{ "username": "user1", "current_index": 1, "queue": [ { "index": 20, "label": "low_health_literacy", "original_text": "Patient A.P., female, born in 1979, has been diagnosed with dilatation cardiomyopathy in 1996. Anamnestically, disease started with tonsillitis, possible myocarditis (which was never proven), with pronounced symptoms of heart failure and general symptoms. She was hospitalized and after one month, the left ventricular ejection fraction was 10% with the aforementioned signs of congestive heart failure. She was hospitalized for 10 months and 9 days, with standard therapy for vitally endangered patient, oxygen support, numerous adjuvant therapy, and intensive monitoring. Therapy was administered (ACE inhibitor - ramipril, cardiotonic - digoxin, beta-blockers - metoprolol and combination of diuretics - furosemide and spironolactone), with the indication of heart transplantation. Clinical improvement occured with an ejection fraction that was gradually increasing and at the age of 21 she entered in remission or stabilization phase, with the ejection fraction value of 48-57% (regular echocardiography was performed every three months). For the following four years therapy remained the same, but in Jun 2004 (after an episode of low immunity), ejection fraction fell to 25%, with a clinical deterioration of the disease. The patient was hospitalized for a period of two months, and the condition stabilized, and she was discharged with therapy that was the same but without cardiotonic. Ejection fraction was stabilized, and in year 2006 it was 50%. At the age of 27, the patient decided on the first pregnancy that was successful with beta blocker (metoprolol) in therapy. After the first pregnancy, the ejection fraction was 40% and she was treated with the same therapy with eplerenone (25 mg) instead of spironolactone. The ejection fraction was controlled and did not fall below 45%. At the end of 2015 the patient became pregnant for the second time, and the pregnancy went neatly until eighth month (35 weeks), when she was urgently admitted to hospital, due to sense of suffocation and inability to walk. Ejection fraction decreased to 18% (brain natriuretic peptide (BNP) was 2600 pg/ mL (reference values are 100-400 pg/ mL)). During pregnancy she received only metoprolol in therapy. Physicians decide to continue with her pregnancy, in the 39th week they performed c-section, and the condition stabilized again after twenty days. In October 2016 new mode of therapy was administered, ramipril (2.5 mg, in the morning), metoprolol (47.5 mg, in the morning), spironolactone (50 mg, once a day) and ivabradine (5 mg, twice a day) with torasemide (5 mg, once a day). LifeVest Defibrillator was carried from 06 December 2016 until 27 February 2017 when it was removed. When removed and after examination (ejection fraction was 44%) she continued with ramipril therapy (1.25 mg) metoprolol (23.75 mg), torasemide (5 mg), spironolactone (25 mg) and ivabradine (7.5 mg, twice a day) with potassium supplements, and compliance with non-pharmacological measures (fluid intake restricted to 1.5 L/ day). The echocardiographic finding in March 2017 showed left ventricular dilatation with moderately reduced left ventricular function and left ventricular wall hypokinesia with ejection fraction of 44% (insignificant pericardial effusion was present, inferior vena cava with physiological flow, preserved valves function - Dopler sonography showed slight insufficiency of mitral valve with dilatation of anulus). Evaluation of a patient with ejection fraction 44% showed no indication for an implantable cardioverter defibrillator (ICD), and conservative procedure and medication therapy were recommended. Regular check-ups and body mass reduction, regular control of renal function parameters and electrolytes were recommended. She is led under the diagnosis of dilated cardiomyopathy and heart failure NYHA stage II without any indication for the ICD prophylactic implantation.", "generated_summary": "A.P. is a 38\u2011year\u2011old woman. At age 17, her heart became big and weak. This may have started after a bad throat infection.\nShe stayed in the hospital for 10 months and 10 days. She was very sick and waiting for a new heart. Her heart rhythm was not dangerously abnormal. Her heart\u2019s pump was very weak.\nDoctors treated her heart failure. They also tried to prevent dangerous heart rhythms and blood clots.\nHer heart got better. This kind of recovery happens in about 16 out of 100 people. The better phase lasted 4 years.\nThen the disease got worse for 2 years.\nAfter that, she was stable. She had her first baby, and the pregnancy was normal.\nIn the middle of her second pregnancy, her heart got worse again. It improved a few months after the birth.\nIn May 2017, she was doing well on medicines. These medicines relax blood vessels, slow the heart, help the body get rid of extra water, and slow the heart\u2019s natural pacemaker. She had no limits in daily activity. She is a mother of two. She did not have a job." }, { "index": 20, "label": "intermediate_health_literacy", "original_text": "Patient A.P., female, born in 1979, has been diagnosed with dilatation cardiomyopathy in 1996. Anamnestically, disease started with tonsillitis, possible myocarditis (which was never proven), with pronounced symptoms of heart failure and general symptoms. She was hospitalized and after one month, the left ventricular ejection fraction was 10% with the aforementioned signs of congestive heart failure. She was hospitalized for 10 months and 9 days, with standard therapy for vitally endangered patient, oxygen support, numerous adjuvant therapy, and intensive monitoring. Therapy was administered (ACE inhibitor - ramipril, cardiotonic - digoxin, beta-blockers - metoprolol and combination of diuretics - furosemide and spironolactone), with the indication of heart transplantation. Clinical improvement occured with an ejection fraction that was gradually increasing and at the age of 21 she entered in remission or stabilization phase, with the ejection fraction value of 48-57% (regular echocardiography was performed every three months). For the following four years therapy remained the same, but in Jun 2004 (after an episode of low immunity), ejection fraction fell to 25%, with a clinical deterioration of the disease. The patient was hospitalized for a period of two months, and the condition stabilized, and she was discharged with therapy that was the same but without cardiotonic. Ejection fraction was stabilized, and in year 2006 it was 50%. At the age of 27, the patient decided on the first pregnancy that was successful with beta blocker (metoprolol) in therapy. After the first pregnancy, the ejection fraction was 40% and she was treated with the same therapy with eplerenone (25 mg) instead of spironolactone. The ejection fraction was controlled and did not fall below 45%. At the end of 2015 the patient became pregnant for the second time, and the pregnancy went neatly until eighth month (35 weeks), when she was urgently admitted to hospital, due to sense of suffocation and inability to walk. Ejection fraction decreased to 18% (brain natriuretic peptide (BNP) was 2600 pg/ mL (reference values are 100-400 pg/ mL)). During pregnancy she received only metoprolol in therapy. Physicians decide to continue with her pregnancy, in the 39th week they performed c-section, and the condition stabilized again after twenty days. In October 2016 new mode of therapy was administered, ramipril (2.5 mg, in the morning), metoprolol (47.5 mg, in the morning), spironolactone (50 mg, once a day) and ivabradine (5 mg, twice a day) with torasemide (5 mg, once a day). LifeVest Defibrillator was carried from 06 December 2016 until 27 February 2017 when it was removed. When removed and after examination (ejection fraction was 44%) she continued with ramipril therapy (1.25 mg) metoprolol (23.75 mg), torasemide (5 mg), spironolactone (25 mg) and ivabradine (7.5 mg, twice a day) with potassium supplements, and compliance with non-pharmacological measures (fluid intake restricted to 1.5 L/ day). The echocardiographic finding in March 2017 showed left ventricular dilatation with moderately reduced left ventricular function and left ventricular wall hypokinesia with ejection fraction of 44% (insignificant pericardial effusion was present, inferior vena cava with physiological flow, preserved valves function - Dopler sonography showed slight insufficiency of mitral valve with dilatation of anulus). Evaluation of a patient with ejection fraction 44% showed no indication for an implantable cardioverter defibrillator (ICD), and conservative procedure and medication therapy were recommended. Regular check-ups and body mass reduction, regular control of renal function parameters and electrolytes were recommended. She is led under the diagnosis of dilated cardiomyopathy and heart failure NYHA stage II without any indication for the ICD prophylactic implantation.", "generated_summary": "A.P. is a 38\u2011year\u2011old woman who developed dilated cardiomyopathy at age 17, likely on the background of infectious myocarditis after a throat infection. She was hospitalized for 10 months and 10 days with severe heart failure and a very low ejection fraction while being evaluated for heart transplantation. There was no clearly dangerous arrhythmia. Treatment focused on heart failure care and on preventing arrhythmias and blood clots.\nHer heart function recovered\u2014a remission seen in about 16% of patients\u2014and that improvement lasted 4 years. She then had a two\u2011year worsening, followed by several stable years and a normal first pregnancy. During her second pregnancy, she experienced a flare in the second trimester with postpartum dilated cardiomyopathy that lasted a couple of months, then improved.\nAs of May 2017, she was stable on guideline\u2011based therapy (an ACE inhibitor, a beta\u2011blocker, diuretics, and an If\u2011channel blocker), reported no limitation in physical activity, and was a mother of two and unemployed." }, { "index": 20, "label": "proficient_health_literacy", "original_text": "Patient A.P., female, born in 1979, has been diagnosed with dilatation cardiomyopathy in 1996. Anamnestically, disease started with tonsillitis, possible myocarditis (which was never proven), with pronounced symptoms of heart failure and general symptoms. She was hospitalized and after one month, the left ventricular ejection fraction was 10% with the aforementioned signs of congestive heart failure. She was hospitalized for 10 months and 9 days, with standard therapy for vitally endangered patient, oxygen support, numerous adjuvant therapy, and intensive monitoring. Therapy was administered (ACE inhibitor - ramipril, cardiotonic - digoxin, beta-blockers - metoprolol and combination of diuretics - furosemide and spironolactone), with the indication of heart transplantation. Clinical improvement occured with an ejection fraction that was gradually increasing and at the age of 21 she entered in remission or stabilization phase, with the ejection fraction value of 48-57% (regular echocardiography was performed every three months). For the following four years therapy remained the same, but in Jun 2004 (after an episode of low immunity), ejection fraction fell to 25%, with a clinical deterioration of the disease. The patient was hospitalized for a period of two months, and the condition stabilized, and she was discharged with therapy that was the same but without cardiotonic. Ejection fraction was stabilized, and in year 2006 it was 50%. At the age of 27, the patient decided on the first pregnancy that was successful with beta blocker (metoprolol) in therapy. After the first pregnancy, the ejection fraction was 40% and she was treated with the same therapy with eplerenone (25 mg) instead of spironolactone. The ejection fraction was controlled and did not fall below 45%. At the end of 2015 the patient became pregnant for the second time, and the pregnancy went neatly until eighth month (35 weeks), when she was urgently admitted to hospital, due to sense of suffocation and inability to walk. Ejection fraction decreased to 18% (brain natriuretic peptide (BNP) was 2600 pg/ mL (reference values are 100-400 pg/ mL)). During pregnancy she received only metoprolol in therapy. Physicians decide to continue with her pregnancy, in the 39th week they performed c-section, and the condition stabilized again after twenty days. In October 2016 new mode of therapy was administered, ramipril (2.5 mg, in the morning), metoprolol (47.5 mg, in the morning), spironolactone (50 mg, once a day) and ivabradine (5 mg, twice a day) with torasemide (5 mg, once a day). LifeVest Defibrillator was carried from 06 December 2016 until 27 February 2017 when it was removed. When removed and after examination (ejection fraction was 44%) she continued with ramipril therapy (1.25 mg) metoprolol (23.75 mg), torasemide (5 mg), spironolactone (25 mg) and ivabradine (7.5 mg, twice a day) with potassium supplements, and compliance with non-pharmacological measures (fluid intake restricted to 1.5 L/ day). The echocardiographic finding in March 2017 showed left ventricular dilatation with moderately reduced left ventricular function and left ventricular wall hypokinesia with ejection fraction of 44% (insignificant pericardial effusion was present, inferior vena cava with physiological flow, preserved valves function - Dopler sonography showed slight insufficiency of mitral valve with dilatation of anulus). Evaluation of a patient with ejection fraction 44% showed no indication for an implantable cardioverter defibrillator (ICD), and conservative procedure and medication therapy were recommended. Regular check-ups and body mass reduction, regular control of renal function parameters and electrolytes were recommended. She is led under the diagnosis of dilated cardiomyopathy and heart failure NYHA stage II without any indication for the ICD prophylactic implantation.", "generated_summary": "Patient A.P., female, born 1979, was diagnosed with dilated cardiomyopathy (DCM) in 1996 after a prodrome of tonsillitis with possible myocarditis (never proven), presenting with pronounced symptoms of heart failure and systemic symptoms. After one month of hospitalization, the left ventricular ejection fraction (LVEF) was 10% with signs of congestive heart failure. She remained hospitalized for 10 months and 9 days with standard therapy for a vitally endangered patient, oxygen support, numerous adjuvant therapies, and intensive monitoring. Pharmacotherapy included an ACE inhibitor (ramipril), a cardiotonic (digoxin), a beta\u2011blocker (metoprolol), and combined diuretics (furosemide and spironolactone), with the indication of heart transplantation.\nClinical improvement ensued with gradual LVEF increase; by age 21 she entered a remission/stabilization phase with LVEF 48\u201357%, with echocardiography every three months. Over the next four years therapy was unchanged. In June 2004, following an episode of low immunity, LVEF fell to 25% with clinical deterioration; she was hospitalized for two months, stabilized, and discharged on the same regimen but without the cardiotonic. LVEF stabilized and was 50% in 2006. At age 27, the first pregnancy was successful on metoprolol. Postpartum, LVEF was 40%, and eplerenone 25 mg replaced spironolactone; LVEF remained \u226545%.\nAt the end of 2015 she became pregnant again. The course was uneventful until 35 weeks, when she was urgently admitted with dyspnea and inability to walk. LVEF was 18% and BNP 2600 pg/mL (reference 100\u2013400 pg/mL). During pregnancy she received only metoprolol. The team decided to continue the pregnancy; at 39 weeks a cesarean section was performed, and the condition stabilized after 20 days.\nIn October 2016, therapy was adjusted to ramipril 2.5 mg qAM, metoprolol 47.5 mg qAM, spironolactone 50 mg daily, ivabradine 5 mg BID, and torasemide 5 mg daily. A LifeVest defibrillator was worn from 06 Dec 2016 to 27 Feb 2017, then removed. On removal/examination, LVEF was 44%. Maintenance therapy was ramipril 1.25 mg, metoprolol 23.75 mg, torasemide 5 mg, spironolactone 25 mg, and ivabradine 7.5 mg BID, plus potassium supplements and non\u2011pharmacological measures (fluid restriction to 1.5 L/day).\nEchocardiography in March 2017 showed left ventricular dilatation with moderately reduced LV systolic function and LV wall hypokinesia; LVEF 44%; insignificant pericardial effusion; inferior vena cava with physiological flow; preserved valvular function with Doppler evidence of slight mitral regurgitation due to annular dilatation. With LVEF 44%, there was no indication for implantable cardioverter\u2011defibrillator (ICD); conservative management and medical therapy were recommended, along with regular follow\u2011up, body mass reduction, and periodic monitoring of renal function and electrolytes. She carries the diagnosis of DCM with heart failure NYHA class II, without indication for prophylactic ICD implantation. As of May 2017 she was clinically stable on ACE inhibitor, beta\u2011blocker, diuretics, and an If\u2011channel blocker, and is a mother of two and unemployed." }, { "index": 21, "label": "low_health_literacy", "original_text": "27-year-old male patient with a history of fibrous dysplasia in the right proximal femur, which was managed prophylactically to reduce the risk of fracture 20 years ago by curettage (intralesional resection), application of bone graft and fixation with osteosynthesis material, which was removed one year after the fixation. Two weeks before admission to hospital, the patient experienced pain after a fall with low energy mechanism characterised by axial load and rotational component of the right hip, which resulted in pain intensity 8/10 on the visual analogue scale (VAS) at the level of the inguinal fold and right thigh, which incapacitated him for walking. Radiological control was performed at four weeks, observing all prosthetic components adequately. The patient was discharged clinically and haemodynamically stable, without the need for transfusion of blood products. During his follow-up in the postoperative period (612 weeks), the patient continued with partial support until day 20, in which he began with full support even accompanied by a walker. Radiological control was performed at four weeks, observing all prosthetic components adequately. The patient is currently carrying out daily activities with slight limitation due to claudicatio intermittens caused by the incision in the middle gluteus. However, he was able to participate in low-impact sports activities, such as walking and expressed great satisfaction with the functional outcome of the procedure.\n", "generated_summary": "A 27-year-old man came to the emergency room with a break at the top of his right thigh bone, near the hip. The break happened after a small fall that twisted his hip and pushed straight down on it. As a child, he had a bone problem in that same area and had surgery to help prevent breaks. The doctors scraped out the weak bone, added graft bone, and used metal to hold it for a time. That metal was removed a year later. To fix the new break for good, the doctors removed the damaged top part of the thigh bone and put in a new artificial hip. They also used metal bands to help hold things steady. They sent a piece of the bone to the lab. The test showed he still had the same bone condition from childhood." }, { "index": 21, "label": "intermediate_health_literacy", "original_text": "27-year-old male patient with a history of fibrous dysplasia in the right proximal femur, which was managed prophylactically to reduce the risk of fracture 20 years ago by curettage (intralesional resection), application of bone graft and fixation with osteosynthesis material, which was removed one year after the fixation. Two weeks before admission to hospital, the patient experienced pain after a fall with low energy mechanism characterised by axial load and rotational component of the right hip, which resulted in pain intensity 8/10 on the visual analogue scale (VAS) at the level of the inguinal fold and right thigh, which incapacitated him for walking. Radiological control was performed at four weeks, observing all prosthetic components adequately. The patient was discharged clinically and haemodynamically stable, without the need for transfusion of blood products. During his follow-up in the postoperative period (612 weeks), the patient continued with partial support until day 20, in which he began with full support even accompanied by a walker. Radiological control was performed at four weeks, observing all prosthetic components adequately. The patient is currently carrying out daily activities with slight limitation due to claudicatio intermittens caused by the incision in the middle gluteus. However, he was able to participate in low-impact sports activities, such as walking and expressed great satisfaction with the functional outcome of the procedure.\n", "generated_summary": "A 27-year-old man presented to the emergency department with a fracture at the base of the neck of the right femur after a low-energy fall that involved axial loading and a twisting motion of the right hip. He had a known history of fibrous dysplasia in the right proximal femur and, 20 years earlier, underwent curettage, bone grafting, and prophylactic fixation; the hardware was removed one year later, and biopsy at that time confirmed fibrous dysplasia. Given the pattern and pathologic nature of the current fracture, the team proceeded with a definitive treatment: wide resection of the proximal femur and a total hip replacement using a modular prosthesis, along with cerclage to secure the construct. An excisional biopsy performed during surgery confirmed the same fibrous dysplasia that had been treated in childhood. He recovered well: imaging at four weeks showed the components in good position, and he progressed from partial weight-bearing to full weight-bearing with a walker around day 20. He returned to daily activities with a mild, intermittent limp related to the gluteus medius incision and was able to do low-impact activities such as walking, reporting high satisfaction with the outcome." }, { "index": 21, "label": "proficient_health_literacy", "original_text": "27-year-old male patient with a history of fibrous dysplasia in the right proximal femur, which was managed prophylactically to reduce the risk of fracture 20 years ago by curettage (intralesional resection), application of bone graft and fixation with osteosynthesis material, which was removed one year after the fixation. Two weeks before admission to hospital, the patient experienced pain after a fall with low energy mechanism characterised by axial load and rotational component of the right hip, which resulted in pain intensity 8/10 on the visual analogue scale (VAS) at the level of the inguinal fold and right thigh, which incapacitated him for walking. Radiological control was performed at four weeks, observing all prosthetic components adequately. The patient was discharged clinically and haemodynamically stable, without the need for transfusion of blood products. During his follow-up in the postoperative period (612 weeks), the patient continued with partial support until day 20, in which he began with full support even accompanied by a walker. Radiological control was performed at four weeks, observing all prosthetic components adequately. The patient is currently carrying out daily activities with slight limitation due to claudicatio intermittens caused by the incision in the middle gluteus. However, he was able to participate in low-impact sports activities, such as walking and expressed great satisfaction with the functional outcome of the procedure.\n", "generated_summary": "We report a 27-year-old male who presented to the emergency department with a right femoral fracture at the base of the neck on pathologic ground, classified as Garden II, Pauwells III, AO 31B2.3r, following a low-energy mechanism characterized by axial load with a rotational component of the right hip. He had a history of fibrous dysplasia (DF) of the right proximal femur managed prophylactically 20 years prior with intralesional resection (curettage), bone grafting, and fixation with unspecified osteosynthesis material in the pertrochanteric region; the biopsy subsequently confirmed DF, and the osteosynthesis was removed one year later. Two weeks before admission he sustained the fall, developed VAS 8/10 pain localized to the right inguinal fold and thigh, and was unable to ambulate. Given the fracture characteristics and pathologic substrate, a definitive, curative approach was undertaken: wide resection of the proximal femur and total hip arthroplasty with a modular prosthesis, including cerclage placement, plus an excisional biopsy. The biopsy corroborated recurrence/persistence of the same DF treated in childhood. Postoperatively, the patient remained clinically and hemodynamically stable without transfusion requirements. He maintained partial weight-bearing until approximately day 20, then advanced to full weight-bearing with a walker. Radiological control at four weeks demonstrated all prosthetic components in adequate position. At follow-up (approximately 6\u201312 weeks), he resumed activities of daily living with slight limitation due to claudicatio intermittens attributed to the middle gluteus incision, participated in low-impact sports (e.g., walking), and expressed high satisfaction with functional outcomes." }, { "index": 22, "label": "low_health_literacy", "original_text": "A 4-year-old boy with stage IV neuroblastoma received four cycles of chemotherapy, including high-dose chemotherapy including busulfan and melphalan, followed by autologous peripheral blood stem cell transplantation with autologous bone marrow supplementation. After eight additional cycles of chemotherapy consisting of temozolomide and irinotecan, which led to stable disease, the patient underwent preparative conditioning with fludarabine (150 mg/m2), melphalan (140 mg/m2), and 12 Gy of TBI for subsequent allogeneic CBT. The patient received tacrolimus and a short-term course of methotrexate for GVHD prophylaxis. The patient underwent engraftment on day 17. He then developed grade 3 GVHD, which was managed by increasing the prednisolone dose and was later discharged on day 85. The patient also received proton beam therapy (39.6 Gy) from days 121 to 150 post-transplantation for a right supra-mediastinum tumor with residual I123-MIBG accumulation in the right adrenal gland.\n\nThe patient remained healthy with no evidence of GVHD until presentation at our hospital with a productive cough on day 159. As his older brother displayed similar cold symptoms, a rapid antigen test for RSV was performed, which revealed a positive result. His respiratory symptoms gradually worsened, and he revisited our hospital on day 194 with dyspnea and intercostal retractions. Upon admission, he was given 0.7-1.0 mg/kg of prednisolone, which failed to improve his respiratory condition. Chest computed tomography on day 231 revealed infiltration, ground-glass opacity, and septal thickening in the bilateral lung fields along with right pleural effusion. Echocardiography showed an elevated tricuspid regurgitation peak velocity of 4.1 m/s and an interventricular septum close to the isobaric, indicating the presence of PH. In addition, pericardial effusion was detected. On day 231, the patient was transferred to the pediatric intensive care unit, where mechanical ventilation and inhaled nitric oxide (NO) were initiated. Thoracoscopic lung biopsy on day 244 revealed diffuse intra-alveolar hemorrhage and edema on hematoxylin-eosin (HE)-stained samples. Elastica van Gieson staining revealed diffuse obstructive lesions due to fibrocellular components with plump endothelial cells in the pre-septal pulmonary veins and venules. While pulmonary muscular arteries and arterioles showed mild medial hypertrophy and focal intimal thickening (Heath-Edwards Grade 2), severe stenosis with concentric intimal fibrosis or plexiform lesions was present. Based on these results, the patient was diagnosed with PVOD with mild pulmonary arterial/arteriolar lesions. Of note, HE staining also revealed enlarged type II pneumocytes with multinucleated and giant cell-like features, indicating the presence of prior lung injury that was likely attributable to his preceding viral infection.", "generated_summary": "A 4-year-old boy had a cancer called neuroblastoma that had spread. He got strong chemotherapy and then had his own stem cells put back. Later, he received a cord blood transplant from a donor. About a month before his lung problem, he had cold-like symptoms and tested positive for RSV. On day 194 after the cord blood transplant, he developed a rare problem where the small veins in the lungs get blocked (PVOD). A lung biopsy showed damage that looked like it came from a virus, along with the PVOD changes. This suggests the RSV infection may have helped trigger the lung problem." }, { "index": 22, "label": "intermediate_health_literacy", "original_text": "A 4-year-old boy with stage IV neuroblastoma received four cycles of chemotherapy, including high-dose chemotherapy including busulfan and melphalan, followed by autologous peripheral blood stem cell transplantation with autologous bone marrow supplementation. After eight additional cycles of chemotherapy consisting of temozolomide and irinotecan, which led to stable disease, the patient underwent preparative conditioning with fludarabine (150 mg/m2), melphalan (140 mg/m2), and 12 Gy of TBI for subsequent allogeneic CBT. The patient received tacrolimus and a short-term course of methotrexate for GVHD prophylaxis. The patient underwent engraftment on day 17. He then developed grade 3 GVHD, which was managed by increasing the prednisolone dose and was later discharged on day 85. The patient also received proton beam therapy (39.6 Gy) from days 121 to 150 post-transplantation for a right supra-mediastinum tumor with residual I123-MIBG accumulation in the right adrenal gland.\n\nThe patient remained healthy with no evidence of GVHD until presentation at our hospital with a productive cough on day 159. As his older brother displayed similar cold symptoms, a rapid antigen test for RSV was performed, which revealed a positive result. His respiratory symptoms gradually worsened, and he revisited our hospital on day 194 with dyspnea and intercostal retractions. Upon admission, he was given 0.7-1.0 mg/kg of prednisolone, which failed to improve his respiratory condition. Chest computed tomography on day 231 revealed infiltration, ground-glass opacity, and septal thickening in the bilateral lung fields along with right pleural effusion. Echocardiography showed an elevated tricuspid regurgitation peak velocity of 4.1 m/s and an interventricular septum close to the isobaric, indicating the presence of PH. In addition, pericardial effusion was detected. On day 231, the patient was transferred to the pediatric intensive care unit, where mechanical ventilation and inhaled nitric oxide (NO) were initiated. Thoracoscopic lung biopsy on day 244 revealed diffuse intra-alveolar hemorrhage and edema on hematoxylin-eosin (HE)-stained samples. Elastica van Gieson staining revealed diffuse obstructive lesions due to fibrocellular components with plump endothelial cells in the pre-septal pulmonary veins and venules. While pulmonary muscular arteries and arterioles showed mild medial hypertrophy and focal intimal thickening (Heath-Edwards Grade 2), severe stenosis with concentric intimal fibrosis or plexiform lesions was present. Based on these results, the patient was diagnosed with PVOD with mild pulmonary arterial/arteriolar lesions. Of note, HE staining also revealed enlarged type II pneumocytes with multinucleated and giant cell-like features, indicating the presence of prior lung injury that was likely attributable to his preceding viral infection.", "generated_summary": "A 4-year-old boy with metastatic neuroblastoma received intensive treatment, including chemotherapy, an autologous stem cell transplant, and then an allogeneic cord blood transplant. About a month after he developed upper respiratory symptoms and tested positive for RSV, he presented on day 194 post\u2013cord blood transplant with worsening breathing problems and was ultimately diagnosed with pulmonary veno-occlusive disease (PVOD), a rare form of pulmonary hypertension caused by blockage of small lung veins. Lung biopsy not only confirmed PVOD-related changes but also showed lung injury patterns consistent with a recent viral infection. Taken together, the timing of his RSV infection and the biopsy findings suggest RSV may have contributed to the onset of PVOD." }, { "index": 22, "label": "proficient_health_literacy", "original_text": "A 4-year-old boy with stage IV neuroblastoma received four cycles of chemotherapy, including high-dose chemotherapy including busulfan and melphalan, followed by autologous peripheral blood stem cell transplantation with autologous bone marrow supplementation. After eight additional cycles of chemotherapy consisting of temozolomide and irinotecan, which led to stable disease, the patient underwent preparative conditioning with fludarabine (150 mg/m2), melphalan (140 mg/m2), and 12 Gy of TBI for subsequent allogeneic CBT. The patient received tacrolimus and a short-term course of methotrexate for GVHD prophylaxis. The patient underwent engraftment on day 17. He then developed grade 3 GVHD, which was managed by increasing the prednisolone dose and was later discharged on day 85. The patient also received proton beam therapy (39.6 Gy) from days 121 to 150 post-transplantation for a right supra-mediastinum tumor with residual I123-MIBG accumulation in the right adrenal gland.\n\nThe patient remained healthy with no evidence of GVHD until presentation at our hospital with a productive cough on day 159. As his older brother displayed similar cold symptoms, a rapid antigen test for RSV was performed, which revealed a positive result. His respiratory symptoms gradually worsened, and he revisited our hospital on day 194 with dyspnea and intercostal retractions. Upon admission, he was given 0.7-1.0 mg/kg of prednisolone, which failed to improve his respiratory condition. Chest computed tomography on day 231 revealed infiltration, ground-glass opacity, and septal thickening in the bilateral lung fields along with right pleural effusion. Echocardiography showed an elevated tricuspid regurgitation peak velocity of 4.1 m/s and an interventricular septum close to the isobaric, indicating the presence of PH. In addition, pericardial effusion was detected. On day 231, the patient was transferred to the pediatric intensive care unit, where mechanical ventilation and inhaled nitric oxide (NO) were initiated. Thoracoscopic lung biopsy on day 244 revealed diffuse intra-alveolar hemorrhage and edema on hematoxylin-eosin (HE)-stained samples. Elastica van Gieson staining revealed diffuse obstructive lesions due to fibrocellular components with plump endothelial cells in the pre-septal pulmonary veins and venules. While pulmonary muscular arteries and arterioles showed mild medial hypertrophy and focal intimal thickening (Heath-Edwards Grade 2), severe stenosis with concentric intimal fibrosis or plexiform lesions was present. Based on these results, the patient was diagnosed with PVOD with mild pulmonary arterial/arteriolar lesions. Of note, HE staining also revealed enlarged type II pneumocytes with multinucleated and giant cell-like features, indicating the presence of prior lung injury that was likely attributable to his preceding viral infection.", "generated_summary": "A 4-year-old boy with stage IV neuroblastoma underwent four cycles of chemotherapy including high-dose busulfan and melphalan, followed by autologous peripheral blood stem cell transplantation with autologous bone marrow supplementation. After eight additional cycles of temozolomide and irinotecan resulting in stable disease, he received conditioning with fludarabine (150 mg/m2), melphalan (140 mg/m2), and 12 Gy total body irradiation for allogeneic cord blood transplantation (CBT). GVHD prophylaxis consisted of tacrolimus and short-course methotrexate; neutrophil engraftment occurred on day 17. He developed grade 3 GVHD managed by escalation of prednisolone, and he was discharged on day 85. Proton beam therapy (39.6 Gy) was administered on days 121\u2013150 for a right supra-mediastinum tumor with residual I123-MIBG accumulation in the right adrenal gland. He remained clinically stable until day 159, when he developed a productive cough; a rapid antigen assay was positive for RSV, concordant with similar symptoms in an older sibling. Symptoms progressed, and on day 194 he re-presented with dyspnea and intercostal retractions. Prednisolone 0.7\u20131.0 mg/kg was initiated without clinical improvement. Chest CT on day 231 demonstrated bilateral infiltrates, ground-glass opacities, and septal thickening with a right pleural effusion. Echocardiography showed tricuspid regurgitation peak velocity of 4.1 m/s and an interventricular septum close to the isobaric position, consistent with pulmonary hypertension; pericardial effusion was also present. He was transferred to the PICU on day 231 for mechanical ventilation and inhaled nitric oxide. Thoracoscopic lung biopsy on day 244 revealed diffuse intra-alveolar hemorrhage and edema on HE staining. Elastica van Gieson staining demonstrated diffuse obstructive fibrocellular lesions with plump endothelial cells in pre-septal pulmonary veins and venules. Pulmonary muscular arteries/arterioles exhibited mild medial hypertrophy and focal intimal thickening (Heath-Edwards Grade 2), while severe stenosis with concentric intimal fibrosis or plexiform lesions was present. Overall, the findings supported a diagnosis of pulmonary veno-occlusive disease (PVOD) with mild pulmonary arterial/arteriolar lesions. Notably, HE staining showed enlarged type II pneumocytes with multinucleation and giant cell-like changes, indicating prior lung injury likely related to the antecedent RSV infection. In this post-CBT setting, the temporal association of RSV positivity (day 159) preceding clinical deterioration (day 194) and the biopsy evidence of viral-type injury support RSV as a potential contributor to PVOD onset, plausibly via endothelial injury in susceptible post-transplant pulmonary microvasculature." }, { "index": 23, "label": "low_health_literacy", "original_text": "65-year-old male with no personal or family history of pathology of relevance. His condition began in 2020 with productive cough that intensified and was accompanied by shortness of breath with small to medium effort; as well as loss of 10 kg of weight in a period of 4 months. He went to a doctor who requested a chest X-ray that showed massive, multilocular right pleural effusion with right bronchial obstruction and mediastinal lymphadenopathy. A thoracocentesis was performed with a biopsy of the right lung and parietal pleura. The histopathological study reported an adeno-squamous carcinoma. His evolution was bad, which is why he was referred to our institution. On admission, a physical examination found him cachectic, with right pulmonary hypoventilation, 92% oxygen saturation and pneumokoccal dysfunction, with no evidence of systemic or haemodynamic compromise. A chest X-ray was performed that showed complete opacity of the right hemithorax, and a pleural catheter was placed with a serohematic flow. In the histopathological study of the revision material, the lung parenchyma was replaced by a poorly differentiated neoplasm with a solid mantle and syncytia, surrounded by abundant lymphocytes and plasma cells. The neoplastic cells had large, ovoid nuclei, fine chromatin, prominent nucleolus and wide, poorly defined cytoplasm. An immunohistochemical study was performed that was positive for CKAE1/AE3, CK 5/6, p63, EBER ISH, and negative for Napsina A, TTF-1 and CK 7, which ruled out the reference diagnosis of adeno-squamous carcinoma and established the diagnosis of CTLP. Molecular study in the paraffin block was positive for PD-L1 (SP263) +++ in approximately 100% of the neoplastic cells, and negative for EGFR, K-RAS, ALK, ROS1. In order to confirm the pulmonary origin of the neoplasm, a nasopharyngeal examination was performed that was negative. In April 2021, a PET-CT was performed that reported a heterogeneous parahilary pulmonary lesion that compromised the main bronchus and caused atelectasis; as well as multiple cervical, mediastinal and peri-gastric lymphadenopathies. The catheter was removed due to partial resolution of the effusion and chemotherapy treatment with gemcitabine/cisplatin was initiated. He received 6 cycles, however, the patient reported hearing loss and AKIN I acute renal failure was documented, so cisplatin was changed to carboplatin, and maintenance durvalumab was continued. In December 2021, disease progression was documented and he died in January 2022 due to respiratory failure.\n", "generated_summary": "A 65-year-old man had a cough, trouble breathing, and lost weight. A chest scan showed a spot in the right lung. A needle test of the spot showed it was a kind of lung cancer. Under the microscope, the cancer cells were large and sat among many infection-fighting cells. Lab tests fit this cancer type and ruled out other common lung cancers. A virus called Epstein\u2013Barr was found inside the tumor cells. Another test showed a protein called PD-L1 was very high on the cancer cells. He was treated with strong chemotherapy and an immune therapy (gemcitabine, cisplatin, and durvalumab). The cancer kept growing. He died 9 months after diagnosis." }, { "index": 23, "label": "intermediate_health_literacy", "original_text": "65-year-old male with no personal or family history of pathology of relevance. His condition began in 2020 with productive cough that intensified and was accompanied by shortness of breath with small to medium effort; as well as loss of 10 kg of weight in a period of 4 months. He went to a doctor who requested a chest X-ray that showed massive, multilocular right pleural effusion with right bronchial obstruction and mediastinal lymphadenopathy. A thoracocentesis was performed with a biopsy of the right lung and parietal pleura. The histopathological study reported an adeno-squamous carcinoma. His evolution was bad, which is why he was referred to our institution. On admission, a physical examination found him cachectic, with right pulmonary hypoventilation, 92% oxygen saturation and pneumokoccal dysfunction, with no evidence of systemic or haemodynamic compromise. A chest X-ray was performed that showed complete opacity of the right hemithorax, and a pleural catheter was placed with a serohematic flow. In the histopathological study of the revision material, the lung parenchyma was replaced by a poorly differentiated neoplasm with a solid mantle and syncytia, surrounded by abundant lymphocytes and plasma cells. The neoplastic cells had large, ovoid nuclei, fine chromatin, prominent nucleolus and wide, poorly defined cytoplasm. An immunohistochemical study was performed that was positive for CKAE1/AE3, CK 5/6, p63, EBER ISH, and negative for Napsina A, TTF-1 and CK 7, which ruled out the reference diagnosis of adeno-squamous carcinoma and established the diagnosis of CTLP. Molecular study in the paraffin block was positive for PD-L1 (SP263) +++ in approximately 100% of the neoplastic cells, and negative for EGFR, K-RAS, ALK, ROS1. In order to confirm the pulmonary origin of the neoplasm, a nasopharyngeal examination was performed that was negative. In April 2021, a PET-CT was performed that reported a heterogeneous parahilary pulmonary lesion that compromised the main bronchus and caused atelectasis; as well as multiple cervical, mediastinal and peri-gastric lymphadenopathies. The catheter was removed due to partial resolution of the effusion and chemotherapy treatment with gemcitabine/cisplatin was initiated. He received 6 cycles, however, the patient reported hearing loss and AKIN I acute renal failure was documented, so cisplatin was changed to carboplatin, and maintenance durvalumab was continued. In December 2021, disease progression was documented and he died in January 2022 due to respiratory failure.\n", "generated_summary": "A 65-year-old man presented with cough, shortness of breath, and weight loss. Chest CT showed a poorly defined nodule in the right lung. A trans-thoracic biopsy confirmed a pulmonary lymphoepithelioma-like carcinoma: large polygonal tumor cells arranged in sheets with abundant lymphocytes and plasma cells. Immunohistochemistry supported this diagnosis (cytokeratin 5/6 and p63 positive; Napsin A and TTF-1 negative). PD-L1 expression was very high (about 100%), and the tumor cells were positive for Epstein\u2013Barr virus by EBER in situ hybridization. To confirm the lung as the primary site, a nasopharyngeal exam was negative. Additional testing from the case showed no EGFR, KRAS, ALK, or ROS1 alterations. Imaging later showed a right perihilar lesion with nodal disease. He received platinum-based chemotherapy (gemcitabine/cisplatin) with durvalumab; cisplatin was later changed to carboplatin because of side effects. Despite treatment, the disease progressed, and he died 9 months after diagnosis." }, { "index": 23, "label": "proficient_health_literacy", "original_text": "65-year-old male with no personal or family history of pathology of relevance. His condition began in 2020 with productive cough that intensified and was accompanied by shortness of breath with small to medium effort; as well as loss of 10 kg of weight in a period of 4 months. He went to a doctor who requested a chest X-ray that showed massive, multilocular right pleural effusion with right bronchial obstruction and mediastinal lymphadenopathy. A thoracocentesis was performed with a biopsy of the right lung and parietal pleura. The histopathological study reported an adeno-squamous carcinoma. His evolution was bad, which is why he was referred to our institution. On admission, a physical examination found him cachectic, with right pulmonary hypoventilation, 92% oxygen saturation and pneumokoccal dysfunction, with no evidence of systemic or haemodynamic compromise. A chest X-ray was performed that showed complete opacity of the right hemithorax, and a pleural catheter was placed with a serohematic flow. In the histopathological study of the revision material, the lung parenchyma was replaced by a poorly differentiated neoplasm with a solid mantle and syncytia, surrounded by abundant lymphocytes and plasma cells. The neoplastic cells had large, ovoid nuclei, fine chromatin, prominent nucleolus and wide, poorly defined cytoplasm. An immunohistochemical study was performed that was positive for CKAE1/AE3, CK 5/6, p63, EBER ISH, and negative for Napsina A, TTF-1 and CK 7, which ruled out the reference diagnosis of adeno-squamous carcinoma and established the diagnosis of CTLP. Molecular study in the paraffin block was positive for PD-L1 (SP263) +++ in approximately 100% of the neoplastic cells, and negative for EGFR, K-RAS, ALK, ROS1. In order to confirm the pulmonary origin of the neoplasm, a nasopharyngeal examination was performed that was negative. In April 2021, a PET-CT was performed that reported a heterogeneous parahilary pulmonary lesion that compromised the main bronchus and caused atelectasis; as well as multiple cervical, mediastinal and peri-gastric lymphadenopathies. The catheter was removed due to partial resolution of the effusion and chemotherapy treatment with gemcitabine/cisplatin was initiated. He received 6 cycles, however, the patient reported hearing loss and AKIN I acute renal failure was documented, so cisplatin was changed to carboplatin, and maintenance durvalumab was continued. In December 2021, disease progression was documented and he died in January 2022 due to respiratory failure.\n", "generated_summary": "A 65-year-old man developed productive cough, dyspnea on exertion, and 10-kg weight loss. Chest imaging included a CT scan demonstrating a poorly defined right-sided pulmonary nodule, and later PET-CT (April 2021) showed a heterogeneous parahilar pulmonary lesion involving the main bronchus with atelectasis, plus multiple cervical, mediastinal, and perigastric lymphadenopathies. Initial outside pathology called adenosquamous carcinoma, but review of trans-thoracic biopsy material (lung and parietal pleura) showed lung parenchyma replaced by a poorly differentiated neoplasm with solid mantles and syncytia, composed of large polygonal/ovoid cells with fine chromatin, prominent nucleoli, and abundant indistinct cytoplasm, in a dense lymphoplasmacytic background\u2014features consistent with pulmonary lymphoepithelioma-like carcinoma (LELC). Immunophenotype: CK AE1/AE3+, CK5/6+, p63+; EBER-ISH nuclear positivity; Napsin A\u2212, TTF-1\u2212, CK7\u2212, excluding conventional adenocarcinoma and supporting LELC. Molecular testing: PD-L1 (SP263) +++ in approximately 100% of tumor cells; no detectable EGFR, KRAS, ALK, or ROS1 alterations. Nasopharyngeal examination was negative, supporting pulmonary origin rather than nasopharyngeal carcinoma. He underwent platinum-based chemotherapy with gemcitabine/cisplatin for six cycles combined with durvalumab; ototoxicity and AKIN I acute kidney injury prompted a switch from cisplatin to carboplatin, with continuation of maintenance durvalumab. The disease progressed (documented December 2021), and he ultimately died of respiratory failure 9 months after diagnosis." }, { "index": 24, "label": "low_health_literacy", "original_text": "A 13-year-old male patient was admitted to the Children\u2019s Hospital in Damascus after noticing a palpable enlarged mass in the left inguinal region. His medical history was unremarkable except for a surgical intervention on his spine 6 years ago due to an accident, which resulted in the loss of motor function and sensation in both of his lower extremities.\n\nDue to the long period he had spent in bed, the patient developed decubitus sores on his left foot. The only finding on clinical examination was a mass in the left inguinal area, which was movable on deep structures and so was the overlaying skin on it. The mass was not tender on palpation, and no signs of local inflammation were observed.\n\nLaboratory tests revealed an Elevated ESR (119 mm/h in the first hour). Other Basic Laboratory tests including (Complete Blood Count, Liver function tests, electrolytes, Urea, Creatinine and LDH) were ordered and were within normal ranges for age. Ordering these tests was essential to rule out systemic diseases. Given the absence of indicative physical findings for systemic disorders or immunodeficiencies, additional tests like those for HIV or Direct Antiglobulin were deemed unnecessary.\n\nA CT of the abdomen, chest, and pelvis showed enlarged lymph nodes inferior to the inguinal ligament, with the largest measuring approximately (3.5\u2009\u00d7\u20092.4 cm). Other organs and nodes were within normal limits.\n\nAll of the above-mentioned investigations were essential to rule other high-risk diagnosis including lymphoma and leukemia. However, these were not sufficient to reach the definite diagnosis, so a decision of surgical resection of the nodes was taken.\n\nTo confirm the diagnoses and exclude other potential differentials presenting with enlarged lymph nodes, surgical removal of all of these enlarged nodes was performed under general anesthesia, and biopsies were sent for microscopic study.\n\nThe biopsy showed hyperplastic nodal architecture with proliferation of histiocytes and plasma cells with vascular proliferation, consistent with Plasma cell subtype of Castleman\u2019s Disease.\n\nThe patient was discharged from the hospital after 14-day period after ensuring that there were no remaining enlarged lymph nodes. The only recommendation was oral prednisolone. The patient underwent follow-up using a whole-body CT scan every three months. During each hospital visit, a comprehensive clinical examination and laboratory tests (e.g. Complete Blood Test, ESR, C-reactive protein, liver function tests, renal function tests) were performed in addition to the CT scan. After a 12-month follow-up period, the patient reported no new symptoms or enlarged lymph nodes. Additionally, no abnormalities were observed during clinical examination or in laboratory tests.", "generated_summary": "A 13-year-old boy felt a lump in his left groin, where the leg meets the body. He felt fine otherwise. The doctors took the lump out to make sure it was not something dangerous. Tests on the lump showed Castleman disease, plasma cell type. This type is very rare in children. This is the first known case of a single Castleman disease lump in the groin. The boy was checked for 12 months after surgery. No new swollen glands or symptoms showed up." }, { "index": 24, "label": "intermediate_health_literacy", "original_text": "A 13-year-old male patient was admitted to the Children\u2019s Hospital in Damascus after noticing a palpable enlarged mass in the left inguinal region. His medical history was unremarkable except for a surgical intervention on his spine 6 years ago due to an accident, which resulted in the loss of motor function and sensation in both of his lower extremities.\n\nDue to the long period he had spent in bed, the patient developed decubitus sores on his left foot. The only finding on clinical examination was a mass in the left inguinal area, which was movable on deep structures and so was the overlaying skin on it. The mass was not tender on palpation, and no signs of local inflammation were observed.\n\nLaboratory tests revealed an Elevated ESR (119 mm/h in the first hour). Other Basic Laboratory tests including (Complete Blood Count, Liver function tests, electrolytes, Urea, Creatinine and LDH) were ordered and were within normal ranges for age. Ordering these tests was essential to rule out systemic diseases. Given the absence of indicative physical findings for systemic disorders or immunodeficiencies, additional tests like those for HIV or Direct Antiglobulin were deemed unnecessary.\n\nA CT of the abdomen, chest, and pelvis showed enlarged lymph nodes inferior to the inguinal ligament, with the largest measuring approximately (3.5\u2009\u00d7\u20092.4 cm). Other organs and nodes were within normal limits.\n\nAll of the above-mentioned investigations were essential to rule other high-risk diagnosis including lymphoma and leukemia. However, these were not sufficient to reach the definite diagnosis, so a decision of surgical resection of the nodes was taken.\n\nTo confirm the diagnoses and exclude other potential differentials presenting with enlarged lymph nodes, surgical removal of all of these enlarged nodes was performed under general anesthesia, and biopsies were sent for microscopic study.\n\nThe biopsy showed hyperplastic nodal architecture with proliferation of histiocytes and plasma cells with vascular proliferation, consistent with Plasma cell subtype of Castleman\u2019s Disease.\n\nThe patient was discharged from the hospital after 14-day period after ensuring that there were no remaining enlarged lymph nodes. The only recommendation was oral prednisolone. The patient underwent follow-up using a whole-body CT scan every three months. During each hospital visit, a comprehensive clinical examination and laboratory tests (e.g. Complete Blood Test, ESR, C-reactive protein, liver function tests, renal function tests) were performed in addition to the CT scan. After a 12-month follow-up period, the patient reported no new symptoms or enlarged lymph nodes. Additionally, no abnormalities were observed during clinical examination or in laboratory tests.", "generated_summary": "A 13-year-old boy presented with a painless, movable mass in his left groin and no constitutional symptoms. To rule out serious causes such as lymphoma and to get a definite diagnosis, surgeons removed the mass. Pathology confirmed unicentric Castleman disease, plasma cell type\u2014a rare form in children\u2014and, to the authors\u2019 knowledge, this is the first reported case of UCD in the inguinal region. Over 12 months of follow-up, he had no new lymph node enlargement and no new symptoms." }, { "index": 24, "label": "proficient_health_literacy", "original_text": "A 13-year-old male patient was admitted to the Children\u2019s Hospital in Damascus after noticing a palpable enlarged mass in the left inguinal region. His medical history was unremarkable except for a surgical intervention on his spine 6 years ago due to an accident, which resulted in the loss of motor function and sensation in both of his lower extremities.\n\nDue to the long period he had spent in bed, the patient developed decubitus sores on his left foot. The only finding on clinical examination was a mass in the left inguinal area, which was movable on deep structures and so was the overlaying skin on it. The mass was not tender on palpation, and no signs of local inflammation were observed.\n\nLaboratory tests revealed an Elevated ESR (119 mm/h in the first hour). Other Basic Laboratory tests including (Complete Blood Count, Liver function tests, electrolytes, Urea, Creatinine and LDH) were ordered and were within normal ranges for age. Ordering these tests was essential to rule out systemic diseases. Given the absence of indicative physical findings for systemic disorders or immunodeficiencies, additional tests like those for HIV or Direct Antiglobulin were deemed unnecessary.\n\nA CT of the abdomen, chest, and pelvis showed enlarged lymph nodes inferior to the inguinal ligament, with the largest measuring approximately (3.5\u2009\u00d7\u20092.4 cm). Other organs and nodes were within normal limits.\n\nAll of the above-mentioned investigations were essential to rule other high-risk diagnosis including lymphoma and leukemia. However, these were not sufficient to reach the definite diagnosis, so a decision of surgical resection of the nodes was taken.\n\nTo confirm the diagnoses and exclude other potential differentials presenting with enlarged lymph nodes, surgical removal of all of these enlarged nodes was performed under general anesthesia, and biopsies were sent for microscopic study.\n\nThe biopsy showed hyperplastic nodal architecture with proliferation of histiocytes and plasma cells with vascular proliferation, consistent with Plasma cell subtype of Castleman\u2019s Disease.\n\nThe patient was discharged from the hospital after 14-day period after ensuring that there were no remaining enlarged lymph nodes. The only recommendation was oral prednisolone. The patient underwent follow-up using a whole-body CT scan every three months. During each hospital visit, a comprehensive clinical examination and laboratory tests (e.g. Complete Blood Test, ESR, C-reactive protein, liver function tests, renal function tests) were performed in addition to the CT scan. After a 12-month follow-up period, the patient reported no new symptoms or enlarged lymph nodes. Additionally, no abnormalities were observed during clinical examination or in laboratory tests.", "generated_summary": "A 13-year-old male with a history of spinal surgery 6 years earlier resulting in loss of motor function and sensation in both lower extremities presented with a palpable, mobile, non-tender mass in the left inguinal region and no constitutional symptoms. He had decubitus sores on the left foot. ESR was elevated at 119 mm/h; CBC, liver function tests, electrolytes, urea, creatinine, and LDH were within age-appropriate reference ranges. Given the lack of clinical indicators for systemic disease or immunodeficiency, additional tests (e.g., HIV, direct antiglobulin) were not pursued. CT of the chest, abdomen, and pelvis demonstrated enlarged lymph nodes inferior to the inguinal ligament, the largest measuring approximately 3.5 \u00d7 2.4 cm; no other organs or nodal stations were involved. Because lymphoma and leukemia were high-risk differential considerations and the work-up was non-diagnostic, excisional resection of all enlarged inguinal nodes was performed under general anesthesia. Histopathologic examination revealed hyperplastic nodal architecture with proliferation of histiocytes and plasma cells with vascular proliferation, consistent with the plasma cell subtype of Castleman\u2019s disease, confirming unicentric Castleman disease localized to the inguinal region. The patient was discharged 14 days postoperatively with no residual lymphadenopathy; oral prednisolone was recommended. Surveillance with whole-body CT every three months plus interval clinical examinations and laboratory tests (CBC, ESR, C-reactive protein, liver and renal function tests) showed no abnormalities. At 12 months, the patient remained asymptomatic with no new lymphadenopathy. To our knowledge, this represents the first reported case of unicentric Castleman disease occurring in the inguinal area; the plasma cell subtype is among the rarest Castleman variants in children." }, { "index": 25, "label": "low_health_literacy", "original_text": "The medical records of patients with a diagnosis of congenital myotonia studied and followed in the pediatric neurology consultation in a third-level hospital between 2015 and 2020 were reviewed. The inclusion criteria were to present a clinical diagnosis \u2013 myotonia, warm-up phenomenon, characteristic electromyographic pattern and/or family history \u2013 and/or a molecular diagnosis (mutation in the CLCN1 gene). The clinical signs and symptoms, as well as the results of the complementary explorations and the genetic mutation found, were collected by reviewing the medical record. Demographic variables (age and sex), course of the disease (age of onset, symptoms and signs, time elapsed until diagnosis and clinical evolution), family history and evaluation of the response to treatment were collected.