{"row_index": 0, "doc_id": 20, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 38-year-old woman had a weak heart since she was 17, after a bad throat infection that might have hurt her heart muscle. Her heart couldn’t pump blood well, and she was in serious danger. She stayed in the hospital for 10 months and got treatment to help her heart work better, including medicines to stop her heart from beating too fast and to reduce fluid buildup. After a while, her heart started to get stronger and stayed that way for 4 years. Then it got worse again for 2 years, but later she got stable again. She had a baby the first time, and her heart stayed strong. During her second pregnancy, in the second trimester, her heart weakened again and stayed weak for a few months. But now, in May 2017, she is doing fine. She takes medicines every day — for her heart, to control fluid, and to keep her heart steady. She can do normal daily activities, has two children, and doesn’t work. Her doctor says her heart is stable and she doesn’t need a special heart device. She just needs to keep taking her medicines, watch her fluid intake, stay healthy, and go to check-ups regularly.\"\n}", "generated_text": "A 38-year-old woman had a weak heart since she was 17, after a bad throat infection that might have hurt her heart muscle. Her heart couldn’t pump blood well, and she was in serious danger. She stayed in the hospital for 10 months and got treatment to help her heart work better, including medicines to stop her heart from beating too fast and to reduce fluid buildup. After a while, her heart started to get stronger and stayed that way for 4 years. Then it got worse again for 2 years, but later she got stable again. She had a baby the first time, and her heart stayed strong. During her second pregnancy, in the second trimester, her heart weakened again and stayed weak for a few months. But now, in May 2017, she is doing fine. She takes medicines every day — for her heart, to control fluid, and to keep her heart steady. She can do normal daily activities, has two children, and doesn’t work. Her doctor says her heart is stable and she doesn’t need a special heart device. She just needs to keep taking her medicines, watch her fluid intake, stay healthy, and go to check-ups regularly."}
{"row_index": 1, "doc_id": 21, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old man broke his right thigh bone after a small fall, where his hip twisted. He had a bone problem called fibrous dysplasia in his thigh years ago, which was fixed with surgery and bone graft 20 years ago. The old surgery part was removed a year later. This time, because the bone broke again, doctors took out a big piece of the upper thigh bone and replaced it with a hip implant. They also took a small tissue sample to make sure it was the same bone problem from when he was a child. Now, he can walk and do light activities, though he still has some pain when walking long distances. He’s doing well and feels happy with how his hip is working.\"\n}", "generated_text": "A 27-year-old man broke his right thigh bone after a small fall, where his hip twisted. He had a bone problem called fibrous dysplasia in his thigh years ago, which was fixed with surgery and bone graft 20 years ago. The old surgery part was removed a year later. This time, because the bone broke again, doctors took out a big piece of the upper thigh bone and replaced it with a hip implant. They also took a small tissue sample to make sure it was the same bone problem from when he was a child. Now, he can walk and do light activities, though he still has some pain when walking long distances. He’s doing well and feels happy with how his hip is working."}
{"row_index": 2, "doc_id": 21, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 27-year-old man came to the emergency department with a broken right femur, specifically at the base of the neck, after a fall that involved pressure and twisting of the hip. The fracture was classified as a serious type (Garden II, Pauwells III, AO 31B2.3r) and occurred despite a low-energy injury. He had a history of fibrous dysplasia — a bone condition — in his right hip area, which was treated 20 years ago with surgery to remove abnormal bone (curettage), bone grafting, and the use of a metal fixation device. This device was removed one year later. A biopsy later confirmed the condition was fibrous dysplasia. Because of the nature of the fracture and the underlying disease, doctors decided on a wide removal of the upper part of the femur and a total hip replacement using a modular prosthesis, along with a biopsy to confirm it was the same fibrous dysplasia from his childhood. The surgery was successful, and the patient is now stable, walking with support and able to do daily activities. He still has some walking limitations due to a scar in the gluteal muscle, but he enjoys low-impact activities like walking and is very satisfied with his recovery.\"\n}", "generated_text": "A 27-year-old man came to the emergency department with a broken right femur, specifically at the base of the neck, after a fall that involved pressure and twisting of the hip. The fracture was classified as a serious type (Garden II, Pauwells III, AO 31B2.3r) and occurred despite a low-energy injury. He had a history of fibrous dysplasia — a bone condition — in his right hip area, which was treated 20 years ago with surgery to remove abnormal bone (curettage), bone grafting, and the use of a metal fixation device. This device was removed one year later. A biopsy later confirmed the condition was fibrous dysplasia. Because of the nature of the fracture and the underlying disease, doctors decided on a wide removal of the upper part of the femur and a total hip replacement using a modular prosthesis, along with a biopsy to confirm it was the same fibrous dysplasia from his childhood. The surgery was successful, and the patient is now stable, walking with support and able to do daily activities. He still has some walking limitations due to a scar in the gluteal muscle, but he enjoys low-impact activities like walking and is very satisfied with his recovery."}
{"row_index": 3, "doc_id": 22, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 4-year-old boy with advanced neuroblastoma received intensive chemotherapy, followed by stem cell transplants — first using his own stem cells (autologous HSCT), then a transplant from a donor using cord blood (allogeneic CBT). After the transplant, he developed symptoms of a respiratory infection about a month before, including upper respiratory issues, and tested positive for RSV (a common virus that causes colds in children). On day 194, he started having severe breathing difficulties and was admitted to the hospital. Tests showed signs of lung damage, including inflammation and scarring in the small blood vessels of the lungs, which led to a diagnosis of PVOD (a condition where the lungs become stiff and hard to breathe). Pathology from a lung biopsy showed both signs of past viral infection and the lung injury linked to PVOD. The doctors believe that the RSV infection may have triggered or worsened the development of PVOD in this child.\"\n}", "generated_text": "A 4-year-old boy with advanced neuroblastoma received intensive chemotherapy, followed by stem cell transplants — first using his own stem cells (autologous HSCT), then a transplant from a donor using cord blood (allogeneic CBT). After the transplant, he developed symptoms of a respiratory infection about a month before, including upper respiratory issues, and tested positive for RSV (a common virus that causes colds in children). On day 194, he started having severe breathing difficulties and was admitted to the hospital. Tests showed signs of lung damage, including inflammation and scarring in the small blood vessels of the lungs, which led to a diagnosis of PVOD (a condition where the lungs become stiff and hard to breathe). Pathology from a lung biopsy showed both signs of past viral infection and the lung injury linked to PVOD. The doctors believe that the RSV infection may have triggered or worsened the development of PVOD in this child."}
{"row_index": 4, "doc_id": 23, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old man started feeling a bad cough, short of breath even doing small things, and lost 10 kilograms in 4 months. Tests showed a lump in his right lung and fluid around it. A small piece of tissue was taken and looked at under a microscope. The cells were large and spread out, with lots of immune cells around them. This type of cancer is rare and not like regular lung cancer. The cancer cells had markers that match a specific kind of cancer called pulmonary lymphoepithelioma-like carcinoma (CTLP). It had a very high level of a protein called PD-L1 and was found to have Epstein-Barr virus. He got 6 rounds of chemo using platinum and durvalumab, but the cancer grew worse. He had side effects like hearing loss and kidney problems, so the chemo was changed. After 9 months, he died from not being able to breathe.\"\n}", "generated_text": "A 65-year-old man started feeling a bad cough, short of breath even doing small things, and lost 10 kilograms in 4 months. Tests showed a lump in his right lung and fluid around it. A small piece of tissue was taken and looked at under a microscope. The cells were large and spread out, with lots of immune cells around them. This type of cancer is rare and not like regular lung cancer. The cancer cells had markers that match a specific kind of cancer called pulmonary lymphoepithelioma-like carcinoma (CTLP). It had a very high level of a protein called PD-L1 and was found to have Epstein-Barr virus. He got 6 rounds of chemo using platinum and durvalumab, but the cancer grew worse. He had side effects like hearing loss and kidney problems, so the chemo was changed. After 9 months, he died from not being able to breathe."}
{"row_index": 5, "doc_id": 24, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old boy found a lump in his groin that could be moved, but wasn't painful or red. No other symptoms were present. Doctors removed the lump to make sure it wasn't cancer or a serious disease. The test results showed the lump was made of special cells called plasma cells, which is a rare kind of disease in kids. This is the first time such a case has been found in the groin area. After 1 year of checking, no new lumps or symptoms came back. The boy is doing fine and has no other problems.\"\n}", "generated_text": "A 13-year-old boy found a lump in his groin that could be moved, but wasn't painful or red. No other symptoms were present. Doctors removed the lump to make sure it wasn't cancer or a serious disease. The test results showed the lump was made of special cells called plasma cells, which is a rare kind of disease in kids. This is the first time such a case has been found in the groin area. After 1 year of checking, no new lumps or symptoms came back. The boy is doing fine and has no other problems."}
{"row_index": 6, "doc_id": 25, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"The medical records of patients diagnosed with congenital myotonia were retrospectively reviewed in the pediatric neurology consultation at a third-level hospital between 2015 and 2020. Inclusion criteria included a clinical diagnosis of myotonia accompanied by a warm-up phenomenon, characteristic electromyographic (EMG) findings, or a family history, as well as a molecular diagnosis involving mutations in the CLCN1 gene. Demographic data (age and sex), disease course (age of onset, symptomatology, time to diagnosis, and clinical progression), family history, and response to therapeutic interventions were systematically extracted from the electronic medical records. All patients underwent comprehensive clinical evaluation, including laboratory testing and EMG assessment.\\n\\nFive patients with a clinical diagnosis of congenital myotonia were identified: three with Becker disease and two with Thomsen disease. The estimated incidence per 10,000 live births was 1:15,000 for the Becker phenotype and 1:21,000 for the Thomsen phenotype. The majority of patients were female; the only male patient presented with onset prior to age six. Initial clinical manifestations included lower-limb myotonia in four patients and upper-limb myotonia in all but one. Age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic testing was performed in all patients approximately two years after symptom onset, except in one case where the family declined testing. All patients exhibited worsening of myotonia with exposure to cold, with the warm-up phenomenon—defined as improvement of muscle tone following prolonged rest—observed exclusively in those with the Becker phenotype.\\n\\nPatients with recessive congenital myotonia demonstrated a progressive clinical course. Family history analysis revealed that patients 2 and 3 were sisters, with no clinical manifestations in their parents, suggesting an autosomal recessive inheritance pattern. The mother of patient 1 exhibited mild, cold-exacerbated myotonia, raising the possibility of subclinical carrier status. The patient who declined genetic testing had a reported history of myotonia in the maternal lineage, consistent with an inherited predisposition.\\n\\nSerum creatine kinase levels were not elevated in any of the patients, indicating that skeletal muscle damage is not a prominent feature of the disease. Electromyographic evaluation was abnormal in all patients except patient 1, who was evaluated at 2.8 years of age (at 2.8/12 years of age); subsequent EMG studies were not repeated due to clinical stability and the established diagnostic certainty. The absence of significant muscle enzyme elevation supports the notion that the pathophysiology is primarily due to impaired chloride channel function rather than active muscle degeneration.\\n\\nInitial pharmacological management primarily involved oxcarbazepine, particularly in patients with the recessive form (Becker disease), with generally favorable responses. However, in patient 2, oxcarbazepine lost efficacy over time, prompting the initiation of mexiletine. Patient 4 required multiple medications, all of which failed due to either therapeutic resistance or adverse effects. Patient 5, who had a mild clinical presentation, declined treatment. Patient 1 was found to carry a previously undescribed, likely pathogenic mutation in the CLCN1 gene (c.824T>C), inherited from his mother. Cases 1 to 3 exhibited the Becker phenotype and displayed composite heterozygosity, involving two distinct CLCN1 mutations. Cases 4 and 5 presented with the Thomsen phenotype, characterized by a more severe, early-onset form of myotonia. Patient 5 declined genetic testing, limiting the ability to confirm the specific inheritance pattern in this individual. The CLCN1 gene encodes the chloride channel subunit responsible for regulating membrane potential in skeletal muscle fibers; mutations in this gene lead to reduced chloride conductance, resulting in prolonged depolarization of the sarcolemma and subsequent muscle hyperexcitability, which manifests clinically as myotonia. This mechanism underlies the pathophysiology of both Becker and Thomsen congenital myotonias, with differences in severity and age of onset likely attributable to the nature and combination of mutations, including the novel c.824T>C variant identified in this cohort.\"\n}", "generated_text": "The medical records of patients diagnosed with congenital myotonia were retrospectively reviewed in the pediatric neurology consultation at a third-level hospital between 2015 and 2020. Inclusion criteria included a clinical diagnosis of myotonia accompanied by a warm-up phenomenon, characteristic electromyographic (EMG) findings, or a family history, as well as a molecular diagnosis involving mutations in the CLCN1 gene. Demographic data (age and sex), disease course (age of onset, symptomatology, time to diagnosis, and clinical progression), family history, and response to therapeutic interventions were systematically extracted from the electronic medical records. All patients underwent comprehensive clinical evaluation, including laboratory testing and EMG assessment.\n\nFive patients with a clinical diagnosis of congenital myotonia were identified: three with Becker disease and two with Thomsen disease. The estimated incidence per 10,000 live births was 1:15,000 for the Becker phenotype and 1:21,000 for the Thomsen phenotype. The majority of patients were female; the only male patient presented with onset prior to age six. Initial clinical manifestations included lower-limb myotonia in four patients and upper-limb myotonia in all but one. Age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic testing was performed in all patients approximately two years after symptom onset, except in one case where the family declined testing. All patients exhibited worsening of myotonia with exposure to cold, with the warm-up phenomenon—defined as improvement of muscle tone following prolonged rest—observed exclusively in those with the Becker phenotype.\n\nPatients with recessive congenital myotonia demonstrated a progressive clinical course. Family history analysis revealed that patients 2 and 3 were sisters, with no clinical manifestations in their parents, suggesting an autosomal recessive inheritance pattern. The mother of patient 1 exhibited mild, cold-exacerbated myotonia, raising the possibility of subclinical carrier status. The patient who declined genetic testing had a reported history of myotonia in the maternal lineage, consistent with an inherited predisposition.\n\nSerum creatine kinase levels were not elevated in any of the patients, indicating that skeletal muscle damage is not a prominent feature of the disease. Electromyographic evaluation was abnormal in all patients except patient 1, who was evaluated at 2.8 years of age (at 2.8/12 years of age); subsequent EMG studies were not repeated due to clinical stability and the established diagnostic certainty. The absence of significant muscle enzyme elevation supports the notion that the pathophysiology is primarily due to impaired chloride channel function rather than active muscle degeneration.\n\nInitial pharmacological management primarily involved oxcarbazepine, particularly in patients with the recessive form (Becker disease), with generally favorable responses. However, in patient 2, oxcarbazepine lost efficacy over time, prompting the initiation of mexiletine. Patient 4 required multiple medications, all of which failed due to either therapeutic resistance or adverse effects. Patient 5, who had a mild clinical presentation, declined treatment. Patient 1 was found to carry a previously undescribed, likely pathogenic mutation in the CLCN1 gene (c.824T>C), inherited from his mother. Cases 1 to 3 exhibited the Becker phenotype and displayed composite heterozygosity, involving two distinct CLCN1 mutations. Cases 4 and 5 presented with the Thomsen phenotype, characterized by a more severe, early-onset form of myotonia. Patient 5 declined genetic testing, limiting the ability to confirm the specific inheritance pattern in this individual. The CLCN1 gene encodes the chloride channel subunit responsible for regulating membrane potential in skeletal muscle fibers; mutations in this gene lead to reduced chloride conductance, resulting in prolonged depolarization of the sarcolemma and subsequent muscle hyperexcitability, which manifests clinically as myotonia. This mechanism underlies the pathophysiology of both Becker and Thomsen congenital myotonias, with differences in severity and age of onset likely attributable to the nature and combination of mutations, including the novel c.824T>C variant identified in this cohort."}
{"row_index": 7, "doc_id": 26, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 67-year-old woman had swelling in her left leg for six years. She already had a problem in her leg's blood vessels called AVMs, which didn’t go away even after treatment. Recently, she started feeling very tired and short of breath, which means her heart was struggling. Doctors found her heart was enlarged and not working well, and her leg swelling was getting worse. The problem was caused by a rare birth defect in her leg’s blood vessels that was sending too much blood to her heart. To fix it, doctors first placed a special stent in her leg to block the bad blood flow. This helped her heart feel better. After that, they did a second treatment to stop the blood from flowing into the wrong veins. After the treatments, her leg swelling went down and her heart started working better. She’s now much stronger and her symptoms are much better.\"\n}", "generated_text": "A 67-year-old woman had swelling in her left leg for six years. She already had a problem in her leg's blood vessels called AVMs, which didn’t go away even after treatment. Recently, she started feeling very tired and short of breath, which means her heart was struggling. Doctors found her heart was enlarged and not working well, and her leg swelling was getting worse. The problem was caused by a rare birth defect in her leg’s blood vessels that was sending too much blood to her heart. To fix it, doctors first placed a special stent in her leg to block the bad blood flow. This helped her heart feel better. After that, they did a second treatment to stop the blood from flowing into the wrong veins. After the treatments, her leg swelling went down and her heart started working better. She’s now much stronger and her symptoms are much better."}
{"row_index": 8, "doc_id": 26, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 67-year-old woman had been suffering from swelling in her left leg for six years. She was previously diagnosed with a complex congenital arteriovenous malformation (AVM) in her lower leg, but treatment with coils did not stop the swelling. Over the past month, she developed symptoms of heart failure, including fatigue and shortness of breath, and was taken to a hospital for further care. Tests showed her heart was enlarged and her heart function had worsened, with high levels of a heart failure marker (BNP). She also had poor blood flow in her leg arteries and no pulses in her lower leg. Imaging revealed a large AVM in the femoral and superficial femoral arteries, along with a swollen femoral artery and vein, which was likely causing the heart to work harder.\\n\\nBecause the AVM was too complex to be fully treated with coils alone, doctors used a covered stent placed in the femoral artery to block part of the abnormal blood flow. This helped reduce the amount of blood flowing into the leg, which in turn improved her heart failure symptoms. The surgery was done under general anesthesia using a catheter inserted through the leg, and the stent was placed exactly where the AVM was most active. After the procedure, her leg swelling and heart function improved significantly. One week later, blood flow in the leg dropped from 3400 ml/min to 1600 ml/min, and her BNP levels dropped, showing better heart health.\\n\\nIn a follow-up treatment, doctors used coils and other materials to block the main drainage veins of the AVM. This further reduced the abnormal blood flow. After one year, her leg swelling had greatly improved, her heart function had recovered, and her BNP levels were much lower. The patient is now doing better, with improved daily function and reduced symptoms of heart failure. This case shows that combining stent placement and embolization can be effective in treating complex congenital AVMs that cause heart failure.\"\n}", "generated_text": "A 67-year-old woman had been suffering from swelling in her left leg for six years. She was previously diagnosed with a complex congenital arteriovenous malformation (AVM) in her lower leg, but treatment with coils did not stop the swelling. Over the past month, she developed symptoms of heart failure, including fatigue and shortness of breath, and was taken to a hospital for further care. Tests showed her heart was enlarged and her heart function had worsened, with high levels of a heart failure marker (BNP). She also had poor blood flow in her leg arteries and no pulses in her lower leg. Imaging revealed a large AVM in the femoral and superficial femoral arteries, along with a swollen femoral artery and vein, which was likely causing the heart to work harder.\n\nBecause the AVM was too complex to be fully treated with coils alone, doctors used a covered stent placed in the femoral artery to block part of the abnormal blood flow. This helped reduce the amount of blood flowing into the leg, which in turn improved her heart failure symptoms. The surgery was done under general anesthesia using a catheter inserted through the leg, and the stent was placed exactly where the AVM was most active. After the procedure, her leg swelling and heart function improved significantly. One week later, blood flow in the leg dropped from 3400 ml/min to 1600 ml/min, and her BNP levels dropped, showing better heart health.\n\nIn a follow-up treatment, doctors used coils and other materials to block the main drainage veins of the AVM. This further reduced the abnormal blood flow. After one year, her leg swelling had greatly improved, her heart function had recovered, and her BNP levels were much lower. The patient is now doing better, with improved daily function and reduced symptoms of heart failure. This case shows that combining stent placement and embolization can be effective in treating complex congenital AVMs that cause heart failure."}
{"row_index": 9, "doc_id": 26, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 67-year-old female patient with a six-year history of progressive left lower limb edema was diagnosed with complex congenital arteriovenous malformations (AVMs) in the lower extremity, following a prior embolization intervention involving two coils (20 mm × 40 cm, BSX, USA) one year prior. Despite this, her lower limb swelling remained unresponsive, and she developed symptomatic acute heart failure characterized by progressive fatigue, dyspnea, and cardiac dysfunction. She was referred to Chengdu University of Traditional Chinese Medicine Hospital for comprehensive evaluation. The patient had no prior history of cardiovascular disease, trauma, or surgical interventions, though she reported lifelong oral estrogen use for menopausal symptoms. Physical examination revealed severe edema, skin sclerosis, absent pulses in the popliteal and distal arteries, and a tremor in the left thigh. Echocardiography demonstrated left ventricular enlargement, moderate mitral regurgitation, severe tricuspid regurgitation, a left ventricular ejection fraction (LVEF) of 60%, and markedly elevated B-type natriuretic peptide (BNP) levels at 2853 ng/L. Electrocardiography showed sinus tachycardia (105 bpm) and left atrial enlargement. Chest CT confirmed cardiac enlargement without pulmonary pathology. Preoperative computed tomography angiography (CTA) revealed a left iliac artery aneurysm, marked dilation of the common femoral artery (CFA; 27 mm), superficial femoral artery (SFA; 22 mm), and complex AVMs involving both the SFA and profunda femoris artery. The femoral and superficial veins were significantly dilated during arterial phase imaging, with non-visualization of the popliteal and anterior tibial arteries. The patient was diagnosed with complex congenital lower limb AVMs, acute decompensated chronic heart failure, and classified as New York Heart Association (NYHA) Class IV. Preoperative CFA flow volume was measured at 3400 ml/min. Given the persistence of high shunt flow and inadequate response to coil embolization, a covered stent graft was deemed necessary to reduce venous shunting and alleviate hemodynamic burden on the heart. Access was achieved via antegrade surgical puncture of the right CFA using a 14 F (Cook Medical, USA) catheter sheath under general anesthesia. A 20 mm × 12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China) was selected based on preoperative CTA measurements showing a middle SFA diameter of 19 mm. A 0.035 guidewire and single-curve catheter were used to navigate to the popliteal artery, followed by transition to a 0.035 super-hard guidewire for stable catheterization during stent deployment. The stent was placed at the distal SFA, where AVM burden was highest. Completion angiography demonstrated marked reduction in venous opacification and restoration of arterial visualization, including the popliteal artery. Postoperatively, the left femoral artery was closed with a 6–0 vascular risk suture. The procedure was performed with minimal duration to avoid exacerbating cardiac stress in the setting of acute heart failure. One week postoperatively, CFA flow decreased to 1600 ml/min, and BNP levels dropped to 1198 ng/L, indicating early improvement in cardiac function. A second-stage embolization was planned to target the nidus of the AVM. Under ultrasound guidance, the draining venous system was punctured via the right CFA, with a 5 F vascular sheath introduced. Contrast injection confirmed the presence of the AVM nidus and its draining veins. Embolization was performed using a 18–20 mm × 40 cm coil (BSX, USA), two microcoils (4 mm × 42 mm and 5 mm × 10 mm, USA), 3% polidocanol (6 mL, Kruelle, Germany), and 99% anhydrous ethanol (10 mL). Completion angiography showed near-complete obliteration of the AVM nidus and draining venous pathways. At one-year follow-up, the CFA flow reduced to 780 ml/min, echocardiography revealed mild atrial enlargement, minor mitral and tricuspid regurgitation, and an improved left ventricular ejection fraction (LVEF) of 71%, with BNP levels significantly reduced. This case illustrates the clinical utility of staged intervention—initial covered stent graft placement to reduce shunt volume and stabilize hemodynamics, followed by targeted embolization to achieve complete nidus occlusion in complex congenital lower", "generated_text": "{\n  \"proficient_health_literacy\": \"A 67-year-old female patient with a six-year history of progressive left lower limb edema was diagnosed with complex congenital arteriovenous malformations (AVMs) in the lower extremity, following a prior embolization intervention involving two coils (20 mm × 40 cm, BSX, USA) one year prior. Despite this, her lower limb swelling remained unresponsive, and she developed symptomatic acute heart failure characterized by progressive fatigue, dyspnea, and cardiac dysfunction. She was referred to Chengdu University of Traditional Chinese Medicine Hospital for comprehensive evaluation. The patient had no prior history of cardiovascular disease, trauma, or surgical interventions, though she reported lifelong oral estrogen use for menopausal symptoms. Physical examination revealed severe edema, skin sclerosis, absent pulses in the popliteal and distal arteries, and a tremor in the left thigh. Echocardiography demonstrated left ventricular enlargement, moderate mitral regurgitation, severe tricuspid regurgitation, a left ventricular ejection fraction (LVEF) of 60%, and markedly elevated B-type natriuretic peptide (BNP) levels at 2853 ng/L. Electrocardiography showed sinus tachycardia (105 bpm) and left atrial enlargement. Chest CT confirmed cardiac enlargement without pulmonary pathology. Preoperative computed tomography angiography (CTA) revealed a left iliac artery aneurysm, marked dilation of the common femoral artery (CFA; 27 mm), superficial femoral artery (SFA; 22 mm), and complex AVMs involving both the SFA and profunda femoris artery. The femoral and superficial veins were significantly dilated during arterial phase imaging, with non-visualization of the popliteal and anterior tibial arteries. The patient was diagnosed with complex congenital lower limb AVMs, acute decompensated chronic heart failure, and classified as New York Heart Association (NYHA) Class IV. Preoperative CFA flow volume was measured at 3400 ml/min. Given the persistence of high shunt flow and inadequate response to coil embolization, a covered stent graft was deemed necessary to reduce venous shunting and alleviate hemodynamic burden on the heart. Access was achieved via antegrade surgical puncture of the right CFA using a 14 F (Cook Medical, USA) catheter sheath under general anesthesia. A 20 mm × 12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China) was selected based on preoperative CTA measurements showing a middle SFA diameter of 19 mm. A 0.035 guidewire and single-curve catheter were used to navigate to the popliteal artery, followed by transition to a 0.035 super-hard guidewire for stable catheterization during stent deployment. The stent was placed at the distal SFA, where AVM burden was highest. Completion angiography demonstrated marked reduction in venous opacification and restoration of arterial visualization, including the popliteal artery. Postoperatively, the left femoral artery was closed with a 6–0 vascular risk suture. The procedure was performed with minimal duration to avoid exacerbating cardiac stress in the setting of acute heart failure. One week postoperatively, CFA flow decreased to 1600 ml/min, and BNP levels dropped to 1198 ng/L, indicating early improvement in cardiac function. A second-stage embolization was planned to target the nidus of the AVM. Under ultrasound guidance, the draining venous system was punctured via the right CFA, with a 5 F vascular sheath introduced. Contrast injection confirmed the presence of the AVM nidus and its draining veins. Embolization was performed using a 18–20 mm × 40 cm coil (BSX, USA), two microcoils (4 mm × 42 mm and 5 mm × 10 mm, USA), 3% polidocanol (6 mL, Kruelle, Germany), and 99% anhydrous ethanol (10 mL). Completion angiography showed near-complete obliteration of the AVM nidus and draining venous pathways. At one-year follow-up, the CFA flow reduced to 780 ml/min, echocardiography revealed mild atrial enlargement, minor mitral and tricuspid regurgitation, and an improved left ventricular ejection fraction (LVEF) of 71%, with BNP levels significantly reduced. This case illustrates the clinical utility of staged intervention—initial covered stent graft placement to reduce shunt volume and stabilize hemodynamics, followed by targeted embolization to achieve complete nidus occlusion in complex congenital lower"}
{"row_index": 10, "doc_id": 27, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 28-year-old man developed two red bumps on his right arm and forearm, with small blisters and sores in the middle, after being on vacation in coastal Ecuador. The area felt hot and itched a lot, but he didn’t have fever or other symptoms. Doctors took a small skin sample and saw signs of irritation and inflammation. Because of the location and his trip to a tropical area, they figured out it was caused by a bug called Paederus. He was treated with anti-itch medicine, creams to calm the skin, and cold compresses. After 8 days, the sores went away, but the skin stayed a bit darker in those areas.\"\n}", "generated_text": "A 28-year-old man developed two red bumps on his right arm and forearm, with small blisters and sores in the middle, after being on vacation in coastal Ecuador. The area felt hot and itched a lot, but he didn’t have fever or other symptoms. Doctors took a small skin sample and saw signs of irritation and inflammation. Because of the location and his trip to a tropical area, they figured out it was caused by a bug called Paederus. He was treated with anti-itch medicine, creams to calm the skin, and cold compresses. After 8 days, the sores went away, but the skin stayed a bit darker in those areas."}
{"row_index": 11, "doc_id": 27, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 28-year-old male with no significant medical history presented to the dermatology department with a 48-hour history of two erythematous plaques exhibiting central vesicular lesions and superficial ulceration situated on the flexor surfaces of the right arm and forearm, symmetrically positioned equidistant from the elbow crease. The lesions were associated with localized burning sensation and pruritus, with no systemic symptoms or evidence of self-medication. The patient reported a recent vacation in the coastal region of Ecuador, which served as a key environmental exposure factor. An incisional biopsy was performed and revealed histopathological features consistent with Paederus dermatitis, including epidermal acanthosis, parakeratosis, and intercellular spongiosis, along with neutrophilic infiltrates in the stratum corneum and perivascular lymphocytic infiltration extending through the superficial, middle, and deep dermis. These findings reflect a type IV hypersensitivity reaction mediated by T-helper 1 (Th1) cells, driven by exposure to Paederus beetles (Paederus fuscipes or Paederus spp.), whose defensive secretions contain cytotoxic compounds such as pederin and other sesquiterpene lactones that induce direct epidermal damage and immune activation. The diagnosis was confirmed based on the clinical presentation, geographic exposure context, and histopathological correlation. Management consisted of antihistamines to mitigate pruritus and histamine-mediated inflammation, topical corticosteroids to suppress dermal immune cell activity and reduce epidermal hyperplasia, and cold compresses to alleviate vascular congestion and symptomatic discomfort. The lesions completely resolved after 8 days of treatment, with residual post-inflammatory hyperpigmentation observed as a consequence of melanocyte activation and prolonged dermal inflammation. This case underscores the importance of considering endemic arthropod exposures in tropical regions when evaluating acute, localized, non-infectious dermatoses with a characteristic vesiculobullous and ulcerative pattern in flexural skin folds.\"\n}", "generated_text": "A 28-year-old male with no significant medical history presented to the dermatology department with a 48-hour history of two erythematous plaques exhibiting central vesicular lesions and superficial ulceration situated on the flexor surfaces of the right arm and forearm, symmetrically positioned equidistant from the elbow crease. The lesions were associated with localized burning sensation and pruritus, with no systemic symptoms or evidence of self-medication. The patient reported a recent vacation in the coastal region of Ecuador, which served as a key environmental exposure factor. An incisional biopsy was performed and revealed histopathological features consistent with Paederus dermatitis, including epidermal acanthosis, parakeratosis, and intercellular spongiosis, along with neutrophilic infiltrates in the stratum corneum and perivascular lymphocytic infiltration extending through the superficial, middle, and deep dermis. These findings reflect a type IV hypersensitivity reaction mediated by T-helper 1 (Th1) cells, driven by exposure to Paederus beetles (Paederus fuscipes or Paederus spp.), whose defensive secretions contain cytotoxic compounds such as pederin and other sesquiterpene lactones that induce direct epidermal damage and immune activation. The diagnosis was confirmed based on the clinical presentation, geographic exposure context, and histopathological correlation. Management consisted of antihistamines to mitigate pruritus and histamine-mediated inflammation, topical corticosteroids to suppress dermal immune cell activity and reduce epidermal hyperplasia, and cold compresses to alleviate vascular congestion and symptomatic discomfort. The lesions completely resolved after 8 days of treatment, with residual post-inflammatory hyperpigmentation observed as a consequence of melanocyte activation and prolonged dermal inflammation. This case underscores the importance of considering endemic arthropod exposures in tropical regions when evaluating acute, localized, non-infectious dermatoses with a characteristic vesiculobullous and ulcerative pattern in flexural skin folds."}
{"row_index": 12, "doc_id": 28, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A man in his 80s had a blocked bile duct causing yellowing of his skin and weight loss. Doctors found a tumor in his bile duct that couldn’t be removed, so they used a light-based treatment called PDT to ease the blockage. Before the treatment, he got a special medicine through his vein 24 hours earlier. During the procedure, a doctor used a tube to look inside the bile duct and guided a light tool through it to shine on the blocked area. The light was turned on slowly, every centimeter, to make sure the whole blockage was treated. Afterward, the doctor checked the bile duct again to make sure everything was okay. The treatment worked well at first — he didn’t feel sick for three months. But later, the blockage came back, and he had infections and other problems. He died 15 months after the treatment because of cancer spreading to his lungs.\"\n}", "generated_text": "A man in his 80s had a blocked bile duct causing yellowing of his skin and weight loss. Doctors found a tumor in his bile duct that couldn’t be removed, so they used a light-based treatment called PDT to ease the blockage. Before the treatment, he got a special medicine through his vein 24 hours earlier. During the procedure, a doctor used a tube to look inside the bile duct and guided a light tool through it to shine on the blocked area. The light was turned on slowly, every centimeter, to make sure the whole blockage was treated. Afterward, the doctor checked the bile duct again to make sure everything was okay. The treatment worked well at first — he didn’t feel sick for three months. But later, the blockage came back, and he had infections and other problems. He died 15 months after the treatment because of cancer spreading to his lungs."}
{"row_index": 13, "doc_id": 28, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"The patient, an 82-year-old male with a two-month history of obstructive jaundice and weight loss, underwent transduodenal photodynamic therapy (TFD) as a palliative intervention for recurrent biliary obstruction. Endoscopic ultrasound (EUS) demonstrated severe dilation of the common bile duct with choledocholithiasis, confirmed by endoscopic retrograde cholangiopancreatography (ERCP), which failed to extract stones due to disproportionate ductal dilation. A plastic biliary stent was placed initially, resulting in transient improvement, but cholestasis recurred at 45 days, with two subsequent ERCP attempts also failing. During the third ERCP, a long, irregular stenosis of the common hepatic duct was identified, and EUS revealed a well-circumscribed hypoechoic solid mass measuring 1.8 × 2 cm compressing the common hepatic duct, with evidence of involvement of the common hepatic artery. Ultrasound-guided needle biopsy confirmed a diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I). Staging determined the tumor to be inoperable, leading to referral for palliative photodynamic therapy (PDT). \\n\\nThe PDT procedure was performed under general anesthesia using intravenous administration of Photogen® (1.5 mg/kg) 24 hours prior to intervention. Photogen® is a porphyrin derivative with peak light absorption at 630 nm, enabling selective activation within tumor tissue upon illumination. Standard duodenoscopy (Olympus TJF-180) was performed to identify the greater duodenal papilla, followed by retrograde cannulation. A digital cholangioscope (SpyGlass™ DS, Boston Scientific) was then advanced into the common bile duct to directly visualize the stenotic segment. Neoplastic stenosis was identified via cholangioscopic examination. Under direct visualization, the illumination catheter (Medlight S.A., RD10-323) was advanced through the cholangioscope. This catheter is a three-way device: the first port features a 1 cm cylindrical light diffuser with two black radiopaque marks defining its distal limits; the second port accommodates a 0.025-inch guidewire for catheter guidance; the third port serves as an injection port for photosensitizer delivery. The illumination was administered at a power of 70 mW/cm² and a total dose of 90 J/cm², with repositioning performed every centimeter to ensure complete coverage of the obstructed area. The procedure lasted 150 minutes and concluded with a final cholangioscopic evaluation to assess immediate outcomes and detect adverse events. A 10 Fr plastic biliary stent was placed at the end of the session due to unavailability of a self-expanding metal stent. \\n\\nPost-procedure, the patient was maintained on a fasted state for 24 hours, with oral diet initiated if no adverse events were observed. Strict photoprotection measures were enforced, including avoidance of light exposure and use of sunglasses, particularly during the first week following PDT, to mitigate photosensitivity risk. The patient exhibited no signs of photosensitivity within the first week. However, early recurrence of cholestasis occurred, complicated by cholangitis. ERCP revealed stent obstruction due to biliary sludge and tumor necrotic debris. A biliary scan followed by re-drainage resolved the acute episode. The patient remained asymptomatic for three months, the longest period since disease onset. Subsequent recurrence was managed with a self-expanding metal stent, and systemic oncologic therapy was continued. Eventually, the patient developed dysphagia, requiring placement of a duodenal stent for palliative relief. He ultimately died from complications of pulmonary metastases, two years after symptom onset and 15 months after the TFD session. The procedure was technically successful with no intra-procedural complications, and the clinical benefit was sustained for a significant duration despite the underlying malignancy progression.\"\n}", "generated_text": "The patient, an 82-year-old male with a two-month history of obstructive jaundice and weight loss, underwent transduodenal photodynamic therapy (TFD) as a palliative intervention for recurrent biliary obstruction. Endoscopic ultrasound (EUS) demonstrated severe dilation of the common bile duct with choledocholithiasis, confirmed by endoscopic retrograde cholangiopancreatography (ERCP), which failed to extract stones due to disproportionate ductal dilation. A plastic biliary stent was placed initially, resulting in transient improvement, but cholestasis recurred at 45 days, with two subsequent ERCP attempts also failing. During the third ERCP, a long, irregular stenosis of the common hepatic duct was identified, and EUS revealed a well-circumscribed hypoechoic solid mass measuring 1.8 × 2 cm compressing the common hepatic duct, with evidence of involvement of the common hepatic artery. Ultrasound-guided needle biopsy confirmed a diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I). Staging determined the tumor to be inoperable, leading to referral for palliative photodynamic therapy (PDT). \n\nThe PDT procedure was performed under general anesthesia using intravenous administration of Photogen® (1.5 mg/kg) 24 hours prior to intervention. Photogen® is a porphyrin derivative with peak light absorption at 630 nm, enabling selective activation within tumor tissue upon illumination. Standard duodenoscopy (Olympus TJF-180) was performed to identify the greater duodenal papilla, followed by retrograde cannulation. A digital cholangioscope (SpyGlass™ DS, Boston Scientific) was then advanced into the common bile duct to directly visualize the stenotic segment. Neoplastic stenosis was identified via cholangioscopic examination. Under direct visualization, the illumination catheter (Medlight S.A., RD10-323) was advanced through the cholangioscope. This catheter is a three-way device: the first port features a 1 cm cylindrical light diffuser with two black radiopaque marks defining its distal limits; the second port accommodates a 0.025-inch guidewire for catheter guidance; the third port serves as an injection port for photosensitizer delivery. The illumination was administered at a power of 70 mW/cm² and a total dose of 90 J/cm², with repositioning performed every centimeter to ensure complete coverage of the obstructed area. The procedure lasted 150 minutes and concluded with a final cholangioscopic evaluation to assess immediate outcomes and detect adverse events. A 10 Fr plastic biliary stent was placed at the end of the session due to unavailability of a self-expanding metal stent. \n\nPost-procedure, the patient was maintained on a fasted state for 24 hours, with oral diet initiated if no adverse events were observed. Strict photoprotection measures were enforced, including avoidance of light exposure and use of sunglasses, particularly during the first week following PDT, to mitigate photosensitivity risk. The patient exhibited no signs of photosensitivity within the first week. However, early recurrence of cholestasis occurred, complicated by cholangitis. ERCP revealed stent obstruction due to biliary sludge and tumor necrotic debris. A biliary scan followed by re-drainage resolved the acute episode. The patient remained asymptomatic for three months, the longest period since disease onset. Subsequent recurrence was managed with a self-expanding metal stent, and systemic oncologic therapy was continued. Eventually, the patient developed dysphagia, requiring placement of a duodenal stent for palliative relief. He ultimately died from complications of pulmonary metastases, two years after symptom onset and 15 months after the TFD session. The procedure was technically successful with no intra-procedural complications, and the clinical benefit was sustained for a significant duration despite the underlying malignancy progression."}
{"row_index": 14, "doc_id": 29, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 77-year-old woman with a history of hypertension and dyslipidaemia presented to the emergency department with haematemesis and signs of shock (heart rate: 100 beats/min, blood pressure: 79/56 mmHg), along with anaemia (haemoglobin: 9.6 g/dL), suggesting upper gastrointestinal bleeding. Non-contrast-enhanced CT was performed due to renal dysfunction and revealed a steeply flexed third part of the duodenum on the right side of the aorta, running caudally without crossing anterior to the aorta. The duodenal-jejunal junction and jejunum were located in the right hemi-abdomen, with dilation of the second part of the duodenum and the stomach, and high-density gastric contents consistent with a gastric haematoma. Upper gastrointestinal endoscopy demonstrated a mucosal laceration at the gastric cardia, consistent with Mallory-Weiss syndrome, a well-documented condition first described by Mallory and Weiss in 1929, wherein forceful vomiting leads to mucosal tears at the gastroesophageal junction. The anatomical configuration of the duodenum—particularly its steep rightward flexion and luminal narrowing—contributed to proximal obstruction, which likely exacerbated repeated vomiting and thus the development of the laceration.\\n\\nInitial CT findings prompted suspicion of intestinal malrotation, given the right-sided displacement of the duodenal-jejunal junction and jejunum. However, repeat CT performed seven days later showed spontaneous resolution of this rightward deviation, indicating a non-malrotational etiology. The patient was discharged after this transient finding. Subsequently, two months later, she presented with a recurrent episode of haematemesis. Dynamic CT revealed contrast extravasation in the dilated stomach, and again, the third part of the duodenum was flexed on the right side of the aorta, with the duodenal-jejunal junction and jejunum displaced to the right hemi-abdomen. Endoscopy confirmed a recurrent gastric cardial laceration, consistent with Mallory-Weiss syndrome.\\n\\nA follow-up non-contrast CT two months after the second haematemesis revealed no persistent duodenal deviation, but demonstrated oedematous wall thickening in the second part of the duodenum. Without prior imaging, this would have been interpreted as duodenitis; however, the clinical context of repeated, spontaneous right-sided deviations of the duodenal-jejunal junction and jejunum—despite their eventual resolution—led to the diagnosis of dysplasia of the ligament of Treitz. This condition is characterized by an abnormal, redundant, or poorly anchored ligament of Treitz, which normally anchors the duodenojejunal junction to the retroperitoneum and stabilizes the small intestine. In this case, the ligament of Treitz was anatomically formed but exhibited incomplete fixation to the upper jejunum, with attachment limited to the duodenum and absence of retroperitoneal anchoring. This results in a fulcrum-like mechanism allowing the jejunum to fold or deviate freely, particularly during increased intra-abdominal pressure (e.g., from vomiting), thereby reproducing transient right-sided displacement of the duodenum and jejunum.\\n\\nLaparotomy was performed, which confirmed the absence of intestinal malrotation and normal relative positioning between the duodenum and jejunum. The jejunum was anatomically located on the left side of the abdomen. The ligament of Treitz was present and formed, but its fixation to the upper jejunum was incomplete, with only partial attachment to the duodenum and no secure retroperitoneal anchoring. The duodenal-jejunal junction was not fixed to the retroperitoneum, allowing for dynamic mobility. Surgically, the upper jejunum was secured with four sutures to the retroperitoneum on the left side to stabilize the anatomical relationship. The postoperative course was uncomplicated, and the patient has remained asymptomatic with no further episodes of haematemesis. The transient, spontaneous rightward deviations observed on CT imaging are attributable to the mechanical instability of the ligament of Treitz, rather than true malrotation, supporting the diagnosis of dysplasia of the ligament of Treitz as the underlying pathophysiological mechanism.\"\n}", "generated_text": "A 77-year-old woman with a history of hypertension and dyslipidaemia presented to the emergency department with haematemesis and signs of shock (heart rate: 100 beats/min, blood pressure: 79/56 mmHg), along with anaemia (haemoglobin: 9.6 g/dL), suggesting upper gastrointestinal bleeding. Non-contrast-enhanced CT was performed due to renal dysfunction and revealed a steeply flexed third part of the duodenum on the right side of the aorta, running caudally without crossing anterior to the aorta. The duodenal-jejunal junction and jejunum were located in the right hemi-abdomen, with dilation of the second part of the duodenum and the stomach, and high-density gastric contents consistent with a gastric haematoma. Upper gastrointestinal endoscopy demonstrated a mucosal laceration at the gastric cardia, consistent with Mallory-Weiss syndrome, a well-documented condition first described by Mallory and Weiss in 1929, wherein forceful vomiting leads to mucosal tears at the gastroesophageal junction. The anatomical configuration of the duodenum—particularly its steep rightward flexion and luminal narrowing—contributed to proximal obstruction, which likely exacerbated repeated vomiting and thus the development of the laceration.\n\nInitial CT findings prompted suspicion of intestinal malrotation, given the right-sided displacement of the duodenal-jejunal junction and jejunum. However, repeat CT performed seven days later showed spontaneous resolution of this rightward deviation, indicating a non-malrotational etiology. The patient was discharged after this transient finding. Subsequently, two months later, she presented with a recurrent episode of haematemesis. Dynamic CT revealed contrast extravasation in the dilated stomach, and again, the third part of the duodenum was flexed on the right side of the aorta, with the duodenal-jejunal junction and jejunum displaced to the right hemi-abdomen. Endoscopy confirmed a recurrent gastric cardial laceration, consistent with Mallory-Weiss syndrome.\n\nA follow-up non-contrast CT two months after the second haematemesis revealed no persistent duodenal deviation, but demonstrated oedematous wall thickening in the second part of the duodenum. Without prior imaging, this would have been interpreted as duodenitis; however, the clinical context of repeated, spontaneous right-sided deviations of the duodenal-jejunal junction and jejunum—despite their eventual resolution—led to the diagnosis of dysplasia of the ligament of Treitz. This condition is characterized by an abnormal, redundant, or poorly anchored ligament of Treitz, which normally anchors the duodenojejunal junction to the retroperitoneum and stabilizes the small intestine. In this case, the ligament of Treitz was anatomically formed but exhibited incomplete fixation to the upper jejunum, with attachment limited to the duodenum and absence of retroperitoneal anchoring. This results in a fulcrum-like mechanism allowing the jejunum to fold or deviate freely, particularly during increased intra-abdominal pressure (e.g., from vomiting), thereby reproducing transient right-sided displacement of the duodenum and jejunum.\n\nLaparotomy was performed, which confirmed the absence of intestinal malrotation and normal relative positioning between the duodenum and jejunum. The jejunum was anatomically located on the left side of the abdomen. The ligament of Treitz was present and formed, but its fixation to the upper jejunum was incomplete, with only partial attachment to the duodenum and no secure retroperitoneal anchoring. The duodenal-jejunal junction was not fixed to the retroperitoneum, allowing for dynamic mobility. Surgically, the upper jejunum was secured with four sutures to the retroperitoneum on the left side to stabilize the anatomical relationship. The postoperative course was uncomplicated, and the patient has remained asymptomatic with no further episodes of haematemesis. The transient, spontaneous rightward deviations observed on CT imaging are attributable to the mechanical instability of the ligament of Treitz, rather than true malrotation, supporting the diagnosis of dysplasia of the ligament of Treitz as the underlying pathophysiological mechanism."}
{"row_index": 15, "doc_id": 30, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 28-year-old man from Morocco had pain in his belly, especially on the right side, and had a fever, chills, and lost weight over a month. He didn’t drink or smoke, and had been vaccinated for tuberculosis. His doctor found a swollen liver with small spots on it that looked like signs of infection. Tests showed these spots were likely caused by tuberculosis, not cancer or another disease. A small surgery was done to take a piece of the liver for testing, and the result confirmed it was tuberculosis. He started taking medicine to fight the tuberculosis, and within days, his fever and pain went away. After three months, the spots on his liver got smaller and fewer. He’s getting better.\"\n}", "generated_text": "A 28-year-old man from Morocco had pain in his belly, especially on the right side, and had a fever, chills, and lost weight over a month. He didn’t drink or smoke, and had been vaccinated for tuberculosis. His doctor found a swollen liver with small spots on it that looked like signs of infection. Tests showed these spots were likely caused by tuberculosis, not cancer or another disease. A small surgery was done to take a piece of the liver for testing, and the result confirmed it was tuberculosis. He started taking medicine to fight the tuberculosis, and within days, his fever and pain went away. After three months, the spots on his liver got smaller and fewer. He’s getting better."}
{"row_index": 16, "doc_id": 30, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 28-year-old Moroccan man with no smoking or drinking habits was admitted to the hospital after experiencing abdominal pain for about a month, along with fever, chills, sweating, loss of appetite, and a 6-kilogram weight loss. The pain was mainly in the upper right part of his abdomen, and he had been experiencing digestive issues like alternating diarrhea and constipation. Initially, his symptoms were mild, but they worsened over time, leading to a significant weight loss of 12 kilograms over three months.\\n\\nPhysical exams showed signs of inflammation, including a high fever and fast heart rate. Blood tests revealed elevated white blood cells and inflammation markers, but no evidence of liver damage or viral hepatitis was found. Imaging scans showed multiple small nodules in the liver that were not enhancing after contrast was given. These nodules were most noticeable in two areas of the liver.\\n\\nAlthough initial tests for tuberculosis (TB) and other infections were negative, the liver biopsies taken during a laparoscopic procedure showed characteristic signs of tuberculosis, including granulomas with caseous necrosis — a hallmark of TB infection. This confirmed a diagnosis of focal liver tuberculosis.\\n\\nThe patient was started on standard anti-tuberculosis medication, which includes four drugs for the first two months, followed by two drugs for the next four months. After starting treatment, his symptoms improved quickly. His fever and inflammation went away, and follow-up scans after three months showed that the liver nodules had shrunk in number and size. The overall clinical and lab results improved significantly, indicating a good response to treatment.\"\n}", "generated_text": "A 28-year-old Moroccan man with no smoking or drinking habits was admitted to the hospital after experiencing abdominal pain for about a month, along with fever, chills, sweating, loss of appetite, and a 6-kilogram weight loss. The pain was mainly in the upper right part of his abdomen, and he had been experiencing digestive issues like alternating diarrhea and constipation. Initially, his symptoms were mild, but they worsened over time, leading to a significant weight loss of 12 kilograms over three months.\n\nPhysical exams showed signs of inflammation, including a high fever and fast heart rate. Blood tests revealed elevated white blood cells and inflammation markers, but no evidence of liver damage or viral hepatitis was found. Imaging scans showed multiple small nodules in the liver that were not enhancing after contrast was given. These nodules were most noticeable in two areas of the liver.\n\nAlthough initial tests for tuberculosis (TB) and other infections were negative, the liver biopsies taken during a laparoscopic procedure showed characteristic signs of tuberculosis, including granulomas with caseous necrosis — a hallmark of TB infection. This confirmed a diagnosis of focal liver tuberculosis.\n\nThe patient was started on standard anti-tuberculosis medication, which includes four drugs for the first two months, followed by two drugs for the next four months. After starting treatment, his symptoms improved quickly. His fever and inflammation went away, and follow-up scans after three months showed that the liver nodules had shrunk in number and size. The overall clinical and lab results improved significantly, indicating a good response to treatment."}
{"row_index": 17, "doc_id": 30, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 28-year-old male, single, without children, active military personnel, presented with a 5-week history of progressive epigastric and right upper quadrant abdominal pain, accompanied by intermittent fever (peak 39.1°C), chills, profuse night sweats, anorexia, and a 6 kg weight loss. No history of alcohol use, tobacco consumption, or significant comorbidities was reported; he had received BCG vaccination and no positive family or personal history of infectious or hepatic disease. Physical examination revealed an asthenic patient with hepatomegaly and moderate right hypochondrial tenderness, consistent with a systemic inflammatory response syndrome (SIRS): tachycardia (124 bpm), tachypnea (22 breaths/min), and elevated body temperature. Laboratory findings included neutrophilic leukocytosis (17,800 cells/mm³), markedly elevated C-reactive protein (323 mg/L), and a positive procalcitonin level (4.1 ng/L), suggesting a bacterial or infectious etiology. Hepatic function tests were within normal limits: ALT 22 IU/L (normal <40 IU/L), AST 17 IU/L (<35 IU/L), GGT 42 IU/L (<50 IU/L), alkaline phosphatase 115 IU/L (normal 40–150 IU/L), bilirubin normal, prothrombin time 78%, and albumin 39 g/L. Renal function and electrolyte balance were unremarkable. Imaging studies, including chest radiography and abdominal ultrasound, were non-contributory. Blood and urine cultures, performed during febrile peaks, were negative. Serological testing for hepatitis B, C, HIV, and syphilis was negative. Lactate dehydrogenase (231 IU/L) and beta-2 microglobulin (2.28 mg/L) were within normal ranges. GeneXpert testing for Mycobacterium tuberculosis in respiratory specimens and biopsy samples was negative; quantiferon tuberculin test was also negative, excluding latent tuberculosis infection. A thoraco-abdomino-pelvic CT scan revealed an enlarged liver (17 cm), with multiple well-defined, rounded hypodense lesions, non-enhancing after contrast administration, primarily in segments I (21×16 mm) and V (36×27 mm). Echo-guided liver biopsy demonstrated subacute fibro-inflammatory changes with no evidence of malignancy or viral hepatitis. Hepatic MRI further characterized the lesions as dysmorphic, with heterogeneous T2 signal intensity, hyperintense perilesional rims on T2, peripheral enhancement post-contrast, and largest lesions in segments I (20×22 mm) and V (33×31 mm). No deep lymphadenopathy was observed. Diagnostic laparoscopy was performed to obtain biopsy specimens from hepatic nodules, which showed histologically confirmed epithelioid and gigantocellular granulomas with caseous necrosis—pathological findings consistent with focal hepatic tuberculosis. The patient was initiated on standard anti-tuberculous therapy: Phase 1 (2 months) of quadritherapy (isoniazid, rifampicin, pyrazinamide, ethambutol) administered orally in the morning on an empty stomach, followed by Phase 2 (4 months) of bithiapine (isoniazid and rifampicin) with identical dosing regimen. Clinical and biological response was observed within days of therapy initiation, with resolution of fever, chills, and systemic inflammatory markers. At three months post-treatment, follow-up imaging demonstrated a significant reduction in both the number and volume of hepatic lesions, supporting a favorable clinical course. This case represents a rare presentation of focal hepatic tuberculosis in a young, previously healthy individual, with non-specific initial symptoms and imaging findings, underscoring the importance of considering tuberculous hepatopathy in patients with chronic abdominal pain, unexplained weight loss, and persistent low-grade fever despite negative standard infectious workups.\"\n}", "generated_text": "A 28-year-old male, single, without children, active military personnel, presented with a 5-week history of progressive epigastric and right upper quadrant abdominal pain, accompanied by intermittent fever (peak 39.1°C), chills, profuse night sweats, anorexia, and a 6 kg weight loss. No history of alcohol use, tobacco consumption, or significant comorbidities was reported; he had received BCG vaccination and no positive family or personal history of infectious or hepatic disease. Physical examination revealed an asthenic patient with hepatomegaly and moderate right hypochondrial tenderness, consistent with a systemic inflammatory response syndrome (SIRS): tachycardia (124 bpm), tachypnea (22 breaths/min), and elevated body temperature. Laboratory findings included neutrophilic leukocytosis (17,800 cells/mm³), markedly elevated C-reactive protein (323 mg/L), and a positive procalcitonin level (4.1 ng/L), suggesting a bacterial or infectious etiology. Hepatic function tests were within normal limits: ALT 22 IU/L (normal <40 IU/L), AST 17 IU/L (<35 IU/L), GGT 42 IU/L (<50 IU/L), alkaline phosphatase 115 IU/L (normal 40–150 IU/L), bilirubin normal, prothrombin time 78%, and albumin 39 g/L. Renal function and electrolyte balance were unremarkable. Imaging studies, including chest radiography and abdominal ultrasound, were non-contributory. Blood and urine cultures, performed during febrile peaks, were negative. Serological testing for hepatitis B, C, HIV, and syphilis was negative. Lactate dehydrogenase (231 IU/L) and beta-2 microglobulin (2.28 mg/L) were within normal ranges. GeneXpert testing for Mycobacterium tuberculosis in respiratory specimens and biopsy samples was negative; quantiferon tuberculin test was also negative, excluding latent tuberculosis infection. A thoraco-abdomino-pelvic CT scan revealed an enlarged liver (17 cm), with multiple well-defined, rounded hypodense lesions, non-enhancing after contrast administration, primarily in segments I (21×16 mm) and V (36×27 mm). Echo-guided liver biopsy demonstrated subacute fibro-inflammatory changes with no evidence of malignancy or viral hepatitis. Hepatic MRI further characterized the lesions as dysmorphic, with heterogeneous T2 signal intensity, hyperintense perilesional rims on T2, peripheral enhancement post-contrast, and largest lesions in segments I (20×22 mm) and V (33×31 mm). No deep lymphadenopathy was observed. Diagnostic laparoscopy was performed to obtain biopsy specimens from hepatic nodules, which showed histologically confirmed epithelioid and gigantocellular granulomas with caseous necrosis—pathological findings consistent with focal hepatic tuberculosis. The patient was initiated on standard anti-tuberculous therapy: Phase 1 (2 months) of quadritherapy (isoniazid, rifampicin, pyrazinamide, ethambutol) administered orally in the morning on an empty stomach, followed by Phase 2 (4 months) of bithiapine (isoniazid and rifampicin) with identical dosing regimen. Clinical and biological response was observed within days of therapy initiation, with resolution of fever, chills, and systemic inflammatory markers. At three months post-treatment, follow-up imaging demonstrated a significant reduction in both the number and volume of hepatic lesions, supporting a favorable clinical course. This case represents a rare presentation of focal hepatic tuberculosis in a young, previously healthy individual, with non-specific initial symptoms and imaging findings, underscoring the importance of considering tuberculous hepatopathy in patients with chronic abdominal pain, unexplained weight loss, and persistent low-grade fever despite negative standard infectious workups."}
{"row_index": 18, "doc_id": 31, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old boy with Down Syndrome and trouble moving his arms and legs had a sore spot on the inside of his tongue. The sore spot was about 1 cm wide, hard around the edge, and had a white-yellow color. His lips were dry and cracked. He had sharp teeth, especially one tooth on the side of his tongue, which kept rubbing against it and caused the soreness. This soreness looked like a serious mouth cancer, but doctors said it was just from long-term rubbing, not cancer. The doctors treated it with salt water, iodine rinse, and lip cream to heal and protect the area. His mom was told to clean his mouth with salt water, use iodine three times a day on the sore spot, and apply lip cream to keep his lips soft. Some of his teeth were broken or gone, so they were taken out and a device was put in to keep space. The boy got better over time, but later had surgery on his neck due to spine problems. After that, he had breathing trouble and passed away.\"\n}", "generated_text": "A 12-year-old boy with Down Syndrome and trouble moving his arms and legs had a sore spot on the inside of his tongue. The sore spot was about 1 cm wide, hard around the edge, and had a white-yellow color. His lips were dry and cracked. He had sharp teeth, especially one tooth on the side of his tongue, which kept rubbing against it and caused the soreness. This soreness looked like a serious mouth cancer, but doctors said it was just from long-term rubbing, not cancer. The doctors treated it with salt water, iodine rinse, and lip cream to heal and protect the area. His mom was told to clean his mouth with salt water, use iodine three times a day on the sore spot, and apply lip cream to keep his lips soft. Some of his teeth were broken or gone, so they were taken out and a device was put in to keep space. The boy got better over time, but later had surgery on his neck due to spine problems. After that, he had breathing trouble and passed away."}
{"row_index": 19, "doc_id": 31, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 12-year-old male with Down Syndrome and myeloradiculopathy was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient's clinical history includes bilateral lower extremity and upper limb weakness, with a prior fall approximately one year prior, leading to hospital admission. His mother reported inconsistent oral hygiene practices, contributing to chronic oral mucosal exposure to trauma and infection. The patient was diagnosed with Down Syndrome, a genetic disorder caused by trisomy 21, and myeloradiculopathy, a neurological condition involving degeneration of spinal nerve roots, likely due to congenital or progressive cervical spinal cord compression.\\n\\nExtraorally, the patient exhibited dysmorphic facial features consistent with Down Syndrome, including a flat facial profile, epicanthal folds, and micrognathia. The vermillion border of the lips demonstrated exfoliative cheilitis, characterized by cracking, desquamation, and desiccation, likely secondary to impaired lip lubrication, reduced mucosal integrity, and altered keratinization. Lymph node assessment was not feasible due to the patient's use of a cervical collar, which restricted neck mobility.\\n\\nIntraorally, a 1×0.7 cm irregular ulcer was observed at the right lateral border of the tongue, with an indurated (hardened) margin and a white-yellowish base. This lesion clinically mimicked oral squamous cell carcinoma (OSCC), a malignant neoplasm of the oral epithelium, due to its well-defined, chronic, non-healing appearance. However, histopathological confirmation was not performed, and the diagnosis of chronic traumatic ulcer was established based on clinical correlation with the patient's occlusal trauma and history of dental malocclusion. The 55 tooth, which was sharp and malpositioned, was identified as the primary source of occlusal trauma, leading to direct mechanical injury to the tongue's lateral border. Additionally, the patient had dentinal caries on tooth 63, reversible pulpitis in 63, and radix gangrene (necrotic root apex) in teeth 55, 62, 74, and 85, indicating advanced dental pathology and potential bacterial invasion.\\n\\nRadiographic and imaging evaluation revealed cervical spine dislocation, confirmed by MRI, which is a known complication in patients with Down Syndrome and myeloradiculopathy, often resulting from developmental anomalies of the cervical vertebrae and ligamentous laxity. This structural abnormality may contribute to neurogenic weakness and impaired motor function. Laboratory findings included hyponatremia (sodium level: 130 mEq/L), likely secondary to impaired renal sodium reabsorption or SIADH (syndrome of inappropriate antidiuretic hormone secretion), and lymphocytosis (lymphocyte percentage: 46%), which may reflect a chronic inflammatory or immune-mediated state.\\n\\nThe patient was managed with a multimodal approach: systemic therapy including paracetamol 120 mg/5 mL oral suspension for pain control and amoxicillin 125 mg/5 mL oral suspension for potential bacterial superinfection; local therapy with 0.9% sodium chloride solution for oral rinsing, 1% povidone-iodine mouthwash applied three times daily for antiseptic and anti-inflammatory effects, and petroleum jelly applied to the lips to address desiccation and promote mucosal hydration. The patient's mother was instructed to perform daily oral care using gauze saturated with 0.9% NaCl, apply povidone-iodine to the ulcer site three times daily, and use petroleum jelly for lip protection.\\n\\nDental management included extraction of teeth 55, 62, 74, and 85 due to extensive root necrosis and irreversible pulpitis, with a space maintainer recommended to preserve arch alignment and prevent malocclusion progression. The diagnosis of the oral lesion was confirmed as a chronic traumatic ulcer, not malignancy, based on clinical features, absence of malignant histopathology, and temporal correlation with occlusal trauma.\\n\\nClinical follow-up showed progressive improvement: at the second visit (3 days post-intervention), the oral lesion showed early signs of healing; at the third visit (1 week), the ulcer size decreased and lip lesions improved; at the fourth visit (10 days), significant ulcer healing was observed. Two days after the fourth visit, the patient underwent neurosurgical intervention to correct the cervical spine dislocation. Postoperative care was provided in the Pediatric Intensive Care Unit (PICU), where the patient developed respiratory failure due to postoperative complications, including possible aspiration, airway compromise, or neurogenic pulmonary edema, and was declared dead two weeks after surgery. This outcome underscores the high morbidity associated with cervical spine instability in pediatric patients with Down Syndrome and associated neurological impair", "generated_text": "{\n  \"proficient_health_literacy\": \"A 12-year-old male with Down Syndrome and myeloradiculopathy was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient's clinical history includes bilateral lower extremity and upper limb weakness, with a prior fall approximately one year prior, leading to hospital admission. His mother reported inconsistent oral hygiene practices, contributing to chronic oral mucosal exposure to trauma and infection. The patient was diagnosed with Down Syndrome, a genetic disorder caused by trisomy 21, and myeloradiculopathy, a neurological condition involving degeneration of spinal nerve roots, likely due to congenital or progressive cervical spinal cord compression.\\n\\nExtraorally, the patient exhibited dysmorphic facial features consistent with Down Syndrome, including a flat facial profile, epicanthal folds, and micrognathia. The vermillion border of the lips demonstrated exfoliative cheilitis, characterized by cracking, desquamation, and desiccation, likely secondary to impaired lip lubrication, reduced mucosal integrity, and altered keratinization. Lymph node assessment was not feasible due to the patient's use of a cervical collar, which restricted neck mobility.\\n\\nIntraorally, a 1×0.7 cm irregular ulcer was observed at the right lateral border of the tongue, with an indurated (hardened) margin and a white-yellowish base. This lesion clinically mimicked oral squamous cell carcinoma (OSCC), a malignant neoplasm of the oral epithelium, due to its well-defined, chronic, non-healing appearance. However, histopathological confirmation was not performed, and the diagnosis of chronic traumatic ulcer was established based on clinical correlation with the patient's occlusal trauma and history of dental malocclusion. The 55 tooth, which was sharp and malpositioned, was identified as the primary source of occlusal trauma, leading to direct mechanical injury to the tongue's lateral border. Additionally, the patient had dentinal caries on tooth 63, reversible pulpitis in 63, and radix gangrene (necrotic root apex) in teeth 55, 62, 74, and 85, indicating advanced dental pathology and potential bacterial invasion.\\n\\nRadiographic and imaging evaluation revealed cervical spine dislocation, confirmed by MRI, which is a known complication in patients with Down Syndrome and myeloradiculopathy, often resulting from developmental anomalies of the cervical vertebrae and ligamentous laxity. This structural abnormality may contribute to neurogenic weakness and impaired motor function. Laboratory findings included hyponatremia (sodium level: 130 mEq/L), likely secondary to impaired renal sodium reabsorption or SIADH (syndrome of inappropriate antidiuretic hormone secretion), and lymphocytosis (lymphocyte percentage: 46%), which may reflect a chronic inflammatory or immune-mediated state.\\n\\nThe patient was managed with a multimodal approach: systemic therapy including paracetamol 120 mg/5 mL oral suspension for pain control and amoxicillin 125 mg/5 mL oral suspension for potential bacterial superinfection; local therapy with 0.9% sodium chloride solution for oral rinsing, 1% povidone-iodine mouthwash applied three times daily for antiseptic and anti-inflammatory effects, and petroleum jelly applied to the lips to address desiccation and promote mucosal hydration. The patient's mother was instructed to perform daily oral care using gauze saturated with 0.9% NaCl, apply povidone-iodine to the ulcer site three times daily, and use petroleum jelly for lip protection.\\n\\nDental management included extraction of teeth 55, 62, 74, and 85 due to extensive root necrosis and irreversible pulpitis, with a space maintainer recommended to preserve arch alignment and prevent malocclusion progression. The diagnosis of the oral lesion was confirmed as a chronic traumatic ulcer, not malignancy, based on clinical features, absence of malignant histopathology, and temporal correlation with occlusal trauma.\\n\\nClinical follow-up showed progressive improvement: at the second visit (3 days post-intervention), the oral lesion showed early signs of healing; at the third visit (1 week), the ulcer size decreased and lip lesions improved; at the fourth visit (10 days), significant ulcer healing was observed. Two days after the fourth visit, the patient underwent neurosurgical intervention to correct the cervical spine dislocation. Postoperative care was provided in the Pediatric Intensive Care Unit (PICU), where the patient developed respiratory failure due to postoperative complications, including possible aspiration, airway compromise, or neurogenic pulmonary edema, and was declared dead two weeks after surgery. This outcome underscores the high morbidity associated with cervical spine instability in pediatric patients with Down Syndrome and associated neurological impair"}
{"row_index": 20, "doc_id": 32, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 59-year-old woman had blurry vision in both eyes for a few weeks. She had multiple sclerosis and was taking medicine for seizures, including levetiracetam. Soon after starting levetiracetam, her vision got worse. Doctors found her corneas were swollen, which can happen when eyes get too full of fluid. When they slowly cut back on levetiracetam, her vision started to get better. After stopping the medicine completely, her vision returned to normal and her corneas stopped being swollen. Six months later, the swelling was gone and her eyes looked healthy again. After 13 months, her vision stayed the same and no changes were seen.\"\n}", "generated_text": "A 59-year-old woman had blurry vision in both eyes for a few weeks. She had multiple sclerosis and was taking medicine for seizures, including levetiracetam. Soon after starting levetiracetam, her vision got worse. Doctors found her corneas were swollen, which can happen when eyes get too full of fluid. When they slowly cut back on levetiracetam, her vision started to get better. After stopping the medicine completely, her vision returned to normal and her corneas stopped being swollen. Six months later, the swelling was gone and her eyes looked healthy again. After 13 months, her vision stayed the same and no changes were seen."}
{"row_index": 21, "doc_id": 32, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 59-year-old woman with secondary progressive multiple sclerosis was referred to ophthalmology because she had been experiencing blurry vision in both eyes for a few weeks. She had been taking levetiracetam, a medication for seizures, a few weeks before the symptoms started. During her eye exam, doctors found swelling in both corneas, a condition called corneal edema, which was confirmed with corneal topography. This swelling was linked to the start of levetiracetam use. After reducing the dose of levetiracetam, her vision began to improve and eventually returned to normal. When the medication was stopped completely, the corneal swelling went away and her vision stabilized. Follow-up tests six months later showed no signs of swelling or vision problems. The doctors made a provisional diagnosis of levetiracetam-induced corneal edema. Her vision has remained stable since then, with no further changes after 13 months.\"\n}", "generated_text": "A 59-year-old woman with secondary progressive multiple sclerosis was referred to ophthalmology because she had been experiencing blurry vision in both eyes for a few weeks. She had been taking levetiracetam, a medication for seizures, a few weeks before the symptoms started. During her eye exam, doctors found swelling in both corneas, a condition called corneal edema, which was confirmed with corneal topography. This swelling was linked to the start of levetiracetam use. After reducing the dose of levetiracetam, her vision began to improve and eventually returned to normal. When the medication was stopped completely, the corneal swelling went away and her vision stabilized. Follow-up tests six months later showed no signs of swelling or vision problems. The doctors made a provisional diagnosis of levetiracetam-induced corneal edema. Her vision has remained stable since then, with no further changes after 13 months."}
{"row_index": 22, "doc_id": 32, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 59-year-old female with a twelve-year history of secondary progressive multiple sclerosis (SPMS) was referred to ophthalmology with a recent onset of bilateral blurring of vision. She had no prior ophthalmic abnormalities or family history of corneal dystrophies, and previous ocular examinations had been unremarkable for signs of Fuchs' endothelial corneal dystrophy. Her medication history included long-term amantadine therapy (100 mg twice daily for 7 years), which is a known cause of corneal edema due to its effect on corneal endothelial cell function, particularly through inhibition of Na⁺/K⁺-ATPase and disruption of ion homeostasis in the endothelium. She was initiated on levetiracetam (250 mg twice daily) as an adjunctive antiepileptic agent for breakthrough seizure activity. Within weeks of starting levetiracetam, she developed progressive bilateral visual deterioration.\\n\\nOphthalmic examination revealed best-corrected visual acuity of 0.5 logMAR in both eyes. Slit-lamp biomicroscopy demonstrated bilateral corneal edema with normal anterior chamber and absence of uveitis. Intraocular pressures were 16 mmHg (right) and 18 mmHg (left), within normal limits. Corneal topography confirmed significant corneal thickening, with central corneal thicknesses of 936 μm (right) and 1134 μm (left), consistent with epithelial and stromal fluid accumulation due to impaired corneal endothelial pump function.\\n\\nGiven the established association between amantadine and corneal edema, the patient and her neurologist agreed to discontinue amantadine and switch to lamotrigine, with levetiracetam continued at the same dose. No improvement in visual acuity was observed after two months, suggesting that the corneal edema was not solely attributable to amantadine withdrawal. The patient then requested a trial discontinuation of levetiracetam due to the temporal correlation between the initiation of levetiracetam and the onset of visual symptoms.\\n\\nLevetiracetam was tapered over several days, and within a few days of dose reduction, visual symptoms began to improve. Upon complete cessation of levetiracetam, vision stabilized and corneal edema resolved. Follow-up corneal topography six months later demonstrated normalization of central corneal thickness to 567 μm (right) and 573 μm (left), with visual acuity improving to 0.2 logMAR in both eyes. Slit-lamp examination confirmed a clear cornea without corneal guttata, indicating resolution of endothelial dysfunction and fluid accumulation.\\n\\nAt a 13-month follow-up, the patient remained stable on amantadine and lamotrigine, with no further changes in medication or ocular findings. Visual acuity remained at 0.2 logMAR bilaterally, and repeat corneal topography showed no progression of corneal thickening. This case supports the hypothesis that levetiracetam may induce corneal edema via endothelial dysfunction, possibly through interference with endothelial cell metabolism, membrane integrity, or ion transport mechanisms, particularly in the context of preexisting neurodegenerative disease and altered neurovascular coupling. While no direct evidence of levetiracetam’s mechanism in corneal endothelium is established, the temporal association, clinical course, and resolution upon discontinuation strongly suggest a causal relationship. This represents a rare but clinically significant adverse effect of levetiracetam, particularly in patients with underlying neurological conditions involving chronic neuroinflammation or altered cellular homeostasis.\"\n}", "generated_text": "A 59-year-old female with a twelve-year history of secondary progressive multiple sclerosis (SPMS) was referred to ophthalmology with a recent onset of bilateral blurring of vision. She had no prior ophthalmic abnormalities or family history of corneal dystrophies, and previous ocular examinations had been unremarkable for signs of Fuchs' endothelial corneal dystrophy. Her medication history included long-term amantadine therapy (100 mg twice daily for 7 years), which is a known cause of corneal edema due to its effect on corneal endothelial cell function, particularly through inhibition of Na⁺/K⁺-ATPase and disruption of ion homeostasis in the endothelium. She was initiated on levetiracetam (250 mg twice daily) as an adjunctive antiepileptic agent for breakthrough seizure activity. Within weeks of starting levetiracetam, she developed progressive bilateral visual deterioration.\n\nOphthalmic examination revealed best-corrected visual acuity of 0.5 logMAR in both eyes. Slit-lamp biomicroscopy demonstrated bilateral corneal edema with normal anterior chamber and absence of uveitis. Intraocular pressures were 16 mmHg (right) and 18 mmHg (left), within normal limits. Corneal topography confirmed significant corneal thickening, with central corneal thicknesses of 936 μm (right) and 1134 μm (left), consistent with epithelial and stromal fluid accumulation due to impaired corneal endothelial pump function.\n\nGiven the established association between amantadine and corneal edema, the patient and her neurologist agreed to discontinue amantadine and switch to lamotrigine, with levetiracetam continued at the same dose. No improvement in visual acuity was observed after two months, suggesting that the corneal edema was not solely attributable to amantadine withdrawal. The patient then requested a trial discontinuation of levetiracetam due to the temporal correlation between the initiation of levetiracetam and the onset of visual symptoms.\n\nLevetiracetam was tapered over several days, and within a few days of dose reduction, visual symptoms began to improve. Upon complete cessation of levetiracetam, vision stabilized and corneal edema resolved. Follow-up corneal topography six months later demonstrated normalization of central corneal thickness to 567 μm (right) and 573 μm (left), with visual acuity improving to 0.2 logMAR in both eyes. Slit-lamp examination confirmed a clear cornea without corneal guttata, indicating resolution of endothelial dysfunction and fluid accumulation.\n\nAt a 13-month follow-up, the patient remained stable on amantadine and lamotrigine, with no further changes in medication or ocular findings. Visual acuity remained at 0.2 logMAR bilaterally, and repeat corneal topography showed no progression of corneal thickening. This case supports the hypothesis that levetiracetam may induce corneal edema via endothelial dysfunction, possibly through interference with endothelial cell metabolism, membrane integrity, or ion transport mechanisms, particularly in the context of preexisting neurodegenerative disease and altered neurovascular coupling. While no direct evidence of levetiracetam’s mechanism in corneal endothelium is established, the temporal association, clinical course, and resolution upon discontinuation strongly suggest a causal relationship. This represents a rare but clinically significant adverse effect of levetiracetam, particularly in patients with underlying neurological conditions involving chronic neuroinflammation or altered cellular homeostasis."}
{"row_index": 23, "doc_id": 33, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 77-year-old man had a seizure at home and fell, causing both hips to pop out of place. He was rushed to the hospital, where doctors found broken bones in his pelvis and both femur heads sticking out. His legs were shorter and twisted, and he couldn’t move them well. He was given fluids and blood to stabilize, and a special brace was used to keep the bones in place. After a few days, doctors did surgery in two steps: first on the left hip, then the right hip, seven days apart. In both surgeries, they fixed the broken hip socket with a ring that holds it in place and replaced the ball of the hip with a new joint that lets it move freely. The new parts were not glued in, so they needed time to settle. The patient had no problems after surgery and was able to walk with a walking stick after six weeks. At one year, he could do all normal activities, had no pain or falls, and his hips were working well. He still has a slight limp on the right side, but everything else is fine.\"\n}", "generated_text": "A 77-year-old man had a seizure at home and fell, causing both hips to pop out of place. He was rushed to the hospital, where doctors found broken bones in his pelvis and both femur heads sticking out. His legs were shorter and twisted, and he couldn’t move them well. He was given fluids and blood to stabilize, and a special brace was used to keep the bones in place. After a few days, doctors did surgery in two steps: first on the left hip, then the right hip, seven days apart. In both surgeries, they fixed the broken hip socket with a ring that holds it in place and replaced the ball of the hip with a new joint that lets it move freely. The new parts were not glued in, so they needed time to settle. The patient had no problems after surgery and was able to walk with a walking stick after six weeks. At one year, he could do all normal activities, had no pain or falls, and his hips were working well. He still has a slight limp on the right side, but everything else is fine."}
{"row_index": 24, "doc_id": 33, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 77-year-old male with a history of moderate cognitive impairment was admitted to the emergency department following a tonic-clonic seizure at home, presenting in a hemodynamically unstable postcritical state with suspected intrapelvic hemorrhage. The activation of a polytrauma protocol was driven by hemodynamic instability, not by the mechanism of injury. The patient was stabilized with intravenous fluid resuscitation and packed red blood cell transfusion. A pelvic binder was applied, and once hemodynamic stability was achieved, a physical examination revealed bilateral lower limb shortening, external rotation, and joint blockage on log roll testing, indicating functional impotence in both hips. No external trauma or bruising was observed; distal pulses were intact, and upper limb mobility was preserved. Initial imaging included anteroposterior pelvic radiography, which revealed bilateral femoral head dislocation. Abdominal-pelvic computed tomography (CT) was performed to assess for intra-abdominal pathology, and a 3D-CT reconstruction confirmed a bilateral transverse acetabular fracture (Letournel classification) and bilateral longitudinal iliac wing fractures, with intrapelvic protrusion of both femoral heads. Supracondylar traction was applied to the femoral heads bilaterally to maintain reduction, and pelvic traction was discontinued. The patient remained in the recovery unit under traction until surgical intervention. Surgical planning was deferred for seven days to allow for fibrovascular consolidation at the fracture sites and to minimize intraoperative bleeding. The procedure was performed in two stages: the left hemipelvis on day 8 and the right hemipelvis on day 15, both under general anesthesia. Tranexamic acid was administered to reduce intraoperative blood loss and transfusion requirements. Cefazolin (2 g preoperatively, 1 g every 8 hours for 24 hours postoperatively) was used as per institutional protocol to prevent surgical site infection. Postoperatively, enoxaparin 40 mg subcutaneously every 24 hours for seven weeks was administered for anticoagulation. The left hemipelvis was operated on first due to greater pelvic protrusion and higher risk of soft tissue hematoma formation during femoral head extraction, which could lead to vascular injury or excessive bleeding. The patient was placed in lateral decubitus position and underwent a posterior-lateral approach with Moore's autograft placement at the acetabular fracture focus. An anti-protrusion ring (Burch Schneider™ Reinforcement Cage, Zimmer Biomet) was implanted, anchored to the ischium and ilium, with medial ischial fixation using screws. Gluteal musculature (gluteus minimus and medius) was dissected to facilitate accurate femoral head positioning. The ring was verified under endoscopic control. A double-mobility cemented acetabular ring was then implanted, followed by a non-cemented femoral stem. Capsular and pelvic musculature closure was achieved using transosseous trochanteric fixation points. The right hemipelvis was operated on seven days later. A first window of the ilio-inguinal approach was utilized to address the longitudinal iliac wing fracture, which was stabilized with a six-hole anatomical plate. The same surgical protocol was repeated: anti-protrusion ring implantation, double-mobility cemented acetabular ring, and non-cemented femoral stem placement. Anti-protrusion rings are indicated in acetabular fractures classified as type IV by the American Academy of Orthopaedic Surgeons (AAOS), where there is disruption of the acetabular background and risk of pelvic disjunction, requiring bony anchorage at the ischium and ilium. They are contraindicated in isolated anterior or posterior wall fractures without acetabular body involvement. The patient remained in bed during admission and was mobilized to prevent pressure ulcer formation. After tolerating the second surgery, he began wheelchair transfers. Full range of motion was permitted in bed without restriction. The patient was discharged at four weeks, with loading initiated only at six weeks using a walking stick. Delayed loading was implemented due to the need for initial graft consolidation in the acetabular background to provide biomechanical support for the anti-protrusion ring, and due to bilateral involvement, which precluded safe partial loading without a stable, healthy hip to serve as a functional baseline. At 12-month follow-up, the patient achieved full weight-bearing with a walking stick, with Harris Hip Score (HHS) of 77 in the right hip and 79 in the left hip, and a WOMAC score of 12. No postoperative complications have been reported. Clinically, the patient is satisfied, reporting occasional discomfort and a mild right-sided limp. Full range of motion is preserved, and no episodes of hip instability have occurred since surgery. The surgical strategy reflects a biomechanically sound approach to managing", "generated_text": "{\n  \"proficient_health_literacy\": \"A 77-year-old male with a history of moderate cognitive impairment was admitted to the emergency department following a tonic-clonic seizure at home, presenting in a hemodynamically unstable postcritical state with suspected intrapelvic hemorrhage. The activation of a polytrauma protocol was driven by hemodynamic instability, not by the mechanism of injury. The patient was stabilized with intravenous fluid resuscitation and packed red blood cell transfusion. A pelvic binder was applied, and once hemodynamic stability was achieved, a physical examination revealed bilateral lower limb shortening, external rotation, and joint blockage on log roll testing, indicating functional impotence in both hips. No external trauma or bruising was observed; distal pulses were intact, and upper limb mobility was preserved. Initial imaging included anteroposterior pelvic radiography, which revealed bilateral femoral head dislocation. Abdominal-pelvic computed tomography (CT) was performed to assess for intra-abdominal pathology, and a 3D-CT reconstruction confirmed a bilateral transverse acetabular fracture (Letournel classification) and bilateral longitudinal iliac wing fractures, with intrapelvic protrusion of both femoral heads. Supracondylar traction was applied to the femoral heads bilaterally to maintain reduction, and pelvic traction was discontinued. The patient remained in the recovery unit under traction until surgical intervention. Surgical planning was deferred for seven days to allow for fibrovascular consolidation at the fracture sites and to minimize intraoperative bleeding. The procedure was performed in two stages: the left hemipelvis on day 8 and the right hemipelvis on day 15, both under general anesthesia. Tranexamic acid was administered to reduce intraoperative blood loss and transfusion requirements. Cefazolin (2 g preoperatively, 1 g every 8 hours for 24 hours postoperatively) was used as per institutional protocol to prevent surgical site infection. Postoperatively, enoxaparin 40 mg subcutaneously every 24 hours for seven weeks was administered for anticoagulation. The left hemipelvis was operated on first due to greater pelvic protrusion and higher risk of soft tissue hematoma formation during femoral head extraction, which could lead to vascular injury or excessive bleeding. The patient was placed in lateral decubitus position and underwent a posterior-lateral approach with Moore's autograft placement at the acetabular fracture focus. An anti-protrusion ring (Burch Schneider™ Reinforcement Cage, Zimmer Biomet) was implanted, anchored to the ischium and ilium, with medial ischial fixation using screws. Gluteal musculature (gluteus minimus and medius) was dissected to facilitate accurate femoral head positioning. The ring was verified under endoscopic control. A double-mobility cemented acetabular ring was then implanted, followed by a non-cemented femoral stem. Capsular and pelvic musculature closure was achieved using transosseous trochanteric fixation points. The right hemipelvis was operated on seven days later. A first window of the ilio-inguinal approach was utilized to address the longitudinal iliac wing fracture, which was stabilized with a six-hole anatomical plate. The same surgical protocol was repeated: anti-protrusion ring implantation, double-mobility cemented acetabular ring, and non-cemented femoral stem placement. Anti-protrusion rings are indicated in acetabular fractures classified as type IV by the American Academy of Orthopaedic Surgeons (AAOS), where there is disruption of the acetabular background and risk of pelvic disjunction, requiring bony anchorage at the ischium and ilium. They are contraindicated in isolated anterior or posterior wall fractures without acetabular body involvement. The patient remained in bed during admission and was mobilized to prevent pressure ulcer formation. After tolerating the second surgery, he began wheelchair transfers. Full range of motion was permitted in bed without restriction. The patient was discharged at four weeks, with loading initiated only at six weeks using a walking stick. Delayed loading was implemented due to the need for initial graft consolidation in the acetabular background to provide biomechanical support for the anti-protrusion ring, and due to bilateral involvement, which precluded safe partial loading without a stable, healthy hip to serve as a functional baseline. At 12-month follow-up, the patient achieved full weight-bearing with a walking stick, with Harris Hip Score (HHS) of 77 in the right hip and 79 in the left hip, and a WOMAC score of 12. No postoperative complications have been reported. Clinically, the patient is satisfied, reporting occasional discomfort and a mild right-sided limp. Full range of motion is preserved, and no episodes of hip instability have occurred since surgery. The surgical strategy reflects a biomechanically sound approach to managing"}
