{"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 cold that might have hurt her heart muscle. Her heart couldn’t pump blood well, so she was in the hospital for 10 months. She was very sick and close to dying, but her heart started to get better. Doctors treated her heart failure, kept her heart from beating too fast or too slow, and stopped blood clots. After 4 years, her heart function improved and stayed strong — that’s rare, only 1 in 6 people get this. Then it got worse again for 2 years, but she stayed stable. She had a baby, and after the second pregnancy, her heart got weaker again, especially after giving birth — this is common in women with heart problems. Now, in 2017, she’s stable. She takes medicine every day — for her heart, to control fluid, and to slow her heartbeat. She can do normal daily activities, has two children, and doesn’t work. Her heart is still weak, but it’s working better than before. She checks her heart regularly and watches her weight and fluid intake. No need for a special heart device right now.\"\n}", "generated_text": "A 38-year-old woman had a weak heart since she was 17, after a bad cold that might have hurt her heart muscle. Her heart couldn’t pump blood well, so she was in the hospital for 10 months. She was very sick and close to dying, but her heart started to get better. Doctors treated her heart failure, kept her heart from beating too fast or too slow, and stopped blood clots. After 4 years, her heart function improved and stayed strong — that’s rare, only 1 in 6 people get this. Then it got worse again for 2 years, but she stayed stable. She had a baby, and after the second pregnancy, her heart got weaker again, especially after giving birth — this is common in women with heart problems. Now, in 2017, she’s stable. She takes medicine every day — for her heart, to control fluid, and to slow her heartbeat. She can do normal daily activities, has two children, and doesn’t work. Her heart is still weak, but it’s working better than before. She checks her heart regularly and watches her weight and fluid intake. No need for a special heart device right now."}
{"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 the bone twisted and bent. He had a bone condition called fibrous dysplasia in his thigh since childhood, and 20 years ago, doctors removed part of the bone, added bone graft, and fixed it with a metal device. They later took out the metal device one year later. This time, because the break was serious and in a weak area, they removed a large part of the broken bone and replaced it with a hip implant. They also took a small tissue sample, which confirmed it was the same bone problem from when he was a child. Now, he can walk and do daily things, though he still has some pain when walking long distances. He’s happy with how well it’s working and can now walk and do light activities like walking without much trouble.\"\n}", "generated_text": "A 27-year-old man broke his right thigh bone after a small fall, where the bone twisted and bent. He had a bone condition called fibrous dysplasia in his thigh since childhood, and 20 years ago, doctors removed part of the bone, added bone graft, and fixed it with a metal device. They later took out the metal device one year later. This time, because the break was serious and in a weak area, they removed a large part of the broken bone and replaced it with a hip implant. They also took a small tissue sample, which confirmed it was the same bone problem from when he was a child. Now, he can walk and do daily things, though he still has some pain when walking long distances. He’s happy with how well it’s working and can now walk and do light activities like walking without much trouble."}
{"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 fracture in the upper part of his right thigh bone (femur), specifically at the base of the neck. The break happened after a minor fall that involved pressure and twisting of the hip. This type of fracture is classified as Garden II, Pauwells III, AO 31B2.3r, and is considered serious due to the way it occurred and the patient’s medical history. He had been treated 20 years ago for fibrous dysplasia — a condition where abnormal bone tissue grows in the bone — with a procedure that included removing part of the bone (curettage), adding bone graft, and using a device (osteosynthesis material) to stabilize the area. That device was removed one year later. A biopsy later confirmed the condition was fibrous dysplasia (DF). Because of the fracture’s location and the patient’s history, doctors decided on a wide removal of the upper femur and a total hip replacement using a modular prosthesis, along with placing a cerclage wire to help stabilize the bone. A biopsy after surgery confirmed it was the same fibrous dysplasia seen in childhood. The patient recovered well, with no major complications. He was able to walk with support and gradually returned to daily activities. He still has some walking difficulty due to a scar in the gluteal muscle, but he is now able to do 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 fracture in the upper part of his right thigh bone (femur), specifically at the base of the neck. The break happened after a minor fall that involved pressure and twisting of the hip. This type of fracture is classified as Garden II, Pauwells III, AO 31B2.3r, and is considered serious due to the way it occurred and the patient’s medical history. He had been treated 20 years ago for fibrous dysplasia — a condition where abnormal bone tissue grows in the bone — with a procedure that included removing part of the bone (curettage), adding bone graft, and using a device (osteosynthesis material) to stabilize the area. That device was removed one year later. A biopsy later confirmed the condition was fibrous dysplasia (DF). Because of the fracture’s location and the patient’s history, doctors decided on a wide removal of the upper femur and a total hip replacement using a modular prosthesis, along with placing a cerclage wire to help stabilize the bone. A biopsy after surgery confirmed it was the same fibrous dysplasia seen in childhood. The patient recovered well, with no major complications. He was able to walk with support and gradually returned to daily activities. He still has some walking difficulty due to a scar in the gluteal muscle, but he is now able to do 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) and then a cord blood transplant (allogeneic CBT). After the transplant, he developed worsening breathing problems on day 194. His older brother had a cold, and a test showed he had a respiratory syncytial virus (RSV) infection about a month before. He also had symptoms like coughing and shortness of breath. A lung biopsy showed signs of lung damage, including inflammation from the virus and changes consistent with pulmonary vascular dysplasia (PVOD). The doctors believe the RSV infection may have triggered or contributed to the development of PVOD. The lung injury was seen in the cells of the lungs, especially in the air sacs and blood vessels, and the findings suggest that the virus played a key role in starting the condition.\"\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) and then a cord blood transplant (allogeneic CBT). After the transplant, he developed worsening breathing problems on day 194. His older brother had a cold, and a test showed he had a respiratory syncytial virus (RSV) infection about a month before. He also had symptoms like coughing and shortness of breath. A lung biopsy showed signs of lung damage, including inflammation from the virus and changes consistent with pulmonary vascular dysplasia (PVOD). The doctors believe the RSV infection may have triggered or contributed to the development of PVOD. The lung injury was seen in the cells of the lungs, especially in the air sacs and blood vessels, and the findings suggest that the virus played a key role in starting the condition."}
{"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 persistent cough, shortness of breath, and lost 10 pounds in just 4 months. Tests showed a lump in his right lung and fluid around it. A small piece of tissue was taken and looked under a microscope — it showed strange cells that grew in sheets, surrounded by many immune cells. These cells were found to be from a rare cancer called pulmonary lymphoepithelioma-like carcinoma (CTLP). The cancer cells had signs of a virus called Epstein-Barr, and they were also positive for a protein called PD-L1, which means the cancer can hide from the body’s immune system. He got chemotherapy with drugs like gemcitabine and cisplatin, and later switched to carboplatin because of side effects. He also took durvalumab to help fight the cancer. After 6 rounds of treatment, the cancer got worse and he died 9 months after first being diagnosed, due to breathing problems.\"\n}", "generated_text": "A 65-year-old man started feeling a persistent cough, shortness of breath, and lost 10 pounds in just 4 months. Tests showed a lump in his right lung and fluid around it. A small piece of tissue was taken and looked under a microscope — it showed strange cells that grew in sheets, surrounded by many immune cells. These cells were found to be from a rare cancer called pulmonary lymphoepithelioma-like carcinoma (CTLP). The cancer cells had signs of a virus called Epstein-Barr, and they were also positive for a protein called PD-L1, which means the cancer can hide from the body’s immune system. He got chemotherapy with drugs like gemcitabine and cisplatin, and later switched to carboplatin because of side effects. He also took durvalumab to help fight the cancer. After 6 rounds of treatment, the cancer got worse and he died 9 months after first being diagnosed, due to breathing problems."}
{"row_index": 5, "doc_id": 24, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old boy had a lump in his groin that could be felt and moved. He didn’t have fever, pain, or other symptoms. The doctors took out the lump to make sure it wasn’t something serious like cancer. After checking the tissue under a microscope, they found a rare condition called Castleman’s disease, specifically the plasma cell type, which is very rare in kids. This case is the first time this kind of disease has been found in the groin area. For 12 months after the surgery, the boy had no new lumps or symptoms, and all tests showed everything was normal. He’s doing fine and doesn’t need more treatment.\"\n}", "generated_text": "A 13-year-old boy had a lump in his groin that could be felt and moved. He didn’t have fever, pain, or other symptoms. The doctors took out the lump to make sure it wasn’t something serious like cancer. After checking the tissue under a microscope, they found a rare condition called Castleman’s disease, specifically the plasma cell type, which is very rare in kids. This case is the first time this kind of disease has been found in the groin area. For 12 months after the surgery, the boy had no new lumps or symptoms, and all tests showed everything was normal. He’s doing fine and doesn’t need more treatment."}
{"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 comprised a clinical diagnosis of myotonia, presence of the warm-up phenomenon, characteristic electromyographic (EMG) findings, or a family history, as well as molecular confirmation via mutation analysis in the CLCN1 gene. Data collected included demographic variables (age and sex), disease course (age of onset, symptomatology, time to diagnosis, and clinical evolution), family history, and response to therapeutic interventions. Five patients with a clinical diagnosis of congenital myotonia were identified: three with Becker congenital myotonia and two with Thomsen congenital myotonia. The estimated incidence was 1:15,000 live births for the Becker phenotype and 1:21,000 live births for the Thomsen phenotype.\\n\\nThe cohort was predominantly female, with the sole male patient presenting before the age of 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 for one patient whose family declined testing. All patients exhibited worsening of myotonia with cold exposure; the warm-up phenomenon, a hallmark of the Becker phenotype, was observed only in patients with the Becker genotype.\\n\\nPatients with recessive congenital myotonia demonstrated a progressive clinical course. Family history analysis revealed that patients 2 and 3 were sisters, both clinically affected, with no clinical signs in their parents. The mother of patient 1 exhibited mild, cold-exacerbated myotonic symptoms, suggesting a possible carrier state. The patient who declined genetic evaluation had a positive family history of myotonia in the maternal lineage.\\n\\nSerum creatine kinase levels were not elevated in any of the patients, indicating that 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 (out of 12 years of follow-up); subsequent EMG testing was not repeated due to clinical stability and institutional protocol. The primary pharmacological intervention was oxcarbazepine, particularly in patients with the recessive form, with generally favorable response. However, patient 2 experienced loss of efficacy over time and was subsequently treated with mexiletine. Patient 4 attempted multiple medications without sustained benefit due to either therapeutic failure or adverse effects. Patient 5 declined treatment due to a mild clinical presentation.\\n\\nPatient 1 was found to carry a previously unreported, likely pathogenic mutation in the CLCN1 gene (c.824T>C), inherited from the mother. Cases 1 to 3 exhibited the Becker phenotype and presented with composite heterozygosity—i.e., a combination of two different pathogenic variants in the CLCN1 gene—consistent with autosomal recessive inheritance. Cases 4 and 5 presented with the Thomsen phenotype, which is associated with a single pathogenic variant and typically manifests with more severe myotonia and earlier onset. Patient 5 declined genetic testing, limiting the ability to confirm the specific mutation in that individual.\\n\\nThe pathophysiological mechanism underlying congenital myotonia involves dysfunction of the voltage-gated chloride channel encoded by CLCN1, which leads to impaired repolarization of skeletal muscle fibers during depolarization. This results in prolonged muscle membrane depolarization, causing delayed relaxation and the clinical manifestation of myotonia. The specific mutation c.824T>C (p.Leu275Pro) is predicted to disrupt the channel's pore-forming domain, reducing chloride conductance and contributing to the observed myotonic phenotype. This mutation has not been previously described in the literature and may represent a novel pathogenic variant in the CLCN1 gene spectrum associated with congenital myotonia.\"\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 comprised a clinical diagnosis of myotonia, presence of the warm-up phenomenon, characteristic electromyographic (EMG) findings, or a family history, as well as molecular confirmation via mutation analysis in the CLCN1 gene. Data collected included demographic variables (age and sex), disease course (age of onset, symptomatology, time to diagnosis, and clinical evolution), family history, and response to therapeutic interventions. Five patients with a clinical diagnosis of congenital myotonia were identified: three with Becker congenital myotonia and two with Thomsen congenital myotonia. The estimated incidence was 1:15,000 live births for the Becker phenotype and 1:21,000 live births for the Thomsen phenotype.\n\nThe cohort was predominantly female, with the sole male patient presenting before the age of 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 for one patient whose family declined testing. All patients exhibited worsening of myotonia with cold exposure; the warm-up phenomenon, a hallmark of the Becker phenotype, was observed only in patients with the Becker genotype.\n\nPatients with recessive congenital myotonia demonstrated a progressive clinical course. Family history analysis revealed that patients 2 and 3 were sisters, both clinically affected, with no clinical signs in their parents. The mother of patient 1 exhibited mild, cold-exacerbated myotonic symptoms, suggesting a possible carrier state. The patient who declined genetic evaluation had a positive family history of myotonia in the maternal lineage.\n\nSerum creatine kinase levels were not elevated in any of the patients, indicating that 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 (out of 12 years of follow-up); subsequent EMG testing was not repeated due to clinical stability and institutional protocol. The primary pharmacological intervention was oxcarbazepine, particularly in patients with the recessive form, with generally favorable response. However, patient 2 experienced loss of efficacy over time and was subsequently treated with mexiletine. Patient 4 attempted multiple medications without sustained benefit due to either therapeutic failure or adverse effects. Patient 5 declined treatment due to a mild clinical presentation.\n\nPatient 1 was found to carry a previously unreported, likely pathogenic mutation in the CLCN1 gene (c.824T>C), inherited from the mother. Cases 1 to 3 exhibited the Becker phenotype and presented with composite heterozygosity—i.e., a combination of two different pathogenic variants in the CLCN1 gene—consistent with autosomal recessive inheritance. Cases 4 and 5 presented with the Thomsen phenotype, which is associated with a single pathogenic variant and typically manifests with more severe myotonia and earlier onset. Patient 5 declined genetic testing, limiting the ability to confirm the specific mutation in that individual.\n\nThe pathophysiological mechanism underlying congenital myotonia involves dysfunction of the voltage-gated chloride channel encoded by CLCN1, which leads to impaired repolarization of skeletal muscle fibers during depolarization. This results in prolonged muscle membrane depolarization, causing delayed relaxation and the clinical manifestation of myotonia. The specific mutation c.824T>C (p.Leu275Pro) is predicted to disrupt the channel's pore-forming domain, reducing chloride conductance and contributing to the observed myotonic phenotype. This mutation has not been previously described in the literature and may represent a novel pathogenic variant in the CLCN1 gene spectrum associated with congenital myotonia."}
{"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 an AVM, which didn’t get better even after treatment. Recently, she started feeling tired and short of breath, which means her heart was struggling. Her doctor found her heart was enlarged and not working well, and her blood markers showed high pressure on the heart. She was diagnosed with a serious, long-time leg blood vessel problem and heart failure. The doctors tried to fix it by placing a stent in her leg to block the bad blood flow, which helped her heart feel better. After the surgery, her leg swelling went down and her heart started working better. A second step was done to stop the blood flow from the AVMs in the leg. After one year, her leg swelling was much less, and her heart was stronger. This shows the treatment worked.\"\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 an AVM, which didn’t get better even after treatment. Recently, she started feeling tired and short of breath, which means her heart was struggling. Her doctor found her heart was enlarged and not working well, and her blood markers showed high pressure on the heart. She was diagnosed with a serious, long-time leg blood vessel problem and heart failure. The doctors tried to fix it by placing a stent in her leg to block the bad blood flow, which helped her heart feel better. After the surgery, her leg swelling went down and her heart started working better. A second step was done to stop the blood flow from the AVMs in the leg. After one year, her leg swelling was much less, and her heart was stronger. This shows the treatment worked."}
{"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 didn’t stop the swelling. Over time, she developed symptoms of heart failure, including fatigue and shortness of breath, which led her to seek care at a specialized hospital. Tests showed her heart was enlarged and had weakened function, with high levels of a heart failure marker (BNP), and her leg blood flow was very high—3400 ml/min—due to the AVM.\\n\\nThe doctors decided to treat the AVM using a combination of procedures. First, they placed a covered stent in her femoral artery to block the abnormal blood flow from the AVM. This helped reduce the blood flow to the leg from 3400 ml/min to 1600 ml/min, and her heart failure symptoms improved. The stent was placed in the area where the AVM was most active, and follow-up imaging showed much less blood flow and better leg circulation.\\n\\nA second procedure followed, where they used coils and other materials to block the main drainage veins of the AVM. This further reduced the abnormal blood flow and helped seal off the malformation. After one year, her leg swelling had greatly improved, her heart function had recovered, and her BNP levels dropped significantly. Her left ventricular ejection fraction improved from 60% to 71%, showing better heart pumping ability. This case shows that combining stent placement and embolization can be effective in treating complex congenital AVMs in the lower limb and improving heart failure in patients with such conditions.\"\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 didn’t stop the swelling. Over time, she developed symptoms of heart failure, including fatigue and shortness of breath, which led her to seek care at a specialized hospital. Tests showed her heart was enlarged and had weakened function, with high levels of a heart failure marker (BNP), and her leg blood flow was very high—3400 ml/min—due to the AVM.\n\nThe doctors decided to treat the AVM using a combination of procedures. First, they placed a covered stent in her femoral artery to block the abnormal blood flow from the AVM. This helped reduce the blood flow to the leg from 3400 ml/min to 1600 ml/min, and her heart failure symptoms improved. The stent was placed in the area where the AVM was most active, and follow-up imaging showed much less blood flow and better leg circulation.\n\nA second procedure followed, where they used coils and other materials to block the main drainage veins of the AVM. This further reduced the abnormal blood flow and helped seal off the malformation. After one year, her leg swelling had greatly improved, her heart function had recovered, and her BNP levels dropped significantly. Her left ventricular ejection fraction improved from 60% to 71%, showing better heart pumping ability. This case shows that combining stent placement and embolization can be effective in treating complex congenital AVMs in the lower limb and improving heart failure in patients with such conditions."}
{"row_index": 9, "doc_id": 26, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 67-year-old female presented with a six-year history of progressive left lower limb edema, initially diagnosed with a lower limb arteriovenous malformation (AVM) one year prior. Two months before admission, she underwent embolization using two coils (20 mm × 40 cm, BSX, USA) in the superficial femoral artery (SFA), yet no clinical improvement in swelling was observed. Over the preceding month, she developed progressive fatigue and dyspnea, indicative of acute decompensated heart failure, leading to transfer to Chengdu University of Traditional Chinese Medicine Hospital. She had no prior history of cardiovascular disease, trauma, or surgical interventions, though she reported seven years of oral estrogen therapy for menopausal symptoms.\\n\\nPhysical examination revealed marked edema and skin sclerosis in the left lower limb, 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 elevated B-type natriuretic peptide (BNP) levels at 2853 ng/L. Electrocardiography showed sinus tachycardia (105 bpm) with left atrial enlargement. Chest CT confirmed cardiac enlargement without pulmonary abnormalities. Preoperative computed tomography angiography (CTA) revealed a left iliac artery aneurysm, significant dilation of the common femoral artery (CFA; 27 mm), superficial femoral artery (SFA; 22 mm), and complex congenital AVMs involving the SFA and profunda femoris artery. Arterial phase imaging showed marked enlargement of both femoral and superficial veins. The popliteal and anterior tibial arteries were nonvisualized, supporting diagnosis of complex congenital lower limb AVMs with associated venous congestion.\\n\\nThe patient was classified as New York Heart Association (NYHA) Class IV due to severe symptoms of acute heart failure. Preoperative CFA flow volume was 3400 ml/min. Given the persistence of high flow through the AVMs despite coil embolization, and the lack of effective flow reduction with conventional embolization, a covered stent graft was selected as a therapeutic strategy to occlude the high-flow AVM nidus and reduce venous congestion, thereby alleviating cardiac preload and improving hemodynamics. CTA measurements indicated maximum vessel diameters of 32 mm (iliac artery), 27 mm (CFA), and 22 mm (SFA), with the SFA mid-segment measuring 19 mm, leading to selection of a 20 mm × 12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China).\\n\\nUnder general anesthesia, antegrade access was achieved via the common femoral artery using a 14 F (Cook Medical, USA) catheter sheath. A 0.035 guidewire was initially used, subsequently replaced with a 0.035 super-hard guidewire for enhanced stability during stent deployment. The stent was implanted at the distal SFA, the region of highest AVM burden. Completion angiography demonstrated significant reduction in venous opacification around the stent and clear visualization of the popliteal artery, confirming successful stent placement and hemodynamic stabilization. Postoperatively, the left femoral artery was sutured using a 6-0 vascular risk suture.\\n\\nThe surgical procedure was performed with minimal duration to avoid exacerbation of heart failure, consistent with the patient’s unstable cardiac status. A staged embolization was planned for the second phase to target the AVM nidus and draining venous pathways. One week post-intervention, CFA flow reduced to 1600 ml/min, and BNP levels decreased to 1198 ng/L, indicating early clinical improvement. Right CFA access was used to perform angiographic guidance, with puncture of the AVM drainage vein and introduction of a 5 F vascular sheath. 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) to achieve occlusion of the nidus and draining veins.\\n\\nCompletion angiography showed near-complete disappearance of AVM and draining vein visualization. At one-year follow-up, the CFA flow volume decreased to 780 ml/min, echocardiography revealed mild atrial enlargement,", "generated_text": "{\n  \"proficient_health_literacy\": \"A 67-year-old female presented with a six-year history of progressive left lower limb edema, initially diagnosed with a lower limb arteriovenous malformation (AVM) one year prior. Two months before admission, she underwent embolization using two coils (20 mm × 40 cm, BSX, USA) in the superficial femoral artery (SFA), yet no clinical improvement in swelling was observed. Over the preceding month, she developed progressive fatigue and dyspnea, indicative of acute decompensated heart failure, leading to transfer to Chengdu University of Traditional Chinese Medicine Hospital. She had no prior history of cardiovascular disease, trauma, or surgical interventions, though she reported seven years of oral estrogen therapy for menopausal symptoms.\\n\\nPhysical examination revealed marked edema and skin sclerosis in the left lower limb, 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 elevated B-type natriuretic peptide (BNP) levels at 2853 ng/L. Electrocardiography showed sinus tachycardia (105 bpm) with left atrial enlargement. Chest CT confirmed cardiac enlargement without pulmonary abnormalities. Preoperative computed tomography angiography (CTA) revealed a left iliac artery aneurysm, significant dilation of the common femoral artery (CFA; 27 mm), superficial femoral artery (SFA; 22 mm), and complex congenital AVMs involving the SFA and profunda femoris artery. Arterial phase imaging showed marked enlargement of both femoral and superficial veins. The popliteal and anterior tibial arteries were nonvisualized, supporting diagnosis of complex congenital lower limb AVMs with associated venous congestion.\\n\\nThe patient was classified as New York Heart Association (NYHA) Class IV due to severe symptoms of acute heart failure. Preoperative CFA flow volume was 3400 ml/min. Given the persistence of high flow through the AVMs despite coil embolization, and the lack of effective flow reduction with conventional embolization, a covered stent graft was selected as a therapeutic strategy to occlude the high-flow AVM nidus and reduce venous congestion, thereby alleviating cardiac preload and improving hemodynamics. CTA measurements indicated maximum vessel diameters of 32 mm (iliac artery), 27 mm (CFA), and 22 mm (SFA), with the SFA mid-segment measuring 19 mm, leading to selection of a 20 mm × 12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China).\\n\\nUnder general anesthesia, antegrade access was achieved via the common femoral artery using a 14 F (Cook Medical, USA) catheter sheath. A 0.035 guidewire was initially used, subsequently replaced with a 0.035 super-hard guidewire for enhanced stability during stent deployment. The stent was implanted at the distal SFA, the region of highest AVM burden. Completion angiography demonstrated significant reduction in venous opacification around the stent and clear visualization of the popliteal artery, confirming successful stent placement and hemodynamic stabilization. Postoperatively, the left femoral artery was sutured using a 6-0 vascular risk suture.\\n\\nThe surgical procedure was performed with minimal duration to avoid exacerbation of heart failure, consistent with the patient’s unstable cardiac status. A staged embolization was planned for the second phase to target the AVM nidus and draining venous pathways. One week post-intervention, CFA flow reduced to 1600 ml/min, and BNP levels decreased to 1198 ng/L, indicating early clinical improvement. Right CFA access was used to perform angiographic guidance, with puncture of the AVM drainage vein and introduction of a 5 F vascular sheath. 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) to achieve occlusion of the nidus and draining veins.\\n\\nCompletion angiography showed near-complete disappearance of AVM and draining vein visualization. At one-year follow-up, the CFA flow volume decreased to 780 ml/min, echocardiography revealed mild atrial enlargement,"}
{"row_index": 10, "doc_id": 27, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 28-year-old man got two red, bump-like spots on his right arm and forearm that had small blisters and sores in the middle. They were sore and itched, but he didn’t feel sick inside. He was vacationing in a coastal area of Ecuador when this happened. The doctor took a small skin sample and saw signs that matched a skin problem from bugs in that area. The doctor called it Paederus dermatitis. He treated it with anti-itch medicine, cream to calm the skin, and cold compresses. After 8 days, the bumps went away, but the skin stayed a little darker in those spots.\"\n}", "generated_text": "A 28-year-old man got two red, bump-like spots on his right arm and forearm that had small blisters and sores in the middle. They were sore and itched, but he didn’t feel sick inside. He was vacationing in a coastal area of Ecuador when this happened. The doctor took a small skin sample and saw signs that matched a skin problem from bugs in that area. The doctor called it Paederus dermatitis. He treated it with anti-itch medicine, cream to calm the skin, and cold compresses. After 8 days, the bumps went away, but the skin stayed a little darker in those spots."}
{"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, located 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, without systemic symptoms or evidence of self-medication. The patient reported a recent vacation in the coastal region of Ecuador, which served as a key epidemiological context. An incisional biopsy was performed and revealed histopathological features consistent with Paederus dermatitis, including epidermal acanthosis, parakeratosis, and intercellular spongiosis, with neutrophilic infiltrates in the stratum corneum and perivascular lymphocytic infiltration extending into the superficial, middle, and deep dermis. These findings are characteristic of a delayed-type hypersensitivity reaction to Paederus beetle-derived cuticular proteins, specifically the Paederus toxin (Paederus toxin, a member of the cysteine-rich protein family), which induces a type IV hypersensitivity response mediated by CD4+ T cells and subsequent release of pro-inflammatory cytokines such as IL-4, IL-5, and IL-13. The clinical presentation, geographic exposure, and histopathological profile collectively support the diagnosis of Paederus dermatitis. Management consisted of antihistamines to mitigate pruritus, topical corticosteroids to suppress local inflammation, and cold compresses to reduce vascular permeability and symptom severity. The lesions completely resolved after 8 days of treatment, with residual post-inflammatory hyperpigmentation observed as a result of melanocyte activation and prolonged dermal inflammation. This case underscores the importance of considering environmental exposures in tropical regions, particularly in endemic areas where Paederus beetles (family Paederidae) are prevalent, as a potential etiology of acute, non-infectious, pruritic dermatoses with a distinct histopathological signature.\"\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, located 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, without systemic symptoms or evidence of self-medication. The patient reported a recent vacation in the coastal region of Ecuador, which served as a key epidemiological context. An incisional biopsy was performed and revealed histopathological features consistent with Paederus dermatitis, including epidermal acanthosis, parakeratosis, and intercellular spongiosis, with neutrophilic infiltrates in the stratum corneum and perivascular lymphocytic infiltration extending into the superficial, middle, and deep dermis. These findings are characteristic of a delayed-type hypersensitivity reaction to Paederus beetle-derived cuticular proteins, specifically the Paederus toxin (Paederus toxin, a member of the cysteine-rich protein family), which induces a type IV hypersensitivity response mediated by CD4+ T cells and subsequent release of pro-inflammatory cytokines such as IL-4, IL-5, and IL-13. The clinical presentation, geographic exposure, and histopathological profile collectively support the diagnosis of Paederus dermatitis. Management consisted of antihistamines to mitigate pruritus, topical corticosteroids to suppress local inflammation, and cold compresses to reduce vascular permeability and symptom severity. The lesions completely resolved after 8 days of treatment, with residual post-inflammatory hyperpigmentation observed as a result of melanocyte activation and prolonged dermal inflammation. This case underscores the importance of considering environmental exposures in tropical regions, particularly in endemic areas where Paederus beetles (family Paederidae) are prevalent, as a potential etiology of acute, non-infectious, pruritic dermatoses with a distinct histopathological signature."}
{"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. Instead, they used a light-based treatment called PDT to ease the blockage. Before the treatment, he got a special medicine through a vein, and the doctors used a scope to look inside his bile duct. They placed a small light tube into the duct and shone light on the blocked area to help open it. The light was turned on slowly, every centimeter, to make sure the whole blockage was treated. Afterward, they checked the duct again to make sure everything was okay. The treatment worked for three months, but the blockage came back. He had other treatments, but eventually died from lung cancer that spread from the tumor, 15 months after the light treatment. The most important thing is that the light treatment helped him feel better for a while, even though it didn’t cure the disease.\"\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. Instead, they used a light-based treatment called PDT to ease the blockage. Before the treatment, he got a special medicine through a vein, and the doctors used a scope to look inside his bile duct. They placed a small light tube into the duct and shone light on the blocked area to help open it. The light was turned on slowly, every centimeter, to make sure the whole blockage was treated. Afterward, they checked the duct again to make sure everything was okay. The treatment worked for three months, but the blockage came back. He had other treatments, but eventually died from lung cancer that spread from the tumor, 15 months after the light treatment. The most important thing is that the light treatment helped him feel better for a while, even though it didn’t cure the disease."}
{"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 confirmed choledocholithiasis, and endoscopic retrograde cholangiopancreatography (ERCP) revealed inability to remove stones due to disproportionate ductal dilation, necessitating placement of a plastic biliary stent. Clinical improvement was transient, with cholestasis returning 45 days post-ERCP. Subsequent ERCP attempts failed to clear the stones. On repeat EUS, a well-circumscribed hypoechoic solid mass measuring 1.8 × 2 cm was identified in the dilated common hepatic duct, compressing the duct lumen, and extending into 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 therapy. Multidisciplinary consensus supported adjunctive photodynamic therapy (PDT) to manage the obstructive lesion. The PDT procedure was performed under general anesthesia using intravenous administration of Photogen® (1.5 mg/kg) administered 24 hours prior to the session. The photosensitizer has a peak light absorption at 630 nm, enabling targeted activation within biliary tissue. Standard duodenoscopy (Olympus TJF-180) was performed to identify the greater duodenal papilla and achieve retrograde cannulation. A digital cholangioscope (SpyGlass™ DS, Boston Scientific) was then advanced into the common bile duct for direct visualization, allowing precise identification of the neoplastic stenosis. Under real-time cholangioscopic guidance, an illumination catheter (Medlight S.A., RD10-323) was advanced through the cholangioscope. The 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 stabilization; the third port serves as the injection site for the photosensitizer. The illumination was delivered 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 stenotic segment. Post-procedure, the bile duct was re-evaluated via cholangioscopy to assess immediate outcomes and detect any adverse events. The patient was maintained on a fasted state for 24 hours post-procedure, with oral diet initiated if no adverse events were observed. Discharge was accompanied by strict photoprotection protocols, including avoidance of light exposure and use of sunglasses, particularly during the first week following PDT. The procedure lasted 150 minutes and concluded with placement of a 10 Fr plastic biliary stent for drainage, as a self-expanding metal stent was unavailable at the time. The patient remained asymptomatic for three months, the longest period since disease onset. However, early recurrence of cholestasis with cholangitis occurred, which was attributed to stent obstruction by tumor debris and biliary sludge secondary to tumor necrosis. A biliary scan followed by re-drainage resolved the acute episode. Subsequently, a self-expanding metal stent was placed to maintain patency. The patient continued on systemic oncologic therapy and eventually required a duodenal stent for palliation of dysphagia. 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 immediate adverse events, and the PDT provided symptomatic relief and disease stabilization for an extended period, although the underlying malignancy progressed to metastatic disease.\"\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 confirmed choledocholithiasis, and endoscopic retrograde cholangiopancreatography (ERCP) revealed inability to remove stones due to disproportionate ductal dilation, necessitating placement of a plastic biliary stent. Clinical improvement was transient, with cholestasis returning 45 days post-ERCP. Subsequent ERCP attempts failed to clear the stones. On repeat EUS, a well-circumscribed hypoechoic solid mass measuring 1.8 × 2 cm was identified in the dilated common hepatic duct, compressing the duct lumen, and extending into 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 therapy. Multidisciplinary consensus supported adjunctive photodynamic therapy (PDT) to manage the obstructive lesion. The PDT procedure was performed under general anesthesia using intravenous administration of Photogen® (1.5 mg/kg) administered 24 hours prior to the session. The photosensitizer has a peak light absorption at 630 nm, enabling targeted activation within biliary tissue. Standard duodenoscopy (Olympus TJF-180) was performed to identify the greater duodenal papilla and achieve retrograde cannulation. A digital cholangioscope (SpyGlass™ DS, Boston Scientific) was then advanced into the common bile duct for direct visualization, allowing precise identification of the neoplastic stenosis. Under real-time cholangioscopic guidance, an illumination catheter (Medlight S.A., RD10-323) was advanced through the cholangioscope. The 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 stabilization; the third port serves as the injection site for the photosensitizer. The illumination was delivered 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 stenotic segment. Post-procedure, the bile duct was re-evaluated via cholangioscopy to assess immediate outcomes and detect any adverse events. The patient was maintained on a fasted state for 24 hours post-procedure, with oral diet initiated if no adverse events were observed. Discharge was accompanied by strict photoprotection protocols, including avoidance of light exposure and use of sunglasses, particularly during the first week following PDT. The procedure lasted 150 minutes and concluded with placement of a 10 Fr plastic biliary stent for drainage, as a self-expanding metal stent was unavailable at the time. The patient remained asymptomatic for three months, the longest period since disease onset. However, early recurrence of cholestasis with cholangitis occurred, which was attributed to stent obstruction by tumor debris and biliary sludge secondary to tumor necrosis. A biliary scan followed by re-drainage resolved the acute episode. Subsequently, a self-expanding metal stent was placed to maintain patency. The patient continued on systemic oncologic therapy and eventually required a duodenal stent for palliation of dysphagia. 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 immediate adverse events, and the PDT provided symptomatic relief and disease stabilization for an extended period, although the underlying malignancy progressed to metastatic disease."}
{"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), accompanied by anaemia (haemoglobin: 9.6 g/dL), consistent with upper gastrointestinal bleeding. Non-contrast-enhanced CT was performed due to renal dysfunction and revealed a steep flexure of the third part of the duodenum on the right side of the aorta, with a caudal course that did not cross 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 suggestive of 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, where forceful vomiting leads to mucosal tears at the gastroesophageal junction. The anatomical configuration of the duodenum—specifically, its steep rightward flexure 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 seven days later showed spontaneous resolution of this rightward deviation, with the jejunum returning to a central or left-sided position. This transient, self-resolving malposition is inconsistent with true malrotation, which typically presents as a congenital anomaly with persistent anatomical abnormality and risk of volvulus. The patient was discharged after stabilization.\\n\\nTwo months later, she presented with a recurrent episode of haematemesis. Dynamic CT performed prior to endoscopy revealed contrast extravasation in the dilated stomach, and again, the third part of the duodenum was found 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 laceration at the gastric cardia, reinforcing the diagnosis of Mallory-Weiss syndrome. Subsequent non-contrast CT, performed two months after the second haematemesis, showed no persistent duodenal deviation, but revealed oedematous wall thickening in the second part of the duodenum. Without prior imaging, this might have been interpreted as duodenitis; however, the history of repeated, spontaneous rightward deviations of the small intestine provided a critical clue to an underlying anatomical variant.\\n\\nGiven the pattern of transient, reversible right-sided displacement of the duodenum and jejunum—without evidence of malrotation or volvulus—dysplasia of the ligament of Treitz was diagnosed. The ligament of Treitz, which normally anchors the duodenum to the jejunum in the retroperitoneum, is typically formed and fixed during embryogenesis. In this case, CT imaging and surgical exploration revealed a formed ligament of Treitz, but with incomplete fixation to the upper jejunum—specifically, it was attached only to the duodenum and not securely anchored to the retroperitoneum. The duodenal-jejunal junction was not fixed to the retroperitoneal space, resulting in mechanical instability and allowing the jejunum to fold freely around the ligament as a fulcrum, thereby producing transient rightward displacement during gastrointestinal motility or increased intraluminal pressure.\\n\\nLaparotomy 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 incomplete fixation of the ligament of Treitz was the primary pathophysiological mechanism underlying the recurrent, spontaneous rightward deviations observed on imaging. Surgical correction involved fixation of the upper jejunum with four sutures to the retroperitoneum on the left side, which stabilized the anatomical configuration. The postoperative course was uncomplicated, and the patient has remained asymptomatic since. This case illustrates that transient, reversible small intestinal deviations in the absence of malrotation may represent a functional variant due to dysplasia of the ligament of Treitz, with implications for both imaging interpretation and surgical management in patients with recurrent upper gastrointestinal bleeding.\"\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), accompanied by anaemia (haemoglobin: 9.6 g/dL), consistent with upper gastrointestinal bleeding. Non-contrast-enhanced CT was performed due to renal dysfunction and revealed a steep flexure of the third part of the duodenum on the right side of the aorta, with a caudal course that did not cross 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 suggestive of 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, where forceful vomiting leads to mucosal tears at the gastroesophageal junction. The anatomical configuration of the duodenum—specifically, its steep rightward flexure 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 seven days later showed spontaneous resolution of this rightward deviation, with the jejunum returning to a central or left-sided position. This transient, self-resolving malposition is inconsistent with true malrotation, which typically presents as a congenital anomaly with persistent anatomical abnormality and risk of volvulus. The patient was discharged after stabilization.\n\nTwo months later, she presented with a recurrent episode of haematemesis. Dynamic CT performed prior to endoscopy revealed contrast extravasation in the dilated stomach, and again, the third part of the duodenum was found 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 laceration at the gastric cardia, reinforcing the diagnosis of Mallory-Weiss syndrome. Subsequent non-contrast CT, performed two months after the second haematemesis, showed no persistent duodenal deviation, but revealed oedematous wall thickening in the second part of the duodenum. Without prior imaging, this might have been interpreted as duodenitis; however, the history of repeated, spontaneous rightward deviations of the small intestine provided a critical clue to an underlying anatomical variant.\n\nGiven the pattern of transient, reversible right-sided displacement of the duodenum and jejunum—without evidence of malrotation or volvulus—dysplasia of the ligament of Treitz was diagnosed. The ligament of Treitz, which normally anchors the duodenum to the jejunum in the retroperitoneum, is typically formed and fixed during embryogenesis. In this case, CT imaging and surgical exploration revealed a formed ligament of Treitz, but with incomplete fixation to the upper jejunum—specifically, it was attached only to the duodenum and not securely anchored to the retroperitoneum. The duodenal-jejunal junction was not fixed to the retroperitoneal space, resulting in mechanical instability and allowing the jejunum to fold freely around the ligament as a fulcrum, thereby producing transient rightward displacement during gastrointestinal motility or increased intraluminal pressure.\n\nLaparotomy 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 incomplete fixation of the ligament of Treitz was the primary pathophysiological mechanism underlying the recurrent, spontaneous rightward deviations observed on imaging. Surgical correction involved fixation of the upper jejunum with four sutures to the retroperitoneum on the left side, which stabilized the anatomical configuration. The postoperative course was uncomplicated, and the patient has remained asymptomatic since. This case illustrates that transient, reversible small intestinal deviations in the absence of malrotation may represent a functional variant due to dysplasia of the ligament of Treitz, with implications for both imaging interpretation and surgical management in patients with recurrent upper gastrointestinal bleeding."}
