaths/min, oxygen saturation of 100% on room air, and oral temperature of 36.9 °C. Physical examination revealed dry, cool skin and bilaterally mid-sized, equal, and reactive pupils; no other abnormalities were noted.\\n\\nInitial point-of-care capillary blood glucose was low, prompting the administration of 50 mL of 50% dextrose (D50) solution. Serum glucose measured 6.3 mg/dL, which transiently rose to 106 mg/dL following D50 infusion. Maintenance infusion with 5% dextrose-water was initiated. Laboratory findings showed a markedly low blood glucose, leukocytosis, hypocalcemia, hyperphosphatemia, and mild elevation in serum creatinine. Initial arterial blood gas analysis revealed a pH of 7.18, PaO2 of 76.9 mmHg, PaCO2 of 40.3 mmHg, and bicarbonate of 14.3 mmol/L, consistent with metabolic acidosis. Baseline lactate was markedly elevated at 8.4 mmol/L, prompting a 1 L bolus of Ringer lactate. Serial blood gas and lactate measurements demonstrated progressive worsening of lactic acidosis, with lact"}
{"row_index": 261, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 59-year-old woman felt confused, was upset, and had trouble moving her right leg. She had been taking medicine for a type of cancer called chronic lymphocytic leukemia (CLL) and a blood problem called hemolytic anemia for months. Her doctor found that her right leg was very weak, her reflexes were uneven, and there was a sign called Babinski on her right side. She was a little overweight and had a low fever. A brain scan showed a spot in the left front part of her brain that looked like a stroke. Later, she got a fever and signs of infection in her brain. A more detailed brain scan showed a large area of damage in the left front brain and small spots that were active. A spinal fluid test found many white blood cells and red blood cells, which means infection. The test found bacteria called Listeria in her blood and spinal fluid. This kind of infection is rare and wasn’t from eating risky food. She started antibiotics and after two days, her fever went away and her brain symptoms got better. After one week, the spinal fluid test showed no more signs of infection. One month later, she was back to normal and could move her legs without trouble.\"\n}"}
{"row_index": 262, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 59-year-old woman was admitted to the hospital because she was confused, agitated, and had weakness in her right leg. She had been treated for chronic lymphocytic leukemia (CLL) with fludarabine for 3 months and for hemolytic anemia with corticosteroids for 2 months. Before admission, she had mild obesity and a slight fever. A neurological exam showed severe weakness in her right leg, abnormal reflexes, and a sign called a Babinski sign on the right side. There were no signs of inflammation in her brain membranes. A brain CT scan showed a small area of damage in the left frontal lobe, which looked like an ischemic stroke. Later, a brain MRI showed a larger area of abnormality in the same region, spreading toward the basal ganglia, and also showed small areas of increased activity after contrast was given. On the second day, she developed a higher fever and signs of meningeal irritation. A spinal fluid test found many white blood cells, red blood cells, and high protein levels, which suggested infection. Cultures from blood and spinal fluid tested positive for Listeria monocytogenes, a type of bacteria that can cause serious brain and spinal infections. She had no recent history of eating high-risk foods like unpasteurized cheeses or deli meats. The diagnosis was Listeria meningoencephalitis. She was started on ampicillin, and within 48 hours, her fever went down and her neurological symptoms improved. After one week of treatment, the spinal fluid showed normal results. One month later, her leg strength and mental status had fully returned to normal.\"\n}"}
{"row_index": 263, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 59-year-old hypertensive white female with a history of chronic lymphocytic leukemia (CLL) diagnosed in 2009 presented with a 24-hour history of confusion, agitation, and mild right-lower extremity weakness. She had received fludarabine-based chemotherapy three months prior for CLL and methylprednisolone therapy two months prior for hemolytic anemia secondary to fludarabine-induced immune-mediated destruction of red blood cells. Physical examination revealed grade 1 obesity and subfebrility (99.32 ºF; 37.4 ºC). Neurological examination demonstrated grade 4 right-lower extremity weakness, reflex asymmetry, and a right-sided Babinski sign, with no signs of meningeal irritation at admission. Laboratory findings included a white blood cell (WBC) count of 3.5 × 10³/μL, hemoglobin of 7.1 g/dL, hematocrit of 21.5%, platelets of 109 × 10³/μL, aspartate aminotransferase (AST) of 59 U/L, and alanine transaminase (ALT) of 79 U/L; all other metabolic parameters (serum glucose, urea nitrogen, creatinine, bilirubin, sodium, potassium) were within normal limits. Cerebral computed tomography (CT) revealed a hypodense lesion in the left frontal lobe, consistent with acute ischemic stroke pathology, likely due to small vessel disease or thrombotic occlusion secondary to hypercoagulable states associated with immunosuppression. On day two of hospitalization, the patient developed fever (101.12 ºF; 38.4 ºC) and new signs of meningeal irritation, including a positive Kernig’s sign. Cerebral magnetic resonance imaging (MRI) showed a hyperintense lesion in the left frontal lobe extending into the basal ganglia on T2 and fluid-attenuated inversion recovery (FLAIR) sequences, with small nodular areas of gadolinium enhancement following intravenous administration, suggesting active inflammatory or infectious intracerebral involvement. Lumbar puncture was performed on day two, yielding cerebrospinal fluid (CSF) analysis revealing 24 red blood cells (RBC"}
{"row_index": 264, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 81-year-old woman felt very tired and weak for 3 days, then got dizzy and had trouble breathing. By November 16, 2021, she fell into a coma. Her oxygen levels dropped to just 70-80%, so she was taken to the ICU. She had long-term lung problems like chronic bronchitis and emphysema, and her lungs were full of infections. Her heart was also not working well, and doctors thought she might have had a heart attack. They did a procedure to check her heart, but found no blockages. She started having belly swelling and constipation, and got a glycerin enema. On day 4, she lost consciousness again, her blood pressure dropped, her belly became swollen and tight, and her bowels stopped working. A scan showed gas in her liver area and dead parts of her intestines. She died on day 5 because her body couldn’t fix the shock from the damage.\"\n}"}
{"row_index": 265, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 81-year-old woman came to the hospital with fatigue, lethargy, fever, chills, cough, and shortness of breath over three days. By November 16, 2021, she fell into a coma. Her oxygen levels dropped to 70%-80%, so she was admitted to the intensive care unit (ICU) for treatment. She had a long history of chronic lung disease, including chronic bronchitis and emphysema, and had been on long-term oxygen therapy. She also had heart problems for five years and was taking medication for heart failure.\\n\\nIn the ICU, her blood pressure dropped, and she needed medicine (norepinephrine) to keep it stable. Tests showed signs of infection in her lungs, with high white blood cell counts and markers of inflammation. Chest CT scans showed chronic lung disease and multiple lung infections, especially in the lower and middle parts of the right lung. Her abdominal CT scan showed no major issues, but her abdominal blood vessels were heavily calcified.\\n\\nHer heart tests showed abnormal heart rhythms and signs of heart damage. Her troponin levels went up, which suggests heart muscle injury. The doctors suspected she had a heart attack (ACS) and performed a procedure called PCI through her femoral artery. No major blockages were found in her coronary arteries.\\n\\nOn the second day, she had constipation, which was treated with a glycerin enema. On day 4, she suddenly lost consciousness, had very low blood pressure, and developed swelling in her abdomen with no bowel sounds. An urgent abdominal CT scan showed gas in the liver portal area and severe damage to her bowel walls. The patient died on day 5 from severe, uncontrolled shock due to these complications.\"\n}"}
{"row_index": 266, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 81-year-old female presented to a local hospital with a three-day history of fatigue, lethargy, fever, chills, productive cough, and wheezing, without prior intervention. On November 16, 2021, she developed acute coma and was transported to the emergency department. Her oxygen saturation declined to 70%–80%, prompting immediate admission to the intensive care unit (ICU) for respiratory and hemodynamic support. Upon ICU admission, she exhibited a progressive hypotensive state, requiring norepinephrine infusion to maintain a mean arterial pressure above 65 mmHg.\\n\\nThe patient had a long-standing history of chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema, with over 50 years of documented disease course, and had been on long-term home oxygen therapy. She also had a five-year history of chronic heart failure, managed with oral bisoprolol, with no prior history of abdominal pain or chronic renal insufficiency. There was no history of tobacco or alcohol use, and no relevant family history of cardiovascular or pulmonary disease.\\n\\nOn initial assessment, vital signs were: temperature 36°C, heart rate 85 beats/min, respiratory rate 18 breaths/min, blood pressure 105/45 mmHg. Physical examination revealed diminished breath sounds bilaterally, with wet rales predominantly at the bases of both lungs. Cardiac and abdominal examinations were unremarkable.\\n\\nLaboratory findings included an initial troponin level of 0.05 ng/mL, which subsequently increased, indicating myocardial injury. B-type natriuretic peptide (BNP) was elevated at 4164 pg/mL, consistent with volume overload and systolic dysfunction. Arterial blood gas analysis demonstrated a partial pressure of carbon dioxide (PaCO₂) of 58.7 mmHg, oxygen partial pressure (PaO₂) of 86.5 mmHg, and an oxygenation index of 172.97 mmHg—indicating severe hypoxemia. Inflammatory markers were markedly elevated: white blood cell count 8.12 × 10⁹/L, neutrophil percentage 93.2%, C-reactive protein 298.38 mg/L, procalcitonin 6"}
{"row_index": 267, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man had a serious brain problem caused by a medicine called ganciclovir, which he was taking for a stomach infection. The medicine made him confused, unsteady on his feet, and eventually fell. Doctors thought it was the medicine, not an infection, because tests showed no signs of virus in his brain fluid. The medicine was stopped, and he got dialysis to clean his blood, which helped his brain feel better. He fully recovered after two dialysis sessions. This was the worst case ever reported for this medicine, with the highest amount ever found in his blood.\"\n}"}
{"row_index": 268, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This case involves a 55-year-old man who had diabetes and kidney failure, leading to a kidney transplant 1.5 years earlier. After the transplant, he developed a severe infection caused by cytomegalovirus (CMV), which required treatment with ganciclovir. Because his infection was serious, he received high doses of the drug without reducing them to standard maintenance levels. Two days after starting the treatment, he began to have balance problems and mild confusion. His condition worsened, leading to delirium and a fall. His brain function declined further, and he could no longer take oral medication. Doctors ruled out other causes of brain inflammation, such as encephalitis, and instead suspected ganciclovir-induced encephalopathy. The drug was stopped, and he received two sessions of therapeutic dialysis, which helped clear the drug from his blood. After the second dialysis, his brain function fully recovered. This patient had the highest known level of ganciclovir in his blood and was the only one in the study with severe symptoms and complete recovery after dialysis.\"\n}"}
{"row_index": 269, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 55-year-old male with a history of diabetic renal failure initiated hemodialysis two years prior, followed by renal transplantation 1.5 years earlier, with subsequent initiation of immunosuppressive therapy. Eight months post-transplantation, his serum creatinine rose to 4.4 mg/dL, indicating progressive renal dysfunction. He presented with CMV enteritis, evidenced by occult gastrointestinal bleeding and a significantly elevated CMV pp65 (C7-HRP) antigen level in peripheral blood mononuclear cells, prompting antiviral intervention. Intravenous ganciclovir was administered at a dose of 150 mg/day for 11 days, followed by transition to valganciclovir at 450 mg/day. Due to the severity of enteritis, the antiviral regimen was not reduced to standard maintenance doses (typically half of initial doses), which is atypical and increases systemic exposure. Two days after initiating valganciclovir, the patient developed gait instability, initially ambulating independently, but within 24 hours required assistance. His level of consciousness deteriorated to E3, V5, M6 on the Glasgow Coma Scale (GCS), indicating mild impairment. The next day, he exhibited intermittent delirium. Two days later, he fell and was found on the floor without significant injury; clinical suspicion initially pointed to exhaustion secondary to severe enteritis. Nine days after starting valganciclovir, his neurological status worsened to E3, V3, M5, and he became unable to ingest oral medications, including valganciclovir. Neurological consultation was obtained; encephalitis was ruled out due to the absence of meningeal signs, fever, and a normal cerebrospinal fluid (CSF) cell count (0.33 cells/μL), with only a marginal elevation in protein concentration (54 mg/dL). Polymerase chain reaction (PCR) testing for CMV, herpes simplex virus (HSV), varicella-zoster virus (VZV), and Epstein-Barr virus (EBV) DNA in the CSF remained negative, supporting exclusion of these viral etiologies. Ganciclovir-induced encephalopathy was therefore clinically and virologically suspected, and the drug was immediately discontinued. To mitigate the risk of further falls and to remove ganciclovir from the systemic circulation,"}
{"row_index": 270, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 59-year-old man had yellow skin and belly pain for over 15 days, and lost 5 pounds. Doctors found a tumor at the opening of the small intestine (duodenal papilla) using a special camera test. The tumor was checked under a microscope and found to be a fast-growing type of cancer called aggressive B-cell lymphoma. Instead of surgery, he started treatment with special medicines that target the cancer cells, along with a standard chemotherapy plan called CHOP.\"\n}"}
{"row_index": 271, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 59-year-old man was seen for jaundice and weight loss. Tests showed a blockage in his bile ducts, and imaging found a tumor at the duodenal papilla. A biopsy was taken and examined under a microscope, which showed a type of lymphoma called aggressive B-cell non-Hodgkin's lymphoma. This type of cancer grows quickly and spreads fast. Based on the results, the doctors decided not to do surgery. Instead, he started treatment with chemotherapy (the CHOP regimen) combined with targeted therapy to fight the cancer more effectively.\"\n}"}
{"row_index": 272, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 59-year-old male was admitted to the Department of Gastroenterology on June 16, 2020, presenting with a 15-day history of pruritic jaundice affecting the skin and sclera, accompanied by progressive weight loss of approximately 5 kg. He had a prior history of brain stem infarction with residual left lower limb weakness and occasional dysphagia, particularly when drinking water. No history of hepatitis, tuberculosis, or other infectious diseases was reported. Physical examination revealed a chronic illness appearance with marked jaundice, absence of palpable superficial lymphadenopathy, and no significant abdominal signs. Laboratory findings at admission included hemoglobin 101 g/L, alanine aminotransferase (ALT) 158 U/L, aspartate aminotransferase (AST) 150 U/L, total bilirubin 217.3 μmol/L, direct bilirubin 152.4 μmol/L, indirect bilirubin 64.9 μmol/L, high-sensitivity C-reactive protein (hs-CRP) 5.8 mg/L, procalcitonin 0.11 ng/mL, carcinoembryonic antigen (CEA) 6.19 μg/L, and carbohydrate antigen 125 (CA125) 117.1 kU/L. Abdominal ultrasonography on June 17 demonstrated gallbladder enlargement, cholecystitis, cholestasis, and significant dilatation of both intrahepatic and extrahepatic bile ducts. Magnetic resonance cholangiopancreatography (MRCP) and abdominal MRI on June 18 confirmed neoplastic involvement of the duodenal papilla, severe bile duct dilatation, bile stasis in the common bile duct, and a markedly enlarged gallbladder. Endoscopic ultrasound (EUS) on June 19 revealed a 2.5 × 2.5 cm neoplasm at the duodenal papilla with surface ulceration, exudative yellow-white slough, and contact bleeding; three biopsy specimens were obtained. The patient was transferred to the surgical oncology department on June 20. Abdominal enhanced computed tomography (CT) on June 23 showed findings consistent with MRI, supporting the"}
{"row_index": 273, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old man woke up with sudden neck pain, numbness in his arms and legs, and weakness. It had started 4 days before he came to the hospital. He had no injury or past history of similar problems. When doctors checked him, his neck muscles were tender, his arms and legs felt numb, and his muscles were strong. Blood tests showed no signs of infection, clotting issues, or cancer. X-rays and CT scans didn’t show broken bones. MRI showed a big lump pressing on his spine in the neck and upper back area, and a small, harmless growth inside his C7 vertebra. This growth is called a vertebral hemangioma. Doctors removed the lump and the growth. After 6 months, his pain and weakness went away and he hasn’t had a return of symptoms. This condition, called IPEH, is rare and can be confused with other spine problems, but it’s treatable with surgery and recovery is good.\"\n}"}
{"row_index": 274, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 27-year-old man came in with sudden neck pain, numbness in his arms and legs, and weakness in his limbs. The symptoms started four days before he visited the hospital, and he had no history of injury or other medical conditions. Earlier, six years ago, he had a similar but brief episode of numbness and weakness. On exam, his neck muscles were tender, and his sensation and muscle strength were reduced, especially in the areas served by the T1 nerve. Blood tests showed no signs of infection, clotting issues, or cancer. X-rays and CT scans didn't show bone damage. MRI scans revealed a large mass pressing on the spinal cord in the C6-T1 region, extending into the C7-T1 area. This mass was bright on T2 images and dark on T1, which is typical for certain types of tumors. Additionally, a small, round mass was found in the C7 vertebra, consistent with a benign vertebral hemangioma (VH). The surgery involved removing the spinal mass through a laminectomy and excising the abnormal tissue. Pathology tests confirmed the presence of abnormal blood vessel growth with blood clots, leading to a diagnosis of intraparenchymal hemangioma of the spine (IPEH). At his six-month follow-up, his symptoms had improved completely, and there was no sign of recurrence. This case highlights the clinical features, imaging signs, possible causes, how it's different from other conditions, and how it's treated.\"\n}"}
{"row_index": 275, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 27-year-old male presented to the Department of Spine Surgery with acute-onset neck pain, unilateral limb numbness, and proximal and distal muscle weakness. Symptoms began four days prior to presentation and were of sudden onset, with no history of trauma. A prior episode of transient sensory disturbance and mild weakness in the extremities occurred six years earlier, suggesting possible recurrent or chronic spinal cord involvement. Physical examination revealed localized tenderness over the paraspinal muscles at the C6-T1 spinous process, diminished sensory perception to light touch in the T1 dermatomal distribution, and preserved motor function with grade IV muscle strength in all four limbs. Laboratory evaluations, including coagulation studies, inflammatory markers (e.g., CRP, ESR), and tumor markers (e.g., CA-125, CEA), were all within normal reference ranges, excluding systemic inflammatory or neoplastic etiologies. Spinal radiography and conventional computed tomography (CT) demonstrated no evidence of bony erosion, lytic lesions, or pathological fractures. Enhanced cervical magnetic resonance imaging (MRI) revealed a homogenously enhancing epidural mass within the C6-T1 spinal canal, compressing the spinal cord and extending into the left C7-T1 foramen. On T1-weighted imaging (T1WIs), the mass appeared hypointense, consistent with high vascular content or fat suppression, while on T2-weighted imaging (T2WIs), it was hyperintense, indicating high water content and susceptibility to edema or hemorrhage. Additionally, a 0.5 cm × 0.5 cm × 0.6 cm heterogeneously enhancing hyperintense lesion was identified within the C7 vertebral body on T2WI, consistent with a benign vertebral hemangioma (VH), a vascular malformation characterized by abnormal proliferation of vascular endothelial cells within the bone marrow. Histopathological examination of the excised epidural mass revealed papillary proliferation of vascular endothelial cells with associated thrombus formation, confirming the diagnosis of intraparenchymal epidural hemangioma (IPEH). The patient underwent C6-T1 laminectomy with radical excision of the epidural mass. Postoperative follow-up at six months demonstrated complete resolution of neurological symptoms without recurrence. This case illustrates the clinical spectrum of IPEH, including its characteristic imaging features (T1 hypointensity, T2 hyperintensity"}
{"row_index": 276, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"Two men who were healthy before got a serious problem after getting the second dose of the Pfizer COVID-19 vaccine, about three weeks later. They both felt sudden, severe tiredness and shortness of breath, even when not moving. Tests showed no active coronavirus in their bodies. Doctors found high pressure in their lungs using heart ultrasound and, in one case, a special test on the heart’s right side. This high lung pressure hurt their hearts and likely caused long-term damage. There was no sign of blood clots in their lungs. Both men now have trouble doing daily activities and likely have lasting heart problems. Their symptoms didn’t go away completely, and the lung pressure stayed high even after months.\"\n}"}
{"row_index": 277, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"Pulmonary hypertension in two previously healthy adult men occurred within three weeks of receiving the second dose of the Pfizer (BNT162b2) mRNA COVID-19 vaccine from different batches. Both men suddenly developed severe fatigue and shortness of breath during physical activity, even at rest, and their SARS-CoV-2 PCR tests came back negative. Doctors diagnosed the condition using heart ultrasounds and, in one case, a more detailed heart catheterization. The diagnosis showed high pressure in the lungs' blood vessels, which is a sign of pulmonary hypertension. Neither patient had blood clots in their lungs. Both cases resulted in lasting symptoms and likely permanent heart damage. The condition led to long-term functional limitations, and in one case, the patient also developed irregular heartbeats. No evidence of pulmonary embolism was found in either case.\"\n}"}
{"row_index": 278, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"Two cases of vaccine-induced pulmonary hypertension are reported in previously healthy adult males following the second dose of the Pfizer BNT162b2 mRNA COVID-19 vaccine, with onset occurring within three weeks of vaccination across different lots. Case #1 involves a 49-year-old male physician-athlete with a BMI of 23, non-smoker, and a history of mild exercise-induced asthma managed with albuterol. He received Dose 1 in December 2020 and Dose 2 in January 2021. Three weeks post-Dose 2, he developed acute severe fatigue, flu-like symptoms, tachycardia, palpitations, orthostasis, right-sided chest pressure, and exertional dyspnea. SARS-CoV-2 PCR testing was negative at symptom onset. Initial transthoracic echocardiography showed normal left ventricular function (ejection fraction 65%), normal right ventricular size and function, and a maximal tricuspid regurgitation velocity (TRVmax) of 3.09 m/s, yielding an estimated right ventricular systolic pressure (RVSP) of 42 mmHg, interpreted as mild to moderate pulmonary hypertension. Laboratory findings included a brain natriuretic peptide (BNP) level of 22 pg/mL (within normal range, <900 pg/mL), elevated low-density lipoprotein (LDL) cholesterol, and hematocrit of 50%. Pulmonary CT angiography with 3D reconstruction of the pulmonary artery (PA) tree demonstrated no evidence of pulmonary emboli. Subsequently, the patient developed 15 lbs of fluid retention, generalized edema, neck pressure, headaches, and a sensation of 'being hung upside down,' consistent with jugular venous distention (JVD) and cerebral venous congestion. Resting oxygen saturation (SpO2) was 92%, and new-onset systolic and diastolic arterial hypertension developed. Symptoms were present at rest and worsened with exertion, with functional capacity limited to New York Heart Association (NYHA) Class 3–4. Serial echocardiographic follow-up over one year showed no progression in RVSP or right ventricular function. Symptoms and exercise tolerance improved to NYHA Class 1–2, with resolution of fluid retention, swelling, tachycardia, and hypertension, and SpO"}
{"row_index": 279, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 21-year-old woman who is overweight had been feeling tired, dizzy, and sweating for a long time. She had episodes of passing out, especially when her blood sugar was too low. Doctors thought it might be a problem with her body making too much insulin, called an insulinoma. Her blood sugar was very low — down to 20 mg/dl — even after giving her sugar. She had been treated as a baby for a similar problem, and doctors found a gene mutation that causes her body to keep making insulin even when sugar is low. She was given medicine called diazoxide, which helped, but she stopped taking it because it caused unwanted side effects like extra hair and swelling. This time, doctors started her on two new medicines: octreotide and diazoxide again. These helped her blood sugar go up and her symptoms like dizziness and passing out went away. She now feels better, and doctors stress that she must keep taking her medicine and check in with a specialist regularly to stay healthy.\"\n}"}
{"row_index": 280, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 21-year-old woman with a history of obesity and low blood sugar since infancy presented to the emergency department with repeated episodes of dizziness, fainting, sweating, and lethargy. Her blood glucose was very low—20 mg/dl when first seen—and remained low even after receiving dextrose (a sugar solution) multiple times. She had previously been diagnosed as a baby with a condition called persistent hyperinsulinemic hypoglycemia of infancy, caused by a mutation in the glucokinase (GCK) gene, specifically a Val452Leu activating mutation. This mutation causes her body to produce too much insulin, leading to low blood sugar. She was once treated with diazoxide and octreotide, which helped control her symptoms, but stopped taking diazoxide due to side effects like increased hair growth and fluid retention. On this visit, she was given octreotide and diazoxide again, and her blood sugar improved, with levels rising to between 55 and 110 mg/dl by discharge. Doctors stressed the importance of continuing her treatment and seeing an endocrinologist regularly to manage her condition.\"\n}"}
{"row_index": 281, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 21-year-old Caucasian female presented to an external emergency department with altered mental status following discovery of lethargy by family members. On arrival, her plasma glucose was 20 mg/dL, consistent with severe hypoglycemia. She was hospitalized and initiated on dextrose infusion (10% dextrose in water), yet remained hypoglycemic with capillary glucose levels persistently between 50 and 60 mg/dL. She was transferred to our facility on suspicion of insulinoma, as she was unable to recall her prior diagnosis of hypoglycemia. Historical records from our neonatal unit revealed a history of persistent hypoglycemia beginning in infancy, including episodes of seizures, syncope, dizziness, headaches, palpitations, and sweating, which were initially intermittent and variable in severity. These symptoms were reported to have onset at birth, with no formal investigation until age 12, when she experienced recurrent episodes. She remained seizure-free and asymptomatic until age 17, when a new syncopal episode prompted an inpatient evaluation for hypoglycemia. During this evaluation, fasting blood glucose was 47 mg/dL after a 2-hour fast, proinsulin levels ranged from 10.4 to 84.1 pmol/L (normal range: 0–10 pmol/L), and C-peptide was 3.1 ng/mL (normal range: 1.1–4.4 ng/mL). Insulin antibody and sulfonylurea screening were negative, ruling out autoimmune or drug-induced causes. Abdominal magnetic resonance imaging (MRI) did not identify any insulinoma, leading to a genetic investigation that revealed a heterozygous Val452Leu activating mutation in the glucokinase (GCK) gene. This mutation results in constitutive activation of glucokinase, a key enzyme in glucose sensing within pancreatic beta cells, leading to excessive insulin secretion even in the absence of elevated blood glucose. The patient was initially managed with diazoxide, a potassium channel opener that reduces insulin release by promoting beta-cell membrane hyperpolarization, resulting in clinical improvement. She was discharged on oral diazoxide 250 mg daily, but discontinued therapy due to adverse effects including hirsutism and fluid retention. On current admission, she received dextrose boluses and was placed on continuous 5% dext"}
{"row_index": 282, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 67-year-old man had psoriasis on his feet that was well controlled. He started treatment for cancer in his stomach, called gastric adenocarcinoma, and took medicine for it for months. Two months before, he began a drug called pembrolizumab to fight the cancer. He started having joint pain in his fingers, toes, knees, and shoulder, with swelling and redness. His skin had psoriasis plaques, and his nails were damaged. Blood tests showed inflammation, but no signs of rheumatoid arthritis. The doctor found inflamed joints, especially in the knees and shoulder, and thought it was psoriatic arthritis. He first tried steroids, but the pain got worse. Then he added two medicines—leflunomide and methotrexate—which helped a little, but the symptoms came back when the steroids were reduced. So, the doctor added a stronger medicine called etanercept, which controls the inflammation and finally stopped the joint pain and swelling.\"\n}"}
{"row_index": 283, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 67-year-old man with a long-standing history of foot psoriasis that was well controlled had recently developed joint pain in multiple areas, including his fingers, toes, left shoulder, and knees. He had been treated for advanced stomach cancer that had spread to lymph nodes, and had previously received pembrolizumab for cancer treatment. Two months before his joint symptoms started, he began pembrolizumab, which is used to help the immune system fight cancer. His psoriasis was already known, and he had signs of psoriatic nail changes and swelling in his finger and toe joints (dactylitis). On exam, his joints were red and swollen, and blood tests showed high levels of inflammation markers like C-reactive protein and erythrocyte sedimentation rate. Tests for rheumatoid arthritis (like rheumatoid factor and anti-CCP) were negative, which helped rule out other types of arthritis. Joint fluid from his knee showed signs of inflammation, and imaging showed fluid buildup and swelling in the knees and shoulder. Initially, he was given methylprednisolone, a steroid, to reduce inflammation, but his symptoms got worse after one week. He then started leflunomide and methotrexate, which helped a little but symptoms came and went with steroid use. Because the condition was not responding well, his treatment was changed to include etanercept, a drug that blocks a specific protein involved in inflammation (a tumor necrosis factor inhibitor). This change led to better control of his psoriatic arthritis.\"\n}"}
{"row_index": 284, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 67-year-old male with a history of well-controlled plaque psoriasis of the feet presented with a two-week history of progressive polyarthralgia and nail dystrophy. He was diagnosed with advanced gastric adenocarcinoma with distant lymph node metastases in March 2020. Endoscopic evaluation revealed a 3-cm ulcerofungating mass in the pre-pyloric antrum, histopathologically confirmed as moderately differentiated adenocarcinoma. Immunohistochemical analysis demonstrated negative staining for human epidermal growth factor receptor 2 (HER2, IHC 1+), Epstein-Barr virus, and deficient DNA mismatch repair (dMMR), characterized by retained nuclear expression of MSH2 and MSH6 and loss of MLH1 and PMS2. Abdominal computed tomography identified multiple enlarged lymph nodes in the para-aortic and aortocaval regions, consistent with nodal involvement. The patient received first-line palliative chemotherapy with capecitabine and oxaliplatin for 11 months, followed by second-line therapy with ramucirumab and paclitaxel. Despite this, progression of disease was observed after two months of ramucirumab and paclitaxel, leading to initiation of pembrolizumab (200 mg every three weeks) in June 2021 as third-line treatment, based on the tumor's dMMR status, which is associated with microsatellite instability and potential responsiveness to immune checkpoint inhibition. Prior to pembrolizumab therapy, his neutrophil-to-lymphocyte ratio (NLR) was 1.1 and prognostic nutritional index (PNI) was 50.5, indicating a relatively preserved immune and nutritional status. Two months after pembrolizumab initiation, laboratory findings showed a normal white blood cell count (7970/µL), with 72.6% neutrophils and 17.9% lymphocytes, an elevated erythrocyte sedimentation rate (ESR) of 89.0 mm/h, and a serum high-sensitivity C-reactive protein (hs-CRP) level of 2.3 mg/L, reflecting systemic inflammation. Serologic testing for autoimmune markers was negative for rheumatoid factor (RF) and anticyclic citrullinated peptide antibody (ACPA), excluding"}
{"row_index": 285, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 75-year-old man had a fever and pain on his right side of the chest. Doctors found a big lump under his diaphragm (the muscle that covers the belly) that was about 10 cm in size. It was attached to the liver and couldn’t be easily separated during surgery. Because of this, they had to remove part of the liver and the diaphragm. The surgery took 8 hours and he lost a lot of blood, but he recovered well and was out of hospital in 14 days. After 1 year, there’s been no sign of the lump coming back. The doctors looked at the tissue and found it was a slow-growing tumor that looked like smooth muscle, even though it wasn’t clearly a known type. They named it a 'spindle cell tumor with smooth muscle features' because it had markers that match muscle cells. The tumor wasn’t spreading, and it didn’t grow fast, so it was not very dangerous.\"\n}"}
{"row_index": 286, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 75-year-old man came in with fever and pain on the right side of his chest. Imaging tests showed a large 10-cm tumor under his diaphragm, which was attached to the liver and hard to separate during surgery. Doctors initially suspected it might be a rare, possibly cancerous tumor from the diaphragm, such as a myxoid sarcoma or schwannoma, but couldn't rule out a benign cause. Blood tests showed mild signs of inflammation and abnormal levels, and a PET scan showed the tumor was active, but not extremely so. Because the tumor was stuck to the liver and near important blood vessels, the surgery had to be more extensive — including removal of part of the liver (right posterior segment) and the diaphragm. The operation took 8 hours and 10 minutes, with about 1,459 mL of blood lost. After surgery, the patient recovered well and was discharged after 14 days. The tumor was found to be just below the liver, touching the diaphragm but not fully connected. Under the microscope, it looked like a low-grade tumor, possibly a solitary fibrous tumor or perivascular epithelioid cell tumor, but tests for those didn’t come back positive. Instead, the final diagnosis was a spindle cell tumor with smooth muscle features, based on positive results for muscle markers like αSMA, desmin, and h-caldesmon. One year after surgery, there has been no sign of the tumor coming back.\"\n}"}
{"row_index": 287, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 75-year-old male presented with fever and right-sided chest pain. Laboratory investigations revealed elevated inflammatory and metabolic markers: lactate dehydrogenase (LDH) 251 IU/L, alkaline phosphatase (ALP) 469 IU/L, gamma-glutamyl transferase (γ-GTP) 125 IU/L, creatinine 1.43 mg/dL, C-reactive protein (CRP) 3.04 mg/dL, squamous cell carcinoma antigen (SCC) 1.8 ng/mL, nerve-specific enolase (NSE) 21.6 ng/mL, and soluble interleukin-2 receptor (SIL-2R) 614 U/mL, suggesting a systemic inflammatory process or malignancy. Contrast-enhanced computed tomography (CT) identified a large, well-circumscribed, 10-cm mass located beneath the right diaphragm, with a smooth margin and heterogeneous, gradually increasing enhancement in both the tumor and adjacent liver parenchyma, particularly in regions adjacent to fatty tissue. The primary arterial supply was identified as the right inferior phrenic artery, supporting a sarcomatoid origin from the diaphragmatic mesenchyme rather than a benign lesion such as schwannoma. No evidence of pulmonary invasion was observed. Magnetic resonance imaging (MRI) demonstrated heterogeneous high signal intensity on T2-weighted imaging (T2WI) and diffusion-weighted imaging (DWI), with progressive, heterogeneous contrast enhancement consistent with CT findings, further indicating active tumor metabolism. FDG-positron emission tomography (FDG-PET) showed abnormal glucose uptake with a maximal standardized uptake value (SUVmax) of 4.6, which, while not extremely high, was sufficient to raise concern for a malignant process, particularly myxoid liposarcoma or other sarcomatoid tumors. Despite imaging suggesting a primary diaphragmatic origin, the possibility of hepatic adhesion was noted due to the tumor's proximity to the hepatic capsule and intraparenchymal space. Given the tumor's adherence to the liver and its close anatomical relationship with the posterior Glisson’s pedicles and segment 8 dorsal Glisson’s pedicle, a diaphragmatic resection was not feasible without risking vascular compromise or hepatic injury. Consequently, an extended right posterior segmentectomy with concomitant diaphragmatic"}
{"row_index": 288, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old man got trapped under a heavy steel frame while fixing a crane. He was bleeding badly from his lower belly, and doctors found serious injuries to his pelvis and bones. Even after trying to stop the bleeding and saving his life, his legs were too damaged to stay attached. Doctors had to cut off both legs — one above the knee on day 8, and the other at the hip on day 13. His body had so much damage that parts of his muscles died and had to be removed. To fix the open wound, doctors used skin from his thigh to cover the exposed bones in his pelvis. This skin stayed in place and helped heal. After months of healing and cleaning the wounds, his skin fully grew back. Now he can sit in a wheelchair, move on his own, and live at home with his parents. The rebuilt pelvis works well with his prosthetic legs.\"\n}"}
{"row_index": 289, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 20-year-old Japanese man was trapped under a 3-ton steel frame while working on a crane. He was rescued and arrived at the hospital with heavy bleeding from his lower right abdomen. His vital signs showed he was in shock, and his injuries were severe: his pelvis was broken, the bones in his lower back and hips were fractured, and there was damage to his spleen. Imaging showed bleeding from both internal iliac arteries, which was treated with a procedure to stop the bleeding. Despite efforts, blood loss continued, and the patient developed tissue damage in both legs. Because of the risk of massive bleeding and the extent of tissue death, doctors decided that amputating both legs was necessary to save his life. He had a right above-knee amputation on day 8 and a left hip disarticulation on day 13. Over the next several weeks, his wounds were cleaned multiple times due to infection, and parts of his muscles were removed. On day 112, a flap of skin from his thigh was used to cover the exposed pelvis, and over time, the wound healed. A skin graft was later applied to finish healing. He now uses a wheelchair and can move independently. The reconstructed pelvis allows him to wear prosthetics properly and live at home with his family.\"\n}"}
{"row_index": 290, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A healthy 20-year-old Japanese male sustained a catastrophic traumatic injury when trapped beneath a 3-ton steel frame during crane maintenance. Upon rescue, he presented with persistent hemorrhage from the right lower abdominal wound, and upon emergency department arrival, exhibited unstable hip mechanics. Vital signs included a respiratory rate of 22 breaths per minute, blood pressure of 97/65 mmHg, and a tachycardia of 140 beats per minute. His Glasgow Coma Scale score was E4 V5 M6, indicating moderate to severe altered mental status. Physical examination revealed active pelvic instability and ongoing exsanguination from the right lower abdominal wound. Immediate interventions included endotracheal intubation and aggressive fluid resuscitation. Computed tomography (CT) imaging demonstrated multiple severe pelvic injuries: splenic laceration, sacral fracture, sacroiliac joint separation, and comminuted fractures of the right pubis, ischium, and acetabulum. Empirical antibiotic therapy with vancomycin and meropenem was initiated to prevent sepsis. Transcatheter arterial embolization (TAE) was performed in the angiography suite to control pelvic hemorrhage; angiographic evaluation revealed extravasation from both bilateral internal iliac arteries, which were successfully embolized. However, bilateral external iliac arteries demonstrated thrombosis, indicating compromised distal perfusion. A SAM® Pelvic Sling™ (SAM Medical, Wilsonville, OR, USA) was applied to stabilize the pelvis and maintain anatomical alignment. Despite TAE, complete hemostasis was not achieved, prompting consultation with a vascular surgeon. Emergency ligation of the right external iliac artery was performed in the operating room, resulting in immediate hemostasis. The wound was then packed and sutured. Follow-up CT imaging revealed ischemic changes in the right lower limb, consistent with distal arterial occlusion. Given the patient’s young age, robust physiological reserve, and strong familial desire to preserve limb function, revascularization was pursued despite the risk of recurrent hemorrhage. A crossover graft using the axillary-femoral artery was performed to restore distal femoral perfusion. Subsequently, a retroperitoneal hemorrhage was identified, likely due to injury to the external iliac artery, prompting a second crossover graft utilizing the axillary-femoral vein. Concurrently, cystostomy and external"}
{"row_index": 291, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 23-year-old man had a fever, no sense of smell, headache, and nausea a week before. Doctors said he had COVID-19 and treated him for 10 days at home. Two weeks later, he came back with fever every two days, feeling cold, then hot, then sweating. Tests showed he also had malaria (P. vivax), and his blood had a lot of clots (high D-dimer). He was given medicine for malaria: DHP for 3 days and primaquine for 14 days, as per local rules. He also got heparin to help stop blood clots. After 6 days, his fever went away and his blood tests got better. He’s now feeling fine and staying at home. Both COVID-19 and malaria can cause blood clots, so having both makes the illness worse. This shows why it’s important to check for both when someone has fever and trouble breathing, especially in areas where malaria is common.\"\n}"}
{"row_index": 292, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 23-year-old man first visited the hospital with fever, loss of smell, headache, and nausea. He was diagnosed with COVID-19 based on a nasal swab test, and treated at home for about 10 days. Even after being cleared, he still tested positive for the virus and continued to self-quarantine.\\n\\nTwo weeks later, he returned with recurring fever every two days, along with chills, fever, and sweating. His temperature reached 39.7°–40°C. The fever came and went, and even with paracetamol, it returned within hours. He also had muscle pain and weakness.\\n\\nLab tests showed high levels of inflammation and a marker called D-dimer, which can indicate blood clotting problems. A malaria test was done, and both the rapid test and blood smear confirmed he had a relapse of P. vivax malaria — a type of malaria he had before, during a trip to Papua.\\n\\nBecause he had both COVID-19 and malaria, doctors treated him for both. He took dihydroartemisinin-piperaquine for 3 days and primaquine for 14 days, following national malaria treatment guidelines. He also received paracetamol and heparin to help with fever and blood clotting. After six days of treatment, his symptoms went away and lab results improved.\\n\\nThis case shows that during the pandemic, people in malaria-endemic areas can get both COVID-19 and malaria at the same time. Both diseases can cause blood clotting issues, so having both can make the illness worse. Early diagnosis and prompt treatment are key to avoiding serious complications.\"\n}"}