{"row_index": 25, "doc_id": 34, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 19-month-old boy fell from a highchair and hit his head. He was acting irritable, vomiting, and had trouble breathing. His breathing was fast and his oxygen levels were very low. When doctors checked him, they saw he was struggling to breathe on his left side. They gave him a tube to help him breathe, but his oxygen kept dropping. Tests showed his left lung was completely collapsed, and there was a blockage in the main airway. A scan found a small piece of almond stuck in the airway, about 2 cm big. The boy had never eaten almonds before and probably swallowed it by accident. After the piece was removed, his breathing got better, and he was able to breathe on his own within 24 hours. He was then taken out of the hospital and sent to a regular pediatric ward to recover.\"\n}", "generated_text": "A 19-month-old boy fell from a highchair and hit his head. He was acting irritable, vomiting, and had trouble breathing. His breathing was fast and his oxygen levels were very low. When doctors checked him, they saw he was struggling to breathe on his left side. They gave him a tube to help him breathe, but his oxygen kept dropping. Tests showed his left lung was completely collapsed, and there was a blockage in the main airway. A scan found a small piece of almond stuck in the airway, about 2 cm big. The boy had never eaten almonds before and probably swallowed it by accident. After the piece was removed, his breathing got better, and he was able to breathe on his own within 24 hours. He was then taken out of the hospital and sent to a regular pediatric ward to recover."}
{"row_index": 26, "doc_id": 34, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-month-old male was admitted to the Emergency Department following a fall from a highchair, during which he initially landed on his gluteal region and subsequently experienced a blunt head impact to the occiput. The child presented without prior warning signs or symptoms, and upon arrival, exhibited three episodes of vomiting and marked irritability. Vital signs revealed a respiratory rate exceeding 60 breaths per minute and a heart rate greater than 150 beats per minute, with oxygen saturation falling below 80%. Physical examination demonstrated subcostal retractions and decreased breath sounds localized to the left basal lung zone. The patient was initially managed with non-invasive ventilation using an AMBU bag connected to oxygen, but despite this intervention, oxygen saturation progressively declined below 70%, indicating worsening hypoxemia. The clinical course suggested a severe impairment in gas exchange, prompting the decision for orotracheal intubation with a cuffed endotracheal tube to secure the airway. Post-intubation, the patient's respiratory status stabilized. Chest computed tomography (CT) revealed complete atelectasis of the left lung, with a discrete abrupt interruption of the main left bronchus at a distance of 12 mm from the bronchial bifurcation, consistent with a foreign body obstruction. The clinical presentation, including the acute onset of severe respiratory distress following a minor trauma, and the history of a prior, self-limiting cough episode in the days preceding the event, led to a high clinical suspicion of foreign body aspiration (FBA). Rigid bronchoscopy was performed, which identified a 2 cm diameter almond lodged in the proximal left main bronchus. The foreign body was successfully removed. Notably, the patient had no prior exposure to nuts or almonds, and the ingestion was accidental. Post-removal, the child demonstrated a progressive clinical recovery, with oxygenation improving steadily. After 24 hours of intensive care, the patient was extubated and transferred to the general pediatrics ward, where he achieved full respiratory function recovery over several days. The radiological and bronchoscopic findings, combined with the clinical trajectory, support the diagnosis of acute left main bronchial obstruction due to accidental almond aspiration, with the respiratory failure secondary to impaired ventilation and alveolar collapse, likely exacerbated by the altered state of consciousness induced by head trauma. The mechanism of respiratory compromise involved obstructive atelectasis, leading to reduced lung compliance and ventilation-perfusion mismatch, which were confirmed by lung ultrasound showing absent A lines and solid, consolidated parenchymal patterns. This case underscores the importance of considering foreign body aspiration in pediatric patients presenting with acute respiratory distress, particularly when there is a history of sudden-onset cough or no prior risk factors, even in the absence of overt aspiration signs.\"\n}", "generated_text": "A 19-month-old male was admitted to the Emergency Department following a fall from a highchair, during which he initially landed on his gluteal region and subsequently experienced a blunt head impact to the occiput. The child presented without prior warning signs or symptoms, and upon arrival, exhibited three episodes of vomiting and marked irritability. Vital signs revealed a respiratory rate exceeding 60 breaths per minute and a heart rate greater than 150 beats per minute, with oxygen saturation falling below 80%. Physical examination demonstrated subcostal retractions and decreased breath sounds localized to the left basal lung zone. The patient was initially managed with non-invasive ventilation using an AMBU bag connected to oxygen, but despite this intervention, oxygen saturation progressively declined below 70%, indicating worsening hypoxemia. The clinical course suggested a severe impairment in gas exchange, prompting the decision for orotracheal intubation with a cuffed endotracheal tube to secure the airway. Post-intubation, the patient's respiratory status stabilized. Chest computed tomography (CT) revealed complete atelectasis of the left lung, with a discrete abrupt interruption of the main left bronchus at a distance of 12 mm from the bronchial bifurcation, consistent with a foreign body obstruction. The clinical presentation, including the acute onset of severe respiratory distress following a minor trauma, and the history of a prior, self-limiting cough episode in the days preceding the event, led to a high clinical suspicion of foreign body aspiration (FBA). Rigid bronchoscopy was performed, which identified a 2 cm diameter almond lodged in the proximal left main bronchus. The foreign body was successfully removed. Notably, the patient had no prior exposure to nuts or almonds, and the ingestion was accidental. Post-removal, the child demonstrated a progressive clinical recovery, with oxygenation improving steadily. After 24 hours of intensive care, the patient was extubated and transferred to the general pediatrics ward, where he achieved full respiratory function recovery over several days. The radiological and bronchoscopic findings, combined with the clinical trajectory, support the diagnosis of acute left main bronchial obstruction due to accidental almond aspiration, with the respiratory failure secondary to impaired ventilation and alveolar collapse, likely exacerbated by the altered state of consciousness induced by head trauma. The mechanism of respiratory compromise involved obstructive atelectasis, leading to reduced lung compliance and ventilation-perfusion mismatch, which were confirmed by lung ultrasound showing absent A lines and solid, consolidated parenchymal patterns. This case underscores the importance of considering foreign body aspiration in pediatric patients presenting with acute respiratory distress, particularly when there is a history of sudden-onset cough or no prior risk factors, even in the absence of overt aspiration signs."}
{"row_index": 27, "doc_id": 35, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 4-month-old male infant from central Mexico presented with a painful, suppurative tumor in the left axillary region. The infant was born to a mother with hypothyroidism during the first trimester of pregnancy, who was receiving pharmacological therapy. The infant had normal birth weight and length, was exclusively breast-fed, and received the BCG vaccine without scarring. The mother resided in a prison cell with the infant and two other individuals, in a crowded environment. At 4 months of age, the infant was evaluated for the axillary mass; a chest X-ray revealed suggestive rib fractures, leading to suspicion of child abuse and hospitalization. Physical examination revealed a weight of 4,190 g (below the third percentile), height of 58 cm, oxygen saturation of 70%, fever, cough, localized swelling, erythema, warmth, and pain in the left axilla. Laboratory findings included hemoglobin of 8.8 g/dL (normal range: 11.0–12.6 g/dL), leukocyte count of 29.3 × 10⁹/L (normal: 6.0–17.5 × 10⁹/L), neutrophil count of 18.4 × 10⁹/L (normal: 1.0–8.5 × 10⁹/L), lymphocyte count of 7.0 × 10⁹/L (normal: 4.0–13.5 × 10⁹/L), monocyte count of 3.5 × 10⁹/L, platelet count of 459 × 10⁹/L (normal: 150–350 × 10⁹/L), and C-reactive protein of 16 mg/L (elevated, normal <3.0 mg/L). A thoracoabdominal tomography demonstrated an axillary abscess, lytic lesions in ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Histopathological examination of the axillary abscess revealed myositis and suppurative panniculitis. Bacterial culture from bronchoalveolar lavage fluid was negative, and PCR testing for Mycobacterium tuberculosis complex was negative. The infant received a 41-day course of dual antimicrobial therapy (ceftriaxone-clindamycin and cefepime-vancomycin) and was discharged. Two months later, at 8 months of age, the infant was readmitted with fever, irritability, and progression of the suppurative process to the left scapula. Repeat laboratory evaluation showed hemoglobin of 10.8 g/dL, leukocyte count of 21.2 × 10⁹/L, neutrophil count of 12.2 × 10⁹/L, lymphocyte count of 7.5 × 10⁹/L, monocyte count of 1.2 × 10⁹/L, and platelet count of 583 × 10⁹/L. Serum HIV testing was negative. Chest imaging revealed left apical consolidation, bronchiectasis, lytic lesions in ribs 2–7 and dorsal vertebrae 2–7, and a multilocular fluid collection. Ultrasound confirmed a fistula connecting the scapular abscess to the underlying tissue. The infant was initially treated with piperacillin-tazobactam, which was later replaced with voriconazole after isolation of Aspergillus fumigatus from secretion culture. Given the recurrent, severe, and progressive nature of the infections, an innate immune deficiency was suspected. A dihydrorhodamine (DHR) assay demonstrated absent production of reactive oxygen species (ROS) in neutrophils, and flow cytometric analysis revealed absent gp91phox protein expression in neutrophils, confirming a defect in the phagocyte NADPH oxidase complex. Next-generation sequencing identified a pathogenic variant in the CYBB gene, c.80_83del/Y (p.Val27Glyfs*33), resulting in a frameshift mutation and premature termination of the gp91phox protein. The mother was found to be a heterozygous carrier (c.80_83del/WT) of this variant, consistent with X-linked recessive inheritance. The two older male siblings, who appeared clinically healthy, were not subjected to genetic testing. The infant was discharged after 65 days of hospitalization and 28 days of voriconazole therapy, with initiation of daily trimethoprim-sulfamethoxazole prophylaxis and weekly fluconazole for antifungal proph", "generated_text": "{\n  \"proficient_health_literacy\": \"A 4-month-old male infant from central Mexico presented with a painful, suppurative tumor in the left axillary region. The infant was born to a mother with hypothyroidism during the first trimester of pregnancy, who was receiving pharmacological therapy. The infant had normal birth weight and length, was exclusively breast-fed, and received the BCG vaccine without scarring. The mother resided in a prison cell with the infant and two other individuals, in a crowded environment. At 4 months of age, the infant was evaluated for the axillary mass; a chest X-ray revealed suggestive rib fractures, leading to suspicion of child abuse and hospitalization. Physical examination revealed a weight of 4,190 g (below the third percentile), height of 58 cm, oxygen saturation of 70%, fever, cough, localized swelling, erythema, warmth, and pain in the left axilla. Laboratory findings included hemoglobin of 8.8 g/dL (normal range: 11.0–12.6 g/dL), leukocyte count of 29.3 × 10⁹/L (normal: 6.0–17.5 × 10⁹/L), neutrophil count of 18.4 × 10⁹/L (normal: 1.0–8.5 × 10⁹/L), lymphocyte count of 7.0 × 10⁹/L (normal: 4.0–13.5 × 10⁹/L), monocyte count of 3.5 × 10⁹/L, platelet count of 459 × 10⁹/L (normal: 150–350 × 10⁹/L), and C-reactive protein of 16 mg/L (elevated, normal <3.0 mg/L). A thoracoabdominal tomography demonstrated an axillary abscess, lytic lesions in ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Histopathological examination of the axillary abscess revealed myositis and suppurative panniculitis. Bacterial culture from bronchoalveolar lavage fluid was negative, and PCR testing for Mycobacterium tuberculosis complex was negative. The infant received a 41-day course of dual antimicrobial therapy (ceftriaxone-clindamycin and cefepime-vancomycin) and was discharged. Two months later, at 8 months of age, the infant was readmitted with fever, irritability, and progression of the suppurative process to the left scapula. Repeat laboratory evaluation showed hemoglobin of 10.8 g/dL, leukocyte count of 21.2 × 10⁹/L, neutrophil count of 12.2 × 10⁹/L, lymphocyte count of 7.5 × 10⁹/L, monocyte count of 1.2 × 10⁹/L, and platelet count of 583 × 10⁹/L. Serum HIV testing was negative. Chest imaging revealed left apical consolidation, bronchiectasis, lytic lesions in ribs 2–7 and dorsal vertebrae 2–7, and a multilocular fluid collection. Ultrasound confirmed a fistula connecting the scapular abscess to the underlying tissue. The infant was initially treated with piperacillin-tazobactam, which was later replaced with voriconazole after isolation of Aspergillus fumigatus from secretion culture. Given the recurrent, severe, and progressive nature of the infections, an innate immune deficiency was suspected. A dihydrorhodamine (DHR) assay demonstrated absent production of reactive oxygen species (ROS) in neutrophils, and flow cytometric analysis revealed absent gp91phox protein expression in neutrophils, confirming a defect in the phagocyte NADPH oxidase complex. Next-generation sequencing identified a pathogenic variant in the CYBB gene, c.80_83del/Y (p.Val27Glyfs*33), resulting in a frameshift mutation and premature termination of the gp91phox protein. The mother was found to be a heterozygous carrier (c.80_83del/WT) of this variant, consistent with X-linked recessive inheritance. The two older male siblings, who appeared clinically healthy, were not subjected to genetic testing. The infant was discharged after 65 days of hospitalization and 28 days of voriconazole therapy, with initiation of daily trimethoprim-sulfamethoxazole prophylaxis and weekly fluconazole for antifungal proph"}
{"row_index": 28, "doc_id": 36, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 25-year-old male patient of Sundanese ethnicity presented to the Department of Oral Medicine at the Dental Hospital of the Faculty of Dentistry, Universitas Padjadjaran, with a chief complaint of painful oral ulcers affecting the upper and lower labial mucosa, exacerbated by eating and speech. The lesions initially appeared as canker sores four days prior to presentation, with subsequent extension to the lips two days later. The patient initially attempted self-treatment with petroleum jelly, which provided no symptomatic relief. He subsequently applied triamcinolone acetonide 0.1% in orabase ointment once daily, which resulted in partial improvement but incomplete healing of the lesions.\\n\\nThe patient reported a preceding one-week history of fever, with no cutaneous or systemic lesions elsewhere. He described a prolonged period of suboptimal nutritional intake—approximately one and a half months—due to high work-related stress. There was no history of medical comorbidities, food allergies, medication use, alcohol consumption, or tobacco use. However, a chronic habit of lip-licking was noted. The patient had a documented history of varicella (chickenpox) in childhood, which is clinically relevant given the role of herpes simplex virus type 1 (HSV-1) in mucocutaneous infections.\\n\\nOn general examination, vital signs were within normal limits, with no lymphadenopathy. Extra-oral examination revealed serosanguineous crusts on the lips that were tender and prone to bleeding. Intra-oral examination demonstrated diffuse, irregular erythematous lesions with well-defined borders on both upper and lower labial mucosa, consistent with mucosal inflammation. Additional findings included hyperkeratotic white plaques with non-scrapable consistency and irregular borders on the left buccal mucosa near tooth 38, yellowish-white, easily scrapable plaques on one-third of the posterior dorsal tongue, and shallow dental impression indentations on the lateral tongue surfaces without pain. A painless, firm nodule measuring 2×1×0.5 cm was identified in the midline of the hard palate. Dental assessment revealed carious lesions, root caries, and edentulous status in teeth 28, 36, 37, and 46, with evidence of reversible pulpitis in tooth 18 and irreversible pulpitis in tooth 47, as well as chronic apical periodontitis due to root caries in tooth 15. Oral hygiene was suboptimal.\\n\\nPsychological evaluation using the DASS-21 scale indicated normal levels of depression (score 0), anxiety (score 6), and stress (score 6), suggesting no significant psychiatric comorbidity. Based on clinical presentation and history, the working diagnosis was suspected to be Herpetic Angina of the Mucosa (HAEM), a condition characterized by recurrent or persistent mucocutaneous ulceration associated with HSV-1 infection. Differential diagnosis considered exfoliative cheilitis, which lacks viral etiology and is typically linked to irritant exposure or chemical dermatitis; however, the presence of HSV-1 seropositivity ruled this out.\\n\\nSerological testing for IgG anti-HSV-1 was performed, yielding a titer of 6.32 (ratio >1.1), confirming prior exposure and active viral involvement. This result, in conjunction with the clinical picture, established a definitive diagnosis of HAEM. The patient’s oral health-related quality of life (OHRQoL) was assessed using the OHIP-14 instrument, with an initial score of 35 (indicating moderate impairment), which improved to 4 (indicating excellent OHRQoL) at the final follow-up.\\n\\nTherapeutic management included both pharmacological and non-pharmacological interventions. Non-pharmacological measures involved patient education on maintaining rigorous oral hygiene—specifically, brushing teeth and tongue twice daily with a soft-bristled brush and non-detergent toothpaste—increasing daily water intake to at least two liters, adopting a balanced nutritional diet, and avoiding acidic, spicy, hard, and monosodium glutamate (MSG)-containing foods. The patient was specifically instructed to discontinue lip-licking and lip-peeling behaviors, which are known to exacerbate mucosal trauma and promote viral replication.\\n\\nPharmacological therapy consisted of topical and systemic agents. Topically, the patient was instructed to apply a thin layer of triamcinolone acetonide 0.1% in orabase three times daily and to compress the lips with gauze soaked in 0.9% NaCl solution at least three times daily to reduce inflammation and promote epithelial healing. Systemically, the patient was prescribed multivitamin supplementation once daily to address potential micronutrient deficiencies, which may contribute to", "generated_text": "{\n  \"proficient_health_literacy\": \"A 25-year-old male patient of Sundanese ethnicity presented to the Department of Oral Medicine at the Dental Hospital of the Faculty of Dentistry, Universitas Padjadjaran, with a chief complaint of painful oral ulcers affecting the upper and lower labial mucosa, exacerbated by eating and speech. The lesions initially appeared as canker sores four days prior to presentation, with subsequent extension to the lips two days later. The patient initially attempted self-treatment with petroleum jelly, which provided no symptomatic relief. He subsequently applied triamcinolone acetonide 0.1% in orabase ointment once daily, which resulted in partial improvement but incomplete healing of the lesions.\\n\\nThe patient reported a preceding one-week history of fever, with no cutaneous or systemic lesions elsewhere. He described a prolonged period of suboptimal nutritional intake—approximately one and a half months—due to high work-related stress. There was no history of medical comorbidities, food allergies, medication use, alcohol consumption, or tobacco use. However, a chronic habit of lip-licking was noted. The patient had a documented history of varicella (chickenpox) in childhood, which is clinically relevant given the role of herpes simplex virus type 1 (HSV-1) in mucocutaneous infections.\\n\\nOn general examination, vital signs were within normal limits, with no lymphadenopathy. Extra-oral examination revealed serosanguineous crusts on the lips that were tender and prone to bleeding. Intra-oral examination demonstrated diffuse, irregular erythematous lesions with well-defined borders on both upper and lower labial mucosa, consistent with mucosal inflammation. Additional findings included hyperkeratotic white plaques with non-scrapable consistency and irregular borders on the left buccal mucosa near tooth 38, yellowish-white, easily scrapable plaques on one-third of the posterior dorsal tongue, and shallow dental impression indentations on the lateral tongue surfaces without pain. A painless, firm nodule measuring 2×1×0.5 cm was identified in the midline of the hard palate. Dental assessment revealed carious lesions, root caries, and edentulous status in teeth 28, 36, 37, and 46, with evidence of reversible pulpitis in tooth 18 and irreversible pulpitis in tooth 47, as well as chronic apical periodontitis due to root caries in tooth 15. Oral hygiene was suboptimal.\\n\\nPsychological evaluation using the DASS-21 scale indicated normal levels of depression (score 0), anxiety (score 6), and stress (score 6), suggesting no significant psychiatric comorbidity. Based on clinical presentation and history, the working diagnosis was suspected to be Herpetic Angina of the Mucosa (HAEM), a condition characterized by recurrent or persistent mucocutaneous ulceration associated with HSV-1 infection. Differential diagnosis considered exfoliative cheilitis, which lacks viral etiology and is typically linked to irritant exposure or chemical dermatitis; however, the presence of HSV-1 seropositivity ruled this out.\\n\\nSerological testing for IgG anti-HSV-1 was performed, yielding a titer of 6.32 (ratio >1.1), confirming prior exposure and active viral involvement. This result, in conjunction with the clinical picture, established a definitive diagnosis of HAEM. The patient’s oral health-related quality of life (OHRQoL) was assessed using the OHIP-14 instrument, with an initial score of 35 (indicating moderate impairment), which improved to 4 (indicating excellent OHRQoL) at the final follow-up.\\n\\nTherapeutic management included both pharmacological and non-pharmacological interventions. Non-pharmacological measures involved patient education on maintaining rigorous oral hygiene—specifically, brushing teeth and tongue twice daily with a soft-bristled brush and non-detergent toothpaste—increasing daily water intake to at least two liters, adopting a balanced nutritional diet, and avoiding acidic, spicy, hard, and monosodium glutamate (MSG)-containing foods. The patient was specifically instructed to discontinue lip-licking and lip-peeling behaviors, which are known to exacerbate mucosal trauma and promote viral replication.\\n\\nPharmacological therapy consisted of topical and systemic agents. Topically, the patient was instructed to apply a thin layer of triamcinolone acetonide 0.1% in orabase three times daily and to compress the lips with gauze soaked in 0.9% NaCl solution at least three times daily to reduce inflammation and promote epithelial healing. Systemically, the patient was prescribed multivitamin supplementation once daily to address potential micronutrient deficiencies, which may contribute to"}
{"row_index": 29, "doc_id": 37, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 29-year-old woman, Para 1, presented with a one-month history of abnormal vaginal bleeding to the gynecology outpatient department of a level 2 hospital. She was HIV-positive, having been diagnosed approximately one year prior to presentation. Antiretroviral therapy (ART) was initiated following diagnosis, but she defaulted treatment for one month during the onset of vaginal bleeding, resulting in virological failure (viral load: 37,400 copies/mL) and immunological deterioration (CD4 count: 26 cells/μL). The timing of initial HIV symptom onset was not clearly established. Physical examination revealed a large cervical mass measuring 8 × 8 cm, extending into the parametrium and bilateral pelvic sidewalls, with bleeding on contact and foul-smelling vaginal discharge. Ultrasonography demonstrated a bulky cervix and bilateral hydronephrosis, supporting a clinical diagnosis of cervical malignancy at International Federation of Gynecology and Obstetrics (FIGO) stage 3B, defined by pelvic wall involvement and hydronephrosis. A punch cervical biopsy was performed, and histopathological examination confirmed an extra-nodal Burkitt lymphoma (BL). Immunohistochemical staining was positive for CD20, CD75a, CD10, PAX5, and BCL6, with additional positivity for CD44 and c-Myc. In situ hybridization for Epstein-Barr virus (EBER-ISH) showed focal positivity, consistent with EBV-associated BL. The Ki67 proliferation index was nearly 100%, indicating aggressive tumor cell proliferation, with moderate PAX5 and BCL6 expression. Laboratory findings included leukopenia (white cell count: 2.67 × 10⁹/L), anemia (hemoglobin: 5.7 g/dL), thrombocytopenia (platelet count: 71 × 10⁹/L), elevated serum creatinine (187 mmol/L), urea (11.1 mmol/L), and reduced albumin (21 g/L), reflecting significant renal and systemic compromise. Aspartate transaminase (41 U/L) and alkaline phosphatase (100 U/L) were within mild upper limits, suggesting minimal hepatic dysfunction. Following histological confirmation, the patient was reviewed at an oncology multidisciplinary team (MDT) meeting, where chemo-radiation therapy was recommended as the standard of care for stage 3B extra-nodal BL. However, due to a prolonged waiting list at the referral oncology unit, treatment initiation was delayed by 43 days—exceeding the recommended 48-hour window for initiating oncological intervention in Burkitt lymphoma, particularly in immunocompromised individuals. During this period, no further imaging (CT or MRI) was conducted due to technical limitations in available equipment. The patient received supportive care, including blood transfusions and analgesia, but ultimately died in the gynecological ward on day 43 while awaiting treatment. Postmortem histopathology was not performed, as both the BL diagnosis and HIV infection were already established. The primary cause of death remains difficult to attribute definitively due to the presence of multiple comorbidities; however, the attending physician concluded that Burkitt lymphoma was the most likely primary cause, given its rapid progression and high mortality in HIV-positive individuals with high viral loads. The secondary cause of death was multiple organ failure, encompassing both renal and hematological failure, which likely resulted from the combined effects of aggressive lymphoma biology, immunosuppression, and progressive organ dysfunction. This case underscores the critical importance of timely diagnosis and intervention in HIV-positive patients with suspected cervical malignancy, especially in the context of EBV-associated extra-nodal BL, where delays in treatment significantly impact survival outcomes.\"\n}", "generated_text": "A 29-year-old woman, Para 1, presented with a one-month history of abnormal vaginal bleeding to the gynecology outpatient department of a level 2 hospital. She was HIV-positive, having been diagnosed approximately one year prior to presentation. Antiretroviral therapy (ART) was initiated following diagnosis, but she defaulted treatment for one month during the onset of vaginal bleeding, resulting in virological failure (viral load: 37,400 copies/mL) and immunological deterioration (CD4 count: 26 cells/μL). The timing of initial HIV symptom onset was not clearly established. Physical examination revealed a large cervical mass measuring 8 × 8 cm, extending into the parametrium and bilateral pelvic sidewalls, with bleeding on contact and foul-smelling vaginal discharge. Ultrasonography demonstrated a bulky cervix and bilateral hydronephrosis, supporting a clinical diagnosis of cervical malignancy at International Federation of Gynecology and Obstetrics (FIGO) stage 3B, defined by pelvic wall involvement and hydronephrosis. A punch cervical biopsy was performed, and histopathological examination confirmed an extra-nodal Burkitt lymphoma (BL). Immunohistochemical staining was positive for CD20, CD75a, CD10, PAX5, and BCL6, with additional positivity for CD44 and c-Myc. In situ hybridization for Epstein-Barr virus (EBER-ISH) showed focal positivity, consistent with EBV-associated BL. The Ki67 proliferation index was nearly 100%, indicating aggressive tumor cell proliferation, with moderate PAX5 and BCL6 expression. Laboratory findings included leukopenia (white cell count: 2.67 × 10⁹/L), anemia (hemoglobin: 5.7 g/dL), thrombocytopenia (platelet count: 71 × 10⁹/L), elevated serum creatinine (187 mmol/L), urea (11.1 mmol/L), and reduced albumin (21 g/L), reflecting significant renal and systemic compromise. Aspartate transaminase (41 U/L) and alkaline phosphatase (100 U/L) were within mild upper limits, suggesting minimal hepatic dysfunction. Following histological confirmation, the patient was reviewed at an oncology multidisciplinary team (MDT) meeting, where chemo-radiation therapy was recommended as the standard of care for stage 3B extra-nodal BL. However, due to a prolonged waiting list at the referral oncology unit, treatment initiation was delayed by 43 days—exceeding the recommended 48-hour window for initiating oncological intervention in Burkitt lymphoma, particularly in immunocompromised individuals. During this period, no further imaging (CT or MRI) was conducted due to technical limitations in available equipment. The patient received supportive care, including blood transfusions and analgesia, but ultimately died in the gynecological ward on day 43 while awaiting treatment. Postmortem histopathology was not performed, as both the BL diagnosis and HIV infection were already established. The primary cause of death remains difficult to attribute definitively due to the presence of multiple comorbidities; however, the attending physician concluded that Burkitt lymphoma was the most likely primary cause, given its rapid progression and high mortality in HIV-positive individuals with high viral loads. The secondary cause of death was multiple organ failure, encompassing both renal and hematological failure, which likely resulted from the combined effects of aggressive lymphoma biology, immunosuppression, and progressive organ dysfunction. This case underscores the critical importance of timely diagnosis and intervention in HIV-positive patients with suspected cervical malignancy, especially in the context of EBV-associated extra-nodal BL, where delays in treatment significantly impact survival outcomes."}
{"row_index": 30, "doc_id": 38, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 56-year-old female patient with connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) was diagnosed in July 2013 with Sjögren’s syndrome complicated by interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH). Initial clinical evaluation revealed dyspnea, productive cough with yellow sputum, and signs of pulmonary vascular congestion on chest X-ray, including interstitial thickening, costophrenic angle blunting, and cardiomegaly. Echocardiography demonstrated a pulmonary artery systolic pressure of 99 mmHg, right atrial and ventricular enlargement, a D-shaped left ventricle, and severe tricuspid regurgitation, consistent with right heart strain. Cardiac catheterization (RHC) in 2017 confirmed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) of approximately 15 Woods, and a wedge pressure of 4 mmHg, classifying the condition as pre-capillary, group I, CTD-related PAH. These findings supported insurance approval for Opsumit (macitentan) 10 mg once daily, which replaced Tracleer (bosentan) in 2017. Treatment with sildenafil (Revatio) 20 mg three times daily and macitentan was initiated and maintained until 2020, during which the patient remained stable with low-to-intermediate risk classification. However, in October 2020, she presented with worsening dyspnea, productive cough with white sputum, and signs of systemic infection. On November 10, 2020, she developed acute severe dyspnea, cold sweats, cyanosis, and hypoxemia (SpO2 = 70%), requiring 100% oxygen via face tent. Arterial blood gas analysis revealed a lactate level of 5.2 mmol/L and brain natriuretic peptide (BNP) exceeding 10,000 pg/mL, indicating cardiogenic shock. She was intubated, admitted to the intensive care unit (ICU), and initiated on four pharmacological agents for PAH management. Her condition stabilized, with successful weaning from vasopressors by November 13, extubation on November 14, and transfer to a general ward on November 21, with oxygen support reduced to nasal cannula at 2 L/min. Follow-up RHC continued to show elevated pulmonary artery pressures, reflecting progressive right ventricular dysfunction due to chronic pulmonary hypertension. Despite stabilization, her 6-minute walk distance progressively declined, and she was reclassified as high-risk. She continues to require frequent hospitalizations for disease control. Physical examination revealed mild rhonchi consistent with ILD and a pansystolic murmur suggestive of severe valvular heart disease. In 2020, Ventavis (iloprost) 10 mcg/ml in 2 ml was added to her regimen. In May 2023, molecular hydrogen therapy was initiated as an adjuvant treatment, consisting of daily administration of 1 capsule of PURE HYDROGEN (HoHo Biotech Co., Ltd., Taipei, Taiwan, ROC). Each capsule contains 170 mg of hydrogen-rich coral calcium with 1.7 × 10²¹ hydrogen molecules, equivalent to 24 cups of water at 1,200 ppb hydrogen or 0.6 mM hydrogen per 200 mL of water. Whole-blood flow cytometry and serological analyses were performed pre- and post-treatment using standard fluorescent dye and antibody reagent kits (Beckman Coulter, Brea, CA, USA), following established immunophenotypic gating protocols. Results demonstrated a significant increase in CD127+ regulatory T cells (Treg), a reduction in anti-Ro autoantibody titers, and a decrease in B cell subsets. These immunological changes correlated with clinical stabilization, including improvement in dyspnea and respiratory function, without any reported adverse events. The study adheres to the CARE (Consolidated Standards of Reporting Trials) 2013 reporting guidelines.\"\n}", "generated_text": "A 56-year-old female patient with connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) was diagnosed in July 2013 with Sjögren’s syndrome complicated by interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH). Initial clinical evaluation revealed dyspnea, productive cough with yellow sputum, and signs of pulmonary vascular congestion on chest X-ray, including interstitial thickening, costophrenic angle blunting, and cardiomegaly. Echocardiography demonstrated a pulmonary artery systolic pressure of 99 mmHg, right atrial and ventricular enlargement, a D-shaped left ventricle, and severe tricuspid regurgitation, consistent with right heart strain. Cardiac catheterization (RHC) in 2017 confirmed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) of approximately 15 Woods, and a wedge pressure of 4 mmHg, classifying the condition as pre-capillary, group I, CTD-related PAH. These findings supported insurance approval for Opsumit (macitentan) 10 mg once daily, which replaced Tracleer (bosentan) in 2017. Treatment with sildenafil (Revatio) 20 mg three times daily and macitentan was initiated and maintained until 2020, during which the patient remained stable with low-to-intermediate risk classification. However, in October 2020, she presented with worsening dyspnea, productive cough with white sputum, and signs of systemic infection. On November 10, 2020, she developed acute severe dyspnea, cold sweats, cyanosis, and hypoxemia (SpO2 = 70%), requiring 100% oxygen via face tent. Arterial blood gas analysis revealed a lactate level of 5.2 mmol/L and brain natriuretic peptide (BNP) exceeding 10,000 pg/mL, indicating cardiogenic shock. She was intubated, admitted to the intensive care unit (ICU), and initiated on four pharmacological agents for PAH management. Her condition stabilized, with successful weaning from vasopressors by November 13, extubation on November 14, and transfer to a general ward on November 21, with oxygen support reduced to nasal cannula at 2 L/min. Follow-up RHC continued to show elevated pulmonary artery pressures, reflecting progressive right ventricular dysfunction due to chronic pulmonary hypertension. Despite stabilization, her 6-minute walk distance progressively declined, and she was reclassified as high-risk. She continues to require frequent hospitalizations for disease control. Physical examination revealed mild rhonchi consistent with ILD and a pansystolic murmur suggestive of severe valvular heart disease. In 2020, Ventavis (iloprost) 10 mcg/ml in 2 ml was added to her regimen. In May 2023, molecular hydrogen therapy was initiated as an adjuvant treatment, consisting of daily administration of 1 capsule of PURE HYDROGEN (HoHo Biotech Co., Ltd., Taipei, Taiwan, ROC). Each capsule contains 170 mg of hydrogen-rich coral calcium with 1.7 × 10²¹ hydrogen molecules, equivalent to 24 cups of water at 1,200 ppb hydrogen or 0.6 mM hydrogen per 200 mL of water. Whole-blood flow cytometry and serological analyses were performed pre- and post-treatment using standard fluorescent dye and antibody reagent kits (Beckman Coulter, Brea, CA, USA), following established immunophenotypic gating protocols. Results demonstrated a significant increase in CD127+ regulatory T cells (Treg), a reduction in anti-Ro autoantibody titers, and a decrease in B cell subsets. These immunological changes correlated with clinical stabilization, including improvement in dyspnea and respiratory function, without any reported adverse events. The study adheres to the CARE (Consolidated Standards of Reporting Trials) 2013 reporting guidelines."}
{"row_index": 31, "doc_id": 39, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 45-year-old man came in sick with pneumonia caused by the SARS-CoV-2 virus. He had no history of brain problems before. After 16 days in the hospital, he suddenly became confused and his eyes turned to the right. His face and chest twitched on one side, then he had a full seizure. After that, he had weakness on his left side. Doctors found the SARS-CoV-2 virus in his brain fluid, which means the virus got into his brain. But he slowly got better over time and is now doing well. He doesn’t need medicine for seizures anymore and is back in a regular room. No serious brain damage was found.\"\n}", "generated_text": "A 45-year-old man came in sick with pneumonia caused by the SARS-CoV-2 virus. He had no history of brain problems before. After 16 days in the hospital, he suddenly became confused and his eyes turned to the right. His face and chest twitched on one side, then he had a full seizure. After that, he had weakness on his left side. Doctors found the SARS-CoV-2 virus in his brain fluid, which means the virus got into his brain. But he slowly got better over time and is now doing well. He doesn’t need medicine for seizures anymore and is back in a regular room. No serious brain damage was found."}
{"row_index": 32, "doc_id": 39, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 45-year-old man was admitted to the hospital with pneumonia caused by SARS-CoV-2, a virus that causes COVID-19. He had no prior neurological problems. For the first few days, he had symptoms like fever, dry cough, shortness of breath, and chest pain. Tests confirmed the pneumonia was due to SARS-CoV-2, and he needed increasing oxygen support as his condition worsened. He was placed in the intensive care unit and given medications including remdesivir, dexamethasone, and antibiotics, which helped reduce inflammation and fight infection.\\n\\nOn the 16th day of hospitalization, he suddenly had a change in consciousness, with his eyes turning to the right and involuntary jerking movements on his left side (face and chest). This was followed by a full seizure. After treatment with midazolam, the seizure stopped. Tests showed no signs of low oxygen, low blood sugar, or other common causes of seizures. A key finding was that the virus SARS-CoV-2 was detected in his cerebrospinal fluid (the fluid around the brain and spinal cord), which suggests the virus may have affected his brain.\\n\\nAfter this event, he remained in a coma-like state for a short time, with no ability to respond to pain or speak, and had weakness on his left side. He was eventually able to wake up and regain some function. His brain scans showed no major damage, and after a few weeks, he was discharged with no need for anti-seizure medication. His overall recovery was favorable, and he continued to improve over time.\"\n}", "generated_text": "A 45-year-old man was admitted to the hospital with pneumonia caused by SARS-CoV-2, a virus that causes COVID-19. He had no prior neurological problems. For the first few days, he had symptoms like fever, dry cough, shortness of breath, and chest pain. Tests confirmed the pneumonia was due to SARS-CoV-2, and he needed increasing oxygen support as his condition worsened. He was placed in the intensive care unit and given medications including remdesivir, dexamethasone, and antibiotics, which helped reduce inflammation and fight infection.\n\nOn the 16th day of hospitalization, he suddenly had a change in consciousness, with his eyes turning to the right and involuntary jerking movements on his left side (face and chest). This was followed by a full seizure. After treatment with midazolam, the seizure stopped. Tests showed no signs of low oxygen, low blood sugar, or other common causes of seizures. A key finding was that the virus SARS-CoV-2 was detected in his cerebrospinal fluid (the fluid around the brain and spinal cord), which suggests the virus may have affected his brain.\n\nAfter this event, he remained in a coma-like state for a short time, with no ability to respond to pain or speak, and had weakness on his left side. He was eventually able to wake up and regain some function. His brain scans showed no major damage, and after a few weeks, he was discharged with no need for anti-seizure medication. His overall recovery was favorable, and he continued to improve over time."}
{"row_index": 33, "doc_id": 39, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 45-year-old male, born in Pakistan and residing in Portugal for seven years, was admitted to the intensive care unit (ICU) with a diagnosis of SARS-CoV-2-associated pneumonia. He had a history of grade 3 obesity and no significant comorbidities or prior pharmacological therapy. The initial presentation included fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia, evolving over four days. On admission, neurological examination was unremarkable, with tachypnea and bilateral rough vesicular breath sounds on pulmonary auscultation, consistent with diffuse pulmonary involvement. Laboratory findings revealed elevated inflammatory markers and type 1 respiratory failure under FiO2 of 21%, with extensive bilateral, peripheral, and basal pulmonary opacities on chest radiography. Reverse-transcription real-time polymerase chain reaction (RT-PCR) testing of nasal and oropharyngeal exudates confirmed active SARS-CoV-2 infection, while tests for influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila were negative, supporting a primary viral etiology of pneumonia.\\n\\nOver the first 48 hours, progressive clinical deterioration was observed, including worsening fatigue, dyspnea, and respiratory failure, necessitating escalation of oxygen therapy. Noninvasive ventilation was initiated but discontinued due to poor patient adherence; high-flow nasal cannula oxygen was then applied without clinical benefit. The patient was subsequently transferred to a level III ICU, where he received sedoanalgesia and orotracheal intubation with invasive mechanical ventilation.\\n\\nOn day 11 of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin, and empirical antibiotic therapy (amoxicillin/clavulanic acid and azithromycin) was continued, administered on suspicion of secondary bacterial superinfection. Persistent fever with suboptimal response to antipyretics was noted, though inflammatory markers improved by day 3 of ICU admission. To rule out alternative infectious sources, intravenous lines were changed, and blood cultures, catheter tip cultures, bronchoalveolar lavage, urinalysis, urine culture, and transthoracic echocardiography were performed. Blood culture yielded Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid—therapy already in use. Echocardiography revealed hypokinesia of the lateral wall and left ventricular apex, with impaired biventricular function, and mild elevation in troponin (1.8 ng/mL) and ST-segment depression in leads I and aVL, consistent with acute coronary syndrome or septic cardiomyopathy. Noninfectious causes of fever, including neuroleptic use and thyroid dysfunction, were excluded.\\n\\nDuring the weaning phase, the patient required inotropic support with dobutamine and continued to need noninvasive ventilation post-extubation, which occurred on day 15. On day 16 (day 19 of symptom onset), the patient experienced a sudden alteration in consciousness, accompanied by conjugate gaze deviation to the right, left-sided myoclonus of the face and thoracic region, and a generalized tonic-clonic seizure, which resolved with midazolam administration. Hypoxic-ischemic encephalopathy was ruled out due to sustained normotension, absence of peri-event hypoxemia or hypoxemia, normal serum lactate, and preserved diuresis. Electrolyte, glucose, and metabolic imbalances were also excluded as etiologies for the seizure.\\n\\nPost-ictal status included a Glasgow Coma Scale (GCS) of 7 (no eye opening, no verbal response, failure to localize to pain), persistent left hemiparesis (grade 3/5), and requirement for airway protection. The patient remained sedated and underwent repeated orotracheal intubation and initiation of anticonvulsant therapy. Cranial computed tomography (CT) showed no acute structural abnormalities. Lumbar puncture revealed turbid cerebrospinal fluid (CSF) with mild proteinorrachia but no pleocytosis and normal opening pressure. CSF analysis included testing for neurotropic viruses, venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria, and RT-PCR for SARS-CoV-2; the latter was positive, confirming the presence of SARS-CoV-2 RNA in the CSF without evidence of bacterial or viral pleocytosis. This finding supported the diagnosis of SARS-CoV-2 encephalitis rather than bacterial meningitis. Electroencephalography (EEG), performed 1 hour after propofol administration under fentanyl, lasted 13 minutes and showed no epileptiform activity.\\n\\nMagnetic resonance imaging (MRI) performed on", "generated_text": "{\n  \"proficient_health_literacy\": \"A 45-year-old male, born in Pakistan and residing in Portugal for seven years, was admitted to the intensive care unit (ICU) with a diagnosis of SARS-CoV-2-associated pneumonia. He had a history of grade 3 obesity and no significant comorbidities or prior pharmacological therapy. The initial presentation included fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia, evolving over four days. On admission, neurological examination was unremarkable, with tachypnea and bilateral rough vesicular breath sounds on pulmonary auscultation, consistent with diffuse pulmonary involvement. Laboratory findings revealed elevated inflammatory markers and type 1 respiratory failure under FiO2 of 21%, with extensive bilateral, peripheral, and basal pulmonary opacities on chest radiography. Reverse-transcription real-time polymerase chain reaction (RT-PCR) testing of nasal and oropharyngeal exudates confirmed active SARS-CoV-2 infection, while tests for influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila were negative, supporting a primary viral etiology of pneumonia.\\n\\nOver the first 48 hours, progressive clinical deterioration was observed, including worsening fatigue, dyspnea, and respiratory failure, necessitating escalation of oxygen therapy. Noninvasive ventilation was initiated but discontinued due to poor patient adherence; high-flow nasal cannula oxygen was then applied without clinical benefit. The patient was subsequently transferred to a level III ICU, where he received sedoanalgesia and orotracheal intubation with invasive mechanical ventilation.\\n\\nOn day 11 of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin, and empirical antibiotic therapy (amoxicillin/clavulanic acid and azithromycin) was continued, administered on suspicion of secondary bacterial superinfection. Persistent fever with suboptimal response to antipyretics was noted, though inflammatory markers improved by day 3 of ICU admission. To rule out alternative infectious sources, intravenous lines were changed, and blood cultures, catheter tip cultures, bronchoalveolar lavage, urinalysis, urine culture, and transthoracic echocardiography were performed. Blood culture yielded Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid—therapy already in use. Echocardiography revealed hypokinesia of the lateral wall and left ventricular apex, with impaired biventricular function, and mild elevation in troponin (1.8 ng/mL) and ST-segment depression in leads I and aVL, consistent with acute coronary syndrome or septic cardiomyopathy. Noninfectious causes of fever, including neuroleptic use and thyroid dysfunction, were excluded.\\n\\nDuring the weaning phase, the patient required inotropic support with dobutamine and continued to need noninvasive ventilation post-extubation, which occurred on day 15. On day 16 (day 19 of symptom onset), the patient experienced a sudden alteration in consciousness, accompanied by conjugate gaze deviation to the right, left-sided myoclonus of the face and thoracic region, and a generalized tonic-clonic seizure, which resolved with midazolam administration. Hypoxic-ischemic encephalopathy was ruled out due to sustained normotension, absence of peri-event hypoxemia or hypoxemia, normal serum lactate, and preserved diuresis. Electrolyte, glucose, and metabolic imbalances were also excluded as etiologies for the seizure.\\n\\nPost-ictal status included a Glasgow Coma Scale (GCS) of 7 (no eye opening, no verbal response, failure to localize to pain), persistent left hemiparesis (grade 3/5), and requirement for airway protection. The patient remained sedated and underwent repeated orotracheal intubation and initiation of anticonvulsant therapy. Cranial computed tomography (CT) showed no acute structural abnormalities. Lumbar puncture revealed turbid cerebrospinal fluid (CSF) with mild proteinorrachia but no pleocytosis and normal opening pressure. CSF analysis included testing for neurotropic viruses, venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria, and RT-PCR for SARS-CoV-2; the latter was positive, confirming the presence of SARS-CoV-2 RNA in the CSF without evidence of bacterial or viral pleocytosis. This finding supported the diagnosis of SARS-CoV-2 encephalitis rather than bacterial meningitis. Electroencephalography (EEG), performed 1 hour after propofol administration under fentanyl, lasted 13 minutes and showed no epileptiform activity.\\n\\nMagnetic resonance imaging (MRI) performed on"}
{"row_index": 34, "doc_id": 40, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"The person had a long-lasting cough, ear pain, and a foul-smelling yellow discharge from one ear. Tests found bacteria that cause tuberculosis in the stomach fluid and in the ear pus. This means they had tuberculosis in both their lungs and middle ear, especially because their immune system was weak from HIV. They were treated with medicine for 6 months to fight the tuberculosis, along with extra medicines to help their body heal. After 6 months, the cough and ear symptoms went away, the bacteria test turned negative, and they felt better. They also started taking HIV medicine again and now have a much lower virus level in their body. The treatment worked and they are fully recovered.\"\n}", "generated_text": "The person had a long-lasting cough, ear pain, and a foul-smelling yellow discharge from one ear. Tests found bacteria that cause tuberculosis in the stomach fluid and in the ear pus. This means they had tuberculosis in both their lungs and middle ear, especially because their immune system was weak from HIV. They were treated with medicine for 6 months to fight the tuberculosis, along with extra medicines to help their body heal. After 6 months, the cough and ear symptoms went away, the bacteria test turned negative, and they felt better. They also started taking HIV medicine again and now have a much lower virus level in their body. The treatment worked and they are fully recovered."}
{"row_index": 35, "doc_id": 40, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"The patient had a long-lasting cough, ear pain, and a chronic foul-smelling discharge from the right ear. Tests found acid-fast bacteria in both the liquid from the stomach and a swab from the ear pus, which pointed to tuberculosis. The patient also had HIV, which weakened their immune system, making them more susceptible to tuberculosis. Despite initial treatment for malaria and ear infection, the symptoms did not improve. Imaging and exams confirmed tuberculosis in both the ear and the lungs. The patient was treated with a 6-month course of anti-tuberculosis medication, including isoniazid, rifampicin, pyrazinamide, and ethambutol in the first two months, followed by isoniazid and rifampicin for the next four months. They also received treatment for HIV, restarted after adjusting their medication, and were given preventive antibiotics and ear cleaning. After 14 days, their symptoms improved, and the bacteria tests became negative. By the end of treatment, the patient was fully recovered with no signs of infection, and their HIV viral load dropped to a very low level.\"\n}", "generated_text": "The patient had a long-lasting cough, ear pain, and a chronic foul-smelling discharge from the right ear. Tests found acid-fast bacteria in both the liquid from the stomach and a swab from the ear pus, which pointed to tuberculosis. The patient also had HIV, which weakened their immune system, making them more susceptible to tuberculosis. Despite initial treatment for malaria and ear infection, the symptoms did not improve. Imaging and exams confirmed tuberculosis in both the ear and the lungs. The patient was treated with a 6-month course of anti-tuberculosis medication, including isoniazid, rifampicin, pyrazinamide, and ethambutol in the first two months, followed by isoniazid and rifampicin for the next four months. They also received treatment for HIV, restarted after adjusting their medication, and were given preventive antibiotics and ear cleaning. After 14 days, their symptoms improved, and the bacteria tests became negative. By the end of treatment, the patient was fully recovered with no signs of infection, and their HIV viral load dropped to a very low level."}
{"row_index": 36, "doc_id": 40, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 32-year-old male baker from Bamako, Mali, was admitted to the Infectious and Tropical Diseases Department of CHU du Point G on 27 April 2023 with a chronic productive cough, otalgia, and a persistent right-sided purulent otorrhea of progressive onset over one month. Initial management at a local medical center with artésunate, paracetamol, and unspecified antibiotics for suspected malaria and acute otitis media was ineffective. The patient is HIV-1 positive, diagnosed seven months prior, and was previously on a triple antiretroviral therapy (TARV) regimen of tenofovir/lamivudine/dolutegravir, which was discontinued due to patient non-adherence. Immunological evaluation at diagnosis revealed a CD4 count of 118 cells/μL and a viral load of 12,370 copies/mL; after six months of ART, the CD4 count increased to 193 cells/μL and viral load decreased to 9,460 copies/mL. At the time of tuberculosis diagnosis (at seven months post-HIV diagnosis), CD4 count was 89 cells/μL and viral load was 10,230 copies/mL, indicating ongoing immunosuppression. Otoscopic examination of the right ear demonstrated inflammation of the external auditory canal with purulent discharge and a single tympanic membrane perforation in the anterior-inferior quadrant; the left ear was normal. Rinne and Weber tests confirmed a right conductive hearing loss. Radiographic findings on frontal chest X-ray showed an accentuated bronchovascular network at the base of the right lung, consistent with pulmonary tuberculosis. Ziehl-Neelsen bacilloscopy was positive in both gastric washings (on admission and at 19 days later) and in the right ear swab due to persistent purulent otorrhea, supporting the presence of acid-fast bacilli. The Xpert-MTB/GeneXpert assay was negative for rifampicin resistance, confirming drug-susceptible Mycobacterium tuberculosis. The diagnosis of concurrent middle ear tuberculosis and pulmonary tuberculosis in the context of HIV-associated immunosuppression was established. The patient was initiated on a standard first-line anti-tuberculosis regimen: a 2-month intensive phase of quadritherapy comprising isoniazid, rifampicin, pyrazinamide, and ethambutol (2RHZE), followed by a 4-month continuation phase of isoniazid and rifampicin (4RH) at a dose of three tablets daily in the morning on an empty stomach, supplemented with vitamin B6 (1 tablet/day) to prevent peripheral neuropathy. Concurrently, the patient received two therapeutic intensifications of antiretroviral therapy (ART), with ART restarted on 4 May 2023 following good tolerance of anti-tuberculosis drugs. The ART regimen was re-established with tenofovir/lamivudine/dolutegravir (1 tablet/day) and an additional dolutegravir 50 mg (1 tablet/day) as per standard HIV management protocols. Chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) was initiated, and the external auditory canal was cleared via aspiration, followed by instillation of ciprofloxacin ear drops (2 drops, three times daily) for 14 days. Clinical improvement was observed within 14 days of therapy, including resolution of fever, improvement in general condition, and amelioration of cough and otorrhea. Bacilloscopy results became negative in both gastric washings and the right ear pus swab during treatment. At the end of the 6-month anti-tuberculosis regimen, complete clinical healing was achieved, with normal ENT and neurological examinations. Sputum and ear swab bacilloscopy, as well as Xpert-MTB/GeneXpert testing, remained negative at the end of the intensive phase (month 2), at month 5, and at the completion of the maintenance phase (month 6). Post-treatment HIV viral load, assessed three months after ART restart, was 329 copies/mL, indicating effective suppression of viral replication. This case demonstrates the clinical and pathological interplay between HIV-induced immunosuppression, pulmonary and otological tuberculosis, and the successful management through integrated anti-tuberculosis and antiretroviral therapy, with sustained virological and microbiological responses.\"\n}", "generated_text": "A 32-year-old male baker from Bamako, Mali, was admitted to the Infectious and Tropical Diseases Department of CHU du Point G on 27 April 2023 with a chronic productive cough, otalgia, and a persistent right-sided purulent otorrhea of progressive onset over one month. Initial management at a local medical center with artésunate, paracetamol, and unspecified antibiotics for suspected malaria and acute otitis media was ineffective. The patient is HIV-1 positive, diagnosed seven months prior, and was previously on a triple antiretroviral therapy (TARV) regimen of tenofovir/lamivudine/dolutegravir, which was discontinued due to patient non-adherence. Immunological evaluation at diagnosis revealed a CD4 count of 118 cells/μL and a viral load of 12,370 copies/mL; after six months of ART, the CD4 count increased to 193 cells/μL and viral load decreased to 9,460 copies/mL. At the time of tuberculosis diagnosis (at seven months post-HIV diagnosis), CD4 count was 89 cells/μL and viral load was 10,230 copies/mL, indicating ongoing immunosuppression. Otoscopic examination of the right ear demonstrated inflammation of the external auditory canal with purulent discharge and a single tympanic membrane perforation in the anterior-inferior quadrant; the left ear was normal. Rinne and Weber tests confirmed a right conductive hearing loss. Radiographic findings on frontal chest X-ray showed an accentuated bronchovascular network at the base of the right lung, consistent with pulmonary tuberculosis. Ziehl-Neelsen bacilloscopy was positive in both gastric washings (on admission and at 19 days later) and in the right ear swab due to persistent purulent otorrhea, supporting the presence of acid-fast bacilli. The Xpert-MTB/GeneXpert assay was negative for rifampicin resistance, confirming drug-susceptible Mycobacterium tuberculosis. The diagnosis of concurrent middle ear tuberculosis and pulmonary tuberculosis in the context of HIV-associated immunosuppression was established. The patient was initiated on a standard first-line anti-tuberculosis regimen: a 2-month intensive phase of quadritherapy comprising isoniazid, rifampicin, pyrazinamide, and ethambutol (2RHZE), followed by a 4-month continuation phase of isoniazid and rifampicin (4RH) at a dose of three tablets daily in the morning on an empty stomach, supplemented with vitamin B6 (1 tablet/day) to prevent peripheral neuropathy. Concurrently, the patient received two therapeutic intensifications of antiretroviral therapy (ART), with ART restarted on 4 May 2023 following good tolerance of anti-tuberculosis drugs. The ART regimen was re-established with tenofovir/lamivudine/dolutegravir (1 tablet/day) and an additional dolutegravir 50 mg (1 tablet/day) as per standard HIV management protocols. Chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) was initiated, and the external auditory canal was cleared via aspiration, followed by instillation of ciprofloxacin ear drops (2 drops, three times daily) for 14 days. Clinical improvement was observed within 14 days of therapy, including resolution of fever, improvement in general condition, and amelioration of cough and otorrhea. Bacilloscopy results became negative in both gastric washings and the right ear pus swab during treatment. At the end of the 6-month anti-tuberculosis regimen, complete clinical healing was achieved, with normal ENT and neurological examinations. Sputum and ear swab bacilloscopy, as well as Xpert-MTB/GeneXpert testing, remained negative at the end of the intensive phase (month 2), at month 5, and at the completion of the maintenance phase (month 6). Post-treatment HIV viral load, assessed three months after ART restart, was 329 copies/mL, indicating effective suppression of viral replication. This case demonstrates the clinical and pathological interplay between HIV-induced immunosuppression, pulmonary and otological tuberculosis, and the successful management through integrated anti-tuberculosis and antiretroviral therapy, with sustained virological and microbiological responses."}
{"row_index": 37, "doc_id": 41, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 16-month-old boy had a weak heart and was put on a list for a heart transplant. At 20 months, he got a special machine outside his body to help his heart work (called a Berlin Heart). At 23 months, he had a stroke on the left side of his brain, which caused weakness on his right side. Doctors used a small tube to clear the blocked blood vessel and fixed it successfully. The boy was only 10 kg at 23 months, which is small for his age, but he stayed healthy. One month after the stroke, he had a successful heart transplant. The only lasting effect from the stroke was a bit of stiffness in his right arm.\"\n}", "generated_text": "A 16-month-old boy had a weak heart and was put on a list for a heart transplant. At 20 months, he got a special machine outside his body to help his heart work (called a Berlin Heart). At 23 months, he had a stroke on the left side of his brain, which caused weakness on his right side. Doctors used a small tube to clear the blocked blood vessel and fixed it successfully. The boy was only 10 kg at 23 months, which is small for his age, but he stayed healthy. One month after the stroke, he had a successful heart transplant. The only lasting effect from the stroke was a bit of stiffness in his right arm."}
{"row_index": 38, "doc_id": 41, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 23-month-old male with a history of hypoxic-ischaemic encephalopathy at birth, exhibiting preserved brain motor potential and normal psychomotor development, was managed for restrictive cardiomyopathy. He was enrolled in a cardiac transplant programme at 16 months of age and subsequently required implantation of an external biventricular support device (Berlin Heart) to maintain circulatory function. To mitigate the risk of embolic complications associated with chronic cardiac dysfunction and mechanical support, he received dual antiplatelet and anticoagulant therapy, including full-dose heparin, resulting in an activated partial thromboplastin time (APTT) of 93 seconds and an international normalised ratio (INR) of 1.08. At 23 months of age, he presented with acute neurological deterioration manifesting as disconnection syndrome and right hemiparesis. A non-contrast computed tomography (CT) scan revealed a hyperdense left middle cerebral artery (MCA), consistent with acute thrombosis, and a chronic right parietotemporal infarction, indicating prior ischemic damage. Given the concomitant anticoagulation, intravenous thrombolytic therapy was contraindicated due to hemorrhagic risk. Therefore, an intra-arterial mechanical thrombectomy was performed under general anaesthesia. The procedure involved puncture of the right femoral artery and insertion of an 11 cm long 4F sheath (Cordis, Ireland). A 4F vertebral Radiofocus catheter (Glidecath, Terumo, Belgium) was advanced to confirm occlusion of the M1 segment of the left MCA. Recanalization was achieved using a 3 mm × 20 mm Trevo XP Pro Vue stentriever (Stryker, The Netherlands), guided by the vertebral catheter as a tutor and positioned in the petrous segment of the internal carotid artery. A straight Rapid Transit microcatheter (Codman Neurovascular, UK) was used to navigate and open the occluded vessel in a single pass. The entire catheter system—including tutor catheter, microcatheter, and stentriever—was removed simultaneously. A control run during the procedure identified an iatrogenic dissection of the left internal carotid artery, which was asymptomatic and did not compromise perfusion, as the left hemisphere remained adequately irrigated via the anterior communicant artery. Post-procedure, the patient underwent a successful heart transplantation one month later. Neurologically, the only persistent long-term sequelae were spasticity of the right upper limb, consistent with the initial stroke lesion. The case highlights the feasibility and efficacy of intra-arterial mechanical thrombectomy in a pediatric population with complex comorbidities, including congenital cardiomyopathy and chronic anticoagulation, and underscores the importance of pre-procedural vascular mapping and intra-procedural monitoring in pediatric neurointerventional practice.\"\n}", "generated_text": "A 23-month-old male with a history of hypoxic-ischaemic encephalopathy at birth, exhibiting preserved brain motor potential and normal psychomotor development, was managed for restrictive cardiomyopathy. He was enrolled in a cardiac transplant programme at 16 months of age and subsequently required implantation of an external biventricular support device (Berlin Heart) to maintain circulatory function. To mitigate the risk of embolic complications associated with chronic cardiac dysfunction and mechanical support, he received dual antiplatelet and anticoagulant therapy, including full-dose heparin, resulting in an activated partial thromboplastin time (APTT) of 93 seconds and an international normalised ratio (INR) of 1.08. At 23 months of age, he presented with acute neurological deterioration manifesting as disconnection syndrome and right hemiparesis. A non-contrast computed tomography (CT) scan revealed a hyperdense left middle cerebral artery (MCA), consistent with acute thrombosis, and a chronic right parietotemporal infarction, indicating prior ischemic damage. Given the concomitant anticoagulation, intravenous thrombolytic therapy was contraindicated due to hemorrhagic risk. Therefore, an intra-arterial mechanical thrombectomy was performed under general anaesthesia. The procedure involved puncture of the right femoral artery and insertion of an 11 cm long 4F sheath (Cordis, Ireland). A 4F vertebral Radiofocus catheter (Glidecath, Terumo, Belgium) was advanced to confirm occlusion of the M1 segment of the left MCA. Recanalization was achieved using a 3 mm × 20 mm Trevo XP Pro Vue stentriever (Stryker, The Netherlands), guided by the vertebral catheter as a tutor and positioned in the petrous segment of the internal carotid artery. A straight Rapid Transit microcatheter (Codman Neurovascular, UK) was used to navigate and open the occluded vessel in a single pass. The entire catheter system—including tutor catheter, microcatheter, and stentriever—was removed simultaneously. A control run during the procedure identified an iatrogenic dissection of the left internal carotid artery, which was asymptomatic and did not compromise perfusion, as the left hemisphere remained adequately irrigated via the anterior communicant artery. Post-procedure, the patient underwent a successful heart transplantation one month later. Neurologically, the only persistent long-term sequelae were spasticity of the right upper limb, consistent with the initial stroke lesion. The case highlights the feasibility and efficacy of intra-arterial mechanical thrombectomy in a pediatric population with complex comorbidities, including congenital cardiomyopathy and chronic anticoagulation, and underscores the importance of pre-procedural vascular mapping and intra-procedural monitoring in pediatric neurointerventional practice."}
{"row_index": 39, "doc_id": 42, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old man came to the hospital after having a seizure due to drinking too much alcohol. He also had a shoulder injury on his right side that wasn't caught at the first hospital. When checked, his right shoulder had a dislocation and his left shoulder had a simple dislocation that wasn't seen before. The doctors found that the left shoulder injury got worse during his stay, probably because he was held down too tightly. They did surgery on both shoulders at once to fix the bones. The right shoulder was fixed with screws and strong stitches. The left shoulder needed two extra surgeries — one to fix the broken piece and another to open the joint. Two years later, he can move his shoulders a little, with scores showing he's doing better than most. He can now work again and is moving toward full recovery.\"\n}", "generated_text": "A 52-year-old man came to the hospital after having a seizure due to drinking too much alcohol. He also had a shoulder injury on his right side that wasn't caught at the first hospital. When checked, his right shoulder had a dislocation and his left shoulder had a simple dislocation that wasn't seen before. The doctors found that the left shoulder injury got worse during his stay, probably because he was held down too tightly. They did surgery on both shoulders at once to fix the bones. The right shoulder was fixed with screws and strong stitches. The left shoulder needed two extra surgeries — one to fix the broken piece and another to open the joint. Two years later, he can move his shoulders a little, with scores showing he's doing better than most. He can now work again and is moving toward full recovery."}
{"row_index": 40, "doc_id": 42, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 52-year-old man was brought to a specialized hospital after having a seizure caused by alcohol withdrawal and a dislocated shoulder on his right side. At first, X-rays showed a right shoulder dislocation and a simple posterior dislocation of his left shoulder — a problem that had not been seen at the previous hospital and took about 48 hours to diagnose. A CT scan later showed that the left shoulder injury had worsened during his hospital stay, likely because of physical restraint. Both shoulders were surgically repaired in one operation using plates and screws to realign and stabilize the bones. The right shoulder had a fragment of bone that was fixed with a screw and strong sutures, while the left shoulder used strong sutures to hold the bone pieces together, since a screw wasn’t needed. After surgery, the patient wore a shoulder immobilizer for four weeks. By the second week, he began gentle exercises to improve movement, but at one month, the left shoulder’s bone alignment started to loosen, so he had a second surgery to fix it with stronger sutures. He then wore the immobilizer for another four weeks and resumed exercises. After 30 sessions of physical therapy, he returned to work five months later. One year after the injury, his right shoulder was doing well, but his left shoulder still had limited motion, especially in rotating outward. A final surgery was done to release the joint and remove the earlier screws in the left shoulder. Two years later, the patient was doing well — he scored 5% on the Quick DASH scale (a measure of shoulder pain and function) and 72 and 76 on the Constant scale (which measures shoulder strength and movement) for his left and right shoulders, respectively. This shows he is making steady progress in recovery.\"\n}", "generated_text": "A 52-year-old man was brought to a specialized hospital after having a seizure caused by alcohol withdrawal and a dislocated shoulder on his right side. At first, X-rays showed a right shoulder dislocation and a simple posterior dislocation of his left shoulder — a problem that had not been seen at the previous hospital and took about 48 hours to diagnose. A CT scan later showed that the left shoulder injury had worsened during his hospital stay, likely because of physical restraint. Both shoulders were surgically repaired in one operation using plates and screws to realign and stabilize the bones. The right shoulder had a fragment of bone that was fixed with a screw and strong sutures, while the left shoulder used strong sutures to hold the bone pieces together, since a screw wasn’t needed. After surgery, the patient wore a shoulder immobilizer for four weeks. By the second week, he began gentle exercises to improve movement, but at one month, the left shoulder’s bone alignment started to loosen, so he had a second surgery to fix it with stronger sutures. He then wore the immobilizer for another four weeks and resumed exercises. After 30 sessions of physical therapy, he returned to work five months later. One year after the injury, his right shoulder was doing well, but his left shoulder still had limited motion, especially in rotating outward. A final surgery was done to release the joint and remove the earlier screws in the left shoulder. Two years later, the patient was doing well — he scored 5% on the Quick DASH scale (a measure of shoulder pain and function) and 72 and 76 on the Constant scale (which measures shoulder strength and movement) for his left and right shoulders, respectively. This shows he is making steady progress in recovery."}
{"row_index": 41, "doc_id": 42, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 52-year-old male with no significant medical history was transferred to a high-complexity trauma center following a tonic-clonic seizure secondary to alcohol withdrawal and a non-reduced right posterior glenohumeral fracture (LFGHP). Upon initial evaluation 24 hours after admission, the patient was conscious but exhibited bilateral shoulder ecchymosis and severe passive external rotation limitation on both shoulders. He was physically restrained due to intermittent psychomotor agitation, with both feet and his left hand secured. The initial radiographic assessment revealed a right LFGHP and a previously undiagnosed simple posterior glenohumeral dislocation of the left shoulder, which had not been identified at the referring facility and was only diagnosed approximately 48 hours after admission.\\n\\nA computed tomography (CT) scan of both shoulders was performed to assess the extent and evolution of the injuries. The CT demonstrated a significant progression of the left shoulder injury from a simple posterior dislocation on admission radiographs to a full posterior glenohumeral fracture (LFGHP) by the 48-hour mark, likely secondary to the mechanical stress imposed by physical restraint during immobilization. This progression highlights the role of external forces in exacerbating glenohumeral instability in the setting of acute trauma.\\n\\nPreoperative imaging of the right shoulder revealed glenoid bone integrity with 40% involvement of the humeral articular surface, including a large fragment that was anatomically positioned to maintain continuity with the lesser tuberosity. This fragment was planned to be stabilized using a 4.0 mm spongy screw with partial threading and high-strength sutures. In contrast, the left shoulder showed intact glenoid bone and a 20% defect in the humeral articular surface, which was addressed by repositioning and osteosynthesizing the lesser tuberosity fragment—mirroring the surgical technique described in McLaughlin’s protocol for humeral head fracture repair.\\n\\nThe surgical approach involved open reduction and internal fixation (ORIF) with bilateral locked-plate fixation using a Philos (Depuy Synthes®) plate. The patient was positioned in a beach chair position, and both shoulders were accessed via a classic deltopectoral approach. For the right shoulder, a posterior mini-open incision (diagnostic arthroscopy-sized) was used for digital manipulation and reduction of the posterior humeral head fragment. A provisional reduction was achieved using high-strength sutures and needles, followed by definitive fixation with a 4.0 mm spongy screw and high-strength sutures. The final reduction and stability were achieved with the Philos plate, supplemented by fixation of the rotator cuff tendons to the plate using high-strength sutures. The right shoulder was closed in layers and immobilized with a universal shoulder immobilizer.\\n\\nThe left shoulder was operated on immediately after the right. A second deltopectoral approach was performed with an accessory posterior portal for digital reduction of the humeral head. Fixation was accomplished similarly to the right shoulder, except that the spongy screw was not used due to the anterior fragment's inability to achieve adequate stability without high-strength suture fixation alone.\\n\\nPostoperative management included bilateral shoulder immobilization for four weeks. Passive and active pendular flexion-extension exercises of the elbow and finger flexion were initiated from the second postoperative week, progressing according to pain tolerance. At the one-month radiographic follow-up, loss of reduction of the greater tuberosity was observed in the left shoulder, prompting a revision surgery to re-stabilize the fragment with high-strength sutures. The patient was then placed in additional immobilization for four weeks on the left shoulder. Bilateral rehabilitation exercises were resumed from the second postoperative week. At the sixth week post-revision, face-to-face kinesiological therapy was initiated twice weekly. After 30 sessions of structured kinesiological rehabilitation, the patient returned to work five months after the initial injury.\\n\\nOne-year follow-up revealed full recovery of strength and range of motion in the right shoulder, while the left shoulder continued to exhibit significant limitations, particularly in external rotation. At this stage, arthroscopic joint release surgery was performed, with removal of the osteosynthesis hardware in the left shoulder to address chronic joint stiffness and functional impairment. Two years after the initial trauma, the patient demonstrated favorable functional outcomes, with a Quick DASH score of 5%, and Constant scores of 72 and 76 in the left and right shoulders, respectively, indicating substantial recovery and satisfactory functional performance despite persistent limitations in the left shoulder. The case underscores the importance of timely diagnosis, accurate imaging interpretation, and surgical intervention in managing complex glenohumeral fractures, particularly in the context of acute trauma and physical restraint-related injury progression.\"\n}", "generated_text": "A 52-year-old male with no significant medical history was transferred to a high-complexity trauma center following a tonic-clonic seizure secondary to alcohol withdrawal and a non-reduced right posterior glenohumeral fracture (LFGHP). Upon initial evaluation 24 hours after admission, the patient was conscious but exhibited bilateral shoulder ecchymosis and severe passive external rotation limitation on both shoulders. He was physically restrained due to intermittent psychomotor agitation, with both feet and his left hand secured. The initial radiographic assessment revealed a right LFGHP and a previously undiagnosed simple posterior glenohumeral dislocation of the left shoulder, which had not been identified at the referring facility and was only diagnosed approximately 48 hours after admission.\n\nA computed tomography (CT) scan of both shoulders was performed to assess the extent and evolution of the injuries. The CT demonstrated a significant progression of the left shoulder injury from a simple posterior dislocation on admission radiographs to a full posterior glenohumeral fracture (LFGHP) by the 48-hour mark, likely secondary to the mechanical stress imposed by physical restraint during immobilization. This progression highlights the role of external forces in exacerbating glenohumeral instability in the setting of acute trauma.\n\nPreoperative imaging of the right shoulder revealed glenoid bone integrity with 40% involvement of the humeral articular surface, including a large fragment that was anatomically positioned to maintain continuity with the lesser tuberosity. This fragment was planned to be stabilized using a 4.0 mm spongy screw with partial threading and high-strength sutures. In contrast, the left shoulder showed intact glenoid bone and a 20% defect in the humeral articular surface, which was addressed by repositioning and osteosynthesizing the lesser tuberosity fragment—mirroring the surgical technique described in McLaughlin’s protocol for humeral head fracture repair.\n\nThe surgical approach involved open reduction and internal fixation (ORIF) with bilateral locked-plate fixation using a Philos (Depuy Synthes®) plate. The patient was positioned in a beach chair position, and both shoulders were accessed via a classic deltopectoral approach. For the right shoulder, a posterior mini-open incision (diagnostic arthroscopy-sized) was used for digital manipulation and reduction of the posterior humeral head fragment. A provisional reduction was achieved using high-strength sutures and needles, followed by definitive fixation with a 4.0 mm spongy screw and high-strength sutures. The final reduction and stability were achieved with the Philos plate, supplemented by fixation of the rotator cuff tendons to the plate using high-strength sutures. The right shoulder was closed in layers and immobilized with a universal shoulder immobilizer.\n\nThe left shoulder was operated on immediately after the right. A second deltopectoral approach was performed with an accessory posterior portal for digital reduction of the humeral head. Fixation was accomplished similarly to the right shoulder, except that the spongy screw was not used due to the anterior fragment's inability to achieve adequate stability without high-strength suture fixation alone.\n\nPostoperative management included bilateral shoulder immobilization for four weeks. Passive and active pendular flexion-extension exercises of the elbow and finger flexion were initiated from the second postoperative week, progressing according to pain tolerance. At the one-month radiographic follow-up, loss of reduction of the greater tuberosity was observed in the left shoulder, prompting a revision surgery to re-stabilize the fragment with high-strength sutures. The patient was then placed in additional immobilization for four weeks on the left shoulder. Bilateral rehabilitation exercises were resumed from the second postoperative week. At the sixth week post-revision, face-to-face kinesiological therapy was initiated twice weekly. After 30 sessions of structured kinesiological rehabilitation, the patient returned to work five months after the initial injury.\n\nOne-year follow-up revealed full recovery of strength and range of motion in the right shoulder, while the left shoulder continued to exhibit significant limitations, particularly in external rotation. At this stage, arthroscopic joint release surgery was performed, with removal of the osteosynthesis hardware in the left shoulder to address chronic joint stiffness and functional impairment. Two years after the initial trauma, the patient demonstrated favorable functional outcomes, with a Quick DASH score of 5%, and Constant scores of 72 and 76 in the left and right shoulders, respectively, indicating substantial recovery and satisfactory functional performance despite persistent limitations in the left shoulder. The case underscores the importance of timely diagnosis, accurate imaging interpretation, and surgical intervention in managing complex glenohumeral fractures, particularly in the context of acute trauma and physical restraint-related injury progression."}
{"row_index": 42, "doc_id": 43, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 70-year-old man had a serious heart problem where blood was leaking backward through the aortic valve. Doctors fixed it with a tiny valve placed inside his heart using a catheter (not open surgery) from the top of his heart. After that, his heart started to fail again, so they added a machine to help his heart pump blood. One year later, the machine showed the valve wasn’t working well, and the leak got worse. The doctors decided to fix the old valve by placing a new one inside it, like putting a new door in an old one. They slowed down the heart machine and set the heart to beat 140 times a minute during the procedure. The new valve went in perfectly, and after 12 months, there was no more leak, his heart was strong, and he could walk much farther without trouble. He’s doing great now.\"\n}", "generated_text": "A 70-year-old man had a serious heart problem where blood was leaking backward through the aortic valve. Doctors fixed it with a tiny valve placed inside his heart using a catheter (not open surgery) from the top of his heart. After that, his heart started to fail again, so they added a machine to help his heart pump blood. One year later, the machine showed the valve wasn’t working well, and the leak got worse. The doctors decided to fix the old valve by placing a new one inside it, like putting a new door in an old one. They slowed down the heart machine and set the heart to beat 140 times a minute during the procedure. The new valve went in perfectly, and after 12 months, there was no more leak, his heart was strong, and he could walk much farther without trouble. He’s doing great now."}
{"row_index": 43, "doc_id": 43, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 70-year-old man with severe heart valve problems was treated with a procedure called transcatheter aortic valve implantation (TAVI) from the apex of his heart. He had a history of heart infection that had healed, and his heart was very weak, with only 20% of its normal pumping ability. Because of his poor heart function and other health issues, surgery was too risky, so TAVI was chosen instead. After the first procedure, his heart improved, but he had a relapse of symptoms four weeks later due to continued weakness. As a result, he received a left ventricular assist device (LVAD), which helps the heart pump blood. He stayed symptom-free for a year, but the LVAD started giving warning signs of high flow, and tests showed worsening leakage through the aortic valve, even though the original valve appeared structurally normal. After careful discussion with his medical team, they decided to perform a second valve procedure — a 'valve-in-valve' approach — where a new valve was placed inside the existing one. This was done while reducing the LVAD flow to the lowest level and using a pacemaker to keep his heart beating at 140 beats per minute during the procedure. The new valve was placed carefully using imaging guidance to avoid damaging the original valve. The procedure was successful, and at 12 months follow-up, the patient had no significant leakage from the aortic valve, his heart function improved to 33%, and he could walk much farther without shortness of breath. He is now doing well and living a normal life.\"\n}", "generated_text": "A 70-year-old man with severe heart valve problems was treated with a procedure called transcatheter aortic valve implantation (TAVI) from the apex of his heart. He had a history of heart infection that had healed, and his heart was very weak, with only 20% of its normal pumping ability. Because of his poor heart function and other health issues, surgery was too risky, so TAVI was chosen instead. After the first procedure, his heart improved, but he had a relapse of symptoms four weeks later due to continued weakness. As a result, he received a left ventricular assist device (LVAD), which helps the heart pump blood. He stayed symptom-free for a year, but the LVAD started giving warning signs of high flow, and tests showed worsening leakage through the aortic valve, even though the original valve appeared structurally normal. After careful discussion with his medical team, they decided to perform a second valve procedure — a 'valve-in-valve' approach — where a new valve was placed inside the existing one. This was done while reducing the LVAD flow to the lowest level and using a pacemaker to keep his heart beating at 140 beats per minute during the procedure. The new valve was placed carefully using imaging guidance to avoid damaging the original valve. The procedure was successful, and at 12 months follow-up, the patient had no significant leakage from the aortic valve, his heart function improved to 33%, and he could walk much farther without shortness of breath. He is now doing well and living a normal life."}
{"row_index": 44, "doc_id": 43, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 70-year-old white male with severe symptomatic aortic regurgitation secondary to healed infective endocarditis was managed with transcatheter aortic valve implantation (TAVI) via an apical approach. The procedure was indicated due to his high surgical risk, assessed using a logistic EuroSCORE I of 24.36%, compounded by secondary pulmonary hypertension, severely impaired left ventricular function (left ventricular ejection fraction [LVEF] of 20%), chronic renal insufficiency (serum creatinine 2.1 mg/dL), and comorbidities including chronic kidney disease and systemic hypertension. Pre-TAVI medical therapy included torasemide 20 mg daily, ramipril 5 mg daily, bisoprolol 2.5 mg twice daily, and spironolactone 12.5 mg daily. On admission, the patient presented with cardiac decompensation and dyspnea (temperature 36.7 °C, pulse 99/min, blood pressure 109/48 mmHg), with no evidence of active infection (normal C-reactive protein and leukocyte count), and no microbiological workup performed. Laboratory findings revealed mild hepatocellular dysfunction (aspartate aminotransferase 59 U/L, alanine aminotransferase 67 U/L) and mild anemia (hemoglobin 10.7 g/dL), with no urine analysis conducted. Coronary angiography, performed prior to TAVI, was normal, supporting the exclusion of coronary artery disease as a contributing factor.\\n\\nThe initial TAVI was performed with a JenaValve 27 mm self-expandable bioprosthesis. Post-procedural imaging demonstrated minimal transvalvular central insufficiency and stable hemodynamics, indicating initial procedural success. However, despite this, the patient experienced recurrent cardiac decompensation due to persistent left ventricular dysfunction, leading to a repeat interdisciplinary evaluation. Four weeks after the initial TAVI, the patient underwent implantation of a left ventricular assist device (LVAD) system (Thoratec® HeartMate II) to support ventricular function. The postoperative course was uneventful, and the patient remained asymptomatic for one year.\\n\\nDuring this period, the LVAD system generated recurrent high-flow alarms, prompting further evaluation. Serial echocardiographic assessments revealed a progressive worsening of transvalvular central aortic insufficiency to a severe level, with no evidence of structural leaflet damage or prosthetic thrombosis in the JenaValve. This suggested a functional impairment of the aortic outflow due to hemodynamic alterations, likely related to the high flow dynamics generated by the LVAD and the inherent geometry of the existing prosthesis. Given the persistent regurgitation and lack of improvement in ventricular function, a valve-in-valve strategy was adopted.\\n\\nThe subsequent TAVI procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm self-expanding valve, without prior valvuloplasty. Hemodynamic management during implantation included reduction of LVAD flow to minimum and maintenance of cardiac pacing at 140 beats per minute to optimize ventricular filling and reduce flow-induced turbulence. Positioning was guided by real-time fluoroscopy and transesophageal echocardiography (TEE), with specific attention to placing the ventricular strut end of the CoreValve Evolut R between the ventricular end and the 'cusp feelers' of the existing JenaValve prosthesis. This positioning was informed by individualized CT imaging, which confirmed optimal alignment of the JenaValve's ventricular edge within the left ventricular outflow tract (LVOT). The initial positioning was successful without repositioning, and the valve was released in the planned anatomical position after final fluoroscopic confirmation. Post-implantation, rapid pacing was discontinued, and LVAD flow was gradually increased to ensure adequate hemodynamic stability.\\n\\nThe postoperative course was uneventful, and follow-up TEE at 12 months demonstrated no significant aortic regurgitation, with only marginal residual insufficiency. The patient reported no symptoms and demonstrated significant functional improvement, with a 6-minute walk distance increasing from 148 meters on admission to 381 meters at 12-month follow-up. Echocardiography also revealed an improvement in left ventricular function, with LVEF rising to 33%. This case illustrates the complex interplay between prosthetic valve dynamics, LVAD-induced hemodynamics, and the risk of transvalvular regurgitation in patients with pre-existing severe aortic regurgitation and severely compromised left ventricular function. The valve-in-valve approach, when carefully planned with precise positioning and optimized hemodynamic support, can", "generated_text": "{\n  \"proficient_health_literacy\": \"A 70-year-old white male with severe symptomatic aortic regurgitation secondary to healed infective endocarditis was managed with transcatheter aortic valve implantation (TAVI) via an apical approach. The procedure was indicated due to his high surgical risk, assessed using a logistic EuroSCORE I of 24.36%, compounded by secondary pulmonary hypertension, severely impaired left ventricular function (left ventricular ejection fraction [LVEF] of 20%), chronic renal insufficiency (serum creatinine 2.1 mg/dL), and comorbidities including chronic kidney disease and systemic hypertension. Pre-TAVI medical therapy included torasemide 20 mg daily, ramipril 5 mg daily, bisoprolol 2.5 mg twice daily, and spironolactone 12.5 mg daily. On admission, the patient presented with cardiac decompensation and dyspnea (temperature 36.7 °C, pulse 99/min, blood pressure 109/48 mmHg), with no evidence of active infection (normal C-reactive protein and leukocyte count), and no microbiological workup performed. Laboratory findings revealed mild hepatocellular dysfunction (aspartate aminotransferase 59 U/L, alanine aminotransferase 67 U/L) and mild anemia (hemoglobin 10.7 g/dL), with no urine analysis conducted. Coronary angiography, performed prior to TAVI, was normal, supporting the exclusion of coronary artery disease as a contributing factor.\\n\\nThe initial TAVI was performed with a JenaValve 27 mm self-expandable bioprosthesis. Post-procedural imaging demonstrated minimal transvalvular central insufficiency and stable hemodynamics, indicating initial procedural success. However, despite this, the patient experienced recurrent cardiac decompensation due to persistent left ventricular dysfunction, leading to a repeat interdisciplinary evaluation. Four weeks after the initial TAVI, the patient underwent implantation of a left ventricular assist device (LVAD) system (Thoratec® HeartMate II) to support ventricular function. The postoperative course was uneventful, and the patient remained asymptomatic for one year.\\n\\nDuring this period, the LVAD system generated recurrent high-flow alarms, prompting further evaluation. Serial echocardiographic assessments revealed a progressive worsening of transvalvular central aortic insufficiency to a severe level, with no evidence of structural leaflet damage or prosthetic thrombosis in the JenaValve. This suggested a functional impairment of the aortic outflow due to hemodynamic alterations, likely related to the high flow dynamics generated by the LVAD and the inherent geometry of the existing prosthesis. Given the persistent regurgitation and lack of improvement in ventricular function, a valve-in-valve strategy was adopted.\\n\\nThe subsequent TAVI procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm self-expanding valve, without prior valvuloplasty. Hemodynamic management during implantation included reduction of LVAD flow to minimum and maintenance of cardiac pacing at 140 beats per minute to optimize ventricular filling and reduce flow-induced turbulence. Positioning was guided by real-time fluoroscopy and transesophageal echocardiography (TEE), with specific attention to placing the ventricular strut end of the CoreValve Evolut R between the ventricular end and the 'cusp feelers' of the existing JenaValve prosthesis. This positioning was informed by individualized CT imaging, which confirmed optimal alignment of the JenaValve's ventricular edge within the left ventricular outflow tract (LVOT). The initial positioning was successful without repositioning, and the valve was released in the planned anatomical position after final fluoroscopic confirmation. Post-implantation, rapid pacing was discontinued, and LVAD flow was gradually increased to ensure adequate hemodynamic stability.\\n\\nThe postoperative course was uneventful, and follow-up TEE at 12 months demonstrated no significant aortic regurgitation, with only marginal residual insufficiency. The patient reported no symptoms and demonstrated significant functional improvement, with a 6-minute walk distance increasing from 148 meters on admission to 381 meters at 12-month follow-up. Echocardiography also revealed an improvement in left ventricular function, with LVEF rising to 33%. This case illustrates the complex interplay between prosthetic valve dynamics, LVAD-induced hemodynamics, and the risk of transvalvular regurgitation in patients with pre-existing severe aortic regurgitation and severely compromised left ventricular function. The valve-in-valve approach, when carefully planned with precise positioning and optimized hemodynamic support, can"}