\n\nFive cases with clinical diagnosis of congenital myotonia were identified (three with Becker's disease and two with Thomsen's disease). The incidence in relation to the number of births was estimated at 1:15,000 newborns for cases with Becker's phenotype and 1:21,000 newborns for Thomsen's phenotypes.\n\nMost of our patients were female, and the male was the only one who started before the age of six. The initial clinical presentation included myotonia in the lower limbs in four of the five patients and in the upper limbs in all but one. The age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic diagnosis was performed in all cases approximately two years after onset, and the family of one patient refused to have it performed. All had a worsening with cold, but the warming phenomenon was only in those with the Becker phenotype.\n\nPatients with recessive congenital myotonia showed some progression. As a family history, it is worth noting that patients 2 and 3 were sisters, without the parents showing any clinical signs, and that the mother of patient 1 showed mild clinical signs that were doubtful with the cold. The patient who refused the study had a history of myotonia in the maternal branch.\n\nBlood tests did not show elevated creatine kinase in any of the patients. The electromyogram was abnormal in all patients except the first one at 2.8/12 years of age. The test was not repeated later because it was not considered necessary.\n\nThe most used treatment initially was oxcarbazepine (in patients with recessive form), with a good response in general. In case 2 it lost efficacy with time and mexiletine was initiated. Patient 4 initiated several drugs without success due to loss of efficacy or side effects. Patient 5 rejected treatment due to mild clinical presentation.\n\nPatient 1 had a previously undescribed, likely pathogenic mutation (CLCN1: c.824T>C) inherited from his mother. Cases 1 to 3 had the Becker phenotype with composite heterozygosity mutations, and cases 4 and 5 had the Thomsen phenotype. Case 5 declined genetic testing.\n", "generated_summary": "Doctors looked back at children\u2019s records from 2015 to 2020 at a large hospital\u2019s nerve clinic. They studied a condition called congenital myotonia. They wrote down age and sex. They noted when symptoms started and how they changed over time. They checked family history. They looked at how treatments worked. They found five children with this condition. Three had the Becker type. Two had the Thomsen type. The Becker type happened in about 1 out of every 15,000 births. The Thomsen type happened in about 1 out of every 21,000 births. They also found a new gene change that likely causes the disease (in a gene called CLCN1: c.824T>C)." }, { "index": 25, "label": "intermediate_health_literacy", "original_text": "The medical records of patients with a diagnosis of congenital myotonia studied and followed in the pediatric neurology consultation in a third-level hospital between 2015 and 2020 were reviewed. The inclusion criteria were to present a clinical diagnosis \u2013 myotonia, warm-up phenomenon, characteristic electromyographic pattern and/or family history \u2013 and/or a molecular diagnosis (mutation in the CLCN1 gene). The clinical signs and symptoms, as well as the results of the complementary explorations and the genetic mutation found, were collected by reviewing the medical record. Demographic variables (age and sex), course of the disease (age of onset, symptoms and signs, time elapsed until diagnosis and clinical evolution), family history and evaluation of the response to treatment were collected.\n\nFive cases with clinical diagnosis of congenital myotonia were identified (three with Becker's disease and two with Thomsen's disease). The incidence in relation to the number of births was estimated at 1:15,000 newborns for cases with Becker's phenotype and 1:21,000 newborns for Thomsen's phenotypes.\n\nMost of our patients were female, and the male was the only one who started before the age of six. The initial clinical presentation included myotonia in the lower limbs in four of the five patients and in the upper limbs in all but one. The age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic diagnosis was performed in all cases approximately two years after onset, and the family of one patient refused to have it performed. All had a worsening with cold, but the warming phenomenon was only in those with the Becker phenotype.\n\nPatients with recessive congenital myotonia showed some progression. As a family history, it is worth noting that patients 2 and 3 were sisters, without the parents showing any clinical signs, and that the mother of patient 1 showed mild clinical signs that were doubtful with the cold. The patient who refused the study had a history of myotonia in the maternal branch.\n\nBlood tests did not show elevated creatine kinase in any of the patients. The electromyogram was abnormal in all patients except the first one at 2.8/12 years of age. The test was not repeated later because it was not considered necessary.\n\nThe most used treatment initially was oxcarbazepine (in patients with recessive form), with a good response in general. In case 2 it lost efficacy with time and mexiletine was initiated. Patient 4 initiated several drugs without success due to loss of efficacy or side effects. Patient 5 rejected treatment due to mild clinical presentation.\n\nPatient 1 had a previously undescribed, likely pathogenic mutation (CLCN1: c.824T>C) inherited from his mother. Cases 1 to 3 had the Becker phenotype with composite heterozygosity mutations, and cases 4 and 5 had the Thomsen phenotype. Case 5 declined genetic testing.\n", "generated_summary": "Researchers reviewed pediatric neurology records from a tertiary hospital (2015\u20132020) to study congenital myotonia. Patients were included based on clinical features (myotonia, a warm\u2011up phenomenon, a characteristic EMG pattern, and/or family history) and/or a molecular finding in the CLCN1 gene. They collected demographics (age, sex), details on disease onset and symptoms, time to diagnosis and clinical course, family history, and response to treatment. Five cases were identified: three with the Becker type and two with the Thomsen type. Using local birth numbers, they estimated an incidence of about 1 in 15,000 births for Becker and 1 in 21,000 for Thomsen. They also identified a previously unreported CLCN1 gene variant (c.824T>C) that is likely disease\u2011causing." }, { "index": 25, "label": "proficient_health_literacy", "original_text": "The medical records of patients with a diagnosis of congenital myotonia studied and followed in the pediatric neurology consultation in a third-level hospital between 2015 and 2020 were reviewed. The inclusion criteria were to present a clinical diagnosis \u2013 myotonia, warm-up phenomenon, characteristic electromyographic pattern and/or family history \u2013 and/or a molecular diagnosis (mutation in the CLCN1 gene). The clinical signs and symptoms, as well as the results of the complementary explorations and the genetic mutation found, were collected by reviewing the medical record. Demographic variables (age and sex), course of the disease (age of onset, symptoms and signs, time elapsed until diagnosis and clinical evolution), family history and evaluation of the response to treatment were collected.\n\nFive cases with clinical diagnosis of congenital myotonia were identified (three with Becker's disease and two with Thomsen's disease). The incidence in relation to the number of births was estimated at 1:15,000 newborns for cases with Becker's phenotype and 1:21,000 newborns for Thomsen's phenotypes.\n\nMost of our patients were female, and the male was the only one who started before the age of six. The initial clinical presentation included myotonia in the lower limbs in four of the five patients and in the upper limbs in all but one. The age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic diagnosis was performed in all cases approximately two years after onset, and the family of one patient refused to have it performed. All had a worsening with cold, but the warming phenomenon was only in those with the Becker phenotype.\n\nPatients with recessive congenital myotonia showed some progression. As a family history, it is worth noting that patients 2 and 3 were sisters, without the parents showing any clinical signs, and that the mother of patient 1 showed mild clinical signs that were doubtful with the cold. The patient who refused the study had a history of myotonia in the maternal branch.\n\nBlood tests did not show elevated creatine kinase in any of the patients. The electromyogram was abnormal in all patients except the first one at 2.8/12 years of age. The test was not repeated later because it was not considered necessary.\n\nThe most used treatment initially was oxcarbazepine (in patients with recessive form), with a good response in general. In case 2 it lost efficacy with time and mexiletine was initiated. Patient 4 initiated several drugs without success due to loss of efficacy or side effects. Patient 5 rejected treatment due to mild clinical presentation.\n\nPatient 1 had a previously undescribed, likely pathogenic mutation (CLCN1: c.824T>C) inherited from his mother. Cases 1 to 3 had the Becker phenotype with composite heterozygosity mutations, and cases 4 and 5 had the Thomsen phenotype. Case 5 declined genetic testing.\n", "generated_summary": "We retrospectively reviewed medical records from a pediatric neurology consultation at a third\u2011level hospital (2015\u20132020) for patients with congenital myotonia. Inclusion criteria comprised a clinical diagnosis (myotonia, warm\u2011up phenomenon, characteristic electromyographic pattern and/or family history) and/or a molecular diagnosis (CLCN1 mutation). For each patient we abstracted demographics (age, sex), disease course (age of onset, symptoms and signs, time to diagnosis, clinical evolution), family history, and treatment response, along with complementary testing and genotypes. Five cases with a clinical diagnosis of congenital myotonia were identified: three with Becker\u2019s disease (recessive phenotype) and two with Thomsen\u2019s disease (dominant phenotype). Incidence relative to births was estimated at 1:15,000 for Becker phenotypes and 1:21,000 for Thomsen phenotypes. Most patients were female; the single male was the only child with onset before age six. Initial presentation included myotonia in the lower limbs in four of five patients and in the upper limbs in all but one. Age at onset ranged from 22 months to 12 years (median 6 years). Genetic diagnosis was pursued approximately two years after onset; one family declined testing. All patients reported worsening with cold; the warming phenomenon was noted only in those with the Becker phenotype. Patients with recessive congenital myotonia showed some progression. Family history included: patients 2 and 3 were sisters with unaffected parents; the mother of patient 1 had mild, cold\u2011provoked, doubtful clinical signs; the patient who declined genetic testing had a maternal\u2011line history of myotonia. Serum creatine kinase was not elevated in any case. The electromyogram was abnormal in all patients except the first one at 2.8/12 years of age (not repeated). Initial therapy most often used was oxcarbazepine in the recessive form, with generally good response; in case 2 it lost efficacy and mexiletine was initiated. Case 4 trialed several drugs without success due to loss of efficacy or adverse effects. Case 5 declined treatment given mild symptoms. Patient 1 harbored a previously undescribed, likely pathogenic variant, CLCN1: c.824T>C, maternally inherited. Cases 1\u20133 (Becker phenotype) carried composite heterozygosity mutations; cases 4\u20135 had the Thomsen phenotype, and case 5 declined genetic testing." }, { "index": 26, "label": "low_health_literacy", "original_text": "A 67-year-old female patient presented with a six-year history of recurrent swelling in the left lower limb. One year prior, she was diagnosed with an AVM in the lower limb at another hospital. Two months before hospitalization, the patient underwent embolization treatment, which included the placement of two coils (20 mm x 40 cm, BSX, USA). Despite this intervention, the patient\u2019s left lower limb swelling did not show any improvement. The patient has been experiencing fatigue and difficulty of breathing for a month. As these symptoms of heart failure progressed and worsened, the patient was transferred to Chengdu University of Traditional Chinese Medicine Hospital for further evaluation and treatment. The patient had no prior history of cardiovascular diseases, injuries, or surgeries. However, she reported a history of oral estrogen use for menopausal syndrome seven years ago.\n\nShe exhibited significant edema and skin sclerosis in the left lower limb. Additionally, absent pulses were observed in the popliteal artery and distal regions. A noticeable tremor was also present in the left thigh. The patient was seated during the examination. Echocardiography revealed cardiac enlargement, along with moderate mitral regurgitation and severe tricuspid regurgitation. The left ventricular ejection fraction (EF) was measured at 60%, and there was an elevation in b-type natriuretic peptide (BNP) levels to 2853 ng/L. The electrocardiogram showed a sinus rhythm with a heart rate of 105 beats per minute and evidence of left atrial enlargement. Chest CT scans confirmed cardiac enlargement, while no respiratory system abnormalities were detected. Preoperative computed tomography angiography (CTA) provided further insights, revealing a left iliac artery aneurysm, a significantly enlarged femoral artery, and complex AVMs in the superficial femoral artery. Additionally, the femoral and superficial veins appeared significantly enlarged on arterial phase imaging. Notably, the left lower limb popliteal artery and anterior tibial artery were not visualized. Based on these findings, the patient was diagnosed with complex congenital lower limb AVMs, acute exacerbation of chronic heart failure, and classified as NYHA Class IV.\n\nThe patient exhibits distinct symptoms of acute heart failure, and preoperative ultrasound assessment has revealed a volume flow of 3400 ml/min in the CFA. Given that embolization using coils may not effectively reduce the flow rate of the AVMs, the utilization of covered stents is a viable option. These stents effectively decrease the flow of lower limb AVMs, thereby improving the patient\u2019s heart failure condition. Additionally, staged embolization treatment can further enhance the treatment outcome by improving the nidus of the lower limb AVMs.\n\nCTA of the patient revealed significant dilatation of blood vessels, with a maximum diameter of 32 mm for the iliac artery, 27 mm for the common femoral artery (CFA), and 22 mm for the superficial femoral artery (SFA). To minimize access site complications, antegrade access was achieved through a surgical approach of the CFA. Under general anesthesia, intravascular covered stents were inserted through an open femoral artery approach, utilizing 14 F (Cook Medical, USA) catheter sheaths intraoperatively. complex AVMs were visualized in the superficial femoral artery and profunda femoris artery, accompanied by early visualization of an enlarged femoral vein.\n\nPreoperative CTA measurements indicated a diameter of 19 mm for the middle segment of the SFA, leading to the selection of a 20 mm\u201312 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China). A 0.035 guidewire, in conjunction with a single-curve catheter, was used to access the popliteal artery. Subsequently, it was replaced with a 0.035 super-hard guidewire to provide support during the implantation of the stent graft. The stent was deployed precisely at the distal end of the superficial femoral artery, the location with the highest concentration of AVMs. Completion angiography revealed a significant reduction in venous opacification around the stent and clear visualization of the popliteal artery. Postoperatively, the left femoral artery was sutured using a 6\u2009\u2212\u20090 vascular risk suture, resulting in a significant improvement in the patient\u2019s heart failure symptoms. The patient has heart failure, so the surgery duration should not be excessive. It is planned to perform embolization treatment in the second phase.\n\nOne week post-treatment, ultrasound examination revealed a reduction in volume flow to 1600 ml/min in the CFA, with a BNP level of 1198ug/l. Targeting the nidus with embolization therapy is expected to further decrease the flow velocity of arteriovenous malformations. The right CFA was punctured, allowing the insertion of a 5 F arterial sheath and a 5 F catheter for angiographic examination. Guided by ultrasound, the drainage vein of the AVM was punctured, and a 5 F vascular sheath was introduced. The contrast agent confirmed the presence of a nidus and its draining veins. The embolization procedure of the draining veins involved the use of a coil (18\u201320 mm x 40 cm, BSX, USA), two microcoils (4 mm x 42 mm, 5 mm x 10 mm, USA), 3% polidocanol (6 mL Kruelle, Germany), and 99% anhydrous ethanol (10 mL).\n\nCompletion angiography showed a significant reduction in the visualization of AVMs and draining veins, indicating their disappearance. During the one-year follow-up, the patient exhibited notable improvement in lower limb swelling and cardiac function. The volume flow in the CFA decreased to 780 ml/min. Echocardiography revealed minor enlargement of the left and right atria, slight mitral and tricuspid regurgitation, and a left ventricular ejection fraction (EF) of 71%. Notably, BNP levels decreased significantly.", "generated_summary": "This report is about a woman with abnormal blood vessel connections in her left leg that she was born with. Her left leg stayed swollen for a long time. She then started having signs of heart trouble. At age 67, doctors confirmed the leg problem was complex and present since birth. The team used a special tube made for the big belly artery, plus a blocking procedure, to slow the bad blood flow in her leg. This was done to help her sudden heart failure caused by the leg problem. The report explains what worked well and what did not." }, { "index": 26, "label": "intermediate_health_literacy", "original_text": "A 67-year-old female patient presented with a six-year history of recurrent swelling in the left lower limb. One year prior, she was diagnosed with an AVM in the lower limb at another hospital. Two months before hospitalization, the patient underwent embolization treatment, which included the placement of two coils (20 mm x 40 cm, BSX, USA). Despite this intervention, the patient\u2019s left lower limb swelling did not show any improvement. The patient has been experiencing fatigue and difficulty of breathing for a month. As these symptoms of heart failure progressed and worsened, the patient was transferred to Chengdu University of Traditional Chinese Medicine Hospital for further evaluation and treatment. The patient had no prior history of cardiovascular diseases, injuries, or surgeries. However, she reported a history of oral estrogen use for menopausal syndrome seven years ago.\n\nShe exhibited significant edema and skin sclerosis in the left lower limb. Additionally, absent pulses were observed in the popliteal artery and distal regions. A noticeable tremor was also present in the left thigh. The patient was seated during the examination. Echocardiography revealed cardiac enlargement, along with moderate mitral regurgitation and severe tricuspid regurgitation. The left ventricular ejection fraction (EF) was measured at 60%, and there was an elevation in b-type natriuretic peptide (BNP) levels to 2853 ng/L. The electrocardiogram showed a sinus rhythm with a heart rate of 105 beats per minute and evidence of left atrial enlargement. Chest CT scans confirmed cardiac enlargement, while no respiratory system abnormalities were detected. Preoperative computed tomography angiography (CTA) provided further insights, revealing a left iliac artery aneurysm, a significantly enlarged femoral artery, and complex AVMs in the superficial femoral artery. Additionally, the femoral and superficial veins appeared significantly enlarged on arterial phase imaging. Notably, the left lower limb popliteal artery and anterior tibial artery were not visualized. Based on these findings, the patient was diagnosed with complex congenital lower limb AVMs, acute exacerbation of chronic heart failure, and classified as NYHA Class IV.\n\nThe patient exhibits distinct symptoms of acute heart failure, and preoperative ultrasound assessment has revealed a volume flow of 3400 ml/min in the CFA. Given that embolization using coils may not effectively reduce the flow rate of the AVMs, the utilization of covered stents is a viable option. These stents effectively decrease the flow of lower limb AVMs, thereby improving the patient\u2019s heart failure condition. Additionally, staged embolization treatment can further enhance the treatment outcome by improving the nidus of the lower limb AVMs.\n\nCTA of the patient revealed significant dilatation of blood vessels, with a maximum diameter of 32 mm for the iliac artery, 27 mm for the common femoral artery (CFA), and 22 mm for the superficial femoral artery (SFA). To minimize access site complications, antegrade access was achieved through a surgical approach of the CFA. Under general anesthesia, intravascular covered stents were inserted through an open femoral artery approach, utilizing 14 F (Cook Medical, USA) catheter sheaths intraoperatively. complex AVMs were visualized in the superficial femoral artery and profunda femoris artery, accompanied by early visualization of an enlarged femoral vein.\n\nPreoperative CTA measurements indicated a diameter of 19 mm for the middle segment of the SFA, leading to the selection of a 20 mm\u201312 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China). A 0.035 guidewire, in conjunction with a single-curve catheter, was used to access the popliteal artery. Subsequently, it was replaced with a 0.035 super-hard guidewire to provide support during the implantation of the stent graft. The stent was deployed precisely at the distal end of the superficial femoral artery, the location with the highest concentration of AVMs. Completion angiography revealed a significant reduction in venous opacification around the stent and clear visualization of the popliteal artery. Postoperatively, the left femoral artery was sutured using a 6\u2009\u2212\u20090 vascular risk suture, resulting in a significant improvement in the patient\u2019s heart failure symptoms. The patient has heart failure, so the surgery duration should not be excessive. It is planned to perform embolization treatment in the second phase.\n\nOne week post-treatment, ultrasound examination revealed a reduction in volume flow to 1600 ml/min in the CFA, with a BNP level of 1198ug/l. Targeting the nidus with embolization therapy is expected to further decrease the flow velocity of arteriovenous malformations. The right CFA was punctured, allowing the insertion of a 5 F arterial sheath and a 5 F catheter for angiographic examination. Guided by ultrasound, the drainage vein of the AVM was punctured, and a 5 F vascular sheath was introduced. The contrast agent confirmed the presence of a nidus and its draining veins. The embolization procedure of the draining veins involved the use of a coil (18\u201320 mm x 40 cm, BSX, USA), two microcoils (4 mm x 42 mm, 5 mm x 10 mm, USA), 3% polidocanol (6 mL Kruelle, Germany), and 99% anhydrous ethanol (10 mL).\n\nCompletion angiography showed a significant reduction in the visualization of AVMs and draining veins, indicating their disappearance. During the one-year follow-up, the patient exhibited notable improvement in lower limb swelling and cardiac function. The volume flow in the CFA decreased to 780 ml/min. Echocardiography revealed minor enlargement of the left and right atria, slight mitral and tricuspid regurgitation, and a left ventricular ejection fraction (EF) of 71%. Notably, BNP levels decreased significantly.", "generated_summary": "A 67-year-old woman with years of left leg swelling developed new symptoms of heart failure and was diagnosed with complex, congenital arteriovenous malformations (AVMs) in the lower limb. These abnormal vessel connections create high-flow shunts that can overload the heart. After a prior coil embolization failed to help, the team used an abdominal aortic stent graft (repurposed in the leg) to quickly reduce blood flow through the AVM, then performed staged embolization to target the AVM nidus and draining veins. Her heart failure and leg swelling improved, with blood flow in the common femoral artery falling stepwise and heart function markers getting better over time. The article highlights real-world lessons and limits: coils alone may not control very high-flow AVMs; covered stents can promptly lower shunt flow but usually need follow-up embolization; and staging helps reduce risk in patients with severe (acute) heart failure." }, { "index": 26, "label": "proficient_health_literacy", "original_text": "A 67-year-old female patient presented with a six-year history of recurrent swelling in the left lower limb. One year prior, she was diagnosed with an AVM in the lower limb at another hospital. Two months before hospitalization, the patient underwent embolization treatment, which included the placement of two coils (20 mm x 40 cm, BSX, USA). Despite this intervention, the patient\u2019s left lower limb swelling did not show any improvement. The patient has been experiencing fatigue and difficulty of breathing for a month. As these symptoms of heart failure progressed and worsened, the patient was transferred to Chengdu University of Traditional Chinese Medicine Hospital for further evaluation and treatment. The patient had no prior history of cardiovascular diseases, injuries, or surgeries. However, she reported a history of oral estrogen use for menopausal syndrome seven years ago.\n\nShe exhibited significant edema and skin sclerosis in the left lower limb. Additionally, absent pulses were observed in the popliteal artery and distal regions. A noticeable tremor was also present in the left thigh. The patient was seated during the examination. Echocardiography revealed cardiac enlargement, along with moderate mitral regurgitation and severe tricuspid regurgitation. The left ventricular ejection fraction (EF) was measured at 60%, and there was an elevation in b-type natriuretic peptide (BNP) levels to 2853 ng/L. The electrocardiogram showed a sinus rhythm with a heart rate of 105 beats per minute and evidence of left atrial enlargement. Chest CT scans confirmed cardiac enlargement, while no respiratory system abnormalities were detected. Preoperative computed tomography angiography (CTA) provided further insights, revealing a left iliac artery aneurysm, a significantly enlarged femoral artery, and complex AVMs in the superficial femoral artery. Additionally, the femoral and superficial veins appeared significantly enlarged on arterial phase imaging. Notably, the left lower limb popliteal artery and anterior tibial artery were not visualized. Based on these findings, the patient was diagnosed with complex congenital lower limb AVMs, acute exacerbation of chronic heart failure, and classified as NYHA Class IV.\n\nThe patient exhibits distinct symptoms of acute heart failure, and preoperative ultrasound assessment has revealed a volume flow of 3400 ml/min in the CFA. Given that embolization using coils may not effectively reduce the flow rate of the AVMs, the utilization of covered stents is a viable option. These stents effectively decrease the flow of lower limb AVMs, thereby improving the patient\u2019s heart failure condition. Additionally, staged embolization treatment can further enhance the treatment outcome by improving the nidus of the lower limb AVMs.\n\nCTA of the patient revealed significant dilatation of blood vessels, with a maximum diameter of 32 mm for the iliac artery, 27 mm for the common femoral artery (CFA), and 22 mm for the superficial femoral artery (SFA). To minimize access site complications, antegrade access was achieved through a surgical approach of the CFA. Under general anesthesia, intravascular covered stents were inserted through an open femoral artery approach, utilizing 14 F (Cook Medical, USA) catheter sheaths intraoperatively. complex AVMs were visualized in the superficial femoral artery and profunda femoris artery, accompanied by early visualization of an enlarged femoral vein.\n\nPreoperative CTA measurements indicated a diameter of 19 mm for the middle segment of the SFA, leading to the selection of a 20 mm\u201312 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China). A 0.035 guidewire, in conjunction with a single-curve catheter, was used to access the popliteal artery. Subsequently, it was replaced with a 0.035 super-hard guidewire to provide support during the implantation of the stent graft. The stent was deployed precisely at the distal end of the superficial femoral artery, the location with the highest concentration of AVMs. Completion angiography revealed a significant reduction in venous opacification around the stent and clear visualization of the popliteal artery. Postoperatively, the left femoral artery was sutured using a 6\u2009\u2212\u20090 vascular risk suture, resulting in a significant improvement in the patient\u2019s heart failure symptoms. The patient has heart failure, so the surgery duration should not be excessive. It is planned to perform embolization treatment in the second phase.\n\nOne week post-treatment, ultrasound examination revealed a reduction in volume flow to 1600 ml/min in the CFA, with a BNP level of 1198ug/l. Targeting the nidus with embolization therapy is expected to further decrease the flow velocity of arteriovenous malformations. The right CFA was punctured, allowing the insertion of a 5 F arterial sheath and a 5 F catheter for angiographic examination. Guided by ultrasound, the drainage vein of the AVM was punctured, and a 5 F vascular sheath was introduced. The contrast agent confirmed the presence of a nidus and its draining veins. The embolization procedure of the draining veins involved the use of a coil (18\u201320 mm x 40 cm, BSX, USA), two microcoils (4 mm x 42 mm, 5 mm x 10 mm, USA), 3% polidocanol (6 mL Kruelle, Germany), and 99% anhydrous ethanol (10 mL).\n\nCompletion angiography showed a significant reduction in the visualization of AVMs and draining veins, indicating their disappearance. During the one-year follow-up, the patient exhibited notable improvement in lower limb swelling and cardiac function. The volume flow in the CFA decreased to 780 ml/min. Echocardiography revealed minor enlargement of the left and right atria, slight mitral and tricuspid regurgitation, and a left ventricular ejection fraction (EF) of 71%. Notably, BNP levels decreased significantly.", "generated_summary": "Case summary: A 67-year-old woman with a six-year history of recurrent left lower limb swelling presented with one month of progressive dyspnea and fatigue consistent with acute exacerbation of chronic heart failure. She had no prior cardiovascular disease, trauma, or surgery; remote oral estrogen use occurred seven years earlier. Examination showed marked left leg edema, skin sclerosis, absent popliteal and distal pulses, and a palpable thrill/tremor in the left thigh. Echocardiography demonstrated cardiomegaly with moderate mitral regurgitation, severe tricuspid regurgitation, and LVEF 60%. BNP was 2853 ng/L. ECG showed sinus tachycardia (105 bpm) with left atrial enlargement. Chest CT confirmed cardiomegaly without pulmonary parenchymal disease. CTA revealed a left iliac artery aneurysm (max 32 mm), marked dilation of the CFA (27 mm) and SFA (22 mm), complex AVMs centered on the SFA with early opacification of an enlarged femoral vein, and nonvisualization of the popliteal and anterior tibial arteries. She was diagnosed with complex congenital lower-limb AVMs and acute exacerbation of chronic heart failure, NYHA class IV.\n\nRationale and strategy: Preoperative duplex showed CFA volume flow of 3400 ml/min, indicating a high-flow shunt. Given prior coil embolization (two coils, 20 mm x 40 cm) failed to reduce flow or swelling, the team prioritized rapid shunt reduction using a covered stent, with staged embolization to address the nidus. This approach repurposed an abdominal aortic stent graft to reduce AVM inflow and improve cardiac load while limiting operative time in the setting of heart failure.\n\nProcedure details: To minimize access complications in dilated vessels (iliac 32 mm, CFA 27 mm, SFA 22 mm), antegrade surgical exposure of the CFA was performed under general anesthesia, placing a 14 F sheath. Complex AVMs were visualized in the SFA and profunda femoris with early venous filling. Based on a preoperative SFA mid-segment diameter of 19 mm, a 20\u201312 mm/120 mm aorto-uni-iliac abdominal aortic covered stent graft (MicroPort, China) was advanced over a 0.035 super-stiff wire (after popliteal access with a single-curve catheter) and deployed at the distal SFA to span the highest AVM density. Completion angiography showed marked reduction of peri-stent venous opacification with clear visualization of the popliteal artery. The femoral arteriotomy was closed with 6-0 vascular suture. The patient\u2019s heart failure symptoms improved postoperatively, and a staged embolization was planned to limit procedure time.\n\nSecond stage and outcomes: At one week, CFA flow decreased to 1600 ml/min and BNP to 1198 \u00b5g/L. Transvenous embolization targeted the nidus and draining veins via right CFA arterial access (5 F sheath/catheter) and ultrasound-guided puncture of the AVM drainage vein (5 F venous sheath). Embolic materials included one 18\u201320 mm x 40 cm coil, two microcoils (4 x 42 mm, 5 x 10 mm), 3% polidocanol (6 mL), and 99% anhydrous ethanol (10 mL). Completion angiography demonstrated near-complete disappearance of AVM/shunting. At one year, leg swelling and cardiac function improved substantially: CFA flow was 780 ml/min; echocardiography showed only mild biatrial enlargement, mild mitral and tricuspid regurgitation, and LVEF 71%; BNP declined markedly.\n\nPractical experience and limitations: In very high-flow, complex congenital lower-limb AVMs causing high-output heart failure, coil-only embolization may be insufficient to meaningfully reduce shunt volume. A covered stent can rapidly downregulate inflow and unload the heart, but often requires adjunctive embolization of the nidus and draining veins to consolidate results. Repurposing an abdominal aortic aorto-uni-iliac covered stent in the SFA is technically feasible but off-label, demands large-bore access (14 F) with surgical exposure, and may be limited by vessel size mismatch, landing zone adequacy, and the need to preserve distal perfusion. Staging is advisable in NYHA IV patients to shorten anesthesia time and manage hemodynamics. This case illustrates that an abdominal aortic stent graft coupled with targeted embolization can effectively address acute heart failure driven by complex congenital lower-limb AVMs, while highlighting device-selection and access considerations that may constrain its use." }, { "index": 27, "label": "low_health_literacy", "original_text": "28-year-old male patient with no significant history presented to the dermatology department with a 48-hour history of a skin condition characterized by two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm equidistant from the elbow crease, accompanied by a burning sensation and pruritus at the site of the lesions. He did not have systemic symptoms or self-medicate. As a background, he reported that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed that reported epidermis with acanthosis, parakeratosis and spongiosis, neutrophils in the stratum corneum and perivascular lymphocyte infiltration in the superficial, middle and deep dermis. Based on the clinical characteristics, the background of travel to a tropical region and the histological findings, a diagnosis of Paederus dermatitis was made. Treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions resolved, leaving a post-inflammatory hyperpigmentation.\n", "generated_summary": "A 28-year-old man had two red patches with small blisters and shallow sores on the inner part of his right arm and forearm for 2 days. The spots burned and itched. He had been on vacation on the coast of Ecuador when this started. The doctor took a small piece of skin to test. The diagnosis was a type of skin irritation called Paederus dermatitis. He was treated with allergy pills, a steroid cream, and cold packs. After 8 days, the rash went away. It left dark marks on the skin." }, { "index": 27, "label": "intermediate_health_literacy", "original_text": "28-year-old male patient with no significant history presented to the dermatology department with a 48-hour history of a skin condition characterized by two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm equidistant from the elbow crease, accompanied by a burning sensation and pruritus at the site of the lesions. He did not have systemic symptoms or self-medicate. As a background, he reported that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed that reported epidermis with acanthosis, parakeratosis and spongiosis, neutrophils in the stratum corneum and perivascular lymphocyte infiltration in the superficial, middle and deep dermis. Based on the clinical characteristics, the background of travel to a tropical region and the histological findings, a diagnosis of Paederus dermatitis was made. Treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions resolved, leaving a post-inflammatory hyperpigmentation.\n", "generated_summary": "A 28-year-old man developed, over 48 hours, two red plaques with small central blisters and shallow ulcers on the inner right arm and forearm. The areas burned and itched. He had no other symptoms and had recently been vacationing on the coast of Ecuador. Doctors performed an incisional skin biopsy. Based on how the rash looked, his recent travel to a tropical area, and the biopsy results, they diagnosed Paederus dermatitis. He was treated with antihistamines, topical steroids, and cold compresses. After 8 days, the lesions resolved, leaving post-inflammatory hyperpigmentation." }, { "index": 27, "label": "proficient_health_literacy", "original_text": "28-year-old male patient with no significant history presented to the dermatology department with a 48-hour history of a skin condition characterized by two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm equidistant from the elbow crease, accompanied by a burning sensation and pruritus at the site of the lesions. He did not have systemic symptoms or self-medicate. As a background, he reported that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed that reported epidermis with acanthosis, parakeratosis and spongiosis, neutrophils in the stratum corneum and perivascular lymphocyte infiltration in the superficial, middle and deep dermis. Based on the clinical characteristics, the background of travel to a tropical region and the histological findings, a diagnosis of Paederus dermatitis was made. Treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions resolved, leaving a post-inflammatory hyperpigmentation.\n", "generated_summary": "A 28-year-old male with no significant past medical history presented with a 48-hour history of two erythematous plaques with central vesicles and superficial ulceration on the flexor surface of the right arm and forearm, equidistant from the antecubital crease, associated with burning and pruritus. He denied systemic symptoms and had not self-medicated. He reported being on vacation in coastal Ecuador at the time of onset. Incisional biopsy demonstrated epidermal acanthosis, parakeratosis, and spongiosis, neutrophils within the stratum corneum, and perivascular lymphocytic infiltrates in the superficial, mid, and deep dermis. Integrating the clinical morphology, tropical travel history, and histopathology, the diagnosis of Paederus dermatitis was made. Management included antihistamines, topical corticosteroids, and cold compresses. By day 8, the eruption resolved, with residual post-inflammatory hyperpigmentation. Paederus dermatitis is an irritant contact dermatitis due to exposure to Paederus species toxin (pederin), typically producing burning, vesiculation, and superficial erosions; the histologic pattern here (spongiotic dermatitis with mixed inflammatory infiltrates) is consistent with this mechanism." }, { "index": 28, "label": "low_health_literacy", "original_text": "Technique\nInformation about the procedure of TFD.\nThe patient receives intravenous photosensitizer (Photogen\u00ae, King of Prussia, PA, USA - 1.5 mg/kg) 24 h before the procedure. Its peak light absorption is at the wavelength of 630 nm. The procedure begins with standard duodenoscopy (Olympus TJF-180) under general anesthesia. After the identification of the greater duodenal papilla and the retrograde cannulation, the digital cholangioscope (SpyGlassTM DS, Boston Scientific, Natick, MA) is introduced into the common bile duct. Then the cholangioscopic examination helps to identify the neoplastic stenosis. Under direct visualization, the illumination catheter (Medlight S.A., RD10-323, Switzerland) is advanced through the cholangioscope. This consists of a typical three-way cannula. The first port has a 1 cm long cylindrical light diffuser at the end. Two black radiopaque marks demarcate the limits of the diffuser. The second port accommodates a 0.025 inch guidewire and the third is a portal for injection. After positioning under cholangioscopic guidance, illumination is initiated. The dose is 90 J/cm\u00b2, with a power of 70 mW/cm\u00b2. Repositioning is recommended every centimeter to cover the entire stenosed area. At the end of the procedure, new cholangioscopy evaluates the bile duct for immediate outcome and adverse events.\n\nPost-procedure care\nThe patient is fasted for the next 24 h. If no adverse event is detected, oral diet is initiated. Discharge from hospital is done under strict guidance on photoprotection (prevention of exposure to light and use of sunglasses), especially during the first week after the session of TFD.\n\nRESULTS\nThis procedure was performed in an 82-year-old man who presented to our tertiary center with obstructive jaundice and weight loss over the previous two months. Endoscopic ultrasound (EUS) revealed severe dilation of the common bile duct associated with choledocholithiasis. ERCP confirmed these findings but was unable to remove the stones due to the disproportionate dilation of the common bile duct. Therefore, a plastic biliary stent was chosen. The patient showed improvement in his clinical condition, but the cholestasis returned 45 days after the first procedure. Two other ERCPs failed to remove the stones. During the third procedure, a long irregular stenosis of the common hepatic duct was apparent and he was referred for another echoendoscopic evaluation.\n\nIn addition to the choledocholithiasis, the new EUS revealed a dilated common hepatic duct with a well-circumscribed hypoechoic solid mass measuring 1.8x2 cm, which was compressing the common hepatic duct. The mass appeared to also involve the common hepatic artery. An ultrasound-guided needle biopsy confirmed the diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I).\n\nAfter staging, the mass was considered inoperable and the patient was referred for palliative treatment. After a multidisciplinary meeting with the oncology team, adjunctive PDT was proposed to treat the recurrent biliary obstruction. The procedure went without complications and lasted 150 minutes. At the end, a biliary drainage was performed with a 10 Fr plastic stent, since a self-expanding metal stent was not available at that time.\n\nThe patient showed no signs or symptoms of photosensitivity in the following week. There was, however, early recurrence of cholestasis complicated with cholangitis. ERCP revealed obstruction of the stent with debris and biliary sludge secondary to tumor necrosis. A biliary scan followed by new drainage resolved the patient's acute condition. Subsequently, he remained asymptomatic for three months, the longest period since the onset of the disease. At his next recurrence, he was drained with a self-expanding metal stent. He continued with systemic treatment and eventually required a duodenal stent for palliation of dysphagia. He died due to complications of pulmonary metastases two years after the onset of symptoms and 15 months after the session of TFD.\n", "generated_summary": "One day before the treatment, you get a light\u2011activated medicine through a vein. During the visit, the doctor slides a flexible camera through your mouth into your gut. They find the small drain where bile comes out. They thread a tiny camera up into the main bile tube. They look for a tight spot caused by a tumor. They slide a thin light cable to that spot while watching on the screen. They turn on the light and move the cable a small step, about 1 centimeter, each time to cover the whole tight area. At the end, they look again to see how it went and to check for any problems. This treatment was used for an 82\u2011year\u2011old man who had yellow skin from blocked bile for two months. Tests showed the main bile tube was very wide and had stones. They also found a firm lump about 1.8 by 2 centimeters pressing on the liver\u2019s main bile tube. Surgery could not fix it. He got this light treatment to ease the blockage. He felt well for three months. He died from complications 15 months after the light treatment." }, { "index": 28, "label": "intermediate_health_literacy", "original_text": "Technique\nInformation about the procedure of TFD.\nThe patient receives intravenous photosensitizer (Photogen\u00ae, King of Prussia, PA, USA - 1.5 mg/kg) 24 h before the procedure. Its peak light absorption is at the wavelength of 630 nm. The procedure begins with standard duodenoscopy (Olympus TJF-180) under general anesthesia. After the identification of the greater duodenal papilla and the retrograde cannulation, the digital cholangioscope (SpyGlassTM DS, Boston Scientific, Natick, MA) is introduced into the common bile duct. Then the cholangioscopic examination helps to identify the neoplastic stenosis. Under direct visualization, the illumination catheter (Medlight S.A., RD10-323, Switzerland) is advanced through the cholangioscope. This consists of a typical three-way cannula. The first port has a 1 cm long cylindrical light diffuser at the end. Two black radiopaque marks demarcate the limits of the diffuser. The second port accommodates a 0.025 inch guidewire and the third is a portal for injection. After positioning under cholangioscopic guidance, illumination is initiated. The dose is 90 J/cm\u00b2, with a power of 70 mW/cm\u00b2. Repositioning is recommended every centimeter to cover the entire stenosed area. At the end of the procedure, new cholangioscopy evaluates the bile duct for immediate outcome and adverse events.\n\nPost-procedure care\nThe patient is fasted for the next 24 h. If no adverse event is detected, oral diet is initiated. Discharge from hospital is done under strict guidance on photoprotection (prevention of exposure to light and use of sunglasses), especially during the first week after the session of TFD.\n\nRESULTS\nThis procedure was performed in an 82-year-old man who presented to our tertiary center with obstructive jaundice and weight loss over the previous two months. Endoscopic ultrasound (EUS) revealed severe dilation of the common bile duct associated with choledocholithiasis. ERCP confirmed these findings but was unable to remove the stones due to the disproportionate dilation of the common bile duct. Therefore, a plastic biliary stent was chosen. The patient showed improvement in his clinical condition, but the cholestasis returned 45 days after the first procedure. Two other ERCPs failed to remove the stones. During the third procedure, a long irregular stenosis of the common hepatic duct was apparent and he was referred for another echoendoscopic evaluation.\n\nIn addition to the choledocholithiasis, the new EUS revealed a dilated common hepatic duct with a well-circumscribed hypoechoic solid mass measuring 1.8x2 cm, which was compressing the common hepatic duct. The mass appeared to also involve the common hepatic artery. An ultrasound-guided needle biopsy confirmed the diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I).\n\nAfter staging, the mass was considered inoperable and the patient was referred for palliative treatment. After a multidisciplinary meeting with the oncology team, adjunctive PDT was proposed to treat the recurrent biliary obstruction. The procedure went without complications and lasted 150 minutes. At the end, a biliary drainage was performed with a 10 Fr plastic stent, since a self-expanding metal stent was not available at that time.\n\nThe patient showed no signs or symptoms of photosensitivity in the following week. There was, however, early recurrence of cholestasis complicated with cholangitis. ERCP revealed obstruction of the stent with debris and biliary sludge secondary to tumor necrosis. A biliary scan followed by new drainage resolved the patient's acute condition. Subsequently, he remained asymptomatic for three months, the longest period since the onset of the disease. At his next recurrence, he was drained with a self-expanding metal stent. He continued with systemic treatment and eventually required a duodenal stent for palliation of dysphagia. He died due to complications of pulmonary metastases two years after the onset of symptoms and 15 months after the session of TFD.\n", "generated_summary": "A light\u2011sensitizing drug is given by IV 24 hours before the procedure. Under general anesthesia, the doctor performs a standard duodenoscopy, locates the papilla (the bile duct opening), and passes a small tube backward into the bile duct. A digital cholangioscope is then advanced into the common bile duct to directly identify a cancer\u2011related narrowing. Under direct vision, a light\u2011delivery catheter is placed through the scope to the stricture. The catheter is moved in 1\u2011cm steps to treat the entire narrowed segment. At the end, the bile duct is re\u2011inspected to assess the immediate result and check for complications. Case outcome: An 82\u2011year\u2011old man had obstructive jaundice for two months. EUS and ERCP showed marked dilation of the common bile duct with choledocholithiasis. They also found dilation of the hepatic duct due to a well\u2011defined hypoechoic mass measuring 1.8 \u00d7 2 cm compressing the common hepatic duct. The tumor was inoperable, so he received palliative photodynamic therapy. He remained symptom\u2011free for three months and died of complications 15 months after the PDT session." }, { "index": 28, "label": "proficient_health_literacy", "original_text": "Technique\nInformation about the procedure of TFD.\nThe patient receives intravenous photosensitizer (Photogen\u00ae, King of Prussia, PA, USA - 1.5 mg/kg) 24 h before the procedure. Its peak light absorption is at the wavelength of 630 nm. The procedure begins with standard duodenoscopy (Olympus TJF-180) under general anesthesia. After the identification of the greater duodenal papilla and the retrograde cannulation, the digital cholangioscope (SpyGlassTM DS, Boston Scientific, Natick, MA) is introduced into the common bile duct. Then the cholangioscopic examination helps to identify the neoplastic stenosis. Under direct visualization, the illumination catheter (Medlight S.A., RD10-323, Switzerland) is advanced through the cholangioscope. This consists of a typical three-way cannula. The first port has a 1 cm long cylindrical light diffuser at the end. Two black radiopaque marks demarcate the limits of the diffuser. The second port accommodates a 0.025 inch guidewire and the third is a portal for injection. After positioning under cholangioscopic guidance, illumination is initiated. The dose is 90 J/cm\u00b2, with a power of 70 mW/cm\u00b2. Repositioning is recommended every centimeter to cover the entire stenosed area. At the end of the procedure, new cholangioscopy evaluates the bile duct for immediate outcome and adverse events.\n\nPost-procedure care\nThe patient is fasted for the next 24 h. If no adverse event is detected, oral diet is initiated. Discharge from hospital is done under strict guidance on photoprotection (prevention of exposure to light and use of sunglasses), especially during the first week after the session of TFD.\n\nRESULTS\nThis procedure was performed in an 82-year-old man who presented to our tertiary center with obstructive jaundice and weight loss over the previous two months. Endoscopic ultrasound (EUS) revealed severe dilation of the common bile duct associated with choledocholithiasis. ERCP confirmed these findings but was unable to remove the stones due to the disproportionate dilation of the common bile duct. Therefore, a plastic biliary stent was chosen. The patient showed improvement in his clinical condition, but the cholestasis returned 45 days after the first procedure. Two other ERCPs failed to remove the stones. During the third procedure, a long irregular stenosis of the common hepatic duct was apparent and he was referred for another echoendoscopic evaluation.\n\nIn addition to the choledocholithiasis, the new EUS revealed a dilated common hepatic duct with a well-circumscribed hypoechoic solid mass measuring 1.8x2 cm, which was compressing the common hepatic duct. The mass appeared to also involve the common hepatic artery. An ultrasound-guided needle biopsy confirmed the diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I).\n\nAfter staging, the mass was considered inoperable and the patient was referred for palliative treatment. After a multidisciplinary meeting with the oncology team, adjunctive PDT was proposed to treat the recurrent biliary obstruction. The procedure went without complications and lasted 150 minutes. At the end, a biliary drainage was performed with a 10 Fr plastic stent, since a self-expanding metal stent was not available at that time.\n\nThe patient showed no signs or symptoms of photosensitivity in the following week. There was, however, early recurrence of cholestasis complicated with cholangitis. ERCP revealed obstruction of the stent with debris and biliary sludge secondary to tumor necrosis. A biliary scan followed by new drainage resolved the patient's acute condition. Subsequently, he remained asymptomatic for three months, the longest period since the onset of the disease. At his next recurrence, he was drained with a self-expanding metal stent. He continued with systemic treatment and eventually required a duodenal stent for palliation of dysphagia. He died due to complications of pulmonary metastases two years after the onset of symptoms and 15 months after the session of TFD.\n", "generated_summary": "Technique (TFD/PDT): The patient receives intravenous photosensitizer (Photogen, 1.5 mg/kg) 24 h pre\u2011procedure; peak absorption is 630 nm. Under general anesthesia, standard duodenoscopy (Olympus TJF\u2011180) is performed. After identification of the greater duodenal papilla and retrograde cannulation, a digital cholangioscope (SpyGlass DS, Boston Scientific) is introduced into the common bile duct. Cholangioscopy is used to identify the neoplastic stenosis. Under direct visualization, the illumination catheter (Medlight S.A., RD10\u2011323) is advanced through the cholangioscope. The catheter is a three\u2011way cannula: port 1 carries a 1\u2011cm cylindrical light diffuser with two black radiopaque markers denoting its limits; port 2 accommodates a 0.025\u2011inch guidewire; port 3 is an injection portal. Following cholangioscopic positioning, illumination is delivered at 90 J/cm\u00b2 with power of 70 mW/cm\u00b2, with 1\u2011cm stepwise repositioning to cover the entire stenosed segment. Completion cholangioscopy assesses immediate outcome and adverse events. Post\u2011procedure care: patients are fasted for 24 h; if no adverse events occur, oral intake is resumed. Discharge includes strict photoprotection instructions (avoidance of light exposure and use of sunglasses), especially during the first week after TFD. Results/Case: An 82\u2011year\u2011old man presented with a 2\u2011month history of obstructive jaundice and weight loss. EUS showed severe dilation of the common bile duct with choledocholithiasis; ERCP confirmed these findings but stone extraction was unsuccessful due to disproportionate ductal dilation, so a plastic biliary stent was placed. Cholestasis recurred 45 days later; two additional ERCPs failed to clear stones. During the third ERCP, a long irregular CHD stenosis was noted, prompting repeat EUS. Repeat EUS revealed a well\u2011circumscribed hypoechoic solid mass (1.8 \u00d7 2 cm) compressing the common hepatic duct, with apparent involvement of the common hepatic artery. Ultrasound\u2011guided needle biopsy confirmed moderately differentiated cholangiocarcinoma (Bismuth I). After staging, the lesion was deemed unresectable and the patient was referred for palliative therapy. Following multidisciplinary discussion, adjunctive PDT was performed to treat recurrent biliary obstruction. The procedure lasted 150 minutes without complications. A 10 Fr plastic stent was placed for biliary drainage (SEMS unavailable at that time). No photosensitivity occurred in the subsequent week. Early recurrence of cholestasis with cholangitis ensued; ERCP demonstrated stent occlusion by debris and biliary sludge secondary to tumor necrosis. A biliary scan and re\u2011drainage resolved the acute episode. He then remained asymptomatic for three months\u2014the longest interval since symptom onset. At subsequent recurrence, a self\u2011expanding metal stent was placed. He continued systemic therapy and later required a duodenal stent for palliation of dysphagia. He died from complications of pulmonary metastases two years after symptom onset and 15 months after the TFD session. Mechanistic context: PDT activates the photosensitizer at 630 nm to generate reactive oxygen species, inducing localized tumor cytotoxicity and microvascular damage, which can debulk malignant biliary strictures and improve ductal patency." }, { "index": 29, "label": "low_health_literacy", "original_text": "A 77-year-old woman with haematemesis presented to the emergency room. Her medical history included only hypertension and dyslipidaemia. When she presented to the emergency room, her vital signs indicated shock (heart rate: 100 beats/min, blood pressure: 79/56\u2009mmHg), and blood tests revealed anaemia (haemoglobin: 9.6\u2009g/dL), which suggested upper gastrointestinal bleeding.