{"row_index": 293, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 23-year-old male patient presented to the Universitas Airlangga Hospital emergency department with a 5-day history of fever, anosmia, headache, and nausea. SARS-CoV-2 RNA was detected by RT-PCR amplification from a nasopharyngeal swab, confirming a diagnosis of COVID-19. Initial laboratory findings included lymphopenia, neutrophilia, thrombocytopenia, and elevated C-reactive protein (CRP), with a normal chest X-ray. The patient was managed according to the Indonesian National COVID-19 Treatment Guidelines, receiving favipiravir at 1600 mg every 12 hours on day 1, followed by 600 mg every 12 hours from day 2 to day 5, intravenous paracetamol 1000 mg every 8 hours, oral vitamin C 500 mg every 8 hours, and oral vitamin D 1000 IU daily. Despite this treatment, the patient remained PCR-positive after 10 days with no clinical symptoms and was discharged to continue self-quarantine at home.\\n\\nTwo weeks later, the patient returned with recurrent fever occurring every 2 days, characterized by a distinct chilling-fever-sweating cycle, with peak temperatures ranging from 39.7° to 40 °C. The fever was partially controlled by paracetamol but recurred within 6 hours, accompanied by malaise and myalgia. The next day, the fever resolved, and the patient was ambulatory with normal physical examination findings: body temperature 38 °C, blood pressure 112/72 mmHg, heart rate 93 bpm, respiratory rate 20 breaths/min, and oxygen saturation 98% on ambient air. Body mass index (BMI) was 22.5 kg/m² (height 170 cm, weight 65 kg). All other physical exam parameters were within normal limits.\\n\\nLaboratory analysis revealed a white blood cell count of 8750/µL with 76.3% neutrophils, 13.5% lymphocytes, and 0.6% eosinophils; hemoglobin 12.2 g/dL, platelet count 231,000/µL; CRP"}
{"row_index": 294, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old man from North Africa who smoked for 30 years came in with chest pain that got worse with activity. He had high blood pressure and bad cholesterol, and had ignored his symptoms for 10 years. His heart exam was normal, and his lungs and legs were fine. His heart’s main pumping chamber (left ventricle) was healthy — it was the right size and working well, even though one major blood vessel in his heart was completely blocked. The right side of his heart was also fine. Doctors found a major blockage in the main artery feeding the left side of the heart, and a narrow spot in the right coronary artery. He had surgery to fix it using grafts from his chest and leg. The surgery went smoothly, and he recovered well. He was out of hospital in 9 days. Six months later, he had no chest pain, no shortness of breath, and his heart was working normally again. His heart test results showed no signs of damage or trouble.\"\n}"}
{"row_index": 295, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 52-year-old North African man with a 30-year history of smoking and high blood pressure presented with unstable angina that had been worsening over the past few days. He had ignored his symptoms for 10 years, including chest pain and shortness of breath during activity. Tests showed a complete blockage in his left main coronary artery, with a significant narrowing in his right coronary artery. Surprisingly, his left ventricle — the main pumping chamber of the heart — was normal in size and function, despite the severe blockage. He underwent successful on-pump coronary artery bypass grafting (CABG) surgery, where blood flow was rerouted around the blocked arteries using grafts taken from his chest and leg. The surgery went smoothly, and he recovered well, being discharged after 9 days. At 6 months follow-up, he had no chest pain or shortness of breath, normal heart function, and a healthy physical exam. His heart rhythm and overall heart health were stable, with no signs of heart failure.\"\n}"}
{"row_index": 296, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 52-year-old North African male with a 30-year history of tobacco smoking presented to our department with unstable angina of 24-hour duration, secondary to a total chronic occlusion of the left main coronary artery (LMCA), with no antegrade flow in the left anterior descending artery (LAD) and circumflex artery (Cx). He had a history of hypertension and dyslipidemia, with controlled blood pressure at 142/83 mmHg during clinical evaluation, and a body mass index of 25 kg/m². Physical examination revealed normal heart sounds, absent murmurs, clear lung auscultation, no peripheral edema, and normal carotid artery flow. Resting electrocardiogram (ECG) demonstrated normal sinus rhythm at 55 bpm without ST-segment elevation, but showed persistent anteroseptal Q waves and inverted T-waves in apical and lateral leads, suggesting prior myocardial injury or ischemia. Transthoracic echocardiography confirmed normal left ventricular (LV) size and systolic function, with an LV ejection fraction of 68%, normal segmental wall motion, and low LV filling pressures. Systolic pulmonary artery pressure was 24 mmHg, and right ventricular size and function were within normal limits, indicating preserved right heart function. Coronary angiography revealed total occlusion of the LMCA, with dominant right coronary artery (RCA) perfusing the left coronary territory via extensive collateral circulation, despite a significant stenosis in the RCA itself. This paradoxical preservation of left ventricular function, despite severe left main disease and extensive ischemia, suggests a robust compensatory collateral network and minimal ischemic myocardial damage. The patient was referred for elective on-pump coronary artery bypass grafting (CABG) two days post-angiography. Anesthesia was induced with cisatracurium besylate, midazolam, thiopental, and propofol, and a median sternotomy was performed for harvesting of the internal thoracic arteries (ITA) and saphenous vein graft (SVG). The right internal thoracic artery (RITA) was anastomosed to the left internal thoracic artery (LITA) to form a composite 'LITA-RITA-Y' graft configuration, enhancing graft viability and flow distribution. Cardiopulmonary bypass was established via aortic and"}
{"row_index": 297, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman had headaches for months, then got a stroke that only affected her senses, like numbness in her face and arm. Doctors first thought it was a virus, but her brain scans and fluid tests didn’t show that. Later, they found tiny worms in her brain fluid — specifically, a type of worm called Taenia solium — which means she had a brain infection from a parasite. Tests confirmed the worm was there, and her body made antibodies to fight it. After taking medicine to kill the worms, the amount of worm DNA in her brain fluid went down a lot. Her headaches got better, and after 3 months, she was feeling fine. The worms didn’t completely disappear, but the infection is now under control.\"\n}"}
{"row_index": 298, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This study describes a woman in her 40s who had headaches for several months, which later turned into a pure sensory stroke — meaning she lost sensation in her face and arm but had no movement problems. Initially, doctors thought it might be a virus, so she was given antiviral medication, but her symptoms didn’t improve. An MRI and other brain scans were normal at first, but later imaging showed small lesions in her brain, and her spinal fluid pressure was very high. After treatment for possible blood clot issues, her headaches remained severe. Tests on her spinal fluid found a high white blood cell count and elevated protein levels. A key test called next-generation sequencing (NGS) detected DNA from a parasite called Taenia solium, which causes cysticercosis. This was confirmed by positive antibodies in her spinal fluid. The patient was treated with antiparasitic medication (praziquantel), and follow-up tests showed a big drop in the parasite DNA levels. Her headaches improved significantly, and after six months, she had no symptoms left. Although some brain lesions remained, the infection was successfully treated.\"\n}"}
{"row_index": 299, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 44-year-old female factory worker presented with a 12-month history of recurrent, temporal and parietal headaches characterized by burst-like pain, initially evaluated at a local hospital in April 2016. Initial brain magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) were normal. Cerebrospinal fluid (CSF) analysis revealed a white blood cell count of 68 cells/μL and an intracranial pressure of 310 mmH₂O, prompting suspicion of viral encephalitis. She was treated with intravenous acyclovir (500 mg every 8 hours for 7 days), but symptoms remained unchanged. Three months later, in July 2016, she presented with worsening headache and paroxysmal numbness of the left face and arm, diagnosed as an ischemic stroke involving the right thalamus. She was initiated on oral aspirin 100 mg and atorvastatin 20 mg daily; numbness improved, but headache persisted. Five days prior to presentation at our institution, she returned to the local hospital due to severe headache on October 26, 2016, with lumbar puncture findings indicating CSF pressure >400 mmH₂O, white cell count of 40 cells/μL, and protein level of 1171 mg/L. Cerebral magnetic resonance venography (MRV) demonstrated underdevelopment of the right lateral sinus, with sinus thrombosis considered as a potential etiology. She was treated with low molecular weight heparin, resulting in partial headache relief. She was subsequently admitted to our hospital for further evaluation.\\n\\nThe patient had no significant past medical history, denied blood transfusions or consumption of raw food. Physical examination was unremarkable except for horizontal nystagmus. Laboratory testing revealed a mild elevation in eosinophil count (3.35%), with all other indices within normal limits. Serologic tests for HIV, syphilis, Herpes simplex virus types 1 and 2, tuberculosis (T-Cell spot test, purified protein derivative), and cryptococcal antigen (latex agglutination) were negative. Three lumbar punctures performed during admission confirmed persistently elevated intracranial pressure and increased white blood cell counts.\\n\\nCerebral MRA showed no abnormalities, while MR"}
{"row_index": 300, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 25-year-old woman from Kuwait, who had her first baby and was not married to someone from her family, was healthy before pregnancy. She went to a private clinic for check-ups, but no ultrasounds were done. She didn’t have diabetes or any past health problems. At 31 weeks, she went to the hospital because her water broke after 3 hours. She was fine when she arrived — no fever, normal breathing, and her heart was okay. The baby was in a breech position (feet first), not in labor yet. The doctors gave her antibiotics to prevent infection and gave her medicine to help her baby’s lungs grow. After 8 hours, she started having labor pains, and the doctor found the cervix was fully open. The baby was born early — weighing 1570 grams — and had a score of 3 out of 10 at first (meaning it needed help). The baby had serious birth problems: legs fused together, unclear genitals, a hole where the bladder and bowel should be, and a tube connecting the windpipe to the esophagus. The baby was taken to a special care unit for help. Doctors found no major chromosome issues, but the baby had missing or fused bones, a single opening for urine, and a blocked part of the intestines. Surgery was done to fix the intestines and create tubes to feed the baby. The left kidney had many small bags, and the right kidney wasn’t seen (might be in a strange place). The baby stayed in the hospital for 123 days and was finally sent home to continue treatment in the USA. The parents agreed to share this story with doctors and pictures, with their full permission.\"\n}"}
{"row_index": 301, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"Mrs. RB, a 25-year-old Kuwaiti woman who was pregnant for the first time, had a normal pregnancy until she was admitted to the Maternity Hospital in Kuwait at 31 weeks of gestation. She had a 3-hour history of ruptured amniotic membranes, which means the sac surrounding the baby had broken. She was not known to have diabetes, and her medical and surgical history was normal. Her family did not have a history of diabetes.\\n\\nAt admission, she was healthy, with normal vital signs and no signs of infection or breathing problems. The baby was in a breech position (feet or buttocks down), and the pregnancy was confirmed to be at 31 weeks. She was given antibiotics to prevent infection and dexamethasone to help the baby’s lungs mature. After 8 hours, she started having labor pains, and the cervix was fully open. The baby was delivered by assisted breech delivery, weighing 1570 grams. The baby’s Apgar score was 3 at 1 minute and 9 at 5 minutes, which means it needed immediate medical support to start breathing.\\n\\nThe newborn had several serious birth defects, including fused lower limbs, ambiguous genitalia, a cloacal anomaly (a single opening for urine, stool, and sometimes waste), and a tracheoesophageal fistula (an abnormal connection between the windpipe and the esophagus). The baby was taken to the neonatal intensive care unit (NICU) for close monitoring and treatment. Tests showed the baby had a normal number of chromosomes (46 XX), but there were major structural problems in the bones and organs.\\n\\nSurgery was needed to fix the bowel issues, including a blocked part of the small intestine and a blocked colon. The esophagus was tied off, and a feeding tube was placed to help the baby get nutrition. The kidneys were also affected — the left kidney had many cysts, and the right kidney was not visible, which may mean it was in an unusual position.\\n\\nThe baby stayed in the hospital for 123 days and was eventually discharged to continue treatment in the USA. The parents gave their consent for the case to be reported, including the use of medical images and details, after discussing it with the doctors.\"\n}"}
{"row_index": 302, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"Mrs RB, a 25-year-old Kuwaiti woman with a primigravida history, married for 18 months to a non-consanguineous partner, presented at 31 weeks of gestation to the Maternity Hospital, Kuwait, with a 3-hour history of ruptured membranes. The pregnancy was spontaneous and had been managed in a private health care setting with no prior antenatal ultrasonographic surveillance; the patient provided no documentation of such imaging. There was no history of diabetes mellitus, and her surgical, medical, and gynecological history was non-contributory. On admission, she was afebrile, hemodynamically stable, with normal vital signs, clear lung sounds, and normal cardiac examination. Obstetric examination confirmed gestational age consistent with 31 weeks, a single fetus in frank breech presentation, and normal fetal heart activity. No signs of intrauterine distress were detected.\\n\\nThe patient was managed conservatively with prophylactic antibiotics to prevent ascending infection and administered a course of dexamethasone (typically 6 mg intramuscularly, repeated every 6 hours for 24 hours) to promote fetal lung maturation in anticipation of premature delivery. She was transferred to the antenatal ward for monitoring. Eight hours later, she was readmitted to the labor ward with onset of labor pains. Pelvic examination revealed complete cervical dilation (10 cm) and a frank breech presentation at station 1 cm below the ischial spine, indicating a clinically significant fetal position for delivery.\\n\\nAn assisted breech delivery was performed due to the non-reassuring fetal position and the premature gestational age. The newborn had a birth weight of 1570 g (approximately 3.46 lbs), and Apgar scores of 3 at 1 minute and 9 at 5 minutes were recorded, indicating initial compromise requiring immediate resuscitation. An endotracheal tube was inserted to secure the airway, and active neonatal resuscitation was initiated, including positive pressure ventilation and chest compressions as needed.\\n\\nThe neonate exhibited multiple congenital anomalies: bilateral lower limb fusion (syndactyly with complete fusion of the tibial and fibular segments), ambiguous genitalia, cloacal anomaly (a single, patent cloaca with malformation of the anorectal and urogenital tracts), and tracheoesophage"}
{"row_index": 303, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old woman had surgery to fix a curved spine and join the bones together using screws and hooks from T3 to T12. After the surgery, on day 2, she had a sudden drop in oxygen levels, so doctors did tests to make sure her lungs weren’t blocked by a blood clot. The tests showed no clot, but the scan found her heart was stretched and had a big hole in the wall between the two upper chambers — a hole that had been there all along but didn’t cause symptoms. They also found one of the screws was bent to the side and was very close to her main blood vessel (aorta). Doctors decided first to fix the heart hole, which was done safely and she recovered well. After that, they checked the screw again with special scans to make sure it wasn’t poking into or touching the blood vessel — and it wasn’t. Two years later, they safely removed the screw and the rest of the hardware. The spine stayed strong and straight, and no problems came back after that. Everyone involved, including heart and spine specialists, watched closely to make sure everything was safe.\"\n}"}
{"row_index": 304, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 20-year-old woman had surgery to correct a curve in her spine (scoliosis) and fuse the spinal bones from T3 to T12 using screws and hooks. After the surgery, on post-operative day 2, she experienced sudden drops in oxygen levels, which led to tests to check for a blood clot in her lungs. These tests were negative, but the CT scan showed that her right side of the heart was enlarged, indicating a large hole in the heart wall (atrial septal defect or ASD) that had been present but not causing symptoms before. During the same scan, a small problem was found with a screw at the left T10 level — the screw tip was very close to the aorta, the main blood vessel in the chest. Because the heart issue was more urgent, the medical team focused on fixing the heart first. She had successful surgery to repair the hole in her heart and recovered well. After that, a follow-up CT scan helped map the position of the screw. Additional imaging, including angiography and ultrasound, showed the screw was not inside or pressing on the aorta. Two years later, the team decided to remove the screw safely, with a vascular surgeon and interventional radiologist on standby. The spine was reopened, the screws were removed, and the fusion site was reinforced with bone graft. The patient has been followed up for two years with no signs of spine curve returning or complications.\"\n}"}
{"row_index": 305, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 20-year-old female underwent posterior spinal deformity correction and spinal fusion for presumed adult idiopathic scoliosis, with posterior spinal instrumentation consisting of pedicle screws and hooks extending from T3 to T12. Preoperative evaluation, including electrocardiography (ECG), revealed no abnormalities, and her medical history was unremarkable, with normal physical activity levels including participation in sports. The anesthetic induction and surgical procedure were uncomplicated, with stable intraoperative neuromonitoring demonstrating consistent motor and sensory nerve potentials throughout the operation. Postoperative course was initially uneventful until post-operative day 2, when the patient experienced episodes of acute desaturation. This prompted evaluation with duplex ultrasound Doppler of the bilateral lower extremities and computed tomography pulmonary angiography (CTPA) to exclude pulmonary embolism. Both studies were negative for pulmonary embolism, but the CTPA revealed a right heart strain pattern and an enlarged right ventricular chamber, consistent with chronic volume overload. Subsequent two-dimensional echocardiography identified a large atrial septal defect (ASD), which had remained clinically asymptomatic until this point. In addition, the CTPA demonstrated a lateral breech at the left T10 pedicle screw level, with the screw tip in close anatomical proximity to the aortic wall, though no evidence of intraluminal penetration was observed. A multidisciplinary team convened and determined that cardiac management should be prioritized due to the significant hemodynamic impact of the ASD, with the malpositioned screw to be monitored and removed in a subsequent staged procedure. The ASD was successfully repaired via a surgical closure technique, with uncomplicated recovery and normalization of cardiac function. Following cardiac repair, a repeat computed tomography (CT) scan was performed to precisely delineate the position of the left T10 pedicle screw relative to the aorta. Angiographic imaging and intravascular ultrasound (IVUS) confirmed the absence of intra-luminal extension of the screw tip into the aortic lumen. A transesophageal echocardiogram (TEE) was additionally performed, which excluded any extra-luminal contact between the screw tip and the aortic wall. Two years after the initial scoliosis correction, a decision was made to proceed with removal of the spinal instrumentation. The midline surgical scar was reopened, and the spine was exposed across the T3–T12 previously fused segments. A solid"}
{"row_index": 306, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old girl was found to have a little bit of protein in her urine during a school health check. She was born very early, at 23 weeks, and was tiny—only 630 grams, like a baby at that stage. She had some breathing problems and eye issues as a baby, but grew up normally. Her blood pressure is normal, and her urine test showed a small amount of protein. Her kidneys were checked, and they were in stage 2 of kidney disease. Her uric acid level was high, which is not normal—her mom and her 16-year-old brother also have high uric acid. A small test on her kidneys showed a pattern that matches a condition called FSGS. After 3 years of medicine to help her kidneys, the protein in her urine went down, but her kidney disease stayed at stage 2. Doctors think her small size at birth was the first problem, and high uric acid later was the second problem that may have made her kidney disease worse.\"\n}"}
{"row_index": 307, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 13-year-old girl was referred to the hospital after a school urine test found mild proteinuria. She was born very prematurely at 23 weeks of pregnancy, weighing only 630 grams — very low for her age. She had some breathing problems as a baby and needed oxygen for a year, but she grew up normally. She has no other major health issues.\\n\\nAt checkup, her urine test showed grade (2+) proteinuria, and her blood test showed a serum creatinine level of 1.02 mg/dL, which led to a diagnosis of stage 2 chronic kidney disease (CKD). Her uric acid level was 7 mg/dL, which is higher than normal (normal is less than 4.6 mg/dL), meaning she had hyperuricemia. Both her mother and her 16-year-old brother also have high uric acid levels.\\n\\nA kidney biopsy showed signs of a condition called FSGS, where parts of the kidney’s filtering units are damaged. The kidney tissue was also showing some scarring and enlarged filtering areas. Tests for common antibodies were negative, supporting this diagnosis.\\n\\nShe has been treated with an angiotensin receptor blocker (ARB) for three years, and her proteinuria has improved. However, her kidney function hasn’t fully recovered — her creatinine level is now 1.07 mg/dL, and she still has stage 2 CKD. Doctors believe her early low birth weight was the first factor that may have damaged her kidneys, and her high uric acid levels (the second factor) may have worsened the damage. This suggests that both factors played a role in the development of her kidney disease.\"\n}"}
{"row_index": 308, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"proficient_health_literacy\": \"A 13-year-old female was referred to our hospital due to mild proteinuria identified during a school-based urinary screening. No prior history of urinary abnormalities existed. She was born at 23 weeks and 6 days of gestation, secondary to maternal fever, with a very low birth weight (LBW) of 630 g, corresponding to the size expected at 23 weeks of gestation. She developed chronic lung disease and retinopathy of prematurity, requiring supplemental oxygen therapy until age 1 year; however, her postnatal growth and neurodevelopmental trajectory normalized by that time. Beyond retinopathy of prematurity, she had no significant comorbidities and remained generally healthy throughout childhood.\\n\\nPhysical examination revealed a height of 154 cm, weight of 50 kg, body mass index (BMI) of 21.1, and blood pressure of 115/73 mmHg. Dipstick urinalysis demonstrated grade (2+) proteinuria. Her serum creatinine level was 1.02 mg/dL, leading to a diagnosis of stage 2 chronic kidney disease (CKD) using age- and sex-matched reference values for Japanese children aged 12–15 years. Her serum uric acid level was 7 mg/dL, which exceeds the normal range of <4.6 mg/dL for female children aged 12–14 years, confirming hyperuricemia. Both her mother and her 16-year-old brother also exhibit hyperuricemia, suggesting a possible familial predisposition.\\n\\nPercutaneous renal biopsy revealed segmental glomerulosclerosis in one of eight glomeruli, characterized by sclerosis with adhesion to the Bowman’s capsule (indicated by black arrow), and partial focal interstitial fibrosis (indicated by white arrow). The mean glomerular diameter measured 348.23 μm, significantly larger than the normal glomerular diameter of 168 ± 12 μm, indicating glomerular hypertrophy—a known pathological feature in focal segmental glomerulosclerosis (FSGS). Immunofluorescence staining for IgG, IgA, IgM, C3, C1q, and C4 was negative, excluding immune-mediated glomerulonephritis and supporting a diagnosis of native FSGS, specifically non-immune, likely of the"}
{"row_index": 309, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 17-year-old girl was taking two medicines for mental illness — lithium and paliperidone — because she had mood swings and heard voices. After a few weeks, she started feeling dizzy, slow, and had a slow heart rate. Her doctor found that her thyroid was not working right and her heart was beating too slowly. These problems went away completely after she stopped taking both medicines. Her heart rate and thyroid levels returned to normal in about 20 days. The doctor thinks the medicines caused these issues, not something else. She now takes a different medicine for her mental health and doesn’t need a pacemaker because her heart fixed itself.\"\n}"}
{"row_index": 310, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 17-year-old Han Chinese girl developed symptoms like dizziness, sluggishness, and chest tightness while being treated with lithium and paliperidone for bipolar disorder with hallucinations. She had been diagnosed with bipolar I disorder and was started on these medications during a prior hospitalization. Two months later, her paliperidone dose was reduced, but one week before her visit, her symptoms worsened. Her heart rate was low at 41 beats per minute, and an ECG showed sinus bradycardia and sinus arrest. Blood tests revealed elevated thyroid-stimulating hormone and low thyroid hormone levels, indicating hypothyroidism. Although the symptoms were mild, they were linked to her medication use. The doctors believed the combination of lithium and paliperidone caused these issues. After stopping both medications, her thyroid function and heart rhythm returned to normal within 20 days. She did not need a pacemaker because her heart rhythm improved on its own. She was switched to olanzapine for her mental health condition. The timing of her symptoms and recovery supports the idea that the medications were responsible, not an underlying heart or thyroid disease.\"\n}"}
{"row_index": 311, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 17-year-old Han Chinese female presented to the psychiatric outpatient clinic with a one-week history of dizziness, lethargy, and impaired school attendance. Her psychiatric history included a prior hospitalization three months earlier for bipolar disorder with psychotic features, specifically auditory hallucinations, meeting DSM-5 criteria for bipolar I disorder based on a documented manic episode and prior major depressive episodes. During admission, she was initiated on lithium carbonate 500 mg twice daily and paliperidone 9 mg (equivalent to 450 mg chlorpromazine) once daily. Two months later, the paliperidone dose was reduced to 6 mg (equivalent to 300 mg chlorpromazine) once daily. One week prior to her outpatient visit, she developed worsening dizziness, chest tightness, and generalized sluggishness. She reported no personal or family history of cardiac or thyroid disease, no smoking, alcohol use, or illicit drug use; however, these reports were self-identified and not corroborated by clinical documentation. Pre-treatment, she had no known history of thyroid dysfunction or bradycardia.\\n\\nOn physical examination, her heart rate was 41 beats per minute, consistent with sinus bradycardia, and blood pressure was 95/57 mmHg. Electrocardiography revealed sinus bradycardia and sinus arrest. Serum electrolytes (calcium, potassium) and myocardial enzymes were within normal limits. Thyroid function tests demonstrated an elevated thyroid-stimulating hormone (TSH) of 9.08 mIU/L (reference range: 0.51–4.94 mIU/L), a decreased total thyroxine (TT4) of 45.05 nmol/L (reference range: 58.1–140.6 nmol/L), and a reduced free thyroxine (FT4) of 10.94 pmol/L (reference range: 11.5–22.7 pmol/L), indicating subclinical hypothyroidism without overt clinical manifestations. The patient and her guardian denied any family or personal history of cardiac or thyroid pathology, and no other medications known to induce conduction delays were identified. Although serum lithium levels were not measured due to assay unavailability, her serum paliperidone concentration was within the therapeutic range.\\n\\nThe clinical presentation—sympt"}
{"row_index": 312, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 56-year-old woman had been bleeding from her intestines for years, causing fatigue and dizziness. She had small blue bumps on her skin since childhood that grew over time. The bleeding got worse and led to a serious blood problem where blood clots formed all over her body. Tests showed her blood was very low in red cells and had too many clotting markers. She was treated with a procedure called argon plasma coagulation during a special camera check of her intestines, and also took a medicine called sirolimus. After about 8 weeks, her blood levels improved and she stopped bleeding. One year later, she was doing well, her blood counts were stable, and she had not had any more bleeding.\"\n}"}
{"row_index": 313, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 56-year-old woman was admitted to the hospital with a 3-year history of fatigue and dizziness, which had worsened over the past 10 days with severe bleeding (melena). She had been hospitalized multiple times before for similar symptoms and had a history of many small, blue growths (venous hemangiomas) since childhood. These growths grew larger and more numerous over time. Tests showed she had severe anemia and a condition called disseminated intravascular coagulation (DIC), where blood clots form throughout the body and then break down, leading to bleeding and low blood clotting. Despite treatment, her hemoglobin levels remained very low, between 39 and 61 g/L, and she required many blood transfusions each year.\\n\\nNo clear source of bleeding was found during endoscopy or colonoscopy. Skin ultrasounds confirmed the blue hemangiomas on her skin. Blood tests showed abnormal clotting times and very low fibrinogen, along with high levels of substances that indicate active clot breakdown.\\n\\nThe doctors diagnosed her with blue rubber bleb nevus syndrome (BRBNS), a rare condition that causes multiple hemangiomas and can lead to bleeding in the intestines. Treatment included argon plasma coagulation (a procedure done during endoscopy to stop bleeding) and the medication sirolimus. After about 8 weeks of treatment, her hemoglobin improved to 100 g/L. At a 12-month follow-up, she was doing well with stable hemoglobin at 102 g/L and no further bleeding.\"\n}"}
{"row_index": 314, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 56-year-old female presented with massive intestinal hemorrhage, characterized by a progressive and persistent bleeding course over three years, with acute exacerbation over the past 10 days manifesting as melena. The patient had a longstanding history of chronic constipation and multiple venous hemangiomas since childhood, which demonstrated progressive increase in both number and size with aging. No familial history of hemangiomas or related vascular disorders was identified. Physical examination revealed significant anemia and multiple cutaneous blue hemangiomas protruding from the skin surface, confirmed by skin ultrasound as vascular malformations. Laboratory findings demonstrated severe hematological abnormalities: white blood cell count of 1.78 × 10¹²/L (normal: 3.80–5.10 × 10¹²/L), hemoglobin of 39 g/L (normal: 115–150 g/L), platelet count of 71 × 10⁹/L (normal: 125–350 × 10⁹/L), and positive fecal occult blood. Coagulation profile revealed marked dysregulation: prothrombin time of 17.7 seconds (normal: 9.5–15.0 sec), activated partial thromboplastin time of 55.8 seconds (normal: 20.0–40.0 sec), prothrombin time-international normalized ratio of 1.65 (normal: 0.80–1.50), fibrinogen level of 0.349 g/L (normal: 1.800–4.000 g/L), D-dimer >10,000 ng/mL (normal: 0–500 µg/mL), tissue plasminogen activator-inhibitor 1 complex of 14.10 ng/mL (normal: 0.00–10.50 ng/mL), and plasmin-α2 cellulase inhibitor complex of 12.23 µg/mL (normal: 0.00–0.80 µg/mL), consistent with a fibrinolytic-type disseminated intravascular coagulation (DIC). Imaging studies, including abdominal computed tomography and digital subtraction angiography with mesenteric arteriography, failed to identify any definitive source"}
{"row_index": 315, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old woman had a cough that got worse and started spitting out a lot of blood. The blood was so big it blocked her airway and she almost died. Doctors couldn’t clear the blockage with normal methods, so they used a thin tube (bronchoscope) to go inside her airway and used a medicine called urokinase to break up the blood clots. The clots were removed, and the airway opened up. After that, she was able to stop using the life-support machine, her breathing tube was removed, and she was taken off the ventilator. Now she’s stable. X-rays and scans show her lungs are getting better.\"\n}"}
{"row_index": 316, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old woman was admitted to the hospital with a cough that had lasted for 7 days and had suddenly worsened with large amounts of blood in her cough (hemoptysis) over the previous 9 hours. She had a history of Hashimoto thyroiditis, but it was not well managed. Chest CT scans showed pneumonia with bleeding in the lungs and thick mucus plugs blocking the airways, especially in the right lung. Her condition quickly got worse, with a large amount of fresh blood and a blood clot in her airway. Her oxygen levels were very low, and her breathing was difficult. Because standard methods to clear the airway were not working, doctors decided to use a procedure called fiberoptic bronchoscopy, combined with a medication called urokinase, to remove the large blood clots. This successfully cleared the blockage in her airway. After treatment, she was able to be taken off the life-support machine (extracorporeal membrane oxygenation), had her breathing tube removed, and was safely taken off the ventilator. Her current condition is stable, and follow-up chest X-rays and CT scans show improvement compared to when she first arrived at the hospital.\"\n}"}
{"row_index": 317, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old female was admitted to the hospital on May 17, 2023, at 15:51 with a chief complaint of a cough lasting seven days that had progressively worsened over the preceding nine hours, presenting with hemoptysis of 100 mL of blood. She had a history of Hashimoto thyroiditis, which was not systematically managed. Initial chest computed tomography (CT) revealed bilateral pneumonia with alveolar hemorrhage, prompting a recommendation for reevaluation post-treatment. Additionally, multiple bronchial mucus plugs were identified in the right main bronchus and in the middle and lower lobes of the right lung, suggesting obstructive airway pathology due to mucopurulent secretions and impaired clearance mechanisms. During the same day's afternoon, she experienced a recurrence of hemoptysis, characterized by a large volume of fresh blood mixed with a small amount of blood clot, indicating active intrapulmonary hemorrhage and potential clot formation within the airway lumen. Physical examination demonstrated a temperature of 36.2 °C, tachycardia (pulse: 128 beats/min), tachypnea (respiration: 25 breaths/min), hypotension (blood pressure: 75/49 mm Hg), and severe hypoxemia (finger-tip oxygen saturation: 50%). Breath sounds were diminished in the right lung, consistent with airway obstruction, while the left lung exhibited prominent moist rales, suggestive of interstitial fluid accumulation or pulmonary edema. Given the severity of airway obstruction and the failure of conventional clearance techniques—including postural drainage and mechanical suction—fiberoptic bronchoscopy was performed in conjunction with urokinase therapy. Urokinase, a serine protease that activates plasminogen to plasmin, was administered to induce fibrinolysis, thereby promoting the dissolution of intrapulmonary blood clots and facilitating their mechanical extraction via bronchoscopic instrumentation. The procedure successfully removed extensive intrapulmonary blood clots, leading to immediate relief of airway obstruction. Subsequent management included weaning from extracorporeal membrane oxygenation (ECMO), successful extubation, and liberation from mechanical ventilation. Post-intervention follow-up imaging, including chest X-ray and high-resolution computed tomography (CT), demonstrated significant improvement in lung parenchymal density and airway pat"}
{"row_index": 318, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man in his 70s had bleeding in his stomach area and pain for a few days. Doctors found a tumor in his small intestine that had spread to his groin. This rare kind of tumor, called GIST, was already growing in his belly and had moved into a hernia in his groin. The doctors first removed the main tumor and the spread parts, then fixed the hernia with surgery. After that, he took medicine to fight the tumor. Later, they found the tumor had grown inside the hernia, so they removed it completely. The man is still doing well, no pain, no return of the hernia, and can go about his daily life. In the past, very few people had this tumor show up in a groin hernia. All known cases needed both tumor removal and hernia repair. After 5 years, about 6 out of every 10 people with this disease are still alive.\"\n}"}
{"row_index": 319, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 71-year-old man came to the hospital with severe abdominal pain and blood in his stool that had lasted for 38 hours. He had no other medical problems or prior surgeries. During the exam, his abdomen was tender, and a mass was found in his small intestine on CT scan, which was causing bleeding. A small mass was also seen in his groin, but it was not noticed at first. The surgery showed a gastrointestinal stromal tumor (GIST) in the jejunum, with spread to other areas of the abdomen. The tumor was removed with a partial resection (R1), and the bowel was reconnected. The patient recovered well and was discharged after 11 days. Pathology confirmed it was a high-risk GIST with fast-growing features. After surgery, he started imatinib chemotherapy for three months. Later, he developed a painful, non-reducible hernia in his right groin, which was confirmed to be a metastasis of the same GIST. The hernia was repaired with surgery, and the tumor was removed along with the hernia sac. The final path report showed the tumor had spread to the groin and was still aggressive. He continued imatinib treatment and has been doing well at his last follow-up in February 2020—still alive and able to work without any signs of recurrence. A review of similar cases shows that GIST presenting as a groin hernia is very rare, and all such cases involved a primary tumor that needed both tumor removal and hernia repair. Long-term survival after diagnosis was about 64.3% at 5 years.\"\n}"}
{"row_index": 320, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 71-year-old male presented to the emergency department with a 38-hour history of diffuse abdominal pain and intermittent hematochezia. He denied other gastrointestinal or genitourinary symptoms and had no prior abdominal surgery or significant comorbidities. Physical examination revealed abdominal tenderness with extensive rebound tenderness; however, the groin was not systematically examined due to the absence of specific complaints. Laboratory evaluation demonstrated hypohemoglobinemia (9.6 g/dL). Contrast-enhanced computed tomography (CT) identified lower gastrointestinal bleeding originating from a ruptured mass measuring 5.2 × 4.1 × 3.0 cm³ located in the small intestine, specifically the third jejunal segment (220 cm from the duodenal-jejunal flexure). Concurrently, CT imaging detected a small mass (2.0 × 1.5 × 0.5 cm³) in the right groin, which was not explicitly noted in the initial emergent report.\\n\\nGiven hemodynamic instability, the patient underwent emergent laparotomy. Intraoperative findings revealed a primary gastrointestinal stromal tumor (GIST) arising from the jejunal wall, with disseminated, multi-focal tumor seeding throughout the peritoneal cavity. A palliative resection was performed, encompassing the primary tumor and all seeding lesions exceeding 2 mm in size, resulting in an R1 resection (resection with microscopic residual disease), followed by side-to-side jejunal anastomosis. The patient was discharged on post-operative day 11 without complications.\\n\\nHistopathological analysis of the primary tumor demonstrated spindle cell morphology, with a high mitotic rate (25/50 high-power fields, HPF) and significant areas of tumor necrosis (see Additional file: Fig. S1). Immunohistochemical (IHC) staining showed strong positivity for CD117, DOG-1, and SDHB; mild positivity for actin and desmin; and negativity for CD34 and S-100. The Ki-67 proliferation index was 20%. Molecular profiling revealed a mutation rate of 18.22% in the c-KIT gene, specifically a duplication at exons 9 (A502_T503dup), classifying the tumor as high-risk jejunal GIST.\\n\\nPostoperative management included imatinib therapy at a dose"}
{"row_index": 321, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 53-year-old woman who had two back surgeries before had a sudden worsening of her back pain, causing her legs to go weak and her bladder to stop working. This is a serious problem called cauda equina syndrome. Her blood tests showed signs of infection, and a scan found a pus-filled bump pressing on her spinal nerves from L4 to S1. The doctors drained the pus and found a small piece of old surgical cotton that had been left behind — it was causing the infection. The cotton was removed and the infection cleared after 2 months of antibiotics. The antibiotics worked, but her leg weakness only got better a little, not fully.\"\n}"}
{"row_index": 322, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 53-year-old woman with a history of two back surgeries at the L4-S1 levels — one 11 years ago and another 2 years ago — developed a sudden, serious condition called cauda equina syndrome. This caused weakness in her legs (paraparesis) and loss of bladder control. She had mild signs of infection in her blood (elevated white blood cell count and C-reactive protein), which matched findings on MRI showing a large abscess in the spine from L4 to S1. The abscess was drained during surgery, and a small, hard lump found inside it was identified as a retained piece of surgical cotton (a known cause of long-term infection). This cottonoid was removed, and the infection was treated with ciprofloxacin for two months. The infection cleared, but her leg weakness only improved partially. The tissue around the cottonoid showed chronic inflammation and scar tissue, and no signs of infection returned after one year.\"\n}"}