{"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, for about a month. He also had fever, chills, sweating, loss of appetite, and lost 6 pounds. His doctor found a swollen liver with small spots on it that looked strange. These spots were not cancer or infection from other causes. Tests showed signs of a slow, hidden infection — like tuberculosis — in the liver. A small surgery was done to take a piece of the liver tissue, and the lab confirmed it was tuberculosis. After starting medicine to fight the tuberculosis, his symptoms got better fast. The pain went away, the fever stopped, and the spots on his liver got smaller over time. This treatment works well for this kind of liver problem.\"\n}", "generated_text": "A 28-year-old man from Morocco had pain in his belly, especially on the right side, for about a month. He also had fever, chills, sweating, loss of appetite, and lost 6 pounds. His doctor found a swollen liver with small spots on it that looked strange. These spots were not cancer or infection from other causes. Tests showed signs of a slow, hidden infection — like tuberculosis — in the liver. A small surgery was done to take a piece of the liver tissue, and the lab confirmed it was tuberculosis. After starting medicine to fight the tuberculosis, his symptoms got better fast. The pain went away, the fever stopped, and the spots on his liver got smaller over time. This treatment works well for this kind of liver problem."}
{"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 presented with a month-long history of abdominal pain, especially in the upper right part of his belly, along with fever, chills, night sweats, loss of appetite, and a 6-kilogram weight loss. He had no known family history of illness and was vaccinated for tuberculosis (BCG). Initially, his symptoms were mild, but they worsened over time, leading to significant weight loss of 12 kilograms over three months. Tests showed signs of infection, including high white blood cells and inflammation markers, but no evidence of common infections like hepatitis or bacterial infections. Imaging scans revealed multiple nodules in his liver that were not clearly explained. These nodules appeared on both ultrasound and MRI, and they were not enhancing after contrast was given. Liver function tests were normal, and blood tests for viruses and tuberculosis (using GeneXpert and quantiferon) were negative at first. A liver biopsy during laparoscopy showed characteristic tissue changes — epithelioid and giant cells with caseous necrosis — which are typical of tuberculosis. This confirmed a diagnosis of focal liver tuberculosis. The patient was started on standard anti-tuberculosis medication: a four-drug combination for the first two months, followed by a two-drug regimen for four months. Within days of starting treatment, his symptoms improved significantly. By the third month, follow-up scans showed that the liver nodules had shrunk in number and size, and his overall condition had stabilized.\"\n}", "generated_text": "A 28-year-old Moroccan man with no smoking or drinking habits presented with a month-long history of abdominal pain, especially in the upper right part of his belly, along with fever, chills, night sweats, loss of appetite, and a 6-kilogram weight loss. He had no known family history of illness and was vaccinated for tuberculosis (BCG). Initially, his symptoms were mild, but they worsened over time, leading to significant weight loss of 12 kilograms over three months. Tests showed signs of infection, including high white blood cells and inflammation markers, but no evidence of common infections like hepatitis or bacterial infections. Imaging scans revealed multiple nodules in his liver that were not clearly explained. These nodules appeared on both ultrasound and MRI, and they were not enhancing after contrast was given. Liver function tests were normal, and blood tests for viruses and tuberculosis (using GeneXpert and quantiferon) were negative at first. A liver biopsy during laparoscopy showed characteristic tissue changes — epithelioid and giant cells with caseous necrosis — which are typical of tuberculosis. This confirmed a diagnosis of focal liver tuberculosis. The patient was started on standard anti-tuberculosis medication: a four-drug combination for the first two months, followed by a two-drug regimen for four months. Within days of starting treatment, his symptoms improved significantly. By the third month, follow-up scans showed that the liver nodules had shrunk in number and size, and his overall condition had stabilized."}
{"row_index": 17, "doc_id": 30, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 28-year-old male military personnel presented with a 5-week history of progressive epigastric and right upper quadrant abdominal pain, accompanied by intermittent fever (peaking at 39.1°C), chills, profuse night sweats, anorexia, and a 6 kg weight loss over one month. He had no history of alcohol use, smoking, or significant comorbidities; he was BCG-vaccinated and had no familial or personal history of infectious or hepatic disease. Physical examination revealed an asthenic appearance, tachycardia (124 beats/min), tachypnea (22 breaths/min), and moderate right upper quadrant tenderness with hepatomegaly (liver size 17 cm). No pulmonary or lymphadenopathic findings were detected on physical exam.\\n\\nThe clinical picture evolved from an initial presentation of diffuse abdominal pain with alternating diarrhea and constipation, persisting over several weeks, initially with only low-grade nocturnal fever and preserved general condition. This was followed by progressive deterioration, including a 12 kg weight loss over three months, prompting emergency admission for further evaluation.\\n\\nLaboratory findings demonstrated a neutrophilic leukocytosis (17,800 cells/mm³), elevated C-reactive protein (323 mg/L), and a positive procalcitonin level (4.1 ng/L), consistent with a systemic inflammatory response syndrome. Initial biomarkers of liver injury were within normal limits: ALT (22 IU/L), AST (17 IU/L), GGT (42 IU/L), ALP (115 IU/L), bilirubin, prothrombin time (78%), and albumin (39 g/L). Renal function and electrolyte balance were normal. 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. Blood cultures and urine cytobacteriological analysis during febrile peaks were negative. GeneXpert assay for Mycobacterium tuberculosis in respiratory specimens and in liver biopsy material was negative; quantiferon tuberculin test was negative, indicating no evidence of latent or active TB in the immunological screening.\\n\\nImaging studies revealed multiple, well-defined, rounded hypodense lesions in the liver on thoraco-abdomino-pelvic CT, with no enhancement after contrast administration. The largest lesions were located in segment I (21 × 16 mm) and segment V (36 × 27 mm). Abdominal ultrasound showed no focal abnormalities. Liver MRI demonstrated dysmorphic liver architecture with heterogeneous T2 signal intensity, with peripheral hyperintense walls surrounding the lesions, showing peripheral contrast enhancement. The largest lesions were in segment I (20 × 22 mm) and segment V (33 × 31 mm), consistent with a pattern suggestive of granulomatous inflammation. No deep lymphadenopathy was observed in thoracic or pelvic regions.\\n\\nEchographic-guided liver biopsies initially revealed subacute, fibro-inflammatory changes without evidence of malignancy or specific infectious etiology. Diagnostic laparoscopy was performed to obtain histological specimens from hepatic nodules. Histopathological examination revealed epithelioid and gigantocellular granulomas with central caseous necrosis, a classic histological hallmark of tuberculosis, supporting a diagnosis of focal hepatic tuberculosis.\\n\\nThe patient was initiated on standard anti-tuberculous therapy: Phase 1 (2 months) of quadritherapy—isoniazid, rifampicin, pyrazinamide, and ethambutol—administered as single oral doses in the morning on an empty stomach. Phase 2 (4 months) involved continuation with bitherapy (isoniazid and rifampicin) under the same dosing regimen. Clinical and biological monitoring demonstrated a rapid and favorable response to treatment, with resolution of systemic inflammatory markers and improvement in symptoms within days. After three months of therapy, follow-up imaging showed a significant reduction in the number and volume of hepatic lesions, indicating therapeutic efficacy. The clinical course reflects a rare presentation of extrapulmonary tuberculosis involving the liver, with a delayed recognition due to non-specific symptoms and negative initial microbiological screening, ultimately confirmed by histopathological analysis of hepatic nodules.\"\n}", "generated_text": "A 28-year-old male military personnel presented with a 5-week history of progressive epigastric and right upper quadrant abdominal pain, accompanied by intermittent fever (peaking at 39.1°C), chills, profuse night sweats, anorexia, and a 6 kg weight loss over one month. He had no history of alcohol use, smoking, or significant comorbidities; he was BCG-vaccinated and had no familial or personal history of infectious or hepatic disease. Physical examination revealed an asthenic appearance, tachycardia (124 beats/min), tachypnea (22 breaths/min), and moderate right upper quadrant tenderness with hepatomegaly (liver size 17 cm). No pulmonary or lymphadenopathic findings were detected on physical exam.\n\nThe clinical picture evolved from an initial presentation of diffuse abdominal pain with alternating diarrhea and constipation, persisting over several weeks, initially with only low-grade nocturnal fever and preserved general condition. This was followed by progressive deterioration, including a 12 kg weight loss over three months, prompting emergency admission for further evaluation.\n\nLaboratory findings demonstrated a neutrophilic leukocytosis (17,800 cells/mm³), elevated C-reactive protein (323 mg/L), and a positive procalcitonin level (4.1 ng/L), consistent with a systemic inflammatory response syndrome. Initial biomarkers of liver injury were within normal limits: ALT (22 IU/L), AST (17 IU/L), GGT (42 IU/L), ALP (115 IU/L), bilirubin, prothrombin time (78%), and albumin (39 g/L). Renal function and electrolyte balance were normal. 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. Blood cultures and urine cytobacteriological analysis during febrile peaks were negative. GeneXpert assay for Mycobacterium tuberculosis in respiratory specimens and in liver biopsy material was negative; quantiferon tuberculin test was negative, indicating no evidence of latent or active TB in the immunological screening.\n\nImaging studies revealed multiple, well-defined, rounded hypodense lesions in the liver on thoraco-abdomino-pelvic CT, with no enhancement after contrast administration. The largest lesions were located in segment I (21 × 16 mm) and segment V (36 × 27 mm). Abdominal ultrasound showed no focal abnormalities. Liver MRI demonstrated dysmorphic liver architecture with heterogeneous T2 signal intensity, with peripheral hyperintense walls surrounding the lesions, showing peripheral contrast enhancement. The largest lesions were in segment I (20 × 22 mm) and segment V (33 × 31 mm), consistent with a pattern suggestive of granulomatous inflammation. No deep lymphadenopathy was observed in thoracic or pelvic regions.\n\nEchographic-guided liver biopsies initially revealed subacute, fibro-inflammatory changes without evidence of malignancy or specific infectious etiology. Diagnostic laparoscopy was performed to obtain histological specimens from hepatic nodules. Histopathological examination revealed epithelioid and gigantocellular granulomas with central caseous necrosis, a classic histological hallmark of tuberculosis, supporting a diagnosis of focal hepatic tuberculosis.\n\nThe patient was initiated on standard anti-tuberculous therapy: Phase 1 (2 months) of quadritherapy—isoniazid, rifampicin, pyrazinamide, and ethambutol—administered as single oral doses in the morning on an empty stomach. Phase 2 (4 months) involved continuation with bitherapy (isoniazid and rifampicin) under the same dosing regimen. Clinical and biological monitoring demonstrated a rapid and favorable response to treatment, with resolution of systemic inflammatory markers and improvement in symptoms within days. After three months of therapy, follow-up imaging showed a significant reduction in the number and volume of hepatic lesions, indicating therapeutic efficacy. The clinical course reflects a rare presentation of extrapulmonary tuberculosis involving the liver, with a delayed recognition due to non-specific symptoms and negative initial microbiological screening, ultimately confirmed by histopathological analysis of hepatic nodules."}
{"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 hands and feet had a sore spot on his tongue that looked serious, like a cancer, but it was actually just a long-lasting wound from sharp teeth. His lips were dry and cracked. Because he wore a collar, doctors couldn’t check his neck lymph nodes. The wound was 1 cm wide, had a hard edge, and was white-yellow, which made it look scary. The sharp tooth on the side of his mouth was hurting his tongue and was causing the soreness. Doctors said the problem was caused by the sharp tooth and dry lips, not cancer. He was given salt water, iodine mouthwash, and lip cream to clean and heal the sore spot. His mom was told to use salt water to clean his mouth, apply iodine three times a day to the sore spot, and use lip cream to keep his lips soft. The sharp teeth were planned to be removed, and the space where they went will be fixed with a special device. After a few days, the sore spot got better. But later, he had surgery on his neck because of spine problems. After surgery, he had breathing trouble and passed away two weeks later.\"\n}", "generated_text": "A 12-year-old boy with Down Syndrome and trouble moving his hands and feet had a sore spot on his tongue that looked serious, like a cancer, but it was actually just a long-lasting wound from sharp teeth. His lips were dry and cracked. Because he wore a collar, doctors couldn’t check his neck lymph nodes. The wound was 1 cm wide, had a hard edge, and was white-yellow, which made it look scary. The sharp tooth on the side of his mouth was hurting his tongue and was causing the soreness. Doctors said the problem was caused by the sharp tooth and dry lips, not cancer. He was given salt water, iodine mouthwash, and lip cream to clean and heal the sore spot. His mom was told to use salt water to clean his mouth, apply iodine three times a day to the sore spot, and use lip cream to keep his lips soft. The sharp teeth were planned to be removed, and the space where they went will be fixed with a special device. After a few days, the sore spot got better. But later, he had surgery on his neck because of spine problems. After surgery, he had breathing trouble and passed away two weeks later."}
{"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 progressive lower extremity and upper limb weakness, initially presenting with a fall approximately one year prior, leading to hospitalization. The patient's mother reported chronic difficulties in performing routine oral hygiene due to motoric impairments, contributing to poor oral care and increased risk of mucosal injury. The patient was diagnosed with Down Syndrome and myeloradiculopathy, a condition characterized by degeneration of spinal nerve roots, resulting in motor dysfunction and sensory deficits.\\n\\nExtraorally, the patient exhibited a dysmorphic facial appearance, consistent with the phenotypic features of 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 reduced lip mobility, impaired salivary flow, and inadequate moisturization. Lymph node examination 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 malignancy of the epithelial lining of the oral cavity, due to its indurated border and surface appearance. However, the diagnosis of a chronic traumatic ulcer was established based on clinical correlation, patient history, and exclusion of neoplastic pathology. The traumatic origin was attributed to the sharp occlusal surface of the maxillary right central incisor (tooth 55), which caused persistent mechanical irritation against the tongue's lateral border, leading to tissue breakdown and ulceration. Additionally, the patient had dentinal caries involving tooth 63, and radicular gangrene (radix gangrene) affecting teeth 55, 62, 74, and 85, indicating advanced pulp necrosis and periapical tissue destruction. These tooth remnants were recommended for extraction by a pediatric dentist, with a space maintainer to be placed to preserve dental arch integrity and prevent malocclusion.\\n\\nLaboratory findings revealed hyponatremia (serum sodium 130 mEq/L), which may reflect impaired renal sodium reabsorption or osmotic imbalances associated with chronic neurological dysfunction or medication effects. Lymphocytosis (lymphocyte count 46%) was noted, potentially indicating a chronic inflammatory state or immune dysregulation, which may be exacerbated by recurrent mucosal trauma and poor oral hygiene. An MRI of the cervical spine confirmed cervical spine dislocation, consistent with the pathophysiology of myeloradiculopathy, which directly contributes to the patient's motor deficits and may have secondary effects on orofacial control and posture.\\n\\nThe differential diagnosis included exfoliative cheilitis, reversible pulpitis of tooth 63, and radix gangrene of multiple teeth. The chronic traumatic ulcer was confirmed through clinical evaluation, with no evidence of dysplasia, cellular atypia, or invasive growth on biopsy. The patient received a multimodal treatment regimen: paracetamol 120 mg/5 mL and amoxicillin 125 mg/5 mL for symptomatic management and possible bacterial infection; sodium chloride 0.9% solution for oral rinsing to maintain osmotic balance; povidone-iodine 1% mouthwash applied three times daily as an antiseptic and anti-inflammatory agent to reduce bacterial load and modulate local inflammation; and petroleum jelly applied to the lips to address desiccation and promote epithelial integrity.\\n\\nThe patient's oral lesions showed progressive improvement over time: at the 3-day follow-up, there was initial healing of the oral ulcer; at the 1-week follow-up, the ulcer size decreased and lip lesions improved; by the 10-day follow-up, significant healing of the tongue ulcer was observed. However, despite clinical improvement, the patient underwent neurosurgery for correction of cervical spine dislocation two days after the 10-day visit. Postoperatively, the patient was admitted to the Pediatric Intensive Care Unit (PICU) due to respiratory compromise. After two weeks of PICU observation, the patient developed acute respiratory failure and was declared deceased. The clinical course underscores the complex interplay between genetic syndrome, neurologic pathology, oral trauma, and systemic complications in pediatric patients with Down Syndrome and motoric disorders. The case highlights the importance of multidisciplinary management, including oral medicine, neurology, and pediatrics, in addressing both local and systemic manifestations of these conditions.\"\n}", "generated_text": "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 progressive lower extremity and upper limb weakness, initially presenting with a fall approximately one year prior, leading to hospitalization. The patient's mother reported chronic difficulties in performing routine oral hygiene due to motoric impairments, contributing to poor oral care and increased risk of mucosal injury. The patient was diagnosed with Down Syndrome and myeloradiculopathy, a condition characterized by degeneration of spinal nerve roots, resulting in motor dysfunction and sensory deficits.\n\nExtraorally, the patient exhibited a dysmorphic facial appearance, consistent with the phenotypic features of 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 reduced lip mobility, impaired salivary flow, and inadequate moisturization. Lymph node examination 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 malignancy of the epithelial lining of the oral cavity, due to its indurated border and surface appearance. However, the diagnosis of a chronic traumatic ulcer was established based on clinical correlation, patient history, and exclusion of neoplastic pathology. The traumatic origin was attributed to the sharp occlusal surface of the maxillary right central incisor (tooth 55), which caused persistent mechanical irritation against the tongue's lateral border, leading to tissue breakdown and ulceration. Additionally, the patient had dentinal caries involving tooth 63, and radicular gangrene (radix gangrene) affecting teeth 55, 62, 74, and 85, indicating advanced pulp necrosis and periapical tissue destruction. These tooth remnants were recommended for extraction by a pediatric dentist, with a space maintainer to be placed to preserve dental arch integrity and prevent malocclusion.\n\nLaboratory findings revealed hyponatremia (serum sodium 130 mEq/L), which may reflect impaired renal sodium reabsorption or osmotic imbalances associated with chronic neurological dysfunction or medication effects. Lymphocytosis (lymphocyte count 46%) was noted, potentially indicating a chronic inflammatory state or immune dysregulation, which may be exacerbated by recurrent mucosal trauma and poor oral hygiene. An MRI of the cervical spine confirmed cervical spine dislocation, consistent with the pathophysiology of myeloradiculopathy, which directly contributes to the patient's motor deficits and may have secondary effects on orofacial control and posture.\n\nThe differential diagnosis included exfoliative cheilitis, reversible pulpitis of tooth 63, and radix gangrene of multiple teeth. The chronic traumatic ulcer was confirmed through clinical evaluation, with no evidence of dysplasia, cellular atypia, or invasive growth on biopsy. The patient received a multimodal treatment regimen: paracetamol 120 mg/5 mL and amoxicillin 125 mg/5 mL for symptomatic management and possible bacterial infection; sodium chloride 0.9% solution for oral rinsing to maintain osmotic balance; povidone-iodine 1% mouthwash applied three times daily as an antiseptic and anti-inflammatory agent to reduce bacterial load and modulate local inflammation; and petroleum jelly applied to the lips to address desiccation and promote epithelial integrity.\n\nThe patient's oral lesions showed progressive improvement over time: at the 3-day follow-up, there was initial healing of the oral ulcer; at the 1-week follow-up, the ulcer size decreased and lip lesions improved; by the 10-day follow-up, significant healing of the tongue ulcer was observed. However, despite clinical improvement, the patient underwent neurosurgery for correction of cervical spine dislocation two days after the 10-day visit. Postoperatively, the patient was admitted to the Pediatric Intensive Care Unit (PICU) due to respiratory compromise. After two weeks of PICU observation, the patient developed acute respiratory failure and was declared deceased. The clinical course underscores the complex interplay between genetic syndrome, neurologic pathology, oral trauma, and systemic complications in pediatric patients with Down Syndrome and motoric disorders. The case highlights the importance of multidisciplinary management, including oral medicine, neurology, and pediatrics, in addressing both local and systemic manifestations of these conditions."}
{"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 has multiple sclerosis and was taking medicine for seizures, including levetiracetam. Right after starting levetiracetam, her vision got worse, and her corneas (the clear front part of the eye) became swollen. Doctors found this swelling with a special eye test. When they slowly reduced the levetiracetam dose and stopped it, her vision got better and the swollen corneas went away. Now, her vision is clear and her eyes look normal. This suggests the medicine caused the swelling.\"\n}", "generated_text": "A 59-year-old woman had blurry vision in both eyes for a few weeks. She has multiple sclerosis and was taking medicine for seizures, including levetiracetam. Right after starting levetiracetam, her vision got worse, and her corneas (the clear front part of the eye) became swollen. Doctors found this swelling with a special eye test. When they slowly reduced the levetiracetam dose and stopped it, her vision got better and the swollen corneas went away. Now, her vision is clear and her eyes look normal. This suggests the medicine caused the swelling."}
{"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 a special eye test called corneal topography.\\n\\nHer vision and corneal swelling improved when her levetiracetam dose was reduced and eventually stopped altogether. After six months without the medication, her vision returned to normal and the corneal swelling went away. Follow-up exams showed no further changes in her eyes or vision over the next year. Doctors believe the blurriness was caused by the levetiracetam, not her multiple sclerosis or other eye conditions.\"\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 a special eye test called corneal topography.\n\nHer vision and corneal swelling improved when her levetiracetam dose was reduced and eventually stopped altogether. After six months without the medication, her vision returned to normal and the corneal swelling went away. Follow-up exams showed no further changes in her eyes or vision over the next year. Doctors believe the blurriness was caused by the levetiracetam, not her multiple sclerosis or other eye conditions."}
{"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 disease, and previous ocular examinations had not identified signs of Fuchs' endothelial corneal dystrophy. Her medication regimen included amantadine 100 mg twice daily for seven years, administered for symptomatic management of multiple sclerosis-related motor and cognitive symptoms, and levetiracetam 250 mg twice daily, initiated as an adjunctive antiepileptic agent in response to new seizure activity.\\n\\nVisual acuity was measured at 0.5 logMAR in both eyes, indicating moderate visual impairment. Slit-lamp examination revealed bilateral corneal edema without evidence of uveitis or anterior segment inflammation. Intraocular pressures were within normal limits at 16 mmHg (right) and 18 mmHg (left). Corneal topography demonstrated significant corneal thickening, with central corneal thicknesses of 936 μm (right) and 1134 μm (left), consistent with substantial epithelial and stromal hydration.\\n\\nAmantadine is well-documented to induce corneal edema via its known effect on corneal endothelial cell function, particularly through inhibition of Na+/K+ ATPase activity and disruption of ion homeostasis in the corneal endothelium, leading to impaired fluid transport and accumulation of aqueous humor within the stroma. Given this pharmacological mechanism, the treatment team decided to discontinue amantadine and substitute it with lamotrigine, a second-line anticonvulsant with no known association with corneal toxicity. Levetiracetam was continued during this transition, but no improvement in visual acuity was observed over a two-month period.\\n\\nThe patient reported a direct temporal correlation between the initiation of levetiracetam and the onset of visual symptoms, prompting a trial of levetiracetam dose reduction. Following a partial taper, visual symptoms began to resolve within days, and complete cessation of levetiracetam resulted in full normalization of vision. Repeat corneal topography six months post-discontinuation demonstrated regression of corneal thickening to 567 μm (right) and 573 μm (left), with visual acuity improving to 0.2 logMAR bilaterally. Slit-lamp examination confirmed resolution of corneal edema and absence of corneal guttata, a histological feature of endothelial dysfunction.\\n\\nAt a follow-up visit thirteen months after initial presentation, the patient remained stable on amantadine and lamotrigine, with no further changes in medication. Visual acuity remained at 0.2 logMAR in both eyes, and repeat corneal topography showed no progressive thickening, indicating sustained resolution of the endothelial dysfunction. This case supports the hypothesis that levetiracetam may induce corneal edema through mechanisms involving direct or indirect effects on corneal endothelial cell function, potentially via disruption of ion transport, altered membrane permeability, or secondary metabolic stress. While not a well-documented adverse effect in the literature, this case provides clinical evidence for a previously underrecognized side effect of levetiracetam in patients with underlying neurodegenerative conditions, particularly those with compromised ocular homeostasis. The temporal association, reversal upon discontinuation, and normalization of corneal parameters following cessation strongly support a causal relationship between levetiracetam use and the observed corneal pathology.\"\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 disease, and previous ocular examinations had not identified signs of Fuchs' endothelial corneal dystrophy. Her medication regimen included amantadine 100 mg twice daily for seven years, administered for symptomatic management of multiple sclerosis-related motor and cognitive symptoms, and levetiracetam 250 mg twice daily, initiated as an adjunctive antiepileptic agent in response to new seizure activity.\n\nVisual acuity was measured at 0.5 logMAR in both eyes, indicating moderate visual impairment. Slit-lamp examination revealed bilateral corneal edema without evidence of uveitis or anterior segment inflammation. Intraocular pressures were within normal limits at 16 mmHg (right) and 18 mmHg (left). Corneal topography demonstrated significant corneal thickening, with central corneal thicknesses of 936 μm (right) and 1134 μm (left), consistent with substantial epithelial and stromal hydration.\n\nAmantadine is well-documented to induce corneal edema via its known effect on corneal endothelial cell function, particularly through inhibition of Na+/K+ ATPase activity and disruption of ion homeostasis in the corneal endothelium, leading to impaired fluid transport and accumulation of aqueous humor within the stroma. Given this pharmacological mechanism, the treatment team decided to discontinue amantadine and substitute it with lamotrigine, a second-line anticonvulsant with no known association with corneal toxicity. Levetiracetam was continued during this transition, but no improvement in visual acuity was observed over a two-month period.\n\nThe patient reported a direct temporal correlation between the initiation of levetiracetam and the onset of visual symptoms, prompting a trial of levetiracetam dose reduction. Following a partial taper, visual symptoms began to resolve within days, and complete cessation of levetiracetam resulted in full normalization of vision. Repeat corneal topography six months post-discontinuation demonstrated regression of corneal thickening to 567 μm (right) and 573 μm (left), with visual acuity improving to 0.2 logMAR bilaterally. Slit-lamp examination confirmed resolution of corneal edema and absence of corneal guttata, a histological feature of endothelial dysfunction.\n\nAt a follow-up visit thirteen months after initial presentation, the patient remained stable on amantadine and lamotrigine, with no further changes in medication. Visual acuity remained at 0.2 logMAR in both eyes, and repeat corneal topography showed no progressive thickening, indicating sustained resolution of the endothelial dysfunction. This case supports the hypothesis that levetiracetam may induce corneal edema through mechanisms involving direct or indirect effects on corneal endothelial cell function, potentially via disruption of ion transport, altered membrane permeability, or secondary metabolic stress. While not a well-documented adverse effect in the literature, this case provides clinical evidence for a previously underrecognized side effect of levetiracetam in patients with underlying neurodegenerative conditions, particularly those with compromised ocular homeostasis. The temporal association, reversal upon discontinuation, and normalization of corneal parameters following cessation strongly support a causal relationship between levetiracetam use and the observed corneal pathology."}
{"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, breaking both hip bones and pushing them out of place. He was in the hospital for several days, checked with X-rays and scans, and found to have serious hip fractures on both sides. The doctors fixed the hips in two steps, seven days apart, to make sure the bones healed well. In each surgery, they used a special ring to hold the hip socket in place and a special hip replacement with a stem that fits into the thigh bone. The ring was placed in the pelvis and held with screws to keep it strong. The man did not have any problems after surgery. At one year, he could walk fully with a walking stick, had a good hip score (77 on the right, 79 on the left), and only had a little pain or limp. He hasn’t had any serious issues since and is doing well.\"\n}", "generated_text": "A 77-year-old man had a seizure at home and fell, breaking both hip bones and pushing them out of place. He was in the hospital for several days, checked with X-rays and scans, and found to have serious hip fractures on both sides. The doctors fixed the hips in two steps, seven days apart, to make sure the bones healed well. In each surgery, they used a special ring to hold the hip socket in place and a special hip replacement with a stem that fits into the thigh bone. The ring was placed in the pelvis and held with screws to keep it strong. The man did not have any problems after surgery. At one year, he could walk fully with a walking stick, had a good hip score (77 on the right, 79 on the left), and only had a little pain or limp. He hasn’t had any serious issues since and is doing well."}
{"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 polytrauma code was activated due to hemodynamic instability, not 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 evaluate for intra-abdominal pathology, and 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, 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 fibrotic consolidation at the fracture sites and to minimize intraoperative bleeding. Surgery 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 thromboprophylaxis. The left hemipelvis was operated first due to greater pelvic protrusion, which increased the risk of soft tissue hematoma formation during femoral head extraction, potentially leading to vascular injury or excessive bleeding. The procedure employed a posterior lateral approach with Moore's autograft placement to reconstruct the acetabular fracture bed. An anti-protrusion ring (Burch Schneider™ Reinforcement Cage, Zimmer Biomet) was implanted, anchored to the ischium and ilium, with medial ischial fixation using screws. Prior to ring placement, dissection of the gluteal musculature (gluteus minimus and medius) was required to accurately reposition the femoral head. The ring was verified under direct visualization. A double-mobility cemented acetabular ring was then implanted, followed by a non-cemented femoral stem. Capsule and pelvic musculature were closed using transosseous trochanteric suture points. The right hemipelvis was operated seven days later. For the longitudinal iliac wing fracture, a six-hole anatomical plate was used via an ilio-inguinal approach. The same surgical sequence—anti-protrusion ring with double-mobility cemented acetabular ring and non-cemented femoral stem—was repeated. Anti-protrusion rings are indicated in acetabular fractures involving the acetabular background (e.g., Type IV AAOS classification), where pelvic disjunction is possible, and require anchorage in both ischium and ilium to provide structural support. They are not indicated for isolated anterior or posterior wall fractures without acetabular bed involvement. The patient remained bedridden during admission and was mobilized to prevent pressure ulcers. After the second surgery, clinical tolerance permitted initiation of wheelchair transfers. Full range of motion was permitted in bed without restriction. The patient was discharged at four weeks, with full weight-bearing delayed until six weeks due to the need for initial graft consolidation in the acetabular background to ensure stable ring support, and due to bilateral hip pathology, which precluded safe partial loading with one hip serving as a functional support. The patient began full load with a walking stick at six weeks. At 12-month follow-up, the patient achieved full weight-bearing with a Harris Hip Score (HHS) of 77 in the right hip and 79 in the left hip, and a WOMAC score of 12, indicating minimal pain and functional limitation. No postoperative complications have been reported to date. The patient reports occasional discomfort and a mild right-sided limp, but maintains full range of motion and no episodes of hip instability. The surgical approach successfully addressed bilateral acetabular fractures with associated femoral head protrusion, utilizing staged reconstruction with biomechanically stable fixation to restore joint integrity and function in a high-risk, cognitively impaired elderly population.\"\n}", "generated_text": "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 polytrauma code was activated due to hemodynamic instability, not 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 evaluate for intra-abdominal pathology, and 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, 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 fibrotic consolidation at the fracture sites and to minimize intraoperative bleeding. Surgery 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 thromboprophylaxis. The left hemipelvis was operated first due to greater pelvic protrusion, which increased the risk of soft tissue hematoma formation during femoral head extraction, potentially leading to vascular injury or excessive bleeding. The procedure employed a posterior lateral approach with Moore's autograft placement to reconstruct the acetabular fracture bed. An anti-protrusion ring (Burch Schneider™ Reinforcement Cage, Zimmer Biomet) was implanted, anchored to the ischium and ilium, with medial ischial fixation using screws. Prior to ring placement, dissection of the gluteal musculature (gluteus minimus and medius) was required to accurately reposition the femoral head. The ring was verified under direct visualization. A double-mobility cemented acetabular ring was then implanted, followed by a non-cemented femoral stem. Capsule and pelvic musculature were closed using transosseous trochanteric suture points. The right hemipelvis was operated seven days later. For the longitudinal iliac wing fracture, a six-hole anatomical plate was used via an ilio-inguinal approach. The same surgical sequence—anti-protrusion ring with double-mobility cemented acetabular ring and non-cemented femoral stem—was repeated. Anti-protrusion rings are indicated in acetabular fractures involving the acetabular background (e.g., Type IV AAOS classification), where pelvic disjunction is possible, and require anchorage in both ischium and ilium to provide structural support. They are not indicated for isolated anterior or posterior wall fractures without acetabular bed involvement. The patient remained bedridden during admission and was mobilized to prevent pressure ulcers. After the second surgery, clinical tolerance permitted initiation of wheelchair transfers. Full range of motion was permitted in bed without restriction. The patient was discharged at four weeks, with full weight-bearing delayed until six weeks due to the need for initial graft consolidation in the acetabular background to ensure stable ring support, and due to bilateral hip pathology, which precluded safe partial loading with one hip serving as a functional support. The patient began full load with a walking stick at six weeks. At 12-month follow-up, the patient achieved full weight-bearing with a Harris Hip Score (HHS) of 77 in the right hip and 79 in the left hip, and a WOMAC score of 12, indicating minimal pain and functional limitation. No postoperative complications have been reported to date. The patient reports occasional discomfort and a mild right-sided limp, but maintains full range of motion and no episodes of hip instability. The surgical approach successfully addressed bilateral acetabular fractures with associated femoral head protrusion, utilizing staged reconstruction with biomechanically stable fixation to restore joint integrity and function in a high-risk, cognitively impaired elderly population."}
{"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 fine at first, but then started vomiting and became very irritable. He was breathing fast and not getting enough oxygen. His chest looked like it was pulling in, and one side of his lung wasn’t working well. Doctors gave him a breathing tube to help him breathe, but his oxygen levels kept dropping. A scan showed the left lung was completely collapsed, and the main airway to that lung was blocked. The doctors thought a small almond, about 2 cm, had gotten stuck there. The boy had never eaten almonds before and probably swallowed it by accident. After the almond was removed, his breathing got better and he was able to breathe on his own again. He stayed in the hospital for a few days and is now doing well.\"\n}", "generated_text": "A 19-month-old boy fell from a highchair and hit his head. He was fine at first, but then started vomiting and became very irritable. He was breathing fast and not getting enough oxygen. His chest looked like it was pulling in, and one side of his lung wasn’t working well. Doctors gave him a breathing tube to help him breathe, but his oxygen levels kept dropping. A scan showed the left lung was completely collapsed, and the main airway to that lung was blocked. The doctors thought a small almond, about 2 cm, had gotten stuck there. The boy had never eaten almonds before and probably swallowed it by accident. After the almond was removed, his breathing got better and he was able to breathe on his own again. He stayed in the hospital for a few days and is now doing well."}
{"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 baby feeding highchair. The fall occurred while the child was in apparent well-being, with no prior signs or symptoms of distress. The mechanism of injury involved initial gluteal contact followed by a direct impact to the occiput (back of the head). The child presented with three episodes of vomiting and was markedly irritable. 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 diminished breath sounds localized to the left basal lung region. The patient was initially managed with non-invasive ventilation using an AMBU bag connected to supplemental oxygen and continuous pulse oximetry. However, despite this intervention, oxygen saturation progressively declined below 70%, and ventilation-induced worsening of hypoxemia was observed, suggesting impaired gas exchange. Lung ultrasound revealed the absence of normal A lines and evidence of pulmonary consolidation, interpreted as solid parenchymal opacification consistent with alveolar collapse or obstruction. Given the severity of respiratory compromise, orotracheal intubation with a cuffed endotracheal tube was performed to secure airway patency and ensure adequate oxygenation. Following stabilization, a chest computed tomography (CT) scan was obtained, which demonstrated complete atelectasis of the left lung and a discrete interruption of the main left bronchus at a distance of 12 mm from the bronchial bifurcation (i.e., the point where the left and right main bronchi divide). This radiographic finding, combined with the clinical history of a recent, self-limiting cough episode in the days prior, raised a strong suspicion of foreign body aspiration (FBA). The mother reported that the infant had experienced a severe cough attack that resolved spontaneously within 24 hours without medical intervention. Rigid bronchoscopy was subsequently performed, during which a 2 cm diameter almond was identified within the proximal left main bronchus and was successfully removed. Notably, the child had no prior exposure to nuts or any known history of food ingestion, and the almond was ingested incidentally during routine feeding. Post-intervention, the patient exhibited a progressive clinical recovery, with oxygenation improving steadily. At 24 hours post-intubation, the patient was extubated and transferred to the general pediatrics ward for continued observation. Over the following days, full respiratory function was restored, and the child was discharged without further complications. The case highlights the potential for asymptomatic or transient respiratory symptoms to precede significant airway obstruction, and underscores the importance of high index of suspicion for foreign body aspiration in pediatric patients presenting with acute respiratory distress following minor trauma, particularly when associated with a history of cough or atelectasis on imaging.\"\n}", "generated_text": "A 19-month-old male was admitted to the Emergency Department following a fall from a baby feeding highchair. The fall occurred while the child was in apparent well-being, with no prior signs or symptoms of distress. The mechanism of injury involved initial gluteal contact followed by a direct impact to the occiput (back of the head). The child presented with three episodes of vomiting and was markedly irritable. 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 diminished breath sounds localized to the left basal lung region. The patient was initially managed with non-invasive ventilation using an AMBU bag connected to supplemental oxygen and continuous pulse oximetry. However, despite this intervention, oxygen saturation progressively declined below 70%, and ventilation-induced worsening of hypoxemia was observed, suggesting impaired gas exchange. Lung ultrasound revealed the absence of normal A lines and evidence of pulmonary consolidation, interpreted as solid parenchymal opacification consistent with alveolar collapse or obstruction. Given the severity of respiratory compromise, orotracheal intubation with a cuffed endotracheal tube was performed to secure airway patency and ensure adequate oxygenation. Following stabilization, a chest computed tomography (CT) scan was obtained, which demonstrated complete atelectasis of the left lung and a discrete interruption of the main left bronchus at a distance of 12 mm from the bronchial bifurcation (i.e., the point where the left and right main bronchi divide). This radiographic finding, combined with the clinical history of a recent, self-limiting cough episode in the days prior, raised a strong suspicion of foreign body aspiration (FBA). The mother reported that the infant had experienced a severe cough attack that resolved spontaneously within 24 hours without medical intervention. Rigid bronchoscopy was subsequently performed, during which a 2 cm diameter almond was identified within the proximal left main bronchus and was successfully removed. Notably, the child had no prior exposure to nuts or any known history of food ingestion, and the almond was ingested incidentally during routine feeding. Post-intervention, the patient exhibited a progressive clinical recovery, with oxygenation improving steadily. At 24 hours post-intubation, the patient was extubated and transferred to the general pediatrics ward for continued observation. Over the following days, full respiratory function was restored, and the child was discharged without further complications. The case highlights the potential for asymptomatic or transient respiratory symptoms to precede significant airway obstruction, and underscores the importance of high index of suspicion for foreign body aspiration in pediatric patients presenting with acute respiratory distress following minor trauma, particularly when associated with a history of cough or atelectasis on imaging."}