{"row_index": 45, "doc_id": 44, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old boy came in with sudden headaches and drinking a lot of water, urinating a lot. Doctors found he had a small cyst in his brain that had burst, but it wasn’t pressing on any parts of his brain or causing serious problems. His hormones were mostly normal, except for a small problem with water balance, which got better with medicine. No surgery was needed because the cyst stayed the same size and didn’t get worse over three years. He grew up normally, started puberty on time, and had no vision issues. But his growth slowed down a bit, so doctors tested him and found he had a little missing growth hormone. After starting treatment, his growth sped up. The cyst stayed stable and didn’t get bigger or smaller much over time.\"\n}", "generated_text": "A 12-year-old boy came in with sudden headaches and drinking a lot of water, urinating a lot. Doctors found he had a small cyst in his brain that had burst, but it wasn’t pressing on any parts of his brain or causing serious problems. His hormones were mostly normal, except for a small problem with water balance, which got better with medicine. No surgery was needed because the cyst stayed the same size and didn’t get worse over three years. He grew up normally, started puberty on time, and had no vision issues. But his growth slowed down a bit, so doctors tested him and found he had a little missing growth hormone. After starting treatment, his growth sped up. The cyst stayed stable and didn’t get bigger or smaller much over time."}
{"row_index": 46, "doc_id": 44, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 12-year-old male presented with acute onset of headache and polyuria-polydipsia, which began one week prior to evaluation. He had no significant past medical history. Physical examination revealed a height of 146.5 cm (−1.4 SD) and weight of 30 kg. No signs of adrenal insufficiency or hypothyroidism were observed. He was at the early stages of puberty, with bilateral gonadal volumes of 3.2 cm and penile length of 6.2 cm (male standard). The polyuria-polydipsia was severe, with urinary fluid excretion reaching up to 113 ml/kg/day, nocturnal enuresis, and excessive fluid intake of 3.8 liters/m². Ophthalmologic assessment, including optical coherence tomography (OCT), showed normal visual function and retinal structure, with no evidence of optic nerve or retinal pathology.\\n\\nEndocrine evaluation revealed diabetes insipidus (DI), characterized by a serum sodium of 140 mEq/L, plasma osmolality of 287 mosm/kg, and urine osmolality of 179 mosm/kg—indicating a profound inability to concentrate urine. All other endocrine markers, including insulin-like growth factor-1 (IGF-1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH), were within normal reference ranges, suggesting intact hypothalamic-pituitary axis function except for the specific deficiency of antidiuretic hormone (ADH) action.\\n\\nMagnetic resonance imaging (MRI) with and without contrast demonstrated apoplexy of a Rathke cleft cyst (RCC), showing spontaneous hyperintensity on both T1 and T2-weighted sequences with dimensions of 15 × 6 × 11 mm. The anterior pituitary exhibited homogeneous contrast enhancement, consistent with normal vascularization and structural integrity. Notably, the posterior pituitary showed loss of typical hyperintensity on T2 sequences, which is a key radiological finding in RCC apoplexy and suggests hemorrhage or disruption of neurohypophyseal tissue. No evidence of craniopharyngioma or other structural lesions was identified. The RCC apoplexy remained stable over a nine-month follow-up period, with size reduction to 12 × 11 × 10 mm, and subsequent imaging at 2 and 3 years revealed progressive stabilization, ultimately measuring 7 × 10 × 6 mm, indicating a non-progressive, possibly self-limiting hemorrhagic event.\\n\\nA multidisciplinary team comprising an endocrinologist, neurosurgeon, and radiologist reviewed the case. Given the absence of compressive neurologic symptoms, normal neuroimaging progression, and stable hormonal profiles (excluding DI), a conservative management strategy was adopted, involving regular clinical, biochemical, and radiological monitoring. Over a three-year follow-up, the patient achieved normal pubertal development without significant endocrine deficiencies, except for a partial growth hormone (GH) deficiency, which emerged later as a secondary finding.\\n\\nGrowth velocity declined from −0.8 SD to −1.1 SD, prompting further investigation. At age 14 years and 9 months, two GH stimulation tests—propranolol-glucagon test and insulin tolerance test—were performed, yielding GH peak values of 19.3 µUI/ml and 10.0 µUI/ml, respectively, both below the threshold for normal pubertal growth, confirming a partial GH deficiency. Following initiation of recombinant human growth hormone (rhGH) therapy, growth velocity improved significantly, increasing from −1.1 SD to +0.2 SD over one year, indicating effective hormonal replacement.\\n\\nRadiological follow-up was conducted at a single center with consistent interpretation by the same radiologist, ensuring longitudinal reliability and minimizing inter-observer variability. The stability of the RCC apoplexy over time, coupled with the absence of expansion or mass effect, supports the conclusion that the lesion is benign and non-encroaching, with no indication for surgical intervention. The case underscores the importance of long-term monitoring in pediatric patients with RCC apoplexy, particularly when initial endocrine and neurologic findings are non-compressive and within normal limits, and highlights the potential for delayed emergence of secondary endocrine deficiencies, such as partial GH deficiency, despite otherwise normal early puberty and hormonal function.\"\n}", "generated_text": "A 12-year-old male presented with acute onset of headache and polyuria-polydipsia, which began one week prior to evaluation. He had no significant past medical history. Physical examination revealed a height of 146.5 cm (−1.4 SD) and weight of 30 kg. No signs of adrenal insufficiency or hypothyroidism were observed. He was at the early stages of puberty, with bilateral gonadal volumes of 3.2 cm and penile length of 6.2 cm (male standard). The polyuria-polydipsia was severe, with urinary fluid excretion reaching up to 113 ml/kg/day, nocturnal enuresis, and excessive fluid intake of 3.8 liters/m². Ophthalmologic assessment, including optical coherence tomography (OCT), showed normal visual function and retinal structure, with no evidence of optic nerve or retinal pathology.\n\nEndocrine evaluation revealed diabetes insipidus (DI), characterized by a serum sodium of 140 mEq/L, plasma osmolality of 287 mosm/kg, and urine osmolality of 179 mosm/kg—indicating a profound inability to concentrate urine. All other endocrine markers, including insulin-like growth factor-1 (IGF-1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH), were within normal reference ranges, suggesting intact hypothalamic-pituitary axis function except for the specific deficiency of antidiuretic hormone (ADH) action.\n\nMagnetic resonance imaging (MRI) with and without contrast demonstrated apoplexy of a Rathke cleft cyst (RCC), showing spontaneous hyperintensity on both T1 and T2-weighted sequences with dimensions of 15 × 6 × 11 mm. The anterior pituitary exhibited homogeneous contrast enhancement, consistent with normal vascularization and structural integrity. Notably, the posterior pituitary showed loss of typical hyperintensity on T2 sequences, which is a key radiological finding in RCC apoplexy and suggests hemorrhage or disruption of neurohypophyseal tissue. No evidence of craniopharyngioma or other structural lesions was identified. The RCC apoplexy remained stable over a nine-month follow-up period, with size reduction to 12 × 11 × 10 mm, and subsequent imaging at 2 and 3 years revealed progressive stabilization, ultimately measuring 7 × 10 × 6 mm, indicating a non-progressive, possibly self-limiting hemorrhagic event.\n\nA multidisciplinary team comprising an endocrinologist, neurosurgeon, and radiologist reviewed the case. Given the absence of compressive neurologic symptoms, normal neuroimaging progression, and stable hormonal profiles (excluding DI), a conservative management strategy was adopted, involving regular clinical, biochemical, and radiological monitoring. Over a three-year follow-up, the patient achieved normal pubertal development without significant endocrine deficiencies, except for a partial growth hormone (GH) deficiency, which emerged later as a secondary finding.\n\nGrowth velocity declined from −0.8 SD to −1.1 SD, prompting further investigation. At age 14 years and 9 months, two GH stimulation tests—propranolol-glucagon test and insulin tolerance test—were performed, yielding GH peak values of 19.3 µUI/ml and 10.0 µUI/ml, respectively, both below the threshold for normal pubertal growth, confirming a partial GH deficiency. Following initiation of recombinant human growth hormone (rhGH) therapy, growth velocity improved significantly, increasing from −1.1 SD to +0.2 SD over one year, indicating effective hormonal replacement.\n\nRadiological follow-up was conducted at a single center with consistent interpretation by the same radiologist, ensuring longitudinal reliability and minimizing inter-observer variability. The stability of the RCC apoplexy over time, coupled with the absence of expansion or mass effect, supports the conclusion that the lesion is benign and non-encroaching, with no indication for surgical intervention. The case underscores the importance of long-term monitoring in pediatric patients with RCC apoplexy, particularly when initial endocrine and neurologic findings are non-compressive and within normal limits, and highlights the potential for delayed emergence of secondary endocrine deficiencies, such as partial GH deficiency, despite otherwise normal early puberty and hormonal function."}
{"row_index": 47, "doc_id": 45, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 67-year-old male with no significant comorbidities presented with a six-month history of progressive dysphonia and dysphagia, culminating in a marked deterioration of general condition accompanied by a 15 kg weight loss over six months. Initial clinical examination revealed a conscious patient with a Glasgow Coma Scale of 15/15, normothermia, blood pressure of 12/8 mmHg, oxygen saturation of 100%, heart rate of 80 beats per minute, and normal conjunctival color. A large mass was identified in the nasopharyngeal cavity, with no evidence of hepatomegaly, splenomegaly, or lymphadenopathy. Physical examination remained otherwise unremarkable.\\n\\nCervico-thoraco-abdomino-pelvic CT imaging demonstrated a 70 mm × 40 mm nasopharyngeal mass extending to 60 mm in size. Laboratory investigations, including complete blood count, renal and hepatic function tests, lactate dehydrogenase, and serologies for HIV, HCV, and HBV, were within normal limits. Histopathological and immunohistochemical analysis of the nasopharyngeal biopsy, performed in two independent laboratories, confirmed a grade 1–2 follicular B-cell non-Hodgkin lymphoma (NHL) characterized by CD20+, CD19+, CD79a+, and CD10+ expression, consistent with a follicular lymphoma subtype. Bone marrow biopsy and pre-therapeutic work-up were normal, excluding hematologic involvement.\\n\\nThe patient received four cycles of R-CHOP chemotherapy (rituximab 375 mg/m² intravenously, cyclophosphamide 750 mg/m² intravenously, oncovin 2 mg intravenously, prednisolone 100 mg orally, doxorubicin 50 mg/m² intravenously), which yielded no clinical or radiological response. Subsequently, three cycles of R-DHAOX chemotherapy (rituximab 375 mg/m² intravenously on day 1, high-dose aracytine 2 g/m² intravenously on day 2 administered over two days, dexamethasone 40 mg intravenously daily from day 1 to day 4, oxalipatin 100 mg/m² intravenously on day 1) were administered, also without response. Persistent growth of the nasopharyngeal mass necessitated tracheostomy due to airway compromise.\\n\\nRepeat biopsy of the nasopharyngeal lesion revealed a complete absence of B-cell lymphoid infiltration and the presence of AL-type amyloid deposits, specifically kappa light chain–associated amyloidosis, suggesting a clonal plasma cell disorder. Immunoelectrophoresis of plasma proteins demonstrated elevated immunoglobulin M (IgM) with kappa light chain specificity, although light chain free light chain quantification was not performed due to institutional resource limitations. Myelogram and a second bone marrow biopsy remained normal, excluding overt multiple myeloma or plasma cell dyscrasia.\\n\\nPositron emission tomography (PET) imaging confirmed a hypermetabolic nasopharyngeal lesion with no evidence of systemic metastatic disease. Cardiac evaluation (electrocardiogram, n-terminal pro-B-type natriuretic peptide, troponin, echocardiography) and renal function were unremarkable. The patient is currently receiving a triplet therapy protocol comprising bortezomib, prednisone, and bendamustine, which has demonstrated favorable clinical response following the initial cycle. The clinical course indicates a possible transformation from follicular lymphoma to a concomitant or secondary amyloidosis, potentially driven by clonal B-cell dysregulation and IgM production, with the nasopharyngeal mass serving as a site of extramedullary amyloid deposition. This case highlights the clinical challenge of distinguishing between primary lymphoma and amyloid-related pathology in the setting of a large, non-lymphomatous-appearing extramedullary mass with immunological features of B-cell dyscrasia.\"\n}", "generated_text": "A 67-year-old male with no significant comorbidities presented with a six-month history of progressive dysphonia and dysphagia, culminating in a marked deterioration of general condition accompanied by a 15 kg weight loss over six months. Initial clinical examination revealed a conscious patient with a Glasgow Coma Scale of 15/15, normothermia, blood pressure of 12/8 mmHg, oxygen saturation of 100%, heart rate of 80 beats per minute, and normal conjunctival color. A large mass was identified in the nasopharyngeal cavity, with no evidence of hepatomegaly, splenomegaly, or lymphadenopathy. Physical examination remained otherwise unremarkable.\n\nCervico-thoraco-abdomino-pelvic CT imaging demonstrated a 70 mm × 40 mm nasopharyngeal mass extending to 60 mm in size. Laboratory investigations, including complete blood count, renal and hepatic function tests, lactate dehydrogenase, and serologies for HIV, HCV, and HBV, were within normal limits. Histopathological and immunohistochemical analysis of the nasopharyngeal biopsy, performed in two independent laboratories, confirmed a grade 1–2 follicular B-cell non-Hodgkin lymphoma (NHL) characterized by CD20+, CD19+, CD79a+, and CD10+ expression, consistent with a follicular lymphoma subtype. Bone marrow biopsy and pre-therapeutic work-up were normal, excluding hematologic involvement.\n\nThe patient received four cycles of R-CHOP chemotherapy (rituximab 375 mg/m² intravenously, cyclophosphamide 750 mg/m² intravenously, oncovin 2 mg intravenously, prednisolone 100 mg orally, doxorubicin 50 mg/m² intravenously), which yielded no clinical or radiological response. Subsequently, three cycles of R-DHAOX chemotherapy (rituximab 375 mg/m² intravenously on day 1, high-dose aracytine 2 g/m² intravenously on day 2 administered over two days, dexamethasone 40 mg intravenously daily from day 1 to day 4, oxalipatin 100 mg/m² intravenously on day 1) were administered, also without response. Persistent growth of the nasopharyngeal mass necessitated tracheostomy due to airway compromise.\n\nRepeat biopsy of the nasopharyngeal lesion revealed a complete absence of B-cell lymphoid infiltration and the presence of AL-type amyloid deposits, specifically kappa light chain–associated amyloidosis, suggesting a clonal plasma cell disorder. Immunoelectrophoresis of plasma proteins demonstrated elevated immunoglobulin M (IgM) with kappa light chain specificity, although light chain free light chain quantification was not performed due to institutional resource limitations. Myelogram and a second bone marrow biopsy remained normal, excluding overt multiple myeloma or plasma cell dyscrasia.\n\nPositron emission tomography (PET) imaging confirmed a hypermetabolic nasopharyngeal lesion with no evidence of systemic metastatic disease. Cardiac evaluation (electrocardiogram, n-terminal pro-B-type natriuretic peptide, troponin, echocardiography) and renal function were unremarkable. The patient is currently receiving a triplet therapy protocol comprising bortezomib, prednisone, and bendamustine, which has demonstrated favorable clinical response following the initial cycle. The clinical course indicates a possible transformation from follicular lymphoma to a concomitant or secondary amyloidosis, potentially driven by clonal B-cell dysregulation and IgM production, with the nasopharyngeal mass serving as a site of extramedullary amyloid deposition. This case highlights the clinical challenge of distinguishing between primary lymphoma and amyloid-related pathology in the setting of a large, non-lymphomatous-appearing extramedullary mass with immunological features of B-cell dyscrasia."}
{"row_index": 48, "doc_id": 46, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 46-year-old man from Haiti who now lives in Chile had warty bumps on his right leg for one year. The bumps started small and got bigger, then began to hurt, bleed, and ooze yellow fluid. Doctors saw the bumps and found a type of fungus called chromoblastomycosis. This fungus shows up in skin samples as thick-walled, brown cells (muriform cells) and grows into black, fuzzy spots in the lab. Under a microscope, the fungus looked like tiny branches with small dots, matching a type called Fonsecaea. He was treated with a medicine (itraconazole) taken twice a day for six months, and had cold treatments (cryotherapy) every 6 to 8 weeks on the thick parts of the bumps. After six months, the bumps went away completely. No signs of the disease came back, and only a little dark spot remains, which is normal after cold treatment.\"\n}", "generated_text": "A 46-year-old man from Haiti who now lives in Chile had warty bumps on his right leg for one year. The bumps started small and got bigger, then began to hurt, bleed, and ooze yellow fluid. Doctors saw the bumps and found a type of fungus called chromoblastomycosis. This fungus shows up in skin samples as thick-walled, brown cells (muriform cells) and grows into black, fuzzy spots in the lab. Under a microscope, the fungus looked like tiny branches with small dots, matching a type called Fonsecaea. He was treated with a medicine (itraconazole) taken twice a day for six months, and had cold treatments (cryotherapy) every 6 to 8 weeks on the thick parts of the bumps. After six months, the bumps went away completely. No signs of the disease came back, and only a little dark spot remains, which is normal after cold treatment."}
{"row_index": 49, "doc_id": 46, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 46-year-old Haitian man who had been living in Chile for one year presented with warty, skin-like plaques on the front of his right leg that had been growing for about a year. He originally had no symptoms, but three months before coming in for care, the area started to itch, hurt, and developed a small ulcer with yellow discharge. On exam, the plaques were about 1 cm to 3 cm in size and had a rough, warty appearance. Dermatoscopy showed thickened skin with dark spots and red blood vessels. Blood tests were normal, and tests for infections like syphilis, HIV, and tuberculosis were negative. A skin biopsy was done and showed thickened skin with inflammation and special cells called muriform cells, which are a key sign of chromoblastomycosis. Fungal culture grew black, velvet-like colonies, and under the microscope, the fungus had long, branching structures and small spores typical of Fonsecaea species. The diagnosis was confirmed as chromoblastomycosis. The patient was treated for six months with itraconazole (an antifungal medicine) and regular cryotherapy (freezing the affected areas with liquid nitrogen) every six to eight weeks. He also used mupirocin ointment to prevent bacterial infections when the skin broke. After six months, the lesions completely went away, and there has been no return of the disease. The only remaining issue is mild skin lightening in the treated areas, which is expected after cryotherapy.\"\n}", "generated_text": "A 46-year-old Haitian man who had been living in Chile for one year presented with warty, skin-like plaques on the front of his right leg that had been growing for about a year. He originally had no symptoms, but three months before coming in for care, the area started to itch, hurt, and developed a small ulcer with yellow discharge. On exam, the plaques were about 1 cm to 3 cm in size and had a rough, warty appearance. Dermatoscopy showed thickened skin with dark spots and red blood vessels. Blood tests were normal, and tests for infections like syphilis, HIV, and tuberculosis were negative. A skin biopsy was done and showed thickened skin with inflammation and special cells called muriform cells, which are a key sign of chromoblastomycosis. Fungal culture grew black, velvet-like colonies, and under the microscope, the fungus had long, branching structures and small spores typical of Fonsecaea species. The diagnosis was confirmed as chromoblastomycosis. The patient was treated for six months with itraconazole (an antifungal medicine) and regular cryotherapy (freezing the affected areas with liquid nitrogen) every six to eight weeks. He also used mupirocin ointment to prevent bacterial infections when the skin broke. After six months, the lesions completely went away, and there has been no return of the disease. The only remaining issue is mild skin lightening in the treated areas, which is expected after cryotherapy."}
{"row_index": 50, "doc_id": 46, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 46-year-old Haitian male, residing in Chile for one year, presented with a one-and-a-half-year history of progressive cutaneous lesions originating as a papule on the anterior right tibial region. Initially asymptomatic, the lesion evolved over time to include pruritus, pain, superficial ulceration, and yellowish exudate. Physical examination revealed three well-demarcated warty plaques measuring 1×1 cm, 2×2 cm, and 3×2 cm on the anterior right leg. Dermatoscopic evaluation demonstrated a hyperkeratotic mass with a central ulcerated area, characterized by reddish-black dots and congested hemorrhagic vessels, consistent with chronic inflammatory and proliferative dermal changes. The patient's general laboratory workup, including VDRL, HIV serology, and PPD, was non-reactive, ruling out syphilis, HIV infection, and latent tuberculosis. Tissue sampling via punch biopsy encompassed epidermis, dermis, and subcutaneous tissue, and was subjected to Gram staining, routine bacterial culture, and anaerobic culture—all of which were negative. Bacilloscopy and Koch complex culture of the same specimen also yielded negative results, excluding mycobacterial and bacillary etiologies. Histopathological analysis using hematoxylin and eosin staining revealed pseudoepitheliomatous hyperplasia of the epidermis, with a dense mixed inflammatory infiltrate containing suppurative foci and foreign body giant cells. Within these giant cells, round, muriform cells with thick, brown-walled walls were observed, morphologically consistent with fungal elements; this finding was further confirmed by periodic acid-Schiff (PAS) staining, which highlighted the fungal wall structure. Mycological culture on Sabouraud dextrose agar at 25°C demonstrated after 15 days of incubation the growth of dematiaceous (black-pigmented), elevated, well-defined, velvety colonies, characteristic of darkly pigmented fungi. Direct microscopic examination using 20% potassium hydroxide (KOH) revealed long, branched, occasionally tortuous hyphae and short chains of acropetal conidia, which are pathognomonic for Fonsecaea spp., a known etiological agent of chromoblastomycosis. The patient was initiated on systemic itraconazole at a dose of 100 mg every 12 hours for a duration of six months, in conjunction with regular cryotherapy using liquid nitrogen applied every six to eight weeks to hypertrophic and ulcerated areas. Topical mupirocin ointment was applied frequently to manage bacterial superinfections resulting from local lesion erosion and ulceration. The clinical course was favorable, with complete regression of all visible lesions and no evidence of relapse at the time of follow-up. Persistent mild local hypopigmentation was noted in treated areas, which is a known sequelae of cryotherapy-induced tissue damage and is expected in the context of repeated cold therapy. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in histopathology, dematiaceous fungal colonies in culture, and conidia morphologically compatible with Fonsecaea spp. in direct microscopy, establishing a definitive fungal etiology with a well-documented clinical and pathological profile.\"\n}", "generated_text": "A 46-year-old Haitian male, residing in Chile for one year, presented with a one-and-a-half-year history of progressive cutaneous lesions originating as a papule on the anterior right tibial region. Initially asymptomatic, the lesion evolved over time to include pruritus, pain, superficial ulceration, and yellowish exudate. Physical examination revealed three well-demarcated warty plaques measuring 1×1 cm, 2×2 cm, and 3×2 cm on the anterior right leg. Dermatoscopic evaluation demonstrated a hyperkeratotic mass with a central ulcerated area, characterized by reddish-black dots and congested hemorrhagic vessels, consistent with chronic inflammatory and proliferative dermal changes. The patient's general laboratory workup, including VDRL, HIV serology, and PPD, was non-reactive, ruling out syphilis, HIV infection, and latent tuberculosis. Tissue sampling via punch biopsy encompassed epidermis, dermis, and subcutaneous tissue, and was subjected to Gram staining, routine bacterial culture, and anaerobic culture—all of which were negative. Bacilloscopy and Koch complex culture of the same specimen also yielded negative results, excluding mycobacterial and bacillary etiologies. Histopathological analysis using hematoxylin and eosin staining revealed pseudoepitheliomatous hyperplasia of the epidermis, with a dense mixed inflammatory infiltrate containing suppurative foci and foreign body giant cells. Within these giant cells, round, muriform cells with thick, brown-walled walls were observed, morphologically consistent with fungal elements; this finding was further confirmed by periodic acid-Schiff (PAS) staining, which highlighted the fungal wall structure. Mycological culture on Sabouraud dextrose agar at 25°C demonstrated after 15 days of incubation the growth of dematiaceous (black-pigmented), elevated, well-defined, velvety colonies, characteristic of darkly pigmented fungi. Direct microscopic examination using 20% potassium hydroxide (KOH) revealed long, branched, occasionally tortuous hyphae and short chains of acropetal conidia, which are pathognomonic for Fonsecaea spp., a known etiological agent of chromoblastomycosis. The patient was initiated on systemic itraconazole at a dose of 100 mg every 12 hours for a duration of six months, in conjunction with regular cryotherapy using liquid nitrogen applied every six to eight weeks to hypertrophic and ulcerated areas. Topical mupirocin ointment was applied frequently to manage bacterial superinfections resulting from local lesion erosion and ulceration. The clinical course was favorable, with complete regression of all visible lesions and no evidence of relapse at the time of follow-up. Persistent mild local hypopigmentation was noted in treated areas, which is a known sequelae of cryotherapy-induced tissue damage and is expected in the context of repeated cold therapy. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in histopathology, dematiaceous fungal colonies in culture, and conidia morphologically compatible with Fonsecaea spp. in direct microscopy, establishing a definitive fungal etiology with a well-documented clinical and pathological profile."}
{"row_index": 51, "doc_id": 47, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 19-year-old man had a painful lump in his scrotum for 8 months that didn’t go away with antibiotics. He also had fever, night sweats, loss of appetite, and lost weight. No one in his family had tuberculosis, but he had the TB vaccine. The lump was surgically removed and tested — it showed signs of tuberculosis in the tube-like part of the testicle. X-rays showed TB in his lungs, lymph nodes, and bones. He started TB medicine, but after 4 months, he had seizures. A brain scan found small TB-related lumps in his brain. He started medicine to stop the seizures and kept taking TB medicine. His symptoms got better — he gained weight, the body lumps went away, and he didn’t have more seizures. The brain lumps slowly got smaller, so he kept taking TB medicine for a long time. After 19 years of treatment, he was fully healed with no long-term problems.\"\n}", "generated_text": "A 19-year-old man had a painful lump in his scrotum for 8 months that didn’t go away with antibiotics. He also had fever, night sweats, loss of appetite, and lost weight. No one in his family had tuberculosis, but he had the TB vaccine. The lump was surgically removed and tested — it showed signs of tuberculosis in the tube-like part of the testicle. X-rays showed TB in his lungs, lymph nodes, and bones. He started TB medicine, but after 4 months, he had seizures. A brain scan found small TB-related lumps in his brain. He started medicine to stop the seizures and kept taking TB medicine. His symptoms got better — he gained weight, the body lumps went away, and he didn’t have more seizures. The brain lumps slowly got smaller, so he kept taking TB medicine for a long time. After 19 years of treatment, he was fully healed with no long-term problems."}
{"row_index": 52, "doc_id": 47, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 19-year-old man with no prior medical problems was admitted to the hospital with a painful lump in his left scrotum that had been growing for 8 months. The lump didn't go away with antibiotics, and he also had symptoms like low-grade fever, night sweats, loss of appetite, and unexplained weight loss. He had no history of tuberculosis in his family or personal history, and he was vaccinated at birth. Exam findings showed a large, tender lump in the scrotum and some firm lumps on his chest. His blood tests showed high inflammation markers, and a chest X-ray showed signs of lung infection. After surgery to remove the scrotal lump, the tissue tested positive for tuberculosis in the epididymis, which is a part of the testicle. Tests also found tuberculosis in his lungs, around the abdomen and chest walls, and in his spine and bones. He started standard tuberculosis treatment with several medications. After four months, he had seizures, and a brain scan showed small areas of tuberculosis in the brain, called tuberculomas. He was then given anti-seizure medication along with continuing tuberculosis treatment. His condition improved over time—he regained his weight, the lung and body infections went away, and the seizures stopped. Although the brain tuberculomas slowly shrank, he needed to stay on tuberculosis treatment for a long time, totaling 234 months (about 19 years), before being declared cured with no long-term effects.\"\n}", "generated_text": "A 19-year-old man with no prior medical problems was admitted to the hospital with a painful lump in his left scrotum that had been growing for 8 months. The lump didn't go away with antibiotics, and he also had symptoms like low-grade fever, night sweats, loss of appetite, and unexplained weight loss. He had no history of tuberculosis in his family or personal history, and he was vaccinated at birth. Exam findings showed a large, tender lump in the scrotum and some firm lumps on his chest. His blood tests showed high inflammation markers, and a chest X-ray showed signs of lung infection. After surgery to remove the scrotal lump, the tissue tested positive for tuberculosis in the epididymis, which is a part of the testicle. Tests also found tuberculosis in his lungs, around the abdomen and chest walls, and in his spine and bones. He started standard tuberculosis treatment with several medications. After four months, he had seizures, and a brain scan showed small areas of tuberculosis in the brain, called tuberculomas. He was then given anti-seizure medication along with continuing tuberculosis treatment. His condition improved over time—he regained his weight, the lung and body infections went away, and the seizures stopped. Although the brain tuberculomas slowly shrank, he needed to stay on tuberculosis treatment for a long time, totaling 234 months (about 19 years), before being declared cured with no long-term effects."}
{"row_index": 53, "doc_id": 47, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-year-old male with no significant medical history presented with a painful left scrotal mass that had persisted for 8 months without improvement following empirical antibiotic therapy for pyogenic infections. He reported intermittent low-grade fever, night sweats, anorexia, and unexplained weight loss since symptom onset, with no history of cough, sputum production, or hemoptysis. There was no personal or familial history of tuberculosis, and he had received standard bacillus Calmette-Guérin (BCG) vaccination at birth. Physical examination revealed a large, tender, slightly warm left scrotal bursa and two elongated, firm, poorly defined subcutaneous masses in the anterior thoracic wall measuring 3–4 cm in length, without audible rales on lung auscultation. The remainder of the systemic examination was unremarkable. Laboratory findings demonstrated a markedly elevated c-reactive protein (CRP) of 90 mg/dL, while complete blood count, serum creatinine, blood glucose, and liver function tests remained within normal limits. Standard chest radiography revealed bilateral reticulonodular infiltrates consistent with pulmonary involvement.\\n\\nUltrasound imaging suggested an epididymal mass, prompting a left orchidectomy. Histopathological analysis of the resected specimen revealed granulomatous epithelioid cell necrosis involving the body and tail of the epididymis, with sparing of the head and testicular tissue, strongly suggestive of active epididymal tuberculosis. The intradermal tuberculin skin test (TST) was positive, supporting the diagnosis. Direct microscopy and culture for acid-fast bacilli (AFB) in sputum and urine over three consecutive days were negative, and serological testing for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Wright's stain (to rule out other hematological disorders) were all negative, excluding alternative infectious or hematologic etiologies.\\n\\nTo evaluate for extrapulmonary dissemination, a thoraco-abdomino-pelvic tomodensitometry was performed, which demonstrated miliary tuberculosis, coelo-mesenteric necrotic lymphadenopathy, two parietal collections (right: 33 × 10 mm; left: 45 × 10 mm) arising from the external oblique muscles, and focal osteolytic lesions at D11 and L5, consistent with early spondylodiscitis. Magnetic resonance imaging (MRI) of the spinal cord confirmed spondylodiscitis at the D7, D11, L4, and L5 levels. This constellation of findings led to a definitive diagnosis of disseminated tuberculosis involving the epididymal, pulmonary, parietal, lymphatic, and osteo-articular compartments.\\n\\nTreatment was initiated with a 2-month intensive phase of quadruple antitubercular chemotherapy consisting of isoniazid, rifampicin, ethambutol, and pyrazinamide, followed by a continuation phase of isoniazid and rifampicin. At the fourth month of therapy, the patient developed generalized tonic-clonic convulsive seizures. Brain MRI revealed multiple nodular lesions located above and below the tentorial membrane, consistent with tuberculomas—focal granulomatous brain lesions caused by Mycobacterium tuberculosis. The patient was promptly started on adjunctive anticonvulsant therapy while continuing anti-tubercular treatment. Clinical and radiological follow-up demonstrated a favorable evolution, including resolution of systemic symptoms, weight gain, and gradual disappearance of thoracic parietal collections, lymphadenopathy, and miliary infiltrates on imaging. However, the tuberculomas showed a slow, progressive reduction in size, necessitating prolonged continuation of antituberculous therapy. The patient was ultimately declared cured at the end of the 234th month of treatment, with a 2-year post-treatment follow-up confirming no recurrence of disease or neurological sequelae. This case illustrates the potential for disseminated tuberculosis to present with extrapulmonary manifestations, including epididymal involvement and central nervous system tuberculomas, and underscores the importance of early diagnosis, comprehensive imaging, and long-term management in young adults with atypical presentations.\"\n}", "generated_text": "A 19-year-old male with no significant medical history presented with a painful left scrotal mass that had persisted for 8 months without improvement following empirical antibiotic therapy for pyogenic infections. He reported intermittent low-grade fever, night sweats, anorexia, and unexplained weight loss since symptom onset, with no history of cough, sputum production, or hemoptysis. There was no personal or familial history of tuberculosis, and he had received standard bacillus Calmette-Guérin (BCG) vaccination at birth. Physical examination revealed a large, tender, slightly warm left scrotal bursa and two elongated, firm, poorly defined subcutaneous masses in the anterior thoracic wall measuring 3–4 cm in length, without audible rales on lung auscultation. The remainder of the systemic examination was unremarkable. Laboratory findings demonstrated a markedly elevated c-reactive protein (CRP) of 90 mg/dL, while complete blood count, serum creatinine, blood glucose, and liver function tests remained within normal limits. Standard chest radiography revealed bilateral reticulonodular infiltrates consistent with pulmonary involvement.\n\nUltrasound imaging suggested an epididymal mass, prompting a left orchidectomy. Histopathological analysis of the resected specimen revealed granulomatous epithelioid cell necrosis involving the body and tail of the epididymis, with sparing of the head and testicular tissue, strongly suggestive of active epididymal tuberculosis. The intradermal tuberculin skin test (TST) was positive, supporting the diagnosis. Direct microscopy and culture for acid-fast bacilli (AFB) in sputum and urine over three consecutive days were negative, and serological testing for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Wright's stain (to rule out other hematological disorders) were all negative, excluding alternative infectious or hematologic etiologies.\n\nTo evaluate for extrapulmonary dissemination, a thoraco-abdomino-pelvic tomodensitometry was performed, which demonstrated miliary tuberculosis, coelo-mesenteric necrotic lymphadenopathy, two parietal collections (right: 33 × 10 mm; left: 45 × 10 mm) arising from the external oblique muscles, and focal osteolytic lesions at D11 and L5, consistent with early spondylodiscitis. Magnetic resonance imaging (MRI) of the spinal cord confirmed spondylodiscitis at the D7, D11, L4, and L5 levels. This constellation of findings led to a definitive diagnosis of disseminated tuberculosis involving the epididymal, pulmonary, parietal, lymphatic, and osteo-articular compartments.\n\nTreatment was initiated with a 2-month intensive phase of quadruple antitubercular chemotherapy consisting of isoniazid, rifampicin, ethambutol, and pyrazinamide, followed by a continuation phase of isoniazid and rifampicin. At the fourth month of therapy, the patient developed generalized tonic-clonic convulsive seizures. Brain MRI revealed multiple nodular lesions located above and below the tentorial membrane, consistent with tuberculomas—focal granulomatous brain lesions caused by Mycobacterium tuberculosis. The patient was promptly started on adjunctive anticonvulsant therapy while continuing anti-tubercular treatment. Clinical and radiological follow-up demonstrated a favorable evolution, including resolution of systemic symptoms, weight gain, and gradual disappearance of thoracic parietal collections, lymphadenopathy, and miliary infiltrates on imaging. However, the tuberculomas showed a slow, progressive reduction in size, necessitating prolonged continuation of antituberculous therapy. The patient was ultimately declared cured at the end of the 234th month of treatment, with a 2-year post-treatment follow-up confirming no recurrence of disease or neurological sequelae. This case illustrates the potential for disseminated tuberculosis to present with extrapulmonary manifestations, including epididymal involvement and central nervous system tuberculomas, and underscores the importance of early diagnosis, comprehensive imaging, and long-term management in young adults with atypical presentations."}
{"row_index": 54, "doc_id": 48, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 10-year-old boy was getting chemotherapy for a serious type of cancer called leukemia. During the early treatment, he got a brain infection caused by a bacteria named B. cereus. Doctors found it using brain scans and a fluid from around the brain. He had a bad headache that didn’t go away, so they checked his brain and found a spot that looked like an infection. Even though he didn’t have a fever, he started to feel very sick and needed help in the hospital. Doctors gave him strong antibiotics, and the infection went away. After a few weeks, his headache stopped and his brain scans showed the infection was getting smaller. He fully recovered and is back to normal.\"\n}", "generated_text": "A 10-year-old boy was getting chemotherapy for a serious type of cancer called leukemia. During the early treatment, he got a brain infection caused by a bacteria named B. cereus. Doctors found it using brain scans and a fluid from around the brain. He had a bad headache that didn’t go away, so they checked his brain and found a spot that looked like an infection. Even though he didn’t have a fever, he started to feel very sick and needed help in the hospital. Doctors gave him strong antibiotics, and the infection went away. After a few weeks, his headache stopped and his brain scans showed the infection was getting smaller. He fully recovered and is back to normal."}
{"row_index": 55, "doc_id": 48, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 10-year-old boy was treated for acute lymphoblastic leukaemia, a type of blood cancer, using a standard chemotherapy protocol. During the early stages of treatment, he developed a serious brain infection called a cerebral abscess caused by a bacteria named B. cereus. This was found through brain imaging and by testing the fluid around the brain (cerebrospinal fluid). Although the infection was severe, it responded well to antibiotics. The boy’s symptoms improved, and he made a full recovery with no lasting brain problems. Follow-up scans showed the infection had shrunk, and he was able to continue his treatment safely.\"\n}", "generated_text": "A 10-year-old boy was treated for acute lymphoblastic leukaemia, a type of blood cancer, using a standard chemotherapy protocol. During the early stages of treatment, he developed a serious brain infection called a cerebral abscess caused by a bacteria named B. cereus. This was found through brain imaging and by testing the fluid around the brain (cerebrospinal fluid). Although the infection was severe, it responded well to antibiotics. The boy’s symptoms improved, and he made a full recovery with no lasting brain problems. Follow-up scans showed the infection had shrunk, and he was able to continue his treatment safely."}
{"row_index": 56, "doc_id": 48, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a case of a 10-year-old male with high-risk early T-cell acute lymphoblastic leukaemia (ALL), managed according to the LAL SEHOP-PETHEMA 2013 protocol. Two years post-diagnosis, he experienced an early central nervous system (CNS) relapse, prompting intervention under the InteReALL HR 2010 protocol, which included bortezomib. During induction therapy, the patient became neutropenic for four weeks (neutrophil count: 20/μL), receiving prophylactic antimicrobials consisting of cefepime, cotrimoxazole, and fluconazole. Concurrently, he was treated with acyclovir for a documented herpes simplex virus 1 (HSV-1) skin infection. On presentation, he developed a severe, treatment-refractory headache, prompting a cranial computed tomography (CT) scan that revealed a hypodense lesion in the right temporal lobe. Given the infectious etiology hypothesis, a lumbar puncture was performed, and empirical therapy was updated to meropenem and vancomycin.\\n\\nDespite the absence of fever, the patient rapidly progressed to septic shock on day one of hospitalization, requiring transfer to the paediatric intensive care unit (PICU) for inotropic and vasoactive support. Antimicrobial coverage was broadened to include gentamicin and caspofungin. Laboratory findings demonstrated a progressive rise in inflammatory markers: C-reactive protein (CRP) reached 312 mg/L and procalcitonin (PCT) peaked at 47.58 ng/mL by day three, consistent with a severe bacterial infection, while no other significant biochemical abnormalities were detected. Complete blood count revealed pancytopenia, attributable to chemotherapy-induced bone marrow suppression. Blood cultures were negative for both bacteremia and fungemia; herpesvirus serologies (HSV-1, HSV-2, HHV-6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus) and urine/fecal cultures were also negative, excluding common pathogens.\\n\\nCerebrospinal fluid (CSF) analysis showed normal glucose (63 mg/dL), protein (16 mg/dL), and leukocyte count (1/μL), indicating a non-inflammatory, non-lymphocytic CSF profile. However, microbiological culture identified *Bacillus cereus* as the causative organism, which was sensitive to meropenem, vancomycin, linezolid, and ciprofloxacin. All other potential CNS pathogens—including *Neisseria meningitidis*, *Listeria monocytogenes*, *Streptococcus pneumoniae*, *Cryptococcus*, and *Toxoplasma gondii*—were ruled out in CSF. Electroencephalography (EEG) revealed diffuse cerebral slowing without epileptiform discharges, suggesting non-epileptic encephalopathy consistent with metabolic or infectious insult.\\n\\nOn day 4, following stabilization of hemodynamics, cranial magnetic resonance imaging (MRI) demonstrated two hyperintense lesions on T2 and FLAIR sequences involving the subcortical regions of the right temporal and parietal lobes. The parietal lesion exhibited ring enhancement after gadolinium administration, and both lesions displayed peripheral diffusion restriction on apparent diffusion coefficient (ADC) mapping, indicative of restricted water diffusion typical of abscess formation. Additionally, scattered small hemorrhagic foci were observed within the brain parenchyma. These imaging findings, in conjunction with the CSF culture result and clinical course, supported a diagnosis of *Bacillus cereus* cerebral abscess, an atypical and rare cause of CNS infection in the immunocompromised setting.\\n\\nThe patient responded favorably to antibiotic therapy, with resolution of headache and absence of new neurological deficits. Follow-up MRI at two weeks showed significant reduction in lesion size. Vancomycin and acyclovir were discontinued after three weeks, and meropenem was continued for a total of six weeks. This case highlights the diagnostic challenge of atypical bacterial CNS infections in children undergoing intensive chemotherapy, particularly in the context of prolonged neutropenia and prophylactic regimens, and underscores the importance of early imaging, CSF analysis, and broad-spectrum empirical therapy in such high-risk populations.\"\n}", "generated_text": "We present a case of a 10-year-old male with high-risk early T-cell acute lymphoblastic leukaemia (ALL), managed according to the LAL SEHOP-PETHEMA 2013 protocol. Two years post-diagnosis, he experienced an early central nervous system (CNS) relapse, prompting intervention under the InteReALL HR 2010 protocol, which included bortezomib. During induction therapy, the patient became neutropenic for four weeks (neutrophil count: 20/μL), receiving prophylactic antimicrobials consisting of cefepime, cotrimoxazole, and fluconazole. Concurrently, he was treated with acyclovir for a documented herpes simplex virus 1 (HSV-1) skin infection. On presentation, he developed a severe, treatment-refractory headache, prompting a cranial computed tomography (CT) scan that revealed a hypodense lesion in the right temporal lobe. Given the infectious etiology hypothesis, a lumbar puncture was performed, and empirical therapy was updated to meropenem and vancomycin.\n\nDespite the absence of fever, the patient rapidly progressed to septic shock on day one of hospitalization, requiring transfer to the paediatric intensive care unit (PICU) for inotropic and vasoactive support. Antimicrobial coverage was broadened to include gentamicin and caspofungin. Laboratory findings demonstrated a progressive rise in inflammatory markers: C-reactive protein (CRP) reached 312 mg/L and procalcitonin (PCT) peaked at 47.58 ng/mL by day three, consistent with a severe bacterial infection, while no other significant biochemical abnormalities were detected. Complete blood count revealed pancytopenia, attributable to chemotherapy-induced bone marrow suppression. Blood cultures were negative for both bacteremia and fungemia; herpesvirus serologies (HSV-1, HSV-2, HHV-6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus) and urine/fecal cultures were also negative, excluding common pathogens.\n\nCerebrospinal fluid (CSF) analysis showed normal glucose (63 mg/dL), protein (16 mg/dL), and leukocyte count (1/μL), indicating a non-inflammatory, non-lymphocytic CSF profile. However, microbiological culture identified *Bacillus cereus* as the causative organism, which was sensitive to meropenem, vancomycin, linezolid, and ciprofloxacin. All other potential CNS pathogens—including *Neisseria meningitidis*, *Listeria monocytogenes*, *Streptococcus pneumoniae*, *Cryptococcus*, and *Toxoplasma gondii*—were ruled out in CSF. Electroencephalography (EEG) revealed diffuse cerebral slowing without epileptiform discharges, suggesting non-epileptic encephalopathy consistent with metabolic or infectious insult.\n\nOn day 4, following stabilization of hemodynamics, cranial magnetic resonance imaging (MRI) demonstrated two hyperintense lesions on T2 and FLAIR sequences involving the subcortical regions of the right temporal and parietal lobes. The parietal lesion exhibited ring enhancement after gadolinium administration, and both lesions displayed peripheral diffusion restriction on apparent diffusion coefficient (ADC) mapping, indicative of restricted water diffusion typical of abscess formation. Additionally, scattered small hemorrhagic foci were observed within the brain parenchyma. These imaging findings, in conjunction with the CSF culture result and clinical course, supported a diagnosis of *Bacillus cereus* cerebral abscess, an atypical and rare cause of CNS infection in the immunocompromised setting.\n\nThe patient responded favorably to antibiotic therapy, with resolution of headache and absence of new neurological deficits. Follow-up MRI at two weeks showed significant reduction in lesion size. Vancomycin and acyclovir were discontinued after three weeks, and meropenem was continued for a total of six weeks. This case highlights the diagnostic challenge of atypical bacterial CNS infections in children undergoing intensive chemotherapy, particularly in the context of prolonged neutropenia and prophylactic regimens, and underscores the importance of early imaging, CSF analysis, and broad-spectrum empirical therapy in such high-risk populations."}
{"row_index": 57, "doc_id": 49, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 16-year-old girl has a flat, gray spot on her left thigh that's been there since birth. The spot is about 10.5 cm wide and 8.0 cm long, and it's got small blood vessels running around the edge. Over time, the spot turned lighter and became flatter. A scan showed that the spot has extra blood vessels in the skin and layer below it, which is normal for this type of growth. There's no sign that it's affecting her legs differently or spreading into muscles or bones.\"\n}", "generated_text": "A 16-year-old girl has a flat, gray spot on her left thigh that's been there since birth. The spot is about 10.5 cm wide and 8.0 cm long, and it's got small blood vessels running around the edge. Over time, the spot turned lighter and became flatter. A scan showed that the spot has extra blood vessels in the skin and layer below it, which is normal for this type of growth. There's no sign that it's affecting her legs differently or spreading into muscles or bones."}
{"row_index": 58, "doc_id": 49, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"16-year-old female presenting with a congenital, depressed gray plaque measuring 10.5 × 8.0 cm located in the lower lateral aspect of the left thigh, characterized by interspersed hypochromic regions and peripheral telangiectatic vessels, including visible superficial veins adjacent to the lesion. The lesion was present at birth and initially exhibited a violaceous hue, evolving over time to become lighter in color and more depressed in elevation. No asymmetry in lower limb length was observed, ruling out significant skeletal or musculoskeletal involvement. Angioresonance imaging revealed a complex vascular malformation involving the dermal and subcutaneous layers, primarily supplied by intermuscular branches of the popliteal artery. Notably, early venous filling was demonstrated both within the lesion and in the surrounding tissue, indicating early venous shunting and possible venous override. No significant dilation of deep draining veins was identified, although a superficial draining vein was observed coursing along the subcutaneous cellular tissue of the anterior thigh. Histopathological and imaging findings confirm thinning of the subcutaneous tissue within the affected region, consistent with chronic vascular remodeling, without evidence of intramuscular or bony extension. The clinical and imaging profile supports a diagnosis of a venous or venous-lymphatic malformation with early venous dominance, likely arising from aberrant vascular development during embryogenesis, involving the popliteal artery-derived vascular plexus.\"\n}", "generated_text": "16-year-old female presenting with a congenital, depressed gray plaque measuring 10.5 × 8.0 cm located in the lower lateral aspect of the left thigh, characterized by interspersed hypochromic regions and peripheral telangiectatic vessels, including visible superficial veins adjacent to the lesion. The lesion was present at birth and initially exhibited a violaceous hue, evolving over time to become lighter in color and more depressed in elevation. No asymmetry in lower limb length was observed, ruling out significant skeletal or musculoskeletal involvement. Angioresonance imaging revealed a complex vascular malformation involving the dermal and subcutaneous layers, primarily supplied by intermuscular branches of the popliteal artery. Notably, early venous filling was demonstrated both within the lesion and in the surrounding tissue, indicating early venous shunting and possible venous override. No significant dilation of deep draining veins was identified, although a superficial draining vein was observed coursing along the subcutaneous cellular tissue of the anterior thigh. Histopathological and imaging findings confirm thinning of the subcutaneous tissue within the affected region, consistent with chronic vascular remodeling, without evidence of intramuscular or bony extension. The clinical and imaging profile supports a diagnosis of a venous or venous-lymphatic malformation with early venous dominance, likely arising from aberrant vascular development during embryogenesis, involving the popliteal artery-derived vascular plexus."}
{"row_index": 59, "doc_id": 50, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 57-year-old woman with a long history of asthma and allergic rhinitis came in with recurring abdominal pain that had been going on for two months. The pain was dull and intermittent, along with nausea, loss of appetite, fatigue, and a 5-kilogram weight loss. She had no fever, no blood or mucus in her stool, and no respiratory symptoms. Tests showed very high levels of a type of white blood cell called eosinophils, and her IgG4 levels were also elevated. After checking for infections, blood disorders, and other conditions that could cause high eosinophils, doctors found no clear cause. A biopsy of her colon tissue showed a large number of eosinophils in the lining of the colon, which confirmed a diagnosis of eosinophilic colitis (EoC). She was treated with corticosteroids and montelukast, and her symptoms improved within two weeks. Her eosinophil levels returned to normal, and after stopping the steroids, she continued on montelukast for three months without any symptoms coming back.\"\n}", "generated_text": "A 57-year-old woman with a long history of asthma and allergic rhinitis came in with recurring abdominal pain that had been going on for two months. The pain was dull and intermittent, along with nausea, loss of appetite, fatigue, and a 5-kilogram weight loss. She had no fever, no blood or mucus in her stool, and no respiratory symptoms. Tests showed very high levels of a type of white blood cell called eosinophils, and her IgG4 levels were also elevated. After checking for infections, blood disorders, and other conditions that could cause high eosinophils, doctors found no clear cause. A biopsy of her colon tissue showed a large number of eosinophils in the lining of the colon, which confirmed a diagnosis of eosinophilic colitis (EoC). She was treated with corticosteroids and montelukast, and her symptoms improved within two weeks. Her eosinophil levels returned to normal, and after stopping the steroids, she continued on montelukast for three months without any symptoms coming back."}
{"row_index": 60, "doc_id": 50, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, managed on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain initiated two months prior. The pain was intermittent, dull, and associated with nausea, anorexia, malaise, and a 5 kg weight loss. Notably, there were no fever, blood or mucus in stool, respiratory symptoms (rhinorrhea, wheezing, cough), or history of alcohol, tobacco, or herbal medicine use. Six weeks before admission, she was diagnosed with an intestinal infection based on a complete blood count (CBC) showing leukocytosis and marked eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotic therapy and mebendazole, which failed to alleviate symptoms. On presentation, vital signs were stable: blood pressure 110/70 mmHg, temperature 37°C, heart rate 88 bpm, respiratory rate 18 bpm. Body mass index was 16.6 kg/m², consistent with severe underweight, and sarcopenia was present, with no skin rash, lymphadenopathy, or edema. Abdominal examination revealed tenderness in the epigastric and umbilical regions without rebound or guarding. Repeat CBC demonstrated persistent leukocytosis and significant eosinophilia (20.8 G/L total WBC, 77.8% eosinophils), with peripheral blood film showing normal eosinophil morphology. Bone marrow aspiration revealed 48% eosinophils without blasts or atypical cells, suggesting a clonal or reactive process but excluding hematologic malignancy. Fluorescence in situ hybridization (FISH) for CHIC2 deletion, a surrogate marker for FIP1L1-PDGFRA fusion in eosinophilic disorders, was negative, ruling out primary myeloid eosinophilia. Autoimmune and vasculitis screening (ANA, anti-dsDNA, p-ANCA, c-ANCA) remained negative, excluding systemic autoimmune conditions. Serum immunoglobulins showed elevated IgG (2760 mg/dL; normal 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal 3.9–86.4 mg/dL), with a mild elevation in IgE (137.5 IU/mL; normal <100 IU/mL) and elevated rheumatoid factor (RF 144.4 IU/mL; normal <20 IU/mL), though these findings were not sufficient to support an autoimmune etiology. All other laboratory parameters—including aminotransferases, blood urea nitrogen, serum creatinine, complement C3/C4, vitamin B12, serum cortisol, and NT-proBNP—were within normal limits. Electrocardiogram and echocardiogram were unremarkable. Chest CT revealed mild pulmonary fibrosis and bronchiectasis, consistent with chronic airway inflammation. Sputum acid-fast bacilli (AFB) smear and bronchoscopy were negative; bronchoalveolar lavage (BAL) cytology showed 35% neutrophils and no eosinophils, indicating that airway eosinophilia was not the primary driver of systemic eosinophilia. Spirometry demonstrated severe obstructive lung disease with a significant bronchodilator response, and fractional exhaled nitric oxide (FeNO) was 15 ppb, supporting a Th2-mediated inflammatory phenotype. Stool analysis revealed leukocyte presence, but no ova, parasites, or evidence of infectious etiology. Serology testing confirmed positive IgG to Toxocara canis (54.2 NovaTec-Units), suggestive of toxocariasis, but remained negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. Abdominal contrast-enhanced CT showed gallbladder stones without acute cholecystitis and no structural abnormalities in the gastrointestinal tract. Upper endoscopy was unremarkable, while colonoscopy revealed mucosal inflammation in the sigmoid, left, transverse, and right colon, prompting systematic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies demonstrated significant eosinophilic infiltration, with counts exceeding 85 eosinophils/HPF in", "generated_text": "{\n  \"proficient_health_literacy\": \"A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, managed on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain initiated two months prior. The pain was intermittent, dull, and associated with nausea, anorexia, malaise, and a 5 kg weight loss. Notably, there were no fever, blood or mucus in stool, respiratory symptoms (rhinorrhea, wheezing, cough), or history of alcohol, tobacco, or herbal medicine use. Six weeks before admission, she was diagnosed with an intestinal infection based on a complete blood count (CBC) showing leukocytosis and marked eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotic therapy and mebendazole, which failed to alleviate symptoms. On presentation, vital signs were stable: blood pressure 110/70 mmHg, temperature 37°C, heart rate 88 bpm, respiratory rate 18 bpm. Body mass index was 16.6 kg/m², consistent with severe underweight, and sarcopenia was present, with no skin rash, lymphadenopathy, or edema. Abdominal examination revealed tenderness in the epigastric and umbilical regions without rebound or guarding. Repeat CBC demonstrated persistent leukocytosis and significant eosinophilia (20.8 G/L total WBC, 77.8% eosinophils), with peripheral blood film showing normal eosinophil morphology. Bone marrow aspiration revealed 48% eosinophils without blasts or atypical cells, suggesting a clonal or reactive process but excluding hematologic malignancy. Fluorescence in situ hybridization (FISH) for CHIC2 deletion, a surrogate marker for FIP1L1-PDGFRA fusion in eosinophilic disorders, was negative, ruling out primary myeloid eosinophilia. Autoimmune and vasculitis screening (ANA, anti-dsDNA, p-ANCA, c-ANCA) remained negative, excluding systemic autoimmune conditions. Serum immunoglobulins showed elevated IgG (2760 mg/dL; normal 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal 3.9–86.4 mg/dL), with a mild elevation in IgE (137.5 IU/mL; normal <100 IU/mL) and elevated rheumatoid factor (RF 144.4 IU/mL; normal <20 IU/mL), though these findings were not sufficient to support an autoimmune etiology. All other laboratory parameters—including aminotransferases, blood urea nitrogen, serum creatinine, complement C3/C4, vitamin B12, serum cortisol, and NT-proBNP—were within normal limits. Electrocardiogram and echocardiogram were unremarkable. Chest CT revealed mild pulmonary fibrosis and bronchiectasis, consistent with chronic airway inflammation. Sputum acid-fast bacilli (AFB) smear and bronchoscopy were negative; bronchoalveolar lavage (BAL) cytology showed 35% neutrophils and no eosinophils, indicating that airway eosinophilia was not the primary driver of systemic eosinophilia. Spirometry demonstrated severe obstructive lung disease with a significant bronchodilator response, and fractional exhaled nitric oxide (FeNO) was 15 ppb, supporting a Th2-mediated inflammatory phenotype. Stool analysis revealed leukocyte presence, but no ova, parasites, or evidence of infectious etiology. Serology testing confirmed positive IgG to Toxocara canis (54.2 NovaTec-Units), suggestive of toxocariasis, but remained negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. Abdominal contrast-enhanced CT showed gallbladder stones without acute cholecystitis and no structural abnormalities in the gastrointestinal tract. Upper endoscopy was unremarkable, while colonoscopy revealed mucosal inflammation in the sigmoid, left, transverse, and right colon, prompting systematic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies demonstrated significant eosinophilic infiltration, with counts exceeding 85 eosinophils/HPF in"}
{"row_index": 61, "doc_id": 51, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 35-year-old man had a heart problem that got worse over time. At first, he had chest pain and trouble breathing, especially after activity. Doctors found a lump in his heart called a cardiac myxoma, and also saw that his heart was getting bigger and weaker — this is called dilated cardiomyopathy. He had signs of Carney syndrome, a rare condition that affects the heart and skin, like dark spots on his ears and small cysts in his kidney. Doctors tested his genes and confirmed the diagnosis. At first, he was treated with medicine but didn’t have surgery. Later, his symptoms got much worse — he could barely breathe, even when lying down, and his heart was failing badly. His heart function was rated as very poor (NYHA Grade IV). Doctors said he needed a heart transplant. On October 1, 2024, he got a new heart from a donor. The surgery was done by cutting open his chest, removing the damaged heart parts, and putting in the new one. The new heart was connected properly with no leaks. After the surgery, he started recovering fast. By day one, he was urinating well and his heart function improved. His blood tests showed his heart was working better. He took medicine to stop his body from rejecting the new heart and to fight infections. After a week, his recovery was good, and by October 20, 2023, his heart was working normally. All tests were normal, and he’s now doing well and living a healthy life.\"\n}", "generated_text": "A 35-year-old man had a heart problem that got worse over time. At first, he had chest pain and trouble breathing, especially after activity. Doctors found a lump in his heart called a cardiac myxoma, and also saw that his heart was getting bigger and weaker — this is called dilated cardiomyopathy. He had signs of Carney syndrome, a rare condition that affects the heart and skin, like dark spots on his ears and small cysts in his kidney. Doctors tested his genes and confirmed the diagnosis. At first, he was treated with medicine but didn’t have surgery. Later, his symptoms got much worse — he could barely breathe, even when lying down, and his heart was failing badly. His heart function was rated as very poor (NYHA Grade IV). Doctors said he needed a heart transplant. On October 1, 2024, he got a new heart from a donor. The surgery was done by cutting open his chest, removing the damaged heart parts, and putting in the new one. The new heart was connected properly with no leaks. After the surgery, he started recovering fast. By day one, he was urinating well and his heart function improved. His blood tests showed his heart was working better. He took medicine to stop his body from rejecting the new heart and to fight infections. After a week, his recovery was good, and by October 20, 2023, his heart was working normally. All tests were normal, and he’s now doing well and living a healthy life."}
{"row_index": 62, "doc_id": 51, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 35-year-old man was diagnosed with heart failure caused by a rare condition called Carney syndrome. This condition leads to the growth of a non-cancerous tumor (called a cardiac myxoma) in the heart and weakens the heart muscle, leading to a condition known as dilated cardiomyopathy. Three years ago, he first had chest tightness and shortness of breath after physical activity. An ultrasound of his heart showed a tumor, and further tests confirmed Carney syndrome. He was treated with medications, but did not have surgery at the time. Over time, his symptoms worsened, and he could no longer lie down without breathing difficulty. His heart function was severely weakened (NYHA Class IV), and new tests showed both the tumor and a weakened heart. Because the heart was no longer able to pump effectively, doctors decided on a heart transplant. On October 1, 2024, he received a new heart from a donor. The surgery involved opening the chest, removing the damaged heart tissue, and connecting the new heart to the major blood vessels. The procedure was successful, and the new heart began working properly. After surgery, he received medicines to prevent his body from rejecting the new heart and to fight infection. His recovery was good, and by October 20, 2024, his heart function was normal, with no signs of problems. He is now doing well and has been followed up regularly since discharge.\"\n}", "generated_text": "A 35-year-old man was diagnosed with heart failure caused by a rare condition called Carney syndrome. This condition leads to the growth of a non-cancerous tumor (called a cardiac myxoma) in the heart and weakens the heart muscle, leading to a condition known as dilated cardiomyopathy. Three years ago, he first had chest tightness and shortness of breath after physical activity. An ultrasound of his heart showed a tumor, and further tests confirmed Carney syndrome. He was treated with medications, but did not have surgery at the time. Over time, his symptoms worsened, and he could no longer lie down without breathing difficulty. His heart function was severely weakened (NYHA Class IV), and new tests showed both the tumor and a weakened heart. Because the heart was no longer able to pump effectively, doctors decided on a heart transplant. On October 1, 2024, he received a new heart from a donor. The surgery involved opening the chest, removing the damaged heart tissue, and connecting the new heart to the major blood vessels. The procedure was successful, and the new heart began working properly. After surgery, he received medicines to prevent his body from rejecting the new heart and to fight infection. His recovery was good, and by October 20, 2024, his heart function was normal, with no signs of problems. He is now doing well and has been followed up regularly since discharge."}
{"row_index": 63, "doc_id": 51, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 38-year-old male presented with recurrent episodes of chest tightness and dyspnea, initially occurring post-exertion three years prior. Outpatient echocardiography revealed a left atrial echogenic mass suggestive of a cardiac myxoma, prompting hospital admission for comprehensive evaluation. Physical examination identified characteristic cutaneous pigmentation in the ears, manifesting as multiple small brown and black macules, consistent with cutaneous manifestations of Carney Complex (CNC). Abdominal computed tomography (CT) demonstrated multiple hepatic lesions and small cystic formations in the left kidney, further supporting the diagnosis. Genetic analysis revealed biallelic pathogenic mutations in both the TTN (titin) and PRKAR1A genes, confirming the diagnosis of Carney syndrome (CNC) through integration of clinical, imaging, and molecular findings. The patient underwent symptomatic management with no surgical intervention, which was voluntarily declined despite the presence of a cardiac myxoma. On September 20, 2023, he presented with worsening dyspnea, including orthopnea and paroxysmal nocturnal dyspnea, necessitating rehospitalization. Physical examination revealed jugular venous distension, leftward and inferior cardiac border displacement, irregular cardiac rhythm (auscultated as atrial fibrillation), a mitral valve murmur of intensity 2/6–3/6 at the fourth intercostal space along the left sternal border, and bilateral wet rales in the middle and lower lung zones. Palpation demonstrated hepatomegaly extending three fingers below the xiphoid process and two fingers below the costal margin, with bilateral lower limb pitting edema. Echocardiography confirmed global left ventricular (LV) dilation, with a left ventricular ejection fraction (LVEF) of 23.1% and fractional shortening (FS) of 10.9%, indicative of severe systolic dysfunction. Additional findings included moderate mitral regurgitation, dilation of the aortic sinus and pulmonary artery, and a well-defined, irregular echogenic mass measuring 54 mm × 43 mm attached to the atrial septum. Electrocardiography revealed atrial fibrillation with an average ventricular rate of 150 beats per minute and abnormal Q waves in leads V1–V3, suggesting prior myocardial injury or infarction. The clinical picture was consistent with both Carney syndrome and dilated cardiomyopathy (DCM), with concomitant cardiac myxoma. Given the progression to end-stage heart failure and the presence of a large, non-resectable myxoma, heart transplantation was deemed the optimal therapeutic strategy to address both the structural and functional cardiac deterioration. A suitable donor heart was available for immediate transplantation on October 1, 2024. The surgical procedure involved a median sternotomy with layer-by-layer dissection of the skin and subcutaneous tissues. The sternum was longitudinally opened using a saw, and bleeding was controlled with electrocoagulation and bone wax. Extracardiac exploration revealed global cardiac enlargement, with marked left ventricular dilation and diminished contractile function. The aorta and main pulmonary artery (PA) were dissected from the supravalvular region. Diseased atrial and ventricular tissues—including the right atrium, left atrium (LA), right ventricle, and left ventricle—were excised, with preservation of portions for anastomotic reconstruction. The excised mass was described as greyish-white and mucoid in consistency, consistent with a myxoma. The donor and residual recipient left atria were sutured using double continuous 3/0 Prolene sutures, with meticulous inspection for bleeding. End-to-end anastomosis of the donor ascending aorta to the recipient pulmonary artery was performed with continuous 5/0 Prolene sutures, and no significant hemorrhage was observed. The donor and recipient left atria were closed with double continuous 5/0 Prolene sutures, and the inferior vena cava of both hearts was similarly sutured with 5/0 Prolene, with multiple inspections confirming hemostasis. Following deflation of the left heart, rewarming was initiated, oxygenation was restored, the ascending aorta was unclamped, and spontaneous return to sinus rhythm was achieved. Continuous 5/0 Prolene sutures were applied to the superior vena cava of both donor and recipient, with careful inspection for bleeding. After successful discontinuation of extracorporeal circulation, venous cannulae were decannulated. Tissue specimens from the patient’s left ventricle and cardiac gray matter were collected for histopathological analysis, confirming the presence of both dilated cardiomyopathy and cardiac myxoma. Postoperatively, the patient exhibited a robust early recovery: on postoperative", "generated_text": "{\n  \"proficient_health_literacy\": \"A 38-year-old male presented with recurrent episodes of chest tightness and dyspnea, initially occurring post-exertion three years prior. Outpatient echocardiography revealed a left atrial echogenic mass suggestive of a cardiac myxoma, prompting hospital admission for comprehensive evaluation. Physical examination identified characteristic cutaneous pigmentation in the ears, manifesting as multiple small brown and black macules, consistent with cutaneous manifestations of Carney Complex (CNC). Abdominal computed tomography (CT) demonstrated multiple hepatic lesions and small cystic formations in the left kidney, further supporting the diagnosis. Genetic analysis revealed biallelic pathogenic mutations in both the TTN (titin) and PRKAR1A genes, confirming the diagnosis of Carney syndrome (CNC) through integration of clinical, imaging, and molecular findings. The patient underwent symptomatic management with no surgical intervention, which was voluntarily declined despite the presence of a cardiac myxoma. On September 20, 2023, he presented with worsening dyspnea, including orthopnea and paroxysmal nocturnal dyspnea, necessitating rehospitalization. Physical examination revealed jugular venous distension, leftward and inferior cardiac border displacement, irregular cardiac rhythm (auscultated as atrial fibrillation), a mitral valve murmur of intensity 2/6–3/6 at the fourth intercostal space along the left sternal border, and bilateral wet rales in the middle and lower lung zones. Palpation demonstrated hepatomegaly extending three fingers below the xiphoid process and two fingers below the costal margin, with bilateral lower limb pitting edema. Echocardiography confirmed global left ventricular (LV) dilation, with a left ventricular ejection fraction (LVEF) of 23.1% and fractional shortening (FS) of 10.9%, indicative of severe systolic dysfunction. Additional findings included moderate mitral regurgitation, dilation of the aortic sinus and pulmonary artery, and a well-defined, irregular echogenic mass measuring 54 mm × 43 mm attached to the atrial septum. Electrocardiography revealed atrial fibrillation with an average ventricular rate of 150 beats per minute and abnormal Q waves in leads V1–V3, suggesting prior myocardial injury or infarction. The clinical picture was consistent with both Carney syndrome and dilated cardiomyopathy (DCM), with concomitant cardiac myxoma. Given the progression to end-stage heart failure and the presence of a large, non-resectable myxoma, heart transplantation was deemed the optimal therapeutic strategy to address both the structural and functional cardiac deterioration. A suitable donor heart was available for immediate transplantation on October 1, 2024. The surgical procedure involved a median sternotomy with layer-by-layer dissection of the skin and subcutaneous tissues. The sternum was longitudinally opened using a saw, and bleeding was controlled with electrocoagulation and bone wax. Extracardiac exploration revealed global cardiac enlargement, with marked left ventricular dilation and diminished contractile function. The aorta and main pulmonary artery (PA) were dissected from the supravalvular region. Diseased atrial and ventricular tissues—including the right atrium, left atrium (LA), right ventricle, and left ventricle—were excised, with preservation of portions for anastomotic reconstruction. The excised mass was described as greyish-white and mucoid in consistency, consistent with a myxoma. The donor and residual recipient left atria were sutured using double continuous 3/0 Prolene sutures, with meticulous inspection for bleeding. End-to-end anastomosis of the donor ascending aorta to the recipient pulmonary artery was performed with continuous 5/0 Prolene sutures, and no significant hemorrhage was observed. The donor and recipient left atria were closed with double continuous 5/0 Prolene sutures, and the inferior vena cava of both hearts was similarly sutured with 5/0 Prolene, with multiple inspections confirming hemostasis. Following deflation of the left heart, rewarming was initiated, oxygenation was restored, the ascending aorta was unclamped, and spontaneous return to sinus rhythm was achieved. Continuous 5/0 Prolene sutures were applied to the superior vena cava of both donor and recipient, with careful inspection for bleeding. After successful discontinuation of extracorporeal circulation, venous cannulae were decannulated. Tissue specimens from the patient’s left ventricle and cardiac gray matter were collected for histopathological analysis, confirming the presence of both dilated cardiomyopathy and cardiac myxoma. Postoperatively, the patient exhibited a robust early recovery: on postoperative"}
{"row_index": 64, "doc_id": 52, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 2.5-year-old girl with a known condition called NF1 has been having diarrhea with blood in it for several weeks. The doctor looked inside her colon with a special tool and saw red, swollen lining from the bottom of the rectum all the way to the start of the colon. A small tissue sample showed long-term inflammation, and tests found a virus called CMV that was causing the problem. This combination of red lining and virus infection means she has a type of chronic colitis, similar to ulcerative colitis. She is being treated with medicine to reduce inflammation and is still having some symptoms, but they are getting better.\"\n}", "generated_text": "A 2.5-year-old girl with a known condition called NF1 has been having diarrhea with blood in it for several weeks. The doctor looked inside her colon with a special tool and saw red, swollen lining from the bottom of the rectum all the way to the start of the colon. A small tissue sample showed long-term inflammation, and tests found a virus called CMV that was causing the problem. This combination of red lining and virus infection means she has a type of chronic colitis, similar to ulcerative colitis. She is being treated with medicine to reduce inflammation and is still having some symptoms, but they are getting better."}
{"row_index": 65, "doc_id": 52, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 2-year-6-month-old female pre-schooler with a prior diagnosis of neurofibromatosis type 1 (NF1), confirmed by genetic testing at 8 months of age via detection of a heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28), presented with a 4-week history of bloody diarrhea, with 5 to 10 episodes of blood-streaked stools per day. Initial evaluation in the emergency department revealed rotavirus infection (positive), with normal inflammatory markers, negative coproculture, and normal abdominal ultrasound. The patient was hospitalized for 3 days to manage dehydration and discharged without active bleeding, though persistent semi-liquid stools remained. Ten days post-discharge, she developed recurrent bloody diarrhea associated with reduced oral intake and a 1 kg weight loss, prompting referral to a pediatric gastroenterologist. A polymerase chain reaction (PCR) panel for gastrointestinal pathogens and PCR for Clostridium difficile were both negative, leading to hospitalization for further investigation.\\n\\nThe clinical history was non-specific for systemic infection: no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions were reported. No pet exposure, recent travel, or dietary changes were noted. The patient has documented skin manifestations (café au lait spots) and bone involvement (requiring ankle arthrodesis at 18 months due to tibial curvature), with no family history of NF1 or inflammatory bowel disease (IBD).\\n\\nPhysical examination revealed a soft, non-distended abdomen with increased air-bubble murmurs, no masses or visceral enlargement. Perianal examination was normal. Multiple brown-coffee-colored stains were observed on the lower extremities and back, consistent with café au lait spots. Laboratory findings included moderate microcytic-hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and mildly elevated inflammatory markers (CRP 1.37 mg/dL, above the normal threshold of ≤0.5 mg/dL).\\n\\nColonoscopy was performed from the anal margin to the cecum, including inspection of the ileocecal valve and appendicular orifice, with the distal ileum also evaluated. The mucosa from the anal margin to the cecum demonstrated erythema and loss of vascular transparency, a feature not observed in the cecal mucosa, which appeared normal. No focal lesions were identified in the anal canal or cecum.\\n\\nHistopathological analysis of biopsies revealed preserved villous architecture and adequate epithelial differentiation in the ileal mucosa with a non-inflamed lamina propria. In the colonic mucosa, there was mild architectural distortion, preserved epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate, and hyperplasia of reactive lymphoid follicles. Isolated microabscesses were identified, consistent with a diagnosis of mild chronic colitis. A PCR assay for cytomegalovirus (CMV) on colonic biopsy was positive. Additional serological testing confirmed positive CMV IgG, negative IgM, and a blood viral load of 79.7 IU/mL, supporting active, recent CMV viremia. Stool PCR for gastrointestinal pathogens and C. difficile were negative. Gram stain of the biopsy showed +++ leukocytes without bacterial presence; culture yielded low-level growth of S. gallolyticus/equinus complex, interpreted as normal commensal flora; acridine orange, Ziehl-Neelsen, Koch culture, and adenovirus PCR were all negative.\\n\\nEndoscopic and histological findings were consistent with ulcerative colitis (UC), with moderate clinical activity (PUCAI score of 50). The patient was initiated on mesalazine (70 mg/kg/day, three times daily), and fecal calprotectin was measured, yielding a value >600 µg/g, confirming active intestinal inflammation. An immunological workup was conducted to evaluate for potential immunodeficiency: lymphocyte subpopulations, immunoglobulin levels, HIV status, memory T-cell populations (showing expected alterations in the context of CMV viremia), and lymphoproliferation test were all within normal limits. A comprehensive genetic panel for primary immunodeficiencies (Invitae, comprising 429 genes, including 68 associated with monogenic inflammatory intestinal disease) was performed, yielding seven variants of uncertain significance, none of which were classified within the monogenic IBD panel.\\n\\nThe patient was treated with intravenous ganciclovir for CMV infection, administered for 15 days, with subsequent PCR monitoring showing undetectable viral load prior to discharge. Clinical", "generated_text": "{\n  \"proficient_health_literacy\": \"A 2-year-6-month-old female pre-schooler with a prior diagnosis of neurofibromatosis type 1 (NF1), confirmed by genetic testing at 8 months of age via detection of a heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28), presented with a 4-week history of bloody diarrhea, with 5 to 10 episodes of blood-streaked stools per day. Initial evaluation in the emergency department revealed rotavirus infection (positive), with normal inflammatory markers, negative coproculture, and normal abdominal ultrasound. The patient was hospitalized for 3 days to manage dehydration and discharged without active bleeding, though persistent semi-liquid stools remained. Ten days post-discharge, she developed recurrent bloody diarrhea associated with reduced oral intake and a 1 kg weight loss, prompting referral to a pediatric gastroenterologist. A polymerase chain reaction (PCR) panel for gastrointestinal pathogens and PCR for Clostridium difficile were both negative, leading to hospitalization for further investigation.\\n\\nThe clinical history was non-specific for systemic infection: no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions were reported. No pet exposure, recent travel, or dietary changes were noted. The patient has documented skin manifestations (café au lait spots) and bone involvement (requiring ankle arthrodesis at 18 months due to tibial curvature), with no family history of NF1 or inflammatory bowel disease (IBD).\\n\\nPhysical examination revealed a soft, non-distended abdomen with increased air-bubble murmurs, no masses or visceral enlargement. Perianal examination was normal. Multiple brown-coffee-colored stains were observed on the lower extremities and back, consistent with café au lait spots. Laboratory findings included moderate microcytic-hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and mildly elevated inflammatory markers (CRP 1.37 mg/dL, above the normal threshold of ≤0.5 mg/dL).\\n\\nColonoscopy was performed from the anal margin to the cecum, including inspection of the ileocecal valve and appendicular orifice, with the distal ileum also evaluated. The mucosa from the anal margin to the cecum demonstrated erythema and loss of vascular transparency, a feature not observed in the cecal mucosa, which appeared normal. No focal lesions were identified in the anal canal or cecum.\\n\\nHistopathological analysis of biopsies revealed preserved villous architecture and adequate epithelial differentiation in the ileal mucosa with a non-inflamed lamina propria. In the colonic mucosa, there was mild architectural distortion, preserved epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate, and hyperplasia of reactive lymphoid follicles. Isolated microabscesses were identified, consistent with a diagnosis of mild chronic colitis. A PCR assay for cytomegalovirus (CMV) on colonic biopsy was positive. Additional serological testing confirmed positive CMV IgG, negative IgM, and a blood viral load of 79.7 IU/mL, supporting active, recent CMV viremia. Stool PCR for gastrointestinal pathogens and C. difficile were negative. Gram stain of the biopsy showed +++ leukocytes without bacterial presence; culture yielded low-level growth of S. gallolyticus/equinus complex, interpreted as normal commensal flora; acridine orange, Ziehl-Neelsen, Koch culture, and adenovirus PCR were all negative.\\n\\nEndoscopic and histological findings were consistent with ulcerative colitis (UC), with moderate clinical activity (PUCAI score of 50). The patient was initiated on mesalazine (70 mg/kg/day, three times daily), and fecal calprotectin was measured, yielding a value >600 µg/g, confirming active intestinal inflammation. An immunological workup was conducted to evaluate for potential immunodeficiency: lymphocyte subpopulations, immunoglobulin levels, HIV status, memory T-cell populations (showing expected alterations in the context of CMV viremia), and lymphoproliferation test were all within normal limits. A comprehensive genetic panel for primary immunodeficiencies (Invitae, comprising 429 genes, including 68 associated with monogenic inflammatory intestinal disease) was performed, yielding seven variants of uncertain significance, none of which were classified within the monogenic IBD panel.\\n\\nThe patient was treated with intravenous ganciclovir for CMV infection, administered for 15 days, with subsequent PCR monitoring showing undetectable viral load prior to discharge. Clinical"}
{"row_index": 66, "doc_id": 53, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 40-year-old HIV-positive male with sustained antiretroviral therapy adherence—documented viral load of 4500 copies/mm³ and CD4 count of 70/mm³ from the prior year—presented with a two-year history of intermittent febrile episodes that lacked a consistent temporal pattern and responded only transiently to non-steroidal anti-inflammatory drugs (NSAIDs). Over the preceding two months, he developed progressive diffuse abdominal pain, with a predominant localization in the upper right quadrant, accompanied by the emergence of a tree-in-bud pulmonary opacification pattern on imaging and bilateral pleural effusions. Abdominal imaging revealed marked hepatosplenomegaly and ascites. Laboratory evaluation demonstrated pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute-phase reactants, indicative of systemic inflammation. Computed tomography (CT) of the thorax, abdomen, and pelvis confirmed generalized lymphadenopathy, hepatosplenomegaly, and the pulmonary tree-in-bud pattern. Multiple microbiological investigations were conducted, including culture-based detection of Mycobacterium species from various specimens, all of which were negative, except for a positive result via RT-PCR for Human Herpesvirus 8 (HHV-8). A left iliac ganglion biopsy was performed, yielding histopathological findings consistent with multicentric Castleman’s disease, a lymphoproliferative disorder characterized by abnormal proliferation of lymphoid tissue and cytokine overproduction, particularly interleukin-6. Despite re-initiation of antiretroviral therapy, clinical deterioration progressed, necessitating the administration of corticosteroids and ganciclovir to address potential HHV-8-driven immune activation. However, within one week, the patient developed multi-organ failure and anasarca, rendering further pharmacologic intervention contraindicated. A repeat chest CT demonstrated worsening pulmonary infiltrates with persistent tree-in-bud morphology and progressive hepato-splenomegaly and ascites. He was transferred to the intensive care unit (ICU) 48 hours after symptom onset, where he rapidly deteriorated and succumbed to fulminant hepatic failure within hours. Postmortem analysis of a tracheal aspirate culture yielded a positive identification of Mycobacterium tuberculosis, confirming latent or active pulmonary tuberculosis as a contributing pathogen. Additionally, a percutaneous liver biopsy revealed non-necrotizing granulomas, consistent with a tuberculous etiology, while the parenchymal architecture remained largely preserved, suggesting a chronic, non-destructive inflammatory process. This case highlights the clinical complexity of HIV-associated lymphoproliferative disorders, particularly Castleman’s disease, in the context of overlapping opportunistic infections and immune dysregulation, and underscores the importance of timely microbiological diagnostics and immune reconstitution in such patients. The study was conducted in accordance with the ethical principles outlined in the World Health Organization’s Declaration of Helsinki.\"\n}", "generated_text": "A 40-year-old HIV-positive male with sustained antiretroviral therapy adherence—documented viral load of 4500 copies/mm³ and CD4 count of 70/mm³ from the prior year—presented with a two-year history of intermittent febrile episodes that lacked a consistent temporal pattern and responded only transiently to non-steroidal anti-inflammatory drugs (NSAIDs). Over the preceding two months, he developed progressive diffuse abdominal pain, with a predominant localization in the upper right quadrant, accompanied by the emergence of a tree-in-bud pulmonary opacification pattern on imaging and bilateral pleural effusions. Abdominal imaging revealed marked hepatosplenomegaly and ascites. Laboratory evaluation demonstrated pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute-phase reactants, indicative of systemic inflammation. Computed tomography (CT) of the thorax, abdomen, and pelvis confirmed generalized lymphadenopathy, hepatosplenomegaly, and the pulmonary tree-in-bud pattern. Multiple microbiological investigations were conducted, including culture-based detection of Mycobacterium species from various specimens, all of which were negative, except for a positive result via RT-PCR for Human Herpesvirus 8 (HHV-8). A left iliac ganglion biopsy was performed, yielding histopathological findings consistent with multicentric Castleman’s disease, a lymphoproliferative disorder characterized by abnormal proliferation of lymphoid tissue and cytokine overproduction, particularly interleukin-6. Despite re-initiation of antiretroviral therapy, clinical deterioration progressed, necessitating the administration of corticosteroids and ganciclovir to address potential HHV-8-driven immune activation. However, within one week, the patient developed multi-organ failure and anasarca, rendering further pharmacologic intervention contraindicated. A repeat chest CT demonstrated worsening pulmonary infiltrates with persistent tree-in-bud morphology and progressive hepato-splenomegaly and ascites. He was transferred to the intensive care unit (ICU) 48 hours after symptom onset, where he rapidly deteriorated and succumbed to fulminant hepatic failure within hours. Postmortem analysis of a tracheal aspirate culture yielded a positive identification of Mycobacterium tuberculosis, confirming latent or active pulmonary tuberculosis as a contributing pathogen. Additionally, a percutaneous liver biopsy revealed non-necrotizing granulomas, consistent with a tuberculous etiology, while the parenchymal architecture remained largely preserved, suggesting a chronic, non-destructive inflammatory process. This case highlights the clinical complexity of HIV-associated lymphoproliferative disorders, particularly Castleman’s disease, in the context of overlapping opportunistic infections and immune dysregulation, and underscores the importance of timely microbiological diagnostics and immune reconstitution in such patients. The study was conducted in accordance with the ethical principles outlined in the World Health Organization’s Declaration of Helsinki."}