\n\nNon-contrast-enhanced CT was performed immediately because of renal dysfunction. CT revealed that the third part of the duodenum flexed steeply on the right side of the aorta and ran caudally, without crossing anterior to the aorta. The jejunum was located on the patient\u2019s right side. The second part of the duodenum and the stomach were dilated, and there were high-density gastric contents that were considered to indicate a haematoma.\n\nUpper gastrointestinal endoscopy was performed following the CT examination, which revealed a mucosal laceration at the gastric cardia. Bleeding from lacerations of the cardia of the stomach as a result of forceful vomiting was first reported by Mallory and Weiss in 1929.1 In our case, the third part of the duodenum flexed steeply, and the lumen was narrowed, which caused an obstruction. As a result, repeat vomiting was considered to have caused Mallory\u2013Weiss syndrome.\n\nOn the basis of the CT findings showing that the duodenal-jejunal junction was located in the right hemi-abdomen, intestinal malrotation was suspected.2 However, 7\u2009days later, when CT was repeated, spontaneous resolution of the malpositioned jejunum was seen. The patient was then discharged from the hospital. However,\u2009months later, she was rushed to the emergency room for repeat haematemesis. Dynamic CT was performed before upper gastrointestinal endoscopy, on admission, and revealed contrast extravasation in the dilated stomach. Additionally, the third part of the duodenum was flexed on the right side of the aorta, and the duodenal-jejunal junction and jejunum were again located in the right hemi-abdomen. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, as in the previous endoscopy, which was considered Mallory\u2013Weiss syndrome.\n\nTwo months after the second episode of haematemesis, the patient presented to the emergency room with nausea. Non-contrast-enhanced CT revealed no abnormalities in the duodenal positioning, but there was oedematous wall thickening in the second part of the duodenum. If we had not had previous CT images, we would have suspected duodenitis, but on the basis of all of the CT findings, we suspected the possibility of an underlying condition after the right-sided deviation of the small intestine had resolved spontaneously.\n\nIn summary, CT was performed 4 times over 5\u2009months. The third and fourth parts of the duodenum and the jejunum deviated repeatedly, but this resolved spontaneously, which is not indicative of intestinal malrotation. Therefore, we diagnosed dysplasia of the ligament of Treitz.\n\nClinical outcomes\nThe patient underwent laparotomy, which revealed no abnormalities in the relative position of the duodenum to the jejunum. Additionally, the jejunum was located on the patient\u2019s left side, and there was no intestinal malrotation. The ligament of Treitz was formed; however, its fixation in the upper jejunum was incomplete as it was attached only to the duodenum. The duodenal-jejunal junction was not fixed to the retroperitoneum, and the jejunum folded easily with the ligament of Treitz as a fulcrum. Surgically, the upper jejunum was fixed with 4 sutures to the retroperitoneum on the patient\u2019s left side. The postoperative course was good, and the patient has remained symptom-free.", "generated_summary": "A 77-year-old woman came to the hospital because she threw up blood. A belly scan (CT) was done. It showed the first part of her small intestine bent sharply on the right side of the body\u2019s main artery and went downward. It did not cross in front of that artery. The meeting point between the first and middle parts of the small intestine was on her right side. The middle part of the small intestine was also on her right side. A camera test of her stomach showed a tear at the top of the stomach where it meets the food pipe. This is called a Mallory\u2013Weiss tear. A week later, another CT showed the intestines moved back to a normal spot by themselves. Two months later, she threw up blood again. The CT again showed that the meeting point and the middle small intestine had slid to the right. The camera test again showed a tear in the same spot. At first, doctors thought she might have been born with her intestines in the wrong place. But because the intestines kept sliding to the right and then moving back on their own, the problem was a weak support band called the ligament of Treitz. Surgery showed the band was there but not firmly attached to the upper small intestine. The scan also showed a nearby tissue space was loose and could move. These issues likely let the small intestine slide to the right." }, { "index": 29, "label": "intermediate_health_literacy", "original_text": "A 77-year-old woman with haematemesis presented to the emergency room. Her medical history included only hypertension and dyslipidaemia. When she presented to the emergency room, her vital signs indicated shock (heart rate: 100 beats/min, blood pressure: 79/56\u2009mmHg), and blood tests revealed anaemia (haemoglobin: 9.6\u2009g/dL), which suggested upper gastrointestinal bleeding.\n\nNon-contrast-enhanced CT was performed immediately because of renal dysfunction. CT revealed that the third part of the duodenum flexed steeply on the right side of the aorta and ran caudally, without crossing anterior to the aorta. The jejunum was located on the patient\u2019s right side. The second part of the duodenum and the stomach were dilated, and there were high-density gastric contents that were considered to indicate a haematoma.\n\nUpper gastrointestinal endoscopy was performed following the CT examination, which revealed a mucosal laceration at the gastric cardia. Bleeding from lacerations of the cardia of the stomach as a result of forceful vomiting was first reported by Mallory and Weiss in 1929.1 In our case, the third part of the duodenum flexed steeply, and the lumen was narrowed, which caused an obstruction. As a result, repeat vomiting was considered to have caused Mallory\u2013Weiss syndrome.\n\nOn the basis of the CT findings showing that the duodenal-jejunal junction was located in the right hemi-abdomen, intestinal malrotation was suspected.2 However, 7\u2009days later, when CT was repeated, spontaneous resolution of the malpositioned jejunum was seen. The patient was then discharged from the hospital. However,\u2009months later, she was rushed to the emergency room for repeat haematemesis. Dynamic CT was performed before upper gastrointestinal endoscopy, on admission, and revealed contrast extravasation in the dilated stomach. Additionally, the third part of the duodenum was flexed on the right side of the aorta, and the duodenal-jejunal junction and jejunum were again located in the right hemi-abdomen. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, as in the previous endoscopy, which was considered Mallory\u2013Weiss syndrome.\n\nTwo months after the second episode of haematemesis, the patient presented to the emergency room with nausea. Non-contrast-enhanced CT revealed no abnormalities in the duodenal positioning, but there was oedematous wall thickening in the second part of the duodenum. If we had not had previous CT images, we would have suspected duodenitis, but on the basis of all of the CT findings, we suspected the possibility of an underlying condition after the right-sided deviation of the small intestine had resolved spontaneously.\n\nIn summary, CT was performed 4 times over 5\u2009months. The third and fourth parts of the duodenum and the jejunum deviated repeatedly, but this resolved spontaneously, which is not indicative of intestinal malrotation. Therefore, we diagnosed dysplasia of the ligament of Treitz.\n\nClinical outcomes\nThe patient underwent laparotomy, which revealed no abnormalities in the relative position of the duodenum to the jejunum. Additionally, the jejunum was located on the patient\u2019s left side, and there was no intestinal malrotation. The ligament of Treitz was formed; however, its fixation in the upper jejunum was incomplete as it was attached only to the duodenum. The duodenal-jejunal junction was not fixed to the retroperitoneum, and the jejunum folded easily with the ligament of Treitz as a fulcrum. Surgically, the upper jejunum was fixed with 4 sutures to the retroperitoneum on the patient\u2019s left side. The postoperative course was good, and the patient has remained symptom-free.", "generated_summary": "A 77-year-old woman presented with haematemesis. CT showed the third part of the duodenum bending steeply on the right side of the aorta and running downward without crossing in front of it. The duodenojejunal junction and the jejunum were located on the patient\u2019s right side. Upper endoscopy found a laceration at the gastric cardia, consistent with a Mallory\u2013Weiss tear. A repeat CT 7 days later showed that the abnormal bowel position had returned to normal on its own. Two months later she had another episode of haematemesis; CT again showed rightward deviation of the duodenojejunal junction and jejunum, and endoscopy again revealed a cardia laceration. The initial CT pattern raised concern for intestinal malrotation, but the intermittent and self-resolving nature of the right-sided deviation argued against a fixed malrotation. Instead, the findings supported dysplasia (incomplete fixation) of the ligament of Treitz. Laparotomy confirmed that the ligament of Treitz was present but incompletely fixed in the upper jejunum. CT also suggested a mobile anterior pararenal space. Together, these factors likely allowed the small intestine to shift to the right." }, { "index": 29, "label": "proficient_health_literacy", "original_text": "A 77-year-old woman with haematemesis presented to the emergency room. Her medical history included only hypertension and dyslipidaemia. When she presented to the emergency room, her vital signs indicated shock (heart rate: 100 beats/min, blood pressure: 79/56\u2009mmHg), and blood tests revealed anaemia (haemoglobin: 9.6\u2009g/dL), which suggested upper gastrointestinal bleeding.\n\nNon-contrast-enhanced CT was performed immediately because of renal dysfunction. CT revealed that the third part of the duodenum flexed steeply on the right side of the aorta and ran caudally, without crossing anterior to the aorta. The jejunum was located on the patient\u2019s right side. The second part of the duodenum and the stomach were dilated, and there were high-density gastric contents that were considered to indicate a haematoma.\n\nUpper gastrointestinal endoscopy was performed following the CT examination, which revealed a mucosal laceration at the gastric cardia. Bleeding from lacerations of the cardia of the stomach as a result of forceful vomiting was first reported by Mallory and Weiss in 1929.1 In our case, the third part of the duodenum flexed steeply, and the lumen was narrowed, which caused an obstruction. As a result, repeat vomiting was considered to have caused Mallory\u2013Weiss syndrome.\n\nOn the basis of the CT findings showing that the duodenal-jejunal junction was located in the right hemi-abdomen, intestinal malrotation was suspected.2 However, 7\u2009days later, when CT was repeated, spontaneous resolution of the malpositioned jejunum was seen. The patient was then discharged from the hospital. However,\u2009months later, she was rushed to the emergency room for repeat haematemesis. Dynamic CT was performed before upper gastrointestinal endoscopy, on admission, and revealed contrast extravasation in the dilated stomach. Additionally, the third part of the duodenum was flexed on the right side of the aorta, and the duodenal-jejunal junction and jejunum were again located in the right hemi-abdomen. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, as in the previous endoscopy, which was considered Mallory\u2013Weiss syndrome.\n\nTwo months after the second episode of haematemesis, the patient presented to the emergency room with nausea. Non-contrast-enhanced CT revealed no abnormalities in the duodenal positioning, but there was oedematous wall thickening in the second part of the duodenum. If we had not had previous CT images, we would have suspected duodenitis, but on the basis of all of the CT findings, we suspected the possibility of an underlying condition after the right-sided deviation of the small intestine had resolved spontaneously.\n\nIn summary, CT was performed 4 times over 5\u2009months. The third and fourth parts of the duodenum and the jejunum deviated repeatedly, but this resolved spontaneously, which is not indicative of intestinal malrotation. Therefore, we diagnosed dysplasia of the ligament of Treitz.\n\nClinical outcomes\nThe patient underwent laparotomy, which revealed no abnormalities in the relative position of the duodenum to the jejunum. Additionally, the jejunum was located on the patient\u2019s left side, and there was no intestinal malrotation. The ligament of Treitz was formed; however, its fixation in the upper jejunum was incomplete as it was attached only to the duodenum. The duodenal-jejunal junction was not fixed to the retroperitoneum, and the jejunum folded easily with the ligament of Treitz as a fulcrum. Surgically, the upper jejunum was fixed with 4 sutures to the retroperitoneum on the patient\u2019s left side. The postoperative course was good, and the patient has remained symptom-free.", "generated_summary": "A 77-year-old woman with haematemesis presented in shock (heart rate 100 beats/min, blood pressure 79/56 mmHg) with anaemia (haemoglobin 9.6 g/dL), consistent with upper gastrointestinal bleeding. Because of renal dysfunction, non-contrast CT was obtained and demonstrated the third portion of the duodenum flexed steeply on the right side of the aorta and coursing caudally without crossing anterior to the aorta. The duodenojejunal (DJ) junction and the jejunum were in the right hemi-abdomen. The second portion of the duodenum and the stomach were dilated, and high-density gastric contents suggested haematoma. Esophagogastroduodenoscopy showed a mucosal laceration at the gastric cardia, consistent with Mallory\u2013Weiss syndrome; in this case, steep flexion with luminal narrowing of the third portion likely caused transient obstruction and repeated vomiting precipitating the tear. Seven days later, repeat CT showed spontaneous resolution of the malpositioned jejunum. Months later she re-presented with haematemesis; dynamic CT on admission demonstrated contrast extravasation in a dilated stomach and again showed the third portion of the duodenum flexed on the right of the aorta with the DJ junction and jejunum in the right hemi-abdomen. Endoscopy again revealed a cardia laceration. Two months after the second haematemesis, she presented with nausea; non-contrast CT showed normal duodenal positioning but oedematous wall thickening in the second portion. Over four CT examinations spanning five months, the third and fourth portions of the duodenum and the jejunum repeatedly deviated to the right and then spontaneously returned to normal position, a pattern incompatible with fixed intestinal malrotation. Dysplasia (incomplete fixation) of the ligament of Treitz was diagnosed. Laparotomy found no intestinal malrotation: the ligament of Treitz was formed, but fixation in the upper jejunum was incomplete (attached only to the duodenum); the DJ junction was not fixed to the retroperitoneum, and the jejunum folded readily with the ligament as a fulcrum. CT also indicated a loosely fixed, mobile anterior pararenal space. These anatomic factors likely permitted intermittent right-sided deviation of the small intestine. Surgically, the upper jejunum was fixed with four sutures to the left retroperitoneum; the postoperative course was uneventful, and she remained symptom-free." }, { "index": 30, "label": "low_health_literacy", "original_text": "Patient and observation\nPatient information (presentation of the patient): he is a 28-year-old single man without children, an active military. He has been present for 5 weeks with progressive abdominal pain, more marked in the epigastrium and the right hypochondrium, followed shortly after by a non-quantified fever, chills, profuse sweats in a context of anorexia and weight loss of 6 kg. Note that the patient is not a drinker or smoker, vaccinated with BCG and has no other contributing personal or family history.\n\nClinical findings: On admission, the physical examination found the patient in a general altered state, asthenic with a weight loss of 6 kg in one month. A clinical systemic inflammatory response syndrome was present with the following elements: a fever of 39.1 \u00b0C, tachycardia (124 beats/min), polypnea (22 cycles/min). The pulmonary examination and exploration of the superficial lymph node areas were without particularity. In the abdominal area, moderate sensitivity in the right hypochondrium with hepatomegaly was found.\n\nChronology: dates back to February 2022 with the onset of diffuse abdominal pain with diarrhea-constipation transit disorder, all in a context of preservation of general condition with low-grade fever predominantly at night. A syntagmatic treatment was unsuccessfully initiated. The evolution is marked by the persistence of low-grade fever associated with anorexia and progressive weight loss of 12 kg over three months. In the face of this transit disorder with unexplained fever and the deterioration of the general condition, the patient will be admitted to the emergency department for further investigation.\n\nDiagnostic approach: upon admission, a biological infectious syndrome was reported with a neutrophilic predominant hyperleucocytosis (17800 cells/mm3) and a high C-reactive protein of 323 mg/L.\n\nIn the face of his abdominal pain, the lipase and troponin tests were normal at 38 IU/L (VN: <3 78 IU/L) and 4 ng/L (VN: 2 to 16 ng/L) respectively. The liver function was stable with ALT (alanine amino transferase) at 22 IU/L (VN: < 40UI/L), AST (aspartate amino transferase) at 17 IU/L (VN: < 35UI/L), GGT (gamma glutamyl transferase) at 42 IU/L (VN: < 50UI/L), PAL (alkaline phosphatase) at 115 IU/L (VN: 40- 150 IU/L) and normal bilirubinemia. The liver function was normal with a prothrombin rate of 78% and an albuminemia of 39 g/L. The blood ionogram and renal function were normal. The chest radiograph and abdominal ultrasound were without particularity.\n\nWith a procalcitonin positive at 4.1 ng/L, an infectious disease assessment to search for the infectious focus was initiated, including a cytobacteriological examination of urine and blood cultures during the febrile peaks at 39\u00b0C, which were both negative. The hepatitis viral B, C and HIV serologies, as well as the syphilis serology performed in hospital were all negative. The lactate dehydrogenase (LDH) and beta-2 microglobulin were normal at 231 IU/L and 2.28 mg/L respectively. The GeneXpert to search for the Mycobacterium on these bioptic pieces was negative. The quantiferon was negative. The search for the Mycobacterium on the morning expectorations of 3 consecutive days was negative.\n\nOn the morphological level, a thoraco-abdomino-pelvic scan showed an enlarged liver (hepatic arrow at 17 cm), the site of multiple, well-defined, rounded hypodensities, which were not enhanced after injection of the contrast agent. The largest lesions were in segment I (21 x 16 mm) and segment V (36 x 27 mm). No suspicious lesions were detected in the thoracic and pelvic levels. The first liver biopsies obtained by echo-guided puncture revealed subacute, fibro-inflammatory liver lesions, with no histological evidence of specificity or malignancy.\n\nA liver MRI following the scan objectified a dysmorphic liver, the site of lesions in heterogeneous signal T2 surrounded by a wall in hyper signal T2, enhanced in the periphery after injection of the contrast agent, the largest of which is located in segment I (20 x 22 mm) and in segment V (33 x 31 mm). No deep lymphadenopathy had been objectified, either in the scan or in the MRI. A diagnostic laparoscopy performed on the hepatic nodules, the histological examination found epithelioid and gigantocellular granulomas of varying size with caseous necrosis in favour of a hepatic tuberculosis.\n\nTherapeutic intervention: the patient was put on anti-tuberculosis treatment according to the standard protocol for months: Phase 1: quadritherapy (Isoniazide + Rifampicine + Pyrazinamide + Ethambutol) in a single oral intake each morning on an empty stomach for 2 months. Phase 2: bithrapia (Isoniazide + Rifampicine) in a single oral intake each morning on an empty stomach for 4 months\n\nFollow-up and results of therapeutic interventions: from the first days of treatment, a good response was obtained with disappearance of the inflammatory syndrome with systemic response both clinically and biologically. After three months of treatment, a control scan of the liver showed a decrease in the number and volume of liver lesions.\n", "generated_summary": "A young man from Morocco had strong liver pain for about a month. He also had mild signs that can come with TB infection. Scans of his belly showed small spots in his liver. Doctors used a small camera surgery to take a tiny piece from one of the spots. The test on that piece proved the spots were TB in the liver. He started TB medicines. He felt better, and his blood tests got better too." }, { "index": 30, "label": "intermediate_health_literacy", "original_text": "Patient and observation\nPatient information (presentation of the patient): he is a 28-year-old single man without children, an active military. He has been present for 5 weeks with progressive abdominal pain, more marked in the epigastrium and the right hypochondrium, followed shortly after by a non-quantified fever, chills, profuse sweats in a context of anorexia and weight loss of 6 kg. Note that the patient is not a drinker or smoker, vaccinated with BCG and has no other contributing personal or family history.\n\nClinical findings: On admission, the physical examination found the patient in a general altered state, asthenic with a weight loss of 6 kg in one month. A clinical systemic inflammatory response syndrome was present with the following elements: a fever of 39.1 \u00b0C, tachycardia (124 beats/min), polypnea (22 cycles/min). The pulmonary examination and exploration of the superficial lymph node areas were without particularity. In the abdominal area, moderate sensitivity in the right hypochondrium with hepatomegaly was found.\n\nChronology: dates back to February 2022 with the onset of diffuse abdominal pain with diarrhea-constipation transit disorder, all in a context of preservation of general condition with low-grade fever predominantly at night. A syntagmatic treatment was unsuccessfully initiated. The evolution is marked by the persistence of low-grade fever associated with anorexia and progressive weight loss of 12 kg over three months. In the face of this transit disorder with unexplained fever and the deterioration of the general condition, the patient will be admitted to the emergency department for further investigation.\n\nDiagnostic approach: upon admission, a biological infectious syndrome was reported with a neutrophilic predominant hyperleucocytosis (17800 cells/mm3) and a high C-reactive protein of 323 mg/L.\n\nIn the face of his abdominal pain, the lipase and troponin tests were normal at 38 IU/L (VN: <3 78 IU/L) and 4 ng/L (VN: 2 to 16 ng/L) respectively. The liver function was stable with ALT (alanine amino transferase) at 22 IU/L (VN: < 40UI/L), AST (aspartate amino transferase) at 17 IU/L (VN: < 35UI/L), GGT (gamma glutamyl transferase) at 42 IU/L (VN: < 50UI/L), PAL (alkaline phosphatase) at 115 IU/L (VN: 40- 150 IU/L) and normal bilirubinemia. The liver function was normal with a prothrombin rate of 78% and an albuminemia of 39 g/L. The blood ionogram and renal function were normal. The chest radiograph and abdominal ultrasound were without particularity.\n\nWith a procalcitonin positive at 4.1 ng/L, an infectious disease assessment to search for the infectious focus was initiated, including a cytobacteriological examination of urine and blood cultures during the febrile peaks at 39\u00b0C, which were both negative. The hepatitis viral B, C and HIV serologies, as well as the syphilis serology performed in hospital were all negative. The lactate dehydrogenase (LDH) and beta-2 microglobulin were normal at 231 IU/L and 2.28 mg/L respectively. The GeneXpert to search for the Mycobacterium on these bioptic pieces was negative. The quantiferon was negative. The search for the Mycobacterium on the morning expectorations of 3 consecutive days was negative.\n\nOn the morphological level, a thoraco-abdomino-pelvic scan showed an enlarged liver (hepatic arrow at 17 cm), the site of multiple, well-defined, rounded hypodensities, which were not enhanced after injection of the contrast agent. The largest lesions were in segment I (21 x 16 mm) and segment V (36 x 27 mm). No suspicious lesions were detected in the thoracic and pelvic levels. The first liver biopsies obtained by echo-guided puncture revealed subacute, fibro-inflammatory liver lesions, with no histological evidence of specificity or malignancy.\n\nA liver MRI following the scan objectified a dysmorphic liver, the site of lesions in heterogeneous signal T2 surrounded by a wall in hyper signal T2, enhanced in the periphery after injection of the contrast agent, the largest of which is located in segment I (20 x 22 mm) and in segment V (33 x 31 mm). No deep lymphadenopathy had been objectified, either in the scan or in the MRI. A diagnostic laparoscopy performed on the hepatic nodules, the histological examination found epithelioid and gigantocellular granulomas of varying size with caseous necrosis in favour of a hepatic tuberculosis.\n\nTherapeutic intervention: the patient was put on anti-tuberculosis treatment according to the standard protocol for months: Phase 1: quadritherapy (Isoniazide + Rifampicine + Pyrazinamide + Ethambutol) in a single oral intake each morning on an empty stomach for 2 months. Phase 2: bithrapia (Isoniazide + Rifampicine) in a single oral intake each morning on an empty stomach for 4 months\n\nFollow-up and results of therapeutic interventions: from the first days of treatment, a good response was obtained with disappearance of the inflammatory syndrome with systemic response both clinically and biologically. After three months of treatment, a control scan of the liver showed a decrease in the number and volume of liver lesions.\n", "generated_summary": "A 28-year-old Moroccan man developed about a month of liver-area pain along with fever, night sweats, and weight loss, which are symptoms that can suggest tuberculosis. CT and MRI showed multiple non-specific nodules in the liver. An initial needle biopsy was not conclusive, so doctors performed a laparoscopy to obtain better tissue samples. Pathology showed granulomas with caseous necrosis, confirming focal hepatic tuberculosis. He started standard anti-tuberculosis therapy: two months of four drugs, then four months of two drugs. He improved quickly, both in how he felt and in his lab results. A follow-up scan at three months showed that the liver nodules were fewer and smaller." }, { "index": 30, "label": "proficient_health_literacy", "original_text": "Patient and observation\nPatient information (presentation of the patient): he is a 28-year-old single man without children, an active military. He has been present for 5 weeks with progressive abdominal pain, more marked in the epigastrium and the right hypochondrium, followed shortly after by a non-quantified fever, chills, profuse sweats in a context of anorexia and weight loss of 6 kg. Note that the patient is not a drinker or smoker, vaccinated with BCG and has no other contributing personal or family history.\n\nClinical findings: On admission, the physical examination found the patient in a general altered state, asthenic with a weight loss of 6 kg in one month. A clinical systemic inflammatory response syndrome was present with the following elements: a fever of 39.1 \u00b0C, tachycardia (124 beats/min), polypnea (22 cycles/min). The pulmonary examination and exploration of the superficial lymph node areas were without particularity. In the abdominal area, moderate sensitivity in the right hypochondrium with hepatomegaly was found.\n\nChronology: dates back to February 2022 with the onset of diffuse abdominal pain with diarrhea-constipation transit disorder, all in a context of preservation of general condition with low-grade fever predominantly at night. A syntagmatic treatment was unsuccessfully initiated. The evolution is marked by the persistence of low-grade fever associated with anorexia and progressive weight loss of 12 kg over three months. In the face of this transit disorder with unexplained fever and the deterioration of the general condition, the patient will be admitted to the emergency department for further investigation.\n\nDiagnostic approach: upon admission, a biological infectious syndrome was reported with a neutrophilic predominant hyperleucocytosis (17800 cells/mm3) and a high C-reactive protein of 323 mg/L.\n\nIn the face of his abdominal pain, the lipase and troponin tests were normal at 38 IU/L (VN: <3 78 IU/L) and 4 ng/L (VN: 2 to 16 ng/L) respectively. The liver function was stable with ALT (alanine amino transferase) at 22 IU/L (VN: < 40UI/L), AST (aspartate amino transferase) at 17 IU/L (VN: < 35UI/L), GGT (gamma glutamyl transferase) at 42 IU/L (VN: < 50UI/L), PAL (alkaline phosphatase) at 115 IU/L (VN: 40- 150 IU/L) and normal bilirubinemia. The liver function was normal with a prothrombin rate of 78% and an albuminemia of 39 g/L. The blood ionogram and renal function were normal. The chest radiograph and abdominal ultrasound were without particularity.\n\nWith a procalcitonin positive at 4.1 ng/L, an infectious disease assessment to search for the infectious focus was initiated, including a cytobacteriological examination of urine and blood cultures during the febrile peaks at 39\u00b0C, which were both negative. The hepatitis viral B, C and HIV serologies, as well as the syphilis serology performed in hospital were all negative. The lactate dehydrogenase (LDH) and beta-2 microglobulin were normal at 231 IU/L and 2.28 mg/L respectively. The GeneXpert to search for the Mycobacterium on these bioptic pieces was negative. The quantiferon was negative. The search for the Mycobacterium on the morning expectorations of 3 consecutive days was negative.\n\nOn the morphological level, a thoraco-abdomino-pelvic scan showed an enlarged liver (hepatic arrow at 17 cm), the site of multiple, well-defined, rounded hypodensities, which were not enhanced after injection of the contrast agent. The largest lesions were in segment I (21 x 16 mm) and segment V (36 x 27 mm). No suspicious lesions were detected in the thoracic and pelvic levels. The first liver biopsies obtained by echo-guided puncture revealed subacute, fibro-inflammatory liver lesions, with no histological evidence of specificity or malignancy.\n\nA liver MRI following the scan objectified a dysmorphic liver, the site of lesions in heterogeneous signal T2 surrounded by a wall in hyper signal T2, enhanced in the periphery after injection of the contrast agent, the largest of which is located in segment I (20 x 22 mm) and in segment V (33 x 31 mm). No deep lymphadenopathy had been objectified, either in the scan or in the MRI. A diagnostic laparoscopy performed on the hepatic nodules, the histological examination found epithelioid and gigantocellular granulomas of varying size with caseous necrosis in favour of a hepatic tuberculosis.\n\nTherapeutic intervention: the patient was put on anti-tuberculosis treatment according to the standard protocol for months: Phase 1: quadritherapy (Isoniazide + Rifampicine + Pyrazinamide + Ethambutol) in a single oral intake each morning on an empty stomach for 2 months. Phase 2: bithrapia (Isoniazide + Rifampicine) in a single oral intake each morning on an empty stomach for 4 months\n\nFollow-up and results of therapeutic interventions: from the first days of treatment, a good response was obtained with disappearance of the inflammatory syndrome with systemic response both clinically and biologically. After three months of treatment, a control scan of the liver showed a decrease in the number and volume of liver lesions.\n", "generated_summary": "A 28-year-old Moroccan active-duty military male, BCG-vaccinated and without alcohol or tobacco use or relevant comorbidities, presented after 5 weeks of progressive abdominal pain maximal in the epigastrium and right hypochondrium, accompanied by fever, chills, profuse sweats, anorexia, and weight loss. On admission, he had SIRS with T 39.1 \u00b0C, HR 124 bpm, RR 22/min, and right hypochondrial tenderness with hepatomegaly; pulmonary exam and superficial lymph node survey were unremarkable. Laboratory data showed neutrophil-predominant leukocytosis (17,800/mm3) and markedly elevated CRP (323 mg/L), with normal lipase (38 IU/L), troponin (4 ng/L), LFTs (ALT 22 IU/L, AST 17 IU/L, GGT 42 IU/L, ALP 115 IU/L, normal bilirubin), PT 78%, albumin 39 g/L, normal electrolytes and renal function, LDH 231 IU/L, and beta-2 microglobulin 2.28 mg/L. Procalcitonin was 4.1 ng/L. Infectious workup including blood and urine cultures during febrile peaks, HBV/HCV/HIV and syphilis serologies, Quantiferon, GeneXpert on biopsy material, and three consecutive morning sputum examinations for mycobacteria were negative. Chest radiograph and abdominal ultrasound were unrevealing.\n\nCross-sectional imaging demonstrated non-specific focal hepatic lesions. Thoraco-abdomino-pelvic CT showed hepatomegaly (liver long axis 17 cm) with multiple, well-circumscribed rounded hypodense lesions lacking post-contrast enhancement; largest lesions were in segment I (21 \u00d7 16 mm) and segment V (36 \u00d7 27 mm). No suspicious thoracic or pelvic lesions were identified. Initial echo-guided liver biopsies showed subacute fibro-inflammatory changes without specific histology or malignancy. Liver MRI revealed a dysmorphic liver containing lesions with heterogeneous T2 signal, a hyperintense T2 rim, and peripheral enhancement after contrast; the largest lesions were in segment I (20 \u00d7 22 mm) and segment V (33 \u00d7 31 mm). No deep lymphadenopathy was seen on CT or MRI. Diagnostic laparoscopy with targeted biopsies demonstrated epithelioid and multinucleated giant-cell granulomas of varying size with caseous necrosis, confirming focal hepatic tuberculosis.\n\nTreatment followed a standard anti-tuberculosis regimen: Phase 1 with isoniazid, rifampicin, pyrazinamide, and ethambutol once daily fasting for 2 months, followed by Phase 2 with isoniazid and rifampicin once daily fasting for 4 months. Clinical and biological improvement occurred within days, with resolution of the inflammatory response. At 3 months, control CT showed a decrease in both number and size of the hepatic lesions. This case underscores that focal hepatic TB can present with non-specific hepatic nodules on imaging and often requires histopathologic confirmation when microbiological tests are negative." }, { "index": 31, "label": "low_health_literacy", "original_text": "A 12-year-old boy with Down Syndrome and motoric disorders was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient was diagnosed with Down Syndrome and myeloradiculopathy. The patient\u2019s mother said that the patient was admitted to the hospital because of weakness in both patient\u2019s hands and feet. The patient had a history of falling down about one year ago. The patient\u2019s mother also had a difficulty in cleaning the patient\u2019s oral cavity regularly.\n\nIn the extraoral examination, the patient had a dysmorphic face. The patient also had a cracking and desquamative condition of the vermillion border of the lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1\u00d70.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. There was dentinal caries on 63 tooth and also the tooth remnants on 55, 62, 74, and 85 teeth. The upper and lower tooth remnants were suggested to be extracted by pediatric dentist. The space of the extracted teeth will be maintained using a space maintainer. The 55 tooth was sharp and caused an occlusion trauma to the right lateral border of the tongue.\n\nLaboratory examination showed a decrease in sodium value (130 mEq/L) and an increase in lymphocyte value (46%). The MRI examination was performed in the Radiology Department to determine the presence of abnormalities in the cervical spine. The results of the MRI examination showed a dislocation of the patient\u2019s cervical spine. The patient\u2019s mother provided informed consent to publish the patient\u2019s case details and any accompanying images.\n\nBased on the history review, the clinical examination, and appropriate investigation, the patient was diagnosed with a chronic traumatic ulcer mimicking OSCC, exfoliative cheilitis, reversible pulpitis of 63 teeth, and radix gangrene on 55, 62, 74, and 85 teeth. The diagnosis of the chronic ulcer was based on clinical examination. There was an indurated margin in the traumatic lesion, which mimicked Oral Squamous Cell Carcinoma clinically. The patient has been hospitalized for 4 days and was given paracetamol 120 mg/5 mL oral suspension and amoxicillin 125 mg/5 mL oral suspension from the Pediatric Department. The patient also was given sodium chloride 0.9% solution, povidone-iodine mouthwash 1%, and petroleum jelly from the Oral Medicine Department. The patient\u2019s mother was instructed to clean the patient\u2019s oral cavity using gauze soaked in sodium chloride 0.9% solution, compress the ulcer using povidone-iodine mouthwashes 1% three times a day as an antiseptic and anti-inflammatory agent to the oral ulcer, and apply petroleum jelly to moisturize the patient\u2019s lips. The patient was also suggested to extract the 55, 62, 74, and 85 teeth.\n\nIn the second visit (3 days follow-up), oral lesions already showed improvement. In the third visit (1-week follow-up), the size of the oral ulcer at the lateral border of the tongue was getting smaller and the lesion of the lips had some improvement.\n\nIn the fourth visit (10 days follow-up), the size of the oral ulcer at the lateral border of the tongue already had significant improvement. Two days after the fourth visit, the patient underwent neurosurgery. The patient was observed in the Pediatric Intensive Care Unit postoperatively. After two weeks of observation in the Pediatric Intensive Care Unit, the experienced respiratory failure and was declared dead.", "generated_summary": "A 12-year-old boy with Down Syndrome and movement problems went to the mouth doctor. His face looked different. His lips were very dry. The doctor could not feel the neck glands because he wore a neck brace. Inside his mouth, there was a sore on the right side of his tongue. It was about 1 by 0.7 centimeters. The edge felt hard. The bottom looked white-yellow. A sharp baby tooth kept rubbing and biting that spot on his tongue. This made a long-lasting injury sore that can look like mouth cancer, but it was from repeated rubbing. The team gave 0.9% salt-water solution, 1% iodine mouthwash, and petroleum jelly for his lips." }, { "index": 31, "label": "intermediate_health_literacy", "original_text": "A 12-year-old boy with Down Syndrome and motoric disorders was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient was diagnosed with Down Syndrome and myeloradiculopathy. The patient\u2019s mother said that the patient was admitted to the hospital because of weakness in both patient\u2019s hands and feet. The patient had a history of falling down about one year ago. The patient\u2019s mother also had a difficulty in cleaning the patient\u2019s oral cavity regularly.\n\nIn the extraoral examination, the patient had a dysmorphic face. The patient also had a cracking and desquamative condition of the vermillion border of the lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1\u00d70.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. There was dentinal caries on 63 tooth and also the tooth remnants on 55, 62, 74, and 85 teeth. The upper and lower tooth remnants were suggested to be extracted by pediatric dentist. The space of the extracted teeth will be maintained using a space maintainer. The 55 tooth was sharp and caused an occlusion trauma to the right lateral border of the tongue.\n\nLaboratory examination showed a decrease in sodium value (130 mEq/L) and an increase in lymphocyte value (46%). The MRI examination was performed in the Radiology Department to determine the presence of abnormalities in the cervical spine. The results of the MRI examination showed a dislocation of the patient\u2019s cervical spine. The patient\u2019s mother provided informed consent to publish the patient\u2019s case details and any accompanying images.\n\nBased on the history review, the clinical examination, and appropriate investigation, the patient was diagnosed with a chronic traumatic ulcer mimicking OSCC, exfoliative cheilitis, reversible pulpitis of 63 teeth, and radix gangrene on 55, 62, 74, and 85 teeth. The diagnosis of the chronic ulcer was based on clinical examination. There was an indurated margin in the traumatic lesion, which mimicked Oral Squamous Cell Carcinoma clinically. The patient has been hospitalized for 4 days and was given paracetamol 120 mg/5 mL oral suspension and amoxicillin 125 mg/5 mL oral suspension from the Pediatric Department. The patient also was given sodium chloride 0.9% solution, povidone-iodine mouthwash 1%, and petroleum jelly from the Oral Medicine Department. The patient\u2019s mother was instructed to clean the patient\u2019s oral cavity using gauze soaked in sodium chloride 0.9% solution, compress the ulcer using povidone-iodine mouthwashes 1% three times a day as an antiseptic and anti-inflammatory agent to the oral ulcer, and apply petroleum jelly to moisturize the patient\u2019s lips. The patient was also suggested to extract the 55, 62, 74, and 85 teeth.\n\nIn the second visit (3 days follow-up), oral lesions already showed improvement. In the third visit (1-week follow-up), the size of the oral ulcer at the lateral border of the tongue was getting smaller and the lesion of the lips had some improvement.\n\nIn the fourth visit (10 days follow-up), the size of the oral ulcer at the lateral border of the tongue already had significant improvement. Two days after the fourth visit, the patient underwent neurosurgery. The patient was observed in the Pediatric Intensive Care Unit postoperatively. After two weeks of observation in the Pediatric Intensive Care Unit, the experienced respiratory failure and was declared dead.", "generated_summary": "A 12-year-old boy with Down Syndrome and motor problems was seen in Oral Medicine. On exam, he had a dysmorphic facial appearance and very dry, cracked lips. Lymph nodes could not be checked because he wore a cervical collar. Inside the mouth, there was an irregular ulcer on the right side of the tongue measuring about 1\u00d70.7 cm, with a firm (indurated) edge and a white\u2011yellow base. A sharp baby tooth (tooth 55) was causing repeated biting trauma to that area. Based on the clinical exam, the team diagnosed a chronic traumatic ulcer that can resemble oral squamous cell carcinoma. Treatment included 0.9% saline, a 1% povidone\u2011iodine mouthwash, and petroleum jelly to moisturize the lips." }, { "index": 31, "label": "proficient_health_literacy", "original_text": "A 12-year-old boy with Down Syndrome and motoric disorders was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient was diagnosed with Down Syndrome and myeloradiculopathy. The patient\u2019s mother said that the patient was admitted to the hospital because of weakness in both patient\u2019s hands and feet. The patient had a history of falling down about one year ago. The patient\u2019s mother also had a difficulty in cleaning the patient\u2019s oral cavity regularly.\n\nIn the extraoral examination, the patient had a dysmorphic face. The patient also had a cracking and desquamative condition of the vermillion border of the lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1\u00d70.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. There was dentinal caries on 63 tooth and also the tooth remnants on 55, 62, 74, and 85 teeth. The upper and lower tooth remnants were suggested to be extracted by pediatric dentist. The space of the extracted teeth will be maintained using a space maintainer. The 55 tooth was sharp and caused an occlusion trauma to the right lateral border of the tongue.\n\nLaboratory examination showed a decrease in sodium value (130 mEq/L) and an increase in lymphocyte value (46%). The MRI examination was performed in the Radiology Department to determine the presence of abnormalities in the cervical spine. The results of the MRI examination showed a dislocation of the patient\u2019s cervical spine. The patient\u2019s mother provided informed consent to publish the patient\u2019s case details and any accompanying images.\n\nBased on the history review, the clinical examination, and appropriate investigation, the patient was diagnosed with a chronic traumatic ulcer mimicking OSCC, exfoliative cheilitis, reversible pulpitis of 63 teeth, and radix gangrene on 55, 62, 74, and 85 teeth. The diagnosis of the chronic ulcer was based on clinical examination. There was an indurated margin in the traumatic lesion, which mimicked Oral Squamous Cell Carcinoma clinically. The patient has been hospitalized for 4 days and was given paracetamol 120 mg/5 mL oral suspension and amoxicillin 125 mg/5 mL oral suspension from the Pediatric Department. The patient also was given sodium chloride 0.9% solution, povidone-iodine mouthwash 1%, and petroleum jelly from the Oral Medicine Department. The patient\u2019s mother was instructed to clean the patient\u2019s oral cavity using gauze soaked in sodium chloride 0.9% solution, compress the ulcer using povidone-iodine mouthwashes 1% three times a day as an antiseptic and anti-inflammatory agent to the oral ulcer, and apply petroleum jelly to moisturize the patient\u2019s lips. The patient was also suggested to extract the 55, 62, 74, and 85 teeth.\n\nIn the second visit (3 days follow-up), oral lesions already showed improvement. In the third visit (1-week follow-up), the size of the oral ulcer at the lateral border of the tongue was getting smaller and the lesion of the lips had some improvement.\n\nIn the fourth visit (10 days follow-up), the size of the oral ulcer at the lateral border of the tongue already had significant improvement. Two days after the fourth visit, the patient underwent neurosurgery. The patient was observed in the Pediatric Intensive Care Unit postoperatively. After two weeks of observation in the Pediatric Intensive Care Unit, the experienced respiratory failure and was declared dead.", "generated_summary": "A 12-year-old boy with Down Syndrome and motoric disorders (diagnosed with myeloradiculopathy) was referred from Pediatrics to the Oral Medicine Department (RS Hasan Sadikin Bandung) for oral evaluation. The mother reported hospitalization for weakness of both hands and feet and difficulty maintaining the child\u2019s oral hygiene; there was a history of a fall approximately one year prior. Extraoral findings: dysmorphic facies; cracking and desquamation of the vermilion border; cervical collar in place, precluding lymph node assessment. Intraorally, there was an irregular 1\u00d70.7 cm ulcer with an indurated margin and a white\u2011yellowish base on the right lateral tongue. Additional findings included dentinal caries on tooth 63 and tooth remnants on 55, 62, 74, and 85. The 55 tooth had a sharp cusp causing occlusal trauma to the right lateral tongue. Pediatric dentistry recommended extraction of the upper and lower tooth remnants with subsequent space maintenance. Laboratory data: hyponatremia (Na 130 mEq/L) and relative lymphocytosis (46%). MRI of the cervical spine demonstrated dislocation; the mother provided informed consent for publication. Working diagnoses, based on history, clinical examination, and investigations: chronic traumatic ulcer mimicking OSCC (clinical diagnosis; indurated margin raised concern for oral squamous cell carcinoma), exfoliative cheilitis, reversible pulpitis of 63, and radix gangrene on 55, 62, 74, and 85. The patient had been hospitalized for 4 days and received paracetamol 120 mg/5 mL oral suspension and amoxicillin 125 mg/5 mL oral suspension from Pediatrics. Oral Medicine management included sodium chloride 0.9% solution, 1% povidone\u2011iodine mouthwash, and petroleum jelly. Caregiver instructions: cleanse the oral cavity with gauze soaked in 0.9% saline; apply 1% povidone\u2011iodine compresses to the ulcer three times daily as an antiseptic/anti\u2011inflammatory; apply petroleum jelly to moisturize the lips. Extractions of 55, 62, 74, and 85 were advised. Follow-up: at 3 days, oral lesions showed improvement; at 1 week, the lateral tongue ulcer decreased in size and lip lesions improved; at 10 days, the ulcer showed significant improvement. Two days later, the patient underwent neurosurgery and was observed in the Pediatric ICU. After two weeks in the ICU, he developed respiratory failure and died." }, { "index": 32, "label": "low_health_literacy", "original_text": "We present a case of a 59-year-old lady with a twelve-year history of secondary progressive multiple sclerosis who was referred to ophthalmology with a few weeks\u2019 history of bilateral blurring of vision.\n\nThe patient had no past ophthalmic history and no drug history other than the anti-epileptic medications related to her multiple sclerosis. Previously documented ophthalmic examinations did not reveal any signs of Fuchs' endothelial corneal dystrophy, and the patient has no family history of corneal pathology.\n\nThe patient had been on amantadine therapy at a dose of 100mg twice daily for the past 7 years and was started on levetiracetam 250mg twice daily as an add-on agent. Visual deterioration was experienced shortly after commencement of levetiracetam therapy for a breakthrough seizure.\n\nOn examination, the patient\u2019s best corrected visual acuity was 0.5 logMAR right eye and 0.5 logMAR left eye. Slit-lamp examination revealed corneal edema involving both eyes and absence of uveitis. Corrected intraocular pressures were 16mmHg right eye and 18mmHg left eye. Corneal topography was performed which confirmed bilateral significant corneal thickening with a right central corneal thickness of 936\u03bcm and left central corneal thickness of 1134\u03bcm. The rest of the eye examination was normal.\n\nSince amantadine is a known cause of corneal edema, it was agreed with the patient and her caring neurologist to switch from amantadine to lamotrigine. Levetiracetam therapy was continued at this stage. No improvement in vision was noted two months after this change in treatment. The patient expressed the wish to temporarily stop levetiracetam on a trial basis in view of the direct temporal association between the onset of symptoms and the commencement of the medication.\n\nAmantadine was re-introduced, while levetiracetam dose was tapered. Improvement in vision was noted a few days after levetiracetam dose reduction. Levetiracetam was stopped altogether, and the patient remained on amantadine and lamotrigine. A provisional diagnosis of levetiracetam-induced corneal edema was made at this stage. Her vision normalized and repeat corneal topography six months after stopping the levetiracetam showed a right central corneal thickness of 567\u03bcm and a left central corneal thickness of 573\u03bcm, and a visual acuity of 0.2 logMAR both eyes. Slit-lamp examination confirmed clear cornea and the absence of corneal guttata in either eye.\n\nThe patient was examined again thirteen months after the first presentation. No further changes in her medications were made, and her vision had remained stable at 0.2 logMAR in both eyes. Repeat corneal topography showed no further changes.", "generated_summary": "A 59-year-old woman has multiple sclerosis. She started a new seizure medicine called levetiracetam. A few weeks later, her vision in both eyes became blurry. The eye doctor found swelling in the clear front window of both eyes. A special eye scan confirmed the swelling. They lowered the dose of the new medicine. Her vision started to get better. They then stopped the medicine. Her vision went back to normal. The swelling went away." }, { "index": 32, "label": "intermediate_health_literacy", "original_text": "We present a case of a 59-year-old lady with a twelve-year history of secondary progressive multiple sclerosis who was referred to ophthalmology with a few weeks\u2019 history of bilateral blurring of vision.\n\nThe patient had no past ophthalmic history and no drug history other than the anti-epileptic medications related to her multiple sclerosis. Previously documented ophthalmic examinations did not reveal any signs of Fuchs' endothelial corneal dystrophy, and the patient has no family history of corneal pathology.\n\nThe patient had been on amantadine therapy at a dose of 100mg twice daily for the past 7 years and was started on levetiracetam 250mg twice daily as an add-on agent. Visual deterioration was experienced shortly after commencement of levetiracetam therapy for a breakthrough seizure.\n\nOn examination, the patient\u2019s best corrected visual acuity was 0.5 logMAR right eye and 0.5 logMAR left eye. Slit-lamp examination revealed corneal edema involving both eyes and absence of uveitis. Corrected intraocular pressures were 16mmHg right eye and 18mmHg left eye. Corneal topography was performed which confirmed bilateral significant corneal thickening with a right central corneal thickness of 936\u03bcm and left central corneal thickness of 1134\u03bcm. The rest of the eye examination was normal.\n\nSince amantadine is a known cause of corneal edema, it was agreed with the patient and her caring neurologist to switch from amantadine to lamotrigine. Levetiracetam therapy was continued at this stage. No improvement in vision was noted two months after this change in treatment. The patient expressed the wish to temporarily stop levetiracetam on a trial basis in view of the direct temporal association between the onset of symptoms and the commencement of the medication.\n\nAmantadine was re-introduced, while levetiracetam dose was tapered. Improvement in vision was noted a few days after levetiracetam dose reduction. Levetiracetam was stopped altogether, and the patient remained on amantadine and lamotrigine. A provisional diagnosis of levetiracetam-induced corneal edema was made at this stage. Her vision normalized and repeat corneal topography six months after stopping the levetiracetam showed a right central corneal thickness of 567\u03bcm and a left central corneal thickness of 573\u03bcm, and a visual acuity of 0.2 logMAR both eyes. Slit-lamp examination confirmed clear cornea and the absence of corneal guttata in either eye.\n\nThe patient was examined again thirteen months after the first presentation. No further changes in her medications were made, and her vision had remained stable at 0.2 logMAR in both eyes. Repeat corneal topography showed no further changes.", "generated_summary": "A 59-year-old woman with secondary progressive multiple sclerosis developed a few weeks of blurry vision in both eyes shortly after starting levetiracetam for new seizures. Eye examination showed corneal edema in both eyes, confirmed by corneal topography. When the levetiracetam dose was reduced, her symptoms improved, and the drug was then stopped. On follow-up, both her vision and the corneal swelling returned to normal. She had no prior eye disease or family history of corneal problems, and changes to other medications did not help beforehand, supporting levetiracetam as the likely cause." }, { "index": 32, "label": "proficient_health_literacy", "original_text": "We present a case of a 59-year-old lady with a twelve-year history of secondary progressive multiple sclerosis who was referred to ophthalmology with a few weeks\u2019 history of bilateral blurring of vision.\n\nThe patient had no past ophthalmic history and no drug history other than the anti-epileptic medications related to her multiple sclerosis. Previously documented ophthalmic examinations did not reveal any signs of Fuchs' endothelial corneal dystrophy, and the patient has no family history of corneal pathology.\n\nThe patient had been on amantadine therapy at a dose of 100mg twice daily for the past 7 years and was started on levetiracetam 250mg twice daily as an add-on agent. Visual deterioration was experienced shortly after commencement of levetiracetam therapy for a breakthrough seizure.\n\nOn examination, the patient\u2019s best corrected visual acuity was 0.5 logMAR right eye and 0.5 logMAR left eye. Slit-lamp examination revealed corneal edema involving both eyes and absence of uveitis. Corrected intraocular pressures were 16mmHg right eye and 18mmHg left eye. Corneal topography was performed which confirmed bilateral significant corneal thickening with a right central corneal thickness of 936\u03bcm and left central corneal thickness of 1134\u03bcm. The rest of the eye examination was normal.\n\nSince amantadine is a known cause of corneal edema, it was agreed with the patient and her caring neurologist to switch from amantadine to lamotrigine. Levetiracetam therapy was continued at this stage. No improvement in vision was noted two months after this change in treatment. The patient expressed the wish to temporarily stop levetiracetam on a trial basis in view of the direct temporal association between the onset of symptoms and the commencement of the medication.\n\nAmantadine was re-introduced, while levetiracetam dose was tapered. Improvement in vision was noted a few days after levetiracetam dose reduction. Levetiracetam was stopped altogether, and the patient remained on amantadine and lamotrigine. A provisional diagnosis of levetiracetam-induced corneal edema was made at this stage. Her vision normalized and repeat corneal topography six months after stopping the levetiracetam showed a right central corneal thickness of 567\u03bcm and a left central corneal thickness of 573\u03bcm, and a visual acuity of 0.2 logMAR both eyes. Slit-lamp examination confirmed clear cornea and the absence of corneal guttata in either eye.\n\nThe patient was examined again thirteen months after the first presentation. No further changes in her medications were made, and her vision had remained stable at 0.2 logMAR in both eyes. Repeat corneal topography showed no further changes.", "generated_summary": "A 59-year-old woman with a 12-year history of secondary progressive multiple sclerosis presented with several weeks of bilateral blurred vision. Past ophthalmic history was unremarkable; there was no family history of corneal pathology, and prior examinations showed no signs of Fuchs' endothelial corneal dystrophy. She had been on amantadine 100 mg twice daily for 7 years and was started on levetiracetam 250 mg twice daily as an add-on agent after a breakthrough seizure; visual deterioration occurred shortly after levetiracetam initiation. On examination, BCVA was 0.5 logMAR OU. Slit-lamp examination revealed bilateral corneal edema without uveitis; IOPs were 16 mmHg OD and 18 mmHg OS. Corneal topography confirmed significant bilateral corneal thickening with CCT 936 \u03bcm OD and 1134 \u03bcm OS; the remainder of the ocular examination was normal. Because amantadine is a known cause of corneal edema, it was switched to lamotrigine while levetiracetam was continued, but there was no improvement after two months. Amantadine was then reintroduced and levetiracetam was tapered; visual improvement was noted within days of levetiracetam dose reduction. Levetiracetam was subsequently discontinued, and the patient remained on amantadine and lamotrigine. A provisional diagnosis of levetiracetam-induced corneal edema was made. Six months after stopping levetiracetam, BCVA improved to 0.2 logMAR OU; corneal topography showed CCT 567 \u03bcm OD and 573 \u03bcm OS, and slit-lamp confirmed clear corneas without guttata. At 13 months after initial presentation, medications were unchanged, vision remained stable at 0.2 logMAR OU, and repeat corneal topography was unchanged. The clinical course is consistent with a drug-induced, reversible corneal endothelial dysfunction temporally related to levetiracetam exposure, with no response to amantadine withdrawal." }, { "index": 33, "label": "low_health_literacy", "original_text": "A 77-year-old male patient presented with a history of moderate cognitive impairment. The patient was admitted to the emergency department for a tonic-clonic seizure at home. The patient presented hemodynamically unstable in the context of a postcritical state and suspected intrapelvic bleeding. The code for a polytraumatized patient was activated, not because of the mechanism of injury, but because of the patient's hemodynamic status. He was stabilized and optimized in the emergency department with intravenous fluid and transfusion of packed red blood cells. A pelvic girdle was placed. Once hemodynamic stability was achieved, a physical examination was performed. Clinically, the patient presented a shortening of the lower limb compared to the contralateral limb, external rotation and joint blockage when performing the log roll test in both limbs. He presented functional impotence in both hips. Given the patient's condition when he arrived at the emergency department, it was not possible to assess the neurological status. He had no signs of external injuries or bruises. Distal pulses were present at the foot level. He could move his upper limbs. A chest and anteroposterior pelvic radiograph was performed as part of the code for a polytraumatized patient, pending completion of an abdominal-pelvic computed tomography (CT) study. A bilateral femoral dislocation was diagnosed in the pelvic radiograph. The patient underwent a procedure to correct the dislocation.