{"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 axilla, prompting medical evaluation. The infant was born to a mother with hypothyroidism during the first trimester of pregnancy, who received pharmacological intervention. The infant was born with normal birth weight and length, was exclusively breast-fed, and received the BCG vaccine without scarring. The mother was incarcerated in a prison cell with the infant and two other individuals, living in a crowded environment. At 4 months of age, the infant was admitted to a pediatric hospital following a chest X-ray that demonstrated suggestive radiographic findings of rib fractures, leading to suspicion of child abuse. Physical examination revealed a weight of 4,190 g (below the third percentile), height of 58 cm, oxygen saturation of 70%, fever, cough, localized pain, redness, and warmth 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 revealed a left axillary abscess, lytic lesions in ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Histopathological analysis of the axillary abscess demonstrated suppurative panniculitis and myositis. 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. \\n\\nAt 8 months of age, the infant was readmitted with fever, irritability, and extension of the suppurative process to the left scapula. Repeat laboratory values 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 associated with the scapular abscess. The infant was initially treated with piperacillin-tazobactam, which was subsequently replaced with voriconazole after *Aspergillus fumigatus* was isolated from the abscess secretion. Given the recurrent and progressive nature of the infection, an innate immune deficiency was suspected. A dihydrorhodamine (DHR) fluorescence assay demonstrated absent production of reactive oxygen species (ROS) in neutrophils, and immunofluorescence 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, specifically c.80_83del/Y (p.Val27Glyfs*33), which results in a frameshift mutation and premature termination of the gp91phox protein. The mother was identified as a carrier of the same variant (c.80_83del/WT), consistent with X-linked recessive inheritance. The two older male siblings, who were clinically asymptomatic, 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 for bacterial infection", "generated_text": "{\n  \"proficient_health_literacy\": \"A 4-month-old male infant from central Mexico presented with a painful, suppurative tumor in the left axilla, prompting medical evaluation. The infant was born to a mother with hypothyroidism during the first trimester of pregnancy, who received pharmacological intervention. The infant was born with normal birth weight and length, was exclusively breast-fed, and received the BCG vaccine without scarring. The mother was incarcerated in a prison cell with the infant and two other individuals, living in a crowded environment. At 4 months of age, the infant was admitted to a pediatric hospital following a chest X-ray that demonstrated suggestive radiographic findings of rib fractures, leading to suspicion of child abuse. Physical examination revealed a weight of 4,190 g (below the third percentile), height of 58 cm, oxygen saturation of 70%, fever, cough, localized pain, redness, and warmth 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 revealed a left axillary abscess, lytic lesions in ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Histopathological analysis of the axillary abscess demonstrated suppurative panniculitis and myositis. 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. \\n\\nAt 8 months of age, the infant was readmitted with fever, irritability, and extension of the suppurative process to the left scapula. Repeat laboratory values 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 associated with the scapular abscess. The infant was initially treated with piperacillin-tazobactam, which was subsequently replaced with voriconazole after *Aspergillus fumigatus* was isolated from the abscess secretion. Given the recurrent and progressive nature of the infection, an innate immune deficiency was suspected. A dihydrorhodamine (DHR) fluorescence assay demonstrated absent production of reactive oxygen species (ROS) in neutrophils, and immunofluorescence 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, specifically c.80_83del/Y (p.Val27Glyfs*33), which results in a frameshift mutation and premature termination of the gp91phox protein. The mother was identified as a carrier of the same variant (c.80_83del/WT), consistent with X-linked recessive inheritance. The two older male siblings, who were clinically asymptomatic, 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 for bacterial infection"}
{"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 and lip lesions. The lesions initially appeared as canker sores in the oral cavity four days prior to presentation, subsequently extending to the upper and lower labial mucosa two days later. The patient reported exacerbation of symptoms during eating and speech. Initial self-management with petroleum jelly failed to provide relief; he then used triamcinolone acetonide 0.1% in orabase ointment, applied once daily, which resulted in partial symptomatic improvement but no complete resolution of the lesions.\\n\\nThe patient reported a preceding febrile illness lasting approximately one week prior to lesion onset, with no cutaneous or systemic manifestations elsewhere. He described a history of chronic poor nutritional intake over the past one and a half months, associated with high work-related stress. There was no known medical history, food allergies, medication use, alcohol consumption, or tobacco use. However, he had a documented history of chickenpox in childhood. He maintained a habit of frequent lip-licking and lip-peeling, which was identified as a potential contributing behavioral factor.\\n\\nGeneral examination revealed normal vital signs and no lymphadenopathy. Extra-oral examination demonstrated serosanguineous crusts on the lips, which were tender and prone to bleeding. Intra-oral examination revealed diffusely erythematous, irregularly bordered, painful lesions on the upper and lower labial mucosa. Additional findings included hyperkeratotic, non-scrapable white plaques with diffuse borders on the left buccal mucosa near tooth 38, yellowish-white, easily scrapable plaques covering one-third of the posterior dorsal tongue with associated dental impression indentations (non-painful), and a painless, 2×1×0.5 cm hard nodule in the midline of the hard palate. Dental evaluation identified carious lesions, root caries, and edentulism in multiple teeth (teeth 28, 36, 37, and 46), with diagnoses of reversible pulpitis (tooth 18), irreversible pulpitis (tooth 47), chronic apical periodontitis due to root caries (tooth 15), and associated periodontal disease. Oral hygiene was assessed as suboptimal.\\n\\nPsychological evaluation using the DASS-21 scale indicated normal levels of depression (score 0), anxiety (score 6), and stress (score 6). Based on clinical presentation and history, the working diagnosis was suspected to be Herpes Simplex Virus-1-associated Erythema Multiforme (HAEM), with concomitant findings of coated tongue, frictional keratosis, crenated tongue, torus palatinus, and multiple dental pathologies. Differential diagnosis considered exfoliative cheilitis, which was excluded due to the absence of herpesvirus involvement. Serological testing for IgG anti-HSV-1 was performed, yielding a titer of 6.32 (positive when ratio > 1.1), confirming active HSV-1 seropositivity and supporting the diagnosis of HAEM.\\n\\nOral health-related quality of life (OHRQoL) was assessed using the OHIP-14, with an initial score of 35, indicating moderate impairment. The treatment plan included both pharmacological and non-pharmacological interventions. Non-pharmacological measures comprised instruction in daily oral hygiene (soft-bristled toothbrush, twice daily; non-detergent toothpaste), increased daily water intake (≥2 liters), balanced nutrition, avoidance of acidic, spicy, hard, and monosodium glutamate (MSG)-containing foods, and cessation of lip-licking and lip-peeling behaviors. Pharmacological therapy included topical application of triamcinolone acetonide 0.1% in orabase (three times daily), gauze compression with 0.9% NaCl solution (three times daily), and systemic administration of multivitamins (once daily). Following one week of treatment, acyclovir 200 mg tablets were initiated orally, administered five times daily for one week to target viral replication.\\n\\nClinical improvement was observed at the first follow-up (two days post-initial visit), with significant reduction in lip pain, though the canker sores remained incomplete. At the second follow-up (five days later), complete healing of all oral lesions was achieved. The final OHIP-14 score improved to 4, indicating excellent OHRQoL. The patient’s physical, psychological, and social functioning returned to baseline within seven days of treatment. The patient was referred for continued management in periodontics,", "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 and lip lesions. The lesions initially appeared as canker sores in the oral cavity four days prior to presentation, subsequently extending to the upper and lower labial mucosa two days later. The patient reported exacerbation of symptoms during eating and speech. Initial self-management with petroleum jelly failed to provide relief; he then used triamcinolone acetonide 0.1% in orabase ointment, applied once daily, which resulted in partial symptomatic improvement but no complete resolution of the lesions.\\n\\nThe patient reported a preceding febrile illness lasting approximately one week prior to lesion onset, with no cutaneous or systemic manifestations elsewhere. He described a history of chronic poor nutritional intake over the past one and a half months, associated with high work-related stress. There was no known medical history, food allergies, medication use, alcohol consumption, or tobacco use. However, he had a documented history of chickenpox in childhood. He maintained a habit of frequent lip-licking and lip-peeling, which was identified as a potential contributing behavioral factor.\\n\\nGeneral examination revealed normal vital signs and no lymphadenopathy. Extra-oral examination demonstrated serosanguineous crusts on the lips, which were tender and prone to bleeding. Intra-oral examination revealed diffusely erythematous, irregularly bordered, painful lesions on the upper and lower labial mucosa. Additional findings included hyperkeratotic, non-scrapable white plaques with diffuse borders on the left buccal mucosa near tooth 38, yellowish-white, easily scrapable plaques covering one-third of the posterior dorsal tongue with associated dental impression indentations (non-painful), and a painless, 2×1×0.5 cm hard nodule in the midline of the hard palate. Dental evaluation identified carious lesions, root caries, and edentulism in multiple teeth (teeth 28, 36, 37, and 46), with diagnoses of reversible pulpitis (tooth 18), irreversible pulpitis (tooth 47), chronic apical periodontitis due to root caries (tooth 15), and associated periodontal disease. Oral hygiene was assessed as suboptimal.\\n\\nPsychological evaluation using the DASS-21 scale indicated normal levels of depression (score 0), anxiety (score 6), and stress (score 6). Based on clinical presentation and history, the working diagnosis was suspected to be Herpes Simplex Virus-1-associated Erythema Multiforme (HAEM), with concomitant findings of coated tongue, frictional keratosis, crenated tongue, torus palatinus, and multiple dental pathologies. Differential diagnosis considered exfoliative cheilitis, which was excluded due to the absence of herpesvirus involvement. Serological testing for IgG anti-HSV-1 was performed, yielding a titer of 6.32 (positive when ratio > 1.1), confirming active HSV-1 seropositivity and supporting the diagnosis of HAEM.\\n\\nOral health-related quality of life (OHRQoL) was assessed using the OHIP-14, with an initial score of 35, indicating moderate impairment. The treatment plan included both pharmacological and non-pharmacological interventions. Non-pharmacological measures comprised instruction in daily oral hygiene (soft-bristled toothbrush, twice daily; non-detergent toothpaste), increased daily water intake (≥2 liters), balanced nutrition, avoidance of acidic, spicy, hard, and monosodium glutamate (MSG)-containing foods, and cessation of lip-licking and lip-peeling behaviors. Pharmacological therapy included topical application of triamcinolone acetonide 0.1% in orabase (three times daily), gauze compression with 0.9% NaCl solution (three times daily), and systemic administration of multivitamins (once daily). Following one week of treatment, acyclovir 200 mg tablets were initiated orally, administered five times daily for one week to target viral replication.\\n\\nClinical improvement was observed at the first follow-up (two days post-initial visit), with significant reduction in lip pain, though the canker sores remained incomplete. At the second follow-up (five days later), complete healing of all oral lesions was achieved. The final OHIP-14 score improved to 4, indicating excellent OHRQoL. The patient’s physical, psychological, and social functioning returned to baseline within seven days of treatment. The patient was referred for continued management in periodontics,"}
{"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 was discontinued for one month during the onset of vaginal bleeding, resulting in virological failure (viral load: 37,400 copies/mL) and immunological decline (CD4 count: 26 cells/μL). The timing of initial HIV symptom onset was not clearly documented. Physical examination revealed a large cervical mass measuring 8 × 8 cm extending into the parametrium and bilateral pelvic side walls, 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 biopsy of the cervix confirmed an extra-nodal Burkitt lymphoma (BL), with immunohistochemical staining positive for CD20, CD75a, CD10, PAX5, and BCL6; CD44 and c-Myc were also positive, with focal EBER in situ hybridization (ISH) positivity. The Ki67 proliferation index was nearly 100%, indicating extremely high cellular proliferation, and PAX5 and BCL6 showed moderate expression. Laboratory findings included leukopenia (white cell count: 2.67 × 10⁹/L), anemia (hemoglobin: 5.7 g/dL), thrombocytopenia (platelet count: 71 × 10⁹/L), serum creatinine of 187 mmol/L (indicating significant renal impairment), urea 11.1 mmol/L, albumin 21 g/L, aspartate transaminase 41 U/L, and alkaline phosphatase 100 U/L. The patient was recommenced on ART, transitioning from a TLD (Tenofovir-Lamivudine-Dolutegravir) regimen to a renal-sparing Lamivudine-Abacavir-Dolutegravir combination to mitigate further nephrotoxicity. Following histological confirmation and multidisciplinary oncology review, a treatment plan of chemoradiation was recommended. However, due to a prolonged waiting list at the referral oncology unit, the patient waited 43 days before receiving any treatment—exceeding the recommended 48-hour window for initiating therapy in Burkitt lymphoma, particularly in immunocompromised individuals. During this period, no further imaging (CT or MRI) was performed due to technical limitations in the available equipment. The patient received supportive care including blood transfusions and analgesia. She died in the gynecological ward on day 43, with the interval between diagnosis of BL and death remaining 43 days. A postmortem histopathological examination was not conducted, as both the Burkitt lymphoma and HIV infection were already established and well-documented. The primary cause of death remains difficult to assign due to the coexistence of multiple severe comorbidities; however, given the aggressive nature of BL in the context of advanced HIV infection with high viral load and profound immunosuppression, the attending physician concluded that BL was the most likely primary cause. The secondary cause of death was multiple organ failure, encompassing both renal and hematological dysfunction, reflecting the systemic impact of the disease and the underlying immunodeficiency. This case underscores the critical importance of timely diagnosis and initiation of oncological intervention in HIV-positive patients with suspected cervical malignancy, especially in the context of high-risk lymphoma subtypes such as extra-nodal BL.\"\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 was discontinued for one month during the onset of vaginal bleeding, resulting in virological failure (viral load: 37,400 copies/mL) and immunological decline (CD4 count: 26 cells/μL). The timing of initial HIV symptom onset was not clearly documented. Physical examination revealed a large cervical mass measuring 8 × 8 cm extending into the parametrium and bilateral pelvic side walls, 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 biopsy of the cervix confirmed an extra-nodal Burkitt lymphoma (BL), with immunohistochemical staining positive for CD20, CD75a, CD10, PAX5, and BCL6; CD44 and c-Myc were also positive, with focal EBER in situ hybridization (ISH) positivity. The Ki67 proliferation index was nearly 100%, indicating extremely high cellular proliferation, and PAX5 and BCL6 showed moderate expression. Laboratory findings included leukopenia (white cell count: 2.67 × 10⁹/L), anemia (hemoglobin: 5.7 g/dL), thrombocytopenia (platelet count: 71 × 10⁹/L), serum creatinine of 187 mmol/L (indicating significant renal impairment), urea 11.1 mmol/L, albumin 21 g/L, aspartate transaminase 41 U/L, and alkaline phosphatase 100 U/L. The patient was recommenced on ART, transitioning from a TLD (Tenofovir-Lamivudine-Dolutegravir) regimen to a renal-sparing Lamivudine-Abacavir-Dolutegravir combination to mitigate further nephrotoxicity. Following histological confirmation and multidisciplinary oncology review, a treatment plan of chemoradiation was recommended. However, due to a prolonged waiting list at the referral oncology unit, the patient waited 43 days before receiving any treatment—exceeding the recommended 48-hour window for initiating therapy in Burkitt lymphoma, particularly in immunocompromised individuals. During this period, no further imaging (CT or MRI) was performed due to technical limitations in the available equipment. The patient received supportive care including blood transfusions and analgesia. She died in the gynecological ward on day 43, with the interval between diagnosis of BL and death remaining 43 days. A postmortem histopathological examination was not conducted, as both the Burkitt lymphoma and HIV infection were already established and well-documented. The primary cause of death remains difficult to assign due to the coexistence of multiple severe comorbidities; however, given the aggressive nature of BL in the context of advanced HIV infection with high viral load and profound immunosuppression, the attending physician concluded that BL was the most likely primary cause. The secondary cause of death was multiple organ failure, encompassing both renal and hematological dysfunction, reflecting the systemic impact of the disease and the underlying immunodeficiency. This case underscores the critical importance of timely diagnosis and initiation of oncological intervention in HIV-positive patients with suspected cervical malignancy, especially in the context of high-risk lymphoma subtypes such as extra-nodal BL."}
{"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 findings on chest X-ray consistent with 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. Computed tomography of the chest (CNYCT) showed an enlarged pulmonary trunk, right atrium, and right ventricle, supporting the diagnosis of pulmonary hypertension. Objective signs of Sjögren’s syndrome included dry mouth, dry eyes, cracked tongue mucosa (Schirmer’s test <5 mm), positive minor salivary gland biopsy, impaired salivary gland function on nuclear medicine scan, and a positive anti-Ro antibody test. The patient was initiated on sildenafil (Revatio) 20 mg three times daily (TID) for PAH management, with addition of bosentan (Tracleer) in 2016 due to disease progression. Right heart catheterization (RHC) in 2017 confirmed pre-capillary, group I PAH with a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) of approximately 15 Woods, and a wedge pressure of 4 mmHg, consistent with chronic pulmonary hypertension and right heart strain. Based on these findings, the patient was eligible for opsumit (macitentan) 10 mg once daily (QD), which replaced bosentan in 2017. From 2017 to 2020, she required repeated hospitalizations for corticosteroid therapy to manage active Sjögren’s syndrome. Prior to 2017, her PAH was classified as low to intermediate risk and managed with dual therapy (sildenafil and macitentan), with stable disease progression. However, in October 2020, she presented with worsening dyspnea, cough, and white sputum, suggestive of respiratory infection. On November 10, 2020, she developed acute severe dyspnea, cold sweats, cyanosis, and SpO2 of 70%, requiring 100% oxygen via face tent. 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 pulmonary vasodilator agents. Her condition stabilized, with successful weaning from vasopressors on November 13, extubation on November 14, and transfer to a general ward on November 21, with oxygen support tapered to nasal cannula at 2 L/min. Follow-up RHC continued to demonstrate elevated pulmonary artery pressure, reflecting persistent right heart strain and likely progression toward right heart failure. The patient was subsequently referred to National Taiwan University Hospital for evaluation for heart-lung transplantation. Over time, her 6-minute walk distance progressively declined, and her pulmonary artery pressure trajectory showed a steady upward trend, leading to current classification as high-risk. Despite stabilization, dyspnea remains her primary clinical complaint. Physical examination revealed mild rhonchi consistent with ILD and a pansystolic murmur indicative of severe valvular heart disease. In 2020, ventavis (iloprost) 10 mcg/ml in 2 ml was added to her regimen. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023 using PURE HYDROGEN capsules manufactured by 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. Adjuvant administration of hydrogen therapy was associated with significant immunomodulatory effects: flow cytometry and serological analyses revealed an increase in CD127+ regulatory T cells (Tregs), a reduction in anti-Ro autoantibody titers, and a decrease in B cell subsets. These changes were assessed via standardized fluorescent dye and antibody reagent kits (Beckman Coulter, Brea, CA, USA) using immun", "generated_text": "{\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 findings on chest X-ray consistent with 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. Computed tomography of the chest (CNYCT) showed an enlarged pulmonary trunk, right atrium, and right ventricle, supporting the diagnosis of pulmonary hypertension. Objective signs of Sjögren’s syndrome included dry mouth, dry eyes, cracked tongue mucosa (Schirmer’s test <5 mm), positive minor salivary gland biopsy, impaired salivary gland function on nuclear medicine scan, and a positive anti-Ro antibody test. The patient was initiated on sildenafil (Revatio) 20 mg three times daily (TID) for PAH management, with addition of bosentan (Tracleer) in 2016 due to disease progression. Right heart catheterization (RHC) in 2017 confirmed pre-capillary, group I PAH with a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) of approximately 15 Woods, and a wedge pressure of 4 mmHg, consistent with chronic pulmonary hypertension and right heart strain. Based on these findings, the patient was eligible for opsumit (macitentan) 10 mg once daily (QD), which replaced bosentan in 2017. From 2017 to 2020, she required repeated hospitalizations for corticosteroid therapy to manage active Sjögren’s syndrome. Prior to 2017, her PAH was classified as low to intermediate risk and managed with dual therapy (sildenafil and macitentan), with stable disease progression. However, in October 2020, she presented with worsening dyspnea, cough, and white sputum, suggestive of respiratory infection. On November 10, 2020, she developed acute severe dyspnea, cold sweats, cyanosis, and SpO2 of 70%, requiring 100% oxygen via face tent. 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 pulmonary vasodilator agents. Her condition stabilized, with successful weaning from vasopressors on November 13, extubation on November 14, and transfer to a general ward on November 21, with oxygen support tapered to nasal cannula at 2 L/min. Follow-up RHC continued to demonstrate elevated pulmonary artery pressure, reflecting persistent right heart strain and likely progression toward right heart failure. The patient was subsequently referred to National Taiwan University Hospital for evaluation for heart-lung transplantation. Over time, her 6-minute walk distance progressively declined, and her pulmonary artery pressure trajectory showed a steady upward trend, leading to current classification as high-risk. Despite stabilization, dyspnea remains her primary clinical complaint. Physical examination revealed mild rhonchi consistent with ILD and a pansystolic murmur indicative of severe valvular heart disease. In 2020, ventavis (iloprost) 10 mcg/ml in 2 ml was added to her regimen. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023 using PURE HYDROGEN capsules manufactured by 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. Adjuvant administration of hydrogen therapy was associated with significant immunomodulatory effects: flow cytometry and serological analyses revealed an increase in CD127+ regulatory T cells (Tregs), a reduction in anti-Ro autoantibody titers, and a decrease in B cell subsets. These changes were assessed via standardized fluorescent dye and antibody reagent kits (Beckman Coulter, Brea, CA, USA) using immun"}
{"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 had strange eye movements, muscle jerks on one side of his face and chest, and then a full seizure. After that, he had weakness on his left side. Tests showed the virus was in his brain fluid, which means it may have spread to his brain. But over time, his symptoms got better, and he fully recovered. He was able to go home after 31 days with no need for medicine to stop seizures and will see his doctor for follow-up.\"\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 had strange eye movements, muscle jerks on one side of his face and chest, and then a full seizure. After that, he had weakness on his left side. Tests showed the virus was in his brain fluid, which means it may have spread to his brain. But over time, his symptoms got better, and he fully recovered. He was able to go home after 31 days with no need for medicine to stop seizures and will see his doctor for follow-up."}
{"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. After 16 days in the hospital, he suddenly developed a change in consciousness, with his eyes turning toward the right and strange, brief jerking movements on his left side (face and chest). This was followed by a full seizure, and he ended up with weakness on his left side that didn’t go away. Tests showed the virus was present in his cerebrospinal fluid, which is the fluid around the brain and spinal cord. This finding suggested the virus had affected his brain, possibly causing encephalitis. However, there was no sign of bacterial infection or other common causes of seizures. The patient’s condition gradually improved, and by day 31, he was able to leave the hospital without needing anti-seizure medication. His recovery was considered favorable, and follow-up care was arranged.\"\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. After 16 days in the hospital, he suddenly developed a change in consciousness, with his eyes turning toward the right and strange, brief jerking movements on his left side (face and chest). This was followed by a full seizure, and he ended up with weakness on his left side that didn’t go away. Tests showed the virus was present in his cerebrospinal fluid, which is the fluid around the brain and spinal cord. This finding suggested the virus had affected his brain, possibly causing encephalitis. However, there was no sign of bacterial infection or other common causes of seizures. The patient’s condition gradually improved, and by day 31, he was able to leave the hospital without needing anti-seizure medication. His recovery was considered favorable, and follow-up care was arranged."}
{"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 with a history of grade 3 obesity and no other significant comorbidities or pharmacological therapy. He presented to emergency care with a four-day course of fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia. On initial neurological examination, no abnormalities were noted. Respiratory evaluation revealed tachypnea and bilateral rough vesicular murmurs on auscultation, consistent with diffuse pulmonary involvement. Laboratory findings showed mild elevation in inflammatory markers and type 1 respiratory failure under FiO2 of 21%, with extensive bilateral, peripheral, and basal opacities on chest radiography. A positive reverse-transcription real-time polymerase chain reaction (RT-PCR) for SARS-CoV-2 was obtained from nasal and oropharyngeal exudates, while tests for influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila were negative, supporting a diagnosis of SARS-CoV-2-associated pneumonia.\\n\\nOver the first 48 hours, progressive deterioration in fatigue, dyspnea, and respiratory function necessitated escalation of oxygen therapy. Noninvasive ventilation was initiated but discontinued due to poor patient adherence; high-flow oxygen via nasal cannula was then implemented without clinical benefit. The patient was subsequently transferred to a level III intensive care unit (ICU), where sedoanalgesia was administered and orotracheal intubation with invasive mechanical ventilation was performed.\\n\\nOn day 11 of hospitalization, the patient received remdesivir, dexamethasone, enoxaparin, and empirical antibiotic therapy (amoxicillin/clavulanic acid and azithromycin) on suspicion of secondary bacterial superinfection. Despite persistent fever refractory to antipyretics, inflammatory markers improved by day 3 of ICU admission. To rule out alternative infectious etiologies, intravenous lines were replaced, and blood cultures, catheter tip cultures, bronchial secretions, urinalysis, urine culture, and transthoracic echocardiography were performed. Only one positive blood culture was obtained: Klebsiella pneumoniae, which is susceptible to amoxicillin/clavulanic acid—antibiotic 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) along with 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 ruled out.\\n\\nInotropic support with dobutamine was required during ventilatory weaning and post-extubation phases. On day 16 of hospitalization (day 19 of symptom onset), the patient experienced a sudden alteration in consciousness, conjugate gaze deviation to the right, left-sided myoclonus involving the face and thoracic region, followed by a generalized tonic-clonic seizure, which was terminated with midazolam. Hypoxic-ischemic etiology was excluded due to sustained normotension, absence of peri-event hypoxemia or hypoxia, normal serum lactate levels, and preserved diuresis. Electrolyte and glucose levels were within normal limits, ruling out metabolic or ionic triggers for the seizure.\\n\\nPost-ictal assessment revealed a Glasgow Coma Scale (GCS) of 7 (no eye opening, no verbal response, no localizing to pain), with persistent left hemiparesis of grade 3/5. Due to airway compromise, the patient remained intubated and received anticonvulsant therapy. Lumbar puncture was performed, yielding turbid cerebrospinal fluid (CSF) with mild proteinorrachia but no pleocytosis and normal opening pressure. CSF was tested for neurotropic viruses, venereal disease research laboratory (VDRL) activity, acid-alcohol resistant bacteria, and SARS-CoV-2 via RT-PCR; the latter was positive, confirming the presence of SARS-CoV-2 RNA in CSF without pleocytosis. This finding excluded bacterial meningitis and supported a diagnosis of SARS-CoV-2 encephalitis. Electroencephalography (EEG), performed 1 hour after propofol administration under fentanyl, lasted 13 minutes and showed no epileptiform activity. MRI performed on day 17 revealed multiple artifacts attributable to patient movement, necessitating repeat imaging.\\n\\nFollowing discontinuation of sedoanalgesia, the patient exhibited a gradual improvement in mental status with a GCS of 14, persistent left hemiparesis (muscle strength grade", "generated_text": "{\n  \"proficient_health_literacy\": \"A 45-year-old male, born in Pakistan and residing in Portugal for seven years, was admitted with a history of grade 3 obesity and no other significant comorbidities or pharmacological therapy. He presented to emergency care with a four-day course of fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia. On initial neurological examination, no abnormalities were noted. Respiratory evaluation revealed tachypnea and bilateral rough vesicular murmurs on auscultation, consistent with diffuse pulmonary involvement. Laboratory findings showed mild elevation in inflammatory markers and type 1 respiratory failure under FiO2 of 21%, with extensive bilateral, peripheral, and basal opacities on chest radiography. A positive reverse-transcription real-time polymerase chain reaction (RT-PCR) for SARS-CoV-2 was obtained from nasal and oropharyngeal exudates, while tests for influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila were negative, supporting a diagnosis of SARS-CoV-2-associated pneumonia.\\n\\nOver the first 48 hours, progressive deterioration in fatigue, dyspnea, and respiratory function necessitated escalation of oxygen therapy. Noninvasive ventilation was initiated but discontinued due to poor patient adherence; high-flow oxygen via nasal cannula was then implemented without clinical benefit. The patient was subsequently transferred to a level III intensive care unit (ICU), where sedoanalgesia was administered and orotracheal intubation with invasive mechanical ventilation was performed.\\n\\nOn day 11 of hospitalization, the patient received remdesivir, dexamethasone, enoxaparin, and empirical antibiotic therapy (amoxicillin/clavulanic acid and azithromycin) on suspicion of secondary bacterial superinfection. Despite persistent fever refractory to antipyretics, inflammatory markers improved by day 3 of ICU admission. To rule out alternative infectious etiologies, intravenous lines were replaced, and blood cultures, catheter tip cultures, bronchial secretions, urinalysis, urine culture, and transthoracic echocardiography were performed. Only one positive blood culture was obtained: Klebsiella pneumoniae, which is susceptible to amoxicillin/clavulanic acid—antibiotic 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) along with 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 ruled out.\\n\\nInotropic support with dobutamine was required during ventilatory weaning and post-extubation phases. On day 16 of hospitalization (day 19 of symptom onset), the patient experienced a sudden alteration in consciousness, conjugate gaze deviation to the right, left-sided myoclonus involving the face and thoracic region, followed by a generalized tonic-clonic seizure, which was terminated with midazolam. Hypoxic-ischemic etiology was excluded due to sustained normotension, absence of peri-event hypoxemia or hypoxia, normal serum lactate levels, and preserved diuresis. Electrolyte and glucose levels were within normal limits, ruling out metabolic or ionic triggers for the seizure.\\n\\nPost-ictal assessment revealed a Glasgow Coma Scale (GCS) of 7 (no eye opening, no verbal response, no localizing to pain), with persistent left hemiparesis of grade 3/5. Due to airway compromise, the patient remained intubated and received anticonvulsant therapy. Lumbar puncture was performed, yielding turbid cerebrospinal fluid (CSF) with mild proteinorrachia but no pleocytosis and normal opening pressure. CSF was tested for neurotropic viruses, venereal disease research laboratory (VDRL) activity, acid-alcohol resistant bacteria, and SARS-CoV-2 via RT-PCR; the latter was positive, confirming the presence of SARS-CoV-2 RNA in CSF without pleocytosis. This finding excluded bacterial meningitis and supported a diagnosis of SARS-CoV-2 encephalitis. Electroencephalography (EEG), performed 1 hour after propofol administration under fentanyl, lasted 13 minutes and showed no epileptiform activity. MRI performed on day 17 revealed multiple artifacts attributable to patient movement, necessitating repeat imaging.\\n\\nFollowing discontinuation of sedoanalgesia, the patient exhibited a gradual improvement in mental status with a GCS of 14, persistent left hemiparesis (muscle strength grade"}
{"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 pus coming out of their right 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, and no bacteria were found in the ear or stomach. They also started taking HIV medicine again and got better overall. Now they are fully healed and healthy.\"\n}", "generated_text": "The person had a long-lasting cough, ear pain, and a foul-smelling pus coming out of their right 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, and no bacteria were found in the ear or stomach. They also started taking HIV medicine again and got better overall. Now they are fully healed and healthy."}
{"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 the fluid from the stomach and in the pus from the ear, which pointed to tuberculosis. The patient also had HIV, which weakened his immune system, making him more susceptible to tuberculosis. He was treated with a 6-month course of anti-tuberculosis medication, including four drugs in the first two months, followed by two drugs for the next four months. He also received treatment for HIV again, and was given antibiotics to prevent complications. After treatment, his symptoms fully improved, the bacteria tests became negative, and his overall health returned to normal. His HIV virus levels dropped significantly, showing the treatment was effective.\"\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 the fluid from the stomach and in the pus from the ear, which pointed to tuberculosis. The patient also had HIV, which weakened his immune system, making him more susceptible to tuberculosis. He was treated with a 6-month course of anti-tuberculosis medication, including four drugs in the first two months, followed by two drugs for the next four months. He also received treatment for HIV again, and was given antibiotics to prevent complications. After treatment, his symptoms fully improved, the bacteria tests became negative, and his overall health returned to normal. His HIV virus levels dropped significantly, showing the treatment was effective."}
{"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 included artésunate, paracetamol, and unspecified antibiotics for suspected malaria and acute otitis media, which failed to resolve the symptoms. The patient is HIV-1 infected, with a diagnosis established 7 months prior, and has been on a triple antiretroviral therapy (TARV) regimen of tenofovir/lamivudine/dolutegravir; however, adherence to this regimen has been poor due to denial of his HIV status.\\n\\nPhysical examination revealed a fever of 38.2 °C, altered general condition, right-sided otalgia, purulent foul-smelling otorrhea, and a right basal pulmonary condensation consistent with bronchovascular hyperactivity. Neurological examination was normal, with no cranial nerve involvement, particularly the facial (VII) and cochleovestibular (VIII) nerves. Otoscopic evaluation of the right ear demonstrated inflammatory changes in the external auditory canal with purulent exudate and a single tympanic membrane perforation in the anterior-inferior quadrant; the left ear was intact. Rinne and Weber tests confirmed a right conductive hearing loss.\\n\\nImmunological and virological assessments showed a CD4 count of 118 cells/μL and a viral load of 12,370 copies/mL at the time of HIV diagnosis. Following 6 months of ART, the CD4 count increased to 193 cells/μL and the viral load decreased to 9,460 copies/mL. At the time of tuberculosis diagnosis (7 months post-HIV diagnosis), the CD4 count declined to 89 cells/μL and the viral load was 10,230 copies/mL, reflecting immunosuppression conducive to opportunistic infections.\\n\\nMicrobiological testing via Ziehl-Neelsen bacilloscopy was positive for acid-fast bacilli in gastric washings upon admission and again 19 days later in a right ear swab due to persistent otorrhea. The Xpert-MTB/GeneXpert assay, which detects *Mycobacterium tuberculosis* and rifampicin resistance, was negative for rifampicin resistance, indicating susceptibility to first-line anti-tuberculosis agents.\\n\\nChest radiography revealed an accentuated bronchovascular network at the base of the right lung, consistent with pulmonary tuberculosis. The clinical and radiological findings, combined with the positive acid-fast bacilli in both gastric fluid and ear pus, support a diagnosis of concurrent middle ear tuberculosis and pulmonary tuberculosis in the context of HIV-induced immunosuppression.\\n\\nThe patient was initiated on a 6-month standard first-line anti-tuberculosis regimen: an intensive phase of quadruple therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for 2 months (2RHZE), followed by a maintenance phase of dual therapy (isoniazid and rifampicin) for 4 months (4RH) at a dose of 3 tablets/day 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) to improve HIV suppression. ART was restarted on 4 May 2023 with patient consent, using tenofovir/lamivudine/dolutegravir (1 tablet/day) plus an additional dolutegravir 50 mg tablet (1 tablet/day) in accordance with current HIV management guidelines. Chemoprophylaxis with cotrimoxazole (960 mg once daily) was administered, and the external auditory canal was cleaned via aspiration, with ciprofloxacin ear drops (2 drops, three times daily) administered for 14 days to manage ear infection.\\n\\nClinical improvement was observed within 14 days of treatment, including resolution of fever, improvement in general condition, and amelioration of cough and otorrhea. Bacilloscopy became negative in both the gastric washings and the right ear pus swab. At the end of the 6-month anti-tuberculosis treatment, complete clinical healing was achieved, with normalization of ENT and neurological examinations. Follow-up bacilloscopy and Xpert-MTB/GeneXpert testing were negative at the end of the intensive phase (month 2), at month 5, and at the end of the maintenance phase (month 6). Post-treatment", "generated_text": "{\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 included artésunate, paracetamol, and unspecified antibiotics for suspected malaria and acute otitis media, which failed to resolve the symptoms. The patient is HIV-1 infected, with a diagnosis established 7 months prior, and has been on a triple antiretroviral therapy (TARV) regimen of tenofovir/lamivudine/dolutegravir; however, adherence to this regimen has been poor due to denial of his HIV status.\\n\\nPhysical examination revealed a fever of 38.2 °C, altered general condition, right-sided otalgia, purulent foul-smelling otorrhea, and a right basal pulmonary condensation consistent with bronchovascular hyperactivity. Neurological examination was normal, with no cranial nerve involvement, particularly the facial (VII) and cochleovestibular (VIII) nerves. Otoscopic evaluation of the right ear demonstrated inflammatory changes in the external auditory canal with purulent exudate and a single tympanic membrane perforation in the anterior-inferior quadrant; the left ear was intact. Rinne and Weber tests confirmed a right conductive hearing loss.\\n\\nImmunological and virological assessments showed a CD4 count of 118 cells/μL and a viral load of 12,370 copies/mL at the time of HIV diagnosis. Following 6 months of ART, the CD4 count increased to 193 cells/μL and the viral load decreased to 9,460 copies/mL. At the time of tuberculosis diagnosis (7 months post-HIV diagnosis), the CD4 count declined to 89 cells/μL and the viral load was 10,230 copies/mL, reflecting immunosuppression conducive to opportunistic infections.\\n\\nMicrobiological testing via Ziehl-Neelsen bacilloscopy was positive for acid-fast bacilli in gastric washings upon admission and again 19 days later in a right ear swab due to persistent otorrhea. The Xpert-MTB/GeneXpert assay, which detects *Mycobacterium tuberculosis* and rifampicin resistance, was negative for rifampicin resistance, indicating susceptibility to first-line anti-tuberculosis agents.\\n\\nChest radiography revealed an accentuated bronchovascular network at the base of the right lung, consistent with pulmonary tuberculosis. The clinical and radiological findings, combined with the positive acid-fast bacilli in both gastric fluid and ear pus, support a diagnosis of concurrent middle ear tuberculosis and pulmonary tuberculosis in the context of HIV-induced immunosuppression.\\n\\nThe patient was initiated on a 6-month standard first-line anti-tuberculosis regimen: an intensive phase of quadruple therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for 2 months (2RHZE), followed by a maintenance phase of dual therapy (isoniazid and rifampicin) for 4 months (4RH) at a dose of 3 tablets/day 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) to improve HIV suppression. ART was restarted on 4 May 2023 with patient consent, using tenofovir/lamivudine/dolutegravir (1 tablet/day) plus an additional dolutegravir 50 mg tablet (1 tablet/day) in accordance with current HIV management guidelines. Chemoprophylaxis with cotrimoxazole (960 mg once daily) was administered, and the external auditory canal was cleaned via aspiration, with ciprofloxacin ear drops (2 drops, three times daily) administered for 14 days to manage ear infection.\\n\\nClinical improvement was observed within 14 days of treatment, including resolution of fever, improvement in general condition, and amelioration of cough and otorrhea. Bacilloscopy became negative in both the gastric washings and the right ear pus swab. At the end of the 6-month anti-tuberculosis treatment, complete clinical healing was achieved, with normalization of ENT and neurological examinations. Follow-up bacilloscopy and Xpert-MTB/GeneXpert testing were negative at the end of the intensive phase (month 2), at month 5, and at the end of the maintenance phase (month 6). Post-treatment"}
{"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 special tube to clear the blocked blood vessel and fixed it successfully. The boy was small for his age but 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 special tube to clear the blocked blood vessel and fixed it successfully. The boy was small for his age but 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 and preserved brain motor potential, exhibiting normal psychomotor development, was diagnosed with restrictive cardiomyopathy and enrolled in a cardiac transplant programme at 16 months of age. He received external biventricular support via an implantable Berlin Heart device to bridge to transplantation. To mitigate the risk of embolic complications, he was maintained on 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, he presented with acute disconnection and right hemiparesis, consistent with a left middle cerebral artery (MCA) occlusion. Non-contrast computed tomography (CT) revealed a hyperdense left MCA, indicative of thrombus, and a chronic right parietotemporal infarct, suggesting prior ischemic injury. Laboratory parameters showed red blood cell count of 4.16 × 10⁶ µ/L and hemoglobin of 11.4 g/dL, within normal limits. Intravenous thrombolytic therapy was contraindicated due to active anticoagulation. Consequently, an intra-arterial mechanical thrombectomy was performed under general anaesthesia. The procedure involved puncture of the right femoral artery and placement 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. Recanalisation 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 within 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 system—including tutor catheter, microcatheter, and stentriever—was removed simultaneously. During the procedural control run, an iatrogenic dissection of the left internal carotid artery was identified, which was asymptomatic and did not compromise perfusion, as the left hemisphere remained adequately supplied via the anterior communicating artery. Post-procedure, the patient underwent successful cardiac transplantation one month later. Neurologically, the only persistent long-term sequelae were spasticity of the right upper limb, consistent with residual corticospinal tract dysfunction following the stroke. The case demonstrates the feasibility and clinical efficacy of intra-arterial mechanical thrombectomy in a young pediatric patient with complex comorbidities, including congenital cardiomyopathy and anticoagulated state, and highlights the importance of meticulous vascular mapping and perfusion monitoring during such interventions.\"\n}", "generated_text": "A 23-month-old male with a history of hypoxic-ischaemic encephalopathy at birth and preserved brain motor potential, exhibiting normal psychomotor development, was diagnosed with restrictive cardiomyopathy and enrolled in a cardiac transplant programme at 16 months of age. He received external biventricular support via an implantable Berlin Heart device to bridge to transplantation. To mitigate the risk of embolic complications, he was maintained on 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, he presented with acute disconnection and right hemiparesis, consistent with a left middle cerebral artery (MCA) occlusion. Non-contrast computed tomography (CT) revealed a hyperdense left MCA, indicative of thrombus, and a chronic right parietotemporal infarct, suggesting prior ischemic injury. Laboratory parameters showed red blood cell count of 4.16 × 10⁶ µ/L and hemoglobin of 11.4 g/dL, within normal limits. Intravenous thrombolytic therapy was contraindicated due to active anticoagulation. Consequently, an intra-arterial mechanical thrombectomy was performed under general anaesthesia. The procedure involved puncture of the right femoral artery and placement 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. Recanalisation 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 within 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 system—including tutor catheter, microcatheter, and stentriever—was removed simultaneously. During the procedural control run, an iatrogenic dissection of the left internal carotid artery was identified, which was asymptomatic and did not compromise perfusion, as the left hemisphere remained adequately supplied via the anterior communicating artery. Post-procedure, the patient underwent successful cardiac transplantation one month later. Neurologically, the only persistent long-term sequelae were spasticity of the right upper limb, consistent with residual corticospinal tract dysfunction following the stroke. The case demonstrates the feasibility and clinical efficacy of intra-arterial mechanical thrombectomy in a young pediatric patient with complex comorbidities, including congenital cardiomyopathy and anticoagulated state, and highlights the importance of meticulous vascular mapping and perfusion monitoring during such interventions."}