{"row_index": 67, "doc_id": 54, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 4-month-old indigenous lactating infant from the rural interior of Panama, specifically from Urracá, approximately 3 hours by canoe from the nearest health subcenter, presented with acute diarrhea and moderate-severe dehydration due to protein-caloric malnutrition. The infant was the fourth daughter, born via vaginal home delivery by a relative without prenatal care; birth weight, height, and Apgar score are unknown. The infant did not receive breast milk and was exclusively fed powdered milk formula with iron (3 ounces every 4 hours), which is inconsistent with recommended infant feeding guidelines for infants under 6 months of age. The household consisted of six members (parents and four children), living in a two-room structure with board walls and palm roof, lacking electricity and relying on kerosene lamps for illumination, well water for hydration, open defecation in a river, and open burning of waste. Household economic activity was based on subsistence agriculture, and the infant received no vaccinations as part of the national expanded programme of immunization. Parents reported normal neurodevelopment prior to hospitalization.\\n\\nThe infant presented to a primary health center with a 4-day history of diarrhea without mucus or blood, accompanied by vomiting of food content; the mother substituted milk with tea due to intolerance. The infant was afebrile and without respiratory symptoms. Initial management included oral rehydration with lactate Ringer's solution (10 ml/kg) and four doses of Enterogermina® (2 billion spores/5 mL), a probiotic containing *Bacillus clausii*. Due to lack of intravenous access (no catheters or intraosseous access), the infant was transferred to a second-level hospital in the provincial capital and subsequently to a tertiary care facility in Panama City, diagnosed with acute gastroenteritis and severe dehydration.\\n\\nOn emergency department admission, the infant exhibited signs of consciousness compromise, profound dehydration (tearless cry, dry oral mucosa), and signs of shock: capillary refill time >2 seconds, cold extremities, filiform pulse, marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. Physical examination revealed +++ edema in hands, feet, abdomen, and face. Anthropometric data: weight 4.7 kg, height 56 cm; height/age Z-score of -2.52, with unquantifiable weight/height and weight/age Z-scores due to severe dehydration. Segmental examination revealed fine crepitus in both lung bases suggestive of pulmonary interstitial involvement, and erythematous-squamous skin lesions with desquamation, as well as hypopigmented patches on trunk and upper limbs, interpreted as pellagroid dermatosis, likely secondary to vitamin B3 deficiency.\\n\\nInitial resuscitation included lactate Ringer's bolus (10 ml/kg), followed by 5% dextrose in 0.33% saline (500 mL) infused at 29 mL/h over 6 hours without KCL until diuresis was achieved. Empirical antibiotic therapy was initiated with ceftriaxone 50 mg/kg/day for suspected sepsis. After stabilization, the patient was transferred to the ward and maintained on 500 mL of 5% dextrose in 0.9% saline at 20 mL/h. Laboratory findings included leukocytosis (39.0 × 10³/μL), severe anemia (5.6 g/dL), and thrombocytosis (502 × 10³/μL). The patient received a transfusion of 50 mL of filtered, leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to coagulopathy. Enteral feeding was initiated via nasogastric tube, and fluid infusion was reduced to 15 mL/h of 5% dextrose in 0.9% saline (500 mL), with a negative water balance maintained.\\n\\nOn day 2, initial peripheral blood culture yielded Gram-positive cocci in clusters, interpreted as *Staphylococcus aureus*. Oxacillin was administered at 200 mg/kg/day, and ceftriaxone was escalated to 75–100 mg/kg/day. Total fluid replacement was increased to 120 mL/kg/day, and calcium was corrected (to 6.38 mg/dL). On day 3, venous access was lost, necessitating placement of a central venous catheter (CVC). The patient remained hypovolemic with subhydrated oral mucosa, increased respiratory effort, cold extremities, and capillary refill time of 3–4 seconds. A rapid Ringer's lactate infusion (", "generated_text": "{\n  \"proficient_health_literacy\": \"A 4-month-old indigenous lactating infant from the rural interior of Panama, specifically from Urracá, approximately 3 hours by canoe from the nearest health subcenter, presented with acute diarrhea and moderate-severe dehydration due to protein-caloric malnutrition. The infant was the fourth daughter, born via vaginal home delivery by a relative without prenatal care; birth weight, height, and Apgar score are unknown. The infant did not receive breast milk and was exclusively fed powdered milk formula with iron (3 ounces every 4 hours), which is inconsistent with recommended infant feeding guidelines for infants under 6 months of age. The household consisted of six members (parents and four children), living in a two-room structure with board walls and palm roof, lacking electricity and relying on kerosene lamps for illumination, well water for hydration, open defecation in a river, and open burning of waste. Household economic activity was based on subsistence agriculture, and the infant received no vaccinations as part of the national expanded programme of immunization. Parents reported normal neurodevelopment prior to hospitalization.\\n\\nThe infant presented to a primary health center with a 4-day history of diarrhea without mucus or blood, accompanied by vomiting of food content; the mother substituted milk with tea due to intolerance. The infant was afebrile and without respiratory symptoms. Initial management included oral rehydration with lactate Ringer's solution (10 ml/kg) and four doses of Enterogermina® (2 billion spores/5 mL), a probiotic containing *Bacillus clausii*. Due to lack of intravenous access (no catheters or intraosseous access), the infant was transferred to a second-level hospital in the provincial capital and subsequently to a tertiary care facility in Panama City, diagnosed with acute gastroenteritis and severe dehydration.\\n\\nOn emergency department admission, the infant exhibited signs of consciousness compromise, profound dehydration (tearless cry, dry oral mucosa), and signs of shock: capillary refill time >2 seconds, cold extremities, filiform pulse, marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. Physical examination revealed +++ edema in hands, feet, abdomen, and face. Anthropometric data: weight 4.7 kg, height 56 cm; height/age Z-score of -2.52, with unquantifiable weight/height and weight/age Z-scores due to severe dehydration. Segmental examination revealed fine crepitus in both lung bases suggestive of pulmonary interstitial involvement, and erythematous-squamous skin lesions with desquamation, as well as hypopigmented patches on trunk and upper limbs, interpreted as pellagroid dermatosis, likely secondary to vitamin B3 deficiency.\\n\\nInitial resuscitation included lactate Ringer's bolus (10 ml/kg), followed by 5% dextrose in 0.33% saline (500 mL) infused at 29 mL/h over 6 hours without KCL until diuresis was achieved. Empirical antibiotic therapy was initiated with ceftriaxone 50 mg/kg/day for suspected sepsis. After stabilization, the patient was transferred to the ward and maintained on 500 mL of 5% dextrose in 0.9% saline at 20 mL/h. Laboratory findings included leukocytosis (39.0 × 10³/μL), severe anemia (5.6 g/dL), and thrombocytosis (502 × 10³/μL). The patient received a transfusion of 50 mL of filtered, leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to coagulopathy. Enteral feeding was initiated via nasogastric tube, and fluid infusion was reduced to 15 mL/h of 5% dextrose in 0.9% saline (500 mL), with a negative water balance maintained.\\n\\nOn day 2, initial peripheral blood culture yielded Gram-positive cocci in clusters, interpreted as *Staphylococcus aureus*. Oxacillin was administered at 200 mg/kg/day, and ceftriaxone was escalated to 75–100 mg/kg/day. Total fluid replacement was increased to 120 mL/kg/day, and calcium was corrected (to 6.38 mg/dL). On day 3, venous access was lost, necessitating placement of a central venous catheter (CVC). The patient remained hypovolemic with subhydrated oral mucosa, increased respiratory effort, cold extremities, and capillary refill time of 3–4 seconds. A rapid Ringer's lactate infusion ("}
{"row_index": 68, "doc_id": 55, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 2-year-old girl had a big lump inside her eye socket that made her eye stick out and move inward and upward. The lump was soft, not painful, and grew slowly over a year. Doctors saw it on a scan and found it was a type of tumor called a teratoma. They removed it through a small cut in the lower eyelid, and during surgery, they saw parts of brain, skin, and cartilage inside the lump. After the surgery, the child’s eye started to sink back in (enophthalmos), her eyelid became red, and her cornea got inflamed because the space in her eye was too small. To fix this, doctors placed a piece of donor eye tissue (sclera) into the socket to fill the space and help the eye sit properly again. One year later, the tumor didn’t come back, and her eye looked better. She still has a little bit of eye sinking and a small eyelid issue, but her vision is the same as before. The eye is now stable and no other problems were seen.\"\n}", "generated_text": "A 2-year-old girl had a big lump inside her eye socket that made her eye stick out and move inward and upward. The lump was soft, not painful, and grew slowly over a year. Doctors saw it on a scan and found it was a type of tumor called a teratoma. They removed it through a small cut in the lower eyelid, and during surgery, they saw parts of brain, skin, and cartilage inside the lump. After the surgery, the child’s eye started to sink back in (enophthalmos), her eyelid became red, and her cornea got inflamed because the space in her eye was too small. To fix this, doctors placed a piece of donor eye tissue (sclera) into the socket to fill the space and help the eye sit properly again. One year later, the tumor didn’t come back, and her eye looked better. She still has a little bit of eye sinking and a small eyelid issue, but her vision is the same as before. The eye is now stable and no other problems were seen."}
{"row_index": 69, "doc_id": 55, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 2-year-old female presented with a 1-year history of painless, progressive left-sided proptosis, without systemic comorbidities or familial predisposition. Ophthalmologic evaluation revealed preserved light perception as the sole visual input in the left eye, accompanied by marked proptosis, inward and upward displacement of the globe, and restricted downward and outward extraocular muscle movements. A palpable, irregularly shaped, well-circumscribed soft mass was identified in the inferior left orbit, associated with left lower eyelid ectropion. The pupil measured 4 mm in diameter and exhibited absent pupillary reaction. Anterior segment examination was otherwise unremarkable, though fundus assessment was compromised due to the child’s small size. Hertel exophthalmometry demonstrated a right eye measurement of 10.5 mm and a left eye measurement of 18 mm, indicating significant orbital expansion. Magnetic resonance imaging (MRI) revealed a well-defined orbital mass with hypointense signal intensity on T1-weighted images (T1WI) and hyperintense signal intensity on T2-weighted images (T2WI), consistent with a cystic or mixed tissue composition. Contrast-enhanced MRI showed no significant enhancement, suggesting a non-vascularized or low-vascularity lesion. A transconjunctival approach via the inferior fornix was employed, with concomitant canthotomy and cantholysis to facilitate access. Surgical exploration revealed a grayish-white, cystic mass with a distinct interface from surrounding orbital tissues. Posterior dissection encountered tight adhesion between the mass and the optic nerve, indicating prior extensive orbital expansion and tissue deformation. Given the substantial size of the lesion and limited surgical field, volume reduction was necessary; approximately 12.5 mL of intralesional fluid was aspirated prior to complete excision. Histopathological analysis confirmed a fibrous capsule lined with squamous and glandular epithelium, with the presence of brain-derived tissue and a cartilaginous matrix, pathologically consistent with an orbital teratoma. One month postoperatively, the patient developed enophthalmos, conjunctival hyperemia, and keratitis. This sequelae was attributed to the preoperative orbital cavity enlargement, leading to postoperative orbital volume collapse and corneal exposure, resulting in inflammation due to inadequate eyelid coverage. With informed consent from the patient’s guardian, a second surgical intervention was performed involving the implantation of allogeneic sclera into the orbital cavity to restore orbital volume, correct fossal pitting, and re-establish corneal apposition. Follow-up over one year demonstrated no recurrence of teratoma or other complications. Persistent minor enophthalmos and outer canthus deformity remained, though visual acuity remained unchanged from preoperative levels. Repeat Hertel exophthalmometry showed a right eye measurement of 10.5 mm and a left eye measurement of 8 mm, indicating partial correction of proptosis. The anterior segment remained clinically stable, with no evidence of recurrent inflammation or structural compromise. The findings support the diagnosis of a complex orbital teratoma with significant orbital expansion, and highlight the importance of surgical volume management and postoperative orbital reconstruction in pediatric cases with large, adherent teratoma masses.\"\n}", "generated_text": "A 2-year-old female presented with a 1-year history of painless, progressive left-sided proptosis, without systemic comorbidities or familial predisposition. Ophthalmologic evaluation revealed preserved light perception as the sole visual input in the left eye, accompanied by marked proptosis, inward and upward displacement of the globe, and restricted downward and outward extraocular muscle movements. A palpable, irregularly shaped, well-circumscribed soft mass was identified in the inferior left orbit, associated with left lower eyelid ectropion. The pupil measured 4 mm in diameter and exhibited absent pupillary reaction. Anterior segment examination was otherwise unremarkable, though fundus assessment was compromised due to the child’s small size. Hertel exophthalmometry demonstrated a right eye measurement of 10.5 mm and a left eye measurement of 18 mm, indicating significant orbital expansion. Magnetic resonance imaging (MRI) revealed a well-defined orbital mass with hypointense signal intensity on T1-weighted images (T1WI) and hyperintense signal intensity on T2-weighted images (T2WI), consistent with a cystic or mixed tissue composition. Contrast-enhanced MRI showed no significant enhancement, suggesting a non-vascularized or low-vascularity lesion. A transconjunctival approach via the inferior fornix was employed, with concomitant canthotomy and cantholysis to facilitate access. Surgical exploration revealed a grayish-white, cystic mass with a distinct interface from surrounding orbital tissues. Posterior dissection encountered tight adhesion between the mass and the optic nerve, indicating prior extensive orbital expansion and tissue deformation. Given the substantial size of the lesion and limited surgical field, volume reduction was necessary; approximately 12.5 mL of intralesional fluid was aspirated prior to complete excision. Histopathological analysis confirmed a fibrous capsule lined with squamous and glandular epithelium, with the presence of brain-derived tissue and a cartilaginous matrix, pathologically consistent with an orbital teratoma. One month postoperatively, the patient developed enophthalmos, conjunctival hyperemia, and keratitis. This sequelae was attributed to the preoperative orbital cavity enlargement, leading to postoperative orbital volume collapse and corneal exposure, resulting in inflammation due to inadequate eyelid coverage. With informed consent from the patient’s guardian, a second surgical intervention was performed involving the implantation of allogeneic sclera into the orbital cavity to restore orbital volume, correct fossal pitting, and re-establish corneal apposition. Follow-up over one year demonstrated no recurrence of teratoma or other complications. Persistent minor enophthalmos and outer canthus deformity remained, though visual acuity remained unchanged from preoperative levels. Repeat Hertel exophthalmometry showed a right eye measurement of 10.5 mm and a left eye measurement of 8 mm, indicating partial correction of proptosis. The anterior segment remained clinically stable, with no evidence of recurrent inflammation or structural compromise. The findings support the diagnosis of a complex orbital teratoma with significant orbital expansion, and highlight the importance of surgical volume management and postoperative orbital reconstruction in pediatric cases with large, adherent teratoma masses."}
{"row_index": 70, "doc_id": 56, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 78-year-old woman was feeling very tired, weak, dizzy, and confused for months. This made it hard for her to leave her house or walk around. She was taking many medicines, and one of the problems might have been her blood pressure medicines. Her kidneys weren’t working as well as they should, which means her body can’t clear some medicines as easily. The doctors checked her kidney function and found it was low. Based on this, they decided to lower the dose of two blood pressure medicines — losartan and manidipine — so her blood pressure wouldn’t go too low. They also switched her pain medicine from pregabalin to gabapentin, which is safer for her kidneys. After two months, her tiredness, dizziness, and confusion went away. Her blood pressure improved, and she felt much better.\"\n}", "generated_text": "A 78-year-old woman was feeling very tired, weak, dizzy, and confused for months. This made it hard for her to leave her house or walk around. She was taking many medicines, and one of the problems might have been her blood pressure medicines. Her kidneys weren’t working as well as they should, which means her body can’t clear some medicines as easily. The doctors checked her kidney function and found it was low. Based on this, they decided to lower the dose of two blood pressure medicines — losartan and manidipine — so her blood pressure wouldn’t go too low. They also switched her pain medicine from pregabalin to gabapentin, which is safer for her kidneys. After two months, her tiredness, dizziness, and confusion went away. Her blood pressure improved, and she felt much better."}
{"row_index": 71, "doc_id": 56, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 78-year-old woman who was taking several medications reported feeling tired, weak, dizzy, and confused for months. These symptoms were making it hard for her to leave her home. She was evaluated at a community pharmacy as part of a personalized medication program. The team checked her medications, especially those processed by the kidneys, using her estimated glomerular filtration rate (eGFR), which was 30 ml/min/1.73 m² — a sign of reduced kidney function. Based on this, they found that her doses of losartan and manidipine, which are blood pressure medicines, needed to be lowered to prevent low blood pressure. The pharmacy sent a report to her primary care doctor, who agreed to reduce losartan to 50 mg per day and manidipine to 10 mg per day. The doctor also switched her pregabalin to gabapentin, which is safer for her kidney function. After two months of follow-up, her blood pressure improved, and the symptoms of tiredness, weakness, dizziness, and confusion went away. The change in medication was successful and her condition stabilized.\"\n}", "generated_text": "A 78-year-old woman who was taking several medications reported feeling tired, weak, dizzy, and confused for months. These symptoms were making it hard for her to leave her home. She was evaluated at a community pharmacy as part of a personalized medication program. The team checked her medications, especially those processed by the kidneys, using her estimated glomerular filtration rate (eGFR), which was 30 ml/min/1.73 m² — a sign of reduced kidney function. Based on this, they found that her doses of losartan and manidipine, which are blood pressure medicines, needed to be lowered to prevent low blood pressure. The pharmacy sent a report to her primary care doctor, who agreed to reduce losartan to 50 mg per day and manidipine to 10 mg per day. The doctor also switched her pregabalin to gabapentin, which is safer for her kidney function. After two months of follow-up, her blood pressure improved, and the symptoms of tiredness, weakness, dizziness, and confusion went away. The change in medication was successful and her condition stabilized."}
{"row_index": 72, "doc_id": 56, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 78-year-old female patient, enrolled in a Personalised Medication Dosage System (PDS), presented with persistent symptoms of fatigue, weakness, dizziness, and confusion over several months, significantly impairing her ability to perform ambulatory activities. Upon clinical evaluation, she was referred to a personalised care setting to assess medication knowledge, adherence, and potential drug-related adverse effects. A comprehensive medication review was conducted, with particular focus on pharmacokinetic parameters relevant to renal function, specifically the estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, which yielded an eGFR of 30 ml/min/1.73 m²—indicative of stage 3 chronic kidney disease (CKD).\\n\\nThe patient's pharmacological regimen includes multiple agents: doxazosin (2 mg/24 h), losartan (100 mg/24 h), manidipine (20 mg/24 h), simvastatin (40 mg/24 h), acetylsalicylic acid (100 mg/24 h), omeprazole (20 mg/24 h), pregabalin (100 mg/12 h), torasemide (10 mg/24 h), dulaglutide (1.5 mg/week), insulin glargine (74 IU/24 h), insulin lispro (20 IU/24 h), and brimonidine (1 drop/12 h). Among these, losartan, manidipine, torasemide, and pregabalin were identified as agents requiring dose adjustment in the context of impaired renal function due to altered pharmacokinetics—specifically, reduced clearance via the kidneys.\\n\\nLosartan, an angiotensin II receptor blocker (ARB), and manidipine, a dihydropyridine calcium channel blocker (DCCB), are primarily eliminated by renal excretion. In patients with eGFR <60 ml/min/1.73 m², their clearance is diminished, increasing the risk of accumulation and adverse effects, including hypotension. According to product monographs and the consensus guidelines developed by the University of Barcelona Faculty of Pharmacy’s practical pharmacy teaching and research group—based on real-world dispensing data and ATC-based therapeutic categorisation—dose reductions are recommended: for losartan, a reduction to 50–75% of the original dose (i.e., 50 mg/24 h) is advised when eGFR ranges from 30 to 59 ml/min/1.73 m²; for manidipine, the recommended dose is adjusted to 10 mg/24 h when eGFR is between 15 and 30 ml/min/1.73 m². These adjustments are grounded in pharmacodynamic and pharmacokinetic evidence showing dose-dependent hypotensive effects in renal impairment.\\n\\nTorasemide, a loop diuretic, also influences blood pressure regulation and may contribute to hypotension when used in patients with reduced renal function due to decreased volume excretion and potential for electrolyte imbalance. Pregabalin, used for neuropathic pain, is metabolised via hepatic pathways but may exhibit increased systemic exposure in renal impairment due to secondary effects on clearance; however, its primary route of elimination is hepatic, and thus, dose adjustment is less critical in this context, though monitoring is advised.\\n\\nAn initial intervention was proposed, recommending a reduction of losartan to 50 mg/24 h and manidipine to 10 mg/24 h, with the option to evaluate pregabalin dose modification post-adjustment of antihypertensives. The patient was informed of the rationale, and a detailed report was submitted to her Primary Care Physician (PCP), outlining the pharmacological basis for the proposed changes. The PCP implemented the recommended dose reductions and substituted pregabalin 100 mg/12 h with gabapentin 300 mg/12 h, a non-narcotic alternative with a more favorable renal clearance profile.\\n\\nA two-month follow-up demonstrated significant clinical improvement: blood pressure values normalized (systolic 128–135 mmHg, diastolic 75–80 mmHg), and the patient reported complete resolution of fatigue, dizziness, and confusion. The gabapentin dose of 300 mg/12 h was confirmed to be within the recommended range for eGFR 30–60 ml/min/1.73 m² (total daily dose: 300–900 mg), indicating appropriate dosing without risk", "generated_text": "{\n  \"proficient_health_literacy\": \"A 78-year-old female patient, enrolled in a Personalised Medication Dosage System (PDS), presented with persistent symptoms of fatigue, weakness, dizziness, and confusion over several months, significantly impairing her ability to perform ambulatory activities. Upon clinical evaluation, she was referred to a personalised care setting to assess medication knowledge, adherence, and potential drug-related adverse effects. A comprehensive medication review was conducted, with particular focus on pharmacokinetic parameters relevant to renal function, specifically the estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, which yielded an eGFR of 30 ml/min/1.73 m²—indicative of stage 3 chronic kidney disease (CKD).\\n\\nThe patient's pharmacological regimen includes multiple agents: doxazosin (2 mg/24 h), losartan (100 mg/24 h), manidipine (20 mg/24 h), simvastatin (40 mg/24 h), acetylsalicylic acid (100 mg/24 h), omeprazole (20 mg/24 h), pregabalin (100 mg/12 h), torasemide (10 mg/24 h), dulaglutide (1.5 mg/week), insulin glargine (74 IU/24 h), insulin lispro (20 IU/24 h), and brimonidine (1 drop/12 h). Among these, losartan, manidipine, torasemide, and pregabalin were identified as agents requiring dose adjustment in the context of impaired renal function due to altered pharmacokinetics—specifically, reduced clearance via the kidneys.\\n\\nLosartan, an angiotensin II receptor blocker (ARB), and manidipine, a dihydropyridine calcium channel blocker (DCCB), are primarily eliminated by renal excretion. In patients with eGFR <60 ml/min/1.73 m², their clearance is diminished, increasing the risk of accumulation and adverse effects, including hypotension. According to product monographs and the consensus guidelines developed by the University of Barcelona Faculty of Pharmacy’s practical pharmacy teaching and research group—based on real-world dispensing data and ATC-based therapeutic categorisation—dose reductions are recommended: for losartan, a reduction to 50–75% of the original dose (i.e., 50 mg/24 h) is advised when eGFR ranges from 30 to 59 ml/min/1.73 m²; for manidipine, the recommended dose is adjusted to 10 mg/24 h when eGFR is between 15 and 30 ml/min/1.73 m². These adjustments are grounded in pharmacodynamic and pharmacokinetic evidence showing dose-dependent hypotensive effects in renal impairment.\\n\\nTorasemide, a loop diuretic, also influences blood pressure regulation and may contribute to hypotension when used in patients with reduced renal function due to decreased volume excretion and potential for electrolyte imbalance. Pregabalin, used for neuropathic pain, is metabolised via hepatic pathways but may exhibit increased systemic exposure in renal impairment due to secondary effects on clearance; however, its primary route of elimination is hepatic, and thus, dose adjustment is less critical in this context, though monitoring is advised.\\n\\nAn initial intervention was proposed, recommending a reduction of losartan to 50 mg/24 h and manidipine to 10 mg/24 h, with the option to evaluate pregabalin dose modification post-adjustment of antihypertensives. The patient was informed of the rationale, and a detailed report was submitted to her Primary Care Physician (PCP), outlining the pharmacological basis for the proposed changes. The PCP implemented the recommended dose reductions and substituted pregabalin 100 mg/12 h with gabapentin 300 mg/12 h, a non-narcotic alternative with a more favorable renal clearance profile.\\n\\nA two-month follow-up demonstrated significant clinical improvement: blood pressure values normalized (systolic 128–135 mmHg, diastolic 75–80 mmHg), and the patient reported complete resolution of fatigue, dizziness, and confusion. The gabapentin dose of 300 mg/12 h was confirmed to be within the recommended range for eGFR 30–60 ml/min/1.73 m² (total daily dose: 300–900 mg), indicating appropriate dosing without risk"}
{"row_index": 73, "doc_id": 57, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"This story is about a 9-year-old girl who has very smart brain skills but struggles with reading and writing because of dyslexia. Before help, she could only read simple letters and had a hard time with sounds and words. She wrote in a messy way, mixing up letters and skipping parts. After getting special reading and sound practice (like playing games to learn how sounds work), she got better. Now she reads faster and more clearly, and her writing is more organized. She still has some trouble with some letters and sounds, but she’s making progress. The help focused on her sound skills, which helped her read and write better, even though she’s still smart and has special abilities.\"\n}", "generated_text": "This story is about a 9-year-old girl who has very smart brain skills but struggles with reading and writing because of dyslexia. Before help, she could only read simple letters and had a hard time with sounds and words. She wrote in a messy way, mixing up letters and skipping parts. After getting special reading and sound practice (like playing games to learn how sounds work), she got better. Now she reads faster and more clearly, and her writing is more organized. She still has some trouble with some letters and sounds, but she’s making progress. The help focused on her sound skills, which helped her read and write better, even though she’s still smart and has special abilities."}
{"row_index": 74, "doc_id": 57, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"This case study reports a longitudinal evaluation and targeted phonological remediation intervention in a 9-year-old female child diagnosed with developmental dyslexia (DD) and high abilities/giftedness (AH/S). The study was approved by the Research Ethics Committee (CEP) under protocol number 1.012.635, with informed consent obtained from both parents and the participant via Free and Informed Consent (TCLE and TALE). The participant, enrolled in the third year of elementary school, was initially assessed at 8 years and 2 months (T1, 2018) and re-evaluated at 9 years and 6 months (T2, 2019), with the interval attributed to public service constraints, weekly appointment scheduling, and school holidays. The child was born at term with typical neuropsychomotor and linguistic development; she was raised in a French-speaking environment until age 2, after which her primary language at home became Brazilian Portuguese, though her first words were in French. Upon return to Brazil, she attended two private schools, initially experiencing communication difficulties due to language mismatch, leading to a transition into a French school at age 3. Over time, she exhibited persistent difficulties in reading and writing, resulting in a repetition of the first year of elementary school. At age 6, she entered a bilingual Portuguese-English school. At age 8, she underwent an interdisciplinary assessment in speech therapy and neuropsychology, leading to a formal diagnosis of developmental dyslexia with concomitant high cognitive abilities. She was subsequently referred to the Laboratory of Written Language, Interdisciplinarity and Learning (LEIA/UFRN) for comprehensive written language evaluation.\\n\\nThe intervention consisted of 20 weekly sessions (60 minutes each) of phonological remediation, conducted during the second semester of 2018, with limited parental engagement due to work commitments. Assessments were administered individually over one hour and included standardized tasks measuring phonological processing, reading, and writing. The following protocols were employed:\\n\\n- **Phonological Awareness**: Evaluated using the Consciência Fonológica Instrumento de Avaliação Sequencial (CONFIAS). This instrument includes tasks assessing syllabic and phonemic awareness (synthesis, segmentation, rhyme, alliteration, initial/final syllable identification, exclusion, transposition). Syllabic awareness comprises 9 items (max 40 points), phonemic awareness 7 items (max 30 points), totaling 70 points. Normative values derived from Ferreiro and Teberosky were used: for syllabic-alphabetic writing hypothesis, expected scores of 27 (syllabic), 12 (phonemic), and 39 (total); for alphabetic writing hypothesis, 31 (syllabic), 15 (phonemic), and 46 (total).\\n\\n- **Phonological Working Memory**: Assessed via the Phonological Working Memory Test. The protocol includes a non-word repetition task (40 invented words), with scoring: 2 points for first correct repetition, 1 point for second, 0 for third. A digits test in direct and reverse order follows, scored similarly. Age-specific norms were applied: for T1 (age 8 years 2 months), expected scores of 69 (pseudo-words), 13 (direct digits), and 6 (reverse digits).\\n\\n- **Mental Lexicon Access**: Evaluated using the Rapid Automatic Naming Test (RAN) at T1 and the Automatic Naming Test (TENA) at T2. Both assess naming speed of visual stimuli (colors, objects, letters, digits) using a left-to-right, top-to-bottom reading movement. For T1 (age 8 years 2 months), RAN normative values were 28 (digits), 29 (letters), 52 (objects), 46 (colors). For T2 (age 9 years 6 months), TENA norms were 35 (digits), 32 (letters), 50 (objects), 53 (colors).\\n\\n- **Reading**: Assessed via two protocols. First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated (LPI), comprising 19 regular words, 20 irregular words, and 20 pseudowords in Arial 24pt font. Correct responses are scored individually (max 59 points). Second, the Assessment of Expository Texts evaluates reading comprehension through directed questions and measures silent and oral reading speed, enabling calculation of words per minute (wpm).\\n\\n- **Writing**: Evaluated through a free narrative task on a topic of interest, followed by oral reading of the written text and a dictation of LPI words and pseudowords. Qualitative analysis was conducted using orthographic criteria", "generated_text": "{\n  \"proficient_health_literacy\": \"This case study reports a longitudinal evaluation and targeted phonological remediation intervention in a 9-year-old female child diagnosed with developmental dyslexia (DD) and high abilities/giftedness (AH/S). The study was approved by the Research Ethics Committee (CEP) under protocol number 1.012.635, with informed consent obtained from both parents and the participant via Free and Informed Consent (TCLE and TALE). The participant, enrolled in the third year of elementary school, was initially assessed at 8 years and 2 months (T1, 2018) and re-evaluated at 9 years and 6 months (T2, 2019), with the interval attributed to public service constraints, weekly appointment scheduling, and school holidays. The child was born at term with typical neuropsychomotor and linguistic development; she was raised in a French-speaking environment until age 2, after which her primary language at home became Brazilian Portuguese, though her first words were in French. Upon return to Brazil, she attended two private schools, initially experiencing communication difficulties due to language mismatch, leading to a transition into a French school at age 3. Over time, she exhibited persistent difficulties in reading and writing, resulting in a repetition of the first year of elementary school. At age 6, she entered a bilingual Portuguese-English school. At age 8, she underwent an interdisciplinary assessment in speech therapy and neuropsychology, leading to a formal diagnosis of developmental dyslexia with concomitant high cognitive abilities. She was subsequently referred to the Laboratory of Written Language, Interdisciplinarity and Learning (LEIA/UFRN) for comprehensive written language evaluation.\\n\\nThe intervention consisted of 20 weekly sessions (60 minutes each) of phonological remediation, conducted during the second semester of 2018, with limited parental engagement due to work commitments. Assessments were administered individually over one hour and included standardized tasks measuring phonological processing, reading, and writing. The following protocols were employed:\\n\\n- **Phonological Awareness**: Evaluated using the Consciência Fonológica Instrumento de Avaliação Sequencial (CONFIAS). This instrument includes tasks assessing syllabic and phonemic awareness (synthesis, segmentation, rhyme, alliteration, initial/final syllable identification, exclusion, transposition). Syllabic awareness comprises 9 items (max 40 points), phonemic awareness 7 items (max 30 points), totaling 70 points. Normative values derived from Ferreiro and Teberosky were used: for syllabic-alphabetic writing hypothesis, expected scores of 27 (syllabic), 12 (phonemic), and 39 (total); for alphabetic writing hypothesis, 31 (syllabic), 15 (phonemic), and 46 (total).\\n\\n- **Phonological Working Memory**: Assessed via the Phonological Working Memory Test. The protocol includes a non-word repetition task (40 invented words), with scoring: 2 points for first correct repetition, 1 point for second, 0 for third. A digits test in direct and reverse order follows, scored similarly. Age-specific norms were applied: for T1 (age 8 years 2 months), expected scores of 69 (pseudo-words), 13 (direct digits), and 6 (reverse digits).\\n\\n- **Mental Lexicon Access**: Evaluated using the Rapid Automatic Naming Test (RAN) at T1 and the Automatic Naming Test (TENA) at T2. Both assess naming speed of visual stimuli (colors, objects, letters, digits) using a left-to-right, top-to-bottom reading movement. For T1 (age 8 years 2 months), RAN normative values were 28 (digits), 29 (letters), 52 (objects), 46 (colors). For T2 (age 9 years 6 months), TENA norms were 35 (digits), 32 (letters), 50 (objects), 53 (colors).\\n\\n- **Reading**: Assessed via two protocols. First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated (LPI), comprising 19 regular words, 20 irregular words, and 20 pseudowords in Arial 24pt font. Correct responses are scored individually (max 59 points). Second, the Assessment of Expository Texts evaluates reading comprehension through directed questions and measures silent and oral reading speed, enabling calculation of words per minute (wpm).\\n\\n- **Writing**: Evaluated through a free narrative task on a topic of interest, followed by oral reading of the written text and a dictation of LPI words and pseudowords. Qualitative analysis was conducted using orthographic criteria"}
{"row_index": 75, "doc_id": 58, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old woman found a lump in the middle of her chest during a knee surgery check-up. Doctors saw it on a chest scan and found it was a round, clear lump, about 6.5 cm long and 4.2 cm wide, sitting in the back part of the chest. The lump didn’t hurt or spread to nearby areas. They took a small sample and looked at it under a microscope. It showed fat and blood-filled areas, along with some blood cell parts that were normal and mature. This told them it was a harmless tumor, called a myelolipoma. Since it wasn’t dangerous, they chose not to remove it and just watched it. She got better and went home without any problems.\"\n}", "generated_text": "A 65-year-old woman found a lump in the middle of her chest during a knee surgery check-up. Doctors saw it on a chest scan and found it was a round, clear lump, about 6.5 cm long and 4.2 cm wide, sitting in the back part of the chest. The lump didn’t hurt or spread to nearby areas. They took a small sample and looked at it under a microscope. It showed fat and blood-filled areas, along with some blood cell parts that were normal and mature. This told them it was a harmless tumor, called a myelolipoma. Since it wasn’t dangerous, they chose not to remove it and just watched it. She got better and went home without any problems."}
{"row_index": 76, "doc_id": 58, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 65-year-old woman was found to have a tumor in the middle of her chest, specifically in the posterior mediastinum, during a preoperative check-up for knee surgery. The tumor measured 6.5 × 4.2 cm, had clear borders, and was made up of fat and solid tissue with no signs of spreading to nearby structures. A biopsy was done using imaging guidance, and the results showed that the tumor contained mature fat tissue along with blood cells and early blood cell precursors, which is consistent with a benign condition called primary mediastinal myelolipoma. Because the tumor was not dangerous and did not show signs of growth or spread, the doctors chose not to treat it surgically. The patient recovered well and was discharged without any complications.\"\n}", "generated_text": "A 65-year-old woman was found to have a tumor in the middle of her chest, specifically in the posterior mediastinum, during a preoperative check-up for knee surgery. The tumor measured 6.5 × 4.2 cm, had clear borders, and was made up of fat and solid tissue with no signs of spreading to nearby structures. A biopsy was done using imaging guidance, and the results showed that the tumor contained mature fat tissue along with blood cells and early blood cell precursors, which is consistent with a benign condition called primary mediastinal myelolipoma. Because the tumor was not dangerous and did not show signs of growth or spread, the doctors chose not to treat it surgically. The patient recovered well and was discharged without any complications."}
{"row_index": 77, "doc_id": 58, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 65-year-old woman with no significant personal or familial medical history presented in August 2022 with a posterior mediastinal tumor identified during preoperative imaging for knee surgery, prompting referral for evaluation. Physical examination at admission was unremarkable, and all laboratory investigations remained within normal limits. A chest computed tomography (CT) scan revealed a well-defined, ovoid lesion measuring 6.5 × 4.2 cm in the posterior right mediastinum, exhibiting mixed fat and solid densities, with no evidence of bone erosion, soft tissue infiltration, or vascular involvement. The tumor was characterized by distinct borders and homogeneous attenuation consistent with adipose tissue intermixed with solid components. A trans-thoracic biopsy was performed using a 18G × 250 mm semiautomatic cutting needle under image guidance via a posterior approach, ensuring precise lesion sampling. Histopathological analysis demonstrated a benign neoplasm composed of mature adipose tissue interspersed with areas of hemorrhage and hematopoietic elements, including erythroid precursors (primarily proerythroblasts and basophilic erythroblasts) and myeloid lineage cells at various stages of differentiation, including promyelocytes, myelocytes, metamyelocytes, and mature granulocytes. Additionally, megakaryocytic elements were observed, indicating active hematopoiesis within the adipose matrix. These findings are consistent with primary mediastinal myelolipoma (MPM), a rare benign tumor of the mediastinum characterized by coexistence of mature adipose tissue and hematopoietic elements, typically arising from a primitive mesenchymal precursor that retains hematopoietic potential. The presence of hematopoietic components, particularly in the context of mature adipose stroma, supports the classification as a myelolipoma rather than a hematologic malignancy. Given the benign histological profile, lack of malignant transformation, and absence of local or systemic signs of disease progression, conservative management was elected. The patient demonstrated stable clinical course, with no evidence of tumor growth, complications, or systemic symptoms, and was discharged without adverse events. This case underscores the importance of accurate imaging interpretation and histopathological characterization in distinguishing benign mediastinal masses from malignant counterparts, particularly in the context of hematopoietic tissue coexistence within adipose stroma.\"\n}", "generated_text": "A 65-year-old woman with no significant personal or familial medical history presented in August 2022 with a posterior mediastinal tumor identified during preoperative imaging for knee surgery, prompting referral for evaluation. Physical examination at admission was unremarkable, and all laboratory investigations remained within normal limits. A chest computed tomography (CT) scan revealed a well-defined, ovoid lesion measuring 6.5 × 4.2 cm in the posterior right mediastinum, exhibiting mixed fat and solid densities, with no evidence of bone erosion, soft tissue infiltration, or vascular involvement. The tumor was characterized by distinct borders and homogeneous attenuation consistent with adipose tissue intermixed with solid components. A trans-thoracic biopsy was performed using a 18G × 250 mm semiautomatic cutting needle under image guidance via a posterior approach, ensuring precise lesion sampling. Histopathological analysis demonstrated a benign neoplasm composed of mature adipose tissue interspersed with areas of hemorrhage and hematopoietic elements, including erythroid precursors (primarily proerythroblasts and basophilic erythroblasts) and myeloid lineage cells at various stages of differentiation, including promyelocytes, myelocytes, metamyelocytes, and mature granulocytes. Additionally, megakaryocytic elements were observed, indicating active hematopoiesis within the adipose matrix. These findings are consistent with primary mediastinal myelolipoma (MPM), a rare benign tumor of the mediastinum characterized by coexistence of mature adipose tissue and hematopoietic elements, typically arising from a primitive mesenchymal precursor that retains hematopoietic potential. The presence of hematopoietic components, particularly in the context of mature adipose stroma, supports the classification as a myelolipoma rather than a hematologic malignancy. Given the benign histological profile, lack of malignant transformation, and absence of local or systemic signs of disease progression, conservative management was elected. The patient demonstrated stable clinical course, with no evidence of tumor growth, complications, or systemic symptoms, and was discharged without adverse events. This case underscores the importance of accurate imaging interpretation and histopathological characterization in distinguishing benign mediastinal masses from malignant counterparts, particularly in the context of hematopoietic tissue coexistence within adipose stroma."}
{"row_index": 78, "doc_id": 59, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old man got sick with both a bad fever and a COVID-19 virus. He worked outside in very hot weather and suddenly lost consciousness. His body temperature reached 104°F, and he fell into a deep coma. Doctors found he had a serious lung infection, damaged liver and kidneys, and a blood problem that made clots form easily. Even with medicine, fluids, and breathing support, he started having trouble breathing and a brain bleed later. He also had a lung infection from other germs, and his body couldn’t fight it well. After days of treatment, his fever and coma went away, but he got worse — he couldn’t breathe properly and had a brain bleed. The damage to his organs, caused by the fever and infections, eventually led to his death.\"\n}", "generated_text": "A 52-year-old man got sick with both a bad fever and a COVID-19 virus. He worked outside in very hot weather and suddenly lost consciousness. His body temperature reached 104°F, and he fell into a deep coma. Doctors found he had a serious lung infection, damaged liver and kidneys, and a blood problem that made clots form easily. Even with medicine, fluids, and breathing support, he started having trouble breathing and a brain bleed later. He also had a lung infection from other germs, and his body couldn’t fight it well. After days of treatment, his fever and coma went away, but he got worse — he couldn’t breathe properly and had a brain bleed. The damage to his organs, caused by the fever and infections, eventually led to his death."}
{"row_index": 79, "doc_id": 59, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 52-year-old male presented with a community-acquired SARS-CoV-2 infection confirmed by reverse-transcription polymerase chain reaction (RT-PCR) of a nasopharyngeal swab, following a self-reported cold. He returned to work after a two-day rest without fever but lost consciousness while working outdoors in an ambient temperature of 35°C for five hours. Upon emergency department admission, his core temperature (Tc) was 40°C, consistent with hyperpyrexia. He presented with persistent coma, dyspnea, and gastrointestinal hemorrhage, with no known comorbidities or family history of disease. Clinical features—including hyperpyrexia, coma, and multi-organ dysfunction—led to a diagnosis of heatstroke (HS). He was admitted to the emergency intensive care unit (ICU) and required mechanical ventilation due to respiratory failure. Initial laboratory findings revealed severe systemic infection, with leukopenia (WBC: 3.13×10⁹/L), profound lymphopenia (lymphocytes: 0.1×10⁹/L), neutrophilic shift (N%: 85.3%), elevated procalcitonin (2.81 ng/mL) and C-reactive protein (32.6 mg/L), indicating a strong bacterial component. Sputum culture identified Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture revealed Staphylococcus epidermidis, while blood cultures remained negative, suggesting a polymicrobial pulmonary infection with possible nosocomial or community-acquired origin. CT imaging demonstrated bilateral frontal subdural effusions, lower lobe consolidation and atelectasis, right upper lobe inflammation, bilateral pleural effusion, and minimal ascites, consistent with severe pulmonary infection and secondary pulmonary edema.\\n\\nThe patient received initial resuscitation with intravenous rehydration using lactated Ringer’s solution and normal saline at 2.5 mL/kg·h, vasoactive support with norepinephrine (0.4 µg/kg·min) to maintain blood pressure (126/77 mmHg), and broad-spectrum antibiotics including piperacillin-tazobactam, later switched to meropenem due to resistance concerns. Immune modulation with thymalfasin was administered for 20 days. Hepatic and renal dysfunction were managed with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and continuous renal replacement therapy (CRRT) for anuria. Coagulopathy was characterized by thrombocytopenia, disseminated intravascular coagulation (DIC), and elevated D-dimer levels, managed with plasma and cryoprecipitate transfusions, continuous intravenous heparin (6000 U/day), and CRRT with sodium citrate anticoagulation (8 g/day). Platelet transfusion was initiated on day 9. Intracranial pressure was managed with mannitol for three days. Despite initial improvement, the patient developed recurrent dyspnea and fever on day 17 (Tc: 39.3°C), requiring reintubation. Bronchoscopy showed reduced sputum volume, and GCS dropped to 3/15, with elevated WBC (14.94×10⁹/L) and neutrophils (13.77×10⁹/L). Laboratory markers worsened: serum total bilirubin increased to 235.2 µmol/L, creatinine to 441 µmol/L. Brain CT revealed ischemic stroke in the right frontal lobe and hemorrhagic infarction in the right occipital lobe, suggesting both vascular injury and microangiopathic damage. Cooling therapy via ice-cold CRRT was initiated. Fungal infection was suspected based on elevated serum Aspergillus galactomannan, Aspergillus IgG, and Candida mannan, leading to addition of carpofungin on day 18. SARS-CoV-2 RT-PCR became negative on day 18, indicating viral clearance or assay limitations.\\n\\nOn day 20, fever and infection resolved, but the patient developed cerebral hemorrhage and brain herniation with bilateral dilated pupils. Dehydration therapy was used to reduce intracranial pressure, but surgical intervention was declined by family. On day 22, inflammatory markers, liver enzymes (aspartate aminotransferase), and creatinine worsened again, with bronchoalveolar lavage fluid cultures positive for carbapenem-resistant Acinetobacter baumannii and Aspergillus fumigatus. Anti-infective therapy was intensified with meropenem, teicoplanin", "generated_text": "{\n  \"proficient_health_literacy\": \"A 52-year-old male presented with a community-acquired SARS-CoV-2 infection confirmed by reverse-transcription polymerase chain reaction (RT-PCR) of a nasopharyngeal swab, following a self-reported cold. He returned to work after a two-day rest without fever but lost consciousness while working outdoors in an ambient temperature of 35°C for five hours. Upon emergency department admission, his core temperature (Tc) was 40°C, consistent with hyperpyrexia. He presented with persistent coma, dyspnea, and gastrointestinal hemorrhage, with no known comorbidities or family history of disease. Clinical features—including hyperpyrexia, coma, and multi-organ dysfunction—led to a diagnosis of heatstroke (HS). He was admitted to the emergency intensive care unit (ICU) and required mechanical ventilation due to respiratory failure. Initial laboratory findings revealed severe systemic infection, with leukopenia (WBC: 3.13×10⁹/L), profound lymphopenia (lymphocytes: 0.1×10⁹/L), neutrophilic shift (N%: 85.3%), elevated procalcitonin (2.81 ng/mL) and C-reactive protein (32.6 mg/L), indicating a strong bacterial component. Sputum culture identified Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture revealed Staphylococcus epidermidis, while blood cultures remained negative, suggesting a polymicrobial pulmonary infection with possible nosocomial or community-acquired origin. CT imaging demonstrated bilateral frontal subdural effusions, lower lobe consolidation and atelectasis, right upper lobe inflammation, bilateral pleural effusion, and minimal ascites, consistent with severe pulmonary infection and secondary pulmonary edema.\\n\\nThe patient received initial resuscitation with intravenous rehydration using lactated Ringer’s solution and normal saline at 2.5 mL/kg·h, vasoactive support with norepinephrine (0.4 µg/kg·min) to maintain blood pressure (126/77 mmHg), and broad-spectrum antibiotics including piperacillin-tazobactam, later switched to meropenem due to resistance concerns. Immune modulation with thymalfasin was administered for 20 days. Hepatic and renal dysfunction were managed with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and continuous renal replacement therapy (CRRT) for anuria. Coagulopathy was characterized by thrombocytopenia, disseminated intravascular coagulation (DIC), and elevated D-dimer levels, managed with plasma and cryoprecipitate transfusions, continuous intravenous heparin (6000 U/day), and CRRT with sodium citrate anticoagulation (8 g/day). Platelet transfusion was initiated on day 9. Intracranial pressure was managed with mannitol for three days. Despite initial improvement, the patient developed recurrent dyspnea and fever on day 17 (Tc: 39.3°C), requiring reintubation. Bronchoscopy showed reduced sputum volume, and GCS dropped to 3/15, with elevated WBC (14.94×10⁹/L) and neutrophils (13.77×10⁹/L). Laboratory markers worsened: serum total bilirubin increased to 235.2 µmol/L, creatinine to 441 µmol/L. Brain CT revealed ischemic stroke in the right frontal lobe and hemorrhagic infarction in the right occipital lobe, suggesting both vascular injury and microangiopathic damage. Cooling therapy via ice-cold CRRT was initiated. Fungal infection was suspected based on elevated serum Aspergillus galactomannan, Aspergillus IgG, and Candida mannan, leading to addition of carpofungin on day 18. SARS-CoV-2 RT-PCR became negative on day 18, indicating viral clearance or assay limitations.\\n\\nOn day 20, fever and infection resolved, but the patient developed cerebral hemorrhage and brain herniation with bilateral dilated pupils. Dehydration therapy was used to reduce intracranial pressure, but surgical intervention was declined by family. On day 22, inflammatory markers, liver enzymes (aspartate aminotransferase), and creatinine worsened again, with bronchoalveolar lavage fluid cultures positive for carbapenem-resistant Acinetobacter baumannii and Aspergillus fumigatus. Anti-infective therapy was intensified with meropenem, teicoplanin"}
{"row_index": 80, "doc_id": 60, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-year-old female presented to the emergency department with a two-day history of headache, recurrent nausea, vomiting, and one-day fever. On admission, she had a high fever of 39.1°C, severe hypertension (189/120 mmHg), and tachycardia (148 beats per minute). Laboratory findings revealed a leukocytosis (14.77×10^9/L) with neutrophilia (13.55×10^9/L), suggestive of systemic inflammation or infection. Empirical antibiotic therapy with moxifloxacin was initiated, but symptoms persisted, prompting admission to the intensive care unit for close monitoring. A year prior, she had been diagnosed with myocarditis at a local hospital, along with hypertension, for which antihypertensive therapy was prescribed; however, she discontinued adherence to medication and failed to monitor blood pressure regularly. Notably, her father had a history of sudden, unexplained death, raising concerns for a hereditary endocrine disorder.\\n\\nA chest CT scan incidentally revealed a left adrenal mass measuring 43 mm × 36 mm with soft tissue density. Head and chest CTs showed no other pathological abnormalities. Electrocardiography demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF, consistent with volume overload or myocardial stress. Transthoracic echocardiography was unremarkable.\\n\\nOn day two of admission, biomarkers including brain natriuretic peptide (BNP) and cardiac troponin I (TnI) increased, supporting a provisional diagnosis of myocarditis of uncertain etiology. Treatment included methylprednisolone (0.25 g/day) for presumed myocardial inflammation, furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) for fluid management, and perindopril amlodipine (10 mg: 5 mg daily) for blood pressure control and afterload reduction. Metoprolol tartrate (25 mg every 12 hours) and esmolol (0.2 g/hour IV infusion) were used to control heart rate and reduce myocardial oxygen demand.\\n\\nGiven the presence of an adrenal mass and sustained hypertension, endocrine workup was initiated, including assessment of aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines and metabolites. In the recumbent position, plasma catecholamines were markedly elevated: dopamine (524.5 pmol/L), norepinephrine (83,975 pmol/L), and epinephrine (10,579.3 pmol/L). Urinary excretion levels included free adrenaline (4,368.89 nmol/24 h), free norepinephrine (>12,697.60 nmol/24 h), normetanephrine (8,312 nmol/24 h), metanephrines (4,078 nmol/24 h), and vanillylmandelic acid (58.1 mg/24 h). These findings are consistent with pheochromocytoma and supported the clinical diagnosis.\\n\\nOn day five post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was replaced with terazosin to provide more precise blood pressure control in the setting of catecholamine excess. An enhanced abdominal CT confirmed the left adrenal mass, highly suggestive of pheochromocytoma. Whole-exome sequencing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), resulting in substitution of cysteine by arginine at codon 634. This mutation is pathogenic and associated with multiple endocrine neoplasia type 2A (MEN2A), prompting further endocrine evaluation of the thyroid and parathyroid glands.\\n\\nThyroid color Doppler ultrasound identified a hypoechoic nodule measuring 6 mm × 4 mm in the left thyroid lobe, with mildly elevated serum calcitonin levels. Parathyroid function tests showed normal serum calcium, phosphate, and parathyroid hormone (PTH) levels. No other significant endocrine abnormalities were detected.\\n\\nFollowing clinical stabilization, plasma cortisol and ACTH levels normalized. The patient underwent surgical resection of the left adrenal tumor, which measured 50 mm × 40 mm × 30 mm. Immunohistochemical analysis confirmed positive staining for vimentin (", "generated_text": "{\n  \"proficient_health_literacy\": \"A 19-year-old female presented to the emergency department with a two-day history of headache, recurrent nausea, vomiting, and one-day fever. On admission, she had a high fever of 39.1°C, severe hypertension (189/120 mmHg), and tachycardia (148 beats per minute). Laboratory findings revealed a leukocytosis (14.77×10^9/L) with neutrophilia (13.55×10^9/L), suggestive of systemic inflammation or infection. Empirical antibiotic therapy with moxifloxacin was initiated, but symptoms persisted, prompting admission to the intensive care unit for close monitoring. A year prior, she had been diagnosed with myocarditis at a local hospital, along with hypertension, for which antihypertensive therapy was prescribed; however, she discontinued adherence to medication and failed to monitor blood pressure regularly. Notably, her father had a history of sudden, unexplained death, raising concerns for a hereditary endocrine disorder.\\n\\nA chest CT scan incidentally revealed a left adrenal mass measuring 43 mm × 36 mm with soft tissue density. Head and chest CTs showed no other pathological abnormalities. Electrocardiography demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF, consistent with volume overload or myocardial stress. Transthoracic echocardiography was unremarkable.\\n\\nOn day two of admission, biomarkers including brain natriuretic peptide (BNP) and cardiac troponin I (TnI) increased, supporting a provisional diagnosis of myocarditis of uncertain etiology. Treatment included methylprednisolone (0.25 g/day) for presumed myocardial inflammation, furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) for fluid management, and perindopril amlodipine (10 mg: 5 mg daily) for blood pressure control and afterload reduction. Metoprolol tartrate (25 mg every 12 hours) and esmolol (0.2 g/hour IV infusion) were used to control heart rate and reduce myocardial oxygen demand.\\n\\nGiven the presence of an adrenal mass and sustained hypertension, endocrine workup was initiated, including assessment of aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines and metabolites. In the recumbent position, plasma catecholamines were markedly elevated: dopamine (524.5 pmol/L), norepinephrine (83,975 pmol/L), and epinephrine (10,579.3 pmol/L). Urinary excretion levels included free adrenaline (4,368.89 nmol/24 h), free norepinephrine (>12,697.60 nmol/24 h), normetanephrine (8,312 nmol/24 h), metanephrines (4,078 nmol/24 h), and vanillylmandelic acid (58.1 mg/24 h). These findings are consistent with pheochromocytoma and supported the clinical diagnosis.\\n\\nOn day five post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was replaced with terazosin to provide more precise blood pressure control in the setting of catecholamine excess. An enhanced abdominal CT confirmed the left adrenal mass, highly suggestive of pheochromocytoma. Whole-exome sequencing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), resulting in substitution of cysteine by arginine at codon 634. This mutation is pathogenic and associated with multiple endocrine neoplasia type 2A (MEN2A), prompting further endocrine evaluation of the thyroid and parathyroid glands.\\n\\nThyroid color Doppler ultrasound identified a hypoechoic nodule measuring 6 mm × 4 mm in the left thyroid lobe, with mildly elevated serum calcitonin levels. Parathyroid function tests showed normal serum calcium, phosphate, and parathyroid hormone (PTH) levels. No other significant endocrine abnormalities were detected.\\n\\nFollowing clinical stabilization, plasma cortisol and ACTH levels normalized. The patient underwent surgical resection of the left adrenal tumor, which measured 50 mm × 40 mm × 30 mm. Immunohistochemical analysis confirmed positive staining for vimentin ("}
{"row_index": 81, "doc_id": 61, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old man had a painful lump on the inside of his penis and scrotum for 5 years. The lump was not causing trouble with urination or weight loss. Doctors found it was a hard, cyst-like growth, about 2 cm big, with lots of blood flow. Imaging showed it was attached to the tube that carries sperm and was deep in the area, not near the testicle or cord. After surgery, the doctors found it was a type of cancer called synovial sarcoma — a kind of tumor that grows in the tissue around joints. The tumor had signs that matched this cancer, and tests confirmed it had a genetic change known in this type of cancer. The first surgery removed the lump, but the cancer came back. The patient had a second surgery to remove more tissue, and even after that, the cancer spread to his liver and spine. He tried several chemotherapy treatments, but none worked. He had more surgeries on his liver, then got a lung tumor. He tried more medicines and radiation, but the cancer kept growing. Eventually, he was moved to palliative care and stopped seeing doctors because the disease was no longer treatable.\"\n}", "generated_text": "A 36-year-old man had a painful lump on the inside of his penis and scrotum for 5 years. The lump was not causing trouble with urination or weight loss. Doctors found it was a hard, cyst-like growth, about 2 cm big, with lots of blood flow. Imaging showed it was attached to the tube that carries sperm and was deep in the area, not near the testicle or cord. After surgery, the doctors found it was a type of cancer called synovial sarcoma — a kind of tumor that grows in the tissue around joints. The tumor had signs that matched this cancer, and tests confirmed it had a genetic change known in this type of cancer. The first surgery removed the lump, but the cancer came back. The patient had a second surgery to remove more tissue, and even after that, the cancer spread to his liver and spine. He tried several chemotherapy treatments, but none worked. He had more surgeries on his liver, then got a lung tumor. He tried more medicines and radiation, but the cancer kept growing. Eventually, he was moved to palliative care and stopped seeing doctors because the disease was no longer treatable."}
{"row_index": 82, "doc_id": 61, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 36-year-old man had a painful lump in the penis and scrotum for 5 years. The lump was about 20 mm in size, not attached to the spermatic cord, and was tender but not causing urinary problems. Imaging showed a well-defined mass with lots of blood flow, and it was connected to the vas deferens. Blood tests were normal. After surgery, the tissue was examined and found to be a type of cancer called synovial sarcoma. The tumor cells were arranged in a specific pattern and tested positive for markers like TLE-1, CD99, BLC2, cytokeratin, and EMA. A genetic test confirmed a known change in the SS18 gene, which is common in this type of cancer. The first surgery removed the mass completely, but the margins were hard to assess because the sample was fragmented. A second surgery was done with wider margins, and the new tissue sample showed no signs of cancer. However, after 16 months of monitoring, the cancer spread to the liver and spine. Despite multiple treatments—including chemotherapy with Ifosfamide and Doxorubicin, surgery to remove liver tumors, and targeted therapy with Pazopanib and radiation—the cancer continued to grow. He tried several other chemotherapy regimens, including Gemcitabine and Docetaxel, and Dacarbazine, but all failed. Eventually, he was moved to palliative care and stopped treatment due to disease progression.\"\n}", "generated_text": "A 36-year-old man had a painful lump in the penis and scrotum for 5 years. The lump was about 20 mm in size, not attached to the spermatic cord, and was tender but not causing urinary problems. Imaging showed a well-defined mass with lots of blood flow, and it was connected to the vas deferens. Blood tests were normal. After surgery, the tissue was examined and found to be a type of cancer called synovial sarcoma. The tumor cells were arranged in a specific pattern and tested positive for markers like TLE-1, CD99, BLC2, cytokeratin, and EMA. A genetic test confirmed a known change in the SS18 gene, which is common in this type of cancer. The first surgery removed the mass completely, but the margins were hard to assess because the sample was fragmented. A second surgery was done with wider margins, and the new tissue sample showed no signs of cancer. However, after 16 months of monitoring, the cancer spread to the liver and spine. Despite multiple treatments—including chemotherapy with Ifosfamide and Doxorubicin, surgery to remove liver tumors, and targeted therapy with Pazopanib and radiation—the cancer continued to grow. He tried several other chemotherapy regimens, including Gemcitabine and Docetaxel, and Dacarbazine, but all failed. Eventually, he was moved to palliative care and stopped treatment due to disease progression."}
{"row_index": 83, "doc_id": 61, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 36-year-old male with no significant past medical history presented with a 5-year history of a left-sided penoscrotal mass. The patient reported no lower urinary tract symptoms, trauma, infections, weight loss, anorexia, or fever. Physical examination revealed a smooth, tender, cystic lesion measuring approximately 20 mm × 20 mm located at the penoscrotal junction, attached to the left side of the bulbar urethra, deep in the tissue, without skin tethering or association with the left spermatic cord, and partially mobile. Doppler ultrasonography demonstrated a well-defined hypoechoic mass measuring 2.7 cm × 3.1 cm × 2.0 cm with markedly increased vascularity on the left penoscrotal junction. Pelvic magnetic resonance imaging (MRI) showed a lesion in the left inferolateral base of the penis with a distinct fat plane, isointense to testicular tissue on T2-weighted, T1-weighted, and diffusion-weighted imaging sequences, and with direct connection to the vas deferens; no regional lymphadenopathy was observed. Serum alpha-fetoprotein and beta-human chorionic gonadotropin levels were within normal limits. Given the chronic pain and imaging findings, surgical resection was performed for both diagnostic and therapeutic purposes. Intraoperatively, a mass was identified in the left posterolateral scrotum and completely resected, with the specimen sent for histopathological evaluation.\\n\\nHistopathological analysis revealed a cellular spindle cell tumor organized in interlacing fascicles, comprising spindle- to oval-shaped cells with vesicular nuclei, evenly distributed chromatin, and inconspicuous nucleoli. The tumor exhibited high mitotic activity, with up to 3 mitotic figures per high-power field. Immunohistochemical staining was positive for TLE-1, CD99, B-cell lymphoma 2 (BCL-2), focal cytokeratin, and focal epithelial membrane antigen (EMA), consistent with synovial sarcoma. Fluorescence in situ hybridization (FISH) analysis confirmed a characteristic rearrangement of the SS18 gene at 18q11.2, a molecular hallmark of synovial sarcoma. Histological assessment of the margins was inconclusive due to fragmentation of the resection specimen.\\n\\nTwo weeks post-initial surgery, the patient returned for a multidisciplinary review. Based on the histopathology, a second surgical resection with wider margins was proposed and accepted. A positron emission tomography–computed tomography (PET/CT) scan of the head, neck, chest, abdomen, pelvis, and musculoskeletal system was performed, revealing a 29 mm × 27 mm thyroid nodule in the lower pole of the left lobe with moderate hypermetabolism (standardized uptake value [SUV] of 4.9). Thyroid ultrasound demonstrated a solid, isoechoic, well-defined nodule without echogenic foci. The nodule was classified as TIRADS category 3 (TR3), indicating a low risk of malignancy.\\n\\nA second surgical resection was performed three weeks after the initial procedure. The resection extended bilaterally to the spermatic cords, deepening to the corpus spongiosum and shaving superiorly to the urethra. The final resected specimen measured 6.0 cm × 6.0 cm × 3.0 cm and was histologically negative for residual tumor. The patient then entered active surveillance. At 16 months, metastatic disease was detected in the sixth segment of the liver and the L1 vertebral body. The oncology team initiated a six-cycle regimen of ifosfamide and doxorubicin, which showed no clinical or radiographic response. Subsequent surgical resection of the fifth and sixth liver segments, along with cholecystectomy, was performed. The patient later developed a new pulmonary lesion, prompting initiation of pazopanib and stereotactic body radiation therapy (SBRT). After six months of surveillance, new lesions emerged in both the liver and lungs. A gemcitabine and docetaxel combination chemotherapy regimen was administered for three cycles, followed by progression. The patient then received two cycles of dacarbazine, with further progression. Subsequently, two cycles of pembrolizumab were administered, also resulting in disease progression. Given the lack of response to all available systemic therapies, the patient was transitioned to palliative care and discontinued follow-up. This case highlights the aggressive clinical course of synovial sarcoma, particularly in the penoscrotal region, with early local recurrence, metastatic spread to liver and bone, and resistance to conventional chemotherapy and immunotherapy regimens, underscoring the need for early detection, comprehensive surgical margins, and exploration of novel targeted or immunother", "generated_text": "{\n  \"proficient_health_literacy\": \"A 36-year-old male with no significant past medical history presented with a 5-year history of a left-sided penoscrotal mass. The patient reported no lower urinary tract symptoms, trauma, infections, weight loss, anorexia, or fever. Physical examination revealed a smooth, tender, cystic lesion measuring approximately 20 mm × 20 mm located at the penoscrotal junction, attached to the left side of the bulbar urethra, deep in the tissue, without skin tethering or association with the left spermatic cord, and partially mobile. Doppler ultrasonography demonstrated a well-defined hypoechoic mass measuring 2.7 cm × 3.1 cm × 2.0 cm with markedly increased vascularity on the left penoscrotal junction. Pelvic magnetic resonance imaging (MRI) showed a lesion in the left inferolateral base of the penis with a distinct fat plane, isointense to testicular tissue on T2-weighted, T1-weighted, and diffusion-weighted imaging sequences, and with direct connection to the vas deferens; no regional lymphadenopathy was observed. Serum alpha-fetoprotein and beta-human chorionic gonadotropin levels were within normal limits. Given the chronic pain and imaging findings, surgical resection was performed for both diagnostic and therapeutic purposes. Intraoperatively, a mass was identified in the left posterolateral scrotum and completely resected, with the specimen sent for histopathological evaluation.\\n\\nHistopathological analysis revealed a cellular spindle cell tumor organized in interlacing fascicles, comprising spindle- to oval-shaped cells with vesicular nuclei, evenly distributed chromatin, and inconspicuous nucleoli. The tumor exhibited high mitotic activity, with up to 3 mitotic figures per high-power field. Immunohistochemical staining was positive for TLE-1, CD99, B-cell lymphoma 2 (BCL-2), focal cytokeratin, and focal epithelial membrane antigen (EMA), consistent with synovial sarcoma. Fluorescence in situ hybridization (FISH) analysis confirmed a characteristic rearrangement of the SS18 gene at 18q11.2, a molecular hallmark of synovial sarcoma. Histological assessment of the margins was inconclusive due to fragmentation of the resection specimen.\\n\\nTwo weeks post-initial surgery, the patient returned for a multidisciplinary review. Based on the histopathology, a second surgical resection with wider margins was proposed and accepted. A positron emission tomography–computed tomography (PET/CT) scan of the head, neck, chest, abdomen, pelvis, and musculoskeletal system was performed, revealing a 29 mm × 27 mm thyroid nodule in the lower pole of the left lobe with moderate hypermetabolism (standardized uptake value [SUV] of 4.9). Thyroid ultrasound demonstrated a solid, isoechoic, well-defined nodule without echogenic foci. The nodule was classified as TIRADS category 3 (TR3), indicating a low risk of malignancy.\\n\\nA second surgical resection was performed three weeks after the initial procedure. The resection extended bilaterally to the spermatic cords, deepening to the corpus spongiosum and shaving superiorly to the urethra. The final resected specimen measured 6.0 cm × 6.0 cm × 3.0 cm and was histologically negative for residual tumor. The patient then entered active surveillance. At 16 months, metastatic disease was detected in the sixth segment of the liver and the L1 vertebral body. The oncology team initiated a six-cycle regimen of ifosfamide and doxorubicin, which showed no clinical or radiographic response. Subsequent surgical resection of the fifth and sixth liver segments, along with cholecystectomy, was performed. The patient later developed a new pulmonary lesion, prompting initiation of pazopanib and stereotactic body radiation therapy (SBRT). After six months of surveillance, new lesions emerged in both the liver and lungs. A gemcitabine and docetaxel combination chemotherapy regimen was administered for three cycles, followed by progression. The patient then received two cycles of dacarbazine, with further progression. Subsequently, two cycles of pembrolizumab were administered, also resulting in disease progression. Given the lack of response to all available systemic therapies, the patient was transitioned to palliative care and discontinued follow-up. This case highlights the aggressive clinical course of synovial sarcoma, particularly in the penoscrotal region, with early local recurrence, metastatic spread to liver and bone, and resistance to conventional chemotherapy and immunotherapy regimens, underscoring the need for early detection, comprehensive surgical margins, and exploration of novel targeted or immunother"}
{"row_index": 84, "doc_id": 62, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old boy came to the emergency room with sudden chest pain on the sides of his chest, especially when coughing. The pain wasn’t linked to fever or other symptoms, and he didn’t feel short of breath. He had a mild cold and a one-time fever, but no joint pain, weight loss, or fatigue. He still played sports regularly. His chest X-ray from 4 years ago showed a similar lung problem, which was treated with an antibiotic called azithromycin and has stayed quiet since. This time, his new chest scan showed a lot of cloudy areas in both lungs, more than two-thirds of them, which points to a rare lung condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including the coronavirus, came back negative. A lung fluid test showed a milky fluid and a sign that matches PAP. His breathing test showed a slight drop in lung function, but he’s still able to breathe and play. No gene changes were found that cause lung problems. A test for a specific immune protein showed it was missing, which makes it likely this is an autoimmune form of PAP. After 20 months, he’s feeling fine, breathing normally, and still plays sports. No treatment is needed right now — just regular check-ups to keep an eye on his lungs.\"\n}", "generated_text": "A 13-year-old boy came to the emergency room with sudden chest pain on the sides of his chest, especially when coughing. The pain wasn’t linked to fever or other symptoms, and he didn’t feel short of breath. He had a mild cold and a one-time fever, but no joint pain, weight loss, or fatigue. He still played sports regularly. His chest X-ray from 4 years ago showed a similar lung problem, which was treated with an antibiotic called azithromycin and has stayed quiet since. This time, his new chest scan showed a lot of cloudy areas in both lungs, more than two-thirds of them, which points to a rare lung condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including the coronavirus, came back negative. A lung fluid test showed a milky fluid and a sign that matches PAP. His breathing test showed a slight drop in lung function, but he’s still able to breathe and play. No gene changes were found that cause lung problems. A test for a specific immune protein showed it was missing, which makes it likely this is an autoimmune form of PAP. After 20 months, he’s feeling fine, breathing normally, and still plays sports. No treatment is needed right now — just regular check-ups to keep an eye on his lungs."}
{"row_index": 85, "doc_id": 62, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 13-year-old male with no significant prior medical history presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain, associated with mild non-productive cough, mild rhinorrhea, and a single febrile episode (38°C). The chest pain was localized to the costal margin and exacerbated by coughing, without diurnal variation or respiratory distress. Symptoms were partially relieved with paracetamol. There were no reports of joint pain, weight loss, anorexia, fatigue, syncope, or exercise intolerance; he maintained regular physical activity, including weekly canoeing. No history of infectious exposure, environmental exposures (e.g., dust, fumes, mineral oils), or familial cardiopulmonary disease was reported. A prior chest radiograph, obtained four years earlier during an acute illness, demonstrated a marked interstitial infiltrate, which was initially treated with azithromycin and has remained asymptomatic since, with no subsequent follow-up.\\n\\nOn admission, vital signs were stable: temperature 37.8°C, oxygen saturation 99% on room air, heart rate 93 bpm, respiratory rate 15 breaths per minute, and blood pressure at the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two-thirds of the lung fields without adventitious sounds, respiratory distress, cyanosis, clubbing, or abnormal cardiac murmurs. Chest radiography showed a persistent interstitial infiltrate, morphologically similar to the prior finding. Thoracic computed tomography (CT) revealed multiple bilateral ground-glass opacities involving greater than 65% of lung parenchyma, with areas of 'crazy paving' pattern—findings highly suggestive of pulmonary alveolar proteinosis (PAP).\\n\\nRespiratory viral testing, including for SARS-CoV-2, was negative. The patient was initially managed with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) for suspected respiratory infection, and symptoms resolved. He was discharged and referred to a pediatric respiratory clinic for further evaluation.\\n\\nOutpatient workup revealed positive antinuclear antibodies (ANA) at a titer of 1/89 with a fine speckled pattern, while other autoantibodies (e.g., anti-dsDNA, anti-Smith, anti-Ro/SSA) were negative, and immunoglobulin levels were within normal ranges. Bronchoalveolar lavage (BAL) fluid exhibited a milky appearance and demonstrated positive periodic acid-Schiff (PAS) staining, indicating the presence of surfactant proteins and alveolar protein accumulation. Microbiological analysis of BAL, including for mycobacteria, was negative, excluding infectious etiologies. Spirometry showed a mild restrictive pattern: forced vital capacity (FVC) of 2.92 L (77%), forced expiratory volume in 1 second (FEV1) of 3.21 L (69.9%), and a normal FEV1/FVC ratio of 109%, consistent with preserved airflow dynamics. Diffusing capacity of the lungs for carbon monoxide (DLCO, single breath) was reduced to 13.8 ml/min/mmHg (48.6%), indicating impaired gas exchange, consistent with alveolar membrane thickening or protein deposition.\\n\\nGenetic testing for mutations associated with surfactant dysfunction (e.g., SFTPA1, SFTPB, SFTPC, ABCA3) was negative, ruling out inherited surfactant-related disorders. Testing for anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibodies was strongly positive, supporting a diagnosis of autoimmune pulmonary alveolar proteinosis (AI-PAP), in which the immune system produces autoantibodies that inhibit GM-CSF function, leading to impaired alveolar macrophage clearance of surfactant proteins and subsequent protein accumulation in alveoli.\\n\\nAt 20-month follow-up, the patient remains asymptomatic and continues to engage in regular physical activity. Repeat spirometry shows normalization of FVC (4.03 L, 81.3%), FEV1 (3.71 L, 87.5%), and FEV1/FVC ratio (91.96%), indicating partial recovery or stabilization of pulmonary function. DLCO has improved to 25.54 ml/min/mmHg (83.7%), suggesting partial restoration of gas exchange. Given the absence of symptoms and stable pulmonary function, treatment was deferred, and the patient is being managed with routine clinical monitoring. The case underscores the clinical and radiological overlap between acute respiratory illness and chronic alveolar proteinosis, particularly in adolescents with recurrent interstitial infiltrates and autoimmune markers,", "generated_text": "{\n  \"proficient_health_literacy\": \"A 13-year-old male with no significant prior medical history presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain, associated with mild non-productive cough, mild rhinorrhea, and a single febrile episode (38°C). The chest pain was localized to the costal margin and exacerbated by coughing, without diurnal variation or respiratory distress. Symptoms were partially relieved with paracetamol. There were no reports of joint pain, weight loss, anorexia, fatigue, syncope, or exercise intolerance; he maintained regular physical activity, including weekly canoeing. No history of infectious exposure, environmental exposures (e.g., dust, fumes, mineral oils), or familial cardiopulmonary disease was reported. A prior chest radiograph, obtained four years earlier during an acute illness, demonstrated a marked interstitial infiltrate, which was initially treated with azithromycin and has remained asymptomatic since, with no subsequent follow-up.\\n\\nOn admission, vital signs were stable: temperature 37.8°C, oxygen saturation 99% on room air, heart rate 93 bpm, respiratory rate 15 breaths per minute, and blood pressure at the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two-thirds of the lung fields without adventitious sounds, respiratory distress, cyanosis, clubbing, or abnormal cardiac murmurs. Chest radiography showed a persistent interstitial infiltrate, morphologically similar to the prior finding. Thoracic computed tomography (CT) revealed multiple bilateral ground-glass opacities involving greater than 65% of lung parenchyma, with areas of 'crazy paving' pattern—findings highly suggestive of pulmonary alveolar proteinosis (PAP).\\n\\nRespiratory viral testing, including for SARS-CoV-2, was negative. The patient was initially managed with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) for suspected respiratory infection, and symptoms resolved. He was discharged and referred to a pediatric respiratory clinic for further evaluation.\\n\\nOutpatient workup revealed positive antinuclear antibodies (ANA) at a titer of 1/89 with a fine speckled pattern, while other autoantibodies (e.g., anti-dsDNA, anti-Smith, anti-Ro/SSA) were negative, and immunoglobulin levels were within normal ranges. Bronchoalveolar lavage (BAL) fluid exhibited a milky appearance and demonstrated positive periodic acid-Schiff (PAS) staining, indicating the presence of surfactant proteins and alveolar protein accumulation. Microbiological analysis of BAL, including for mycobacteria, was negative, excluding infectious etiologies. Spirometry showed a mild restrictive pattern: forced vital capacity (FVC) of 2.92 L (77%), forced expiratory volume in 1 second (FEV1) of 3.21 L (69.9%), and a normal FEV1/FVC ratio of 109%, consistent with preserved airflow dynamics. Diffusing capacity of the lungs for carbon monoxide (DLCO, single breath) was reduced to 13.8 ml/min/mmHg (48.6%), indicating impaired gas exchange, consistent with alveolar membrane thickening or protein deposition.\\n\\nGenetic testing for mutations associated with surfactant dysfunction (e.g., SFTPA1, SFTPB, SFTPC, ABCA3) was negative, ruling out inherited surfactant-related disorders. Testing for anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibodies was strongly positive, supporting a diagnosis of autoimmune pulmonary alveolar proteinosis (AI-PAP), in which the immune system produces autoantibodies that inhibit GM-CSF function, leading to impaired alveolar macrophage clearance of surfactant proteins and subsequent protein accumulation in alveoli.\\n\\nAt 20-month follow-up, the patient remains asymptomatic and continues to engage in regular physical activity. Repeat spirometry shows normalization of FVC (4.03 L, 81.3%), FEV1 (3.71 L, 87.5%), and FEV1/FVC ratio (91.96%), indicating partial recovery or stabilization of pulmonary function. DLCO has improved to 25.54 ml/min/mmHg (83.7%), suggesting partial restoration of gas exchange. Given the absence of symptoms and stable pulmonary function, treatment was deferred, and the patient is being managed with routine clinical monitoring. The case underscores the clinical and radiological overlap between acute respiratory illness and chronic alveolar proteinosis, particularly in adolescents with recurrent interstitial infiltrates and autoimmune markers,"}
{"row_index": 86, "doc_id": 63, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old woman had swelling on her face and trouble opening her mouth 48 hours after taking antibiotics for a tooth infection. A scan of her neck showed a big blood clot in a vein, and a chest scan found clots in her lungs. She was treated right away with strong antibiotics and medicine to thin her blood to stop the clots from getting worse. She got better after a few days of this treatment.\"\n}", "generated_text": "A 27-year-old woman had swelling on her face and trouble opening her mouth 48 hours after taking antibiotics for a tooth infection. A scan of her neck showed a big blood clot in a vein, and a chest scan found clots in her lungs. She was treated right away with strong antibiotics and medicine to thin her blood to stop the clots from getting worse. She got better after a few days of this treatment."}
{"row_index": 87, "doc_id": 63, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 27-year-old woman developed facial swelling and difficulty opening her mouth (trismus) 48 hours after taking phenoxymethylpenicillin for a throat infection. Tests showed a large blood clot in the internal jugular vein of her neck and lung clots from the infection spreading to her lungs (pulmonary septic embolism). She was treated with strong intravenous antibiotics and anticoagulant medication to stop the clot from growing and to fight the infection. Her symptoms improved over several days, and after 14 days of treatment, she was able to go home on oral antibiotics and continued anticoagulation therapy.\"\n}", "generated_text": "A 27-year-old woman developed facial swelling and difficulty opening her mouth (trismus) 48 hours after taking phenoxymethylpenicillin for a throat infection. Tests showed a large blood clot in the internal jugular vein of her neck and lung clots from the infection spreading to her lungs (pulmonary septic embolism). She was treated with strong intravenous antibiotics and anticoagulant medication to stop the clot from growing and to fight the infection. Her symptoms improved over several days, and after 14 days of treatment, she was able to go home on oral antibiotics and continued anticoagulation therapy."}
{"row_index": 88, "doc_id": 63, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 27-year-old woman with a history of uncontrolled asthma and a prior mild SARS-CoV-2 infection presented 48 hours after completing oral phenoxymethylpenicillin 1,000,000 IU daily for five days, administered for a peritonsillar abscess, with new-onset facial edema and trismus. Physical examination revealed hemodynamic stability, absence of respiratory distress, and a palpable, homolateral, tender cervical adenopathy consistent with regional lymphadenopathy. Laboratory findings demonstrated leukocytosis, thrombocytopenia, and elevated acute-phase reactants, with no significant abnormalities in other parameters. Imaging studies included a head and neck CT, which revealed a large thrombus involving both the internal and external carotid arteries, consistent with a potentially infectious or inflammatory etiology triggering vasculopathy. A chest CT scan identified bilateral pulmonary septic emboli, indicating the dissemination of infectious material via venous thromboembolism from the head and neck region. Arterial Doppler ultrasound of the neck vessels was unremarkable, and cardiac Doppler ultrasound excluded cardiac vegetations, suggesting a non-cardiac source of embolic material. Initial empiric intravenous therapy consisted of ceftriaxone 1 g every 12 hours and clindamycin 300 mg every 6 hours to cover both gram-negative and gram-positive pathogens, including potential anaerobes. Concurrent anticoagulation was initiated with enoxaparin, dosed at 60 mg subcutaneously every 12 hours, adjusted for body weight and renal function, to manage the thrombotic burden. Over the subsequent 72 hours, the patient developed a fever of 38.5 °C and further leukocytosis, prompting repeat imaging and hemocultures. Hemocultures remained negative, and pharyngeal exudate culture was obtained. Given the clinical progression and lack of microbial growth in cultures, the antibiotic regimen was escalated to piperacillin-tazobactam 4.5 g every 6 hours intravenously to enhance coverage against multidrug-resistant or extended-spectrum pathogens. The patient responded favorably to this regimen, with resolution of fever and clinical signs of infection, and by day 14, chest CT showed complete absence of pulmonary embolic lesions. At that point, oral clindamycin 300 mg every 6 hours was transitioned to continue coverage for anaerobic flora, and anticoagulation was switched to acenocumarol, adjusted to body weight, to maintain therapeutic anticoagulation levels. The patient was discharged without residual complications. The clinical course reflects a rare but serious complication of odontogenic infection—namely, infectious thrombophlebitis of the carotid arteries leading to septic pulmonary embolism—likely mediated by a systemic inflammatory response and endothelial activation due to bacterial endotoxin exposure, potentially exacerbated by underlying immunological vulnerabilities such as uncontrolled asthma and prior viral infection. The thrombotic event may represent a direct effect of bacterial toxins on vascular endothelium or a hypercoagulable state induced by acute inflammation, with subsequent embolic seeding of the pulmonary circulation. This case underscores the importance of early recognition of systemic complications in odontogenic infections, particularly in patients with comorbidities or immunological predispositions, and highlights the need for prompt initiation of broad-spectrum antibiotics and anticoagulation in the setting of suspected septic embolism.\"\n}", "generated_text": "A 27-year-old woman with a history of uncontrolled asthma and a prior mild SARS-CoV-2 infection presented 48 hours after completing oral phenoxymethylpenicillin 1,000,000 IU daily for five days, administered for a peritonsillar abscess, with new-onset facial edema and trismus. Physical examination revealed hemodynamic stability, absence of respiratory distress, and a palpable, homolateral, tender cervical adenopathy consistent with regional lymphadenopathy. Laboratory findings demonstrated leukocytosis, thrombocytopenia, and elevated acute-phase reactants, with no significant abnormalities in other parameters. Imaging studies included a head and neck CT, which revealed a large thrombus involving both the internal and external carotid arteries, consistent with a potentially infectious or inflammatory etiology triggering vasculopathy. A chest CT scan identified bilateral pulmonary septic emboli, indicating the dissemination of infectious material via venous thromboembolism from the head and neck region. Arterial Doppler ultrasound of the neck vessels was unremarkable, and cardiac Doppler ultrasound excluded cardiac vegetations, suggesting a non-cardiac source of embolic material. Initial empiric intravenous therapy consisted of ceftriaxone 1 g every 12 hours and clindamycin 300 mg every 6 hours to cover both gram-negative and gram-positive pathogens, including potential anaerobes. Concurrent anticoagulation was initiated with enoxaparin, dosed at 60 mg subcutaneously every 12 hours, adjusted for body weight and renal function, to manage the thrombotic burden. Over the subsequent 72 hours, the patient developed a fever of 38.5 °C and further leukocytosis, prompting repeat imaging and hemocultures. Hemocultures remained negative, and pharyngeal exudate culture was obtained. Given the clinical progression and lack of microbial growth in cultures, the antibiotic regimen was escalated to piperacillin-tazobactam 4.5 g every 6 hours intravenously to enhance coverage against multidrug-resistant or extended-spectrum pathogens. The patient responded favorably to this regimen, with resolution of fever and clinical signs of infection, and by day 14, chest CT showed complete absence of pulmonary embolic lesions. At that point, oral clindamycin 300 mg every 6 hours was transitioned to continue coverage for anaerobic flora, and anticoagulation was switched to acenocumarol, adjusted to body weight, to maintain therapeutic anticoagulation levels. The patient was discharged without residual complications. The clinical course reflects a rare but serious complication of odontogenic infection—namely, infectious thrombophlebitis of the carotid arteries leading to septic pulmonary embolism—likely mediated by a systemic inflammatory response and endothelial activation due to bacterial endotoxin exposure, potentially exacerbated by underlying immunological vulnerabilities such as uncontrolled asthma and prior viral infection. The thrombotic event may represent a direct effect of bacterial toxins on vascular endothelium or a hypercoagulable state induced by acute inflammation, with subsequent embolic seeding of the pulmonary circulation. This case underscores the importance of early recognition of systemic complications in odontogenic infections, particularly in patients with comorbidities or immunological predispositions, and highlights the need for prompt initiation of broad-spectrum antibiotics and anticoagulation in the setting of suspected septic embolism."}