\n\n\n\nComputed tomography angiography to rule out vascular lesions given the instability in hemodynamic that presented itself on admission. Vascular lesions were ruled out after the angiography. In the 3D-CT reconstruction of the pelvis, a bilateral transverse acetabular fracture was found, according to the classification of Letournel and a bilateral longitudinal fracture of the iliac wing was found, along with intrapelvic protrusion of both femoral heads. After initial evaluation, supracondylar traction was placed on the femoral head in both extremities and the pelvic traction was removed. The patient was admitted to the recovery unit until surgery, where he remained with the traction supracondylar femoral head in both extremities and the pelvic traction was removed. The patient was operated on the eighth day of admission. In our service, the acetabular fractures were ruled out after seven days waiting for the formation of a fibrosis in the focus of fracture and the decrease of intraoperative bleeding during surgical procedures. It was decided to perform the surgery in two stages due to the long duration of each intervention. Both surgeries were performed with general anaesthesia, tranexamic acid was administered to prevent intraoperative bleeding and decrease blood transfusions in relation to the surgeries; and antibiotic (cefazolin 2 g preoperatively and 1 g of cefazolin every 8 hours postoperatively for 24 hours) as an intrahospital protocol. During the postoperative period, enoxaparin 40 mg was administered subcutaneously every 24 hours for seven weeks. Initially, the surgery of the left hemipelvis was performed since, at the radiographic level, it presented greater pelvic protrusion and it was not desirable that a hematoma in the soft tissue phase could generate complications at the time of extraction of the femoral head (vascular injuries, intraoperative bleeding). The supracondylar traction was removed. The patient was placed in lateral decubitus, and a posterior lateral approach was performed with a Moore's autograft in the acetabular background (fracture focus). Subsequently, the anti-protrusion ring was implanted (Burch SchneiderTM Reinforcement Cage, Zimmer Biomet) anchored to the ischium and ilium. Prior to the implantation of the ring, it was necessary to perform dissection of the gluteal musculature (gluteus minimus and medius) to correctly place the femoral head. The medial ischial fracture of the ring was also anchored with screws. The check was performed under the control of a scope to verify the correct implantation. Subsequently, a double mobility cementaed acetabular ring was implanted and then the non-cemented femoral stem was implanted. After finishing the placement of the components, the capsule and pelvic musculature were closed by means of transosseous trochanteric points. The surgery of the right hemipelvis was performed seven days later. The patient was placed in lateral decubitus. To address the longitudinal fracture of the iliac wing, the first window of the ilio-inguinal approach was performed. It was synthesised with a six-hole anatomical plate. Subsequently, the same procedure as the previous surgery was performed, using an anti-protrusion ring with a double mobility cemented femoral stem and non-cemented femoral stem. This type of anti-protrusion rings are used when there are acetabular fractures that could be equivalent to a pelvic disjunction (type IV classification of acetabular defects of the AAOS) and an anchorage in the ischium and ilium of the ring is needed to support the ring. They are not indicated for isolated fractures of the anterior or posterior wall of the acetabulum where there is no involvement of the acetabular background. During admission, the patient remained in bed and was mobilised to avoid decubitus ulcers. Once the second intervention was performed and when the patient tolerated it clinically, he began to transfer with the use of a wheelchair. In bed he was allowed to have a full range of motion without restriction. The patient was discharged four weeks later and did not begin to load or walk until six weeks. He began to load with the use of a walking stick. We decided to delay loading because, despite the use of arthroplasty as a treatment, it was decided to wait until there was an initial consolidation of the graft in the acetabular background that provided better support for the ring. It was also added that the patient presented bilateral involvement and it would be difficult to start partial loading, given that he did not have a healthy hip to support. During the follow-up of the patient, at 12 months of the intervention he was already doing full load with the use of a walking stick, with a Harris hip score of 79 in the left hip and 77 in the right hip; and a score of 12 on the WOMAC scale. He has not presented any postoperative complications to date. The patient is satisfied clinically, he reports occasional discomfort and a slight limp of the right side. He has a full range of motion in the examination and does not report having had any episode of instability since the surgery.\n", "generated_summary": "A 77-year-old man has memory and thinking problems. He had a big seizure. Both hip joints popped inward into the pelvis. In the emergency room, his right leg looked shorter than the left. Both legs were turned outward. Both hips were stuck when staff gently rolled his legs. Scans and medical checks were done to get him ready for surgery. The surgeries were done in two steps. The left hip was done on day 8. The right hip was done on day 15. In both surgeries, doctors put in a support ring and a special hip socket that helps keep the joint stable. They also put in a new thigh-bone piece that does not use cement. Right after surgery, there were no problems from the operation. At 12 months, he could put full weight on his legs. His right hip score was 77. His left hip score was 79. His WOMAC score was 12. He has had no problems since the surgery." }, { "index": 33, "label": "intermediate_health_literacy", "original_text": "A 77-year-old male patient presented with a history of moderate cognitive impairment. The patient was admitted to the emergency department for a tonic-clonic seizure at home. The patient presented hemodynamically unstable in the context of a postcritical state and suspected intrapelvic bleeding. The code for a polytraumatized patient was activated, not because of the mechanism of injury, but because of the patient's hemodynamic status. He was stabilized and optimized in the emergency department with intravenous fluid and transfusion of packed red blood cells. A pelvic girdle was placed. Once hemodynamic stability was achieved, a physical examination was performed. Clinically, the patient presented a shortening of the lower limb compared to the contralateral limb, external rotation and joint blockage when performing the log roll test in both limbs. He presented functional impotence in both hips. Given the patient's condition when he arrived at the emergency department, it was not possible to assess the neurological status. He had no signs of external injuries or bruises. Distal pulses were present at the foot level. He could move his upper limbs. A chest and anteroposterior pelvic radiograph was performed as part of the code for a polytraumatized patient, pending completion of an abdominal-pelvic computed tomography (CT) study. A bilateral femoral dislocation was diagnosed in the pelvic radiograph. The patient underwent a procedure to correct the dislocation.\n\n\n\nComputed tomography angiography to rule out vascular lesions given the instability in hemodynamic that presented itself on admission. Vascular lesions were ruled out after the angiography. In the 3D-CT reconstruction of the pelvis, a bilateral transverse acetabular fracture was found, according to the classification of Letournel and a bilateral longitudinal fracture of the iliac wing was found, along with intrapelvic protrusion of both femoral heads. After initial evaluation, supracondylar traction was placed on the femoral head in both extremities and the pelvic traction was removed. The patient was admitted to the recovery unit until surgery, where he remained with the traction supracondylar femoral head in both extremities and the pelvic traction was removed. The patient was operated on the eighth day of admission. In our service, the acetabular fractures were ruled out after seven days waiting for the formation of a fibrosis in the focus of fracture and the decrease of intraoperative bleeding during surgical procedures. It was decided to perform the surgery in two stages due to the long duration of each intervention. Both surgeries were performed with general anaesthesia, tranexamic acid was administered to prevent intraoperative bleeding and decrease blood transfusions in relation to the surgeries; and antibiotic (cefazolin 2 g preoperatively and 1 g of cefazolin every 8 hours postoperatively for 24 hours) as an intrahospital protocol. During the postoperative period, enoxaparin 40 mg was administered subcutaneously every 24 hours for seven weeks. Initially, the surgery of the left hemipelvis was performed since, at the radiographic level, it presented greater pelvic protrusion and it was not desirable that a hematoma in the soft tissue phase could generate complications at the time of extraction of the femoral head (vascular injuries, intraoperative bleeding). The supracondylar traction was removed. The patient was placed in lateral decubitus, and a posterior lateral approach was performed with a Moore's autograft in the acetabular background (fracture focus). Subsequently, the anti-protrusion ring was implanted (Burch SchneiderTM Reinforcement Cage, Zimmer Biomet) anchored to the ischium and ilium. Prior to the implantation of the ring, it was necessary to perform dissection of the gluteal musculature (gluteus minimus and medius) to correctly place the femoral head. The medial ischial fracture of the ring was also anchored with screws. The check was performed under the control of a scope to verify the correct implantation. Subsequently, a double mobility cementaed acetabular ring was implanted and then the non-cemented femoral stem was implanted. After finishing the placement of the components, the capsule and pelvic musculature were closed by means of transosseous trochanteric points. The surgery of the right hemipelvis was performed seven days later. The patient was placed in lateral decubitus. To address the longitudinal fracture of the iliac wing, the first window of the ilio-inguinal approach was performed. It was synthesised with a six-hole anatomical plate. Subsequently, the same procedure as the previous surgery was performed, using an anti-protrusion ring with a double mobility cemented femoral stem and non-cemented femoral stem. This type of anti-protrusion rings are used when there are acetabular fractures that could be equivalent to a pelvic disjunction (type IV classification of acetabular defects of the AAOS) and an anchorage in the ischium and ilium of the ring is needed to support the ring. They are not indicated for isolated fractures of the anterior or posterior wall of the acetabulum where there is no involvement of the acetabular background. During admission, the patient remained in bed and was mobilised to avoid decubitus ulcers. Once the second intervention was performed and when the patient tolerated it clinically, he began to transfer with the use of a wheelchair. In bed he was allowed to have a full range of motion without restriction. The patient was discharged four weeks later and did not begin to load or walk until six weeks. He began to load with the use of a walking stick. We decided to delay loading because, despite the use of arthroplasty as a treatment, it was decided to wait until there was an initial consolidation of the graft in the acetabular background that provided better support for the ring. It was also added that the patient presented bilateral involvement and it would be difficult to start partial loading, given that he did not have a healthy hip to support. During the follow-up of the patient, at 12 months of the intervention he was already doing full load with the use of a walking stick, with a Harris hip score of 79 in the left hip and 77 in the right hip; and a score of 12 on the WOMAC scale. He has not presented any postoperative complications to date. The patient is satisfied clinically, he reports occasional discomfort and a slight limp of the right side. He has a full range of motion in the examination and does not report having had any episode of instability since the surgery.\n", "generated_summary": "A 77-year-old man with moderate cognitive impairment had a generalized seizure, which caused both hips to dislocate inward (central dislocation). In the emergency department, his exam showed a shorter right leg compared with the left, outward rotation of both legs, and the hips locked with the log-roll test on both sides. He underwent imaging and medical optimization before surgery. Surgeons staged the operations: the left hip on hospital day 8 and the right hip on day 15. On both sides they implanted an anti-protrusion ring and a dual-mobility acetabular component, along with an uncemented femoral stem. There were no immediate surgical complications. At the 12-month follow-up, he was fully weight-bearing, with Harris Hip Scores of 79 on the left and 77 on the right, and a WOMAC score of 12. He has had no postoperative complications to date." }, { "index": 33, "label": "proficient_health_literacy", "original_text": "A 77-year-old male patient presented with a history of moderate cognitive impairment. The patient was admitted to the emergency department for a tonic-clonic seizure at home. The patient presented hemodynamically unstable in the context of a postcritical state and suspected intrapelvic bleeding. The code for a polytraumatized patient was activated, not because of the mechanism of injury, but because of the patient's hemodynamic status. He was stabilized and optimized in the emergency department with intravenous fluid and transfusion of packed red blood cells. A pelvic girdle was placed. Once hemodynamic stability was achieved, a physical examination was performed. Clinically, the patient presented a shortening of the lower limb compared to the contralateral limb, external rotation and joint blockage when performing the log roll test in both limbs. He presented functional impotence in both hips. Given the patient's condition when he arrived at the emergency department, it was not possible to assess the neurological status. He had no signs of external injuries or bruises. Distal pulses were present at the foot level. He could move his upper limbs. A chest and anteroposterior pelvic radiograph was performed as part of the code for a polytraumatized patient, pending completion of an abdominal-pelvic computed tomography (CT) study. A bilateral femoral dislocation was diagnosed in the pelvic radiograph. The patient underwent a procedure to correct the dislocation.\n\n\n\nComputed tomography angiography to rule out vascular lesions given the instability in hemodynamic that presented itself on admission. Vascular lesions were ruled out after the angiography. In the 3D-CT reconstruction of the pelvis, a bilateral transverse acetabular fracture was found, according to the classification of Letournel and a bilateral longitudinal fracture of the iliac wing was found, along with intrapelvic protrusion of both femoral heads. After initial evaluation, supracondylar traction was placed on the femoral head in both extremities and the pelvic traction was removed. The patient was admitted to the recovery unit until surgery, where he remained with the traction supracondylar femoral head in both extremities and the pelvic traction was removed. The patient was operated on the eighth day of admission. In our service, the acetabular fractures were ruled out after seven days waiting for the formation of a fibrosis in the focus of fracture and the decrease of intraoperative bleeding during surgical procedures. It was decided to perform the surgery in two stages due to the long duration of each intervention. Both surgeries were performed with general anaesthesia, tranexamic acid was administered to prevent intraoperative bleeding and decrease blood transfusions in relation to the surgeries; and antibiotic (cefazolin 2 g preoperatively and 1 g of cefazolin every 8 hours postoperatively for 24 hours) as an intrahospital protocol. During the postoperative period, enoxaparin 40 mg was administered subcutaneously every 24 hours for seven weeks. Initially, the surgery of the left hemipelvis was performed since, at the radiographic level, it presented greater pelvic protrusion and it was not desirable that a hematoma in the soft tissue phase could generate complications at the time of extraction of the femoral head (vascular injuries, intraoperative bleeding). The supracondylar traction was removed. The patient was placed in lateral decubitus, and a posterior lateral approach was performed with a Moore's autograft in the acetabular background (fracture focus). Subsequently, the anti-protrusion ring was implanted (Burch SchneiderTM Reinforcement Cage, Zimmer Biomet) anchored to the ischium and ilium. Prior to the implantation of the ring, it was necessary to perform dissection of the gluteal musculature (gluteus minimus and medius) to correctly place the femoral head. The medial ischial fracture of the ring was also anchored with screws. The check was performed under the control of a scope to verify the correct implantation. Subsequently, a double mobility cementaed acetabular ring was implanted and then the non-cemented femoral stem was implanted. After finishing the placement of the components, the capsule and pelvic musculature were closed by means of transosseous trochanteric points. The surgery of the right hemipelvis was performed seven days later. The patient was placed in lateral decubitus. To address the longitudinal fracture of the iliac wing, the first window of the ilio-inguinal approach was performed. It was synthesised with a six-hole anatomical plate. Subsequently, the same procedure as the previous surgery was performed, using an anti-protrusion ring with a double mobility cemented femoral stem and non-cemented femoral stem. This type of anti-protrusion rings are used when there are acetabular fractures that could be equivalent to a pelvic disjunction (type IV classification of acetabular defects of the AAOS) and an anchorage in the ischium and ilium of the ring is needed to support the ring. They are not indicated for isolated fractures of the anterior or posterior wall of the acetabulum where there is no involvement of the acetabular background. During admission, the patient remained in bed and was mobilised to avoid decubitus ulcers. Once the second intervention was performed and when the patient tolerated it clinically, he began to transfer with the use of a wheelchair. In bed he was allowed to have a full range of motion without restriction. The patient was discharged four weeks later and did not begin to load or walk until six weeks. He began to load with the use of a walking stick. We decided to delay loading because, despite the use of arthroplasty as a treatment, it was decided to wait until there was an initial consolidation of the graft in the acetabular background that provided better support for the ring. It was also added that the patient presented bilateral involvement and it would be difficult to start partial loading, given that he did not have a healthy hip to support. During the follow-up of the patient, at 12 months of the intervention he was already doing full load with the use of a walking stick, with a Harris hip score of 79 in the left hip and 77 in the right hip; and a score of 12 on the WOMAC scale. He has not presented any postoperative complications to date. The patient is satisfied clinically, he reports occasional discomfort and a slight limp of the right side. He has a full range of motion in the examination and does not report having had any episode of instability since the surgery.\n", "generated_summary": "A 77-year-old male with a history of moderate cognitive impairment presented after a tonic\u2013clonic seizure at home. On arrival to the ED he was hemodynamically unstable in a postictal state with suspected intrapelvic bleeding, triggering activation of the polytrauma code (for physiology rather than mechanism). He was stabilized with intravenous fluids and transfusion of packed red blood cells, and a pelvic girdle was applied. Once stable, examination showed shortening of the lower limb compared with the contralateral side, external rotation, and joint blockage on log-roll testing in both limbs, with functional impotence of both hips. Neurologic assessment was initially limited. There were no external injuries; distal foot pulses were present, and he could move his upper limbs. Chest and AP pelvic radiographs were obtained; the pelvic film demonstrated bilateral femoral dislocation, and a reduction procedure was performed. Computed tomography angiography was then used to exclude vascular injury (none identified). 3D-CT reconstructions revealed bilateral transverse acetabular fractures per Letournel, bilateral longitudinal iliac wing fractures, and intrapelvic protrusion of both femoral heads. Bilateral supracondylar femoral traction was applied and pelvic traction was removed. The patient was operated on hospital day 8, in accordance with the service protocol to delay acetabular fracture surgery approximately 7 days to allow fibrosis at the fracture site and reduce intraoperative bleeding. Given anticipated operative duration, a staged approach was selected. Perioperatively, both procedures were performed under general anesthesia with tranexamic acid to limit bleeding and cefazolin prophylaxis (2 g pre-op, then 1 g q8h for 24 h). Postoperatively, enoxaparin 40 mg SC daily was administered for 7 weeks. The left hemipelvis was addressed first due to greater radiographic protrusion and concern that a soft-tissue hematoma could complicate femoral head extraction (risk of vascular injury/bleeding). With the patient in lateral decubitus, a posterolateral approach was used. A Moore\u2019s autograft was placed in the acetabular background (fracture focus). A Burch-Schneider Reinforcement Cage (Zimmer Biomet) was implanted, anchored to the ischium and ilium; dissection of the gluteus minimus and medius was required to position the femoral head. The ischial fixation was secured with screws, and fluoroscopy confirmed component positioning. A cemented dual-mobility acetabular construct was then implanted, followed by a non-cemented femoral stem. Closure included the capsule and pelvic musculature with transosseous trochanteric sutures. Seven days later, the right side was performed in lateral decubitus. The longitudinal iliac wing fracture was addressed first via the first window of the ilioinguinal approach and fixed with a six-hole anatomical plate. The hip reconstruction then mirrored the left: anti-protrusion ring with a cemented dual-mobility acetabular component and a non-cemented femoral stem. The authors note that anti-protrusion rings are indicated for acetabular fractures equivalent to pelvic discontinuity (AAOS type IV acetabular defects), requiring ischial and iliac anchorage, and are not indicated for isolated anterior or posterior wall fractures without acetabular floor involvement. During admission, the patient remained in bed with mobilization to prevent pressure ulcers. After the second operation and as tolerated, he transferred using a wheelchair; in bed he had unrestricted range of motion. He was discharged at 4 weeks and remained non\u2013weight bearing until 6 weeks, then progressed to loading with a cane. Loading was delayed to allow initial consolidation of the acetabular background graft to support the ring and because bilateral involvement precluded practical partial weight bearing. At 12 months, he was fully weight bearing with a cane, with Harris Hip Scores of 79 (left) and 77 (right), WOMAC 12, and no postoperative complications. He reported occasional discomfort and a mild right-sided limp, had full range of motion on examination, and no episodes of instability since surgery." }, { "index": 34, "label": "low_health_literacy", "original_text": "A 19-month-old boy was admitted to the Emergency Department because he fell from his baby feeding highchair. This fall occurred in apparent well-being, without the presence of anticipatory signs or symptoms. First, he fell on his gluteus and then he banged his head (occiput) on the ground. He presented with vomiting (three episodes) and he was very irritable. His respiratory rate and heart rate were >60 breaths and >150 beats per minute, while oxygen saturation was <80%. Upon physical examination, the child was hydrated and conscious, but irritable. More importantly, we noted subcostal retractions, and, at the auscultation, decreased breath sounds in the left basal part of chest. The patient was ventilated with an AMBU balloon connected to an oxygen source and monitored with a pulse oximeter. Despite our intervention, oxygen saturation fell below 70% and the more we ventilated, the more the saturation dropped down. The lung ultrasound showed the absence of the typical A lines and the consolidation of the lung, which was directly visualized as a solid parenchyma. On the basis of the poor clinical condition, the patient underwent orotracheal intubation with a cuffed endotracheal tube. After the baby was stabilized, he underwent a chest computed tomography (CT) showing complete atelectasis of the left lung with an interruption of the main left bronchus at 12 cm from bronchial bifurcation. An FBA was suspected as the mother also stated that the baby in the previous days had an intensive cough attack and disappeared within 24 h without any treatment. Therefore, a rigid bronchoscopy was performed and an almond of 2 cm in diameter in the main left bronchus was found and promptly removed.\n\nThe patient had never consumed almonds or other nuts before and in this circumstance ingested the almond by chance.\n\nThe baby had a progressive clinical improvement, and after 24 h, he was extubated and discharged from intensive care to be admitted to the general pediatrics ward for a few days with gradual and a total respiratory function recovery.", "generated_summary": "A 19\u2011month\u2011old boy went to the emergency room because he hit his head. Doctors saw that he was fighting to breathe. They put in a breathing tube to help him. The team believed the breathing problem likely started first. It may have made him less alert, and then he fell and hit his head. Scans showed the left lung was not filling with air, like a balloon that stays flat. This made doctors think something was stuck in his airway. A CT scan showed a sudden stop in the main airway to the left lung. Doctors used a small camera to look inside. They found and removed a 2\u2011cm almond that was blocking the airway." }, { "index": 34, "label": "intermediate_health_literacy", "original_text": "A 19-month-old boy was admitted to the Emergency Department because he fell from his baby feeding highchair. This fall occurred in apparent well-being, without the presence of anticipatory signs or symptoms. First, he fell on his gluteus and then he banged his head (occiput) on the ground. He presented with vomiting (three episodes) and he was very irritable. His respiratory rate and heart rate were >60 breaths and >150 beats per minute, while oxygen saturation was <80%. Upon physical examination, the child was hydrated and conscious, but irritable. More importantly, we noted subcostal retractions, and, at the auscultation, decreased breath sounds in the left basal part of chest. The patient was ventilated with an AMBU balloon connected to an oxygen source and monitored with a pulse oximeter. Despite our intervention, oxygen saturation fell below 70% and the more we ventilated, the more the saturation dropped down. The lung ultrasound showed the absence of the typical A lines and the consolidation of the lung, which was directly visualized as a solid parenchyma. On the basis of the poor clinical condition, the patient underwent orotracheal intubation with a cuffed endotracheal tube. After the baby was stabilized, he underwent a chest computed tomography (CT) showing complete atelectasis of the left lung with an interruption of the main left bronchus at 12 cm from bronchial bifurcation. An FBA was suspected as the mother also stated that the baby in the previous days had an intensive cough attack and disappeared within 24 h without any treatment. Therefore, a rigid bronchoscopy was performed and an almond of 2 cm in diameter in the main left bronchus was found and promptly removed.\n\nThe patient had never consumed almonds or other nuts before and in this circumstance ingested the almond by chance.\n\nThe baby had a progressive clinical improvement, and after 24 h, he was extubated and discharged from intensive care to be admitted to the general pediatrics ward for a few days with gradual and a total respiratory function recovery.", "generated_summary": "A 19\u2011month\u2011old boy presented to the ER after a fall with head trauma. During evaluation, clinicians discovered severe respiratory distress, so he required tracheal intubation. The team later suspected the breathing crisis likely began first and caused altered consciousness, which led to the fall. Imaging showed complete collapse (atelectasis) of the entire left lung, raising concern for foreign body aspiration. CT demonstrated an abrupt cutoff of the left main bronchus. Bronchoscopy then confirmed and removed a 2\u2011cm almond. A recent history of a brief coughing spell supported the diagnosis. The child improved after removal." }, { "index": 34, "label": "proficient_health_literacy", "original_text": "A 19-month-old boy was admitted to the Emergency Department because he fell from his baby feeding highchair. This fall occurred in apparent well-being, without the presence of anticipatory signs or symptoms. First, he fell on his gluteus and then he banged his head (occiput) on the ground. He presented with vomiting (three episodes) and he was very irritable. His respiratory rate and heart rate were >60 breaths and >150 beats per minute, while oxygen saturation was <80%. Upon physical examination, the child was hydrated and conscious, but irritable. More importantly, we noted subcostal retractions, and, at the auscultation, decreased breath sounds in the left basal part of chest. The patient was ventilated with an AMBU balloon connected to an oxygen source and monitored with a pulse oximeter. Despite our intervention, oxygen saturation fell below 70% and the more we ventilated, the more the saturation dropped down. The lung ultrasound showed the absence of the typical A lines and the consolidation of the lung, which was directly visualized as a solid parenchyma. On the basis of the poor clinical condition, the patient underwent orotracheal intubation with a cuffed endotracheal tube. After the baby was stabilized, he underwent a chest computed tomography (CT) showing complete atelectasis of the left lung with an interruption of the main left bronchus at 12 cm from bronchial bifurcation. An FBA was suspected as the mother also stated that the baby in the previous days had an intensive cough attack and disappeared within 24 h without any treatment. Therefore, a rigid bronchoscopy was performed and an almond of 2 cm in diameter in the main left bronchus was found and promptly removed.\n\nThe patient had never consumed almonds or other nuts before and in this circumstance ingested the almond by chance.\n\nThe baby had a progressive clinical improvement, and after 24 h, he was extubated and discharged from intensive care to be admitted to the general pediatrics ward for a few days with gradual and a total respiratory function recovery.", "generated_summary": "A 19\u2011month\u2011old boy was admitted following a fall from a feeding highchair, landing on his gluteal region and striking the occiput. He had three episodes of vomiting, marked irritability, RR >60/min, HR >150/min, and SpO2 <80%. On exam, he was hydrated and conscious but irritable, with subcostal retractions and decreased breath sounds at the left base. Bag\u2011mask ventilation with supplemental oxygen and pulse oximetry monitoring were initiated; paradoxically, SpO2 fell below 70% with ongoing ventilation. Lung ultrasound demonstrated absent A\u2011lines and consolidation, visualizing the lung as solid parenchyma. Given the poor clinical condition, orotracheal intubation with a cuffed endotracheal tube was performed. Post\u2011stabilization chest CT revealed complete atelectasis of the left lung with interruption of the main left bronchus at 12 cm from the bronchial bifurcation. In the context of maternal history of an intensive coughing episode in the preceding days that resolved spontaneously within 24 h, foreign body aspiration was suspected. Rigid bronchoscopy identified and removed a 2\u2011cm almond lodged in the left main bronchus. The patient improved progressively, was extubated at 24 h, transferred from intensive care to the general pediatrics ward, and achieved full recovery of respiratory function. Based on the clinical course, the team hypothesized that severe respiratory compromise likely preceded the event, causing altered consciousness and subsequent head trauma." }, { "index": 35, "label": "low_health_literacy", "original_text": "The patient was a 4-month-old male from central Mexico with two healthy male siblings. His mother was hypothyroid during the first trimester of pregnancy and took drugs. The infant was born with normal weight and size, was breast-fed, and received the BCG vaccine with no scarring. The mother of the patient was a prisoner in a jail cell with the infant in a crowded cell with two others.At 4 months, the patient was medically evaluated for a painful tumor in the left axilla. A chest X-ray showed suggestive images of rib fractures; the mother was suspected of child abuse, and the infant was admitted to a pediatric hospital. The infant was weighed (4,190 g) and measured (58 cm) below the third percentile, oxygen saturation of 70%, fever, cough, increased volume in the left axilla, and pain, redness, and warmth. The blood count showed: hemoglobin of 8.8 g/dL (11.0-12.6), 29.3 \u00d7 109 leukocytes/L (6.0-17.5), 18.4 \u00d7 109 neutrophils/L (1.0-8.5), 7.0 \u00d7 109 lymphocytes/L (4.0-13.5), 3.5 \u00d7 109 monocytes/L, 459 \u00d7 109 platelets/L (150-350), and C-reactive protein of 16 mg/L (< 3.0). The first thoracoabdominal tomography showed an abscess in the left axilla, lytic lesions in ribs 3-6, left apical pneumonia, pulmonary nodules in both lungs, and enlarged cervical and mediastinal lymph nodes. The biopsy of the left axilla abscess reported myositis and suppurative panniculitis. Only the culture for bacteria from the bronchoalveolar liquid was negative, and the PCR for the Mycobacterium tuberculosis complex was negative. After 41 days of hospitalization and receiving two antimicrobial regimens of ceftriaxone-clindamycin and cefepime-vancomycin, the patient was discharged.\n\nTwo months later, at eight months of age, he was readmitted to hospital with a fever, irritability and a suppurating abscess in the left scapula. The blood count showed haemoglobin of 10.8 g/dl (10.5-12), 21.2 \u00d7 109 leukocytes/L (6-17), 12.2 \u00d7 109 neutrophils/L (1.5-8.5), 7.5 \u00d7 109 lymphocytes/L (4-10.5), 1.2 \u00d7 109 monocytes/L (600), and 583 \u00d7 109 platelets/L (150-350); the serum test for HIV was negative. A left apical consolidation, bronchiectasis, lytic lesions in ribs 2-7 and dorsal vertebrae 2-7, and a multilocular fluid collection were observed on a chest scan; ultrasound showed a fistula associated with the scapular abscess. The patient received piperacillin-tazobactam, which was later replaced with voriconazole after Aspergillus fumigatus was detected in the secretion sample culture. Given the recurrence and severity of the infection, an innate immunity defect was suspected. The dihydrorhodamine test showed no production of reactive oxygen species and the gp91phox expression in neutrophils was absent, establishing a diagnosis of X-linked chronic granulomatous disease. The pathogenic variant detected by next-generation sequencing was c.80_83del/Y (p.Val27Glyfs*33) in CYBB. The mother was a carrier of the variant (c.80_83del/WT). The two older male siblings, who were apparently healthy, could not be genetically tested. The patient was discharged after 65 days of hospitalisation and 28 days of voriconazole treatment. Daily antibiotic prophylaxis with trimethoprim-sulfamethoxazole and antifungal prophylaxis with fluconazole twice a week were initiated. Two months later, at one year of age, the infant was readmitted due to multifocal pneumonia, for which mechanical respiratory assistance was required. The galactomannan antigen was detected in the serum and A. fumigatus was detected in the culture of the lavage fluid, so treatment with voriconazole was initiated again. The patient suffered a multiple organ failure and died one month after admission.\n", "generated_summary": "A baby boy was 4 months old. He lived with his mother in a prison cell. A painful lump grew in his left armpit. A chest X-ray looked like some ribs were broken. Doctors worried he might have been hurt. The pictures also showed a pocket of pus in his armpit, damage to his ribs, a lung infection, and small spots in his lungs. He got strong antibiotics. He went home. When he was 8 months old, he got a fever. The pus spread toward his left shoulder. New chest pictures looked worse. Tests found a mold called Aspergillus fumigatus in the pus. The doctors said he had a serious mold infection. He took a strong antifungal medicine called voriconazole for 28 days. A special blood test showed his germ-fighting cells did not work well. He had a rare immune problem called chronic granulomatous disease. It was caused by a change in a gene called CYBB. His mother carried this gene change. When he was 12 months old, the mold infection came back. The treatments did not work. He died." }, { "index": 35, "label": "intermediate_health_literacy", "original_text": "The patient was a 4-month-old male from central Mexico with two healthy male siblings. His mother was hypothyroid during the first trimester of pregnancy and took drugs. The infant was born with normal weight and size, was breast-fed, and received the BCG vaccine with no scarring. The mother of the patient was a prisoner in a jail cell with the infant in a crowded cell with two others.At 4 months, the patient was medically evaluated for a painful tumor in the left axilla. A chest X-ray showed suggestive images of rib fractures; the mother was suspected of child abuse, and the infant was admitted to a pediatric hospital. The infant was weighed (4,190 g) and measured (58 cm) below the third percentile, oxygen saturation of 70%, fever, cough, increased volume in the left axilla, and pain, redness, and warmth. The blood count showed: hemoglobin of 8.8 g/dL (11.0-12.6), 29.3 \u00d7 109 leukocytes/L (6.0-17.5), 18.4 \u00d7 109 neutrophils/L (1.0-8.5), 7.0 \u00d7 109 lymphocytes/L (4.0-13.5), 3.5 \u00d7 109 monocytes/L, 459 \u00d7 109 platelets/L (150-350), and C-reactive protein of 16 mg/L (< 3.0). The first thoracoabdominal tomography showed an abscess in the left axilla, lytic lesions in ribs 3-6, left apical pneumonia, pulmonary nodules in both lungs, and enlarged cervical and mediastinal lymph nodes. The biopsy of the left axilla abscess reported myositis and suppurative panniculitis. Only the culture for bacteria from the bronchoalveolar liquid was negative, and the PCR for the Mycobacterium tuberculosis complex was negative. After 41 days of hospitalization and receiving two antimicrobial regimens of ceftriaxone-clindamycin and cefepime-vancomycin, the patient was discharged.\n\nTwo months later, at eight months of age, he was readmitted to hospital with a fever, irritability and a suppurating abscess in the left scapula. The blood count showed haemoglobin of 10.8 g/dl (10.5-12), 21.2 \u00d7 109 leukocytes/L (6-17), 12.2 \u00d7 109 neutrophils/L (1.5-8.5), 7.5 \u00d7 109 lymphocytes/L (4-10.5), 1.2 \u00d7 109 monocytes/L (600), and 583 \u00d7 109 platelets/L (150-350); the serum test for HIV was negative. A left apical consolidation, bronchiectasis, lytic lesions in ribs 2-7 and dorsal vertebrae 2-7, and a multilocular fluid collection were observed on a chest scan; ultrasound showed a fistula associated with the scapular abscess. The patient received piperacillin-tazobactam, which was later replaced with voriconazole after Aspergillus fumigatus was detected in the secretion sample culture. Given the recurrence and severity of the infection, an innate immunity defect was suspected. The dihydrorhodamine test showed no production of reactive oxygen species and the gp91phox expression in neutrophils was absent, establishing a diagnosis of X-linked chronic granulomatous disease. The pathogenic variant detected by next-generation sequencing was c.80_83del/Y (p.Val27Glyfs*33) in CYBB. The mother was a carrier of the variant (c.80_83del/WT). The two older male siblings, who were apparently healthy, could not be genetically tested. The patient was discharged after 65 days of hospitalisation and 28 days of voriconazole treatment. Daily antibiotic prophylaxis with trimethoprim-sulfamethoxazole and antifungal prophylaxis with fluconazole twice a week were initiated. Two months later, at one year of age, the infant was readmitted due to multifocal pneumonia, for which mechanical respiratory assistance was required. The galactomannan antigen was detected in the serum and A. fumigatus was detected in the culture of the lavage fluid, so treatment with voriconazole was initiated again. The patient suffered a multiple organ failure and died one month after admission.\n", "generated_summary": "This case describes a 4\u2011month\u2011old boy who lived with his mother in a crowded prison cell and developed a painful mass in his left armpit. Initial imaging raised concern for rib fractures, so he was hospitalized for possible child abuse. Imaging also showed an axillary abscess, rib damage, pneumonia, and small nodules in both lungs. He received broad\u2011spectrum antibiotics and was discharged. At 8 months, he returned with fever and an enlarging, pus\u2011draining abscess extending toward the left shoulder. Imaging showed progression. Culture of the abscess grew Aspergillus fumigatus, confirming invasive aspergillosis, and he was treated with 28 days of voriconazole. Because the infection was severe and recurrent, doctors tested his innate immune function. A dihydrorhodamine assay showed a defect consistent with chronic granulomatous disease (CGD). Genetic testing identified an X\u2011linked CYBB pathogenic variant (c.80_83del/Y); his mother was a carrier (c.80_83del/WT). At 12 months, he was readmitted with recurrent invasive aspergillosis that did not respond to treatment and he died." }, { "index": 35, "label": "proficient_health_literacy", "original_text": "The patient was a 4-month-old male from central Mexico with two healthy male siblings. His mother was hypothyroid during the first trimester of pregnancy and took drugs. The infant was born with normal weight and size, was breast-fed, and received the BCG vaccine with no scarring. The mother of the patient was a prisoner in a jail cell with the infant in a crowded cell with two others.At 4 months, the patient was medically evaluated for a painful tumor in the left axilla. A chest X-ray showed suggestive images of rib fractures; the mother was suspected of child abuse, and the infant was admitted to a pediatric hospital. The infant was weighed (4,190 g) and measured (58 cm) below the third percentile, oxygen saturation of 70%, fever, cough, increased volume in the left axilla, and pain, redness, and warmth. The blood count showed: hemoglobin of 8.8 g/dL (11.0-12.6), 29.3 \u00d7 109 leukocytes/L (6.0-17.5), 18.4 \u00d7 109 neutrophils/L (1.0-8.5), 7.0 \u00d7 109 lymphocytes/L (4.0-13.5), 3.5 \u00d7 109 monocytes/L, 459 \u00d7 109 platelets/L (150-350), and C-reactive protein of 16 mg/L (< 3.0). The first thoracoabdominal tomography showed an abscess in the left axilla, lytic lesions in ribs 3-6, left apical pneumonia, pulmonary nodules in both lungs, and enlarged cervical and mediastinal lymph nodes. The biopsy of the left axilla abscess reported myositis and suppurative panniculitis. Only the culture for bacteria from the bronchoalveolar liquid was negative, and the PCR for the Mycobacterium tuberculosis complex was negative. After 41 days of hospitalization and receiving two antimicrobial regimens of ceftriaxone-clindamycin and cefepime-vancomycin, the patient was discharged.\n\nTwo months later, at eight months of age, he was readmitted to hospital with a fever, irritability and a suppurating abscess in the left scapula. The blood count showed haemoglobin of 10.8 g/dl (10.5-12), 21.2 \u00d7 109 leukocytes/L (6-17), 12.2 \u00d7 109 neutrophils/L (1.5-8.5), 7.5 \u00d7 109 lymphocytes/L (4-10.5), 1.2 \u00d7 109 monocytes/L (600), and 583 \u00d7 109 platelets/L (150-350); the serum test for HIV was negative. A left apical consolidation, bronchiectasis, lytic lesions in ribs 2-7 and dorsal vertebrae 2-7, and a multilocular fluid collection were observed on a chest scan; ultrasound showed a fistula associated with the scapular abscess. The patient received piperacillin-tazobactam, which was later replaced with voriconazole after Aspergillus fumigatus was detected in the secretion sample culture. Given the recurrence and severity of the infection, an innate immunity defect was suspected. The dihydrorhodamine test showed no production of reactive oxygen species and the gp91phox expression in neutrophils was absent, establishing a diagnosis of X-linked chronic granulomatous disease. The pathogenic variant detected by next-generation sequencing was c.80_83del/Y (p.Val27Glyfs*33) in CYBB. The mother was a carrier of the variant (c.80_83del/WT). The two older male siblings, who were apparently healthy, could not be genetically tested. The patient was discharged after 65 days of hospitalisation and 28 days of voriconazole treatment. Daily antibiotic prophylaxis with trimethoprim-sulfamethoxazole and antifungal prophylaxis with fluconazole twice a week were initiated. Two months later, at one year of age, the infant was readmitted due to multifocal pneumonia, for which mechanical respiratory assistance was required. The galactomannan antigen was detected in the serum and A. fumigatus was detected in the culture of the lavage fluid, so treatment with voriconazole was initiated again. The patient suffered a multiple organ failure and died one month after admission.\n", "generated_summary": "A 4\u2011month\u2011old male from central Mexico with two apparently healthy older male siblings presented with a painful tumor in the left axilla while living with his hypothyroid mother in a crowded prison cell. He was born appropriate for gestational age, was breast\u2011fed, and had received BCG without scarring. On admission he was below the 3rd percentile for weight (4,190 g) and length (58 cm), with oxygen saturation of 70%, fever, cough, and a tender, erythematous, warm left axillary mass. CBC: hemoglobin 8.8 g/dL (11.0\u201312.6), leukocytes 29.3 \u00d7 10^9/L (6.0\u201317.5), neutrophils 18.4 \u00d7 10^9/L (1.0\u20138.5), lymphocytes 7.0 \u00d7 10^9/L (4.0\u201313.5), monocytes 3.5 \u00d7 10^9/L, platelets 459 \u00d7 10^9/L (150\u2013350), CRP 16 mg/L (< 3.0). Chest radiography showed images suggestive of rib fractures, prompting concern for child abuse and admission. Thoracoabdominal CT demonstrated a left axillary abscess, lytic lesions of ribs 3\u20136, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Biopsy of the axillary lesion showed myositis and suppurative panniculitis. BAL bacterial culture was negative, and PCR for Mycobacterium tuberculosis complex was negative. He received ceftriaxone\u2013clindamycin, then cefepime\u2013vancomycin, and was discharged after 41 days. \n\nAt 8 months, he was readmitted with fever, irritability, and a suppurating abscess over the left scapula. CBC: hemoglobin 10.8 g/dL (10.5\u201312), leukocytes 21.2 \u00d7 10^9/L (6\u201317), neutrophils 12.2 \u00d7 10^9/L (1.5\u20138.5), lymphocytes 7.5 \u00d7 10^9/L (4\u201310.5), monocytes 1.2 \u00d7 10^9/L (~0.6), platelets 583 \u00d7 10^9/L (150\u2013350); HIV serology was negative. Chest imaging showed left apical consolidation, bronchiectasis, lytic lesions in ribs 2\u20137 and thoracic vertebrae T2\u2013T7, and a multilocular fluid collection; ultrasound identified a fistula linked to the scapular abscess. Initial piperacillin\u2013tazobactam was switched to voriconazole when Aspergillus fumigatus grew from abscess secretion culture, establishing invasive aspergillosis. Given the recurrence and severity, an innate immune defect was suspected. Dihydrorhodamine (DHR) testing demonstrated absent reactive oxygen species production with absent gp91phox expression in neutrophils, confirming X\u2011linked chronic granulomatous disease. Next\u2011generation sequencing identified CYBB c.80_83del/Y (p.Val27Glyfs*33); the mother was a heterozygous carrier (c.80_83del/WT). The patient was discharged after 65 days of hospitalization, including 28 days of voriconazole, and was started on prophylaxis with daily trimethoprim\u2013sulfamethoxazole and fluconazole twice weekly. \n\nAt 12 months, he was readmitted with multifocal pneumonia requiring mechanical respiratory assistance. Serum galactomannan was positive, and A. fumigatus was recovered from lavage fluid; voriconazole was re\u2011initiated. Despite therapy, he developed multiple organ failure and died one month after admission. \n\nContext: CGD is caused by NADPH oxidase dysfunction in phagocytes, leading to impaired oxidative burst and susceptibility to catalase\u2011positive organisms, especially Aspergillus spp. X\u2011linked CYBB variants frequently present in infancy with invasive aspergillosis and osteolytic lesions; A. fumigatus remains a leading cause of mortality in CGD." }, { "index": 36, "label": "low_health_literacy", "original_text": "Male patient, 25 years old, Sundanese, presented at the Dental Hospital of the Faculty of Dentistry Universitas Padjadjaran with the chief complaint of mouth sores, which are painful on the upper and lower lips and exacerbated when eating and talking. Initially, four days ago, canker sores started in the oral cavity, then appeared on the lips two days later. The patient tried to self-medicate by applying petroleum jelly which he used to relieve his symptoms, but it did not improve. The patient replaced the drug with triamcinolone acetonide 0.1% in orabase ointment purchased at the pharmacy and applied it once a day. Canker sores were getting better but did not cure.\n\nThe patient had history a of fever for about a week before the canker sores appeared and there were no lesions on other parts of the body. He stated that the workload was quite heavy and he had not consumed a balanced nutritional diet for about one and a half months. He had no medical history, history of food allergies, or history of taking medication. He had no history of alcohol consumption or smoking, but he had a frequent habit of licking his lips. He also had a history of chickenpox when he was a child.\n\nThe patient had no fever with all vital signs within normal limits on general examination. Extra-oral examination showed no abnormalities in the lymph nodes. There were serosanguineous crusts that felt painful and bleed easily on the lips. Intra-oral examination revealed erythematous lesions, irregular in shape, and had diffuse borders, accompanied by pain in the upper and lower labial mucosa. Hyperkeratotic white plaque that could not be scraped off, irregular in shape, has diffuse borders, without pain in the region of tooth 38 left buccal mucosa. Yellowish-white plaques were seen on 1/3 of the posterior surface of the dorsal tongue, which could be scraped off without leaving an erythematous area, and there were indentations in the form of dental impressions without pain on the lateral right and left sides of the tongue. A painless hard nodule about 2\u00d71 x 0.5 cm in size was seen in the midline of the hard palate. Several teeth were found in caries, radix, and edentulous conditions in all regions. The oral hygiene was poor.\n\nExamination of psychological conditions was evaluated using the DASS-21 questionnaire and showed normal depression level (score 0), normal anxiety level (score 6), and normal stress level (score 6). Based on history and clinical examination, the working diagnosis was suspected HAEM, accompanied by the coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis of tooth 18, irreversible pulpitis of tooth 47, chronic apical periodontitis et causa radix of tooth 15, and edentulous teeth 28, 37, 36, and 46. The differential diagnosis of suspected HAEM lesions on the lips was exfoliative cheilitis. However, exfoliative cheilitis did not have herpes virus involvement. The patient was indicated for serological testing (IgG anti-HSV-1) to confirm the diagnosis. Oral health-related quality of life was measured, and the results of the OHIP-14 examination at the first visit were 35 (moderate OHRQol).\n\nThe non-pharmacological therapy included instruction to maintain oral hygiene by brushing the teeth and tongue using a soft-bristled toothbrush two times a day and using non-detergent toothpaste. Education was given such as increasing the intake of water by at least two liters per day, consuming a balanced nutritional diet, avoiding acidic, spicy, hard, and monosodium glutamate-containing foods, and stopping the bad habit of licking and peeling the skin of the lips. The pharmacological therapy included topical and systemic medications. The topical medications included instructions to compress the lips with gauze moistened with 0.9% NaCl solution at least three times a day and to apply a thin layer of triamcinolone acetonide 0.1% in orabase to the lips three times a day. The systemic medications included instruction to take a multivitamin once a day.\n\nThe progress of improvement was visible in the first follow-up, two days after the initial visit. The pain in the lips was reduced, but the canker sores have not healed. Extra-oral examination revealed serosanguinous crusts on the lips which were still painful and bled easily. The serological test result (IgG anti-HSV-1) was positive with a ratio of: 6.32 (positive: ratio > 1.1). The definitive diagnosis was established based on the history, clinical examination, and serological tests as HAEM. The non-pharmacological and pharmacological therapy was continued, and systemic medication was added in the form of instructions to consume acyclovir 200 mg tablets five times a day for one week.\n\nSignificant improvement was visible in the second follow-up, five days after the previous visit, showing excellent healing in all of the patient\u2019s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient\u2019s physical, psychological, and social conditions showed improvement and returned to normal after 7 days of treatment. Patient was referred to continue dental and oral care in the periodontics, dental conservation, oral surgery, and prosthodontics departments. The patient has approved and written informed consent for the case details to be published included publication of the images, and the institution has also approved for publication. This case had complied with the Declaration of Helsinki.", "generated_summary": "A 25-year-old man went to the mouth clinic because he had painful canker sores on his lips. The outside of his lips had crusty scabs that hurt and bled easily. Inside his mouth, the inner parts of his upper and lower lips had red, sore, uneven patches. A blood test for the cold sore virus (HSV-1) was positive. The doctor said he had a condition called HAEM. His treatment included a steroid mouth paste (triamcinolone acetonide 0.1% in orabase), acyclovir pills, multivitamins, and salt-water (0.9% NaCl). He was also told to keep his mouth clean, avoid spicy and sour foods, and stop licking his lips." }, { "index": 36, "label": "intermediate_health_literacy", "original_text": "Male patient, 25 years old, Sundanese, presented at the Dental Hospital of the Faculty of Dentistry Universitas Padjadjaran with the chief complaint of mouth sores, which are painful on the upper and lower lips and exacerbated when eating and talking. Initially, four days ago, canker sores started in the oral cavity, then appeared on the lips two days later. The patient tried to self-medicate by applying petroleum jelly which he used to relieve his symptoms, but it did not improve. The patient replaced the drug with triamcinolone acetonide 0.1% in orabase ointment purchased at the pharmacy and applied it once a day. Canker sores were getting better but did not cure.\n\nThe patient had history a of fever for about a week before the canker sores appeared and there were no lesions on other parts of the body. He stated that the workload was quite heavy and he had not consumed a balanced nutritional diet for about one and a half months. He had no medical history, history of food allergies, or history of taking medication. He had no history of alcohol consumption or smoking, but he had a frequent habit of licking his lips. He also had a history of chickenpox when he was a child.\n\nThe patient had no fever with all vital signs within normal limits on general examination. Extra-oral examination showed no abnormalities in the lymph nodes. There were serosanguineous crusts that felt painful and bleed easily on the lips. Intra-oral examination revealed erythematous lesions, irregular in shape, and had diffuse borders, accompanied by pain in the upper and lower labial mucosa. Hyperkeratotic white plaque that could not be scraped off, irregular in shape, has diffuse borders, without pain in the region of tooth 38 left buccal mucosa. Yellowish-white plaques were seen on 1/3 of the posterior surface of the dorsal tongue, which could be scraped off without leaving an erythematous area, and there were indentations in the form of dental impressions without pain on the lateral right and left sides of the tongue. A painless hard nodule about 2\u00d71 x 0.5 cm in size was seen in the midline of the hard palate. Several teeth were found in caries, radix, and edentulous conditions in all regions. The oral hygiene was poor.