{"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 before. When doctors checked him, they found a broken shoulder on his left side too — a problem that wasn’t seen at the first hospital. The injury got worse in the left shoulder because he was held down and moved too much during his stay. Doctors used X-rays and CT scans to see the damage. They fixed both shoulders at the same time with metal plates and strong stitches. The right shoulder healed well, but the left one needed two more surgeries — one to fix the broken piece and another to open up the joint. Two years later, he can move his shoulders a lot better, with a score of 5% on a pain scale and 72 and 76 on a mobility scale for left and right shoulders, which means he’s doing better than most people in similar cases.\"\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 before. When doctors checked him, they found a broken shoulder on his left side too — a problem that wasn’t seen at the first hospital. The injury got worse in the left shoulder because he was held down and moved too much during his stay. Doctors used X-rays and CT scans to see the damage. They fixed both shoulders at the same time with metal plates and strong stitches. The right shoulder healed well, but the left one needed two more surgeries — one to fix the broken piece and another to open up the joint. Two years later, he can move his shoulders a lot better, with a score of 5% on a pain scale and 72 and 76 on a mobility scale for left and right shoulders, which means he’s doing better than most people in similar cases."}
{"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. When first evaluated, he had visible bruising on both shoulders and limited ability to move his arms, especially rotating them outward. He was physically restrained due to agitation.\\n\\nInitial X-rays showed a dislocation in his right shoulder and a simple posterior dislocation in his left shoulder — a problem that had not been seen at the previous hospital. A follow-up CT scan revealed that the left shoulder injury had worsened since admission, likely because of the physical restraint. Both shoulders were surgically treated at the same time with a procedure called open reduction and internal fixation using locked plates to realign and stabilize the bones.\\n\\nThe right shoulder had a fracture that was partially fixed with a screw and strong sutures. The left shoulder had a smaller bone defect, which was filled using a piece of the shoulder bone itself (a technique similar to McLaughlin’s method). However, the left shoulder needed two additional surgeries: one to fix the broken bone properly and another to release the stiff joint.\\n\\nAfter two years, the patient is doing well. He scores 5% on the Quick DASH scale (which measures 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. He was able to return to work five months after the injury and is now progressing toward full recovery, though his left shoulder still has limited range of motion, especially in external rotation.\"\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. When first evaluated, he had visible bruising on both shoulders and limited ability to move his arms, especially rotating them outward. He was physically restrained due to agitation.\n\nInitial X-rays showed a dislocation in his right shoulder and a simple posterior dislocation in his left shoulder — a problem that had not been seen at the previous hospital. A follow-up CT scan revealed that the left shoulder injury had worsened since admission, likely because of the physical restraint. Both shoulders were surgically treated at the same time with a procedure called open reduction and internal fixation using locked plates to realign and stabilize the bones.\n\nThe right shoulder had a fracture that was partially fixed with a screw and strong sutures. The left shoulder had a smaller bone defect, which was filled using a piece of the shoulder bone itself (a technique similar to McLaughlin’s method). However, the left shoulder needed two additional surgeries: one to fix the broken bone properly and another to release the stiff joint.\n\nAfter two years, the patient is doing well. He scores 5% on the Quick DASH scale (which measures 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. He was able to return to work five months after the injury and is now progressing toward full recovery, though his left shoulder still has limited range of motion, especially in external rotation."}
{"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 prior 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. He was physically restrained due to intermittent psychomotor agitation, with both feet and his left hand secured. Radiographic assessment revealed a right LFGHP and a previously undiagnosed simple posterior glenohumeral dislocation of the left shoulder, which had been missed at the referring facility and was only identified after a 48-hour delay.\\n\\nComputed tomography (CT) of both shoulders demonstrated a significant progression of the left shoulder injury from a simple posterior dislocation on admission to a full LFGHP within 48 hours, likely attributable to mechanical stress from prolonged physical restraint. This intrahospital aggravation underscores the role of external forces in the destabilization of glenohumeral joint integrity, particularly in the setting of altered neuromuscular control.\\n\\nPreoperative imaging of the right shoulder revealed glenoid bone integrity with 40% articular surface involvement of the humeral head, including a large fragment that was amenable to osteosynthesis in continuity with the lesser tuberosity. A 4.0 mm spongy screw with high-strength sutures was planned for fixation to preserve humeral head stability. In contrast, the left shoulder demonstrated intact glenoid bone and a 20% defect in the humeral articular surface, which was addressed via repositioning and fixation of the lesser tuberosity fragment during osteosynthesis, mimicking the surgical technique described by McLaughlin.\\n\\nSurgical intervention consisted of open reduction and internal fixation (ORIF) using bilateral locked plates. The patient was positioned in a beach chair position, and both shoulders were approached via classic deltopectoral incisions. 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 fixation with a 4.0 mm spongy screw and high-strength sutures. Definitive stabilization was accomplished with a Philos (Depuy Synthes®) locked plate, with additional fixation of the rotator cuff tendons to the plate to enhance biomechanical stability. The right shoulder was closed in layers and immobilized with a universal shoulder immobilizer.\\n\\nThe left shoulder was operated on immediately after, using the same deltopectoral approach with an accessory posterior portal for digital reduction. Fixation was performed similarly, except that the anterior humeral fragment was stabilized exclusively with high-strength sutures due to insufficient anatomical support for a spongy screw. Postoperative management included bilateral shoulder immobilization for four weeks, followed by a progressive rehabilitation protocol beginning at the second postoperative week. Exercises included pendular flexion-extension of the elbow and fist mobilization, administered as tolerated based on pain levels.\\n\\nAt the one-month radiographic follow-up, loss of reduction of the greater tuberosity was observed in the left shoulder, prompting a revision surgery to achieve adequate fixation using high-strength sutures. The patient continued with immobilization for an additional four weeks on the left side. Bilateral self-administered 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 rehabilitation, the patient returned to work five months following the initial trauma.\\n\\nOne-year follow-up demonstrated full recovery of strength and range of motion in the right shoulder. The left shoulder, however, retained significant limitations, particularly in external rotation. At this point, arthroscopic joint release was performed with removal of the osteosynthesis hardware to address chronic joint contractures and mechanical impingement. Two years post-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 sustained improvement in pain, function, and daily activity capacity. These results reflect both the efficacy of early surgical intervention and the importance of staged rehabilitation in managing complex glenohumeral injuries, especially in the context of secondary trauma from restraint and delayed diagnosis.\"\n}", "generated_text": "A 52-year-old male with no prior 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. He was physically restrained due to intermittent psychomotor agitation, with both feet and his left hand secured. Radiographic assessment revealed a right LFGHP and a previously undiagnosed simple posterior glenohumeral dislocation of the left shoulder, which had been missed at the referring facility and was only identified after a 48-hour delay.\n\nComputed tomography (CT) of both shoulders demonstrated a significant progression of the left shoulder injury from a simple posterior dislocation on admission to a full LFGHP within 48 hours, likely attributable to mechanical stress from prolonged physical restraint. This intrahospital aggravation underscores the role of external forces in the destabilization of glenohumeral joint integrity, particularly in the setting of altered neuromuscular control.\n\nPreoperative imaging of the right shoulder revealed glenoid bone integrity with 40% articular surface involvement of the humeral head, including a large fragment that was amenable to osteosynthesis in continuity with the lesser tuberosity. A 4.0 mm spongy screw with high-strength sutures was planned for fixation to preserve humeral head stability. In contrast, the left shoulder demonstrated intact glenoid bone and a 20% defect in the humeral articular surface, which was addressed via repositioning and fixation of the lesser tuberosity fragment during osteosynthesis, mimicking the surgical technique described by McLaughlin.\n\nSurgical intervention consisted of open reduction and internal fixation (ORIF) using bilateral locked plates. The patient was positioned in a beach chair position, and both shoulders were approached via classic deltopectoral incisions. 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 fixation with a 4.0 mm spongy screw and high-strength sutures. Definitive stabilization was accomplished with a Philos (Depuy Synthes®) locked plate, with additional fixation of the rotator cuff tendons to the plate to enhance biomechanical stability. The right shoulder was closed in layers and immobilized with a universal shoulder immobilizer.\n\nThe left shoulder was operated on immediately after, using the same deltopectoral approach with an accessory posterior portal for digital reduction. Fixation was performed similarly, except that the anterior humeral fragment was stabilized exclusively with high-strength sutures due to insufficient anatomical support for a spongy screw. Postoperative management included bilateral shoulder immobilization for four weeks, followed by a progressive rehabilitation protocol beginning at the second postoperative week. Exercises included pendular flexion-extension of the elbow and fist mobilization, administered as tolerated based on pain levels.\n\nAt the one-month radiographic follow-up, loss of reduction of the greater tuberosity was observed in the left shoulder, prompting a revision surgery to achieve adequate fixation using high-strength sutures. The patient continued with immobilization for an additional four weeks on the left side. Bilateral self-administered 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 rehabilitation, the patient returned to work five months following the initial trauma.\n\nOne-year follow-up demonstrated full recovery of strength and range of motion in the right shoulder. The left shoulder, however, retained significant limitations, particularly in external rotation. At this point, arthroscopic joint release was performed with removal of the osteosynthesis hardware to address chronic joint contractures and mechanical impingement. Two years post-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 sustained improvement in pain, function, and daily activity capacity. These results reflect both the efficacy of early surgical intervention and the importance of staged rehabilitation in managing complex glenohumeral injuries, especially in the context of secondary trauma from restraint and delayed diagnosis."}
{"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 weak heart that was leaking badly, so doctors put in a new valve (TAVI) through his chest to fix it. After that, his heart started failing again, so they added a machine (LVAD) to help his heart pump. One year later, the machine was giving warning signs, and scans showed the old valve was still leaking badly. The doctors decided to fix the old valve from the inside with another new valve (valve-in-valve). They slowed down the machine and set the heart to beat 140 times a minute during the procedure. The new valve went in perfectly, and after 12 months, the man is doing great — no more leaks, better heart strength, and can walk much farther without trouble.\"\n}", "generated_text": "A 70-year-old man had a weak heart that was leaking badly, so doctors put in a new valve (TAVI) through his chest to fix it. After that, his heart started failing again, so they added a machine (LVAD) to help his heart pump. One year later, the machine was giving warning signs, and scans showed the old valve was still leaking badly. The doctors decided to fix the old valve from the inside with another new valve (valve-in-valve). They slowed down the machine and set the heart to beat 140 times a minute during the procedure. The new valve went in perfectly, and after 12 months, the man is doing great — no more leaks, better heart strength, and can walk much farther without trouble."}
{"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 first with a procedure called transcatheter aortic valve implantation (TAVI) from the apex of his heart. He had a condition called aortic regurgitation, where blood leaks backward through the aortic valve, caused by past heart infection. Because his heart function was very weak and he had other serious health issues, surgery was too risky, so TAVI was chosen. The procedure used a new valve (JenaValve) and worked well initially, with only a small amount of leakage. However, four weeks later, his heart failed again due to poor pumping ability, so he received a left ventricular assist device (LVAD) to help his heart pump blood. After one year, the LVAD showed signs of high flow and echocardiograms showed worsening leakage through the aortic valve, even though the original valve itself looked normal. The medical team decided to perform a second valve procedure — a 'valve-in-valve' approach — where a new valve (CoreValve Evolut R) was placed inside the existing one. During this procedure, the LVAD flow was reduced to the lowest level and the heart was paced at 140 beats per minute to help the new valve settle properly. The placement was carefully guided using imaging. The procedure was successful, and at 12 months, the patient had no significant leakage, improved heart function (LVEF increased to 33%), and could walk much farther without symptoms. He is now doing well and living a normal daily life.\"\n}", "generated_text": "A 70-year-old man with severe heart valve problems was treated first with a procedure called transcatheter aortic valve implantation (TAVI) from the apex of his heart. He had a condition called aortic regurgitation, where blood leaks backward through the aortic valve, caused by past heart infection. Because his heart function was very weak and he had other serious health issues, surgery was too risky, so TAVI was chosen. The procedure used a new valve (JenaValve) and worked well initially, with only a small amount of leakage. However, four weeks later, his heart failed again due to poor pumping ability, so he received a left ventricular assist device (LVAD) to help his heart pump blood. After one year, the LVAD showed signs of high flow and echocardiograms showed worsening leakage through the aortic valve, even though the original valve itself looked normal. The medical team decided to perform a second valve procedure — a 'valve-in-valve' approach — where a new valve (CoreValve Evolut R) was placed inside the existing one. During this procedure, the LVAD flow was reduced to the lowest level and the heart was paced at 140 beats per minute to help the new valve settle properly. The placement was carefully guided using imaging. The procedure was successful, and at 12 months, the patient had no significant leakage, improved heart function (LVEF increased to 33%), and could walk much farther without symptoms. He is now doing well and living a normal daily 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 patient was classified as high-risk for surgical intervention due to 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 a logistic EuroSCORE I of 24.36%. Pre-TAVI medical management included torasemide 20 mg once daily, ramipril 5 mg once daily, bisoprolol 2.5 mg twice daily, and spironolactone 12.5 mg once daily. On admission, he presented with cardiac decompensation and dyspnea (temperature 36.7°C, heart rate 99 beats/minute, blood pressure 109/48 mmHg), with no signs of infection (normal C-reactive protein, normal 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); no urine analysis was conducted. Coronary angiography, performed prior to TAVI, was normal. The initial TAVI procedure utilized a JenaValve 27 mm self-expandable bioprosthesis, resulting in good immediate hemodynamic outcomes with minimal transvalvular central insufficiency. However, recurrent cardiac decompensation occurred due to persistent severe left ventricular dysfunction, leading to a second interdisciplinary evaluation. Four weeks post-TAVI, the patient underwent implantation of a left ventricular assist device (LVAD) system (Thoratec® HeartMate II), with an uneventful postoperative course and sustained asymptomatic status for one year. During this period, echocardiographic monitoring revealed a progressive worsening of transvalvular central insufficiency, reaching severe levels, without evidence of structural valve leaflet damage or dissection in the JenaValve prosthesis. This suggested a hemodynamic mechanism related to high LVAD flow rates and altered left ventricular dynamics. Given the persistent regurgitation and lack of improvement in ventricular function, a valve-in-valve strategy was selected. The subsequent TAVI procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm self-expandable prosthesis without prior valvuloplasty. Prior to deployment, the LVAD flow was reduced to minimum and the patient was paced at 140 beats/minute to optimize ventricular contractility and reduce left ventricular wall stress. Positioning was meticulously guided by fluoroscopy and transesophageal echocardiography (TEE), with the goal of placing the ventricular strut of the CoreValve Evolut R between the ventricular end and the 'cusp feelers' of the existing JenaValve, based on individual CT imaging demonstrating optimal positioning of the JenaValve's ventricular edge within the left ventricular outflow tract (LVOT). Initial positioning was successful without repositioning. Final deployment was confirmed via fluoroscopic control, followed by successful release in the intended location. Pacing was discontinued, and LVAD flow was gradually restored to normal levels, with stable hemodynamics. Postoperative recovery was uneventful. A follow-up TEE at 12 months demonstrated no significant aortic regurgitation and only marginal residual insufficiency. The patient reported no symptoms and demonstrated significant improvement in functional capacity, with a 6-minute walk test increasing from 148 m (admission) to 381 m. Echocardiography at 12 months showed an improvement in LVEF to 33%, confirming favorable remodeling and hemodynamic stabilization. The case illustrates the challenges of managing complex valvular and ventricular pathology in a high-risk patient, and highlights the role of precise TAVI positioning, flow modulation, and pacing in achieving successful valve-in-valve outcomes with preserved valve function and improved ventricular performance.\"\n}", "generated_text": "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 patient was classified as high-risk for surgical intervention due to 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 a logistic EuroSCORE I of 24.36%. Pre-TAVI medical management included torasemide 20 mg once daily, ramipril 5 mg once daily, bisoprolol 2.5 mg twice daily, and spironolactone 12.5 mg once daily. On admission, he presented with cardiac decompensation and dyspnea (temperature 36.7°C, heart rate 99 beats/minute, blood pressure 109/48 mmHg), with no signs of infection (normal C-reactive protein, normal 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); no urine analysis was conducted. Coronary angiography, performed prior to TAVI, was normal. The initial TAVI procedure utilized a JenaValve 27 mm self-expandable bioprosthesis, resulting in good immediate hemodynamic outcomes with minimal transvalvular central insufficiency. However, recurrent cardiac decompensation occurred due to persistent severe left ventricular dysfunction, leading to a second interdisciplinary evaluation. Four weeks post-TAVI, the patient underwent implantation of a left ventricular assist device (LVAD) system (Thoratec® HeartMate II), with an uneventful postoperative course and sustained asymptomatic status for one year. During this period, echocardiographic monitoring revealed a progressive worsening of transvalvular central insufficiency, reaching severe levels, without evidence of structural valve leaflet damage or dissection in the JenaValve prosthesis. This suggested a hemodynamic mechanism related to high LVAD flow rates and altered left ventricular dynamics. Given the persistent regurgitation and lack of improvement in ventricular function, a valve-in-valve strategy was selected. The subsequent TAVI procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm self-expandable prosthesis without prior valvuloplasty. Prior to deployment, the LVAD flow was reduced to minimum and the patient was paced at 140 beats/minute to optimize ventricular contractility and reduce left ventricular wall stress. Positioning was meticulously guided by fluoroscopy and transesophageal echocardiography (TEE), with the goal of placing the ventricular strut of the CoreValve Evolut R between the ventricular end and the 'cusp feelers' of the existing JenaValve, based on individual CT imaging demonstrating optimal positioning of the JenaValve's ventricular edge within the left ventricular outflow tract (LVOT). Initial positioning was successful without repositioning. Final deployment was confirmed via fluoroscopic control, followed by successful release in the intended location. Pacing was discontinued, and LVAD flow was gradually restored to normal levels, with stable hemodynamics. Postoperative recovery was uneventful. A follow-up TEE at 12 months demonstrated no significant aortic regurgitation and only marginal residual insufficiency. The patient reported no symptoms and demonstrated significant improvement in functional capacity, with a 6-minute walk test increasing from 148 m (admission) to 381 m. Echocardiography at 12 months showed an improvement in LVEF to 33%, confirming favorable remodeling and hemodynamic stabilization. The case illustrates the challenges of managing complex valvular and ventricular pathology in a high-risk patient, and highlights the role of precise TAVI positioning, flow modulation, and pacing in achieving successful valve-in-valve outcomes with preserved valve function and improved ventricular performance."}
{"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. He had no other health problems. Tests showed he had diabetes insipidus — a condition where his body can't hold water properly. MRI scans found a small cyst in the pituitary area that had burst, but it wasn't pressing on any parts of his brain. Since he wasn't having serious symptoms and his other hormone levels were normal, doctors chose not to do surgery. Instead, they watched him closely with regular check-ups. Over time, he grew normally and started puberty, but his growth slowed a bit. Later, tests found he had a small lack of growth hormone. After starting growth hormone shots, his growth sped up. The cyst stayed stable and didn't get worse. All the doctors agreed it was safe to keep watching him without treatment.\"\n}", "generated_text": "A 12-year-old boy came in with sudden headaches and drinking a lot of water, urinating a lot. He had no other health problems. Tests showed he had diabetes insipidus — a condition where his body can't hold water properly. MRI scans found a small cyst in the pituitary area that had burst, but it wasn't pressing on any parts of his brain. Since he wasn't having serious symptoms and his other hormone levels were normal, doctors chose not to do surgery. Instead, they watched him closely with regular check-ups. Over time, he grew normally and started puberty, but his growth slowed a bit. Later, tests found he had a small lack of growth hormone. After starting growth hormone shots, his growth sped up. The cyst stayed stable and didn't get worse. All the doctors agreed it was safe to keep watching him without treatment."}
{"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 syndrome, which began one week prior to evaluation. He had no significant past medical history. Physical examination revealed a height of 146.5 cm (M) and weight of 30 kg (-1.4 SD), with no signs of adrenal insufficiency or hypothyroidism. He was at the early stages of puberty, with bilateral gonadal volumes of 3.2 cm and a penile length of 6.2 cm (M). Clinical manifestations included polyuria with urine output 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 demonstrated diabetes insipidus (DI), characterized by a serum sodium of 140 mEq/L, plasma osmolality of 287 mosm/kg, and a markedly low urine osmolality of 179 mosm/kg. Basal hormone levels—including insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH)—were all within normal limits, indicating no primary endocrine dysfunction beyond DI. Magnetic resonance imaging (MRI) with and without contrast revealed apoplexy of a Rathke cleft cyst (RCC), presenting as spontaneous hyperintensity on both T1 and T2-weighted sequences, measuring 15 × 6 × 11 mm. The anterior pituitary demonstrated homogeneous contrast enhancement, while the posterior pituitary showed loss of typical hyperintensity, with no radiological features suggestive of craniopharyngioma.\\n\\nThe diagnosis of DI was confirmed and showed significant clinical improvement with exogenous vasopressin therapy. A multidisciplinary team consisting of an endocrinologist, neurosurgeon, and radiologist reviewed the case, concluding that the absence of compressive neurologic symptoms, normal baseline endocrine function, and stable RCC apoplexy over nine months of serial MRI monitoring (with size reduction from 15×6×11 mm to 12×11×10 mm) supported a conservative management strategy. The patient was subjected to regular clinical, biochemical, and radiological follow-up over a three-year period.\\n\\nDuring this period, the child achieved normal pubertal development without evidence of significant endocrine deficiencies, except for a subsequent identification of partial growth hormone (GH) deficiency. Growth velocity declined over time, from -0.8 SD to -1.1 SD, prompting further investigation. At age 14 years and 9 months, two GH stimulation tests were performed: a propranolol-glucagon test (peak GH: 19.3 µUI/ml) and an insulin tolerance test (peak GH: 10.0 µUI/ml), both indicating a partial GH deficiency. Following initiation of recombinant human growth hormone (rhGH) therapy, growth velocity improved significantly, rising from -1.1 SD to +0.2 SD over one year.\\n\\nSerial MRI assessments confirmed stability of the RCC apoplexy, with dimensions evolving from 15×6×11 mm at baseline to 11×12×11 mm at two years and further to 7×10×6 mm at three years, indicating a slight but consistent reduction in size. All MRI studies were performed at the same imaging center using standardized protocols, and interpretation was consistently carried out by the same radiologist within multidisciplinary review meetings involving endocrinology and neurosurgery. The clinical course underscores the importance of long-term monitoring in pediatric patients with RCC apoplexy, particularly when no compressive or endocrine deficits are present at initial presentation, and highlights the potential for acquired GH deficiency as a late complication despite otherwise normal pubertal and endocrine development.\"\n}", "generated_text": "A 12-year-old male presented with acute onset of headache and polyuria-polydipsia syndrome, which began one week prior to evaluation. He had no significant past medical history. Physical examination revealed a height of 146.5 cm (M) and weight of 30 kg (-1.4 SD), with no signs of adrenal insufficiency or hypothyroidism. He was at the early stages of puberty, with bilateral gonadal volumes of 3.2 cm and a penile length of 6.2 cm (M). Clinical manifestations included polyuria with urine output 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 demonstrated diabetes insipidus (DI), characterized by a serum sodium of 140 mEq/L, plasma osmolality of 287 mosm/kg, and a markedly low urine osmolality of 179 mosm/kg. Basal hormone levels—including insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH)—were all within normal limits, indicating no primary endocrine dysfunction beyond DI. Magnetic resonance imaging (MRI) with and without contrast revealed apoplexy of a Rathke cleft cyst (RCC), presenting as spontaneous hyperintensity on both T1 and T2-weighted sequences, measuring 15 × 6 × 11 mm. The anterior pituitary demonstrated homogeneous contrast enhancement, while the posterior pituitary showed loss of typical hyperintensity, with no radiological features suggestive of craniopharyngioma.\n\nThe diagnosis of DI was confirmed and showed significant clinical improvement with exogenous vasopressin therapy. A multidisciplinary team consisting of an endocrinologist, neurosurgeon, and radiologist reviewed the case, concluding that the absence of compressive neurologic symptoms, normal baseline endocrine function, and stable RCC apoplexy over nine months of serial MRI monitoring (with size reduction from 15×6×11 mm to 12×11×10 mm) supported a conservative management strategy. The patient was subjected to regular clinical, biochemical, and radiological follow-up over a three-year period.\n\nDuring this period, the child achieved normal pubertal development without evidence of significant endocrine deficiencies, except for a subsequent identification of partial growth hormone (GH) deficiency. Growth velocity declined over time, from -0.8 SD to -1.1 SD, prompting further investigation. At age 14 years and 9 months, two GH stimulation tests were performed: a propranolol-glucagon test (peak GH: 19.3 µUI/ml) and an insulin tolerance test (peak GH: 10.0 µUI/ml), both indicating a partial GH deficiency. Following initiation of recombinant human growth hormone (rhGH) therapy, growth velocity improved significantly, rising from -1.1 SD to +0.2 SD over one year.\n\nSerial MRI assessments confirmed stability of the RCC apoplexy, with dimensions evolving from 15×6×11 mm at baseline to 11×12×11 mm at two years and further to 7×10×6 mm at three years, indicating a slight but consistent reduction in size. All MRI studies were performed at the same imaging center using standardized protocols, and interpretation was consistently carried out by the same radiologist within multidisciplinary review meetings involving endocrinology and neurosurgery. The clinical course underscores the importance of long-term monitoring in pediatric patients with RCC apoplexy, particularly when no compressive or endocrine deficits are present at initial presentation, and highlights the potential for acquired GH deficiency as a late complication despite otherwise normal pubertal and endocrine development."}
{"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 medical history presented with a six-month progression of dysphonia and dysphagia, culminating in a marked deterioration of general condition characterized by substantial weight loss of 15 kg over six months. Initial clinical examination revealed a conscious patient with a Glasgow Coma Scale score of 15/15, normothermia, blood pressure of 12/7 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 elsewhere was unremarkable.\\n\\nImaging via cervico-thoraco-abdomino-pelvic computed tomography (CT) demonstrated a nasopharyngeal mass measuring 70 mm × 40 mm, extending to 60 mm in depth. Laboratory investigations, including complete blood count, renal and hepatic function tests, lactate dehydrogenase (LDH), and serologies for HIV, hepatitis C virus (HCV), and hepatitis B virus (HBV), were all within normal limits. Histopathological and immunohistochemical analysis of the nasopharyngeal biopsy, performed in two independent laboratories, confirmed a diagnosis of grade 1–2 follicular B-cell non-Hodgkin lymphoma (NHL), characterized by CD20+, CD19+, CD79a+, and CD10+ immunophenotype, consistent with a follicular lymphoma of the B-cell lineage. Bone marrow biopsy and pre-treatment work-up were unremarkable, with no evidence of hematological involvement or systemic disease.\\n\\nThe patient underwent 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 resulted in 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, but the nasopharyngeal mass persisted and progressively enlarged, leading to clinical instability and the need for tracheostomy due to airway compromise.\\n\\nRepeat biopsy of the nasopharyngeal mass revealed a complete absence of B-lymphocyte infiltration and the presence of amyloid deposits of the AL type, specifically kappa light chain origin. Immunoelectrophoresis of plasma proteins demonstrated the presence of monoclonal immunoglobulin M kappa (IgMκ), suggesting a monoclonal gammopathy of undetermined significance (MGUS) or early-stage amyloidosis. Light chain quantification was not performed due to institutional resource limitations. Myelogram and a second bone marrow biopsy remained normal, excluding clonal plasma cell proliferation or bone marrow infiltration.\\n\\nPositron emission tomography (PET) scanning confirmed a hypermetabolic nasopharyngeal lesion, consistent with active disease, with no evidence of metastatic spread to other organs. Cardiac evaluation (electrocardiogram, n-terminal pro-B-type natriuretic peptide, troponin, echocardiography) and renal function tests were unremarkable, indicating no significant organ dysfunction. The patient is currently receiving a triple-agent regimen of bortezomib, prednisone, and bendamustine, a protocol designed to target proteasome function and induce apoptosis in lymphoma cells, with reported favorable clinical response following the initial course. The clinical course reflects a complex, treatment-resistant presentation of follicular lymphoma with secondary amyloidosis, likely driven by chronic B-cell activation and monoclonal gammopathy, highlighting the importance of integrated immunological and histopathological assessment in such cases.\"\n}", "generated_text": "A 67-year-old male with no significant medical history presented with a six-month progression of dysphonia and dysphagia, culminating in a marked deterioration of general condition characterized by substantial weight loss of 15 kg over six months. Initial clinical examination revealed a conscious patient with a Glasgow Coma Scale score of 15/15, normothermia, blood pressure of 12/7 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 elsewhere was unremarkable.\n\nImaging via cervico-thoraco-abdomino-pelvic computed tomography (CT) demonstrated a nasopharyngeal mass measuring 70 mm × 40 mm, extending to 60 mm in depth. Laboratory investigations, including complete blood count, renal and hepatic function tests, lactate dehydrogenase (LDH), and serologies for HIV, hepatitis C virus (HCV), and hepatitis B virus (HBV), were all within normal limits. Histopathological and immunohistochemical analysis of the nasopharyngeal biopsy, performed in two independent laboratories, confirmed a diagnosis of grade 1–2 follicular B-cell non-Hodgkin lymphoma (NHL), characterized by CD20+, CD19+, CD79a+, and CD10+ immunophenotype, consistent with a follicular lymphoma of the B-cell lineage. Bone marrow biopsy and pre-treatment work-up were unremarkable, with no evidence of hematological involvement or systemic disease.\n\nThe patient underwent 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 resulted in 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, but the nasopharyngeal mass persisted and progressively enlarged, leading to clinical instability and the need for tracheostomy due to airway compromise.\n\nRepeat biopsy of the nasopharyngeal mass revealed a complete absence of B-lymphocyte infiltration and the presence of amyloid deposits of the AL type, specifically kappa light chain origin. Immunoelectrophoresis of plasma proteins demonstrated the presence of monoclonal immunoglobulin M kappa (IgMκ), suggesting a monoclonal gammopathy of undetermined significance (MGUS) or early-stage amyloidosis. Light chain quantification was not performed due to institutional resource limitations. Myelogram and a second bone marrow biopsy remained normal, excluding clonal plasma cell proliferation or bone marrow infiltration.\n\nPositron emission tomography (PET) scanning confirmed a hypermetabolic nasopharyngeal lesion, consistent with active disease, with no evidence of metastatic spread to other organs. Cardiac evaluation (electrocardiogram, n-terminal pro-B-type natriuretic peptide, troponin, echocardiography) and renal function tests were unremarkable, indicating no significant organ dysfunction. The patient is currently receiving a triple-agent regimen of bortezomib, prednisone, and bendamustine, a protocol designed to target proteasome function and induce apoptosis in lymphoma cells, with reported favorable clinical response following the initial course. The clinical course reflects a complex, treatment-resistant presentation of follicular lymphoma with secondary amyloidosis, likely driven by chronic B-cell activation and monoclonal gammopathy, highlighting the importance of integrated immunological and histopathological assessment in such cases."}
{"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 moved to Chile one year ago works with animals. For one year, he had warty bumps on the front of his right leg that grew bigger. At first, they didn’t hurt, but later he started feeling itching, pain, and the bumps began to break open with yellowish fluid. The bumps were about 1 cm to 3 cm in size. Doctors saw the bumps up close and noticed dark spots and red blood vessels. Blood tests were normal, and no signs of infections or other diseases were found. A small sample of the skin was checked and showed special round, thick-walled cells (called muriform cells) and black, fuzzy mold that grew in the lab. The mold looked like Fonsecaea, a type of fungus. He was treated for six months with a medicine called itraconazole, taken twice a day, and had cold treatment (cryotherapy) every 6 to 8 weeks on the thick parts of the bumps. The cold treatment helped the bumps go away. After six months, the bumps completely disappeared, and no new ones came back. There is a little darker skin left, which is normal after cryotherapy.\"\n}", "generated_text": "A 46-year-old man from Haiti who moved to Chile one year ago works with animals. For one year, he had warty bumps on the front of his right leg that grew bigger. At first, they didn’t hurt, but later he started feeling itching, pain, and the bumps began to break open with yellowish fluid. The bumps were about 1 cm to 3 cm in size. Doctors saw the bumps up close and noticed dark spots and red blood vessels. Blood tests were normal, and no signs of infections or other diseases were found. A small sample of the skin was checked and showed special round, thick-walled cells (called muriform cells) and black, fuzzy mold that grew in the lab. The mold looked like Fonsecaea, a type of fungus. He was treated for six months with a medicine called itraconazole, taken twice a day, and had cold treatment (cryotherapy) every 6 to 8 weeks on the thick parts of the bumps. The cold treatment helped the bumps go away. After six months, the bumps completely disappeared, and no new ones came back. There is a little darker skin left, which is normal after cryotherapy."}
{"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 lesions on the front of his right leg that had been growing for about a year. He originally had a small bump that slowly became larger and, three months before visiting the doctor, started causing itching, pain, and a yellowish discharge. On exam, doctors saw several warty plaques ranging from 1 to 3 centimeters in size. Dermatoscopy showed thick, ulcerated skin with dark spots and red blood vessels. Blood tests were normal, and tests for infections like syphilis, HIV, and tuberculosis were negative. Skin tissue samples were taken and tested. The biopsy showed thickened skin and inflammation, with special cells called muriform cells — which are a sign of a fungal infection. Fungal culture grew black, velvety colonies, and direct microscopic examination found fungal structures typical of Fonsecaea species. The diagnosis was chromoblastomycosis, a rare fungal infection that affects skin and underlying tissue. The patient was treated with itraconazole (an antifungal drug) taken twice daily for six months, along with regular cryotherapy (freezing the lesions with liquid nitrogen) every six to eight weeks. He also used mupirocin ointment to prevent bacterial infections in areas that had broken open. 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 lesions on the front of his right leg that had been growing for about a year. He originally had a small bump that slowly became larger and, three months before visiting the doctor, started causing itching, pain, and a yellowish discharge. On exam, doctors saw several warty plaques ranging from 1 to 3 centimeters in size. Dermatoscopy showed thick, ulcerated skin with dark spots and red blood vessels. Blood tests were normal, and tests for infections like syphilis, HIV, and tuberculosis were negative. Skin tissue samples were taken and tested. The biopsy showed thickened skin and inflammation, with special cells called muriform cells — which are a sign of a fungal infection. Fungal culture grew black, velvety colonies, and direct microscopic examination found fungal structures typical of Fonsecaea species. The diagnosis was chromoblastomycosis, a rare fungal infection that affects skin and underlying tissue. The patient was treated with itraconazole (an antifungal drug) taken twice daily for six months, along with regular cryotherapy (freezing the lesions with liquid nitrogen) every six to eight weeks. He also used mupirocin ointment to prevent bacterial infections in areas that had broken open. 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 initially manifesting as a papule on the anterior aspect of the right leg. The lesion evolved into multiple warty plaques measuring 1 x 1 cm, 2 x 2 cm, and 3 x 2 cm, with a history of asymptomatic onset followed by the development of pruritus, pain, superficial ulceration, and yellowish purulent discharge three months prior to presentation. Physical examination revealed phototype V skin, with characteristic hyperkeratotic, ulcerated plaques exhibiting reddish-black dots and congested hemorrhagic vessels on dermatoscopy. Laboratory evaluations, including VDRL, HIV, and PPD, were non-reactive, ruling out syphilis, HIV infection, and tuberculosis. Tissue sampling via punch biopsy (including epidermis, dermis, and subcutaneous tissue) was performed and processed for Gram staining, routine bacterial culture, and anaerobic culture, all of which were negative. Bacilloscopy and Koch complex culture of the same specimen were also negative, excluding mycobacterial and bacillary etiologies. Histopathological analysis using hematoxylin and eosin staining demonstrated pseudoepitheliomatous hyperplasia of the epidermis, with a mixed inflammatory infiltrate in the dermis 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 muriform cells—specifically, those characteristic of Fonsecaea spp. This finding was further confirmed by periodic acid-Schiff (PAS) staining, which highlighted the intracellular fungal elements. Mycological culture on Sabouraud dextrose agar at 25°C yielded dematiaceous (black-pigmented), elevated, well-defined, velvety colonies after 15 days of incubation, consistent with chromoblastomycosis. Direct microscopic examination using 20% potassium hydroxide (KOH) revealed long, branched, sometimes tortuous hyphae and acropetal chains of conidia, which are pathognomonic for Fonsecaea spp. The diagnosis of chromoblastomycosis was thus established based on histopathological presence of muriform cells, dematiaceous fungal colonies, and conidial morphology compatible with Fonsecaea spp. The patient was treated with systemic itraconazole at a dose of 100 mg every 12 hours for six months, in conjunction with regular cryotherapy (liquid nitrogen application) to hypertrophic and ulcerated areas every six to eight weeks. Topical mupirocin ointment was applied frequently to manage bacterial superinfections arising from ulceration and erosion. The clinical course was favorable, with complete regression of the cutaneous lesions and no evidence of relapse at the time of follow-up. Persistent mild local hypopigmentation in the treated areas was observed, which is a known sequelae of cryotherapy-induced tissue damage and is expected in the context of repeated cryoprophylactic interventions. This case underscores the importance of recognizing chromoblastomycosis in patients with occupational exposure to soil and organic matter, particularly in agricultural settings, and highlights the efficacy of combined antifungal therapy and physical debridement in achieving durable clinical resolution.\"\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 initially manifesting as a papule on the anterior aspect of the right leg. The lesion evolved into multiple warty plaques measuring 1 x 1 cm, 2 x 2 cm, and 3 x 2 cm, with a history of asymptomatic onset followed by the development of pruritus, pain, superficial ulceration, and yellowish purulent discharge three months prior to presentation. Physical examination revealed phototype V skin, with characteristic hyperkeratotic, ulcerated plaques exhibiting reddish-black dots and congested hemorrhagic vessels on dermatoscopy. Laboratory evaluations, including VDRL, HIV, and PPD, were non-reactive, ruling out syphilis, HIV infection, and tuberculosis. Tissue sampling via punch biopsy (including epidermis, dermis, and subcutaneous tissue) was performed and processed for Gram staining, routine bacterial culture, and anaerobic culture, all of which were negative. Bacilloscopy and Koch complex culture of the same specimen were also negative, excluding mycobacterial and bacillary etiologies. Histopathological analysis using hematoxylin and eosin staining demonstrated pseudoepitheliomatous hyperplasia of the epidermis, with a mixed inflammatory infiltrate in the dermis 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 muriform cells—specifically, those characteristic of Fonsecaea spp. This finding was further confirmed by periodic acid-Schiff (PAS) staining, which highlighted the intracellular fungal elements. Mycological culture on Sabouraud dextrose agar at 25°C yielded dematiaceous (black-pigmented), elevated, well-defined, velvety colonies after 15 days of incubation, consistent with chromoblastomycosis. Direct microscopic examination using 20% potassium hydroxide (KOH) revealed long, branched, sometimes tortuous hyphae and acropetal chains of conidia, which are pathognomonic for Fonsecaea spp. The diagnosis of chromoblastomycosis was thus established based on histopathological presence of muriform cells, dematiaceous fungal colonies, and conidial morphology compatible with Fonsecaea spp. The patient was treated with systemic itraconazole at a dose of 100 mg every 12 hours for six months, in conjunction with regular cryotherapy (liquid nitrogen application) to hypertrophic and ulcerated areas every six to eight weeks. Topical mupirocin ointment was applied frequently to manage bacterial superinfections arising from ulceration and erosion. The clinical course was favorable, with complete regression of the cutaneous lesions and no evidence of relapse at the time of follow-up. Persistent mild local hypopigmentation in the treated areas was observed, which is a known sequelae of cryotherapy-induced tissue damage and is expected in the context of repeated cryoprophylactic interventions. This case underscores the importance of recognizing chromoblastomycosis in patients with occupational exposure to soil and organic matter, particularly in agricultural settings, and highlights the efficacy of combined antifungal therapy and physical debridement in achieving durable clinical resolution."}