{"row_index": 89, "doc_id": 64, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 5-year-old child swallowed a toxic substance called chlorpyrifos, which hurt his body badly. He also breathed in a mix of charcoal and palm oil, which made his lungs worse. He started with fast breathing, sweating, shaking, and couldn’t breathe properly. He fell into a deep sleep (coma) and had very weak limbs. His breathing was so bad that he needed help right away. Doctors gave him breathing support at home (like a mask), medicine to stop the poison, and drugs to help his heart and blood pressure. He also had blood changes that needed fixing — they replaced part of his blood to clean it. His body slowly got better, he woke up fully, and stopped having trouble breathing. After 10 days, he was strong enough to go home. He didn’t have any serious late problems like some other kids with this poison might. But he didn’t come back for check-ups after leaving the hospital.\"\n}", "generated_text": "A 5-year-old child swallowed a toxic substance called chlorpyrifos, which hurt his body badly. He also breathed in a mix of charcoal and palm oil, which made his lungs worse. He started with fast breathing, sweating, shaking, and couldn’t breathe properly. He fell into a deep sleep (coma) and had very weak limbs. His breathing was so bad that he needed help right away. Doctors gave him breathing support at home (like a mask), medicine to stop the poison, and drugs to help his heart and blood pressure. He also had blood changes that needed fixing — they replaced part of his blood to clean it. His body slowly got better, he woke up fully, and stopped having trouble breathing. After 10 days, he was strong enough to go home. He didn’t have any serious late problems like some other kids with this poison might. But he didn’t come back for check-ups after leaving the hospital."}
{"row_index": 90, "doc_id": 64, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 5-year-old child suffered severe poisoning from chlorpyrifos, a type of organophosphate pesticide, after swallowing it. Shortly after, the child also inhaled a mixture of charcoal and palm oil, which worsened the condition. The poisoning caused serious symptoms including fast breathing, excessive sweating, vomiting, muscle jerks, and eventually coma. At the time of arrival at the emergency department, the child had a very low level of consciousness, pinpoint pupils, weak limbs, and dangerously low oxygen levels in the blood. The heart was beating very fast, and blood pressure was low.\\n\\nThe child was diagnosed with severe organophosphate poisoning and lung damage from aspiration. Treatment included non-invasive breathing support (using bubble CPAP), intravenous atropine to help with the poisoning, antibiotics for the lung infection, and steroids to reduce inflammation. Because the family could not afford intensive care, the treatment was managed with available resources. The child received two blood exchange transfusions to help remove toxic substances from the blood.\\n\\nOver the next few days, the child’s breathing improved, consciousness returned, and symptoms slowly went away. Blood sugar levels were unstable at first but stabilized with treatment. The child was able to regain full awareness by the 39th hour and started eating regular food again. After 10 days of hospitalization, the child was discharged home, though no follow-up care was arranged afterward. The child did not develop a known complication called intermediate syndrome and responded well to treatment.\"\n}", "generated_text": "A 5-year-old child suffered severe poisoning from chlorpyrifos, a type of organophosphate pesticide, after swallowing it. Shortly after, the child also inhaled a mixture of charcoal and palm oil, which worsened the condition. The poisoning caused serious symptoms including fast breathing, excessive sweating, vomiting, muscle jerks, and eventually coma. At the time of arrival at the emergency department, the child had a very low level of consciousness, pinpoint pupils, weak limbs, and dangerously low oxygen levels in the blood. The heart was beating very fast, and blood pressure was low.\n\nThe child was diagnosed with severe organophosphate poisoning and lung damage from aspiration. Treatment included non-invasive breathing support (using bubble CPAP), intravenous atropine to help with the poisoning, antibiotics for the lung infection, and steroids to reduce inflammation. Because the family could not afford intensive care, the treatment was managed with available resources. The child received two blood exchange transfusions to help remove toxic substances from the blood.\n\nOver the next few days, the child’s breathing improved, consciousness returned, and symptoms slowly went away. Blood sugar levels were unstable at first but stabilized with treatment. The child was able to regain full awareness by the 39th hour and started eating regular food again. After 10 days of hospitalization, the child was discharged home, though no follow-up care was arranged afterward. The child did not develop a known complication called intermediate syndrome and responded well to treatment."}
{"row_index": 91, "doc_id": 64, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 5-year-old child presented to the pediatric emergency department (ED) 13 hours after ingestion of chlorpyrifos, a potent organophosphate pesticide, followed by aspiration of a charcoal-palm oil mixture. The clinical presentation included acute cholinergic crisis characterized by abnormal muscle jerks, tachypnea (respiratory rate of 48 breaths per minute with intermittent sighing), dyspnea, excessive sweating, polyuria, increased secretions, and involuntary limb movements. The patient lapsed into coma prior to arrival, with presentation parameters including a core temperature of 38.3°C, Glasgow Coma Scale (GCS) of 3, pinpoint pupils, and global hypotonia. Vital signs at presentation revealed tachycardia (pulse 180 beats per minute), normotensive blood pressure (120/80 mmHg), and hypoglycemia (random blood glucose 14 mg/dL). Physical examination noted severe respiratory distress with oxygen saturation of 88% and widespread bilateral crackles on auscultation, indicative of pulmonary edema and aspiration-related pneumonitis.\\n\\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. Given the lack of ICU resources and affordability constraints, non-invasive ventilation (NIV) was initiated using bubble continuous positive airway pressure (b-CPAP), which successfully improved oxygenation to 99–100%. Hypoglycemia was promptly corrected with a dextrose bolus, and tachycardia was managed with 20 mL/kg of normal saline. Empirical intravenous antibiotics were administered to address suspected aspiration pneumonia. Intravenous atropine was administered at a dose of 0.02 mg/kg/dose to counteract excessive parasympathetic stimulation, with the first dose leading to a significant tachycardic response, prompting discontinuation due to risk of arrhythmia. Dexamethasone and mannitol were administered for cerebral protection and intracranial pressure control, respectively.\\n\\nDue to the severity of the cholinergic crisis and ongoing respiratory compromise, the patient underwent two episodes of fresh-whole-blood exchange blood transfusion (FWB-EBT), each involving 500 mL of blood, within the first 30 hours of admission. This intervention was likely aimed at rapidly removing circulating organophosphate metabolites and potentially mitigating neuromuscular and metabolic toxicity, though the exact mechanism remains under investigation in the context of acute OPP.\\n\\nOver the course of the first 30 hours, the patient’s neurological status improved, with GCS rising from 3 to 9/15, and respiratory distress gradually resolving. By day 2, rhonchi developed, managed with nebulized salbutamol and budesonide, and the patient transitioned to nasal prong oxygen therapy with sustained saturation at 97%. A chest radiograph confirmed bilateral pulmonary infiltrates consistent with pneumonia, likely secondary to aspiration and possible secondary infection.\\n\\nConsciousness was fully restored by the 39th hour of admission. Antioxidant therapy was initiated with intravenous vitamin C and B complex, and oral vitamin E and zinc to counteract oxidative stress induced by organophosphate toxicity and inflammation. A graded dietary reintroduction was implemented over the subsequent 48 hours. The patient’s clinical course remained stable, with progressive recovery of physiological parameters. He was discharged home after 10 days of hospitalization, though subsequent follow-up was lost to contact.\\n\\nPathophysiologically, chlorpyrifos inhibits acetylcholinesterase (AChE) in synaptic and neuromuscular junctions, leading to accumulation of acetylcholine, resulting in overstimulation of muscarinic and nicotinic receptors. This manifests as the classic cholinergic symptoms (e.g., bronchorrhea, bradycardia, miosis, sweating) and neuromuscular effects (e.g., fasciculations, paralysis). In this case, the severe respiratory failure and type I paralysis (flaccid paralysis) reflect profound neuromuscular blockade due to AChE inhibition. The development of intermediate syndrome, which typically occurs 24–96 hours post-exposure with delayed neuromuscular weakness, was absent, suggesting either a rapid clinical response to treatment or a possible protective effect of early exchange transfusion. The absence of pralidoxime administration (an oxime reactivator of AChE) due to unavailability may have limited the potential for early enzyme reactivation, though the patient’s favorable outcome suggests that supportive care and timely intervention were sufficient to prevent progression to irreversible neurological damage. Serum cholinesterase levels, which are typically suppressed in OPP, were not measured due to institutional limitations, limiting direct biochemical confirmation of enzyme", "generated_text": "{\n  \"proficient_health_literacy\": \"A 5-year-old child presented to the pediatric emergency department (ED) 13 hours after ingestion of chlorpyrifos, a potent organophosphate pesticide, followed by aspiration of a charcoal-palm oil mixture. The clinical presentation included acute cholinergic crisis characterized by abnormal muscle jerks, tachypnea (respiratory rate of 48 breaths per minute with intermittent sighing), dyspnea, excessive sweating, polyuria, increased secretions, and involuntary limb movements. The patient lapsed into coma prior to arrival, with presentation parameters including a core temperature of 38.3°C, Glasgow Coma Scale (GCS) of 3, pinpoint pupils, and global hypotonia. Vital signs at presentation revealed tachycardia (pulse 180 beats per minute), normotensive blood pressure (120/80 mmHg), and hypoglycemia (random blood glucose 14 mg/dL). Physical examination noted severe respiratory distress with oxygen saturation of 88% and widespread bilateral crackles on auscultation, indicative of pulmonary edema and aspiration-related pneumonitis.\\n\\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. Given the lack of ICU resources and affordability constraints, non-invasive ventilation (NIV) was initiated using bubble continuous positive airway pressure (b-CPAP), which successfully improved oxygenation to 99–100%. Hypoglycemia was promptly corrected with a dextrose bolus, and tachycardia was managed with 20 mL/kg of normal saline. Empirical intravenous antibiotics were administered to address suspected aspiration pneumonia. Intravenous atropine was administered at a dose of 0.02 mg/kg/dose to counteract excessive parasympathetic stimulation, with the first dose leading to a significant tachycardic response, prompting discontinuation due to risk of arrhythmia. Dexamethasone and mannitol were administered for cerebral protection and intracranial pressure control, respectively.\\n\\nDue to the severity of the cholinergic crisis and ongoing respiratory compromise, the patient underwent two episodes of fresh-whole-blood exchange blood transfusion (FWB-EBT), each involving 500 mL of blood, within the first 30 hours of admission. This intervention was likely aimed at rapidly removing circulating organophosphate metabolites and potentially mitigating neuromuscular and metabolic toxicity, though the exact mechanism remains under investigation in the context of acute OPP.\\n\\nOver the course of the first 30 hours, the patient’s neurological status improved, with GCS rising from 3 to 9/15, and respiratory distress gradually resolving. By day 2, rhonchi developed, managed with nebulized salbutamol and budesonide, and the patient transitioned to nasal prong oxygen therapy with sustained saturation at 97%. A chest radiograph confirmed bilateral pulmonary infiltrates consistent with pneumonia, likely secondary to aspiration and possible secondary infection.\\n\\nConsciousness was fully restored by the 39th hour of admission. Antioxidant therapy was initiated with intravenous vitamin C and B complex, and oral vitamin E and zinc to counteract oxidative stress induced by organophosphate toxicity and inflammation. A graded dietary reintroduction was implemented over the subsequent 48 hours. The patient’s clinical course remained stable, with progressive recovery of physiological parameters. He was discharged home after 10 days of hospitalization, though subsequent follow-up was lost to contact.\\n\\nPathophysiologically, chlorpyrifos inhibits acetylcholinesterase (AChE) in synaptic and neuromuscular junctions, leading to accumulation of acetylcholine, resulting in overstimulation of muscarinic and nicotinic receptors. This manifests as the classic cholinergic symptoms (e.g., bronchorrhea, bradycardia, miosis, sweating) and neuromuscular effects (e.g., fasciculations, paralysis). In this case, the severe respiratory failure and type I paralysis (flaccid paralysis) reflect profound neuromuscular blockade due to AChE inhibition. The development of intermediate syndrome, which typically occurs 24–96 hours post-exposure with delayed neuromuscular weakness, was absent, suggesting either a rapid clinical response to treatment or a possible protective effect of early exchange transfusion. The absence of pralidoxime administration (an oxime reactivator of AChE) due to unavailability may have limited the potential for early enzyme reactivation, though the patient’s favorable outcome suggests that supportive care and timely intervention were sufficient to prevent progression to irreversible neurological damage. Serum cholinesterase levels, which are typically suppressed in OPP, were not measured due to institutional limitations, limiting direct biochemical confirmation of enzyme"}
{"row_index": 92, "doc_id": 65, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 19-year-old woman came to the hospital with a fast, irregular heartbeat and signs that her heart wasn't pumping well. Tests showed her heart was working poorly, and the doctors thought it might be because of a birth defect in her heart. They checked her heart with different scans: one ruled out a heart attack, another didn’t find heart muscle damage, and a special scan (CCTA) found that the main blood vessel to her right side of the heart was missing at the start. Instead, a small blood vessel grew around it to supply the heart. The doctors found the problem spot on a part of the heart muscle called the posteromedial papillary muscle, which was causing the fast heartbeat. They fixed it with a procedure that stops the abnormal heartbeat. Since then, she hasn’t had any symptoms and is feeling fine.\"\n}", "generated_text": "A 19-year-old woman came to the hospital with a fast, irregular heartbeat and signs that her heart wasn't pumping well. Tests showed her heart was working poorly, and the doctors thought it might be because of a birth defect in her heart. They checked her heart with different scans: one ruled out a heart attack, another didn’t find heart muscle damage, and a special scan (CCTA) found that the main blood vessel to her right side of the heart was missing at the start. Instead, a small blood vessel grew around it to supply the heart. The doctors found the problem spot on a part of the heart muscle called the posteromedial papillary muscle, which was causing the fast heartbeat. They fixed it with a procedure that stops the abnormal heartbeat. Since then, she hasn’t had any symptoms and is feeling fine."}
{"row_index": 93, "doc_id": 65, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 19-year-old woman came to the emergency department with sudden palpitations and signs of cardiogenic shock. Her electrocardiogram showed a fast heart rhythm and other abnormal patterns, and her blood tests showed elevated markers of heart stress. A 12-lead ECG ruled out a heart attack, and cardiac MRI did not show signs of heart muscle disease. Because of this, doctors performed a cardiac CT scan (CCTA) to look for a possible congenital heart problem. The scan revealed that the opening of the right coronary artery was missing, and the heart was relying on a collateral blood vessel to supply blood to that area. This is a rare congenital condition. She was referred to a specialist center for congenital heart disease. There, an electrophysiological study found that the arrhythmia was originating from the posteromedial papillary muscle, and this area was successfully treated with radiofrequency ablation. Since the procedure, she has not had any symptoms and is doing well with regular follow-up.\"\n}", "generated_text": "A 19-year-old woman came to the emergency department with sudden palpitations and signs of cardiogenic shock. Her electrocardiogram showed a fast heart rhythm and other abnormal patterns, and her blood tests showed elevated markers of heart stress. A 12-lead ECG ruled out a heart attack, and cardiac MRI did not show signs of heart muscle disease. Because of this, doctors performed a cardiac CT scan (CCTA) to look for a possible congenital heart problem. The scan revealed that the opening of the right coronary artery was missing, and the heart was relying on a collateral blood vessel to supply blood to that area. This is a rare congenital condition. She was referred to a specialist center for congenital heart disease. There, an electrophysiological study found that the arrhythmia was originating from the posteromedial papillary muscle, and this area was successfully treated with radiofrequency ablation. Since the procedure, she has not had any symptoms and is doing well with regular follow-up."}
{"row_index": 94, "doc_id": 65, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-year-old woman presented to the emergency department with acute onset of palpitations. Initial 12-lead electrocardiogram (ECG) revealed ventricular tachycardia with right branch bundle block and left posterior hemiblock, accompanied by T-wave inversion in inferior and precordial leads. Laboratory findings demonstrated elevated serum troponin (27 ng/L; normal <14 ng/L) and NT-pro BNP (2225 pg/mL; normal <130 pg/mL), indicating myocardial injury and volume overload consistent with cardiogenic shock. She was admitted to the coronary care unit.\\n\\nFive years prior, she had presented with cardiogenic shock secondary to fascicular ventricular tachycardia. Subsequent evaluation included cardiac magnetic resonance (CMR) and transesophageal electrophysiological study, both of which were inconclusive. She was diagnosed with tachycardiomiopathy and initiated standard medical therapy comprising angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and beta-blockers, with routine follow-up scheduled. Her clinical course remained stable thereafter.\\n\\nDuring the current admission, no additional episodes of hyperkinetic arrhythmias were observed. Baseline 12-lead ECG and echocardiography revealed diffuse hypokinesia of both ventricles, consistent with global systolic dysfunction. CMR remained inconclusive for underlying cardiomyopathy. Given the persistence of symptoms despite exclusion of acute myocardial infarction and structural cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed to evaluate for undiagnosed congenital coronary anomalies. The CCTA was conducted using a GE Lightspeed scanner (GE HealthCare, Chicago, USA) with retrospective gating, at 100 kVp, 696 mAs, gantry rotation time of 0.35 s, and 0.625 mm slice thickness, with intravenous administration of 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).\\n\\nDifferential diagnosis of cardiogenic shock includes myocardial infarction, arrhythmias, and various forms of cardiomyopathy. In otherwise healthy adult patients, undiagnosed congenital heart disease represents a significant and often underrecognized etiology. When acute myocardial infarction is excluded by 12-lead ECG and cardiomyopathy is not confirmed by CMR, CCTA becomes the preferred imaging modality to differentiate between obstructive coronary disease and congenital coronary anatomical variants.\\n\\nCCTA findings demonstrated a regular origin of the left main coronary artery, with a well-developed left anterior descending (LAD) artery exhibiting a wide ramus intermedium, two diagonal branches, and a thin, non-dominant left circumflex artery. No obstructive lesions were identified in any of these vessels. However, the ostium and proximal segment of the right coronary artery (RCA) were completely absent. Instead, the mid and distal RCA was supplied by a large collateral branch originating from the distal LAD, which encircles the lateral wall of the right ventricle, traverses the distal atrioventricular groove, and gives rise to thin posterior interventricular and posterolateral arteries. Additionally, a fine branch arising from the mid-LAD was observed to supply the sinoatrial node, potentially contributing to autonomic instability.\\n\\nBased on these findings, the patient underwent stress echocardiography, which confirmed inducible myocardial ischemia in the inferior wall—consistent with the anatomical location of the arrhythmic focus. She was subsequently transferred to a specialized center for congenital cardiovascular disease. There, she underwent transcatheter radiofrequency ablation targeting the sustained ventricular tachycardia originating from the posteromedial papillary muscle. Post-procedural follow-up revealed complete suppression of arrhythmias. At 6-month follow-up, she remains asymptomatic with no recurrence of ventricular tachycardia. Medical therapy post-ablation includes acetylsalicylic acid and verapamil for antiplatelet and rate control, respectively. The case underscores the importance of advanced imaging in diagnosing rare congenital coronary anomalies that may present with phenotypes mimicking acquired cardiomyopathy or acute coronary syndromes, particularly in young patients with recurrent arrhythmias and elevated biomarkers despite negative acute infarction workup.\"\n}", "generated_text": "A 19-year-old woman presented to the emergency department with acute onset of palpitations. Initial 12-lead electrocardiogram (ECG) revealed ventricular tachycardia with right branch bundle block and left posterior hemiblock, accompanied by T-wave inversion in inferior and precordial leads. Laboratory findings demonstrated elevated serum troponin (27 ng/L; normal <14 ng/L) and NT-pro BNP (2225 pg/mL; normal <130 pg/mL), indicating myocardial injury and volume overload consistent with cardiogenic shock. She was admitted to the coronary care unit.\n\nFive years prior, she had presented with cardiogenic shock secondary to fascicular ventricular tachycardia. Subsequent evaluation included cardiac magnetic resonance (CMR) and transesophageal electrophysiological study, both of which were inconclusive. She was diagnosed with tachycardiomiopathy and initiated standard medical therapy comprising angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and beta-blockers, with routine follow-up scheduled. Her clinical course remained stable thereafter.\n\nDuring the current admission, no additional episodes of hyperkinetic arrhythmias were observed. Baseline 12-lead ECG and echocardiography revealed diffuse hypokinesia of both ventricles, consistent with global systolic dysfunction. CMR remained inconclusive for underlying cardiomyopathy. Given the persistence of symptoms despite exclusion of acute myocardial infarction and structural cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed to evaluate for undiagnosed congenital coronary anomalies. The CCTA was conducted using a GE Lightspeed scanner (GE HealthCare, Chicago, USA) with retrospective gating, at 100 kVp, 696 mAs, gantry rotation time of 0.35 s, and 0.625 mm slice thickness, with intravenous administration of 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).\n\nDifferential diagnosis of cardiogenic shock includes myocardial infarction, arrhythmias, and various forms of cardiomyopathy. In otherwise healthy adult patients, undiagnosed congenital heart disease represents a significant and often underrecognized etiology. When acute myocardial infarction is excluded by 12-lead ECG and cardiomyopathy is not confirmed by CMR, CCTA becomes the preferred imaging modality to differentiate between obstructive coronary disease and congenital coronary anatomical variants.\n\nCCTA findings demonstrated a regular origin of the left main coronary artery, with a well-developed left anterior descending (LAD) artery exhibiting a wide ramus intermedium, two diagonal branches, and a thin, non-dominant left circumflex artery. No obstructive lesions were identified in any of these vessels. However, the ostium and proximal segment of the right coronary artery (RCA) were completely absent. Instead, the mid and distal RCA was supplied by a large collateral branch originating from the distal LAD, which encircles the lateral wall of the right ventricle, traverses the distal atrioventricular groove, and gives rise to thin posterior interventricular and posterolateral arteries. Additionally, a fine branch arising from the mid-LAD was observed to supply the sinoatrial node, potentially contributing to autonomic instability.\n\nBased on these findings, the patient underwent stress echocardiography, which confirmed inducible myocardial ischemia in the inferior wall—consistent with the anatomical location of the arrhythmic focus. She was subsequently transferred to a specialized center for congenital cardiovascular disease. There, she underwent transcatheter radiofrequency ablation targeting the sustained ventricular tachycardia originating from the posteromedial papillary muscle. Post-procedural follow-up revealed complete suppression of arrhythmias. At 6-month follow-up, she remains asymptomatic with no recurrence of ventricular tachycardia. Medical therapy post-ablation includes acetylsalicylic acid and verapamil for antiplatelet and rate control, respectively. The case underscores the importance of advanced imaging in diagnosing rare congenital coronary anomalies that may present with phenotypes mimicking acquired cardiomyopathy or acute coronary syndromes, particularly in young patients with recurrent arrhythmias and elevated biomarkers despite negative acute infarction workup."}
{"row_index": 95, "doc_id": 66, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 17-year-old boy was found to have a small metal button stuck in his nose during a dental check-up. He had no symptoms like nose blockage, bleeding, or pain. The button had been there for over 10 years, probably since he was 7 years old when he put it in. It was hidden in the bottom part of his nose, covered with mucus and dirt, and looked shiny — that’s how doctors knew it was metal. X-rays showed the button clearly, and doctors confirmed it was safe and not hurting any bones or sinuses. The family had ignored earlier advice to remove it, thinking it would fall out on its own. The button was safely taken out in the clinic with local numbing spray and a small tool, with no serious bleeding. After removal, the nose healed well, and the boy is now doing fine with regular nose rinses.\"\n}", "generated_text": "A 17-year-old boy was found to have a small metal button stuck in his nose during a dental check-up. He had no symptoms like nose blockage, bleeding, or pain. The button had been there for over 10 years, probably since he was 7 years old when he put it in. It was hidden in the bottom part of his nose, covered with mucus and dirt, and looked shiny — that’s how doctors knew it was metal. X-rays showed the button clearly, and doctors confirmed it was safe and not hurting any bones or sinuses. The family had ignored earlier advice to remove it, thinking it would fall out on its own. The button was safely taken out in the clinic with local numbing spray and a small tool, with no serious bleeding. After removal, the nose healed well, and the boy is now doing fine with regular nose rinses."}
{"row_index": 96, "doc_id": 67, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"An 18-year-old Hispanic male with no significant past medical history presented to the emergency department (ED) with acute onset of substernal, non-radiating chest pain, orthopnoea, dry non-productive cough, and subjective fevers lasting 3–4 days. Family history is notable for paternal grandfather with non-ischaemic cardiomyopathy and pacemaker implantation at age 86. The patient lives with both parents, denies smoking, alcohol use, recreational drug use, or abuse. He works at an auto parts shop and plans to begin college. Initial workup revealed elevated serum troponin I, diffuse ST-segment elevation on electrocardiogram (ECG), and an enlarged cardiac silhouette with mild pulmonary oedema on chest X-ray. Transthoracic echocardiography (TTE) demonstrated a left ventricular ejection fraction (LVEF) of 40%, severe left ventricular (LV) concentric hypertrophy (septal thickness 1.9 cm, inferolateral wall 2.2 cm), and mild posterior pericardial effusion. Coxsackie virus A and B titres were elevated, prompting initial consideration of viral myopericarditis. Symptoms initially improved with ibuprofen and colchicine, and cardiac catheterization confirmed absence of coronary artery disease. Repeat TTE showed LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral walls, and elevated LV end-diastolic pressure consistent with diastolic dysfunction. Chest CT angiogram revealed pneumonitis and pericardial effusion, supporting a diagnosis of Coxsackie virus-induced myopericarditis. On day 4 of admission, the patient developed diaphoresis, tachycardia, and hypotension with undetectable blood pressure. Repeat TTE revealed large pericardial effusion with signs of impending cardiac tamponade, necessitating emergent pericardiocentesis. During the procedure, the patient experienced pulseless electrical activity (PEA) cardiac arrest, requiring 30 minutes of advanced cardiovascular life support. He was intubated, placed on veno-arterial extracorporeal membrane oxygenation (VA ECMO), and initiated vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min). Significant bleeding from ECMO cannulae necessitated multiple transfusions (9 packed red blood cells, 10 platelets, 10 cryoprecipitate, 4 fresh frozen plasma). The patient was transferred to a tertiary center for endomyocardial biopsy (EMB) due to concern for fulminant myocarditis or infiltrative cardiomyopathy. EMB showed no evidence of inflammatory or infiltrative process. Repeat Coxsackie serology confirmed positivity for Coxsackie A9, B2, and B6, and quantitative PCR for Epstein-Barr virus (EBV) DNA was elevated at 133,000 IU/mL. A subsequent TTE revealed a severely reduced LVEF of 10%–15% with persistent severe concentric LV hypertrophy. Intravenous immunoglobulin (IVIG) was initiated for suspected Coxsackie myocarditis, broad-spectrum antibiotics were administered for worsening leucocytosis without identifiable focus, and colchicine was discontinued due to concern for rhabdomyolysis (serum creatine kinase elevated to 2874 U/L). Vasopressors were discontinued and the patient was extubated. He subsequently developed flushing, fever, dyspnoea, and hypoxaemia with chest X-ray showing congested lung parenchyma suggestive of acute respiratory distress syndrome (ARDS), leading to IVIG discontinuation. Despite initial decompensation, cardiac function improved with a subsequent TTE showing LVEF of 25%–30%, prompting consideration of ECMO removal—this was unsuccessful. The patient remained on VA ECMO and was evaluated for left ventricular assist device (LVAD) placement, which was deemed contraindicated due to extensive global concentric LV hypertrophy. A multidisciplinary team concluded that emergency listing for heart transplantation was appropriate, with consideration of transition to intra-aortic balloon pump and inotrope support. During evaluation for transplantation, an incisional biopsy of a 1×1 inch, painless, rubbery, mobile lesion in the right upper extremity was performed. Pathology revealed aggressive EBV-positive natural killer/T-cell lymphoma (ENKTCL) with cytotoxic immunophenotype (positive for CD2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1, and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybrid", "generated_text": "{\n  \"proficient_health_literacy\": \"An 18-year-old Hispanic male with no significant past medical history presented to the emergency department (ED) with acute onset of substernal, non-radiating chest pain, orthopnoea, dry non-productive cough, and subjective fevers lasting 3–4 days. Family history is notable for paternal grandfather with non-ischaemic cardiomyopathy and pacemaker implantation at age 86. The patient lives with both parents, denies smoking, alcohol use, recreational drug use, or abuse. He works at an auto parts shop and plans to begin college. Initial workup revealed elevated serum troponin I, diffuse ST-segment elevation on electrocardiogram (ECG), and an enlarged cardiac silhouette with mild pulmonary oedema on chest X-ray. Transthoracic echocardiography (TTE) demonstrated a left ventricular ejection fraction (LVEF) of 40%, severe left ventricular (LV) concentric hypertrophy (septal thickness 1.9 cm, inferolateral wall 2.2 cm), and mild posterior pericardial effusion. Coxsackie virus A and B titres were elevated, prompting initial consideration of viral myopericarditis. Symptoms initially improved with ibuprofen and colchicine, and cardiac catheterization confirmed absence of coronary artery disease. Repeat TTE showed LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral walls, and elevated LV end-diastolic pressure consistent with diastolic dysfunction. Chest CT angiogram revealed pneumonitis and pericardial effusion, supporting a diagnosis of Coxsackie virus-induced myopericarditis. On day 4 of admission, the patient developed diaphoresis, tachycardia, and hypotension with undetectable blood pressure. Repeat TTE revealed large pericardial effusion with signs of impending cardiac tamponade, necessitating emergent pericardiocentesis. During the procedure, the patient experienced pulseless electrical activity (PEA) cardiac arrest, requiring 30 minutes of advanced cardiovascular life support. He was intubated, placed on veno-arterial extracorporeal membrane oxygenation (VA ECMO), and initiated vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min). Significant bleeding from ECMO cannulae necessitated multiple transfusions (9 packed red blood cells, 10 platelets, 10 cryoprecipitate, 4 fresh frozen plasma). The patient was transferred to a tertiary center for endomyocardial biopsy (EMB) due to concern for fulminant myocarditis or infiltrative cardiomyopathy. EMB showed no evidence of inflammatory or infiltrative process. Repeat Coxsackie serology confirmed positivity for Coxsackie A9, B2, and B6, and quantitative PCR for Epstein-Barr virus (EBV) DNA was elevated at 133,000 IU/mL. A subsequent TTE revealed a severely reduced LVEF of 10%–15% with persistent severe concentric LV hypertrophy. Intravenous immunoglobulin (IVIG) was initiated for suspected Coxsackie myocarditis, broad-spectrum antibiotics were administered for worsening leucocytosis without identifiable focus, and colchicine was discontinued due to concern for rhabdomyolysis (serum creatine kinase elevated to 2874 U/L). Vasopressors were discontinued and the patient was extubated. He subsequently developed flushing, fever, dyspnoea, and hypoxaemia with chest X-ray showing congested lung parenchyma suggestive of acute respiratory distress syndrome (ARDS), leading to IVIG discontinuation. Despite initial decompensation, cardiac function improved with a subsequent TTE showing LVEF of 25%–30%, prompting consideration of ECMO removal—this was unsuccessful. The patient remained on VA ECMO and was evaluated for left ventricular assist device (LVAD) placement, which was deemed contraindicated due to extensive global concentric LV hypertrophy. A multidisciplinary team concluded that emergency listing for heart transplantation was appropriate, with consideration of transition to intra-aortic balloon pump and inotrope support. During evaluation for transplantation, an incisional biopsy of a 1×1 inch, painless, rubbery, mobile lesion in the right upper extremity was performed. Pathology revealed aggressive EBV-positive natural killer/T-cell lymphoma (ENKTCL) with cytotoxic immunophenotype (positive for CD2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1, and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybrid"}
{"row_index": 97, "doc_id": 68, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 50-year-old man who smoked a lot and had bad cholesterol levels for years got a serious problem in one eye. The eye swelled fast, caused constant double vision (diplopia), and the eye movement got very weak. Even though his thyroid was normal, the eye tissue in one muscle (the right inferior rectus) turned hard and stiff, like fibrous tissue. This made the double vision worse and stayed bad even after steroid shots. The doctor tried medicine first, then surgery to open up the eye socket, which helped a little. The biopsy showed the muscle was completely filled with scar tissue. This case is rare and shows how serious eye problems can be in people with no thyroid issues.\"\n}", "generated_text": "A 50-year-old man who smoked a lot and had bad cholesterol levels for years got a serious problem in one eye. The eye swelled fast, caused constant double vision (diplopia), and the eye movement got very weak. Even though his thyroid was normal, the eye tissue in one muscle (the right inferior rectus) turned hard and stiff, like fibrous tissue. This made the double vision worse and stayed bad even after steroid shots. The doctor tried medicine first, then surgery to open up the eye socket, which helped a little. The biopsy showed the muscle was completely filled with scar tissue. This case is rare and shows how serious eye problems can be in people with no thyroid issues."}
{"row_index": 98, "doc_id": 68, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 50-year-old man with a long history of smoking and high cholesterol developed a rare eye condition called euthyroid single muscular Graves' ophthalmopathy. He had no family or personal history of thyroid disease. Over several months, his right eye swelled rapidly, causing severe pain and constant double vision (diplopia) that made daily activities difficult. His vision was normal, but he could no longer move his eye properly, especially upward, which worsened his quality of life. Tests showed mild signs of thyroid autoimmunity, but his thyroid function was normal. Inflammation in the eye area was moderate, and imaging showed significant swelling only in the right inferior rectus muscle, while other eye muscles were unaffected. A biopsy confirmed massive fibrosis (scarring) in that muscle. Initial treatment with high-dose steroid injections helped reduce inflammation but did not improve double vision or eye movement. Two surgeries to relieve pressure in the eye socket were needed. The scarring in the muscle was the main reason the symptoms didn’t improve. This case highlights a rare form of eye disease that can cause serious vision problems even when the thyroid is healthy.\"\n}", "generated_text": "A 50-year-old man with a long history of smoking and high cholesterol developed a rare eye condition called euthyroid single muscular Graves' ophthalmopathy. He had no family or personal history of thyroid disease. Over several months, his right eye swelled rapidly, causing severe pain and constant double vision (diplopia) that made daily activities difficult. His vision was normal, but he could no longer move his eye properly, especially upward, which worsened his quality of life. Tests showed mild signs of thyroid autoimmunity, but his thyroid function was normal. Inflammation in the eye area was moderate, and imaging showed significant swelling only in the right inferior rectus muscle, while other eye muscles were unaffected. A biopsy confirmed massive fibrosis (scarring) in that muscle. Initial treatment with high-dose steroid injections helped reduce inflammation but did not improve double vision or eye movement. Two surgeries to relieve pressure in the eye socket were needed. The scarring in the muscle was the main reason the symptoms didn’t improve. This case highlights a rare form of eye disease that can cause serious vision problems even when the thyroid is healthy."}
{"row_index": 99, "doc_id": 68, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a rare case of euthyroid unilateral Graves' ophthalmopathy (GO) characterized by early and massive mono-muscular fibrosis involving the right inferior rectus muscle in a 50-year-old male patient. The patient has a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no personal or familial history of thyroid autoimmune disorders. He is a long-term smoker (20 cigarettes/day since age 30) and has had chronic dyslipidemia for several years, with laboratory findings showing total cholesterol of 220 mg/dL, triglycerides of 297 mg/dL, and low high-density lipoprotein cholesterol (HDL) of 38 mg/dL—indicating a pro-atherogenic lipid profile. Since June 2020, the patient developed rapid and progressive soft tissue swelling in the right orbit, moderate pain during ocular movements, eyelid redness, and persistent diplopia. Visual acuity remained normal (16/17 and 17/17 in right and left eyes, respectively), and color vision was preserved. Ocular motility evaluation revealed severe depression of elevation and persistent primary position depression of the right globe, as quantified by the Gorman score, with constant diplopia. Clinical Activity Score (CAS) was 3/7, indicating moderate active inflammation, and Hertel measurements were 24 mm (right) and 18 mm (left), with a right orbital muscle orbit area ratio of 0.25 (in-house Autocad-based method; normal threshold vn ≤ 0.20±0.03), confirming significant enlargement of the inferior rectus muscle. CT imaging (1.25 mm contiguous slices, 200 mA, 120 kV, pitch 0.5) demonstrated marked expansion of the lower rectus body to the level of its tendon insertion, while all other extraocular muscles in both orbits exhibited normal morphology. Thyroid function tests were within normal limits, with only a slight elevation in thyroid-stimulating hormone receptor antibody (TSH-R-Ab) levels at 1.75 mU/L (normal <1.5 mU/L), consistent with subclinical autoimmune thyroid stimulation. Thyroid ultrasound revealed a thyroiditis-like pattern, suggestive of non-autoimmune thyroid inflammation. Electrophysiological assessment showed a slight reduction in the amplitude of the p100 wave in the right eye, indicating early neuro-ocular dysfunction. Routine systemic laboratory evaluations were unremarkable, excluding hematological or systemic diseases. Initial treatment with intravenous corticosteroid pulse therapy (Solumedrol, 4500 mg cumulative dose over 12 weeks) resulted in resolution of inflammatory signs and symptoms, but failed to improve ocular motility, Hertel measurements, or quality of life as measured by the Graves’ Ophthalmopathy Quality of Life Questionnaire (GO-QOL), where functional subscale scores (12.5) remained significantly lower than appearance subscale (50), despite normal visual acuity. Notably, electrophysiological parameters and visual function deteriorated during this period. As a result, second-line therapy with two-wall orbital surgical decompression combined with continued parenteral glucocorticoids was initiated. Histopathological examination of the right inferior rectus muscle biopsy revealed extensive fibrosis with significant adipose tissue infiltration, confirming the presence of early, severe, and isolated mono-muscular fibrotic change. This case highlights the potential for rapid progression of unilateral, euthyroid GO with prominent fibrotic transformation, even in the absence of significant thyroid autoimmunity, and underscores the importance of early surgical intervention in patients with persistent diplopia and progressive muscle enlargement despite medical therapy. The observed fibrosis may reflect a dysregulated fibroproliferative response to chronic inflammation, possibly driven by local cytokine milieu and metabolic factors such as dyslipidemia and smoking-related oxidative stress, which are known contributors to extracellular matrix remodeling in orbital tissues.\"\n}", "generated_text": "We present a rare case of euthyroid unilateral Graves' ophthalmopathy (GO) characterized by early and massive mono-muscular fibrosis involving the right inferior rectus muscle in a 50-year-old male patient. The patient has a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no personal or familial history of thyroid autoimmune disorders. He is a long-term smoker (20 cigarettes/day since age 30) and has had chronic dyslipidemia for several years, with laboratory findings showing total cholesterol of 220 mg/dL, triglycerides of 297 mg/dL, and low high-density lipoprotein cholesterol (HDL) of 38 mg/dL—indicating a pro-atherogenic lipid profile. Since June 2020, the patient developed rapid and progressive soft tissue swelling in the right orbit, moderate pain during ocular movements, eyelid redness, and persistent diplopia. Visual acuity remained normal (16/17 and 17/17 in right and left eyes, respectively), and color vision was preserved. Ocular motility evaluation revealed severe depression of elevation and persistent primary position depression of the right globe, as quantified by the Gorman score, with constant diplopia. Clinical Activity Score (CAS) was 3/7, indicating moderate active inflammation, and Hertel measurements were 24 mm (right) and 18 mm (left), with a right orbital muscle orbit area ratio of 0.25 (in-house Autocad-based method; normal threshold vn ≤ 0.20±0.03), confirming significant enlargement of the inferior rectus muscle. CT imaging (1.25 mm contiguous slices, 200 mA, 120 kV, pitch 0.5) demonstrated marked expansion of the lower rectus body to the level of its tendon insertion, while all other extraocular muscles in both orbits exhibited normal morphology. Thyroid function tests were within normal limits, with only a slight elevation in thyroid-stimulating hormone receptor antibody (TSH-R-Ab) levels at 1.75 mU/L (normal <1.5 mU/L), consistent with subclinical autoimmune thyroid stimulation. Thyroid ultrasound revealed a thyroiditis-like pattern, suggestive of non-autoimmune thyroid inflammation. Electrophysiological assessment showed a slight reduction in the amplitude of the p100 wave in the right eye, indicating early neuro-ocular dysfunction. Routine systemic laboratory evaluations were unremarkable, excluding hematological or systemic diseases. Initial treatment with intravenous corticosteroid pulse therapy (Solumedrol, 4500 mg cumulative dose over 12 weeks) resulted in resolution of inflammatory signs and symptoms, but failed to improve ocular motility, Hertel measurements, or quality of life as measured by the Graves’ Ophthalmopathy Quality of Life Questionnaire (GO-QOL), where functional subscale scores (12.5) remained significantly lower than appearance subscale (50), despite normal visual acuity. Notably, electrophysiological parameters and visual function deteriorated during this period. As a result, second-line therapy with two-wall orbital surgical decompression combined with continued parenteral glucocorticoids was initiated. Histopathological examination of the right inferior rectus muscle biopsy revealed extensive fibrosis with significant adipose tissue infiltration, confirming the presence of early, severe, and isolated mono-muscular fibrotic change. This case highlights the potential for rapid progression of unilateral, euthyroid GO with prominent fibrotic transformation, even in the absence of significant thyroid autoimmunity, and underscores the importance of early surgical intervention in patients with persistent diplopia and progressive muscle enlargement despite medical therapy. The observed fibrosis may reflect a dysregulated fibroproliferative response to chronic inflammation, possibly driven by local cytokine milieu and metabolic factors such as dyslipidemia and smoking-related oxidative stress, which are known contributors to extracellular matrix remodeling in orbital tissues."}
{"row_index": 100, "doc_id": 69, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 15-year-old boy had stomach pain and vomiting for four days. Doctors first thought it was a stomach bug, but it didn’t go away. His belly was swollen, and tests showed his intestines were blocked. A scan found a piece of intestine stuck in a small opening in his belly, called the Winslow hiatus. This caused the blockage. The doctors tried a small surgery first, but couldn’t see clearly, so they did a bigger cut in the middle of his belly to fix it. They pulled the stuck piece of intestine back into place and found it was just a small part of the small intestine that had slipped through the opening. No part of the intestine had to be cut off. They didn’t do any extra steps to prevent it from happening again. After surgery, he had a small pocket of fluid in his pelvis, which was treated with medicine and didn’t get worse. He’s now recovering at the pediatric surgery clinic and doing well.\"\n}", "generated_text": "A 15-year-old boy had stomach pain and vomiting for four days. Doctors first thought it was a stomach bug, but it didn’t go away. His belly was swollen, and tests showed his intestines were blocked. A scan found a piece of intestine stuck in a small opening in his belly, called the Winslow hiatus. This caused the blockage. The doctors tried a small surgery first, but couldn’t see clearly, so they did a bigger cut in the middle of his belly to fix it. They pulled the stuck piece of intestine back into place and found it was just a small part of the small intestine that had slipped through the opening. No part of the intestine had to be cut off. They didn’t do any extra steps to prevent it from happening again. After surgery, he had a small pocket of fluid in his pelvis, which was treated with medicine and didn’t get worse. He’s now recovering at the pediatric surgery clinic and doing well."}
{"row_index": 101, "doc_id": 69, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 15-year-old boy with no prior medical issues came in with vomiting and abdominal pain that had lasted four days. At first, doctors thought it was gastroenteritis, but the symptoms didn’t go away. He was admitted to the hospital after tests showed signs of intestinal obstruction.\\n\\nAn abdominal CT scan found that a loop of small intestine had gotten stuck at the Winslow hiatus — a key opening in the abdomen — causing a blockage. The doctors tried to fix it with laparoscopy (a minimally invasive surgery), but poor visibility made it difficult. They switched to a larger open surgery (supraumbilical midline laparotomy) to safely see and treat the problem.\\n\\nDuring the surgery, they found a section of the ileum (part of the small intestine) that had herniated through the Winslow hiatus. The loop was about 5 centimeters long and was causing the blockage. The area around the opening looked normal, so no extra steps were taken to prevent it from coming back.\\n\\nAfter surgery, the boy had a temporary stop in bowel movement (paralytic ileus), which resolved after five days. He started eating again and did well. He also developed a small fluid collection in his pelvis, which was treated with antibiotics and improved over time. He was discharged ten days after surgery and is now being followed up in outpatient paediatric surgery. No further surgery is planned to prevent recurrence.\"\n}", "generated_text": "A 15-year-old boy with no prior medical issues came in with vomiting and abdominal pain that had lasted four days. At first, doctors thought it was gastroenteritis, but the symptoms didn’t go away. He was admitted to the hospital after tests showed signs of intestinal obstruction.\n\nAn abdominal CT scan found that a loop of small intestine had gotten stuck at the Winslow hiatus — a key opening in the abdomen — causing a blockage. The doctors tried to fix it with laparoscopy (a minimally invasive surgery), but poor visibility made it difficult. They switched to a larger open surgery (supraumbilical midline laparotomy) to safely see and treat the problem.\n\nDuring the surgery, they found a section of the ileum (part of the small intestine) that had herniated through the Winslow hiatus. The loop was about 5 centimeters long and was causing the blockage. The area around the opening looked normal, so no extra steps were taken to prevent it from coming back.\n\nAfter surgery, the boy had a temporary stop in bowel movement (paralytic ileus), which resolved after five days. He started eating again and did well. He also developed a small fluid collection in his pelvis, which was treated with antibiotics and improved over time. He was discharged ten days after surgery and is now being followed up in outpatient paediatric surgery. No further surgery is planned to prevent recurrence."}
{"row_index": 102, "doc_id": 69, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a clinical case of a 15-year-old male with no prior medical history or surgical interventions, who presented to the paediatric emergency department with a four-day history of vomiting and epigastric abdominal pain, remaining afebrile throughout. Initial evaluation was consistent with gastroenteritis, but symptoms persisted, including biliary vomiting and ongoing epigastric discomfort, prompting admission for further investigation.\\n\\nPhysical examination revealed an otherwise stable general condition, afebrile status, and mild signs of dehydration. The abdomen was distended, with absent peritoneal signs and diminished bowel sounds. Laboratory findings were non-contributory. Abdominal radiography demonstrated features consistent with small bowel obstruction.\\n\\nUrgent computed tomography (CT) was performed, revealing ascites and significant dilatation of small intestinal loops, with a focal change in caliber at the level of the Winslow hiatus, indicating interposition of a small intestinal loop within the trans-cavity of the epiploic foramen. The CT findings suggested a mechanical obstruction due to internal herniation of a segment of the ileum.\\n\\nSurgical management began with exploratory laparoscopy. Intraoperatively, dilated loops of the small intestine, including the terminal ileum, cecum, and ascending colon, were observed in the right hypochondrium. The cecum was noted to be highly mobile without adhesions to the right parietocolic space. Proximal to the terminal ileum, small intestinal loops were identified in the region corresponding to the theoretical location of the Winslow hiatus. Attempts to mobilize the cecum and terminal ileum toward the right iliac fossa were unsuccessful due to obstruction by the lower edge of the liver and the distended bowel loops. Percutaneous puncture of a dilated loop to decompress gas was attempted but did not improve visualization or facilitate reduction.\\n\\nDue to poor visualization and failure to identify the precise site of caliber change, a conversion to supraumbilical midline laparotomy was performed. In the open laparotomy, a clear change in intestinal caliber was observed approximately 40 cm distal to the ileocecal valve, confirming a herniation of a 5-cm segment of ileum through the Winslow hiatus. The herniated loop exhibited characteristic congestive imprints at both ends, consistent with compression and ischemic changes due to entrapment. The normal anatomical caliber of the Winslow hiatus was confirmed, and no preventive surgical technique (e.g., hernia repair or reinforcement) was performed to reduce the risk of recurrence.\\n\\nPostoperatively, the patient developed a paralytic ileus, which resolved over five days, allowing for nasogastric tube removal and initiation of oral intake with good tolerance. Concurrently, a pelvic collection was identified and managed conservatively with antibiotic therapy, with favorable clinical evolution. The patient was discharged ten days after surgery with preserved bowel transit, absence of fever, and stable general condition. He is currently under outpatient follow-up in the paediatric surgery clinic.\\n\\nThis case highlights the diagnostic challenge of internal hernias in adolescents, particularly those involving the Winslow hiatus, which may present with nonspecific gastrointestinal symptoms and mimic other conditions such as gastroenteritis or acute appendicitis. The anatomical complexity of the trans-cavity epiploic foramen, combined with the distension and mobility of bowel loops, contributes to the difficulty in both preoperative diagnosis and intraoperative identification. Internal hernias are often missed on routine imaging and require high index of suspicion, especially in young patients with prolonged abdominal pain and obstructive features. The lack of preventive intervention in this case underscores the potential for recurrence, although the absence of recurrence in the current follow-up suggests a favorable outcome in the absence of anatomical reinforcement.\"\n}", "generated_text": "We present a clinical case of a 15-year-old male with no prior medical history or surgical interventions, who presented to the paediatric emergency department with a four-day history of vomiting and epigastric abdominal pain, remaining afebrile throughout. Initial evaluation was consistent with gastroenteritis, but symptoms persisted, including biliary vomiting and ongoing epigastric discomfort, prompting admission for further investigation.\n\nPhysical examination revealed an otherwise stable general condition, afebrile status, and mild signs of dehydration. The abdomen was distended, with absent peritoneal signs and diminished bowel sounds. Laboratory findings were non-contributory. Abdominal radiography demonstrated features consistent with small bowel obstruction.\n\nUrgent computed tomography (CT) was performed, revealing ascites and significant dilatation of small intestinal loops, with a focal change in caliber at the level of the Winslow hiatus, indicating interposition of a small intestinal loop within the trans-cavity of the epiploic foramen. The CT findings suggested a mechanical obstruction due to internal herniation of a segment of the ileum.\n\nSurgical management began with exploratory laparoscopy. Intraoperatively, dilated loops of the small intestine, including the terminal ileum, cecum, and ascending colon, were observed in the right hypochondrium. The cecum was noted to be highly mobile without adhesions to the right parietocolic space. Proximal to the terminal ileum, small intestinal loops were identified in the region corresponding to the theoretical location of the Winslow hiatus. Attempts to mobilize the cecum and terminal ileum toward the right iliac fossa were unsuccessful due to obstruction by the lower edge of the liver and the distended bowel loops. Percutaneous puncture of a dilated loop to decompress gas was attempted but did not improve visualization or facilitate reduction.\n\nDue to poor visualization and failure to identify the precise site of caliber change, a conversion to supraumbilical midline laparotomy was performed. In the open laparotomy, a clear change in intestinal caliber was observed approximately 40 cm distal to the ileocecal valve, confirming a herniation of a 5-cm segment of ileum through the Winslow hiatus. The herniated loop exhibited characteristic congestive imprints at both ends, consistent with compression and ischemic changes due to entrapment. The normal anatomical caliber of the Winslow hiatus was confirmed, and no preventive surgical technique (e.g., hernia repair or reinforcement) was performed to reduce the risk of recurrence.\n\nPostoperatively, the patient developed a paralytic ileus, which resolved over five days, allowing for nasogastric tube removal and initiation of oral intake with good tolerance. Concurrently, a pelvic collection was identified and managed conservatively with antibiotic therapy, with favorable clinical evolution. The patient was discharged ten days after surgery with preserved bowel transit, absence of fever, and stable general condition. He is currently under outpatient follow-up in the paediatric surgery clinic.\n\nThis case highlights the diagnostic challenge of internal hernias in adolescents, particularly those involving the Winslow hiatus, which may present with nonspecific gastrointestinal symptoms and mimic other conditions such as gastroenteritis or acute appendicitis. The anatomical complexity of the trans-cavity epiploic foramen, combined with the distension and mobility of bowel loops, contributes to the difficulty in both preoperative diagnosis and intraoperative identification. Internal hernias are often missed on routine imaging and require high index of suspicion, especially in young patients with prolonged abdominal pain and obstructive features. The lack of preventive intervention in this case underscores the potential for recurrence, although the absence of recurrence in the current follow-up suggests a favorable outcome in the absence of anatomical reinforcement."}
{"row_index": 103, "doc_id": 70, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 75-year-old woman from Western Ethiopia had a small birth control device (IUD) put in her uterus 40 years ago. Since then, she never checked it or saw a doctor. Now, she has pain in her lower belly and vagina, which started 3 years ago and got worse. The doctor found the old IUD still inside, near the opening of her cervix. It was easy to pull out using simple tools. She was given pain medicine and doxycycline to help her feel better and get rid of any infection. She went home after being watched for 4 hours and her pain went away.\"\n}", "generated_text": "A 75-year-old woman from Western Ethiopia had a small birth control device (IUD) put in her uterus 40 years ago. Since then, she never checked it or saw a doctor. Now, she has pain in her lower belly and vagina, which started 3 years ago and got worse. The doctor found the old IUD still inside, near the opening of her cervix. It was easy to pull out using simple tools. She was given pain medicine and doxycycline to help her feel better and get rid of any infection. She went home after being watched for 4 hours and her pain went away."}
{"row_index": 104, "doc_id": 70, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 75-year-old woman from Western Ethiopia, who had her last period 25 years ago, came to the hospital with ongoing lower abdominal pain and discomfort in her vagina. She had been using an intrauterine device (IUD), specifically a Lippes loop, since she was 18 years old — meaning it had been in place for 40 years. She had never had a gynecological checkup since then and didn’t know it was still inside her. During a pelvic exam, doctors found part of the IUD at the opening of her cervix. It was easily removed using special forceps. The patient was given pain relief and doxycycline for 3 days to prevent infection. She was discharged after being observed for 4 hours and her pain went away after treatment.\"\n}", "generated_text": "A 75-year-old woman from Western Ethiopia, who had her last period 25 years ago, came to the hospital with ongoing lower abdominal pain and discomfort in her vagina. She had been using an intrauterine device (IUD), specifically a Lippes loop, since she was 18 years old — meaning it had been in place for 40 years. She had never had a gynecological checkup since then and didn’t know it was still inside her. During a pelvic exam, doctors found part of the IUD at the opening of her cervix. It was easily removed using special forceps. The patient was given pain relief and doxycycline for 3 days to prevent infection. She was discharged after being observed for 4 hours and her pain went away after treatment."}
{"row_index": 105, "doc_id": 71, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 71-year-old man had a long-time skin condition called vitiligo and started losing vision in his right eye six months before hospital visit. He also lost hearing in both ears, worse on the right side. He had bad headaches, fever, and lost weight without trying. When doctors checked his eyes, the right eye was very sensitive to light and had redness, while the left eye could only see blurry shapes. The right eye’s back part had dark spots and the optic nerve was damaged (atrophied), and the left eye had swelling around the nerve and early nerve damage (optic neuritis). Doctors checked for infections and diseases like TB, herpes, or autoimmune problems, but none were found. A spinal fluid test showed normal pressure but a bit high protein, which could mean nerve issues. Nerve tests showed damage to nerves in arms and legs, worse in the legs. Brain and eye scans didn’t show tumors, but showed signs of infection in the sinuses and lining of the brain. Sarcoidosis was ruled out with blood and scan tests. Because of the eye and nerve damage, doctors started high-dose steroid pills to reduce inflammation. After a few weeks, the man’s vision and headaches got better, and he started feeling stronger. He’s now being followed up in the clinic for ongoing care.\"\n}", "generated_text": "A 71-year-old man had a long-time skin condition called vitiligo and started losing vision in his right eye six months before hospital visit. He also lost hearing in both ears, worse on the right side. He had bad headaches, fever, and lost weight without trying. When doctors checked his eyes, the right eye was very sensitive to light and had redness, while the left eye could only see blurry shapes. The right eye’s back part had dark spots and the optic nerve was damaged (atrophied), and the left eye had swelling around the nerve and early nerve damage (optic neuritis). Doctors checked for infections and diseases like TB, herpes, or autoimmune problems, but none were found. A spinal fluid test showed normal pressure but a bit high protein, which could mean nerve issues. Nerve tests showed damage to nerves in arms and legs, worse in the legs. Brain and eye scans didn’t show tumors, but showed signs of infection in the sinuses and lining of the brain. Sarcoidosis was ruled out with blood and scan tests. Because of the eye and nerve damage, doctors started high-dose steroid pills to reduce inflammation. After a few weeks, the man’s vision and headaches got better, and he started feeling stronger. He’s now being followed up in the clinic for ongoing care."}
{"row_index": 106, "doc_id": 71, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 71-year-old man with long-standing vitiligo had lost vision in his right eye six months before hospitalization, along with hearing loss in both ears, worse on the right side. He also had chronic headaches, fever, and lost a lot of weight without trying. On eye exams, his right eye had very poor vision, was sensitive to light, and showed signs of damage including a swollen optic nerve and pigment spots. His left eye had good vision (20/200), but the optic nerve was swollen and there was early nerve damage. The right eye also showed signs of nerve degeneration. Tests were done to check for conditions like tuberculosis, infections, or autoimmune diseases, and none were found. A spinal fluid test showed normal pressure but slightly high protein levels. Nerve tests showed damage to multiple nerves, especially in the legs. Brain and eye MRI scans found no tumors, but showed signs of sinus infection and inflammation around the brain lining. Sarcoidosis was ruled out with normal blood and imaging tests. After further eye evaluation, the doctor confirmed ongoing eye nerve damage, including optic atrophy on the right and optic neuritis on the left. The patient started high-dose steroid treatment, which was slowly reduced over time. He improved over time, with better vision and less nerve-related symptoms, and was referred for ongoing follow-up care.\"\n}", "generated_text": "A 71-year-old man with long-standing vitiligo had lost vision in his right eye six months before hospitalization, along with hearing loss in both ears, worse on the right side. He also had chronic headaches, fever, and lost a lot of weight without trying. On eye exams, his right eye had very poor vision, was sensitive to light, and showed signs of damage including a swollen optic nerve and pigment spots. His left eye had good vision (20/200), but the optic nerve was swollen and there was early nerve damage. The right eye also showed signs of nerve degeneration. Tests were done to check for conditions like tuberculosis, infections, or autoimmune diseases, and none were found. A spinal fluid test showed normal pressure but slightly high protein levels. Nerve tests showed damage to multiple nerves, especially in the legs. Brain and eye MRI scans found no tumors, but showed signs of sinus infection and inflammation around the brain lining. Sarcoidosis was ruled out with normal blood and imaging tests. After further eye evaluation, the doctor confirmed ongoing eye nerve damage, including optic atrophy on the right and optic neuritis on the left. The patient started high-dose steroid treatment, which was slowly reduced over time. He improved over time, with better vision and less nerve-related symptoms, and was referred for ongoing follow-up care."}
{"row_index": 107, "doc_id": 71, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 71-year-old male with a history of untreated vitiligo presented with right-sided visual loss six months prior to admission, accompanied by bilateral sensorineural hearing loss with predilection for the right ear. He also reported chronic headaches, intermittent fever, and significant unintentional weight loss, along with generalized weakness and cutaneous thickening. Ophthalmologic examination revealed reduced visual acuity in the right eye (RO) to light perception with impaired color discrimination, and 20/200 visual acuity in the left eye (LO), with an afferent pupillary defect in both eyes. Both eyes exhibited hyperemic bulbar conjunctiva and ciliary injection. Corneal findings included peripheral, nummular, subepithelial infiltrates in both eyes, with aqueous anterior chamber (AAC) clear and no cellular infiltrate. Iris and lens were normal, though both demonstrated nuclear opacities. Fundus examination of the right eye showed a pale ++ papilla with 50% excavation, blunt nasal border, thinned and raised vascular pattern, macular involvement, and scattered pigmentary deposits. The left eye fundus demonstrated vitreous haze 2+, edematous papilla, blurred borders, peripapillary streaked hemorrhages, an unevaluable excavation, thinned vascular pattern, macular changes, and scattered pigment. Notably, the right optic nerve exhibited atrophy, and the left eye showed signs of anterior optic neuritis. Additional neurological evaluation included lumbar puncture, which revealed normal opening pressure and a cerebrospinal fluid (CSF) protein level of 54 mg/dL, consistent with non-inflammatory or mild neuroinflammatory processes. Nerve conduction studies demonstrated a pattern of symmetric polyradiculoneuropathy with moderate to severe axonal degeneration affecting all four extremities, with greater involvement in the lower limbs, suggesting a distal symmetric polyneuropathy. Contrast-enhanced magnetic resonance imaging (MRI) of the skull and orbits showed no evidence of optic nerve enhancement or intracranial tumors, but did reveal sinusitis and meningeal enhancement, indicating possible meningeal inflammation. Sarcoidosis was excluded based on normal angiotensin-converting enzyme (ACE) levels and a whole-body gamma scan without focal or diffuse uptake. Anti-neutrophil cytoplasmic antibody (ANCA)-positive and ANCA-negative vasculitides were also ruled out. The ocular and neurological manifestations progressed over time, confirming persistent disease activity. High-dose pulse corticosteroid therapy was initiated, followed by a stepwise tapering regimen, resulting in clinically and functionally significant improvement in both ophthalmological and neurological parameters. The patient was subsequently referred for ongoing outpatient follow-up. The clinical course supports a diagnosis of a chronic, immune-mediated neuro-ophthalmic disorder, likely involving autoimmune-mediated optic nerve damage, with features consistent with a vasculitic or inflammatory process affecting the optic pathways, possibly related to the underlying vitiligo, which may represent a chronic autoimmune skin condition with systemic immune dysregulation.\"\n}", "generated_text": "A 71-year-old male with a history of untreated vitiligo presented with right-sided visual loss six months prior to admission, accompanied by bilateral sensorineural hearing loss with predilection for the right ear. He also reported chronic headaches, intermittent fever, and significant unintentional weight loss, along with generalized weakness and cutaneous thickening. Ophthalmologic examination revealed reduced visual acuity in the right eye (RO) to light perception with impaired color discrimination, and 20/200 visual acuity in the left eye (LO), with an afferent pupillary defect in both eyes. Both eyes exhibited hyperemic bulbar conjunctiva and ciliary injection. Corneal findings included peripheral, nummular, subepithelial infiltrates in both eyes, with aqueous anterior chamber (AAC) clear and no cellular infiltrate. Iris and lens were normal, though both demonstrated nuclear opacities. Fundus examination of the right eye showed a pale ++ papilla with 50% excavation, blunt nasal border, thinned and raised vascular pattern, macular involvement, and scattered pigmentary deposits. The left eye fundus demonstrated vitreous haze 2+, edematous papilla, blurred borders, peripapillary streaked hemorrhages, an unevaluable excavation, thinned vascular pattern, macular changes, and scattered pigment. Notably, the right optic nerve exhibited atrophy, and the left eye showed signs of anterior optic neuritis. Additional neurological evaluation included lumbar puncture, which revealed normal opening pressure and a cerebrospinal fluid (CSF) protein level of 54 mg/dL, consistent with non-inflammatory or mild neuroinflammatory processes. Nerve conduction studies demonstrated a pattern of symmetric polyradiculoneuropathy with moderate to severe axonal degeneration affecting all four extremities, with greater involvement in the lower limbs, suggesting a distal symmetric polyneuropathy. Contrast-enhanced magnetic resonance imaging (MRI) of the skull and orbits showed no evidence of optic nerve enhancement or intracranial tumors, but did reveal sinusitis and meningeal enhancement, indicating possible meningeal inflammation. Sarcoidosis was excluded based on normal angiotensin-converting enzyme (ACE) levels and a whole-body gamma scan without focal or diffuse uptake. Anti-neutrophil cytoplasmic antibody (ANCA)-positive and ANCA-negative vasculitides were also ruled out. The ocular and neurological manifestations progressed over time, confirming persistent disease activity. High-dose pulse corticosteroid therapy was initiated, followed by a stepwise tapering regimen, resulting in clinically and functionally significant improvement in both ophthalmological and neurological parameters. The patient was subsequently referred for ongoing outpatient follow-up. The clinical course supports a diagnosis of a chronic, immune-mediated neuro-ophthalmic disorder, likely involving autoimmune-mediated optic nerve damage, with features consistent with a vasculitic or inflammatory process affecting the optic pathways, possibly related to the underlying vitiligo, which may represent a chronic autoimmune skin condition with systemic immune dysregulation."}
{"row_index": 108, "doc_id": 72, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 39-year-old female with peripartum cardiomyopathy underwent heart transplantation in October 2014. Induction therapy consisted of basiliximab and methylprednisolone, with maintenance immunosuppression comprising tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. During the first post-transplant year, she experienced two episodes of acute rejection, both managed effectively with methylprednisolone pulse therapy. No prior history of renal disease was noted, and early post-transplant renal function was stable, with serum creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m². Routine monitoring for polyomavirus infection, including BK virus viral load and urinary cytology, was not performed during follow-up. In 2016, serum creatinine elevated to a peak of 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m². At that time, minimum tacrolimus level was 7.2 ng/mL and everolimus 5.2 ng/mL, prompting suspicion of calcineurin inhibitor toxicity. Tacrolimus was reduced to 4 mg daily, resulting in a partial recovery of renal function (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m²); no renal biopsy was conducted. In March 2017, creatinine rose to 2.69 mg/dL and GFR dropped to 21.4 mL/min/1.73m², necessitating hospitalization despite the absence of clinical symptoms. Physical examination revealed normal general condition, heart rate of 80 bpm, blood pressure 130/90 mmHg, respiratory rate of 15/min, and no fever. Imaging and laboratory studies, including renal ultrasound (normal size, increased echogenicity), urinalysis (negative for hematuria, pyuria, and casts), urine culture, echocardiography (normal cardiac function), and serologic screening for HIV, syphilis, hepatitis B and C (all negative), were unremarkable. Minimum immunosuppressant levels remained within therapeutic range (tacrolimus 5.2 ng/mL, everolimus 5.98 ng/mL). Intravenous hydration and further reduction of tacrolimus to 2 mg daily were initiated, but renal function did not improve, leading to the decision for renal biopsy. The biopsy revealed active chronic tubulointerstitial nephritis with evidence of late-stage BK virus nephropathy. BK virus PCR detected a viral load of 33,800 copies/mL in serum (log 4.5), confirming active viral replication. Tacrolimus was discontinued due to its nephrotoxic potential in the context of BK virus infection. Post-treatment, serum creatinine stabilized between 2.2 and 2.4 mg/dL without further elevation, and the viral load progressively declined to undetectable levels. Over a three-year follow-up period, the patient remained free of cardiac rejection episodes. The most recent serum creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m², indicating stable but significantly reduced renal function consistent with chronic tubulointerstitial injury secondary to BK virus infection. The pathophysiological mechanism involves BK virus-induced tubular epithelial cell damage, leading to interstitial inflammation, fibrosis, and progressive glomerular dysfunction, exacerbated by immunosuppressive therapy that impairs viral clearance. The clinical course highlights the importance of vigilant monitoring for polyomavirus infection in solid organ transplant recipients, particularly in the setting of prolonged immunosuppression and declining renal function, even in the absence of overt symptoms.\"\n}", "generated_text": "A 39-year-old female with peripartum cardiomyopathy underwent heart transplantation in October 2014. Induction therapy consisted of basiliximab and methylprednisolone, with maintenance immunosuppression comprising tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. During the first post-transplant year, she experienced two episodes of acute rejection, both managed effectively with methylprednisolone pulse therapy. No prior history of renal disease was noted, and early post-transplant renal function was stable, with serum creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m². Routine monitoring for polyomavirus infection, including BK virus viral load and urinary cytology, was not performed during follow-up. In 2016, serum creatinine elevated to a peak of 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m². At that time, minimum tacrolimus level was 7.2 ng/mL and everolimus 5.2 ng/mL, prompting suspicion of calcineurin inhibitor toxicity. Tacrolimus was reduced to 4 mg daily, resulting in a partial recovery of renal function (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m²); no renal biopsy was conducted. In March 2017, creatinine rose to 2.69 mg/dL and GFR dropped to 21.4 mL/min/1.73m², necessitating hospitalization despite the absence of clinical symptoms. Physical examination revealed normal general condition, heart rate of 80 bpm, blood pressure 130/90 mmHg, respiratory rate of 15/min, and no fever. Imaging and laboratory studies, including renal ultrasound (normal size, increased echogenicity), urinalysis (negative for hematuria, pyuria, and casts), urine culture, echocardiography (normal cardiac function), and serologic screening for HIV, syphilis, hepatitis B and C (all negative), were unremarkable. Minimum immunosuppressant levels remained within therapeutic range (tacrolimus 5.2 ng/mL, everolimus 5.98 ng/mL). Intravenous hydration and further reduction of tacrolimus to 2 mg daily were initiated, but renal function did not improve, leading to the decision for renal biopsy. The biopsy revealed active chronic tubulointerstitial nephritis with evidence of late-stage BK virus nephropathy. BK virus PCR detected a viral load of 33,800 copies/mL in serum (log 4.5), confirming active viral replication. Tacrolimus was discontinued due to its nephrotoxic potential in the context of BK virus infection. Post-treatment, serum creatinine stabilized between 2.2 and 2.4 mg/dL without further elevation, and the viral load progressively declined to undetectable levels. Over a three-year follow-up period, the patient remained free of cardiac rejection episodes. The most recent serum creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m², indicating stable but significantly reduced renal function consistent with chronic tubulointerstitial injury secondary to BK virus infection. The pathophysiological mechanism involves BK virus-induced tubular epithelial cell damage, leading to interstitial inflammation, fibrosis, and progressive glomerular dysfunction, exacerbated by immunosuppressive therapy that impairs viral clearance. The clinical course highlights the importance of vigilant monitoring for polyomavirus infection in solid organ transplant recipients, particularly in the setting of prolonged immunosuppression and declining renal function, even in the absence of overt symptoms."}
{"row_index": 109, "doc_id": 73, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 14-year-old boy who had a cough and breathing trouble was found to have a lump in his chest, likely cancer called non-Hodgkin lymphoma. He was treated with a medicine called L-asp and prednisone. During this treatment, he started having high fat levels in his blood and low sodium levels, which doctors thought might be a side effect of the medicines. They checked this using a special method and found it was definitely caused by the mix of L-asp and prednisone. He was given a low-fat diet, plus medicines to lower his fat levels. His fat levels went back to normal in 14 days. The medicines were not stopped because the cancer treatment was still going. His body got better without any serious problems.\"\n}", "generated_text": "A 14-year-old boy who had a cough and breathing trouble was found to have a lump in his chest, likely cancer called non-Hodgkin lymphoma. He was treated with a medicine called L-asp and prednisone. During this treatment, he started having high fat levels in his blood and low sodium levels, which doctors thought might be a side effect of the medicines. They checked this using a special method and found it was definitely caused by the mix of L-asp and prednisone. He was given a low-fat diet, plus medicines to lower his fat levels. His fat levels went back to normal in 14 days. The medicines were not stopped because the cancer treatment was still going. His body got better without any serious problems."}
{"row_index": 110, "doc_id": 73, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 14-year-old boy with a history of a nighttime cough was admitted to the hospital after developing severe breathing problems and abdominal pain. Tests showed a mass in the middle of his chest, leading to a suspicion of non-Hodgkin lymphoma. He was treated with chemotherapy, including L-asp and prednisone, as part of a standard protocol. During treatment, he developed high levels of triglycerides in his blood and low sodium levels (a condition called pseudohyponatraemia), which are known to be linked to certain medications. Doctors suspected this was a drug reaction (ADR) caused by the combination of L-asp and prednisone. Using a standard method to evaluate drug reactions, they concluded it was a 'definitive' drug reaction. He was given a low-fat, high-fiber diet and medications to lower his triglycerides, which improved within 14 days. His condition stabilized, and the drug reaction resolved without complications. The medications were not stopped because the treatment for lymphoma was still ongoing, as per the treatment plan.\"\n}", "generated_text": "A 14-year-old boy with a history of a nighttime cough was admitted to the hospital after developing severe breathing problems and abdominal pain. Tests showed a mass in the middle of his chest, leading to a suspicion of non-Hodgkin lymphoma. He was treated with chemotherapy, including L-asp and prednisone, as part of a standard protocol. During treatment, he developed high levels of triglycerides in his blood and low sodium levels (a condition called pseudohyponatraemia), which are known to be linked to certain medications. Doctors suspected this was a drug reaction (ADR) caused by the combination of L-asp and prednisone. Using a standard method to evaluate drug reactions, they concluded it was a 'definitive' drug reaction. He was given a low-fat, high-fiber diet and medications to lower his triglycerides, which improved within 14 days. His condition stabilized, and the drug reaction resolved without complications. The medications were not stopped because the treatment for lymphoma was still ongoing, as per the treatment plan."}
{"row_index": 111, "doc_id": 73, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 14-year-old previously healthy adolescent presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of nocturnal irritative cough, progressing to dyspnoea and orthopnoea. Upon evaluation at the Osorno Base Hospital (OBH), he was found to have severe respiratory distress, intolerance to supine positioning, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU) in a tachycardic, hypertensive, polypneic state with oxygen saturation of 96% on 35% FiO2, rosy peripheries, adequate hydration, and well-perfused tissues, with flat jugular veins and small bilateral supraclavicular lymphadenopathies. Physical examination revealed no soft tissue retraction, maintained genupectoral posture, decreased pulmonary murmurs in both lung bases, and muffled cardiac tones without breath sounds. Abdominal examination showed non-depressible, tender soft tissue in both hypochondria with doubtful visceral enlargement and no trauma. Chest radiography demonstrated a superior mediastinal mass, atelectasis of the right middle lobe, and ipsilateral pleural effusion. Contrast-enhanced chest imaging was not performed due to contraindication of anaesthesia, as noted in the transfer summary. The patient was transferred to the PICU HBV with a diagnosis of mediastinal compression syndrome and clinical suspicion of non-Hodgkin lymphoma. Multidisciplinary evaluation by paediatric haemato-oncology, surgery, intensive care, imaging, radiotherapy, and oncology teams confirmed a normal pulmonary murmur and muffled cardiac auscultation, with no breath sounds, and persistent abdominal tenderness and suspected visceral enlargement. The chest radiograph remained consistent with a superior mediastinal mass and right middle lobe atelectasis with pleural effusion. A nephrological assessment revealed acute renal failure secondary to tumor lysis syndrome, with serum creatinine of 1.54 mg/dL, phosphoria of 11 mg/dL, and no hypernatremia. No dialysis was required, and the patient was managed with furosemide for volume control and amlodipine for hypertension. Respiratory support was initiated with Venturi mask at 35% FiO2, which was discontinued on day three due to clinical improvement. Episodes of psychomotor agitation, attributed to diagnostic stress, were managed according to institutional protocols with psychological and psychiatric support, resulting in satisfactory clinical course. On day three, a contrast-enhanced CT of the thorax, abdomen, and pelvis was performed, revealing thymic enlargement with homogeneous appearance, suggestive of a lymphoproliferative process, and findings consistent with pulmonary thromboembolism. AngioCT of the thorax confirmed jugular vein thrombosis, extensive bilateral pleural effusion, atelectasis in both lung bases, and signs of bilateral nephrotic syndrome. Anticoagulation with enoxaparin (1 mg/kg every 12 hours) was initiated for 20 days, with follow-up angioCT showing complete resolution of thrombosis. On day four, comprehensive diagnostic workup was completed, including complete biochemical profile (including lipid panel), bone marrow myelogram showing granulopoietic hyperplasia, flow cytometry of bone marrow and peripheral blood, which was negative for clonal or neoplastic haematopoietic immunophenotypes, and cytological analysis of pleural fluid, which was negative for neoplastic cells. Flow cytometry of pleural fluid also failed to detect haematological neoplasia. The patient was referred to the paediatric oncology committee, where, due to the absence of a viable biopsy specimen (as the mediastinal mass resolved with cytoreductive therapy), a diagnosis of lymphoblastic lymphoma was established based on clinical presentation and response to treatment, in accordance with the PINDA 0516 induction protocol. This protocol includes eight doses of L-asp (L-asparaginase) at 10,000 IU/m² in Induction IA. The patient received seven doses of L-asp, accumulating a total of 90,000 IU, in combination with prednisone glucocorticoids. During this period, he developed clinical deterioration with vomiting, abdominal pain, and mild dehydration. Pancreatitis was suspected but ruled out by normal amylase and lipase levels and normal hepatic function tests. Laboratory findings included hyponatraemia (126 mOsm/kg) and hypertriglyceridaemia, with urinary osmolality of 510 mOsm/kg (within normal range), leading to suspicion of a drug-induced metabolic disturbance—specifically, pseudohyponatraemia secondary to hypertriglyceridaemia. This was further supported", "generated_text": "{\n  \"proficient_health_literacy\": \"A 14-year-old previously healthy adolescent presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of nocturnal irritative cough, progressing to dyspnoea and orthopnoea. Upon evaluation at the Osorno Base Hospital (OBH), he was found to have severe respiratory distress, intolerance to supine positioning, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU) in a tachycardic, hypertensive, polypneic state with oxygen saturation of 96% on 35% FiO2, rosy peripheries, adequate hydration, and well-perfused tissues, with flat jugular veins and small bilateral supraclavicular lymphadenopathies. Physical examination revealed no soft tissue retraction, maintained genupectoral posture, decreased pulmonary murmurs in both lung bases, and muffled cardiac tones without breath sounds. Abdominal examination showed non-depressible, tender soft tissue in both hypochondria with doubtful visceral enlargement and no trauma. Chest radiography demonstrated a superior mediastinal mass, atelectasis of the right middle lobe, and ipsilateral pleural effusion. Contrast-enhanced chest imaging was not performed due to contraindication of anaesthesia, as noted in the transfer summary. The patient was transferred to the PICU HBV with a diagnosis of mediastinal compression syndrome and clinical suspicion of non-Hodgkin lymphoma. Multidisciplinary evaluation by paediatric haemato-oncology, surgery, intensive care, imaging, radiotherapy, and oncology teams confirmed a normal pulmonary murmur and muffled cardiac auscultation, with no breath sounds, and persistent abdominal tenderness and suspected visceral enlargement. The chest radiograph remained consistent with a superior mediastinal mass and right middle lobe atelectasis with pleural effusion. A nephrological assessment revealed acute renal failure secondary to tumor lysis syndrome, with serum creatinine of 1.54 mg/dL, phosphoria of 11 mg/dL, and no hypernatremia. No dialysis was required, and the patient was managed with furosemide for volume control and amlodipine for hypertension. Respiratory support was initiated with Venturi mask at 35% FiO2, which was discontinued on day three due to clinical improvement. Episodes of psychomotor agitation, attributed to diagnostic stress, were managed according to institutional protocols with psychological and psychiatric support, resulting in satisfactory clinical course. On day three, a contrast-enhanced CT of the thorax, abdomen, and pelvis was performed, revealing thymic enlargement with homogeneous appearance, suggestive of a lymphoproliferative process, and findings consistent with pulmonary thromboembolism. AngioCT of the thorax confirmed jugular vein thrombosis, extensive bilateral pleural effusion, atelectasis in both lung bases, and signs of bilateral nephrotic syndrome. Anticoagulation with enoxaparin (1 mg/kg every 12 hours) was initiated for 20 days, with follow-up angioCT showing complete resolution of thrombosis. On day four, comprehensive diagnostic workup was completed, including complete biochemical profile (including lipid panel), bone marrow myelogram showing granulopoietic hyperplasia, flow cytometry of bone marrow and peripheral blood, which was negative for clonal or neoplastic haematopoietic immunophenotypes, and cytological analysis of pleural fluid, which was negative for neoplastic cells. Flow cytometry of pleural fluid also failed to detect haematological neoplasia. The patient was referred to the paediatric oncology committee, where, due to the absence of a viable biopsy specimen (as the mediastinal mass resolved with cytoreductive therapy), a diagnosis of lymphoblastic lymphoma was established based on clinical presentation and response to treatment, in accordance with the PINDA 0516 induction protocol. This protocol includes eight doses of L-asp (L-asparaginase) at 10,000 IU/m² in Induction IA. The patient received seven doses of L-asp, accumulating a total of 90,000 IU, in combination with prednisone glucocorticoids. During this period, he developed clinical deterioration with vomiting, abdominal pain, and mild dehydration. Pancreatitis was suspected but ruled out by normal amylase and lipase levels and normal hepatic function tests. Laboratory findings included hyponatraemia (126 mOsm/kg) and hypertriglyceridaemia, with urinary osmolality of 510 mOsm/kg (within normal range), leading to suspicion of a drug-induced metabolic disturbance—specifically, pseudohyponatraemia secondary to hypertriglyceridaemia. This was further supported"}