{"row_index": 323, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 53-year-old female with a longstanding history of low back pain underwent two prior spinal surgical interventions: an L5-S1 discectomy performed 11 years earlier and an L4-L5 decompressive laminectomy 2 years prior. Over a period of several weeks, she presented with an acute cauda equina syndrome, clinically manifesting as paraparesis and acute urinary incontinence. Physical examination revealed mild tenderness in the lower back region. Laboratory evaluation demonstrated a mildly elevated white blood cell count (12,600/mm³) and a significantly increased C-reactive protein level, consistent with acute inflammation, without evidence of urinary tract infection. Plain radiographic imaging confirmed the anatomical defects attributable to prior laminectomies at the L4-L5 and L5-S1 levels. Magnetic resonance imaging (MRI) revealed an oblong posterior epidural lesion extending from the L4 to S1 levels, which was hypointense on T1-weighted sequences and hyperintense on T2-weighted sequences, exhibiting ring enhancement after gadolinium administration—findings consistent with a post-infectious epidural abscess. Given the clinical and imaging features, a decompressive laminectomy was performed to relieve spinal cord compression. Intraoperatively, a well-encapsulated posterior epidural abscess was identified and drained. Histopathological analysis of the abscess wall revealed a granulomatous lesion, subsequently identified as a retained surgical cottonoid, located at the antero-inferior aspect of the abscess wall at the S1 level. This lesion was completely excised, along with adjacent marginal fibrotic capsular tissue. Microbiological culture of the thick, fibrotic abscess capsule yielded Klebsiella oxytoca, a Gram-negative bacillus commonly associated with nosocomial and postoperative infections. The patient was treated with intravenous ciprofloxacin for a duration of two months, after which the infection was fully resolved. However, despite successful eradication of the infectious process, the motor deficit associated with the cauda equina syndrome only partially recovered. Postoperative histopathology confirmed the presence of a textiloma, a fibrogranulomatous reaction to foreign body material, with chronic inflammation and extensive fibrosis surrounding the retained cottonoid. At one-year follow-up, no recurrence of infection was observed, indicating complete resolution of the infectious component and stable surgical outcome, though neuro"}
{"row_index": 324, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 72-year-old man had cancer in his bile duct, so doctors removed part of his pancreas and small intestine (pancreaticoduodenectomy). After the surgery, his bile duct got blocked in one part, which made it hard for bile to flow. To fix this, doctors used a special test (DIC-CT) to see exactly where the bile duct was and how it was blocked. They found the blockage was in a small part of the bile duct, and the small intestine was raised up, which made it hard to connect. Using a tiny needle and CT guidance, they pierced the bile duct and checked it with a small camera. They pushed a thin wire through the needle and felt the wall of the bile duct vibrate — this showed the needle went right into the blocked area. When they did this, they saw the raised part of the small intestine was squeezed a little, which confirmed the needle was in the right spot. Then they placed a small tube (8.5-Fr pigtail catheter) into the raised small intestine to help bile flow. After that, they put in a metal stent to keep the tube open. The patient recovered well, went back to regular visits, and had no problems with the stent even after 6 months.\"\n}"}
{"row_index": 325, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 72-year-old Japanese man had middle bile duct cancer and underwent surgery called a pancreaticoduodenectomy to remove the tumor. During the surgery, a complication occurred: a blockage in the posterior segment of the bile duct, which is a part of the bile duct system. To figure out how the bile duct and the elevated jejunum (a part of the small intestine) were positioned, doctors performed a drip infusion cholecystocholangiography-computed tomography (DIC-CT) test. This test showed that the bile duct was isolated and that there was no tissue or organ between it and the elevated jejunum, making it safe to connect them. Using CT guidance, the doctors made a small puncture in the bile duct and used an endoscope to see the connection site. They inserted a guide wire through a needle and felt vibrations in the bile duct wall, which confirmed the needle had reached the correct spot. When the wire was placed, they saw that the elevated jejunum was partially compressed, which helped confirm the puncture was successful. They then successfully placed an 8.5-Fr pigtail catheter into the elevated jejunum. After that, all drains were removed, and a metal stent was placed directly into the bile duct to keep it open. The patient recovered well and now visits the clinic as an outpatient. Six months later, the stent is still open and working without any problems.\"\n}"}
{"row_index": 326, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 72-year-old Japanese male with no significant prior medical history was referred for evaluation of jaundice and impaired hepatic function identified during a routine health screening. Preoperative endoscopic retrograde cholangiopancreatography (ERCP) revealed stenosis in the middle bile duct, and biliary abrasive cytology confirmed a Class V adenocarcinoma, consistent with malignant obstruction. Imaging demonstrated a low bifurcation in the posterior segmental bile duct branch, which informed the surgical planning for pancreaticoduodenectomy due to middle bile duct cancer. Postoperatively, the patient remained asymptomatic with only mild postoperative inflammation, and was discharged on postoperative day 22. However, on postoperative day 30, blood work revealed elevated inflammatory markers, prompting further investigation. Contrast-enhanced computed tomography (CT) showed abscess formation adjacent to the hepaticojejunal anastomosis site and posterior segmental bile duct dilatation, suggesting bile leak or ischemic injury. Initial management included percutaneous transhepatic biliary drainage (PTBD), which demonstrated contrast filling only in the posterior segmental branch, with no evidence of bile leakage into the elevated jejunum. Subsequent endoscopic contrast radiography from the hepaticojejunal anastomosis site revealed visualization of only the anterior segmental branch and left branch, confirming the anatomical lesion was localized to the low bifurcation of the posterior segmental bile duct. Bile output via PTBD averaged approximately 250 ml/day over consecutive days. To assess the spatial relationship between the posterior segmental bile duct and the elevated jejunum, a drip infusion cholecystocholangiography-computed tomography (DIC-CT) test was performed. This imaging modality demonstrated contrast reflux into the elevated jejunum from the anterior segmental and left branches, while the posterior segmental branch was dorsally visualized with a poorly defined anatomical relationship to the jejunum. Notably, no intervening abdominal organs were identified between the bile duct and the elevated jejunum, supporting the feasibility of percutaneous transhepatic internal biliary drainage of the isolated posterior segmental bile duct into the elevated jejunum. Under computed tomography (CT) guidance, a precise puncture was made into the posterior segmental bile duct, followed by endoscopic visualization of the hepaticojejunal anastomosis site. A guide"}
{"row_index": 327, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 19-year-old young man had surgery on his nose and nose bones. He was healthy before surgery, no problems with his voice or breathing, and no other medical issues. The doctors thought his airway was normal and safely able to handle anesthesia. During the surgery, they put a breathing tube in easily without any trouble. After the surgery, he started to have a hoarse voice, which lasted for several days. On the sixth day, doctors saw that one of the small bones in his voice box (the arytenoid cartilage) had slipped out of place. They fixed it with a small surgery under anesthesia, and his voice slowly got better over six weeks. He had no other symptoms or problems.\"\n}"}
{"row_index": 328, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 19-year-old Caucasian male had a routine surgery for nose and nasal bone correction (septorhinoplasty). He had no known medical problems, such as diabetes, lung issues, or weakened joints, and was considered healthy before surgery (ASA Class I). His airway was normal, and intubation (inserting a tube into the windpipe) went smoothly without complications. The patient did not cough during the procedure, and the surgery lasted four hours with no issues. After surgery, he developed moderate hoarseness, which lasted for several days. On the sixth day, a doctor found that the left arytenoid cartilage — a small bone in the voice box — had moved out of place. This caused the hoarseness. The cartilage was gently repositioned under anesthesia using a bronchoscope and steroid injection. Over the next six weeks, his voice improved. He had no other symptoms and was discharged on the second day. This case shows that even in healthy young patients, a rare condition like arytenoid cartilage dislocation can occur after surgery, though it is usually treatable.\"\n}"}
{"row_index": 329, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 19-year-old Caucasian male underwent septorhinoplasty under general anesthesia. His medical history was unremarkable, with no prior laryngeal pathology, diabetes mellitus, chronic renal failure, chronic corticosteroid use, laryngeal malacia, or acromegaly—all of which are known risk factors for cricoarytenoid joint instability. Preoperative evaluation, including physical examination and laboratory workup, was normal, consistent with an American Society of Anesthesiologists (ASA) physical status classification of I. Airway assessment revealed a class 2 airway, with normal Mallampati score and other standard airway parameters. Anesthesia was induced with thiopental (8 mg.kg⁻¹), rocuronium (0.6 mg.kg⁻¹), and remifentanyl (0.5 mcg.kg⁻¹), achieving complete muscle relaxation prior to endotracheal intubation. Using a Macintosh 4 laryngoscope blade, direct laryngoscopy demonstrated a short epiglottis and a glottis grade II according to the Cormack-Lahene classification, indicating a relatively straightforward visualization. A 8.0-mm endotracheal tube was successfully inserted on the first attempt without resistance, and was secured at the mid-trachea. The patient did not experience coughing or other reflexive responses during intubation. Intraoperative anesthesia was maintained with a mixture of nitrous oxide, oxygen, isoflurane, remifentanyl (0.25 mcg.kg⁻¹.min⁻¹), and rocuronium, with no complications during the four-hour surgical procedure. Postoperatively, the endotracheal tube was removed without incident, and the patient did not exhibit severe coughing or vomiting. On postoperative day 1, he reported moderate hoarseness, which persisted through day 6. No other symptoms were present. On day 6, fiberoptic laryngoscopy performed by an otorhinolaryngologist revealed anteromedial dislocation of the left arytenoid cartilage—a rare but clinically significant finding. This dislocation is likely due to a transient biomechanical disruption during the surgical maneuver or anesthesia-induced relaxation of the laryngeal musculature, possibly exacerbated by the inherent structural variability of the arytenoid cartilage in young individuals, though no predisposing conditions were identified"}
{"row_index": 330, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A young, healthy woman found a lump on her small finger that had been growing for months. It got bigger during her pregnancy, almost the size of an olive, and caused pain when her baby grabbed it. First, doctors thought it was a common cyst, but it didn’t go away. Later, tests showed it was a type of cancer called leiomyosarcoma. There was a small bump in her armpit, but doctors said it wasn’t serious. The cancer was caught early and only in her finger. She had surgery to remove the finger (a ray amputation) and the cut was clean with no cancer left behind. After surgery, she had no pain, no new lumps, and her hand worked well. She’s been cancer-free for months and is doing great with physical therapy. Her scar is noticeable but she’s working on it. No signs of cancer have come back.\"\n}"}
{"row_index": 331, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 24-year-old woman with no major health problems was diagnosed with a primary leiomyosarcoma in her small finger. The tumor had been growing for months, and its size changed depending on her pregnancy — it sometimes grew as large as an olive. She first visited urgent care, where the mass was thought to be a ganglion cyst, but it wasn't removed. Later, the mass became painful and started bleeding, leading to a biopsy that confirmed it was a low-grade leiomyosarcoma. Imaging showed a suspicious lymph node in her armpit, but doctors believed it was just a normal reaction, not cancer. The cancer was classified as stage 1A, meaning it was localized and early. A second opinion confirmed the diagnosis. After discussion with her medical team, she had a ray amputation of her small finger, removing the tumor at the level of the mid-metacarpal bone. The surgery was successful, with clear margins and no signs of cancer left behind. She also had nerve reinnervation to help preserve hand function. Following surgery, she had regular follow-ups and imaging, all of which showed no signs of cancer. She is now disease-free, with good hand function and no pain or new masses. She continues to do well and is recovering well with physical therapy.\"\n}"}
{"row_index": 332, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 24-year-old right-hand dominant Hispanic female presented to an urgent care clinic in October 2021 with a palpable mass on the ulnar aspect of the proximal interphalangeal (PIP) joint of her right small finger, which had been present for several months. She reported cyclical changes in mass size, with growth during pregnancy—reaching up to the size of an olive—and worsening pain associated with her newborn's frequent grasping of the finger. Initial attempts at aspiration were unsuccessful, and the mass was initially diagnosed as a ganglion cyst. Subsequent evaluation by a local hand surgeon was planned but never executed. In March 2022, she returned with progressive pain and an open, bleeding wound at the original site, prompting imaging. Plain radiographs revealed a soft tissue mass near the PIP joint with incidental punctate calcifications. An excisional biopsy was performed on March 15, 2022, and reviewed by two independent pathologists, confirming a diagnosis of low-grade leiomyosarcoma of the finger. Immunohistochemical staining and histopathological analysis supported this diagnosis, showing characteristic expression of smooth muscle markers (e.g., desmin, caldesmon, SMA) and absence of features consistent with benign fibroblastic or epithelial tumors. A PET/CT scan performed in early April 2022 identified a suspicious right axillary lymph node, which the treating oncologist and general surgeon interpreted as reactive and benign, consistent with inflammatory or post-traumatic changes. The clinical and pathologic staging aligns with AJCC stage IIA, indicating a localized tumor with no regional lymph node metastasis. The primary lesion was also visible on PET/CT. A second opinion from a general surgeon reinforced the benign nature of the lymphadenopathy. In early May 2022, the tumor board at the treating institution recommended ray amputation as the most appropriate oncologic intervention given the tumor's location, histologic grade, and lack of evidence of systemic spread. Concurrent laboratory studies were unremarkable, with no signs of infection or systemic inflammation. On the same day, a new mass was noted distal to the original lesion on the small finger, with imaging consistent with a potential second focus of leiomyosarcoma. On June 15, 2022, the patient underwent successful right-hand minor finger ray amputation, with the small finger amputated"}
{"row_index": 333, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 64-year-old woman who had cancer in her ovaries and was already treated before, now has pain, belly swelling, and trouble moving food through her gut. The cancer spread to her belly lining and intestines. After first treatment, she got better and had no cancer signs for a while. Then, the cancer came back. She tried a new drug combo — trabectedin and PLD — which worked well, and after a few cycles, she stayed in good shape. Even when she only took trabectedin alone, she kept getting better and stayed healthy for over two years. She had no major side effects and could do everyday things. This shows that trabectedin, even by itself, can help control this cancer for a long time.\"\n}"}
{"row_index": 334, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 64-year-old woman who had recurrent ovarian cancer after menopause was treated with a second-line chemotherapy combination of trabectedin and PLD, followed by trabectedin alone. She had symptoms like abdominal pain, bloating, and changes in bowel movement, and imaging showed widespread cancer in her abdomen and pelvis. After initial treatment with chemotherapy and surgery, her cancer went into complete remission. However, it returned seven months later, prompting a switch to trabectedin and PLD, which worked well — her cancer markers dropped significantly. Although she had side effects like low blood counts, the treatment was well tolerated. After the combination was stopped due to toxicity, she continued with trabectedin alone, which kept her cancer under control for over two years. Even after a later recurrence, she responded to further treatment with bevacizumab, which she continues to take to maintain her response. The case shows that trabectedin, especially when used alone, can be effective and well tolerated in managing recurrent ovarian cancer over a long period.\"\n}"}
{"row_index": 335, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 64-year-old Caucasian postmenopausal woman presented with persistent pain, abdominal distension, and altered intestinal transit, consistent with advanced gastrointestinal malignancy. Imaging via thoracic and abdominopelvic computed tomography (CT) revealed extensive peritoneal carcinomatosis, massive ascites, involvement of the greater omentum, diffuse mesenteric spread involving the small intestine, diffuse parietal peritoneal implants, and suspicious lesions at the base of the Douglas pouch with probable ovarian surface involvement despite normal ovarian size. Plasma CA-125 levels were 1,110.9 U/mL, with other tumor markers within normal limits. Omental biopsy confirmed high-grade serous carcinoma (HGSC), demonstrating positive immunohistochemical expression for WT-1, p53, and CK-7, and negative expression for CK20 and TTF-1, supporting a gynecological origin (tube-ovarian-peritoneal). The diagnosis was classified as primary peritoneal carcinoma of gynecological origin, stage IIIC, with unresectable disease due to extensive mesenteric infiltration.\\n\\nNeoadjuvant chemotherapy was initiated with intravenous paclitaxel 175 mg/m² and intravenous carboplatin AUC 6 administered every 21 days for three cycles. Follow-up CT imaging demonstrated a significant partial response, with CA-125 levels dropping to 65 U/mL (a 95% reduction from baseline). Subsequently, surgical cytoreduction was performed, achieving optimal tumor resection, and an intraperitoneal (i.p.) catheter was placed for future delivery of i.p. chemotherapy. Pathological evaluation of resected specimens confirmed high-grade serous carcinoma.\\n\\nAdjuvant intraperitoneal chemotherapy was delivered over four cycles: i.v. paclitaxel 175 mg/m² on day 1, i.p. cisplatin 75 mg/m² on day 2, and i.p. paclitaxel 60 mg/m² on day 8. The patient achieved a complete clinical response, although treatment-related toxicity included grade-2 asthenia and grade-3 neutropenia, necessitating dose delay and granulocyte-colony stimulating factor (G-CSF) support.\\n\\nSeven months after completion of platinum-based therapy, follow-up CT imaging revealed mediastinal"}
{"row_index": 336, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old woman who is overweight fell down the stairs and broke her right elbow. She had a break in the middle of her radius bone, a break near the top of the radius with a 15-degree twist, and her elbow popped out of place. First, the doctors fixed the popped-out elbow. Then they used surgery to fix the two breaks in the radius bone and put the elbow back in place. They made sure the elbow stayed stable and the soft parts around it were reattached. She wore a splint for 6 weeks and started moving her arm early, first with bending and straightening, then with turning her hand. After 6 weeks, she could only bend a little and turn her hand a little. By 3 months, she could bend and straighten much better and turn her hand more. By 5 months, she could move her arm almost normally again, and her thumb worked well. She was able to go back to work as a funeral director after 5 months.\"\n}"}
{"row_index": 337, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 36-year-old woman with obesity suffered a fall down the stairs, which caused a break in her right radial bone (radial diaphyseal fracture), a break in the neck of the radius with about 15° angulation, and a dislocation of her elbow (posterolateral elbow dislocation). She was admitted for treatment. First, the doctors reduced the elbow dislocation and stabilized the broken radius bones using surgery. They also repaired the damaged structures around the elbow. A CT scan was done to check for damage to the elbow’s stabilizing parts, and no coronoid bone injury was found. The radial neck fracture did not fully heal initially, so a second surgery was performed using a specific approach between two muscles to fix the fracture and reattach the elbow’s posterior structures. The radial nerve was protected during surgery by keeping the elbow in a pronated position. After surgery, she wore a splint for 6 weeks and began physical therapy early, starting with gentle movement. By 3 months, she had regained most of her elbow motion, though she still had some numbness in her radial nerve area. By 5 months, her range of motion improved significantly, including full recovery of thumb movement, and she was able to return to her job as a funeral director.\"\n}"}
{"row_index": 338, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 36-year-old female with obesity (BMI 34) was admitted following a low-energy fall down stairs, resulting in indirect trauma to the right elbow. Clinical examination revealed upper limb trauma without distal neurovascular compromise. Radiographic imaging demonstrated a 2R2A2 radial diaphyseal fracture and a 2R1A2 radial neck fracture with approximately 15° of angulation, along with a posterolateral humeroulnar dislocation. The initial intervention was emergency reduction of the humeroulnar dislocation, during which ligamentous stability was compromised due to the concomitant diaphyseal fracture. The patient was immobilized in a brachio-antebrachial-palmar (BABP) splint, and a computed tomography (CT) scan was performed to evaluate the integrity of the elbow's stabilizing ligamentous and bony structures, with no evidence of coronoid involvement identified.\\n\\nOsteosynthesis of the radial diaphysis was performed under regional anesthesia using a Synthes compression plate with a working length of two screw holes and a lever arm spanning six contiguous cortices on both sides, providing biomechanical stability through cortical interlocking. Post-reduction elbow assessment demonstrated no recurrent dislocation up to −40° of extension, though persistent displacement of the radial neck fracture remained.\\n\\nA Cadenat approach was employed to access the radial neck fracture, performed between the ulnar extensor and anconeus muscle, allowing direct visualization of the metaphyseal fragment shift while preserving the motor branch of the radial nerve by maintaining elbow pronation. The fracture was stabilized using an anatomical radial head plate (Trilock Radial Head Plates, Medartis), and the posterolateral elbow structures were reattached. Given the achieved joint stability, no additional medial stabilization procedures were indicated.\\n\\nPostoperative immobilization was maintained for 6 weeks in a BABP splint, with early rehabilitation initiated for flexion and extension. Pronation and supination were permitted beginning at the third week. At 6 weeks, range of motion was: flexion-extension 10°/0°/20°; pronation-supination 0°/0°/10°, with a deficit in thumb flexion. At 3 months, motion improved to flexion-extension 0°/40°/120°;"}
{"row_index": 339, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman with a tough-to-treat ovarian cancer that kept coming back got sick and lost a lot of weight because of the tumors. Her cancer didn’t show the usual signs that help doctors treat it, and tests found it had low cancer activity, but two small changes in the tumor genes. The doctors tried a new treatment: a drug called pembrolizumab and another called bevacizumab, given every three weeks. After just one round, her cancer marker went down a lot. By the seventh round, it was back to normal. A scan showed the tumors shrunk a lot, and after nine rounds, the cancer was completely gone. She started to get better, gained weight, and her muscles and fat returned. The only side effect was mild joint pain in her hands. No other serious problems happened.\"\n}"}
{"row_index": 340, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 42-year-old woman with advanced ovarian clear cell carcinoma (OCCC) had multiple surgeries and chemotherapy treatments, but her cancer returned and became difficult to control. Her tumors spread widely and caused severe weight loss (cachexia) and other symptoms. Tests showed her cancer had low mutation activity, no PD-L1 protein, and two specific gene mutations (ARID1A), which made her a candidate for a new type of treatment. Instead of traditional chemo, she received pembrolizumab and bevacizumab together every three weeks. After just one cycle, her tumor marker CA-125 dropped sharply and returned to normal after seven cycles. CT scans showed a big reduction in tumor size, and she achieved complete remission after nine cycles. Her weight and strength improved significantly, and she recovered from severe wasting. The only side effect was mild joint pain in her hands. No other serious side effects were seen, and she has remained free of cancer since then.\"\n}"}
{"row_index": 341, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 42-year-old Asian woman, gravida 0, para 0, initially presented with a suspected ovarian chocolate cyst at Kaiser Hospital in southern California in March 2014, which was pathologically diagnosed as clear cell carcinoma. Following optimal debulking surgery, she was found to have FIGO stage II disease and received adjuvant chemotherapy with paclitaxel and carboplatin for seven cycles. Recurrent disease was detected in January 2016, evidenced by rising serum CA-125 levels and pelvic tumor recurrence, prompting a secondary debulking procedure and subsequent treatment with carboplatin and gemcitabine. Despite this, deep pelvic recurrence near the sigmoid colon, rectum, and bladder emerged in September 2017, progressing despite salvage chemotherapy regimens including liposomal doxorubicin and topotecan. In February 2019, she presented to a medical center in Taiwan for a third debulking surgery involving resection of the sigmoid colon, rectum, and bladder, followed by small bowel bypass, T-colostomy, and bilateral percutaneous nephrostomy. Postoperative tumor recurrence occurred, with two major pelvic and abdominal masses forming shortly thereafter, leading to palliative management due to treatment refractoriness. An experimental immune cell therapy with undefined immunological cells was attempted but was ineffective. She subsequently presented to our institution in April 2019 with elevated serum CA-125 (1236.6 U/mL), a pelvic mass causing vaginal bleeding, and severe cachexia. Comprehensive genomic profiling using FoundationOne CDx, covering over 300 cancer-related genes, revealed a stable microsatellite instability (MSI) status, low tumor mutational burden (TMB), and two somatic mutations in the ARID1A gene, a component of the SWI/SNF chromatin remodeling complex implicated in transcriptional regulation and tumor suppression. Immunohistochemical analysis of tumor tissue demonstrated PD-L1 negativity, indicating absence of programmed death-ligand 1 expression, which is a key immune checkpoint molecule that typically enables tumor immune evasion. Given the absence of PD-L1 expression and the known limitations of immune checkpoint inhibitors in epithelial ovarian cancer (EOC) based on prior clinical trial data, a combination therapy approach was selected with pembrolizumab (200 mg) and bevacizumab (15 mg/kg,"}
{"row_index": 342, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 15-year-old boy had pain and swelling in his lower back for 4 months. Doctors found a growing lump on his spine, mostly on the left side, using X-rays, MRI, and CT scans. They called it an ABC. To fix it, they first blocked the blood supply to the lump, then removed it completely with a special surgery. They also fused the bones in his lower back to stabilize it. Two years later, he had no pain and the lump didn’t come back. The only small problem was a loose screw on one side, but it wasn’t causing any symptoms.\"\n}"}
{"row_index": 343, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 15-year-old boy had been experiencing a slowly worsening painful swelling in his lower back for four months, but no nerve problems. X-rays, MRI, and CT scans showed a large, expanding lesion on the left side of his sacrum and lower back bones (L4-S2), which was consistent with a condition called an ABC. This condition involves bone destruction and abnormal tissue growth. To treat it, the boy first had a procedure to block blood flow to the lesion (selective arterial embolization), then had surgery to remove the affected tissue (extended curettage). He also had spinal fusion surgery to stabilize the area (posterior fusion from L4 to S2). Pathology tests confirmed the diagnosis. Two years later, he was doing well with no pain and no signs of the lesion coming back. The only small finding on X-rays was a loose screw from the surgery, which was not causing any symptoms.\"\n}"}
{"row_index": 344, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 15-year-old male presented with a gradually progressive painful lower back swelling over a 4-month period, without associated neurological deficit. Plain lumbosacral radiography revealed an enlarged lytic lesion predominantly involving the left sacrum and lower lumbar vertebrae from L4 to S2. Magnetic resonance imaging (MRI) demonstrated a large, multi-loculated, expansile mass with a characteristic soap-bubble-like appearance extending from L4 to S2, involving the neural foramina, sacroiliac joints, and paravertebral musculature, findings consistent with an aneurysmal bone cyst (ABC). Lumbosacral computed tomography (CT) further delineated the lytic lesion, showing involvement of the sacral alae, partial destruction of the S1 and S2 vertebral bodies, and complete destruction of the left L5 pedicle. Arterial angiography confirmed the vascularity of the lesion, supporting the diagnosis of an ABC. Preoperative selective arterial embolization was performed on the day of surgery to reduce vascular supply and minimize intraoperative bleeding. The patient then underwent extended surgical excision via curettage, followed by posterior pedicle screw and rod lumbopelvic reconstruction (L4-S2). Histopathological examination of the resected tissue confirmed the diagnosis of an aneurysmal bone cyst, demonstrating osteoid foci, spindle cells, multinucleated giant cells, and reactive osteoblastic changes. Two years postoperatively, the patient remained neurologically intact and asymptomatic, with no radiographic evidence of lesion recurrence. The only radiographic finding on follow-up was asymptomatic loosening of the inferior left-sided set screw, indicating mechanical wear rather than biological recurrence or progression of disease.\"\n}"}
{"row_index": 345, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old woman who was healthy had a fever for two days and went to the doctor. She had sex for the first time six months before. Tests showed she got infected with a virus called CMV first. About five months later, she had a fever again and swollen lymph nodes in her neck. Tests at that time showed she had a new virus infection called EBV. This means she got infected with EBV after already having CMV. Both infections were new ones at that time, and she recovered fully without serious problems.\"\n}"}
{"row_index": 346, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 20-year-old healthy Japanese woman first had a two-day fever and visited the clinic. She had sex for the first time six months earlier. Tests showed she was infected with cytomegalovirus (CMV) for the first time. About five months later, she had a fever and swollen lymph nodes in her neck. Tests at that time showed she was infected with Epstein-Barr virus (EBV) for the first time. This means she got CMV first, then EBV a few months later. Both infections were confirmed by blood tests that detect specific antibodies. Her symptoms improved with treatment, and follow-up tests showed the CMV infection had fully cleared after three months. The sequence of infections was clear and matched the timeline of her symptoms.\"\n}"}
{"row_index": 347, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 20-year-old healthy Japanese female presented with a 2-day history of high fever to the emergency department at Kawasaki Medical School. Her medical history included prior episodes of mycoplasma pneumonia at ages 1 and 18. She reported her first sexual encounter six months prior. On examination, she exhibited pharyngeal erythema and lymphadenopathy in the posterior cervical and left axillary regions, with no significant findings on neurological or physical assessment. Vital signs at admission included a heart rate of 108 beats/minute, blood pressure of 101/58 mmHg, and a temperature of 38.9°C. Laboratory findings revealed leukocytopenia (white blood cell count: 1710/μL; neutrophils 76.0%, monocytes 5.0%, lymphocytes 18.0%, atypical lymphocytes 1.0%) and elevated C-reactive protein (CRP: 3.92 mg/dL). Mild hepatic dysfunction was noted: γ-glutamyl transferase (γ-GTP) 78 U/L, alkaline phosphatase (ALP) 276 U/L, aspartate aminotransferase (AST) 30 U/L, alanine aminotransferase (ALT) 28 U/L. Chest X-ray and computed tomography (CT) showed no evidence of pneumonia; abdominal CT revealed slight hepatomegaly and splenomegaly. Serological testing for influenza A/B antigens and Mycoplasma pneumonia antigen was negative. Hepatitis B surface antigen and hepatitis C antibody were negative. Human immunodeficiency virus (HIV) antigen/antibody test was negative (cutoff index <0.3). Treponema pallidum hemagglutination (TPHA) was negative. Urine culture yielded small amounts of Corynebacterium sp. and Gram-positive cocci, consistent with bacteriuria, though no pathogenic bacteria were isolated. Given the elevated CRP, levofloxacin (500 mg/day) was initiated empirically for suspected bacterial infection. The patient had a history of suspected bladder infection by her primary care provider. Viral serology demonstrated: CMV IgM antibody 3.89 (+) (enzyme immunoassay, EIA), CMV IgG antibody"}
{"row_index": 348, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 37-year-old woman had a swollen belly, swollen feet, and yellow eyes because of a blockage in her liver blood vessels. Doctors found the problem was Budd Chiari syndrome, where the veins carrying blood from the liver were blocked. She had a surgery called a side-to-side portacaval shunt to fix the blockage, using a vein from her leg as a bridge. After the surgery, the shunt got blocked early, so doctors placed a small metal tube (stent) inside it to open it up again. This worked, and she has been feeling better for five years with no symptoms and is on blood-thinning medicine to prevent clots.\"\n}"}
{"row_index": 349, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 37-year-old woman had a condition called Budd Chiari syndrome, which caused her liver to swell and fluid to build up in her abdomen. She had yellowing of the eyes, swelling in her legs, and a firm, enlarged liver. Tests showed that the veins carrying blood from her liver were blocked, especially the hepatic veins. Imaging confirmed a narrowed inferior vena cava and complete blockage of the hepatic veins. She underwent a side-to-side portacaval shunt using a vein from her leg as a graft to reroute blood flow. However, the shunt became blocked early, and this was fixed by placing a metallic stent across the shunt. After treatment, her symptoms improved, and she has been symptom-free for five years with regular follow-up and blood thinners.\"\n}"}
{"row_index": 350, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 37-year-old female presented with a two-week history of progressive abdominal distension, pedal edema, and jaundice. Physical examination revealed icterus, an enlarged and firm liver, and gross ascites. Laboratory findings demonstrated conjugated hyperbilirubinemia, mild derangement of transaminases, and elevated alkaline phosphatase. Imaging via ultrasonography with color Doppler identified an enlarged liver with hypertrophied caudate lobe, a 1.1 cm portal vein with hepatopetal flow, complete occlusion of the right hepatic vein, patent but narrowed inferior vena cava (IVC) compressed by the caudate lobe, and free abdominal fluid. Splenic and superior mesenteric veins were intact. Liver biopsy confirmed the diagnosis of Budd Chiari syndrome. Prothrombotic workup was negative for underlying thrombophilic disorders. Transjugular venography revealed 90% stenosis of the IVC with a 14 mmHg pressure gradient across the narrowing and non-cannulation of the hepatic veins beyond their origins, indicating complete occlusion at the hepatic vein ostia. An 18 × 63 mm metallic stent was deployed across the IVC segment, followed by balloon dilatation using a 16 mm balloon. Percutaneous transhepatic venography under ultrasound guidance demonstrated that the left hepatic vein was patent only in its proximal segment, with distal occlusion (2–3 cm) and collateral drainage; the right hepatic vein was completely occluded, and the middle hepatic vein exhibited long-segment total occlusion (>3 cm). Attempted recanalization of the left hepatic vein failed due to extensive fibrosis and long segmental occlusion. The patient subsequently underwent a side-to-side portocaval shunt using the right external iliac vein as the H-graft. Postoperative course was uneventful, with initiation of anticoagulation. Six weeks postoperatively, she was re-admitted with recurrent pedal edema and ascites. Doppler ultrasound revealed patchy flow through the shunt. Transjugular venography confirmed patency of the IVC stent but demonstrated narrowing of the portosystemic graft with a gradient exceeding 15 mmHg at the IVC end. Given the acute angulation of the shunt relative to the IVC, a"}
{"row_index": 351, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 70-year-old man had belly pain for 2 days, his stomach was swollen, he was feeling sick and threw up, and hadn’t had a bowel movement in 2 days. A scan showed his last part of small intestine was swollen and had a sharp object stuck in it — like a fish bone — that had pierced through the wall. The doctors took out the fish bone and cleaned the area. The man got better and was home in 6 days. He said he accidentally swallowed the fish bone 5 days before.\"\n}"}
{"row_index": 352, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 70-year-old man came to the emergency room with abdominal pain that had been worsening for 48 hours, along with swelling in his abdomen, nausea, vomiting, and not having a bowel movement for two days. An abdominal CT scan showed that the end of the small intestine (terminal ileum) was swollen, measuring 30mm, and there was a sharp foreign object located 15 centimeters from the end of this section. The object had pierced through the wall of the intestine. During surgery, the fish bone was removed, and the damaged area was cleaned and closed. The patient recovered well and was discharged after six days. He later admitted that he had accidentally swallowed the fish bone five days earlier. His overall condition improved during recovery and there were no serious complications.\"\n}"}
{"row_index": 353, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 70-year-old male with no significant comorbidities was referred to the emergency department by his family physician with a 48-hour history of progressive abdominal pain, marked abdominal distension, nausea, vomiting, and a last bowel movement reported two days prior. On physical examination, vital signs were: temperature 37.3 °C, pulse 110 beats per minute, respiratory rate 24 breaths per minute, and blood pressure 110/60 mmHg. Abdominal examination revealed right iliac fossa tenderness, generalized abdominal distension, and an empty rectal ampulla on digital rectal examination. Laboratory findings included hyperleukocytosis (white blood cell count: 15,700/mm³), hemoglobin 11 g/dL, platelet count 159,000/mm³, and elevated C-reactive protein (180 mg/L); hepatic and renal function tests were within normal limits. Abdominal X-ray demonstrated hydro-aeric levels in the ileal segments, consistent with ileal obstruction, without evidence of pneumoperitoneum. Abdomino-pelvic CT imaging revealed a 30 mm distension of the terminal ileum, upstream of a transitional zone where a rectangular, planar foreign body was identified. Based on these findings, the patient was diagnosed with ileal perforation secondary to foreign body penetration. Prior to surgery, the patient underwent optimization of his hemodynamic status with nasogastric tube suction and intravenous fluid resuscitation. An emergency laparotomy was performed under general anesthesia with endotracheal intubation, conducted by a fifth-year and fourth-year surgical resident. Preoperative prophylactic antibiotics were administered. Intraoperatively, a sharp foreign body measuring 3 cm × 2 cm was identified at the 15 proximal centimeters of the terminal ileum, penetrating through the ileal wall. The foreign body was successfully removed and identified as a fish bone. The margins of the perforation were excised, and primary anastomosis was performed. Postoperative recovery was uneventful; the patient was discharged on postoperative day 6. Patient history confirmed incidental ingestion of the fish bone five days prior to presentation. The postoperative course was uncomplicated, with resolution of systemic inflammation and restoration of gastrointestinal continuity. The pathophysiological mechanism involved mechanical obstruction and subsequent perforation"}
{"row_index": 354, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 74-year-old man had blurry vision in both eyes because of cataracts. His eye doctor planned to fix his right eye with cataract surgery. During the surgery, heat damaged the front and outer layer of his right eye. The damage was serious — his eye could only see with his hand moving, and the pressure inside the eye was very low. The front part of the eye became cloudy, and fluid leaked out. The surgery team could not sew the damaged part back together because it was too loose and broken. So, they took a piece of healthy tissue from a donor and put it into the damaged area to fix the eye. After that, they removed the cloudy lens part and placed a clear lens inside the eye. It took 7 months for the new lens to settle in place. Now, his vision is better — it’s 2/20 in his right eye, and the eye is stable with less cloudiness.\"\n}"}
{"row_index": 355, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 74-year-old man had severe eye damage during cataract surgery in his right eye. He had prostate enlargement but no history of dementia. Before surgery, he had blurry vision due to cataracts, with good vision and normal eye pressure. During the procedure, heat from the surgery caused serious injury to both the cornea and sclera (the white part of the eye). The injury led to heavy clouding of the cornea and fluid leaking into the eye. The wound was initially closed with stitches, but fluid kept leaking, so more material was injected. The next day, he was transferred to our hospital, where his vision had dropped to hand motion and eye pressure was only 3 mm Hg. The sclera was badly damaged and could not be repaired directly because it was too loose. Instead, a donor scleral graft was transplanted to cover the damaged area using 10-0 nylon sutures. After the graft healed and fluid stopped leaking, the lens nucleus was removed from the wound. Pathology showed the damaged tissue had coagulation necrosis with no inflammation. Three months later, inflammation caused macular edema, which was treated with anterior vitrectomy. Finally, an intraocular lens was placed in the ciliary sulcus seven months after surgery. His vision improved to 2/20 in the right eye, and his eye pressure stabilized with less corneal clouding.\"\n}"}
{"row_index": 356, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 74-year-old male presented in October 2015 with blurred vision in both eyes due to senile cataract, with baseline visual acuity of 6/20 in the right eye (OD) and 8/20 in the left eye (OS), and normal intraocular pressure (IOP). Slit-lamp examination revealed mild cortical cataract in both eyes, with no notable fundus abnormalities. The initial ophthalmologic management plan included phacoemulsification for the right eye. The patient had a history of benign prostatic hyperplasia (BPH) but no history of dementia. Prior to phacoemulsification, viscoelastic agents with high cohesive properties were injected into the anterior chamber to induce pupillary dilation following miosis induced by hydrodissection in the right eye. Shortly after initiating phacoemulsification, a severe thermal corneoscleral injury occurred, characterized by extensive thermal damage to the corneal stroma and sclera. The wound was initially managed with tight suturing using pedunculated conjunctiva; however, persistent intraocular fluid leakage necessitated repeated injection of viscoelastic material. The next day, the patient was transferred to our institution, where he presented with hand motion vision and an IOP of 3 mm Hg OD. Histological evaluation of the injured sclera revealed coagulation necrosis with eosinophilic material accumulation, consistent with thermal injury and lack of inflammatory cell infiltration, indicating a direct thermal insult without significant immune response. The scleral wound was found to be actively opening upon conjunctival incision, and due to marked scleral mobility, direct suture closure was not feasible. As a result, a donor scleral graft was transplanted to the injured site using 10-0 nylon sutures. Post-transplantation, intraocular fluid leakage was confirmed to be absent, allowing safe extraction of the lens nucleus from the newly formed temporal wound. Histopathological analysis confirmed favorable graft attachment and restoration of IOP to normal levels. Three months postoperatively, macular edema developed secondary to intraocular inflammation driven by residual lens cortex, leading to anterior vitrectomy, which resolved the edema. An intraocular lens (IOL) was ultimately implanted in the ciliary sulcus seven months after surgery. At the final follow-up in October 2016, the patient achieved a visual acuity of 2"}