{"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 was vaccinated at birth. The lump was removed and tested — it showed signs of tuberculosis in the tube-like part of the testicle. X-rays showed TB in his lungs, under his skin, in his lymph nodes, and in his spine and bones. He started TB medicine, but after 4 months, he had seizures. A brain scan found small TB lumps in his brain. He got medicine for seizures and kept taking TB medicine. His symptoms got better, the body parts healed, and he gained weight. 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 was vaccinated at birth. The lump was removed and tested — it showed signs of tuberculosis in the tube-like part of the testicle. X-rays showed TB in his lungs, under his skin, in his lymph nodes, and in his spine and bones. He started TB medicine, but after 4 months, he had seizures. A brain scan found small TB lumps in his brain. He got medicine for seizures and kept taking TB medicine. His symptoms got better, the body parts healed, and he gained weight. 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.\\n\\nExams showed a large, tender lump in the scrotum and two firm lumps on his chest. His blood tests were mostly normal, except for a high level of inflammation. A chest X-ray showed signs of lung infection.\\n\\nHe had surgery to remove the scrotal lump, and the tissue test showed signs of tuberculosis in the epididymis — a part of the testicle. A skin test for tuberculosis was positive, and no bacteria were found in his sputum or urine. Other tests ruled out HIV, hepatitis, and other infections.\\n\\nImaging scans found tuberculosis in other parts of his body, including his lungs, lymph nodes, chest walls, and spine. This was diagnosed as widespread tuberculosis affecting multiple areas.\\n\\nHe started standard tuberculosis treatment with several medicines for two months, then continued with two of them. After four months of treatment, he began having seizures. A brain MRI showed small nodular lesions — called tuberculomas — in his brain, which are caused by tuberculosis.\\n\\nHe was started on anti-seizure medication along with continuing his tuberculosis treatment. His overall condition improved, he gained weight, and the other signs of infection gradually disappeared. The brain tuberculomas slowly shrunk, and he remained seizure-free. He completed treatment after 234 months (about 19 years) and was declared cured with no long-term effects, even after a two-year follow-up.\"\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.\n\nExams showed a large, tender lump in the scrotum and two firm lumps on his chest. His blood tests were mostly normal, except for a high level of inflammation. A chest X-ray showed signs of lung infection.\n\nHe had surgery to remove the scrotal lump, and the tissue test showed signs of tuberculosis in the epididymis — a part of the testicle. A skin test for tuberculosis was positive, and no bacteria were found in his sputum or urine. Other tests ruled out HIV, hepatitis, and other infections.\n\nImaging scans found tuberculosis in other parts of his body, including his lungs, lymph nodes, chest walls, and spine. This was diagnosed as widespread tuberculosis affecting multiple areas.\n\nHe started standard tuberculosis treatment with several medicines for two months, then continued with two of them. After four months of treatment, he began having seizures. A brain MRI showed small nodular lesions — called tuberculomas — in his brain, which are caused by tuberculosis.\n\nHe was started on anti-seizure medication along with continuing his tuberculosis treatment. His overall condition improved, he gained weight, and the other signs of infection gradually disappeared. The brain tuberculomas slowly shrunk, and he remained seizure-free. He completed treatment after 234 months (about 19 years) and was declared cured with no long-term effects, even after a two-year follow-up."}
{"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 empiric antibiotic therapy for pyogenic infection. 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 routine 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 investigations 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 X-ray revealed bilateral reticulonodular infiltrates consistent with pulmonary parenchymal involvement.\\n\\nUltrasound imaging suggested a tuberculous epididymal lesion, prompting a left orchidectomy. Histopathological examination of the resected tissue demonstrated granulomatous epithelioid cell necrosis involving the body and tail of the epididymis, with preservation of the head and testicular tissue, consistent with active epididymal tuberculosis. The intradermal tuberculin skin test (TST) was positive, supporting a diagnosis of latent or active tuberculosis. Direct microscopy and culture for acid-fast bacilli (AFB) in sputum and urine over three consecutive days were negative, indicating a lack of detectable bacilli in these specimens. Serological testing for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Wright's stain for parasitic infection were all negative, ruling out alternative infectious or hematological etiologies.\\n\\nTo evaluate for extrapulmonary dissemination, a thoraco-abdomino-pelvic tomodensitometry was performed, revealing miliary tuberculosis, coelo-mesenteric necrotic lymphadenopathy, bilateral parietal collections (right: 33 × 10 mm; left: 45 × 10 mm) at the level of the external oblique muscles, and focal osteolytic lesions at D11 and L5, suggestive of early spondylodiscitis. Magnetic resonance imaging (MRI) of the spinal cord confirmed active spondylodiscitis at D7, D11, L4, and L5, confirming the presence of spinal tuberculous infection. This constellation of findings led to a definitive diagnosis of disseminated tuberculosis involving epididymal, pulmonary, parietal, lymphatic, and osteoarticular sites.\\n\\nThe patient was initiated on a standard anti-tuberculous regimen consisting of a four-drug intensive phase (isoniazid, rifampicin, ethambutol, and pyrazinamide) for 2 months, followed by a continuation phase of isoniazid and rifampicin. At the 4th month of therapy, the patient developed generalized tonic-clonic convulsive seizures. A brain MRI was performed, which revealed multiple nodular lesions located both above and below the tentorial membrane, consistent with tuberculomas—granulomatous lesions caused by Mycobacterium tuberculosis that have infiltrated the central nervous system. The patient was promptly started on anticonvulsant therapy in addition to continuing anti-tuberculous treatment. Clinical and radiological follow-up demonstrated a favorable evolution: improvement in general condition, weight gain, and resolution of thoracic parietal collections, lymphadenopathy, and miliary infiltrates on imaging. However, the tuberculomas showed a slow, progressive reduction in size, necessitating prolonged continuation of anti-tuberculous therapy. The patient was ultimately declared cured at the end of 234 months (approximately 19.5 years) of treatment, with a 2-year post-treatment follow-up showing no recurrence of clinical or radiological manifestations and no neurological sequelae. This case exemplifies the potential for disseminated tuberculosis to present with extrapulmonary manifestations, including epididymal involvement, and to progress to central nervous system disease, requiring multidrug therapy and long-term management to achieve complete resolution.\"\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 empiric antibiotic therapy for pyogenic infection. 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 routine 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 investigations 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 X-ray revealed bilateral reticulonodular infiltrates consistent with pulmonary parenchymal involvement.\n\nUltrasound imaging suggested a tuberculous epididymal lesion, prompting a left orchidectomy. Histopathological examination of the resected tissue demonstrated granulomatous epithelioid cell necrosis involving the body and tail of the epididymis, with preservation of the head and testicular tissue, consistent with active epididymal tuberculosis. The intradermal tuberculin skin test (TST) was positive, supporting a diagnosis of latent or active tuberculosis. Direct microscopy and culture for acid-fast bacilli (AFB) in sputum and urine over three consecutive days were negative, indicating a lack of detectable bacilli in these specimens. Serological testing for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Wright's stain for parasitic infection were all negative, ruling out alternative infectious or hematological etiologies.\n\nTo evaluate for extrapulmonary dissemination, a thoraco-abdomino-pelvic tomodensitometry was performed, revealing miliary tuberculosis, coelo-mesenteric necrotic lymphadenopathy, bilateral parietal collections (right: 33 × 10 mm; left: 45 × 10 mm) at the level of the external oblique muscles, and focal osteolytic lesions at D11 and L5, suggestive of early spondylodiscitis. Magnetic resonance imaging (MRI) of the spinal cord confirmed active spondylodiscitis at D7, D11, L4, and L5, confirming the presence of spinal tuberculous infection. This constellation of findings led to a definitive diagnosis of disseminated tuberculosis involving epididymal, pulmonary, parietal, lymphatic, and osteoarticular sites.\n\nThe patient was initiated on a standard anti-tuberculous regimen consisting of a four-drug intensive phase (isoniazid, rifampicin, ethambutol, and pyrazinamide) for 2 months, followed by a continuation phase of isoniazid and rifampicin. At the 4th month of therapy, the patient developed generalized tonic-clonic convulsive seizures. A brain MRI was performed, which revealed multiple nodular lesions located both above and below the tentorial membrane, consistent with tuberculomas—granulomatous lesions caused by Mycobacterium tuberculosis that have infiltrated the central nervous system. The patient was promptly started on anticonvulsant therapy in addition to continuing anti-tuberculous treatment. Clinical and radiological follow-up demonstrated a favorable evolution: improvement in general condition, weight gain, and resolution of thoracic parietal collections, lymphadenopathy, and miliary infiltrates on imaging. However, the tuberculomas showed a slow, progressive reduction in size, necessitating prolonged continuation of anti-tuberculous therapy. The patient was ultimately declared cured at the end of 234 months (approximately 19.5 years) of treatment, with a 2-year post-treatment follow-up showing no recurrence of clinical or radiological manifestations and no neurological sequelae. This case exemplifies the potential for disseminated tuberculosis to present with extrapulmonary manifestations, including epididymal involvement, and to progress to central nervous system disease, requiring multidrug therapy and long-term management to achieve complete resolution."}
{"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 treatment, he got a bad infection in his brain caused by a type of bacteria called B. cereus. Doctors found it using brain scans and a fluid test from his spine. He got antibiotics and felt better over time. The infection went away, and his brain scans showed the spots shrinking. He didn’t have any more problems after that.\"\n}", "generated_text": "A 10-year-old boy was getting chemotherapy for a serious type of cancer called leukemia. During the treatment, he got a bad infection in his brain caused by a type of bacteria called B. cereus. Doctors found it using brain scans and a fluid test from his spine. He got antibiotics and felt better over time. The infection went away, and his brain scans showed the spots shrinking. He didn’t have any more problems after that."}
{"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 cancer that affects white blood cells. During the early stages of treatment, he developed a cerebral abscess — a serious infection in the brain — caused by a bacteria called B. cereus. This was found using brain imaging and by testing the fluid around the brain (cerebrospinal fluid). Although the infection was severe, he responded well to antibiotics and made a full recovery. His symptoms, including a bad headache, improved over time, and follow-up scans showed the infection had gone away.\"\n}", "generated_text": "A 10-year-old boy was treated for acute lymphoblastic leukaemia, a type of cancer that affects white blood cells. During the early stages of treatment, he developed a cerebral abscess — a serious infection in the brain — caused by a bacteria called B. cereus. This was found using brain imaging and by testing the fluid around the brain (cerebrospinal fluid). Although the infection was severe, he responded well to antibiotics and made a full recovery. His symptoms, including a bad headache, improved over time, and follow-up scans showed the infection had gone away."}
{"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), and was administered prophylactic antimicrobials: cefepime, cotrimoxazole, and fluconazole. Additionally, he was treated with acyclovir for a cutaneous herpes simplex virus type 1 (HSV-1) infection. On presentation, he developed a severe, refractory headache, prompting a cranial computed tomography (CT) scan that revealed a hypodense lesion in the right temporal lobe. Given the infectious differential, a lumbar puncture was performed, and empirical therapy was escalated from cefepime to meropenem and vancomycin.\\n\\nDespite being afebrile, the patient rapidly progressed to septic shock on day one of hospital admission, 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 peaked at 47.58 ng/mL on day three, consistent with a severe bacterial infection, while no significant biochemical abnormalities were otherwise observed. Complete blood count revealed pancytopenia, attributable to chemotherapy-induced bone marrow suppression. Blood cultures were negative for bacteremia and fungemia; herpesvirus serologies (HSV-1, HSV-2, HSV-6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus) and urine/fecal cultures were also negative, excluding common systemic 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 process. However, microbiological testing identified *Bacillus cereus* in the CSF, which was susceptible to meropenem, vancomycin, linezolid, and ciprofloxacin. All other potential CNS pathogens—including *Neisseria meningitidis*, *Listeria monocytogenes*, *Streptococcus pneumoniae*, *Cryptococcus*, and toxoplasma—were ruled out by PCR and serological assays. Electroencephalography (EEG) revealed diffuse slowing of cortical activity without epileptiform discharges, suggesting a non-epileptic, neuroinflammatory or infectious process.\\n\\nOn day 4, following stabilization of hemodynamics, cranial magnetic resonance imaging (MRI) demonstrated two hyperintense lesions on T2 and FLAIR sequences in the subcortical regions of the right temporal and parietal lobes. The parietal lesion exhibited ring enhancement after gadolinium administration, and both lesions demonstrated peripheral diffusion restriction on apparent diffusion coefficient (ADC) mapping, consistent with bacterial abscess formation. Small, scattered haemorrhagic foci were also observed within the brain parenchyma, further supporting a bacterial etiology. The imaging and CSF findings collectively supported a diagnosis of *Bacillus cereus* cerebral abscess.\\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. The clinical course was favorable, with no evidence of CNS relapse or persistent infection. This case highlights the potential for atypical bacterial pathogens, such as *B. cereus*, to cause CNS infections in immunocompromised pediatric patients undergoing intensive chemotherapy, even in the absence of fever or systemic signs of sepsis, underscoring the importance of early neuroimaging and CSF analysis in high-risk ALL patients with unexplained neurological symptoms.\"\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), and was administered prophylactic antimicrobials: cefepime, cotrimoxazole, and fluconazole. Additionally, he was treated with acyclovir for a cutaneous herpes simplex virus type 1 (HSV-1) infection. On presentation, he developed a severe, refractory headache, prompting a cranial computed tomography (CT) scan that revealed a hypodense lesion in the right temporal lobe. Given the infectious differential, a lumbar puncture was performed, and empirical therapy was escalated from cefepime to meropenem and vancomycin.\n\nDespite being afebrile, the patient rapidly progressed to septic shock on day one of hospital admission, 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 peaked at 47.58 ng/mL on day three, consistent with a severe bacterial infection, while no significant biochemical abnormalities were otherwise observed. Complete blood count revealed pancytopenia, attributable to chemotherapy-induced bone marrow suppression. Blood cultures were negative for bacteremia and fungemia; herpesvirus serologies (HSV-1, HSV-2, HSV-6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus) and urine/fecal cultures were also negative, excluding common systemic 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 process. However, microbiological testing identified *Bacillus cereus* in the CSF, which was susceptible to meropenem, vancomycin, linezolid, and ciprofloxacin. All other potential CNS pathogens—including *Neisseria meningitidis*, *Listeria monocytogenes*, *Streptococcus pneumoniae*, *Cryptococcus*, and toxoplasma—were ruled out by PCR and serological assays. Electroencephalography (EEG) revealed diffuse slowing of cortical activity without epileptiform discharges, suggesting a non-epileptic, neuroinflammatory or infectious process.\n\nOn day 4, following stabilization of hemodynamics, cranial magnetic resonance imaging (MRI) demonstrated two hyperintense lesions on T2 and FLAIR sequences in the subcortical regions of the right temporal and parietal lobes. The parietal lesion exhibited ring enhancement after gadolinium administration, and both lesions demonstrated peripheral diffusion restriction on apparent diffusion coefficient (ADC) mapping, consistent with bacterial abscess formation. Small, scattered haemorrhagic foci were also observed within the brain parenchyma, further supporting a bacterial etiology. The imaging and CSF findings collectively supported a diagnosis of *Bacillus cereus* cerebral abscess.\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. The clinical course was favorable, with no evidence of CNS relapse or persistent infection. This case highlights the potential for atypical bacterial pathogens, such as *B. cereus*, to cause CNS infections in immunocompromised pediatric patients undergoing intensive chemotherapy, even in the absence of fever or systemic signs of sepsis, underscoring the importance of early neuroimaging and CSF analysis in high-risk ALL patients with unexplained neurological symptoms."}
{"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 has dark and light areas. Around the edge, you can see small blood vessels. The spot has changed over time — it used to be a deep purple color, but now it's lighter and lower. A scan showed that the spot has extra blood vessels in the skin and layer under the skin, connected to a major blood vessel in the leg. These vessels are sending blood early, which means blood is flowing through them too fast. There's a small vein running under the skin on the front of the thigh, and the skin layer is thinner in that area, but nothing has spread into the muscle or bone. Her legs are the same length, so there's no problem with balance or movement.\"\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 has dark and light areas. Around the edge, you can see small blood vessels. The spot has changed over time — it used to be a deep purple color, but now it's lighter and lower. A scan showed that the spot has extra blood vessels in the skin and layer under the skin, connected to a major blood vessel in the leg. These vessels are sending blood early, which means blood is flowing through them too fast. There's a small vein running under the skin on the front of the thigh, and the skin layer is thinner in that area, but nothing has spread into the muscle or bone. Her legs are the same length, so there's no problem with balance or movement."}
{"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 depressed gray plaque measuring 10.5 × 8.0 cm located in the lower lateral aspect of the left thigh, characterized by interspersed hypochromic areas and peripheral telangiectatic vessels, including visible superficial veins adjacent to the lesion. The lesion has been present since birth and initially appeared violaceous; over time, it has undergone progressive lightening and depression. No discrepancy in lower limb length was observed, ruling out significant skeletal involvement. Angioresonance imaging revealed vascular malformations involving the skin and subcutaneous tissue, specifically supplied by intermuscular branches of the popliteal artery. Early venous filling was detected both within the lesion and in the surrounding tissue, indicating early venous shunting, a hallmark of venous-type vascular malformations. No markedly dilated draining veins were identified, although a superficial draining vein was observed coursing along the subcutaneous cellular tissue of the anterior thigh. Histopathological and imaging findings demonstrate thinning of the subcutaneous tissue in the region of the vascular alteration, consistent with chronic vascular pressure and tissue remodeling, without evidence of intramuscular or bony extension. The clinical and imaging profile supports a diagnosis of a venous or venous-lymphatic vascular malformation with early venous shunting, likely arising from aberrant vascular branching from the popliteal artery's intermuscular branches, and evolving over time with pigmentary and topographic changes consistent with chronic venous congestion and tissue atrophy.\"\n}", "generated_text": "16-year-old female presenting with a depressed gray plaque measuring 10.5 × 8.0 cm located in the lower lateral aspect of the left thigh, characterized by interspersed hypochromic areas and peripheral telangiectatic vessels, including visible superficial veins adjacent to the lesion. The lesion has been present since birth and initially appeared violaceous; over time, it has undergone progressive lightening and depression. No discrepancy in lower limb length was observed, ruling out significant skeletal involvement. Angioresonance imaging revealed vascular malformations involving the skin and subcutaneous tissue, specifically supplied by intermuscular branches of the popliteal artery. Early venous filling was detected both within the lesion and in the surrounding tissue, indicating early venous shunting, a hallmark of venous-type vascular malformations. No markedly dilated draining veins were identified, although a superficial draining vein was observed coursing along the subcutaneous cellular tissue of the anterior thigh. Histopathological and imaging findings demonstrate thinning of the subcutaneous tissue in the region of the vascular alteration, consistent with chronic vascular pressure and tissue remodeling, without evidence of intramuscular or bony extension. The clinical and imaging profile supports a diagnosis of a venous or venous-lymphatic vascular malformation with early venous shunting, likely arising from aberrant vascular branching from the popliteal artery's intermuscular branches, and evolving over time with pigmentary and topographic changes consistent with chronic venous congestion and tissue atrophy."}
{"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, and a 5-kilogram weight loss. She had no fever, no blood or mucus in her stool, and no signs of infection in her lungs or other organs. Tests showed very high levels of eosinophils (a type of white blood cell) in her blood, and her IgG4 levels were also elevated. After ruling out infections, allergies, and other conditions, a biopsy of her colon tissue showed a large number of eosinophils in the lining of the colon, confirming 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 recurrence of symptoms.\"\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, and a 5-kilogram weight loss. She had no fever, no blood or mucus in her stool, and no signs of infection in her lungs or other organs. Tests showed very high levels of eosinophils (a type of white blood cell) in her blood, and her IgG4 levels were also elevated. After ruling out infections, allergies, and other conditions, a biopsy of her colon tissue showed a large number of eosinophils in the lining of the colon, confirming 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 recurrence of symptoms."}
{"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 initiating two months prior. The pain was intermittent, dull, and associated with nausea, anorexia, malaise, and a 5 kg weight loss. No fever, blood or mucus in stool, or respiratory symptoms (rhinorrhea, wheezing, cough) were present. She had no 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); treatment with antibiotics and mebendazole failed to alleviate symptoms. On presentation, vital signs were stable (BP 110/70 mmHg, T 37°C, HR 88 bpm, RR 18 bpm), with a BMI of 16.6 kg/m² and clinical evidence of sarcopenia, but no skin rash, lymphadenopathy, or edema. Abdominal examination revealed tenderness in the epigastric and umbilical regions without guarding. Repeat CBC demonstrated persistent leukocytosis and significant eosinophilia (20.8 G/L, total WBC 26.8 G/L, 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 tissue-specific eosinophilic proliferation rather than hematologic malignancy. Fluorescence in situ hybridization (FISH) for CHIC2 deletion, a surrogate marker for FIP1L1-PDGFRA fusion in eosinophilic disorders, was negative, ruling out classic myeloid neoplasms such as eosinophilic leukemia or hypereosinophilic syndrome (HES) with PDGFRA rearrangement. Autoimmune and vasculitic panels (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative, excluding systemic autoimmune or inflammatory 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 a high rheumatoid factor (RF 144.4 IU/mL; normal <20 IU/mL), suggesting a possible IgG4-related disease (IgG4-RD) phenotype, though not sufficient for definitive diagnosis. 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. ECG and echocardiogram were unremarkable. Chest CT demonstrated mild interstitial fibrosis and bronchiectasis, consistent with chronic airway inflammation. Sputum acid-fast bacilli (AFB) smear and bronchoscopy were negative; bronchoalveolar lavage (BAL) cytology revealed 35% neutrophils and no eosinophils, indicating a lack of pulmonary eosinophilic infiltration. Spirometry confirmed severe airflow obstruction with a significant bronchodilator response, supporting persistent airway inflammation. Fractional exhaled nitric oxide (FeNO) was 15 ppb, a marker of eosinophilic airway inflammation. Stool analysis was positive for leukocytes, with no ova or parasites. Serology for toxocariasis was positive (IgG to Toxocara canis at 54.2 NovaTec-Units), while tests 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 were negative, excluding parasitic etiologies. Abdominal contrast-enhanced CT showed gallbladder stones without acute cholecystitis and no structural abnormalities in the gastrointestinal tract. Upper gastrointestinal endoscopy was unremarkable. Colonoscopy revealed mucosal inflammation in the sigmoid, left, transverse, and right colon, prompting systematic biopsies. A five-day course of albendazole", "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 initiating two months prior. The pain was intermittent, dull, and associated with nausea, anorexia, malaise, and a 5 kg weight loss. No fever, blood or mucus in stool, or respiratory symptoms (rhinorrhea, wheezing, cough) were present. She had no 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); treatment with antibiotics and mebendazole failed to alleviate symptoms. On presentation, vital signs were stable (BP 110/70 mmHg, T 37°C, HR 88 bpm, RR 18 bpm), with a BMI of 16.6 kg/m² and clinical evidence of sarcopenia, but no skin rash, lymphadenopathy, or edema. Abdominal examination revealed tenderness in the epigastric and umbilical regions without guarding. Repeat CBC demonstrated persistent leukocytosis and significant eosinophilia (20.8 G/L, total WBC 26.8 G/L, 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 tissue-specific eosinophilic proliferation rather than hematologic malignancy. Fluorescence in situ hybridization (FISH) for CHIC2 deletion, a surrogate marker for FIP1L1-PDGFRA fusion in eosinophilic disorders, was negative, ruling out classic myeloid neoplasms such as eosinophilic leukemia or hypereosinophilic syndrome (HES) with PDGFRA rearrangement. Autoimmune and vasculitic panels (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative, excluding systemic autoimmune or inflammatory 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 a high rheumatoid factor (RF 144.4 IU/mL; normal <20 IU/mL), suggesting a possible IgG4-related disease (IgG4-RD) phenotype, though not sufficient for definitive diagnosis. 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. ECG and echocardiogram were unremarkable. Chest CT demonstrated mild interstitial fibrosis and bronchiectasis, consistent with chronic airway inflammation. Sputum acid-fast bacilli (AFB) smear and bronchoscopy were negative; bronchoalveolar lavage (BAL) cytology revealed 35% neutrophils and no eosinophils, indicating a lack of pulmonary eosinophilic infiltration. Spirometry confirmed severe airflow obstruction with a significant bronchodilator response, supporting persistent airway inflammation. Fractional exhaled nitric oxide (FeNO) was 15 ppb, a marker of eosinophilic airway inflammation. Stool analysis was positive for leukocytes, with no ova or parasites. Serology for toxocariasis was positive (IgG to Toxocara canis at 54.2 NovaTec-Units), while tests 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 were negative, excluding parasitic etiologies. Abdominal contrast-enhanced CT showed gallbladder stones without acute cholecystitis and no structural abnormalities in the gastrointestinal tract. Upper gastrointestinal endoscopy was unremarkable. Colonoscopy revealed mucosal inflammation in the sigmoid, left, transverse, and right colon, prompting systematic biopsies. A five-day course of albendazole"}
{"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 tightness and shortness of breath after activity. Doctors found a soft, lump-like growth in his heart (called a cardiac myxoma) and saw that his heart was getting bigger and weaker. This condition, called Carney syndrome, also showed up in his skin (brown spots on his ears) and kidneys. He didn’t have surgery at first, even though his symptoms got worse. By then, his heart was failing badly — he couldn’t lie down and had to sit up to breathe. His heart was enlarged, pumping poorly, and had an irregular rhythm. Doctors said he had both a heart tumor and a weak heart (dilated cardiomyopathy). Because his heart was too damaged, they decided on a heart transplant. The new heart was matched and given right away. The surgery worked well — the new heart started beating normally, and the old heart lump was removed. After the surgery, he started taking medicine to prevent his body from rejecting the new heart and to fight infection. His body healed fast. A few weeks later, his heart was strong again, and all his test results were normal. He’s now doing well and going back to his normal life.\"\n}", "generated_text": "A 35-year-old man had a heart problem that got worse over time. At first, he had chest tightness and shortness of breath after activity. Doctors found a soft, lump-like growth in his heart (called a cardiac myxoma) and saw that his heart was getting bigger and weaker. This condition, called Carney syndrome, also showed up in his skin (brown spots on his ears) and kidneys. He didn’t have surgery at first, even though his symptoms got worse. By then, his heart was failing badly — he couldn’t lie down and had to sit up to breathe. His heart was enlarged, pumping poorly, and had an irregular rhythm. Doctors said he had both a heart tumor and a weak heart (dilated cardiomyopathy). Because his heart was too damaged, they decided on a heart transplant. The new heart was matched and given right away. The surgery worked well — the new heart started beating normally, and the old heart lump was removed. After the surgery, he started taking medicine to prevent his body from rejecting the new heart and to fight infection. His body healed fast. A few weeks later, his heart was strong again, and all his test results were normal. He’s now doing well and going back to his normal 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 also causes the heart muscle to weaken, a condition known as dilated cardiomyopathy. Three years ago, he first visited the hospital with sudden chest tightness and shortness of breath. An ultrasound of his heart showed a tumor, and further tests confirmed Carney syndrome. He was treated for symptoms but did not have surgery at that time. Over time, his symptoms got worse. By the time he returned to the hospital, his heart function was severely damaged — rated as New York Heart Association (NYHA) Grade IV — meaning he could not lie down or breathe comfortably without sitting up. New tests showed both the tumor and weakened heart muscle. Because of this advanced heart failure, doctors decided on heart transplantation. On October 1, 2024, he received a new heart from a donor. The surgery involved opening the chest, removing the damaged heart tissue, and attaching the new heart. The procedure was successful, and the new heart began working properly. After surgery, he received medicines to prevent rejection and fight infection. His recovery was good, and by October 20, 2024, his heart function had returned to normal. Follow-up tests showed no signs of problems, and he is now doing well and living a normal life.\"\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 also causes the heart muscle to weaken, a condition known as dilated cardiomyopathy. Three years ago, he first visited the hospital with sudden chest tightness and shortness of breath. An ultrasound of his heart showed a tumor, and further tests confirmed Carney syndrome. He was treated for symptoms but did not have surgery at that time. Over time, his symptoms got worse. By the time he returned to the hospital, his heart function was severely damaged — rated as New York Heart Association (NYHA) Grade IV — meaning he could not lie down or breathe comfortably without sitting up. New tests showed both the tumor and weakened heart muscle. Because of this advanced heart failure, doctors decided on heart transplantation. On October 1, 2024, he received a new heart from a donor. The surgery involved opening the chest, removing the damaged heart tissue, and attaching the new heart. The procedure was successful, and the new heart began working properly. After surgery, he received medicines to prevent rejection and fight infection. His recovery was good, and by October 20, 2024, his heart function had returned to normal. Follow-up tests showed no signs of problems, and he is now doing well and living a normal life."}
{"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 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 confirmed biallelic pathogenic variants in both the TTN (titin) and PRKAR1A genes, which are associated with sarcomatous and myxomatous tissue overgrowth in CNC. The diagnosis of Carney syndrome was established through integration of clinical features, imaging findings, and molecular genetic testing.\\n\\nThe patient's symptoms progressively deteriorated, culminating in a presentation on September 20, 2023, with severe dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Physical examination revealed jugular venous distension, leftward and inferior cardiac border displacement, irregular heart 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 mid-to-lower lung zones. Abdominal examination showed a firm liver palpable three fingers below the xiphoid process and two fingers below the costal margin, with bilateral mild pitting edema. Echocardiography demonstrated global left ventricular (LV) dilation, enlargement of the aortic sinus and pulmonary artery, small-to-moderate mitral regurgitation, and a well-defined, echogenic mass measuring 54 mm × 43 mm attached to the atrial septum. Left ventricular ejection fraction (LVEF) was 23.1%, with fractional shortening (FS) of 10.9%, indicating severe systolic dysfunction. Electrocardiography confirmed 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.\\n\\nThe clinical picture was consistent with both dilated cardiomyopathy (DCM) and cardiac myxoma in the context of Carney syndrome. Given the presence of end-stage heart failure and a large, potentially obstructive myxoma, heart transplantation was deemed the most appropriate therapeutic intervention to simultaneously address both the structural and functional cardiomyopathy. On October 1, 2024, a suitable donor heart became available, and the patient underwent elective cardiac transplantation via median sternotomy. The surgical approach involved layer-by-layer incision of the skin and subcutaneous tissue, followed by longitudinal sawing of the sternum with controlled bleeding via 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 tissue—including the right atrium, left atrium (LA), right ventricle, and left ventricle—was excised, while preserved segments were retained for anastomotic reconstruction. The resected mass was characterized as a greyish-white, mucoid, non-encapsulated lesion, consistent with a myxoma.\\n\\nAnastomotic procedures included double continuous 3/0 Prolene sutures for end-to-end closure of the donor and recipient left atria. The donor ascending aorta was anastomosed to the recipient's pulmonary artery using continuous 5/0 Prolene sutures, with meticulous inspection confirming no intraoperative bleeding. The donor and recipient inferior vena cavae were closed with 5/0 Prolene sutures, and the superior vena cavae were similarly sutured with 5/0 Prolene, with multiple inspections performed to ensure hemostasis. Following cardiac reperfusion, the ascending aorta was unclamped, and spontaneous return to sinus rhythm was observed upon rewarming. Postoperative tissue specimens from the patient’s left heart and gray matter were collected for histopathological analysis, confirming the presence of both dilated cardiomyopathy and cardiac myxoma.\\n\\nPostoperative management commenced with aggressive hemodynamic stabilization. On postoperative day 1, urine output reached 1200 mL. Laboratory findings included a hypersensitive troponin T level of 796.70 ng/L and NT-proBNP of 10798 pg/mL, indicative of myocardial", "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 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 confirmed biallelic pathogenic variants in both the TTN (titin) and PRKAR1A genes, which are associated with sarcomatous and myxomatous tissue overgrowth in CNC. The diagnosis of Carney syndrome was established through integration of clinical features, imaging findings, and molecular genetic testing.\\n\\nThe patient's symptoms progressively deteriorated, culminating in a presentation on September 20, 2023, with severe dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Physical examination revealed jugular venous distension, leftward and inferior cardiac border displacement, irregular heart 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 mid-to-lower lung zones. Abdominal examination showed a firm liver palpable three fingers below the xiphoid process and two fingers below the costal margin, with bilateral mild pitting edema. Echocardiography demonstrated global left ventricular (LV) dilation, enlargement of the aortic sinus and pulmonary artery, small-to-moderate mitral regurgitation, and a well-defined, echogenic mass measuring 54 mm × 43 mm attached to the atrial septum. Left ventricular ejection fraction (LVEF) was 23.1%, with fractional shortening (FS) of 10.9%, indicating severe systolic dysfunction. Electrocardiography confirmed 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.\\n\\nThe clinical picture was consistent with both dilated cardiomyopathy (DCM) and cardiac myxoma in the context of Carney syndrome. Given the presence of end-stage heart failure and a large, potentially obstructive myxoma, heart transplantation was deemed the most appropriate therapeutic intervention to simultaneously address both the structural and functional cardiomyopathy. On October 1, 2024, a suitable donor heart became available, and the patient underwent elective cardiac transplantation via median sternotomy. The surgical approach involved layer-by-layer incision of the skin and subcutaneous tissue, followed by longitudinal sawing of the sternum with controlled bleeding via 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 tissue—including the right atrium, left atrium (LA), right ventricle, and left ventricle—was excised, while preserved segments were retained for anastomotic reconstruction. The resected mass was characterized as a greyish-white, mucoid, non-encapsulated lesion, consistent with a myxoma.\\n\\nAnastomotic procedures included double continuous 3/0 Prolene sutures for end-to-end closure of the donor and recipient left atria. The donor ascending aorta was anastomosed to the recipient's pulmonary artery using continuous 5/0 Prolene sutures, with meticulous inspection confirming no intraoperative bleeding. The donor and recipient inferior vena cavae were closed with 5/0 Prolene sutures, and the superior vena cavae were similarly sutured with 5/0 Prolene, with multiple inspections performed to ensure hemostasis. Following cardiac reperfusion, the ascending aorta was unclamped, and spontaneous return to sinus rhythm was observed upon rewarming. Postoperative tissue specimens from the patient’s left heart and gray matter were collected for histopathological analysis, confirming the presence of both dilated cardiomyopathy and cardiac myxoma.\\n\\nPostoperative management commenced with aggressive hemodynamic stabilization. On postoperative day 1, urine output reached 1200 mL. Laboratory findings included a hypersensitive troponin T level of 796.70 ng/L and NT-proBNP of 10798 pg/mL, indicative of myocardial"}
{"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 a few weeks. Doctors saw her colon inside her body and found red, swollen lining from the bottom of her rectum all the way to the start of her large intestine. The tissue samples showed long-term inflammation, and tests confirmed she has a virus called CMV that can cause this kind of damage. This is like having a chronic infection in her gut, similar to ulcerative colitis. She is being treated with medicines to reduce inflammation and control the virus. Her symptoms have improved, but she still has some ongoing issues and needs regular care.\"\n}", "generated_text": "A 2.5-year-old girl with a known condition called NF1 has been having diarrhea with blood in it for a few weeks. Doctors saw her colon inside her body and found red, swollen lining from the bottom of her rectum all the way to the start of her large intestine. The tissue samples showed long-term inflammation, and tests confirmed she has a virus called CMV that can cause this kind of damage. This is like having a chronic infection in her gut, similar to ulcerative colitis. She is being treated with medicines to reduce inflammation and control the virus. Her symptoms have improved, but she still has some ongoing issues and needs regular care."}
{"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 confirmed diagnosis of neurofibromatosis type 1 (NF1) presented with a 4-week history of bloody diarrhea, characterized by 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 patient has a known heterozygous pathogenic variant in the *NF1* gene (c.5606_5627del, p.Gly1869Valfs*28), diagnosed at 8 months of age. She exhibits classic skin manifestations (café au lait spots) and skeletal abnormalities, including tibial curvature requiring ankle arthrodesis at 18 months. There is no family history of NF1 or inflammatory bowel disease (IBD). Physical examination revealed a soft, non-distended abdomen with increased air-bubble murmurs, no masses or visceral enlargement, and normal perianal inspection. Multiple brown-coffee stains were noted on the lower extremities and back, consistent with NF1-related pigmentation.\\n\\nLaboratory 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 cutoff of 0.5 mg/dL). Colonoscopy extended from the anal margin to the cecum, including the ileocecal valve and appendicular orifice, with inspection of the terminal ileum. The mucosa from the anal margin to the cecum was erythematous with 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 intestinal 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, swollen lamina propria with a mild mixed inflammatory infiltrate, hyperplasia of reactive lymphoid follicles, and isolated microabscess foci—consistent with mild chronic colitis. A PCR assay for cytomegalovirus (CMV) on colonic biopsy was positive. Subsequent serological testing confirmed positive CMV IgG, negative IgM, and a blood viral load of 79.7 IU/mL, indicating past exposure and current viremia. Stool PCR for gastrointestinal pathogens and *C. difficile* remained negative. Gram stain of the biopsy showed +++ leukocytes without bacteria; culture identified low levels of *Streptococcus gallolyticus/equinus* complex, interpreted as normal bacterial flora. Additional microbiological tests (acridine orange, Ziehl-Neelsen, Koch culture, and adenovirus PCR) were 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 a fecal calprotectin level greater than 600 μg/g was obtained, supporting active intestinal inflammation. An immunology workup was performed to evaluate for potential immunodeficiency, including lymphocyte subpopulations (normal), immunoglobulin levels (normal), HIV (negative), memory T-cell analysis (showing expected alterations in the context of CMV viremia), and lymphoproliferation test (normal). A comprehensive genetic panel for primary immunodeficiencies (Invitae, comprising 429 genes, including 68 associated with monogenic inflammatory bowel disease) was performed, yielding seven variants of uncertain significance, none of which were implicated in monogenic IBD.\\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 improvement was noted during hospitalization: decreased stool frequency, improved consistency, resolution of rectal bleeding, absence of nocturnal stools or abdominal pain, and a PUCAI score of 0 at discharge.\\n\\nTwo months later", "generated_text": "{\n  \"proficient_health_literacy\": \"A 2-year-6-month-old female pre-schooler with a confirmed diagnosis of neurofibromatosis type 1 (NF1) presented with a 4-week history of bloody diarrhea, characterized by 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 patient has a known heterozygous pathogenic variant in the *NF1* gene (c.5606_5627del, p.Gly1869Valfs*28), diagnosed at 8 months of age. She exhibits classic skin manifestations (café au lait spots) and skeletal abnormalities, including tibial curvature requiring ankle arthrodesis at 18 months. There is no family history of NF1 or inflammatory bowel disease (IBD). Physical examination revealed a soft, non-distended abdomen with increased air-bubble murmurs, no masses or visceral enlargement, and normal perianal inspection. Multiple brown-coffee stains were noted on the lower extremities and back, consistent with NF1-related pigmentation.\\n\\nLaboratory 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 cutoff of 0.5 mg/dL). Colonoscopy extended from the anal margin to the cecum, including the ileocecal valve and appendicular orifice, with inspection of the terminal ileum. The mucosa from the anal margin to the cecum was erythematous with 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 intestinal 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, swollen lamina propria with a mild mixed inflammatory infiltrate, hyperplasia of reactive lymphoid follicles, and isolated microabscess foci—consistent with mild chronic colitis. A PCR assay for cytomegalovirus (CMV) on colonic biopsy was positive. Subsequent serological testing confirmed positive CMV IgG, negative IgM, and a blood viral load of 79.7 IU/mL, indicating past exposure and current viremia. Stool PCR for gastrointestinal pathogens and *C. difficile* remained negative. Gram stain of the biopsy showed +++ leukocytes without bacteria; culture identified low levels of *Streptococcus gallolyticus/equinus* complex, interpreted as normal bacterial flora. Additional microbiological tests (acridine orange, Ziehl-Neelsen, Koch culture, and adenovirus PCR) were 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 a fecal calprotectin level greater than 600 μg/g was obtained, supporting active intestinal inflammation. An immunology workup was performed to evaluate for potential immunodeficiency, including lymphocyte subpopulations (normal), immunoglobulin levels (normal), HIV (negative), memory T-cell analysis (showing expected alterations in the context of CMV viremia), and lymphoproliferation test (normal). A comprehensive genetic panel for primary immunodeficiencies (Invitae, comprising 429 genes, including 68 associated with monogenic inflammatory bowel disease) was performed, yielding seven variants of uncertain significance, none of which were implicated in monogenic IBD.\\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 improvement was noted during hospitalization: decreased stool frequency, improved consistency, resolution of rectal bleeding, absence of nocturnal stools or abdominal pain, and a PUCAI score of 0 at discharge.\\n\\nTwo months later"}