{"row_index": 112, "doc_id": 74, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 56-year-old Italian female with β-thalassemia major underwent magnetic resonance imaging (MRI) to quantify myocardial, hepatic, and pancreatic iron deposition. Her clinical history includes transfusion-dependent β-thalassemia with genotype HBB:c.118C>T/HBB:c.93-21G>A, diagnosed at age 7 years, with the first red blood cell transfusion administered at 2 years of age. As a consequence of chronic transfusion and associated bone marrow pathology, she underwent splenectomy and cholecystectomy. At the time of MRI, she was negative for Hepatitis C virus RNA (HCV-RNA), had no evidence of osteoporosis or endocrine, cardiac, or hepatic complications, and maintained stable iron levels despite long-term iron overload. Her current therapy includes deferasirox for iron chelation, vitamin D supplementation, and luspatercept, an erythropoiesis-stimulating agent initiated two years prior to imaging, which demonstrated a 35% increase in transfusion interval duration, indicating a clinically significant response. Transfusion regimen consists of two units of concentrated and filtered red blood cells every 25 days, with pre-transfusion hemoglobin levels maintained between 10–10.5 g/dL.\\n\\nOn MRI, a solid, lobulated mass with regular contours was identified in the prevascular mediastinum. The lesion exhibited mild hyperintensity on T2-weighted imaging (T2-wi) and isointensity on T1-wi, and was previously detected in a prior MRI performed in 2020 before luspatercept initiation, with marginal enlargement over time. No other mediastinal abnormalities, pleural or pericardial effusions, or neurovascular compression symptoms were observed. Neurological examination was normal, and the patient reported no symptoms of mediastinal syndrome, fever, or weight loss.\\n\\nFurther evaluation via 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) revealed mild FDG uptake in the mediastinal mass (SUVmax = 4.3), with no abnormal radiotracer accumulation in the neck, chest, abdomen, or skeleton. Chest CT with contrast demonstrated a well-defined, solid lesion with mild contrast enhancement, no evidence of invasion into adjacent structures, and absence of lymphadenopathy or extra-thoracic metastases. These imaging features—indolent temporal progression, lack of systemic symptoms, and low metabolic activity—support a diagnosis of thymoma.\\n\\nHowever, on lung window analysis, multiple symmetric, thin-walled cystic lesions were identified throughout both lungs, with normal intervening parenchyma, no associated nodules, and no pneumothorax. These findings are consistent with lymphangioleiomyomatosis (LAM), a rare cystic lung disease characterized by proliferation of smooth muscle-like cells in the lung interstitium. The patient is a never-smoker and denies chronic cough, recurrent respiratory infections, or cutaneous fibrofolliculomas. Physical examination revealed clear lung fields, normal peripheral capillary oxygen saturation (98%), heart rate of 75 bpm, and significantly reduced diffusing capacity of the lungs for carbon monoxide (DLCO: 42% of predicted), partially attributable to anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of predicted. These pulmonary function abnormalities are consistent with advanced LAM pathology.\\n\\nFollowing multidisciplinary tumor board review involving a pulmonologist and thoracic surgeon, the patient underwent left thoracoscopic thymectomy with concomitant lingual segment wedge resection. Histopathological analysis confirmed a type B2 thymoma with focal capsule infiltration, no extracapsular extension, and presence at the resection margin, classifying the tumor as stage IIa by the Masaoka–Koga system and stage 1a by the TNM classification (indicating microscopically incomplete resection, R1). The pulmonary lesion demonstrated cysts of variable size lined by spindle cells with a myoid morphology, immunoreactive for actin, estrogen, progesterone receptors, and focal HMB45 positivity, with moderate chronic interstitial inflammation, vascular congestion, and recent blood extravasation—findings consistent with pulmonary LAM.\\n\\nFinal diagnosis is dual pathology: type B2 thymoma and pulmonary lymphangioleiomyomatosis. Given the R1 resection margin status, adjuvant radiation therapy is indicated for the thymoma to reduce risk of recurrence. For the LAM, which is associated with chronic iron overload in β-thalassemia, sirolimus therapy is recommended due to its ability to inhibit mTOR signaling, thereby suppressing the proliferation of abnormal smooth muscle-like cells in the lung paren", "generated_text": "{\n  \"proficient_health_literacy\": \"A 56-year-old Italian female with β-thalassemia major underwent magnetic resonance imaging (MRI) to quantify myocardial, hepatic, and pancreatic iron deposition. Her clinical history includes transfusion-dependent β-thalassemia with genotype HBB:c.118C>T/HBB:c.93-21G>A, diagnosed at age 7 years, with the first red blood cell transfusion administered at 2 years of age. As a consequence of chronic transfusion and associated bone marrow pathology, she underwent splenectomy and cholecystectomy. At the time of MRI, she was negative for Hepatitis C virus RNA (HCV-RNA), had no evidence of osteoporosis or endocrine, cardiac, or hepatic complications, and maintained stable iron levels despite long-term iron overload. Her current therapy includes deferasirox for iron chelation, vitamin D supplementation, and luspatercept, an erythropoiesis-stimulating agent initiated two years prior to imaging, which demonstrated a 35% increase in transfusion interval duration, indicating a clinically significant response. Transfusion regimen consists of two units of concentrated and filtered red blood cells every 25 days, with pre-transfusion hemoglobin levels maintained between 10–10.5 g/dL.\\n\\nOn MRI, a solid, lobulated mass with regular contours was identified in the prevascular mediastinum. The lesion exhibited mild hyperintensity on T2-weighted imaging (T2-wi) and isointensity on T1-wi, and was previously detected in a prior MRI performed in 2020 before luspatercept initiation, with marginal enlargement over time. No other mediastinal abnormalities, pleural or pericardial effusions, or neurovascular compression symptoms were observed. Neurological examination was normal, and the patient reported no symptoms of mediastinal syndrome, fever, or weight loss.\\n\\nFurther evaluation via 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) revealed mild FDG uptake in the mediastinal mass (SUVmax = 4.3), with no abnormal radiotracer accumulation in the neck, chest, abdomen, or skeleton. Chest CT with contrast demonstrated a well-defined, solid lesion with mild contrast enhancement, no evidence of invasion into adjacent structures, and absence of lymphadenopathy or extra-thoracic metastases. These imaging features—indolent temporal progression, lack of systemic symptoms, and low metabolic activity—support a diagnosis of thymoma.\\n\\nHowever, on lung window analysis, multiple symmetric, thin-walled cystic lesions were identified throughout both lungs, with normal intervening parenchyma, no associated nodules, and no pneumothorax. These findings are consistent with lymphangioleiomyomatosis (LAM), a rare cystic lung disease characterized by proliferation of smooth muscle-like cells in the lung interstitium. The patient is a never-smoker and denies chronic cough, recurrent respiratory infections, or cutaneous fibrofolliculomas. Physical examination revealed clear lung fields, normal peripheral capillary oxygen saturation (98%), heart rate of 75 bpm, and significantly reduced diffusing capacity of the lungs for carbon monoxide (DLCO: 42% of predicted), partially attributable to anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of predicted. These pulmonary function abnormalities are consistent with advanced LAM pathology.\\n\\nFollowing multidisciplinary tumor board review involving a pulmonologist and thoracic surgeon, the patient underwent left thoracoscopic thymectomy with concomitant lingual segment wedge resection. Histopathological analysis confirmed a type B2 thymoma with focal capsule infiltration, no extracapsular extension, and presence at the resection margin, classifying the tumor as stage IIa by the Masaoka–Koga system and stage 1a by the TNM classification (indicating microscopically incomplete resection, R1). The pulmonary lesion demonstrated cysts of variable size lined by spindle cells with a myoid morphology, immunoreactive for actin, estrogen, progesterone receptors, and focal HMB45 positivity, with moderate chronic interstitial inflammation, vascular congestion, and recent blood extravasation—findings consistent with pulmonary LAM.\\n\\nFinal diagnosis is dual pathology: type B2 thymoma and pulmonary lymphangioleiomyomatosis. Given the R1 resection margin status, adjuvant radiation therapy is indicated for the thymoma to reduce risk of recurrence. For the LAM, which is associated with chronic iron overload in β-thalassemia, sirolimus therapy is recommended due to its ability to inhibit mTOR signaling, thereby suppressing the proliferation of abnormal smooth muscle-like cells in the lung paren"}
{"row_index": 113, "doc_id": 75, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 49-year-old woman had a long sickness called lupus that started when she was a child. Over time, her kidneys and heart got weaker because of the disease. She needed dialysis for 4 years until she got a new kidney. Before the surgery, her heart was very weak — only pumping 26% of the blood it should — so doctors gave her a medicine called Levosimendan to help her heart work better. The surgery was hard, but she survived. Afterward, her heart got stronger: now it pumps better, and her kidney function is normal. Her ability to walk stairs improved, and her heart problems got much better over time. She is now doing well after the transplant.\"\n}", "generated_text": "A 49-year-old woman had a long sickness called lupus that started when she was a child. Over time, her kidneys and heart got weaker because of the disease. She needed dialysis for 4 years until she got a new kidney. Before the surgery, her heart was very weak — only pumping 26% of the blood it should — so doctors gave her a medicine called Levosimendan to help her heart work better. The surgery was hard, but she survived. Afterward, her heart got stronger: now it pumps better, and her kidney function is normal. Her ability to walk stairs improved, and her heart problems got much better over time. She is now doing well after the transplant."}
{"row_index": 114, "doc_id": 75, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a case of a 49-year-old woman with chronic renal and cardiac failure secondary to long-standing systemic lupus erythematosus (SLE), spanning from childhood (initiated at age 13). The patient had a history of lupus nephritis (LN), initially class III and later progressing to class IV, managed with early steroid therapy, followed by cyclophosphamide, subsequently replaced by methotrexate and azathioprine. Partial remission of nephrotic syndrome was achieved, and immunosuppressive therapy was discontinued in 2002 due to active hepatitis C virus (HCV) replication. SLE-related vascular involvement manifested as early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at age 20. In 2007, declining renal function (serum creatinine 2.2 mg/dL) and proteinuria (2 g/day) prompted a kidney biopsy, which revealed active and sclerotic focal proliferative lupus nephritis; immunosuppression was withheld due to HCV activity. Over time, renal function progressively deteriorated. Despite percutaneous coronary intervention (PCI) of the right coronary artery (RCA), the patient developed severe post-infarction dilated cardiomyopathy and required implantation of an implantable cardioverter-defibrillator (ICD) for primary prevention in 2009. Subsequently, significant mitral and tricuspid valve regurgitation developed on the background of lupus-related and secondary cardiomyopathic pathology, necessitating mitral and tricuspid valve repair, followed by left ventricular volume reduction surgery in 2014, complicated by low cardiac output syndrome requiring intra-aortic balloon pump (IABP) support. Postoperatively, renal function further declined, leading to initiation of chronic renal replacement therapy (dialysis), which has been sustained for 4 years. During active waiting for kidney transplantation, laboratory markers of lupus entered remission (normal C3: 0.93 g/L, C4: 0.4 g/L, ANA negative), though circulatory insufficiency persisted, evidenced by markedly reduced exercise tolerance (limited to one flight of stairs) and elevated B-type natriuretic peptide (BNP) of 619 pg/mL (normal range: 0–100 pg/mL). Transthoracic echocardiography prior to transplantation demonstrated significant left ventricular and left atrial enlargement, with severely impaired systolic function: left ventricular ejection fraction (LVEF) of 26% and global longitudinal strain (GLS) of −3. Due to mitral ring implantation, left ventricular diastolic function could not be assessed. A high tricuspid regurgitant flow gradient and a widened, poorly respiratory mobile inferior vena cava (IVC) suggested a high probability of pulmonary hypertension. Given the extremely low ejection fraction and complex cardiac pathology, cardioprotective therapy with levosimendan was initiated during pre-transplant preparation. Levosimendan was administered at a dose of 0.1 μg/kg/min immediately after cross-match confirmation and dialysis session, and continued postoperatively for 24 hours. The anesthetic and perioperative management was optimized to ensure adequate transplanted kidney perfusion, avoiding nephrotoxic agents (including those excreted by functional kidneys), and utilizing nephroprotective strategies. Due to recurrent ventricular extrasystoles and risk of circulatory decompensation, and the necessity of ICD disconnection during transplantation, Swan-Ganz catheterization for hemodynamic monitoring was avoided. Anesthesia was monitored via ECG, central venous pressure (CVP) via central catheter, direct radial artery blood pressure, and continuous cardiac ultrasound. CVP was used to guide fluid management during anesthesia, and postoperatively, cardiac ultrasound and inferior vena cava respiratory fill and motility were used to assess hemodynamic stability. Therapy was guided by goal-directed therapy (GDT) principles. Anesthesia included fentanyl, triacrium, propofol, desflurane, standard antibiotic prophylaxis, and immunosuppressive regimens (steroids, tacrolimus, mycophenolate mofetil), with mycophenolate mofetil discontinued due to persistent leukopenia and cytomegalovirus (CMV) infection. Delayed graft function was observed, requiring hemodialysis for nearly 6 weeks, primarily due to fluid overload. BNP levels peaked at 2996 pg/mL and gradually declined. A kidney biopsy performed two weeks post-transplant revealed acute rejection (AR II B, Banff 2015 classification) with acute tubular necrosis (ATN). The", "generated_text": "{\n  \"proficient_health_literacy\": \"We present a case of a 49-year-old woman with chronic renal and cardiac failure secondary to long-standing systemic lupus erythematosus (SLE), spanning from childhood (initiated at age 13). The patient had a history of lupus nephritis (LN), initially class III and later progressing to class IV, managed with early steroid therapy, followed by cyclophosphamide, subsequently replaced by methotrexate and azathioprine. Partial remission of nephrotic syndrome was achieved, and immunosuppressive therapy was discontinued in 2002 due to active hepatitis C virus (HCV) replication. SLE-related vascular involvement manifested as early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at age 20. In 2007, declining renal function (serum creatinine 2.2 mg/dL) and proteinuria (2 g/day) prompted a kidney biopsy, which revealed active and sclerotic focal proliferative lupus nephritis; immunosuppression was withheld due to HCV activity. Over time, renal function progressively deteriorated. Despite percutaneous coronary intervention (PCI) of the right coronary artery (RCA), the patient developed severe post-infarction dilated cardiomyopathy and required implantation of an implantable cardioverter-defibrillator (ICD) for primary prevention in 2009. Subsequently, significant mitral and tricuspid valve regurgitation developed on the background of lupus-related and secondary cardiomyopathic pathology, necessitating mitral and tricuspid valve repair, followed by left ventricular volume reduction surgery in 2014, complicated by low cardiac output syndrome requiring intra-aortic balloon pump (IABP) support. Postoperatively, renal function further declined, leading to initiation of chronic renal replacement therapy (dialysis), which has been sustained for 4 years. During active waiting for kidney transplantation, laboratory markers of lupus entered remission (normal C3: 0.93 g/L, C4: 0.4 g/L, ANA negative), though circulatory insufficiency persisted, evidenced by markedly reduced exercise tolerance (limited to one flight of stairs) and elevated B-type natriuretic peptide (BNP) of 619 pg/mL (normal range: 0–100 pg/mL). Transthoracic echocardiography prior to transplantation demonstrated significant left ventricular and left atrial enlargement, with severely impaired systolic function: left ventricular ejection fraction (LVEF) of 26% and global longitudinal strain (GLS) of −3. Due to mitral ring implantation, left ventricular diastolic function could not be assessed. A high tricuspid regurgitant flow gradient and a widened, poorly respiratory mobile inferior vena cava (IVC) suggested a high probability of pulmonary hypertension. Given the extremely low ejection fraction and complex cardiac pathology, cardioprotective therapy with levosimendan was initiated during pre-transplant preparation. Levosimendan was administered at a dose of 0.1 μg/kg/min immediately after cross-match confirmation and dialysis session, and continued postoperatively for 24 hours. The anesthetic and perioperative management was optimized to ensure adequate transplanted kidney perfusion, avoiding nephrotoxic agents (including those excreted by functional kidneys), and utilizing nephroprotective strategies. Due to recurrent ventricular extrasystoles and risk of circulatory decompensation, and the necessity of ICD disconnection during transplantation, Swan-Ganz catheterization for hemodynamic monitoring was avoided. Anesthesia was monitored via ECG, central venous pressure (CVP) via central catheter, direct radial artery blood pressure, and continuous cardiac ultrasound. CVP was used to guide fluid management during anesthesia, and postoperatively, cardiac ultrasound and inferior vena cava respiratory fill and motility were used to assess hemodynamic stability. Therapy was guided by goal-directed therapy (GDT) principles. Anesthesia included fentanyl, triacrium, propofol, desflurane, standard antibiotic prophylaxis, and immunosuppressive regimens (steroids, tacrolimus, mycophenolate mofetil), with mycophenolate mofetil discontinued due to persistent leukopenia and cytomegalovirus (CMV) infection. Delayed graft function was observed, requiring hemodialysis for nearly 6 weeks, primarily due to fluid overload. BNP levels peaked at 2996 pg/mL and gradually declined. A kidney biopsy performed two weeks post-transplant revealed acute rejection (AR II B, Banff 2015 classification) with acute tubular necrosis (ATN). The"}
{"row_index": 115, "doc_id": 76, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 42-year-old woman had bad headaches that were very sharp and strong, like a storm inside her head. The pain came on suddenly, lasted about 30 minutes, and happened many times a day when she coughed or lifted things. She tried medicines, but they caused stomach problems and didn’t work. When the pain got too bad, she went to a pain clinic. There, doctors used an ultrasound to guide a needle to block the nerve causing the pain. The medicine used was bupivacaine. After the first block, her pain went from 9 out of 10 to just 2 out of 10. She had this block once a week for a month. After two months, the headaches became much less frequent and weaker. By the sixth month, she didn’t have any more attacks and no side effects.\"\n}", "generated_text": "A 42-year-old woman had bad headaches that were very sharp and strong, like a storm inside her head. The pain came on suddenly, lasted about 30 minutes, and happened many times a day when she coughed or lifted things. She tried medicines, but they caused stomach problems and didn’t work. When the pain got too bad, she went to a pain clinic. There, doctors used an ultrasound to guide a needle to block the nerve causing the pain. The medicine used was bupivacaine. After the first block, her pain went from 9 out of 10 to just 2 out of 10. She had this block once a week for a month. After two months, the headaches became much less frequent and weaker. By the sixth month, she didn’t have any more attacks and no side effects."}
{"row_index": 116, "doc_id": 76, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 42-year-old female with a history of menstrual migraine, Hashimoto thyroiditis, familial Mediterranean fever (FMF), and dyspepsia was evaluated for refractory headache. She was on stable therapy including 75 mg daily levothyroxine, 30 mg daily lansoprazole, and 1.5 mg daily colchicine. In February 2023, she developed acute bronchitis treated with antibiotics and bronchodilators, followed by the onset of daily headache episodes manifesting as more than ten brief, self-limiting attacks per day, each lasting approximately 30 minutes, provoked by coughing, straining, or lifting. The pain was bilaterally distributed from the neck to the vertex of the skull, described as sharp and severe, with a characteristic sensation of 'storm-like fluid movement' within the head. Pain intensity was quantified using a 0–10 numeric rating scale (NRS), consistently reaching 9/10 during attacks, which frequently required emergency department visits. Neurological and physical examinations were normal, and laboratory evaluations—including thyroid function, electrolytes, hepatic and renal function, and serological markers—were negative. Brain MRI with and without contrast, cervical spinal MRI, magnetic resonance venography (MRV), and magnetic resonance angiography (MRA) were all unremarkable. Lumbar puncture was not performed due to patient refusal. Prior to presentation to the pain clinic, she was on 25 mg of indomethacin daily; her headache attacks ceased after increasing lansoprazole to 60 mg and raising indomethacin to 150 mg, but gastrointestinal adverse effects led to discontinuation of indomethacin on day three. Concomitant medications, including topiramate and propranolol, were not initiated due to intolerance. Fifteen days after initial evaluation, she presented with a recurrent attack of NRS 9/10 and was taken to the local operating room for ultrasound-guided proximal greater occipital nerve block (PGONB). The procedure was performed using a GE Healthcare Voluson™ E6 ultrasound system with a linear 13–5 MHz probe. The patient’s neck was in a position of flexion, and the probe was initially transversely placed over the occipital protuberance, then advanced caudally to visualize the C2 spinous process, which was observed to have a bicondylar appearance resembling two horns. Lateral probe movement allowed identification of the inferior fibers of the obliquus capitis and semispinalis capitis muscles. The greater occipital nerve (GON) was localized superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle. A 22-gauge spinal needle was inserted at this site, and 3 cc of 0.5% bupivacaine was injected. Within 20 minutes of injection, the headache intensity dropped from 9/10 to 2/10. The procedure was repeated weekly for one month. By the second month, the frequency of attacks reduced to two per month, with an average intensity of 4/10. By the sixth month, no attacks were reported, and no adverse effects were observed. This case demonstrates the efficacy of ultrasound-guided PGONB in managing refractory, non-migraine-like headaches with a distinct mechanical trigger profile, particularly in patients with comorbidities and intolerance to conventional pharmacologic therapies.\"\n}", "generated_text": "A 42-year-old female with a history of menstrual migraine, Hashimoto thyroiditis, familial Mediterranean fever (FMF), and dyspepsia was evaluated for refractory headache. She was on stable therapy including 75 mg daily levothyroxine, 30 mg daily lansoprazole, and 1.5 mg daily colchicine. In February 2023, she developed acute bronchitis treated with antibiotics and bronchodilators, followed by the onset of daily headache episodes manifesting as more than ten brief, self-limiting attacks per day, each lasting approximately 30 minutes, provoked by coughing, straining, or lifting. The pain was bilaterally distributed from the neck to the vertex of the skull, described as sharp and severe, with a characteristic sensation of 'storm-like fluid movement' within the head. Pain intensity was quantified using a 0–10 numeric rating scale (NRS), consistently reaching 9/10 during attacks, which frequently required emergency department visits. Neurological and physical examinations were normal, and laboratory evaluations—including thyroid function, electrolytes, hepatic and renal function, and serological markers—were negative. Brain MRI with and without contrast, cervical spinal MRI, magnetic resonance venography (MRV), and magnetic resonance angiography (MRA) were all unremarkable. Lumbar puncture was not performed due to patient refusal. Prior to presentation to the pain clinic, she was on 25 mg of indomethacin daily; her headache attacks ceased after increasing lansoprazole to 60 mg and raising indomethacin to 150 mg, but gastrointestinal adverse effects led to discontinuation of indomethacin on day three. Concomitant medications, including topiramate and propranolol, were not initiated due to intolerance. Fifteen days after initial evaluation, she presented with a recurrent attack of NRS 9/10 and was taken to the local operating room for ultrasound-guided proximal greater occipital nerve block (PGONB). The procedure was performed using a GE Healthcare Voluson™ E6 ultrasound system with a linear 13–5 MHz probe. The patient’s neck was in a position of flexion, and the probe was initially transversely placed over the occipital protuberance, then advanced caudally to visualize the C2 spinous process, which was observed to have a bicondylar appearance resembling two horns. Lateral probe movement allowed identification of the inferior fibers of the obliquus capitis and semispinalis capitis muscles. The greater occipital nerve (GON) was localized superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle. A 22-gauge spinal needle was inserted at this site, and 3 cc of 0.5% bupivacaine was injected. Within 20 minutes of injection, the headache intensity dropped from 9/10 to 2/10. The procedure was repeated weekly for one month. By the second month, the frequency of attacks reduced to two per month, with an average intensity of 4/10. By the sixth month, no attacks were reported, and no adverse effects were observed. This case demonstrates the efficacy of ultrasound-guided PGONB in managing refractory, non-migraine-like headaches with a distinct mechanical trigger profile, particularly in patients with comorbidities and intolerance to conventional pharmacologic therapies."}
{"row_index": 117, "doc_id": 77, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old male martial artist had pain in the back of his left thigh for 5 weeks. The pain started after a short sprint in soccer, and he heard a pop. He couldn’t move his knee well and had to stop all sports. Even with pain medicine, ice, and bandages, the pain didn’t go away. The doctor checked and ruled out other serious problems. He couldn’t bend or straighten his knee properly and walked with a limp. His pain was 5 out of 10 at rest and 7 during activity. A special treatment was done: a gentle movement technique to help the nerve slide smoothly, done 3 times a day for 3 days. He also learned how to stand and move better. After 3 days, his pain dropped to 2 out of 10 at rest and 4 during activity. His knee could move much better. At 2 months, he was pain-free and could go back to martial arts without any trouble.\"\n}", "generated_text": "A 20-year-old male martial artist had pain in the back of his left thigh for 5 weeks. The pain started after a short sprint in soccer, and he heard a pop. He couldn’t move his knee well and had to stop all sports. Even with pain medicine, ice, and bandages, the pain didn’t go away. The doctor checked and ruled out other serious problems. He couldn’t bend or straighten his knee properly and walked with a limp. His pain was 5 out of 10 at rest and 7 during activity. A special treatment was done: a gentle movement technique to help the nerve slide smoothly, done 3 times a day for 3 days. He also learned how to stand and move better. After 3 days, his pain dropped to 2 out of 10 at rest and 4 during activity. His knee could move much better. At 2 months, he was pain-free and could go back to martial arts without any trouble."}
{"row_index": 118, "doc_id": 77, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 20-year-old male Arabic martial artist had a left hamstring strain that lasted for 5 weeks. He tried medications and physical therapy, but his pain didn’t improve. He stopped all sports activities because the pain was severe. After checking with a doctor, other causes like nerve problems or back issues were ruled out. The patient was treated with a modified slump mobilization technique, done four times a day for three days, along with postural retraining. Before treatment, his pain was 5 out of 10 at rest and 7 out of 10 during activity. After three days, pain dropped to 2 out of 10 at rest and 4 out of 10 during activity. His knee function also improved significantly: the Knee Society score went from 22 to 61 for pain and from 30 to 80 for movement. At a 2-month follow-up, he had fully recovered and was able to return to sports without any problems.\"\n}", "generated_text": "A 20-year-old male Arabic martial artist had a left hamstring strain that lasted for 5 weeks. He tried medications and physical therapy, but his pain didn’t improve. He stopped all sports activities because the pain was severe. After checking with a doctor, other causes like nerve problems or back issues were ruled out. The patient was treated with a modified slump mobilization technique, done four times a day for three days, along with postural retraining. Before treatment, his pain was 5 out of 10 at rest and 7 out of 10 during activity. After three days, pain dropped to 2 out of 10 at rest and 4 out of 10 during activity. His knee function also improved significantly: the Knee Society score went from 22 to 61 for pain and from 30 to 80 for movement. At a 2-month follow-up, he had fully recovered and was able to return to sports without any problems."}
{"row_index": 119, "doc_id": 77, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, BMI 28.24) presented with a left hamstring strain with a five-week history of persistent pain in the posterior left thigh, initially precipitated by a sudden sprint during soccer play, during which he reported a 'pop' sensation. The pain was severe enough to cause immediate cessation of activity and was rated at 5/10 at rest and 7/10 during activity. There was no associated bruising or significant swelling, and the patient denied prior lower back or leg injuries. Clinical examination revealed a progressive loss of knee joint mobility, with active range of motion (AROM) limited to 10–15° in the left knee versus 0–130° in the contralateral right knee. The patient exhibited an analgesic gait pattern with reduced heel strike and was unable to fully extend or flex the knee when maintained at a 15° flexion position. Palpation identified tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles, consistent with hamstring muscle strain or fascial tightness. Manual muscle testing and isometric assessments were contraindicated due to persistent pain. The patient reported using crutches for ambulation, stair climbing via single-step ascents, and avoiding direct pressure on the thigh, including sitting at the edge of a chair. Despite adherence to nonsteroidal anti-inflammatory drugs (NSAIDs), cryotherapy, and compression bandaging, symptoms worsened over time, leading to referral for specialized evaluation. Diagnostic workup excluded lumbar disc pathology, gluteal tunnel syndrome, and ischial nerve entrapment based on clinical and neurodynamic screening, including a negative slump test for peripheral nerve tension. The clinical picture was consistent with hamstring strain syndrome (HSI), though conventional treatments had failed to yield improvement. The therapeutic intervention consisted of a modified slump mobilization technique involving sequential spinal and joint mobilization under controlled neurodynamic conditions. The protocol included three sets of daily sessions, each comprising thoracic and cervical spine flexion, maximal knee extension under tolerable pain thresholds, and dynamic neck and ankle movements (15 repetitions) to facilitate neural glide. The patient was also instructed to progressively mobilize the mid- and upper back until pain was elicited in the knee region, followed by repetition of the sequence. This neurodynamic approach was based on the biomechanical proximity of the tibial nerve and sciatic nerve to the hamstring musculature and the functional interplay between neural tension and lower limb joint mechanics. By the third day of intervention, active knee extension improved from 5° to 15°, and standing posture normalized. Concurrently, the patient was introduced to a structured postural retraining program including active chin flexion, passive stretching of cervical extensors in prone position, and dynamic shoulder retraction exercises (T-to-Y, Y-to-W) performed with limb weight bearing. Additional interventions included active chest stretches at wall corners to correct kyphotic posture, with exercise duration increased from 5 to 10 seconds, performed in 10 repetitions across three sets daily. Outcomes were quantified using the Numeric Pain Rating Scale (NPRS) and the Knee Society Score (KSS). Pre-intervention NPRS scores were 5/10 at rest and 7/10 during activity; post-intervention (on day 3) these improved to 2/10 at rest and 4/10 during activity. KSS scores increased from 22 to 61 in the pain domain and from 30 to 80 in the functional domain. Pain medication was discontinued following clinical improvement. At the end of a two-week home exercise program, the patient achieved full active straight leg raise (SLR). At the two-month follow-up, the patient reported complete resolution of symptoms, regained full functional mobility, and resumed participation in martial arts without limitations. The intervention demonstrates the efficacy of a neurodynamic mobilization approach in addressing chronic hamstring-related pain when conventional treatments fail, particularly in patients with structural and functional neural-tissue interactions affecting joint mechanics and posture.\"\n}", "generated_text": "A 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, BMI 28.24) presented with a left hamstring strain with a five-week history of persistent pain in the posterior left thigh, initially precipitated by a sudden sprint during soccer play, during which he reported a 'pop' sensation. The pain was severe enough to cause immediate cessation of activity and was rated at 5/10 at rest and 7/10 during activity. There was no associated bruising or significant swelling, and the patient denied prior lower back or leg injuries. Clinical examination revealed a progressive loss of knee joint mobility, with active range of motion (AROM) limited to 10–15° in the left knee versus 0–130° in the contralateral right knee. The patient exhibited an analgesic gait pattern with reduced heel strike and was unable to fully extend or flex the knee when maintained at a 15° flexion position. Palpation identified tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles, consistent with hamstring muscle strain or fascial tightness. Manual muscle testing and isometric assessments were contraindicated due to persistent pain. The patient reported using crutches for ambulation, stair climbing via single-step ascents, and avoiding direct pressure on the thigh, including sitting at the edge of a chair. Despite adherence to nonsteroidal anti-inflammatory drugs (NSAIDs), cryotherapy, and compression bandaging, symptoms worsened over time, leading to referral for specialized evaluation. Diagnostic workup excluded lumbar disc pathology, gluteal tunnel syndrome, and ischial nerve entrapment based on clinical and neurodynamic screening, including a negative slump test for peripheral nerve tension. The clinical picture was consistent with hamstring strain syndrome (HSI), though conventional treatments had failed to yield improvement. The therapeutic intervention consisted of a modified slump mobilization technique involving sequential spinal and joint mobilization under controlled neurodynamic conditions. The protocol included three sets of daily sessions, each comprising thoracic and cervical spine flexion, maximal knee extension under tolerable pain thresholds, and dynamic neck and ankle movements (15 repetitions) to facilitate neural glide. The patient was also instructed to progressively mobilize the mid- and upper back until pain was elicited in the knee region, followed by repetition of the sequence. This neurodynamic approach was based on the biomechanical proximity of the tibial nerve and sciatic nerve to the hamstring musculature and the functional interplay between neural tension and lower limb joint mechanics. By the third day of intervention, active knee extension improved from 5° to 15°, and standing posture normalized. Concurrently, the patient was introduced to a structured postural retraining program including active chin flexion, passive stretching of cervical extensors in prone position, and dynamic shoulder retraction exercises (T-to-Y, Y-to-W) performed with limb weight bearing. Additional interventions included active chest stretches at wall corners to correct kyphotic posture, with exercise duration increased from 5 to 10 seconds, performed in 10 repetitions across three sets daily. Outcomes were quantified using the Numeric Pain Rating Scale (NPRS) and the Knee Society Score (KSS). Pre-intervention NPRS scores were 5/10 at rest and 7/10 during activity; post-intervention (on day 3) these improved to 2/10 at rest and 4/10 during activity. KSS scores increased from 22 to 61 in the pain domain and from 30 to 80 in the functional domain. Pain medication was discontinued following clinical improvement. At the end of a two-week home exercise program, the patient achieved full active straight leg raise (SLR). At the two-month follow-up, the patient reported complete resolution of symptoms, regained full functional mobility, and resumed participation in martial arts without limitations. The intervention demonstrates the efficacy of a neurodynamic mobilization approach in addressing chronic hamstring-related pain when conventional treatments fail, particularly in patients with structural and functional neural-tissue interactions affecting joint mechanics and posture."}
{"row_index": 120, "doc_id": 78, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A male infant was delivered via emergency cesarean section at 40 weeks' gestation due to fetal distress. The mother was 33 years old, gravida 1, para 1, with no family history of congenital anomalies, aortic disease, or sudden cardiac death. Prenatal ultrasonography revealed a femur length 1–3 weeks above the expected gestational age, suggesting disproportionate growth. Fetal echocardiography demonstrated cardiomegaly with a fetal cardiothoracic circumference ratio of ≥0.5, a larger-than-normal foramen ovale, and left aortic constriction adjacent to the subclavian artery basin; no other structural abnormalities were identified.\\n\\nAt birth, the infant weighed 3560 g (75th percentile), measured 56.5 cm (above 90th percentile), and had a head circumference of 36 cm (above 90th percentile). Apgar scores were 4 at 1 minute and 6 at 5 minutes. The newborn exhibited absent spontaneous breathing, bradycardia, and cyanosis upon delivery, necessitating immediate neonatal intensive care unit (NICU) admission.\\n\\nPhysical examination revealed multiple severe musculoskeletal manifestations consistent with Marfan syndrome (MFS), including bilateral arachnodactyly, camptodactyly, flat feet, joint contractures at the elbows and knees, malar hypoplasia, a senile facial appearance, deep-set eyes with down-slanting palpebral fissures, hypoplastic and crumpled external ear cartilage, a sagging mouth, prominent coronal suture, and brachycephaly. Ophthalmologic evaluation confirmed bilateral ectopia lentis with lens subluxation. The musculoskeletal severity was assessed using the Ghent criteria, yielding a total score of 11 points, supporting a diagnosis of severe MFS.\\n\\nCardiac evaluation revealed a grade V/VI systolic murmur at the upper and left lower sternal borders, accompanied by a parasternal heave. Echocardiography demonstrated poor left ventricular contractility, severe pulmonary hypertension, a dilated aortic sinus (20.2 mm), with Z-scores of 8.08 (Boston), 6.37 (Detroit), and 5.97 (Halifax), indicating extreme dilation. Multiple valvular abnormalities were present: moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation. These findings are consistent with progressive valvular degeneration due to impaired extracellular matrix integrity.\\n\\nGenetic analysis via Sanger sequencing and polymerase chain reaction (PCR) of the fibrillin-1 (FBN1) gene identified a novel heterozygous mutation at nucleotide position c.3964 + 1G > T, located in intron 32 of the FBN1 gene. This mutation affects the splice site of exon 32 and is classified as a pathogenic variant based on the 2015 ACMG/AMP guidelines. The mutation lies within the previously defined 'neonatal region' of the FBN1 gene (exons 24–32), which is associated with a more severe, early-onset phenotype of MFS, including neonatal cardiac involvement and rapid progression of valvular and musculoskeletal pathology.\\n\\nOn postnatal day 1, refractory hypoxemia was observed despite >60% oxygen supplementation, indicating inadequate cardiac output and pulmonary perfusion. Medical management was initiated to address low cardiac output secondary to severe mitral and aortic regurgitation. Therapeutic interventions included milrinone (an inodilator) for afterload reduction, continuous fentanyl sedation to suppress myocardial oxygen demand, and diuretic therapy to manage oliguria and fluid overload. Despite these measures, the infant developed progressive respiratory failure, worsening pulmonary hypertension, and deteriorating cardiac contractility. Echocardiographic follow-up confirmed progressive worsening of aortic and mitral regurgitation, with sustained severe pulmonary hypertension.\\n\\nMultidisciplinary team consultations with the family and clinical staff concluded that surgical intervention—such as valve repair or replacement—was not feasible given the rapid disease progression and poor prognosis. Palliative care was initiated instead. Over the following weeks, the infant developed hepatic and pulmonary congestion, pulmonary hemorrhage, and ultimately progressed to multiple organ dysfunction syndrome (MODS). The patient died 32 days after birth. This case exemplifies the severe, early-onset form of Marfan syndrome associated with a novel FBN1 mutation in the neonatal region, characterized by profound cardiac dysfunction, valvular deterioration, and multisystem involvement, underscoring the critical need for early genetic diagnosis and the limitations of medical therapy", "generated_text": "{\n  \"proficient_health_literacy\": \"A male infant was delivered via emergency cesarean section at 40 weeks' gestation due to fetal distress. The mother was 33 years old, gravida 1, para 1, with no family history of congenital anomalies, aortic disease, or sudden cardiac death. Prenatal ultrasonography revealed a femur length 1–3 weeks above the expected gestational age, suggesting disproportionate growth. Fetal echocardiography demonstrated cardiomegaly with a fetal cardiothoracic circumference ratio of ≥0.5, a larger-than-normal foramen ovale, and left aortic constriction adjacent to the subclavian artery basin; no other structural abnormalities were identified.\\n\\nAt birth, the infant weighed 3560 g (75th percentile), measured 56.5 cm (above 90th percentile), and had a head circumference of 36 cm (above 90th percentile). Apgar scores were 4 at 1 minute and 6 at 5 minutes. The newborn exhibited absent spontaneous breathing, bradycardia, and cyanosis upon delivery, necessitating immediate neonatal intensive care unit (NICU) admission.\\n\\nPhysical examination revealed multiple severe musculoskeletal manifestations consistent with Marfan syndrome (MFS), including bilateral arachnodactyly, camptodactyly, flat feet, joint contractures at the elbows and knees, malar hypoplasia, a senile facial appearance, deep-set eyes with down-slanting palpebral fissures, hypoplastic and crumpled external ear cartilage, a sagging mouth, prominent coronal suture, and brachycephaly. Ophthalmologic evaluation confirmed bilateral ectopia lentis with lens subluxation. The musculoskeletal severity was assessed using the Ghent criteria, yielding a total score of 11 points, supporting a diagnosis of severe MFS.\\n\\nCardiac evaluation revealed a grade V/VI systolic murmur at the upper and left lower sternal borders, accompanied by a parasternal heave. Echocardiography demonstrated poor left ventricular contractility, severe pulmonary hypertension, a dilated aortic sinus (20.2 mm), with Z-scores of 8.08 (Boston), 6.37 (Detroit), and 5.97 (Halifax), indicating extreme dilation. Multiple valvular abnormalities were present: moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation. These findings are consistent with progressive valvular degeneration due to impaired extracellular matrix integrity.\\n\\nGenetic analysis via Sanger sequencing and polymerase chain reaction (PCR) of the fibrillin-1 (FBN1) gene identified a novel heterozygous mutation at nucleotide position c.3964 + 1G > T, located in intron 32 of the FBN1 gene. This mutation affects the splice site of exon 32 and is classified as a pathogenic variant based on the 2015 ACMG/AMP guidelines. The mutation lies within the previously defined 'neonatal region' of the FBN1 gene (exons 24–32), which is associated with a more severe, early-onset phenotype of MFS, including neonatal cardiac involvement and rapid progression of valvular and musculoskeletal pathology.\\n\\nOn postnatal day 1, refractory hypoxemia was observed despite >60% oxygen supplementation, indicating inadequate cardiac output and pulmonary perfusion. Medical management was initiated to address low cardiac output secondary to severe mitral and aortic regurgitation. Therapeutic interventions included milrinone (an inodilator) for afterload reduction, continuous fentanyl sedation to suppress myocardial oxygen demand, and diuretic therapy to manage oliguria and fluid overload. Despite these measures, the infant developed progressive respiratory failure, worsening pulmonary hypertension, and deteriorating cardiac contractility. Echocardiographic follow-up confirmed progressive worsening of aortic and mitral regurgitation, with sustained severe pulmonary hypertension.\\n\\nMultidisciplinary team consultations with the family and clinical staff concluded that surgical intervention—such as valve repair or replacement—was not feasible given the rapid disease progression and poor prognosis. Palliative care was initiated instead. Over the following weeks, the infant developed hepatic and pulmonary congestion, pulmonary hemorrhage, and ultimately progressed to multiple organ dysfunction syndrome (MODS). The patient died 32 days after birth. This case exemplifies the severe, early-onset form of Marfan syndrome associated with a novel FBN1 mutation in the neonatal region, characterized by profound cardiac dysfunction, valvular deterioration, and multisystem involvement, underscoring the critical need for early genetic diagnosis and the limitations of medical therapy"}
{"row_index": 121, "doc_id": 79, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old woman with a long-term blood condition called beta thalassemia has been having swollen, bleeding gums and bad breath since she became pregnant. She is 16 weeks pregnant and has not seen a dentist before or since. Her gums are red, soft, and bleed easily, and her lips are dry and peeling. This is common when you have both thalassemia and are pregnant. She also has a weak body and was once diagnosed with knee pain from thalassemia-related arthritis. Her blood tests show signs of infection and anemia, which is why she needs regular blood transfusions — but she stopped them during pregnancy. The doctors treated her gums with a special mouth rinse (chlorine dioxide), a hydrogen peroxide swab, antibiotics, and cleaning of her teeth. They also gave her instructions to brush gently and use a small toothbrush between her teeth. After three months of care, her gums healed, the bleeding stopped, and she no longer has bad breath or swollen gums. She is now doing well and keeps her mouth clean with daily care. The team of doctors, dentists, and nurses worked together to fix her problem.\"\n}", "generated_text": "A 27-year-old woman with a long-term blood condition called beta thalassemia has been having swollen, bleeding gums and bad breath since she became pregnant. She is 16 weeks pregnant and has not seen a dentist before or since. Her gums are red, soft, and bleed easily, and her lips are dry and peeling. This is common when you have both thalassemia and are pregnant. She also has a weak body and was once diagnosed with knee pain from thalassemia-related arthritis. Her blood tests show signs of infection and anemia, which is why she needs regular blood transfusions — but she stopped them during pregnancy. The doctors treated her gums with a special mouth rinse (chlorine dioxide), a hydrogen peroxide swab, antibiotics, and cleaning of her teeth. They also gave her instructions to brush gently and use a small toothbrush between her teeth. After three months of care, her gums healed, the bleeding stopped, and she no longer has bad breath or swollen gums. She is now doing well and keeps her mouth clean with daily care. The team of doctors, dentists, and nurses worked together to fix her problem."}
{"row_index": 122, "doc_id": 79, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 27-year-old woman with beta thalassemia major, a condition that requires monthly blood transfusions and iron-lowering drugs, is now pregnant at 16 weeks. Because of her pregnancy, she stopped her blood transfusions and iron treatments. She has been experiencing swollen, bleeding gums, bad breath, and dry, peeling lips. She has never seen a dentist before or since. During her check-up, her dentist found that her gums were red, soft, and swollen with bleeding, and there were deep pockets in her mouth — signs of gum disease. Her blood tests showed anemia and signs of infection, which are common in beta thalassemia. The doctors diagnosed her with gum enlargement and chronic periodontitis (gum disease) linked to both her pregnancy and beta thalassemia. \\n\\nTo treat her condition, she received a combination of care: her gums were cleaned with a 3% hydrogen peroxide solution, she used a chlorine dioxide mouthwash (Oxyfresh®) three times a day, and took antibiotics for a short time. Her dentist also removed tartar and gave her instructions on how to brush and floss properly. Blood transfusions were given monthly during treatment. After three months of care from an oral medicine specialist, a periodontist, and an internist, her symptoms improved greatly. By the end of the treatment, her gums had healed, she no longer had bleeding or bad breath, and she was able to brush without pain. She is now following a routine at home, including using mouthwash, applying petroleum jelly to her lips, and using an interdental brush to keep her mouth clean. The overall outcome was positive because she followed the treatment plan and stayed consistent with her care.\"\n}", "generated_text": "A 27-year-old woman with beta thalassemia major, a condition that requires monthly blood transfusions and iron-lowering drugs, is now pregnant at 16 weeks. Because of her pregnancy, she stopped her blood transfusions and iron treatments. She has been experiencing swollen, bleeding gums, bad breath, and dry, peeling lips. She has never seen a dentist before or since. During her check-up, her dentist found that her gums were red, soft, and swollen with bleeding, and there were deep pockets in her mouth — signs of gum disease. Her blood tests showed anemia and signs of infection, which are common in beta thalassemia. The doctors diagnosed her with gum enlargement and chronic periodontitis (gum disease) linked to both her pregnancy and beta thalassemia. \n\nTo treat her condition, she received a combination of care: her gums were cleaned with a 3% hydrogen peroxide solution, she used a chlorine dioxide mouthwash (Oxyfresh®) three times a day, and took antibiotics for a short time. Her dentist also removed tartar and gave her instructions on how to brush and floss properly. Blood transfusions were given monthly during treatment. After three months of care from an oral medicine specialist, a periodontist, and an internist, her symptoms improved greatly. By the end of the treatment, her gums had healed, she no longer had bleeding or bad breath, and she was able to brush without pain. She is now following a routine at home, including using mouthwash, applying petroleum jelly to her lips, and using an interdental brush to keep her mouth clean. The overall outcome was positive because she followed the treatment plan and stayed consistent with her care."}
{"row_index": 123, "doc_id": 20, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 38-year-old woman named A.P. was diagnosed with dilated cardiomyopathy at age 17, after having a severe case of tonsillitis that may have led to heart inflammation (myocarditis), though this was never proven. She developed serious heart failure symptoms and was hospitalized for 10 months and 9 days. At the time, her heart was not pumping effectively — her ejection fraction was only 10%, and she was at high risk of dying. She received treatment to support heart function, prevent dangerous heart rhythms, and reduce blood clots. Over time, her heart function improved, and by age 21, her ejection fraction reached 48–57%, marking a period of remission. This improvement lasted for 4 years, after which her condition worsened, and her ejection fraction dropped to 25%. She was hospitalized again for two months and then stabilized with adjusted treatment. By 2006, her heart function had recovered to 50%.\\n\\nAt age 27, she had a successful first pregnancy. After giving birth, her heart function remained stable at around 40%, and she continued with heart medications. In 2015, she became pregnant again. During the second trimester, at 35 weeks, she was hospitalized due to shortness of breath and inability to walk. Her ejection fraction dropped to 18%, and her heart failure worsened. Despite this, her doctors decided to continue the pregnancy. She had a C-section at 39 weeks, and her condition improved within 20 days.\\n\\nIn October 2016, her treatment was updated to include medications like ramipril, metoprolol, spironolactone, and ivabradine, along with a daily fluid limit of 1.5 liters. She also wore a life-saving device called a LifeVest defibrillator from December 2016 to February 2017, when it was removed. After removal, her ejection fraction was 44%, and doctors found no need for a permanent defibrillator. She is now stable on medication, can do normal daily activities, and is a mother of two children. She is not working, but her heart condition is well-controlled with regular check-ups, weight management, and monitoring of kidney function and electrolytes. Her diagnosis remains dilated cardiomyopathy with heart failure stage II, and no further device is needed at this time.\"\n}", "generated_text": "A 38-year-old woman named A.P. was diagnosed with dilated cardiomyopathy at age 17, after having a severe case of tonsillitis that may have led to heart inflammation (myocarditis), though this was never proven. She developed serious heart failure symptoms and was hospitalized for 10 months and 9 days. At the time, her heart was not pumping effectively — her ejection fraction was only 10%, and she was at high risk of dying. She received treatment to support heart function, prevent dangerous heart rhythms, and reduce blood clots. Over time, her heart function improved, and by age 21, her ejection fraction reached 48–57%, marking a period of remission. This improvement lasted for 4 years, after which her condition worsened, and her ejection fraction dropped to 25%. She was hospitalized again for two months and then stabilized with adjusted treatment. By 2006, her heart function had recovered to 50%.\n\nAt age 27, she had a successful first pregnancy. After giving birth, her heart function remained stable at around 40%, and she continued with heart medications. In 2015, she became pregnant again. During the second trimester, at 35 weeks, she was hospitalized due to shortness of breath and inability to walk. Her ejection fraction dropped to 18%, and her heart failure worsened. Despite this, her doctors decided to continue the pregnancy. She had a C-section at 39 weeks, and her condition improved within 20 days.\n\nIn October 2016, her treatment was updated to include medications like ramipril, metoprolol, spironolactone, and ivabradine, along with a daily fluid limit of 1.5 liters. She also wore a life-saving device called a LifeVest defibrillator from December 2016 to February 2017, when it was removed. After removal, her ejection fraction was 44%, and doctors found no need for a permanent defibrillator. She is now stable on medication, can do normal daily activities, and is a mother of two children. She is not working, but her heart condition is well-controlled with regular check-ups, weight management, and monitoring of kidney function and electrolytes. Her diagnosis remains dilated cardiomyopathy with heart failure stage II, and no further device is needed at this time."}
{"row_index": 124, "doc_id": 24, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 13-year-old boy was brought to the hospital after finding a noticeable lump in his left groin area. He had no fever, weight loss, or other general symptoms. The lump was soft, movable, and not painful. His medical history included a past spinal surgery six years ago that left him with limited movement and sensation in his legs, and he had developed pressure sores from being in bed for a long time. Blood tests showed a slightly high inflammation marker (ESR), but all other blood and organ function tests were normal. A CT scan found enlarged lymph nodes in the groin area, the largest being about 3.5 cm in size, but no other abnormalities were seen. Since the lump could have been a sign of serious conditions like lymphoma or leukemia, surgery was done to remove the lymph nodes for testing. The tissue sample showed changes consistent with a rare form of Castleman’s disease called plasma cell type, which is very uncommon in children. This case is the first reported instance of unicentric Castleman disease (UCD) in the groin area. After 12 months of follow-up, the boy had no new symptoms, no further lymph node swelling, and all test results remained normal. He was given a short course of prednisolone and continues to be monitored every three months with regular check-ups and imaging.\"\n}", "generated_text": "A 13-year-old boy was brought to the hospital after finding a noticeable lump in his left groin area. He had no fever, weight loss, or other general symptoms. The lump was soft, movable, and not painful. His medical history included a past spinal surgery six years ago that left him with limited movement and sensation in his legs, and he had developed pressure sores from being in bed for a long time. Blood tests showed a slightly high inflammation marker (ESR), but all other blood and organ function tests were normal. A CT scan found enlarged lymph nodes in the groin area, the largest being about 3.5 cm in size, but no other abnormalities were seen. Since the lump could have been a sign of serious conditions like lymphoma or leukemia, surgery was done to remove the lymph nodes for testing. The tissue sample showed changes consistent with a rare form of Castleman’s disease called plasma cell type, which is very uncommon in children. This case is the first reported instance of unicentric Castleman disease (UCD) in the groin area. After 12 months of follow-up, the boy had no new symptoms, no further lymph node swelling, and all test results remained normal. He was given a short course of prednisolone and continues to be monitored every three months with regular check-ups and imaging."}
{"row_index": 125, "doc_id": 27, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 28-year-old man developed two red, raised patches on his right arm and forearm, each with small blisters and a shallow ulcer, about halfway between the elbow and the wrist. The areas were painful and itchy, but he had no fever or other systemic symptoms. He had been on vacation in a coastal area of Ecuador when the rash appeared. A small skin sample was taken and examined under a microscope, which showed signs consistent with a skin condition caused by exposure to a type of beetle found in tropical regions. The diagnosis was Paederus dermatitis, a rash caused by contact with the beetle’s secretion. He was treated with antihistamines, a topical steroid cream, and cold compresses. After 8 days, the rash went away, though the skin remained slightly darker in those areas as a result of the inflammation.\"\n}", "generated_text": "A 28-year-old man developed two red, raised patches on his right arm and forearm, each with small blisters and a shallow ulcer, about halfway between the elbow and the wrist. The areas were painful and itchy, but he had no fever or other systemic symptoms. He had been on vacation in a coastal area of Ecuador when the rash appeared. A small skin sample was taken and examined under a microscope, which showed signs consistent with a skin condition caused by exposure to a type of beetle found in tropical regions. The diagnosis was Paederus dermatitis, a rash caused by contact with the beetle’s secretion. He was treated with antihistamines, a topical steroid cream, and cold compresses. After 8 days, the rash went away, though the skin remained slightly darker in those areas as a result of the inflammation."}
{"row_index": 126, "doc_id": 29, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 77-year-old woman had repeated episodes of vomiting blood (haematemesis). She had high blood pressure and high cholesterol, but no other major health problems. When she first came to the emergency room, she was shaky and had low blood pressure, and her blood tests showed anaemia, which pointed to bleeding in her upper digestive tract.\\n\\nA CT scan was done to check the cause. It showed that the third part of the duodenum (a section of the small intestine) bent sharply to the right side of the aorta and went downward without crossing in front of it. The duodenal-jejunal junction (where the duodenum meets the jejunum) and the jejunum were also on the right side. This raised concern that she might have intestinal malrotation — a condition where the intestines are abnormally positioned.\\n\\nHowever, seven days later, a repeat CT scan showed that the intestines had moved back to the normal position on their own. This didn’t match typical malrotation, which is usually permanent. Instead, it suggested a different problem: dysplasia of the ligament of Treitz — a condition where the ligament that normally holds the small intestine in place is abnormally formed or weak.\\n\\nA few months later, she had another episode of vomiting blood. The CT scan again showed the duodenum and jejunum on the right side. Endoscopy (a procedure to look inside the stomach) found a tear at the gastric cardia (the area where the stomach meets the esophagus), which is a known cause of bleeding called Mallory-Weiss syndrome.\\n\\nLater, during surgery (laparotomy), doctors found that the ligament of Treitz was present but not properly fixed to the jejunum. It was only attached to the duodenum, so it could move easily and caused the intestine to shift to the right side. The rest of the intestines were in normal position, and there was no malrotation.\\n\\nThe surgery fixed the upper jejunum to the back of the abdomen, and the patient recovered well and has not had any further bleeding since.\\n\\nIn short, the repeated, temporary shifts of the small intestine were not due to malrotation, but to a weak or abnormal ligament of Treitz, which allowed the intestine to move freely and cause symptoms during vomiting.\"\n}", "generated_text": "A 77-year-old woman had repeated episodes of vomiting blood (haematemesis). She had high blood pressure and high cholesterol, but no other major health problems. When she first came to the emergency room, she was shaky and had low blood pressure, and her blood tests showed anaemia, which pointed to bleeding in her upper digestive tract.\n\nA CT scan was done to check the cause. It showed that the third part of the duodenum (a section of the small intestine) bent sharply to the right side of the aorta and went downward without crossing in front of it. The duodenal-jejunal junction (where the duodenum meets the jejunum) and the jejunum were also on the right side. This raised concern that she might have intestinal malrotation — a condition where the intestines are abnormally positioned.\n\nHowever, seven days later, a repeat CT scan showed that the intestines had moved back to the normal position on their own. This didn’t match typical malrotation, which is usually permanent. Instead, it suggested a different problem: dysplasia of the ligament of Treitz — a condition where the ligament that normally holds the small intestine in place is abnormally formed or weak.\n\nA few months later, she had another episode of vomiting blood. The CT scan again showed the duodenum and jejunum on the right side. Endoscopy (a procedure to look inside the stomach) found a tear at the gastric cardia (the area where the stomach meets the esophagus), which is a known cause of bleeding called Mallory-Weiss syndrome.\n\nLater, during surgery (laparotomy), doctors found that the ligament of Treitz was present but not properly fixed to the jejunum. It was only attached to the duodenum, so it could move easily and caused the intestine to shift to the right side. The rest of the intestines were in normal position, and there was no malrotation.\n\nThe surgery fixed the upper jejunum to the back of the abdomen, and the patient recovered well and has not had any further bleeding since.\n\nIn short, the repeated, temporary shifts of the small intestine were not due to malrotation, but to a weak or abnormal ligament of Treitz, which allowed the intestine to move freely and cause symptoms during vomiting."}
{"row_index": 127, "doc_id": 31, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 12-year-old boy with Down Syndrome and movement problems was referred to the Oral Medicine Department. He had a distinctive facial appearance and dry, cracked lips. Because he wore a cervical collar, doctors could not check his lymph nodes. Inside his mouth, there was a 1×0.7 cm ulcer on the right side of his tongue, with a hard edge and a white-yellow base. The ulcer looked like oral cancer (OSCC) at first, but doctors found it was actually a chronic traumatic ulcer caused by sharp teeth. The tooth at the back of the upper jaw (tooth 55) was sharp and was rubbing against the tongue, causing the injury. The patient also had damaged teeth and tooth remnants on several teeth, which were recommended to be removed and replaced with a space maintainer to prevent shifting of other teeth.\\n\\nThe boy had low sodium levels and higher lymphocyte counts, and an MRI showed dislocation in his neck spine. He was given treatments including salt water (0.9% sodium chloride), povidone-iodine mouthwash (1%) to clean and reduce inflammation, and petroleum jelly to keep his lips moist. His mother was taught how to care for his mouth at home: using gauze soaked in salt water, applying the mouthwash three times a day to the ulcer, and using petroleum jelly on his lips.\\n\\nAfter a few days, the ulcer and lip condition improved. By the 10-day follow-up, the ulcer had greatly reduced. Two days after that, the boy had surgery on his neck spine. He was then admitted to the Pediatric Intensive Care Unit, where he later developed respiratory failure and passed away after two weeks of care.\"\n}", "generated_text": "A 12-year-old boy with Down Syndrome and movement problems was referred to the Oral Medicine Department. He had a distinctive facial appearance and dry, cracked lips. Because he wore a cervical collar, doctors could not check his lymph nodes. Inside his mouth, there was a 1×0.7 cm ulcer on the right side of his tongue, with a hard edge and a white-yellow base. The ulcer looked like oral cancer (OSCC) at first, but doctors found it was actually a chronic traumatic ulcer caused by sharp teeth. The tooth at the back of the upper jaw (tooth 55) was sharp and was rubbing against the tongue, causing the injury. The patient also had damaged teeth and tooth remnants on several teeth, which were recommended to be removed and replaced with a space maintainer to prevent shifting of other teeth.\n\nThe boy had low sodium levels and higher lymphocyte counts, and an MRI showed dislocation in his neck spine. He was given treatments including salt water (0.9% sodium chloride), povidone-iodine mouthwash (1%) to clean and reduce inflammation, and petroleum jelly to keep his lips moist. His mother was taught how to care for his mouth at home: using gauze soaked in salt water, applying the mouthwash three times a day to the ulcer, and using petroleum jelly on his lips.\n\nAfter a few days, the ulcer and lip condition improved. By the 10-day follow-up, the ulcer had greatly reduced. Two days after that, the boy had surgery on his neck spine. He was then admitted to the Pediatric Intensive Care Unit, where he later developed respiratory failure and passed away after two weeks of care."}
{"row_index": 128, "doc_id": 34, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 19-month-old boy was brought to the emergency room after falling from his highchair. He hit his head and started vomiting, became very irritable, and had fast breathing and heart rate. His oxygen levels were low, and he showed signs of serious breathing difficulty, including pulling in his stomach muscles and weak breath sounds on the left side of his chest. Despite treatment with a breathing tube and oxygen, his oxygen levels kept dropping, so doctors decided to insert a tube into his windpipe to help him breathe. A lung ultrasound showed signs of lung collapse, and a chest CT scan revealed that the entire left lung was collapsed, with a sudden blockage in the main airway of the left lung, about 12 mm from the main branch. This raised suspicion of a foreign object — an almond — being stuck in the airway. The mother reported that the child had had a sudden, intense cough a few days before that went away on its own. A rigid bronchoscopy was performed, and a 2 cm almond was found and removed. The boy had never eaten almonds before and likely swallowed it by accident. After recovery, his breathing improved, and he was able to breathe on his own again within 24 hours. He was then moved to a regular pediatric ward for further care and full recovery.\"\n}", "generated_text": "A 19-month-old boy was brought to the emergency room after falling from his highchair. He hit his head and started vomiting, became very irritable, and had fast breathing and heart rate. His oxygen levels were low, and he showed signs of serious breathing difficulty, including pulling in his stomach muscles and weak breath sounds on the left side of his chest. Despite treatment with a breathing tube and oxygen, his oxygen levels kept dropping, so doctors decided to insert a tube into his windpipe to help him breathe. A lung ultrasound showed signs of lung collapse, and a chest CT scan revealed that the entire left lung was collapsed, with a sudden blockage in the main airway of the left lung, about 12 mm from the main branch. This raised suspicion of a foreign object — an almond — being stuck in the airway. The mother reported that the child had had a sudden, intense cough a few days before that went away on its own. A rigid bronchoscopy was performed, and a 2 cm almond was found and removed. The boy had never eaten almonds before and likely swallowed it by accident. After recovery, his breathing improved, and he was able to breathe on his own again within 24 hours. He was then moved to a regular pediatric ward for further care and full recovery."}
{"row_index": 129, "doc_id": 35, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 4-month-old boy lived in a prison cell with his mom and two other people. He had a painful lump in his armpit and X-rays showed broken ribs and lung problems. Doctors thought it might be abuse, so he went to the hospital. He was very sick — low oxygen, fever, and swelling — and had a big abscess. Tests showed his body couldn’t fight off infections well. Bacteria were not found, but a fungus called Aspergillus fumigatus was found in the abscess. He got antibiotics and then antifungal medicine (voriconazole) for 28 days. A test showed he had a rare immune problem called chronic granulomatous disease, caused by a gene fault passed from his mom. At 8 months, the infection got worse and spread to his shoulder. He had more lung damage and needed more medicine. At 12 months, he got sick again with the same fungus, even after treatment, and died.\"\n}", "generated_text": "A 4-month-old boy lived in a prison cell with his mom and two other people. He had a painful lump in his armpit and X-rays showed broken ribs and lung problems. Doctors thought it might be abuse, so he went to the hospital. He was very sick — low oxygen, fever, and swelling — and had a big abscess. Tests showed his body couldn’t fight off infections well. Bacteria were not found, but a fungus called Aspergillus fumigatus was found in the abscess. He got antibiotics and then antifungal medicine (voriconazole) for 28 days. A test showed he had a rare immune problem called chronic granulomatous disease, caused by a gene fault passed from his mom. At 8 months, the infection got worse and spread to his shoulder. He had more lung damage and needed more medicine. At 12 months, he got sick again with the same fungus, even after treatment, and died."}
{"row_index": 130, "doc_id": 36, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 25-year-old man had painful sores on his lips and inside his mouth. The sores started a few days ago, got worse when he ate or talked, and he tried using petroleum jelly but it didn’t help. He started using a medicine ointment (triamcinolone) on his lips, and the pain got better, but the sores didn’t go away. He had a fever before the sores came, didn’t eat well for a long time, and often licked his lips. He had chickenpox as a child. The sores were red, bumpy, and bled easily. A test showed he had a virus called HSV-1, which means the sores were caused by a common virus. The doctor said it was HAEM — a condition where the body reacts to stress and poor diet with mouth sores. To fix it, he took vitamins, used an antiviral medicine (acyclovir), and used a salt water rinse. He was also told to brush his teeth and tongue gently, avoid spicy or sour foods, stop licking his lips, and eat better. After a few days, his sores healed completely and he felt much better. Now he needs to keep going to the dentist for more care.\"\n}", "generated_text": "A 25-year-old man had painful sores on his lips and inside his mouth. The sores started a few days ago, got worse when he ate or talked, and he tried using petroleum jelly but it didn’t help. He started using a medicine ointment (triamcinolone) on his lips, and the pain got better, but the sores didn’t go away. He had a fever before the sores came, didn’t eat well for a long time, and often licked his lips. He had chickenpox as a child. The sores were red, bumpy, and bled easily. A test showed he had a virus called HSV-1, which means the sores were caused by a common virus. The doctor said it was HAEM — a condition where the body reacts to stress and poor diet with mouth sores. To fix it, he took vitamins, used an antiviral medicine (acyclovir), and used a salt water rinse. He was also told to brush his teeth and tongue gently, avoid spicy or sour foods, stop licking his lips, and eat better. After a few days, his sores healed completely and he felt much better. Now he needs to keep going to the dentist for more care."}
{"row_index": 131, "doc_id": 36, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 25-year-old man came to the dental clinic with painful sores on his lips that started about four days ago and spread to his upper and lower lips two days later. The sores were painful, especially when eating or talking, and didn't improve with self-treatment like petroleum jelly. He tried using triamcinolone ointment, which helped a little, but the sores didn’t fully heal.\\n\\nHe had a fever a week before the sores appeared and had been under a lot of stress with poor nutrition for about a month. He didn’t have any medical conditions, allergies, or habits like smoking or drinking alcohol. However, he often licked his lips, which may have worsened the sores. He also had chickenpox as a child.\\n\\nOn examination, his lips had red, painful sores with crusts that bled easily. His tongue had white patches, and there were other minor oral issues like tooth decay and poor hygiene. A blood test for herpes virus (HSV-1) came back positive, which confirmed the diagnosis of HAEM — a condition caused by herpes virus that affects the mouth and lips, especially in people under stress or with poor nutrition.\\n\\nTreatment included applying a topical ointment (triamcinolone) to the lips, taking oral multivitamins, and using acyclovir tablets to fight the virus. He was also advised to improve his diet, avoid spicy or acidic foods, stop licking his lips, and keep his mouth clean by brushing teeth and tongue daily.\\n\\nAfter a few days, his pain improved and the sores began to heal. By the second follow-up, all the sores had healed completely. His quality of life improved significantly, and he was referred to continue regular dental care. The case was reviewed and approved for publication, following ethical guidelines.\"\n}", "generated_text": "A 25-year-old man came to the dental clinic with painful sores on his lips that started about four days ago and spread to his upper and lower lips two days later. The sores were painful, especially when eating or talking, and didn't improve with self-treatment like petroleum jelly. He tried using triamcinolone ointment, which helped a little, but the sores didn’t fully heal.\n\nHe had a fever a week before the sores appeared and had been under a lot of stress with poor nutrition for about a month. He didn’t have any medical conditions, allergies, or habits like smoking or drinking alcohol. However, he often licked his lips, which may have worsened the sores. He also had chickenpox as a child.\n\nOn examination, his lips had red, painful sores with crusts that bled easily. His tongue had white patches, and there were other minor oral issues like tooth decay and poor hygiene. A blood test for herpes virus (HSV-1) came back positive, which confirmed the diagnosis of HAEM — a condition caused by herpes virus that affects the mouth and lips, especially in people under stress or with poor nutrition.\n\nTreatment included applying a topical ointment (triamcinolone) to the lips, taking oral multivitamins, and using acyclovir tablets to fight the virus. He was also advised to improve his diet, avoid spicy or acidic foods, stop licking his lips, and keep his mouth clean by brushing teeth and tongue daily.\n\nAfter a few days, his pain improved and the sores began to heal. By the second follow-up, all the sores had healed completely. His quality of life improved significantly, and he was referred to continue regular dental care. The case was reviewed and approved for publication, following ethical guidelines."}
{"row_index": 132, "doc_id": 37, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 29-year-old woman had heavy vaginal bleeding for a month and was living with HIV. Her immune cells (CD4) were very low at 26, meaning her body was weak. A biopsy showed a serious cancer in her cervix that spread beyond the cervix, called extra-nodal BL. This cancer was stage 3B, meaning it had reached her kidneys and pelvic walls. Doctors said she needed chemo and radiation, but it took her 43 days to get treatment because of a long waiting list. That delay was too long — doctors say treatment should start within 48 hours. She died 43 days after diagnosis, before getting treatment. During those days, no more scans could be done because the machines were broken. She got blood transfusions and pain relief, but still passed away. The main reason she died was likely the fast-spreading cancer, especially since she had weak immunity and high virus levels. But her body also failed in many ways — her kidneys and blood system stopped working. Doctors couldn’t do a final test after she died, but they believe the cancer was the main cause, with organ failure as the final result.\"\n}", "generated_text": "A 29-year-old woman had heavy vaginal bleeding for a month and was living with HIV. Her immune cells (CD4) were very low at 26, meaning her body was weak. A biopsy showed a serious cancer in her cervix that spread beyond the cervix, called extra-nodal BL. This cancer was stage 3B, meaning it had reached her kidneys and pelvic walls. Doctors said she needed chemo and radiation, but it took her 43 days to get treatment because of a long waiting list. That delay was too long — doctors say treatment should start within 48 hours. She died 43 days after diagnosis, before getting treatment. During those days, no more scans could be done because the machines were broken. She got blood transfusions and pain relief, but still passed away. The main reason she died was likely the fast-spreading cancer, especially since she had weak immunity and high virus levels. But her body also failed in many ways — her kidneys and blood system stopped working. Doctors couldn’t do a final test after she died, but they believe the cancer was the main cause, with organ failure as the final result."}
{"row_index": 133, "doc_id": 38, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 56-year-old woman was diagnosed in 2013 with Sjogren’s syndrome, a condition that affects dryness in the mouth and eyes, and which also led to lung disease (interstitial lung disease) and pulmonary arterial hypertension (PAH). She was treated with several medications, including sildenafil, bosentan, macitentan, iloprost, and corticosteroids, but her condition continued to worsen. By 2020, she was experiencing severe shortness of breath, cough, and signs of heart failure, including low oxygen levels and high levels of a heart-related marker (BNP), which led to cardiogenic shock. She was hospitalized, treated in the ICU, and stabilized, but her condition remained serious and required frequent hospital visits.\\n\\nIn May 2023, she started a new treatment called molecular hydrogen therapy, taking one capsule per day. This therapy involved hydrogen-rich capsules made from coral calcium. After starting the treatment, tests showed an increase in certain immune cells (CD127+ Treg cells) and a decrease in harmful autoantibodies (anti-Ro) and B cell activity. Her symptoms, such as shortness of breath, stabilized without any side effects. Blood tests confirmed these changes in her immune system. This treatment is being used as an added support, not a replacement for standard care, and so far, it has helped improve her health without causing harm.\"\n}", "generated_text": "A 56-year-old woman was diagnosed in 2013 with Sjogren’s syndrome, a condition that affects dryness in the mouth and eyes, and which also led to lung disease (interstitial lung disease) and pulmonary arterial hypertension (PAH). She was treated with several medications, including sildenafil, bosentan, macitentan, iloprost, and corticosteroids, but her condition continued to worsen. By 2020, she was experiencing severe shortness of breath, cough, and signs of heart failure, including low oxygen levels and high levels of a heart-related marker (BNP), which led to cardiogenic shock. She was hospitalized, treated in the ICU, and stabilized, but her condition remained serious and required frequent hospital visits.\n\nIn May 2023, she started a new treatment called molecular hydrogen therapy, taking one capsule per day. This therapy involved hydrogen-rich capsules made from coral calcium. After starting the treatment, tests showed an increase in certain immune cells (CD127+ Treg cells) and a decrease in harmful autoantibodies (anti-Ro) and B cell activity. Her symptoms, such as shortness of breath, stabilized without any side effects. Blood tests confirmed these changes in her immune system. This treatment is being used as an added support, not a replacement for standard care, and so far, it has helped improve her health without causing harm."}
{"row_index": 134, "doc_id": 44, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 12-year-old boy was admitted because he had recently started getting headaches and was drinking and urinating a lot. He had no other medical problems. Tests showed he had diabetes insipidus (DI), a condition where the body can't properly regulate water balance, causing excessive urination and thirst. MRI scans found a rare condition called Rathke cleft cyst apoplexy, which is a sudden bleeding or swelling in a cyst in the pituitary area, but it wasn't pressing on any brain parts or causing serious issues. His hormone levels were mostly normal, and there were no signs of other endocrine problems. Because the cyst was stable and not causing harm, the doctors chose a watchful approach — regular check-ups with blood tests, physical exams, and MRI scans instead of surgery. Over three years, the boy developed normally, including puberty, with no major hormone problems except for a small deficiency in growth hormone. His growth slowed slightly, and after testing, it was found he had a partial growth hormone deficiency. He started treatment with growth hormone, and his growth improved over the next year. The cyst on the MRI stayed stable and even slightly decreased in size over time. The team of doctors, including endocrinologists and neurosurgeons, agreed that ongoing monitoring was safe and effective.\"\n}", "generated_text": "A 12-year-old boy was admitted because he had recently started getting headaches and was drinking and urinating a lot. He had no other medical problems. Tests showed he had diabetes insipidus (DI), a condition where the body can't properly regulate water balance, causing excessive urination and thirst. MRI scans found a rare condition called Rathke cleft cyst apoplexy, which is a sudden bleeding or swelling in a cyst in the pituitary area, but it wasn't pressing on any brain parts or causing serious issues. His hormone levels were mostly normal, and there were no signs of other endocrine problems. Because the cyst was stable and not causing harm, the doctors chose a watchful approach — regular check-ups with blood tests, physical exams, and MRI scans instead of surgery. Over three years, the boy developed normally, including puberty, with no major hormone problems except for a small deficiency in growth hormone. His growth slowed slightly, and after testing, it was found he had a partial growth hormone deficiency. He started treatment with growth hormone, and his growth improved over the next year. The cyst on the MRI stayed stable and even slightly decreased in size over time. The team of doctors, including endocrinologists and neurosurgeons, agreed that ongoing monitoring was safe and effective."}
{"row_index": 135, "doc_id": 45, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 67-year-old man with no prior medical problems started having trouble swallowing, a hoarse voice, and a general decline in health over six months. He developed a large mass in his neck that was confirmed by biopsy to be a slow-growing type of lymphoma called grade 1 and 2 follicular non-Hodgkin lymphoma. Imaging showed the mass was 70 mm by 40 mm and had spread into nearby areas. Blood tests and bone marrow checks were normal at the start of treatment. The patient received four courses of chemotherapy (rituximab plus CHOP — a combination of drugs including cyclophosphamide, doxorubicin, prednisone, and oncovin) with no improvement. He then had three more courses of a different chemotherapy (rituximab plus DHAOX) with no response either. During follow-up, the biopsy of the mass showed that the lymphoma cells had disappeared and were replaced by AL amyloid deposits, which are a sign of abnormal protein buildup. Blood tests found high levels of immunoglobulin M, a type of antibody. A PET scan showed the mass was very active (hypermetabolic), which is a sign of ongoing disease. The patient is now on a new treatment plan with bortezomib, prednisone, and bendamustine, and is showing improvement after the first dose.\"\n}", "generated_text": "A 67-year-old man with no prior medical problems started having trouble swallowing, a hoarse voice, and a general decline in health over six months. He developed a large mass in his neck that was confirmed by biopsy to be a slow-growing type of lymphoma called grade 1 and 2 follicular non-Hodgkin lymphoma. Imaging showed the mass was 70 mm by 40 mm and had spread into nearby areas. Blood tests and bone marrow checks were normal at the start of treatment. The patient received four courses of chemotherapy (rituximab plus CHOP — a combination of drugs including cyclophosphamide, doxorubicin, prednisone, and oncovin) with no improvement. He then had three more courses of a different chemotherapy (rituximab plus DHAOX) with no response either. During follow-up, the biopsy of the mass showed that the lymphoma cells had disappeared and were replaced by AL amyloid deposits, which are a sign of abnormal protein buildup. Blood tests found high levels of immunoglobulin M, a type of antibody. A PET scan showed the mass was very active (hypermetabolic), which is a sign of ongoing disease. The patient is now on a new treatment plan with bortezomib, prednisone, and bendamustine, and is showing improvement after the first dose."}
{"row_index": 136, "doc_id": 49, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 16-year-old girl has a flat, grayish patch on her left thigh that has been there since birth. The patch is about 10.5 cm wide and 8.0 cm long, and it has darkened and become depressed over time. It has small blood vessels running around the edge, and the area shows signs of abnormal blood flow. Imaging tests (angioresonance) found that the patch is caused by a vascular malformation in the skin and layer beneath the skin, fed by branches of the popliteal artery. The blood flow shows early signs of shunting, meaning blood is taking an unusual path. There is a small visible vein running under the skin, but no blood vessels have spread into the muscle or bone. The patch does not affect the length of her legs.\"\n}", "generated_text": "A 16-year-old girl has a flat, grayish patch on her left thigh that has been there since birth. The patch is about 10.5 cm wide and 8.0 cm long, and it has darkened and become depressed over time. It has small blood vessels running around the edge, and the area shows signs of abnormal blood flow. Imaging tests (angioresonance) found that the patch is caused by a vascular malformation in the skin and layer beneath the skin, fed by branches of the popliteal artery. The blood flow shows early signs of shunting, meaning blood is taking an unusual path. There is a small visible vein running under the skin, but no blood vessels have spread into the muscle or bone. The patch does not affect the length of her legs."}
{"row_index": 137, "doc_id": 50, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 57-year-old woman with asthma and allergies had stomach pain that came and went for two months. She lost weight and felt tired, but had no fever or diarrhea. Blood tests showed a high number of a type of white blood cell called eosinophils, and her IgG4 levels were high. Doctors checked for infections and other causes, but nothing was found. A tissue sample from her colon showed too many eosinophils, which confirmed a condition called eosinophilic colitis. She was treated with steroids and a medicine called montelukast. Her symptoms went away in two weeks, and after that, she stayed on montelukast for three months with no pain coming back.\"\n}", "generated_text": "A 57-year-old woman with asthma and allergies had stomach pain that came and went for two months. She lost weight and felt tired, but had no fever or diarrhea. Blood tests showed a high number of a type of white blood cell called eosinophils, and her IgG4 levels were high. Doctors checked for infections and other causes, but nothing was found. A tissue sample from her colon showed too many eosinophils, which confirmed a condition called eosinophilic colitis. She was treated with steroids and a medicine called montelukast. Her symptoms went away in two weeks, and after that, she stayed on montelukast for three months with no pain coming back."}
{"row_index": 138, "doc_id": 52, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 2.5-year-old girl with a history of neurofibromatosis type 1 (NF1) was brought in with bloody diarrhea that had lasted for several weeks. She had been having 5 to 10 episodes of diarrhea per day, with blood streaks, and had lost some weight. Tests initially showed a rotavirus infection, but that didn’t explain the ongoing symptoms. After being hospitalized for dehydration, her symptoms returned with blood in the stool, low appetite, and weight loss.\\n\\nAn endoscopy exam showed red, inflamed lining in her colon from the anus all the way to the beginning of the large intestine (the cecum), with loss of normal blood vessel visibility. Biopsies of the colon tissue showed signs of chronic inflammation, which is consistent with ulcerative colitis. Additionally, a test for cytomegalovirus (CMV) found a positive result, meaning the child had an active CMV infection.\\n\\nThe child was treated with antiviral medication (ganciclovir) for the CMV, which helped reduce the virus load. Her symptoms improved during hospitalization, and she stopped having bloody stools and abdominal pain. However, after two months, the inflammation returned, with bloody diarrhea again. A repeat endoscopy confirmed ongoing inflammation throughout the colon. She was treated with antibiotics and corticosteroids, which worked well, and she now has mild, ongoing symptoms.\\n\\nShe continues to be managed with a medication called mesalazine to help control the inflammation and is being monitored regularly. Her condition is stable, but she needs long-term care due to the chronic nature of the disease and her underlying NF1.\"\n}", "generated_text": "A 2.5-year-old girl with a history of neurofibromatosis type 1 (NF1) was brought in with bloody diarrhea that had lasted for several weeks. She had been having 5 to 10 episodes of diarrhea per day, with blood streaks, and had lost some weight. Tests initially showed a rotavirus infection, but that didn’t explain the ongoing symptoms. After being hospitalized for dehydration, her symptoms returned with blood in the stool, low appetite, and weight loss.\n\nAn endoscopy exam showed red, inflamed lining in her colon from the anus all the way to the beginning of the large intestine (the cecum), with loss of normal blood vessel visibility. Biopsies of the colon tissue showed signs of chronic inflammation, which is consistent with ulcerative colitis. Additionally, a test for cytomegalovirus (CMV) found a positive result, meaning the child had an active CMV infection.\n\nThe child was treated with antiviral medication (ganciclovir) for the CMV, which helped reduce the virus load. Her symptoms improved during hospitalization, and she stopped having bloody stools and abdominal pain. However, after two months, the inflammation returned, with bloody diarrhea again. A repeat endoscopy confirmed ongoing inflammation throughout the colon. She was treated with antibiotics and corticosteroids, which worked well, and she now has mild, ongoing symptoms.\n\nShe continues to be managed with a medication called mesalazine to help control the inflammation and is being monitored regularly. Her condition is stable, but she needs long-term care due to the chronic nature of the disease and her underlying NF1."}
{"row_index": 139, "doc_id": 53, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 40-year-old man with HIV who was taking his medicine regularly came in with fevers that came and went for two years. Recently, he started having bad pain in his belly, especially on the right side, and his organs — liver and spleen — got bigger. He also had swollen lymph nodes all over. Lab tests showed his blood was weak, his body was fighting off infections, and his proteins were low. X-rays showed big liver and spleen, swollen lymph nodes, and a tree-like pattern in his lung, plus fluid in his lungs and belly. He got worse fast, had liver failure, and ended up in the ICU. He died a few hours later. After he died, doctors found tuberculosis in his lung sample and saw small, harmless spots in his liver that didn’t destroy tissue. This case shows how HIV can lead to serious infections when the body is weak.\"\n}", "generated_text": "A 40-year-old man with HIV who was taking his medicine regularly came in with fevers that came and went for two years. Recently, he started having bad pain in his belly, especially on the right side, and his organs — liver and spleen — got bigger. He also had swollen lymph nodes all over. Lab tests showed his blood was weak, his body was fighting off infections, and his proteins were low. X-rays showed big liver and spleen, swollen lymph nodes, and a tree-like pattern in his lung, plus fluid in his lungs and belly. He got worse fast, had liver failure, and ended up in the ICU. He died a few hours later. After he died, doctors found tuberculosis in his lung sample and saw small, harmless spots in his liver that didn’t destroy tissue. This case shows how HIV can lead to serious infections when the body is weak."}
{"row_index": 140, "doc_id": 53, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 40-year-old man with HIV who had been consistently taking his medication came in with recurring fevers over two years. These fevers didn’t follow a regular pattern and were only temporarily relieved with anti-inflammatory drugs. In the past two months, he developed widespread abdominal pain, especially on the right side, along with swelling in his liver and spleen. He also had enlarged lymph nodes throughout his body. Lab tests showed low blood cell counts, blood clotting problems, low protein levels, and signs of inflammation. Imaging scans showed enlarged liver and spleen and widespread lymph node swelling. Tests for bacteria like Mycobacterium were mostly negative, except for a detection of HHV-8 in a lab test. A biopsy of a lymph node in his pelvis found signs of Castleman’s disease. Even after restarting his HIV treatment, his symptoms got worse. He was started on corticosteroids and ganciclovir, but after one week, he developed severe organ failure and swelling (anasarca), which made the treatment unsafe. A new chest scan showed tree-like patterns in the upper right lung and fluid around both lungs, and his liver and spleen continued to grow larger with more abdominal fluid. He was admitted to the intensive care unit 48 hours later and died shortly after from sudden liver failure. After death, tests on a sample from his airway found Mycobacterium tuberculosis, and a liver biopsy showed small, non-destructive granulomas.\"\n}", "generated_text": "A 40-year-old man with HIV who had been consistently taking his medication came in with recurring fevers over two years. These fevers didn’t follow a regular pattern and were only temporarily relieved with anti-inflammatory drugs. In the past two months, he developed widespread abdominal pain, especially on the right side, along with swelling in his liver and spleen. He also had enlarged lymph nodes throughout his body. Lab tests showed low blood cell counts, blood clotting problems, low protein levels, and signs of inflammation. Imaging scans showed enlarged liver and spleen and widespread lymph node swelling. Tests for bacteria like Mycobacterium were mostly negative, except for a detection of HHV-8 in a lab test. A biopsy of a lymph node in his pelvis found signs of Castleman’s disease. Even after restarting his HIV treatment, his symptoms got worse. He was started on corticosteroids and ganciclovir, but after one week, he developed severe organ failure and swelling (anasarca), which made the treatment unsafe. A new chest scan showed tree-like patterns in the upper right lung and fluid around both lungs, and his liver and spleen continued to grow larger with more abdominal fluid. He was admitted to the intensive care unit 48 hours later and died shortly after from sudden liver failure. After death, tests on a sample from his airway found Mycobacterium tuberculosis, and a liver biopsy showed small, non-destructive granulomas."}
{"row_index": 141, "doc_id": 54, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 4-month-old baby from a rural village in Panama, far from any hospital, was sick with diarrhea and could not keep fluids down. She was very weak, had no weight, and was dehydrated — her body was dry and she couldn’t cry properly. She didn’t get breast milk and was fed powdered milk, which wasn’t enough. Her family had no electricity, no clean water, and lived in a simple house with a thatched roof. She didn’t get vaccines or any medical care for the first four months of life. When she came to a health center, she had diarrhea for four days, no fever, no cough, but she was vomiting. Doctors gave her a medicine called Enterogermina to help her gut. Because she kept getting worse, she was taken to a bigger hospital and then to a major hospital in Panama City. There, she had trouble breathing, her skin was cold and pale, her heart was racing, and her blood pressure was very low. Tests showed she had a dangerous bacteria in her blood called MRSA and also had a gut infection from Clostridiodes difficile. A good bacteria called Bacillus clausii was found in her blood over several days. Even with strong antibiotics, she kept getting sicker. She developed heart problems, her kidneys stopped working, and her body failed in many ways. After 12 days, she died. No autopsy was done because the mother didn’t want to.\"\n}", "generated_text": "A 4-month-old baby from a rural village in Panama, far from any hospital, was sick with diarrhea and could not keep fluids down. She was very weak, had no weight, and was dehydrated — her body was dry and she couldn’t cry properly. She didn’t get breast milk and was fed powdered milk, which wasn’t enough. Her family had no electricity, no clean water, and lived in a simple house with a thatched roof. She didn’t get vaccines or any medical care for the first four months of life. When she came to a health center, she had diarrhea for four days, no fever, no cough, but she was vomiting. Doctors gave her a medicine called Enterogermina to help her gut. Because she kept getting worse, she was taken to a bigger hospital and then to a major hospital in Panama City. There, she had trouble breathing, her skin was cold and pale, her heart was racing, and her blood pressure was very low. Tests showed she had a dangerous bacteria in her blood called MRSA and also had a gut infection from Clostridiodes difficile. A good bacteria called Bacillus clausii was found in her blood over several days. Even with strong antibiotics, she kept getting sicker. She developed heart problems, her kidneys stopped working, and her body failed in many ways. After 12 days, she died. No autopsy was done because the mother didn’t want to."}