{"row_index": 357, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A baby boy, just 4 days old, had a small, yellowish-white spot found on the inside of his left eye's back part. The spot was about the size of 1.5 eye circles. When doctors looked at it with a special eye test, it showed bright spots and a little leaking. Seven months later, the spot was gone and the eye looked normal. The blood vessels in the eye were a bit twisted but didn't leak anymore. No treatment was needed because the spot just disappeared on its own.\"\n}"}
{"row_index": 358, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 4-day-old male infant was found to have a small, harmless growth called an isolated retinal astrocytic hamartoma in the nasal retina of his left eye. At first, it appeared as a yellowish-white flat spot about 1.5 times the size of a normal retina disc. Fluorescein angiography showed the area was abnormally bright with a little leakage, which is a common finding in such growths. Seven months later, the spot had completely disappeared during a fundus exam, and the eye’s blood vessels looked slightly twisted but without any leakage. The right eye was normal throughout. This suggests that the growth may have gone away on its own without treatment, a process known as spontaneous regression.\"\n}"}
{"row_index": 359, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 4-day-old male infant, delivered at 40 weeks' gestation with a birth weight of 3660 g, was admitted to the Department of Neonatology at The Second Hospital of Jilin University in February 2022 due to dyspnea. Delivery was via episiotomy combined with forceps. No cutaneous abnormalities were noted. Brain magnetic resonance imaging (MRI) revealed bilateral short T1 signal abnormalities beneath the occipital cranial plate, consistent with subarachnoid hemorrhage, though no associated neurological deficits or family history of congenital or genetic disorders were present. Routine retinal screening using RetCam 3 (Clarity Medical Systems, Inc.) demonstrated a normal right retina. In contrast, a color fundus photograph of the left eye identified a solitary, yellowish-white, flat retinal lesion measuring approximately 1.5 disc diameters in the nasal retina. Fluorescein angiography (FA) demonstrated diffuse hyperfluorescence with mild fluorescence leakage, suggesting abnormal vascular permeability and perfusion within the lesion. B-scan ultrasound was unremarkable, showing no distinct calcifications or structural abnormalities, and the mass was inapparent on imaging. No therapeutic intervention was initiated, and the patient was followed clinically. At three months post-initial presentation, a reduction in lesion size was observed, with FA revealing decreased vascularization and mild mottled hyperfluorescence, indicating partial vascular normalization and possible resolution of the vascular dysregulation. Seven months after initial detection, fundus examination confirmed complete absence of the retinal lesion in the left eye. Repeat fluorescein angiography showed mild tortuosity of the surrounding retinal vessels without evidence of leakage, consistent with restored vascular integrity. The right retina remained unaffected. These findings support the clinical observation that isolated retinal astrocytic hamartoma (RAH) may exhibit spontaneous regression, likely due to the self-limiting nature of the lesion's vascular and cellular architecture, with a probable mechanism involving gradual resolution of the astrocytic proliferation and vascular remodeling over time. The absence of systemic involvement, familial predisposition, or associated anomalies further suggests a sporadic, non-malignant, and benign developmental origin of the lesion.\"\n}"}
{"row_index": 360, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 78-year-old man with liver damage from years of drinking alcohol had a cancer in his liver that broke into pieces and started bleeding. The bleeding was so bad it filled his belly with blood, and he needed surgery right away. Doctors opened his belly and saw a lot of blood and two spots where the liver had torn. The bleeding wouldn’t stop with normal methods. So they used a special machine that sends heat to the blood vessels feeding the cancer, and it worked — the bleeding stopped. The surgery took 90 minutes and he needed blood and medicine to stay alive. After the surgery, he went to the hospital room to recover. Two days later, he was moved to a regular room and didn’t need more medicine. His liver was still strong enough to heal, even though it was damaged. Later, he got a serious problem called hepatorenal syndrome, but didn’t need dialysis. He stayed in the hospital and was followed by a team that helps people with serious illness. Sadly, he passed away two months later because the cancer kept getting worse.\"\n}"}
{"row_index": 361, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 78-year-old man with long-term alcohol-related liver damage (cirrhosis) and several liver tumors (multifocal hepatocellular carcinoma) was admitted to the hospital after his abdomen suddenly filled with blood due to ruptured tumors. An abdominal CT scan showed multiple bleeding spots in both sides of his liver. He was in serious condition and urgently taken to the operating room, where a large amount of blood (4 liters) was found in his abdominal cavity (hemoperitoneum). During surgery, it was found that his liver was heavily damaged and covered by tumors, with two areas (segments II and IV) bleeding uncontrollably. Standard methods to stop the bleeding failed. To control the bleeding, doctors used a procedure called radiofrequency ablation (RFA), which applies heat to the blood vessels feeding the tumors, sealing them off. This was done around both tumors for a total of 40 minutes, and the bleeding stopped successfully. The surgery took 90 minutes, and he needed blood transfusions and medication to support his blood pressure. After surgery, he was moved to the intensive care unit and stayed there for two days before being transferred to a regular medical floor. His liver enzymes were very high after surgery, but he did not develop liver failure. He later developed a complication called hepatorenal syndrome on day 9, which affected his kidneys, but he did not need dialysis. His overall condition remained stable, and he was followed up by a palliative care team. Unfortunately, he passed away two months later due to worsening liver disease.\"\n}"}
{"row_index": 362, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"We present a case report of a 78-year-old white male with alcoholic cirrhosis and multifocal hepatocellular carcinoma (HCC), complicated by ascites and portosystemic encephalopathy. The patient's history includes a prior wedge resection of segment II for HCC (G2) two years prior, followed by annual surveillance including computed tomography (CT) imaging. Due to advanced age and poor liver function, he was not considered a candidate for liver transplantation (LT). He presented to the emergency department with decompensated ascites, abdominal tension, and lower limb edema. During hospitalization, his hematocrit dropped abruptly (hemoglobin from 9.3 g/L to 6.7 g/L over a 3-hour period), indicating significant hemorrhage. Abdominal CT revealed multiple bilateral foci of HCC with active acute bleeding from one lesion. His Model for End-Stage Liver Disease (MELD) score was 19, Child–Pugh score C11, total bilirubin 8 mg/dL, and alpha-fetoprotein (AFP) level of 604 μg/L—indicative of aggressive HCC. The patient was hemodynamically unstable and required urgent surgical intervention for hemorrhagic shock. A midline laparotomy was performed, revealing a massive hemoperitoneum (4 L) with a cirrhotic liver exhibiting recanalization of the umbilical vein and development of collateral circulation. The liver was completely subverted by tumor mass, with two spontaneous, uncontrollable lacerations identified in segments II and IV. Conventional hemostatic measures—including argon beam coagulation, oxidized regenerated cellulose, and fibrin glue—failed to achieve hemostasis. Given the multifocal nature of the HCC, poor hepatic reserve, and the presence of active bleeding from multiple vascular afferents, a strategy of radiofrequency ablation (RFA) was employed to coagulate the feeding vessels of each tumor nodule. Circumferential RFA cycles were applied to both nodules, totaling 40 minutes of ablation duration. This approach successfully achieved hemostasis and controlled the bleeding from the ruptured hepatocellular carcinoma. The surgical procedure lasted 90 minutes, during which the patient required three units of packed red blood cells (PRBCs) and vasopressor support with noradrenal"}
{"row_index": 363, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old woman had a hard, rubbery lump in her right upper belly that had been there for two months. She didn’t have any other health problems. Doctors found the lump was big — about 13 to 14 centimeters — and it had a small, bright part inside. A scan showed the lump was in her liver and also spread a little to her lower belly. She had surgery to remove part of her liver and a piece of tissue called the omentum. After the surgery, doctors looked at the tissue and found it was a rare kind of cancer called low-grade malignant epithelioid mesothelioma. This type of cancer grows slowly and doesn’t spread easily. Six months after surgery, she has not had any signs of cancer coming back. This is a good sign. It’s very rare for this kind of cancer to start in the liver, and even rarer for it to be in both the liver and the omentum at the same time.\"\n}"}
{"row_index": 364, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 36-year-old woman was admitted to the hospital after discovering a hard, elastic lump in her right upper abdomen that had been causing pain for two months. Imaging tests showed a large cystic mass in her right liver, about 13 to 14 centimeters in size, with a small blood-filled spot inside. A PET scan also showed abnormal activity in the liver and lower abdomen, suggesting a tumor. The patient had no history of asbestos exposure or other known risk factors. She underwent surgery to remove part of her liver and a portion of the omentum (a fatty tissue layer in the abdomen). Pathology results showed that the tumors were low-grade malignant epithelioid mesothelioma — a rare type of cancer that usually starts in the lining of organs. This type of cancer is very uncommon in the liver, and this case is one of the youngest reported in women. The tumors in both the liver and omentum had similar features, including a fibrous capsule and low growth rate, which suggests they are separate, primary tumors rather than spread from one area. After six months of follow-up, the patient has shown no signs of cancer returning. While rare, mesothelioma can sometimes occur in the liver or omentum, and in this case, both tumors were considered low-grade, meaning they are less aggressive and have a better prognosis.\"\n}"}
{"row_index": 365, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 36-year-old woman presented with a 2-month history of abdominal and back pain, leading to referral and admission for evaluation of a hard, elastic, poorly flexible mass in the right upper abdomen. No signs of obstructive jaundice or abdominal tenderness were present. Laboratory findings revealed anemia (hemoglobin = 10.6 g/dL), thrombocytosis (43.9 × 10⁴/μL), and elevated C-reactive protein (2.71 mg/dL); all other laboratory parameters, including tumor markers α-fetoprotein (AFP), carcinoembryonic antigen (CEA), and cancer antigen (CA)19-9, were within normal limits. Abdominal ultrasonography identified a large, heterogeneous space-occupying lesion in the right lobe of the liver, measuring 15 cm in diameter, with evidence of hemorrhage and a hypervascular mural nodule. Contrast-enhanced computed tomography (CT) demonstrated a cystic mass measuring 13 × 14 × 11 cm in the right liver lobe with an enhanced mural nodule. Magnetic resonance imaging (MRI) showed hyperintense T2-weighted components consistent with hemorrhagic content. 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) revealed abnormal metabolic accumulation in the liver and lower abdominal region, prompting surgical intervention. The procedure included hepatectomy of the posterior segment and partial resection of the omentum, which was identified as a lesion on FDG-PET. Gross examination revealed a massive cystic tumor measuring 18 × 15 cm containing hemorrhagic fluid, with multinodular, mucinous, brownish or yellowish lesions observed in the extra-cystic wall. The omental lesions were two nodular tumors measuring 2.1 × 1.3 cm and 0.3 × 0.3 cm, both slightly brownish in appearance. Microscopic evaluation demonstrated tubular, cystic, and spindle arrangements of epithelioid cells with clear or eosinophilic cytoplasm in both hepatic and omental tumors. Immunohistochemical analysis showed positive staining for AE1/AE3, EMA, CK19, CK7, CD10, and calretinin; partial or weak positivity for CK5/6, D2-40"}
{"row_index": 366, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 82-year-old man had pain in his belly for nine days, along with vomiting and belly swelling. He had a history of gallstones before. Tests showed his gallbladder was small and his intestines were stretched out, with a gallstone stuck in the small intestine, blocking the flow. This caused air to show up in the bile duct, which means a gallstone got into the intestine through a hole between the gallbladder and the small intestine. The doctors did an emergency surgery to remove the stone from the intestine. They left the hole alone because cutting it could have hurt the small intestine. After surgery, he recovered well and went home without problems. He stayed healthy for 16 months after that.\"\n}"}
{"row_index": 367, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 82-year-old man with a history of gallstones presented with abdominal pain, distension, and vomiting that had lasted for nine days. His abdomen was swollen, and the bowel sounds were loud. Ultrasound showed a shrunken gallbladder and swollen intestines. A CT scan found a gallstone stuck in the small intestine, blocking it, along with air in the bile ducts — a sign of gallstone ileus and a connection between the gallbladder and the duodenum (cholecystoduodenal fistula). The patient underwent emergency surgery, where the gallstone was removed from the intestine (enterolithotomy). The connection between the gallbladder and duodenum was not repaired because it could have caused serious injury to the duodenum. After surgery, he recovered well and was discharged on day six. He has remained symptom-free for 16 months.\"\n}"}
{"row_index": 368, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 82-year-old frail male with a history of hypertension for 15 years and previously diagnosed cholelithiasis (eight years prior) presented with a nine-day history of abdominal distension, constipation, localized periumbilical pain described as intermittent, nonradiating, and multiple episodes of nonprojectile, nonbilious vomiting containing food particles. He denied fever, jaundice, hematochezia, melena, urinary changes, or recent abdominal trauma. His recent diagnosis of bronchiectasis was managed with low-flow oxygen therapy. Physical examination revealed normal vital signs, a distended abdomen without tenderness, and hyperactive bowel sounds. Laboratory investigations, including complete blood count and biochemistry, were within normal limits. Abdominal ultrasound demonstrated a contracted gallbladder with distended bowel loops, consistent with intestinal obstruction. Abdominal computed tomography (CT) of the abdomen and pelvis revealed dilated loops of the small intestine with hyperdense intramural calculi and air within the biliary tree, confirming the diagnosis of gallstone ileus with associated cholecystoduodenal fistula. Initial management included intravenous fluid resuscitation, nasogastric tube insertion, analgesia, and nil-by-mouth status. A Foley catheter was placed, and urinary output was monitored closely. The patient underwent an emergency exploratory laparotomy via a lower midline incision under spinal anesthesia, performed within 24 hours due to concerns for chest morbidity. Intraoperatively, a single 4.5 × 2 cm gallstone was identified impacted in the terminal ileum, located 10 cm proximal to the ileocaecal junction. The ileal segment at the site of impaction was intact and healthy, with proximal bowel dilation. An incidental finding was a Meckel's diverticulum measuring 60 cm proximal to the ileocaecal junction, characterized by a wide base. A longitudinal enterotomy was performed proximal to the stone impaction to facilitate stone extraction via milking, followed by transverse repair of the enterotomy. The gallstone responsible for the intestinal obstruction was successfully removed. The cholecystoduodenal fistula was not ligated or repaired, as the procedure would have carried a high risk of duodenal injury, particularly given the anatomical proximity and the potential for bile-induced duodenal perforation or stricture. Postoperative course was un"}
{"row_index": 369, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old man with high blood pressure, diabetes, obesity, and liver disease had been on dialysis for two years. He often missed his dialysis sessions and didn’t follow his diet, which made his body weak. During one session, he felt tired, dizzy, and confused. His blood pressure was very low (50/30), and his heart was not working well. Tests showed his heart was wrapped in a thick, stiff layer (pericardium) that was squeezing it, making it hard to pump blood. This condition, called constrictive pericarditis, was caused by long-term dialysis. The doctors removed the thick layer (pericardiectomy) and found it was full of scar tissue and calcium, not infection. After the surgery, he started dialysis more regularly and followed his diet. He’s now feeling better and going to dialysis every week as planned.\"\n}"}
{"row_index": 370, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 65-year-old man with long-standing conditions like high blood pressure, diabetes, obesity, and liver disease on hemodialysis for two years began feeling unwell during one of his dialysis sessions. He reported feeling tired, lightheaded, and confused, but no chest pain or shortness of breath. He had a history of missing dialysis sessions and not following his diet, which likely worsened his condition.\\n\\nAt the time of admission, he was very weak, had a dangerously low blood pressure (50/30 mmHg), and showed signs of shock. His heart exam revealed weak sounds and a slow refill time, and his ECG showed low electrical activity in the heart. An echocardiogram found a thickened pericardium (the sac around the heart) with no fluid buildup, and cardiac catheterization confirmed that the pressures in all heart chambers were equal—this is a key sign of constrictive pericarditis.\\n\\nTests ruled out infection, heart disease, and other causes. Pathology of the removed pericardium showed heavy scarring and calcium deposits, with no signs of infection or inflammation. These findings point to dialysis-related constrictive pericarditis (DICP), a condition that can develop in people on long-term hemodialysis due to poor dialysis adherence and high fluid retention.\\n\\nThe patient underwent surgery to remove the thickened pericardium (pericardiectomy), which improved his symptoms. After recovery, he started attending dialysis more regularly, followed his diet, and now manages his condition better. This case highlights the importance of consistent dialysis attendance and dietary control in preventing serious complications like constrictive pericarditis.\"\n}"}
{"row_index": 371, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 65-year-old male with a history of hypertension, type 2 diabetes mellitus, morbid obesity, and cirrhosis secondary to non-alcoholic steatohepatitis (NASH) presented with symptoms of malaise, lightheadedness, and confusion during a hemodialysis session. He had been on hemodialysis for two years due to diabetic nephropathy, but exhibited chronic non-adherence to treatment, with only three to four sessions per week attended, resulting in an actual Kt/V of 1.5–2.0, significantly below the calculated standard Kt/V of 2.45 under ideal adherence. His dialysis prescription included a high-flux polysulfone membrane with a surface area of 2.2 m², a blood flow rate (Qb) of 370 mL/min, and a dialysate flow rate (Qd) of 800 mL/min. Dialysate composition consisted of calcium 2.5 mEq/L, potassium 1 mEq/L, sodium 138 mEq/L, bicarbonate 36 mmol/L, and unfractionated heparin 5000 IU/session. He was also prescribed allopurinol 100 mg/day, sertraline 50 mg/day, esomeprazole 40 mg/day, and sevelamer 2.4 g three times daily.\\n\\nAt presentation, the patient was anuric and in hypotensive shock with a blood pressure of 50/30 mmHg, prolonged capillary refill time, and jugular venous stasis. Physical examination revealed pallor, cyanosis, and hypophonic heart murmurs; respiratory rate was 16 breaths per minute, oxygen saturation 88% in room air, and no signs of pulmonary pathology. Cardiac auscultation showed no parasternal or apex murmurs, with a heart rate of 88 bpm. Neurological examination demonstrated altered mental status and bradykinesia. Electrocardiography revealed sinus rhythm, low diffuse QRS voltage, and evidence of altered ventricular repolarization, consistent with impaired conduction and reduced myocardial voltage.\\n\\nLaboratory findings included: hemoglobin 9.8 g/dL, hematocrit 29.5%, leukocytes 5,230/mm³,"}
{"row_index": 372, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 4-year-old girl was born with her index finger and thumb bigger than the other fingers. These fingers have gotten larger over time and now cause pain, tingling, and sometimes a bluish color, especially at night. The fingers are stiff, especially on the right hand, but she can still grip things she needs to hold. The big fingers are not normal — they have extra fat and fibrous tissue, like soft, firm stuff that grows around the nerves. This is called macrodactyly. Her siblings are healthy, and she had a normal birth. The doctors saw this on X-rays, which showed thick soft tissue and bigger bones in those fingers. Before surgery, everything looked the same. They planned surgery to fix the second finger, which was the worst, because it hurt the most and made her hand stiff. They removed the extra soft tissue (fat and fibrous stuff) without touching the bone or nerve. Then they cut a small piece of bone to straighten the finger and used a tiny metal wire to hold it in place while it healed. After surgery, she had regular check-ups and physical therapy to move her fingers better and reduce stiffness. She is getting better — her grip is stronger, her fingers move more, and the pain and stiffness are going down. She will keep being checked to make sure everything is healing well.\"\n}"}
{"row_index": 373, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 4-year-old girl has had enlarged index and thumb fingers since birth. Over time, these fingers have gotten larger, causing pain, tingling, and occasional bluish coloring—especially at night. The enlargement is most noticeable in the right hand, where the index and second fingers are much bigger than the others. The fingers feel firm and are slightly stiff, especially when gripping things. She can still hold objects, but her right hand has noticeable stiffness.\\n\\nThe condition is called macrodactyly, a type of FLH (fibrolipomatous hamartoma), which means abnormal growth of soft tissues like fat and fibrous tissue around the nerves in the hand. The swelling is not in the bones, but in the soft tissue, and it’s most prominent near the median nerve. X-rays showed increased soft tissue and bone growth in the affected fingers, which matches what’s seen in this condition.\\n\\nBefore surgery, doctors confirmed the diagnosis using X-rays. Since MRI was not available due to long wait times, they relied on X-rays to plan treatment. The surgery focused on the second finger, which was the most enlarged and caused the most problems. The procedure included removing the excess soft tissue (fibroadipose tissue), correcting the bent angle of the finger with a bone cut (wedge osteotomy), and using a small metal wire (K-Wire) to help the bone heal in the right position.\\n\\nThe surgery was done to reduce pain, improve finger movement, and make daily activities easier. After surgery, the child had regular follow-ups and physical therapy to improve hand strength and flexibility. Over time, she showed better grip, less stiffness, and improved hand function. She continues to be monitored for long-term results.\"\n}"}
{"row_index": 374, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 4-year-old female patient presents with congenital macrodactyly of the right index finger and thumb, a hallmark feature of fibrolipomatous hamartoma (FLH). The enlargement is disproportionate, with the index and thumb significantly larger than adjacent digits, and is characterized by firm, swollen tissue upon palpation consistent with fibroadipose proliferation. Radiographic evaluation reveals increased soft tissue density and bony enlargement of the first and second phalanges of the right hand, particularly on the palmar surface, confirming the radiological pattern typical of FLH involving both soft tissue and bone. The condition has been progressive since birth, with symptoms including nocturnal pain, paresthesia (tingling), and episodic cyanosis of the affected digits, suggesting compromised microvascular perfusion and/or nerve compression. These symptoms correlate anatomically with the course of the median nerve through the wrist and hand, a region commonly involved in FLH due to the infiltrative nature of the fibroadipose lesion.\\n\\nDetailed measurements show the right first finger measures 6 × 2.0 cm and the second finger 6 × 1.9 cm, with a 20-degree angulation directed toward the ulnar side at the distal and middle phalanges. Sensory function is preserved throughout the affected digits—base, middle, and tip—comparable to contralateral and non-affected sides, with no evidence of sensory loss or tenderness. The mother’s first finger measures 4 × 1.5 cm and second finger 5 × 1.5 cm, indicating a relative degree of familial variation, though not a direct hereditary pattern.\\n\\nPreoperative imaging, including initial X-rays, demonstrated widespread soft tissue edema and hyperdensity consistent with fibroadipose tissue expansion. Although MRI was planned as the gold standard for detailed soft tissue characterization and to confirm the diagnosis of fibrolipomatous hamartoma, its unavailability due to prolonged waiting lists necessitated reliance on X-ray findings for diagnostic and surgical planning. The absence of significant bony involvement in the excised tissue confirms that FLH is primarily a soft tissue hamartoma, with fibrous tissue derived from proliferative fibroblasts and collagen deposition around the nerve sheath, and adipose tissue representing abnormal fat accumulation within and adjacent to the nerve bundles. The excised mass exhibited a soft, pliable consistency with intermixed fibrous nodules,"}
{"row_index": 375, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 60-year-old woman who wears dentures had a sore spot on the inside of her lower right cheek for a month. She also had dry mouth. The doctor saw redness at the corners of her mouth and a small, painless lump near her tooth area, likely caused by a bad-fitting denture. A test found a rare type of yeast called C. calyptogenae, which is not common and usually lives in seawater or clams. This yeast matched almost perfectly with a known strain. After two weeks of using a mouth spray and a cream with miconazole and fusidic acid, the redness went down. The yeast was no longer found in her mouth after checking again. The doctor fixed her denture to prevent it from happening again. Her symptoms got better, and she’s now doing well.\"\n}"}
{"row_index": 376, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 60-year-old woman who wore dentures was diagnosed with angular cheilitis, a condition causing irritation and redness at the corners of her mouth. She also had a small, painless lump on the inside of her lower right cheek, likely caused by a poorly fitting denture. Testing of her mouth samples showed a rare yeast called C. calyptogenae, which is not commonly found in the mouth. The yeast was identified through laboratory tests that compared its genetic code to known strains, showing 99.6% similarity in one part of its DNA and 100% in another. After two weeks of treatment with a mouthwash and a topical cream containing miconazole and fusidic acid, her symptoms improved, with less redness. Follow-up testing showed no trace of the yeast. The doctor also recommended a new denture to better fit her mouth and prevent the problem from coming back.\"\n}"}
{"row_index": 377, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 60-year-old denture-wearing Malaysian woman was referred to the Oral Medicine Clinic, Universiti Malaya, in February 2020, presenting with a painless swelling on the lower right cheek that had persisted for one month. She reported moderate xerostomia, quantified by a Clinical Oral Dryness Score of five. On clinical examination, she was partially edentulous, with no facial swelling or palpable lymphadenopathy. Slight erythema was observed at the bilateral angles of the mouth, consistent with angular cheilitis. A non-tender, non-indurated lesion measuring 0.5 × 0.5 cm was identified on the lower right buccal sulcus over the premolar region, morphologically resembling an irritation fibroma, likely secondary to ill-fitting denture pressure. An oral swab was collected from the bilateral angles for Gram staining and Candida culture on Brilliance Candida Agar™ (BCA, Oxoid, UK). An expectorated oral rinse sample (20 ml saline) was obtained, centrifuged at 9600 rpm at 4°C for 10 minutes, and the resulting pellet (100 μl) was cultured for Candida isolation. Gram staining of the swab revealed scanty Gram-positive and Gram-negative bacteria and epithelial cells, with no evidence of blastoconidia or hyphal filaments. Primary cultures from both the oral swab and oral rinse yielded dark blue colonies along initial streak lines on BCA after 48 hours of incubation at 37°C. Colonies were subcultured onto fresh BCA and Sabouraud’s Dextrose Agar (SDA) plates, incubated at both room temperature and 37°C. On SDA, smooth, mucoid, light orange to beige colonies were observed at both temperatures; on BCA, similar colonies were seen at room temperature, while dark blue pigmentation was observed at 37°C. Yeast growth was faster at room temperature compared to 37°C on both media. Gram stain of the pure culture demonstrated round-to-oval yeast morphology. The isolate was designated as *C. calyptogenae* strain D1.\\n\\nSpecies-level identification was achieved via polymerase chain reaction (PCR) amplification and sequencing of the internal transcribed spacer (ITS) region and the D1/D2 domain of"}
{"row_index": 378, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man with a weak immune system stayed infected with the COVID-19 virus for 189 days. Even after treatment, the virus kept coming back, and tests showed it was the same strain each time. This wasn’t a new infection — it was the same virus returning. Doctors used medicines like dexamethasone, remdesivir, and IV immune shots to help him. His body slowly got better, and by day 189, the virus was no longer detectable. Tests confirmed the virus didn’t change — it stayed the same. He got the vaccine later, and after that, his tests came back negative. Now he’s getting stronger and can do more activities.\"\n}"}
{"row_index": 379, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 58-year-old man with weakened immunity due to lymphoma treatment developed a long-lasting SARS-CoV-2 infection that lasted for 189 days. Even after initial treatment, the virus kept coming back in the same form, as confirmed by genetic testing showing the exact same strain each time. This was not a new infection with a different virus, but a relapse of the original virus. The patient had a cough, fever, and breathing problems that returned multiple times, requiring hospital visits and treatments like dexamethasone, remdesivir, and intravenous immunoglobulin. His immune system was weakened by prior chemotherapy and rituximab, which likely contributed to the prolonged infection. Viral culture and PCR tests showed the virus remained detectable for months, and even after treatment, the virus was still present until day 189. Once the infection was fully cleared, he received the COVID-19 vaccine, and follow-up tests showed no virus. His symptoms gradually improved, and he is now able to do more physical activity. The case shows that some immunocompromised patients can have very long-lasting viral infections that require a combination of treatments to manage.\"\n}"}
{"row_index": 380, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 58-year-old Caucasian male with a history of follicular lymphoma, previously treated with six cycles of bendamustine and rituximab followed by maintenance rituximab, presented prior to widespread COVID-19 vaccination with a one-week course of cough, low-grade fever, and systemic malaise. Oropharyngeal swab testing was positive for SARS-CoV-2, and he was managed outpatient without hospitalization. Twenty-seven days later, he developed hypoxemia requiring hospital admission. Initial nasopharyngeal (NP) swab was negative, and high-resolution computed tomography (CT) revealed recurrent ground glass opacities and bilateral interstitial pneumonia, consistent with COVID-19. Laboratory findings included severe lymphopenia (0.1 × 10⁹/L, normal: 0.7–3.5 × 10⁹/L), elevated C-reactive protein (57.0 mg/L, normal: 0.0–8.0 mg/L), and markedly increased ferritin (2047 μg/L, normal: 30–500 μg/L), indicating significant inflammatory and immune dysregulation. He responded initially to dexamethasone 6 mg daily for 10 days; however, recurrent hypoxemia and progressive radiographic changes led to a diagnosis of organizing pneumonia as a post-COVID-19 sequelae. Bronchoscopy was declined, and oral prednisone 50 mg daily was initiated with a planned taper. On day 90 (73 days post-admission), following prednisone reduction to 10 mg, he developed new pyrexia and relapse of hypoxemia. Repeat NP swab RT-PCR was positive (Ct 18.7), and bronchoscopy was performed. Bronchoalveolar lavage (BAL) demonstrated both RT-PCR (Ct 18.7) and culture positivity (1.17 × 10⁴ pfu/mL) for wild-type SARS-CoV-2, belonging to the G clade, B.1.160 sublineage, with no growth of bacteria, mycobacteria, other viruses, or fungi. Histopathology of transbronchial biopsies revealed active pneumonitis with focal organizing pneumonia and patchy interstitial fibrosis, confirming a clinical"}
{"row_index": 381, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 54-year-old man had a sudden heart attack, his heart stopped, and he needed CPR and medicine to restore blood flow. Doctors used a clot-busting drug and placed stents in his heart arteries to fix the blockage. He ended up in the heart care unit with a weak heart and severe muscle damage. The muscle damage was caused by a cholesterol medicine (atorvastatin) he was taking, so they stopped it. He needed help to filter his blood because his kidneys weren’t working well, and had to get dialysis. His muscles were damaged so badly that a muscle biopsy was done. After recovering, he was finally released to a regular hospital room.\"\n}"}
{"row_index": 382, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 54-year-old man had a severe heart attack (AMI) that led to cardiogenic shock and cardiac arrest. He required cardiopulmonary resuscitation, fibrinolysis with tenecteplase, and successful coronary angiography with stents placed in key heart arteries. He was admitted to the coronary care unit (CCU) with deep sedation, mechanical ventilation, and a SOFA score of 7, indicating serious organ dysfunction. He developed post-extubation complications including delirium, stridor, and a pneumothorax, which required reintubation. During his hospital stay, he received medications that can cause muscle damage, including haloperidol, olanzapine, and hydrocortisone. Shortly after reintubation, he developed severe rhabdomyolysis — a condition where muscle breakdown releases harmful substances into the blood — linked to his atorvastatin medication. His creatine phosphokinase (CPK) levels rose over 10 times normal, peaking five days later, prompting the discontinuation of atorvastatin. He also developed kidney failure (oliguria), requiring temporary hemodialysis. After recovery, he was successfully extubated and discharged to a general hospital room. The rhabdomyolysis was directly tied to atorvastatin use, which was stopped due to the severe muscle damage.\"\n}"}
{"row_index": 383, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 54-year-old male presented with acute myocardial infarction (AMI) complicated by cardiogenic shock and cardiac arrest, requiring immediate advanced airway management in the emergency department. Tenecteplase 0.5 mg/kg was administered, with an ischemic time of 1 hour 40 minutes, and no reperfusion was achieved during the initial intervention. The patient experienced two episodes of pulseless tachyarrhythmias, each requiring defibrillation with 200 J biphasic shocks, advanced cardiopulmonary resuscitation (CPR), and intravenous amiodarone 300 mg to restore spontaneous circulation. Total duration of cardiac arrest was approximately 11 minutes.\\n\\nRescue coronary angiography revealed significant coronary artery occlusion, resulting in the placement of a medicated stent in the anterior descending artery and an unmedicated stent in the first diagonal artery. Post-procedural coronary flow was confirmed with a final TIMI flow grade of 3 and a blush grade of 3, indicating adequate reperfusion. The patient was admitted to the coronary care unit (CCU) in a state of deep sedation, under mechanical ventilation, with clinical evidence of cardiogenic shock and a SOFA score of 7, reflecting moderate organ dysfunction.\\n\\nPost-extubation complications included delirium, stridor, and iatrogenic pneumothorax, necessitating reintubation 48 hours after initial extubation. During this period, the patient received medications known to induce myositis, including intravenous haloperidol (5 mg intermittent doses, cumulative 30 mg), olanzapine (cumulative 20 mg), and hydrocortisone (200 mg). Subsequently, the patient developed septic shock, prompting initiation of broad-spectrum antibiotic therapy with vancomycin and meropenem at full initial doses, adjusted according to renal function, for six days as treatment for nosocomial pneumonia.\\n\\nAtorvastatin was continued enterally at a fixed dose of 80 mg every 24 hours for a total duration of 15 days. Two days after reintubation (10 days post-admission to CCU), serum creatine phosphokinase (CPK) levels rose to more than 10 times the upper limit of normal, peaking five days later, at which"}
{"row_index": 384, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 24-year-old woman had a big, growing lump on her left upper back and shoulder that caused severe pain and made her unable to use her left arm. She had been treated before for a similar problem in the same area, and had surgery and chemo back then. The lump kept getting worse, and her wound wouldn’t heal. Doctors tried chemo several times, but it didn’t work. She refused an amputation of her arm, so she came to our hospital. When she arrived, the lump was huge, bleeding, and smelly. Tests showed it was cancer called Ewing’s sarcoma, and it had spread into the muscles but not into her arm joint or chest. She had surgery to remove the entire lump and surrounding tissue, including part of her shoulder blade and muscles. The area was cleaned and covered with a flap of skin from her back to close it. After surgery, she got radiation and chemotherapy, and also had a special treatment to help her body recover. Now, after 3 years, she has no signs of cancer, can use her left arm normally, and is back to her regular work.\"\n}"}
{"row_index": 385, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 24-year-old woman was diagnosed with Ewing’s sarcoma in her left scapula (shoulder blade) and had previously undergone surgery and chemotherapy. Over time, the tumor grew large, causing a massive, bleeding mass on her left upper back and shoulder, severe pain, and inability to use her left arm. The tumor was so large that it caused an open ulcer that wouldn’t heal. After multiple failed treatment attempts and being offered a limb amputation, she refused and was referred to our hospital. There, she received a surgery to remove the entire tumor, including part of the shoulder blade, surrounding muscles, and skin, with no cancer cells left behind. Before surgery, she received antibiotics, blood transfusions, and treatment to stop the tumor’s blood supply. After surgery, she received radiation therapy and chemotherapy, followed by a stem cell transplant to help her body recover. She has been disease-free for three years and now has full use of her left arm and is back to her normal work activities.\"\n}"}
{"row_index": 386, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 24-year-old female presented with a massive fungating mass over the left upper back and shoulder region, characterized by active bleeding and foul-smelling purulent discharge from a large, non-healing ulcer. The lesion had been progressively enlarging over the prior two years, with an insidious onset of swelling. An incisional biopsy performed one year prior yielded a provisional diagnosis of Ewing’s sarcoma (ES) of the left scapula, prompting initiation of chemotherapy and subsequent surgical resection after three months of chemotherapeutic intervention. However, the surgical wound failed to heal, resulting in a rapidly expanding ulcer that persisted despite treatment. Neoadjuvant chemotherapy was initiated to shrink the tumor, but due to poor response—manifested by continued progressive growth and lack of tumor reduction—the regimen was modified multiple times over nine months without clinical benefit. Given the extensive size, invasive nature, and associated complications, multiple referral centers recommended forequarter amputation of the left upper limb, which was declined by the patient. She was ultimately referred to our institution for definitive management.\\n\\nOn presentation, magnetic resonance imaging (MRI) of the shoulder and upper back revealed a large, heterogeneous lesion measuring 18 cm × 27 cm × 26 cm, with T1 isointense and T2 heterogeneous high-signal intensity, consistent with a highly cellular, necrotic, and cystic tumor. The imaging demonstrated multiple fluid levels, degenerative cystic changes, hemorrhagic foci, areas of necrosis, and significant infiltration of periscapular musculature. Computed tomography (CT) scanning confirmed an ill-defined, heterogeneous tumor with prominent cystic components and gross osteolysis of the scapular bone, while no evidence of involvement was observed in the shoulder joint, chest wall, or brachial plexus. The axillary vascular bundle was displaced anteriorly without signs of vascular infiltration. Whole-body positron emission tomography-CT (PET-CT) scan showed no evidence of pulmonary or distant metastatic disease, supporting a localized, primary malignancy.\\n\\nHistopathological examination of a needle biopsy confirmed the diagnosis of Ewing’s sarcoma, demonstrating sheets of small, round, uniform cells with scant cytoplasm, separated by fibrous strands, and exhibiting minimal stromal component and few mitotic figures. Immunohistochemical staining was positive for CD99, a hallmark marker of Ewing’s sarcoma,"}
{"row_index": 387, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 25-year-old man got into a fast car crash and hurt his wrist badly. His hand was stuck against the steering wheel, which broke the bone in his wrist. He was in extreme pain, even with pain medicine, and couldn’t have anyone touch his arm without it hurting. To fix the pain without putting him to sleep, doctors used a needle guided by ultrasound to inject numbing medicine into the nerves in his shoulder area. This made his arm completely numb and pain-free. After that, they were able to fix the broken bone without him feeling any pain. He went home the same day with a splint and will see a doctor for follow-up. The next day, he said his arm felt normal — no numbness or tingling.\"\n}"}
{"row_index": 388, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 25-year-old man came to the emergency department after a high-speed car crash. He had a Colles fracture in his right wrist, caused when his hand hit the steering wheel during the collision. Despite taking strong pain medications, he continued to have severe pain and couldn't tolerate having his wrist moved. To control the pain without using sedation, doctors performed an ultrasound-guided nerve block called a CCBPB. This block numbs the nerves in the upper arm, providing strong pain relief. After the procedure, the patient had complete numbness in his right arm and reported no pain at all. The broken bone was successfully realigned without further pain. He was given a splint and sent home with follow-up care. The next day, he reported no numbness, tingling, or weakness, and felt fully recovered.\"\n}"}