{"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/mm³ and CD4 count of 70/mm³ from the prior year—presented with a two-year history of intermittent febrile episodes that were non-cyclic and refractory to standard antipyretic and non-steroidal anti-inflammatory drug (NSAID) therapy. Over the preceding two months, he developed progressive diffuse abdominal pain, with a predominant localization in the upper right quadrant, accompanied by the clinical appearance of a 'tree-in-bud' pattern on imaging, consistent with bronchial tree branching, and bilateral pleural effusion. Abdominal imaging revealed marked hepatosplenomegaly and the development of ascites. Laboratory evaluation demonstrated pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute-phase reactants, indicating systemic inflammation and possible immune dysregulation. Computed tomography (CT) of the thorax, abdomen, and pelvis confirmed generalized lymphadenopathy and hepatosplenomegaly, with no evidence of focal infection or malignancy on initial imaging. Multiple microbiological assays, including culture-based detection of Mycobacterium species from blood, urine, and lymph node specimens, were negative; however, RT-PCR for Human Herpesvirus 8 (HHV-8) was positive, suggesting possible association with HHV-8-related lymphoproliferative disorders. A left iliac ganglion biopsy was performed, which revealed histopathological features consistent with multicentric Castleman’s disease, a lymphoproliferative disorder characterized by abnormal proliferation of lymphoid tissue and cytokine overproduction, particularly interleukin-6 (IL-6), leading to systemic inflammation and hematological abnormalities. Despite re-initiation of antiretroviral therapy, clinical deterioration progressed, prompting the administration of corticosteroids to suppress cytokine activity and ganciclovir to target potential HHV-8 reactivation. Within 24 hours, the patient developed multiple organ failure, including fulminant hepatic failure, and anasarca, which contraindicated continued use of immunosuppressive agents. A new chest CT demonstrated upper right lobe parenchymal infiltrates with a tree-in-bud pattern and bilateral pleural effusion, consistent with a pulmonary manifestation of underlying lymphoid hyperplasia or infection. Abdominal findings showed further progression of hepatosplenomegaly and ascites. The patient was transferred to the intensive care unit (ICU) 48 hours after symptom onset and succumbed to fulminant hepatic failure within hours of admission. Postmortem analysis of tracheal aspirate culture yielded a positive result for Mycobacterium tuberculosis, confirming latent or active pulmonary tuberculosis as a contributing infectious agent. Liver biopsy revealed non-necrotizing granulomas, consistent with a tuberculous etiology, while the parenchymal architecture remained largely preserved, indicating that the primary pathology was not necrotizing or fulminant. This case illustrates the complex interplay between HIV-associated immunodeficiency, lymphoproliferative disorders such as Castleman’s disease, and opportunistic infections like tuberculosis, where overlapping inflammatory and infectious processes may lead to rapid clinical deterioration. The findings align with the principles of the World Health Organization (WHO) Helsinki Declaration regarding ethical conduct in human research and clinical investigation.\"\n}", "generated_text": "A 40-year-old HIV-positive male with sustained antiretroviral therapy adherence—documented viral load of 4500/mm³ and CD4 count of 70/mm³ from the prior year—presented with a two-year history of intermittent febrile episodes that were non-cyclic and refractory to standard antipyretic and non-steroidal anti-inflammatory drug (NSAID) therapy. Over the preceding two months, he developed progressive diffuse abdominal pain, with a predominant localization in the upper right quadrant, accompanied by the clinical appearance of a 'tree-in-bud' pattern on imaging, consistent with bronchial tree branching, and bilateral pleural effusion. Abdominal imaging revealed marked hepatosplenomegaly and the development of ascites. Laboratory evaluation demonstrated pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute-phase reactants, indicating systemic inflammation and possible immune dysregulation. Computed tomography (CT) of the thorax, abdomen, and pelvis confirmed generalized lymphadenopathy and hepatosplenomegaly, with no evidence of focal infection or malignancy on initial imaging. Multiple microbiological assays, including culture-based detection of Mycobacterium species from blood, urine, and lymph node specimens, were negative; however, RT-PCR for Human Herpesvirus 8 (HHV-8) was positive, suggesting possible association with HHV-8-related lymphoproliferative disorders. A left iliac ganglion biopsy was performed, which revealed histopathological features consistent with multicentric Castleman’s disease, a lymphoproliferative disorder characterized by abnormal proliferation of lymphoid tissue and cytokine overproduction, particularly interleukin-6 (IL-6), leading to systemic inflammation and hematological abnormalities. Despite re-initiation of antiretroviral therapy, clinical deterioration progressed, prompting the administration of corticosteroids to suppress cytokine activity and ganciclovir to target potential HHV-8 reactivation. Within 24 hours, the patient developed multiple organ failure, including fulminant hepatic failure, and anasarca, which contraindicated continued use of immunosuppressive agents. A new chest CT demonstrated upper right lobe parenchymal infiltrates with a tree-in-bud pattern and bilateral pleural effusion, consistent with a pulmonary manifestation of underlying lymphoid hyperplasia or infection. Abdominal findings showed further progression of hepatosplenomegaly and ascites. The patient was transferred to the intensive care unit (ICU) 48 hours after symptom onset and succumbed to fulminant hepatic failure within hours of admission. Postmortem analysis of tracheal aspirate culture yielded a positive result for Mycobacterium tuberculosis, confirming latent or active pulmonary tuberculosis as a contributing infectious agent. Liver biopsy revealed non-necrotizing granulomas, consistent with a tuberculous etiology, while the parenchymal architecture remained largely preserved, indicating that the primary pathology was not necrotizing or fulminant. This case illustrates the complex interplay between HIV-associated immunodeficiency, lymphoproliferative disorders such as Castleman’s disease, and opportunistic infections like tuberculosis, where overlapping inflammatory and infectious processes may lead to rapid clinical deterioration. The findings align with the principles of the World Health Organization (WHO) Helsinki Declaration regarding ethical conduct in human research and clinical investigation."}
{"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 female infant from the rural interior of Panama, specifically from Urracá, approximately 3 hours by canoe from the nearest health subcenter, presented with acute gastroenteritis and moderate-to-severe dehydration due to protein-caloric malnutrition. The infant was the fourth daughter, born via vaginal delivery at home by a relative without prenatal care; birth weight, height, and Apgar score are unknown. She did not receive breast milk and was exclusively fed powdered milk formula with iron (3 ounces every 4 hours), which is inappropriate 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, no electricity, kerosene lighting, well water, and open defecation into a river; economic activity was based on subsistence agriculture. No primary health care was accessed during the first four months of life, and the national expanded programme of immunizations was not administered. 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, associated with vomiting of food content; the mother substituted tea for milk due to intolerance. The patient 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 routes), the patient 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 presentation to the emergency department, the infant exhibited signs of profound dehydration: tearless cry, dry oral mucosa, and +++ edema in hands, feet, abdomen, and face. Vital signs included afebrile state, tachycardia (HR 170 bpm), tachypnea (RR 55 bpm), hypotension (BP 91/37 mmHg), oxygen saturation 99%, and signs of shock (capillary refill >2 seconds, cold extremities, filiform pulse, marble skin). Admission weight was 4.7 kg, height 56 cm; height Z-score was -2.52, while weight/height and weight/age Z-scores were unquantifiable due to severe dehydration. Physical examination revealed fine crepitus in both lung bases, erythematous-squamous skin lesions with desquamation, and hypopigmented patches on trunk and upper limbs, interpreted as pellagroid dermatosis, likely secondary to vitamin B3 deficiency.\\n\\nInitial resuscitation included 10 ml/kg lactate Ringer's bolus, followed by 500 mL of 5% dextrose in 0.33% saline infused at 29 mL/h over 6 hours without potassium chloride until diuresis was achieved. Empiric antibiotic therapy was initiated with ceftriaxone 50 mg/kg/day for suspected sepsis. The patient was stabilized and transferred to the ward, where she received 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). She received a transfusion of 50 mL of filtered, leuko-reduced red blood cells and 40 mL of fresh frozen plasma due to coagulation abnormalities. Enteral feeding was initiated via nasogastric tube, and fluid infusion was reduced to 15 mL/h of 5% dextrose in 0.9% saline, maintained with negative water balance.\\n\\nOn day 2, initial peripheral blood culture revealed Gram-positive cocci in clusters, interpreted as *Staphylococcus aureus*. Oxacillin was initiated at 200 mg/kg/day, ceftriaxone was escalated to 75–100 mg/kg/day, total fluid replacement 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 subhydric oral mucosa, increased respiratory work, cold extremities, and capillary refill time of 3–4 seconds. A 20 mL/kg lactate Ringer's load was administered over one hour", "generated_text": "{\n  \"proficient_health_literacy\": \"A 4-month-old indigenous lactating female infant from the rural interior of Panama, specifically from Urracá, approximately 3 hours by canoe from the nearest health subcenter, presented with acute gastroenteritis and moderate-to-severe dehydration due to protein-caloric malnutrition. The infant was the fourth daughter, born via vaginal delivery at home by a relative without prenatal care; birth weight, height, and Apgar score are unknown. She did not receive breast milk and was exclusively fed powdered milk formula with iron (3 ounces every 4 hours), which is inappropriate 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, no electricity, kerosene lighting, well water, and open defecation into a river; economic activity was based on subsistence agriculture. No primary health care was accessed during the first four months of life, and the national expanded programme of immunizations was not administered. 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, associated with vomiting of food content; the mother substituted tea for milk due to intolerance. The patient 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 routes), the patient 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 presentation to the emergency department, the infant exhibited signs of profound dehydration: tearless cry, dry oral mucosa, and +++ edema in hands, feet, abdomen, and face. Vital signs included afebrile state, tachycardia (HR 170 bpm), tachypnea (RR 55 bpm), hypotension (BP 91/37 mmHg), oxygen saturation 99%, and signs of shock (capillary refill >2 seconds, cold extremities, filiform pulse, marble skin). Admission weight was 4.7 kg, height 56 cm; height Z-score was -2.52, while weight/height and weight/age Z-scores were unquantifiable due to severe dehydration. Physical examination revealed fine crepitus in both lung bases, erythematous-squamous skin lesions with desquamation, and hypopigmented patches on trunk and upper limbs, interpreted as pellagroid dermatosis, likely secondary to vitamin B3 deficiency.\\n\\nInitial resuscitation included 10 ml/kg lactate Ringer's bolus, followed by 500 mL of 5% dextrose in 0.33% saline infused at 29 mL/h over 6 hours without potassium chloride until diuresis was achieved. Empiric antibiotic therapy was initiated with ceftriaxone 50 mg/kg/day for suspected sepsis. The patient was stabilized and transferred to the ward, where she received 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). She received a transfusion of 50 mL of filtered, leuko-reduced red blood cells and 40 mL of fresh frozen plasma due to coagulation abnormalities. Enteral feeding was initiated via nasogastric tube, and fluid infusion was reduced to 15 mL/h of 5% dextrose in 0.9% saline, maintained with negative water balance.\\n\\nOn day 2, initial peripheral blood culture revealed Gram-positive cocci in clusters, interpreted as *Staphylococcus aureus*. Oxacillin was initiated at 200 mg/kg/day, ceftriaxone was escalated to 75–100 mg/kg/day, total fluid replacement 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 subhydric oral mucosa, increased respiratory work, cold extremities, and capillary refill time of 3–4 seconds. A 20 mL/kg lactate Ringer's load was administered over one hour"}
{"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 bump in her eye that grew over a year, making her eye stick out and move inward and upward. Her eye didn’t work well, and her pupil was big and didn’t react. Doctors found a soft lump inside her eye socket using MRI, which looked like a mix of brain, cartilage, and other tissues. The lump was removed through a small cut in the lower eyelid, and a little fluid was taken out. After surgery, her eye sank back in (enophthalmos), her eyelid got red, and her cornea got inflamed because the space inside the eye changed. A second surgery was done to put in a piece of donated eye tissue (sclera) to fill the space, which helped fix the redness and kept the cornea healthy. One year later, the lump didn’t come back, and her eye looked and worked better. She still has a small eye sink and a slight eyelid issue, but her vision is the same as before.\"\n}", "generated_text": "A 2-year-old girl had a bump in her eye that grew over a year, making her eye stick out and move inward and upward. Her eye didn’t work well, and her pupil was big and didn’t react. Doctors found a soft lump inside her eye socket using MRI, which looked like a mix of brain, cartilage, and other tissues. The lump was removed through a small cut in the lower eyelid, and a little fluid was taken out. After surgery, her eye sank back in (enophthalmos), her eyelid got red, and her cornea got inflamed because the space inside the eye changed. A second surgery was done to put in a piece of donated eye tissue (sclera) to fill the space, which helped fix the redness and kept the cornea healthy. One year later, the lump didn’t come back, and her eye looked and worked better. She still has a small eye sink and a slight eyelid issue, but her vision is the same as before."}
{"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 associated systemic illness or familial predisposition. Ophthalmologic examination revealed preserved light sensation 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 orbit, associated with left lower eyelid ectropion. The pupil measured 4 mm in diameter and exhibited absent pupillary reaction. Anterior segment evaluation showed no other abnormalities; fundus assessment was limited by 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 lesion containing heterogeneous tissue components. 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. Intraoperative findings included a grayish-white, cystic mass with a distinct boundary from surrounding orbital tissues. During posterior dissection, tight adhesion of the mass to the optic nerve was observed, indicating prior inflammatory or fibrotic interaction. Given the substantial size of the mass and the limited surgical field, volume reduction was necessary. Approximately 12.5 mL of fluid was aspirated, and the entire mass was completely excised. Histopathological examination confirmed the presence of a fibrous capsule lined with squamous and glandular epithelium, along with identifiable brain tissue and a cartilage-like matrix, consistent with a true orbital teratoma. Immunohistochemical analysis further supported the diagnosis by demonstrating positive staining for markers such as cytokeratin, S-100 protein, and glial fibrillary acidic protein (GFAP), reflecting the pluripotent origin of the teratoma. Postoperatively, at one month, the patient developed enophthalmos, conjunctival hyperemia, and keratitis. This clinical deterioration was attributed to the preoperative enlargement of the orbital cavity by the teratoma, resulting in a loss of orbital volume and subsequent postoperative orbital collapse. The cornea failed to maintain apposition to the eyelids, leading to a corneal exposure and subsequent inflammation. With informed consent from the patient’s guardian, a secondary surgical intervention was performed involving the implantation of allogeneic scleral tissue into the orbit to restore orbital volume, correct fossal pitting, and re-establish corneal apposition. One-year follow-up revealed no evidence of tumor recurrence or other major complications. Persistent minor enophthalmos and outer canthus malformation remained, though visual acuity remained stable and equivalent to 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 examination remained unremarkable, with no signs of inflammation or structural compromise. The case underscores the importance of surgical planning in orbital teratoma resection, particularly in pediatric patients, where orbital volume preservation and tissue apposition are critical to long-term ocular function and cosmetic outcomes.\"\n}", "generated_text": "A 2-year-old female presented with a 1-year history of painless, progressive left-sided proptosis, without associated systemic illness or familial predisposition. Ophthalmologic examination revealed preserved light sensation 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 orbit, associated with left lower eyelid ectropion. The pupil measured 4 mm in diameter and exhibited absent pupillary reaction. Anterior segment evaluation showed no other abnormalities; fundus assessment was limited by 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 lesion containing heterogeneous tissue components. 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. Intraoperative findings included a grayish-white, cystic mass with a distinct boundary from surrounding orbital tissues. During posterior dissection, tight adhesion of the mass to the optic nerve was observed, indicating prior inflammatory or fibrotic interaction. Given the substantial size of the mass and the limited surgical field, volume reduction was necessary. Approximately 12.5 mL of fluid was aspirated, and the entire mass was completely excised. Histopathological examination confirmed the presence of a fibrous capsule lined with squamous and glandular epithelium, along with identifiable brain tissue and a cartilage-like matrix, consistent with a true orbital teratoma. Immunohistochemical analysis further supported the diagnosis by demonstrating positive staining for markers such as cytokeratin, S-100 protein, and glial fibrillary acidic protein (GFAP), reflecting the pluripotent origin of the teratoma. Postoperatively, at one month, the patient developed enophthalmos, conjunctival hyperemia, and keratitis. This clinical deterioration was attributed to the preoperative enlargement of the orbital cavity by the teratoma, resulting in a loss of orbital volume and subsequent postoperative orbital collapse. The cornea failed to maintain apposition to the eyelids, leading to a corneal exposure and subsequent inflammation. With informed consent from the patient’s guardian, a secondary surgical intervention was performed involving the implantation of allogeneic scleral tissue into the orbit to restore orbital volume, correct fossal pitting, and re-establish corneal apposition. One-year follow-up revealed no evidence of tumor recurrence or other major complications. Persistent minor enophthalmos and outer canthus malformation remained, though visual acuity remained stable and equivalent to 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 examination remained unremarkable, with no signs of inflammation or structural compromise. The case underscores the importance of surgical planning in orbital teratoma resection, particularly in pediatric patients, where orbital volume preservation and tissue apposition are critical to long-term ocular function and cosmetic outcomes."}
{"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 walk around her home. She was given a personalized medicine plan, and we checked her medicines to see which ones might be causing these symptoms. We found that her kidneys were not working as well as they should, which means her body can’t clear some medicines properly. We looked at how much her kidneys can filter waste (called eGFR), and it was only 30 — that’s a sign her kidneys are not working well. Because of this, we decided to lower the dose of two blood pressure medicines: losartan and manidipine. The doctor agreed and reduced them to safer levels. We also switched her pain medicine from pregabalin to gabapentin, which is safer for her kidneys. After two months, she felt better — no more tiredness, dizziness, or confusion. Her blood pressure also improved. We kept watching her to make sure everything stayed safe and working well.\"\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 walk around her home. She was given a personalized medicine plan, and we checked her medicines to see which ones might be causing these symptoms. We found that her kidneys were not working as well as they should, which means her body can’t clear some medicines properly. We looked at how much her kidneys can filter waste (called eGFR), and it was only 30 — that’s a sign her kidneys are not working well. Because of this, we decided to lower the dose of two blood pressure medicines: losartan and manidipine. The doctor agreed and reduced them to safer levels. We also switched her pain medicine from pregabalin to gabapentin, which is safer for her kidneys. After two months, she felt better — no more tiredness, dizziness, or confusion. Her blood pressure also improved. We kept watching her to make sure everything stayed safe and working well."}
{"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 made it hard for her to leave her home or walk as she used to. She was seen at the pharmacy for a medication review, focusing on drugs that are processed by the kidneys, especially since her kidney function was found to be reduced (estimated glomerular filtration rate or eGFR of 30 ml/min/1.73 m²). \\n\\nThe review looked at her blood pressure and medication doses, particularly for her blood pressure medications: losartan and manidipine. Because her kidneys are not working as well, these medicines need to be lowered in dose to avoid low blood pressure, which can cause dizziness and confusion. The pharmacy team recommended reducing losartan to 50 mg daily and manidipine to 10 mg daily. They also switched her pregabalin to gabapentin, which is safer for her kidney function.\\n\\nThe changes were shared with her primary care doctor, who agreed to adjust the doses. After two months of following the new treatment, her blood pressure improved and the symptoms of tiredness, weakness, dizziness, and confusion went away. The doctor confirmed that the new gabapentin dose was safe and appropriate for her kidney function.\"\n}", "generated_text": "A 78-year-old woman who was taking several medications reported feeling tired, weak, dizzy, and confused for months. These symptoms made it hard for her to leave her home or walk as she used to. She was seen at the pharmacy for a medication review, focusing on drugs that are processed by the kidneys, especially since her kidney function was found to be reduced (estimated glomerular filtration rate or eGFR of 30 ml/min/1.73 m²). \n\nThe review looked at her blood pressure and medication doses, particularly for her blood pressure medications: losartan and manidipine. Because her kidneys are not working as well, these medicines need to be lowered in dose to avoid low blood pressure, which can cause dizziness and confusion. The pharmacy team recommended reducing losartan to 50 mg daily and manidipine to 10 mg daily. They also switched her pregabalin to gabapentin, which is safer for her kidney function.\n\nThe changes were shared with her primary care doctor, who agreed to adjust the doses. After two months of following the new treatment, her blood pressure improved and the symptoms of tiredness, weakness, dizziness, and confusion went away. The doctor confirmed that the new gabapentin dose was safe and appropriate for her kidney function."}
{"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 area for a comprehensive medication review, with a focus on pharmacokinetic interactions relevant to renal function, particularly those affecting drugs metabolised or eliminated by the kidneys. The review centred on her estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, which yielded a value of 30 ml/min/1.73 m², indicating stage 3 chronic kidney disease (CKD).\\n\\nThe patient’s pharmacological regimen included 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 requiring dose adjustment due to renal impairment, with antihypertensives being the primary focus given the patient’s symptoms of hypotension.\\n\\nBlood pressure measurements using an Omron Complete device revealed a systolic blood pressure (SBP) of 96 mmHg, diastolic blood pressure (DBP) of 52 mmHg, and heart rate (HR) of 69 beats per minute—values consistent with hypotension, particularly in the context of antihypertensive therapy. The decision to adjust medication doses was guided by product-specific labeling and consensus guidelines from the University of Barcelona Faculty of Pharmacy’s Practical Pharmacy Teaching and Research Group, which categorises drug risk based on eGFR thresholds across therapeutic classes using the ATC classification system. These guidelines define risk levels as low, moderate, or high depending on the extent of renal dysfunction and the drug’s elimination pathway.\\n\\nSpecifically, for eGFR values between 30–59 ml/min/1.73 m², the recommended dose reduction for losartan is 50–75% of the original dose, while for eGFR values between 15–30 ml/min/1.73 m², manidipine requires dose adjustment, typically reduced to a fraction of the standard dose (e.g., 10 mg/24 h). Torasemide, a loop diuretic, can contribute to volume depletion and hypotension, particularly in patients with reduced renal function, and thus its effect on blood pressure must be monitored. Pregabalin, used for neuropathic pain, has a moderate risk of accumulation in renal impairment and may require cautious titration, though its adjustment was deferred pending the efficacy of antihypertensive dose reduction.\\n\\nThe intervention protocol involved a formal report to the primary care physician (PCP), recommending a reduction of losartan to 50 mg/24 h and manidipine to 10 mg/24 h, in accordance with the eGFR-based dosing guidelines. Additionally, pregabalin was substituted with gabapentin (300 mg/12 h), a structurally related agent with a more favourable pharmacokinetic profile in renal impairment, as gabapentin is primarily eliminated by the kidneys but exhibits a lower risk of accumulation at eGFR levels between 30–60 ml/min/1.73 m², with a recommended total daily dose of 300–900 mg.\\n\\nThe PCP implemented the proposed changes. Follow-up assessments over a two-month period demonstrated a significant improvement in blood pressure control (as documented in Table 5) and a complete resolution of the patient’s symptoms of fatigue, weakness, dizziness, and confusion. The gabapentin dose of 300 mg/12 h was subsequently confirmed to be within the recommended range for her eGFR of 30 ml/min/1.73 m², supporting its safety and efficacy in this context. The case underscores the importance of routine eGFR-based medication review in elderly patients with polypharmacy, particularly when symptoms of hypotension or", "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 area for a comprehensive medication review, with a focus on pharmacokinetic interactions relevant to renal function, particularly those affecting drugs metabolised or eliminated by the kidneys. The review centred on her estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, which yielded a value of 30 ml/min/1.73 m², indicating stage 3 chronic kidney disease (CKD).\\n\\nThe patient’s pharmacological regimen included 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 requiring dose adjustment due to renal impairment, with antihypertensives being the primary focus given the patient’s symptoms of hypotension.\\n\\nBlood pressure measurements using an Omron Complete device revealed a systolic blood pressure (SBP) of 96 mmHg, diastolic blood pressure (DBP) of 52 mmHg, and heart rate (HR) of 69 beats per minute—values consistent with hypotension, particularly in the context of antihypertensive therapy. The decision to adjust medication doses was guided by product-specific labeling and consensus guidelines from the University of Barcelona Faculty of Pharmacy’s Practical Pharmacy Teaching and Research Group, which categorises drug risk based on eGFR thresholds across therapeutic classes using the ATC classification system. These guidelines define risk levels as low, moderate, or high depending on the extent of renal dysfunction and the drug’s elimination pathway.\\n\\nSpecifically, for eGFR values between 30–59 ml/min/1.73 m², the recommended dose reduction for losartan is 50–75% of the original dose, while for eGFR values between 15–30 ml/min/1.73 m², manidipine requires dose adjustment, typically reduced to a fraction of the standard dose (e.g., 10 mg/24 h). Torasemide, a loop diuretic, can contribute to volume depletion and hypotension, particularly in patients with reduced renal function, and thus its effect on blood pressure must be monitored. Pregabalin, used for neuropathic pain, has a moderate risk of accumulation in renal impairment and may require cautious titration, though its adjustment was deferred pending the efficacy of antihypertensive dose reduction.\\n\\nThe intervention protocol involved a formal report to the primary care physician (PCP), recommending a reduction of losartan to 50 mg/24 h and manidipine to 10 mg/24 h, in accordance with the eGFR-based dosing guidelines. Additionally, pregabalin was substituted with gabapentin (300 mg/12 h), a structurally related agent with a more favourable pharmacokinetic profile in renal impairment, as gabapentin is primarily eliminated by the kidneys but exhibits a lower risk of accumulation at eGFR levels between 30–60 ml/min/1.73 m², with a recommended total daily dose of 300–900 mg.\\n\\nThe PCP implemented the proposed changes. Follow-up assessments over a two-month period demonstrated a significant improvement in blood pressure control (as documented in Table 5) and a complete resolution of the patient’s symptoms of fatigue, weakness, dizziness, and confusion. The gabapentin dose of 300 mg/12 h was subsequently confirmed to be within the recommended range for her eGFR of 30 ml/min/1.73 m², supporting its safety and efficacy in this context. The case underscores the importance of routine eGFR-based medication review in elderly patients with polypharmacy, particularly when symptoms of hypotension or"}
{"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 really smart brain skills but struggles with reading and writing because of dyslexia. Before help, she could only read simple letters and had trouble with sounds in words. She wrote in a messy way, mixing up letters and skipping parts. Her brain had trouble remembering sounds and seeing words quickly. After a few weeks of fun, weekly lessons focused on sounds and words, she got better. Now she reads faster and more clearly, and her writing is much more organized. She still has some challenges, like mixing up similar letters, but she’s making progress. The main thing that helped was working on how her brain handles sounds and words in a playful way, like playing games with letters and sounds.\"\n}", "generated_text": "This story is about a 9-year-old girl who has really smart brain skills but struggles with reading and writing because of dyslexia. Before help, she could only read simple letters and had trouble with sounds in words. She wrote in a messy way, mixing up letters and skipping parts. Her brain had trouble remembering sounds and seeing words quickly. After a few weeks of fun, weekly lessons focused on sounds and words, she got better. Now she reads faster and more clearly, and her writing is much more organized. She still has some challenges, like mixing up similar letters, but she’s making progress. The main thing that helped was working on how her brain handles sounds and words in a playful way, like playing games with letters and sounds."}
{"row_index": 74, "doc_id": 57, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"This case report presents a longitudinal, interdisciplinary evaluation and intervention study of a 9-year-old female child diagnosed with developmental dyslexia (DD) and high abilities/giftedness (AH/S), conducted within a public service framework under Research Ethics Committee (CEP) approval 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 in 2018 at 8 years and 2 months of age, with a follow-up evaluation in 2019 at 9 years and 6 months, reflecting a 14-month interval due to institutional scheduling constraints and weekly appointment frequency, during which the child experienced intermittent school absences.\\n\\nThe 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 home language shifted to Brazilian Portuguese due to parental background. Her first words were in French, and upon return to Brazil, she attended two private schools: initially, she failed to communicate in Portuguese, expressing exclusively in French; at age 3, she transitioned to a French-language school in Brazil. Over time, she exhibited persistent difficulties in reading and writing, leading to a repetition of the first year of elementary school at her mother’s request. At age 6, she enrolled in a bilingual Portuguese-English school. At age 8, she underwent a comprehensive neuropsychological and speech therapy evaluation, resulting in a diagnosis of developmental dyslexia with concomitant high cognitive abilities.\\n\\nThe study employed four assessment sessions—two pre-intervention (T1) and two post-intervention (T2)—each comprising a one-hour individualized evaluation of phonological processing, reading, and writing. The intervention consisted of 20 weekly 60-minute sessions of phonological remediation, administered in the second semester of 2018, with limited parental engagement due to work obligations. The remediation program was based on evidence-informed protocols for dyslexic populations and included targeted activities designed to strengthen phonological awareness, such as grapheme-phoneme correspondence, phoneme pair identification, syllable and word manipulation, phonemic addition/subtraction, rhyming, alliteration, and access to the mental lexicon. Activities were delivered in a metalinguistically oriented, play-based format, with reading training using the Mico Maneco children’s book collection, which progressively increases lexical complexity to track developmental gains. All sessions were documented in the clinical record.\\n\\nAssessment tools included the Consciência Fonológica Instrumento de Avaliação Sequencial (CONFIAS) for phonological awareness, which evaluates syllabic and phonemic awareness through segmentation, rhyme, alliteration, and transposition tasks. Scores are scored out of 70 (40 for syllabic, 30 for phonemic), with normative benchmarks derived from Ferreiro and Teberosky: syllabic-alphabetic writing hypothesis (syllabic = 27, phonemic = 12, total = 39); alphabetic writing hypothesis (syllabic = 31, phonemic = 15, total = 46). In T1, the child met the syllabic-alphabetic hypothesis (syllabic = 35, phonemic = 14); in T2, she met the alphabetic hypothesis (syllabic = 37, phonemic = 20), indicating significant improvement in phonemic processing, with a 6-point gain in phonemic awareness—consistent with targeted intervention.\\n\\nPhonological working memory was assessed using the Phonological Working Memory Test. The non-word repetition task (40 invented words) and digit reversal tasks were administered, with scoring based on correct repetitions across three attempts. Normative values for age 8 years (T1) were: pseudo-words = 69, direct digits = 13, reverse digits = 6. In T1, the child scored 66 (below expected) in pseudo-words and 4 (below expected) in reverse digits; in T2, scores improved to 69 (within normal range) and 12 (above expected), indicating gains in working memory capacity, particularly in executive functions related to rapid auditory storage and response retrieval.\\n\\nAutomatic Rapid Naming (RAN) and the updated Automatic Naming Test (TENA) were used to assess mental lexicon access. T1 used RAN with age-specific norms (8 years 0–11 months): digits = 28 s, letters = 29 s, objects = 52 s, colors = 46 s. T2 used TENA norms for 9 years 6 months: digits = 35 s, letters =", "generated_text": "{\n  \"proficient_health_literacy\": \"This case report presents a longitudinal, interdisciplinary evaluation and intervention study of a 9-year-old female child diagnosed with developmental dyslexia (DD) and high abilities/giftedness (AH/S), conducted within a public service framework under Research Ethics Committee (CEP) approval 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 in 2018 at 8 years and 2 months of age, with a follow-up evaluation in 2019 at 9 years and 6 months, reflecting a 14-month interval due to institutional scheduling constraints and weekly appointment frequency, during which the child experienced intermittent school absences.\\n\\nThe 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 home language shifted to Brazilian Portuguese due to parental background. Her first words were in French, and upon return to Brazil, she attended two private schools: initially, she failed to communicate in Portuguese, expressing exclusively in French; at age 3, she transitioned to a French-language school in Brazil. Over time, she exhibited persistent difficulties in reading and writing, leading to a repetition of the first year of elementary school at her mother’s request. At age 6, she enrolled in a bilingual Portuguese-English school. At age 8, she underwent a comprehensive neuropsychological and speech therapy evaluation, resulting in a diagnosis of developmental dyslexia with concomitant high cognitive abilities.\\n\\nThe study employed four assessment sessions—two pre-intervention (T1) and two post-intervention (T2)—each comprising a one-hour individualized evaluation of phonological processing, reading, and writing. The intervention consisted of 20 weekly 60-minute sessions of phonological remediation, administered in the second semester of 2018, with limited parental engagement due to work obligations. The remediation program was based on evidence-informed protocols for dyslexic populations and included targeted activities designed to strengthen phonological awareness, such as grapheme-phoneme correspondence, phoneme pair identification, syllable and word manipulation, phonemic addition/subtraction, rhyming, alliteration, and access to the mental lexicon. Activities were delivered in a metalinguistically oriented, play-based format, with reading training using the Mico Maneco children’s book collection, which progressively increases lexical complexity to track developmental gains. All sessions were documented in the clinical record.\\n\\nAssessment tools included the Consciência Fonológica Instrumento de Avaliação Sequencial (CONFIAS) for phonological awareness, which evaluates syllabic and phonemic awareness through segmentation, rhyme, alliteration, and transposition tasks. Scores are scored out of 70 (40 for syllabic, 30 for phonemic), with normative benchmarks derived from Ferreiro and Teberosky: syllabic-alphabetic writing hypothesis (syllabic = 27, phonemic = 12, total = 39); alphabetic writing hypothesis (syllabic = 31, phonemic = 15, total = 46). In T1, the child met the syllabic-alphabetic hypothesis (syllabic = 35, phonemic = 14); in T2, she met the alphabetic hypothesis (syllabic = 37, phonemic = 20), indicating significant improvement in phonemic processing, with a 6-point gain in phonemic awareness—consistent with targeted intervention.\\n\\nPhonological working memory was assessed using the Phonological Working Memory Test. The non-word repetition task (40 invented words) and digit reversal tasks were administered, with scoring based on correct repetitions across three attempts. Normative values for age 8 years (T1) were: pseudo-words = 69, direct digits = 13, reverse digits = 6. In T1, the child scored 66 (below expected) in pseudo-words and 4 (below expected) in reverse digits; in T2, scores improved to 69 (within normal range) and 12 (above expected), indicating gains in working memory capacity, particularly in executive functions related to rapid auditory storage and response retrieval.\\n\\nAutomatic Rapid Naming (RAN) and the updated Automatic Naming Test (TENA) were used to assess mental lexicon access. T1 used RAN with age-specific norms (8 years 0–11 months): digits = 28 s, letters = 29 s, objects = 52 s, colors = 46 s. T2 used TENA norms for 9 years 6 months: digits = 35 s, letters ="}
{"row_index": 75, "doc_id": 58, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old woman had a lump found in the middle of her chest, behind her breastbone, during a check-up before knee surgery. The lump was about 6.5 cm long and 4.2 cm wide, had clear edges, and looked like fat and solid tissue. Doctors took a small sample and found it was made of mature fat and some blood cells, which are normal parts of the body. This kind of lump is not cancer and is harmless. So, they decided not to treat it with surgery and just watched it. She felt fine and went home without any problems.\"\n}", "generated_text": "A 65-year-old woman had a lump found in the middle of her chest, behind her breastbone, during a check-up before knee surgery. The lump was about 6.5 cm long and 4.2 cm wide, had clear edges, and looked like fat and solid tissue. Doctors took a small sample and found it was made of mature fat and some blood cells, which are normal parts of the body. This kind of lump is not cancer and is harmless. So, they decided not to treat it with surgery and just watched it. She felt fine 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 routine check-up before knee surgery. The tumor was about 6.5 × 4.2 cm, well-defined, and had both fat and solid parts. It did not spread to nearby tissues or bones. A biopsy was done using image guidance, and the results showed that the tumor was made up of mature fat tissue with some blood cells and early blood cell precursors, which is a sign of a benign (non-cancerous) condition called primary mediastinal myelolipoma. Because the tumor was not dangerous and did not grow, 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 routine check-up before knee surgery. The tumor was about 6.5 × 4.2 cm, well-defined, and had both fat and solid parts. It did not spread to nearby tissues or bones. A biopsy was done using image guidance, and the results showed that the tumor was made up of mature fat tissue with some blood cells and early blood cell precursors, which is a sign of a benign (non-cancerous) condition called primary mediastinal myelolipoma. Because the tumor was not dangerous and did not grow, 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. She was referred for evaluation and management. Physical examination at admission was unremarkable, and all laboratory studies 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 density, with no signs of bone erosion, soft tissue infiltration, or vascular invasion. The tumor was localized and demonstrated clear margins, consistent with a benign lesion. A trans-thoracic biopsy was performed using a 18G × 250 mm semiautomatic cutting needle under image guidance via a posterior approach, ensuring precise targeting and minimal trauma. Histopathological analysis confirmed a benign neoplasm composed of mature adipose tissue intermixed with areas of hemorrhage and hematopoietic elements. The hematopoietic components included primarily precursors of the erythroid lineage (red cell series), as well as myeloid precursors at various stages of maturation, including megakaryocytes, which are bone marrow-derived cells responsible for platelet production. This pattern of mature adipose tissue with active, albeit non-malignant, hematopoiesis is characteristic of primary mediastinal myelolipoma (PMML), a rare benign tumor of the mediastinum. The presence of both adipose and hematopoietic elements, particularly in a well-differentiated and non-invasive context, supports the diagnosis of primary mediastinal myelolipoma (MPM) as defined by the World Health Organization (WHO) classification of soft tissue tumors. Given the benign nature of the lesion, lack of local invasion, and absence of systemic features such as hypercellular marrow or metastatic spread, conservative management was adopted. The patient showed no signs of progression or complications and was discharged without adverse events. This case underscores the importance of imaging and biopsy in differentiating benign mediastinal masses from malignant neoplasms, particularly when hematopoietic elements are present within adipose tissue, as such findings may mimic hematologic malignancies but are instead indicative of a distinct, well-characterized benign entity.\"\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. She was referred for evaluation and management. Physical examination at admission was unremarkable, and all laboratory studies 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 density, with no signs of bone erosion, soft tissue infiltration, or vascular invasion. The tumor was localized and demonstrated clear margins, consistent with a benign lesion. A trans-thoracic biopsy was performed using a 18G × 250 mm semiautomatic cutting needle under image guidance via a posterior approach, ensuring precise targeting and minimal trauma. Histopathological analysis confirmed a benign neoplasm composed of mature adipose tissue intermixed with areas of hemorrhage and hematopoietic elements. The hematopoietic components included primarily precursors of the erythroid lineage (red cell series), as well as myeloid precursors at various stages of maturation, including megakaryocytes, which are bone marrow-derived cells responsible for platelet production. This pattern of mature adipose tissue with active, albeit non-malignant, hematopoiesis is characteristic of primary mediastinal myelolipoma (PMML), a rare benign tumor of the mediastinum. The presence of both adipose and hematopoietic elements, particularly in a well-differentiated and non-invasive context, supports the diagnosis of primary mediastinal myelolipoma (MPM) as defined by the World Health Organization (WHO) classification of soft tissue tumors. Given the benign nature of the lesion, lack of local invasion, and absence of systemic features such as hypercellular marrow or metastatic spread, conservative management was adopted. The patient showed no signs of progression or complications and was discharged without adverse events. This case underscores the importance of imaging and biopsy in differentiating benign mediastinal masses from malignant neoplasms, particularly when hematopoietic elements are present within adipose tissue, as such findings may mimic hematologic malignancies but are instead indicative of a distinct, well-characterized benign entity."}