{"row_index": 142, "doc_id": 54, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 4-month-old indigenous infant from a rural area in Panama, living 3 hours by canoe from the nearest health center, arrived at a hospital with severe diarrhea and dehydration. She had not been breastfed and was given powdered milk instead, which may have contributed to her poor health. Her family lived in a basic home without electricity or running water, relying on a well and a river for waste disposal. She did not receive any vaccines or prenatal care during her early life.\\n\\nShe first visited a local health center with 4 days of diarrhea, vomiting, and no fever or breathing problems. Doctors gave her oral fluids and a medication called Enterogermina (which contains B. clausii bacteria) to help her gut recover. Because she was severely dehydrated, she was transferred to a larger hospital and then to a major hospital in Panama City.\\n\\nWhen she arrived at the hospital, she was very weak, with dry mouth, no tears, and signs of shock — including cold hands and feet, a fast heartbeat, and low blood pressure. She had swelling in her hands, feet, face, and belly. Tests showed she had a serious infection, including methicillin-resistant Staphylococcus aureus (MRSA) in her blood, and later, Clostridiodes difficile (a harmful gut bacteria) was found. B. clausii, a beneficial bacteria, was also found in her blood over several days.\\n\\nShe received multiple antibiotics, but the infection kept getting worse. Her body began to fail in many systems — her heart, kidneys, and organs stopped working properly. She developed acute heart inflammation (myocarditis) and kidney failure. Despite treatment, including IV antibiotics, fluids, and medications to support her organs, she died 12 days after being admitted to the hospital. No autopsy was done because the mother refused, due to cultural reasons.\"\n}", "generated_text": "A 4-month-old indigenous infant from a rural area in Panama, living 3 hours by canoe from the nearest health center, arrived at a hospital with severe diarrhea and dehydration. She had not been breastfed and was given powdered milk instead, which may have contributed to her poor health. Her family lived in a basic home without electricity or running water, relying on a well and a river for waste disposal. She did not receive any vaccines or prenatal care during her early life.\n\nShe first visited a local health center with 4 days of diarrhea, vomiting, and no fever or breathing problems. Doctors gave her oral fluids and a medication called Enterogermina (which contains B. clausii bacteria) to help her gut recover. Because she was severely dehydrated, she was transferred to a larger hospital and then to a major hospital in Panama City.\n\nWhen she arrived at the hospital, she was very weak, with dry mouth, no tears, and signs of shock — including cold hands and feet, a fast heartbeat, and low blood pressure. She had swelling in her hands, feet, face, and belly. Tests showed she had a serious infection, including methicillin-resistant Staphylococcus aureus (MRSA) in her blood, and later, Clostridiodes difficile (a harmful gut bacteria) was found. B. clausii, a beneficial bacteria, was also found in her blood over several days.\n\nShe received multiple antibiotics, but the infection kept getting worse. Her body began to fail in many systems — her heart, kidneys, and organs stopped working properly. She developed acute heart inflammation (myocarditis) and kidney failure. Despite treatment, including IV antibiotics, fluids, and medications to support her organs, she died 12 days after being admitted to the hospital. No autopsy was done because the mother refused, due to cultural reasons."}
{"row_index": 143, "doc_id": 55, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 2-year-old girl was brought in with a 1-year history of painless swelling in her left eye, where the eye had slowly moved forward and was pointing inward and upward. Her vision was very limited, with only light sensation in the left eye. Examining her eye, doctors found that the eye was stuck in position and couldn’t move properly. A soft, well-defined lump was felt in the lower part of her left eye socket, and her lower eyelid was turned outward. The pupil was large and didn’t react to light. MRI scans showed a clear mass inside the eye socket that appeared dark on T1-weighted images and bright on T2-weighted images. The mass did not take up contrast, which helped rule out some other conditions. The diagnosis of orbital teratoma — a type of tumor containing different tissues like skin, cartilage, and brain tissue — was confirmed through tissue testing and lab analysis. The doctors removed the tumor using a small incision inside the lower eyelid, along with cutting the lower eyelid and outer corner of the eye to give better access. During surgery, they found a grayish-white cystic mass with a clear border, and it was tightly attached to the optic nerve. Because the tumor was large and the space was limited, they removed most of the fluid and completely excised the mass. One month after surgery, the child developed a sunken eye (enophthalmos), redness of the eyelid (conjunctival hyperemia), and inflammation of the cornea (keratitis). This happened because the tumor had previously stretched the eye socket, and after removal, the space collapsed. To fix this, a second surgery was done, where a donated sclera (the white part of the eye) was implanted into the socket to restore volume and help the eye sit properly again. After one year of follow-up, no tumor came back, and there were no other serious complications. The child’s vision stayed the same, though she still has a slight sunken eye and a small issue with the outer corner of her eye.\"\n}", "generated_text": "A 2-year-old girl was brought in with a 1-year history of painless swelling in her left eye, where the eye had slowly moved forward and was pointing inward and upward. Her vision was very limited, with only light sensation in the left eye. Examining her eye, doctors found that the eye was stuck in position and couldn’t move properly. A soft, well-defined lump was felt in the lower part of her left eye socket, and her lower eyelid was turned outward. The pupil was large and didn’t react to light. MRI scans showed a clear mass inside the eye socket that appeared dark on T1-weighted images and bright on T2-weighted images. The mass did not take up contrast, which helped rule out some other conditions. The diagnosis of orbital teratoma — a type of tumor containing different tissues like skin, cartilage, and brain tissue — was confirmed through tissue testing and lab analysis. The doctors removed the tumor using a small incision inside the lower eyelid, along with cutting the lower eyelid and outer corner of the eye to give better access. During surgery, they found a grayish-white cystic mass with a clear border, and it was tightly attached to the optic nerve. Because the tumor was large and the space was limited, they removed most of the fluid and completely excised the mass. One month after surgery, the child developed a sunken eye (enophthalmos), redness of the eyelid (conjunctival hyperemia), and inflammation of the cornea (keratitis). This happened because the tumor had previously stretched the eye socket, and after removal, the space collapsed. To fix this, a second surgery was done, where a donated sclera (the white part of the eye) was implanted into the socket to restore volume and help the eye sit properly again. After one year of follow-up, no tumor came back, and there were no other serious complications. The child’s vision stayed the same, though she still has a slight sunken eye and a small issue with the outer corner of her eye."}
{"row_index": 144, "doc_id": 57, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"This study follows a 9-year-old girl who has both high intellectual abilities and dyslexia, a learning disorder that makes reading and writing difficult. The goal was to see how her reading, writing, and phonological skills improved after targeted therapy. Before the intervention, she was reading at an early stage (alphabetic level), writing in a transitional phase between syllabic and alphabetic systems, and had weak phonological processing skills. After six months of weekly therapy focused on phonological skills—like recognizing sounds, blending sounds, and improving memory—the child showed clear progress. Her phonological processing improved, her writing became more consistent and reached the alphabetic level, and her reading speed increased significantly—from about 20 to 94 words per minute. She also showed better ability to access words quickly in her mind. However, some writing problems remained, such as mixing up similar letters and making small spelling errors. The therapy helped her catch up in key areas, especially in reading and sound processing, even though she still faces some challenges typical of dyslexia. This case shows that with focused support, children with high abilities and dyslexia can make meaningful progress in learning to read and write.\"\n}", "generated_text": "This study follows a 9-year-old girl who has both high intellectual abilities and dyslexia, a learning disorder that makes reading and writing difficult. The goal was to see how her reading, writing, and phonological skills improved after targeted therapy. Before the intervention, she was reading at an early stage (alphabetic level), writing in a transitional phase between syllabic and alphabetic systems, and had weak phonological processing skills. After six months of weekly therapy focused on phonological skills—like recognizing sounds, blending sounds, and improving memory—the child showed clear progress. Her phonological processing improved, her writing became more consistent and reached the alphabetic level, and her reading speed increased significantly—from about 20 to 94 words per minute. She also showed better ability to access words quickly in her mind. However, some writing problems remained, such as mixing up similar letters and making small spelling errors. The therapy helped her catch up in key areas, especially in reading and sound processing, even though she still faces some challenges typical of dyslexia. This case shows that with focused support, children with high abilities and dyslexia can make meaningful progress in learning to read and write."}
{"row_index": 145, "doc_id": 59, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"We report the first case of heatstroke occurring at the same time as a severe SARS-CoV-2 infection in a 52-year-old man. He first tested positive for the virus after having a cold, then returned to work without fever. But while working outdoors in very hot weather (35°C) for five hours, he lost consciousness. When brought to the hospital, his body temperature was extremely high at 40°C, and he was in a coma. Doctors diagnosed him with heatstroke and a serious COVID-19 infection, which caused multiple organ damage. He received treatment including intravenous antibiotics, fluids, blood pressure support, mechanical ventilation, and care for his blood clotting problems. Despite initial improvement, he later developed shortness of breath and a brain bleed. He also had a multi-pathogen lung infection and a severe blood clotting disorder that led to failure of several organs (MODS), which ultimately caused his death. This case shows that heatstroke can happen alongside severe COVID-19, and it can lead to serious complications even in people with no known health problems.\"\n}", "generated_text": "We report the first case of heatstroke occurring at the same time as a severe SARS-CoV-2 infection in a 52-year-old man. He first tested positive for the virus after having a cold, then returned to work without fever. But while working outdoors in very hot weather (35°C) for five hours, he lost consciousness. When brought to the hospital, his body temperature was extremely high at 40°C, and he was in a coma. Doctors diagnosed him with heatstroke and a serious COVID-19 infection, which caused multiple organ damage. He received treatment including intravenous antibiotics, fluids, blood pressure support, mechanical ventilation, and care for his blood clotting problems. Despite initial improvement, he later developed shortness of breath and a brain bleed. He also had a multi-pathogen lung infection and a severe blood clotting disorder that led to failure of several organs (MODS), which ultimately caused his death. This case shows that heatstroke can happen alongside severe COVID-19, and it can lead to serious complications even in people with no known health problems."}
{"row_index": 146, "doc_id": 60, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 19-year-old woman was admitted to the hospital with severe headaches, nausea, vomiting, fever, and very high blood pressure. She had a large adrenal mass found on imaging, and initial tests suggested possible infection or heart inflammation. Her blood pressure was extremely high (189/120 mmHg), and her heart rate was fast, leading to concerns about heart damage. She had a history of similar symptoms a year earlier, when she was diagnosed with myocarditis and hypertension, but she did not follow up on her blood pressure treatment. Her father had a history of sudden death, which raised concerns about a genetic condition.\\n\\nTests showed very high levels of certain hormones, including catecholamines, which are produced by the adrenal glands. These findings pointed to a condition called pheochromocytoma — a tumor of the adrenal gland that can cause high blood pressure and other symptoms. Genetic testing revealed a mutation in the RET gene, linked to a condition called MEN2A, which can cause tumors in multiple endocrine glands.\\n\\nFurther testing found a small thyroid nodule with slightly elevated calcitonin levels, but normal parathyroid hormone and calcium levels. After surgery to remove the adrenal tumor, the patient remained stable. Over the next 15 months, her thyroid nodule stayed the same size, and her calcitonin levels remained mildly high. However, her parathyroid hormone and blood calcium levels slowly increased. A scan for parathyroid tumors came back negative, meaning no parathyroid tumor was found.\\n\\nThe patient is now doing well after surgery and is being followed up regularly without any signs of recurrence.\"\n}", "generated_text": "A 19-year-old woman was admitted to the hospital with severe headaches, nausea, vomiting, fever, and very high blood pressure. She had a large adrenal mass found on imaging, and initial tests suggested possible infection or heart inflammation. Her blood pressure was extremely high (189/120 mmHg), and her heart rate was fast, leading to concerns about heart damage. She had a history of similar symptoms a year earlier, when she was diagnosed with myocarditis and hypertension, but she did not follow up on her blood pressure treatment. Her father had a history of sudden death, which raised concerns about a genetic condition.\n\nTests showed very high levels of certain hormones, including catecholamines, which are produced by the adrenal glands. These findings pointed to a condition called pheochromocytoma — a tumor of the adrenal gland that can cause high blood pressure and other symptoms. Genetic testing revealed a mutation in the RET gene, linked to a condition called MEN2A, which can cause tumors in multiple endocrine glands.\n\nFurther testing found a small thyroid nodule with slightly elevated calcitonin levels, but normal parathyroid hormone and calcium levels. After surgery to remove the adrenal tumor, the patient remained stable. Over the next 15 months, her thyroid nodule stayed the same size, and her calcitonin levels remained mildly high. However, her parathyroid hormone and blood calcium levels slowly increased. A scan for parathyroid tumors came back negative, meaning no parathyroid tumor was found.\n\nThe patient is now doing well after surgery and is being followed up regularly without any signs of recurrence."}
{"row_index": 147, "doc_id": 62, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 13-year-old boy came to the emergency department with sudden chest pain on the sides of his chest, which worsened when he coughed. The pain was not severe, and he didn’t have shortness of breath, fever, or other symptoms like joint pain or fatigue. He had a mild cold and a single fever spike, but otherwise felt fine. He was active, doing canoeing twice a week, and had no known exposure to infections or environmental irritants. His past chest X-ray, taken four years earlier during a cold, showed a similar lung pattern that was treated with azithromycin and has not returned since.\\n\\nAt the hospital, his breathing was normal, oxygen levels were good, and his physical exam showed reduced breath sounds in the lower part of his lungs. A new chest X-ray showed a similar lung pattern as before. A detailed lung scan (CT) found widespread, cloudy areas in both lungs, covering more than 65% of the lung tissue, which is typical of a condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including COVID-19, came back negative. A lung fluid sample (bronchoalveolar lavage) showed a milky appearance and tested positive for a specific stain (periodic acid-Schiff), which supports the diagnosis of PAP. Lung function tests showed a mild restriction in how much air he could breathe out (FVC at 77%) and a moderate drop in lung capacity to transfer oxygen (DLCO at 48.6%).\\n\\nGenetic testing ruled out known causes of PAP related to surfactant problems. Testing for antibodies against a protein called GM-CSF was strongly positive, which suggests the body is attacking its own lung cells — pointing to an autoimmune form of PAP. At 20 months of follow-up, the boy is still symptom-free, breathing normally, and continues to exercise regularly. His lung function has improved slightly and remains stable. Since he has no symptoms and is doing well, treatment has been delayed, and he is being monitored regularly at the clinic.\"\n}", "generated_text": "A 13-year-old boy came to the emergency department with sudden chest pain on the sides of his chest, which worsened when he coughed. The pain was not severe, and he didn’t have shortness of breath, fever, or other symptoms like joint pain or fatigue. He had a mild cold and a single fever spike, but otherwise felt fine. He was active, doing canoeing twice a week, and had no known exposure to infections or environmental irritants. His past chest X-ray, taken four years earlier during a cold, showed a similar lung pattern that was treated with azithromycin and has not returned since.\n\nAt the hospital, his breathing was normal, oxygen levels were good, and his physical exam showed reduced breath sounds in the lower part of his lungs. A new chest X-ray showed a similar lung pattern as before. A detailed lung scan (CT) found widespread, cloudy areas in both lungs, covering more than 65% of the lung tissue, which is typical of a condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including COVID-19, came back negative. A lung fluid sample (bronchoalveolar lavage) showed a milky appearance and tested positive for a specific stain (periodic acid-Schiff), which supports the diagnosis of PAP. Lung function tests showed a mild restriction in how much air he could breathe out (FVC at 77%) and a moderate drop in lung capacity to transfer oxygen (DLCO at 48.6%).\n\nGenetic testing ruled out known causes of PAP related to surfactant problems. Testing for antibodies against a protein called GM-CSF was strongly positive, which suggests the body is attacking its own lung cells — pointing to an autoimmune form of PAP. At 20 months of follow-up, the boy is still symptom-free, breathing normally, and continues to exercise regularly. His lung function has improved slightly and remains stable. Since he has no symptoms and is doing well, treatment has been delayed, and he is being monitored regularly at the clinic."}
{"row_index": 148, "doc_id": 66, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 17-year-old boy was found to have a small metal object in his nose during a routine dental exam. He had no symptoms like nosebleeds, congestion, or discomfort. His parents remembered when he was seven that he had inserted a small object into his nose, but at that time, no imaging was done and the issue was never followed up. Over the years, they thought the object had fallen out on its own. Later, imaging showed a shiny, metallic snap button stuck in the floor of his right nasal cavity, likely there for over 10 years. The object was covered in mucus and crust, showing signs of long-term exposure. It was safely removed under local anesthesia with a simple procedure that caused little bleeding. After removal, the nose healed well, and the patient is doing fine now. He’s being given nasal rinses to keep the area clean and is doing well at his follow-up visit.\"\n}", "generated_text": "A 17-year-old boy was found to have a small metal object in his nose during a routine dental exam. He had no symptoms like nosebleeds, congestion, or discomfort. His parents remembered when he was seven that he had inserted a small object into his nose, but at that time, no imaging was done and the issue was never followed up. Over the years, they thought the object had fallen out on its own. Later, imaging showed a shiny, metallic snap button stuck in the floor of his right nasal cavity, likely there for over 10 years. The object was covered in mucus and crust, showing signs of long-term exposure. It was safely removed under local anesthesia with a simple procedure that caused little bleeding. After removal, the nose healed well, and the patient is doing fine now. He’s being given nasal rinses to keep the area clean and is doing well at his follow-up visit."}
{"row_index": 149, "doc_id": 66, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 17-year-old male with no significant past medical or family history was referred to the clinic from the dental department following an incidental discovery of a nasal foreign body (NFB) during preoperative orthodontic planning, which included routine dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. Parental recall indicated that at age seven, the patient had inserted a small object into his nose; at that time, no imaging was performed, and an anterior rhinoscopy was attempted due to non-cooperative behavior, leading the physician to recommend removal under sedation. However, the family did not pursue follow-up, and given the absence of symptoms, they assumed the foreign body had spontaneously expelled. Endoscopic evaluation of the right nasal cavity revealed a deviated nasal septum with inferior turbinate hypertrophy, erythematous and mildly edematous mucosa, and a foreign body lodged and adherent to the floor of the nasal cavity beneath the inferior turbinate. The object was partially obscured by mucus and crusted material, exhibiting a shiny surface consistent with metallic composition. Radiographic assessment using lateral and frontal x-rays demonstrated a circular, radiopaque lesion located in the floor of the right nasal cavity, morphologically consistent with a metallic snap button. No abnormalities in adjacent bony structures were observed. CBCT further confirmed the presence of the foreign body and revealed mild inflammatory changes within the nasal mucosa, with no evidence of significant bony erosion, sinus involvement, or spread to adjacent anatomic spaces. With informed parental consent, the foreign body was removed under local anesthesia in a semi-sitting position to minimize the risk of dislodgment into the airway. Prior to retrieval, the nasal cavity was decongested with Xylometazoline 0.1%, and Lidocaine spray (10 mg/spray) was administered to the right nostril. A hook was used to disengage the object, which was then extracted using bayonet forceps. The procedure was uncomplicated, with minimal bleeding effectively controlled by saline irrigation. Post-removal examination showed no significant mucosal injury or tissue necrosis. The retrieved object, identified as a metallic snap button measuring 1 cm in diameter, demonstrated extensive corrosion and accumulation of biological material, consistent with prolonged retention over a period exceeding ten years. The patient was discharged in stable condition and prescribed daily nasal rinses with 0.9% sodium chloride irrigation solution. At a two-week follow-up, the patient was clinically stable with no signs of recurrence, inflammation, or obstruction, and endoscopic examination remained unremarkable. This case underscores the potential for long-term retention of small metallic foreign bodies in the nasal cavity, particularly in children, with delayed presentation due to asymptomatic course, highlighting the importance of thorough imaging evaluation and timely intervention when such objects are incidentally detected, even in the absence of clinical symptoms. The presence of corrosion and biofilm formation suggests prolonged exposure, which may contribute to chronic local inflammation and tissue remodeling, although no structural damage was observed in this case.\"\n}", "generated_text": "A 17-year-old male with no significant past medical or family history was referred to the clinic from the dental department following an incidental discovery of a nasal foreign body (NFB) during preoperative orthodontic planning, which included routine dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. Parental recall indicated that at age seven, the patient had inserted a small object into his nose; at that time, no imaging was performed, and an anterior rhinoscopy was attempted due to non-cooperative behavior, leading the physician to recommend removal under sedation. However, the family did not pursue follow-up, and given the absence of symptoms, they assumed the foreign body had spontaneously expelled. Endoscopic evaluation of the right nasal cavity revealed a deviated nasal septum with inferior turbinate hypertrophy, erythematous and mildly edematous mucosa, and a foreign body lodged and adherent to the floor of the nasal cavity beneath the inferior turbinate. The object was partially obscured by mucus and crusted material, exhibiting a shiny surface consistent with metallic composition. Radiographic assessment using lateral and frontal x-rays demonstrated a circular, radiopaque lesion located in the floor of the right nasal cavity, morphologically consistent with a metallic snap button. No abnormalities in adjacent bony structures were observed. CBCT further confirmed the presence of the foreign body and revealed mild inflammatory changes within the nasal mucosa, with no evidence of significant bony erosion, sinus involvement, or spread to adjacent anatomic spaces. With informed parental consent, the foreign body was removed under local anesthesia in a semi-sitting position to minimize the risk of dislodgment into the airway. Prior to retrieval, the nasal cavity was decongested with Xylometazoline 0.1%, and Lidocaine spray (10 mg/spray) was administered to the right nostril. A hook was used to disengage the object, which was then extracted using bayonet forceps. The procedure was uncomplicated, with minimal bleeding effectively controlled by saline irrigation. Post-removal examination showed no significant mucosal injury or tissue necrosis. The retrieved object, identified as a metallic snap button measuring 1 cm in diameter, demonstrated extensive corrosion and accumulation of biological material, consistent with prolonged retention over a period exceeding ten years. The patient was discharged in stable condition and prescribed daily nasal rinses with 0.9% sodium chloride irrigation solution. At a two-week follow-up, the patient was clinically stable with no signs of recurrence, inflammation, or obstruction, and endoscopic examination remained unremarkable. This case underscores the potential for long-term retention of small metallic foreign bodies in the nasal cavity, particularly in children, with delayed presentation due to asymptomatic course, highlighting the importance of thorough imaging evaluation and timely intervention when such objects are incidentally detected, even in the absence of clinical symptoms. The presence of corrosion and biofilm formation suggests prolonged exposure, which may contribute to chronic local inflammation and tissue remodeling, although no structural damage was observed in this case."}
{"row_index": 150, "doc_id": 67, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 18-year-old boy came to the emergency room with sudden chest pain, fever, and trouble breathing, especially when lying down. He had no history of heart problems, but his family had a heart condition in the past. Tests showed his heart was enlarged, his heart muscles were thick, and there was fluid around the heart. Doctors thought it was a virus called Coxsackie, which can cause heart and chest lining inflammation. He got medicine for that, but his breathing got worse and his blood pressure dropped. The fluid around the heart grew so big it was pressing on his heart, causing a life-threatening situation. They drained the fluid, but during that, he had a sudden stop in his heart rhythm and needed a machine to keep his heart and lungs working. Tests on his heart tissue showed no virus or inflammation, but a small lump on his arm was found to have a rare cancer called Epstein-Barr virus (EBV) positive natural killer/T-cell lymphoma. This cancer was likely causing the heart and heart lining problems. After starting cancer treatment, his heart function improved — the thick heart muscles got thinner, the fluid went away, and his breathing got better. He’s now on heart failure medicine and is doing well, with plans to finish chemotherapy and possibly get radiation or a stem cell transplant in the future.\"\n}", "generated_text": "A 18-year-old boy came to the emergency room with sudden chest pain, fever, and trouble breathing, especially when lying down. He had no history of heart problems, but his family had a heart condition in the past. Tests showed his heart was enlarged, his heart muscles were thick, and there was fluid around the heart. Doctors thought it was a virus called Coxsackie, which can cause heart and chest lining inflammation. He got medicine for that, but his breathing got worse and his blood pressure dropped. The fluid around the heart grew so big it was pressing on his heart, causing a life-threatening situation. They drained the fluid, but during that, he had a sudden stop in his heart rhythm and needed a machine to keep his heart and lungs working. Tests on his heart tissue showed no virus or inflammation, but a small lump on his arm was found to have a rare cancer called Epstein-Barr virus (EBV) positive natural killer/T-cell lymphoma. This cancer was likely causing the heart and heart lining problems. After starting cancer treatment, his heart function improved — the thick heart muscles got thinner, the fluid went away, and his breathing got better. He’s now on heart failure medicine and is doing well, with plans to finish chemotherapy and possibly get radiation or a stem cell transplant in the future."}
{"row_index": 151, "doc_id": 67, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"An 18-year-old male came to the emergency department with new chest pain, fever, and shortness of breath, especially when lying down. He had a dry cough and felt unwell for 3 to 4 days. His family history included a grandfather with heart disease, but he had no known heart problems himself. He worked at a car parts shop and planned to go to college.\\n\\nInitial tests showed high levels of a heart damage marker (troponin), widespread changes on his ECG, and an enlarged heart on X-ray. An echo test (TTE) revealed thickened heart muscle (severe biventricular concentric hypertrophy) and a small amount of fluid around the heart (pericardial effusion). Viral tests found high levels of Coxsackie virus A and B, which can cause viral pericarditis. His symptoms improved slightly with medications like ibuprofen and colchicine, and a heart catheterization showed no blocked arteries.\\n\\nHowever, by the fourth day, his condition worsened. He became very weak, had very low blood pressure, and developed a large pericardial effusion that was threatening to stop his heart (cardiac tamponade). A needle was inserted to remove the fluid (pericardiocentesis), but during the procedure, he went into cardiac arrest with no pulse. He needed emergency life support with a machine that takes over heart and lung functions (VA ECMO), and received blood transfusions due to bleeding.\\n\\nA biopsy of his heart tissue showed no signs of inflammation or infection, which made the initial diagnosis of viral pericarditis less likely. A skin biopsy from a small, painless lump on his right arm revealed a rare type of cancer called Epstein-Barr virus (EBV)-positive natural killer/T-cell lymphoma. This finding changed the diagnosis — the heart and pericardium were likely affected by this cancer, not just a virus.\\n\\nHe started chemotherapy for the lymphoma, and within days, his heart function began to improve. His heart pump strength (ejection fraction) increased from 10%–15% to 55%, the fluid around the heart went away, and the thickened heart muscle started to normalize. He is now on heart failure treatment and cardiac rehab.\\n\\nHe has completed five out of six chemotherapy sessions and is expected to finish the full course. He may now receive radiation therapy or a stem cell transplant. His care involves both cardiology and oncology teams, and he is doing much better overall.\"\n}", "generated_text": "An 18-year-old male came to the emergency department with new chest pain, fever, and shortness of breath, especially when lying down. He had a dry cough and felt unwell for 3 to 4 days. His family history included a grandfather with heart disease, but he had no known heart problems himself. He worked at a car parts shop and planned to go to college.\n\nInitial tests showed high levels of a heart damage marker (troponin), widespread changes on his ECG, and an enlarged heart on X-ray. An echo test (TTE) revealed thickened heart muscle (severe biventricular concentric hypertrophy) and a small amount of fluid around the heart (pericardial effusion). Viral tests found high levels of Coxsackie virus A and B, which can cause viral pericarditis. His symptoms improved slightly with medications like ibuprofen and colchicine, and a heart catheterization showed no blocked arteries.\n\nHowever, by the fourth day, his condition worsened. He became very weak, had very low blood pressure, and developed a large pericardial effusion that was threatening to stop his heart (cardiac tamponade). A needle was inserted to remove the fluid (pericardiocentesis), but during the procedure, he went into cardiac arrest with no pulse. He needed emergency life support with a machine that takes over heart and lung functions (VA ECMO), and received blood transfusions due to bleeding.\n\nA biopsy of his heart tissue showed no signs of inflammation or infection, which made the initial diagnosis of viral pericarditis less likely. A skin biopsy from a small, painless lump on his right arm revealed a rare type of cancer called Epstein-Barr virus (EBV)-positive natural killer/T-cell lymphoma. This finding changed the diagnosis — the heart and pericardium were likely affected by this cancer, not just a virus.\n\nHe started chemotherapy for the lymphoma, and within days, his heart function began to improve. His heart pump strength (ejection fraction) increased from 10%–15% to 55%, the fluid around the heart went away, and the thickened heart muscle started to normalize. He is now on heart failure treatment and cardiac rehab.\n\nHe has completed five out of six chemotherapy sessions and is expected to finish the full course. He may now receive radiation therapy or a stem cell transplant. His care involves both cardiology and oncology teams, and he is doing much better overall."}
{"row_index": 152, "doc_id": 72, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A woman had a weak heart after giving birth and got a new heart transplant. After the transplant, her kidneys were working fine at first. But later, her kidneys started to fail because of a virus called BK virus. The doctors found the virus in her blood and saw damage in her kidney tissue. They cut back on the medicines that weaken the immune system, which helped. After two years, her kidneys stayed stable, with a kidney function level that is still okay, even though her kidney numbers are low.\"\n}", "generated_text": "A woman had a weak heart after giving birth and got a new heart transplant. After the transplant, her kidneys were working fine at first. But later, her kidneys started to fail because of a virus called BK virus. The doctors found the virus in her blood and saw damage in her kidney tissue. They cut back on the medicines that weaken the immune system, which helped. After two years, her kidneys stayed stable, with a kidney function level that is still okay, even though her kidney numbers are low."}
{"row_index": 153, "doc_id": 72, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 39-year-old woman had a heart transplant due to peripartum cardiomyopathy. After the transplant, her kidneys initially worked well, with normal kidney function and no signs of kidney disease. However, in 2016, her kidney function started to decline, and by 2017, her creatinine had risen to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2. She was hospitalized, and tests showed no signs of infection or other common causes of kidney problems. A kidney biopsy was done and found to have active chronic tubulointerstitial nephritis linked to late-stage BK virus infection. The blood test showed a high BK virus load (log 4.5). Her immunosuppressive medications, especially tacrolimus, were reduced. After two years of follow-up, her kidney function stabilized at a serum creatinine of 2.5 mg/dL and a GFR of 23.4 mL/min/1.73m2. The virus load gradually decreased to undetectable levels, and she has had no further kidney issues or heart rejection episodes.\"\n}", "generated_text": "A 39-year-old woman had a heart transplant due to peripartum cardiomyopathy. After the transplant, her kidneys initially worked well, with normal kidney function and no signs of kidney disease. However, in 2016, her kidney function started to decline, and by 2017, her creatinine had risen to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2. She was hospitalized, and tests showed no signs of infection or other common causes of kidney problems. A kidney biopsy was done and found to have active chronic tubulointerstitial nephritis linked to late-stage BK virus infection. The blood test showed a high BK virus load (log 4.5). Her immunosuppressive medications, especially tacrolimus, were reduced. After two years of follow-up, her kidney function stabilized at a serum creatinine of 2.5 mg/dL and a GFR of 23.4 mL/min/1.73m2. The virus load gradually decreased to undetectable levels, and she has had no further kidney issues or heart rejection episodes."}
{"row_index": 154, "doc_id": 74, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 56-year-old Italian woman with a serious blood disorder called β-thalassemia major had a magnetic resonance imaging (MRI) scan to check how much iron was building up in her heart, liver, and pancreas. She has been needing regular blood transfusions since she was 7 years old and had previously had her spleen and gallbladder removed. At the time of the scan, she had no major problems with her heart, liver, or hormones, and was taking medications including deferasirox to remove iron, vitamin D, and luspatercept to help reduce her need for transfusions.\\n\\nThe MRI found a mass in the mediastinum (the area in the chest between the lungs), which had been seen before in a 2020 scan but had slightly grown. This mass showed only mild activity on a PET scan, which made doctors think it might be a type of thymoma — a tumor that develops in the thymus gland. However, a chest CT scan revealed multiple thin-walled cysts in both lungs, which are a sign of a condition called lymphangioleiomyomatosis (LAM), a rare lung disease often linked to certain conditions like thalassemia.\\n\\nThe patient had no symptoms like coughing or shortness of breath and was not a smoker. After a team of specialists reviewed her case, she had surgery to remove the thymoma mass and a small piece of lung tissue affected by LAM. The surgery results showed a type B2 thymoma with some cells at the edge of the removed tissue, meaning it wasn’t completely removed. The lung tissue showed signs of LAM, with cysts lined by specific cells and mild inflammation.\\n\\nFollowing surgery, she was recommended to receive adjuvant radiation therapy for the thymoma and to take sirolimus, a medication that helps control LAM, especially in people with thalassemia. This treatment plan is designed to manage both conditions and reduce the risk of future complications.\"\n}", "generated_text": "A 56-year-old Italian woman with a serious blood disorder called β-thalassemia major had a magnetic resonance imaging (MRI) scan to check how much iron was building up in her heart, liver, and pancreas. She has been needing regular blood transfusions since she was 7 years old and had previously had her spleen and gallbladder removed. At the time of the scan, she had no major problems with her heart, liver, or hormones, and was taking medications including deferasirox to remove iron, vitamin D, and luspatercept to help reduce her need for transfusions.\n\nThe MRI found a mass in the mediastinum (the area in the chest between the lungs), which had been seen before in a 2020 scan but had slightly grown. This mass showed only mild activity on a PET scan, which made doctors think it might be a type of thymoma — a tumor that develops in the thymus gland. However, a chest CT scan revealed multiple thin-walled cysts in both lungs, which are a sign of a condition called lymphangioleiomyomatosis (LAM), a rare lung disease often linked to certain conditions like thalassemia.\n\nThe patient had no symptoms like coughing or shortness of breath and was not a smoker. After a team of specialists reviewed her case, she had surgery to remove the thymoma mass and a small piece of lung tissue affected by LAM. The surgery results showed a type B2 thymoma with some cells at the edge of the removed tissue, meaning it wasn’t completely removed. The lung tissue showed signs of LAM, with cysts lined by specific cells and mild inflammation.\n\nFollowing surgery, she was recommended to receive adjuvant radiation therapy for the thymoma and to take sirolimus, a medication that helps control LAM, especially in people with thalassemia. This treatment plan is designed to manage both conditions and reduce the risk of future complications."}
{"row_index": 155, "doc_id": 75, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 49-year-old woman with long-term lupus (SLE) developed both kidney and heart failure over many years. She had lupus since childhood and was treated with several medications, including steroids and immunosuppressants, but stopped in 2002 due to hepatitis C. Over time, her kidneys failed, requiring dialysis, and her heart suffered damage, including heart attacks and weakened heart muscle. By 2007, her kidney function had worsened enough to need a biopsy, which showed active kidney disease. Despite treatments, her heart continued to fail, leading to serious heart problems like valve damage and a need for surgery in 2014. After surgery, her heart function remained poor, and she needed dialysis for 4 years before being ready for a kidney transplant.\\n\\nBefore the transplant, her heart was very weak—only 26% of its normal pumping ability—and she had high levels of a heart stress marker (BNP). Because of this, doctors added a heart-protective drug called Levosimendan to help her heart during surgery. The transplant was done with careful planning to protect her kidneys and heart, avoiding harmful medications and using fluid therapy to keep her stable. During recovery, her heart function slowly improved: by one month after surgery, her heart was pumping better (EF improved to 30%) and her exercise ability increased from very limited to normal. By five months, her heart function was much better, her BNP dropped to normal levels, and her kidneys were working properly again. The transplant was successful, and she is now recovering well.\"\n}", "generated_text": "A 49-year-old woman with long-term lupus (SLE) developed both kidney and heart failure over many years. She had lupus since childhood and was treated with several medications, including steroids and immunosuppressants, but stopped in 2002 due to hepatitis C. Over time, her kidneys failed, requiring dialysis, and her heart suffered damage, including heart attacks and weakened heart muscle. By 2007, her kidney function had worsened enough to need a biopsy, which showed active kidney disease. Despite treatments, her heart continued to fail, leading to serious heart problems like valve damage and a need for surgery in 2014. After surgery, her heart function remained poor, and she needed dialysis for 4 years before being ready for a kidney transplant.\n\nBefore the transplant, her heart was very weak—only 26% of its normal pumping ability—and she had high levels of a heart stress marker (BNP). Because of this, doctors added a heart-protective drug called Levosimendan to help her heart during surgery. The transplant was done with careful planning to protect her kidneys and heart, avoiding harmful medications and using fluid therapy to keep her stable. During recovery, her heart function slowly improved: by one month after surgery, her heart was pumping better (EF improved to 30%) and her exercise ability increased from very limited to normal. By five months, her heart function was much better, her BNP dropped to normal levels, and her kidneys were working properly again. The transplant was successful, and she is now recovering well."}
{"row_index": 156, "doc_id": 76, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 42-year-old woman with a chronic headache condition could not use certain medications because of side effects. When her headaches were very severe — scoring 9 out of 10 — she came to the pain clinic. Doctors took her to a local operating room and performed a nerve block using ultrasound guidance. This procedure targeted the greater occipital nerve in the neck and used a local anesthetic called bupivacaine. Right after the block, her headache pain dropped from 9/10 to just 2/10. The block was repeated once a week for a month. By the end of two months, her headaches had greatly improved: the number of attacks dropped from daily to just two per month, and the pain intensity decreased to 4/10. She had no side effects from the treatment and hasn’t had any attacks by the sixth month.\"\n}", "generated_text": "A 42-year-old woman with a chronic headache condition could not use certain medications because of side effects. When her headaches were very severe — scoring 9 out of 10 — she came to the pain clinic. Doctors took her to a local operating room and performed a nerve block using ultrasound guidance. This procedure targeted the greater occipital nerve in the neck and used a local anesthetic called bupivacaine. Right after the block, her headache pain dropped from 9/10 to just 2/10. The block was repeated once a week for a month. By the end of two months, her headaches had greatly improved: the number of attacks dropped from daily to just two per month, and the pain intensity decreased to 4/10. She had no side effects from the treatment and hasn’t had any attacks by the sixth month."}
{"row_index": 157, "doc_id": 78, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A baby was born early by C-section because the baby was not getting enough oxygen. The baby had a weak heart from birth and had serious problems with the heart valves, making it hard for blood to flow properly. The baby’s hands and feet were long and bent, the fingers couldn’t straighten, and the joints at elbows and knees were stuck. The face looked old, the eyes were deep-set and slanted, the ears were small and soft, and the mouth hung down. The baby also had a flat foot and a swollen belly. Tests showed the heart was too big, the blood pressure in the lungs was too high, and the lens in the eyes had moved out of place. A genetic test found a new change in a gene that causes a rare condition called neonatal MFS, which affects the body’s connective tissue. Doctors tried medicines to help the heart pump better, used sedation, and gave diuretics to reduce swelling, but the heart problems got worse. The baby’s breathing and heart function kept getting worse, and the body started to shut down. Even with treatment, the baby could not survive. The family chose to focus on comfort instead of surgery, and the baby passed away 32 days after birth.\"\n}", "generated_text": "A baby was born early by C-section because the baby was not getting enough oxygen. The baby had a weak heart from birth and had serious problems with the heart valves, making it hard for blood to flow properly. The baby’s hands and feet were long and bent, the fingers couldn’t straighten, and the joints at elbows and knees were stuck. The face looked old, the eyes were deep-set and slanted, the ears were small and soft, and the mouth hung down. The baby also had a flat foot and a swollen belly. Tests showed the heart was too big, the blood pressure in the lungs was too high, and the lens in the eyes had moved out of place. A genetic test found a new change in a gene that causes a rare condition called neonatal MFS, which affects the body’s connective tissue. Doctors tried medicines to help the heart pump better, used sedation, and gave diuretics to reduce swelling, but the heart problems got worse. The baby’s breathing and heart function kept getting worse, and the body started to shut down. Even with treatment, the baby could not survive. The family chose to focus on comfort instead of surgery, and the baby passed away 32 days after birth."}
{"row_index": 158, "doc_id": 78, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A newborn boy was born early via emergency cesarean section because of fetal distress. He had several serious physical problems from birth, including long, thin fingers and toes (arachnodactyly), fingers that could not fully straighten (camptodactyly), stiff elbows and knees, a wrinkled, aged-looking face, flat feet, and a deep, downward-slanting eye opening. His ears were small and soft, and his mouth sagged. He also had a short head shape (brachycephaly) and a lens that was out of place in his eyes (ectopia lentis), which is a sign of a genetic condition called Marfan syndrome.\\n\\nGenetic testing found a new mutation in a gene called fibrillin-1, specifically in a section known as the neonatal region (exons 24 to 32). This mutation is linked to a severe form of Marfan syndrome that affects the heart and blood vessels.\\n\\nAt birth, the baby had a weak heart, severe heart valve problems (especially mitral and aortic regurgitation), and high blood pressure in the lungs (pulmonary hypertension). These issues led to low blood pressure, poor breathing, and heart failure. Doctors tried medications to help, including drugs to reduce the heart’s workload, sedation, and diuretics to manage fluid buildup. However, the heart problems continued to get worse.\\n\\nBecause the disease was progressing too quickly and surgery was not expected to help, the family chose to focus on palliative care — care aimed at making the child comfortable rather than trying to cure the condition. Over the next few months, the baby developed severe lung and liver problems, including bleeding in the lungs, and eventually died at 32 days old.\"\n}", "generated_text": "A newborn boy was born early via emergency cesarean section because of fetal distress. He had several serious physical problems from birth, including long, thin fingers and toes (arachnodactyly), fingers that could not fully straighten (camptodactyly), stiff elbows and knees, a wrinkled, aged-looking face, flat feet, and a deep, downward-slanting eye opening. His ears were small and soft, and his mouth sagged. He also had a short head shape (brachycephaly) and a lens that was out of place in his eyes (ectopia lentis), which is a sign of a genetic condition called Marfan syndrome.\n\nGenetic testing found a new mutation in a gene called fibrillin-1, specifically in a section known as the neonatal region (exons 24 to 32). This mutation is linked to a severe form of Marfan syndrome that affects the heart and blood vessels.\n\nAt birth, the baby had a weak heart, severe heart valve problems (especially mitral and aortic regurgitation), and high blood pressure in the lungs (pulmonary hypertension). These issues led to low blood pressure, poor breathing, and heart failure. Doctors tried medications to help, including drugs to reduce the heart’s workload, sedation, and diuretics to manage fluid buildup. However, the heart problems continued to get worse.\n\nBecause the disease was progressing too quickly and surgery was not expected to help, the family chose to focus on palliative care — care aimed at making the child comfortable rather than trying to cure the condition. Over the next few months, the baby developed severe lung and liver problems, including bleeding in the lungs, and eventually died at 32 days old."}
{"row_index": 159, "doc_id": 0, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 20-year-old woman had a long history of nephrotic syndrome (NS) that started when she was 8 years old. Her condition was first noticed after she developed a blood clot in her brain veins and a large blood clot in her lungs. She didn’t have any lasting effects from this. Tests showed no family history of blood clots, and no other signs pointed to a secondary cause of her NS. She was treated with blood-thinning medication (anticoagulation) and steroid pills, which worked well. Over time, she had several relapses of her disease, each controlled with high-dose steroids. To reduce the need for steroids and support her growth, she started taking mycophenolate mofetil (MMF). Thrombophilia tests — which check for blood clotting disorders — came back normal. After nine years, her blood thinners were stopped. From 2017 onward, she stayed in remission and didn’t have any relapses. Her MMF was stopped in 2019, and she remained healthy without symptoms. One year later, she suddenly developed severe abdominal pain, vomiting after eating, and swelling in both legs. Lab tests confirmed a relapse of her nephrotic syndrome. An abdominal CT scan showed a blood clot in the superior mesenteric artery, causing acute mesenteric ischemia (lack of blood flow to the intestines). During surgery, doctors found widespread tissue death in her small intestine, and the damage was so severe that removing the affected parts was not possible. The patient died four days later.\"\n}", "generated_text": "A 20-year-old woman had a long history of nephrotic syndrome (NS) that started when she was 8 years old. Her condition was first noticed after she developed a blood clot in her brain veins and a large blood clot in her lungs. She didn’t have any lasting effects from this. Tests showed no family history of blood clots, and no other signs pointed to a secondary cause of her NS. She was treated with blood-thinning medication (anticoagulation) and steroid pills, which worked well. Over time, she had several relapses of her disease, each controlled with high-dose steroids. To reduce the need for steroids and support her growth, she started taking mycophenolate mofetil (MMF). Thrombophilia tests — which check for blood clotting disorders — came back normal. After nine years, her blood thinners were stopped. From 2017 onward, she stayed in remission and didn’t have any relapses. Her MMF was stopped in 2019, and she remained healthy without symptoms. One year later, she suddenly developed severe abdominal pain, vomiting after eating, and swelling in both legs. Lab tests confirmed a relapse of her nephrotic syndrome. An abdominal CT scan showed a blood clot in the superior mesenteric artery, causing acute mesenteric ischemia (lack of blood flow to the intestines). During surgery, doctors found widespread tissue death in her small intestine, and the damage was so severe that removing the affected parts was not possible. The patient died four days later."}
{"row_index": 160, "doc_id": 0, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old girl had a kidney disease called nephrotic syndrome since she was 8 years old. It started with blood clots in her brain and lungs, but she got better. She was treated with medicine to stop clots and steroids to calm her kidneys. Over time, she had several flare-ups that were controlled with steroids, but after 2017, her kidneys stayed healthy and no more flares happened. So, her doctors stopped the clot medicine and the kidney medicine (MMF). One year later, she got sudden, severe stomach pain, threw up after eating, and her legs swelled. Tests showed her kidney disease came back. A scan found a blood clot in a major blood vessel in her abdomen, cutting off blood to part of her intestines. When doctors opened her belly, they saw that most of her small intestine was dead and could not be saved. She died two days later.\"\n}", "generated_text": "A 20-year-old girl had a kidney disease called nephrotic syndrome since she was 8 years old. It started with blood clots in her brain and lungs, but she got better. She was treated with medicine to stop clots and steroids to calm her kidneys. Over time, she had several flare-ups that were controlled with steroids, but after 2017, her kidneys stayed healthy and no more flares happened. So, her doctors stopped the clot medicine and the kidney medicine (MMF). One year later, she got sudden, severe stomach pain, threw up after eating, and her legs swelled. Tests showed her kidney disease came back. A scan found a blood clot in a major blood vessel in her abdomen, cutting off blood to part of her intestines. When doctors opened her belly, they saw that most of her small intestine was dead and could not be saved. She died two days later."}
{"row_index": 161, "doc_id": 0, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 20-year-old female with a 12-year history of idiopathic nephrotic syndrome (NS) presented with a clinical course initiated at age eight, marked by cerebral venous thrombosis extending to the right jugular vein and a massive pulmonary embolism, which resolved without sequelae. No history of medical comorbidities, surgical interventions, or family history of thrombotic events was reported. Initial evaluation excluded secondary causes of nephrotic syndrome, as she lacked gross hematuria, hypertension, or renal biopsy findings, and no extra-renal manifestations were present. Consequently, she was initiated on anticoagulation therapy with oral vitamin K antagonist and oral corticosteroids, which resulted in stable disease control. Subsequent relapses of NS were managed with high-dose corticosteroid pulses, leading to long-term maintenance therapy with mycophenolate mofetil (MMF) to reduce corticosteroid dependence and support normal growth and development. A comprehensive thrombophilia workup—including homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and beta-1-glycoprotein antibodies—was performed and all results were within normal limits, ruling out inherited or acquired thrombophilic predispositions. Anticoagulant therapy was discontinued after nine years of use. The patient experienced multiple relapses of NS, all of which were controlled with oral corticosteroids, achieving sustained remission by 2017. MMF was gradually tapered and discontinued in 2019, with no further relapses or clinical symptoms observed thereafter.\\n\\nOne year after the last remission, the patient presented to the emergency department with severe, diffuse acute abdominal pain, non-radiating, associated with postprandial vomiting and bilateral lower limb edema lasting six hours. Physical examination revealed intense epigastric tenderness, with normal vital signs (blood pressure 120/70 mm Hg, heart rate 83 bpm, oxygen saturation 100% on room air), afebrile status, and intact consciousness. No other systemic abnormalities were identified. Urinalysis using labstix demonstrated proteinuria. Arterial blood gas analysis revealed metabolic acidosis with respiratory compensation. Laboratory findings included hypoalbuminemia, hypercholesterolemia, a prolonged prothrombin time (90%), markedly elevated D-dimer, lactate dehydrogenase, and creatine phosphokinase, and a systemic inflammatory response characterized by a C-reactive protein (CRP) level of 37 mg/L and leukocytosis (26.4 × 10³/µL). Renal and hepatic function tests remained within normal ranges.\\n\\nThe patient was admitted to the intensive care unit for close hemodynamic and metabolic monitoring. An urgent abdominal ultrasound revealed a low-to-moderate volume intra-abdominal effusion. Abdominal computed tomography (CT) demonstrated acute thrombosis of the superior mesenteric artery with concomitant acute mesenteric ischemia. Immediate surgical intervention was performed. Intraoperative exploration confirmed extensive mesenteric ischemia with nearly complete necrosis of the small intestine, rendering resection of the bowel segments non-viable and incompatible with survival. The patient succumbed to multi-organ failure within 48 hours of presentation. This case highlights the potential for severe, life-threatening complications in patients with long-standing idiopathic nephrotic syndrome, particularly in the context of underlying hypercoagulable states or unrecognized vascular vulnerability, even in the absence of thrombophilia. The pathophysiological link between chronic immune dysregulation in NS and a pro-thrombotic milieu—potentially mediated by persistent inflammation, endothelial dysfunction, and increased expression of tissue factor—may contribute to the development of acute arterial thrombosis in critical vascular territories such as the superior mesenteric artery, leading to ischemic bowel necrosis and death.\"\n}", "generated_text": "A 20-year-old female with a 12-year history of idiopathic nephrotic syndrome (NS) presented with a clinical course initiated at age eight, marked by cerebral venous thrombosis extending to the right jugular vein and a massive pulmonary embolism, which resolved without sequelae. No history of medical comorbidities, surgical interventions, or family history of thrombotic events was reported. Initial evaluation excluded secondary causes of nephrotic syndrome, as she lacked gross hematuria, hypertension, or renal biopsy findings, and no extra-renal manifestations were present. Consequently, she was initiated on anticoagulation therapy with oral vitamin K antagonist and oral corticosteroids, which resulted in stable disease control. Subsequent relapses of NS were managed with high-dose corticosteroid pulses, leading to long-term maintenance therapy with mycophenolate mofetil (MMF) to reduce corticosteroid dependence and support normal growth and development. A comprehensive thrombophilia workup—including homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and beta-1-glycoprotein antibodies—was performed and all results were within normal limits, ruling out inherited or acquired thrombophilic predispositions. Anticoagulant therapy was discontinued after nine years of use. The patient experienced multiple relapses of NS, all of which were controlled with oral corticosteroids, achieving sustained remission by 2017. MMF was gradually tapered and discontinued in 2019, with no further relapses or clinical symptoms observed thereafter.\n\nOne year after the last remission, the patient presented to the emergency department with severe, diffuse acute abdominal pain, non-radiating, associated with postprandial vomiting and bilateral lower limb edema lasting six hours. Physical examination revealed intense epigastric tenderness, with normal vital signs (blood pressure 120/70 mm Hg, heart rate 83 bpm, oxygen saturation 100% on room air), afebrile status, and intact consciousness. No other systemic abnormalities were identified. Urinalysis using labstix demonstrated proteinuria. Arterial blood gas analysis revealed metabolic acidosis with respiratory compensation. Laboratory findings included hypoalbuminemia, hypercholesterolemia, a prolonged prothrombin time (90%), markedly elevated D-dimer, lactate dehydrogenase, and creatine phosphokinase, and a systemic inflammatory response characterized by a C-reactive protein (CRP) level of 37 mg/L and leukocytosis (26.4 × 10³/µL). Renal and hepatic function tests remained within normal ranges.\n\nThe patient was admitted to the intensive care unit for close hemodynamic and metabolic monitoring. An urgent abdominal ultrasound revealed a low-to-moderate volume intra-abdominal effusion. Abdominal computed tomography (CT) demonstrated acute thrombosis of the superior mesenteric artery with concomitant acute mesenteric ischemia. Immediate surgical intervention was performed. Intraoperative exploration confirmed extensive mesenteric ischemia with nearly complete necrosis of the small intestine, rendering resection of the bowel segments non-viable and incompatible with survival. The patient succumbed to multi-organ failure within 48 hours of presentation. This case highlights the potential for severe, life-threatening complications in patients with long-standing idiopathic nephrotic syndrome, particularly in the context of underlying hypercoagulable states or unrecognized vascular vulnerability, even in the absence of thrombophilia. The pathophysiological link between chronic immune dysregulation in NS and a pro-thrombotic milieu—potentially mediated by persistent inflammation, endothelial dysfunction, and increased expression of tissue factor—may contribute to the development of acute arterial thrombosis in critical vascular territories such as the superior mesenteric artery, leading to ischemic bowel necrosis and death."}
{"row_index": 162, "doc_id": 1, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 34-year-old pregnant woman had seizures and trouble speaking, which went away in less than two hours. She had no other health problems. Doctors did an MRI of her brain and saw a special pattern called the 'Medusa head' sign. This means there’s a problem with how veins develop in the brain, with some blood clots at the edges and slow blood flow near the center. The brain tissue around the veins is swollen, which causes the symptoms. She started taking medicine to prevent more seizures and clots, and her symptoms got better in a week.\"\n}", "generated_text": "A 34-year-old pregnant woman had seizures and trouble speaking, which went away in less than two hours. She had no other health problems. Doctors did an MRI of her brain and saw a special pattern called the 'Medusa head' sign. This means there’s a problem with how veins develop in the brain, with some blood clots at the edges and slow blood flow near the center. The brain tissue around the veins is swollen, which causes the symptoms. She started taking medicine to prevent more seizures and clots, and her symptoms got better in a week."}
{"row_index": 163, "doc_id": 2, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 22-year-old woman visited the Oral Medicine Department with painful mouth sores that had been bothering her for one month. The sores started with a fever and appeared as small, pimple-like bumps on her lips. She had been using pod-type vapes for about a year, mostly during free time or with friends, and had recently switched to a new e-liquid flavor without telling anyone. She had never smoked cigarettes before and had no history of taking medications or having allergies. She also didn’t eat healthy foods regularly, often skipping vegetables and fruits. \\n\\nOn examination, her lips had crusts that looked like a mix of blood and fluid, and the corner of her mouth was sore and easily bled. Inside her mouth, she had white ulcers with yellow edges, of different sizes, on the lips, tongue, and floor of her mouth. There were no signs of illness on her body outside the mouth. Lab tests showed no evidence of a common virus (HSV-1) linked to these sores, which helped doctors rule out other causes.\\n\\nThe diagnosis was oral erythema multiforme, a condition that can be triggered by vaping, and it was classified as mild. Treatment included applying a saltwater solution (0.9% NaCl) to her lips three times a day, using a mouthwash with dexamethasone and hyaluronic acid three times a day (after waiting 30 minutes before eating or drinking), applying a 2% miconazole cream to the sore corner of her mouth twice daily, and using vaseline album cream for dry lips. She was also advised to stop vaping and avoid foods with MSG. \\n\\nAfter one week of treatment, her mouth sores improved significantly. The case was reviewed with her consent, and it followed ethical medical guidelines.\"\n}", "generated_text": "A 22-year-old woman visited the Oral Medicine Department with painful mouth sores that had been bothering her for one month. The sores started with a fever and appeared as small, pimple-like bumps on her lips. She had been using pod-type vapes for about a year, mostly during free time or with friends, and had recently switched to a new e-liquid flavor without telling anyone. She had never smoked cigarettes before and had no history of taking medications or having allergies. She also didn’t eat healthy foods regularly, often skipping vegetables and fruits. \n\nOn examination, her lips had crusts that looked like a mix of blood and fluid, and the corner of her mouth was sore and easily bled. Inside her mouth, she had white ulcers with yellow edges, of different sizes, on the lips, tongue, and floor of her mouth. There were no signs of illness on her body outside the mouth. Lab tests showed no evidence of a common virus (HSV-1) linked to these sores, which helped doctors rule out other causes.\n\nThe diagnosis was oral erythema multiforme, a condition that can be triggered by vaping, and it was classified as mild. Treatment included applying a saltwater solution (0.9% NaCl) to her lips three times a day, using a mouthwash with dexamethasone and hyaluronic acid three times a day (after waiting 30 minutes before eating or drinking), applying a 2% miconazole cream to the sore corner of her mouth twice daily, and using vaseline album cream for dry lips. She was also advised to stop vaping and avoid foods with MSG. \n\nAfter one week of treatment, her mouth sores improved significantly. The case was reviewed with her consent, and it followed ethical medical guidelines."}
{"row_index": 164, "doc_id": 3, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A baby was born at 39 weeks and had a small, harmless lump inside the heart that was found during pregnancy. The lump didn’t grow or shrink, and the baby didn’t have any seizures or skin spots. The doctor checked the baby right after birth, at 1 month, 7 months, and 1 year, and everything was normal. The baby grew well, stayed healthy, and developed like other babies her age. The heart lump was only in the heart and didn’t cause any problems. No other signs of a rare condition called tuberous sclerosis were found, so the baby doesn’t have that condition.\"\n}", "generated_text": "A baby was born at 39 weeks and had a small, harmless lump inside the heart that was found during pregnancy. The lump didn’t grow or shrink, and the baby didn’t have any seizures or skin spots. The doctor checked the baby right after birth, at 1 month, 7 months, and 1 year, and everything was normal. The baby grew well, stayed healthy, and developed like other babies her age. The heart lump was only in the heart and didn’t cause any problems. No other signs of a rare condition called tuberous sclerosis were found, so the baby doesn’t have that condition."}
{"row_index": 165, "doc_id": 3, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 29-year-old gravida V par IV woman, with a history of three spontaneous vaginal deliveries and one previous cesarean section for failed induction of labor (four years prior), presented for antenatal care follow-up at 32 weeks' gestation based on her last normal menstrual period (LNMP). Comprehensive medical history revealed that all four of her children are healthy, thriving in school, and have no known genetic or seizure-related disorders. Laboratory investigations including Venereal Disease Research Laboratory (VDRL) testing, Hepatitis B surface antigen (HBsAg), and urine analysis were negative. Complete Blood Count (CBC) showed normal cellular parameters; blood group was A, Rh-positive. Obstetric ultrasound demonstrated a normal fetal anatomy except for the cardiac structure. Detailed fetal echocardiography revealed normal atrial size and situs, with appropriately positioned and functioning atrioventricular and semilunar valves. Both ventricles exhibited comparable size and contractile function, with normal left ventricular apex formation and no ventricular septal defect. However, two circumscribed, round, echogenic masses were identified on the left ventricular papillary muscles, measuring 18.2 mm × 8.3 mm and 13.5 mm × 8.3 mm, respectively. The left ventricular outflow tract (LVOT) and right ventricular outflow tract (RVOT) demonstrated normal anatomy and hemodynamics on two-dimensional (2D) and color flow (CF) ultrasound assessment. Based on these findings, a diagnosis of isolated fetal cardiac rhabdomyoma was established. Given the strong association between cardiac rhabdomyoma and tuberous sclerosis complex (TSC), a comprehensive evaluation for TSC was performed, including neurosonography and systemic screening for cutaneous, renal, and neurological manifestations. No additional features consistent with TSC were identified beyond the cardiac mass. The patient maintained regular antenatal care from 32 weeks through 39 weeks plus 1 day, with no complications. At 39 weeks plus 1 day, a cesarean section was performed for full-term delivery and patient request for repeat cesarean delivery, resulting in the birth of a 3200-gram female infant with an APGAR score of 10 at both 1 and 5 minutes. Both maternal and neonatal postoperative courses were uncomplicated, and both were discharged on postoperative day three. Postnatal evaluations were conducted on days 1, 7, and 30, with no evidence of tumor regression, growth, or emergence of skin lesions or seizures. Physical examination findings remained normal, and the cardiac mass size was stable compared to the prenatal assessment. At 7 months of age, developmental history and neurodevelopmental screening were performed, revealing age-appropriate developmental progress. Anthropometric measurements confirmed normal growth. A pediatric echocardiogram revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles, measuring 21.8 mm × 9.2 mm and 14.7 mm × 8.5 mm, respectively, with no evidence of left ventricular inflow obstruction or functional compromise. At 12 months of age, comprehensive evaluation including physical examination, anthropometric assessment, and neurobehavioral testing was completed. The child demonstrated healthy growth parameters and normal neurobehavioral development, consistent with age-matched peers. The cardiac rhabdomyoma remained stable in size and did not exhibit any growth or regression. No clinical criteria for tuberous sclerosis complex were met, including absence of cutaneous hamartomas, subependymal nodules, renal angiomyolipomas, or other systemic manifestations. This case represents an isolated, asymptomatic cardiac rhabdomyoma without evidence of tuberous sclerosis complex, with stable tumor morphology and normal developmental and physiological outcomes through one year of age.\"\n}", "generated_text": "A 29-year-old gravida V par IV woman, with a history of three spontaneous vaginal deliveries and one previous cesarean section for failed induction of labor (four years prior), presented for antenatal care follow-up at 32 weeks' gestation based on her last normal menstrual period (LNMP). Comprehensive medical history revealed that all four of her children are healthy, thriving in school, and have no known genetic or seizure-related disorders. Laboratory investigations including Venereal Disease Research Laboratory (VDRL) testing, Hepatitis B surface antigen (HBsAg), and urine analysis were negative. Complete Blood Count (CBC) showed normal cellular parameters; blood group was A, Rh-positive. Obstetric ultrasound demonstrated a normal fetal anatomy except for the cardiac structure. Detailed fetal echocardiography revealed normal atrial size and situs, with appropriately positioned and functioning atrioventricular and semilunar valves. Both ventricles exhibited comparable size and contractile function, with normal left ventricular apex formation and no ventricular septal defect. However, two circumscribed, round, echogenic masses were identified on the left ventricular papillary muscles, measuring 18.2 mm × 8.3 mm and 13.5 mm × 8.3 mm, respectively. The left ventricular outflow tract (LVOT) and right ventricular outflow tract (RVOT) demonstrated normal anatomy and hemodynamics on two-dimensional (2D) and color flow (CF) ultrasound assessment. Based on these findings, a diagnosis of isolated fetal cardiac rhabdomyoma was established. Given the strong association between cardiac rhabdomyoma and tuberous sclerosis complex (TSC), a comprehensive evaluation for TSC was performed, including neurosonography and systemic screening for cutaneous, renal, and neurological manifestations. No additional features consistent with TSC were identified beyond the cardiac mass. The patient maintained regular antenatal care from 32 weeks through 39 weeks plus 1 day, with no complications. At 39 weeks plus 1 day, a cesarean section was performed for full-term delivery and patient request for repeat cesarean delivery, resulting in the birth of a 3200-gram female infant with an APGAR score of 10 at both 1 and 5 minutes. Both maternal and neonatal postoperative courses were uncomplicated, and both were discharged on postoperative day three. Postnatal evaluations were conducted on days 1, 7, and 30, with no evidence of tumor regression, growth, or emergence of skin lesions or seizures. Physical examination findings remained normal, and the cardiac mass size was stable compared to the prenatal assessment. At 7 months of age, developmental history and neurodevelopmental screening were performed, revealing age-appropriate developmental progress. Anthropometric measurements confirmed normal growth. A pediatric echocardiogram revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles, measuring 21.8 mm × 9.2 mm and 14.7 mm × 8.5 mm, respectively, with no evidence of left ventricular inflow obstruction or functional compromise. At 12 months of age, comprehensive evaluation including physical examination, anthropometric assessment, and neurobehavioral testing was completed. The child demonstrated healthy growth parameters and normal neurobehavioral development, consistent with age-matched peers. The cardiac rhabdomyoma remained stable in size and did not exhibit any growth or regression. No clinical criteria for tuberous sclerosis complex were met, including absence of cutaneous hamartomas, subependymal nodules, renal angiomyolipomas, or other systemic manifestations. This case represents an isolated, asymptomatic cardiac rhabdomyoma without evidence of tuberous sclerosis complex, with stable tumor morphology and normal developmental and physiological outcomes through one year of age."}
{"row_index": 166, "doc_id": 4, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old boy had a problem in his throat since he was 2 years old, with small growths called papillomas that blocked his airway. By age 3, he needed a tube (tracheostomy) to breathe. His mom also had a similar skin growth. The boy had trouble breathing, especially at night, with a loud breathing sound and hoarseness. He got medicine and oxygen but it didn’t help. Tests showed growths in his voice box and windpipe, and small lung pockets. After surgery, the doctor removed the growths and put in a breathing tube. He got one shot of a medicine called bevacizumab to help stop the growths. He started breathing better and didn’t need oxygen after a few days. He stayed in the hospital for 7 days and then went to another hospital. After 8 months, the family said the problem didn’t come back. He is doing well and no signs of return.\"\n}", "generated_text": "A 13-year-old boy had a problem in his throat since he was 2 years old, with small growths called papillomas that blocked his airway. By age 3, he needed a tube (tracheostomy) to breathe. His mom also had a similar skin growth. The boy had trouble breathing, especially at night, with a loud breathing sound and hoarseness. He got medicine and oxygen but it didn’t help. Tests showed growths in his voice box and windpipe, and small lung pockets. After surgery, the doctor removed the growths and put in a breathing tube. He got one shot of a medicine called bevacizumab to help stop the growths. He started breathing better and didn’t need oxygen after a few days. He stayed in the hospital for 7 days and then went to another hospital. After 8 months, the family said the problem didn’t come back. He is doing well and no signs of return."}
{"row_index": 167, "doc_id": 4, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 13-year-old male from Cusco with a longstanding history of laryngeal papillomatosis since age two, who required tracheostomy at age three, was admitted to the San Borja National Institute of Child Health in Lima following a 16-day course of progressive respiratory distress, primarily nocturnal, characterized by inspiratory laryngeal stridor and moderate dysphonia. Prior treatment with azithromycin and supplemental oxygen failed to improve symptoms. Physical examination revealed mild subcostal retraction, diminished vesicular breath sounds in the left hemithorax, and scattered wheezing predominantly in the right hemithorax, necessitating oxygen via binasal cannula at 4 liters per minute. Laboratory findings included leukocyte count of 8.03 × 10³/μL, platelets at 209 × 10³/μL, hemoglobin 13.2 g/dL, and C-reactive protein of 36.6 mg/L, indicating a moderate inflammatory response without evidence of sepsis. Imaging studies consisted of chest radiography and head and neck tomography, which revealed multiple stenosing nodules involving the larynx and trachea, as well as several pulmonary cysts consistent with chronic airway obstruction and alveolar damage. At 48 hours post-admission, the patient experienced worsening stridor and respiratory compromise, prompting urgent intervention in the emergency operating room. The procedure included tracheostomy, microsurgical excision of papillomatosis lesions, and removal of a large appendicular tumor with papillomatous morphology and ventricular banding structures involving the epiglottis, glottic region, vocal cords, subglottis, and trachea extending to tracheal ring 5. Histopathological analysis confirmed coilocytic atypia and mild focal dysplasia, consistent with human papillomavirus (HPV)-induced epithelial dysregulation, most likely HPV-16 or HPV-18 based on typical patterns of HPV-associated laryngeal papillomatosis. Postoperatively, the patient was transferred to the pediatric intensive care unit (PICU) for close respiratory monitoring and initiated weaning from oxygen, which was successfully achieved by 48 hours post-surgery. He received a single intravenous dose of 400 mg bevacizumab, a monoclonal antibody targeting vascular endothelial growth factor (VEGF), administered to inhibit angiogenesis and reduce tumor neovascularization in recurrent or persistent papillomatosis. Clinically, the patient showed significant improvement within 72 hours, with normalization of oxygen saturation and progressive reduction in respiratory support. He remained hospitalized for seven days before being transferred to the Hospital in Breña for continued outpatient management. Eight-month follow-up via telemonitoring demonstrated no evidence of disease recurrence, no new lesions, and no additional respiratory complications, supporting the durability of the intervention. The clinical course underscores the role of HPV-driven epithelial proliferation in laryngeal and tracheal stenosis, the efficacy of combined surgical excision and anti-angiogenic therapy, and the importance of long-term surveillance in patients with familial or recurrent papillomatosis, particularly in those with a maternal history of genital human papillomavirus infection.\"\n}", "generated_text": "A 13-year-old male from Cusco with a longstanding history of laryngeal papillomatosis since age two, who required tracheostomy at age three, was admitted to the San Borja National Institute of Child Health in Lima following a 16-day course of progressive respiratory distress, primarily nocturnal, characterized by inspiratory laryngeal stridor and moderate dysphonia. Prior treatment with azithromycin and supplemental oxygen failed to improve symptoms. Physical examination revealed mild subcostal retraction, diminished vesicular breath sounds in the left hemithorax, and scattered wheezing predominantly in the right hemithorax, necessitating oxygen via binasal cannula at 4 liters per minute. Laboratory findings included leukocyte count of 8.03 × 10³/μL, platelets at 209 × 10³/μL, hemoglobin 13.2 g/dL, and C-reactive protein of 36.6 mg/L, indicating a moderate inflammatory response without evidence of sepsis. Imaging studies consisted of chest radiography and head and neck tomography, which revealed multiple stenosing nodules involving the larynx and trachea, as well as several pulmonary cysts consistent with chronic airway obstruction and alveolar damage. At 48 hours post-admission, the patient experienced worsening stridor and respiratory compromise, prompting urgent intervention in the emergency operating room. The procedure included tracheostomy, microsurgical excision of papillomatosis lesions, and removal of a large appendicular tumor with papillomatous morphology and ventricular banding structures involving the epiglottis, glottic region, vocal cords, subglottis, and trachea extending to tracheal ring 5. Histopathological analysis confirmed coilocytic atypia and mild focal dysplasia, consistent with human papillomavirus (HPV)-induced epithelial dysregulation, most likely HPV-16 or HPV-18 based on typical patterns of HPV-associated laryngeal papillomatosis. Postoperatively, the patient was transferred to the pediatric intensive care unit (PICU) for close respiratory monitoring and initiated weaning from oxygen, which was successfully achieved by 48 hours post-surgery. He received a single intravenous dose of 400 mg bevacizumab, a monoclonal antibody targeting vascular endothelial growth factor (VEGF), administered to inhibit angiogenesis and reduce tumor neovascularization in recurrent or persistent papillomatosis. Clinically, the patient showed significant improvement within 72 hours, with normalization of oxygen saturation and progressive reduction in respiratory support. He remained hospitalized for seven days before being transferred to the Hospital in Breña for continued outpatient management. Eight-month follow-up via telemonitoring demonstrated no evidence of disease recurrence, no new lesions, and no additional respiratory complications, supporting the durability of the intervention. The clinical course underscores the role of HPV-driven epithelial proliferation in laryngeal and tracheal stenosis, the efficacy of combined surgical excision and anti-angiogenic therapy, and the importance of long-term surveillance in patients with familial or recurrent papillomatosis, particularly in those with a maternal history of genital human papillomavirus infection."}
{"row_index": 168, "doc_id": 5, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 54-year-old man with a long history of kidney problems and medicines that weaken his immune system got sick with fever, cough, and trouble breathing. He had been smoking for a long time and was on strong medicines for his kidneys. Before he got sick, his chest X-ray was normal. When he got sick, he had a high fever, shortness of breath, and his body wasn’t getting enough oxygen. His lungs made crackling sounds, and scans showed cloudy spots in both lungs. Tests showed signs of infection — bacteria, virus, or fungus — and he had antibodies for RSV, a common virus. Because his immune system was weak from long-term medicine use, he couldn’t fight off the infection well. Doctors gave him antibiotics, antifungal medicine, and steroids to calm his body’s reaction. Even with all this care, his condition got worse fast. He needed a breathing machine, but still didn’t improve. Two days later, he passed away from not being able to breathe.\"\n}", "generated_text": "A 54-year-old man with a long history of kidney problems and medicines that weaken his immune system got sick with fever, cough, and trouble breathing. He had been smoking for a long time and was on strong medicines for his kidneys. Before he got sick, his chest X-ray was normal. When he got sick, he had a high fever, shortness of breath, and his body wasn’t getting enough oxygen. His lungs made crackling sounds, and scans showed cloudy spots in both lungs. Tests showed signs of infection — bacteria, virus, or fungus — and he had antibodies for RSV, a common virus. Because his immune system was weak from long-term medicine use, he couldn’t fight off the infection well. Doctors gave him antibiotics, antifungal medicine, and steroids to calm his body’s reaction. Even with all this care, his condition got worse fast. He needed a breathing machine, but still didn’t improve. Two days later, he passed away from not being able to breathe."}
{"row_index": 169, "doc_id": 6, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 34-year-old woman had lower back pain and blood in her urine. She also had a big bruise on her right buttock and no history of bleeding before. The bleeding started after she had a C-section during pregnancy two months ago. Doctors found that her body couldn't stop bleeding properly because of a problem with a blood protein called factor VIII. This problem was made worse after giving birth. Tests showed she had a high level of an antibody that attacks this protein. This confirmed she had acquired haemophilia, which happened after childbirth. She got treatment with medicines to stop the bleeding and help her blood work, and her symptoms got better over time. She is now doing well and can go home.\"\n}", "generated_text": "A 34-year-old woman had lower back pain and blood in her urine. She also had a big bruise on her right buttock and no history of bleeding before. The bleeding started after she had a C-section during pregnancy two months ago. Doctors found that her body couldn't stop bleeding properly because of a problem with a blood protein called factor VIII. This problem was made worse after giving birth. Tests showed she had a high level of an antibody that attacks this protein. This confirmed she had acquired haemophilia, which happened after childbirth. She got treatment with medicines to stop the bleeding and help her blood work, and her symptoms got better over time. She is now doing well and can go home."}
{"row_index": 170, "doc_id": 7, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A two-day-old baby was admitted to Children’s Hospital with a swelling on the right side of the scrotum that had been present since birth. The baby was born at full term by cesarean section at a private hospital and stayed in the nursery for one day before being referred for surgery. When they arrived at the hospital, the baby was healthy, well-hydrated, pink, and had good circulation. On exam, the right testis was enlarged, firm, not painful, and had a red color with skin damage. The testis did not allow light to pass through (negative trans-illumination), while the left one did (positive). Both testicles had normal openings, with no signs of hernia. An ultrasound showed the right testis was enlarged (15.6 mm x 9.4 mm), had an uneven texture, and showed a thickened network of tissue (rete testis) with no blood flow, which is a sign of poor circulation. The left testis was normal in size and shape, with only a small amount of fluid around it. Surgery was urgently performed. During the operation, the right testis was found to be completely dead (necrotic) and twisted inside the scrotum (intravaginal torsion), with only a small amount of fluid. The doctors removed the damaged right testis (right orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to prevent future issues.\"\n}", "generated_text": "A two-day-old baby was admitted to Children’s Hospital with a swelling on the right side of the scrotum that had been present since birth. The baby was born at full term by cesarean section at a private hospital and stayed in the nursery for one day before being referred for surgery. When they arrived at the hospital, the baby was healthy, well-hydrated, pink, and had good circulation. On exam, the right testis was enlarged, firm, not painful, and had a red color with skin damage. The testis did not allow light to pass through (negative trans-illumination), while the left one did (positive). Both testicles had normal openings, with no signs of hernia. An ultrasound showed the right testis was enlarged (15.6 mm x 9.4 mm), had an uneven texture, and showed a thickened network of tissue (rete testis) with no blood flow, which is a sign of poor circulation. The left testis was normal in size and shape, with only a small amount of fluid around it. Surgery was urgently performed. During the operation, the right testis was found to be completely dead (necrotic) and twisted inside the scrotum (intravaginal torsion), with only a small amount of fluid. The doctors removed the damaged right testis (right orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to prevent future issues."}
{"row_index": 171, "doc_id": 7, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A two-day-old baby was born by C-section and had a swelling on the right side of his scrotum from the start. When they checked him, he was healthy, warm, and breathing well. The swollen testicle was big, stiff, red, and had small skin scratches. A light test showed the right side didn’t let light through (which means it’s not normal), but the left side did. The baby’s groin openings were fine. A scan showed the right testicle was enlarged and had a bad, patchy look with no blood flow — this means it was dying. The left testicle was normal but had a little fluid. Doctors had to do an emergency surgery. Inside, they found the right testicle was dead and twisted, with only a small amount of fluid. They removed the dead testicle (right orchidectomy) and fixed the left testicle (contralateral orchidopexy) to keep it in place.\"\n}", "generated_text": "A two-day-old baby was born by C-section and had a swelling on the right side of his scrotum from the start. When they checked him, he was healthy, warm, and breathing well. The swollen testicle was big, stiff, red, and had small skin scratches. A light test showed the right side didn’t let light through (which means it’s not normal), but the left side did. The baby’s groin openings were fine. A scan showed the right testicle was enlarged and had a bad, patchy look with no blood flow — this means it was dying. The left testicle was normal but had a little fluid. Doctors had to do an emergency surgery. Inside, they found the right testicle was dead and twisted, with only a small amount of fluid. They removed the dead testicle (right orchidectomy) and fixed the left testicle (contralateral orchidopexy) to keep it in place."}
{"row_index": 172, "doc_id": 7, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a case of a two-day-old male neonate presenting with an inborn right scrotal swelling admitted to the pediatric emergency department of Children’s Hospital. The infant was born at term via cesarean section at a private facility and remained in the nursery for one day prior to referral for urgent surgical evaluation. Transfer to our institution was delayed by a full day, during which time the clinical condition was stable. On arrival, the neonate was well-hydrated, had normal room temperature skin color, and exhibited adequate peripheral perfusion, indicating no signs of systemic compromise. Physical examination revealed a markedly enlarged, tense, non-tender right testis with visible erythema and overlying skin excoriation, suggestive of localized ischemia or inflammatory processes. Trans-illumination testing was negative in the right testis (indicating a non-reflective, solid tissue mass), while it was positive in the left contralateral testis, consistent with a normal, fluid-containing structure. Both inguinal hernial orifices were anatomically intact, ruling out inguinal hernia as a primary etiology. An urgent Doppler ultrasound of the inguinoscrotal region was performed, revealing the right testis to be enlarged (dimensions: 15.6 × 9.4 mm) with a heterogeneous hypoechoic echotexture, characterized by prominent rete testis architecture and absence of detectable arterial or venous flow on color Doppler imaging—findings consistent with ischemic compromise and loss of vascular perfusion. The left testis was normal in size, shape, and echotexture, with a minimal hydrocele present, indicating preserved vascular integrity and normal testicular development. Intraoperative findings confirmed a frank necrotic right testis with intravaginal torsion (i.e., twisting of the testicular parenchyma around its vascular pedicle), leading to complete arterial occlusion and irreversible tissue damage. Minimal hydrocele was also noted in the right scrotum. The surgical intervention consisted of a right orchidectomy (removal of the necrotic testis) and contralateral orchidopexy (surgical fixation of the normally developing left testis to the scrotal wall) to prevent future complications such as testicular descent failure or torsion. The absence of flow on Doppler imaging is a critical indicator of testicular ischemia, and the presence of necrosis and intravaginal torsion confirms a diagnosis of testicular torsion with secondary ischemic necrosis, likely occurring in the perinatal period due to delayed presentation and inadequate perfusion. This case underscores the importance of prompt evaluation and intervention in neonates with scrotal swelling, as delayed diagnosis significantly increases the risk of irreversible testicular loss.\"\n}", "generated_text": "We present a case of a two-day-old male neonate presenting with an inborn right scrotal swelling admitted to the pediatric emergency department of Children’s Hospital. The infant was born at term via cesarean section at a private facility and remained in the nursery for one day prior to referral for urgent surgical evaluation. Transfer to our institution was delayed by a full day, during which time the clinical condition was stable. On arrival, the neonate was well-hydrated, had normal room temperature skin color, and exhibited adequate peripheral perfusion, indicating no signs of systemic compromise. Physical examination revealed a markedly enlarged, tense, non-tender right testis with visible erythema and overlying skin excoriation, suggestive of localized ischemia or inflammatory processes. Trans-illumination testing was negative in the right testis (indicating a non-reflective, solid tissue mass), while it was positive in the left contralateral testis, consistent with a normal, fluid-containing structure. Both inguinal hernial orifices were anatomically intact, ruling out inguinal hernia as a primary etiology. An urgent Doppler ultrasound of the inguinoscrotal region was performed, revealing the right testis to be enlarged (dimensions: 15.6 × 9.4 mm) with a heterogeneous hypoechoic echotexture, characterized by prominent rete testis architecture and absence of detectable arterial or venous flow on color Doppler imaging—findings consistent with ischemic compromise and loss of vascular perfusion. The left testis was normal in size, shape, and echotexture, with a minimal hydrocele present, indicating preserved vascular integrity and normal testicular development. Intraoperative findings confirmed a frank necrotic right testis with intravaginal torsion (i.e., twisting of the testicular parenchyma around its vascular pedicle), leading to complete arterial occlusion and irreversible tissue damage. Minimal hydrocele was also noted in the right scrotum. The surgical intervention consisted of a right orchidectomy (removal of the necrotic testis) and contralateral orchidopexy (surgical fixation of the normally developing left testis to the scrotal wall) to prevent future complications such as testicular descent failure or torsion. The absence of flow on Doppler imaging is a critical indicator of testicular ischemia, and the presence of necrosis and intravaginal torsion confirms a diagnosis of testicular torsion with secondary ischemic necrosis, likely occurring in the perinatal period due to delayed presentation and inadequate perfusion. This case underscores the importance of prompt evaluation and intervention in neonates with scrotal swelling, as delayed diagnosis significantly increases the risk of irreversible testicular loss."}