{"row_index": 389, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 25-year-old male with no significant past medical history presented to the emergency department via ambulance following a high-speed motor vehicle collision in which he served as a restrained driver. During impact, he braced his outstretched right hand against the steering wheel, resulting in a traumatic injury to the wrist. On arrival, vital signs were stable, but the patient exhibited profound distress, reporting pain at 10/10 on the numeric rating scale. Physical examination revealed a grossly deformed right wrist with prominent dorsal swelling and severe tenderness to palpation, with no signs of neurovascular compromise. Radiographic evaluation demonstrated a transverse fracture of the distal radius with dorsal angulation of the distal fragment—consistent with a Colles fracture—and an associated ulnar styloid fracture.\\n\\nDespite administration of multimodal analgesia including intravenous opioids and nonsteroidal anti-inflammatory drugs (NSAIDs), the patient continued to experience intractable, severe pain, with absolute intolerance to radial manipulation, which precluded safe and effective manual reduction. To avoid the need for procedural sedation, an ultrasound-guided costoclavicular brachial plexus block (CCBPB) was performed as a targeted regional anesthesia strategy to achieve dense surgical anesthesia of the upper extremity and facilitate fracture reduction.\\n\\nInformed consent was obtained. The patient was monitored via continuous cardiac telemetry and had intravenous access established. He was positioned supine with the right arm abducted to 90 degrees to optimize anatomical exposure by stretching the pectoralis major and minor muscles, thereby bringing the costoclavicular brachial plexus into a more superficial and accessible position. Standard sterile technique was maintained throughout the procedure. A high-frequency linear ultrasound probe was positioned transversely just inferior to the midpoint of the right clavicle within the infraclavicular fossa, with the beam angled slightly cephalad to visualize the costoclavicular space posterior to the clavicular body. The costoclavicular brachial plexus cords were identified in the region lateral to the axillary artery and situated between the subclavius and serratus anterior (upper slips) muscles. Using an in-plane, lateral-to-medial approach, a 22-gauge, 50-millimeter echogenic needle was advanced between the lateral and posterior cords of the brachial plexus. Twenty milliliters of 0.5% rop"}
{"row_index": 390, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"Ms. B is an 86-year-old woman who came to the hospital with a four-day history of not being able to move her bowels, not eating, feeling sick, and vomiting. She had pain in her belly, especially after eating, and her stomach was swollen. She had a history of some health problems like cancer of the skin (Kaposi sarcoma), high blood pressure, joint pain, and low vitamin D. She had had a C-section and a tonsil removal before. She lived alone but could still take care of herself.\\n\\nWhen checked, her belly was swollen and painful, especially on the lower side. Her blood tests showed signs of infection and a slightly swollen liver, which means something was blocking the flow of bile. Her kidneys were a little affected, likely because she wasn’t eating much and was dehydrated. Her urine was normal.\\n\\nA scan showed two big gallstones — one stuck in the first part of the small intestine (duodenum) and one in the end of the large intestine (colon). The gallbladder was swollen and had gas, which means it was leaking into the intestines. This is called a gallstone fistula. The doctor diagnosed her with Bouveret syndrome and gallstone coleus.\\n\\nShe got IV fluids and a tube put in her nose to drain her stomach. She started antibiotics to fight infection. The doctors decided to do an open surgery (not laparoscopy) because the stones were big and hard to reach, and there was likely scar tissue. During surgery, they found two places where the stones were blocking the intestines. They tried to push one stone into her stomach but couldn’t. They cut open the first part of the small intestine and removed the stone. They also opened the end of the large intestine and removed the second stone. There was no cancer or serious damage found. The cuts were closed with stitches, and the small intestine was reinforced with a piece of healthy tissue.\\n\\nThe surgery went well. She didn’t need extra help like breathing machines or heart medicine. Her diet was slowly restarted. She was sent home to her family and will keep checking in with a general surgery doctor.\"\n}"}
{"row_index": 391, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"Ms. B is an 86-year-old Italian woman who came to the emergency department with worsening bowel blockage. She had been experiencing four days of severe abdominal pain, nausea, vomiting, loss of appetite, and trouble passing stool. Her medical history includes Kaposi sarcoma, high blood pressure, joint pain (osteoarthritis), and low vitamin D. She had previously had gallbladder inflammation but never had surgery to remove it. She also had a caesarean section and tonsillectomy. She lived alone but could care for herself.\\n\\nOn exam, her vital signs were normal, but her abdomen was swollen and tender, especially in the lower part. Bowel sounds were still present. Lab tests showed mild signs of inflammation and early kidney issues due to dehydration. Liver tests showed a pattern consistent with a blockage in the bile flow. The CT scan found two large gallstones — one in the first part of the small intestine (duodenum) and one in the lower large intestine (distal colon). The gallbladder was inflamed and had gas, which suggested a connection between the gallbladder and the intestine (a fistula). The common bile duct was enlarged, confirming the diagnosis of Bouveret syndrome with gallstone coleus.\\n\\nShe was given IV fluids, antibiotics, and a tube to drain stomach contents. A laparotomy (open surgery) was performed because laparoscopy was too risky due to the stones and possible scar tissue. During surgery, both stones were found and removed — one from the duodenum and one from the sigmoid colon. The duodenal stone could not be moved, so it was removed by cutting open the first part of the small intestine. The colon stone was removed after making a small incision. There was no sign of a serious infection or tumor. The area around the gallbladder and duodenum showed signs of inflammation, which suggested a possible connection between the gallbladder and the intestine.\\n\\nNo gallbladder removal or bile duct surgery was done because the exact anatomy was unclear and the patient had many health problems that made those procedures too risky. Her recovery after surgery was smooth. She did not need extra support like breathing or heart medications. Her diet was gradually restarted, and she was discharged to her family. She is now being followed up in a general surgery clinic.\"\n}"}
{"row_index": 392, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"Ms. B is an 86-year-old Italian woman with a complex medical history including Kaposi sarcoma, hypertension, osteoarthritis, and vitamin D deficiency. She presented to the emergency department with a four-day history of obstipation, anorexia, nausea, vomiting, worsening colicky abdominal pain, and postprandial reflux. Her surgical history includes a lower abdominal midline cesarean section and tonsillectomy; she lives independently and has no significant functional limitations. On physical examination, vital signs were normal, but the abdomen was distended, tender on palpation and percussion, with localized guarding, particularly in the lower quadrant. Bowel sounds were present, suggesting preserved peristalsis despite obstruction.\\n\\nLaboratory findings revealed a mildly elevated white cell count of 15.6 × 10⁹/L (normal: 4.0–11.0 × 10⁹/L) and C-reactive protein of 67 mg/L (normal <6.0 mg/L), indicating acute inflammation. Liver function tests showed bilirubin of 25 μmol/L (normal 2–20 μmol/L), alanine aminotransferase (ALT) of 18 U/L (normal <33 U/L), alkaline phosphatase (ALP) of 135 U/L (normal 30–110 U/L), and gamma-glutamyl transpeptidase (GGT) of 56 U/L (normal <56 U/L), consistent with an obstructive liver pattern. Serum creatinine was 99 μmol/L (normal 45–90 μmol/L) and urea was 8.6 mmol/L (normal 2.5–7.5 mmol/L), reflecting mild acute kidney injury secondary to reduced oral intake and dehydration. Electrolytes were within normal limits, and urinalysis was unremarkable.\\n\\nAbdominal computed tomography (CT) demonstrated two gallstones: one measuring 3.0 cm lodged in the proximal duodenum and another 3.3 cm located in the distal sigmoid colon. The gallbladder was contracted and inflamed, with gas detectable within the biliary tree (pneumobilia), suggesting a fistulous communication between the gallbladder and gastrointestinal tract. The common bile duct"}
{"row_index": 393, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 43-year-old man has had a long problem with a type of white blood cell called eosinophils for 13 years. This has caused him to have shortness of breath, skin rashes, joint pain, stomach issues, and even problems with his breasts and kidneys. His breasts got swollen and painful, so he had surgery to remove both. His kidneys showed damage that needed treatment. He was given steroids to help his body calm down, and after a few days of strong IV steroids, his breathing and lung problem got better. Now he takes steroids every day to keep his symptoms under control. His condition is stable, and he can live a normal life with this treatment.\"\n}"}
{"row_index": 394, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 43-year-old Chinese man has had a 13-year history of high levels of a type of white blood cell called eosinophils, along with shortness of breath for the past 7 days. Over the years, he has had a range of symptoms including stomach problems, skin rashes (like eczema and vitiligo), joint pain, breast inflammation, and kidney issues. The chronic breast inflammation was so severe that he needed a bilateral mastectomy. A bone marrow biopsy confirmed the eosinophilia, and a kidney biopsy showed a condition called focal segmental glomerulosclerosis, which is a type of kidney disease. He has been treated with steroids, starting with intravenous methylprednisolone for 3 days, followed by oral steroids at the same dose. After treatment, a chest CT scan showed improvement in his lung condition. He is now on a long-term oral steroid regimen and his condition is stable. Steroids help control his symptoms, but symptoms often return when the medication is stopped. He also had episodes of high blood pressure and protein in his urine, which were signs of nephrotic syndrome, but these have improved with treatment.\"\n}"}
{"row_index": 395, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 43-year-old Chinese male with a 13-year history of peripheral blood eosinophilia and progressive respiratory symptoms presenting with exertional dyspnea for 7 days was admitted to our institution. His initial presentation in August 2005 revealed a white blood cell count of 8.5 × 10⁹/L with 24.2% eosinophils (2 × 10⁹/L), prompting evaluation for eosinophilic disorders. Bone marrow biopsy demonstrated 13.5% eosinophils, predominantly with normally segmented rod nuclei, consistent with chronic eosinophilic infiltration. Upon initiation of oral triamcinolone (4 mg, three times daily), eosinophil counts rapidly normalized, indicating a strong corticosteroid-responsive phenotype. However, after a 6-month taper and eventual discontinuation, progressive hyperplastic and nodular changes developed in both breasts, accompanied by abnormal lactation and bilateral axillary lymphadenopathy, leading to a diagnosis of chronic mastitis. Bilateral mastectomy was performed in January 2006, with postoperative histopathology revealing male breast development and severe chronic interstitial inflammation characterized by dilatation of mammary ducts and dense eosinophilic infiltration.\\n\\nOne month later, the patient presented with trunk and limb joint pain, movement dysfunction, and a worsening erythematous skin rash. Treatment with dexamethasone and prednisone was initiated, and briefly, an herbal extract (Tripterygium wilfordii) was administered due to its anti-inflammatory properties, but was discontinued owing to severe treatment-related alopecia. Joint symptoms gradually improved, allowing functional recovery and return to work.\\n\\nIn April 2017, spontaneous bilateral lower extremity edema emerged, with clinical features consistent with nephrotic syndrome: blood pressure of 150/100 mmHg, plasma albumin of 15.6 g/L, low-density lipoprotein of 6.87 mmol/L, and 24-hour urinary protein excretion of 14.78 g/d. A renal biopsy confirmed focal segmental glomerulosclerosis (FSGS), non-specific type, a histopathological pattern commonly associated with chronic eosinophilic inflammation and immune dysregulation. Repeat bone marrow aspiration confirmed persistent eosinophilia, though qualitative polymerase chain reaction (PCR)"}
{"row_index": 396, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 4-month-old boy came to the hospital with a lump on his head that was swollen, painful, and leaking pus. The lump got bigger and turned into a sore, and doctors found tiny worms inside it. Even after giving antibiotics and removing the worms, the boy still had fever and pus. X-rays and a 3D scan showed the bone around the lump was infected. The doctors changed the antibiotics and gave them for six weeks, plus used a skin flap to cover the area. After all this, the boy started feeling better and was sent home with more medicine and follow-up visits.\"\n}"}
{"row_index": 397, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 4-month-old male boy from a low-income area in Cartagena, Colombia, was brought to the emergency room with a painful, swollen bump on his skull that had pus draining from it. The bump had grown and turned into an open sore, and doctors found larvae inside it. He had a history of skin conditions like seborrheic dermatitis and fungal hair disease. He was given antibiotics at first, but the infection did not improve. The lesion worsened, and despite removing the larvae surgically, the boy continued to have fever, pain, and drainage. A skull X-ray showed a bone breakdown, and a 3D CT scan confirmed that the infection had spread to the outer part of the skull bone (osteomyelitis). The treatment was changed to include clindamycin and ivermectin, and he received antibiotics for six weeks, followed by four weeks of rifampicin. A skin flap surgery was also done to cover the damaged area. Tests for HIV were negative. After treatment, the boy’s symptoms improved, and he was discharged with ongoing antibiotic therapy and follow-up visits.\"\n}"}
{"row_index": 398, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"Male patient, 4 months old, from a low-income neighborhood in Cartagena de Indias, Colombia, with a prior history of seborrheic dermatitis and tinea capitis, presented to the emergency department with a one-week history of fever accompanied by a nodular lesion localized on the parietal region of the skull. The lesion was characterized by significant edema, tenderness, pain, and spontaneous purulent drainage. Initial empiric therapy with cefalotin was initiated, but no clinical improvement was observed. Over the course of hospitalization, the lesion evolved into a 3 cm diameter ulcer, and at admission, Dermatophagoides hominis larvae were directly visualized within the ulcerated orifice. Surgical debridement was performed, resulting in the removal of approximately ten larvae. Despite this intervention, the patient continued to exhibit fever, purulent exudate, and persistent larval presence even after six days of antibiotic therapy. Consequently, a combination regimen of clindamycin and ivermectin was introduced. Imaging evaluation revealed a skull radiograph demonstrating an osteolytic lesion, with 3D reconstructed computed tomography confirming osteomyelitis affecting the outer parietal bone surface. The patient received a total of six weeks of clindamycin therapy and four weeks of rifampicin, in addition to surgical intervention involving a scalp flap. Human immunodeficiency virus (HIV) testing, including both primary and secondary assays, was performed and returned negative, ruling out HIV as a contributing factor. Clinical improvement was achieved following the combined antimicrobial and surgical approach, and the patient was discharged with continued outpatient antibiotic therapy and scheduled follow-up visits. The clinical course reflects a complex case of cutaneous larva migrans with secondary osteomyelitis, likely secondary to deep tissue invasion by D. hominis larvae, which may have been facilitated by compromised skin integrity due to preexisting dermatological conditions and potential immunological vulnerability. The persistence of infection despite initial antibiotic coverage underscores the importance of accurate parasitic identification and the need for targeted antimicrobial and surgical management in pediatric cases involving deep cutaneous and osseous involvement.\"\n}"}
{"row_index": 399, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A very small baby born early had a lung problem where air got trapped in the chest. Even after putting in a tube to fix it, the air stayed and the lung kept collapsing. Doctors had to cut open the chest to find a small hole in the air pipe (bronchus) that was letting air in. They fixed the hole with a patch and stitched it closed. After that, the lung started to work better. The baby had to have this surgery twice because the hole kept leaking air. After both surgeries, the air stopped coming back, and the baby finally got better. He’s now home with a small machine to help breathe and uses only a little oxygen.\"\n}"}
{"row_index": 400, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A preterm baby born at 27 weeks developed pneumomediastinum and pneumothorax, both of which did not go away even after inserting a chest tube. The pneumothorax kept coming back, and doctors eventually had to perform a thoracotomy to find and fix a tear in the bronchus. During the surgery, they found a 1 cm hole between the left bronchus and the carina, repaired it with a patch, and used stitches and medical glue to secure it. After the first surgery, the baby still had another episode of air leak, so they did a second thoracotomy at the same site and repaired it again. The hole was fixed, and no air leaks were found after the procedure. The baby also had a small heart issue (patent ductus arteriosus) that was managed during the surgery. After recovery, the chest tubes were removed, and the baby was discharged home on day 161 with a home ventilator and oxygen support.\"\n}"}
{"row_index": 401, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 27-week 4-day preterm male infant, born via cesarean section from a dichorionic diamniotic twin pregnancy with a birth weight of 1135 grams, presented with severe respiratory distress following premature rupture of membranes at 27 weeks, accompanied by uterine contractions and vaginal bleeding. Antenatal corticosteroids were administered, and delivery was planned due to arrested labor. At birth, the neonate exhibited hypotonia and apnea, requiring immediate intubation within one minute due to respiratory failure with an uncuffed endotracheal tube. APGAR scores were 4 at 1 minute, 6 at 5 minutes, and 7 at 10 minutes. The infant was admitted to the newborn intensive care unit (NICU) where a diagnosis of respiratory distress syndrome (RDS) was established. Treatment included endotracheal administration of poractant alfa (200 mg/kg), parenteral ampicillin-gentamicin for broad-spectrum coverage, and caffeine citrate to mitigate apnea. Mechanical ventilation was initiated in assist-control mode with volume guarantee and a maximum inspiratory pressure of 20 cm/H₂O. Cranial ultrasound revealed no structural abnormalities. On day 3, the infant was extubated and transitioned to nasal intermittent positive pressure ventilation (NIPPV), but required reintubation due to recurrent respiratory failure. Antibiotic therapy was escalated to vancomycin-meropenem due to clinical deterioration. On day 5, the infant developed worsening acute hypoxic respiratory failure. Chest radiography demonstrated mediastinal pneumothorax, with follow-up imaging showing rapid progression of pneumothorax on the left side and rightward mediastinal shift. A chest tube was inserted through the left 5th intercostal space to manage the pneumothorax. Repeat imaging showed expansion of the left lung and air bronchograms on the right. Ten hours later, persistent acidosis and hypoxia were noted, with a subsequent chest x-ray confirming recurrence of left-sided pneumothorax. The chest tube was set to continuous suction, resulting in progressive resolution of the pneumothorax on serial imaging. On day 6, echocardiography revealed a 3 mm patent ductus arteriosus (PDA) with predominantly left-to-right shunting and evidence of pulmonary hypertension. Oxygen saturation was approximately 80%, and"}
{"row_index": 402, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 40-year-old man who worked in construction suddenly lost strength in his right arm and leg six days before he went to the hospital. He didn’t have any injury or neck pain from hitting his head. His neck didn’t hurt, and he didn’t have diabetes or high blood pressure. He had smoked for 10 years. When doctors checked him, his brain and speech were normal, but his right side was weak — he couldn’t lift his right arm or stand on his right leg. His right leg had no feeling, and his right hand had weak touch. The doctors found that the problem was in the spine, specifically in the neck area, and it was called Brown-Séquard syndrome on the right side. The brain scan was normal, but the neck spine scan showed a blockage in the blood vessel that supplies the spine — a torn blood vessel (vertebral artery dissection). This blockage caused damage to the spinal cord. After three months of medicine to stop blood clots and prevent blood from sticking together (anticoagulation and antiplatelets), the blood vessel healed and the strength returned. He felt much better and could walk again. Doctors said he should keep coming back for check-ups, but he didn’t.\"\n}"}
{"row_index": 403, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 40-year-old man who was otherwise healthy suddenly developed weakness on his right side six days before coming to the hospital. The weakness started about 16 hours before admission and made it hard for him to lift his right arm or stand on his right leg. He had no history of neck injury, surgery, or infections, and had no diabetes or high blood pressure. He had smoked for 10 years.\\n\\nNeurological tests showed that his brain and speech were normal, but his right side had significant weakness. His right arm had only mild strength, his right leg had no strength, and his left side was normal. Sensation to pain and temperature was reduced on the left side below the neck, and reflexes were weak. These signs pointed to a condition called right-sided Brown-Séquard syndrome at the C3 level of the spinal cord.\\n\\nBrain scans (head CT and MRI) were normal. Cervical spine MRI showed swelling and damage to the right side of the spinal cord at the C1-C3 level, indicating a spinal cord infarction (blockage of blood flow). A high-resolution MRI scan (VISTA) revealed a tear in the vertebral artery on the right side at the same level, which is known as vertebral artery dissection (VAD). This dissection likely caused the blood clot that damaged the spinal cord.\\n\\nThe patient was treated with anticoagulation (to prevent blood clots) and antiplatelet medications (to reduce clotting) for three months. After this treatment, follow-up MRI scans showed that the spinal cord damage improved and the vertebral artery had begun to heal. His symptoms greatly improved, and he was able to walk again. He was discharged with a good recovery score and advised to follow up, though he chose not to.\"\n}"}
{"row_index": 404, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 40-year-old male building worker presented with acute onset of right-sided body weakness, initially manifesting as inability to lift the right upper limb and inability to stand on the right lower limb, which began 16 hours prior to hospital admission. There was no history of trauma, neck manipulation, surgery, or prior infectious illness. The patient had no history of diabetes and was normotensive. He was a chronic smoker with a 10-year history of tobacco use. Neurologic examination revealed intact consciousness and speech, with normal cranial nerve function. Using the Medical Research Council muscle grading scale, the right upper proximal limb demonstrated muscle power of 4/5, the right distal limb 2/5, and the right lower limb 0/5; contralateral limbs were intact at 5/5. Sensory deficits included loss of joint position and vibration sense in the right lower limb, impaired position sense in the right hand, and reduced pain and temperature sensation on the left side below the C3 level. The right ankle reflex was diminished. These findings are consistent with a right-sided Brown-Séquard syndrome at the C3 level. Deep sensation was preserved on the left side of the body. The Kernig sign was negative. Laboratory evaluations—including hematologic, biochemical, and immunologic parameters—were within normal limits. Cerebrospinal fluid obtained via lumbar puncture was unremarkable. Head CT and MRI were normal, excluding intracranial pathology. Cervical spine sagittal T2-weighted MRI demonstrated spinal cord swelling with a hyperintense lesion at the C1–C3 level. Axial T2-weighted sequences confirmed hyperintensity of the right spinal cord, consistent with spinal cord infarction (SCI). High-resolution 3D volumetric isotropic turbo spin echo (VISTA) MRI revealed asymmetric narrowing of the right vertebral artery at the C1–C3 level, with an eccentric high-signal intensity lesion parallel to the vessel lumen, indicative of vertebral artery dissection (VAD) with intramural hematoma. This finding established a pathophysiological link between the VAD and the ischemic spinal cord injury. The patient was treated with a combination of anticoagulant (AC) and antiplatelet (AP) therapy for a duration of 3 months. Follow-up MRI demonstrated a significant reduction in the abnormal spinal cord signal intensity, and VISTA imaging confirmed"}
{"row_index": 405, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 76-year-old man had pain in his right leg when walking, which meant his leg blood flow was blocked. Doctors found the blockage in the right leg artery using a scan. They fixed it with a small tube (stent-graft) placed inside the artery. After the fix, the man started having pain and swelling in his right thigh, but no fever or infection was found. Blood tests showed his body was inflamed, like it was fighting something. A scan showed swelling around the artery and signs of inflammation. Doctors gave him steroids to calm the swelling, and within 7 days, the pain went away. The steroid dose was slowly lowered over 3 weeks. A follow-up scan after 3 months showed the swelling and inflammation had mostly gone away. The fix worked and his leg pain is now better.\"\n}"}
{"row_index": 406, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 76-year-old man with pain in his right leg (claudication) was found to have a blockage in his right superficial femoral artery, confirmed by a CT scan. He had a history of high blood pressure, high cholesterol, and smoked in the past. Treatment involved endovascular therapy, where a stent-graft named Viabahn (25 cm, 5 mm diameter) was placed to open the blocked artery. During the procedure, ultrasound was used to guide the stent through the artery safely. After the procedure, the patient developed pain and swelling in his right thigh about 5 days later. Blood tests showed high levels of inflammation, and MRI scans showed swelling in the surrounding tissue and increased signal around the artery, suggesting inflammation around the stent. There was no sign of infection or blood clot. The doctors started steroid medication (prednisolone) to reduce the inflammation, and within 7 days, the symptoms went away. The steroid dose was slowly reduced over 3 weeks and stopped. Follow-up MRI scans showed that the swelling and inflammation had greatly improved over the next few months. The patient recovered well and his condition stabilized.\"\n}"}
{"row_index": 407, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 76-year-old male with peripheral arterial disease classified as Fontaine Stage IIB presented with right leg claudication. He had a history of hypertension, dyslipidemia, and current smoking. Preoperative contrast-enhanced computed tomography (CT) demonstrated a complete occlusion of the right superficial femoral artery (SFA). Antiplatelet therapy was initiated with 100 mg/day aspirin and 75 mg/day clopidogrel. Digital subtraction angiography revealed a 16-cm chronic total occlusion of the right SFA. Endovascular treatment (EVT) was performed under intra-arterial heparinization (5000 units). A 6-French guiding sheath was introduced via the left femoral artery. Intravascular ultrasound (IVUS) was utilized to navigate through the true lumen and confirm vessel patency, with no evidence of major dissection observed during pre-dilatation. A 4-mm semi-compliant balloon was used for pre-dilatation, followed by deployment of a 25-cm Viabahn stent-graft (diameter 5 mm) and post-dilatation with a 5-mm non-compliant balloon. Final angiographic assessment showed no edge dissection and confirmed adequate luminal patency and hemodynamic flow. The patient experienced symptomatic improvement and was discharged after 4 days. However, 6 days post-procedure, he developed acute pain and localized swelling in the right thigh. Venous thrombosis was ruled out by duplex ultrasound. Laboratory evaluation showed no signs of systemic infection: negative blood culture, procalcitonin level of 0.1 ng/ml (normal ≤0.5 ng/ml), and no fever. Nevertheless, inflammatory markers were significantly elevated: white blood cell (WBC) count of 12,000 cells/μl (normal range 4500–7500 cells/μl) and C-reactive protein (CRP) of 11.83 mg/dl (normal ≤1.0 mg/dl). Magnetic resonance imaging (MRI) revealed extensive soft-tissue edema and a high perivascular T2 signal surrounding the right SFA, consistent with perigraft inflammation. The stent-graft remained patent, indicating that the inflammatory response was localized to the perivascular tissue rather than involving graft failure. The clinical"}
{"row_index": 408, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old woman who drank a lot of vodka every day for years came to the hospital because she was scared and heard voices, thinking people were trying to hurt her. She had been drinking for a while and had been treated before for withdrawal, but left early. When doctors gave her a medicine called chlordiazepoxide to calm her down, she got worse—she became confused, saw things, and heard voices. But when they switched to another medicine, lorazepam, she started feeling better and soon stopped having those scary thoughts. After stopping all the medicines, she felt normal and stayed that way for hours. She’s now in a program to stop drinking and hasn’t had any more problems.\"\n}"}
{"row_index": 409, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 27-year-old white woman with a long history of heavy alcohol use developed symptoms of withdrawal when she stopped drinking. She was admitted to another hospital for withdrawal but left before being fully discharged. When she came to our hospital, she was paranoid, believed people were trying to harm her, and heard voices. Tests showed no signs of other illnesses or drug use, and her symptoms were linked to her alcohol dependence. She was given chlordiazepoxide, a benzodiazepine used to treat withdrawal, but within hours of each dose, she became more confused, agitated, and started hearing and seeing things that weren’t there. This worsened her delirium. After stopping chlordiazepoxide, she was given lorazepam, which helped calm her and improved her mental state. By the next day, she was calm, thinking clearly, and no longer had hallucinations or paranoia. She remained stable over the next 10 hours and was referred to a program for alcohol treatment, where she did not have any further mental health issues and did not need more benzodiazepines.\"\n}"}
{"row_index": 410, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 27-year-old Caucasian female with a established history of ethanol dependence presented to the emergency department (ED) for evaluation of possible psychosis in the context of ethanol withdrawal. Two days prior, she had been admitted to an external hospital for management of ethanol withdrawal, receiving intravenous fluids but not benzodiazepines (BNZs). She removed her intravenous line and left the facility prior to formal discharge. Her family subsequently brought her to our institution, reporting symptoms of paranoia and the belief that individuals outside her home were attempting to kill her. Her last known alcohol consumption occurred four days prior, and toxicology screening for ethanol, benzodiazepines, and barbiturates was negative in both serum and urine. She reported consuming at least five 'heavy pours' of vodka daily for several years, consistent with chronic heavy alcohol use. Physical examination revealed tachycardia (127–132 beats per minute), elevated blood pressure (143–149/102–103 mmHg), and mild tenderness on bilateral upper abdominal quadrant palpation. Despite these findings, she was calm, fully oriented, and exhibited organized thought processes, though she reported persistent paranoia involving family members intending harm and auditory hallucinations. A comprehensive medical workup for delirium was performed, including a normal complete blood count, a comprehensive metabolic panel showing mildly elevated transaminases [aspartate aminotransferase (AST) 94 U/L; alanine transaminase (ALT) 72 U/L], and a noncontrast computed tomography (CT) of the brain demonstrating mild diffuse cerebral volume loss exceeding age-matched expectations. These findings were attributed to chronic alcohol exposure and were not indicative of an independent neurodegenerative or infectious process. Urine and serum toxicology screens were negative for coronavirus (SARS-CoV-2), human immunodeficiency virus (HIV), and hepatitis B and C. The patient expressed a strong interest in achieving sustained sobriety. Initial management included oral lorazepam 2 mg, followed by initiation of chlordiazepoxide 25 mg twice daily due to persistent tachycardia and hypertension. Within two hours of each chlordiazepoxide dose, she developed acute confusion, agitation, and vivid visual and auditory hallucinations, including the perception of individuals on the other side of the door attempting to enter her room. After two doses ("}
{"row_index": 411, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 76-year-old woman noticed a small, slow-growing spot on her left breast for 5 years. It started growing faster recently, but she didn’t feel pain or any other symptoms. The spot was about 10 mm by 8 mm, blue-gray and looked like tiny pearls. Doctors checked her body and found no signs of cancer spreading. Tests showed no cancer in her chest, lymph nodes, or other parts of her body. A small biopsy confirmed it was a type of skin cancer called pigmented superficial BCC. She had surgery to remove the spot with a 10 mm safe edge around it. The doctors checked the edges right after surgery and found no cancer left. She went home the second day after surgery and has been feeling fine. At a 3-month check-up, there was no sign of the cancer coming back or spreading.\"\n}"}
{"row_index": 412, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 76-year-old Asian woman had a slowly growing spot on her left breast for 5 years, with recent faster growth. She had no pain, itching, or other symptoms. She did not have a history of cancer or major health conditions like high blood pressure, heart disease, or diabetes. Her family and personal history of skin or breast cancer was negative, and she had no significant sun exposure or radiation exposure.\\n\\nOn exam, a 10 mm × 8 mm blue-gray, pearl-like spot was found on the breast, with slight surface erosion. The rest of her body was normal. Imaging tests — including breast ultrasound, chest CT, SPECT-CT, and lymph node ultrasound — showed no signs of cancer spreading to other parts of the body.\\n\\nA biopsy confirmed the lesion was a type of skin cancer called pigmented superficial basal cell carcinoma (BCC). The cancer started in the top layer of the skin and had a characteristic appearance under the microscope.\\n\\nThe patient had surgery to remove the lesion, including the nipple and areola, with a 10 mm safety margin around it. During surgery, the doctors checked the edges of the removed tissue and found no remaining cancer cells. After the procedure, the patient was discharged on the second day and had a follow-up visit at 3 months. She remained symptom-free and showed no signs of cancer returning or spreading.\"\n}"}
{"row_index": 413, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 76-year-old Asian female presented with a 5-year history of a slowly enlarging lesion on the left breast, with recent acceleration in growth. She reported no pain, pruritus, or systemic symptoms. Medical history was notable for hyperlipidemia, with no comorbidities including hypertension, cardiovascular disease, diabetes, hepatitis, tuberculosis, immunosuppression, or arsenic exposure. There was no personal or familial history of skin or breast cancer, and no significant history of solar or ionizing radiation exposure.\\n\\nPhysical examination revealed a stable, otherwise well-appearing elderly patient without distress. The left breast demonstrated a 10 mm × 8 mm pigmented plaque with superficial erosion; surrounding skin was intact and unremarkable. No other abnormalities were detected.\\n\\nImaging modalities including breast ultrasound, chest computed tomography (CT), SPECT-CT, and axillary lymph node ultrasound were performed to assess for metastatic disease, all of which returned negative results, indicating no evidence of distant spread.\\n\\nDermoscopic evaluation of the lesion revealed characteristic features including multiple blue-gray globules, spoke-wheel patterns, leaf-like structures, and areas of erosion—findings consistent with pigmented basal cell carcinoma (BCC). Histopathological examination confirmed the presence of tumor nests originating from the superficial epidermis, exhibiting a palisading pattern of tumor cells with a narrow, pigmented cleft surrounding the nests—pathognomonic for pigmented superficial basal cell carcinoma.\\n\\nGiven the patient’s age, the absence of metastatic disease, and the benign clinical course, standard surgical excision was selected after shared decision-making with the patient and her family. The procedure involved complete removal of the nipple and areola with a 10 mm circumferential margin, followed by primary closure. The excised specimen measured 2.0 × 1.8 cm and extended into the subcutaneous adipose tissue layer. Intraoperative frozen section analysis and subsequent postoperative histopathological evaluation both confirmed clear margins, with no residual tumor cells at the surgical edges.\\n\\nThe patient was discharged on postoperative day 2. No adjuvant therapy was required due to the absence of microscopic residual disease. At a 3-month follow-up, the patient remained asymptomatic, with no clinical signs of local recurrence or metastatic progression. The lesion is currently considered fully resected with no evidence of disease recurrence in the"}
{"row_index": 414, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old woman had kidney problems and needed dialysis for 3 years. She started having bad shaking in her arms, neck, and legs, which got worse over 5 days. The shaking wasn’t just in one part — it spread to both sides of her body. A brain scan showed spots in the deep part of her brain (the basal ganglia) that were damaged, and these spots were the same on both sides. Doctors found that the shaking was likely caused by two things: bad waste from her kidneys and an overactive thyroid. She was treated with stronger dialysis, oxygen therapy, and medicine to fix her thyroid. After a month, the shaking stopped completely, and she could move her body normally again. Her brain scans showed the spots were mostly gone, and her blood tests showed her kidney and thyroid levels were getting better.\"\n}"}
{"row_index": 415, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old woman with chronic kidney disease had been on hemodialysis for 3 years. She started experiencing severe involuntary movements in her shoulders and neck about 5 days before being admitted to the hospital, which later spread to her limbs. Brain scans showed symmetric, non-hemorrhagic lesions in both sides of her brain’s basal ganglia, areas involved in movement control. These lesions were linked to a combination of uremic toxins (build-up from kidney failure) and hyperthyroidism (overactive thyroid). After treatment with high-frequency, high-flux dialysis, hyperbaric oxygen therapy, and medication to lower her parathyroid hormone levels, her symptoms improved significantly. Within a month, she regained full control of her movements and was discharged. Follow-up scans showed the brain lesions had mostly disappeared, and her blood tests showed improved levels of toxins and thyroid-related markers. The condition was diagnosed as a movement disorder caused by damage to the basal ganglia from kidney disease and thyroid issues.\"\n}"}
{"row_index": 416, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old female with non-diabetic chronic kidney disease underwent regular hemodialysis via a right forearm arteriovenous fistula for three years. She was admitted due to a five-day history of progressive involuntary movement, initially manifesting as a resting tremor in the shoulders and neck, which progressively evolved into generalized, uncontrolled limb movements. Vital signs were stable, with no evidence of headache, fever, visual disturbance, or cognitive impairment. Neurological examination revealed normal myodynamic parameters and deep tendon reflexes, with suspiciously positive Babinski signs indicating upper motor neuron involvement. Prior to admission, there was a documented history of significant blood creatinine fluctuations, primarily attributed to suboptimal dialysis, and a concurrent severe hyperthyroid state characterized by intact parathyroid hormone (iPTH) levels of 3200 pg/mL, with no prior history of hypertension, diabetes mellitus, respiratory infection, stroke, hepatic disease, hypoxia, or toxic exposure.\\n\\nBrain magnetic resonance imaging (MRI) performed five days after symptom onset demonstrated symmetrical hyperintense non-hemorrhagic lesions on T2-weighted imaging (T2WI) and T2/fluid-attenuated inversion recovery (T2FLAIR) sequences in the bilateral basal ganglia, consistent with acute or subacute neurotoxic injury. Additional findings included mild diffusion restriction in the corona radiata, suggestive of early ischemic or cytotoxic edema, while T1-weighted imaging (T1WI) and diffusion-weighted imaging (DWI) remained within normal limits, indicating no acute cytotoxic or hemorrhagic change. These findings are consistent with a neurodegenerative or neurotoxic process affecting the basal ganglia circuitry, particularly the striatum, which is critical for motor control.\\n\\nInitial blood work upon admission revealed markedly elevated uremic toxin levels: urea nitrogen 25.80 mmol/L, serum creatinine 1206 μmol/L, uric acid 548 μmol/L, phosphorus 1.88 mmol/L, calcium 2.33 mmol/L, and anion gap 23.9 mmol/L—indicative of severe uremic burden and metabolic derangement. Hyperthyroidism was confirmed with iPTH of 2487 pg/mL, suggesting a state of secondary hyperparathyroidism likely secondary to chronic uremia and"}
{"row_index": 417, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 68-year-old woman had numbness in her left arm and pain in her neck. Doctors found a problem with blood vessels in her neck that were pressing on her nerves and spine. This caused her arm to feel numb and weak, and her shoulder to hurt. Tests showed a strange blood vessel connection (like a leak) between her left neck blood vessel and a vein near the spine, at the C5 level. The doctors fixed it using a small tube and special coils placed through her leg artery. They used a balloon to hold the tube in place and put the coils tightly to stop the leak. After the fix, the pain and numbness went away. The woman fully recovered, with no return of the leak or symptoms, and her nerves were no longer being pressed. Four years later, MRI showed the blood vessel problem was completely gone and her arm and neck were back to normal.\"\n}"}
{"row_index": 418, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old woman came in with numbness in her left arm and pain in her neck. At first, doctors thought it was a musculoskeletal issue, but her symptoms got worse over time. Imaging tests showed abnormal blood vessels pressing on the nerves and spinal cord in her neck, specifically between the C4 and C6 levels. This was confirmed by MRI and angiography, which found a large blood vessel connection — called a VVAVF — between the left vertebral artery and the vertebral venous plexus at the C5 level. This abnormal connection was causing the nerve compression and pain.\\n\\nTo fix it, the patient underwent a minimally invasive procedure under general anesthesia. A small catheter was inserted through her right femoral artery and guided to the area of the blood vessel connection in her neck. Using a special technique with tiny coils and a balloon to keep the catheter stable, doctors successfully blocked the abnormal blood flow. The procedure was done carefully to avoid damaging nearby blood vessels.\\n\\nAfter the treatment, the patient’s pain and numbness improved within a month. Four years later, she is doing well with no return of symptoms. Follow-up MRI scans show that the abnormal blood vessel is gone and the nerves are no longer compressed. The left vertebral artery remains open and healthy, and there has been no leakage or complications. She was able to recover fully and has returned to normal daily life.\"\n}"}