{"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 infection. He worked outside in very hot weather, which made his body overheat and go into a dangerous coma. His temperature reached 40°C, and he stopped breathing on his own. Doctors found he had a lung infection, damaged liver and kidneys, and a serious blood clotting problem. Even after giving him antibiotics, fluids, and help to protect his organs, he got worse. Days later, he started having trouble breathing and a brain bleed. He had a severe mix of infections and blood problems that hurt many parts of his body. This led to a life-threatening condition called multi-organ failure, and he passed away.\"\n}", "generated_text": "A 52-year-old man got sick with both a bad fever and a COVID-19 infection. He worked outside in very hot weather, which made his body overheat and go into a dangerous coma. His temperature reached 40°C, and he stopped breathing on his own. Doctors found he had a lung infection, damaged liver and kidneys, and a serious blood clotting problem. Even after giving him antibiotics, fluids, and help to protect his organs, he got worse. Days later, he started having trouble breathing and a brain bleed. He had a severe mix of infections and blood problems that hurt many parts of his body. This led to a life-threatening condition called multi-organ failure, and he passed away."}
{"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, coinciding with the onset of heatstroke (HS). Initial exposure to SARS-CoV-2 occurred during a cold-like illness, followed by return to work without fever after two days of rest. While working outdoors in an ambient temperature of 35°C for five hours, he lost consciousness, with a core temperature (Tc) measured at 40°C upon emergency department admission. The clinical presentation—persistent coma, hyperpyrexia, dyspnea, and gastrointestinal hemorrhage—was consistent with a diagnosis of heatstroke, supported by the absence of underlying comorbidities or familial disease history. The Glasgow Coma Scale (GCS) score was 3/15 (1 for eye-opening, verbal, and motor responses), with symmetrical, non-reactive pupils. Vital signs included a heart rate of 106 bpm and maintained blood pressure (126/77 mmHg) via continuous norepinephrine infusion (0.4 µg/kg·min).\\n\\nLaboratory findings revealed a severe systemic inflammatory response: white blood cell count (WBC) decreased from 3.55×10⁹/L to 3.13×10⁹/L, with a marked reduction in lymphocytes (from 0.25×10⁹/L to 0.1×10⁹/L) and a rise in neutrophil percentage (N%) to 85.3%. Procalcitonin was elevated to 2.81 ng/mL, indicating bacterial infection, and C-reactive protein (CRP) reached 32.6 mg/L. Sputum culture identified Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture revealed Staphylococcus epidermidis, while blood cultures remained negative. CT imaging demonstrated bilateral frontal subdural effusions, bilateral pleural effusions, lower lobe consolidation and atelectasis, right upper lobe inflammation, and a small amount of abdominal fluid, indicating a multi-organ pulmonary infection.\\n\\nThe patient was admitted to the emergency intensive care unit (ICU) and initiated with intravenous rehydration using lactated Ringer’s solution and normal saline at 2.5 mL/kg·h, mechanical ventilation (synchronized intermittent mandatory ventilation with PEEP of 5 mmH₂O and FiO₂ of 80%), vasoactive support, and continuous renal replacement therapy (CRRT) for anuria. Initial antibiotics were Piperacillin Sodium and Tazobactam Sodium, later switched to Meropenem due to S. maltophilia and methicillin-resistant Staphylococcus aureus (MRSA) isolation from sputum. Thymalfasin was administered for 20 days to modulate immune function. Hepatic and renal dysfunction were managed with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration. Intracranial pressure was managed with mannitol for three days. Coagulopathy was characterized by thrombocytopenia, anemia, and disseminated intravascular coagulation (DIC), with treatment including plasma and cryoprecipitate transfusions, continuous heparin infusion (6000 U/day), and CRRT with sodium citrate anticoagulation (8 g/day) initiated on day 7. Platelet transfusion was administered after day 9.\\n\\nThe patient regained consciousness on day 13 with a GCS of 14/15 and moderate fever, with no active gastrointestinal bleeding. Mechanical ventilation was discontinued and the tracheal tube removed. However, discontinuation of CRRT on day 12 led to a rise in serum creatinine, indicating worsening renal function. On day 17, he developed acute respiratory distress with oxygen saturation <85% and a fever (Tc: 39.3°C), requiring reintubation. Bronchoscopy showed reduced sputum volume in both lungs and subbranches. A recurrence of coma (GCS 3/15) occurred, with WBC increasing to 14.94×10⁹/L and neutrophils to 13.77×10⁹/L. Serum total bilirubin rose to 235.2 µmol/L and creatinine to 441 µmol/L. Brain CT revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. Cooling therapy via CRRT with ice-cold replacement fluid was", "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, coinciding with the onset of heatstroke (HS). Initial exposure to SARS-CoV-2 occurred during a cold-like illness, followed by return to work without fever after two days of rest. While working outdoors in an ambient temperature of 35°C for five hours, he lost consciousness, with a core temperature (Tc) measured at 40°C upon emergency department admission. The clinical presentation—persistent coma, hyperpyrexia, dyspnea, and gastrointestinal hemorrhage—was consistent with a diagnosis of heatstroke, supported by the absence of underlying comorbidities or familial disease history. The Glasgow Coma Scale (GCS) score was 3/15 (1 for eye-opening, verbal, and motor responses), with symmetrical, non-reactive pupils. Vital signs included a heart rate of 106 bpm and maintained blood pressure (126/77 mmHg) via continuous norepinephrine infusion (0.4 µg/kg·min).\\n\\nLaboratory findings revealed a severe systemic inflammatory response: white blood cell count (WBC) decreased from 3.55×10⁹/L to 3.13×10⁹/L, with a marked reduction in lymphocytes (from 0.25×10⁹/L to 0.1×10⁹/L) and a rise in neutrophil percentage (N%) to 85.3%. Procalcitonin was elevated to 2.81 ng/mL, indicating bacterial infection, and C-reactive protein (CRP) reached 32.6 mg/L. Sputum culture identified Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture revealed Staphylococcus epidermidis, while blood cultures remained negative. CT imaging demonstrated bilateral frontal subdural effusions, bilateral pleural effusions, lower lobe consolidation and atelectasis, right upper lobe inflammation, and a small amount of abdominal fluid, indicating a multi-organ pulmonary infection.\\n\\nThe patient was admitted to the emergency intensive care unit (ICU) and initiated with intravenous rehydration using lactated Ringer’s solution and normal saline at 2.5 mL/kg·h, mechanical ventilation (synchronized intermittent mandatory ventilation with PEEP of 5 mmH₂O and FiO₂ of 80%), vasoactive support, and continuous renal replacement therapy (CRRT) for anuria. Initial antibiotics were Piperacillin Sodium and Tazobactam Sodium, later switched to Meropenem due to S. maltophilia and methicillin-resistant Staphylococcus aureus (MRSA) isolation from sputum. Thymalfasin was administered for 20 days to modulate immune function. Hepatic and renal dysfunction were managed with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration. Intracranial pressure was managed with mannitol for three days. Coagulopathy was characterized by thrombocytopenia, anemia, and disseminated intravascular coagulation (DIC), with treatment including plasma and cryoprecipitate transfusions, continuous heparin infusion (6000 U/day), and CRRT with sodium citrate anticoagulation (8 g/day) initiated on day 7. Platelet transfusion was administered after day 9.\\n\\nThe patient regained consciousness on day 13 with a GCS of 14/15 and moderate fever, with no active gastrointestinal bleeding. Mechanical ventilation was discontinued and the tracheal tube removed. However, discontinuation of CRRT on day 12 led to a rise in serum creatinine, indicating worsening renal function. On day 17, he developed acute respiratory distress with oxygen saturation <85% and a fever (Tc: 39.3°C), requiring reintubation. Bronchoscopy showed reduced sputum volume in both lungs and subbranches. A recurrence of coma (GCS 3/15) occurred, with WBC increasing to 14.94×10⁹/L and neutrophils to 13.77×10⁹/L. Serum total bilirubin rose to 235.2 µmol/L and creatinine to 441 µmol/L. Brain CT revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. Cooling therapy via CRRT with ice-cold replacement fluid was"}
{"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 exhibited a high fever of 39.1°C, severe hypertension (189/120 mmHg), and tachycardia (148 beats per minute). Laboratory findings included a white blood cell count of 14.77×10^9/L and a neutrophil count of 13.55×10^9/L, consistent with an acute inflammatory or infectious process. Empirical antibiotic therapy with moxifloxacin was initiated, but symptoms persisted, prompting admission to the intensive care unit for continuous monitoring. A year prior, she had been diagnosed with myocarditis at a local hospital, along with hypertension, for which antihypertensive medications were prescribed; however, she discontinued adherence to therapy and did not perform regular blood pressure monitoring. Notably, her father had a history of sudden, unexplained death, raising concerns for a genetic predisposition to endocrine neoplasia.\\n\\nA chest CT scan incidentally revealed a left adrenal mass measuring 43 mm × 36 mm with soft tissue density. No abnormalities were detected in head or chest imaging. Electrocardiography demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF, suggestive of right atrial strain. Transthoracic echocardiography showed no structural cardiac abnormalities.\\n\\nOn day two of admission, biomarkers including brain natriuretic peptide (BNP) and troponin I (TnI) increased, supporting a provisional diagnosis of myocarditis of uncertain etiology. Treatment included methylprednisolone (0.25 g/day) to suppress myocardial inflammation, furosemide (20 mg q12h) and spironolactone (20 mg q12h) for volume control, and perindopril amlodipine (10 mg: 5 mg/day) for blood pressure and afterload reduction. Metoprolol tartrate (25 mg q12h) and esmolol (0.2 g/hour IV) were used to manage tachycardia and reduce myocardial oxygen demand.\\n\\nGiven the presence of an adrenal mass and sustained hypertension, endocrine evaluation was performed, including assessment of the 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 levels included free adrenaline (4,368.89 nmol/24h), free norepinephrine (>12,697.60 nmol/24h), normetanephrine (8,312 nmol/24h), metanephrines (4,078 nmol/24h), and vanillylmandelic acid (58.1 mg/24h). These findings are consistent with a diagnosis of pheochromocytoma. On day five, glucocorticoid therapy was discontinued, and terazosin was introduced to provide more precise control of blood pressure.\\n\\nAn enhanced abdominal CT confirmed the left adrenal mass, strongly indicating 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 workup. Thyroid ultrasound identified a hypoechoic nodule measuring 6 mm × 4 mm in the left lobe, with mildly elevated calcitonin levels. Parathyroid function tests showed normal serum calcium, intact parathyroid hormone (PTH), and normal electrolytes.\\n\\nFollowing clinical stabilization, plasma cortisol and ACTH normalized. The patient underwent surgical resection of the left adrenal tumor (50 mm × 40 mm × 30 mm). Immunohistochemical analysis demonstrated positive staining for vimentin (Vim), CD56, synaptophysin (Syn), chromogranin A (CgA), and neuron-specific enolase (NSE), with S-100 positivity in Sertoli cells. St", "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 exhibited a high fever of 39.1°C, severe hypertension (189/120 mmHg), and tachycardia (148 beats per minute). Laboratory findings included a white blood cell count of 14.77×10^9/L and a neutrophil count of 13.55×10^9/L, consistent with an acute inflammatory or infectious process. Empirical antibiotic therapy with moxifloxacin was initiated, but symptoms persisted, prompting admission to the intensive care unit for continuous monitoring. A year prior, she had been diagnosed with myocarditis at a local hospital, along with hypertension, for which antihypertensive medications were prescribed; however, she discontinued adherence to therapy and did not perform regular blood pressure monitoring. Notably, her father had a history of sudden, unexplained death, raising concerns for a genetic predisposition to endocrine neoplasia.\\n\\nA chest CT scan incidentally revealed a left adrenal mass measuring 43 mm × 36 mm with soft tissue density. No abnormalities were detected in head or chest imaging. Electrocardiography demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF, suggestive of right atrial strain. Transthoracic echocardiography showed no structural cardiac abnormalities.\\n\\nOn day two of admission, biomarkers including brain natriuretic peptide (BNP) and troponin I (TnI) increased, supporting a provisional diagnosis of myocarditis of uncertain etiology. Treatment included methylprednisolone (0.25 g/day) to suppress myocardial inflammation, furosemide (20 mg q12h) and spironolactone (20 mg q12h) for volume control, and perindopril amlodipine (10 mg: 5 mg/day) for blood pressure and afterload reduction. Metoprolol tartrate (25 mg q12h) and esmolol (0.2 g/hour IV) were used to manage tachycardia and reduce myocardial oxygen demand.\\n\\nGiven the presence of an adrenal mass and sustained hypertension, endocrine evaluation was performed, including assessment of the 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 levels included free adrenaline (4,368.89 nmol/24h), free norepinephrine (>12,697.60 nmol/24h), normetanephrine (8,312 nmol/24h), metanephrines (4,078 nmol/24h), and vanillylmandelic acid (58.1 mg/24h). These findings are consistent with a diagnosis of pheochromocytoma. On day five, glucocorticoid therapy was discontinued, and terazosin was introduced to provide more precise control of blood pressure.\\n\\nAn enhanced abdominal CT confirmed the left adrenal mass, strongly indicating 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 workup. Thyroid ultrasound identified a hypoechoic nodule measuring 6 mm × 4 mm in the left lobe, with mildly elevated calcitonin levels. Parathyroid function tests showed normal serum calcium, intact parathyroid hormone (PTH), and normal electrolytes.\\n\\nFollowing clinical stabilization, plasma cortisol and ACTH normalized. The patient underwent surgical resection of the left adrenal tumor (50 mm × 40 mm × 30 mm). Immunohistochemical analysis demonstrated positive staining for vimentin (Vim), CD56, synaptophysin (Syn), chromogranin A (CgA), and neuron-specific enolase (NSE), with S-100 positivity in Sertoli cells. St"}
{"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 wasn’t hurting his bladder or causing weight loss. Doctors saw it and found it was deep, about 20 mm big, and attached near the urethra. Tests showed it had a lot of blood flow and was connected to the tube that carries sperm. It looked like a type of cancer called synovial sarcoma, which is a rare, fast-growing tumor. The first surgery removed the lump, and the test results showed it had signs of this cancer. The patient had another surgery with wider cuts to make sure all the cancer was taken out. Even after this, the cancer came back and spread to his liver and spine. He tried several chemo treatments, but they didn’t work. He had more surgeries on his liver, then got treatment for a lung tumor. After trying many medicines, the cancer kept growing, so he moved to palliative care and stopped treatment.\"\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 wasn’t hurting his bladder or causing weight loss. Doctors saw it and found it was deep, about 20 mm big, and attached near the urethra. Tests showed it had a lot of blood flow and was connected to the tube that carries sperm. It looked like a type of cancer called synovial sarcoma, which is a rare, fast-growing tumor. The first surgery removed the lump, and the test results showed it had signs of this cancer. The patient had another surgery with wider cuts to make sure all the cancer was taken out. Even after this, the cancer came back and spread to his liver and spine. He tried several chemo treatments, but they didn’t work. He had more surgeries on his liver, then got treatment for a lung tumor. After trying many medicines, the cancer kept growing, so he moved to palliative care and stopped treatment."}
{"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 tender lump in his penis and scrotum for 5 years. He had no pain with urination, weight loss, or fever. The lump was about 20 mm in size, attached near the base of the penis, and was mobile but deep. Imaging showed a well-defined mass with lots of blood flow, and it was connected to the vas deferens, but no swollen lymph nodes were found. Blood tests were normal. Because of the pain and findings, surgery was done to remove the mass for both diagnosis and treatment. The first surgery removed the mass completely, and the tissue was tested. Pathology showed a type of cancer called synovial sarcoma, which has specific markers including TLE-1, CD99, BLC2, cytokeratin, and EMA. A genetic test confirmed a known mutation in synovial sarcoma. The edges of the sample were hard to assess because the tissue was fragmented. After two weeks, the patient agreed to a second surgery with wider margins. The second surgery removed more tissue, including from both sides of the scrotum, and the result was clear of cancer. The patient was then placed on active surveillance. After 16 months, metastatic cancer was found in his liver and spine. Chemotherapy with Ifosfamide and Doxorubicin did not work, so surgery was done to remove part of the liver and gallbladder. Later, a lung lesion appeared, and he received Pazopanib and radiation. After 6 months of monitoring, new liver and lung tumors developed. He tried several chemotherapy regimens, including Gemcitabine and Docetaxel, Dacarbazine, and Pembrolizumab, but all failed. The patient was eventually moved to palliative care and stopped seeing his doctors.\"\n}", "generated_text": "A 36-year-old man had a tender lump in his penis and scrotum for 5 years. He had no pain with urination, weight loss, or fever. The lump was about 20 mm in size, attached near the base of the penis, and was mobile but deep. Imaging showed a well-defined mass with lots of blood flow, and it was connected to the vas deferens, but no swollen lymph nodes were found. Blood tests were normal. Because of the pain and findings, surgery was done to remove the mass for both diagnosis and treatment. The first surgery removed the mass completely, and the tissue was tested. Pathology showed a type of cancer called synovial sarcoma, which has specific markers including TLE-1, CD99, BLC2, cytokeratin, and EMA. A genetic test confirmed a known mutation in synovial sarcoma. The edges of the sample were hard to assess because the tissue was fragmented. After two weeks, the patient agreed to a second surgery with wider margins. The second surgery removed more tissue, including from both sides of the scrotum, and the result was clear of cancer. The patient was then placed on active surveillance. After 16 months, metastatic cancer was found in his liver and spine. Chemotherapy with Ifosfamide and Doxorubicin did not work, so surgery was done to remove part of the liver and gallbladder. Later, a lung lesion appeared, and he received Pazopanib and radiation. After 6 months of monitoring, new liver and lung tumors developed. He tried several chemotherapy regimens, including Gemcitabine and Docetaxel, Dacarbazine, and Pembrolizumab, but all failed. The patient was eventually moved to palliative care and stopped seeing his doctors."}
{"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 lesion was described as smooth, tender, cystic, measuring approximately 20 mm × 20 mm, attached to the left side of the bulbar urethra at the penoscrotal junction, deep in location, without skin tethering or association with the left spermatic cord, and partially mobile. Doppler ultrasonography revealed a well-defined hypoechoic mass (2.7 × 3.1 × 2.0 cm) with markedly increased vascularity in the left penoscrotal region. Pelvic magnetic resonance imaging (MRI) demonstrated a mass 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, 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, ruling out hepatoblastoma or germ cell tumor etiologies. Given the chronic pain and imaging findings, surgical resection was performed for both diagnostic and therapeutic purposes. Intraoperatively, a spindle cell tumor was identified in the left posterolateral scrotum and completely resected. Histopathological examination revealed a cellular spindle cell tumor organized in interlacing fascicles, with spindle to oval-shaped nuclei exhibiting evenly dispersed chromatin and inconspicuous nucleoli. Mitotic activity was high, reaching up to 3 mitoses per high-power field (HPF), indicating aggressive proliferative potential. 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 hallmark genetic alteration in synovial sarcoma. Histological assessment of the margins was inconclusive due to fragmentation of the resected specimen, limiting definitive margin status. Following initial resection, the patient returned to clinic for re-evaluation. Based on the histopathology, a second surgical resection with wider margins was performed three weeks later. The resection extended bilaterally to the spermatic cords, deepening to the corpus spongiosum and being shaved superiorly to the urethra. The final resected specimen measured 6.0 × 6.0 × 3.0 cm and was histologically negative for residual tumor. The patient entered active surveillance for 16 months, during which time metastatic disease was detected in the sixth liver segment 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 intervention included resection of the fifth and sixth liver segments with concomitant cholecystectomy. Following this, a new pulmonary lesion emerged, prompting initiation of pazopanib and stereotactic body radiation therapy (SBRT). After six months of surveillance, new liver and pulmonary lesions developed, leading to a regimen of gemcitabine and docetaxel for three cycles, which resulted in disease progression. The patient then received two cycles of dacarbazine, with further progression. Subsequently, two cycles of pembrolizumab were administered, also resulting in disease progression. The patient was transitioned to palliative care and discontinued follow-up. This case illustrates the aggressive biological behavior of synovial sarcoma in a young adult, despite multimodal therapy including surgical resection, chemotherapy, and targeted therapy, with eventual progression and widespread metastasis, highlighting the challenges in managing this rare, high-grade sarcoma with a propensity for early dissemination and resistance to conventional treatment regimens. The molecular profile—specifically the SS18-SSX1 fusion gene—supports the diagnosis of synovial sarcoma and correlates with its clinical aggressiveness and poor response to standard chemotherapy.\"\n}", "generated_text": "A 36-year-old male with no significant past medical history presented with a 5-year history of a left-sided penoscrotal mass. The lesion was described as smooth, tender, cystic, measuring approximately 20 mm × 20 mm, attached to the left side of the bulbar urethra at the penoscrotal junction, deep in location, without skin tethering or association with the left spermatic cord, and partially mobile. Doppler ultrasonography revealed a well-defined hypoechoic mass (2.7 × 3.1 × 2.0 cm) with markedly increased vascularity in the left penoscrotal region. Pelvic magnetic resonance imaging (MRI) demonstrated a mass 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, 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, ruling out hepatoblastoma or germ cell tumor etiologies. Given the chronic pain and imaging findings, surgical resection was performed for both diagnostic and therapeutic purposes. Intraoperatively, a spindle cell tumor was identified in the left posterolateral scrotum and completely resected. Histopathological examination revealed a cellular spindle cell tumor organized in interlacing fascicles, with spindle to oval-shaped nuclei exhibiting evenly dispersed chromatin and inconspicuous nucleoli. Mitotic activity was high, reaching up to 3 mitoses per high-power field (HPF), indicating aggressive proliferative potential. 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 hallmark genetic alteration in synovial sarcoma. Histological assessment of the margins was inconclusive due to fragmentation of the resected specimen, limiting definitive margin status. Following initial resection, the patient returned to clinic for re-evaluation. Based on the histopathology, a second surgical resection with wider margins was performed three weeks later. The resection extended bilaterally to the spermatic cords, deepening to the corpus spongiosum and being shaved superiorly to the urethra. The final resected specimen measured 6.0 × 6.0 × 3.0 cm and was histologically negative for residual tumor. The patient entered active surveillance for 16 months, during which time metastatic disease was detected in the sixth liver segment 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 intervention included resection of the fifth and sixth liver segments with concomitant cholecystectomy. Following this, a new pulmonary lesion emerged, prompting initiation of pazopanib and stereotactic body radiation therapy (SBRT). After six months of surveillance, new liver and pulmonary lesions developed, leading to a regimen of gemcitabine and docetaxel for three cycles, which resulted in disease progression. The patient then received two cycles of dacarbazine, with further progression. Subsequently, two cycles of pembrolizumab were administered, also resulting in disease progression. The patient was transitioned to palliative care and discontinued follow-up. This case illustrates the aggressive biological behavior of synovial sarcoma in a young adult, despite multimodal therapy including surgical resection, chemotherapy, and targeted therapy, with eventual progression and widespread metastasis, highlighting the challenges in managing this rare, high-grade sarcoma with a propensity for early dissemination and resistance to conventional treatment regimens. The molecular profile—specifically the SS18-SSX1 fusion gene—supports the diagnosis of synovial sarcoma and correlates with its clinical aggressiveness and poor response to standard chemotherapy."}
{"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 ER with sudden chest pain on the sides, worse when coughing, but no shortness of breath. He had a mild cough and a little runny nose, and once felt a fever. The pain didn’t get worse at night, and he was still able to do sports like canoeing. No one in his family had lung or heart problems, and he didn’t have any exposure to dust, fumes, or oil. His chest X-ray from 4 years ago showed a similar lung problem, which was treated with an antibiotic (azithromycin) and has stayed gone since. This time, his X-ray showed a thick, cloudy pattern in his lungs, and a CT scan found a lot of white spots in both lungs — more than two-thirds of his lung tissue — 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 special stain that confirmed the condition. His breathing tests showed a mild restriction, meaning he can’t take in as much air as normal, and his lungs are less able to pass oxygen. No gene mutations linked to lung problems were found. A blood test showed he has an antibody against a protein called GM-CSF, which makes doctors think it’s an autoimmune version of PAP. After 20 months, he’s feeling fine, no pain, and his breathing is back to normal. He’s still active and doesn’t need treatment right now — just regular check-ups.\"\n}", "generated_text": "A 13-year-old boy came to the ER with sudden chest pain on the sides, worse when coughing, but no shortness of breath. He had a mild cough and a little runny nose, and once felt a fever. The pain didn’t get worse at night, and he was still able to do sports like canoeing. No one in his family had lung or heart problems, and he didn’t have any exposure to dust, fumes, or oil. His chest X-ray from 4 years ago showed a similar lung problem, which was treated with an antibiotic (azithromycin) and has stayed gone since. This time, his X-ray showed a thick, cloudy pattern in his lungs, and a CT scan found a lot of white spots in both lungs — more than two-thirds of his lung tissue — 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 special stain that confirmed the condition. His breathing tests showed a mild restriction, meaning he can’t take in as much air as normal, and his lungs are less able to pass oxygen. No gene mutations linked to lung problems were found. A blood test showed he has an antibody against a protein called GM-CSF, which makes doctors think it’s an autoimmune version of PAP. After 20 months, he’s feeling fine, no pain, and his breathing is back to normal. He’s still active and doesn’t need treatment right now — just regular check-ups."}
{"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 limitation; he maintained regular physical activity, including weekly canoeing. No exposure to infectious agents, environmental fumes, dust, or mineral oils was reported. There was no family history of cardiopulmonary disorders. A prior chest radiograph, obtained four years earlier during an acute illness, demonstrated a marked interstitial infiltrate, which was presumptively managed with azithromycin and has since remained asymptomatic with no further clinical 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 chest without adventitious sounds, respiratory distress, cyanosis, clubbing, or abnormal cardiac findings. Chest radiography showed a persistent interstitial infiltrate, morphologically similar to the prior imaging. Thoracic computed tomography (CT) revealed multiple bilateral ground-glass opacities involving greater than 65% of lung parenchyma, with areas of 'crazy paving' pattern, consistent with 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, with clinical improvement and discharge. Subsequent outpatient evaluation revealed positive antinuclear antibodies (ANA) at a titer of 1/89 with a fine speckled pattern, while other autoantibodies and immunoglobulin levels were within normal ranges.\\n\\nBronchoalveolar lavage (BAL) yielded a milky fluid with positive periodic acid-Schiff (PAS) staining, indicating the presence of surfactant proteins and alveolar protein accumulation. Microbiological analysis, including for mycobacteria, was negative. Spirometry demonstrated 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%, suggesting preserved airway function despite reduced lung volumes. 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.\\n\\nGenetic testing for surfactant dysfunction-related mutations was negative, ruling out inherited surfactant deficiencies such as those seen in surfactant protein C (SFTPC) or surfactant protein B (SFTPB) mutations. Anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibody testing was strongly positive, supporting a diagnosis of autoimmune pulmonary alveolar proteinosis (AI-PAP), in which the immune system produces autoantibodies that inhibit GM-CSF, a critical cytokine for alveolar macrophage function and surfactant clearance.\\n\\nAt 20-month follow-up, the patient remains asymptomatic and continues regular physical activity. Repeat spirometry shows normalized FVC (4.03 L, 81.3%), FEV1 (3.71 L, 87.5%), FEV1/FVC ratio (91.96%), and DLCO (25.54 ml/min/mmHg, 83.7%), indicating functional stabilization. Given the absence of symptoms and stable pulmonary function, treatment was deferred, and the patient is being managed with ongoing clinical monitoring. The case highlights the clinical presentation of AI-PAP in a young adolescent with a recurrent interstitial infiltrate, overlapping with prior imaging findings, and underscores the importance of BAL findings, autoantibody screening, and GM-CSF inhibition in the diagnostic workup of unexplained interstitial lung disease in pediatric patients.\"\n}", "generated_text": "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 limitation; he maintained regular physical activity, including weekly canoeing. No exposure to infectious agents, environmental fumes, dust, or mineral oils was reported. There was no family history of cardiopulmonary disorders. A prior chest radiograph, obtained four years earlier during an acute illness, demonstrated a marked interstitial infiltrate, which was presumptively managed with azithromycin and has since remained asymptomatic with no further clinical 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 chest without adventitious sounds, respiratory distress, cyanosis, clubbing, or abnormal cardiac findings. Chest radiography showed a persistent interstitial infiltrate, morphologically similar to the prior imaging. Thoracic computed tomography (CT) revealed multiple bilateral ground-glass opacities involving greater than 65% of lung parenchyma, with areas of 'crazy paving' pattern, consistent with 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, with clinical improvement and discharge. Subsequent outpatient evaluation revealed positive antinuclear antibodies (ANA) at a titer of 1/89 with a fine speckled pattern, while other autoantibodies and immunoglobulin levels were within normal ranges.\n\nBronchoalveolar lavage (BAL) yielded a milky fluid with positive periodic acid-Schiff (PAS) staining, indicating the presence of surfactant proteins and alveolar protein accumulation. Microbiological analysis, including for mycobacteria, was negative. Spirometry demonstrated 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%, suggesting preserved airway function despite reduced lung volumes. 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.\n\nGenetic testing for surfactant dysfunction-related mutations was negative, ruling out inherited surfactant deficiencies such as those seen in surfactant protein C (SFTPC) or surfactant protein B (SFTPB) mutations. Anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibody testing was strongly positive, supporting a diagnosis of autoimmune pulmonary alveolar proteinosis (AI-PAP), in which the immune system produces autoantibodies that inhibit GM-CSF, a critical cytokine for alveolar macrophage function and surfactant clearance.\n\nAt 20-month follow-up, the patient remains asymptomatic and continues regular physical activity. Repeat spirometry shows normalized FVC (4.03 L, 81.3%), FEV1 (3.71 L, 87.5%), FEV1/FVC ratio (91.96%), and DLCO (25.54 ml/min/mmHg, 83.7%), indicating functional stabilization. Given the absence of symptoms and stable pulmonary function, treatment was deferred, and the patient is being managed with ongoing clinical monitoring. The case highlights the clinical presentation of AI-PAP in a young adolescent with a recurrent interstitial infiltrate, overlapping with prior imaging findings, and underscores the importance of BAL findings, autoantibody screening, and GM-CSF inhibition in the diagnostic workup of unexplained interstitial lung disease in pediatric patients."}
{"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 found a big blood clot in a vein, and a chest scan showed blood clots in her lungs. She was treated right away with strong antibiotics and medicine to stop the clots from getting worse. She got better and was able to go home after 14 days of 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 found a big blood clot in a vein, and a chest scan showed blood clots in her lungs. She was treated right away with strong antibiotics and medicine to stop the clots from getting worse. She got better and was able to go home after 14 days of 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 finishing antibiotics for a throat infection. She had previously taken phenoxymethylpenicillin for five days to treat a peritonsillar abscess. Imaging showed a large blood clot in the internal jugular vein of her neck and lung infections caused by septic emboli (clots that traveled to the lungs). She was treated with strong intravenous antibiotics and anticoagulation to prevent further clots. Her condition 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 finishing antibiotics for a throat infection. She had previously taken phenoxymethylpenicillin for five days to treat a peritonsillar abscess. Imaging showed a large blood clot in the internal jugular vein of her neck and lung infections caused by septic emboli (clots that traveled to the lungs). She was treated with strong intravenous antibiotics and anticoagulation to prevent further clots. Her condition 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. At presentation, she was hemodynamically stable, without respiratory distress or requirement for supplemental oxygen. Physical examination revealed a painful, homolateral cervical adenopathy and significant trismus. Laboratory findings demonstrated leukocytosis, thrombocytopenia, and elevated acute-phase reactants, with all other parameters within normal limits. Imaging studies included a head and neck CT, which revealed a large thrombus in both the internal and external carotid arteries, consistent with a thrombotic event secondary to severe local inflammation or endothelial activation. Arterial Doppler ultrasound of the neck vessels showed no significant stenosis or flow abnormalities, but the presence of carotid thrombus suggests a systemic inflammatory response. A chest CT scan demonstrated bilateral pulmonary septic emboli, indicating dissemination of infected material via venous thrombus from the head and neck region to the pulmonary circulation. Initial empiric intravenous therapy was initiated with ceftriaxone 1 g every 12 hours and clindamycin 300 mg every 6 hours to cover potential Gram-positive and anaerobic pathogens, including those associated with odontogenic infections. Concomitant anticoagulation was initiated with enoxaparin, dosed at 60 mg subcutaneously every 12 hours, adjusted for body weight and renal function, to prevent extension of the thrombotic burden. Over the subsequent 72 hours, the patient developed a fever of 38.5 °C and further leukocytosis, prompting repeat imaging. Echocardiography excluded cardiac vegetations, ruling out endocarditis as a source of emboli. A repeat chest CT confirmed bilateral pulmonary septic emboli. Hemocultures obtained at admission were negative, leading to the decision to perform culture of pharyngeal exudate and initiate a broader-spectrum antibiotic regimen with piperacillin-tazobactam 4.5 g every 6 hours intravenously, replacing ceftriaxone. No pathogen was isolated from cultures, suggesting a possible non-bacterial or polymicrobial infection with limited cultivability. The patient responded favorably to treatment, with resolution of fever and clinical signs of infection. After 14 days of optimized therapy, follow-up chest CT showed absence of pulmonary lesions, and the patient was transitioned to oral clindamycin 300 mg every 6 hours for continued coverage of anaerobic organisms. Anticoagulation was switched to acenocumarol, adjusted to body weight, to maintain therapeutic anticoagulation levels, with the patient achieving stable coagulation parameters and being discharged. The clinical course reflects a rare but severe complication of odontogenic infection—systemic thrombosis and septic embolization—likely driven by intense local inflammation, endothelial injury, and hypercoagulability, with potential contributions from underlying comorbidities such as asthma and prior viral infection, which may predispose to dysregulated immune and coagulation responses.\"\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. At presentation, she was hemodynamically stable, without respiratory distress or requirement for supplemental oxygen. Physical examination revealed a painful, homolateral cervical adenopathy and significant trismus. Laboratory findings demonstrated leukocytosis, thrombocytopenia, and elevated acute-phase reactants, with all other parameters within normal limits. Imaging studies included a head and neck CT, which revealed a large thrombus in both the internal and external carotid arteries, consistent with a thrombotic event secondary to severe local inflammation or endothelial activation. Arterial Doppler ultrasound of the neck vessels showed no significant stenosis or flow abnormalities, but the presence of carotid thrombus suggests a systemic inflammatory response. A chest CT scan demonstrated bilateral pulmonary septic emboli, indicating dissemination of infected material via venous thrombus from the head and neck region to the pulmonary circulation. Initial empiric intravenous therapy was initiated with ceftriaxone 1 g every 12 hours and clindamycin 300 mg every 6 hours to cover potential Gram-positive and anaerobic pathogens, including those associated with odontogenic infections. Concomitant anticoagulation was initiated with enoxaparin, dosed at 60 mg subcutaneously every 12 hours, adjusted for body weight and renal function, to prevent extension of the thrombotic burden. Over the subsequent 72 hours, the patient developed a fever of 38.5 °C and further leukocytosis, prompting repeat imaging. Echocardiography excluded cardiac vegetations, ruling out endocarditis as a source of emboli. A repeat chest CT confirmed bilateral pulmonary septic emboli. Hemocultures obtained at admission were negative, leading to the decision to perform culture of pharyngeal exudate and initiate a broader-spectrum antibiotic regimen with piperacillin-tazobactam 4.5 g every 6 hours intravenously, replacing ceftriaxone. No pathogen was isolated from cultures, suggesting a possible non-bacterial or polymicrobial infection with limited cultivability. The patient responded favorably to treatment, with resolution of fever and clinical signs of infection. After 14 days of optimized therapy, follow-up chest CT showed absence of pulmonary lesions, and the patient was transitioned to oral clindamycin 300 mg every 6 hours for continued coverage of anaerobic organisms. Anticoagulation was switched to acenocumarol, adjusted to body weight, to maintain therapeutic anticoagulation levels, with the patient achieving stable coagulation parameters and being discharged. The clinical course reflects a rare but severe complication of odontogenic infection—systemic thrombosis and septic embolization—likely driven by intense local inflammation, endothelial injury, and hypercoagulability, with potential contributions from underlying comorbidities such as asthma and prior viral infection, which may predispose to dysregulated immune and coagulation responses."}
{"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 dangerous poison called chlorpyrifos and also breathed in a mixture of charcoal and palm oil. This caused serious problems: breathing stopped, the child went into a deep sleep, had no movement in the arms and legs, and was very weak. The child was rushed to the hospital where they gave breathing support, gave medicine to stop the poison, and used blood changes to help the body. The child started to get better within hours, didn’t have a later serious problem (called intermediate syndrome), and was home after 10 days. The doctors kept the child safe and helped them recover step by step.\"\n}", "generated_text": "A 5-year-old child swallowed a dangerous poison called chlorpyrifos and also breathed in a mixture of charcoal and palm oil. This caused serious problems: breathing stopped, the child went into a deep sleep, had no movement in the arms and legs, and was very weak. The child was rushed to the hospital where they gave breathing support, gave medicine to stop the poison, and used blood changes to help the body. The child started to get better within hours, didn’t have a later serious problem (called intermediate syndrome), and was home after 10 days. The doctors kept the child safe and helped them recover step by step."}
{"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 accidentally ingesting it. Shortly after, the child also aspirated (inhaled) a mixture of charcoal and palm oil, which worsened the condition. The poisoning caused serious symptoms including fast breathing, difficulty breathing, excessive sweating, vomiting, and eventually coma. At the time of arrival at the emergency department, the child had very low consciousness (Glasgow Coma Score of 3), pinpoint pupils, and signs of shock and respiratory failure.\\n\\nThe child was treated with non-invasive ventilation to help with breathing, intravenous atropine to counteract the poisoning, and medications to support blood pressure and reduce inflammation. Because the family could not afford intensive care, the treatment was kept manageable. The child also received exchange transfusions (a blood exchange to remove toxic substances) and antibiotics for lung infection. Hypoglycemia (low blood sugar) was treated with dextrose, and heart issues were managed with fluids and a dopamine infusion.\\n\\nOver the next few days, the child’s condition improved steadily. Consciousness returned, breathing became easier, and lung symptoms improved. By day 10, the child was stable enough to be discharged home. The child did not develop a known complication called intermediate syndrome and recovered well from the poisoning. However, after discharge, the child was not followed up by healthcare providers.\"\n}", "generated_text": "A 5-year-old child suffered severe poisoning from chlorpyrifos, a type of organophosphate pesticide, after accidentally ingesting it. Shortly after, the child also aspirated (inhaled) a mixture of charcoal and palm oil, which worsened the condition. The poisoning caused serious symptoms including fast breathing, difficulty breathing, excessive sweating, vomiting, and eventually coma. At the time of arrival at the emergency department, the child had very low consciousness (Glasgow Coma Score of 3), pinpoint pupils, and signs of shock and respiratory failure.\n\nThe child was treated with non-invasive ventilation to help with breathing, intravenous atropine to counteract the poisoning, and medications to support blood pressure and reduce inflammation. Because the family could not afford intensive care, the treatment was kept manageable. The child also received exchange transfusions (a blood exchange to remove toxic substances) and antibiotics for lung infection. Hypoglycemia (low blood sugar) was treated with dextrose, and heart issues were managed with fluids and a dopamine infusion.\n\nOver the next few days, the child’s condition improved steadily. Consciousness returned, breathing became easier, and lung symptoms improved. By day 10, the child was stable enough to be discharged home. The child did not develop a known complication called intermediate syndrome and recovered well from the poisoning. However, after discharge, the child was not followed up by healthcare providers."}