\n\nExamination of psychological conditions was evaluated using the DASS-21 questionnaire and showed normal depression level (score 0), normal anxiety level (score 6), and normal stress level (score 6). Based on history and clinical examination, the working diagnosis was suspected HAEM, accompanied by the coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis of tooth 18, irreversible pulpitis of tooth 47, chronic apical periodontitis et causa radix of tooth 15, and edentulous teeth 28, 37, 36, and 46. The differential diagnosis of suspected HAEM lesions on the lips was exfoliative cheilitis. However, exfoliative cheilitis did not have herpes virus involvement. The patient was indicated for serological testing (IgG anti-HSV-1) to confirm the diagnosis. Oral health-related quality of life was measured, and the results of the OHIP-14 examination at the first visit were 35 (moderate OHRQol).\n\nThe non-pharmacological therapy included instruction to maintain oral hygiene by brushing the teeth and tongue using a soft-bristled toothbrush two times a day and using non-detergent toothpaste. Education was given such as increasing the intake of water by at least two liters per day, consuming a balanced nutritional diet, avoiding acidic, spicy, hard, and monosodium glutamate-containing foods, and stopping the bad habit of licking and peeling the skin of the lips. The pharmacological therapy included topical and systemic medications. The topical medications included instructions to compress the lips with gauze moistened with 0.9% NaCl solution at least three times a day and to apply a thin layer of triamcinolone acetonide 0.1% in orabase to the lips three times a day. The systemic medications included instruction to take a multivitamin once a day.\n\nThe progress of improvement was visible in the first follow-up, two days after the initial visit. The pain in the lips was reduced, but the canker sores have not healed. Extra-oral examination revealed serosanguinous crusts on the lips which were still painful and bled easily. The serological test result (IgG anti-HSV-1) was positive with a ratio of: 6.32 (positive: ratio > 1.1). The definitive diagnosis was established based on the history, clinical examination, and serological tests as HAEM. The non-pharmacological and pharmacological therapy was continued, and systemic medication was added in the form of instructions to consume acyclovir 200 mg tablets five times a day for one week.\n\nSignificant improvement was visible in the second follow-up, five days after the previous visit, showing excellent healing in all of the patient\u2019s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient\u2019s physical, psychological, and social conditions showed improvement and returned to normal after 7 days of treatment. Patient was referred to continue dental and oral care in the periodontics, dental conservation, oral surgery, and prosthodontics departments. The patient has approved and written informed consent for the case details to be published included publication of the images, and the institution has also approved for publication. This case had complied with the Declaration of Helsinki.", "generated_summary": "A 25-year-old man presented with painful canker sores on the upper and lower lips, worse with eating and talking. On exam, his lips had painful serosanguineous crusts that bled easily, and the inner surfaces of the upper and lower lips showed diffuse, irregular erythematous lesions. Serology for anti-HSV-1 IgG was positive, supporting a diagnosis of HAEM. Management included triamcinolone acetonide 0.1% in orabase applied to the lips, saline (0.9% NaCl) compresses, and a daily multivitamin; acyclovir tablets were also prescribed. He was advised to maintain good oral hygiene, avoid spicy and sour foods, and stop lip-licking. The lesions and pain improved with this approach over the following days." }, { "index": 36, "label": "proficient_health_literacy", "original_text": "Male patient, 25 years old, Sundanese, presented at the Dental Hospital of the Faculty of Dentistry Universitas Padjadjaran with the chief complaint of mouth sores, which are painful on the upper and lower lips and exacerbated when eating and talking. Initially, four days ago, canker sores started in the oral cavity, then appeared on the lips two days later. The patient tried to self-medicate by applying petroleum jelly which he used to relieve his symptoms, but it did not improve. The patient replaced the drug with triamcinolone acetonide 0.1% in orabase ointment purchased at the pharmacy and applied it once a day. Canker sores were getting better but did not cure.\n\nThe patient had history a of fever for about a week before the canker sores appeared and there were no lesions on other parts of the body. He stated that the workload was quite heavy and he had not consumed a balanced nutritional diet for about one and a half months. He had no medical history, history of food allergies, or history of taking medication. He had no history of alcohol consumption or smoking, but he had a frequent habit of licking his lips. He also had a history of chickenpox when he was a child.\n\nThe patient had no fever with all vital signs within normal limits on general examination. Extra-oral examination showed no abnormalities in the lymph nodes. There were serosanguineous crusts that felt painful and bleed easily on the lips. Intra-oral examination revealed erythematous lesions, irregular in shape, and had diffuse borders, accompanied by pain in the upper and lower labial mucosa. Hyperkeratotic white plaque that could not be scraped off, irregular in shape, has diffuse borders, without pain in the region of tooth 38 left buccal mucosa. Yellowish-white plaques were seen on 1/3 of the posterior surface of the dorsal tongue, which could be scraped off without leaving an erythematous area, and there were indentations in the form of dental impressions without pain on the lateral right and left sides of the tongue. A painless hard nodule about 2\u00d71 x 0.5 cm in size was seen in the midline of the hard palate. Several teeth were found in caries, radix, and edentulous conditions in all regions. The oral hygiene was poor.\n\nExamination of psychological conditions was evaluated using the DASS-21 questionnaire and showed normal depression level (score 0), normal anxiety level (score 6), and normal stress level (score 6). Based on history and clinical examination, the working diagnosis was suspected HAEM, accompanied by the coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis of tooth 18, irreversible pulpitis of tooth 47, chronic apical periodontitis et causa radix of tooth 15, and edentulous teeth 28, 37, 36, and 46. The differential diagnosis of suspected HAEM lesions on the lips was exfoliative cheilitis. However, exfoliative cheilitis did not have herpes virus involvement. The patient was indicated for serological testing (IgG anti-HSV-1) to confirm the diagnosis. Oral health-related quality of life was measured, and the results of the OHIP-14 examination at the first visit were 35 (moderate OHRQol).\n\nThe non-pharmacological therapy included instruction to maintain oral hygiene by brushing the teeth and tongue using a soft-bristled toothbrush two times a day and using non-detergent toothpaste. Education was given such as increasing the intake of water by at least two liters per day, consuming a balanced nutritional diet, avoiding acidic, spicy, hard, and monosodium glutamate-containing foods, and stopping the bad habit of licking and peeling the skin of the lips. The pharmacological therapy included topical and systemic medications. The topical medications included instructions to compress the lips with gauze moistened with 0.9% NaCl solution at least three times a day and to apply a thin layer of triamcinolone acetonide 0.1% in orabase to the lips three times a day. The systemic medications included instruction to take a multivitamin once a day.\n\nThe progress of improvement was visible in the first follow-up, two days after the initial visit. The pain in the lips was reduced, but the canker sores have not healed. Extra-oral examination revealed serosanguinous crusts on the lips which were still painful and bled easily. The serological test result (IgG anti-HSV-1) was positive with a ratio of: 6.32 (positive: ratio > 1.1). The definitive diagnosis was established based on the history, clinical examination, and serological tests as HAEM. The non-pharmacological and pharmacological therapy was continued, and systemic medication was added in the form of instructions to consume acyclovir 200 mg tablets five times a day for one week.\n\nSignificant improvement was visible in the second follow-up, five days after the previous visit, showing excellent healing in all of the patient\u2019s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient\u2019s physical, psychological, and social conditions showed improvement and returned to normal after 7 days of treatment. Patient was referred to continue dental and oral care in the periodontics, dental conservation, oral surgery, and prosthodontics departments. The patient has approved and written informed consent for the case details to be published included publication of the images, and the institution has also approved for publication. This case had complied with the Declaration of Helsinki.", "generated_summary": "A 25-year-old Sundanese male presented to the Dental Hospital, Faculty of Dentistry, Universitas Padjadjaran with a 4-day history of painful oral ulcerations that appeared intraorally first and extended to the lips 2 days later, exacerbated by eating and speaking. He initially self-treated with petroleum jelly without benefit, then applied triamcinolone acetonide 0.1% in orabase once daily from a pharmacy, with partial but incomplete improvement. One week prior to lesion onset he reported a febrile episode; he also reported heavy workload and approximately 1.5 months of suboptimal nutrition. He denied systemic disease, drug or food allergies, alcohol, and tobacco, but reported frequent lip-licking; childhood varicella was noted.\n\nGeneral examination showed normal vital signs and no lymphadenopathy. Extraoral findings: serosanguineous crusts on the lips that were painful and bled easily. Intraoral findings: irregular, diffuse-bordered erythematous lesions with pain on the upper and lower labial mucosa. Additional findings included a non-scrapable hyperkeratotic white plaque of irregular shape with diffuse borders on the left buccal mucosa near tooth 38; scrapable yellowish-white plaques on the posterior third of the dorsal tongue without underlying erythema; crenated tongue with dental impressions laterally; a painless, hard torus palatinus (~2 \u00d7 1 \u00d7 0.5 cm) at the hard palate midline; multiple teeth with caries, radix, and edentulous areas; poor oral hygiene.\n\nPsychological assessment (DASS-21): normal depression (0), anxiety (6), and stress (6). Working diagnosis: suspected HAEM, with concurrent findings of coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis (tooth 18), irreversible pulpitis (tooth 47), chronic apical periodontitis et causa radix (tooth 15), and edentulous teeth 28, 37, 36, and 46. Differential diagnosis for the lip lesions included exfoliative cheilitis, which lacks herpesvirus involvement. Serologic testing (IgG anti\u2013HSV-1) was indicated to support the diagnosis. Baseline OHRQoL (OHIP-14) was 35 (moderate).\n\nInitial management combined non-pharmacologic and pharmacologic therapy. Non-pharmacologic: oral hygiene instructions (brush teeth and tongue twice daily with a soft-bristled brush and non-detergent toothpaste), hydrate with \u22652 L water/day, consume a balanced diet, avoid acidic, spicy, hard, and MSG-containing foods, and cease lip-licking and peeling. Pharmacologic: topical lip compresses with 0.9% NaCl at least three times daily and triamcinolone acetonide 0.1% in orabase applied thinly to the lips three times daily; a daily multivitamin was prescribed.\n\nAt 2-day follow-up, pain had decreased though serosanguineous crusts persisted. Serology returned positive for anti\u2013HSV-1 IgG, ratio 6.32 (positive >1.1). A definitive diagnosis of HAEM (herpes-associated erythema multiforme) was established based on history, clinical findings, and serology. Existing therapy was continued, and acyclovir 200 mg orally five times daily for 7 days was added.\n\nAt 5 days after the prior visit, there was significant improvement with excellent healing of all oral lesions. Final OHIP-14 was 4, and physical, psychological, and social conditions normalized after 7 days of treatment. The patient was referred for definitive dental and oral care in periodontics, dental conservation, oral surgery, and prosthodontics. Written informed consent and institutional approval were obtained; the case complies with the Declaration of Helsinki.\n\nContext: HAEM is an immune-mediated mucocutaneous reaction pattern commonly triggered by HSV-1. Positive HSV-1 serology in the appropriate clinical context, together with characteristic labial crusting and diffuse labial mucosal erythema, supports the diagnosis. Management typically combines topical corticosteroids and systemic antiviral therapy, along with supportive oral care and trigger avoidance." }, { "index": 37, "label": "low_health_literacy", "original_text": "A 29-year-old woman, Para 1, with abnormal vaginal bleeding of one-month duration presented to the gynecology outpatient department of a level 2 hospital. She was HIV positive, commenced on antiretroviral treatment following diagnosis, but had defaulted the antiretroviral treatment for one month when she became ill with vaginal bleeding, resulting in virological and immunological failures (viral load 37400 copies/mL and CD4 count 26 cells/\u03bcL). Of note, it was unclear when the patient first started showing HIV symptoms. However, she was diagnosed with HIV about a year prior to presentation. Physical examination revealed a large mass on the cervix measuring 8 \u00d7 8 cm extending to the parametrium and to the pelvic side walls bilaterally. There was bleeding on contact and foul-smelling vaginal discharge. Ultrasonography detected a bulky cervix and bilateral hydronephrosis. The patient was clinically diagnosed with cervical malignancy stage 3B. She was recommenced on antiretroviral therapy with a treatment change from TLD (Tenofovir-Lamivudine-Dolutegravir combination) to a preferable renal friendly regimen (Lamivudine-Abacavir-Dolutegravir combination). A punch biopsy of the cervix was performed, and the histopathological report revealed the diagnosis of an extra-nodal BL. The immunohistochemical and in situ hybridization confirmed the diagnosis, with CD20, CD75a, CD10, PAX5 and Bcl-6 positive. In addition, the CD44 and c-Myc were positive, with the EBER-ISH demonstrating focal positivity. The Ki67 demonstrated a proliferation index of almost 100% and PAX5 moderately positive BCL6. She had white cell count of 2.67 x109/L, haemoglobin of 5.7g/dl and platelet count of 71 \u00d7 109/L. Results of other investigations were serum creatinine 187 mmol/L, urea 11.1 mmol/l, albumin 21 g/l, aspartate transaminase 41 U/l and alkaline phosphatase 100 U/l.\n\nFollowing histological confirmation of the diagnosis and review at an oncology multidisciplinary meeting, she spent 43 days waiting to start treatment at oncology unit. The delay was due to long waiting list. This delay exceeded the 48 hours waiting period during which oncological treatment for BL should commence following diagnosis. The treatment plan was chemo-radiation therapy, and the patient gave written informed consent for the case to be published. However, she demised in the gynaecological ward on the 43rd day while waiting to start the treatment. During the 43 days, further imaging could not be performed due to poor functionality of the available CT and MRI machines. In addition to antiretroviral therapy, the patient received other supportive care such as blood transfusion and analgesia. Again, the number of days between the diagnosis of the BL and her death was 43 days. Histopathological postmortem was not performed as the diagnoses (BL and retroviral disease) were known. We reckon that the main primary cause of death is challenging to assign because of the multiple principal diagnoses. Because BL has rapid progression and high mortality rate in persons living with HIV particularly with high viral load, the attending physician certifying the death assigned BL as the most likely cause of death. However, the secondary cause of death was multiple organ failure (renal and haematological inclusive).", "generated_summary": "She was 29 years old and had one child. She had HIV and a very weak immune system (CD4 count of 26). She had abnormal vaginal bleeding for one month. A tissue test from her cervix showed a blood cancer called Burkitt lymphoma in the cervix, outside the lymph nodes. Doctors also said the cervical cancer was stage 3B because it reached the pelvic wall and caused the kidneys to swell from blocked urine. A team of cancer doctors said she needed chemotherapy and radiation together. There was a long waiting list for this treatment. The start of care was delayed. She died 43 days after the diagnosis. She did not get the planned treatment." }, { "index": 37, "label": "intermediate_health_literacy", "original_text": "A 29-year-old woman, Para 1, with abnormal vaginal bleeding of one-month duration presented to the gynecology outpatient department of a level 2 hospital. She was HIV positive, commenced on antiretroviral treatment following diagnosis, but had defaulted the antiretroviral treatment for one month when she became ill with vaginal bleeding, resulting in virological and immunological failures (viral load 37400 copies/mL and CD4 count 26 cells/\u03bcL). Of note, it was unclear when the patient first started showing HIV symptoms. However, she was diagnosed with HIV about a year prior to presentation. Physical examination revealed a large mass on the cervix measuring 8 \u00d7 8 cm extending to the parametrium and to the pelvic side walls bilaterally. There was bleeding on contact and foul-smelling vaginal discharge. Ultrasonography detected a bulky cervix and bilateral hydronephrosis. The patient was clinically diagnosed with cervical malignancy stage 3B. She was recommenced on antiretroviral therapy with a treatment change from TLD (Tenofovir-Lamivudine-Dolutegravir combination) to a preferable renal friendly regimen (Lamivudine-Abacavir-Dolutegravir combination). A punch biopsy of the cervix was performed, and the histopathological report revealed the diagnosis of an extra-nodal BL. The immunohistochemical and in situ hybridization confirmed the diagnosis, with CD20, CD75a, CD10, PAX5 and Bcl-6 positive. In addition, the CD44 and c-Myc were positive, with the EBER-ISH demonstrating focal positivity. The Ki67 demonstrated a proliferation index of almost 100% and PAX5 moderately positive BCL6. She had white cell count of 2.67 x109/L, haemoglobin of 5.7g/dl and platelet count of 71 \u00d7 109/L. Results of other investigations were serum creatinine 187 mmol/L, urea 11.1 mmol/l, albumin 21 g/l, aspartate transaminase 41 U/l and alkaline phosphatase 100 U/l.\n\nFollowing histological confirmation of the diagnosis and review at an oncology multidisciplinary meeting, she spent 43 days waiting to start treatment at oncology unit. The delay was due to long waiting list. This delay exceeded the 48 hours waiting period during which oncological treatment for BL should commence following diagnosis. The treatment plan was chemo-radiation therapy, and the patient gave written informed consent for the case to be published. However, she demised in the gynaecological ward on the 43rd day while waiting to start the treatment. During the 43 days, further imaging could not be performed due to poor functionality of the available CT and MRI machines. In addition to antiretroviral therapy, the patient received other supportive care such as blood transfusion and analgesia. Again, the number of days between the diagnosis of the BL and her death was 43 days. Histopathological postmortem was not performed as the diagnoses (BL and retroviral disease) were known. We reckon that the main primary cause of death is challenging to assign because of the multiple principal diagnoses. Because BL has rapid progression and high mortality rate in persons living with HIV particularly with high viral load, the attending physician certifying the death assigned BL as the most likely cause of death. However, the secondary cause of death was multiple organ failure (renal and haematological inclusive).", "generated_summary": "A 29-year-old woman (Para 1) presented with a month of abnormal vaginal bleeding. She was living with HIV and had severe immunosuppression (CD4 26 cells/\u03bcL). Examination and ultrasound showed a large cervical mass with pelvic wall involvement and bilateral hydronephrosis, meeting FIGO stage 3B criteria for cervical cancer. Cervical biopsy confirmed extra-nodal Burkitt lymphoma involving the cervix. Her case was reviewed at a multidisciplinary oncology meeting, and chemoradiation was recommended. Because of a long waiting list at the referral oncology unit, treatment did not begin. She died 43 days after diagnosis, before receiving chemoradiation." }, { "index": 37, "label": "proficient_health_literacy", "original_text": "A 29-year-old woman, Para 1, with abnormal vaginal bleeding of one-month duration presented to the gynecology outpatient department of a level 2 hospital. She was HIV positive, commenced on antiretroviral treatment following diagnosis, but had defaulted the antiretroviral treatment for one month when she became ill with vaginal bleeding, resulting in virological and immunological failures (viral load 37400 copies/mL and CD4 count 26 cells/\u03bcL). Of note, it was unclear when the patient first started showing HIV symptoms. However, she was diagnosed with HIV about a year prior to presentation. Physical examination revealed a large mass on the cervix measuring 8 \u00d7 8 cm extending to the parametrium and to the pelvic side walls bilaterally. There was bleeding on contact and foul-smelling vaginal discharge. Ultrasonography detected a bulky cervix and bilateral hydronephrosis. The patient was clinically diagnosed with cervical malignancy stage 3B. She was recommenced on antiretroviral therapy with a treatment change from TLD (Tenofovir-Lamivudine-Dolutegravir combination) to a preferable renal friendly regimen (Lamivudine-Abacavir-Dolutegravir combination). A punch biopsy of the cervix was performed, and the histopathological report revealed the diagnosis of an extra-nodal BL. The immunohistochemical and in situ hybridization confirmed the diagnosis, with CD20, CD75a, CD10, PAX5 and Bcl-6 positive. In addition, the CD44 and c-Myc were positive, with the EBER-ISH demonstrating focal positivity. The Ki67 demonstrated a proliferation index of almost 100% and PAX5 moderately positive BCL6. She had white cell count of 2.67 x109/L, haemoglobin of 5.7g/dl and platelet count of 71 \u00d7 109/L. Results of other investigations were serum creatinine 187 mmol/L, urea 11.1 mmol/l, albumin 21 g/l, aspartate transaminase 41 U/l and alkaline phosphatase 100 U/l.\n\nFollowing histological confirmation of the diagnosis and review at an oncology multidisciplinary meeting, she spent 43 days waiting to start treatment at oncology unit. The delay was due to long waiting list. This delay exceeded the 48 hours waiting period during which oncological treatment for BL should commence following diagnosis. The treatment plan was chemo-radiation therapy, and the patient gave written informed consent for the case to be published. However, she demised in the gynaecological ward on the 43rd day while waiting to start the treatment. During the 43 days, further imaging could not be performed due to poor functionality of the available CT and MRI machines. In addition to antiretroviral therapy, the patient received other supportive care such as blood transfusion and analgesia. Again, the number of days between the diagnosis of the BL and her death was 43 days. Histopathological postmortem was not performed as the diagnoses (BL and retroviral disease) were known. We reckon that the main primary cause of death is challenging to assign because of the multiple principal diagnoses. Because BL has rapid progression and high mortality rate in persons living with HIV particularly with high viral load, the attending physician certifying the death assigned BL as the most likely cause of death. However, the secondary cause of death was multiple organ failure (renal and haematological inclusive).", "generated_summary": "A 29-year-old woman, Para 1, presented with one month of abnormal vaginal bleeding to a level 2 hospital. She was HIV positive, had been commenced on antiretroviral therapy (ART) after diagnosis approximately one year earlier, but defaulted ART for one month when she became ill with vaginal bleeding, resulting in virological and immunological failure (viral load 37,400 copies/mL; CD4 26 cells/\u03bcL). On exam, there was an 8 \u00d7 8 cm friable cervical mass extending to the parametrium and bilaterally to the pelvic sidewalls, with contact bleeding and foul-smelling discharge. Ultrasonography showed a bulky cervix and bilateral hydronephrosis. She was clinically staged as FIGO stage 3B cervical malignancy based on pelvic wall involvement and hydronephrosis. ART was re-initiated with a switch from TLD (Tenofovir\u2013Lamivudine\u2013Dolutegravir) to a renal-friendly regimen (Lamivudine\u2013Abacavir\u2013Dolutegravir). A punch cervical biopsy revealed extra-nodal BL (Burkitt lymphoma). Immunohistochemistry and in situ hybridization confirmed the diagnosis: CD20, CD75a, CD10, PAX5, and Bcl-6 positive; CD44 and c-Myc positive; EBER-ISH focally positive. Ki-67 showed an almost 100% proliferation index, and PAX5 moderately positive BCL6. Baseline labs included WBC 2.67 \u00d7 10^9/L, hemoglobin 5.7 g/dL, platelets 71 \u00d7 10^9/L; creatinine 187 mmol/L, urea 11.1 mmol/L, albumin 21 g/L, AST 41 U/L, ALP 100 U/L. After histologic confirmation and multidisciplinary review, the plan was chemoradiation. She then waited 43 days to start treatment at the oncology unit due to a long waiting list\u2014exceeding the recommended \u226448-hour window for initiating BL therapy. During this interval, further CT/MRI imaging could not be performed due to equipment dysfunction. Supportive care included ART, blood transfusion, and analgesia. She died on day 43 post-diagnosis while awaiting treatment and received no chemoradiation. No histopathological postmortem was performed because BL and HIV were established. Given BL\u2019s rapid progression and high mortality in people with HIV and high viral load, the attending physician certified BL as the most likely primary cause of death, with multiple organ failure (including renal and hematologic) as a secondary cause." }, { "index": 38, "label": "low_health_literacy", "original_text": "A 56-year-old female patient presented with complaints of dyspnea that required oxygen supplementation. Her medical history dates back to July 2013 when she was hospitalized in the chest ward for dyspnea and cough with yellow sputum. She was subsequently diagnosed with Sjogren\u2019s syndrome complicated with interstitial lung disease (ILD) and PAH (Table I). Her chest X-ray at that time showed vascular markings with interstitial thickening, costophrenic (CP) angle blunting and cardiomegaly. An echocardiogram revealed a pulmonary arterial (PA) systolic pressure of 99 mmHg, enlargement of the right atrium and ventricle, D-shaped left ventricle (LV), and severe tricuspid regurgitation. Chest CNYCT showed no filling defects, excluding pulmonary embolism; it also displayed an enlarged pulmonary trunk, right atrium (RA), and right ventricle (RV), further evidencing pulmonary hypertension. Symptoms of dry mouth, dry eyes, and cracked tongue mucosa, with a Schirmer\u2019s test showing <5 cm, oculus uterque (OU). A positive minor salivary gland biopsy, nuclear medicine scan showing impaired salivary gland function, and a positive anti-Ro test, confirmed Sjogren\u2019s syndrome. She started on Revatio (Sildenafil) 20 mg three times a day (TID) for pulmonary hypertension control, adding Tracleer (Bosentan) in 2016 due to disease progression. A right heart catheterization (RHC) revealed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) nearly 15 Woods, and a wedge pressure of 4, indicating pre-capillary type, group I, CTD-related PAH in 2017. The right heart catheterization (RHC) report allowed for insurance coverage of Opsumit (Macitentan) 10 mg once a day (QD), replacing Tracleer (Bosentan) in 2017. From 2017 to 2020, she was hospitalized multiple times for steroid treatments to manage her underlying Sjogren\u2019s syndrome.\n\nPulmonary hypertension treatment is risk-based, and until 2017, the patient was considered low to intermediate risk, controlled with two medications (Sildenafil + Macitentan). Her condition remained stable until October 2020, when she experienced worsened dyspnea accompanied by cough and expectoration of white sputum, suggestive of infection. On November 10, 2020, the patient experienced severe dyspnea, cold sweats, and cyanosis, with SpO2 dropping to 70%, necessitating 100% O2 via face tent. Blood gas and lab tests revealed a lactate level of 5.2 mmol/l and brain natriuretic peptide (BNP) over 10,000 pg/ml, strongly suggesting cardiogenic shock. She was prepped for intensive care unit (ICU) admission, intubated, and initiated on four pulmonary hypertension medications. Her condition stabilized and showed improvement, preventing further deterioration. On November 12, 2020, evaluation for heart-lung transplantation began. Her condition continued to improve with off vasopressors on November 13, 2020, and extubating on November 14, 2020, and transferred to a general ward on November 21, 2020, with O2 tapered to nasal cannula 2l/min. A follow-up RHC continued to show elevated pulmonary artery pressure, likely attributed to chronic hypertension leading to right heart strain and eventual failure. After intensive care unit (ICU) treatment, she was referred to National Taiwan University Hospital for evaluation for heart-lung transplant.\n\nReviewing the records since the onset of her illness, it was evident that pulmonary artery pressure had steadily increased, and the distance covered in the 6-minute walk test was progressively shortened. Currently, the patient is classified as high risk. She continues regular hospitalizations for control. Despite the relatively stable condition, her chief complaint during the admission is still dyspnea. The physical examination revealed mild rhonchi ILD and a pansystolic murmur indicative of severe valvular heart disease, with no other significant findings. Ventavis (Iloprost) 10 mcg/ml 2 ml was added in 2020. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023. Hydrogen capsules (PURE HYDROGEN) were purchased from HoHo Biotech Co., Ltd. (Taipei, Taiwan, ROC). Each capsule contained 170 mg of hydrogen-rich coral calcium containing 1.7\u00d71,021 molecules of hydrogen, which is equivalent to 24 cups of water with 1,200 ppb of hydrogen or 0.6 mM of hydrogen per 200 ml of water. Adjuvant therapy with hydrogen capsules resulted in increased CD127 + Treg, decreased anti-Ro antibody, decreased B cell subsets, and stabilization of clinical symptoms and signs was observed following the addition of hydrogen therapy in this patient. No adverse reactions or events were observed following the administration of hydrogen capsules. Flow cytometry and serological examination were employed for whole-blood analysis to assess changes in immune cells and autoantibody before and after hydrogen therapy. For subsequent whole-blood analysis via flow cytometry, blood samples were prepared using standard fluorescent dye preparation methods and fluorescent antibody reagent kits with dried reagents (Beckman Coulter, Brea, CA, USA). The methods, steps, immunophenotypic analysis, and cell gating were conducted following previously described procedures. Our analysis of immunophenotypic markers before and after hydrogen therapy revealed increased CD127 + Treg and decreased B cell subsets after treatment. Moreover, this study adheres to the CARE reporting guidelines (2013 CARE Checklist).", "generated_summary": "This report is about a 56-year-old woman with Sjogren\u2019s syndrome. It caused lung scarring and high blood pressure in the lungs. Doctors found this in 2013. She took medicines for lung pressure and for her immune disease: sildenafil, bosentan, macitentan, iloprost, and steroids. Even with treatment, she got worse. In 2020, she had very hard breathing and went into heart-related shock. In May 2023, her care team added daily hydrogen capsules to help. After starting the hydrogen capsules, tests showed more immune cells that calm the body (CD127+ Tregs). A Sjogren\u2019s antibody called anti-Ro went down. Some B cells, another kind of immune cell, also went down. Her symptoms became stable. She had no side effects." }, { "index": 38, "label": "intermediate_health_literacy", "original_text": "A 56-year-old female patient presented with complaints of dyspnea that required oxygen supplementation. Her medical history dates back to July 2013 when she was hospitalized in the chest ward for dyspnea and cough with yellow sputum. She was subsequently diagnosed with Sjogren\u2019s syndrome complicated with interstitial lung disease (ILD) and PAH (Table I). Her chest X-ray at that time showed vascular markings with interstitial thickening, costophrenic (CP) angle blunting and cardiomegaly. An echocardiogram revealed a pulmonary arterial (PA) systolic pressure of 99 mmHg, enlargement of the right atrium and ventricle, D-shaped left ventricle (LV), and severe tricuspid regurgitation. Chest CNYCT showed no filling defects, excluding pulmonary embolism; it also displayed an enlarged pulmonary trunk, right atrium (RA), and right ventricle (RV), further evidencing pulmonary hypertension. Symptoms of dry mouth, dry eyes, and cracked tongue mucosa, with a Schirmer\u2019s test showing <5 cm, oculus uterque (OU). A positive minor salivary gland biopsy, nuclear medicine scan showing impaired salivary gland function, and a positive anti-Ro test, confirmed Sjogren\u2019s syndrome. She started on Revatio (Sildenafil) 20 mg three times a day (TID) for pulmonary hypertension control, adding Tracleer (Bosentan) in 2016 due to disease progression. A right heart catheterization (RHC) revealed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) nearly 15 Woods, and a wedge pressure of 4, indicating pre-capillary type, group I, CTD-related PAH in 2017. The right heart catheterization (RHC) report allowed for insurance coverage of Opsumit (Macitentan) 10 mg once a day (QD), replacing Tracleer (Bosentan) in 2017. From 2017 to 2020, she was hospitalized multiple times for steroid treatments to manage her underlying Sjogren\u2019s syndrome.\n\nPulmonary hypertension treatment is risk-based, and until 2017, the patient was considered low to intermediate risk, controlled with two medications (Sildenafil + Macitentan). Her condition remained stable until October 2020, when she experienced worsened dyspnea accompanied by cough and expectoration of white sputum, suggestive of infection. On November 10, 2020, the patient experienced severe dyspnea, cold sweats, and cyanosis, with SpO2 dropping to 70%, necessitating 100% O2 via face tent. Blood gas and lab tests revealed a lactate level of 5.2 mmol/l and brain natriuretic peptide (BNP) over 10,000 pg/ml, strongly suggesting cardiogenic shock. She was prepped for intensive care unit (ICU) admission, intubated, and initiated on four pulmonary hypertension medications. Her condition stabilized and showed improvement, preventing further deterioration. On November 12, 2020, evaluation for heart-lung transplantation began. Her condition continued to improve with off vasopressors on November 13, 2020, and extubating on November 14, 2020, and transferred to a general ward on November 21, 2020, with O2 tapered to nasal cannula 2l/min. A follow-up RHC continued to show elevated pulmonary artery pressure, likely attributed to chronic hypertension leading to right heart strain and eventual failure. After intensive care unit (ICU) treatment, she was referred to National Taiwan University Hospital for evaluation for heart-lung transplant.\n\nReviewing the records since the onset of her illness, it was evident that pulmonary artery pressure had steadily increased, and the distance covered in the 6-minute walk test was progressively shortened. Currently, the patient is classified as high risk. She continues regular hospitalizations for control. Despite the relatively stable condition, her chief complaint during the admission is still dyspnea. The physical examination revealed mild rhonchi ILD and a pansystolic murmur indicative of severe valvular heart disease, with no other significant findings. Ventavis (Iloprost) 10 mcg/ml 2 ml was added in 2020. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023. Hydrogen capsules (PURE HYDROGEN) were purchased from HoHo Biotech Co., Ltd. (Taipei, Taiwan, ROC). Each capsule contained 170 mg of hydrogen-rich coral calcium containing 1.7\u00d71,021 molecules of hydrogen, which is equivalent to 24 cups of water with 1,200 ppb of hydrogen or 0.6 mM of hydrogen per 200 ml of water. Adjuvant therapy with hydrogen capsules resulted in increased CD127 + Treg, decreased anti-Ro antibody, decreased B cell subsets, and stabilization of clinical symptoms and signs was observed following the addition of hydrogen therapy in this patient. No adverse reactions or events were observed following the administration of hydrogen capsules. Flow cytometry and serological examination were employed for whole-blood analysis to assess changes in immune cells and autoantibody before and after hydrogen therapy. For subsequent whole-blood analysis via flow cytometry, blood samples were prepared using standard fluorescent dye preparation methods and fluorescent antibody reagent kits with dried reagents (Beckman Coulter, Brea, CA, USA). The methods, steps, immunophenotypic analysis, and cell gating were conducted following previously described procedures. Our analysis of immunophenotypic markers before and after hydrogen therapy revealed increased CD127 + Treg and decreased B cell subsets after treatment. Moreover, this study adheres to the CARE reporting guidelines (2013 CARE Checklist).", "generated_summary": "A 56-year-old woman with connective tissue disease\u2013associated pulmonary arterial hypertension (CTD-PAH) from Sjogren\u2019s syndrome, diagnosed in 2013 with interstitial lung disease, was treated over the years with sildenafil, bosentan (later switched to macitentan), iloprost, and corticosteroids. Despite these therapies, her condition worsened and she developed severe dyspnea and cardiogenic shock in 2020. In May 2023, molecular hydrogen was added as an adjuvant therapy in the form of daily hydrogen capsules. After starting hydrogen, immune testing showed an increase in regulatory T cells (CD127+ Tregs), a reduction in anti-Ro antibodies, and a decrease in B cell subsets. Clinically, her symptoms stabilized, and no adverse effects were reported." }, { "index": 38, "label": "proficient_health_literacy", "original_text": "A 56-year-old female patient presented with complaints of dyspnea that required oxygen supplementation. Her medical history dates back to July 2013 when she was hospitalized in the chest ward for dyspnea and cough with yellow sputum. She was subsequently diagnosed with Sjogren\u2019s syndrome complicated with interstitial lung disease (ILD) and PAH (Table I). Her chest X-ray at that time showed vascular markings with interstitial thickening, costophrenic (CP) angle blunting and cardiomegaly. An echocardiogram revealed a pulmonary arterial (PA) systolic pressure of 99 mmHg, enlargement of the right atrium and ventricle, D-shaped left ventricle (LV), and severe tricuspid regurgitation. Chest CNYCT showed no filling defects, excluding pulmonary embolism; it also displayed an enlarged pulmonary trunk, right atrium (RA), and right ventricle (RV), further evidencing pulmonary hypertension. Symptoms of dry mouth, dry eyes, and cracked tongue mucosa, with a Schirmer\u2019s test showing <5 cm, oculus uterque (OU). A positive minor salivary gland biopsy, nuclear medicine scan showing impaired salivary gland function, and a positive anti-Ro test, confirmed Sjogren\u2019s syndrome. She started on Revatio (Sildenafil) 20 mg three times a day (TID) for pulmonary hypertension control, adding Tracleer (Bosentan) in 2016 due to disease progression. A right heart catheterization (RHC) revealed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) nearly 15 Woods, and a wedge pressure of 4, indicating pre-capillary type, group I, CTD-related PAH in 2017. The right heart catheterization (RHC) report allowed for insurance coverage of Opsumit (Macitentan) 10 mg once a day (QD), replacing Tracleer (Bosentan) in 2017. From 2017 to 2020, she was hospitalized multiple times for steroid treatments to manage her underlying Sjogren\u2019s syndrome.\n\nPulmonary hypertension treatment is risk-based, and until 2017, the patient was considered low to intermediate risk, controlled with two medications (Sildenafil + Macitentan). Her condition remained stable until October 2020, when she experienced worsened dyspnea accompanied by cough and expectoration of white sputum, suggestive of infection. On November 10, 2020, the patient experienced severe dyspnea, cold sweats, and cyanosis, with SpO2 dropping to 70%, necessitating 100% O2 via face tent. Blood gas and lab tests revealed a lactate level of 5.2 mmol/l and brain natriuretic peptide (BNP) over 10,000 pg/ml, strongly suggesting cardiogenic shock. She was prepped for intensive care unit (ICU) admission, intubated, and initiated on four pulmonary hypertension medications. Her condition stabilized and showed improvement, preventing further deterioration. On November 12, 2020, evaluation for heart-lung transplantation began. Her condition continued to improve with off vasopressors on November 13, 2020, and extubating on November 14, 2020, and transferred to a general ward on November 21, 2020, with O2 tapered to nasal cannula 2l/min. A follow-up RHC continued to show elevated pulmonary artery pressure, likely attributed to chronic hypertension leading to right heart strain and eventual failure. After intensive care unit (ICU) treatment, she was referred to National Taiwan University Hospital for evaluation for heart-lung transplant.\n\nReviewing the records since the onset of her illness, it was evident that pulmonary artery pressure had steadily increased, and the distance covered in the 6-minute walk test was progressively shortened. Currently, the patient is classified as high risk. She continues regular hospitalizations for control. Despite the relatively stable condition, her chief complaint during the admission is still dyspnea. The physical examination revealed mild rhonchi ILD and a pansystolic murmur indicative of severe valvular heart disease, with no other significant findings. Ventavis (Iloprost) 10 mcg/ml 2 ml was added in 2020. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023. Hydrogen capsules (PURE HYDROGEN) were purchased from HoHo Biotech Co., Ltd. (Taipei, Taiwan, ROC). Each capsule contained 170 mg of hydrogen-rich coral calcium containing 1.7\u00d71,021 molecules of hydrogen, which is equivalent to 24 cups of water with 1,200 ppb of hydrogen or 0.6 mM of hydrogen per 200 ml of water. Adjuvant therapy with hydrogen capsules resulted in increased CD127 + Treg, decreased anti-Ro antibody, decreased B cell subsets, and stabilization of clinical symptoms and signs was observed following the addition of hydrogen therapy in this patient. No adverse reactions or events were observed following the administration of hydrogen capsules. Flow cytometry and serological examination were employed for whole-blood analysis to assess changes in immune cells and autoantibody before and after hydrogen therapy. For subsequent whole-blood analysis via flow cytometry, blood samples were prepared using standard fluorescent dye preparation methods and fluorescent antibody reagent kits with dried reagents (Beckman Coulter, Brea, CA, USA). The methods, steps, immunophenotypic analysis, and cell gating were conducted following previously described procedures. Our analysis of immunophenotypic markers before and after hydrogen therapy revealed increased CD127 + Treg and decreased B cell subsets after treatment. Moreover, this study adheres to the CARE reporting guidelines (2013 CARE Checklist).", "generated_summary": "A 56-year-old female with CTD-PAH secondary to Sjogren\u2019s syndrome (diagnosed 2013) complicated by ILD initially presented with dyspnea. Early studies showed interstitial changes and cardiomegaly on chest X-ray; echocardiography demonstrated PASP 99 mmHg, RA/RV enlargement, D-shaped LV, and severe TR. Chest CNYCT showed no filling defects to suggest PE, with enlarged pulmonary trunk, RA, and RV, consistent with PH. Sjogren\u2019s was confirmed by sicca symptoms with Schirmer\u2019s <5 cm OU, positive minor salivary gland biopsy, impaired salivary gland function on nuclear medicine scan, and positive anti-Ro. She began Revatio (sildenafil) 20 mg TID in 2013; Tracleer (bosentan) was added in 2016. Right heart catheterization in 2017 showed mPAP 39 mmHg, PVR nearly 15 Woods, and wedge 4 mmHg, indicating pre-capillary, group I CTD-PAH; Opsumit (macitentan) 10 mg QD replaced bosentan. From 2017 to 2020 she required repeated steroid hospitalizations for Sjogren\u2019s control. Her risk status was low-to-intermediate on dual therapy until October\u2013November 2020, when she developed worsened dyspnea and signs of infection, then severe decompensation on November 10 with SpO2 70% requiring 100% O2 via face tent, lactate 5.2 mmol/L, and BNP >10,000 pg/mL, consistent with cardiogenic shock. She was intubated in the ICU, started on four PH agents, stabilized, and improved; heart\u2013lung transplant evaluation began November 12, vasopressors were discontinued November 13, she was extubated November 14, and transferred to the ward November 21 on nasal cannula 2 L/min. Follow-up RHC showed persistently elevated PA pressures attributed to chronic PH with right heart strain. She was reclassified as high risk; Ventavis (iloprost) 10 mcg/ml 2 ml was added in 2020. In May 2023, molecular hydrogen was initiated as adjuvant therapy: 1 capsule/day (PURE HYDROGEN; HoHo Biotech, Taipei, Taiwan), each containing 170 mg of hydrogen-rich coral calcium with 1.7\u00d71,021 molecules of hydrogen, equivalent to 24 cups of water at 1,200 ppb H2 or 0.6 mM H2 per 200 ml water. Flow cytometry and serology (standard fluorescent dye preparation; dried reagent kits, Beckman Coulter; immunophenotyping and gating per prior methods) before and after hydrogen therapy demonstrated increased CD127+ Treg populations and decreased B cell subsets; anti-Ro antibody levels declined. Clinically, signs and symptoms stabilized following the addition of hydrogen therapy, and no adverse reactions occurred. The case adheres to CARE reporting guidelines (2013 CARE Checklist)." }, { "index": 39, "label": "low_health_literacy", "original_text": "The patient was a 45-year-old male born in Pakistan who had resided in Portugal for 7 years. He had a history of grade 3 obesity, with no other known personal history or usual pharmacological therapy.\n\nThe patient sought emergency care for fever, dry cough, dyspnea, chest pain, dysgeusia, headache and myalgia with 4 days of evolution. In the summary neurological examination at admission, there were no reported changes. In the evaluation of the respiratory system, tachypnea and pulmonary auscultation with bilateral rough vesicular murmur, without other adventitious sounds, were noted. The remainder of the objective examination showed no changes.\n\nOf the complementary diagnostic tests performed at admission, there was a slight increase in inflammatory parameters and in arterial blood gases under an inspired oxygen fraction (FiO2) of 21%, with type 1 respiratory failure and extensive predominant bilateral, peripheral and basal opacities on chest teleradiography. After a positive reverse-transcription real-time polymerase chain reaction (RT-PCR) test for SARS-CoV-2 (nasal and oropharyngeal exudate) and negative tests for influenza A and B, Streptococcus pneumoniae and Legionella pneumophila, a diagnosis of pneumonia by SARS-CoV-2 infection was established.\n\nOver the first 48 hours, progressive worsening of fatigue, dyspnea and type 1 respiratory failure, requiring an increase in supplemental oxygen therapy, were observed. Due to the lack of improvement, noninvasive mechanical ventilation was initiated; however, due to poor adherence, high-flow oxygen therapy was initiated through a nasal cannula, without a response to therapy.\n\nIn this context, the patient was admitted to the intensive care unit (ICU), level III, where he underwent sedoanalgesia and orotracheal intubation with connection to invasive mechanical ventilation.\n\nOn the eleventh day of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin and empirical antibiotic therapy with amoxicillin/clavulanic acid and azithromycin, administered on suspicion of bacterial overinfection, was continued. During this period, sustained fever was observed, with a weak response to antipyretic therapy, with improvements in inflammatory parameters after the third day of hospitalization in the ICU.\n\nTo exclude any concomitant infectious etiology, intravenous devices were replaced, and blood cultures, cultures of the tip of the central catheter and bronchial secretions, urinalysis, urine culture and transthoracic echocardiography were performed. Among the cultures, the blood culture yielded the only positive result, i.e., Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid, which the patient was already receiving. The summary echocardiogram did not reveal valve changes suggestive of endocarditis, but the patient presented hypokinesia of the lateral wall and left ventricular apex, as well as poor biventricular function. A slight increase in troponins (1.8ng/mL) and ST-segment depression in leads I and aVL were confirmed, suggesting the existence of acute coronary syndrome or septic cardiomyopathy.\n\nOther noninfectious causes of febrile symptoms in the critically ill patient were excluded, including treatment with neuroleptics or altered thyroid function.\n\nNotably, there was a need for inotropic support with dobutamine in the ventilatory weaning phase as well as noninvasive ventilatory support after orotracheal extubation, which occurred on the fifteenth day of hospitalization.\n\nOn the sixteenth day of hospitalization (nineteenth day of confirmed disease), there was an episode of altered state of consciousness, conjugated deviation of gaze to the right and myoclonus of the face and thoracic region to the left followed by a generalized tonic-clonic seizure crisis, which ceased after midazolam therapy. The hypothesis that the seizure occurred in the context of a hypoxic-ischemic event was excluded because the patient remained normotensive, there was never a peri-event or hypoxemia, serum lactate level was normal, and diuresis remained preserved. Any ionic or glycemic disorders that could explain the inaugural seizure episode were excluded.\n\nIn the post-critical period, there was an absence of eye opening, no verbal response, failure to localize to pain (coma scale of Glasgow 7), and persistent left hemiparesis grade 3 out of 5. Due to the need for airway protection, the patient was sedated, subjected to orotracheal intubation and started on anticonvulsant therapy.\n\nIn the process of diagnosis of the convulsive episode, after cranial computed tomography confirmed no changes, the patient was subjected to lumbar puncture, with turbid CSF output and mild proteinorrachia but without pleocytosis and with normal opening pressure. In the CSF, neurotropic virus and venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria tests and an RT-PCR test for SARS-CoV-2 were requested, and samples were collected for culture. Electroencephalography was performed 1 hour after propofol suspension and under fentanyl, with a single record and total duration of 13 minutes; the findings indicated no changes.\n\nAfter confirmation of a positive RT-PCR test for SARS-CoV-2 RNA in the CSF, without CSF pleiocytosis, the hypothesis of bacterial but nonviral meningitis was excluded, considering the hypothesis of encephalitis. Magnetic resonance imaging (MRI) performed on the seventeenth day of hospitalization showed multiple image artifacts associated with patient movement during the procedure, suggesting the need to repeat the examination.\n\nAfter discontinuation of sedoanalgesia, a change in consciousness was observed, with a Glasgow coma scale score of 14, persistent left hemiparesis with muscle strength grade 4 in 5 and an absence of involuntary movements, allowing safe orotracheal extubation in 24 hours. Given the favorable clinical outcome, brain biopsy was excluded. On the twenty-first day of hospitalization, the patient was transferred to the ward.\n\nThe patient maintained apyrexia without altered state of consciousness. No new episodes of involuntary movements were observed, and on the twenty-sixth day of hospitalization, he underwent a reassessment MRI, which revealed no pathological changes. As he maintained a favorable clinical evolution, the patient was discharged on the thirty-first day of hospitalization without antiepileptic drugs and with an appointment for follow-up with the internal medicine department.\n", "generated_summary": "A 45-year-old man was in the hospital with lung infection from the virus that causes COVID-19. He had no past brain or nerve problems. On day 16 in the hospital, he suddenly became less awake. Both eyes pulled to the right. His left face and chest had quick jerks. Then he had a full-body seizure. After that, the left side of his body stayed weak. A lab test on the fluid around his brain and spine found the COVID-19 virus. He slowly got better, and the final result was good." }, { "index": 39, "label": "intermediate_health_literacy", "original_text": "The patient was a 45-year-old male born in Pakistan who had resided in Portugal for 7 years. He had a history of grade 3 obesity, with no other known personal history or usual pharmacological therapy.\n\nThe patient sought emergency care for fever, dry cough, dyspnea, chest pain, dysgeusia, headache and myalgia with 4 days of evolution. In the summary neurological examination at admission, there were no reported changes. In the evaluation of the respiratory system, tachypnea and pulmonary auscultation with bilateral rough vesicular murmur, without other adventitious sounds, were noted. The remainder of the objective examination showed no changes.\n\nOf the complementary diagnostic tests performed at admission, there was a slight increase in inflammatory parameters and in arterial blood gases under an inspired oxygen fraction (FiO2) of 21%, with type 1 respiratory failure and extensive predominant bilateral, peripheral and basal opacities on chest teleradiography. After a positive reverse-transcription real-time polymerase chain reaction (RT-PCR) test for SARS-CoV-2 (nasal and oropharyngeal exudate) and negative tests for influenza A and B, Streptococcus pneumoniae and Legionella pneumophila, a diagnosis of pneumonia by SARS-CoV-2 infection was established.\n\nOver the first 48 hours, progressive worsening of fatigue, dyspnea and type 1 respiratory failure, requiring an increase in supplemental oxygen therapy, were observed. Due to the lack of improvement, noninvasive mechanical ventilation was initiated; however, due to poor adherence, high-flow oxygen therapy was initiated through a nasal cannula, without a response to therapy.\n\nIn this context, the patient was admitted to the intensive care unit (ICU), level III, where he underwent sedoanalgesia and orotracheal intubation with connection to invasive mechanical ventilation.\n\nOn the eleventh day of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin and empirical antibiotic therapy with amoxicillin/clavulanic acid and azithromycin, administered on suspicion of bacterial overinfection, was continued. During this period, sustained fever was observed, with a weak response to antipyretic therapy, with improvements in inflammatory parameters after the third day of hospitalization in the ICU.\n\nTo exclude any concomitant infectious etiology, intravenous devices were replaced, and blood cultures, cultures of the tip of the central catheter and bronchial secretions, urinalysis, urine culture and transthoracic echocardiography were performed. Among the cultures, the blood culture yielded the only positive result, i.e., Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid, which the patient was already receiving. The summary echocardiogram did not reveal valve changes suggestive of endocarditis, but the patient presented hypokinesia of the lateral wall and left ventricular apex, as well as poor biventricular function. A slight increase in troponins (1.8ng/mL) and ST-segment depression in leads I and aVL were confirmed, suggesting the existence of acute coronary syndrome or septic cardiomyopathy.\n\nOther noninfectious causes of febrile symptoms in the critically ill patient were excluded, including treatment with neuroleptics or altered thyroid function.\n\nNotably, there was a need for inotropic support with dobutamine in the ventilatory weaning phase as well as noninvasive ventilatory support after orotracheal extubation, which occurred on the fifteenth day of hospitalization.\n\nOn the sixteenth day of hospitalization (nineteenth day of confirmed disease), there was an episode of altered state of consciousness, conjugated deviation of gaze to the right and myoclonus of the face and thoracic region to the left followed by a generalized tonic-clonic seizure crisis, which ceased after midazolam therapy. The hypothesis that the seizure occurred in the context of a hypoxic-ischemic event was excluded because the patient remained normotensive, there was never a peri-event or hypoxemia, serum lactate level was normal, and diuresis remained preserved. Any ionic or glycemic disorders that could explain the inaugural seizure episode were excluded.\n\nIn the post-critical period, there was an absence of eye opening, no verbal response, failure to localize to pain (coma scale of Glasgow 7), and persistent left hemiparesis grade 3 out of 5. Due to the need for airway protection, the patient was sedated, subjected to orotracheal intubation and started on anticonvulsant therapy.\n\nIn the process of diagnosis of the convulsive episode, after cranial computed tomography confirmed no changes, the patient was subjected to lumbar puncture, with turbid CSF output and mild proteinorrachia but without pleocytosis and with normal opening pressure. In the CSF, neurotropic virus and venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria tests and an RT-PCR test for SARS-CoV-2 were requested, and samples were collected for culture. Electroencephalography was performed 1 hour after propofol suspension and under fentanyl, with a single record and total duration of 13 minutes; the findings indicated no changes.\n\nAfter confirmation of a positive RT-PCR test for SARS-CoV-2 RNA in the CSF, without CSF pleiocytosis, the hypothesis of bacterial but nonviral meningitis was excluded, considering the hypothesis of encephalitis. Magnetic resonance imaging (MRI) performed on the seventeenth day of hospitalization showed multiple image artifacts associated with patient movement during the procedure, suggesting the need to repeat the examination.\n\nAfter discontinuation of sedoanalgesia, a change in consciousness was observed, with a Glasgow coma scale score of 14, persistent left hemiparesis with muscle strength grade 4 in 5 and an absence of involuntary movements, allowing safe orotracheal extubation in 24 hours. Given the favorable clinical outcome, brain biopsy was excluded. On the twenty-first day of hospitalization, the patient was transferred to the ward.\n\nThe patient maintained apyrexia without altered state of consciousness. No new episodes of involuntary movements were observed, and on the twenty-sixth day of hospitalization, he underwent a reassessment MRI, which revealed no pathological changes. As he maintained a favorable clinical evolution, the patient was discharged on the thirty-first day of hospitalization without antiepileptic drugs and with an appointment for follow-up with the internal medicine department.