{"row_index": 173, "doc_id": 8, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 4-year-old boy had a skin infection (impetigo) two weeks before his illness. For 5 days, he had blood in his urine and swelling in his legs. Then he started having headaches, nausea, vomiting, and suddenly had a seizure. His blood pressure became very high, causing a dangerous situation. Tests showed his body was missing some important proteins (C3) and had high levels of a strep infection marker (ASO), which pointed to a condition called GNAPE. Because of the high blood pressure, his brain started to swell (PRES), which can cause brain damage. He also developed a type of anemia where his red blood cells were being destroyed, and his hemoglobin dropped to 5 g/dL. He needed medicine to lower his blood pressure, protect his brain, and stop the body from attacking his red blood cells (steroids). He stayed in the hospital for 31 days, and after that, he was back to normal. Six months later, he had no symptoms and was doing well with medicine to keep his blood pressure and kidneys healthy.\"\n}", "generated_text": "A 4-year-old boy had a skin infection (impetigo) two weeks before his illness. For 5 days, he had blood in his urine and swelling in his legs. Then he started having headaches, nausea, vomiting, and suddenly had a seizure. His blood pressure became very high, causing a dangerous situation. Tests showed his body was missing some important proteins (C3) and had high levels of a strep infection marker (ASO), which pointed to a condition called GNAPE. Because of the high blood pressure, his brain started to swell (PRES), which can cause brain damage. He also developed a type of anemia where his red blood cells were being destroyed, and his hemoglobin dropped to 5 g/dL. He needed medicine to lower his blood pressure, protect his brain, and stop the body from attacking his red blood cells (steroids). He stayed in the hospital for 31 days, and after that, he was back to normal. Six months later, he had no symptoms and was doing well with medicine to keep his blood pressure and kidneys healthy."}
{"row_index": 174, "doc_id": 8, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 4-year-old male presented with a 5-day history of macroscopic glomerular hematuria and lower extremity edema, which progressed over the preceding 12 hours to include headaches, nausea, vomiting, and a generalised tonic-clonic seizure. On emergency department admission, the patient was afebrile, with non-evaluable blood pressure, and exhibited quantitative consciousness impairment, generalized hypertonia, and bilateral pretibial edema. Endotracheal intubation was performed, and phenobarbital (10 mg/kg) was administered to control seizure activity.\\n\\nPhysical examination in the intensive care unit (ICU) revealed a blood pressure of 134/94 mmHg (BP 110 mmHg), with a p95 of 108/66 mmHg and p95+12 of 120/78 mmHg. Initial laboratory findings included hematuria (>100 erythrocytes per field), proteinuria 3+, leucocyturia (10–25 per field), creatinine 0.3 mg/dL, hemoglobin 7 g/dL, hematocrit 21%, normal mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC), leukocytosis (23,900/mm³), thrombocytosis (756,000/mm³), absence of acute-phase reactants, hypocomplementemia (C3 25 mg/dL; normal range 80–150 mg/dL), and normal C4. A rapid antigen test for Streptococcus pyogenes (group A beta-hemolytic streptococcus) was positive, and Anti-Streptolysin O (ASO) titers were elevated, consistent with recent streptococcal infection. Non-contrast brain CT showed no acute abnormalities. Renal ultrasound revealed bilateral nephromegaly with increased cortical echogenicity and reduced corticomedullary differentiation.\\n\\nThe patient was diagnosed with nephritic syndrome secondary to group A streptococcal infection (GNAPE) complicated by hypertensive emergency and convulsive status. Within 24 hours of ICU admission, mechanical ventilation and continued phenobarbital therapy were required. Electroencephalography (EEG) and cerebrospinal fluid analysis were normal on day one. Empirical antibiotic therapy with cefotaxime was initiated for eradication of Streptococcus pyogenes, and furosemide was administered for diuresis.\\n\\nOn post-admission day two, the patient developed acute kidney injury with creatinine rising to 0.99 mg/dL, persistent hypertension, and 24-hour proteinuria of 36.6 mg/m²/h, without oliguria. Antihypertensive therapy was initiated with amlodipine and intravenous labetalol, achieving initial control. At 48 hours, extubation was performed, which was well tolerated. However, within 24 hours of extubation, the patient's mental status deteriorated to Glasgow Coma Scale (GCS) 8 (ocular opening and limb withdrawal only to painful stimuli), with poor verbal response, and blood pressure remained above p95+12 despite continuous infusion of labetalol (up to 3 mg/kg/h), amlodipine (10 mg/day), and furosemide. This necessitated reintroduction of mechanical ventilation and administration of sodium nitroprusside (up to 3 mcg/kg/min) to achieve a gradual reduction of blood pressure by 25% per day to prevent secondary neurological injury. Given the presence of acute neurological symptoms in the context of severe hypertension in a patient with glomerulonephritis, posterior reversible encephalopathy syndrome (PRES) was suspected and confirmed by magnetic resonance imaging (MRI) on day 5. MRI demonstrated bilateral, symmetric subcortical hyperintensities in the occipital regions, without diffusion restriction, consistent with vasogenic edema. Ophthalmological examination was normal, and subsequent EEG showed occasional episodes of generalized voltage depression.\\n\\nHemoglobin declined to 5 g/dL during ICU stay, with normal MCV and MCHC, and no plateletopenia, prompting suspicion of autoimmune hemolytic anemia. A positive direct Coombs test and hemoglobinuria supported this diagnosis. Two red blood cell transfusions were required. Corticosteroid therapy with methylprednisolone (1 mg/kg/day) was initiated for 72 hours. Serological testing for Epstein-Barr virus, parvovirus B19, extractable nuclear antigens (ENA), anti-neutrophil cytoplasmic antibodies (AN", "generated_text": "{\n  \"proficient_health_literacy\": \"A 4-year-old male presented with a 5-day history of macroscopic glomerular hematuria and lower extremity edema, which progressed over the preceding 12 hours to include headaches, nausea, vomiting, and a generalised tonic-clonic seizure. On emergency department admission, the patient was afebrile, with non-evaluable blood pressure, and exhibited quantitative consciousness impairment, generalized hypertonia, and bilateral pretibial edema. Endotracheal intubation was performed, and phenobarbital (10 mg/kg) was administered to control seizure activity.\\n\\nPhysical examination in the intensive care unit (ICU) revealed a blood pressure of 134/94 mmHg (BP 110 mmHg), with a p95 of 108/66 mmHg and p95+12 of 120/78 mmHg. Initial laboratory findings included hematuria (>100 erythrocytes per field), proteinuria 3+, leucocyturia (10–25 per field), creatinine 0.3 mg/dL, hemoglobin 7 g/dL, hematocrit 21%, normal mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC), leukocytosis (23,900/mm³), thrombocytosis (756,000/mm³), absence of acute-phase reactants, hypocomplementemia (C3 25 mg/dL; normal range 80–150 mg/dL), and normal C4. A rapid antigen test for Streptococcus pyogenes (group A beta-hemolytic streptococcus) was positive, and Anti-Streptolysin O (ASO) titers were elevated, consistent with recent streptococcal infection. Non-contrast brain CT showed no acute abnormalities. Renal ultrasound revealed bilateral nephromegaly with increased cortical echogenicity and reduced corticomedullary differentiation.\\n\\nThe patient was diagnosed with nephritic syndrome secondary to group A streptococcal infection (GNAPE) complicated by hypertensive emergency and convulsive status. Within 24 hours of ICU admission, mechanical ventilation and continued phenobarbital therapy were required. Electroencephalography (EEG) and cerebrospinal fluid analysis were normal on day one. Empirical antibiotic therapy with cefotaxime was initiated for eradication of Streptococcus pyogenes, and furosemide was administered for diuresis.\\n\\nOn post-admission day two, the patient developed acute kidney injury with creatinine rising to 0.99 mg/dL, persistent hypertension, and 24-hour proteinuria of 36.6 mg/m²/h, without oliguria. Antihypertensive therapy was initiated with amlodipine and intravenous labetalol, achieving initial control. At 48 hours, extubation was performed, which was well tolerated. However, within 24 hours of extubation, the patient's mental status deteriorated to Glasgow Coma Scale (GCS) 8 (ocular opening and limb withdrawal only to painful stimuli), with poor verbal response, and blood pressure remained above p95+12 despite continuous infusion of labetalol (up to 3 mg/kg/h), amlodipine (10 mg/day), and furosemide. This necessitated reintroduction of mechanical ventilation and administration of sodium nitroprusside (up to 3 mcg/kg/min) to achieve a gradual reduction of blood pressure by 25% per day to prevent secondary neurological injury. Given the presence of acute neurological symptoms in the context of severe hypertension in a patient with glomerulonephritis, posterior reversible encephalopathy syndrome (PRES) was suspected and confirmed by magnetic resonance imaging (MRI) on day 5. MRI demonstrated bilateral, symmetric subcortical hyperintensities in the occipital regions, without diffusion restriction, consistent with vasogenic edema. Ophthalmological examination was normal, and subsequent EEG showed occasional episodes of generalized voltage depression.\\n\\nHemoglobin declined to 5 g/dL during ICU stay, with normal MCV and MCHC, and no plateletopenia, prompting suspicion of autoimmune hemolytic anemia. A positive direct Coombs test and hemoglobinuria supported this diagnosis. Two red blood cell transfusions were required. Corticosteroid therapy with methylprednisolone (1 mg/kg/day) was initiated for 72 hours. Serological testing for Epstein-Barr virus, parvovirus B19, extractable nuclear antigens (ENA), anti-neutrophil cytoplasmic antibodies (AN"}
{"row_index": 175, "doc_id": 9, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 69-year-old man with a history of heart surgery (coronary artery bypass grafting) came in with severe shortness of breath even during light activity, which had been going on for two months. He was diagnosed with heart failure caused by reduced blood flow to part of his heart, specifically due to a blockage in the right coronary artery (RCA) that had previously failed to work properly. This diagnosis was made based on his heart test results, blood markers, and a detailed heart imaging study (coronary angiogram). \\n\\nTo fix the blocked artery, doctors used a technique called 'retrograde recanalization' — meaning they started from the opposite side of the heart, using natural blood channels (collaterals) from the left side to reach the blocked RCA. They first cleared a major blockage in the left coronary artery, then used a method called 'septal surfing' to travel through the septal branches and reach the blocked RCA. Once there, they opened the blockage with a balloon and placed two drug-coated stents to keep the artery open.\\n\\nAfter the procedure, his shortness of breath improved and went away by the time he was discharged. At a 6-month check-up, he had no return of symptoms and was doing much better.\"\n}", "generated_text": "A 69-year-old man with a history of heart surgery (coronary artery bypass grafting) came in with severe shortness of breath even during light activity, which had been going on for two months. He was diagnosed with heart failure caused by reduced blood flow to part of his heart, specifically due to a blockage in the right coronary artery (RCA) that had previously failed to work properly. This diagnosis was made based on his heart test results, blood markers, and a detailed heart imaging study (coronary angiogram). \n\nTo fix the blocked artery, doctors used a technique called 'retrograde recanalization' — meaning they started from the opposite side of the heart, using natural blood channels (collaterals) from the left side to reach the blocked RCA. They first cleared a major blockage in the left coronary artery, then used a method called 'septal surfing' to travel through the septal branches and reach the blocked RCA. Once there, they opened the blockage with a balloon and placed two drug-coated stents to keep the artery open.\n\nAfter the procedure, his shortness of breath improved and went away by the time he was discharged. At a 6-month check-up, he had no return of symptoms and was doing much better."}
{"row_index": 176, "doc_id": 9, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 69-year-old man had trouble breathing even when doing small things like walking, for two months. He had had heart surgery before (CABG) and now his heart isn’t pumping well, which caused this breathing problem. Doctors found that a part of his heart’s blood supply (the right coronary artery) was completely blocked, and that damage from a heart attack years ago made the heart weaker. They fixed the blocked blood vessel by going backward through a small channel in the heart muscle, using a special method called 'septal surfing.' After fixing it, his breathing got better right away. Six months later, he still doesn’t have any breathing problems.\"\n}", "generated_text": "A 69-year-old man had trouble breathing even when doing small things like walking, for two months. He had had heart surgery before (CABG) and now his heart isn’t pumping well, which caused this breathing problem. Doctors found that a part of his heart’s blood supply (the right coronary artery) was completely blocked, and that damage from a heart attack years ago made the heart weaker. They fixed the blocked blood vessel by going backward through a small channel in the heart muscle, using a special method called 'septal surfing.' After fixing it, his breathing got better right away. Six months later, he still doesn’t have any breathing problems."}
{"row_index": 177, "doc_id": 9, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 69-year-old male with a prior history of coronary artery bypass grafting (CABG) presented with severe dyspnea at mild exertion, classified as New York Heart Association (NYHA) class III, lasting for two months. The patient had a documented history of inferior ST-segment-elevation myocardial infarction (STEMI) in 2009 at age 59, with coronary angiography at that time revealing severe three-vessel disease, including a complete occlusion (CTO) in the proximal left anterior descending artery (LAD), 90% stenosis in the mid and distal left circumflex artery, and 95% stenosis in the mid-right coronary artery (RCA). In 2009, he underwent CABG utilizing the left internal mammary artery (LIMA) to the LAD, followed by sequential saphenous vein graft (SVG) to the first obtuse marginal branch (OM1), second obtuse marginal branch (OM2), and posterolateral artery (PL). At presentation, coronary angiography via 6 French left radial artery access demonstrated patency of the LIMA-to-LAD and SVG-to-OM1, OM2 conduits, but a complete occlusion of the SVG-to-PL graft. Native left main coronary artery was occluded at its ostium, and the native RCA was occluded in the mid-portion with bridging collaterals. Given the functional significance of the occluded native RCA, a targeted intervention was initiated to recanalize the native right coronary artery CTO. Dual arterial access was established using a second 6 Fr sheath in the right femoral artery. Left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic) and 6 Fr EBU 3.5 (Launcher; Medtronic) guide catheters, respectively. An antegrade approach via the left radial artery was attempted; however, neither the Fielder XTR wire (Asahi Intec) nor the Gaia 3 wire (Asahi Intec) with Finecross microcatheter (Terumo) successfully navigated to the true lumen of the distal RCA. A parallel wire technique using Crusade microcatheter (Kaneka) and two Gaia 3 wires was attempted but failed to achieve coronary artery crossing. Consequently, a retrograde approach via the septal collaterals originating from the left anterior descending artery (LAD) through the occluded left main coronary artery was employed. The Gaia 3 wire crossed the occluded left main (LM) and LAD and reached the true lumen of the distal LAD. The Sion wire was then exchanged for a Finecross microcatheter (Terumo) and advanced into the distal LAD. The left main and proximal LAD were predilated with a 2.0 × 15 mm balloon. Subsequently, the septal surfing technique (SST) was applied to facilitate retrograde crossing of the CTO. Multiple septal channels were evaluated from proximal to distal LAD, and the Sion wire was retrogradely delivered through a distal septal branch into the distal RCA, supported by a 150-cm Finecross microcatheter. The Gaia 3 wire successfully traversed the CTO lesion retrogradely into the true lumen of the proximal RCA and was advanced into the Guidezilla guide extension catheter (Boston Scientific) positioned within the antegrade guiding catheter. The Finecross microcatheter was then delivered to the antegrade catheter, and an RG3 wire (Asahi Intec) was externalized. The CTO was predilated with a 2.0 × 15 mm balloon and treated with two overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm), resulting in excellent angiographic restoration with TIMI 3 flow in all distal coronary branches. Post-procedure, the patient’s dyspnea improved significantly and was fully resolved at discharge. At 6-month follow-up, there was no recurrence of dyspnea. The diagnosis of heart failure due to ischemic etiology was established based on electrocardiographic findings of ST depression in leads II, III, aVF, and V4–V6, elevated plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels (2640 pg/mL), and echocardiographic evidence of left ventricular systolic dysfunction with a left ventricular ejection fraction of 30%, consistent with ischemic cardiomyopathy secondary to prior SVG failure in the right coronary artery.\"\n}", "generated_text": "A 69-year-old male with a prior history of coronary artery bypass grafting (CABG) presented with severe dyspnea at mild exertion, classified as New York Heart Association (NYHA) class III, lasting for two months. The patient had a documented history of inferior ST-segment-elevation myocardial infarction (STEMI) in 2009 at age 59, with coronary angiography at that time revealing severe three-vessel disease, including a complete occlusion (CTO) in the proximal left anterior descending artery (LAD), 90% stenosis in the mid and distal left circumflex artery, and 95% stenosis in the mid-right coronary artery (RCA). In 2009, he underwent CABG utilizing the left internal mammary artery (LIMA) to the LAD, followed by sequential saphenous vein graft (SVG) to the first obtuse marginal branch (OM1), second obtuse marginal branch (OM2), and posterolateral artery (PL). At presentation, coronary angiography via 6 French left radial artery access demonstrated patency of the LIMA-to-LAD and SVG-to-OM1, OM2 conduits, but a complete occlusion of the SVG-to-PL graft. Native left main coronary artery was occluded at its ostium, and the native RCA was occluded in the mid-portion with bridging collaterals. Given the functional significance of the occluded native RCA, a targeted intervention was initiated to recanalize the native right coronary artery CTO. Dual arterial access was established using a second 6 Fr sheath in the right femoral artery. Left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic) and 6 Fr EBU 3.5 (Launcher; Medtronic) guide catheters, respectively. An antegrade approach via the left radial artery was attempted; however, neither the Fielder XTR wire (Asahi Intec) nor the Gaia 3 wire (Asahi Intec) with Finecross microcatheter (Terumo) successfully navigated to the true lumen of the distal RCA. A parallel wire technique using Crusade microcatheter (Kaneka) and two Gaia 3 wires was attempted but failed to achieve coronary artery crossing. Consequently, a retrograde approach via the septal collaterals originating from the left anterior descending artery (LAD) through the occluded left main coronary artery was employed. The Gaia 3 wire crossed the occluded left main (LM) and LAD and reached the true lumen of the distal LAD. The Sion wire was then exchanged for a Finecross microcatheter (Terumo) and advanced into the distal LAD. The left main and proximal LAD were predilated with a 2.0 × 15 mm balloon. Subsequently, the septal surfing technique (SST) was applied to facilitate retrograde crossing of the CTO. Multiple septal channels were evaluated from proximal to distal LAD, and the Sion wire was retrogradely delivered through a distal septal branch into the distal RCA, supported by a 150-cm Finecross microcatheter. The Gaia 3 wire successfully traversed the CTO lesion retrogradely into the true lumen of the proximal RCA and was advanced into the Guidezilla guide extension catheter (Boston Scientific) positioned within the antegrade guiding catheter. The Finecross microcatheter was then delivered to the antegrade catheter, and an RG3 wire (Asahi Intec) was externalized. The CTO was predilated with a 2.0 × 15 mm balloon and treated with two overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm), resulting in excellent angiographic restoration with TIMI 3 flow in all distal coronary branches. Post-procedure, the patient’s dyspnea improved significantly and was fully resolved at discharge. At 6-month follow-up, there was no recurrence of dyspnea. The diagnosis of heart failure due to ischemic etiology was established based on electrocardiographic findings of ST depression in leads II, III, aVF, and V4–V6, elevated plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels (2640 pg/mL), and echocardiographic evidence of left ventricular systolic dysfunction with a left ventricular ejection fraction of 30%, consistent with ischemic cardiomyopathy secondary to prior SVG failure in the right coronary artery."}
{"row_index": 178, "doc_id": 10, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 51-year-old man came in with sudden, painful vision loss in his left eye three days earlier. His right eye had normal vision, but his left eye could only see hand movements. Examining the back of his left eye showed swelling around the optic nerve, bulging of the choroid, fluid buildup under the retina, and wrinkling of the retinal pigment epithelium. Imaging tests, including MRI of the orbit and brain, showed a nodular mass at the junction of the optic nerve and sclera. Tests for cancer and autoimmune diseases were normal. Based on these findings, the doctor diagnosed nodular posterior scleritis, a type of eye inflammation. The patient was started on oral prednisolone at 50 mg per kilogram of body weight. After surgery to remove a small nodule, the fluid in the eye improved, and vision stabilized. The treatment was gradually reduced over three months. All tests and follow-up showed no signs of serious disease.\"\n}", "generated_text": "A 51-year-old man came in with sudden, painful vision loss in his left eye three days earlier. His right eye had normal vision, but his left eye could only see hand movements. Examining the back of his left eye showed swelling around the optic nerve, bulging of the choroid, fluid buildup under the retina, and wrinkling of the retinal pigment epithelium. Imaging tests, including MRI of the orbit and brain, showed a nodular mass at the junction of the optic nerve and sclera. Tests for cancer and autoimmune diseases were normal. Based on these findings, the doctor diagnosed nodular posterior scleritis, a type of eye inflammation. The patient was started on oral prednisolone at 50 mg per kilogram of body weight. After surgery to remove a small nodule, the fluid in the eye improved, and vision stabilized. The treatment was gradually reduced over three months. All tests and follow-up showed no signs of serious disease."}
{"row_index": 179, "doc_id": 10, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 51-year-old man woke up 3 days ago with a sudden, painful blurry vision in his left eye. His right eye was fine. He could see clearly with his best eye, but the left eye only showed hand motion. When doctors looked inside his left eye, they saw swelling around the back of the eye, bulging tissue, fluid buildup, and wrinkled layers of the eye’s lining. A scan of his eye and brain showed a small lump near where the optic nerve meets the eye socket. Tests for cancer and other diseases came back normal. The doctor diagnosed it as a type of eye inflammation called nodular posterior scleritis. He started taking a strong steroid pill (prednisolone) at a high dose to reduce the swelling and pain. The lump went down, the fluid cleared, and his vision improved. After a week, he had surgery to remove a small part of the eye socket tissue, and the steroid was injected. He didn’t go to the hospital for IV medicine, but still got better with the pills. After three months, the medicine was slowly stopped. His vision stayed good.\"\n}", "generated_text": "A 51-year-old man woke up 3 days ago with a sudden, painful blurry vision in his left eye. His right eye was fine. He could see clearly with his best eye, but the left eye only showed hand motion. When doctors looked inside his left eye, they saw swelling around the back of the eye, bulging tissue, fluid buildup, and wrinkled layers of the eye’s lining. A scan of his eye and brain showed a small lump near where the optic nerve meets the eye socket. Tests for cancer and other diseases came back normal. The doctor diagnosed it as a type of eye inflammation called nodular posterior scleritis. He started taking a strong steroid pill (prednisolone) at a high dose to reduce the swelling and pain. The lump went down, the fluid cleared, and his vision improved. After a week, he had surgery to remove a small part of the eye socket tissue, and the steroid was injected. He didn’t go to the hospital for IV medicine, but still got better with the pills. After three months, the medicine was slowly stopped. His vision stayed good."}
{"row_index": 180, "doc_id": 10, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 51-year-old male presented with acute, painful visual loss of the left eye (LE) onset three days prior. Best-corrected distance visual acuity (BCDVA) was 20/20 in the right eye (RE) and hand motion (HM) in the LE. Ocular motility was intact bilaterally. Anterior segment examination was normal. Fundus examination of the LE revealed optic disc (ONH) swelling, choroidal bulging, multiple subretinal fluid accumulations, and retinal pigment epithelial (RPE) corrugations. The RE fundus was unremarkable. Multimodal imaging was performed: Optical coherence tomography (OCT; OptoVue, Inc., software version 2018,0,0,18) demonstrated mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid, and mild retinal thickening. Fundus blue-autofluorescence (BAF) showed a geographic area of speckled autofluorescence at the macula, consistent with RPE disruption. Indocyanin green angiography (ICGA) revealed a geographic hypofluorescent area with speckled hyperfluorescent margins measuring three disc diameters (DD), suggesting focal vascular leakage and RPE dysfunction. Fluorescein angiography (FA; Heidelberg Eye Explorer v1.9.13.0, Spectralis Viewing Module 6.5.2.0) demonstrated vascular leakage at the optic disc (hot spot), supporting active inflammation. B-scan ultrasonography confirmed optic nerve enlargement, consistent with retrobulbar infiltration. Orbital and brain MRI with gadolinium enhancement identified a retrobulbar nodular mass at the optic nerve-sclera junction, showing intense enhancement, raising concern for both inflammatory and neoplastic etiologies. Oncology evaluation was negative for malignancy. Rheumatology work-up, including PPD (tuberculosis), chest X-ray, serum ACE (sarcoidosis), and C-ANCA (Wegener granulomatosis), was unremarkable. Given the clinical suspicion of nodular posterior scleritis, the patient underwent transconjunctival lateral orbitotomy one week after presentation, revealing a pink, localized scleral nodule with edematous tenon. Sub-tenon triamcinolone acetonide was administered as a local anti-inflammatory intervention. The patient declined admission and intravenous corticosteroid therapy. Oral prednisolone was initiated at a dose of 50 mg/kg/day, targeting immunomodulation and suppression of inflammatory cascades within the ocular and orbital tissues. At follow-up one week post-intervention, BCDVA remained 20/20, with counting fingers at 2 meters in both eyes. Subretinal fluid (SRF) was completely absorbed, and the macular region exhibited atrophy, indicating resolution of active fluid accumulation and chronic RPE damage. Oral prednisolone was tapered over a three-month period to minimize long-term corticosteroid effects. The clinical course supports a diagnosis of nodular posterior scleritis, with imaging findings consistent with inflammatory-mediated RPE and choroidal disruption, optic nerve edema, and focal vascular leakage, all without evidence of systemic autoimmune or infectious pathology or malignancy. The pathophysiological mechanism likely involves chronic inflammation at the posterior sclera-optic nerve interface, leading to RPE dysfunction, fluid accumulation, and structural changes in the retinal layers, with potential activation of local cytokine networks (e.g., IL-1, IL-6, TNF-α) contributing to tissue swelling and vascular permeability.\"\n}", "generated_text": "A 51-year-old male presented with acute, painful visual loss of the left eye (LE) onset three days prior. Best-corrected distance visual acuity (BCDVA) was 20/20 in the right eye (RE) and hand motion (HM) in the LE. Ocular motility was intact bilaterally. Anterior segment examination was normal. Fundus examination of the LE revealed optic disc (ONH) swelling, choroidal bulging, multiple subretinal fluid accumulations, and retinal pigment epithelial (RPE) corrugations. The RE fundus was unremarkable. Multimodal imaging was performed: Optical coherence tomography (OCT; OptoVue, Inc., software version 2018,0,0,18) demonstrated mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid, and mild retinal thickening. Fundus blue-autofluorescence (BAF) showed a geographic area of speckled autofluorescence at the macula, consistent with RPE disruption. Indocyanin green angiography (ICGA) revealed a geographic hypofluorescent area with speckled hyperfluorescent margins measuring three disc diameters (DD), suggesting focal vascular leakage and RPE dysfunction. Fluorescein angiography (FA; Heidelberg Eye Explorer v1.9.13.0, Spectralis Viewing Module 6.5.2.0) demonstrated vascular leakage at the optic disc (hot spot), supporting active inflammation. B-scan ultrasonography confirmed optic nerve enlargement, consistent with retrobulbar infiltration. Orbital and brain MRI with gadolinium enhancement identified a retrobulbar nodular mass at the optic nerve-sclera junction, showing intense enhancement, raising concern for both inflammatory and neoplastic etiologies. Oncology evaluation was negative for malignancy. Rheumatology work-up, including PPD (tuberculosis), chest X-ray, serum ACE (sarcoidosis), and C-ANCA (Wegener granulomatosis), was unremarkable. Given the clinical suspicion of nodular posterior scleritis, the patient underwent transconjunctival lateral orbitotomy one week after presentation, revealing a pink, localized scleral nodule with edematous tenon. Sub-tenon triamcinolone acetonide was administered as a local anti-inflammatory intervention. The patient declined admission and intravenous corticosteroid therapy. Oral prednisolone was initiated at a dose of 50 mg/kg/day, targeting immunomodulation and suppression of inflammatory cascades within the ocular and orbital tissues. At follow-up one week post-intervention, BCDVA remained 20/20, with counting fingers at 2 meters in both eyes. Subretinal fluid (SRF) was completely absorbed, and the macular region exhibited atrophy, indicating resolution of active fluid accumulation and chronic RPE damage. Oral prednisolone was tapered over a three-month period to minimize long-term corticosteroid effects. The clinical course supports a diagnosis of nodular posterior scleritis, with imaging findings consistent with inflammatory-mediated RPE and choroidal disruption, optic nerve edema, and focal vascular leakage, all without evidence of systemic autoimmune or infectious pathology or malignancy. The pathophysiological mechanism likely involves chronic inflammation at the posterior sclera-optic nerve interface, leading to RPE dysfunction, fluid accumulation, and structural changes in the retinal layers, with potential activation of local cytokine networks (e.g., IL-1, IL-6, TNF-α) contributing to tissue swelling and vascular permeability."}
{"row_index": 181, "doc_id": 11, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 78-year-old man from the Amhara region of Ethiopia had a permanent pacemaker because he had complete heart block. He needed surgery for an enlarged prostate (benign prostatic hyperplasia), which had developed after a previous prostate procedure. Before surgery, doctors checked his heart and overall health and found that his heart function was stable, though he had high blood pressure and type 2 diabetes. His pacemaker was set to a mode that could be risky during surgery, so doctors recommended changing it to a safer setting. However, the patient could not afford the cost of reprogramming the device due to limited access to cardiac care in Ethiopia and the long wait times for specialists. After discussing the risks, he chose to proceed with the surgery using his current pacemaker setup. Informed consent was given, and the surgery went ahead. He received combined epidural-spinal anesthesia (a mix of bupivacaine and fentanyl) at the L3-L4 level, which provided good pain relief. His vital signs stayed stable during surgery and recovery, with no major heart or breathing issues. After the operation, he was monitored in the recovery room for 12 hours, then moved to the ward. He got pain relief after 4 hours and had a small dose of epidural medicine to keep pain under control. He stayed in the hospital for about 24 hours and was discharged after 88 hours of recovery, in stable condition. He continues to take his medications and is advised to have regular check-ups to ensure his pacemaker is working properly.\"\n}", "generated_text": "A 78-year-old man from the Amhara region of Ethiopia had a permanent pacemaker because he had complete heart block. He needed surgery for an enlarged prostate (benign prostatic hyperplasia), which had developed after a previous prostate procedure. Before surgery, doctors checked his heart and overall health and found that his heart function was stable, though he had high blood pressure and type 2 diabetes. His pacemaker was set to a mode that could be risky during surgery, so doctors recommended changing it to a safer setting. However, the patient could not afford the cost of reprogramming the device due to limited access to cardiac care in Ethiopia and the long wait times for specialists. After discussing the risks, he chose to proceed with the surgery using his current pacemaker setup. Informed consent was given, and the surgery went ahead. He received combined epidural-spinal anesthesia (a mix of bupivacaine and fentanyl) at the L3-L4 level, which provided good pain relief. His vital signs stayed stable during surgery and recovery, with no major heart or breathing issues. After the operation, he was monitored in the recovery room for 12 hours, then moved to the ward. He got pain relief after 4 hours and had a small dose of epidural medicine to keep pain under control. He stayed in the hospital for about 24 hours and was discharged after 88 hours of recovery, in stable condition. He continues to take his medications and is advised to have regular check-ups to ensure his pacemaker is working properly."}
{"row_index": 182, "doc_id": 11, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 78-year-old man from Ethiopia had a pacemaker in his heart because his heart wasn’t beating properly. He needed surgery to fix a swollen prostate, and the doctors said his pacemaker was set in a way that could be risky during surgery. They suggested changing the pacemaker setting to make it safer, but he couldn’t afford the cost and chose to go ahead with the old setting. He gave permission to have the surgery and to share his story later. Before surgery, he was checked well and had normal blood tests. He was given pain medicine through a tube in his back (epidural) and a small shot of pain medicine (fentanyl) to help him stay comfortable. The doctors watched his heart and blood pressure closely and found nothing wrong. During the surgery, the team kept his heart safe by staying away from the pacemaker and having emergency tools ready. His body stayed steady the whole time. After surgery, he stayed in a recovery room for 12 hours, got more pain medicine, and was moved to a regular room. He stayed in the hospital for about 2 days and got pain relief for 3 days. He was finally sent home after 88 hours, and the doctors said he’s doing well and should keep checking his pacemaker regularly.\"\n}", "generated_text": "A 78-year-old man from Ethiopia had a pacemaker in his heart because his heart wasn’t beating properly. He needed surgery to fix a swollen prostate, and the doctors said his pacemaker was set in a way that could be risky during surgery. They suggested changing the pacemaker setting to make it safer, but he couldn’t afford the cost and chose to go ahead with the old setting. He gave permission to have the surgery and to share his story later. Before surgery, he was checked well and had normal blood tests. He was given pain medicine through a tube in his back (epidural) and a small shot of pain medicine (fentanyl) to help him stay comfortable. The doctors watched his heart and blood pressure closely and found nothing wrong. During the surgery, the team kept his heart safe by staying away from the pacemaker and having emergency tools ready. His body stayed steady the whole time. After surgery, he stayed in a recovery room for 12 hours, got more pain medicine, and was moved to a regular room. He stayed in the hospital for about 2 days and got pain relief for 3 days. He was finally sent home after 88 hours, and the doctors said he’s doing well and should keep checking his pacemaker regularly."}
{"row_index": 183, "doc_id": 12, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old woman had trouble urinating for years, going to the bathroom often and feeling pain when she did. She saw red and black thread-like stuff in her urine, and sometimes had headaches, fever, and chills. She tried many treatments for infections, but nothing helped. No bugs or travel was linked to her symptoms. She had surgery before, but that didn’t fix it. Tests showed no infections or blockages. A bladder check showed redness and dirt in the bladder. Doctors thought it might be a worm, so they gave medicine, but symptoms stayed. Later, a tiny worm was found in her urine under a microscope. It was a type of fly larva. The doctor told her to clean herself better and drink at least 3 liters of water every day. That helped her feel better.\"\n}", "generated_text": "A 52-year-old woman had trouble urinating for years, going to the bathroom often and feeling pain when she did. She saw red and black thread-like stuff in her urine, and sometimes had headaches, fever, and chills. She tried many treatments for infections, but nothing helped. No bugs or travel was linked to her symptoms. She had surgery before, but that didn’t fix it. Tests showed no infections or blockages. A bladder check showed redness and dirt in the bladder. Doctors thought it might be a worm, so they gave medicine, but symptoms stayed. Later, a tiny worm was found in her urine under a microscope. It was a type of fly larva. The doctor told her to clean herself better and drink at least 3 liters of water every day. That helped her feel better."}
{"row_index": 184, "doc_id": 13, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 36-year-old woman with ulcerative colitis had been doing well on medication but started experiencing worsening chest pain, shortness of breath, and symptoms like fatigue and night sweats. Her electrocardiogram showed abnormal changes in the lower part of her heart, and tests revealed signs of inflammation and heart damage. An emergency heart scan found severe blockages in two major coronary arteries, with the worst blockage in the right coronary artery. She had successful treatment with a stent placed in that artery. During the procedure, doctors noticed signs that might point to a condition called aortitis, which can cause inflammation in the aorta and its branches. Further testing, including blood work and a detailed imaging scan (CTA), showed thickening of the aortic walls and narrowing in several arteries, strongly suggesting Takayasu arteritis — a rare inflammatory disease that affects large arteries. She was started on prednisone and methotrexate to reduce inflammation. After three weeks, she had surgery to improve blood flow to her heart using a blood vessel from her chest. The surgery was successful, and she is now recovering well at home with regular follow-up.\"\n}", "generated_text": "A 36-year-old woman with ulcerative colitis had been doing well on medication but started experiencing worsening chest pain, shortness of breath, and symptoms like fatigue and night sweats. Her electrocardiogram showed abnormal changes in the lower part of her heart, and tests revealed signs of inflammation and heart damage. An emergency heart scan found severe blockages in two major coronary arteries, with the worst blockage in the right coronary artery. She had successful treatment with a stent placed in that artery. During the procedure, doctors noticed signs that might point to a condition called aortitis, which can cause inflammation in the aorta and its branches. Further testing, including blood work and a detailed imaging scan (CTA), showed thickening of the aortic walls and narrowing in several arteries, strongly suggesting Takayasu arteritis — a rare inflammatory disease that affects large arteries. She was started on prednisone and methotrexate to reduce inflammation. After three weeks, she had surgery to improve blood flow to her heart using a blood vessel from her chest. The surgery was successful, and she is now recovering well at home with regular follow-up."}
{"row_index": 185, "doc_id": 13, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old woman had a long-time stomach problem called ulcerative colitis, which she was managing with medicine. She started feeling chest pain that got worse over a week, along with shortness of breath and feeling tired and sweating at night. Tests showed her heart had damage, especially in the lower part, and two major blood vessels feeding the heart were badly blocked. Doctors fixed one of the blocked vessels with a stent and did a surgery later to fix the other. They also found signs of a rare inflammation in her blood vessels, especially around the aorta, which pointed to a condition called Takayasu arteritis. She was given steroids and a medicine to calm her immune system. After a few weeks, she had heart surgery that worked well, and she’s now doing fine at home.\"\n}", "generated_text": "A 36-year-old woman had a long-time stomach problem called ulcerative colitis, which she was managing with medicine. She started feeling chest pain that got worse over a week, along with shortness of breath and feeling tired and sweating at night. Tests showed her heart had damage, especially in the lower part, and two major blood vessels feeding the heart were badly blocked. Doctors fixed one of the blocked vessels with a stent and did a surgery later to fix the other. They also found signs of a rare inflammation in her blood vessels, especially around the aorta, which pointed to a condition called Takayasu arteritis. She was given steroids and a medicine to calm her immune system. After a few weeks, she had heart surgery that worked well, and she’s now doing fine at home."}
{"row_index": 186, "doc_id": 13, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 36-year-old female with a history of ulcerative colitis, well-controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares, was admitted to the emergency department with a one-week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms, including fatigue and night sweats. She reported a six-month history of generalized malaise, with prior episodes of effort-related precordial pain that had progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.\\n\\nElectrocardiography demonstrated sinus rhythm with supradesnivel (supra- or superior) ST-segment elevation in the inferior wall, indicating acute ischemia or infarction. Emergency coronary angiography revealed severe two-vessel coronary artery disease: a 90% ostial lesion in the left coronary trunk and a 99–100% subocclusive lesion at the ostial level of the right coronary artery (culprit vessel). Primary percutaneous coronary intervention (PCI) was performed with successful deployment of a drug-eluting stent in the right coronary artery. The hemodynamic team observed vascular friability during balloon advancement in the aortic arch, raising suspicion for aortic inflammation, prompting a targeted evaluation for systemic inflammatory or autoimmune etiology prior to surgical revascularization of the left coronary trunk.\\n\\nLaboratory findings included mild anemia (hemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm³), elevated erythrocyte sedimentation rate (ESR: 42 mm/h), elevated C-reactive protein (CRP: 4.9 mg/L; normal <1 mg/L), and elevated ultra-sensitive troponin, consistent with myocardial injury. Autoimmune workup showed normal complement levels (C3 and C4), negative anti-nuclear antibodies (ANA), anti-double-stranded DNA, negative extracellular nuclear antigen (ENA) profile, and non-reactive VDRL, excluding systemic lupus erythematosus and syphilis.\\n\\nCardiac magnetic resonance (CMR) with contrast revealed acute non-transmural infarction of the inferior wall of the left ventricle and subendocardial ischemia in the anteroseptoapical region at rest. Mild aortic and mitral regurgitation were noted, with preserved biventricular systolic function.\\n\\nComputed tomography angiography (CTA) of the chest, abdomen, and pelvis demonstrated periaortic fibrotic wall thickening involving the aortic root, aortic arch, and abdominal aorta, with severe stenosis of the left coronary trunk and mild stenosis of the left subclavian and left vertebral arteries. Severe stenosis of the lower mesenteric artery was also identified. These findings are consistent with Takayasu arteritis, a rare large-vessel vasculitis primarily affecting young women. Immunological evaluation revealed IgG level of 1,600 mg/dL (within reference range of 700–1,600 mg/dL), with elevated IgG1 (1024 mg/dL), and normal IgG2 (456 mg/dL), IgG3 (98.8 mg/dL), and IgG4 (13.6 mg/dL)—a pattern suggestive of IgG4-related disease, although the clinical diagnosis of Takayasu arteritis was established primarily through imaging and clinical context.\\n\\nThe patient was diagnosed with Takayasu arteritis based on clinical presentation, inflammatory markers, and imaging findings. Treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by intramuscular injection, and folic acid 1 mg daily to mitigate methotrexate-induced toxicity. After three weeks of immunosuppressive therapy, the patient underwent delayed myocardial revascularization surgery using the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta were found to be structurally intact, without evidence of significant inflammatory or fibrotic involvement. Postoperative recovery was uneventful, and the patient is currently stable at home under ambulatory follow-up with ongoing monitoring for disease activity and cardiovascular complications. The case illustrates the importance of considering large-vessel vasculitides in young patients with unexplained cardiovascular symptoms, particularly in the context of chronic inflammatory conditions such as inflammatory bowel disease.\"\n}", "generated_text": "A 36-year-old female with a history of ulcerative colitis, well-controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares, was admitted to the emergency department with a one-week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms, including fatigue and night sweats. She reported a six-month history of generalized malaise, with prior episodes of effort-related precordial pain that had progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.\n\nElectrocardiography demonstrated sinus rhythm with supradesnivel (supra- or superior) ST-segment elevation in the inferior wall, indicating acute ischemia or infarction. Emergency coronary angiography revealed severe two-vessel coronary artery disease: a 90% ostial lesion in the left coronary trunk and a 99–100% subocclusive lesion at the ostial level of the right coronary artery (culprit vessel). Primary percutaneous coronary intervention (PCI) was performed with successful deployment of a drug-eluting stent in the right coronary artery. The hemodynamic team observed vascular friability during balloon advancement in the aortic arch, raising suspicion for aortic inflammation, prompting a targeted evaluation for systemic inflammatory or autoimmune etiology prior to surgical revascularization of the left coronary trunk.\n\nLaboratory findings included mild anemia (hemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm³), elevated erythrocyte sedimentation rate (ESR: 42 mm/h), elevated C-reactive protein (CRP: 4.9 mg/L; normal <1 mg/L), and elevated ultra-sensitive troponin, consistent with myocardial injury. Autoimmune workup showed normal complement levels (C3 and C4), negative anti-nuclear antibodies (ANA), anti-double-stranded DNA, negative extracellular nuclear antigen (ENA) profile, and non-reactive VDRL, excluding systemic lupus erythematosus and syphilis.\n\nCardiac magnetic resonance (CMR) with contrast revealed acute non-transmural infarction of the inferior wall of the left ventricle and subendocardial ischemia in the anteroseptoapical region at rest. Mild aortic and mitral regurgitation were noted, with preserved biventricular systolic function.\n\nComputed tomography angiography (CTA) of the chest, abdomen, and pelvis demonstrated periaortic fibrotic wall thickening involving the aortic root, aortic arch, and abdominal aorta, with severe stenosis of the left coronary trunk and mild stenosis of the left subclavian and left vertebral arteries. Severe stenosis of the lower mesenteric artery was also identified. These findings are consistent with Takayasu arteritis, a rare large-vessel vasculitis primarily affecting young women. Immunological evaluation revealed IgG level of 1,600 mg/dL (within reference range of 700–1,600 mg/dL), with elevated IgG1 (1024 mg/dL), and normal IgG2 (456 mg/dL), IgG3 (98.8 mg/dL), and IgG4 (13.6 mg/dL)—a pattern suggestive of IgG4-related disease, although the clinical diagnosis of Takayasu arteritis was established primarily through imaging and clinical context.\n\nThe patient was diagnosed with Takayasu arteritis based on clinical presentation, inflammatory markers, and imaging findings. Treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by intramuscular injection, and folic acid 1 mg daily to mitigate methotrexate-induced toxicity. After three weeks of immunosuppressive therapy, the patient underwent delayed myocardial revascularization surgery using the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta were found to be structurally intact, without evidence of significant inflammatory or fibrotic involvement. Postoperative recovery was uneventful, and the patient is currently stable at home under ambulatory follow-up with ongoing monitoring for disease activity and cardiovascular complications. The case illustrates the importance of considering large-vessel vasculitides in young patients with unexplained cardiovascular symptoms, particularly in the context of chronic inflammatory conditions such as inflammatory bowel disease."}
{"row_index": 187, "doc_id": 14, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 36-year-old woman had trouble swallowing (dysphagia) and long-standing pain in her neck and upper chest. She also had a multinodular goiter, but no other major health issues. Imaging tests showed a rare birth defect called a mirror image right aortic arch. In this condition, the aorta (the main blood vessel from the heart) forms around the right bronchus and the arteries that supply the neck and arms develop in the opposite order to normal. This creates a ring around the esophagus and trachea, which can press on them and cause symptoms. In her case, the aortic arch and a small pouch called a Kommerell diverticulum (1.3 cm) were pressing on the esophagus, causing a narrowing of 60%. However, she had no serious complications like breathing problems, aneurysms, or aortic dissection, and her symptoms improved on their own over time. Because her condition was not causing major harm and she was doing well, no surgery was done. This rare condition usually doesn’t cause problems unless there is significant pressure on the airway or esophagus, or if there are other serious complications. Treatment is not standard and depends on the individual case.\"\n}", "generated_text": "A 36-year-old woman had trouble swallowing (dysphagia) and long-standing pain in her neck and upper chest. She also had a multinodular goiter, but no other major health issues. Imaging tests showed a rare birth defect called a mirror image right aortic arch. In this condition, the aorta (the main blood vessel from the heart) forms around the right bronchus and the arteries that supply the neck and arms develop in the opposite order to normal. This creates a ring around the esophagus and trachea, which can press on them and cause symptoms. In her case, the aortic arch and a small pouch called a Kommerell diverticulum (1.3 cm) were pressing on the esophagus, causing a narrowing of 60%. However, she had no serious complications like breathing problems, aneurysms, or aortic dissection, and her symptoms improved on their own over time. Because her condition was not causing major harm and she was doing well, no surgery was done. This rare condition usually doesn’t cause problems unless there is significant pressure on the airway or esophagus, or if there are other serious complications. Treatment is not standard and depends on the individual case."}
{"row_index": 188, "doc_id": 14, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old woman had trouble swallowing and pain in her neck and upper chest. She didn’t have other health problems. Doctors found a rare birth difference in her chest where the main blood vessel (aorta) loops around the right side of her airway and windpipe. This causes a small pouch (called Kommerell diverticulum) that presses on her esophagus. Most people with this don’t have symptoms, but if the pressure is strong or the blood vessel weakens or bursts, surgery might be needed. In this case, her symptoms were mild and didn’t affect her eating or health, so no surgery was done. Her symptoms got better on their own over time.\"\n}", "generated_text": "A 36-year-old woman had trouble swallowing and pain in her neck and upper chest. She didn’t have other health problems. Doctors found a rare birth difference in her chest where the main blood vessel (aorta) loops around the right side of her airway and windpipe. This causes a small pouch (called Kommerell diverticulum) that presses on her esophagus. Most people with this don’t have symptoms, but if the pressure is strong or the blood vessel weakens or bursts, surgery might be needed. In this case, her symptoms were mild and didn’t affect her eating or health, so no surgery was done. Her symptoms got better on their own over time."}
{"row_index": 189, "doc_id": 15, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 62-year-old woman of North African descent, diagnosed with Von Hippel-Lindau disease in 2021, had several tumors involving her kidneys, adrenal glands, pancreas, and ovaries. She had a left bone tumor, a pheochromocytoma in her adrenal gland, a kidney cancer on the left side, a multi-cystic right kidney, and masses in her pancreas. She also had ovarian cysts that were found during imaging and surgery.\\n\\nShe underwent several surgeries: radiotherapy for a bone tumor, removal of her left adrenal gland and left kidney, and a major surgery to remove part of her pancreas. A tumor in her left ovary was found during a scan and later confirmed with imaging, raising concerns for cancer. Laparoscopic surgery revealed cystic tumors in both fallopian tubes and the area around the uterus. After a hysterectomy with removal of both ovaries, tissue tests showed clear-cell papillary cystadenomas in both tubes and the broad ligament — a known sign of Von Hippel-Lindau disease.\\n\\nShe recovered well after surgery and has been followed every four months with normal ultrasounds. However, she recently returned to the hospital for a new brain tumor, which is a known possible complication of this condition.\"\n}", "generated_text": "A 62-year-old woman of North African descent, diagnosed with Von Hippel-Lindau disease in 2021, had several tumors involving her kidneys, adrenal glands, pancreas, and ovaries. She had a left bone tumor, a pheochromocytoma in her adrenal gland, a kidney cancer on the left side, a multi-cystic right kidney, and masses in her pancreas. She also had ovarian cysts that were found during imaging and surgery.\n\nShe underwent several surgeries: radiotherapy for a bone tumor, removal of her left adrenal gland and left kidney, and a major surgery to remove part of her pancreas. A tumor in her left ovary was found during a scan and later confirmed with imaging, raising concerns for cancer. Laparoscopic surgery revealed cystic tumors in both fallopian tubes and the area around the uterus. After a hysterectomy with removal of both ovaries, tissue tests showed clear-cell papillary cystadenomas in both tubes and the broad ligament — a known sign of Von Hippel-Lindau disease.\n\nShe recovered well after surgery and has been followed every four months with normal ultrasounds. However, she recently returned to the hospital for a new brain tumor, which is a known possible complication of this condition."}
{"row_index": 190, "doc_id": 15, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 62-year-old woman from Tunisia had a rare disease called Von Hippel-Lindau. In 2021, she was found to have tumors in several parts of her body, including her brain, kidneys, adrenal glands, pancreas, and ovaries. She had surgeries to remove tumors from her left kidney, left adrenal gland, and part of her pancreas. A tumor in her left ear bone was treated with radiation. An ovarian tumor was found during a scan and later confirmed as a cystic mass. Surgery showed tumors in her fallopian tubes and pelvic area, which are normal for this disease. After removing her uterus and both ovaries, the doctors found the tumors were clear-cell papillary cystadenomas, which match the disease. She has been doing well since, with no new problems, but recently came back because a brain tumor came back.\"\n}", "generated_text": "A 62-year-old woman from Tunisia had a rare disease called Von Hippel-Lindau. In 2021, she was found to have tumors in several parts of her body, including her brain, kidneys, adrenal glands, pancreas, and ovaries. She had surgeries to remove tumors from her left kidney, left adrenal gland, and part of her pancreas. A tumor in her left ear bone was treated with radiation. An ovarian tumor was found during a scan and later confirmed as a cystic mass. Surgery showed tumors in her fallopian tubes and pelvic area, which are normal for this disease. After removing her uterus and both ovaries, the doctors found the tumors were clear-cell papillary cystadenomas, which match the disease. She has been doing well since, with no new problems, but recently came back because a brain tumor came back."}
{"row_index": 191, "doc_id": 16, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 59-year-old man with type 1 diabetes developed heart failure and was found to have infections on his heart valves. Tests showed large growths (vegetations) on both the mitral and aortic valves, which are signs of native valve endocarditis (NVE) — an infection of the heart valves caused by bacteria. The bacteria identified was Staphylococcus warneri, a type of common skin bacteria that can cause serious infections in people with weakened hearts or poor blood sugar control. He had no history of medical devices or immune problems, and the infection likely started from bacteria that had been living in his body for years. Before getting sick, he had mild signs like slight lab abnormalities, weight loss, and low blood counts, which may have been early warning signs of the infection. He was treated with antibiotics first, and after four weeks, he had surgery where both his mitral and aortic valves were replaced with mechanical valves. His heart function improved, and he has not had any problems since, over two years later. His poor diabetes control and high blood sugar likely made the surgery risky, so it was delayed until his health stabilized.\"\n}", "generated_text": "A 59-year-old man with type 1 diabetes developed heart failure and was found to have infections on his heart valves. Tests showed large growths (vegetations) on both the mitral and aortic valves, which are signs of native valve endocarditis (NVE) — an infection of the heart valves caused by bacteria. The bacteria identified was Staphylococcus warneri, a type of common skin bacteria that can cause serious infections in people with weakened hearts or poor blood sugar control. He had no history of medical devices or immune problems, and the infection likely started from bacteria that had been living in his body for years. Before getting sick, he had mild signs like slight lab abnormalities, weight loss, and low blood counts, which may have been early warning signs of the infection. He was treated with antibiotics first, and after four weeks, he had surgery where both his mitral and aortic valves were replaced with mechanical valves. His heart function improved, and he has not had any problems since, over two years later. His poor diabetes control and high blood sugar likely made the surgery risky, so it was delayed until his health stabilized."}
{"row_index": 192, "doc_id": 16, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A man in his 50s with type 1 diabetes had heart problems that got worse. He started feeling short of breath and had a fever, but didn’t notice any other symptoms before. Doctors found big, sticky spots on his heart valves — these are signs of an infection called endocarditis. The infection was caused by a type of bacteria that lived in his body all along, not from a cut or injury. Before this, he had been losing weight slowly and had small signs like a slightly high white blood cell count and low blood proteins, which might have been early warning signs. He didn’t have any devices or medicines that weaken his immune system. Doctors treated him with antibiotics first, which helped his heart stop failing. After his heart stabilized, they did surgery to replace both his aortic and mitral heart valves because the infections were too serious. He recovered well and hasn’t had any problems since, two years later.\"\n}", "generated_text": "A man in his 50s with type 1 diabetes had heart problems that got worse. He started feeling short of breath and had a fever, but didn’t notice any other symptoms before. Doctors found big, sticky spots on his heart valves — these are signs of an infection called endocarditis. The infection was caused by a type of bacteria that lived in his body all along, not from a cut or injury. Before this, he had been losing weight slowly and had small signs like a slightly high white blood cell count and low blood proteins, which might have been early warning signs. He didn’t have any devices or medicines that weaken his immune system. Doctors treated him with antibiotics first, which helped his heart stop failing. After his heart stabilized, they did surgery to replace both his aortic and mitral heart valves because the infections were too serious. He recovered well and hasn’t had any problems since, two years later."}
{"row_index": 193, "doc_id": 16, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 59-year-old Japanese man with a 28-year history of type 1 diabetes presented with acute heart failure and was diagnosed with native valve endocarditis (NVE) caused by Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS). The patient had long-standing, poorly controlled diabetes, evidenced by severely depleted insulin secretion (serum C-peptide undetectable), persistent hyperglycemia (HbA1c ≈ 9.0%), and marked glycemic variability despite intensive multiple-dose insulin therapy. His body mass index was 18.4 kg/m² (height 168 cm, weight 52 kg), indicating underweight status, which may have contributed to impaired immune surveillance and increased susceptibility to infection. He had a pre-existing diagnosis of asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years prior, which he had actively declined to monitor, leading to progressive valvular deterioration. No prosthetic devices or immunosuppressive therapies were implanted, and no prior history of medical device use or immunocompromise was reported.\\n\\nEight days prior to presentation, the patient presented to an emergency clinic with acute dyspnea and fever (>38°C), with no prior history of fever, chills, weakness, or systemic symptoms. On admission, vital signs included hypertension (192/82 mmHg) and tachycardia (118 bpm), orthopnea, and hypoxemia (SpO₂ 80%). Physical examination revealed a Levine 3/6 systolic murmur, a finding not previously documented during routine follow-up. No classic signs of infective endocarditis (IE) such as Osler nodes, Janeway lesions, or conjunctival petechiae were observed. Laboratory findings showed marked leukocytosis (WBC 20,800 /μL), elevated C-reactive protein (CRP 6.06 mg/dL), normal serum creatine phosphokinase MB (6.0 IU/L), and negative troponin T, suggesting myocardial injury was not present. Chest X-ray demonstrated pulmonary congestion and cardiac enlargement (cardiothoracic ratio 55%). Electrocardiography showed ST elevation in leads V1–V4, consistent with acute strain or ischemia, but emergency transthoracic echocardiography revealed preserved left ventricular contractility, indicating that the hemodynamic compromise was primarily due to valvular dysfunction.\\n\\nTransthoracic echocardiography revealed severe aortic and mitral regurgitation, with a mobile vegetation detected on the mitral valve. Transesophageal echocardiography confirmed a 16.5×6-mm mobile vegetation on the anterior mitral valve leaflet and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings met the clinical criteria for native valve endocarditis, particularly given the size and mobility of the vegetations. Imaging with head CT and MRI showed no evidence of cerebral infarction or hemorrhage, though the presence of a mobile vegetation was confirmed, raising concern for embolic risk. Retrospective review of pre-admission laboratory data revealed subtle abnormalities: four months prior to admission, a slight elevation in WBC was noted; subsequently, serum albumin declined to 3.0 g/dL, hemoglobin showed a gradual decline over two months, and the patient experienced a 4-kg weight loss. These findings, though non-specific, may represent early signs of systemic infection or malignancy. Esophagogastroduodenoscopy and whole-body CT were unremarkable. One month later, the patient regained weight and laboratory values nearly normalized (except for mild CRP elevation at 0.54 mg/dL). However, at the visit eight days before admission, WBC rose to 9,300 /μL, Hb and albumin dropped again to 13.1 g/dL and 3.0 g/dL, and CRP increased to 4.18 mg/dL, with a concomitant drop in diastolic blood pressure, suggesting a recurrent inflammatory or infectious process.\\n\\nEmpirical intravenous antibiotic therapy was initiated with 12 g/day ampicillin sulbactam (ABPC/S) and 120 mg/day gentamicin (GM). Three blood culture sets obtained upon admission were positive for S. warneri, with minimal inhibitory concentrations (MICs) of ≤8 μg/mL for ABPC/S, ≤1 μg/mL for GM, and ≤2 μg/mL for cefazolin (CEZ), confirming susceptibility to these agents. The organism was identified as a member of the CoNS family, known for its", "generated_text": "{\n  \"proficient_health_literacy\": \"A 59-year-old Japanese man with a 28-year history of type 1 diabetes presented with acute heart failure and was diagnosed with native valve endocarditis (NVE) caused by Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS). The patient had long-standing, poorly controlled diabetes, evidenced by severely depleted insulin secretion (serum C-peptide undetectable), persistent hyperglycemia (HbA1c ≈ 9.0%), and marked glycemic variability despite intensive multiple-dose insulin therapy. His body mass index was 18.4 kg/m² (height 168 cm, weight 52 kg), indicating underweight status, which may have contributed to impaired immune surveillance and increased susceptibility to infection. He had a pre-existing diagnosis of asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years prior, which he had actively declined to monitor, leading to progressive valvular deterioration. No prosthetic devices or immunosuppressive therapies were implanted, and no prior history of medical device use or immunocompromise was reported.\\n\\nEight days prior to presentation, the patient presented to an emergency clinic with acute dyspnea and fever (>38°C), with no prior history of fever, chills, weakness, or systemic symptoms. On admission, vital signs included hypertension (192/82 mmHg) and tachycardia (118 bpm), orthopnea, and hypoxemia (SpO₂ 80%). Physical examination revealed a Levine 3/6 systolic murmur, a finding not previously documented during routine follow-up. No classic signs of infective endocarditis (IE) such as Osler nodes, Janeway lesions, or conjunctival petechiae were observed. Laboratory findings showed marked leukocytosis (WBC 20,800 /μL), elevated C-reactive protein (CRP 6.06 mg/dL), normal serum creatine phosphokinase MB (6.0 IU/L), and negative troponin T, suggesting myocardial injury was not present. Chest X-ray demonstrated pulmonary congestion and cardiac enlargement (cardiothoracic ratio 55%). Electrocardiography showed ST elevation in leads V1–V4, consistent with acute strain or ischemia, but emergency transthoracic echocardiography revealed preserved left ventricular contractility, indicating that the hemodynamic compromise was primarily due to valvular dysfunction.\\n\\nTransthoracic echocardiography revealed severe aortic and mitral regurgitation, with a mobile vegetation detected on the mitral valve. Transesophageal echocardiography confirmed a 16.5×6-mm mobile vegetation on the anterior mitral valve leaflet and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings met the clinical criteria for native valve endocarditis, particularly given the size and mobility of the vegetations. Imaging with head CT and MRI showed no evidence of cerebral infarction or hemorrhage, though the presence of a mobile vegetation was confirmed, raising concern for embolic risk. Retrospective review of pre-admission laboratory data revealed subtle abnormalities: four months prior to admission, a slight elevation in WBC was noted; subsequently, serum albumin declined to 3.0 g/dL, hemoglobin showed a gradual decline over two months, and the patient experienced a 4-kg weight loss. These findings, though non-specific, may represent early signs of systemic infection or malignancy. Esophagogastroduodenoscopy and whole-body CT were unremarkable. One month later, the patient regained weight and laboratory values nearly normalized (except for mild CRP elevation at 0.54 mg/dL). However, at the visit eight days before admission, WBC rose to 9,300 /μL, Hb and albumin dropped again to 13.1 g/dL and 3.0 g/dL, and CRP increased to 4.18 mg/dL, with a concomitant drop in diastolic blood pressure, suggesting a recurrent inflammatory or infectious process.\\n\\nEmpirical intravenous antibiotic therapy was initiated with 12 g/day ampicillin sulbactam (ABPC/S) and 120 mg/day gentamicin (GM). Three blood culture sets obtained upon admission were positive for S. warneri, with minimal inhibitory concentrations (MICs) of ≤8 μg/mL for ABPC/S, ≤1 μg/mL for GM, and ≤2 μg/mL for cefazolin (CEZ), confirming susceptibility to these agents. The organism was identified as a member of the CoNS family, known for its"}
{"row_index": 194, "doc_id": 17, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 27-year-old woman with a family history of colorectal cancer (familial adenomatous polyposis) had multiple cancers in her colon and rectum. To treat this, she underwent a complex robotic surgery called robot-assisted total proctocolectomy (TPC), which included removing lymph nodes from the entire colorectal area using the Hugo RAS system. The surgery was done in three main steps: first, the ascending colon was removed along with its surrounding tissue (complete mesocolic excision) while the patient was in a Trendelenburg position; second, the descending colon was removed, and the rectum was fully excised with detailed lymph node removal (D3 dissection); and third, the superior mesenteric artery was ligated to stop blood flow to the colon. After the surgery, the tumor sample was removed through the anus, and a new pouch made from part of the small intestine was created and connected to the anus (ileal pouch-anal anastomosis). The entire procedure took 632 minutes and involved only minimal blood loss. The patient recovered smoothly, started eating liquids on day 1, and returned to a regular diet by day 3. Pathology showed two sigmoid colon cancers and one rectal cancer, with 18 of 89 lymph nodes found to be positive, indicating the cancer had spread to nearby lymph nodes. The cancer stage was classified as pT1bN2b.\"\n}", "generated_text": "A 27-year-old woman with a family history of colorectal cancer (familial adenomatous polyposis) had multiple cancers in her colon and rectum. To treat this, she underwent a complex robotic surgery called robot-assisted total proctocolectomy (TPC), which included removing lymph nodes from the entire colorectal area using the Hugo RAS system. The surgery was done in three main steps: first, the ascending colon was removed along with its surrounding tissue (complete mesocolic excision) while the patient was in a Trendelenburg position; second, the descending colon was removed, and the rectum was fully excised with detailed lymph node removal (D3 dissection); and third, the superior mesenteric artery was ligated to stop blood flow to the colon. After the surgery, the tumor sample was removed through the anus, and a new pouch made from part of the small intestine was created and connected to the anus (ileal pouch-anal anastomosis). The entire procedure took 632 minutes and involved only minimal blood loss. The patient recovered smoothly, started eating liquids on day 1, and returned to a regular diet by day 3. Pathology showed two sigmoid colon cancers and one rectal cancer, with 18 of 89 lymph nodes found to be positive, indicating the cancer had spread to nearby lymph nodes. The cancer stage was classified as pT1bN2b."}
{"row_index": 195, "doc_id": 18, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 65-year-old man had a motorcycle accident six months ago, which injured his right middle finger. After the fall, he couldn't fully extend his finger and noticed swelling. Over time, the finger developed a deformity called boutonniere deformity, where the middle joint bends and the tip of the finger extends too far. An X-ray showed no bone damage, so the problem was caused by soft tissue injury — specifically, a tear in the central slip of the finger's extensor tendon.\\n\\nThe doctor repaired the injury by using a part of the ulnar side of the flexor tendon (FDS) to replace the damaged central slip. The surgery was done under anesthesia, with the finger carefully opened and the damaged tissue removed. The new tendon was passed through a small tunnel in the bone and secured with sutures to restore normal movement.\\n\\nAfter surgery, the patient wore a splint for two weeks to keep the finger extended. Once the wound healed, he started gentle exercises to improve finger movement. After one month, his middle finger could move from 0 to 100 degrees, and after two months, movement returned to normal (0 to 110 degrees). His hand function improved dramatically, as shown by the DASH score, which went from 50 (indicating poor function) to 4.2 (indicating nearly normal function). He was able to return to work and daily activities with much better finger control.\"\n}", "generated_text": "A 65-year-old man had a motorcycle accident six months ago, which injured his right middle finger. After the fall, he couldn't fully extend his finger and noticed swelling. Over time, the finger developed a deformity called boutonniere deformity, where the middle joint bends and the tip of the finger extends too far. An X-ray showed no bone damage, so the problem was caused by soft tissue injury — specifically, a tear in the central slip of the finger's extensor tendon.\n\nThe doctor repaired the injury by using a part of the ulnar side of the flexor tendon (FDS) to replace the damaged central slip. The surgery was done under anesthesia, with the finger carefully opened and the damaged tissue removed. The new tendon was passed through a small tunnel in the bone and secured with sutures to restore normal movement.\n\nAfter surgery, the patient wore a splint for two weeks to keep the finger extended. Once the wound healed, he started gentle exercises to improve finger movement. After one month, his middle finger could move from 0 to 100 degrees, and after two months, movement returned to normal (0 to 110 degrees). His hand function improved dramatically, as shown by the DASH score, which went from 50 (indicating poor function) to 4.2 (indicating nearly normal function). He was able to return to work and daily activities with much better finger control."}
{"row_index": 196, "doc_id": 18, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 65-year-old male patient presented with a six-month history of swelling and boutonniere deformity involving the right middle finger (digiti III) following a motorcycle accident on January 1, 2023. The initial injury resulted in traumatic disruption of the central slip of the flexor digitorum superficialis (FDS) tendon, leading to impaired extension of the proximal interphalangeal (PIP) joint. The patient initially managed symptoms with analgesics without seeking medical evaluation. Clinical examination revealed persistent edema, active range of motion (ROM) of the PIP joint limited to 45–110 degrees, and passive ROM within normal limits, indicating a soft tissue pathology rather than bony involvement. Radiographic assessment via anteroposterior (AP) and lateral views of the right hand demonstrated no osseous abnormalities, confirming the deformity as originating from a central slip defect.\\n\\nSurgical intervention was performed via a midlateral incision on the ulnar aspect of the right middle phalanx, centered at the PIP joint, extending dorsally in an oblique fashion. A transverse incision was made proximal to the A1 pulley at the metacarpophalangeal (MCP) joint flexion crease. The ulnar neurovascular bundle was identified and preserved throughout the procedure. The central slip was exposed, and interposed scar tissue and pseudotendinous tissue were excised. Due to the inability to repair the central slip primarily, reconstruction was achieved using the ulnar slip of the FDS tendon.\\n\\nThe extensor tendon was mobilized and tenolyzed, and the dorsal capsule of the PIP joint was incised and debrided. The A3 pulley's periosteal insertion was longitudinally incised, and the volar capsule of the PIP joint was similarly opened. The ulnar slip of the FDS tendon was isolated and transected to release it from its proximal attachment, avoiding entrapment of the radial slip. A 2–0 non-absorbable monofilament suture was placed around the ulnar slip at the PIP joint level and used to release the distal portion of the FDS tendon slip, enabling distal transposition of the ulnar slip. A 2.8-mm drill was used to create a vertically oriented dorsal bone tunnel, positioned posterior to the volar plate. An elevator was placed between the flexor digitorum profundus (FDP) tendon, the volar plate, and the volar base of the middle phalanx to protect adjacent anatomic structures. The FDS tendon slip was passed through the tunnel while maintaining the PIP joint in full extension and reduced position, traversing the intact proximal segment of the central slip and extensor tendon. A pulvertaft weave was completed using a tendon weaver to ensure proper tension and biomechanical stability, with a 3–0 non-absorbable suture securing the weave. The margins of the joint capsule and central slip reconstruction were approximated, and adhesions were released with mobilization of the lateral bands.\\n\\nPostoperative care included a 4-day follow-up for wound management, with administration of oral meloxicam 7.5 mg twice daily and doxycycline 100 mg twice daily for three days. A second follow-up was conducted three days later. At two weeks postoperatively, the posterior splint was removed, external sutures were discontinued, and both active and passive range of motion exercises were initiated. At three weeks, wound healing was confirmed, and the PIP joint ROM improved to 0–90 degrees. One month postoperatively, ROM reached 0–100 degrees, with significant functional improvement. By seven weeks, the patient achieved full active ROM of 0–110 degrees and returned to work. Functional outcome was assessed using the DASH (Disability of Arm, Shoulder, and Hand) score, which decreased from 50 (indicating moderate disability) to 4.2 (indicating minimal disability), reflecting a substantial restoration of hand function. The surgical reconstruction successfully restored biomechanical alignment, joint stability, and functional capacity of the PIP joint through precise tendon transfer and pulvertaft tenodesis, with no evidence of bony pathology on imaging.\"\n}", "generated_text": "A 65-year-old male patient presented with a six-month history of swelling and boutonniere deformity involving the right middle finger (digiti III) following a motorcycle accident on January 1, 2023. The initial injury resulted in traumatic disruption of the central slip of the flexor digitorum superficialis (FDS) tendon, leading to impaired extension of the proximal interphalangeal (PIP) joint. The patient initially managed symptoms with analgesics without seeking medical evaluation. Clinical examination revealed persistent edema, active range of motion (ROM) of the PIP joint limited to 45–110 degrees, and passive ROM within normal limits, indicating a soft tissue pathology rather than bony involvement. Radiographic assessment via anteroposterior (AP) and lateral views of the right hand demonstrated no osseous abnormalities, confirming the deformity as originating from a central slip defect.\n\nSurgical intervention was performed via a midlateral incision on the ulnar aspect of the right middle phalanx, centered at the PIP joint, extending dorsally in an oblique fashion. A transverse incision was made proximal to the A1 pulley at the metacarpophalangeal (MCP) joint flexion crease. The ulnar neurovascular bundle was identified and preserved throughout the procedure. The central slip was exposed, and interposed scar tissue and pseudotendinous tissue were excised. Due to the inability to repair the central slip primarily, reconstruction was achieved using the ulnar slip of the FDS tendon.\n\nThe extensor tendon was mobilized and tenolyzed, and the dorsal capsule of the PIP joint was incised and debrided. The A3 pulley's periosteal insertion was longitudinally incised, and the volar capsule of the PIP joint was similarly opened. The ulnar slip of the FDS tendon was isolated and transected to release it from its proximal attachment, avoiding entrapment of the radial slip. A 2–0 non-absorbable monofilament suture was placed around the ulnar slip at the PIP joint level and used to release the distal portion of the FDS tendon slip, enabling distal transposition of the ulnar slip. A 2.8-mm drill was used to create a vertically oriented dorsal bone tunnel, positioned posterior to the volar plate. An elevator was placed between the flexor digitorum profundus (FDP) tendon, the volar plate, and the volar base of the middle phalanx to protect adjacent anatomic structures. The FDS tendon slip was passed through the tunnel while maintaining the PIP joint in full extension and reduced position, traversing the intact proximal segment of the central slip and extensor tendon. A pulvertaft weave was completed using a tendon weaver to ensure proper tension and biomechanical stability, with a 3–0 non-absorbable suture securing the weave. The margins of the joint capsule and central slip reconstruction were approximated, and adhesions were released with mobilization of the lateral bands.\n\nPostoperative care included a 4-day follow-up for wound management, with administration of oral meloxicam 7.5 mg twice daily and doxycycline 100 mg twice daily for three days. A second follow-up was conducted three days later. At two weeks postoperatively, the posterior splint was removed, external sutures were discontinued, and both active and passive range of motion exercises were initiated. At three weeks, wound healing was confirmed, and the PIP joint ROM improved to 0–90 degrees. One month postoperatively, ROM reached 0–100 degrees, with significant functional improvement. By seven weeks, the patient achieved full active ROM of 0–110 degrees and returned to work. Functional outcome was assessed using the DASH (Disability of Arm, Shoulder, and Hand) score, which decreased from 50 (indicating moderate disability) to 4.2 (indicating minimal disability), reflecting a substantial restoration of hand function. The surgical reconstruction successfully restored biomechanical alignment, joint stability, and functional capacity of the PIP joint through precise tendon transfer and pulvertaft tenodesis, with no evidence of bony pathology on imaging."}
{"row_index": 197, "doc_id": 19, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 23-year-old man came to the emergency room with a sudden, very severe headache that lasted for two hours, along with nausea, vomiting, and a feeling of chest heaviness. He had high blood pressure and a fast breathing rate. An emergency heart test (ECG) showed signs of a heart attack (STEMI), so he was quickly taken to a specialized center for treatment. During the procedure, his coronary arteries were found to be normal, meaning there was no blockage. However, a brain scan (CT) later revealed a cisternal subarachnoid hemorrhage (SAH), which is bleeding in the space around the brain. This condition was likely the cause of his symptoms. Despite being treated with medications, monitored closely, and given supportive care, his condition worsened rapidly. He suffered a cardiac arrest and could not be revived. He died after seven days in the intensive care unit.\"\n}", "generated_text": "A 23-year-old man came to the emergency room with a sudden, very severe headache that lasted for two hours, along with nausea, vomiting, and a feeling of chest heaviness. He had high blood pressure and a fast breathing rate. An emergency heart test (ECG) showed signs of a heart attack (STEMI), so he was quickly taken to a specialized center for treatment. During the procedure, his coronary arteries were found to be normal, meaning there was no blockage. However, a brain scan (CT) later revealed a cisternal subarachnoid hemorrhage (SAH), which is bleeding in the space around the brain. This condition was likely the cause of his symptoms. Despite being treated with medications, monitored closely, and given supportive care, his condition worsened rapidly. He suffered a cardiac arrest and could not be revived. He died after seven days in the intensive care unit."}
{"row_index": 198, "doc_id": 19, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 23-year-old man came to the hospital with a sudden, very bad headache that lasted two hours. He also had nausea, vomiting, and felt like his chest was heavy. His blood pressure was very high, and he was breathing fast. An emergency heart test showed a sign of a heart attack, so they rushed him to get treated. But when they looked at his heart tubes, they found no blockage — the heart was fine. Instead, a brain scan showed bleeding around the brain, which can be deadly. Even with doctors working together to help, his condition got worse quickly. He had a heart stoppage and couldn't be saved. He passed away.\"\n}", "generated_text": "A 23-year-old man came to the hospital with a sudden, very bad headache that lasted two hours. He also had nausea, vomiting, and felt like his chest was heavy. His blood pressure was very high, and he was breathing fast. An emergency heart test showed a sign of a heart attack, so they rushed him to get treated. But when they looked at his heart tubes, they found no blockage — the heart was fine. Instead, a brain scan showed bleeding around the brain, which can be deadly. Even with doctors working together to help, his condition got worse quickly. He had a heart stoppage and couldn't be saved. He passed away."}
{"row_index": 199, "doc_id": 19, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 23-year-old male presented to the emergency department with a sudden onset of severe frontal headache lasting two hours, accompanied by nausea, vomiting, and chest heaviness. His medical history was unremarkable, with no known illicit drug use; however, he had a significant smoking history of 23 pack-years and denied alcohol consumption. Physical examination revealed acute distress, full consciousness, and orientation to time, place, and person. Chest auscultation demonstrated normal vesicular breath sounds, while cardiovascular and abdominal examinations were non-specific. Neurological assessment identified neck stiffness, bilateral dilated pupils with intact light reflexes, normal plantar responses, and no focal neurological deficits. Vital signs showed hypertension (blood pressure 178/103 mmHg), tachypnea (respiratory rate 26 breaths/min), fever (temperature 38.9°C), heart rate of 87 beats/min, and oxygen saturation of 94%.\\n\\nEmergency evaluation included an electrocardiogram (ECG), which demonstrated ST-segment elevation greater than 2 mm in leads V2–V5, consistent with acute ST-elevation myocardial infarction (STEMI) as the primary differential diagnosis. This prompted immediate referral to a tertiary cardiac center for percutaneous coronary intervention (PCI). Prior to transfer, a 300 mg aspirin loading dose was administered. Cardiac biomarkers revealed markedly elevated troponin levels (1.48 mg/dL, normal <0.16 mg/dL), confirming myocardial injury. PCI via the femoral artery was performed, with coronary angiography showing normal coronary artery anatomy and TIMI flow grade 3, indicating patent vessel flow. Post-procedure ECG showed normal sinus rhythm with evidence of left ventricular hypertrophy (LVH). Echocardiography confirmed preserved left ventricular systolic function with no regional wall motion abnormalities (RWMA), suggesting no acute ischemic injury to myocardial segments.\\n\\nFollowing PCI, the patient was admitted to the medical ward for further workup. Laboratory tests included complete blood count (CBC), random blood glucose, renal function tests, and C-reactive protein (CRP), which revealed lymphocytosis and a mildly elevated CRP, suggestive of inflammatory or infectious processes. A non-contrast head CT was performed to evaluate the cause of the headache, which identified a cisternal subarachnoid hemorrhage (SAH) extending anterior to the right temporal lobe. Abdominal ultrasound was conducted to exclude polycystic kidney disease, which was negative. Cerebral CT angiography was planned to assess for the presence of a cerebral aneurysm, a common source of spontaneous SAH. Nimodipine 60 mg every 4 hours was initiated to prevent cerebral vasospasm, with a target mean arterial pressure of 160/100 mmHg to optimize cerebral perfusion.\\n\\nOn day two, the patient experienced a rapid clinical deterioration, culminating in in-hospital cardiac arrest. Cardiopulmonary resuscitation (CPR) was initiated, resulting in a Glasgow Coma Scale (GCS) score of 6, indicating severe neurological impairment. The patient was intubated and placed on mechanical ventilation in the intensive care unit (ICU). Due to hemodynamic instability and deteriorating neurological status, repeated neuroimaging and the planned cerebral CT angiography were not performed.\\n\\nOver the subsequent seven days, the patient was managed with a multidisciplinary approach, including nasogastric tube placement for enteral nutrition and fluid resuscitation. Medications administered included intravenous fluids, broad-spectrum antibiotics (to rule out systemic infection), proton pump inhibitors (to prevent stress-induced gastric mucosal injury), and continued nimodipine therapy.\\n\\nOn day eight, the patient developed sudden ventricular fibrillation, which persisted despite multiple defibrillation attempts (greater than five shocks). Despite aggressive resuscitation efforts, return of spontaneous circulation was not achieved, and the patient died. The case highlights the diagnostic challenge of differentiating between acute coronary syndrome and subarachnoid hemorrhage in a young patient with non-classic risk factors, where initial ECG findings may misdirect early management. The presence of SAH in a young individual without known vascular pathology or hypertension underscores the importance of neuroimaging in the evaluation of acute headaches with systemic symptoms, particularly when cardiovascular findings are initially suggestive of myocardial infarction. The coexistence of SAH and STEMI in this patient may reflect a rare, potentially shared pathophysiological mechanism, such as vasospasm or microvascular injury, though no direct causal link has been established. The absence of coronary atherosclerosis in this patient further emphasizes that STEMI in young individuals can arise from non-atherosclerotic etiologies, including coronary vasospasm, thrombosis, or", "generated_text": "{\n  \"proficient_health_literacy\": \"A 23-year-old male presented to the emergency department with a sudden onset of severe frontal headache lasting two hours, accompanied by nausea, vomiting, and chest heaviness. His medical history was unremarkable, with no known illicit drug use; however, he had a significant smoking history of 23 pack-years and denied alcohol consumption. Physical examination revealed acute distress, full consciousness, and orientation to time, place, and person. Chest auscultation demonstrated normal vesicular breath sounds, while cardiovascular and abdominal examinations were non-specific. Neurological assessment identified neck stiffness, bilateral dilated pupils with intact light reflexes, normal plantar responses, and no focal neurological deficits. Vital signs showed hypertension (blood pressure 178/103 mmHg), tachypnea (respiratory rate 26 breaths/min), fever (temperature 38.9°C), heart rate of 87 beats/min, and oxygen saturation of 94%.\\n\\nEmergency evaluation included an electrocardiogram (ECG), which demonstrated ST-segment elevation greater than 2 mm in leads V2–V5, consistent with acute ST-elevation myocardial infarction (STEMI) as the primary differential diagnosis. This prompted immediate referral to a tertiary cardiac center for percutaneous coronary intervention (PCI). Prior to transfer, a 300 mg aspirin loading dose was administered. Cardiac biomarkers revealed markedly elevated troponin levels (1.48 mg/dL, normal <0.16 mg/dL), confirming myocardial injury. PCI via the femoral artery was performed, with coronary angiography showing normal coronary artery anatomy and TIMI flow grade 3, indicating patent vessel flow. Post-procedure ECG showed normal sinus rhythm with evidence of left ventricular hypertrophy (LVH). Echocardiography confirmed preserved left ventricular systolic function with no regional wall motion abnormalities (RWMA), suggesting no acute ischemic injury to myocardial segments.\\n\\nFollowing PCI, the patient was admitted to the medical ward for further workup. Laboratory tests included complete blood count (CBC), random blood glucose, renal function tests, and C-reactive protein (CRP), which revealed lymphocytosis and a mildly elevated CRP, suggestive of inflammatory or infectious processes. A non-contrast head CT was performed to evaluate the cause of the headache, which identified a cisternal subarachnoid hemorrhage (SAH) extending anterior to the right temporal lobe. Abdominal ultrasound was conducted to exclude polycystic kidney disease, which was negative. Cerebral CT angiography was planned to assess for the presence of a cerebral aneurysm, a common source of spontaneous SAH. Nimodipine 60 mg every 4 hours was initiated to prevent cerebral vasospasm, with a target mean arterial pressure of 160/100 mmHg to optimize cerebral perfusion.\\n\\nOn day two, the patient experienced a rapid clinical deterioration, culminating in in-hospital cardiac arrest. Cardiopulmonary resuscitation (CPR) was initiated, resulting in a Glasgow Coma Scale (GCS) score of 6, indicating severe neurological impairment. The patient was intubated and placed on mechanical ventilation in the intensive care unit (ICU). Due to hemodynamic instability and deteriorating neurological status, repeated neuroimaging and the planned cerebral CT angiography were not performed.\\n\\nOver the subsequent seven days, the patient was managed with a multidisciplinary approach, including nasogastric tube placement for enteral nutrition and fluid resuscitation. Medications administered included intravenous fluids, broad-spectrum antibiotics (to rule out systemic infection), proton pump inhibitors (to prevent stress-induced gastric mucosal injury), and continued nimodipine therapy.\\n\\nOn day eight, the patient developed sudden ventricular fibrillation, which persisted despite multiple defibrillation attempts (greater than five shocks). Despite aggressive resuscitation efforts, return of spontaneous circulation was not achieved, and the patient died. The case highlights the diagnostic challenge of differentiating between acute coronary syndrome and subarachnoid hemorrhage in a young patient with non-classic risk factors, where initial ECG findings may misdirect early management. The presence of SAH in a young individual without known vascular pathology or hypertension underscores the importance of neuroimaging in the evaluation of acute headaches with systemic symptoms, particularly when cardiovascular findings are initially suggestive of myocardial infarction. The coexistence of SAH and STEMI in this patient may reflect a rare, potentially shared pathophysiological mechanism, such as vasospasm or microvascular injury, though no direct causal link has been established. The absence of coronary atherosclerosis in this patient further emphasizes that STEMI in young individuals can arise from non-atherosclerotic etiologies, including coronary vasospasm, thrombosis, or"}