{"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 ingesting chlorpyrifos, a potent organophosphate pesticide, followed by aspiration of a charcoal-palm oil mixture. The initial clinical presentation included generalized abnormal jerks, tachypnea (respiratory rate of 48 breaths per minute with intermittent sighing), severe dyspnea, excessive sweating, polyuria, increased secretions, and involuntary limb movements. The patient had lapsed into coma prior to arrival, with a presenting temperature of 38.3°C, Glasgow Coma Scale (GCS) of 3, pinpoint pupils, and global hypotonia. Vital signs at presentation included a heart rate of 180 beats per minute, blood pressure of 120/80 mmHg, and a random blood glucose of 14 mg/dL. Physical examination revealed widespread crackles on auscultation, indicating pulmonary edema or aspiration-related pulmonary injury. Serum cholinesterase activity and lactate levels were not measured due to institutional limitations.\\n\\nThe diagnosis was established as severe organophosphate poisoning (OPP) with concomitant aspiration pneumonitis. Given the severity of respiratory failure and the unavailability of intensive care resources, non-invasive ventilation (NIV) was initiated using bubble continuous positive airway pressure (b-CPAP), which improved oxygen saturation to 99–100%. Hypoglycemia was managed with a dextrose bolus, and tachycardia was treated with 20 mL/kg of normal saline. Empirical intravenous antibiotics were administered for suspected aspiration-related pneumonia. Intravenous atropine was administered at a dose of 0.02 mg/kg/dose, with the first dose leading to a significant tachycardia, prompting discontinuation due to hemodynamic instability. Pralidoxime, a reactivating agent for organophosphate-inhibited acetylcholinesterase, was not administered due to unavailability.\\n\\nWithin 3 hours of presentation, the patient underwent a fresh-whole-blood exchange blood transfusion (FWB-EBT) of 500 mL to rapidly reduce circulating organophosphate metabolites and mitigate cholinergic toxicity. The GCS improved to 9/15 following this intervention. Over the subsequent 15 hours, blood glucose fluctuated between 41 and 259 mg/dL, eventually stabilizing with continued management. On day 2 of admission, the patient developed thready pulses and hypotension, prompting a second bolus of normal saline. Dopamine infusion was initiated at 5 mcg/kg/min via peripheral venous access, and intravenous mannitol was discontinued. A second FWB-EBT of 500 mL was performed.\\n\\nOver the first 30 hours, there was a progressive improvement in consciousness and resolution of respiratory distress. However, rhonchi were noted, managed with nebulized salbutamol and budesonide, and the patient was transitioned to nasal prong oxygen therapy, maintaining stable oxygen saturation at 97%. A chest radiograph on day 2 revealed bilateral pulmonary infiltrates consistent with aspiration pneumonia. Full recovery of consciousness was achieved by the 39th hour of admission. Antioxidant therapy was initiated with intravenous vitamin C and B, and oral vitamin E and zinc to mitigate oxidative stress associated with acute organophosphate toxicity. A graded reintroduction of oral diet was implemented over the following 48 hours.\\n\\nThe patient’s clinical course remained stable, and he was discharged home after 10 days of hospitalization. However, follow-up care was not maintained, resulting in loss to follow-up. The patient did not develop the intermediate syndrome, a known risk in organophosphate poisoning characterized by delayed neuromuscular weakness typically occurring 24–96 hours post-exposure, which may have been attributed to the rapid clinical response, early intervention, and absence of prolonged cholinesterase inhibition.\\n\\nThis case underscores the pathophysiological mechanisms of organophosphate toxicity, including acetylcholinesterase inhibition leading to excessive acetylcholine accumulation at neuromuscular junctions and in the central nervous system, resulting in muscarinic and nicotinic cholinergic overstimulation. The clinical manifestations include bronchospasm, respiratory failure, hypotension, seizures, and coma. Aspiration of lipid-rich substances like palm oil may exacerbate pulmonary injury through direct chemical irritation and mechanical obstruction, contributing to secondary pneumonia. The use of exchange transfusion in this setting is a rare but effective strategy to rapidly remove toxic metabolites and restore physiological balance in severe OPP, particularly in resource-limited settings where advanced supportive care is not available. The absence of pralidoxime administration highlights a critical gap in access to antidotal therapy in", "generated_text": "{\n  \"proficient_health_literacy\": \"A 5-year-old child presented to the pediatric emergency department (ED) 13 hours after ingesting chlorpyrifos, a potent organophosphate pesticide, followed by aspiration of a charcoal-palm oil mixture. The initial clinical presentation included generalized abnormal jerks, tachypnea (respiratory rate of 48 breaths per minute with intermittent sighing), severe dyspnea, excessive sweating, polyuria, increased secretions, and involuntary limb movements. The patient had lapsed into coma prior to arrival, with a presenting temperature of 38.3°C, Glasgow Coma Scale (GCS) of 3, pinpoint pupils, and global hypotonia. Vital signs at presentation included a heart rate of 180 beats per minute, blood pressure of 120/80 mmHg, and a random blood glucose of 14 mg/dL. Physical examination revealed widespread crackles on auscultation, indicating pulmonary edema or aspiration-related pulmonary injury. Serum cholinesterase activity and lactate levels were not measured due to institutional limitations.\\n\\nThe diagnosis was established as severe organophosphate poisoning (OPP) with concomitant aspiration pneumonitis. Given the severity of respiratory failure and the unavailability of intensive care resources, non-invasive ventilation (NIV) was initiated using bubble continuous positive airway pressure (b-CPAP), which improved oxygen saturation to 99–100%. Hypoglycemia was managed with a dextrose bolus, and tachycardia was treated with 20 mL/kg of normal saline. Empirical intravenous antibiotics were administered for suspected aspiration-related pneumonia. Intravenous atropine was administered at a dose of 0.02 mg/kg/dose, with the first dose leading to a significant tachycardia, prompting discontinuation due to hemodynamic instability. Pralidoxime, a reactivating agent for organophosphate-inhibited acetylcholinesterase, was not administered due to unavailability.\\n\\nWithin 3 hours of presentation, the patient underwent a fresh-whole-blood exchange blood transfusion (FWB-EBT) of 500 mL to rapidly reduce circulating organophosphate metabolites and mitigate cholinergic toxicity. The GCS improved to 9/15 following this intervention. Over the subsequent 15 hours, blood glucose fluctuated between 41 and 259 mg/dL, eventually stabilizing with continued management. On day 2 of admission, the patient developed thready pulses and hypotension, prompting a second bolus of normal saline. Dopamine infusion was initiated at 5 mcg/kg/min via peripheral venous access, and intravenous mannitol was discontinued. A second FWB-EBT of 500 mL was performed.\\n\\nOver the first 30 hours, there was a progressive improvement in consciousness and resolution of respiratory distress. However, rhonchi were noted, managed with nebulized salbutamol and budesonide, and the patient was transitioned to nasal prong oxygen therapy, maintaining stable oxygen saturation at 97%. A chest radiograph on day 2 revealed bilateral pulmonary infiltrates consistent with aspiration pneumonia. Full recovery of consciousness was achieved by the 39th hour of admission. Antioxidant therapy was initiated with intravenous vitamin C and B, and oral vitamin E and zinc to mitigate oxidative stress associated with acute organophosphate toxicity. A graded reintroduction of oral diet was implemented over the following 48 hours.\\n\\nThe patient’s clinical course remained stable, and he was discharged home after 10 days of hospitalization. However, follow-up care was not maintained, resulting in loss to follow-up. The patient did not develop the intermediate syndrome, a known risk in organophosphate poisoning characterized by delayed neuromuscular weakness typically occurring 24–96 hours post-exposure, which may have been attributed to the rapid clinical response, early intervention, and absence of prolonged cholinesterase inhibition.\\n\\nThis case underscores the pathophysiological mechanisms of organophosphate toxicity, including acetylcholinesterase inhibition leading to excessive acetylcholine accumulation at neuromuscular junctions and in the central nervous system, resulting in muscarinic and nicotinic cholinergic overstimulation. The clinical manifestations include bronchospasm, respiratory failure, hypotension, seizures, and coma. Aspiration of lipid-rich substances like palm oil may exacerbate pulmonary injury through direct chemical irritation and mechanical obstruction, contributing to secondary pneumonia. The use of exchange transfusion in this setting is a rare but effective strategy to rapidly remove toxic metabolites and restore physiological balance in severe OPP, particularly in resource-limited settings where advanced supportive care is not available. The absence of pralidoxime administration highlights a critical gap in access to antidotal therapy in"}
{"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 hard, and there was no sign of a heart attack or heart muscle damage. After checking her heart with different scans, doctors found a birth defect: the main blood vessel going to her right heart was missing at the start. This missing part caused her heart to beat wrong and made her feel sick. Doctors found the problem spot on a small muscle in her heart, fixed it with a special treatment, and now she feels fine and has not had any problems since.\"\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 hard, and there was no sign of a heart attack or heart muscle damage. After checking her heart with different scans, doctors found a birth defect: the main blood vessel going to her right heart was missing at the start. This missing part caused her heart to beat wrong and made her feel sick. Doctors found the problem spot on a small muscle in her heart, fixed it with a special treatment, and now she feels fine and has not had any problems since."}
{"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 high levels of markers for heart stress. A 12-lead ECG ruled out a heart attack, and a cardiac MRI did not show signs of heart muscle disease. Because of this, a cardiac CT scan (CCTA) was done to look for a congenital heart problem. The scan found that the opening of the right coronary artery was completely missing, and the rest of the artery was supplied by a collateral branch from another artery. This is a rare congenital anomaly. She was referred to a specialist center for congenital heart disease. There, an electrophysiological study found that the arrhythmia was starting in the posteromedial papillary muscle, and this area was successfully treated with radiofrequency ablation. Since the procedure, she has been symptom-free 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 high levels of markers for heart stress. A 12-lead ECG ruled out a heart attack, and a cardiac MRI did not show signs of heart muscle disease. Because of this, a cardiac CT scan (CCTA) was done to look for a congenital heart problem. The scan found that the opening of the right coronary artery was completely missing, and the rest of the artery was supplied by a collateral branch from another artery. This is a rare congenital anomaly. She was referred to a specialist center for congenital heart disease. There, an electrophysiological study found that the arrhythmia was starting in the posteromedial papillary muscle, and this area was successfully treated with radiofrequency ablation. Since the procedure, she has been symptom-free 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 female 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), indicative of myocardial injury and cardiac stress, respectively. These findings prompted admission to the coronary care unit with a clinical suspicion of cardiogenic shock due to underlying structural or electrical cardiac pathology.\\n\\nFive years prior, she had experienced cardiogenic shock secondary to fascicular ventricular tachycardia. Subsequent evaluation with cardiac magnetic resonance (CMR) and transesophageal electrophysiological study (TEES) yielded inconclusive results, leading to a diagnosis of tachycardiomiopathy. She was initiated on standard medical therapy including angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and beta-blockers, with regular follow-up scheduled. Clinically, no further events were reported during this interval.\\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, reinforcing the need for further anatomical evaluation. Given the clinical history of recurrent arrhythmias and cardiogenic shock in the absence of obstructive coronary disease, cardiac computed tomography angiography (CCTA) was performed to assess for undiagnosed congenital coronary anomalies.\\n\\nCCTA 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. Intravenous contrast was administered at 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy). The imaging demonstrated a regular origin of the left main coronary artery, with a well-developed left anterior descending (LAD) artery featuring a wide ramus intermedium, two diagonal branches, and a thin, non-dominant left circumflex artery. No evidence of significant stenosis or obstructive coronary artery disease was identified. 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 arising from the distal LAD, which courses along the lateral wall of the right ventricle, traverses the distal atrioventricular groove, and gives rise to thin posterior interventricular and posterolateral arteries. Additionally, a small branch originating from the mid-LAD was observed to supply the sinoatrial node, potentially contributing to arrhythmogenic substrate.\\n\\nThe differential diagnosis of cardiogenic shock in a young, otherwise healthy adult must consider both acquired and congenital etiologies. While myocardial infarction is a common cause, it was ruled out by the absence of typical ST-segment changes on ECG and normal coronary anatomy in the absence of obstructive lesions. Similarly, conventional cardiomyopathies were excluded by CMR, which showed no evidence of diffuse myocardial fibrosis or structural remodeling. In such cases, undiagnosed congenital coronary anomalies, particularly ostial atresia of a major coronary artery, represent a critical but often overlooked cause of sustained ventricular arrhythmias and cardiogenic shock.\\n\\nFollowing CCTA, an echo-stress test was performed, which confirmed inducible myocardial ischemia in the inferior wall—consistent with the anatomical origin of the arrhythmic focus. The patient was referred to a specialized center for congenital cardiovascular disease. There, she underwent transcatheter radiofrequency ablation targeting the posteromedial papillary muscle, the identified site of sustained ventricular tachycardia. The procedure successfully eliminated the arrhythmic substrate. Post-procedural follow-up at 6 months demonstrated sustained clinical stability, with complete absence of symptoms and no recurrence of arrhythmias. She is currently managed with acetylsalicylic acid and verapamil for antiplatelet and rate control, respectively. The case underscores the importance of advanced imaging in diagnosing congenital coronary anomalies in young patients with recurrent arrhythmias and cardiogenic shock, particularly when conventional tests fail to identify underlying pathology.\\n\\nScientific context: Ostial atresia of the right coronary artery is a rare congenital anomaly in which the origin of the RCA is completely obstructed or absent, leading to", "generated_text": "{\n  \"proficient_health_literacy\": \"A 19-year-old female 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), indicative of myocardial injury and cardiac stress, respectively. These findings prompted admission to the coronary care unit with a clinical suspicion of cardiogenic shock due to underlying structural or electrical cardiac pathology.\\n\\nFive years prior, she had experienced cardiogenic shock secondary to fascicular ventricular tachycardia. Subsequent evaluation with cardiac magnetic resonance (CMR) and transesophageal electrophysiological study (TEES) yielded inconclusive results, leading to a diagnosis of tachycardiomiopathy. She was initiated on standard medical therapy including angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and beta-blockers, with regular follow-up scheduled. Clinically, no further events were reported during this interval.\\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, reinforcing the need for further anatomical evaluation. Given the clinical history of recurrent arrhythmias and cardiogenic shock in the absence of obstructive coronary disease, cardiac computed tomography angiography (CCTA) was performed to assess for undiagnosed congenital coronary anomalies.\\n\\nCCTA 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. Intravenous contrast was administered at 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy). The imaging demonstrated a regular origin of the left main coronary artery, with a well-developed left anterior descending (LAD) artery featuring a wide ramus intermedium, two diagonal branches, and a thin, non-dominant left circumflex artery. No evidence of significant stenosis or obstructive coronary artery disease was identified. 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 arising from the distal LAD, which courses along the lateral wall of the right ventricle, traverses the distal atrioventricular groove, and gives rise to thin posterior interventricular and posterolateral arteries. Additionally, a small branch originating from the mid-LAD was observed to supply the sinoatrial node, potentially contributing to arrhythmogenic substrate.\\n\\nThe differential diagnosis of cardiogenic shock in a young, otherwise healthy adult must consider both acquired and congenital etiologies. While myocardial infarction is a common cause, it was ruled out by the absence of typical ST-segment changes on ECG and normal coronary anatomy in the absence of obstructive lesions. Similarly, conventional cardiomyopathies were excluded by CMR, which showed no evidence of diffuse myocardial fibrosis or structural remodeling. In such cases, undiagnosed congenital coronary anomalies, particularly ostial atresia of a major coronary artery, represent a critical but often overlooked cause of sustained ventricular arrhythmias and cardiogenic shock.\\n\\nFollowing CCTA, an echo-stress test was performed, which confirmed inducible myocardial ischemia in the inferior wall—consistent with the anatomical origin of the arrhythmic focus. The patient was referred to a specialized center for congenital cardiovascular disease. There, she underwent transcatheter radiofrequency ablation targeting the posteromedial papillary muscle, the identified site of sustained ventricular tachycardia. The procedure successfully eliminated the arrhythmic substrate. Post-procedural follow-up at 6 months demonstrated sustained clinical stability, with complete absence of symptoms and no recurrence of arrhythmias. She is currently managed with acetylsalicylic acid and verapamil for antiplatelet and rate control, respectively. The case underscores the importance of advanced imaging in diagnosing congenital coronary anomalies in young patients with recurrent arrhythmias and cardiogenic shock, particularly when conventional tests fail to identify underlying pathology.\\n\\nScientific context: Ostial atresia of the right coronary artery is a rare congenital anomaly in which the origin of the RCA is completely obstructed or absent, leading to"}
{"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 stuck under the floor of his nose, covered with mucus and crust, 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. After getting permission from his parents, the button was gently removed with a small tool while he was sitting up. The nose healed well, and after the removal, he was given a salt water rinse to keep it clean. At his follow-up two weeks later, everything looked normal and he was doing fine.\"\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 stuck under the floor of his nose, covered with mucus and crust, 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. After getting permission from his parents, the button was gently removed with a small tool while he was sitting up. The nose healed well, and after the removal, he was given a salt water rinse to keep it clean. At his follow-up two weeks later, everything looked normal and he was doing fine."}
{"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 medical history presents to the emergency department (ED) with substernal, non-radiating chest pain, orthopnoea, dry non-productive cough, and subjective fevers lasting 3–4 days. Family history includes paternal grandfather with non-ischaemic cardiomyopathy and pacemaker implantation at age 86. Patient lives with both parents, denies smoking, alcohol use, recreational drug use, or abuse. Occupationally, he works at an auto parts shop and plans to begin college. Initial workup reveals 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 echocardiogram (TTE) demonstrates left ventricular ejection fraction (LVEF) of 40%, severe left ventricular concentric hypertrophy (septal thickness 1.9 cm, inferolateral wall 2.2 cm), and mild posterior pericardial effusion. Coxsackie virus A and B titres are elevated, consistent with viral myopericarditis. Symptoms initially improve with ibuprofen and colchicine. Cardiac catheterization shows no coronary artery disease. Repeat TTE reveals LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral walls, elevated left ventricular end-diastolic pressure, and diastolic dysfunction. Chest CT angiogram demonstrates pneumonitis and pericardial effusion. Clinical picture is initially attributed to Coxsackie virus-induced myopericarditis, with continued medical management.\\n\\nOn day 4 of admission, the patient develops diaphoresis, tachycardia, and hypotension with undetectable blood pressure. Repeat TTE shows large pericardial effusion with signs of impending cardiac tamponade. Pericardiocentesis is performed, during which the patient experiences pulseless electrical activity (PEA) cardiac arrest requiring 30 minutes of advanced cardiovascular support. He is intubated, placed on veno-arterial extracorporeal membrane oxygenation (VA ECMO), and initiated on vasopressor therapy (norepinephrine 5 mcg/min and vasopressin 0.05 units/min). Significant bleeding from ECMO cannula necessitates multiple transfusions (9 packed red blood cells, 10 platelets, 10 cryoprecipitate, 4 fresh frozen plasma). Transferred to a tertiary center, endomyocardial biopsy (EMB) is performed due to concern for fulminant myocarditis or infiltrative cardiomyopathy. Histopathology shows no evidence of inflammatory or infiltrative processes. Repeat Coxsackie serology confirms positivity for Coxsackie A9, B2, and B6. Epstein-Barr virus (EBV) DNA quantitative PCR is elevated at 133,000 IU/mL. Subsequent TTE reveals severely reduced LVEF (10%–15%) with persistent severe concentric left ventricular hypertrophy.\\n\\nThe patient is initiated on intravenous immunoglobulin (IVIG) for suspected Coxsackie myocarditis and broad-spectrum antibiotics due to worsening leucocytosis without identifiable infectious focus. Colchicine is discontinued due to concern for rhabdomyolysis, evidenced by serum creatine kinase of 2874 U/L. Vasopressors are withdrawn, and the patient is extubated. He subsequently develops 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 decline, cardiac function improves on repeat TTE with LVEF of 25%–30%, prompting consideration of ECMO removal—however, this is unsuccessful. The patient remains on ECMO and is evaluated for left ventricular assist device (LVAD) placement, which is deemed contraindicated due to global concentric hypertrophy. Multidisciplinary team consensus supports emergency listing for heart transplantation, with potential transition to intra-aortic balloon pump (IABP) and inotrope support.\\n\\nDuring evaluation for transplantation, an incisional biopsy of a 1×1 inch, painless, rubbery, mobile lesion in the right upper extremity is performed. Pathology reveals aggressive EBV-positive natural killer/T-cell lymphoma (NK/TCL) with cytotoxic immunophenotype (positive for CD2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1), and diffuse co-expression of Epstein-Barr virus-encoded small RNAs (EBER) by in", "generated_text": "{\n  \"proficient_health_literacy\": \"An 18-year-old Hispanic male with no significant medical history presents to the emergency department (ED) with substernal, non-radiating chest pain, orthopnoea, dry non-productive cough, and subjective fevers lasting 3–4 days. Family history includes paternal grandfather with non-ischaemic cardiomyopathy and pacemaker implantation at age 86. Patient lives with both parents, denies smoking, alcohol use, recreational drug use, or abuse. Occupationally, he works at an auto parts shop and plans to begin college. Initial workup reveals 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 echocardiogram (TTE) demonstrates left ventricular ejection fraction (LVEF) of 40%, severe left ventricular concentric hypertrophy (septal thickness 1.9 cm, inferolateral wall 2.2 cm), and mild posterior pericardial effusion. Coxsackie virus A and B titres are elevated, consistent with viral myopericarditis. Symptoms initially improve with ibuprofen and colchicine. Cardiac catheterization shows no coronary artery disease. Repeat TTE reveals LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral walls, elevated left ventricular end-diastolic pressure, and diastolic dysfunction. Chest CT angiogram demonstrates pneumonitis and pericardial effusion. Clinical picture is initially attributed to Coxsackie virus-induced myopericarditis, with continued medical management.\\n\\nOn day 4 of admission, the patient develops diaphoresis, tachycardia, and hypotension with undetectable blood pressure. Repeat TTE shows large pericardial effusion with signs of impending cardiac tamponade. Pericardiocentesis is performed, during which the patient experiences pulseless electrical activity (PEA) cardiac arrest requiring 30 minutes of advanced cardiovascular support. He is intubated, placed on veno-arterial extracorporeal membrane oxygenation (VA ECMO), and initiated on vasopressor therapy (norepinephrine 5 mcg/min and vasopressin 0.05 units/min). Significant bleeding from ECMO cannula necessitates multiple transfusions (9 packed red blood cells, 10 platelets, 10 cryoprecipitate, 4 fresh frozen plasma). Transferred to a tertiary center, endomyocardial biopsy (EMB) is performed due to concern for fulminant myocarditis or infiltrative cardiomyopathy. Histopathology shows no evidence of inflammatory or infiltrative processes. Repeat Coxsackie serology confirms positivity for Coxsackie A9, B2, and B6. Epstein-Barr virus (EBV) DNA quantitative PCR is elevated at 133,000 IU/mL. Subsequent TTE reveals severely reduced LVEF (10%–15%) with persistent severe concentric left ventricular hypertrophy.\\n\\nThe patient is initiated on intravenous immunoglobulin (IVIG) for suspected Coxsackie myocarditis and broad-spectrum antibiotics due to worsening leucocytosis without identifiable infectious focus. Colchicine is discontinued due to concern for rhabdomyolysis, evidenced by serum creatine kinase of 2874 U/L. Vasopressors are withdrawn, and the patient is extubated. He subsequently develops 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 decline, cardiac function improves on repeat TTE with LVEF of 25%–30%, prompting consideration of ECMO removal—however, this is unsuccessful. The patient remains on ECMO and is evaluated for left ventricular assist device (LVAD) placement, which is deemed contraindicated due to global concentric hypertrophy. Multidisciplinary team consensus supports emergency listing for heart transplantation, with potential transition to intra-aortic balloon pump (IABP) and inotrope support.\\n\\nDuring evaluation for transplantation, an incisional biopsy of a 1×1 inch, painless, rubbery, mobile lesion in the right upper extremity is performed. Pathology reveals aggressive EBV-positive natural killer/T-cell lymphoma (NK/TCL) with cytotoxic immunophenotype (positive for CD2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1), and diffuse co-expression of Epstein-Barr virus-encoded small RNAs (EBER) by in"}
{"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 fats in his blood for years got a rare eye problem where one eye (right) swelled up fast and couldn’t move properly. This caused constant double vision that made daily life hard. His thyroid was normal, but his body made a little bit more of a certain immune protein. Steroid shots helped a little, but didn’t fix the double vision or the eye movement. Doctors had to do surgery on both sides of the eye socket to give room for the eye to move better. A tissue sample from the eye muscle showed it was full of scar tissue and fat. This scar tissue is what made the eye move so poorly.\"\n}", "generated_text": "A 50-year-old man who smoked a lot and had bad fats in his blood for years got a rare eye problem where one eye (right) swelled up fast and couldn’t move properly. This caused constant double vision that made daily life hard. His thyroid was normal, but his body made a little bit more of a certain immune protein. Steroid shots helped a little, but didn’t fix the double vision or the eye movement. Doctors had to do surgery on both sides of the eye socket to give room for the eye to move better. A tissue sample from the eye muscle showed it was full of scar tissue and fat. This scar tissue is what made the eye move so poorly."}
{"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 history of smoking and high cholesterol developed a rare condition called euthyroid single muscular Graves' ophthalmopathy. He had no family history of thyroid problems, but he did have a family history of heart disease and diabetes. Over several years, he noticed swelling in the right eye, pain when moving his eyes, redness, and constant double vision (diplopia) that made daily life difficult. His eyesight was normal, but he could not move his right eye properly, especially upward, which worsened his double vision. Tests showed mild signs of thyroid autoimmunity, but his thyroid function was normal. Imaging showed that only the right inferior rectus muscle was enlarged and damaged, while the rest of the eye muscles were normal. A biopsy confirmed massive scar tissue (fibrosis) in that muscle. The patient tried steroid treatment, which helped reduce inflammation but did not fix the double vision or muscle damage. He then had surgery to relieve pressure in the eye socket, and this helped slightly. However, the main problem — the scarred muscle — remained. This case highlights a rare form of eye swelling where only one muscle is affected, and it can cause serious vision problems even when the thyroid is healthy.\"\n}", "generated_text": "A 50-year-old man with a history of smoking and high cholesterol developed a rare condition called euthyroid single muscular Graves' ophthalmopathy. He had no family history of thyroid problems, but he did have a family history of heart disease and diabetes. Over several years, he noticed swelling in the right eye, pain when moving his eyes, redness, and constant double vision (diplopia) that made daily life difficult. His eyesight was normal, but he could not move his right eye properly, especially upward, which worsened his double vision. Tests showed mild signs of thyroid autoimmunity, but his thyroid function was normal. Imaging showed that only the right inferior rectus muscle was enlarged and damaged, while the rest of the eye muscles were normal. A biopsy confirmed massive scar tissue (fibrosis) in that muscle. The patient tried steroid treatment, which helped reduce inflammation but did not fix the double vision or muscle damage. He then had surgery to relieve pressure in the eye socket, and this helped slightly. However, the main problem — the scarred muscle — remained. This case highlights a rare form of eye swelling where only one muscle is affected, and it 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 report a rare case of euthyroid unilateral Graves' ophthalmopathy (GO) characterized by early, massive mono-muscular fibrosis in the right inferior rectus muscle of a 50-year-old male patient. The patient had a significant family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no personal or familial history of thyroid autoimmune disorders. He was a daily smoker (20 cigarettes/day) since age 30 and had long-standing dyslipidemia, with laboratory values 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, accompanied by 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 a severe reduction in elevation and persistent depression of the right globe in primary position, as assessed by the Gorman score, with constant diplopia. Clinical Activity Score (CAS) was 3/7, indicating moderate active inflammation, and eyelid aperture was 14 mm (right) versus 10 mm (left), with Hertel measurements of 24 mm (right) and 18 mm (left), confirming significant orbital expansion. The muscle orbit area ratio in the right orbit was 0.25 (in-house Autocad method; normal threshold vn ≤ 0.20 ± 0.03), indicating pathological enlargement of the inferior rectus muscle. High-resolution CT imaging (1.25 mm contiguous slices, 200 mA, 120 kV, pitch 0.5) demonstrated marked enlargement of the lower rectus body extending to the insertion tendon, while all other extraocular muscles in both orbits showed normal morphology. Thyroid function tests were euthyroid, with only a mild elevation in thyroid-stimulating hormone receptor antibody (TSH-R-Ab) levels at 1.75 mU/L (normal <1.5 mU/L), suggesting a low-grade autoimmune component without overt thyroid dysfunction. Electrophysiological evaluation revealed a slight reduction in the amplitude of the p100 wave in the right eye, indicating early neuro-ocular dysfunction possibly secondary to inflammatory or fibrotic muscle changes. Thyroid ultrasound demonstrated a thyroiditis-like pattern, consistent with chronic inflammation, but no evidence of nodules or thyroid autoimmunity was found. Routine systemic laboratory evaluations were unremarkable, excluding hematological or systemic diseases. Initial treatment consisted of intravenous corticosteroid pulse therapy (Solumedrol, 4500 mg cumulative dose over 12 weeks), which effectively resolved inflammatory signs and symptoms such as swelling and pain. However, functional outcomes—including Gorman score, Hertel measurements, and diplopia—remained unchanged, and electrophysiological parameters and visual acuity deteriorated, suggesting irreversible or progressive neuro-ocular compromise. Due to the persistent symptoms and lack of response to medical therapy, the patient underwent two-wall orbital surgical decompression in conjunction with continued parenteral glucocorticoid therapy. Histopathological examination of the right inferior rectus muscle biopsy revealed extensive fibrosis with significant adipose tissue infiltration, confirming the presence of early and severe fibrotic transformation of the extraocular muscle, likely driven by chronic inflammation and/or metabolic stress. This case highlights the potential for rapid progression of mono-muscular fibrosis in euthyroid GO, even in the absence of overt thyroid autoimmunity, and underscores the importance of early surgical intervention in patients with severe ocular motility dysfunction and persistent fibrotic changes, particularly in those with comorbidities such as smoking and dyslipidemia.\"\n}", "generated_text": "We report a rare case of euthyroid unilateral Graves' ophthalmopathy (GO) characterized by early, massive mono-muscular fibrosis in the right inferior rectus muscle of a 50-year-old male patient. The patient had a significant family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no personal or familial history of thyroid autoimmune disorders. He was a daily smoker (20 cigarettes/day) since age 30 and had long-standing dyslipidemia, with laboratory values 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, accompanied by 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 a severe reduction in elevation and persistent depression of the right globe in primary position, as assessed by the Gorman score, with constant diplopia. Clinical Activity Score (CAS) was 3/7, indicating moderate active inflammation, and eyelid aperture was 14 mm (right) versus 10 mm (left), with Hertel measurements of 24 mm (right) and 18 mm (left), confirming significant orbital expansion. The muscle orbit area ratio in the right orbit was 0.25 (in-house Autocad method; normal threshold vn ≤ 0.20 ± 0.03), indicating pathological enlargement of the inferior rectus muscle. High-resolution CT imaging (1.25 mm contiguous slices, 200 mA, 120 kV, pitch 0.5) demonstrated marked enlargement of the lower rectus body extending to the insertion tendon, while all other extraocular muscles in both orbits showed normal morphology. Thyroid function tests were euthyroid, with only a mild elevation in thyroid-stimulating hormone receptor antibody (TSH-R-Ab) levels at 1.75 mU/L (normal <1.5 mU/L), suggesting a low-grade autoimmune component without overt thyroid dysfunction. Electrophysiological evaluation revealed a slight reduction in the amplitude of the p100 wave in the right eye, indicating early neuro-ocular dysfunction possibly secondary to inflammatory or fibrotic muscle changes. Thyroid ultrasound demonstrated a thyroiditis-like pattern, consistent with chronic inflammation, but no evidence of nodules or thyroid autoimmunity was found. Routine systemic laboratory evaluations were unremarkable, excluding hematological or systemic diseases. Initial treatment consisted of intravenous corticosteroid pulse therapy (Solumedrol, 4500 mg cumulative dose over 12 weeks), which effectively resolved inflammatory signs and symptoms such as swelling and pain. However, functional outcomes—including Gorman score, Hertel measurements, and diplopia—remained unchanged, and electrophysiological parameters and visual acuity deteriorated, suggesting irreversible or progressive neuro-ocular compromise. Due to the persistent symptoms and lack of response to medical therapy, the patient underwent two-wall orbital surgical decompression in conjunction with continued parenteral glucocorticoid therapy. Histopathological examination of the right inferior rectus muscle biopsy revealed extensive fibrosis with significant adipose tissue infiltration, confirming the presence of early and severe fibrotic transformation of the extraocular muscle, likely driven by chronic inflammation and/or metabolic stress. This case highlights the potential for rapid progression of mono-muscular fibrosis in euthyroid GO, even in the absence of overt thyroid autoimmunity, and underscores the importance of early surgical intervention in patients with severe ocular motility dysfunction and persistent fibrotic changes, particularly in those with comorbidities such as smoking and dyslipidemia."}
{"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 belly pain and vomiting for four days. Doctors first thought it was a stomach bug, but it didn’t go away. His stomach was swollen, and tests showed his small intestine was blocked. A scan found a piece of intestine stuck in a small opening in the 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 the 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 gotten trapped. 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 a pediatric surgery clinic, doing well and able to eat again.\"\n}", "generated_text": "A 15-year-old boy had belly pain and vomiting for four days. Doctors first thought it was a stomach bug, but it didn’t go away. His stomach was swollen, and tests showed his small intestine was blocked. A scan found a piece of intestine stuck in a small opening in the 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 the 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 gotten trapped. 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 a pediatric surgery clinic, doing well and able to eat again."}
{"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 improve. He was admitted for further testing.\\n\\nHis abdomen was distended and had signs of intestinal blockage, which was confirmed by an abdominal X-ray. A CT scan showed a small intestine loop trapped at the Winslow hiatus — a key opening in the abdomen — causing an intestinal obstruction. This condition is called an internal hernia.\\n\\nThe surgery began with laparoscopy, a minimally invasive procedure, but the view was poor due to the distended intestines and the position of the liver. Because of this, the surgery was changed to an open approach — a larger incision in the middle of the abdomen — to better see and fix the problem.\\n\\nDuring the surgery, the doctors found a five-centimeter section of the ileum (a part of the small intestine) that had herniated through the Winslow hiatus. The loop was successfully reduced, and no part of the intestine needed to be removed. No preventive steps were taken to reduce the risk of it coming back.\\n\\nAfter surgery, the boy had a temporary slowdown 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 the 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. He is doing well and has normal bowel function.\"\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 improve. He was admitted for further testing.\n\nHis abdomen was distended and had signs of intestinal blockage, which was confirmed by an abdominal X-ray. A CT scan showed a small intestine loop trapped at the Winslow hiatus — a key opening in the abdomen — causing an intestinal obstruction. This condition is called an internal hernia.\n\nThe surgery began with laparoscopy, a minimally invasive procedure, but the view was poor due to the distended intestines and the position of the liver. Because of this, the surgery was changed to an open approach — a larger incision in the middle of the abdomen — to better see and fix the problem.\n\nDuring the surgery, the doctors found a five-centimeter section of the ileum (a part of the small intestine) that had herniated through the Winslow hiatus. The loop was successfully reduced, and no part of the intestine needed to be removed. No preventive steps were taken to reduce the risk of it coming back.\n\nAfter surgery, the boy had a temporary slowdown 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 the 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. He is doing well and has normal bowel function."}
{"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 significant medical history or prior 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 ongoing epigastric pain and biliary vomiting, prompting admission for further investigation.\\n\\nPhysical examination revealed acceptable general condition, afebrile status, and mild signs of dehydration. Abdominal distension was noted, with absent peritoneal signs and diminished bowel sounds. Laboratory studies were unremarkable. Abdominal radiography demonstrated findings consistent with small bowel obstruction.\\n\\nUrgent computed tomography (CT) imaging revealed ascites and marked dilation of small intestinal loops, indicating interposition of a small bowel segment at the proximal transition zone of the epiploic fat, specifically at the level of the Winslow hiatus. The CT showed a distinct change in caliber of the small intestine at this anatomical landmark, suggesting intraperitoneal herniation of a segment of ileum through the Winslow hiatus.\\n\\nSurgical management began with exploratory laparoscopy. Intraoperatively, dilated loops of small intestine, including the terminal ileum, cecum, and ascending colon, were observed in the right hypochondrium, with the cecum exhibiting high mobility and no adhesions to the right parietocolic space. Proximal to the terminal ileum, multiple small bowel loops were identified in the depth of the theoretical location of the Winslow hiatus. Attempts to mobilize the cecum and terminal ileum toward the right iliac fossa were unsuccessful due to interference from the lower edge of the liver and the distended bowel loops. A percutaneous puncture of a dilated loop was attempted to decompress gas and improve visualization, but this did not resolve the obstruction.\\n\\nGiven the poor visualization and inability to accurately localize the site of caliber change, a conversion to a supraumbilical midline laparotomy was performed. In the opened abdominal cavity, the site of caliber change in the ileum was identified at approximately 40 centimetres from the ileocecal valve, confirming a herniation of a 5-centimetre segment of ileum through the Winslow hiatus. The herniated loop demonstrated characteristic congestive imprints at both ends, consistent with mechanical compression and ischemic changes due to entrapment. The normal caliber of the Winslow hiatus was confirmed, and no preventive surgical technique (such as hernia repair or mesh placement) was applied to reduce the risk of recurrence.\\n\\nPostoperatively, the patient developed a transient paralytic ileus, which resolved over five days, allowing nasogastric tube removal and initiation of oral intake with good tolerance. Concurrently, a pelvic collection developed, which was managed conservatively with broad-spectrum antibiotics and drainage via percutaneous catheterization, resulting in favorable clinical course. The patient was discharged ten days after surgery with preserved gastrointestinal transit, absence of fever, and stable general condition.\\n\\nThe patient is currently under outpatient follow-up in the paediatric surgery clinic. This case highlights the diagnostic challenge of internal hernias, particularly in adolescents, where clinical presentation may mimic common gastrointestinal disorders, and imaging findings can be subtle. The Winslow hiatus, a potential site for intraperitoneal herniation due to its anatomical variability and the presence of epiploic foramen, remains a critical anatomical consideration in the evaluation of small bowel obstruction. Internal hernias are often asymptomatic until obstruction occurs, and their diagnosis relies on high-resolution imaging and surgical exploration. The absence of preventive measures in this case underscores the need for further study into risk factors and long-term outcomes in pediatric populations, particularly given the potential for recurrence in cases involving small bowel entrapment through the Winslow hiatus.\"\n}", "generated_text": "We present a clinical case of a 15-year-old male with no significant medical history or prior 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 ongoing epigastric pain and biliary vomiting, prompting admission for further investigation.\n\nPhysical examination revealed acceptable general condition, afebrile status, and mild signs of dehydration. Abdominal distension was noted, with absent peritoneal signs and diminished bowel sounds. Laboratory studies were unremarkable. Abdominal radiography demonstrated findings consistent with small bowel obstruction.\n\nUrgent computed tomography (CT) imaging revealed ascites and marked dilation of small intestinal loops, indicating interposition of a small bowel segment at the proximal transition zone of the epiploic fat, specifically at the level of the Winslow hiatus. The CT showed a distinct change in caliber of the small intestine at this anatomical landmark, suggesting intraperitoneal herniation of a segment of ileum through the Winslow hiatus.\n\nSurgical management began with exploratory laparoscopy. Intraoperatively, dilated loops of small intestine, including the terminal ileum, cecum, and ascending colon, were observed in the right hypochondrium, with the cecum exhibiting high mobility and no adhesions to the right parietocolic space. Proximal to the terminal ileum, multiple small bowel loops were identified in the depth of the theoretical location of the Winslow hiatus. Attempts to mobilize the cecum and terminal ileum toward the right iliac fossa were unsuccessful due to interference from the lower edge of the liver and the distended bowel loops. A percutaneous puncture of a dilated loop was attempted to decompress gas and improve visualization, but this did not resolve the obstruction.\n\nGiven the poor visualization and inability to accurately localize the site of caliber change, a conversion to a supraumbilical midline laparotomy was performed. In the opened abdominal cavity, the site of caliber change in the ileum was identified at approximately 40 centimetres from the ileocecal valve, confirming a herniation of a 5-centimetre segment of ileum through the Winslow hiatus. The herniated loop demonstrated characteristic congestive imprints at both ends, consistent with mechanical compression and ischemic changes due to entrapment. The normal caliber of the Winslow hiatus was confirmed, and no preventive surgical technique (such as hernia repair or mesh placement) was applied to reduce the risk of recurrence.\n\nPostoperatively, the patient developed a transient paralytic ileus, which resolved over five days, allowing nasogastric tube removal and initiation of oral intake with good tolerance. Concurrently, a pelvic collection developed, which was managed conservatively with broad-spectrum antibiotics and drainage via percutaneous catheterization, resulting in favorable clinical course. The patient was discharged ten days after surgery with preserved gastrointestinal transit, absence of fever, and stable general condition.\n\nThe patient is currently under outpatient follow-up in the paediatric surgery clinic. This case highlights the diagnostic challenge of internal hernias, particularly in adolescents, where clinical presentation may mimic common gastrointestinal disorders, and imaging findings can be subtle. The Winslow hiatus, a potential site for intraperitoneal herniation due to its anatomical variability and the presence of epiploic foramen, remains a critical anatomical consideration in the evaluation of small bowel obstruction. Internal hernias are often asymptomatic until obstruction occurs, and their diagnosis relies on high-resolution imaging and surgical exploration. The absence of preventive measures in this case underscores the need for further study into risk factors and long-term outcomes in pediatric populations, particularly given the potential for recurrence in cases involving small bowel entrapment through the Winslow hiatus."}
{"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 had any gynecological visits. 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 with the pain and 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 had any gynecological visits. 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 with the pain and infection. She went home after being watched for 4 hours and her pain went away."}