\n", "generated_summary": "A 45-year-old man was hospitalized with COVID-19 pneumonia and had no prior neurologic history. On hospital day 16, he suddenly developed reduced consciousness, his eyes deviated to the right, and he had jerking movements on the left side of his face and chest, followed by a generalized tonic\u2013clonic seizure. After the seizure, he was left with persistent weakness on the left side (left hemiparesis). Brain CT was normal, and a spinal tap showed slightly elevated protein but no increase in white blood cells. Importantly, the cerebrospinal fluid tested positive for SARS-CoV-2 by RT-PCR, making viral involvement of the brain (encephalitis) likely and bacterial meningitis unlikely. An EEG did not show clear abnormalities, and later MRI was also unremarkable. He improved gradually, his condition stabilized, and his overall outcome was favorable." }, { "index": 39, "label": "proficient_health_literacy", "original_text": "The patient was a 45-year-old male born in Pakistan who had resided in Portugal for 7 years. He had a history of grade 3 obesity, with no other known personal history or usual pharmacological therapy.\n\nThe patient sought emergency care for fever, dry cough, dyspnea, chest pain, dysgeusia, headache and myalgia with 4 days of evolution. In the summary neurological examination at admission, there were no reported changes. In the evaluation of the respiratory system, tachypnea and pulmonary auscultation with bilateral rough vesicular murmur, without other adventitious sounds, were noted. The remainder of the objective examination showed no changes.\n\nOf the complementary diagnostic tests performed at admission, there was a slight increase in inflammatory parameters and in arterial blood gases under an inspired oxygen fraction (FiO2) of 21%, with type 1 respiratory failure and extensive predominant bilateral, peripheral and basal opacities on chest teleradiography. After a positive reverse-transcription real-time polymerase chain reaction (RT-PCR) test for SARS-CoV-2 (nasal and oropharyngeal exudate) and negative tests for influenza A and B, Streptococcus pneumoniae and Legionella pneumophila, a diagnosis of pneumonia by SARS-CoV-2 infection was established.\n\nOver the first 48 hours, progressive worsening of fatigue, dyspnea and type 1 respiratory failure, requiring an increase in supplemental oxygen therapy, were observed. Due to the lack of improvement, noninvasive mechanical ventilation was initiated; however, due to poor adherence, high-flow oxygen therapy was initiated through a nasal cannula, without a response to therapy.\n\nIn this context, the patient was admitted to the intensive care unit (ICU), level III, where he underwent sedoanalgesia and orotracheal intubation with connection to invasive mechanical ventilation.\n\nOn the eleventh day of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin and empirical antibiotic therapy with amoxicillin/clavulanic acid and azithromycin, administered on suspicion of bacterial overinfection, was continued. During this period, sustained fever was observed, with a weak response to antipyretic therapy, with improvements in inflammatory parameters after the third day of hospitalization in the ICU.\n\nTo exclude any concomitant infectious etiology, intravenous devices were replaced, and blood cultures, cultures of the tip of the central catheter and bronchial secretions, urinalysis, urine culture and transthoracic echocardiography were performed. Among the cultures, the blood culture yielded the only positive result, i.e., Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid, which the patient was already receiving. The summary echocardiogram did not reveal valve changes suggestive of endocarditis, but the patient presented hypokinesia of the lateral wall and left ventricular apex, as well as poor biventricular function. A slight increase in troponins (1.8ng/mL) and ST-segment depression in leads I and aVL were confirmed, suggesting the existence of acute coronary syndrome or septic cardiomyopathy.\n\nOther noninfectious causes of febrile symptoms in the critically ill patient were excluded, including treatment with neuroleptics or altered thyroid function.\n\nNotably, there was a need for inotropic support with dobutamine in the ventilatory weaning phase as well as noninvasive ventilatory support after orotracheal extubation, which occurred on the fifteenth day of hospitalization.\n\nOn the sixteenth day of hospitalization (nineteenth day of confirmed disease), there was an episode of altered state of consciousness, conjugated deviation of gaze to the right and myoclonus of the face and thoracic region to the left followed by a generalized tonic-clonic seizure crisis, which ceased after midazolam therapy. The hypothesis that the seizure occurred in the context of a hypoxic-ischemic event was excluded because the patient remained normotensive, there was never a peri-event or hypoxemia, serum lactate level was normal, and diuresis remained preserved. Any ionic or glycemic disorders that could explain the inaugural seizure episode were excluded.\n\nIn the post-critical period, there was an absence of eye opening, no verbal response, failure to localize to pain (coma scale of Glasgow 7), and persistent left hemiparesis grade 3 out of 5. Due to the need for airway protection, the patient was sedated, subjected to orotracheal intubation and started on anticonvulsant therapy.\n\nIn the process of diagnosis of the convulsive episode, after cranial computed tomography confirmed no changes, the patient was subjected to lumbar puncture, with turbid CSF output and mild proteinorrachia but without pleocytosis and with normal opening pressure. In the CSF, neurotropic virus and venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria tests and an RT-PCR test for SARS-CoV-2 were requested, and samples were collected for culture. Electroencephalography was performed 1 hour after propofol suspension and under fentanyl, with a single record and total duration of 13 minutes; the findings indicated no changes.\n\nAfter confirmation of a positive RT-PCR test for SARS-CoV-2 RNA in the CSF, without CSF pleiocytosis, the hypothesis of bacterial but nonviral meningitis was excluded, considering the hypothesis of encephalitis. Magnetic resonance imaging (MRI) performed on the seventeenth day of hospitalization showed multiple image artifacts associated with patient movement during the procedure, suggesting the need to repeat the examination.\n\nAfter discontinuation of sedoanalgesia, a change in consciousness was observed, with a Glasgow coma scale score of 14, persistent left hemiparesis with muscle strength grade 4 in 5 and an absence of involuntary movements, allowing safe orotracheal extubation in 24 hours. Given the favorable clinical outcome, brain biopsy was excluded. On the twenty-first day of hospitalization, the patient was transferred to the ward.\n\nThe patient maintained apyrexia without altered state of consciousness. No new episodes of involuntary movements were observed, and on the twenty-sixth day of hospitalization, he underwent a reassessment MRI, which revealed no pathological changes. As he maintained a favorable clinical evolution, the patient was discharged on the thirty-first day of hospitalization without antiepileptic drugs and with an appointment for follow-up with the internal medicine department.\n", "generated_summary": "A 45-year-old male (Pakistan-born, 7 years in Portugal) with grade 3 obesity and no neurologic history presented with 4 days of fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia. Admission exam: no focal neurologic findings; tachypnea; bilateral rough vesicular murmur; otherwise unremarkable. Labs showed mildly elevated inflammatory markers; on room air (FiO2 21%) arterial gases were consistent with type 1 respiratory failure. Chest teleradiography: extensive bilateral, predominantly peripheral and basal opacities. Nasal/oropharyngeal RT-PCR for SARS-CoV-2 was positive; influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila tests were negative, confirming COVID-19 pneumonia. Respiratory status worsened over 48 hours, escalating from supplemental O2 to noninvasive ventilation, then high-flow nasal cannula without response. He was transferred to a level III ICU for sedoanalgesia, orotracheal intubation, and invasive mechanical ventilation.\nBy ICU day 11, he was on remdesivir, dexamethasone, enoxaparin, and empirical amoxicillin/clavulanic acid plus azithromycin for suspected bacterial superinfection. He had sustained fever with poor antipyretic response; inflammatory markers improved by ICU day 3. A sepsis workup included line changes; blood, catheter tip, bronchial secretion, urine cultures; urinalysis; and transthoracic echocardiography. Only blood cultures were positive (Klebsiella pneumoniae), sensitive to amoxicillin/clavulanic acid already in use. Echocardiogram: no valvular vegetations; hypokinesia of the lateral wall and LV apex with poor biventricular function. Troponin was mildly elevated (1.8 ng/mL) with ST-segment depression in leads I and aVL, raising concern for ACS vs septic cardiomyopathy. Noninfectious fever causes (e.g., neuroleptics, thyroid dysfunction) were excluded. He required dobutamine during ventilatory weaning and needed noninvasive ventilatory support post-extubation; first extubation occurred on hospital day 15.\nOn hospital day 16 (day 19 of illness), he developed an acute alteration in consciousness with conjugate rightward gaze deviation and left facial and thoracic myoclonus, progressing to a generalized tonic\u2013clonic seizure that terminated after midazolam. Hypoxic-ischemic seizure etiology was deemed unlikely: he remained normotensive, without peri-event hypoxemia, had normal serum lactate, and preserved diuresis. No ionic or glycemic disturbances were identified. Postictally: no eye opening, no verbal response, no localization to pain (GCS 7), and persistent left hemiparesis (3/5). For airway protection, he was resedated, reintubated, and started on anticonvulsant therapy. Head CT was unremarkable. Lumbar puncture yielded turbid CSF with mild proteinorrachia, no pleocytosis, and normal opening pressure. CSF studies included panels for neurotropic viruses, VDRL, acid\u2013alcohol resistant bacteria, cultures, and RT-PCR for SARS-CoV-2. EEG performed 1 hour after propofol discontinuation (under fentanyl; single 13-minute recording) showed no significant abnormalities. CSF RT-PCR returned positive for SARS-CoV-2 RNA, and in the absence of CSF pleocytosis, bacterial (but not viral) meningitis was excluded; encephalitis was considered the leading diagnosis. Brain MRI on hospital day 17 was limited by motion artifacts. After withdrawal of sedoanalgesia, his mental status improved (GCS 14); left hemiparesis improved to 4/5; no recurrent involuntary movements; he was safely extubated within 24 hours. Given the favorable trajectory, brain biopsy was not pursued. He was transferred to the ward on day 21, remained afebrile with stable mentation, had no further seizures or myoclonus, and a repeat MRI on day 26 was normal. He was discharged home on day 31 without antiepileptic drugs, with internal medicine follow-up. This case highlights COVID-19\u2013associated encephalitic presentation with a generalized seizure and persistent unilateral deficits, supported by detection of SARS-CoV-2 RNA in CSF despite absent pleocytosis, and a favorable clinical outcome with gradual recovery." }, { "index": 40, "label": "low_health_literacy", "original_text": "This is a 32-year-old patient, a baker, from Bamako, who was admitted to the Infectious and Tropical Diseases department of the CHU du Point G (Bamako, Mali) on 27 April 2023 for chronic productive cough, otalgia and a chronic right-sided purulent otorrhea.\n\nThe symptomatology would be of progressive installation in 1 month, initially treated in a medical center with art\u00e9sunate, paracetamol and unspecified antibiotics for confirmed malaria and acute otitis media, without success. He is immunosuppressed by a HIV1 infection, diagnosed and put on a tritherapy antiretroviral (TARV) Tenofovir/Lamivudine/Dolut\u00e9gravir 7 months ago, not observed due to denial of his illness.\n\nThe general physical examination found a fever (38.2 \u00b0C), altered general condition, otalgia, purulent right foul-smelling otorrhea, a right basal pulmonary condensation syndrome, a normal neurological examination, without the involvement of the cranial nerves, mainly the facial nerve VII and the VIII cochleovestibular nerve.\n\nIn the ENT examination, the otoscopy of the right ear showed an inflammatory external auditory canal with purulent secretions and the presence of a single tympanic perforation in the anterior-inferior quadrant. The left ear is normal. The Rinne and Weber test is in favor of a right conductive hearing loss.\n\nImmuno-virological evaluation shows a CD4 count of 118 cells/pl and a viral load of 12,370 copies/ml at the time of diagnosis of HIV infection, compared to a viral load of 9,460 copies/ml and a CD4 lymphocyte count of 193 cells/pl at the 6th month of antiretroviral treatment. At the time of diagnosis of tuberculosis at the 7th month, the immuno-virological evaluation shows a CD4 count of 89 cells/pl and a viral load of 10,230 copies/ml.\n\nThe Ziehl Neelsen bacilloscopy was positive with a cross in the gastric washings on admission and 19 days later in the right ear swab because of the persistent otorrhea. The Xpert-MTB/GeneXpert test did not detect rifampicin-resistant Mycobacterium tuberculosis.\n\nThe frontal chest radiograph shows a more accentuated bronchovascular network at the base of the right lung.\n\nThe diagnosis of tuberculosis of the middle ear concomitant to a pulmonary localization in the field of immunosuppression by HIV1 is therefore retained.\n\nThe patient is put on oral first-line anti-tuberculosis for 6 months, a fixed dose of a quadra-therapy in the intensive phase of isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months (2RHZE), followed by a bi-therapy in the maintenance phase of isoniazid and rifampicin for 4 months (4RH) at a dose of 3 tablets/day in the morning on an empty stomach, associated with vitamin B6 (1 tablet/day). He benefits from two sessions of therapeutic reinforcement with anti-retroviral drugs. The ART is restarted on 4 May 2023 with his consent, given the good tolerance of the anti-tuberculosis drugs, with the combination of tenofovir/lamivudine/dolutegravir at a dose of 1 tablet/day associated with dolutegravir 50 mg as a supplement (1 tablet/day) according to the protocol for the management of HIV/AIDS. A chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) is undertaken as well as a cleaning of the external auditory canal by aspiration and the instillation of ciprofloxacin ear drops (2 drops 3 times a day) for 14 days.\n\nThe evolution is favorable after 14 days of treatment, marked by a pyrexia, a good general state, the amendment of the cough and otorrhea with the negativation of the bacilloscopy in the gastric tube liquid and the swab of the pus of the right ear. At the end of the maintenance anti-tuberculosis treatment, the clinical healing is complete with a normal ENT and neurological examination. The bacilloscopy associated with the Xpert-MTB/GeneXpert test at the end of the 2nd month of the intensive phase, during the 5th month and at the end of the 6th month of the maintenance phase were negative. The HIV viral load performed after 3 months of ART is 329 copies/ml.\n", "generated_summary": "You had a long-lasting cough with mucus. Your right ear hurt and kept leaking pus.\nDoctors looked for TB germs. They found these germs in fluid taken from a tube from your stomach and in the pus from your right ear.\nYou took TB medicine for 6 months, along with other helpful medicines. You got completely better." }, { "index": 40, "label": "intermediate_health_literacy", "original_text": "This is a 32-year-old patient, a baker, from Bamako, who was admitted to the Infectious and Tropical Diseases department of the CHU du Point G (Bamako, Mali) on 27 April 2023 for chronic productive cough, otalgia and a chronic right-sided purulent otorrhea.\n\nThe symptomatology would be of progressive installation in 1 month, initially treated in a medical center with art\u00e9sunate, paracetamol and unspecified antibiotics for confirmed malaria and acute otitis media, without success. He is immunosuppressed by a HIV1 infection, diagnosed and put on a tritherapy antiretroviral (TARV) Tenofovir/Lamivudine/Dolut\u00e9gravir 7 months ago, not observed due to denial of his illness.\n\nThe general physical examination found a fever (38.2 \u00b0C), altered general condition, otalgia, purulent right foul-smelling otorrhea, a right basal pulmonary condensation syndrome, a normal neurological examination, without the involvement of the cranial nerves, mainly the facial nerve VII and the VIII cochleovestibular nerve.\n\nIn the ENT examination, the otoscopy of the right ear showed an inflammatory external auditory canal with purulent secretions and the presence of a single tympanic perforation in the anterior-inferior quadrant. The left ear is normal. The Rinne and Weber test is in favor of a right conductive hearing loss.\n\nImmuno-virological evaluation shows a CD4 count of 118 cells/pl and a viral load of 12,370 copies/ml at the time of diagnosis of HIV infection, compared to a viral load of 9,460 copies/ml and a CD4 lymphocyte count of 193 cells/pl at the 6th month of antiretroviral treatment. At the time of diagnosis of tuberculosis at the 7th month, the immuno-virological evaluation shows a CD4 count of 89 cells/pl and a viral load of 10,230 copies/ml.\n\nThe Ziehl Neelsen bacilloscopy was positive with a cross in the gastric washings on admission and 19 days later in the right ear swab because of the persistent otorrhea. The Xpert-MTB/GeneXpert test did not detect rifampicin-resistant Mycobacterium tuberculosis.\n\nThe frontal chest radiograph shows a more accentuated bronchovascular network at the base of the right lung.\n\nThe diagnosis of tuberculosis of the middle ear concomitant to a pulmonary localization in the field of immunosuppression by HIV1 is therefore retained.\n\nThe patient is put on oral first-line anti-tuberculosis for 6 months, a fixed dose of a quadra-therapy in the intensive phase of isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months (2RHZE), followed by a bi-therapy in the maintenance phase of isoniazid and rifampicin for 4 months (4RH) at a dose of 3 tablets/day in the morning on an empty stomach, associated with vitamin B6 (1 tablet/day). He benefits from two sessions of therapeutic reinforcement with anti-retroviral drugs. The ART is restarted on 4 May 2023 with his consent, given the good tolerance of the anti-tuberculosis drugs, with the combination of tenofovir/lamivudine/dolutegravir at a dose of 1 tablet/day associated with dolutegravir 50 mg as a supplement (1 tablet/day) according to the protocol for the management of HIV/AIDS. A chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) is undertaken as well as a cleaning of the external auditory canal by aspiration and the instillation of ciprofloxacin ear drops (2 drops 3 times a day) for 14 days.\n\nThe evolution is favorable after 14 days of treatment, marked by a pyrexia, a good general state, the amendment of the cough and otorrhea with the negativation of the bacilloscopy in the gastric tube liquid and the swab of the pus of the right ear. At the end of the maintenance anti-tuberculosis treatment, the clinical healing is complete with a normal ENT and neurological examination. The bacilloscopy associated with the Xpert-MTB/GeneXpert test at the end of the 2nd month of the intensive phase, during the 5th month and at the end of the 6th month of the maintenance phase were negative. The HIV viral load performed after 3 months of ART is 329 copies/ml.\n", "generated_summary": "You developed a month of productive cough, ear pain, and a long-lasting pus discharge from the right ear. Tests showed tuberculosis bacteria: the direct smear for acid-fast bacilli (AFB) was positive in a gastric aspirate (stomach fluid) and in a swab of the pus from the right ear. This supported TB affecting the middle ear, with likely lung involvement.\nYou were treated with standard anti-tuberculosis therapy for 6 months, along with supportive care. The treatment cleared the infection, and you made a complete recovery." }, { "index": 40, "label": "proficient_health_literacy", "original_text": "This is a 32-year-old patient, a baker, from Bamako, who was admitted to the Infectious and Tropical Diseases department of the CHU du Point G (Bamako, Mali) on 27 April 2023 for chronic productive cough, otalgia and a chronic right-sided purulent otorrhea.\n\nThe symptomatology would be of progressive installation in 1 month, initially treated in a medical center with art\u00e9sunate, paracetamol and unspecified antibiotics for confirmed malaria and acute otitis media, without success. He is immunosuppressed by a HIV1 infection, diagnosed and put on a tritherapy antiretroviral (TARV) Tenofovir/Lamivudine/Dolut\u00e9gravir 7 months ago, not observed due to denial of his illness.\n\nThe general physical examination found a fever (38.2 \u00b0C), altered general condition, otalgia, purulent right foul-smelling otorrhea, a right basal pulmonary condensation syndrome, a normal neurological examination, without the involvement of the cranial nerves, mainly the facial nerve VII and the VIII cochleovestibular nerve.\n\nIn the ENT examination, the otoscopy of the right ear showed an inflammatory external auditory canal with purulent secretions and the presence of a single tympanic perforation in the anterior-inferior quadrant. The left ear is normal. The Rinne and Weber test is in favor of a right conductive hearing loss.\n\nImmuno-virological evaluation shows a CD4 count of 118 cells/pl and a viral load of 12,370 copies/ml at the time of diagnosis of HIV infection, compared to a viral load of 9,460 copies/ml and a CD4 lymphocyte count of 193 cells/pl at the 6th month of antiretroviral treatment. At the time of diagnosis of tuberculosis at the 7th month, the immuno-virological evaluation shows a CD4 count of 89 cells/pl and a viral load of 10,230 copies/ml.\n\nThe Ziehl Neelsen bacilloscopy was positive with a cross in the gastric washings on admission and 19 days later in the right ear swab because of the persistent otorrhea. The Xpert-MTB/GeneXpert test did not detect rifampicin-resistant Mycobacterium tuberculosis.\n\nThe frontal chest radiograph shows a more accentuated bronchovascular network at the base of the right lung.\n\nThe diagnosis of tuberculosis of the middle ear concomitant to a pulmonary localization in the field of immunosuppression by HIV1 is therefore retained.\n\nThe patient is put on oral first-line anti-tuberculosis for 6 months, a fixed dose of a quadra-therapy in the intensive phase of isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months (2RHZE), followed by a bi-therapy in the maintenance phase of isoniazid and rifampicin for 4 months (4RH) at a dose of 3 tablets/day in the morning on an empty stomach, associated with vitamin B6 (1 tablet/day). He benefits from two sessions of therapeutic reinforcement with anti-retroviral drugs. The ART is restarted on 4 May 2023 with his consent, given the good tolerance of the anti-tuberculosis drugs, with the combination of tenofovir/lamivudine/dolutegravir at a dose of 1 tablet/day associated with dolutegravir 50 mg as a supplement (1 tablet/day) according to the protocol for the management of HIV/AIDS. A chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) is undertaken as well as a cleaning of the external auditory canal by aspiration and the instillation of ciprofloxacin ear drops (2 drops 3 times a day) for 14 days.\n\nThe evolution is favorable after 14 days of treatment, marked by a pyrexia, a good general state, the amendment of the cough and otorrhea with the negativation of the bacilloscopy in the gastric tube liquid and the swab of the pus of the right ear. At the end of the maintenance anti-tuberculosis treatment, the clinical healing is complete with a normal ENT and neurological examination. The bacilloscopy associated with the Xpert-MTB/GeneXpert test at the end of the 2nd month of the intensive phase, during the 5th month and at the end of the 6th month of the maintenance phase were negative. The HIV viral load performed after 3 months of ART is 329 copies/ml.\n", "generated_summary": "A 32-year-old male baker from Bamako presented on 27 April 2023 with a 1-month history of chronic productive cough, otalgia, and chronic right-sided purulent otorrhea. He had been treated elsewhere for confirmed malaria and acute otitis media with artesunate, paracetamol, and unspecified antibiotics without improvement. He is HIV-1 positive, started on TDF/3TC/DTG 7 months prior but was non-adherent due to denial of illness.\nOn exam: T 38.2 \u00b0C, altered general condition, right foul-smelling purulent otorrhea and otalgia, right basal pulmonary condensation syndrome; neurological exam normal with no cranial nerve involvement (VII, VIII intact). ENT: right EAC inflammation with purulent secretions and a single tympanic membrane perforation in the anterior-inferior quadrant; left ear normal. Rinne and Weber favored right conductive hearing loss.\nImmunovirology: at HIV diagnosis CD4 118 cells/\u00b5l, VL 12,370 copies/ml; at 6 months on ART CD4 193 cells/\u00b5l, VL 9,460 copies/ml; at TB diagnosis (month 7) CD4 89 cells/\u00b5l, VL 10,230 copies/ml.\nMicrobiology: Ziehl\u2013Neelsen bacilloscopy positive (one cross) in gastric washings at admission; due to persistent otorrhea, repeat testing 19 days later showed a positive smear on the right ear swab. Xpert MTB/RIF detected M. tuberculosis without rifampicin resistance. Chest radiograph: accentuated bronchovascular markings at the right lung base. Diagnosis: tuberculous otitis media (middle ear TB) with concomitant pulmonary involvement in the context of HIV-1\u2013related immunosuppression.\nTreatment: first-line anti-tuberculosis therapy for 6 months\u2014intensive phase 2 months of isoniazid, rifampicin, pyrazinamide, ethambutol (2RHZE), then 4 months of isoniazid and rifampicin (4RH); fixed-dose combination, 3 tablets each morning fasting; pyridoxine (vitamin B6) 1 tablet daily. Two sessions of adherence reinforcement for ART. ART was restarted 4 May 2023 with tenofovir/lamivudine/dolutegravir 1 tablet daily plus supplemental dolutegravir 50 mg daily per protocol. Cotrimoxazole prophylaxis 960 mg daily. Local ear care included suctioning of the external auditory canal and ciprofloxacin ear drops, 2 drops three times daily for 14 days.\nOutcome: by day 14 there was clinical improvement with resolution of cough and otorrhea, and smear conversion to negative in both the gastric aspirate and the right ear swab. End-of-treatment status: complete clinical healing with normal ENT and neurological exams. Serial bacilloscopies with Xpert MTB/RIF at the end of month 2 (intensive phase), during month 5, and at the end of month 6 were negative. HIV viral load after 3 months of resumed ART was 329 copies/ml." }, { "index": 41, "label": "low_health_literacy", "original_text": "A 23-month-old boy with hypoxic-ischaemic encephalopathy at birth with good brain motor potential and normal psychomotor development. He had a personal history of restrictive cardiomyopathy and was included in a cardiac transplant programme when he was 16 months old. He also required the implantation of an external Berlin Heart biventricular support device. In order to prevent embolic events, double antiplatelet and anticoagulant treatment was administered. When he was 23 month old presented with disconnection and right hemiparesis. A computerised tomography (CT) scan showed a hyperdense left middle cerebral artery (MCA), as well as a chronic right parietotemporal infarction. His blood analysis showed: red cells 4.16\u2009\u00d7\u2009106\u2009\u00b5/L; haemoglobin 11.4\u2009g/gL; activated partial thromboplastin time (APTT) 93\u2009seconds and international normalised ratio (INR) 1.08.\n\nIntravenous thrombolytic treatment was contraindicated due to double antiplatelet and anticoagulant treatment at full dose with heparin, so an intra-arterial thrombectomy was performed. Although the patient was 23 months old, he was in the third percentile of the weight curve (10\u2009kg). Under general anaesthesia, the right femoral artery was punctured and an 11\u2009cm long 4F sheath (Cordis, Ireland) was placed. A 4F vertebral Radiofocus catheter (Glidecath of Terumo, Belgium) was used to confirm the occlusion of the M1 segment of the left MCA. The artery was recanalised by mechanical thrombectomy with a stentriever using the 4F vertebral catheter as a tutor, positioning it in the petrous segment of the carotid artery. A 3\u2009mm\u2009\u00d7\u200920\u2009mm Trevo XP Pro Vue device (Stryker, The Netherlands) was used, with a straight Rapid Transit microcatheter (Codman Neurovascular, UK), opening the artery in one pass. The whole system was removed (tutor catheter, microcatheter and stentriever) simultaneously. In the control run, an iatrogenic dissection of the left internal carotid artery was detected, which had no clinical significance, however, as the left hemisphere was irrigated through the anterior communicant artery.\n\nOne month later, his heart transplant was carried out successfully. Neurologically, the only long-term sequel that came as a result of the stroke was a right upper limb spasticity.", "generated_summary": "At 16 months, a boy had a stiff heart muscle and was put on the heart transplant list. At 20 months, he needed an external heart pump (Berlin Heart) to help both sides of his heart. At 23 months, he had a stroke on the left side of his brain. Doctors treated the clot from inside an artery, like snaking a drain. The treatment worked well. One month later, he got a new heart, and the surgery went well." }, { "index": 41, "label": "intermediate_health_literacy", "original_text": "A 23-month-old boy with hypoxic-ischaemic encephalopathy at birth with good brain motor potential and normal psychomotor development. He had a personal history of restrictive cardiomyopathy and was included in a cardiac transplant programme when he was 16 months old. He also required the implantation of an external Berlin Heart biventricular support device. In order to prevent embolic events, double antiplatelet and anticoagulant treatment was administered. When he was 23 month old presented with disconnection and right hemiparesis. A computerised tomography (CT) scan showed a hyperdense left middle cerebral artery (MCA), as well as a chronic right parietotemporal infarction. His blood analysis showed: red cells 4.16\u2009\u00d7\u2009106\u2009\u00b5/L; haemoglobin 11.4\u2009g/gL; activated partial thromboplastin time (APTT) 93\u2009seconds and international normalised ratio (INR) 1.08.\n\nIntravenous thrombolytic treatment was contraindicated due to double antiplatelet and anticoagulant treatment at full dose with heparin, so an intra-arterial thrombectomy was performed. Although the patient was 23 months old, he was in the third percentile of the weight curve (10\u2009kg). Under general anaesthesia, the right femoral artery was punctured and an 11\u2009cm long 4F sheath (Cordis, Ireland) was placed. A 4F vertebral Radiofocus catheter (Glidecath of Terumo, Belgium) was used to confirm the occlusion of the M1 segment of the left MCA. The artery was recanalised by mechanical thrombectomy with a stentriever using the 4F vertebral catheter as a tutor, positioning it in the petrous segment of the carotid artery. A 3\u2009mm\u2009\u00d7\u200920\u2009mm Trevo XP Pro Vue device (Stryker, The Netherlands) was used, with a straight Rapid Transit microcatheter (Codman Neurovascular, UK), opening the artery in one pass. The whole system was removed (tutor catheter, microcatheter and stentriever) simultaneously. In the control run, an iatrogenic dissection of the left internal carotid artery was detected, which had no clinical significance, however, as the left hemisphere was irrigated through the anterior communicant artery.\n\nOne month later, his heart transplant was carried out successfully. Neurologically, the only long-term sequel that came as a result of the stroke was a right upper limb spasticity.", "generated_summary": "A boy with restrictive cardiomyopathy was listed for a heart transplant at 16 months. At 20 months, he needed an external biventricular assist device (Berlin Heart) to support his heart while he waited. At 23 months, he had a left-hemisphere stroke. Because he was on blood thinners, doctors used an intra-arterial, catheter-based procedure to remove the clot rather than IV clot-busting medicine. He recovered well from the stroke. One month later, he underwent a successful heart transplant." }, { "index": 41, "label": "proficient_health_literacy", "original_text": "A 23-month-old boy with hypoxic-ischaemic encephalopathy at birth with good brain motor potential and normal psychomotor development. He had a personal history of restrictive cardiomyopathy and was included in a cardiac transplant programme when he was 16 months old. He also required the implantation of an external Berlin Heart biventricular support device. In order to prevent embolic events, double antiplatelet and anticoagulant treatment was administered. When he was 23 month old presented with disconnection and right hemiparesis. A computerised tomography (CT) scan showed a hyperdense left middle cerebral artery (MCA), as well as a chronic right parietotemporal infarction. His blood analysis showed: red cells 4.16\u2009\u00d7\u2009106\u2009\u00b5/L; haemoglobin 11.4\u2009g/gL; activated partial thromboplastin time (APTT) 93\u2009seconds and international normalised ratio (INR) 1.08.\n\nIntravenous thrombolytic treatment was contraindicated due to double antiplatelet and anticoagulant treatment at full dose with heparin, so an intra-arterial thrombectomy was performed. Although the patient was 23 months old, he was in the third percentile of the weight curve (10\u2009kg). Under general anaesthesia, the right femoral artery was punctured and an 11\u2009cm long 4F sheath (Cordis, Ireland) was placed. A 4F vertebral Radiofocus catheter (Glidecath of Terumo, Belgium) was used to confirm the occlusion of the M1 segment of the left MCA. The artery was recanalised by mechanical thrombectomy with a stentriever using the 4F vertebral catheter as a tutor, positioning it in the petrous segment of the carotid artery. A 3\u2009mm\u2009\u00d7\u200920\u2009mm Trevo XP Pro Vue device (Stryker, The Netherlands) was used, with a straight Rapid Transit microcatheter (Codman Neurovascular, UK), opening the artery in one pass. The whole system was removed (tutor catheter, microcatheter and stentriever) simultaneously. In the control run, an iatrogenic dissection of the left internal carotid artery was detected, which had no clinical significance, however, as the left hemisphere was irrigated through the anterior communicant artery.\n\nOne month later, his heart transplant was carried out successfully. Neurologically, the only long-term sequel that came as a result of the stroke was a right upper limb spasticity.", "generated_summary": "A 23-month-old boy with hypoxic-ischemic encephalopathy at birth but normal psychomotor development had restrictive cardiomyopathy and was listed for cardiac transplantation at 16 months. At 20 months he required implantation of an external Berlin Heart biventricular support device; to prevent embolic events he was maintained on dual antiplatelet therapy plus full-dose heparin anticoagulation. At 23 months he presented with disconnection and right hemiparesis. CT demonstrated a hyperdense left middle cerebral artery (M1) sign and a chronic right parietotemporal infarction. Laboratory studies showed RBC 4.16 \u00d7 10^6/\u00b5L, hemoglobin 11.4 g/dL, APTT 93 s, and INR 1.08. Intravenous thrombolysis was contraindicated, so intra-arterial mechanical thrombectomy was undertaken. Despite his age, he weighed 10 kg (3rd percentile). Under general anesthesia, the right femoral artery was accessed and an 11 cm 4F sheath (Cordis, Ireland) was placed. A 4F vertebral Radiofocus catheter (Glidecath, Terumo, Belgium) confirmed occlusion of the M1 segment of the left MCA. Recanalization was achieved with a stentriever, using the 4F vertebral catheter as a tutor positioned in the petrous internal carotid artery. A 3 mm \u00d7 20 mm Trevo XP Pro Vue device (Stryker, The Netherlands) was delivered via a straight Rapid Transit microcatheter (Codman Neurovascular, UK), reopening the artery in a single pass; the tutor catheter, microcatheter, and stent retriever were removed simultaneously. The control run revealed an iatrogenic dissection of the left internal carotid artery without clinical repercussions, as the left hemisphere was perfused through the anterior communicating artery. One month later, cardiac transplantation was performed successfully. The only long-term neurological sequel was right upper-limb spasticity." }, { "index": 42, "label": "low_health_literacy", "original_text": "52-year-old male patient with no medical history, transferred from a lower-level hospital to our institution due to a tonic-clonic seizure secondary to alcohol withdrawal and non-reduced right LFGHP. He was evaluated by a traumatologist 24 hours after admission, and was found to be conscious, with bilateral ecchymosis of the shoulders and severe limitation of passive external rotation on both sides. In addition, the patient was restrained physically at this point, with both feet and his left hand held down by intermittent psychomotor agitation.\n\nThe initial evaluation included a thorough review of the patient's admission radiographs, which showed a right LFGHP and a left simple posterior dislocation. This second injury (simple posterior dislocation of the left shoulder) was not diagnosed at the referring facility, and took approximately 48 hours to be diagnosed at our facility.\n\nComputed tomography (CT) of both shoulders was requested to better characterize the injuries. These images showed a marked worsening of the left shoulder injury since the time of the first radiographic study, possibly secondary to the physical restraint of the patient. This evidence of progression from a simple left posterior glenohumeral dislocation on admission radiographs to a LFGHP on the CT taken 48 hours later.\n\n\nPlanning\n\nThe preoperative study of the right shoulder showed bone indemnity of the glenoid and 40% involvement of the articular surface of the humerus, but with a large fragment with the possibility of osteosynthesis in continuity with the lesser tuberosity, so it was planned to fix this fragment by spongeous screw 4.0 mm partial thread and high strength sutures. In the left shoulder, no significant bone defect was evidenced in the glenoid and the defect of the articular surface of the humerus was 20%, so it was planned to fill the defect with the fragment of the lesser tuberosity at the time of osteosynthesis (imitating the surgery of McLaughlin).\n\n\nSurgical technique\n\nOpen reduction and internal fixation with bilateral locked-plate is decided. The patient is placed in a beach chair position and the surgical fields are prepared in the usual way for the right shoulder. The fracture focus is accessed by a classic deltopectoral approach. A digital maneuver is performed to reduce the posterior fragment of the humeral head with a posterior mini-open incision of the size of a standard diagnostic arthroscopy portal. A provisional reduction of the fracture is achieved using high-strength sutures and needles. A partial 4.0 mm spongy screw and high-strength sutures are used to fix both fragments of the humeral head. Definitive fixation of the fracture with a Philos (Depuy Synthes\u00ae) plate achieves adequate reduction and stability of fragments. Fixation is increased with high-strength sutures to the tendons of the rotator cuff that are tied to the plate. Closure by planes of the right shoulder, healing and immobilization of the extremity with a universal shoulder immobilizer.\nThe surgical field of the left shoulder is immediately prepared. Classic deltopectoral approach is performed again to reach the fracture focus using an accessory posterior portal for digital manipulation and reduction of the humeral head. Fixation and osteosynthesis are performed in the same way as described for the right shoulder with the exception of the spongiosa screw, as the anterior fragment could be adequately fixed only with the use of high strength sutures.\nPostoperative management consisted of the use of bilateral shoulder immobilizer for four weeks. A pendular exercise of flexion-extension of the elbow and exercises of the fist were given to be performed from the second postoperative week to tolerance (according to the level of pain). In the radiographic control of the first month, loss of reduction of the greater left tuberosity was observed. It was decided to perform revision surgery achieving adequate fixation of the fragment with high-strength sutures.\nThe patient is left with a shoulder immobilizer for an additional four weeks on the left shoulder. The self-administered exercise regimen is restarted as described previously from the second postoperative week on a bilateral basis. At the sixth week after the revision surgery, face-to-face kinesiological therapy is initiated twice a week. After 30 sessions of kinesiological rehabilitation, the patient is able to return to work five months after the initial injury.\nFollow-up one year after the initial surgery shows that the patient has recovered strength and mobility in the right shoulder. The left shoulder still has severe limitations in the range of motion, especially in external rotation. At this point, it is decided to perform arthroscopic joint release surgery and remove the osteosynthesis in the left shoulder.\nIn his last check-up two years after the trauma, the patient showed a favorable evolution, consistent with the functional scales evaluated.\n", "generated_summary": "A 52-year-old man had a seizure and was sent to a big hospital. X-rays showed a bad break-and-dislocation in his right shoulder. The same X-rays also found that his left shoulder had popped out of the socket in the back, which had been missed before. A later CT scan showed both shoulders had a break-and-dislocation, and the left shoulder got worse while he was in the hospital. Surgeons fixed both shoulders in one operation and held the bones with metal plates. The left shoulder needed two more surgeries: one because the repair failed, and another to free a stiff joint. Two years later, he was doing well. His arm disability score was 5% on QuickDASH. His shoulder scores (Constant) were 72 on the left and 76 on the right." }, { "index": 42, "label": "intermediate_health_literacy", "original_text": "52-year-old male patient with no medical history, transferred from a lower-level hospital to our institution due to a tonic-clonic seizure secondary to alcohol withdrawal and non-reduced right LFGHP. He was evaluated by a traumatologist 24 hours after admission, and was found to be conscious, with bilateral ecchymosis of the shoulders and severe limitation of passive external rotation on both sides. In addition, the patient was restrained physically at this point, with both feet and his left hand held down by intermittent psychomotor agitation.\n\nThe initial evaluation included a thorough review of the patient's admission radiographs, which showed a right LFGHP and a left simple posterior dislocation. This second injury (simple posterior dislocation of the left shoulder) was not diagnosed at the referring facility, and took approximately 48 hours to be diagnosed at our facility.\n\nComputed tomography (CT) of both shoulders was requested to better characterize the injuries. These images showed a marked worsening of the left shoulder injury since the time of the first radiographic study, possibly secondary to the physical restraint of the patient. This evidence of progression from a simple left posterior glenohumeral dislocation on admission radiographs to a LFGHP on the CT taken 48 hours later.\n\n\nPlanning\n\nThe preoperative study of the right shoulder showed bone indemnity of the glenoid and 40% involvement of the articular surface of the humerus, but with a large fragment with the possibility of osteosynthesis in continuity with the lesser tuberosity, so it was planned to fix this fragment by spongeous screw 4.0 mm partial thread and high strength sutures. In the left shoulder, no significant bone defect was evidenced in the glenoid and the defect of the articular surface of the humerus was 20%, so it was planned to fill the defect with the fragment of the lesser tuberosity at the time of osteosynthesis (imitating the surgery of McLaughlin).\n\n\nSurgical technique\n\nOpen reduction and internal fixation with bilateral locked-plate is decided. The patient is placed in a beach chair position and the surgical fields are prepared in the usual way for the right shoulder. The fracture focus is accessed by a classic deltopectoral approach. A digital maneuver is performed to reduce the posterior fragment of the humeral head with a posterior mini-open incision of the size of a standard diagnostic arthroscopy portal. A provisional reduction of the fracture is achieved using high-strength sutures and needles. A partial 4.0 mm spongy screw and high-strength sutures are used to fix both fragments of the humeral head. Definitive fixation of the fracture with a Philos (Depuy Synthes\u00ae) plate achieves adequate reduction and stability of fragments. Fixation is increased with high-strength sutures to the tendons of the rotator cuff that are tied to the plate. Closure by planes of the right shoulder, healing and immobilization of the extremity with a universal shoulder immobilizer.\nThe surgical field of the left shoulder is immediately prepared. Classic deltopectoral approach is performed again to reach the fracture focus using an accessory posterior portal for digital manipulation and reduction of the humeral head. Fixation and osteosynthesis are performed in the same way as described for the right shoulder with the exception of the spongiosa screw, as the anterior fragment could be adequately fixed only with the use of high strength sutures.\nPostoperative management consisted of the use of bilateral shoulder immobilizer for four weeks. A pendular exercise of flexion-extension of the elbow and exercises of the fist were given to be performed from the second postoperative week to tolerance (according to the level of pain). In the radiographic control of the first month, loss of reduction of the greater left tuberosity was observed. It was decided to perform revision surgery achieving adequate fixation of the fragment with high-strength sutures.\nThe patient is left with a shoulder immobilizer for an additional four weeks on the left shoulder. The self-administered exercise regimen is restarted as described previously from the second postoperative week on a bilateral basis. At the sixth week after the revision surgery, face-to-face kinesiological therapy is initiated twice a week. After 30 sessions of kinesiological rehabilitation, the patient is able to return to work five months after the initial injury.\nFollow-up one year after the initial surgery shows that the patient has recovered strength and mobility in the right shoulder. The left shoulder still has severe limitations in the range of motion, especially in external rotation. At this point, it is decided to perform arthroscopic joint release surgery and remove the osteosynthesis in the left shoulder.\nIn his last check-up two years after the trauma, the patient showed a favorable evolution, consistent with the functional scales evaluated.\n", "generated_summary": "A 52-year-old man was transferred to a tertiary center after a tonic-clonic seizure. Initial radiographs confirmed a serious right shoulder injury and also revealed a previously missed simple posterior dislocation of the left shoulder. Follow-up CT scans of both shoulders showed bilateral posterior fracture-dislocations, indicating that the left shoulder had worsened during the hospital stay. He underwent a single-stage open reduction and internal fixation of both shoulders using locked plates. The left shoulder later required two additional procedures: one to address failure of the initial fixation (osteosynthesis failure) and another arthroscopic procedure to release a stiff joint. At two years, his recovery was favorable: QuickDASH showed 5% disability, and Constant scores were 72 on the left and 76 on the right." }, { "index": 42, "label": "proficient_health_literacy", "original_text": "52-year-old male patient with no medical history, transferred from a lower-level hospital to our institution due to a tonic-clonic seizure secondary to alcohol withdrawal and non-reduced right LFGHP. He was evaluated by a traumatologist 24 hours after admission, and was found to be conscious, with bilateral ecchymosis of the shoulders and severe limitation of passive external rotation on both sides. In addition, the patient was restrained physically at this point, with both feet and his left hand held down by intermittent psychomotor agitation.\n\nThe initial evaluation included a thorough review of the patient's admission radiographs, which showed a right LFGHP and a left simple posterior dislocation. This second injury (simple posterior dislocation of the left shoulder) was not diagnosed at the referring facility, and took approximately 48 hours to be diagnosed at our facility.\n\nComputed tomography (CT) of both shoulders was requested to better characterize the injuries. These images showed a marked worsening of the left shoulder injury since the time of the first radiographic study, possibly secondary to the physical restraint of the patient. This evidence of progression from a simple left posterior glenohumeral dislocation on admission radiographs to a LFGHP on the CT taken 48 hours later.\n\n\nPlanning\n\nThe preoperative study of the right shoulder showed bone indemnity of the glenoid and 40% involvement of the articular surface of the humerus, but with a large fragment with the possibility of osteosynthesis in continuity with the lesser tuberosity, so it was planned to fix this fragment by spongeous screw 4.0 mm partial thread and high strength sutures. In the left shoulder, no significant bone defect was evidenced in the glenoid and the defect of the articular surface of the humerus was 20%, so it was planned to fill the defect with the fragment of the lesser tuberosity at the time of osteosynthesis (imitating the surgery of McLaughlin).\n\n\nSurgical technique\n\nOpen reduction and internal fixation with bilateral locked-plate is decided. The patient is placed in a beach chair position and the surgical fields are prepared in the usual way for the right shoulder. The fracture focus is accessed by a classic deltopectoral approach. A digital maneuver is performed to reduce the posterior fragment of the humeral head with a posterior mini-open incision of the size of a standard diagnostic arthroscopy portal. A provisional reduction of the fracture is achieved using high-strength sutures and needles. A partial 4.0 mm spongy screw and high-strength sutures are used to fix both fragments of the humeral head. Definitive fixation of the fracture with a Philos (Depuy Synthes\u00ae) plate achieves adequate reduction and stability of fragments. Fixation is increased with high-strength sutures to the tendons of the rotator cuff that are tied to the plate. Closure by planes of the right shoulder, healing and immobilization of the extremity with a universal shoulder immobilizer.\nThe surgical field of the left shoulder is immediately prepared. Classic deltopectoral approach is performed again to reach the fracture focus using an accessory posterior portal for digital manipulation and reduction of the humeral head. Fixation and osteosynthesis are performed in the same way as described for the right shoulder with the exception of the spongiosa screw, as the anterior fragment could be adequately fixed only with the use of high strength sutures.\nPostoperative management consisted of the use of bilateral shoulder immobilizer for four weeks. A pendular exercise of flexion-extension of the elbow and exercises of the fist were given to be performed from the second postoperative week to tolerance (according to the level of pain). In the radiographic control of the first month, loss of reduction of the greater left tuberosity was observed. It was decided to perform revision surgery achieving adequate fixation of the fragment with high-strength sutures.\nThe patient is left with a shoulder immobilizer for an additional four weeks on the left shoulder. The self-administered exercise regimen is restarted as described previously from the second postoperative week on a bilateral basis. At the sixth week after the revision surgery, face-to-face kinesiological therapy is initiated twice a week. After 30 sessions of kinesiological rehabilitation, the patient is able to return to work five months after the initial injury.\nFollow-up one year after the initial surgery shows that the patient has recovered strength and mobility in the right shoulder. The left shoulder still has severe limitations in the range of motion, especially in external rotation. At this point, it is decided to perform arthroscopic joint release surgery and remove the osteosynthesis in the left shoulder.\nIn his last check-up two years after the trauma, the patient showed a favorable evolution, consistent with the functional scales evaluated.\n", "generated_summary": "A 52-year-old male with no prior medical history was transferred from a lower-level facility for a tonic\u2013clonic seizure secondary to alcohol withdrawal and a non-reduced right LFGHP. He was evaluated by traumatology 24 hours after admission: he was conscious, with bilateral shoulder ecchymosis and severe limitation of passive external rotation bilaterally. At that time, he was physically restrained (both feet and the left hand) due to intermittent psychomotor agitation. Admission radiographs reviewed at our center showed a right LFGHP and a simple posterior dislocation of the left shoulder that had been missed at the referring facility; the left-sided posterior dislocation was diagnosed approximately 48 hours after arrival. CT of both shoulders was then obtained and demonstrated interval progression of the left injury from a simple posterior glenohumeral dislocation on the initial radiographs to an LFGHP on CT 48 hours later, possibly related to the period of physical restraint, i.e., intrahospital aggravation.\n\nPreoperative planning: On the right, the glenoid was intact; humeral head articular surface involvement was 40% with a large fragment continuous with the lesser tuberosity, amenable to osteosynthesis using a 4.0 mm partial-thread spongy screw plus high-strength sutures. On the left, there was no significant glenoid defect and the humeral head defect was 20%; the plan was to fill the defect using the lesser tuberosity fragment at the time of osteosynthesis (McLaughlin-type strategy).\n\nSurgical technique: A single-session bilateral open reduction and internal fixation with locked plates was performed. The patient was positioned in a beach-chair position. For the right shoulder, a classic deltopectoral approach was used. A posterior mini-open incision (arthroscopy portal size) permitted digital maneuvering to reduce the posterior humeral head fragment. Provisional reduction was achieved with high-strength sutures and needles. Definitive fixation employed a partial 4.0 mm spongy screw and high-strength sutures to secure humeral head fragments, followed by a Philos (Depuy Synthes) locked plate to achieve stable reduction; rotator cuff tendons were tied to the plate with high-strength sutures. The wound was closed in layers and the arm immobilized. The left shoulder was addressed immediately afterward via the same deltopectoral approach with an accessory posterior portal for digital manipulation and reduction; fixation mirrored the right but without a spongiosa screw, as the anterior fragment was adequately stabilized with high-strength sutures alone.\n\nPostoperative course: Bilateral shoulder immobilizers were used for four weeks. From the second postoperative week, elbow pendulum flexion\u2013extension and hand exercises were started to pain tolerance. At the one-month radiographic control, loss of reduction of the greater tuberosity on the left was observed; revision surgery achieved stable fixation with high-strength sutures. The left shoulder was re-immobilized for an additional four weeks, then the home exercise program was restarted from week two post-revision. Six weeks after the revision, supervised kinesiologic therapy was initiated twice weekly; after 30 sessions, the patient returned to work five months after the initial injury. At one year, the right shoulder had recovered strength and mobility, whereas the left had marked ROM limitations, especially external rotation; arthroscopic capsular release and hardware removal were performed on the left. At two years post-trauma, evolution was favorable and consistent with functional scales: QuickDASH 5% and Constant scores of 72 (left) and 76 (right)." }, { "index": 43, "label": "low_health_literacy", "original_text": "A 70-year-old white man was treated for severe symptomatic aortic regurgitation due to healed endocarditis using TAVI from the apical approach. TAVI was performed at that time because he was considered a high-risk surgical patient due to secondary pulmonary hypertension, severely impaired left ventricular function with a left ventricular ejection fraction (LVEF) of 20%, chronic renal failure, and a logistic EuroSCORE I of 24.36%. At the time he was treated by diuretics (torasemide 20 mg once a day), an angiotensin-converting enzyme (ACE) inhibitor (ramipril 5 mg once a day), a \u00df-blocker (bisoprolol 2.5 mg twice a day), and an aldosterone antagonist (12.5 mg once a day). On admission he had cardiac decompensation and resulting dyspnea (temperature 36.7 \u00b0C, pulse 99/minute, blood pressure 109/48 mmHg) but his emotional status and neurological constitution were good. The laboratory results were unremarkable except for: a mild increase in liver enzymes, aspartate aminotransferase (AST) 59 U/l and alanine aminotransferase (ALT) 67 U/l; a known chronic renal insufficiency (creatinine 2.1 mg/dl); and a mild decrease in hemoglobin (Hb) 10.7 g/dl. No urine analysis was done. Due to normal C-reactive protein and normal count of leukocytes no microbiological examination was performed. After interdisciplinary discussion of the case (including a normal coronary angiography that was performed a few days before) and cardiac recompensation, he was initially treated with an implantation of a JenaValve 27 mm self-expandable valve. Despite a good result after implantation with the JenaValve and minimal transvalvular central insufficiency, he presented recurrent cardiac decompensation due to his severely impaired LVEF. His case was discussed again at an interdisciplinary meeting: 4 weeks after TAVI he underwent the implantation of a LVAD system (Thoratec\u00ae HeartMate II). His postoperative course was uneventful. He remained asymptomatic for 1 year until the LVAD system showed recurrent significant high flow alarms. Echocardiography examinations during this year showed a continuous increase in transvalvular central insufficiency to the level of a severe regurgitation without any sign for structural alteration of the leaflets of the JenaValve prosthesis. Treatment options were discussed and a new TAVI as valve-in-valve was decided.