{"row_index": 419, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old woman with no prior history of trauma or vascular disease presented to the orthopedic surgery department for progressive left upper limb numbness and left neck pain. Noncontrast head CT and cervical spine X-ray were unremarkable, and initial management included analgesics, with no improvement over a 12-month period. Cervical magnetic resonance imaging (MRI) revealed an extramedullary lesion characterized by flow voids and abnormal vascular morphology adjacent to the left neural foramen from C4 to C6, demonstrating compression of spinal nerve roots and the spinal cord. Neurological examination confirmed left C5 radiculopathy, with hyperesthesia in the left arm and scapula, and weakness in the left deltoid and biceps brachii muscles. A vascular murmur was auscultated in the left neck, suggesting a high-flow vascular abnormality.\\n\\nMR angiography (MRA) identified a left vertebral-vertebral venous arteriovenous fistula (VVAVF) with ectasia of the left vertebral artery (VA), but could not precisely localize the fistulous point. Left vertebral artery digital subtraction angiography (DSA) confirmed a high-flow VVAVF connecting the left VA to the vertebral venous plexus, with a single, well-defined fistulous origin at the C5 level within the V2 segment. The fistula drained into the anterior internal vertebral venous plexus, forming a large venous network. No filling of the fistula was observed from the anterior cerebral circulation, confirming the absence of collateral flow from the anterior circulation. The contralateral vertebrobasilar circulation remained intact, with no evidence of steal phenomenon, indicating that the fistula was isolated to the left side.\\n\\nThe treatment strategy involved targeted microballoon-assisted coil embolization of the expanded paravertebral venous plexus to achieve complete occlusion of the shunt. Preoperatively, heparin (3000 IU intravenously) was administered to prevent thrombosis. Under general anesthesia, a 10 cm, 7-French femoral short sheath (TERUMO) was inserted into the right common femoral artery. A 90 cm, 7-French Guider Guiding Catheter ST (Stryker Japan) was advanced into the left vertebral artery. A 150 cm,"}
{"row_index": 420, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 26-year-old man had fever, chills, headache, nausea, vomiting, and diarrhea 5 weeks after getting COVID-19. Tests showed he had been infected before, even though the virus wasn't found in his body anymore. He suddenly got very weak and his heart stopped pumping well — it was in shock. Doctors gave him medicine to help his heart beat and to get rid of extra fluid. They were worried it might be a serious heart infection, so they took a small sample of heart tissue. The test showed the heart was inflamed, but mostly with macrophages (a type of immune cell), not the kind that usually means a serious heart attack. This matched what's seen in some people who had COVID-19 and got a bad heart reaction. They called it MIS-A. He also had blood clots in his lungs, which made him short of breath. He got IVIG, steroids, and blood thinners, and started feeling better. His heart function improved, and by the end, it was working normally again. He can now exercise without limits, but is advised to avoid very intense activity. He’s on heart medicine and going to a cardiac rehab program. A follow-up scan will check how his heart is doing long-term.\"\n}"}
{"row_index": 421, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 26-year-old man developed high fever, chills, headache, nausea, vomiting, and diarrhea about 5 weeks after recovering from COVID-19. Tests showed he had been infected with the virus in the past, but no active virus was found in his body. He was found to be in severe heart failure, with both sides of his heart not pumping properly, leading to low blood pressure and poor oxygen levels. He needed strong medications like inotropes and diuretics to support his heart function. Doctors were worried he might have had a serious heart inflammation called myocarditis, so they performed a heart tissue biopsy. The results showed mainly inflammation from macrophages (a type of immune cell), with only a few T cells, which is similar to what's seen in some COVID-19 patients. This helped rule out full-blown myocarditis and supported a diagnosis of MIS-A (Multisystem Inflammatory Syndrome in Adults), a rare condition that can occur after a COVID-19 infection. He also had blood clots in his lungs, which were treated with anticoagulation therapy. He received intravenous immunoglobulin (IVIg) and steroids to reduce inflammation, and his condition improved quickly. After recovery, his heart function returned to normal, and he was able to resume normal activities. He is now on long-term heart medications, advised to avoid very intense exercise, and is following a cardiac rehabilitation program. A follow-up heart MRI is planned to better understand the heart damage.\"\n}"}
{"row_index": 422, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 26-year-old male presented with a 1-week history of fevers (peak 39.2°C), chills, headache, nausea, vomiting, and diarrhea. On emergency department evaluation, he was hypotensive (75/35 mmHg), tachycardic (126 beats per minute), and had an oxygen saturation of 96% on 6 L nasal cannula. Laboratory findings included leukocytosis (WBC 17.1 × 10⁹/L), lymphopenia (absolute lymphocyte count 0.73 × 10⁹/L), acute kidney injury (serum creatinine 1.9 mg/dL), lactic acidosis (lactate 4.1 mmol/L), and elevated cardiac troponin T (0.218 µg/L, above normal range <0.09 µg/L). SARS-CoV-2 PCR was negative, but SARS-CoV-2 IgG was positive, confirming prior infection. Point-of-care ultrasound revealed severely reduced biventricular function, consistent with cardiogenic shock. The patient was admitted to the cardiac care unit and initiated on intravenous diuresis and inotropes for hemodynamic support.\\n\\nFurther laboratory evaluation demonstrated elevations in transaminases, procalcitonin, NT-proBNP, ferritin, D-dimer, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP), indicating systemic inflammation and organ stress. Chest x-ray showed right lower lobe and left lower lobe opacities, with a borderline enlarged cardiac silhouette. Electrocardiogram revealed sinus tachycardia and right axis deviation. Echocardiography revealed a left ventricular ejection fraction (LVEF) of 20%, global hypokinesis, mild left ventricular dilation, biatrial enlargement, hypokinetic and dilated right ventricle, moderate to severe mitral regurgitation due to leaflet tethering, severe tricuspid regurgitation, small pericardial effusion, and an estimated pulmonary artery systolic pressure of 53 mmHg with a right atrial pressure of 15 mmHg.\\n\\nA bedside pulmonary artery catheter was placed on admission, revealing right atrial pressure (RA) of 17 mmHg"}
{"row_index": 423, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A young man from Serbia had a very weak heart and couldn't get enough oxygen, so doctors put in a machine to help his heart work. His heart was failing on both sides, and tests showed his heart muscle was full of iron, which made it weak. This iron buildup was causing his heart to stop working properly. Doctors found a gene problem that causes a rare condition called juvenile hemochromatosis — a condition where the body absorbs too much iron. This iron damage also hurt his pancreas, making him develop diabetes, and his body wasn’t making enough hormones for energy. He got a special heart pump to help his heart, and after a few months, his heart started to get better. The iron was removed with medicine, and his heart function improved so much that the pump was safely taken out after 131 days. His heart is now working well, and his iron levels are back to normal. He still needs insulin and regular blood removal to keep iron low, and he’s doing well and back to work.\"\n}"}
{"row_index": 424, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 31-year-old Serbian man with severe heart failure due to iron overload was treated with life-support devices and eventually recovered. He had been diagnosed with iron buildup in his body four months earlier, which caused fatigue and other symptoms. His iron levels were very high — serum ferritin was 2,541 μg/L (normal is 30–500) and transferrin saturation was 90% (normal is 10–45%). Despite normal liver and kidney function, tests showed iron was damaging his heart, leading to very weak heart function with an ejection fraction of only 5–10%. He also developed diabetes due to iron damage to the pancreas, with poor insulin production.\\n\\nHe was admitted to the ICU and started on extracorporeal membrane oxygenation (ECMO) to support his heart and lungs. After a few days, he received biventricular assist devices (BiVAD) to help his heart pump blood. A heart biopsy showed iron deposits in the heart muscle, confirming iron overload as the cause of his heart failure. He began iron chelation therapy with desferrioxamine, which quickly reduced his iron levels. His heart function improved over time, and after 131 days, the BiVAD was successfully removed.\\n\\nGenetic testing revealed a mutation in the HJV gene (called G320V), which is linked to a rare condition called juvenile hemochromatosis — a form of iron overload that can affect the heart and pancreas, especially in young people. This condition often has no family history, which is what this patient had. He continues to receive insulin for diabetes, testosterone for low hormone levels, and regular blood removals (venesections) to manage iron. After 12 months, his heart function had returned to near normal, and follow-up scans showed no significant iron left in his heart or liver. He has returned to work and is doing well.\"\n}"}
{"row_index": 425, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 31-year-old male of Serbian origin presented to a quaternary intensive care unit (ICU) with severe biventricular heart failure refractory to maximal inotropic support, characterized by a cardiac index of 1.3 L/min/m² on noradrenaline and dobutamine infusion. He presented with acute shortness of breath, extreme lethargy, and abdominal pain, with clinical signs of hypotension and sinus tachycardia (HR 105 bpm). Physical examination revealed a hyperdynamic apex beat with heave, jugular venous pulsation of 2–3 cm, and dual heart sounds without murmurs. Neurological status was assessed as Glasgow Coma Score 14 (E3, M5, V6). Abdominal examination showed tenderness in the right upper and lower quadrants without guarding. Notably, he had a tanned skin appearance and no peripheral edema. Laboratory investigations on admission revealed normal hemoglobin, platelets, renal function, and electrolytes, but mild derangement of liver function with elevated alanine aminotransferase (88 U/L), bilirubin (62 μmol/L), and decreased albumin (30 g/L). C-reactive protein (9 mg/L) and neutrophil count (10.27 ×10⁹/L) were mildly elevated, while white blood cell count remained within normal limits. High-sensitivity troponin I was mildly elevated (64 ng/L), suggesting subclinical myocardial injury. Urine and blood cultures were negative. Imaging demonstrated a dilated heart with pleural effusions, ascites, and liver congestion. Transthoracic echocardiography revealed severe global systolic dysfunction with left ventricular ejection fraction (LVEF) of 5–10%, right ventricular dysfunction, and mild to moderate mitral and pulmonary regurgitation, with no evidence of myocarditis or coronary artery disease.\\n\\nThe patient had a prior diagnosis of iron overload, initially identified 4 months earlier, with serum ferritin of 2541 μg/L (reference range 30–500) and transferrin saturation (TS) of 90% (reference range 10–45%). Liver biopsy showed extensive intrahepatocyte iron accumulation with minimal inflammatory infiltrate and fibrosis (hepatic iron index 1"}
{"row_index": 426, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 43-year-old Black woman had a painful lump on the outside of her vagina on the left side. Doctors thought it was a common infection called a Bartholin's abscess and cut it out to drain the fluid. While doing that, they found a small, tan-brown bump nearby. That bump turned out to be a harmless growth called hidradenoma papilliferum, which is like a small, slow-growing bump in the skin that can sometimes get confused with an infection. It’s not serious and doesn’t need treatment unless it causes trouble.\"\n}"}
{"row_index": 427, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 43-year-old African American woman had a painful lump on her left labia majora. Doctors initially diagnosed it as a Bartholin's abscess, which is a common infection in the glands near the vaginal opening. During surgery to remove and drain the abscess, they found an additional tan-brown lump nearby. This second lump was tested under a microscope and showed features of a condition called hidradenoma papilliferum, which is a type of benign (non-cancerous) growth that can develop in the skin. The findings suggest that the abscess formed inside this existing growth. Both conditions are not serious and were successfully treated.\"\n}"}
{"row_index": 428, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 43-year-old African American woman presented with a painful cystic mass on the left labia majora. Preoperative imaging and clinical evaluation led to a diagnosis of Bartholin's abscess, a common benign inflammatory condition resulting from obstruction and infection of the Bartholin's gland ducts, typically involving ductal epithelial proliferation and subsequent suppuration. During surgical excision and drainage of the abscess, an additional dermal nodule measuring 2.0 × 0.8 × 0.8 cm was identified and removed for histopathological assessment. The nodule exhibited a tan-brown color consistent with chronic dermal fibrosis and adipocytic infiltration. Microscopic examination revealed fibro-necrotic foci intermingled with a well-circumscribed papillary neoplasm characterized by cystic dilation of the glandular projections. The papillary architecture was lined by basophilic cuboidal to columnar epithelial cells, with a distinct layer of compressed myoepithelial cells at the basal margin, indicating a differentiated glandular origin. Immunohistochemical staining confirmed apocrine differentiation, evidenced by the presence of foci of active decapitation secretion—where secretory vesicles are cleaved off the apical surface of the epithelial cells—suggesting functional apocrine glandular activity. The presence of these features, particularly the well-defined papillary architecture with apocrine and decapitation secretion, is consistent with Hidradenoma papilliferum, a rare benign adnexal tumor of the eccrine or apocrine sweat glands, often arising in the perineal region. The clinical scenario demonstrates a rare overlap where a Bartholin's abscess develops in the context of a pre-existing hidradenoma papilliferum, suggesting that the underlying dermal lesion may have been a latent neoplasm that became inflamed and infected. This finding underscores the importance of thorough histopathological evaluation in perineal masses, as the presence of a hidradenoma papilliferum may be missed in routine diagnosis and may have implications for long-term monitoring due to its potential for local recurrence or transformation in rare cases. The diagnosis was ultimately established as a Bartholin's abscess arising within a hidradenoma papilliferum, with the histological features supporting both the inflammatory and neoplastic components of the lesion.\"\n}"}
{"row_index": 429, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 71-year-old man had heart problems since he was a kid. His heart didn’t work well because of a big hole in the heart and a blocked lung valve, which doctors call unrepaired TOF. He had a small tube (shunt) put in when he was 19 to help blood flow, but never had the full fix. Over the years, he had heart failure three times — at 50, 70, and 71 — but kept playing golf and living a normal life until then. When he came to our hospital, his heart was weak, had high pressure, and was not pumping blood well. Tests showed his heart had a big hole, a thick right ventricle, and a narrow lung valve. His blood was thick and his heart was working hard. Even though he couldn’t have the full surgery because of his other health issues, his doctors fixed his heart rhythm with medicine and a tiny device that shocks the heart if it goes wrong. They also gave him medicine to help his heart pump better. After a month in the hospital, his heart started working much better. One year later, he’s doing great — no more shortness of breath, and he’s still playing golf.\"\n}"}
{"row_index": 430, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 71-year-old man with a history of heart failure had a sudden heart stoppage (cardiopulmonary arrest) caused by a fast, irregular heart rhythm (ventricular fibrillation). Thanks to quick action by bystanders, he survived without brain damage. His low potassium levels were thought to have triggered the heart rhythm problem. He was referred to our clinic for further care.\\n\\nHe had a heart murmur since childhood and was diagnosed with a serious heart condition called tetralogy of Fallot (TOF) at age 19. At 21, he had a shunt procedure (Blalock-Taussig) to help blood flow, but he never had the full repair surgery, which was recommended. For years, he was able to work and play golf without symptoms, but started having heart failure at ages 50, 70, and 71.\\n\\nAt the clinic, his blood pressure and heart rate were normal, but he had low oxygen levels and signs of poor heart function, like blue lips and clubbing. His heart scan showed a large hole in the heart (ventricular septal defect) with the aorta overriding it, thickened right ventricle, and severe narrowing of the pulmonary valve—all signs of an unrepaired TOF. A shunt from his childhood was still present. His heart was not pumping well, and the right side of the heart was enlarged and weak.\\n\\nTests showed he had blocked coronary arteries, which can damage the heart muscle. Because of his many health problems, the full heart surgery was not done. Instead, he received medication to control his heart rhythm and improve blood flow. He had a device implanted to prevent sudden, dangerous heart rhythms. His doctors carefully adjusted his medications, which helped his symptoms improve.\\n\\nOne year after being discharged, he was doing well and was able to play golf again. His heart failure symptoms had improved enough that he could now walk around without severe shortness of breath.\"\n}"}
{"row_index": 431, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 71-year-old male with a history of chronic kidney disease, paroxysmal atrial fibrillation (AF), and chronic heart failure experienced cardiopulmonary arrest secondary to unexpected ventricular fibrillation (VF). Bystander-initiated cardiopulmonary resuscitation was promptly initiated, resulting in complete recovery without neurological sequelae. Upon prior admission, serum potassium was found to be hypokalemic at 3.3 mEq/L, leading to the hypothesis that incidental hypokalaemia contributed to the induction of VF. The patient was referred to our institution for comprehensive evaluation of his cardiac and systemic status.\\n\\nClinical history revealed a lifelong presence of a heart murmur, initially unrecognized and uninvestigated. At age 19, the patient was diagnosed with tetralogy of Fallot (TOF) and underwent palliative Blalock–Taussig shunt placement at age 21. Despite recommendations for radical intracardiac repair, the patient declined further surgical intervention. For several decades, he maintained an active lifestyle, including employment and regular participation in golf, without overt symptoms of heart failure; however, he was hospitalized at ages 50, 70, and 71 due to progressive decompensated heart failure.\\n\\nOn presentation, vital signs included a blood pressure of 114/58 mmHg, heart rate of 69 beats per minute, and oxygen saturation of 89% in ambient air. Physical examination demonstrated lip cyanosis and clubbing, with no evidence of peripheral edema. Cardiac auscultation revealed a harsh systolic ejection murmur localized to the 2nd to 4th intercostal spaces along the left sternal border. Laboratory findings included polycythaemia (hemoglobin 18.0 g/dL, hematocrit 52.6%), serum creatinine of 1.8 mg/dL, and markedly elevated brain natriuretic peptide (BNP) at 697 pg/mL. Chest radiography showed a characteristic 'boot-shaped' cardiac silhouette with bilateral pleural effusions. Electrocardiography confirmed the presence of atrial fibrillation.\\n\\nTransthoracic echocardiography demonstrated aortic overriding over a large ventricular septal defect (VSD) measuring 32 mm in diameter, right ventricular (RV) hypertrophy, and severe pulmonary sten"}
{"row_index": 432, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man took simvastatin for seven years to lower his cholesterol. Over time, he started getting weaker, especially in his arms and legs, and couldn't climb stairs or stand up on his own. He also lost a lot of weight. Tests showed his muscle damage was very bad — his muscle enzyme level was very high, and his body made antibodies against a protein that helps make cholesterol. A muscle biopsy showed dead muscle fibers, some new ones growing, and signs of inflammation. This condition is called SINAM, which happens when a statin drug causes the body’s immune system to attack muscles. The doctor stopped the statin and gave him strong steroids, immune shots, and methotrexate to calm the immune attack. After three months, his muscle strength came back, the enzyme level went back to normal, and he could move around again without help.\"\n}"}
{"row_index": 433, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 70-year-old woman had been taking simvastatin for seven years to lower her cholesterol. Over time, she started feeling increasing weakness in her muscles, especially when climbing stairs or getting up from a chair. Her weakness got worse until she could no longer walk without help or do basic tasks like combing her hair or bathing. She also lost 15% of her weight over 10 months and had no fever, rash, or other signs of infection.\\n\\nTests showed very high levels of creatine kinase (a marker of muscle damage) at 2,954 U/L, and blood tests found positive antibodies to HMG-CoA reductase, a protein targeted by statins. A muscle biopsy showed signs of muscle damage, including dead muscle fibers, some new growing fibers, and inflammation around the muscle tissue. The muscle also had a higher-than-normal level of a protein called MHC class I, which is linked to immune activity.\\n\\nAfter doctors ruled out infections, cancer, and other conditions, they diagnosed her with SINAM — a rare condition where a statin drug causes an autoimmune reaction that attacks the muscles. The simvastatin was stopped immediately. She started treatment with high-dose corticosteroids (a type of anti-inflammatory drug), intravenous immunoglobulin (to calm the immune system), and methotrexate (an immune-suppressing medication).\\n\\nAfter three months, her muscle strength improved significantly, and her creatine kinase level dropped back to normal (15 U/L). She is now on a lower dose of steroids and methotrexate, and her symptoms have mostly gone away.\"\n}"}
{"row_index": 434, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 70-year-old woman with a history of hypertension, type 2 diabetes mellitus, hyperlipidemia, ischemic heart disease, and degenerative joint disease presented with progressive proximal muscle weakness and myalgia over several months. She had been on simvastatin 20 mg/day for the prior seven years, which was discontinued upon diagnosis. Clinical manifestations included impaired functional mobility—difficulty climbing stairs, rising from a chair, combing hair, and bathing—accompanied by a 15% weight loss over 10 months. She denied systemic symptoms such as fever, rash, oral ulcers, dyspnea, chest pain, dysphagia, or visual disturbances, and there was no family history of neuromuscular disorders.\\n\\nPhysical examination revealed significant proximal muscle weakness on the Medical Research Council (MRC) scale: shoulder abduction 3/5, elbow flexion 4/5, hip flexion 3/5, knee flexion 4/5 bilaterally. She was unable to rise from a sitting position. Deep tendon reflexes, sensory function, and coordination were preserved. No abnormalities were detected on cardiac, pulmonary, or abdominal examination. Cutaneous signs suggestive of dermatomyositis were absent.\\n\\nLaboratory findings demonstrated markedly elevated creatine kinase (CK) at 2,954 U/L (reference range: 10–149 U/L), aldolase at 45.6 U/L (reference <7.6 U/L), aspartate transaminase (124 U/L, reference 10–31 U/L), and alanine transaminase (95 U/L, reference 10–31 U/L), indicating muscle damage and hepatocellular involvement. Serologic testing for viral infections—including herpes simplex virus, Epstein-Barr virus, cytomegalovirus, varicella-zoster virus, human immunodeficiency virus, and hepatitis C—was negative. Hepatitis B serology revealed past exposure (HBV DNA negative), and thyroid function tests were within normal limits.\\n\\nNerve conduction studies and electromyography (EMG) revealed abnormal spontaneous electrical activity in proximal muscles of the upper and lower extremities, consistent with an irritable myopathy. Muscle biopsy of the right deltoid demonstrated deep myopathic pathology characterized by widespread necrotic muscle fibers, scattered regenerating fibers"}
{"row_index": 435, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A Chinese boy had two bad episodes when he was 6 and 8 years old. Each time, he got very sick with vomiting, diarrhea, and belly pain, which made his body not get enough blood. His blood pressure dropped very low, and he was very weak. Doctors gave him fluids to help, but the second time, even after giving lots of fluids, his blood pressure stayed low. His heart was not working well — the walls of his heart were thick and stiff. Tests showed his heart wasn’t pumping properly, and he needed a machine called ECMO to help his heart and lungs breathe. After using the machine, his heart started to work better again. The thick heart walls went back to normal over time. Doctors found that his body had swelling in the heart that went away. All his tests matched a condition called ISCLS. Now, he’s healthy, has no symptoms for over a year, and his heart is fully back to normal. He still has a little nerve problem in his leg, but it’s not hurting him anymore.\"\n}"}
{"row_index": 436, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A Chinese boy had two serious episodes of hypovolaemic shock, starting at age 6 and again at age 8. The first time, he had symptoms like cold, runny nose, vomiting, and stomach pain, which led to low blood pressure and a fast heart rate. He was treated with fluids and antibiotics, and his condition improved. An echo test showed a thickened heart muscle, but it returned to normal a month later. After being healthy again, he had a second episode at age 8 with similar symptoms, but this time his blood pressure stayed very low despite large fluid doses. His heart function was severely weakened, and he needed emergency treatment with powerful medications and was transferred to a specialized cardiac unit. He received extracorporeal membrane oxygenation (ECMO) support, which helped stabilize his heart and lungs. During recovery, his heart function improved significantly, and follow-up echo tests showed normal heart wall thickness and full recovery of heart function. The medical team found that his symptoms were consistent with a rare condition called ISCLS, which is linked to immune system issues. He now takes montelukast daily and receives regular immunoglobulin infusions to prevent future episodes. While he still has some lingering nerve issues, he has been symptom-free for over a year and his heart function is fully recovered.\"\n}"}
{"row_index": 437, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A Chinese boy with a history of eczema and obesity presented with two distinct episodes of anasarca and hypovolaemic shock. The first episode occurred at age 6 years, following a two-day course of coryzal symptoms, followed by one day of vomiting, diarrhoea, and generalized abdominal pain. On presentation, his blood pressure was 85/66 mmHg and heart rate was 144 beats per minute. He rapidly progressed to hypovolaemic shock requiring admission to a paediatric intensive care unit for fluid resuscitation. Laboratory findings included haemoconcentration, hypoalbuminemia, renal impairment, and metabolic acidosis. Echocardiography revealed left ventricular wall thickening. Blood culture yielded coagulase-negative staphylococci, interpreted as a skin contaminant. The patient was managed with intravenous fluid resuscitation and a seven-day course of ceftriaxone; renal function normalized following fluid therapy, and he was discharged after one week. A follow-up echocardiogram one month later demonstrated normal ventricular wall thickness, structure, and function.\\n\\nBetween episodes, the patient remained asymptomatic until age 8 years, when he presented with one-day history of vomiting, diarrhoea, abdominal pain, and low-grade fever. He was admitted again and developed lethargy, hypotension (76/52 mmHg), tachycardia (141 bpm), and signs of poor perfusion. Despite administration of a total of 3500 mL (70 mL/kg) of normal saline boluses over 8 hours, only transient improvements were observed, with persistent hypotension. Laboratory findings mirrored the first episode: haemoconcentration, hypoalbuminemia, impaired renal function, and metabolic acidosis. Echocardiography from the referring hospital showed significant left ventricular wall thickening, with interventricular septum thickness of 11.9 mm (Z-score +13.34) and free wall thickness of 14.2 mm (Z-score +16.22).\\n\\nHis haemodynamic instability persisted despite additional fluid resuscitation (total 3500 mL over 12 hours) and administration of multiple inotropic agents, including dopamine, dobutamine, noradrenaline, and stress-dose hydrocortisone."}
{"row_index": 438, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 66-year-old man came to the hospital because his right leg was swollen and painful. Tests showed a blood clot in the right leg vein. Doctors found a strange connection in his veins: instead of the usual path, the vein on the left side drained into a different vein called the hemiazygos vein, and his liver vein went straight into the heart. This changed how blood flowed in his body, and it was likely caused by a blockage in the main vein behind the spine. His right leg had a clot, and the left leg’s vein was wider and better able to carry blood, which helped compensate. There was no normal vein behind the liver, and the blood from the liver went directly into the heart. This is a rare way blood flows, but it's not dangerous on its own.\"\n}"}
{"row_index": 439, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 66-year-old man was admitted to the hospital because of a blood clot in his right leg. Imaging showed that his body’s main vein on the left side (the IVC) had abnormally drained into the hemiazygos vein instead of going to the heart normally. His liver’s vein drained directly into the heart, bypassing the usual path. This unusual connection was likely caused by a previous blockage in the pelvic veins, which led to the left side of his venous system forming a new path. The clot was in the right leg, and the patient had no other symptoms like fever or chest pain. Tests showed elevated levels of a clot marker (D-dimer) and confirmed the clot in the femoral vein. The imaging also revealed that the right common iliac vein was compressed and narrowed, leading to poor blood flow and the development of collateral veins. This condition is rare and affects how blood flows from the legs to the heart, especially on the left side of the body.\"\n}"}
{"row_index": 440, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 66-year-old male was admitted to the hospital with a 2-day history of pain and edema in the right lower extremity, without fever, chest pain, or dyspnea. Prior to admission, he had sustained multiple soft tissue injuries from falls 12 days earlier. There was no significant personal or family history of vascular disease or thrombotic events. Physical examination revealed bilateral swelling of the right leg with palpable pitting edema, normal skin temperature, and intact arterial pulsations. Laboratory evaluation showed a D-dimer level of 2789 ng/mL (normal range: 0–500 ng/mL), indicating a high probability of thrombosis. Color Doppler ultrasonography confirmed right iliac-femoral vein thrombosis with markedly reduced distal blood flow velocity. Following thrombolysis, contrast-enhanced computed tomography was performed to evaluate the retroperitoneal venous anatomy and revealed a congenital anomaly of venous drainage: the right common iliac vein was located posterior to the left common iliac artery and exhibited significant compression and stenosis, resulting in collateral vessel formation in the pelvic region. The left iliac vein was markedly wider than the right, suggesting asymmetrical venous development. An abnormal left-sided inferior vena cava (IVC) was identified, formed by the union of the two common iliac veins at the level of the fourth lumbar vertebra. This left IVC ascended vertically to the left of the abdominal aorta, where it received contributions from the left renal vein at the level of the second lumbar vertebra and the right renal vein at the level of the third lumbar vertebra, with the latter crossing posteriorly over the abdominal aorta. The left IVC continued its ascent, intersecting the hemiazygos vein at the level of the second lumbar vertebra, then traversed posterior to the left diaphragmatic crura and entered the thorax. It ascended through the posterior mediastinum, passing posterior to the thoracic aorta and the azygos vein at the level of the eighth thoracic vertebra, arching over the root of the right lung, and ultimately joining the right superior vena cava at the level of the fifth thoracic vertebra. Notably, this patient lacked a retrohepatic IVC or a right-sided IVC, and the hepatic veins drained directly into the right atrium"}
{"row_index": 441, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 7-month-old baby started having trouble sitting up and her body started shaking, especially in her head, arms, and legs, about 48 hours after getting the second dose of the MenB vaccine. She had a fever and threw up before, but those went away when she came to the hospital. The doctors checked everything — blood tests, brain scans, and tests for infections — and found nothing wrong. No virus, no bacteria, no other cause could explain her symptoms. The doctors looked at past cases of similar problems in children and found that shaking and balance issues after infections or vaccines are very rare in babies under one year old. They studied 1663 cases from the last 30 years to understand this. The baby’s symptoms got better over 8 days, and by one month, she was sitting still without shaking or falling again. The doctors think the vaccine might have started the problem, but it was very rare and not something that happens often.\"\n}"}
{"row_index": 442, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 7-month-old girl developed acute ataxia and cerebellitis within 24 hours of receiving the second dose of the MenB vaccine. She had previously been healthy and had no known medical problems. Her symptoms included difficulty sitting steadily, uncontrolled shaking movements in her head, arms, and body, and fever that resolved by the time she was admitted to the hospital. She had received the first dose of the MenB vaccine at 5 months, and the second dose 72 hours before her symptoms started.\\n\\nDoctors performed a wide range of tests — including blood work, spinal fluid analysis, imaging scans of the brain and spine, and tests for viruses and bacteria — to rule out infections, genetic conditions, or other serious causes. All tests came back normal. No infection or autoimmune cause was found.\\n\\nBecause the symptoms began right after the vaccine, doctors considered a possible link to the vaccine. They reviewed 20 studies from the past 30 years involving 1,663 patients with similar symptoms, and found that ataxia or cerebellitis caused by infections or other conditions is very rare in children under one year old. This case is unusual because it happened so soon after vaccination and in such a young child.\\n\\nThe girl’s condition improved over 8 days, and by one month, she was able to sit steadily without any shaking or balance problems. No long-term effects were found. A report was filed with health authorities to monitor similar cases in the future.\"\n}"}
{"row_index": 443, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 7-month-old female presented with acute cerebellar ataxia (ACA) within 24 hours of receiving the second dose of MenB vaccine (Bexsero, Novartis Vaccines and Diagnostics S.r.l., Siena, Italy). The clinical presentation included impaired sitting balance, previously achieved at 3 weeks of age, with new-onset abnormal involuntary and oscillatory movements affecting the head, limbs, and trunk. Postural control while unsupported was severely compromised, with sustained oscillations and falls. Symptoms began approximately 48 hours prior to presentation and were accompanied by fever and vomiting, both of which resolved at admission. The patient had a unremarkable prenatal and perinatal history, including spontaneous vaginal delivery at 39 weeks gestation, birth weight of 3020 g, Apgar score of 9 at 1 minute, and normal neonatal screening for congenital hypothyroidism, phenylketonuria, cystic fibrosis, and 17-hydroxyprogesterone. She was exclusively breastfed, with a transient episode of cyanosis on day two of life, which was managed appropriately. Vital signs and echocardiography were within normal limits; a mild thrombocytopenia at birth resolved by follow-up. Developmental milestones were otherwise age-appropriate.\\n\\nVaccination history revealed prior administration of the hexavalent vaccine (DTaP-Hib-IPV-HepB) at 3 and 5 months of age, with no adverse events reported. The MenB vaccine was administered at 5 months, coinciding with the onset of symptoms. On physical examination, the patient was alert, without nystagmus or saccadic eye movements, with normal optic fundi and cranial nerve function, and intact tendon reflexes.\\n\\nTo exclude infectious meningoencephalitis, a comprehensive diagnostic workup was performed, including blood chemistry, leukocyte count, acute phase proteins, electrolytes, and serologies for adenovirus, cytomegalovirus, Epstein-Barr virus, coxsackievirus, herpes simplex virus, human herpesvirus 6, Mycoplasma pneumoniae, and parvovirus B19—all of which were negative. Cerebrospinal fluid (CSF) analysis revealed a white blood cell count of 1/μL, protein level of 17 mg/dL"}
{"row_index": 444, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 33-year-old woman was in a car crash going fast and didn't wear a seatbelt. She hit hard and broke bones in her right hip, thigh, and lower leg. Her hip was out of place and had a big crack in the back wall of the hip socket and in the top of the thigh bone. The doctors tried to push the hip back into place in the emergency room but couldn't because of the other broken bones. So they took her to the operating room right away. In there, they used a small pin to push the hip back into place, fixed the thigh and lower leg bones with metal rods, and checked the hip while she was under anesthesia to make sure it was stable. After the surgery, she could start walking with just a little weight and was able to walk fully six weeks later. The bones were healing well, and the hip stayed in place. She never came back for a follow-up visit.\"\n}"}
{"row_index": 445, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 33-year-old woman arrived at the trauma center after a high-speed car crash where she was not wearing a seatbelt. She had severe injuries to her right hip and leg, including a dislocated hip, a fracture of the femoral head, fractures of the femur and tibia, and an open wound on her lower leg with exposed bone. Initial attempts to realign her hip in the emergency room failed due to the complexity of her fractures. She was then taken to the operating room for surgery. During the procedure, a small pin was inserted to help realign the hip, and the broken femur and tibia were stabilized using metal rods inserted into the center of the bones. A special X-ray exam under anesthesia was done to check if the hip joint was stable and properly aligned. The results showed that the hip was stable and the fracture pieces were in place. After surgery, she could begin walking with minimal weight and was discharged after 16 days. Six weeks later, she returned to the clinic and was able to fully bear weight on her right leg, with X-rays showing that the hip and leg fractures were healing well. However, she did not return for follow-up care after that.\"\n}"}
{"row_index": 446, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 33-year-old female with a history of schizophrenia and bipolar disorder presented to the trauma center following a high-impact motor vehicle collision at approximately 50 miles per hour, during which she was an unrestrained driver. The mechanism of injury resulted in significant blunt force trauma to the pelvis and lower extremity. Upon arrival in the trauma bay, she reported acute pain in the right hip and leg, with physical examination revealing shortening and deformity of the right lower extremity. A 2 cm × 1 cm open laceration was observed over the distal tibia with exposed bone fragments, indicating a comminuted open tibial fracture. The patient was intubated for airway protection due to potential respiratory compromise from pain and shock. Initial radiographic evaluation of the right hip, femur, and tibia revealed a right hip dislocation with associated fractures of the femoral shaft and tibial shaft. Computed tomography (CT) of the pelvis confirmed a posterosuperior acetabular hip dislocation with specific involvement of the posterior wall of the acetabulum and an inferior infrafoveal femoral head impaction fracture, consistent with a posterior wall fracture dislocation. The presence of these fractures raises concerns for avascular necrosis (AVN) of the femoral head due to disruption of the vascular supply from the femoral neck. Attempts at closed reduction of the hip dislocation in the emergency department were unsuccessful, primarily due to the presence of concomitant femoral and tibial shaft fractures, which limited the feasibility of manual reduction and introduced biomechanical instability. Given the severity of the injuries and the risk of AVN, the patient was transferred urgently to the operating room for surgical intervention. In the operating room, she was placed in supine position on a radiolucent table with a small elevation under the right buttock to facilitate optimal pelvic alignment. A 5 mm Schanz pin was inserted percutaneously along the anatomical axis of the femoral neck to provide temporary stabilization and serve as a guide for reduction. Traction and controlled rotational forces were applied to achieve reduction of the femoral head into the acetabulum, confirming the presence of an inferior infrafoveal impaction fracture. The open tibial fracture was debrided to remove contaminated bone fragments and soft tissue debris, followed by primary closure. Both the femoral and tibial shaft fractures were stabilized using intramedullary nailing"}
{"row_index": 447, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 50-year-old woman was bleeding from her vagina for 4 months, had lower belly pain, and trouble with sex. Doctors found her uterus was big and hard, and a sample from inside it showed a rare type of cancer called uterine carcinosarcoma (MMT). At the same time, they saw a lump in her left kidney that looked like kidney cancer (RCC) on scans. They tried to check the kidney lump with a tiny needle, but it only came back with blood. So they did surgery to check both the uterus and the kidney. The uterus cancer was confirmed, and the kidney lump was not cancer — it was a very rare, harmless tumor called RH. The woman had surgery to remove the uterus and both ovaries, and also the kidney. She recovered well and is now on chemo for the uterine cancer. The kidney tumor was not dangerous, and no family history of cancer was found. She’s doing fine and is being followed up regularly.\"\n}"}
{"row_index": 448, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 50-year-old woman came in with vaginal bleeding that had been going on for 4 months, along with lower abdominal pain and discomfort during sex. She had regular periods before this, but now her bleeding was heavy, with clots and pain. She had two children from normal deliveries and had no history of family cancer. She was also diagnosed with hypothyroidism a few years ago, which she manages with medication.\\n\\nOn exam, her abdomen was normal, but her cervix was enlarged and firm. Her uterus was bulky and firm. A sample of the uterine lining (endometrial sampling) showed a rare type of cancer called uterine carcinosarcoma (MMT), which is a serious but uncommon cancer. Blood tests were normal, and her thyroid and other liver/kidney levels were within range.\\n\\nImaging scans showed a large, abnormal uterus and a mass in the left kidney. The kidney mass looked very vascular (full of blood) and was initially thought to be renal cell carcinoma (RCC), a common kidney cancer. A needle biopsy (FNAC) of the kidney mass was done twice, but it only showed blood — no cancer cells were found.\\n\\nThe patient had surgery to remove the uterus and both ovaries and fallopian tubes (staging laparotomy), and a frozen section of the kidney mass was checked. The results were unclear, with only a few unusual cells seen. Because of this uncertainty, a full kidney removal (radical nephrectomy) was done.\\n\\nAfter surgery, the tissue samples were examined under a microscope. The uterine tumor was confirmed as MMT — a rare cancer with both glandular and connective tissue parts. The kidney tumor was found to be a very rare benign tumor called renal hemangioma (RH), not cancer. This tumor is not aggressive and does not spread.\\n\\nThe patient recovered well and was discharged after 6 days. Tests for a genetic condition linked to such tumors (VHL) were normal. She started chemotherapy for her uterine cancer using paclitaxel and carboplatin, and she is now doing well with regular follow-up for 15 months.\"\n}"}
{"row_index": 449, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 50-year-old female presented to the Gynecology Outpatient Department with a four-month history of abnormal vaginal bleeding, including passage of clots, accompanied by lower abdominal pain and dyspareunia for two months. Her menstrual cycles had previously been regular, lasting six days every 28 days, until four months prior when bleeding commenced. She reported no use of oral contraceptives or other forms of contraception. She has two term deliveries via vaginal birth, with the most recent delivery occurring 17 years ago. She was diagnosed with hypothyroidism two years prior and is currently maintained on thyroxine 50 μg daily with euthyroid status. There is no family history of genital, colonic, or renal malignancies.\\n\\nOn physical examination, she was afebrile, with a pulse of 76 beats per minute, blood pressure of 110/74 mmHg, and mild pallor. Abdominal examination was unremarkable, with no palpable mass. Speculum examination revealed a hypertrophied cervix with active bleeding at the external os. Vaginal examination demonstrated a firm cervix and a bulky, firm uterus with normal mobility and no palpable adnexal mass. Rectal examination showed normal rectal mucosa and soft parametrium.\\n\\nEndometrial sampling revealed a high-grade endometrial adenocarcinoma, specifically the villonodular subtype. Hemoglobin was 8.9 g/dL, and all liver and renal function tests were within normal limits. Serum TSH was 2.6 uIU/mL, and CA-125 was elevated at 165 IU/L. Pap smear was negative for intraepithelial lesions or malignancy. Pelvic ultrasonography showed a bulky uterus with increased endometrial thickness and an intracavitary lesion. Contrast-enhanced computed tomography (CT) demonstrated a heterogeneous, centrally enhancing mass in the lower pole of the left kidney, suggestive of a highly vascular lesion with mitotic activity, most likely renal cell carcinoma (RCC). MRI of the abdomen and pelvis further revealed a lobulated, ill-defined myometrial-based endometrial mass measuring 2.4 × 1.1 × 2.0 cm, extending into the endometrium and distorting the endometrial cavity, consistent with adenomyosis. A heterogeneously enhancing renal lesion measuring"}
{"row_index": 450, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old man had a lump on the back of his right hand for 5 years. It started small and got bigger over time, now measuring about 4 cm long. The lump was hard, stayed in one place, and didn’t move when he moved his hand. It didn’t hurt much, only when he did heavy work, and it didn’t bother him at night or stop him from doing daily tasks. Doctors saw the lump and used X-rays and MRI to check it. The MRI showed a bony growth coming from the hand bone, with a soft part on top, which matched a condition called osteochondroma. The lump was removed in surgery, and the tissue was tested. The test confirmed it was an osteochondroma. After surgery, the man had no pain, could move his hand freely, and at one year later, the doctors said he was doing well with no signs of the lump coming back.\"\n}"}
{"row_index": 451, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 20-year-old man had a swelling on the right hand for 5 years that slowly got bigger, reaching 4 cm × 3 cm × 2 cm. The swelling was on the palm side, near the inside of the hand, and felt hard with no pain except when doing heavy activities. It didn’t cause night pain or limit daily tasks. On exam, it was fixed to the bone and couldn’t move. X-rays showed a bony growth coming from the end of the fifth metacarpal bone. MRI confirmed the growth, showing it was made of bone and cartilage, and it was pushing on nearby tendons and muscles. A diagnosis of osteochondroma was made. The swelling was surgically removed under general anesthesia through a small incision on the back and inside of the hand. The removed tissue was tested under a microscope and confirmed to be an osteochondroma — a benign bone and cartilage growth. The surgery went smoothly, with no complications. The patient recovered well, had no pain, and could move his hand normally. At one-year follow-up, the results were good with no signs of recurrence.\"\n}"}
{"row_index": 452, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 20-year-old male presented in January 2021 with a progressive, insidious-onset swelling of the right hand, localized to the palmar medial border, lasting for five years. The lesion gradually increased in size, reaching dimensions of 4 cm × 3 cm × 2 cm, and was characterized clinically as bony, hard, with an irregular surface, adherent to the underlying bone, and fixed in both coronal and sagittal planes. Palpation revealed no fluctuance, local warmth, or signs of inflammation, and there was no associated fever, regional lymphadenopathy, skin changes, sinuses, dilated veins, or systemic symptoms. The swelling was not present elsewhere in the body and was not associated with nocturnal pain or functional limitation during daily activities, though it was aggravated by excessive mechanical loading and relieved with rest.\\n\\nClinical examination confirmed the lesion's fixed, bony nature and its position on the ulnar aspect of the hand. Radiographic evaluation (X-ray) demonstrated a pedunculated bony lesion originating from the distal metaphyseal region of the fifth metacarpal bone, consistent with an exophytic bony outgrowth. Magnetic resonance imaging (MRI) further characterized the lesion as measuring 2 × 2.5 × 3 cm (anteroposterior × transverse × sagittal), arising from the distal metaphysis of the fifth metacarpal and exhibiting continuity with the medullary cavity, extending away from the epiphysis. The MRI also revealed displacement of the fifth flexor digitorum profundus tendon laterally and compression of the flexor digiti minimi and abductor digiti minimi muscles. Additionally, a bursa with inflammatory fluid accumulation was identified within the soft tissue compartment adjacent to the lesion. Based on these imaging and clinical findings, a provisional diagnosis of osteochondroma was established.\\n\\nThe lesion was surgically excised under general anesthesia with tourniquet control via a posteromedial incision. The excision was performed at the base of the pedicle, removing a tumor mass of approximately 3 × 2 cm. The resected specimen was sent for histopathological evaluation. Histopathology confirmed the presence of a cartilaginous cap overlying a bony component, with well-organized bony trabeculae. The cartilaginous layer was lined by perichondrium and"}
{"row_index": 453, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 68-year-old man who had never had any heart problems before suddenly became confused and stopped breathing normally. His wife called emergency services when she found him not responding. When doctors arrived, he was unresponsive and had a heart stoppage. They revived him with life-saving steps, including shock and breathing support. An electrical test of his heart showed signs that match a rare heart condition called Brugada syndrome. This condition can cause the heart to stop suddenly, even without any blockage or heart attack. Doctors found no heart damage, and his heart’s blood flow was normal. He was given medicine for a slow thyroid and later agreed to get a small device in his chest to prevent future heart problems. The doctors confirmed the diagnosis based on the heart test results and his history of no symptoms before this event.\"\n}"}
{"row_index": 454, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old Hispanic man was brought to the emergency department after his wife found him breathing badly and unresponsive. When doctors arrived, he was confused and had a sudden heart rhythm problem that led to cardiac arrest. He was revived with emergency treatment, including defibrillation and CPR. An electrocardiogram (ECG) taken during this event showed abnormal heart patterns, specifically ST-segment elevations in the chest leads V1 to V3 and unusual repolarization changes in V1 and V2 — findings that are typical of Brugada syndrome. Other ECG results showed a slow heart signal (first-degree AV block) and a normal QRS duration. Blood tests revealed low levels of sodium, potassium, magnesium, and thyroid hormone, indicating severe hypothyroidism, which was treated with hormone replacement. No blockages were found in the heart arteries during catheterization. After recovery, the patient was found to have small brain injuries from previous events, but no major heart problems were present. He was discharged with medications for heart and brain health. Later testing confirmed that his heart rhythm abnormalities matched the pattern of Brugada syndrome, a condition that can cause sudden cardiac death. The doctors recommended he get an implantable cardioverter defibrillator (ICD) to help prevent future heart problems.\"\n}"}
{"row_index": 455, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old Hispanic male with no significant past medical history was evaluated in the emergency department (ED) following an acute episode of confusion and altered mental status. Emergency medical services (EMS) were dispatched by the patient's wife after she observed erratic breathing and inability to rouse him. Upon ED arrival, the patient was obtunded and experienced in-hospital cardiac arrest due to ventricular fibrillation. Immediate advanced cardiac life support (ACLS) was initiated, including endotracheal intubation, cardiopulmonary resuscitation (CPR), and defibrillation, resulting in return of spontaneous circulation (ROSC). An electrocardiogram (ECG) obtained during the cardiac arrest event revealed ST-segment elevations in leads V1–V3, consistent with a type 1 Brugada pattern, along with prominent repolarization abnormalities in V1 and V2. Additional ECG findings included first-degree atrioventricular (AV) block with a PR interval of 220 milliseconds (normal range: 120–200 ms), and a QRS duration of 0.11 seconds (normal: 0.08–0.12 s), both of which are non-specific but support the presence of underlying conduction system abnormalities.\\n\\nInitial laboratory values demonstrated hyponatremia (sodium: 132 meq/L; normal: 136–145 meq/L), hypokalemia (potassium: 3.3 meq/L; normal: 3.5–5.0 meq/L), hypomagnesemia (magnesium: 3.3 mg/dL; normal: 1.5–2.4 mg/dL), hyperglycemia (glucose: 197 mg/dL), normal troponin (<0.02 ng/mL), mild elevation of brain natriuretic peptide (BNP: 65 pg/mL), prolonged prothrombin time (PT: 13.6 s; normal: 11–13 s) and international normalized ratio (INR: 1.3), and severe primary hypothyroidism (thyroid-stimulating hormone [TSH]: 59.4 mU/L; normal: 0.5–5.0 mU/L). These abnormalities were not attributable to acute ischemia"}
{"row_index": 456, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old woman had dry eyes and dry mouth for years, and finally got checked. Doctors found she had Sjögren’s syndrome — a condition where her body stops making enough saliva and tears. This was confirmed by blood tests showing antibodies to Ro (SS-A), a biopsy of her salivary glands, and a scan that showed no saliva flow. She also had kidney damage, called membranous glomerulonephritis, which was seen in a kidney biopsy. Three months later, she had a serious stomach problem — a hole in her small intestine that let air in (pneumoperitoneum), and the tissue sample showed a cancer called Epstein-Barr virus-positive diffuse large B-cell lymphoma (DLBCL). She didn’t get chemotherapy because she was too weak, poor, and didn’t want to. But she was taking low-dose steroids and hydroxychloroquine for her Sjögren’s, and after one year, her dry symptoms and protein in her urine got better. A scan showed the cancer wasn’t getting worse.\"\n}"}
{"row_index": 457, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 52-year-old woman was diagnosed with primary Sjögren's syndrome, a condition that causes dry eyes and dry mouth, based on her symptoms, blood tests, salivary gland biopsy, and imaging. She had positive results for anti-nuclear antibody (ANA) and anti-Ro (SS-A) antibodies, and her salivary glands showed signs of inflammation. A kidney biopsy later confirmed she had membranous glomerulonephritis, a type of kidney disease that causes protein in the urine. Three months after her diagnosis, she developed a serious abdominal complication: a perforation in her small bowel, which led to infection. A biopsy of the bowel tissue showed Epstein-Barr virus-positive diffuse large B-cell lymphoma (DLBCL), a type of aggressive cancer. Despite being diagnosed with both Sjögren's syndrome and lymphoma, she did not receive chemotherapy due to poor health, low motivation, and financial hardship. However, over the course of one year, her proteinuria improved and her dry eye and dry mouth symptoms got better. A follow-up scan showed that the lymphoma was stable, meaning it did not get worse.\"\n}"}
{"row_index": 458, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 52-year-old woman presented with intermittent abdominal tenderness, chronic dry eyes, and dry mouth, which had persisted for several years without prior medical evaluation. She had a history of dilated cardiomyopathy and left-eye glaucoma, managed with loop diuretics, proton pump inhibitors, and anthocyanosides. Physical examination revealed lower extremity edema, with normal body temperature (36.5°C) and blood pressure. Laboratory findings included a white blood cell count of 8,600/mm³ (neutrophilic predominance, 73.4%), sodium 141 mEq/L, chloride 108 mEq/L, blood urea nitrogen 15.7 mg/dL, and creatinine 0.6 mg/dL. Serum total protein was 5.5 g/dL, albumin 1.5 g/dL, and total cholesterol 257 mg/dL. Urinalysis demonstrated significant proteinuria (6.3 g/day), 30–49 red blood cells per high-power field, and no casts. Serologic testing revealed a positive anti-nuclear antibody (ANA; 1:80, homogeneous and speckled pattern), rheumatoid factor (390 IU/mL), and anti-Ro (SS-A) autoantibody (>200 U/mL). Notably, antibodies against double-stranded DNA, La (SS-B), Sm, ribonucleoproteins, antineutrophil cytoplasmic antibodies, lupus anticoagulant, IgG/IgM anti-cardiolipin, and IgG β2-glycoprotein-1 were absent. Complement levels showed a marked reduction in C3 (38 mg/dL; normal range 90–180 mg/dL), while C4 (16 mg/dL; normal 10–40 mg/dL) and complement component 50 (33.1 U/mL; normal 23–46 U/mL) remained within normal limits. Hepatitis B surface antigen, hepatitis C antibodies, cryoglobulins, and human immunodeficiency virus were all negative. Minor salivary gland biopsy demonstrated diffuse lymphocytic infiltrates with a focus score of 3, consistent with lymphoid infiltration in the exocrine glands. Salivary scintigraphy showed non-visualization"}
{"row_index": 459, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 47-year-old woman had numbness in her toes and trouble urinating for a year. Tests showed her spine's end part was stuck low, like a string tied to the bottom of the spine. The doctors fixed it by cutting part of her spine at the L2 level to free it up. They used screws at L1 and L3 to hold the spine in place, and made sure they were straight and lined up right. They removed part of the bone on the top and sides of L2, and took out the disc between L1 and L2. Then they removed the top part of the L2 bone. A metal rod was attached to the screws and pressed in to hold the spine together. Two soft tapes were placed on the spine to keep it stable. After surgery, her leg numbness got better right away, and her bladder problems improved after one year. The bone healed fully, and the metal parts were taken out after a year. She hasn’t had any problems since then.\"\n}"}
{"row_index": 460, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 47-year-old Asian woman was admitted to the hospital with a 1-year history of leg numbness and trouble with urination. She had first noticed numbness in her third and fourth toes five years ago, and over time, her entire toes became numb. She also started having frequent urination. After imaging tests, doctors found that her spinal cord was low in position, extending to the S2 level and surrounded by fat, which led to the diagnosis of adult tethered cord syndrome. To fix this, surgeons performed a spine-shortening procedure at the L2 level.\\n\\nThe surgery involved making a cut from T11 to L4, placing screws at L1 and L3 to help stabilize the spine. The screws were inserted carefully, parallel to the top surfaces of the vertebrae, to make sure the bones aligned properly. The upper part of the L2 lamina (the back part of the bone) and part of the L2 pedicle were removed. The disc between L1 and L2 was also removed. Then, the top part of the L2 vertebra was taken out using a drill. After removing the vertebra, a straight rod was attached to the screws and used to press the bones together. Two polyethylene tapes were placed to support the spine.\\n\\nThe surgery took 5 hours and 13 minutes, with only 108 ml of blood loss. The patient’s leg numbness improved right after the surgery, and her urinary problems improved one year later. A year after surgery, CT scans showed the bones had fully healed, and the hardware was removed. No symptoms returned after two years. This procedure helps free the spinal cord and improve nerve function in patients with tethered cord syndrome.\"\n}"}
{"row_index": 461, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 47-year-old Asian woman presented with a 1-year history of progressive bilateral leg numbness, initially affecting the third and fourth toes for 5 years, and subsequent involvement of all toes, along with a 1-year history of urinary frequency. Physical examination revealed intact motor function and normal deep tendon reflexes; sensory disturbance was localized to the anal region. Her finger-to-floor distance was 10 cm, and straight leg raise testing yielded 80 degrees, indicating no significant hamstring tightness. Magnetic resonance imaging (MRI) demonstrated a low-lying conus medullaris extending to the S2 level, surrounded by fat tissue, with no other structural abnormalities identified. This finding was consistent with adult tethered cord syndrome (ATCS), a condition characterized by a fixed, low-lying conus medullaris that is tethered to the spinal column, leading to chronic neurologic compression and progressive sensory and motor deficits. Given the clinical and imaging findings, a spine-shortening vertebral osteotomy was planned at the L2 level to decompress the conus medullaris by reducing spinal length and relieving tethering forces.\\n\\nAfter obtaining informed consent, the patient underwent surgical intervention under general anesthesia, positioned on a Jackson Spinal Table (Mizuho Co. Ltd., Tokyo, Japan). Neurophysiological monitoring using motor evoked potentials was performed to assess real-time spinal cord function during the procedure. A midline incision was extended from the T11 to L4 spinous process level, allowing extensive exposure of the L2 vertebral segment, including posterior elements and transverse processes bilaterally. Bilateral pedicle screws were placed at L1 and L3 using an anterior-posterior image intensifier. Critical to surgical precision, monoaxial screws were inserted parallel to the rostral endplates of each vertebral body to ensure optimal alignment between the L1 caudal endplate and the L2 osteotomy surface, minimizing the risk of postoperative spinal misalignment and neurological compromise.\\n\\nThe osteotomy procedure commenced after screw placement. Initial resections included the lower half of the L1 lamina, bilateral inferior articular processes of L1, and bilateral superior articular processes of L2. Subsequently, the upper one-third of the L2 lamina was resected, and the bilateral two-thirds of the L2 pedicle were removed using a surgical air drill. This lamina resection is clinically significant because complete preservation"}
{"row_index": 462, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 60-year-old man had a tumor in his bladder that wasn't painful or linked to other health problems. After tests, doctors found it was a serious type of cancer called small cell bladder cancer. They removed the tumor first, then gave him chemotherapy and radiation to kill any leftover cancer cells. He also had surgery to remove his bladder and part of his prostate, and replaced it with a new bladder made from part of his intestine. The surgery and treatment worked well — no cancer came back even 33 months later. He’s now healthy and being checked every 6 months to make sure everything stays clear.\"\n}"}
{"row_index": 463, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 60-year-old man was diagnosed with a rare type of bladder cancer called small cell bladder cancer (SCBC) two and a half years ago. He had no risk factors like smoking or family history, and his symptoms were mild—just painless blood in his urine. After tests, a 6 cm tumor was found on the bladder wall, and initial tests showed no signs of spread. The tumor was removed, and further testing confirmed it was muscle-invasive and aggressive, with a very high growth rate.\\n\\nBecause this type of cancer can spread quickly, the patient received four cycles of chemotherapy using cisplatin and etoposide, followed by radiation to the brain to prevent spread. He then had surgery to remove his bladder and prostate, along with nearby lymph nodes. The surgery was successful, and final tests showed no cancer cells left in the tissue or lymph nodes.\\n\\nSince the treatment, the patient has remained free of cancer for 33 months. He now has regular check-ups every six months, including urine tests and imaging, and no signs of recurrence have been found. This case shows an unusually long period of disease-free survival for someone with this type of cancer.\"\n}"}
{"row_index": 464, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 60-year-old male presented with painless gross hematuria, with no identifiable risk factors including smoking, prior radiation exposure, occupational hazards, or hereditary predisposition. No systemic symptoms such as weight loss, night sweats, or B-symptoms were present, and no neurological deficits were reported. Urinary infection was excluded by appropriate laboratory and microbiological workup. Cystoscopy revealed a 6 cm solid tumor on the right bladder wall, which was completely resected via transurethral resection of the bladder tumor (TURBT). Primary histopathological evaluation confirmed a muscle-invasive small cell neuroendocrine carcinoma (SCBC) with pT2a GIII classification. Immunohistochemical staining demonstrated strong positivity for synaptophysin and AE1/AE3, consistent with neuroendocrine differentiation, while chromogranin A, CD56, CD3, CD20, TdT, S-100, and HMB45 were negative, supporting the diagnosis of small cell carcinoma without features of other neuroendocrine or epithelial tumors. The tumor exhibited a high proliferative index, with a KI-67 labeling index of 95%, indicating aggressive cellular turnover. An 18F-FDG PET/CT scan at initial diagnosis showed no evidence of lymph node or visceral metastasis, and cranial magnetic resonance tomography (MRT) confirmed absence of brain infiltration, supporting a localized disease at presentation. Given the established evidence in the literature that neoadjuvant chemotherapy improves outcomes in SCBC, the patient received four cycles of cisplatin (25 mg/m²) and etoposide (100 mg/m²), administered every 21 days (days 1–3 per cycle), with no treatment-related adverse events. Concurrently, prophylactic whole-brain radiotherapy (WBRT) was delivered at a total dose of 26 Gray to mitigate the risk of central nervous system relapse, a known site of early dissemination in SCBC. Following chemotherapy, the patient underwent radical cystoprostatectomy with ileal neobladder reconstruction and bilateral extended pelvic lymphadenectomy, including the resection of 32 lymph nodes, all of which were tumor-free. Final pathological assessment confirmed a complete pathological response (ypT0, N0, L0, V0, Pn0), indicating absence of viable small cell carcinoma in the"}
{"row_index": 465, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 72-year-old man who had been sick with a type of cancer called chronic lymphocytic leukemia (CLL) for years started getting worse symptoms two weeks before he was admitted to the hospital. He had a fever, chills, night sweats, tiredness, trouble swallowing, and fast-growing swollen lymph nodes in his neck. Tests showed his cancer had changed into a more serious form called diffuse large B-cell lymphoma. He began chemotherapy called DA-R-EPOCH, which helped shrink the swollen nodes but also caused serious side effects. Soon after, he had trouble breathing because the swollen neck nodes blocked his airway, so doctors had to put a tube in his throat to keep his airway open. After a few days, the swelling went down, but he stayed unconscious and started having severe, hard-to-stop seizures. Brain scans showed swelling in the back part of his brain, which is a condition called PRES. This swelling was likely caused by the chemotherapy, his damaged kidneys, and a serious infection. Even with treatment, he did not get better and eventually had a heart stop. His brain problem was caused by a mix of these factors.\"\n}"}
{"row_index": 466, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 72-year-old man with a history of chronic lymphocytic leukemia (CLL) that had changed to a more aggressive form of lymphoma called diffuse large B-cell lymphoma (DLBCL) presented with a two-week history of low-grade fever, chills, night sweats, fatigue, difficulty swallowing, and fast-growing swollen lymph nodes in his neck. Tests showed his lymphocyte count had risen and his platelet count had dropped, and a scan revealed widespread swelling in his neck, chest, abdomen, and pelvis. A biopsy confirmed the lymphoma had transformed from his original CLL, a condition known as Richter syndrome. He began treatment with DA-R-EPOCH chemotherapy, but soon developed complications including tumor lysis syndrome, kidney damage, and a bacterial infection caused by Pseudomonas aeruginosa. A few days later, his neck swelling became so severe that he needed emergency intubation to protect his airway. Although the swelling improved, he did not regain consciousness and started having severe, uncontrolled seizures. Brain imaging showed swelling in the back part of his brain, specifically in the occipital and inferior temporal lobes, which is consistent with posterior reversible encephalopathy syndrome (PRES). His seizures were hard to control with standard medications but responded to midazolam and propofol. Additional infections were found, and antibiotics were adjusted, but due to his poor outlook, care was not escalated. His condition eventually worsened, and he suffered a cardiac arrest. Experts believe his PRES was caused by a combination of the new chemotherapy, kidney injury, and sepsis.\"\n}"}
{"row_index": 467, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 72-year-old White man with an 8-year history of chronic lymphocytic leukemia (CLL), previously treated with four cycles of fludarabine, cyclophosphamide, and rituximab in 2012, and subsequent maintenance therapy with ibrutinib since 2014, presented to the oncology clinic with a 2-week history of low-grade fever, chills, night sweats, fatigue, dysphagia, and rapidly progressive cervical lymphadenopathy. Laboratory evaluation revealed a significant increase in lymphocyte percentage (61% at presentation versus 40.2% at 6 months prior), along with thrombocytopenia (42 vs. 92 K/mm³). Positron emission tomography (PET) imaging demonstrated extensive, confluent hypermetabolic lymphadenopathy involving bilateral neck, chest, abdomen, and pelvis, suggestive of disease progression. Lymph node biopsy confirmed transformation of CLL to high-grade diffuse large B-cell lymphoma (DLBCL), consistent with Richter syndrome. The patient was initiated on dose-adjusted rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-R-EPOCH) chemotherapy. Concurrently, he developed tumor lysis syndrome, acute kidney injury, and neutropenic fever with Pseudomonas aeruginosa bacteremia, requiring broad-spectrum antibacterial and antifungal therapy, as well as granulocyte colony-stimulating factor (G-CSF) support. On day 9 of hospitalization, the patient experienced severe airway obstruction due to extensive cervical lymphadenopathy, necessitating emergency endotracheal intubation and transfer to the intensive care unit (ICU). Neck magnetic resonance imaging (MRI) revealed marked soft-tissue edema, which was treated with high-dose hydrocortisone without clinical improvement. On day 10, after sedation was withdrawn, the patient remained unresponsive and developed two episodes of generalized, refractory seizures. Head computed tomography (CT) showed no acute structural abnormalities; electroencephalography (EEG) failed to detect focal or generalized epileptiform activity. Brain MRI revealed bilateral occipital and inferior temporal lobe edema involving cortical gray matter and subcortical white matter, consistent with posterior reversible encephalopathy syndrome"}
{"row_index": 468, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 84-year-old man had eye pressure problems from glaucoma. His doctor tried medicines for years, but the pressure stayed high and his vision got worse, especially in his right eye. So, they did a small surgery in his right eye to help lower the pressure using a tiny device called XEN45. Right after, his eye pressure dropped too low, and a small part of the eye (the choroid) detached, but doctors fixed it with eye drops and steroids. Eight months later, they did the same surgery in his left eye. After that, the same problem happened — the choroid detached again — so they did a second surgery to fix it. Both eyes now have normal eye pressure and the problem is gone. The man also had cloudy lenses in both eyes, which made it hard to see clearly, so they did cataract surgery in both eyes. After that, his vision improved a little, but some parts of his eye still have changes from aging, and that doesn’t hurt his daily vision much.\"\n}"}
{"row_index": 469, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 84-year-old man with glaucoma had surgery to lower pressure in his eyes using the XEN45 device. The procedure was done in his right eye first in July 2020 and went smoothly. After surgery, his eye pressure dropped very low (to 10 mmHg), which caused a temporary condition called hypotony and a type of detachment in the choroid (a layer behind the retina). This was treated with steroid eye drops and eye drops that reduce muscle activity (cycloplegic drops), and it improved over time. By month eight, the left eye had the same surgery, and again, choroidal detachment occurred. This time, a small surgical procedure was needed to drain the fluid and fix the problem. After that, pressure stabilized between 10 and 12 mmHg, and the detachment fully resolved. Both eyes now have the XEN45 device in place and the pressure is well controlled. The patient also had cataract surgery in both eyes later in 2022. After the surgery, his vision improved in the right eye to 10/10, and in the left eye to 6/10. Although there were some eye conditions like lens clouding and age-related changes in the back of the eye, these did not significantly affect his daily vision.\"\n}"}
{"row_index": 470, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 84-year-old male with primary open-angle glaucoma (POAG) presented with decompensated intraocular pressure (IOP) in the right eye, despite maximal medical therapy. His preoperative topical regimen included tafluprost (15 µg/mL once daily), brinzolamide (twice daily), and timolol (twice daily), with addition of oral acetazolamide (250 mg twice daily) in the prior year. Preoperative best-corrected visual acuity (BCVA) was 6/10 in the right eye and 4/10 in the left eye (Snellen chart). Slit-lamp examination revealed transparent corneas, normal anterior chambers, and nuclear cataract opacities in both eyes, with no other anterior segment abnormalities. Preoperative IOP was 24 mmHg in the right eye and 20 mmHg in the left eye. Fundus examination demonstrated a large cup-to-disc ratio (CDR = 0.9) and neuroretinal rim narrowing in all disc sectors bilaterally. Despite optimization of both oral and topical glaucoma medications, a progressive bilateral visual field defect was documented in June 2020, with the most significant decline observed in the right eye.\\n\\nGiven the patient’s age, bilateral glaucomatous optic nerve damage, and failure of medical therapy to achieve target IOP (ideally <21 mmHg in this population), ab interno XEN45 glaucoma drainage device implantation was selected as the most appropriate surgical intervention. In July 2020, a subconjunctival injection of mitomycin C (0.2 mg/mL) was administered during the right eye XEN45 implantation, which proceeded without intraoperative complications. Postoperatively, IOP dropped to 10 mmHg on day 1, with a diffusely distributed filtration bleb and flat anterior chamber. Fundus examination revealed serous nasal and temporal choroidal detachments, confirmed by eco-B scan as serous choroidal detachments (SCDs), consistent with hypotonic stress-induced fluid accumulation due to excessive outflow and reduced intraocular pressure.\\n\\nTo mitigate postoperative inflammation and prevent further complications associated with hypotony, a combination of topical dexamethasone (2 mg/mL, three times daily), atropine"}
{"row_index": 471, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 22-year-old man had a big, soft lump in his belly that made him feel full and sick. Years ago, he had a tube (VPS) put in to drain fluid from his brain, because of a birth condition called spina bifida. The tube had been in place for 21 years, and no other surgeries were done. Doctors found a fluid-filled bag near the tube’s end, which was blocking his stomach. This bag, called a pseudocyst, was filled with cerebrospinal fluid — the same fluid that flows in the brain. The fluid looked like brain fluid, and tests showed no infection. The bag was in the upper left part of his belly, between his stomach and colon. Surgeons opened it, drained 1500 ml of clear fluid, and moved the tube out of the bag. The problem was confirmed as a rare complication of the brain drain tube. This kind of cyst can happen years after the tube is placed, even after 20 years. It causes belly swelling and a lump, and if not treated, can be dangerous. The only way to fix it is to remove the bag and move the tube safely. In this case, surgery was needed because the belly had too much scar tissue to do it with small tools.\"\n}"}
{"row_index": 472, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 22-year-old man was admitted to the hospital because of a swollen, distended abdomen and nausea. He had a ventriculoperitoneal shunt (VPS) placed 21 years earlier to treat fluid buildup in his brain due to spina bifida. This shunt was originally placed when he was just a few months old, and he had no other abdominal surgeries since then. No history of cancer, liver, or pancreas problems was found.\\n\\nOn exam, a large, soft mass was felt in his upper abdomen. Blood tests were normal, and imaging showed a fluid-filled collection near the tip of the VPS catheter. This suggested a cyst formed around the shunt, likely filled with cerebrospinal fluid (CSF), a type of fluid that normally flows in the brain and spinal cord.\\n\\nThe doctors suspected a peritoneal pseudocyst — a rare complication of VPS — and performed emergency surgery. The cyst was located in the left upper abdomen, between the stomach and the colon, in a space called the omental bursa. During surgery, 1500 ml of clear fluid was drained, and the VPS catheter was moved outside the cyst. The cyst wall was removed, and the tissue was found to be fibrous with some inflammation.\\n\\nThe fluid from the cyst matched cerebrospinal fluid in appearance and had no signs of infection. This confirmed the diagnosis: an abdominal cerebrospinal fluid pseudocyst as a complication of the VPS. This condition is rare but can be serious, especially if it causes blockage or swelling in the abdomen.\\n\\nThis case is notable because the symptoms appeared 21 years after the initial VPS surgery — the longest time reported in the medical literature for such a complication. In most cases, these cysts form within a few weeks to a decade after shunt placement, but this one developed much later.\\n\\nSymptoms in adults usually include abdominal pain, bloating, and a noticeable mass. Children more often have symptoms like headaches or nausea due to shunt issues. In this case, the patient had no signs of infection or inflammation, making it unlikely to be an abscess or a pancreatic cyst.\\n\\nThe treatment involved open surgery to remove the cyst and drain the fluid. While some doctors now use smaller, less invasive procedures like laparoscopy, this patient had severe scar tissue (adhesions"}
{"row_index": 473, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 22-year-old male presented with progressive abdominal distention and nausea. He had a ventriculoperitoneal shunt (VPS) implanted 21 years earlier to manage hydrocephalus secondary to spina bifida. Shunt revision occurred only at age 10 months, with no subsequent abdominal surgical interventions. No history of malignancy, pancreatic disease, or liver pathology was reported. Physical examination revealed a large, elastic, palpable mass in the upper abdomen, with no neurological deficits. Laboratory findings, including white blood cell count and serum amylase, were within normal limits. Supine abdominal radiography demonstrated the VPS in the left upper quadrant and a soft-tissue mass in the upper abdomen. Unenhanced abdominal computed tomography (CT) revealed a homogeneous low-density fluid collection adjacent to the VPS catheter tip, consistent with a cystic lesion arising in the peritoneal cavity. The mass was anatomically localized between the stomach and the mesentery of the transverse colon, specifically within the omental bursa, and was independent of the pancreas. The fluid collection exhibited characteristics consistent with cerebrospinal fluid (CSF), including negative microbial cultures and absence of detectable bacterial flora, as confirmed by fluid analysis. Histopathological examination of the resected pseudocyst wall revealed fibrous tissue with mild inflammatory cell infiltration, confirming the absence of epithelial lining, which is characteristic of a pseudocyst rather than a true cyst or neoplasm.\\n\\nEmergency laparotomy was performed to address the obstructive effect of the mass on the gastric outlet. The cystic mass was excised, and 1500 ml of clear fluid was drained. A portion of the pseudocyst wall, comprising the posterior gastric wall and adjacent colonic mesentery, was completely resected to facilitate decompression and prevent recurrence. The distal end of the VPS catheter was repositioned externally to the cystic mass to ensure proper drainage and avoid further complications. Postoperatively, the patient's appetite improved, and he was discharged on postoperative day 8 in stable condition. His recovery has been uneventful over the subsequent 4 months.\\n\\nAbdominal cerebrospinal fluid pseudocyst is a rare but potentially life-threatening complication of VPS placement, typically manifesting as a thin-walled, fluid-filled cystic mass adjacent to the shunt tip. The"}
{"row_index": 474, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"low_health_literacy\": \"An 8-month-old boy had a fever for 9 days and started with a droopy left eye (ptosis) right from the beginning. His eye also pointed down and out. The pupil reacted normally, and tests showed no measles or virus in his spinal fluid. The fever was mild and not linked to rash, seizures, or brain problems. His muscles and nerves were normal. Tests for infections and blood were normal. Brain and eye scans were clear, and no serious issues were found. The eye problem went away on its own in about 3 weeks without any medicine. This kind of eye problem in young kids is rare, and it often happens after a virus. In this case, the virus was likely the cause, but no specific test could confirm it. The child fully recovered with no long-term effects.\"\n}"}
{"row_index": 475, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 8-month-old boy had a fever for 9 days and developed left-sided ptosis (drooping eyelid) from the first day of fever. His eye was also turned down and out, but his pupil reacted normally. There was no rash, seizures, or other neurological problems. The child was otherwise active and healthy. Tests showed normal blood work, no signs of infection like measles or other autoimmune conditions, and normal brain and eye scans. The spinal fluid (CSF) showed mild inflammation (lymphocytic pleocytosis), with normal protein and sugar levels, and no detectable measles antibodies. No steroids were given, and the ptosis and eye deviation improved within 2 weeks, fully resolving after 3 weeks. Oculomotor nerve palsy in children is rare and often linked to trauma, infection, or inflammation. In this case, the fever and short duration of symptoms suggest a viral cause, even though measles antibodies were normal. Since the scans were normal and no other serious conditions were found, this appears to be a rare case of temporary viral nerve damage that fully recovered without treatment.\"\n}"}
{"row_index": 476, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 8-month-old boy presented with a 9-day history of moderate, intermittent fever, accompanied from the first day by left-sided ptosis and infero-lateral deviation of the left eye. There was no associated rash, joint pain, convulsions, altered sensorium, or neurologic deficits; the child remained otherwise playful and interactive. On clinical examination, left-sided ptosis was present with downward and outward deviation of the globe, and the pupil exhibited normal reactivity. Inability to elevate the left eyelid was noted, but there were no abnormalities in motor strength, tone, or reflexes in any of the four limbs. Laboratory investigations, including complete blood count, electrolytes, urea, and creatinine, were within normal limits. Autoimmune markers—ANA, ASO titer, pANCA, and cANCA—were all within normal ranges. Magnetic resonance imaging (MRI) of the brain and both orbits, along with MRI angiography, was unremarkable, excluding structural abnormalities, including intracranial aneurysms of the internal carotid artery or posterior communicating artery, which are well-documented causes of pediatric oculomotor nerve (CN-III) palsy. Cerebrospinal fluid (CSF) analysis revealed lymphocytic pleocytosis (10 cells/HPF), with normal protein and glucose levels, consistent with aseptic meningitis. IgM and IgG antimeasles antibody titers in CSF were within normal limits, and CSF norovirus polymerase chain reaction was not performed due to financial constraints. The clinical course was self-limiting: ptosis and eye deviation resolved almost completely within 2 weeks and fully after 3 weeks, without the use of corticosteroids. Pediatric oculomotor nerve palsy is a rare entity, with reported etiologies including trauma, infection, congenital causes, and inflammatory processes. In a series by Keith (n=28), trauma, infection, and idiopathic causes were the most common; in Miller’s series (n=30), congenital or traumatic/inflammatory origins predominated. Schumacher-Feero et al. reported that 47% of patients with partial CN-III palsy achieved full recovery without surgical intervention due to spontaneous resolution or partial functional recovery. Viral infections, particularly measles and norovirus, have been linked to postviral oculomotor nerve"}
{"row_index": 477, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 6-year-old boy kept getting sick with bacterial meningitis, caused by a type of bacteria called Streptococcus Pneumoniae 23F. He had headaches, vomiting, and fever, and the doctors found this bacteria in his spinal fluid and blood. After treating him with antibiotics for 14 days, he got better and went home. But the infections kept coming back. The doctors looked for a reason and found that fluid from his brain was leaking out through a small hole in his skull, into his middle ear — this happened on the right side. This leak likely let bacteria get into his brain again. Tests showed damage to the bone near his ear and brain, especially around the facial nerve and areas near the ear. The doctors confirmed the leak was coming from the right side of his skull, and that’s why the infections kept coming back. The family didn’t want surgery, so the boy just got vaccinated with Prevenar 7 to help prevent future infections. This vaccine is not part of the regular national vaccine schedule and had to be paid for himself.\"\n}"}
{"row_index": 478, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 6-year-old boy had repeated episodes of bacterial meningitis caused by Streptococcus Pneumoniae type 23F. He had been treated before with antibiotics, and after one episode, he was discharged without complications. However, the infections kept coming back. Tests showed his immune system was normal, so the cause was likely a problem in his skull bone related to chronic sinusitis. Initial imaging showed sinus inflammation on the right side, but no bone damage. A nuclear scan found that cerebrospinal fluid (CSF) was leaking from the right petroocipital region into the middle ear. Further high-resolution CT and MRI scans showed damage to the bone around the right side of his skull, including areas near the facial nerve and the carotid and jugular canals. These changes showed that the CSF leak was likely the reason for the repeated meningitis. Doctors recommended surgery to fix the bone defect, but the family chose not to proceed. The boy completed antibiotic treatment with vancomycin for 14 days and was sent home. He later received the Prevenar 7 vaccine for pneumococcal infection, though it was not part of the national vaccination program at that time.\"\n}"}