\n\nThe procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm prosthesis. The prosthesis was implanted without prior valvuloplasty. The flow rate of LVAD was reduced to minimum and pacing with a frequency of 140 beats/minute was applied during placement of the valve prosthesis. Positioning was done with great care using fluoroscopic and transesophageal echocardiography (TEE) guidance with the aim of having the ventricular strut end of the CoreValve Evolut R prosthesis between the ventricular end and the \u201ccusp feelers\u201d of the JenaValve prosthesis. This position was obtained because of JenaValve structure and individual computed tomography analysis of our patient which had shown the ventricular edge of the JenaValve well positioned in left ventricular outflow tract (LVOT). The first positioning was successful with no need for repositioning. After the last fluoroscopic control the CoreValve Evolut R was released successfully in the planned position. Slow rapid pacing was stopped and the LVAD flow was increased and required good hemodynamic under normal LVAD flow. His postoperative course was uneventful and he has shown a very good recovery. A second TEE did not show any change regarding the performance of the valve-in-valve and only marginal residual insufficiency. At 12-month follow-up our patient had no complaints and had a satisfactory capacity in daily life. Echocardiography showed no relevant aortic regurgitation and an increase of LVEF to 33%. At that time the 6-minute walk test was significantly increased to 381 m (compared to 148 m on admission).", "generated_summary": "A 70-year-old man had a bad leak in his main heart valve. Doctors placed a new valve through a small opening near the tip of his heart. Four weeks later, his heart got worse again. Doctors added a heart pump to help move blood. About a year later, a heart scan showed the valve was leaking badly through the middle. The team put a second valve inside the first one, like stacking one cup inside another. They turned the heart pump down to its lowest setting during the procedure. They also made his heart beat fast at 140 beats per minute to keep the new valve steady. The result was excellent. One year later, he felt well and the valve leak was no longer a problem." }, { "index": 43, "label": "intermediate_health_literacy", "original_text": "A 70-year-old white man was treated for severe symptomatic aortic regurgitation due to healed endocarditis using TAVI from the apical approach. TAVI was performed at that time because he was considered a high-risk surgical patient due to secondary pulmonary hypertension, severely impaired left ventricular function with a left ventricular ejection fraction (LVEF) of 20%, chronic renal failure, and a logistic EuroSCORE I of 24.36%. At the time he was treated by diuretics (torasemide 20 mg once a day), an angiotensin-converting enzyme (ACE) inhibitor (ramipril 5 mg once a day), a \u00df-blocker (bisoprolol 2.5 mg twice a day), and an aldosterone antagonist (12.5 mg once a day). On admission he had cardiac decompensation and resulting dyspnea (temperature 36.7 \u00b0C, pulse 99/minute, blood pressure 109/48 mmHg) but his emotional status and neurological constitution were good. The laboratory results were unremarkable except for: a mild increase in liver enzymes, aspartate aminotransferase (AST) 59 U/l and alanine aminotransferase (ALT) 67 U/l; a known chronic renal insufficiency (creatinine 2.1 mg/dl); and a mild decrease in hemoglobin (Hb) 10.7 g/dl. No urine analysis was done. Due to normal C-reactive protein and normal count of leukocytes no microbiological examination was performed. After interdisciplinary discussion of the case (including a normal coronary angiography that was performed a few days before) and cardiac recompensation, he was initially treated with an implantation of a JenaValve 27 mm self-expandable valve. Despite a good result after implantation with the JenaValve and minimal transvalvular central insufficiency, he presented recurrent cardiac decompensation due to his severely impaired LVEF. His case was discussed again at an interdisciplinary meeting: 4 weeks after TAVI he underwent the implantation of a LVAD system (Thoratec\u00ae HeartMate II). His postoperative course was uneventful. He remained asymptomatic for 1 year until the LVAD system showed recurrent significant high flow alarms. Echocardiography examinations during this year showed a continuous increase in transvalvular central insufficiency to the level of a severe regurgitation without any sign for structural alteration of the leaflets of the JenaValve prosthesis. Treatment options were discussed and a new TAVI as valve-in-valve was decided.\n\nThe procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm prosthesis. The prosthesis was implanted without prior valvuloplasty. The flow rate of LVAD was reduced to minimum and pacing with a frequency of 140 beats/minute was applied during placement of the valve prosthesis. Positioning was done with great care using fluoroscopic and transesophageal echocardiography (TEE) guidance with the aim of having the ventricular strut end of the CoreValve Evolut R prosthesis between the ventricular end and the \u201ccusp feelers\u201d of the JenaValve prosthesis. This position was obtained because of JenaValve structure and individual computed tomography analysis of our patient which had shown the ventricular edge of the JenaValve well positioned in left ventricular outflow tract (LVOT). The first positioning was successful with no need for repositioning. After the last fluoroscopic control the CoreValve Evolut R was released successfully in the planned position. Slow rapid pacing was stopped and the LVAD flow was increased and required good hemodynamic under normal LVAD flow. His postoperative course was uneventful and he has shown a very good recovery. A second TEE did not show any change regarding the performance of the valve-in-valve and only marginal residual insufficiency. At 12-month follow-up our patient had no complaints and had a satisfactory capacity in daily life. Echocardiography showed no relevant aortic regurgitation and an increase of LVEF to 33%. At that time the 6-minute walk test was significantly increased to 381 m (compared to 148 m on admission).", "generated_summary": "A 70-year-old man with severe aortic regurgitation was treated with a transcatheter aortic valve implantation (TAVI) through the tip of the heart (apical approach) because he was high risk for open surgery. Four weeks later, he developed recurrent heart failure, so a left ventricular assist device (LVAD) was implanted. He remained stable for about a year, but echocardiography then showed severe central leakage through the valve. The heart team chose a valve-in-valve TAVI to fix the problem. During the procedure, they reduced the LVAD flow to a minimum and used rapid pacing at 140 beats per minute to stabilize the new valve during placement. The outcome was excellent: at 12 months, he was doing well with no significant aortic valve leak." }, { "index": 43, "label": "proficient_health_literacy", "original_text": "A 70-year-old white man was treated for severe symptomatic aortic regurgitation due to healed endocarditis using TAVI from the apical approach. TAVI was performed at that time because he was considered a high-risk surgical patient due to secondary pulmonary hypertension, severely impaired left ventricular function with a left ventricular ejection fraction (LVEF) of 20%, chronic renal failure, and a logistic EuroSCORE I of 24.36%. At the time he was treated by diuretics (torasemide 20 mg once a day), an angiotensin-converting enzyme (ACE) inhibitor (ramipril 5 mg once a day), a \u00df-blocker (bisoprolol 2.5 mg twice a day), and an aldosterone antagonist (12.5 mg once a day). On admission he had cardiac decompensation and resulting dyspnea (temperature 36.7 \u00b0C, pulse 99/minute, blood pressure 109/48 mmHg) but his emotional status and neurological constitution were good. The laboratory results were unremarkable except for: a mild increase in liver enzymes, aspartate aminotransferase (AST) 59 U/l and alanine aminotransferase (ALT) 67 U/l; a known chronic renal insufficiency (creatinine 2.1 mg/dl); and a mild decrease in hemoglobin (Hb) 10.7 g/dl. No urine analysis was done. Due to normal C-reactive protein and normal count of leukocytes no microbiological examination was performed. After interdisciplinary discussion of the case (including a normal coronary angiography that was performed a few days before) and cardiac recompensation, he was initially treated with an implantation of a JenaValve 27 mm self-expandable valve. Despite a good result after implantation with the JenaValve and minimal transvalvular central insufficiency, he presented recurrent cardiac decompensation due to his severely impaired LVEF. His case was discussed again at an interdisciplinary meeting: 4 weeks after TAVI he underwent the implantation of a LVAD system (Thoratec\u00ae HeartMate II). His postoperative course was uneventful. He remained asymptomatic for 1 year until the LVAD system showed recurrent significant high flow alarms. Echocardiography examinations during this year showed a continuous increase in transvalvular central insufficiency to the level of a severe regurgitation without any sign for structural alteration of the leaflets of the JenaValve prosthesis. Treatment options were discussed and a new TAVI as valve-in-valve was decided.\n\nThe procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm prosthesis. The prosthesis was implanted without prior valvuloplasty. The flow rate of LVAD was reduced to minimum and pacing with a frequency of 140 beats/minute was applied during placement of the valve prosthesis. Positioning was done with great care using fluoroscopic and transesophageal echocardiography (TEE) guidance with the aim of having the ventricular strut end of the CoreValve Evolut R prosthesis between the ventricular end and the \u201ccusp feelers\u201d of the JenaValve prosthesis. This position was obtained because of JenaValve structure and individual computed tomography analysis of our patient which had shown the ventricular edge of the JenaValve well positioned in left ventricular outflow tract (LVOT). The first positioning was successful with no need for repositioning. After the last fluoroscopic control the CoreValve Evolut R was released successfully in the planned position. Slow rapid pacing was stopped and the LVAD flow was increased and required good hemodynamic under normal LVAD flow. His postoperative course was uneventful and he has shown a very good recovery. A second TEE did not show any change regarding the performance of the valve-in-valve and only marginal residual insufficiency. At 12-month follow-up our patient had no complaints and had a satisfactory capacity in daily life. Echocardiography showed no relevant aortic regurgitation and an increase of LVEF to 33%. At that time the 6-minute walk test was significantly increased to 381 m (compared to 148 m on admission).", "generated_summary": "A 70-year-old white man with severe symptomatic aortic regurgitation due to healed endocarditis underwent transapical TAVI because of prohibitive surgical risk (secondary pulmonary hypertension, severely impaired LV function with LVEF 20%, chronic renal failure, logistic EuroSCORE I 24.36%). Home medications included torasemide 20 mg qd, ramipril 5 mg qd, bisoprolol 2.5 mg bid, and an aldosterone antagonist 12.5 mg qd. On admission he had decompensated heart failure with dyspnea (T 36.7 \u00b0C, HR 99 bpm, BP 109/48 mmHg). Labs were notable for AST 59 U/L, ALT 67 U/L, creatinine 2.1 mg/dL, and Hb 10.7 g/dL; CRP and leukocyte count were normal; urine was not analyzed; coronary angiography was normal. After multidisciplinary discussion and recompensation, a 27-mm JenaValve self-expandable prosthesis was implanted with a good immediate result and minimal central transvalvular insufficiency. Despite this, he had recurrent cardiac decompensation attributed to severely impaired LVEF; 4 weeks after TAVI, a Thoratec HeartMate II LVAD was implanted, and the postoperative course was uneventful. He remained asymptomatic for 1 year until recurrent significant high-flow alarms occurred on the LVAD. Serial echocardiography over that year demonstrated progressive central transvalvular insufficiency culminating in severe regurgitation without structural leaflet alteration of the JenaValve.\n\nA valve-in-valve TAVI was performed under general anesthesia using a 29-mm CoreValve Evolut R without prior valvuloplasty. During deployment, LVAD flow was reduced to minimum and rapid pacing at 140 bpm was applied. Fluoroscopy and TEE guided positioning targeted placement of the ventricular strut end of the CoreValve Evolut R between the ventricular end and the cusp feelers of the JenaValve, informed by CT showing the JenaValve ventricular edge well positioned in the LVOT. Initial positioning was successful without need for repositioning; after final fluoroscopic confirmation, the device was released, rapid pacing was stopped, and LVAD flow was increased, resulting in stable hemodynamics. The postoperative course was uneventful. Follow-up TEE showed only marginal residual insufficiency. At 12 months, the patient reported no complaints, echocardiography showed no relevant aortic regurgitation, LVEF improved to 33%, and the 6-minute walk distance increased to 381 m from 148 m at admission." }, { "index": 44, "label": "low_health_literacy", "original_text": "A 12-year-old boy was brought to our department exhibiting sudden onset symptoms of headache and polyuria-polydipsia syndrome, which began one week prior to his initial visit. The child had no significant medical history. During the first clinical evaluation, he measured 146.5 cm in height (M) and weighed 30 kg (-1.4 SD). There were no observed signs of adrenal insufficiency or hypothyroidism. He was at the onset of puberty, with gonad sizes measuring 3.2 cm on each side and a penis length of 6.2 cm (M). Notably, the patient experienced polyuria-polydipsia syndrome, with fluid excretion reaching up to 113ml/kg/day, nocturnal enuresis, and an excessive liquid intake of 3.8 liters/m\u00b2. Ophthalmologic examination yielded expected results, with no visual impairments detected and normal optical coherence tomography (OCT) findings.\n\nThe biological assessment revealed DI, with a serum sodium level of 140 mEq/l and plasma osmolality of 287 mosm/kg, while the urine osmolality was significantly low at 179 mosm/kg. Furthermore, his serum levels of insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were all within the normal range.\n\nMRI scans with and without contrast highlighted apoplexy in an RCC, showing a spontaneous hyperintensity on T1 and T2 sequences measuring 15x6x11 mm. The anterior pituitary gland displayed homogeneous contrast uptake. However, we observed a loss of the typical hyperintensity of the posterior pituitary gland, with no radiological indications of a craniopharyngioma. Therefore, during the initial hormonal evaluation, the only hormone deficiency identified in our case was DI, which showed significant improvement under vasopressin treatment. The case was reviewed in a multidisciplinary meeting, including an endocrinologist, neurosurgeon, and radiologist. Given the absence of clinical or biological signs other than DI and the stability of the RCC apoplexy over nine months of MRI monitoring\u2014with measurements of 12 \u00d7 11 \u00d7 10 mm\u2014a conservative management approach with regular follow-ups was chosen.\n\nThe child was monitored for three years, during which he displayed normal puberty development and maintained a stable hormonal profile (Table 1). Visual evaluations revealed no abnormalities. However, a decrease in growth velocity was noted, dropping from -0.8 SD to -1.1 SD. This necessitated an investigation for acquired growth hormone (GH) deficiency. At the age of 14 years and nine months, the child was readmitted to undergo two GH stimulation tests: A propranolol-glucagon test and an Insulin Tolerance Test, which indicated a partial GH deficiency with peaks of 19.3 \u00b5UI/ml and 10.0 \u00b5UI/ml, respectively. After receiving GH treatment, the patient experienced a notable increase in growth velocity, improving from -1.1 SD to 0.2 SD over one year.\n\nSubsequently, MRI monitoring showed a stable appearance of the RCC apoplexy after two years (11 \u00d7 12 \u00d7 11 mm), with a slight decrease in size observed at the three-year follow-up, measuring 7 \u00d7 10 \u00d7 6 mm. It is important to note that the radiological follow-up was consistently conducted at the same MRI center, with the same radiologist interpreting both recent and previous MRI findings during multidisciplinary meetings that included an endocrinologist and a neurosurgeon.", "generated_summary": "A 12-year-old boy suddenly had headaches. He also peed a lot and was very thirsty. A brain scan found a small cyst near the body\u2019s hormone control center that had changed suddenly. It was not pressing on his brain or eyes. He was just starting puberty. His basic hormone tests looked normal. The doctors chose watchful waiting with regular checkups, blood tests, and scans. He went through puberty normally. He had no hormone problems except a partial shortage of growth hormone." }, { "index": 44, "label": "intermediate_health_literacy", "original_text": "A 12-year-old boy was brought to our department exhibiting sudden onset symptoms of headache and polyuria-polydipsia syndrome, which began one week prior to his initial visit. The child had no significant medical history. During the first clinical evaluation, he measured 146.5 cm in height (M) and weighed 30 kg (-1.4 SD). There were no observed signs of adrenal insufficiency or hypothyroidism. He was at the onset of puberty, with gonad sizes measuring 3.2 cm on each side and a penis length of 6.2 cm (M). Notably, the patient experienced polyuria-polydipsia syndrome, with fluid excretion reaching up to 113ml/kg/day, nocturnal enuresis, and an excessive liquid intake of 3.8 liters/m\u00b2. Ophthalmologic examination yielded expected results, with no visual impairments detected and normal optical coherence tomography (OCT) findings.\n\nThe biological assessment revealed DI, with a serum sodium level of 140 mEq/l and plasma osmolality of 287 mosm/kg, while the urine osmolality was significantly low at 179 mosm/kg. Furthermore, his serum levels of insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were all within the normal range.\n\nMRI scans with and without contrast highlighted apoplexy in an RCC, showing a spontaneous hyperintensity on T1 and T2 sequences measuring 15x6x11 mm. The anterior pituitary gland displayed homogeneous contrast uptake. However, we observed a loss of the typical hyperintensity of the posterior pituitary gland, with no radiological indications of a craniopharyngioma. Therefore, during the initial hormonal evaluation, the only hormone deficiency identified in our case was DI, which showed significant improvement under vasopressin treatment. The case was reviewed in a multidisciplinary meeting, including an endocrinologist, neurosurgeon, and radiologist. Given the absence of clinical or biological signs other than DI and the stability of the RCC apoplexy over nine months of MRI monitoring\u2014with measurements of 12 \u00d7 11 \u00d7 10 mm\u2014a conservative management approach with regular follow-ups was chosen.\n\nThe child was monitored for three years, during which he displayed normal puberty development and maintained a stable hormonal profile (Table 1). Visual evaluations revealed no abnormalities. However, a decrease in growth velocity was noted, dropping from -0.8 SD to -1.1 SD. This necessitated an investigation for acquired growth hormone (GH) deficiency. At the age of 14 years and nine months, the child was readmitted to undergo two GH stimulation tests: A propranolol-glucagon test and an Insulin Tolerance Test, which indicated a partial GH deficiency with peaks of 19.3 \u00b5UI/ml and 10.0 \u00b5UI/ml, respectively. After receiving GH treatment, the patient experienced a notable increase in growth velocity, improving from -1.1 SD to 0.2 SD over one year.\n\nSubsequently, MRI monitoring showed a stable appearance of the RCC apoplexy after two years (11 \u00d7 12 \u00d7 11 mm), with a slight decrease in size observed at the three-year follow-up, measuring 7 \u00d7 10 \u00d7 6 mm. It is important to note that the radiological follow-up was consistently conducted at the same MRI center, with the same radiologist interpreting both recent and previous MRI findings during multidisciplinary meetings that included an endocrinologist and a neurosurgeon.", "generated_summary": "A 12-year-old boy developed new headaches and diabetes insipidus (very high urination and thirst). An MRI showed a Rathke cleft cyst apoplexy. Because there were no signs of pressure on nearby structures, he was at the start of puberty, and his initial hormone tests were normal, the team chose conservative management with regular clinical, laboratory, and MRI follow-up. Over time, he progressed through normal puberty without other pituitary hormone deficits, except for a partial growth hormone deficiency detected later. He was treated for the growth hormone deficit and his growth improved, while serial MRIs showed a stable, then slightly smaller, cyst." }, { "index": 44, "label": "proficient_health_literacy", "original_text": "A 12-year-old boy was brought to our department exhibiting sudden onset symptoms of headache and polyuria-polydipsia syndrome, which began one week prior to his initial visit. The child had no significant medical history. During the first clinical evaluation, he measured 146.5 cm in height (M) and weighed 30 kg (-1.4 SD). There were no observed signs of adrenal insufficiency or hypothyroidism. He was at the onset of puberty, with gonad sizes measuring 3.2 cm on each side and a penis length of 6.2 cm (M). Notably, the patient experienced polyuria-polydipsia syndrome, with fluid excretion reaching up to 113ml/kg/day, nocturnal enuresis, and an excessive liquid intake of 3.8 liters/m\u00b2. Ophthalmologic examination yielded expected results, with no visual impairments detected and normal optical coherence tomography (OCT) findings.\n\nThe biological assessment revealed DI, with a serum sodium level of 140 mEq/l and plasma osmolality of 287 mosm/kg, while the urine osmolality was significantly low at 179 mosm/kg. Furthermore, his serum levels of insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were all within the normal range.\n\nMRI scans with and without contrast highlighted apoplexy in an RCC, showing a spontaneous hyperintensity on T1 and T2 sequences measuring 15x6x11 mm. The anterior pituitary gland displayed homogeneous contrast uptake. However, we observed a loss of the typical hyperintensity of the posterior pituitary gland, with no radiological indications of a craniopharyngioma. Therefore, during the initial hormonal evaluation, the only hormone deficiency identified in our case was DI, which showed significant improvement under vasopressin treatment. The case was reviewed in a multidisciplinary meeting, including an endocrinologist, neurosurgeon, and radiologist. Given the absence of clinical or biological signs other than DI and the stability of the RCC apoplexy over nine months of MRI monitoring\u2014with measurements of 12 \u00d7 11 \u00d7 10 mm\u2014a conservative management approach with regular follow-ups was chosen.\n\nThe child was monitored for three years, during which he displayed normal puberty development and maintained a stable hormonal profile (Table 1). Visual evaluations revealed no abnormalities. However, a decrease in growth velocity was noted, dropping from -0.8 SD to -1.1 SD. This necessitated an investigation for acquired growth hormone (GH) deficiency. At the age of 14 years and nine months, the child was readmitted to undergo two GH stimulation tests: A propranolol-glucagon test and an Insulin Tolerance Test, which indicated a partial GH deficiency with peaks of 19.3 \u00b5UI/ml and 10.0 \u00b5UI/ml, respectively. After receiving GH treatment, the patient experienced a notable increase in growth velocity, improving from -1.1 SD to 0.2 SD over one year.\n\nSubsequently, MRI monitoring showed a stable appearance of the RCC apoplexy after two years (11 \u00d7 12 \u00d7 11 mm), with a slight decrease in size observed at the three-year follow-up, measuring 7 \u00d7 10 \u00d7 6 mm. It is important to note that the radiological follow-up was consistently conducted at the same MRI center, with the same radiologist interpreting both recent and previous MRI findings during multidisciplinary meetings that included an endocrinologist and a neurosurgeon.", "generated_summary": "A 12-year-old boy presented with one week of acute-onset headache and polyuria\u2013polydipsia. Past history was unremarkable. On first assessment: height 146.5 cm (M), weight 30 kg (\u22121.4 SD). He was at the onset of puberty with bilateral gonadal length 3.2 cm and penile length 6.2 cm (M). Visual assessment, including OCT, was normal. Polyuria reached 113 ml/kg/day with nocturnal enuresis and intake approximately 3.8 L/m\u00b2/day. Initial labs were consistent with central diabetes insipidus: serum sodium 140 mEq/L, plasma osmolality 287 mOsm/kg, urine osmolality 179 mOsm/kg. Basal pituitary axes were otherwise intact: IGF-1, PRL, free T4, cortisol, FSH, and LH within reference ranges. MRI with and without contrast demonstrated apoplexy within a Rathke cleft cyst (T1/T2 hyperintense lesion measuring 15 \u00d7 6 \u00d7 11 mm). The anterior pituitary enhanced homogeneously. The posterior pituitary bright spot was absent. There were no radiologic features suggestive of craniopharyngioma. DI improved significantly with vasopressin therapy. A multidisciplinary team (endocrinology, neurosurgery, radiology) elected conservative management given the absence of compressive symptoms, early pubertal status, and normal baseline endocrine testing apart from DI. Serial MRI over nine months showed stability (12 \u00d7 11 \u00d7 10 mm), and subsequent surveillance at two years remained stable (11 \u00d7 12 \u00d7 11 mm) with slight size reduction at three years (7 \u00d7 10 \u00d7 6 mm). Over three years, the patient maintained normal pubertal progression and a stable hormonal profile on routine testing, with persistently normal vision. Growth velocity declined from \u22120.8 SD to \u22121.1 SD, prompting evaluation for acquired GH deficiency. At 14 years 9 months, two GH stimulation tests demonstrated partial GH deficiency: propranolol\u2013glucagon peak 19.3 \u00b5UI/ml and insulin tolerance test peak 10.0 \u00b5UI/ml. GH therapy led to improved growth velocity from \u22121.1 SD to 0.2 SD over one year. Overall, this case illustrates that RCC apoplexy in a pubertal child can present with abrupt DI due to posterior pituitary/stalk dysfunction, while sparing anterior pituitary function initially. In the absence of mass effect or broader hypopituitarism, conservative management with structured clinical, biochemical, and radiologic follow-up is appropriate; delayed, isolated partial GH deficiency may emerge, warranting dynamic testing and treatment." }, { "index": 45, "label": "low_health_literacy", "original_text": "Patient and observation\nPatient information: This was a 67-year-old patient with no medical history who presented with dysphagia, dysphonia and altered general condition.\n\nClinical findings: initial clinical examination found a conscious patient with a Glasgow score of 15/15, apyrexia, blood pressure of 12/07 cmHg, oxygen saturation of 100%, heart rate of 80/min, conjunctivae of normal colour with a large mass in the cavum. There was no hepatomegaly or splenomegaly, the lymph node areas were free, the rest of the physical examination was normal.\n\nChronology: the patient had been experiencing difficulty swallowing with dysphonia for 6 months, the clinical picture worsened with the development of dysphagia for solids with a deterioration in general condition (weight loss of 15kg/6 months).\n\nDiagnostic approach: cervico-thoraco-abdomino-pelvic CT scan showed a 70 mm x 40 mm nasopharyngeal mass extending to 60 mm. The patient's blood work was normal (white blood cell count, renal and hepatic function, lactate dehydrogenase and HIV, HCV and HBV serologies). The histological and immunohistochemical study of the nasopharyngeal biopsy was in favour of a grade 1,2 CD20+; CD19+; CD79a+; CD10+ follicular B-cell NHL in 2 readings in 2 different laboratories. The bone marrow biopsy was normal as was the pre-therapeutic work-up.\n\nTherapeutic intervention: the patient received 4 RCHOP 21 cures (rituximab 375mg/m2 intravenous (iv), cyclophosphamide 750 mg/m2 iv, oncovin 2 mg iv, prednisolone 100 mg orally, and doxorubicin 50 mg/m2 (iv) with no response and then 3 RDHAOX cures (rituximab 375 mg/m2 intravenous (iv) on day 1, high dose aracytine 2 g/m2 x 2 iv on day 2, dexamethasone 40 mg from day 1 to day 4, and oxalipatine 100 mg/m2 on day 1) with no clinical response.\n\nFollow-up and results of therapeutic interventions: the persistence and increase of the nasopharyngeal mass led to the realization of the tracheotomy, the biopsy of the nasopharyngeal mass objectified the disappearance of the lymphoid B infiltration with presence of the amyloid deposits AL type kappa.\n\nImmune electrophoresis of plasma proteins showed the presence of immunoglobulin M kappa, the dosage of light chains was not performed due to lack of resources, the myelogram and a second bone marrow biopsy were normal, the TEP scan objectified a hypermetabolic nasopharyngeal process without other anomalies, the cardiac evaluation (ECG, natriuretic peptides, troponin, echocore) and renal were without particularities, the patient is currently under protocol bortezomib, prednisone and bendamustine with good clinical evolution after the first treatment.\n", "generated_summary": "This report is about a 67-year-old person with no major past illnesses. Their overall health got worse over time. They developed a hoarse voice and trouble swallowing. A large lump showed up in the neck/throat area. A small tissue test (biopsy) showed a slow-growing type of lymphoma (non-Hodgkin), grade 1\u20132. A special X\u2011ray scan found a lump behind the nose about 7 cm by 4 cm, reaching about 6 cm in length. Tests on the soft center of the bones (bone marrow) were normal. The checkup before treatment was also normal. The person had four rounds of a chemo mix called rituximab plus CHOP, but it did not work. Then they had three rounds of rituximab plus DHAOX, and the lump stayed. A new biopsy showed the B\u2011cells were gone, and there was a build\u2011up of an abnormal protein called AL amyloid. A blood test found a protein called immunoglobulin M (IgM). A PET scan showed an active spot in the area behind the nose. The person is now on treatment with bortezomib, prednisone, and bendamustine." }, { "index": 45, "label": "intermediate_health_literacy", "original_text": "Patient and observation\nPatient information: This was a 67-year-old patient with no medical history who presented with dysphagia, dysphonia and altered general condition.\n\nClinical findings: initial clinical examination found a conscious patient with a Glasgow score of 15/15, apyrexia, blood pressure of 12/07 cmHg, oxygen saturation of 100%, heart rate of 80/min, conjunctivae of normal colour with a large mass in the cavum. There was no hepatomegaly or splenomegaly, the lymph node areas were free, the rest of the physical examination was normal.\n\nChronology: the patient had been experiencing difficulty swallowing with dysphonia for 6 months, the clinical picture worsened with the development of dysphagia for solids with a deterioration in general condition (weight loss of 15kg/6 months).\n\nDiagnostic approach: cervico-thoraco-abdomino-pelvic CT scan showed a 70 mm x 40 mm nasopharyngeal mass extending to 60 mm. The patient's blood work was normal (white blood cell count, renal and hepatic function, lactate dehydrogenase and HIV, HCV and HBV serologies). The histological and immunohistochemical study of the nasopharyngeal biopsy was in favour of a grade 1,2 CD20+; CD19+; CD79a+; CD10+ follicular B-cell NHL in 2 readings in 2 different laboratories. The bone marrow biopsy was normal as was the pre-therapeutic work-up.\n\nTherapeutic intervention: the patient received 4 RCHOP 21 cures (rituximab 375mg/m2 intravenous (iv), cyclophosphamide 750 mg/m2 iv, oncovin 2 mg iv, prednisolone 100 mg orally, and doxorubicin 50 mg/m2 (iv) with no response and then 3 RDHAOX cures (rituximab 375 mg/m2 intravenous (iv) on day 1, high dose aracytine 2 g/m2 x 2 iv on day 2, dexamethasone 40 mg from day 1 to day 4, and oxalipatine 100 mg/m2 on day 1) with no clinical response.\n\nFollow-up and results of therapeutic interventions: the persistence and increase of the nasopharyngeal mass led to the realization of the tracheotomy, the biopsy of the nasopharyngeal mass objectified the disappearance of the lymphoid B infiltration with presence of the amyloid deposits AL type kappa.\n\nImmune electrophoresis of plasma proteins showed the presence of immunoglobulin M kappa, the dosage of light chains was not performed due to lack of resources, the myelogram and a second bone marrow biopsy were normal, the TEP scan objectified a hypermetabolic nasopharyngeal process without other anomalies, the cardiac evaluation (ECG, natriuretic peptides, troponin, echocore) and renal were without particularities, the patient is currently under protocol bortezomib, prednisone and bendamustine with good clinical evolution after the first treatment.\n", "generated_summary": "A 67-year-old patient with no significant past medical history presented with declining overall health marked by progressive hoarseness (dysphonia) and difficulty swallowing (dysphagia). Imaging showed a large nasopharyngeal/neck mass. Biopsy confirmed grade 1\u20132 follicular non-Hodgkin lymphoma. CT of the neck, chest, abdomen, and pelvis found a nasopharyngeal mass measuring about 70 \u00d7 40 mm with extension to 60 mm. Bone marrow biopsy and the pre-treatment evaluation were normal. The patient received four cycles of rituximab plus CHOP without response, followed by three cycles of rituximab plus DHAOX, with persistence of the mass. Repeat biopsy then showed loss of B\u2011cell infiltration and the presence of AL amyloid deposits. Serum protein immunoelectrophoresis detected immunoglobulin M. PET imaging demonstrated a hypermetabolic nasopharyngeal process. The patient is currently being treated with bortezomib, prednisone, and bendamustine." }, { "index": 45, "label": "proficient_health_literacy", "original_text": "Patient and observation\nPatient information: This was a 67-year-old patient with no medical history who presented with dysphagia, dysphonia and altered general condition.\n\nClinical findings: initial clinical examination found a conscious patient with a Glasgow score of 15/15, apyrexia, blood pressure of 12/07 cmHg, oxygen saturation of 100%, heart rate of 80/min, conjunctivae of normal colour with a large mass in the cavum. There was no hepatomegaly or splenomegaly, the lymph node areas were free, the rest of the physical examination was normal.\n\nChronology: the patient had been experiencing difficulty swallowing with dysphonia for 6 months, the clinical picture worsened with the development of dysphagia for solids with a deterioration in general condition (weight loss of 15kg/6 months).\n\nDiagnostic approach: cervico-thoraco-abdomino-pelvic CT scan showed a 70 mm x 40 mm nasopharyngeal mass extending to 60 mm. The patient's blood work was normal (white blood cell count, renal and hepatic function, lactate dehydrogenase and HIV, HCV and HBV serologies). The histological and immunohistochemical study of the nasopharyngeal biopsy was in favour of a grade 1,2 CD20+; CD19+; CD79a+; CD10+ follicular B-cell NHL in 2 readings in 2 different laboratories. The bone marrow biopsy was normal as was the pre-therapeutic work-up.\n\nTherapeutic intervention: the patient received 4 RCHOP 21 cures (rituximab 375mg/m2 intravenous (iv), cyclophosphamide 750 mg/m2 iv, oncovin 2 mg iv, prednisolone 100 mg orally, and doxorubicin 50 mg/m2 (iv) with no response and then 3 RDHAOX cures (rituximab 375 mg/m2 intravenous (iv) on day 1, high dose aracytine 2 g/m2 x 2 iv on day 2, dexamethasone 40 mg from day 1 to day 4, and oxalipatine 100 mg/m2 on day 1) with no clinical response.\n\nFollow-up and results of therapeutic interventions: the persistence and increase of the nasopharyngeal mass led to the realization of the tracheotomy, the biopsy of the nasopharyngeal mass objectified the disappearance of the lymphoid B infiltration with presence of the amyloid deposits AL type kappa.\n\nImmune electrophoresis of plasma proteins showed the presence of immunoglobulin M kappa, the dosage of light chains was not performed due to lack of resources, the myelogram and a second bone marrow biopsy were normal, the TEP scan objectified a hypermetabolic nasopharyngeal process without other anomalies, the cardiac evaluation (ECG, natriuretic peptides, troponin, echocore) and renal were without particularities, the patient is currently under protocol bortezomib, prednisone and bendamustine with good clinical evolution after the first treatment.\n", "generated_summary": "A 67-year-old patient with no medical history presented with a 6\u2011month course of dysphagia and dysphonia and deterioration of general condition (15 kg weight loss over 6 months). On examination: GCS 15/15, afebrile, BP 12/07 cmHg, SpO2 100%, HR 80/min, normal conjunctivae, and a large mass in the cavum; no hepatosplenomegaly or peripheral adenopathy; otherwise unremarkable exam. Cervico-thoraco-abdomino-pelvic CT identified a 70 \u00d7 40 mm nasopharyngeal mass extending to 60 mm. Laboratory studies were normal (WBC, renal and hepatic function, LDH) with negative HIV, HCV, and HBV serologies. Nasopharyngeal biopsy with histology and immunohistochemistry in two independent readings supported a grade 1\u20132 follicular B\u2011cell NHL: CD20+, CD19+, CD79a+, CD10+. Bone marrow biopsy and the pre\u2011therapeutic work\u2011up were normal. The patient received 4 cures of R\u2011CHOP\u201121 (rituximab 375 mg/m2 IV, cyclophosphamide 750 mg/m2 IV, oncovin 2 mg IV, prednisolone 100 mg PO, doxorubicin 50 mg/m2 IV) without response, followed by 3 cures of R\u2011DHAOX (rituximab 375 mg/m2 IV D1, high\u2011dose aracytine 2 g/m2 \u00d7 2 IV D2, dexamethasone 40 mg D1\u2013D4, oxaliplatine 100 mg/m2 D1) with no clinical response. Due to persistence and increase of the nasopharyngeal mass, a tracheotomy was performed. Repeat biopsy of the mass objectified disappearance of lymphoid B infiltration with presence of AL\u2011type kappa amyloid deposits. Immune electrophoresis of plasma proteins revealed immunoglobulin M kappa; serum free light chains were not dosed due to resource limitations. Myelogram and a second bone marrow biopsy were normal. PET (TEP) showed a hypermetabolic nasopharyngeal process without other anomalies. Cardiac evaluation (ECG, natriuretic peptides, troponin, echocore) and renal assessment were unremarkable. The patient is currently under a bortezomib, prednisone, and bendamustine protocol, with good clinical evolution after the first treatment. This trajectory suggests an IgM\u2011associated localized AL amyloid process emerging in the site of the prior follicular lymphoma, despite systemic evaluations (including marrow and organ assessments) remaining normal." }, { "index": 46, "label": "low_health_literacy", "original_text": "46-year-old Haitian male, residing in Chile for one year. In Haiti he was a livestock farmer. He presented a one-and-a-half-year history of a lesion that began as a papule on the anterior aspect of the right leg, which increased in size progressively. Initially asymptomatic, three months prior to the consultation he developed pruritus, pain, superficial ulceration and yellowish discharge. On physical examination, the patient was found to be of phototype V, with 1 x 1 cm, 2 x 2 cm and 3 x 2 cm warty plaques on the anterior aspect of the right leg. A dermatoscopy revealed a hyperkeratotic mass with ulcerated center, with reddish-black dots and congested hemorrhagic vessels. The general laboratory was normal; VDRL, HIV and PPD were non-reactive. Tissue samples were taken by a punch biopsy, including epidermis, dermis and subcutaneous tissue, and stained with Gram, routine bacteriological culture and anaerobic culture, which were negative. Bacilloscopy and Koch culture of the same tissue were also negative. The histopathological study was performed with hematoxylin and eosin stain, and showed a pseudoepitheliomatous epidermis with irregular hyperplasia, a dermis with abundant mixed inflammatory infiltrate with suppurative foci and giant cells of the foreign body type, some of which contained round cells with a thick brown wall, compatible with muriform cells; these cells were more evident when evaluated with PAS stain. Fungal culture was performed on Sabouraud dextrose agar at 25\u00b0C, which showed, after 15 days of incubation, the growth of black or dematiaceous, elevated, well-defined, velvety colonies. Direct microscopic examination with 20% KOH showed long, branched, sometimes tortuous, hyphae, and short chains of acropetal conidia, suggestive of Fonsecaea spp. Itraconazole was administered at 100 mg every 12 h for six months, in association with physical measures, which consisted of cryotherapy (liquid nitrogen) application to hypertrophic areas every six to eight weeks. Due to local complications, such as erosion or ulceration of the lesions, frequent healing was performed with application of mupirocin ointment topically for signs of bacterial superinfection.\n\nThe patient had a favorable evolution, with regression of the lesions and no evidence of relapses to date, remaining with a mild local hypopigmentation, expected in areas of treatment with cryotherapy.\n", "generated_summary": "A 46-year-old man from Haiti now lives in Chile. He had wart-like bumps on the front of his shin for about a year. Tests showed a long-lasting skin fungus called chromoblastomycosis. The skin sample had special cells that prove this infection. The lab also grew dark-colored fungus from the sample. Under the microscope, the germ looked like a kind called Fonsecaea. He took antifungal pills and got freezing treatments on the spots. Treatment lasted six months. All the bumps went away." }, { "index": 46, "label": "intermediate_health_literacy", "original_text": "46-year-old Haitian male, residing in Chile for one year. In Haiti he was a livestock farmer. He presented a one-and-a-half-year history of a lesion that began as a papule on the anterior aspect of the right leg, which increased in size progressively. Initially asymptomatic, three months prior to the consultation he developed pruritus, pain, superficial ulceration and yellowish discharge. On physical examination, the patient was found to be of phototype V, with 1 x 1 cm, 2 x 2 cm and 3 x 2 cm warty plaques on the anterior aspect of the right leg. A dermatoscopy revealed a hyperkeratotic mass with ulcerated center, with reddish-black dots and congested hemorrhagic vessels. The general laboratory was normal; VDRL, HIV and PPD were non-reactive. Tissue samples were taken by a punch biopsy, including epidermis, dermis and subcutaneous tissue, and stained with Gram, routine bacteriological culture and anaerobic culture, which were negative. Bacilloscopy and Koch culture of the same tissue were also negative. The histopathological study was performed with hematoxylin and eosin stain, and showed a pseudoepitheliomatous epidermis with irregular hyperplasia, a dermis with abundant mixed inflammatory infiltrate with suppurative foci and giant cells of the foreign body type, some of which contained round cells with a thick brown wall, compatible with muriform cells; these cells were more evident when evaluated with PAS stain. Fungal culture was performed on Sabouraud dextrose agar at 25\u00b0C, which showed, after 15 days of incubation, the growth of black or dematiaceous, elevated, well-defined, velvety colonies. Direct microscopic examination with 20% KOH showed long, branched, sometimes tortuous, hyphae, and short chains of acropetal conidia, suggestive of Fonsecaea spp. Itraconazole was administered at 100 mg every 12 h for six months, in association with physical measures, which consisted of cryotherapy (liquid nitrogen) application to hypertrophic areas every six to eight weeks. Due to local complications, such as erosion or ulceration of the lesions, frequent healing was performed with application of mupirocin ointment topically for signs of bacterial superinfection.\n\nThe patient had a favorable evolution, with regression of the lesions and no evidence of relapses to date, remaining with a mild local hypopigmentation, expected in areas of treatment with cryotherapy.\n", "generated_summary": "A 46-year-old Haitian man living in Chile developed wart-like plaques on the front of his right shin for about a year. Doctors diagnosed chromoblastomycosis after a skin biopsy showed the characteristic cells of this infection and a fungal culture grew dark (dematiaceous) colonies; direct microscopy suggested a Fonsecaea-type fungus. He was treated for six months with itraconazole taken twice daily and cryotherapy to the thickened areas. The lesions cleared completely. Additional context: The problem began as a small bump that slowly enlarged, later causing itch, pain, shallow ulcers, and yellowish drainage. Routine blood tests and screening for syphilis, HIV, and tuberculosis were negative. Local wound care was provided, including antibiotic ointment when signs of bacterial infection appeared. After therapy, there has been no relapse, with only mild lightening of the treated skin, which is expected after cryotherapy." }, { "index": 46, "label": "proficient_health_literacy", "original_text": "46-year-old Haitian male, residing in Chile for one year. In Haiti he was a livestock farmer. He presented a one-and-a-half-year history of a lesion that began as a papule on the anterior aspect of the right leg, which increased in size progressively. Initially asymptomatic, three months prior to the consultation he developed pruritus, pain, superficial ulceration and yellowish discharge. On physical examination, the patient was found to be of phototype V, with 1 x 1 cm, 2 x 2 cm and 3 x 2 cm warty plaques on the anterior aspect of the right leg. A dermatoscopy revealed a hyperkeratotic mass with ulcerated center, with reddish-black dots and congested hemorrhagic vessels. The general laboratory was normal; VDRL, HIV and PPD were non-reactive. Tissue samples were taken by a punch biopsy, including epidermis, dermis and subcutaneous tissue, and stained with Gram, routine bacteriological culture and anaerobic culture, which were negative. Bacilloscopy and Koch culture of the same tissue were also negative. The histopathological study was performed with hematoxylin and eosin stain, and showed a pseudoepitheliomatous epidermis with irregular hyperplasia, a dermis with abundant mixed inflammatory infiltrate with suppurative foci and giant cells of the foreign body type, some of which contained round cells with a thick brown wall, compatible with muriform cells; these cells were more evident when evaluated with PAS stain. Fungal culture was performed on Sabouraud dextrose agar at 25\u00b0C, which showed, after 15 days of incubation, the growth of black or dematiaceous, elevated, well-defined, velvety colonies. Direct microscopic examination with 20% KOH showed long, branched, sometimes tortuous, hyphae, and short chains of acropetal conidia, suggestive of Fonsecaea spp. Itraconazole was administered at 100 mg every 12 h for six months, in association with physical measures, which consisted of cryotherapy (liquid nitrogen) application to hypertrophic areas every six to eight weeks. Due to local complications, such as erosion or ulceration of the lesions, frequent healing was performed with application of mupirocin ointment topically for signs of bacterial superinfection.\n\nThe patient had a favorable evolution, with regression of the lesions and no evidence of relapses to date, remaining with a mild local hypopigmentation, expected in areas of treatment with cryotherapy.\n", "generated_summary": "A 46-year-old Haitian male, residing in Chile for one year, presented with a one-and-a-half-year history of a lesion that began as a papule on the anterior aspect of the right leg, with progressive enlargement. Initially asymptomatic, pruritus, pain, superficial ulceration, and yellowish discharge developed three months prior to consultation. On examination (phototype V), there were warty plaques measuring 1 \u00d7 1 cm, 2 \u00d7 2 cm, and 3 \u00d7 2 cm on the anterior right leg. Dermatoscopy revealed a hyperkeratotic mass with an ulcerated center, reddish-black dots, and congested hemorrhagic vessels. General laboratories were normal; VDRL, HIV, and PPD were non-reactive. Punch biopsy including epidermis, dermis, and subcutis was performed; Gram stain, routine bacteriological culture, and anaerobic culture were negative. Bacilloscopy and Koch culture were also negative. Histopathology (hematoxylin and eosin) showed pseudoepitheliomatous epidermal hyperplasia with irregular hyperplasia; the dermis contained abundant mixed inflammatory infiltrate with suppurative foci and foreign body-type giant cells, some containing round, thick-walled brown cells compatible with muriform (sclerotic) cells; these were more evident with PAS stain. Fungal culture on Sabouraud dextrose agar at 25\u00b0C demonstrated, after 15 days, growth of black/dematiaceous, elevated, well-defined, velvety colonies. Direct microscopic examination with 20% KOH showed long, branched, sometimes tortuous hyphae and short chains of acropetal conidia, suggestive of Fonsecaea spp. The diagnosis was chromoblastomycosis. Treatment included itraconazole 100 mg every 12 hours for six months, combined with physical measures consisting of cryotherapy (liquid nitrogen) applied to hypertrophic areas every 6\u20138 weeks. Due to local complications (erosion/ulceration), frequent wound care was provided, with topical mupirocin for signs of bacterial superinfection. The patient had a favorable evolution, with regression of lesions and no evidence of relapse to date, remaining with mild local hypopigmentation expected after cryotherapy. Contextual note: Chromoblastomycosis is a chronic cutaneous and subcutaneous mycosis caused by dematiaceous fungi (classically Fonsecaea, Cladophialophora, and Phialophora), with muriform cells being pathognomonic; combined antifungal therapy and cryotherapy are standard strategies, with itraconazole commonly dosed at 200 mg/day as used here." }, { "index": 47, "label": "low_health_literacy", "original_text": "Patient information: A 19-year-old male with no significant medical history was admitted to our department with a painful left scrotal mass that had been present for 8 months and had not improved with antibiotics for pyogenic organisms. The patient reported intermittent low grade fever, night sweats, anorexia and unexplained weight loss since the onset of symptoms. He did not have a cough, sputum or haemoptysis. There was no history of tuberculosis in his personal or family medical history. He was vaccinated against tuberculosis at birth.\n\nClinical findings: Physical examination revealed a large, painful, slightly hot left bursa and two elongated, poorly defined, firm, painful subcutaneous formations in the anterior thoracic wall, 3 to 4 cm long. There were no rales on auscultation. The remainder of the examination was normal. Laboratory studies revealed a high c-reactive protein of 90 mg/dl. The blood count, creatinine, blood glucose and liver function tests were within normal limits. The standard chest X-ray showed reticulonodular infiltrates in both lung fields.\n\nDiagnostic approach: In the presence of an ultrasound finding in favour of an epididymal tumour, the patient underwent a left orchidectomy. However, the pathological examination of the surgical specimen showed a granulomatous epitheloid necrosis of the epididymis, suggestive of active epididymal tuberculosis involving the body and tail of the epididymis and sparing the head and testicle. The intradermal tuberculin reaction was positive. The search for acid-fast bacilli (AFB) in sputum and urine for 3 consecutive days was negative on direct examination and culture. The serologies for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV) and Wright's stain were also negative. In search of other tuberculous sites, a thoraco-abdomino-pelvic tomodensitometry was performed, which showed a miliary tuberculosis, coelo-mesenteric necrotic adenopathies, two thoracic parietal collections (at the expense of the external oblique muscles measuring 33 \u00d7 10 mm on the right and 45 \u00d7 10 mm on the left) and a focal osteolysis of D11 and L5, suggestive of a spondylodiscitis in the early stages. The magnetic resonance imaging (MRI) of the spinal cord confirmed the existence of a spondylodiscitis at the level of D7, D11, L4 and L5. The diagnosis of disseminated tuberculosis with epididymal, pulmonary, parietal, ganglionary and osteo-articular sites was retained.\n\nTherapeutic intervention: a poly-chemotherapy for tuberculosis with isoniazid, rifampicin, ethambutol and pyrazinamide for 2 months, followed by the association of isoniazid and rifampicin, was initiated.\n\nFollow-up and results: however, at the 4th month of treatment, the patient had presented generalised tonic-clonic convulsive seizures. A brain MRI was performed, showing multiple nodular lesions above and below the tentorial membrane corresponding to tuberculomas. The patient was put on anticonvulsive treatment and anti-tuberculosis treatment was continued. The evolution was favourable with recovery of the general condition and weight gain from the first months of treatment as well as a disappearance of thoracic parietal formations, adenopathies and tuberculous milia on the tomodensitometry with absence of recurrence of convulsive seizures. However, the slow decrease of the size of the tuberculomas obliged us to continue the anti-tuberculosis treatment for a long period. Finally, the patient was declared cured, without sequelae, at the end of the 234th month of treatment with a 2-year follow-up.\n", "generated_summary": "A 19-year-old man had a painful lump in his left scrotum for 8 months. Doctors removed the left testicle. Lab tests showed the lump was from TB in the small tube behind the testicle that carries sperm. Scans showed the TB germs had also spread to his lymph nodes, lungs, chest wall, and his bones and joints. He started TB medicines. After 4 months, he had seizures. A brain scan showed small TB lumps in his brain. The doctors kept the TB treatment and added seizure medicine. He got better, and his scans looked better too." }, { "index": 47, "label": "intermediate_health_literacy", "original_text": "Patient information: A 19-year-old male with no significant medical history was admitted to our department with a painful left scrotal mass that had been present for 8 months and had not improved with antibiotics for pyogenic organisms. The patient reported intermittent low grade fever, night sweats, anorexia and unexplained weight loss since the onset of symptoms. He did not have a cough, sputum or haemoptysis. There was no history of tuberculosis in his personal or family medical history. He was vaccinated against tuberculosis at birth.\n\nClinical findings: Physical examination revealed a large, painful, slightly hot left bursa and two elongated, poorly defined, firm, painful subcutaneous formations in the anterior thoracic wall, 3 to 4 cm long. There were no rales on auscultation. The remainder of the examination was normal. Laboratory studies revealed a high c-reactive protein of 90 mg/dl. The blood count, creatinine, blood glucose and liver function tests were within normal limits. The standard chest X-ray showed reticulonodular infiltrates in both lung fields.\n\nDiagnostic approach: In the presence of an ultrasound finding in favour of an epididymal tumour, the patient underwent a left orchidectomy. However, the pathological examination of the surgical specimen showed a granulomatous epitheloid necrosis of the epididymis, suggestive of active epididymal tuberculosis involving the body and tail of the epididymis and sparing the head and testicle. The intradermal tuberculin reaction was positive. The search for acid-fast bacilli (AFB) in sputum and urine for 3 consecutive days was negative on direct examination and culture. The serologies for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV) and Wright's stain were also negative. In search of other tuberculous sites, a thoraco-abdomino-pelvic tomodensitometry was performed, which showed a miliary tuberculosis, coelo-mesenteric necrotic adenopathies, two thoracic parietal collections (at the expense of the external oblique muscles measuring 33 \u00d7 10 mm on the right and 45 \u00d7 10 mm on the left) and a focal osteolysis of D11 and L5, suggestive of a spondylodiscitis in the early stages. The magnetic resonance imaging (MRI) of the spinal cord confirmed the existence of a spondylodiscitis at the level of D7, D11, L4 and L5. The diagnosis of disseminated tuberculosis with epididymal, pulmonary, parietal, ganglionary and osteo-articular sites was retained.\n\nTherapeutic intervention: a poly-chemotherapy for tuberculosis with isoniazid, rifampicin, ethambutol and pyrazinamide for 2 months, followed by the association of isoniazid and rifampicin, was initiated.\n\nFollow-up and results: however, at the 4th month of treatment, the patient had presented generalised tonic-clonic convulsive seizures. A brain MRI was performed, showing multiple nodular lesions above and below the tentorial membrane corresponding to tuberculomas. The patient was put on anticonvulsive treatment and anti-tuberculosis treatment was continued. The evolution was favourable with recovery of the general condition and weight gain from the first months of treatment as well as a disappearance of thoracic parietal formations, adenopathies and tuberculous milia on the tomodensitometry with absence of recurrence of convulsive seizures. However, the slow decrease of the size of the tuberculomas obliged us to continue the anti-tuberculosis treatment for a long period. Finally, the patient was declared cured, without sequelae, at the end of the 234th month of treatment with a 2-year follow-up.\n", "generated_summary": "A 19-year-old man was admitted with an 8-month history of a painful left scrotal mass. He underwent an orchidectomy, and pathology favored epididymal tuberculosis. Imaging then revealed additional TB sites: lymph nodes, lungs, the chest wall (parietal), and the bones and joints (osteoarticular). Standard anti-tuberculosis therapy was started. In the fourth month of treatment he developed generalized seizures, and brain MRI showed tuberculomas. Treatment was continued along with an anticonvulsant, leading to good clinical and radiologic improvement." }, { "index": 47, "label": "proficient_health_literacy", "original_text": "Patient information: A 19-year-old male with no significant medical history was admitted to our department with a painful left scrotal mass that had been present for 8 months and had not improved with antibiotics for pyogenic organisms. The patient reported intermittent low grade fever, night sweats, anorexia and unexplained weight loss since the onset of symptoms. He did not have a cough, sputum or haemoptysis. There was no history of tuberculosis in his personal or family medical history. He was vaccinated against tuberculosis at birth.\n\nClinical findings: Physical examination revealed a large, painful, slightly hot left bursa and two elongated, poorly defined, firm, painful subcutaneous formations in the anterior thoracic wall, 3 to 4 cm long. There were no rales on auscultation. The remainder of the examination was normal. Laboratory studies revealed a high c-reactive protein of 90 mg/dl. The blood count, creatinine, blood glucose and liver function tests were within normal limits. The standard chest X-ray showed reticulonodular infiltrates in both lung fields.\n\nDiagnostic approach: In the presence of an ultrasound finding in favour of an epididymal tumour, the patient underwent a left orchidectomy. However, the pathological examination of the surgical specimen showed a granulomatous epitheloid necrosis of the epididymis, suggestive of active epididymal tuberculosis involving the body and tail of the epididymis and sparing the head and testicle. The intradermal tuberculin reaction was positive. The search for acid-fast bacilli (AFB) in sputum and urine for 3 consecutive days was negative on direct examination and culture. The serologies for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV) and Wright's stain were also negative. In search of other tuberculous sites, a thoraco-abdomino-pelvic tomodensitometry was performed, which showed a miliary tuberculosis, coelo-mesenteric necrotic adenopathies, two thoracic parietal collections (at the expense of the external oblique muscles measuring 33 \u00d7 10 mm on the right and 45 \u00d7 10 mm on the left) and a focal osteolysis of D11 and L5, suggestive of a spondylodiscitis in the early stages. The magnetic resonance imaging (MRI) of the spinal cord confirmed the existence of a spondylodiscitis at the level of D7, D11, L4 and L5. The diagnosis of disseminated tuberculosis with epididymal, pulmonary, parietal, ganglionary and osteo-articular sites was retained.