{"row_index": 479, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 6-year-old male presented with a one-week history of nausea, vomiting, and headache, initially managed at outpatient clinics without improvement. Progression of symptoms, including fever, led to emergency department (ED) admission. Family history revealed a prior episode of acute otitis media (AOM) in infancy and a single episode of acute sinusitis approximately two months prior to admission. No history of skull trauma was reported. Physical examination demonstrated lethargy, neck stiffness, and positive meningeal signs (Brudzinski’s and Kerning signs), consistent with meningitis. Laboratory evaluation included complete blood count (CBC) with differential (WBC: 29,190/mm³, with 4% bands), biochemistry, glucose, and blood culture. Lumbar puncture was performed, yielding cerebrospinal fluid (CSF) analysis, bacterial/viral culture, and CSF biochemistry. CSF showed a WBC count of 3,240/uL with 91% neutrophils, glucose of 55 mg/dL, and total protein of 160.5 mg/dL. Gram stain of CSF identified Streptococcus pneumoniae, prompting immediate initiation of vancomycin and cefotaxime. Both CSF and blood cultures confirmed Streptococcus pneumoniae serotype 23F. Antibiotic sensitivity testing indicated vancomycin efficacy against this serotype, leading to continued therapy for 14 days. The patient had previously suffered from bacterial meningitis six months prior, with identical findings: CSF gram stain positive for Streptococcus pneumoniae 23F, and positive CSF and blood cultures. Immunological assessment, including complement levels and immunoglobulin profiles, was performed and revealed no abnormalities, ruling out primary immunodeficiency as a cause. Given the history of recurrent sinusitis and the temporal association with recurrent meningitis, a chronic bony defect secondary to persistent sinus inflammation was hypothesized. Initial sinus CT imaging demonstrated right maxillary sinusitis without bony erosion. A nuclear scan was subsequently performed to evaluate for cerebrospinal fluid (CSF) leakage, which revealed CSF leakage originating from the right petroocciptital region into the middle ear. High-resolution CT (HRCT) of the temporal bones demonstrated focal enlargement of the right facial nerve canal, erosion of the bony canal at the geniculate ganglion and tympanic"}
{"row_index": 480, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman had problems with her feet, especially the big toe and second toe, that made walking hard and painful. Her toes were bent wrong, and she had thick, painful calluses on her feet. She tried wearing big, soft shoes for years, but it didn’t help much. She kept falling and felt unbalanced. Her doctor found that her big toe was out of place and her second toe was crossing over it. The second toe was bent inward (varus), and this made walking feel like stepping on a pebble. On one foot, the second toe was much worse than on the other. She had surgery on both feet using a soft tissue method called syndesmosis, which didn’t cut any bone. The surgery fixed the big toe position by tying the first and second metatarsal bones together with a special suture. Surprisingly, after this, the second toe bent inward problem fixed itself — it didn’t need any extra surgery. On both feet, the second toe straightened out on its own. Only the right foot’s second toe still had a small problem, so a little extra work was done to fix it. The surgery looked good and felt good after she walked again. This shows that sometimes, fixing one part of the foot can help fix another part without doing extra work.\"\n}"}
{"row_index": 481, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 60-year-old woman had long-standing foot problems, including bilateral hallux valgus (HV) deformities and crossover deformities between her first and second toes. She tried wearing wider, softer shoes for years, but the pain from walking—especially on uneven ground or stairs—got worse. She developed thick, painful calluses on her feet and had trouble balancing, leading to several falls. Her mother had a similar issue but didn’t need surgery and managed it without intervention.\\n\\nOn exam, her feet showed that the first metatarsal bones were unstable and the second toe on her right foot was severely bent inward (varus deformity), crossing over the big toe. This deformity was causing discomfort and affecting her walking. X-rays and pressure studies showed that her weight was shifting to the second and third toes, worsening the calluses and foot pain.\\n\\nShe chose surgery to fix both her HV and crossover issues. Instead of cutting bones (osteotomy), her doctor used a soft tissue procedure called a syndesmosis procedure, which involves using sutures to realign the first and second metatarsal bones without removing any bone.\\n\\nDuring surgery, the first and second metatarsals were tied together with dissolvable sutures. To our surprise, once the first metatarsal was properly aligned, the second toe’s varus deformity corrected itself—both on the right and left feet—without any extra surgery. The only remaining issue on the right foot was a mild bend in the second toe, which was fixed with a small soft tissue release.\\n\\nAfter surgery, she wore a forefoot cast for three months and returned to normal walking and shoes after six months. She now has good function and appearance in her feet. The case raises an interesting question: why does the second toe deformity correct itself when the first metatarsal is realigned? This may be due to how the bones and soft tissues are connected and how movement affects the toe alignment.\"\n}"}
{"row_index": 482, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 60-year-old female presented with progressive hallux valgus (HV) and bunion deformities, compounded by a bilateral crossover deformity between the first and second toes. Despite initial management with increasingly accommodating footwear—characterized by a widened forefoot region and soft, roomy toe box—she experienced persistent metatarsalgia, with significant pain localized to the first metatarsal head, described as a constant sensation of walking on a pebble. This led to the development of thick, painful metatarsal calluses bilaterally, particularly under the forefoot, and impaired ambulation, including difficulties with balance on uneven terrain and stair descent. She had experienced multiple falls, reflecting functional compromise. Her mother had a milder HV deformity and managed without surgical intervention, suggesting a familial predisposition. Physical examination revealed bilateral HV deformities with only partial correction possible passively. Passive range of motion at the first metatarsophalangeal joint (MPJ) was 45° in extension and 60° in flexion on the right foot, and 60° and 45° on the left foot, indicating hypermobility. The right second toe exhibited a severe varus deformity, crossing over the hallux without notable clawing, while the left second toe had a milder varus deformity. Manual realignment of the left second toe was complete, whereas the right toe remained resistant to realignment. Both second MPJs were moderately tender and demonstrated reduced passive flexion due to pain. First metatarsals displayed hypermobility in both sagittal and frontal planes, consistent with joint instability. Dorsoplantar standing radiographs revealed a right foot first intermetatarsal angle (IMA) of 17.5° (above the normal upper limit of 9°) and metatarsophalangeal angle (MPA) of 33.7° (exceeding the normal upper limit of 15°), with a left foot IMA of 16.8° and MPA of 27.9°. All first and second MPJs were incongruent, and the right second MPJ showed dorsomedial subluxation. Both tibial and fibular sesamoids were dissociated from the first metatarsal, indicating ligamentous insufficiency and joint instability. Preoperative plantar pressure analysis using F-Scan (Tekscan, USA) demonstrated"}
{"row_index": 483, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 34-year-old woman fell and hit her head, lost consciousness for a few minutes, then woke up. She didn’t go to the hospital right away. Three days later, she started having a mild headache and went to a clinic. Doctors saw her brain scan and found a blood clot on the side of her head — a big one, but not pressing on her brain yet. Her brain’s spaces were bigger than normal, which means she had a condition called hydrocephalus since birth, but it didn’t cause problems in her growing up. She didn’t have seizures in years, and she’s been doing well in school and work. She didn’t show any signs of brain damage. The headache got worse at first, but by day 5, it was getting better. Doctors decided not to do surgery — just gave her pain medicine and watched her closely. Her headache went away, and she stayed healthy. After 3 weeks, the blood clot got smaller. A year later, she was still fine with no symptoms. This is rare — people with this kind of hydrocephalus can get a brain bleed after a fall, even if they don’t feel sick at first. The hydrocephalus might have helped keep the brain from getting too full, so symptoms came later.\"\n}"}
{"row_index": 484, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 34-year-old woman with a history of congenital hydrocephalus (a condition where fluid builds up in the brain) due to a narrow aqueduct, did not have surgery. She had no symptoms from the condition and lived a normal life, going to school, earning a bachelor’s degree, and working full time. After falling in the bathroom, she lost consciousness briefly and regained it quickly. She didn’t seek medical help at first but started having a mild headache three days later. A CT scan showed a large blood clot (epidural hematoma) on the right side of her brain, which was causing slight pressure. Her brain’s ventricles were enlarged, a sign of hydrocephalus, but there was no serious fluid buildup or brain swelling. She had a small fracture in her skull but no other injuries. Despite the injury, she remained asymptomatic except for the headache. Because she had no serious symptoms and the blood clot was stable, doctors chose not to operate and instead treated her with pain relief and close monitoring. Her headache improved over time, and by day 8, she was able to go home. Follow-up scans showed the blood clot was shrinking, and her brain pressure was normal. At 10 months after the injury, she was fully recovered with no symptoms. This case is rare — adults with arrested hydrocephalus (where brain fluid buildup stops or slows) may still develop brain bleeds after head injuries, even without noticeable symptoms. The hydrocephalus may have helped reduce pressure in the brain, delaying the appearance of symptoms.\"\n}"}
{"row_index": 485, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 34-year-old female presented with traumatic brain injury following a fall on the bathroom floor, resulting in transient loss of consciousness and subsequent development of an acute right temporal epidural hematoma measuring 41 cc in volume, with a midline shift of 0.4 cm on initial cranial CT. The hematoma was associated with effacement of cerebral sulci and enlargement of the lateral and third ventricles, consistent with increased intracranial volume, but without transependymal effusion. A linear, nondisplaced fracture of the right temporal bone was identified. Despite the presence of a large epidural hematoma, the patient remained asymptomatic except for a mild, intermittent right-sided headache that began on day 3 postinjury. Neurological examination revealed a Glasgow Coma Scale (GCS) of 15, with equal and briskly reactive pupils, normal visual acuity (20/25 bilaterally), and absence of papilledema, sensory, or motor deficits. Head circumference of 59 cm was noted to be in the upper 97th percentile for her height, consistent with chronic macrocephaly, likely secondary to congenital hydrocephalus due to aqueductal stenosis, which had been managed without surgical intervention. The patient had a history of epilepsy controlled with phenobarbital, with the last seizure occurring approximately 15 years prior, and a recent mild COVID-19 infection five months before the injury. She had no developmental delays, completed high school at the top of her class, earned a bachelor’s degree at age 20, and was actively pursuing a master’s degree while maintaining full-time employment. The patient was initially advised to seek neurosurgical evaluation but delayed consultation until day 5 postinjury. Repeat cranial CT on day 5 demonstrated stable hematoma size, with a marked reduction in headache severity. Conservative management was initiated, including analgesic therapy and close clinical monitoring, with resolution of headache by day 8. Follow-up imaging at 3 weeks postinjury showed progressive reduction in hematoma volume and attenuation, indicating resolution of the hematoma without significant intracranial pressure elevation. Transcranial Doppler study revealed normal pulsatility indices across all intracranial arteries, confirming the absence of significant cerebral perfusion abnormalities or increased intracranial pressure. At 10-month follow-up, the patient remained asymptomatic with no neurological deficits"}
{"row_index": 486, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 67-year-old woman from a area where leishmaniasis is common had a swollen face that lasted two months. The swelling was red, puffy, and had bleeding crusts on her nose. She first got treated for a common facial infection with antibiotics, but it didn’t help. Doctors then guessed it was a type of skin infection called cutaneous leishmaniasis, and checked a small skin sample that showed the tiny parasites causing it. She was given two medicines—metronidazole and clarithromycin—for 30 days, and her symptoms got better.\"\n}"}
{"row_index": 487, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 67-year-old woman from a region in Morocco where leishmaniasis is common had swelling on her face and nose that lasted for two months. The swelling was red, swollen, and had crusts, and was initially treated for a bacterial infection called facial erysipelas with antibiotics. However, the symptoms did not improve. Based on her medical history and the appearance of the skin, doctors suspected a type of leishmaniasis known as erysipeloid form. This was confirmed by a skin test that showed the presence of Leishmania parasites. She was then treated with metronidazole and clarithromycin for 30 days, and her condition improved significantly. She had a heart condition called left bundle branch block, so the doctors chose this treatment instead of the usual antimonial drugs.\"\n}"}
{"row_index": 488, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 67-year-old female from Chichaoua, Morocco—a known endemic zone for Leishmania tropica—presented with a two-month history of progressive swelling in the centrofacial region, characterized by an erythematous and edematous plaque extending to the eyelids, accompanied by hemorrhagic crusts at the nasal tip. The clinical presentation was initially managed as facial erysipelas with a course of amoxicillin-clavulanic acid and ciprofloxacin for 15 days, which failed to result in clinical improvement. Given the patient's residence in an endemic area for Leishmania tropica and the presence of a family history of leishmaniasis (her grandson having been previously treated for the disease), the differential diagnosis was strongly shifted toward cutaneous leishmaniasis in its erysipeloid form. Confirmation was achieved via skin smear, which demonstrated the presence of Leishmania amastigotes, confirming the diagnosis. The specific species of Leishmania could not be identified at the institutional level. Notably, the patient had a left bundle branch block on electrocardiography, which contraindicated the use of pentavalent antimonial agents due to potential cardiac toxicity. As such, a combination therapy of metronidazole (1.5 g daily) and clarithromycin (15 mg/kg body weight) was selected as a safer alternative, based on its efficacy in treating erysipeloid cutaneous leishmaniasis in patients with cardiac comorbidities. The patient received this regimen for 30 days and demonstrated a good clinical response with progressive resolution of the lesion. The erysipeloid form of cutaneous leishmaniasis is a self-limiting but persistent infection, typically presenting with erythematous, edematous plaques and hemorrhagic crusts, and is caused by Leishmania tropica, which resides in the dermal layers and replicates intracellularly within macrophages as amastigotes. The pathogenesis involves the invasion of dermal macrophages, leading to local inflammation, edema, and tissue damage. Metronidazole and clarithromycin are effective due to their ability to penetrate the macrophage phagolysosome and exert activity against intracellular amastigotes, with clarithromycin showing particularly favorable pharmacokinetic properties in this setting. This case underscores the importance of considering leish"}
{"row_index": 489, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 57-year-old woman had high potassium levels in her blood for years, always between 5.3 and 5.9. Her doctor checked her closely, but she had no symptoms or problems. Her blood pressure was under control, and her heart test was normal. She was referred to a kidney specialist because the high potassium didn’t go down, even when she followed a low-potassium diet. The doctor checked everything — her blood, urine, and other tests — to find the cause. Nothing was wrong with her kidneys, no signs of blood cell breakdown, no infections, no muscle damage, and no other known causes. Even after testing for possible rare conditions, nothing explained the high levels. The doctors thought it might be a rare issue where the blood sample shows high potassium even when it’s not real — like a trick in the lab. They tested the blood under different conditions to see if the high number was just a mistake. The results showed the high level didn’t happen. So, the cause of the high potassium could not be found. The patient’s body is just doing something unusual, and no treatment is needed right now.\"\n}"}
{"row_index": 490, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 57-year-old woman had high potassium levels in her blood for four years, ranging from 5.3 to 5.9 mmol/L (normal is 3.5–5.1 mmol/L). She had no symptoms or signs of illness, and her heart tests were normal. She was on medication for high blood pressure, which was well controlled. After being referred to a nephrology specialist, doctors checked for possible causes like kidney problems, broken cells, or acidosis. All tests came back normal, including blood cell counts, kidney function, and urine tests. A diet low in potassium was recommended, but it didn’t lower her potassium levels. Even after checking for conditions like blood disorders or tissue damage, no cause was found. The doctors considered a rare condition called familial pseudohyperkalemia, where blood samples might show falsely high potassium due to how they’re stored or transported. They tested the blood under different conditions (cold, room temperature, body temperature) and found that the high potassium level only appeared when the sample was left uncentrifuged and exposed to certain conditions. When the sample was properly processed, the potassium level returned to normal. This suggests the high reading was not real, and the cause of the elevated levels could not be confirmed.\"\n}"}
{"row_index": 491, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"We present a case of a 57-year-old female with a four-year history of persistent mild hyperkalemia, defined by serum potassium levels ranging from 5.3 to 5.9 mmol/L (reference range: 3.5–5.1 mmol/L), without associated clinical manifestations such as muscle weakness, cardiac arrhythmias, or hemolysis. Spectrophotometric hemolysis index remained below 6 mg/dL across all laboratory reports, excluding intravascular hemolysis as a contributing factor. Electrocardiographic monitoring was normal, with no evidence of electrolyte-induced conduction abnormalities. The patient's medical history included chronic arterial hypertension, which was well-controlled with angiotensin-converting enzyme (ACE) inhibitor therapy. No significant findings were noted during physical examination or anamnesis. She was receiving amlodipine for blood pressure control, with stable clinical outcomes.\\n\\nThe patient was referred to the Nephrology Unit for further evaluation due to the persistent elevation of serum potassium despite the absence of identifiable clinical or laboratory triggers. Initial management included a potassium-restricted diet, which was implemented for a three-month period. At the three-month follow-up, a serum sample was collected and analyzed; the sample was non-hemolyzed (hemolysis index <6 mg/dL) and revealed a potassium concentration of 5.5 mmol/L, confirming the continued presence of hyperkalemia.\\n\\nA comprehensive differential diagnosis was conducted to exclude common etiologies of hyperkalemia, including: (1) renal insufficiency, (2) intravascular hemolysis, (3) metabolic acidosis, (4) tissue breakdown (e.g., rhabdomyolysis), and (5) pseudohyperkalemia secondary to oncohematologic conditions such as essential thrombocytosis or acute or chronic leukemia. Laboratory workup included a hemogram with reticulocyte count and blood smear, general biochemistry (including ions, hemolysis index, hepatic enzymes—GOT, GPT, GGT, LDH, ALP, renal function—creatinine, urea, and estimated glomerular filtration rate via CKD-EPI equation), creatine kinase (CK), haptoglobin, phosphocalcic parameters, and iron metabolism (iron, transferrin saturation, transferrin, ferritin),"}
{"row_index": 492, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A family has a rare condition called Noonan syndrome. The girl, her sister, mother, maternal aunt, grandmother, and one female cousin all have signs of this condition. Three of them had genetic testing, and it showed that the girl and her sister both got the same change in a gene called LZTR1 from their mom. The girl also has a problem with growth hormone, which makes her grow slower than others. She has some typical features like wide-set eyes, a short nose, low ears, and a curved spine. She also has a weak heart rhythm and a small jaw. Her growth hormone level is low, and her bones are not growing as fast as they should. Doctors said she has Noonan syndrome with growth hormone deficiency, and because of her spine problems, they don’t recommend giving her growth hormone treatment right now.\"\n}"}
{"row_index": 493, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A family has been studied where multiple members have Noonan syndrome, a genetic condition that can cause physical and developmental differences. The proband, a 6.6-year-old girl, along with her sister, mother, maternal aunt, grandmother, and a female cousin, showed signs of Noonan syndrome, either typical or atypical. Only three family members had genetic testing, and the results showed that both the proband and her sister inherited the same genetic change in the LZTR1 gene (c.1149+1G>T) from their mother. This gene mutation is linked to the condition. The girl also had growth hormone deficiency, which means her body doesn't produce enough growth hormone, and she did not have any other genetic changes. She had short stature, delayed development, and physical features common in Noonan syndrome, such as widely spaced eyes, a short nose, low-set ears, and a webbed appearance of the upper lip. She also had scoliosis and a bone deformity in her spine. Her growth hormone levels were low, and her bone age was younger than her actual age. Her heart, liver, kidneys, and brain were normal. Because of her severe spinal issues, treatment with growth hormone was not recommended.\"\n}"}
{"row_index": 494, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"We herein describe a family with LZTR1-related Noonan syndrome. The proband, a 6.6-year-old female, was referred for evaluation of short stature as the first child of nonconsanguineous parents, born at 41 weeks of gestation via vaginal delivery with a birth weight of 1800 g (<P3rd) and length of 47 cm (<P3rd). She exhibited significant prenatal and postnatal growth retardation, with current height of 90.5 cm (−6.3 SD), weight of 11 kg (−4.9 SD), and BMI of 13.4 kg/m² (P10–25th). Her arm span/height ratio was 0.92 (−2 SD) and sitting height/height ratio was 0.58 (+3 SD), both deviating from standard reference values. Psychomotor development was mildly delayed. Clinical examination revealed typical Noonan syndrome features including hypertelorism, downslanting palpebral fissures, epicanthal folds, low-set oval posteriorly rotated ears with thick helix, short broad nose with depressed root and full tip, deeply grooved long philtrum, high and wide vermilion peaks, highly arched palate, micrognathia, short neck, cubitus valgus, scoliosis, café au lait spots, and mild hypertrichosis. Additional findings included squinting, refractive errors, and nystagmus. Laboratory investigations showed IGF-1 level of 61 μg/L (−1.9 SD), and growth hormone (GH) stimulation testing (insulin and levodopa protocols) demonstrated a GH peak of 5.54 ng/mL, below the cut-off value of 7 ng/mL, confirming growth hormone deficiency. Electrocardiography revealed frequent premature ventricular beats (second and third rhythms). Imaging studies, including X-ray and MRI of the spine, identified a hemivertebral deformity of the third thoracic vertebra and scoliosis with a Cobb’s angle of 28°; bone age was assessed at 5.5 years. Hormonal evaluations of the adrenal, thyroid, and gonadal axes were within normal limits, and tumor markers (AFP, HCG, CEA) were negative. No structural abnormalities were detected on cardiac, hepatic, renal, gynecological,"}
{"row_index": 495, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 82-year-old man had surgery to remove his bladder and prostate because of cancer. Four days after surgery, he suddenly lost movement in all four limbs — his arms and legs — but didn’t feel pain or have trouble speaking. Doctors thought it might be a problem in his spine, but scans showed no blockage or bleeding in the spine. Instead, the problem was found in his brain: two small strokes happened at the same time on both sides, in areas that control movement. These strokes were caused by a lack of blood flow, likely because of a blood clot that came from his heart, maybe linked to his cancer. Since there was no clear reason found, doctors started giving him medicine to prevent more clots. His arms got better over time, but his legs stayed weak. This case shows that even after major surgery, a stroke can happen due to blood clots, and early treatment helps prevent more problems.\"\n}"}
{"row_index": 496, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 82-year-old man had surgery to remove his bladder and prostate due to cancer. Four days after the surgery, he suddenly developed severe weakness in all four limbs — arms and legs — without pain or loss of sensation. His brain scans showed acute bilateral strokes in the areas of the brain that control movement (precentral gyri), which explains the weakness. These strokes were caused by a sudden blockage of blood flow, likely due to a blood clot that traveled from his heart. Although the spinal cord was checked and found normal, the brain imaging revealed the strokes. The patient had no history of falls or trauma, and his blood clotting tests were normal, making the cause harder to find. Because of the surgery and anesthesia, doctors suspected a clot from the heart. He was started on anticoagulant medication to prevent future clots. After recovery, he began taking aspirin for long-term prevention. The key point is that this rare case shows that strokes can happen after major surgery, even without obvious risk factors, and brain imaging is essential for diagnosis.\"\n}"}
{"row_index": 497, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 82-year-old Caucasian male was admitted to the urology department for radical cystoprostatectomy due to localized prostate adenocarcinoma. On the fourth postoperative day, he abruptly developed severe painless tetraparesis, characterized by Medical Research Council (MRC) grade 2/5 muscle strength in proximal upper limb muscles bilaterally and 0/5 in both lower limbs, with no involvement of cranial nerves, impaired consciousness, or sensory deficits. There were no cerebellar signs. Neurological examination revealed brisk tendon reflexes and positive pyramidal signs bilaterally, strongly suggesting a lesion affecting the central nervous system, such as acute spinal cord compression, subdural hemorrhage, or ischemia. No recent trauma or fall was reported prior to symptom onset. A peridural catheter had been placed for analgesia postoperatively and was removed the previous day without complications.\\n\\nAn emergency magnetic resonance imaging (MRI) study was performed, requiring the removal of metal brackets from subcutaneous tissue due to surgical implants. Spinal MRI did not demonstrate any evidence of spinal cord compression, subarachnoid hemorrhage, or ischemic changes (Figure A), thereby excluding a primary spinal cord pathology. In contrast, cranial MRI revealed acute bilateral ischemic infarctions localized to the precentral gyri—specifically, the median portion of the precentral gyrus on both sides (Figure B and C; arrows)—with no involvement of the internal capsule (Figure D). T2-weighted imaging at the level of the primary motor cortex showed no abnormal signal intensity at the time of presentation, which is consistent with acute ischemia and supports a time-dependent pathophysiological mechanism (Figure E). The precentral gyrus is supplied by the anterior cerebral artery (supplying the medial one-third) and the middle cerebral artery (supplying the lateral two-thirds) bilaterally.\\n\\nOver the subsequent days, upper extremity weakness gradually resolved, while lower limb paralysis persisted, indicating a regionally selective motor cortex infarction. Comprehensive diagnostic evaluation, including carotid duplex sonography, 24-hour electrocardiography (ECG), and transesophageal echocardiography, failed to identify any structural vascular disease, cardiac thrombus, or paroxysmal atrial fibrillation. While hypercoagulability associated with prostate cancer may have contributed to the cerebral ischemia,"}
{"row_index": 498, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 60-year-old man had cancer in the back part of his pancreas. He didn’t have diabetes at first, and his blood sugar was normal. Doctors found the cancer with a blood test and imaging. They removed the cancer with surgery and gave him chemo to help fight it. Two years later, the cancer came back in one spot in his liver. The blood test for sugar started going up fast, and his blood sugar got worse as the cancer grew. So, doctors started giving him insulin to control his blood sugar. Even though the liver cancer didn’t respond well to chemo, it was only one spot, so they did surgery to remove it. After that surgery, his blood sugar got better right away and he stopped needing insulin. Now, two years later, he’s still alive and the cancer hasn’t come back.\"\n}"}
{"row_index": 499, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 60-year-old man was diagnosed with cancer in the tail of the pancreas, and his blood sugar levels were normal at the time of diagnosis. He had no history of diabetes or family history of pancreatic cancer. After surgery to remove the tumor (distal pancreatectomy) with lymph node removal, he received chemotherapy (S-1) to reduce the risk of the cancer coming back. Two years later, a single tumor was found in his liver, which was treated with two rounds of chemotherapy—first gemcitabine/nab-paclitaxel, then modified FOLFIRINOX. However, his blood sugar control worsened over time, rising from 5.6% to over 10%, and matched the growth of the tumor. Because of this, insulin therapy was started to manage his high blood sugar. Despite the liver tumor not responding well to chemotherapy, it was completely removed with a left hepatectomy since only one tumor was present. After the surgery, his blood sugar improved right away, and insulin was stopped. Two years after the second surgery, the patient is still alive and has not had any signs of cancer coming back.\"\n}"}
{"row_index": 500, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 60-year-old male with a history of past smoking (Brinkman Index: 800) and chronic alcohol consumption (20 g/day for 20 years) was referred for evaluation of suspected pancreatic tail adenocarcinoma based on an elevated carbohydrate antigen 19-9 (CA19-9) concentration of 286.8 U/mL during a routine medical screening. He had no prior history of diabetes, significant comorbidities, or familial predisposition to pancreatic cancer. His body mass index was 20.8 kg/m², and he reported no weight loss. Dynamic contrast-enhanced computed tomography (dCECT) demonstrated a hypovascular lesion in the pancreatic tail, consistent with a resectable tumor. Endoscopic ultrasonographic fine-needle aspiration confirmed the diagnosis of adenocarcinoma. Positron emission tomography (PET) revealed a high standardized uptake value (SUVmax = 6.6), supporting malignant activity. Magnetic resonance imaging with gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA) showed no synchronous liver metastases, and the tumor was deemed anatomically resectable. The patient underwent a curative-intent distal pancreatectomy with regional lymph node dissection via radical antegrade modular pancreatosplenectomy. The pancreatic parenchyma was resected just above the superior mesenteric vein using tri-stapler technology, resulting in an operative time of 251 minutes and extraoperative blood loss of 720 mL. A clinically significant postoperative pancreatic fistula developed but resolved spontaneously without intervention, and the patient was discharged on postoperative day 40. Pathological examination revealed a 36 × 18 × 17-mm moderately differentiated tubular adenocarcinoma with no lymph node metastasis (0/27), absence of microscopic lymphatic invasion, but presence of microscopic venous invasion. The tumor margin was negative for extrapancreatic extension, and the resection margins were clear. The postoperative stage was classified as IB (T2N0M0) according to the Union for International Cancer Control 8th edition. Adjuvant S-1 chemotherapy (120 mg/m²/day) was administered for six months postoperatively.\\n\\nTwo years following the initial pan"}
{"row_index": 501, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 61-year-old man had high blood pressure and a small cancer in his kidney called chromophobe renal cell carcinoma. Later, a tumor was found in his seminal vesicle (a part of the male reproductive system). Doctors thought it might be a spread from the kidney cancer, but tests showed it was actually a separate tumor called a primary paraganglioma. This new tumor did not spread to other parts of the body and was not made from cancer cells. It had features that match a normal type of tumor in that area. The tumor cells showed signs of a specific protein (synaptophysin and chromogranin), and some surrounding cells had S100 protein. Tests for genetic changes found nothing in either tumor, which supports it being a new, original tumor. The man had surgery to remove the tumor, and his blood pressure is now under control. He is still alive after 14 months.\"\n}"}
{"row_index": 502, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This report describes a rare case of a primary paraganglioma in the seminal vesicle of a 61-year-old man. He had been dealing with high blood pressure and previously had a tumor in his kidney, diagnosed as chromophobe renal cell carcinoma. When a new tumor appeared in his left seminal vesicle, doctors considered it a possible spread (metastasis) from the kidney cancer. However, tests showed that the seminal vesicle tumor was not made of cancer cells and did not match the kidney tumor's characteristics. Instead, it showed markers typical of a paraganglioma — a type of tumor that arises from nerve tissue. The tumor cells expressed synaptophysin and chromogranin, and the surrounding cells showed S100 protein, which is common in such tumors. Both the kidney tumor and the seminal vesicle tumor had normal levels of SDHA and SDHB proteins, and no gene mutations were found in these genes. Imaging confirmed no other tumors were present, supporting the diagnosis that this was a primary tumor in the seminal vesicle, not a spread from the kidney. The patient recovered well and remains alive with controlled blood pressure after 14 months of follow-up.\"\n}"}
{"row_index": 503, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 61-year-old obese male presented with persistent arterial hypertension and was evaluated for an incidental renal tumor discovered during imaging for hypertension. Laparoscopic partial nephrectomy revealed a chromophobe renal cell carcinoma (cRCC), a rare subtype of clear cell carcinoma characterized by minimal cytoplasmic visibility and low mitochondrial content, typically associated with intact von Hippel-Lindau (VHL) pathway function. Following one year of surveillance, a new lesion was identified in the left seminal vesicle. Magnetic resonance imaging (MRI) demonstrated a well-circumscribed, heterogeneous solid tumor measuring 32 mm in maximum dimension, with clear anatomical separation from the rectal and bladder walls, suggesting a benign or low-aggressiveness growth pattern. The patient underwent laparoscopic excision of the left seminal vesicle.\\n\\nGross examination revealed a seminal vesicle measuring 6 × 3 × 2 cm, with a solid, smooth, brownish nodule of 30 mm in greatest diameter. Surgical margins were negative for residual tumor, indicating complete resection. Microscopic evaluation showed well-defined nests of cuboidal tumor cells separated by vascular fibrous septa, with no evidence of vascular invasion, mitotic activity, or necrosis. Focal glandular structures were observed, and individual tumor cells exhibited a large central nucleus with small to medium-sized nucleoli and granular eosinophilic cytoplasm, consistent with neuroendocrine differentiation.\\n\\nDifferential diagnoses included metastatic chromophobe renal cell carcinoma, primary adenocarcinoma of the seminal vesicle, and paraganglioma. Immunohistochemical analysis was performed to discriminate between these entities. Tumor cells demonstrated strong positive immunoreactivity for synaptophysin and chromogranin, markers of neuroendocrine differentiation, supporting a neuroendocrine origin. Peripheral S100 protein-positive cells, likely corresponding to sustentacular cells, were identified at the tumor nest margins, further supporting a paraganglioma phenotype. Absence of keratin expression (AE1/AE3, CK7, CK8/18) excluded both primary and metastatic adenocarcinoma, reinforcing the diagnosis of a primary paraganglioma of the seminal vesicle. The Ki-67 labeling index was less than 2%, indicating a very low proliferative rate and favorable biological behavior.\\n\\nGenomic analysis was conducted on paraffin-"}
{"row_index": 504, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old Chinese woman had pain in her upper belly for 6 months. A scan found a small spot in her left liver, about 1.1 x 1.3 cm in size. The spot looked different on the scan — dark on one setting and bright on another — which made doctors think it might be cancer. After checking the tissue from the surgery, they found it was a rare type of liver cancer called LEL-ICC. She had the surgery using a small camera (laparoscopic) and recovered well, going home after 5 days. No signs of cancer were found after 28 months of follow-up. She still checks in every 3 months for blood tests and scans to stay safe.\"\n}"}
{"row_index": 505, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old Chinese woman had been experiencing upper abdominal pain for six months. An MRI scan found a 1.1×1.3 cm lesion in the left part of her liver. The lesion looked different on the scan — it appeared dark on T1-weighted images and bright on T2-weighted images — which made doctors think it could be liver cancer. However, after surgery, the tissue was examined closely. The results showed it was a rare type of liver cancer called LEL-ICC. This type of cancer is linked to Epstein-Barr virus (EBV) and has specific markers that helped confirm the diagnosis. The patient had hepatitis B for six years, but her virus was inactive and not actively causing harm. Her other cancer markers were within normal ranges. She had a laparoscopic surgery to remove the part of the liver, and she recovered well, being discharged on postoperative day 5. After surgery, she had regular check-ups every three months for the first two years, then every six months. All tests remained normal, and she has not had any signs of cancer recurrence even after 28 months of follow-up. She is currently healthy and doing well.\"\n}"}
{"row_index": 506, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old Chinese female presented to Sichuan University West China Hospital with a 6-month history of upper abdominal pain. She had no history of radiotherapy, industrial chemical exposure, hormonal therapy, or contraceptive use. She reported one prior pregnancy and delivery of a male child. No personal or family history of hypertension, diabetes, smoking, or alcohol consumption was noted. Physical examination was unremarkable. Laboratory findings included hemoglobin 14.2 g/dL (normal range: 13–17.5 g/dL), white blood cells 7.12×10⁹/L (normal: 3.5–9.5×10⁹/L), platelets 249×10⁹/L (normal: 100–300×10⁹/L), total bilirubin 12.5 μmol/L (normal: 5.0–28 μmol/L), and aspartate aminotransferase (AST) 35 IU/L (normal <50 IU/L). Serological testing revealed carcinoembryonic antigen (CEA) of 5.54 ng/mL (abnormal threshold: ≥3.4 ng/mL), hepatitis B surface antigen (HBsAg) positive, and hepatitis B virus DNA (HBV-DNA) less than 1×10² IU/mL (indicating inactive HBV infection). Tumor markers CA19-9, CA125, and α-fetoprotein were 25.6 U/mL (normal <30 U/mL), 13.3 U/mL (normal <24 U/mL), and 3.37 ng/mL (normal <7 ng/mL), respectively. Abdominal computed tomography (CT) identified a lesion in the left lobe of the liver with no evidence of metastatic disease. Magnetic resonance imaging (MRI) of the upper abdomen revealed a 1.1×1.3 cm lesion in the left hepatic lobe exhibiting low signal intensity on T1-weighted sequences and high signal intensity on T2-weighted sequences, findings consistent with hepatocellular carcinoma (HCC) on initial preoperative evaluation. The patient underwent laparoscopic left lateral sectionectomy. Macroscopic examination revealed a yellowish solid mass measuring 12 mm in diameter. Microscopic analysis demonstrated an undifferentiated"}
{"row_index": 507, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 66-year-old man suddenly lost movement on his right side and had trouble speaking. Doctors found a blocked blood vessel in his brain, on the left side, that was causing the stroke. They gave him a medicine called alteplase to open the blockage, then used a special tool to remove the clot. The blood vessel didn’t fully open at first, so they used a balloon to stretch it out while keeping blood flowing to other parts of the body. This helped the blood vessel open up again. After 15 minutes, the blockage was fixed and the man’s symptoms went away. He didn’t have any brain damage, and by the next day, he could move and speak normally. The doctors said the treatment worked well and the blockage improved over time. He’s now back to normal, with no problems after a year.\"\n}"}
{"row_index": 508, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 66-year-old man suddenly developed weakness on his right side and difficulty speaking. MRI scans showed a blockage in the left middle cerebral artery, which supplies blood to part of the brain. He received alteplase, a clot-dissolving drug, and then underwent a procedure to remove the clot using a catheter (mechanical thrombectomy). The clot was partially removed, but the artery remained narrowed (stenosis), leading to a recurrence of blockage. To fix this, a special balloon catheter was used for a 15-minute angioplasty while keeping blood flow to other parts of the body. This helped reopen the artery and improved blood flow. The patient’s symptoms improved significantly, and by the next day, his neurological score was back to normal. Follow-up scans showed the blockage had improved, and he was able to go home without any lasting brain damage. He was prescribed medications to prevent future clots, and after three months, his artery showed better flow. No major problems occurred for over a year. The treatment used a device not yet officially approved, but it was approved by the hospital after careful review and with the patient’s informed consent.\"\n}"}
{"row_index": 509, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 66-year-old male presented with an acute onset of right hemiplegia and dysarthria at 7:30 a.m. while driving, prompting immediate transport to the hospital. Clinical examination revealed right facial paralysis, dysarthria, right upper extremity paralysis, and right upper and lower extremity paresthesia, with an initial National Institutes of Health Stroke Scale (NIHSS) score of 6/42. Magnetic resonance imaging (MRI) diffusion-weighted imaging (DWI) demonstrated hyperintense signals in the left putamen, corona radiata, and partial region of the middle cerebral artery, consistent with acute ischemic infarction. Magnetic resonance angiography (MRA) confirmed a distal occlusion of the left middle cerebral artery (MCA), while T2-weighted imaging showed no visible thrombus within the occluded segment, suggesting a thrombus-free occlusion with possible vasospasm or plaque-induced stenosis. A perfusion-diffusion mismatch was identified, supporting the indication for intravenous alteplase therapy, which was administered at 9:27 a.m. after correction of hypotension with nicardipine. The treatment protocol was guided by current stroke guidelines, with no contraindications identified.\\n\\nEndovascular recanalization was initiated using a 9 Fr sheath placed in the right femoral artery, with subsequent guidance of a 9 Fr OPTIMO catheter into the left internal carotid artery. Internal carotid arteriography revealed a distal occlusion of the left MCA. In the delayed phase, collateral circulation was observed via anastomosis of the cerebral pia mater, providing anterior-to-middle cerebral artery perfusion. A rebar (Medtronic) was advanced distal to the occlusion using a CHIKAI 14 × 200 cm catheter to secure the distal vessel, and a Trevo XP ProVue Retriever (4.0 × 30 mm, Stryker) was deployed. Post-deployment imaging demonstrated immediate flow restoration, but poor stent dilation was noted in the occluded segment, indicating significant arterial stenosis. The proximal diameter of the stenosis was 2.6 mm, and the distal diameter was 2.1 mm, confirming a moderate to severe stenotic lesion. Following retrieval of the Trevo, a 1"}