\n\nTherapeutic intervention: a poly-chemotherapy for tuberculosis with isoniazid, rifampicin, ethambutol and pyrazinamide for 2 months, followed by the association of isoniazid and rifampicin, was initiated.\n\nFollow-up and results: however, at the 4th month of treatment, the patient had presented generalised tonic-clonic convulsive seizures. A brain MRI was performed, showing multiple nodular lesions above and below the tentorial membrane corresponding to tuberculomas. The patient was put on anticonvulsive treatment and anti-tuberculosis treatment was continued. The evolution was favourable with recovery of the general condition and weight gain from the first months of treatment as well as a disappearance of thoracic parietal formations, adenopathies and tuberculous milia on the tomodensitometry with absence of recurrence of convulsive seizures. However, the slow decrease of the size of the tuberculomas obliged us to continue the anti-tuberculosis treatment for a long period. Finally, the patient was declared cured, without sequelae, at the end of the 234th month of treatment with a 2-year follow-up.\n", "generated_summary": "A 19-year-old male with no significant history presented with an 8-month painful left scrotal mass unresponsive to antibiotics for presumed pyogenic infection, along with intermittent low-grade fever, night sweats, anorexia, and weight loss. Exam showed a large, painful, slightly warm left bursa and two firm, painful subcutaneous formations on the anterior thoracic wall (3\u20134 cm). CRP was 90 mg/dl; CBC, creatinine, glucose, and liver function tests were normal. Chest radiograph demonstrated bilateral reticulonodular infiltrates. Scrotal ultrasound suggested an epididymal tumor, and a left orchidectomy was performed. Histopathology revealed granulomatous epithelioid necrosis of the epididymis, consistent with active epididymal tuberculosis involving the body and tail and sparing the head and testis. The tuberculin skin test was positive. AFB studies of sputum and urine on 3 consecutive days were negative on direct smear and culture. HIV, HBV, HCV serologies and Wright's were negative. Thoraco-abdomino-pelvic CT identified miliary tuberculosis, coelo-mesenteric necrotic adenopathies, two thoracic parietal collections within the external oblique muscles (33 \u00d7 10 mm right, 45 \u00d7 10 mm left), and focal osteolysis of D11 and L5 suggestive of early spondylodiscitis; spinal MRI confirmed spondylodiscitis at D7, D11, L4, and L5. The diagnosis was disseminated tuberculosis with epididymal, pulmonary, parietal, ganglionary, and osteo-articular involvement. Treatment consisted of isoniazid, rifampicin, ethambutol, and pyrazinamide for 2 months, followed by isoniazid plus rifampicin. At month 4 of therapy he developed generalized tonic-clonic seizures; brain MRI showed multiple supra- and infratentorial nodular lesions compatible with tuberculomas. An anticonvulsant was added and anti-tuberculous therapy was continued. Evolution was favorable with early weight gain and disappearance of thoracic parietal formations, adenopathies, and miliary lesions on CT; there was no recurrence of seizures. Because the tuberculomas regressed slowly, therapy was prolonged; he was ultimately declared cured without sequelae at the end of the 234th month of treatment (as reported) with 2-year follow-up. Context: Epididymal tuberculosis can mimic neoplasm and may occur with negative AFB studies; CNS tuberculomas emerging during therapy are a recognized phenomenon, typically managed by continuing anti-tuberculous treatment with seizure control." }, { "index": 48, "label": "low_health_literacy", "original_text": "We present the case of a 10-year-old male diagnosed with high-risk early T-cell acute lymphoblastic leukaemia, who was treated according to the LAL SEHOP-PETHEMA 2013 protocol. Two years after diagnosis, he developed an early CNS relapse, so he was treated according to the InteReALL HR 2010 protocol with bortezomib. During induction, after being neutropenic for four weeks (20 neutrophils/\u03bcL), he was receiving prophylaxis with cefepime, cotrimoxazole and fluconazole. In addition, he was being treated with acyclovir for a herpes simplex virus 1 skin infection. In this context, he developed a severe headache that did not respond to usual analgesia. A cranial computed tomographic scan was performed that showed a hypodens lesion in the right temporal lobe. When the possibility of an infectious origin was considered, a lumbar puncture was performed and cefepime was replaced with meropenem and vancomycin.\n\nDespite remaining afebrile, he developed signs of septic shock on the first day after admission to the clinic and was transferred to the paediatric intensive care unit for inotropic and vasoactive support. In addition, the antimicrobial spectrum was extended with gentamicin and caspofungin.\n\nThe blood analysis showed a progressive increase in C-reactive protein and procalcitonin (up to 312 mg/L and 47.58 ng/mL, respectively, on the third day of evolution), with no other relevant biochemical alterations. The blood count showed pancytopenia due to chemotherapy. The blood cultures ruled out bacteremia and fungemia, and herpes virus serologies were negative. The urine culture and the fecal culture were also negative. The biochemical analysis of the cerebrospinal fluid was completely normal (glucose, 63 mg/dL; proteins, 16 mg/dL; leukocytes 1/\u00b5L), but the presence of B. cereus was detected in the microbiological study (sensitive to meropenem, vancomycin, linezolid and ciprofloxacin). The presence of herpes simplex 1 and 2, herpes virus 6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus, toxoplasma, Neisseria meningitidis, Listeria monocytogenes, Streptococcus pneumoniae and Cryptococcus was ruled out in the cerebrospinal fluid.\n\nThe EEG showed diffuse slowing of brain activity with no clear epileptiform activity. On day 4, after the haemodynamic support was removed, a cranial MRI showed two hyperintense lesions in T2 and FLAIR that involved the subcortical region of the right temporal and parietal lobes. The parietal lesion had ring enhancement after administration of gadolinium and both lesions showed peripheral diffusion restriction. In addition, small haemorrhagic foci were observed scattered in the brain parenchyma. The image suggested a bacterial origin with an atypical germ, and these findings, together with those of the cerebrospinal fluid, led to the diagnosis of B. cereus abscess.\n\nAfter two weeks of treatment, the patient had a favorable outcome with resolution of the headache and no neurological findings. A follow-up MRI showed a decrease in the size of the lesions. Vancomycin and acyclovir were discontinued after three weeks and meropenem was continued for six weeks.\n", "generated_summary": "A 10-year-old boy was getting cancer medicine for leukemia. During the first phase of treatment, he got a pocket of infection in his brain. The germ was called Bacillus cereus. Doctors found it with brain scans and by testing the fluid around his brain and spine. He got better after taking antibiotics." }, { "index": 48, "label": "intermediate_health_literacy", "original_text": "We present the case of a 10-year-old male diagnosed with high-risk early T-cell acute lymphoblastic leukaemia, who was treated according to the LAL SEHOP-PETHEMA 2013 protocol. Two years after diagnosis, he developed an early CNS relapse, so he was treated according to the InteReALL HR 2010 protocol with bortezomib. During induction, after being neutropenic for four weeks (20 neutrophils/\u03bcL), he was receiving prophylaxis with cefepime, cotrimoxazole and fluconazole. In addition, he was being treated with acyclovir for a herpes simplex virus 1 skin infection. In this context, he developed a severe headache that did not respond to usual analgesia. A cranial computed tomographic scan was performed that showed a hypodens lesion in the right temporal lobe. When the possibility of an infectious origin was considered, a lumbar puncture was performed and cefepime was replaced with meropenem and vancomycin.\n\nDespite remaining afebrile, he developed signs of septic shock on the first day after admission to the clinic and was transferred to the paediatric intensive care unit for inotropic and vasoactive support. In addition, the antimicrobial spectrum was extended with gentamicin and caspofungin.\n\nThe blood analysis showed a progressive increase in C-reactive protein and procalcitonin (up to 312 mg/L and 47.58 ng/mL, respectively, on the third day of evolution), with no other relevant biochemical alterations. The blood count showed pancytopenia due to chemotherapy. The blood cultures ruled out bacteremia and fungemia, and herpes virus serologies were negative. The urine culture and the fecal culture were also negative. The biochemical analysis of the cerebrospinal fluid was completely normal (glucose, 63 mg/dL; proteins, 16 mg/dL; leukocytes 1/\u00b5L), but the presence of B. cereus was detected in the microbiological study (sensitive to meropenem, vancomycin, linezolid and ciprofloxacin). The presence of herpes simplex 1 and 2, herpes virus 6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus, toxoplasma, Neisseria meningitidis, Listeria monocytogenes, Streptococcus pneumoniae and Cryptococcus was ruled out in the cerebrospinal fluid.\n\nThe EEG showed diffuse slowing of brain activity with no clear epileptiform activity. On day 4, after the haemodynamic support was removed, a cranial MRI showed two hyperintense lesions in T2 and FLAIR that involved the subcortical region of the right temporal and parietal lobes. The parietal lesion had ring enhancement after administration of gadolinium and both lesions showed peripheral diffusion restriction. In addition, small haemorrhagic foci were observed scattered in the brain parenchyma. The image suggested a bacterial origin with an atypical germ, and these findings, together with those of the cerebrospinal fluid, led to the diagnosis of B. cereus abscess.\n\nAfter two weeks of treatment, the patient had a favorable outcome with resolution of the headache and no neurological findings. A follow-up MRI showed a decrease in the size of the lesions. Vancomycin and acyclovir were discontinued after three weeks and meropenem was continued for six weeks.\n", "generated_summary": "A 10-year-old boy receiving chemotherapy for acute lymphoblastic leukemia developed a brain abscess during induction therapy. He had a severe headache, and brain scans (CT/MRI) showed lesions that looked like an infection. Tests on his spinal fluid directly detected Bacillus cereus, confirming the cause. He was treated with antibiotics (such as meropenem and vancomycin). His symptoms resolved, follow-up imaging showed the abscess shrinking, and he recovered well." }, { "index": 48, "label": "proficient_health_literacy", "original_text": "We present the case of a 10-year-old male diagnosed with high-risk early T-cell acute lymphoblastic leukaemia, who was treated according to the LAL SEHOP-PETHEMA 2013 protocol. Two years after diagnosis, he developed an early CNS relapse, so he was treated according to the InteReALL HR 2010 protocol with bortezomib. During induction, after being neutropenic for four weeks (20 neutrophils/\u03bcL), he was receiving prophylaxis with cefepime, cotrimoxazole and fluconazole. In addition, he was being treated with acyclovir for a herpes simplex virus 1 skin infection. In this context, he developed a severe headache that did not respond to usual analgesia. A cranial computed tomographic scan was performed that showed a hypodens lesion in the right temporal lobe. When the possibility of an infectious origin was considered, a lumbar puncture was performed and cefepime was replaced with meropenem and vancomycin.\n\nDespite remaining afebrile, he developed signs of septic shock on the first day after admission to the clinic and was transferred to the paediatric intensive care unit for inotropic and vasoactive support. In addition, the antimicrobial spectrum was extended with gentamicin and caspofungin.\n\nThe blood analysis showed a progressive increase in C-reactive protein and procalcitonin (up to 312 mg/L and 47.58 ng/mL, respectively, on the third day of evolution), with no other relevant biochemical alterations. The blood count showed pancytopenia due to chemotherapy. The blood cultures ruled out bacteremia and fungemia, and herpes virus serologies were negative. The urine culture and the fecal culture were also negative. The biochemical analysis of the cerebrospinal fluid was completely normal (glucose, 63 mg/dL; proteins, 16 mg/dL; leukocytes 1/\u00b5L), but the presence of B. cereus was detected in the microbiological study (sensitive to meropenem, vancomycin, linezolid and ciprofloxacin). The presence of herpes simplex 1 and 2, herpes virus 6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus, toxoplasma, Neisseria meningitidis, Listeria monocytogenes, Streptococcus pneumoniae and Cryptococcus was ruled out in the cerebrospinal fluid.\n\nThe EEG showed diffuse slowing of brain activity with no clear epileptiform activity. On day 4, after the haemodynamic support was removed, a cranial MRI showed two hyperintense lesions in T2 and FLAIR that involved the subcortical region of the right temporal and parietal lobes. The parietal lesion had ring enhancement after administration of gadolinium and both lesions showed peripheral diffusion restriction. In addition, small haemorrhagic foci were observed scattered in the brain parenchyma. The image suggested a bacterial origin with an atypical germ, and these findings, together with those of the cerebrospinal fluid, led to the diagnosis of B. cereus abscess.\n\nAfter two weeks of treatment, the patient had a favorable outcome with resolution of the headache and no neurological findings. A follow-up MRI showed a decrease in the size of the lesions. Vancomycin and acyclovir were discontinued after three weeks and meropenem was continued for six weeks.\n", "generated_summary": "A 10-year-old male with high-risk early T-cell acute lymphoblastic leukaemia (initially treated per LAL SEHOP-PETHEMA 2013) experienced an early CNS relapse two years after diagnosis and began InteReALL HR 2010 induction with bortezomib. After four weeks of profound neutropenia (20 neutrophils/\u00b5L) on prophylaxis (cefepime, cotrimoxazole, fluconazole) and acyclovir for HSV-1 skin infection, he developed a severe, analgesia-refractory headache. Head CT revealed a right temporal hypodense lesion. Suspecting infection, a lumbar puncture was performed and cefepime was switched to meropenem plus vancomycin. Despite being afebrile, he showed signs of septic shock on day 1 and required PICU admission for inotropic/vasoactive support; antimicrobials were broadened with gentamicin and caspofungin. Inflammatory markers rose (CRP 312 mg/L, procalcitonin 47.58 ng/mL by day 3), with pancytopenia attributable to chemotherapy and no other major biochemical abnormalities. Blood, urine, and fecal cultures were negative; viral serologies were negative. CSF biochemistry was normal (glucose 63 mg/dL; protein 16 mg/dL; leukocytes 1/\u00b5L), but microbiology detected Bacillus cereus, susceptible to meropenem, vancomycin, linezolid, and ciprofloxacin; CSF PCR/assays were negative for HSV-1/2, HHV-6, CMV, VZV, enterovirus, parechovirus, Toxoplasma, Neisseria meningitidis, Listeria monocytogenes, Streptococcus pneumoniae, and Cryptococcus. EEG showed diffuse slowing without epileptiform activity. On day 4, once off haemodynamic support, brain MRI demonstrated two T2/FLAIR hyperintense subcortical lesions in the right temporal and parietal lobes; the parietal lesion exhibited ring enhancement post-gadolinium, both lesions had peripheral diffusion restriction, and scattered parenchymal microhaemorrhages were present\u2014an appearance suggestive of bacterial abscess due to an atypical pathogen. Integrating imaging with direct CSF detection established the diagnosis of B. cereus cerebral abscess. After two weeks of therapy, his headache resolved with no focal neurological deficits; interval MRI showed lesion size reduction. Vancomycin and acyclovir were discontinued after three weeks, and meropenem was continued to complete six weeks, with a favourable clinical course." }, { "index": 49, "label": "low_health_literacy", "original_text": "Female patient, 16 years old, presenting a depressed gray plaque of 10.5 \u00d7 8.0 cm interspersed with hypochromic areas in the lower lateral part of the left thigh. Telangiectatic vessels overlap the lesion peripherally, with visible veins close to it. The plaque was present from birth, but was initially violaceous. It evolved with the passing of the years, with lightening and depression. There is no discrepancy in the length of the lower limbs.\n\nAngioresonance showed vascular malformations in the skin and subcutaneous tissue supplied by intermuscular branches of the popliteal artery. Early venous filling was found in both the region and the malformations, suggesting early venous shunting. Dilated draining veins were not documented, except for a superficial draining vein running along the subcutaneous cellular tissue of the anterior thigh. In addition, thinning of the subcutaneous tissue was noted in the topography of the vascular alteration, but without intramuscular or bone extension.\n", "generated_summary": "A 16-year-old girl has a sunken, gray patch on her left thigh. A special scan that looks at blood vessels showed a blood vessel problem in the skin and in the layer just under the skin." }, { "index": 49, "label": "intermediate_health_literacy", "original_text": "Female patient, 16 years old, presenting a depressed gray plaque of 10.5 \u00d7 8.0 cm interspersed with hypochromic areas in the lower lateral part of the left thigh. Telangiectatic vessels overlap the lesion peripherally, with visible veins close to it. The plaque was present from birth, but was initially violaceous. It evolved with the passing of the years, with lightening and depression. There is no discrepancy in the length of the lower limbs.\n\nAngioresonance showed vascular malformations in the skin and subcutaneous tissue supplied by intermuscular branches of the popliteal artery. Early venous filling was found in both the region and the malformations, suggesting early venous shunting. Dilated draining veins were not documented, except for a superficial draining vein running along the subcutaneous cellular tissue of the anterior thigh. In addition, thinning of the subcutaneous tissue was noted in the topography of the vascular alteration, but without intramuscular or bone extension.\n", "generated_summary": "A 16-year-old girl has a depressed gray plaque on the lower outer part of her left thigh, measuring about 10.5 by 8 cm. It has been present since birth, was initially purple, and gradually became lighter and sunken. Small surface blood vessels can be seen around it, with some nearby veins. An angioresonance (vascular MRI) shows a vascular malformation limited to the skin and subcutaneous tissue, supplied by branches from the popliteal artery, with early venous filling that suggests some artery-to-vein shunting. The subcutaneous tissue in that spot is thinned, with no spread into muscle or bone, and there is no difference in leg length. No large draining veins were seen, aside from one superficial vein in the front of the thigh." }, { "index": 49, "label": "proficient_health_literacy", "original_text": "Female patient, 16 years old, presenting a depressed gray plaque of 10.5 \u00d7 8.0 cm interspersed with hypochromic areas in the lower lateral part of the left thigh. Telangiectatic vessels overlap the lesion peripherally, with visible veins close to it. The plaque was present from birth, but was initially violaceous. It evolved with the passing of the years, with lightening and depression. There is no discrepancy in the length of the lower limbs.\n\nAngioresonance showed vascular malformations in the skin and subcutaneous tissue supplied by intermuscular branches of the popliteal artery. Early venous filling was found in both the region and the malformations, suggesting early venous shunting. Dilated draining veins were not documented, except for a superficial draining vein running along the subcutaneous cellular tissue of the anterior thigh. In addition, thinning of the subcutaneous tissue was noted in the topography of the vascular alteration, but without intramuscular or bone extension.\n", "generated_summary": "Female patient, 16 years old, with a depressed gray plaque measuring 10.5 \u00d7 8.0 cm, interspersed with hypochromic areas on the lower lateral left thigh. Telangiectatic vessels overlap the lesion peripherally, with visible veins adjacent to it. The plaque has been present since birth, initially violaceous, and evolved over the years with lightening and progressive depression. No discrepancy in lower limb length. Angioresonance demonstrated vascular malformations confined to the skin and subcutaneous tissue, supplied by intermuscular branches of the popliteal artery. There is early venous filling in both the region and the malformations, suggesting early venous shunting. Dilated draining veins were not documented, except for a superficial draining vein coursing along the subcutaneous cellular tissue of the anterior thigh. There is thinning of the subcutaneous tissue at the site of the vascular alteration, without intramuscular or bone extension." }, { "index": 50, "label": "low_health_literacy", "original_text": "A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain that began two months earlier. The pain was intermittent and dull, accompanied by nausea, anorexia, malaise, and a weight loss of 5 kg. There was no fever, blood / mucus in the stool, or respiratory symptoms (rhinorrhea, wheezing, coughing). She had no history of alcohol/tobacco use or traditional herbal medicines. Six weeks before admission, she was diagnosed with an intestinal infection in a local clinic after a complete blood count (CBC) revealed leukocytosis and significant eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotics and mebendazole without relief of symptoms. At presentation, the patient was alerted and oriented with stable vitals (BP 110/70 mmHg, T 37\u00b0C, HR 88 bpm, RR 18 bpm). She had a BMI of 16.6 kg/m\u00b2 and sarcopenia, but no skin rash, lymphadenopathy, or edema. The abdominal exam showed tenderness in the epigastric and umbilical regions without guarding. CBC revealed leukocytosis and significant eosinophilia (20.8 G/L, with a total white blood cell count of 26.8 G/L, comprising 77.8% eosinophils). Peripheral blood film examination showed normal eosinophils. Bone marrow aspiration reveals 48% eosinophils without blasts, atypical cells. Fluorescence in situ hybridization (FISH) for CHIC2 deletion as a surrogate marker for FIP1L1-PDGFRA showed no rearrangements of the PDGFRA gene. Autoimmune and vasculitis screenings (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative. Elevated serum IgG (2760 mg/dL; normal range, 700\u20131600 mg/dL) and IgG4 (1260 mg/dL; normal range, 3.9\u201386.4 mg/dL), slightly elevated IgE (137.5 IU/mL; normal range, <100 IU/mL) and high RF (144.4 IU/mL; normal range, <20 IU/mL) were observed. Other parameters were normal, including aminotransferase, blood urea nitrogen, serum creatinine, complement C3, complement C4, vitamin B12, serum cortisol, and NT-proBNP. ECG and echocardiogram were normal. Chest CT scans showed mild fibrosis and bronchiectasis. Sputum AFB smears and bronchoscopy were negative. The cytology of the bronchoalveolar lavage fluid showed 35% neutrophils, no eosinophils. Spirometry indicated severe obstruction with bronchodilator response. The fractional exhaled nitric oxide (FeNO) level was 15 ppb. Stool samples were tested positive for leukocytes, with no signs of ova or parasites. Serology tests were positive for toxocariasis (positive IgG of Toxocara canis at 54.2 NovaTec-Units) but negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. An abdominal contrast-enhanced computed tomography scan revealed gallbladder stones without acute cholecystitis and showed no gastrointestinal tract abnormalities. The upper gastrointestinal endoscopy showed unremarkable results with a normal appearance. Colonoscopy showed mucosal inflammation in the sigmoid, left, transverse, and right colon with systemic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies revealed significant eosinophilic infiltration (>85 eosinophils/High-power field (HPF) in the left colon, >100 eosinophils/HPF in the transverse and right colon). Given the patient\u2019s nonresponse to toxocariasis treatment and the significant eosinophilic infiltration observed in the colon mucosa biopsy, a diagnosis of eosinophilic colitis was confirmed. The patient was treated with oral methylprednisolone (16 mg) and montelukast (5 mg). Symptoms resolved in two weeks and eosinophil counts normalized (0.3 G/L). The corticosteroid was reduced and discontinued, and the patient was maintained on montelukast for three months without symptom recurrence.", "generated_summary": "A 57-year-old patient had asthma and nose allergies. She kept having stomach pain. Her blood showed very high levels of allergy-fighting white cells. A certain immune protein (IgG4) was also high. The doctors checked for blood cancers and other causes and did not find them. They gently took tiny samples from the lining of her large intestine. The samples showed too many of those allergy cells sitting in the tissue. This meant she had eosinophilic colitis, which is swelling of the colon from a build-up of allergy cells. She took a steroid medicine to calm the swelling. Then she stayed on montelukast to keep the problem quiet. Her pain went away and did not come back for three months." }, { "index": 50, "label": "intermediate_health_literacy", "original_text": "A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain that began two months earlier. The pain was intermittent and dull, accompanied by nausea, anorexia, malaise, and a weight loss of 5 kg. There was no fever, blood / mucus in the stool, or respiratory symptoms (rhinorrhea, wheezing, coughing). She had no history of alcohol/tobacco use or traditional herbal medicines. Six weeks before admission, she was diagnosed with an intestinal infection in a local clinic after a complete blood count (CBC) revealed leukocytosis and significant eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotics and mebendazole without relief of symptoms. At presentation, the patient was alerted and oriented with stable vitals (BP 110/70 mmHg, T 37\u00b0C, HR 88 bpm, RR 18 bpm). She had a BMI of 16.6 kg/m\u00b2 and sarcopenia, but no skin rash, lymphadenopathy, or edema. The abdominal exam showed tenderness in the epigastric and umbilical regions without guarding. CBC revealed leukocytosis and significant eosinophilia (20.8 G/L, with a total white blood cell count of 26.8 G/L, comprising 77.8% eosinophils). Peripheral blood film examination showed normal eosinophils. Bone marrow aspiration reveals 48% eosinophils without blasts, atypical cells. Fluorescence in situ hybridization (FISH) for CHIC2 deletion as a surrogate marker for FIP1L1-PDGFRA showed no rearrangements of the PDGFRA gene. Autoimmune and vasculitis screenings (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative. Elevated serum IgG (2760 mg/dL; normal range, 700\u20131600 mg/dL) and IgG4 (1260 mg/dL; normal range, 3.9\u201386.4 mg/dL), slightly elevated IgE (137.5 IU/mL; normal range, <100 IU/mL) and high RF (144.4 IU/mL; normal range, <20 IU/mL) were observed. Other parameters were normal, including aminotransferase, blood urea nitrogen, serum creatinine, complement C3, complement C4, vitamin B12, serum cortisol, and NT-proBNP. ECG and echocardiogram were normal. Chest CT scans showed mild fibrosis and bronchiectasis. Sputum AFB smears and bronchoscopy were negative. The cytology of the bronchoalveolar lavage fluid showed 35% neutrophils, no eosinophils. Spirometry indicated severe obstruction with bronchodilator response. The fractional exhaled nitric oxide (FeNO) level was 15 ppb. Stool samples were tested positive for leukocytes, with no signs of ova or parasites. Serology tests were positive for toxocariasis (positive IgG of Toxocara canis at 54.2 NovaTec-Units) but negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. An abdominal contrast-enhanced computed tomography scan revealed gallbladder stones without acute cholecystitis and showed no gastrointestinal tract abnormalities. The upper gastrointestinal endoscopy showed unremarkable results with a normal appearance. Colonoscopy showed mucosal inflammation in the sigmoid, left, transverse, and right colon with systemic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies revealed significant eosinophilic infiltration (>85 eosinophils/High-power field (HPF) in the left colon, >100 eosinophils/HPF in the transverse and right colon). Given the patient\u2019s nonresponse to toxocariasis treatment and the significant eosinophilic infiltration observed in the colon mucosa biopsy, a diagnosis of eosinophilic colitis was confirmed. The patient was treated with oral methylprednisolone (16 mg) and montelukast (5 mg). Symptoms resolved in two weeks and eosinophil counts normalized (0.3 G/L). The corticosteroid was reduced and discontinued, and the patient was maintained on montelukast for three months without symptom recurrence.", "generated_summary": "A 57-year-old woman with longstanding asthma and allergic rhinitis developed recurrent abdominal pain. Blood tests showed marked eosinophilia (very high levels of allergy-type white blood cells) and an elevated IgG4 level. After doctors ruled out blood cancers and other secondary causes of eosinophilia, they performed a colon biopsy. The biopsy showed an excess of eosinophils in the colon lining, confirming eosinophilic colitis. She improved quickly on corticosteroids and was then maintained on montelukast. Over the next three months, her symptoms did not return." }, { "index": 50, "label": "proficient_health_literacy", "original_text": "A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain that began two months earlier. The pain was intermittent and dull, accompanied by nausea, anorexia, malaise, and a weight loss of 5 kg. There was no fever, blood / mucus in the stool, or respiratory symptoms (rhinorrhea, wheezing, coughing). She had no history of alcohol/tobacco use or traditional herbal medicines. Six weeks before admission, she was diagnosed with an intestinal infection in a local clinic after a complete blood count (CBC) revealed leukocytosis and significant eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotics and mebendazole without relief of symptoms. At presentation, the patient was alerted and oriented with stable vitals (BP 110/70 mmHg, T 37\u00b0C, HR 88 bpm, RR 18 bpm). She had a BMI of 16.6 kg/m\u00b2 and sarcopenia, but no skin rash, lymphadenopathy, or edema. The abdominal exam showed tenderness in the epigastric and umbilical regions without guarding. CBC revealed leukocytosis and significant eosinophilia (20.8 G/L, with a total white blood cell count of 26.8 G/L, comprising 77.8% eosinophils). Peripheral blood film examination showed normal eosinophils. Bone marrow aspiration reveals 48% eosinophils without blasts, atypical cells. Fluorescence in situ hybridization (FISH) for CHIC2 deletion as a surrogate marker for FIP1L1-PDGFRA showed no rearrangements of the PDGFRA gene. Autoimmune and vasculitis screenings (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative. Elevated serum IgG (2760 mg/dL; normal range, 700\u20131600 mg/dL) and IgG4 (1260 mg/dL; normal range, 3.9\u201386.4 mg/dL), slightly elevated IgE (137.5 IU/mL; normal range, <100 IU/mL) and high RF (144.4 IU/mL; normal range, <20 IU/mL) were observed. Other parameters were normal, including aminotransferase, blood urea nitrogen, serum creatinine, complement C3, complement C4, vitamin B12, serum cortisol, and NT-proBNP. ECG and echocardiogram were normal. Chest CT scans showed mild fibrosis and bronchiectasis. Sputum AFB smears and bronchoscopy were negative. The cytology of the bronchoalveolar lavage fluid showed 35% neutrophils, no eosinophils. Spirometry indicated severe obstruction with bronchodilator response. The fractional exhaled nitric oxide (FeNO) level was 15 ppb. Stool samples were tested positive for leukocytes, with no signs of ova or parasites. Serology tests were positive for toxocariasis (positive IgG of Toxocara canis at 54.2 NovaTec-Units) but negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. An abdominal contrast-enhanced computed tomography scan revealed gallbladder stones without acute cholecystitis and showed no gastrointestinal tract abnormalities. The upper gastrointestinal endoscopy showed unremarkable results with a normal appearance. Colonoscopy showed mucosal inflammation in the sigmoid, left, transverse, and right colon with systemic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies revealed significant eosinophilic infiltration (>85 eosinophils/High-power field (HPF) in the left colon, >100 eosinophils/HPF in the transverse and right colon). Given the patient\u2019s nonresponse to toxocariasis treatment and the significant eosinophilic infiltration observed in the colon mucosa biopsy, a diagnosis of eosinophilic colitis was confirmed. The patient was treated with oral methylprednisolone (16 mg) and montelukast (5 mg). Symptoms resolved in two weeks and eosinophil counts normalized (0.3 G/L). The corticosteroid was reduced and discontinued, and the patient was maintained on montelukast for three months without symptom recurrence.", "generated_summary": "A 57-year-old woman with a 14-year history of asthma and allergic rhinitis on salmeterol/fluticasone presented with two months of intermittent, dull abdominal pain, nausea, anorexia, malaise, and 5-kg weight loss. She was afebrile, hemodynamically stable, underweight (BMI 16.6 kg/m\u00b2) with sarcopenia, and had epigastric/umbilical tenderness without guarding. CBC showed leukocytosis with marked eosinophilia (WBC 26.8 G/L with 20.8 G/L eosinophils; 77.8%). Peripheral smear showed morphologically normal eosinophils. Bone marrow aspiration revealed 48% eosinophils without blasts or atypia. FISH for CHIC2 deletion (surrogate for FIP1L1-PDGFRA) was negative. Autoimmune/vasculitis screens (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative. Serum immunoglobulins demonstrated elevated IgG (2760 mg/dL) and IgG4 (1260 mg/dL), mildly elevated IgE (137.5 IU/mL), and high RF (144.4 IU/mL). Liver enzymes, BUN/creatinine, C3/C4, vitamin B12, cortisol, and NT-proBNP were within normal limits. ECG/echocardiogram were normal. Chest CT showed mild fibrosis and bronchiectasis. Bronchoscopy and AFB smears were negative; BAL cytology had 35% neutrophils and no eosinophils. Spirometry demonstrated severe obstruction with bronchodilator responsiveness; FeNO was 15 ppb. Stool leukocytes were present, but ova/parasite exams were negative. Serology was positive for Toxocara canis IgG (54.2 NovaTec-Units) and negative for other helminths and HIV. Empiric albendazole (400 mg twice daily for 5 days) was ineffective. Abdominal contrast-enhanced CT showed cholelithiasis without cholecystitis and no GI structural abnormality. Upper GI endoscopy was unremarkable. Colonoscopy demonstrated mucosal inflammation in the sigmoid, left, transverse, and right colon. Systematic colonic biopsies showed dense eosinophilic infiltration (>85 eosinophils/HPF in the left colon; >100 eosinophils/HPF in the transverse and right colon). Given the exclusion of hematologic neoplasms and secondary causes (including lack of response to anti-parasitic therapy and negative work-up for vasculitis/autoimmune disease), the findings were diagnostic of eosinophilic colitis. She was treated with oral methylprednisolone 16 mg and montelukast 5 mg. Symptoms resolved within two weeks with normalization of eosinophils to 0.3 G/L. Corticosteroids were tapered and discontinued, and montelukast was continued for three months with no symptom recurrence. This case illustrates eosinophilic colitis in an atopic patient with marked peripheral and tissue eosinophilia, elevated IgG4, negative myeloid neoplasm markers, and steroid-responsiveness, consistent with primary eosinophilic gastrointestinal disease after exclusion of secondary etiologies." }, { "index": 51, "label": "low_health_literacy", "original_text": "A 38-year-old male presented to the hospital with chest tightness and shortness of breath. Three years prior, he had experienced similar symptoms post-activity and received treatment at our hospital. Outpatient echocardiography indicated a left heart echomass suggestive of a myxoma, which led to his admission for further evaluation. Physical examination revealed pigmentation of the patient\u2019s ears characterized by multiple small brown and black spots. Abdominal computed tomography (CT) showed multiple livers and small cysts in the left kidney. Genetic testing identified mutations in the TTN and PRKAR1A genes. The diagnosis of CNC was confirmed through clinical examination, imaging, and genetic testing. Following symptomatic treatment, the patient\u2019s condition improved; however, he refused surgical intervention. On September 20, 2023, the patient presented to our hospital with exacerbated chest tightness and dyspnea. He reported difficulty lying supine and needing to sit upright to breathe. Physical examination revealed jugular vein distension, leftward and downward displacement of the heart boundary, irregular heart rhythm on auscultation, and a mitral valve murmur of intensity 2/6\u20133/6 in the fourth intercostal space along the left sternal margin. Wet rales were audible in both middle and lower lung fields. Palpation revealed a firm liver extending three fingers below the xiphoid process and two fingers below the rib cage, along with mild pitting edema in both lower limbs. Echocardiographic images indicated global heart enlargement, dilation of the aortic sinus and pulmonary artery, small-to-moderate mitral valve regurgitation, and an irregular echoic mass measuring 54 mm \u00d743 mm in the left chamber attached to the atrial septum. The left ventricular (LV) ejection fraction (EF) was 23.1%, with fractional shortening (FS) of 10.9%. Electrocardiography demonstrated atrial fibrillation (average ventricular rate, 150 beats/min) and abnormal Q waves in leads V1-V3. Based on the patient\u2019s history, the diagnosis included DCM and CNC with cardiac myxoma. Given the presence of end-stage heart failure and concurrent cardiac myxoma, the patient was hospitalized, and heart transplantation was considered a viable therapeutic option to address both conditions simultaneously. A suitable donor heart became available for immediate transplantation on October 1, 2024.\n\n\nSurgical procedure\n\nThe skin and subcutaneous tissues were carefully incised layer-by-layer through a median sternotomy. The sternum was sawed longitudinally open, and bleeding was controlled using electrocoagulation and bone wax. Extracardiac exploration uncovered global heart enlargement, most prominent in the LV. The heart showed diminished contractile strength. The aorta and the main pulmonary artery (PA) were dissected from the supravalvular region. Some tissues were preserved for posterior suturing, whereas most diseased right atrium, left atrium(LA), right ventricle, and LV were excised. Resection revealed a greyish-white mucoid mass. The donor and residual recipient LA tissues were sutured using double continuous 3/0 Prolene threads. The anastomosis was meticulously inspected multiple times, and no significant bleeding was observed. Similarly, end-to-end anastomosis of the donor ascending aorta and recipient PA was performed using continuous 5/0 Prolene sutures, and careful inspection revealed no bleeding.\n\nFurthermore, the donor\u2019s LA and recipient\u2019s PA were securely closed using double continuous 5/0 Prolene sutures. The inferior vena cava tissues of both the donor and recipient were similarly sutured with 5/0 Prolene sutures, and several inspections were performed to confirm no significant bleeding was present. The left side of the heart was then deflated, and as rewarming commenced, oxygenation was restored, the ascending aorta was unclamped, and the heart spontaneously returned to sinus rhythm. Continuous suturing with 5/0 Prolene was applied to both the donor and recipient\u2019s superior vena cava and diligently inspected to ensure the absence of significant bleeding. After the successful discontinuation of assisted circulation, the venous cavity was decannulated. Tissue samples from the patient\u2019s left heart and gray matter were collected for histopathological examination, and the diagnosis of DCM and cardiac myxoma were confirmed.\n\n\nPostoperative management\n\nOn the first day after heart transplantation, the patient produced 1200 ml of urine. Laboratory tests revealed a hypersensitive troponin T level of 796.70ng/L and an NT-proBNP level of 10798pg/ml. The complete blood count showed white blood cells at 17.15\u2009\u00d7\u2009109/L, with no significant abnormalities in other test results. The echocardiograph displayed an LVEF of 65%, FS of 35%, normal ventricular wall thickness and echogenicity, and no discernible abnormalities in valve morphology and structure. After heart transplantation, Methylprednisolone Sodium Succinate (0.25 g)intravenous hormone therapy was administered to enhance immunity, and Cefoperazone and Sulbactam Sodium (2 g) intravenous anti-infection treatment was provided. The patient was given a nutrient solution and liver and tiopronin on the first day post-surgery. On postoperative day three, Methylprednisolone Sodium Succinate was replaced with oral Prednisone Acetate (25 mg). Mycophenolate Mofetil capsules (0.5 g) were administered orally to minimize heart rejection, and (50 mg) of Carpofungin Acetate was administered intravenously to prevent fungal infections. The patient\u2019s urine output was 2000 ml, with hypersensitive troponin T levels of 390ng/L, NT-proBNP levels of 7877pg/ml, and a leukocyte count of 12.15\u2009\u00d7\u2009109/L. On the 7th day post-surgery, tacrolimus capsules were introduced at an oral dose of (1 mg) to minimize the patient\u2019s rejection of the donor heart, with careful monitoring of blood concentrations. Subsequently, the oral dosage of Prednisone Acetate was gradually decreased to (10 mg) while adjusting the tacrolimus blood concentration to 10.90ng/ml. The patient\u2019s recovery improved. On October 20, 2023, follow-up echocardiography (Fig. 6) indicated no abnormalities, with troponin levels of 85 ng/L, NT-proBNP of 210pg/ml, and all other test results within normal ranges. The patient exhibited excellent postoperative recovery and was discharged. Regular follow-up visits to our department after discharge showed that the patient remains in good condition.", "generated_summary": "This is the story of a 35-year-old man with a rare condition called Carney syndrome. This condition led to a growth in his heart (a myxoma) and made his heart large and weak (dilated cardiomyopathy). Three years ago, he went to the hospital for sudden chest tightness and shortness of breath. Heart pictures showed the growth. Exams and genetic tests confirmed Carney syndrome. His symptoms got better with medicines, and he went home. No surgery was done then. Later, his chest tightness and shortness of breath got much worse. Doctors said he had very severe heart failure. Tests showed the weak, enlarged heart was still there along with the heart growth. He received a heart transplant. The transplant successfully treated his heart failure." }, { "index": 51, "label": "intermediate_health_literacy", "original_text": "A 38-year-old male presented to the hospital with chest tightness and shortness of breath. Three years prior, he had experienced similar symptoms post-activity and received treatment at our hospital. Outpatient echocardiography indicated a left heart echomass suggestive of a myxoma, which led to his admission for further evaluation. Physical examination revealed pigmentation of the patient\u2019s ears characterized by multiple small brown and black spots. Abdominal computed tomography (CT) showed multiple livers and small cysts in the left kidney. Genetic testing identified mutations in the TTN and PRKAR1A genes. The diagnosis of CNC was confirmed through clinical examination, imaging, and genetic testing. Following symptomatic treatment, the patient\u2019s condition improved; however, he refused surgical intervention. On September 20, 2023, the patient presented to our hospital with exacerbated chest tightness and dyspnea. He reported difficulty lying supine and needing to sit upright to breathe. Physical examination revealed jugular vein distension, leftward and downward displacement of the heart boundary, irregular heart rhythm on auscultation, and a mitral valve murmur of intensity 2/6\u20133/6 in the fourth intercostal space along the left sternal margin. Wet rales were audible in both middle and lower lung fields. Palpation revealed a firm liver extending three fingers below the xiphoid process and two fingers below the rib cage, along with mild pitting edema in both lower limbs. Echocardiographic images indicated global heart enlargement, dilation of the aortic sinus and pulmonary artery, small-to-moderate mitral valve regurgitation, and an irregular echoic mass measuring 54 mm \u00d743 mm in the left chamber attached to the atrial septum. The left ventricular (LV) ejection fraction (EF) was 23.1%, with fractional shortening (FS) of 10.9%. Electrocardiography demonstrated atrial fibrillation (average ventricular rate, 150 beats/min) and abnormal Q waves in leads V1-V3. Based on the patient\u2019s history, the diagnosis included DCM and CNC with cardiac myxoma. Given the presence of end-stage heart failure and concurrent cardiac myxoma, the patient was hospitalized, and heart transplantation was considered a viable therapeutic option to address both conditions simultaneously. A suitable donor heart became available for immediate transplantation on October 1, 2024.\n\n\nSurgical procedure\n\nThe skin and subcutaneous tissues were carefully incised layer-by-layer through a median sternotomy. The sternum was sawed longitudinally open, and bleeding was controlled using electrocoagulation and bone wax. Extracardiac exploration uncovered global heart enlargement, most prominent in the LV. The heart showed diminished contractile strength. The aorta and the main pulmonary artery (PA) were dissected from the supravalvular region. Some tissues were preserved for posterior suturing, whereas most diseased right atrium, left atrium(LA), right ventricle, and LV were excised. Resection revealed a greyish-white mucoid mass. The donor and residual recipient LA tissues were sutured using double continuous 3/0 Prolene threads. The anastomosis was meticulously inspected multiple times, and no significant bleeding was observed. Similarly, end-to-end anastomosis of the donor ascending aorta and recipient PA was performed using continuous 5/0 Prolene sutures, and careful inspection revealed no bleeding.\n\nFurthermore, the donor\u2019s LA and recipient\u2019s PA were securely closed using double continuous 5/0 Prolene sutures. The inferior vena cava tissues of both the donor and recipient were similarly sutured with 5/0 Prolene sutures, and several inspections were performed to confirm no significant bleeding was present. The left side of the heart was then deflated, and as rewarming commenced, oxygenation was restored, the ascending aorta was unclamped, and the heart spontaneously returned to sinus rhythm. Continuous suturing with 5/0 Prolene was applied to both the donor and recipient\u2019s superior vena cava and diligently inspected to ensure the absence of significant bleeding. After the successful discontinuation of assisted circulation, the venous cavity was decannulated. Tissue samples from the patient\u2019s left heart and gray matter were collected for histopathological examination, and the diagnosis of DCM and cardiac myxoma were confirmed.\n\n\nPostoperative management\n\nOn the first day after heart transplantation, the patient produced 1200 ml of urine. Laboratory tests revealed a hypersensitive troponin T level of 796.70ng/L and an NT-proBNP level of 10798pg/ml. The complete blood count showed white blood cells at 17.15\u2009\u00d7\u2009109/L, with no significant abnormalities in other test results. The echocardiograph displayed an LVEF of 65%, FS of 35%, normal ventricular wall thickness and echogenicity, and no discernible abnormalities in valve morphology and structure. After heart transplantation, Methylprednisolone Sodium Succinate (0.25 g)intravenous hormone therapy was administered to enhance immunity, and Cefoperazone and Sulbactam Sodium (2 g) intravenous anti-infection treatment was provided. The patient was given a nutrient solution and liver and tiopronin on the first day post-surgery. On postoperative day three, Methylprednisolone Sodium Succinate was replaced with oral Prednisone Acetate (25 mg). Mycophenolate Mofetil capsules (0.5 g) were administered orally to minimize heart rejection, and (50 mg) of Carpofungin Acetate was administered intravenously to prevent fungal infections. The patient\u2019s urine output was 2000 ml, with hypersensitive troponin T levels of 390ng/L, NT-proBNP levels of 7877pg/ml, and a leukocyte count of 12.15\u2009\u00d7\u2009109/L. On the 7th day post-surgery, tacrolimus capsules were introduced at an oral dose of (1 mg) to minimize the patient\u2019s rejection of the donor heart, with careful monitoring of blood concentrations. Subsequently, the oral dosage of Prednisone Acetate was gradually decreased to (10 mg) while adjusting the tacrolimus blood concentration to 10.90ng/ml. The patient\u2019s recovery improved. On October 20, 2023, follow-up echocardiography (Fig. 6) indicated no abnormalities, with troponin levels of 85 ng/L, NT-proBNP of 210pg/ml, and all other test results within normal ranges. The patient exhibited excellent postoperative recovery and was discharged. Regular follow-up visits to our department after discharge showed that the patient remains in good condition.", "generated_summary": "A 35-year-old man developed heart failure due to Carney syndrome, which caused a cardiac myxoma and dilated cardiomyopathy. Three years earlier, he presented with sudden chest tightness and shortness of breath. Echocardiography suggested a myxoma, and the diagnosis of Carney syndrome with cardiac myxoma was confirmed by physical examination and genetic screening. He improved with symptomatic treatment and was discharged; surgery was not performed at that time. His symptoms later worsened, and he returned with severe (New York Heart Association class IV) heart failure. Echocardiography then showed dilated cardiomyopathy accompanied by a cardiac myxoma. He ultimately underwent heart transplantation, which successfully treated his heart failure." }, { "index": 51, "label": "proficient_health_literacy", "original_text": "A 38-year-old male presented to the hospital with chest tightness and shortness of breath. Three years prior, he had experienced similar symptoms post-activity and received treatment at our hospital. Outpatient echocardiography indicated a left heart echomass suggestive of a myxoma, which led to his admission for further evaluation. Physical examination revealed pigmentation of the patient\u2019s ears characterized by multiple small brown and black spots. Abdominal computed tomography (CT) showed multiple livers and small cysts in the left kidney. Genetic testing identified mutations in the TTN and PRKAR1A genes. The diagnosis of CNC was confirmed through clinical examination, imaging, and genetic testing. Following symptomatic treatment, the patient\u2019s condition improved; however, he refused surgical intervention. On September 20, 2023, the patient presented to our hospital with exacerbated chest tightness and dyspnea. He reported difficulty lying supine and needing to sit upright to breathe. Physical examination revealed jugular vein distension, leftward and downward displacement of the heart boundary, irregular heart rhythm on auscultation, and a mitral valve murmur of intensity 2/6\u20133/6 in the fourth intercostal space along the left sternal margin. Wet rales were audible in both middle and lower lung fields. Palpation revealed a firm liver extending three fingers below the xiphoid process and two fingers below the rib cage, along with mild pitting edema in both lower limbs. Echocardiographic images indicated global heart enlargement, dilation of the aortic sinus and pulmonary artery, small-to-moderate mitral valve regurgitation, and an irregular echoic mass measuring 54 mm \u00d743 mm in the left chamber attached to the atrial septum. The left ventricular (LV) ejection fraction (EF) was 23.1%, with fractional shortening (FS) of 10.9%. Electrocardiography demonstrated atrial fibrillation (average ventricular rate, 150 beats/min) and abnormal Q waves in leads V1-V3. Based on the patient\u2019s history, the diagnosis included DCM and CNC with cardiac myxoma. Given the presence of end-stage heart failure and concurrent cardiac myxoma, the patient was hospitalized, and heart transplantation was considered a viable therapeutic option to address both conditions simultaneously. A suitable donor heart became available for immediate transplantation on October 1, 2024.\n\n\nSurgical procedure\n\nThe skin and subcutaneous tissues were carefully incised layer-by-layer through a median sternotomy. The sternum was sawed longitudinally open, and bleeding was controlled using electrocoagulation and bone wax. Extracardiac exploration uncovered global heart enlargement, most prominent in the LV. The heart showed diminished contractile strength. The aorta and the main pulmonary artery (PA) were dissected from the supravalvular region. Some tissues were preserved for posterior suturing, whereas most diseased right atrium, left atrium(LA), right ventricle, and LV were excised. Resection revealed a greyish-white mucoid mass. The donor and residual recipient LA tissues were sutured using double continuous 3/0 Prolene threads. The anastomosis was meticulously inspected multiple times, and no significant bleeding was observed. Similarly, end-to-end anastomosis of the donor ascending aorta and recipient PA was performed using continuous 5/0 Prolene sutures, and careful inspection revealed no bleeding.\n\nFurthermore, the donor\u2019s LA and recipient\u2019s PA were securely closed using double continuous 5/0 Prolene sutures. The inferior vena cava tissues of both the donor and recipient were similarly sutured with 5/0 Prolene sutures, and several inspections were performed to confirm no significant bleeding was present. The left side of the heart was then deflated, and as rewarming commenced, oxygenation was restored, the ascending aorta was unclamped, and the heart spontaneously returned to sinus rhythm. Continuous suturing with 5/0 Prolene was applied to both the donor and recipient\u2019s superior vena cava and diligently inspected to ensure the absence of significant bleeding. After the successful discontinuation of assisted circulation, the venous cavity was decannulated. Tissue samples from the patient\u2019s left heart and gray matter were collected for histopathological examination, and the diagnosis of DCM and cardiac myxoma were confirmed.\n\n\nPostoperative management\n\nOn the first day after heart transplantation, the patient produced 1200 ml of urine. Laboratory tests revealed a hypersensitive troponin T level of 796.70ng/L and an NT-proBNP level of 10798pg/ml. The complete blood count showed white blood cells at 17.15\u2009\u00d7\u2009109/L, with no significant abnormalities in other test results. The echocardiograph displayed an LVEF of 65%, FS of 35%, normal ventricular wall thickness and echogenicity, and no discernible abnormalities in valve morphology and structure. After heart transplantation, Methylprednisolone Sodium Succinate (0.25 g)intravenous hormone therapy was administered to enhance immunity, and Cefoperazone and Sulbactam Sodium (2 g) intravenous anti-infection treatment was provided. The patient was given a nutrient solution and liver and tiopronin on the first day post-surgery. On postoperative day three, Methylprednisolone Sodium Succinate was replaced with oral Prednisone Acetate (25 mg). Mycophenolate Mofetil capsules (0.5 g) were administered orally to minimize heart rejection, and (50 mg) of Carpofungin Acetate was administered intravenously to prevent fungal infections. The patient\u2019s urine output was 2000 ml, with hypersensitive troponin T levels of 390ng/L, NT-proBNP levels of 7877pg/ml, and a leukocyte count of 12.15\u2009\u00d7\u2009109/L. On the 7th day post-surgery, tacrolimus capsules were introduced at an oral dose of (1 mg) to minimize the patient\u2019s rejection of the donor heart, with careful monitoring of blood concentrations. Subsequently, the oral dosage of Prednisone Acetate was gradually decreased to (10 mg) while adjusting the tacrolimus blood concentration to 10.90ng/ml. The patient\u2019s recovery improved. On October 20, 2023, follow-up echocardiography (Fig. 6) indicated no abnormalities, with troponin levels of 85 ng/L, NT-proBNP of 210pg/ml, and all other test results within normal ranges. The patient exhibited excellent postoperative recovery and was discharged. Regular follow-up visits to our department after discharge showed that the patient remains in good condition.", "generated_summary": "A 38-year-old male with a three-year history of exertional chest tightness and dyspnea re-presented with progressive orthopnea and decompensated heart failure. Three years prior, outpatient echocardiography had identified a left-sided intracardiac echogenic mass consistent with myxoma, prompting admission. Physical examination at that time noted auricular hyperpigmentation with multiple brown-black macules. Abdominal imaging reported extracardiac findings, and genetic testing revealed TTN and PRKAR1A mutations. The diagnosis of Carney complex (CNC) with cardiac myxoma was established by clinical findings, imaging, and genetics. He improved with symptomatic therapy but declined definitive surgery. \n\nOn re-presentation (September 20, 2023), exam showed jugular venous distension, cardiomegaly with leftward/downward displacement, an irregular rhythm, a 2/6\u20133/6 mitral murmur at the left sternal border (fourth intercostal space), bilateral mid-to-lower lung wet rales, hepatomegaly (firm liver palpable 3 fingerbreadths below the xiphoid and 2 fingerbreadths below the costal margin), and mild bilateral pitting edema. ECG demonstrated atrial fibrillation (average ventricular rate ~150 bpm) with abnormal Q waves in V1\u2013V3. Transthoracic echocardiography showed global cardiac enlargement, dilation of the aortic sinus and main pulmonary artery, small-to-moderate mitral regurgitation, and an irregular echogenic mass measuring 54 \u00d7 43 mm in the left chamber attached to the atrial septum. LV systolic function was severely depressed (LVEF 23.1%, FS 10.9%). The working diagnosis was end-stage heart failure due to dilated cardiomyopathy (DCM) in the setting of CNC with a cardiac myxoma. Given concomitant end-stage DCM and intracardiac tumor, heart transplantation was pursued when a suitable donor became available.\n\nOperative course: Median sternotomy was performed with cardiopulmonary bypass. Exploration confirmed global cardiomegaly, most pronounced in the LV, with poor contractility. Diseased native right atrium, left atrium, right ventricle, and left ventricle were resected, revealing a gray-white mucoid mass consistent with myxoma. Standard orthotopic heart transplantation anastomoses were completed (including left atrial cuff, great vessels, and caval anastomoses) using continuous Prolene sutures (3/0 and 5/0), with meticulous hemostasis. After rewarming and aortic unclamping, the graft resumed sinus rhythm spontaneously. Assisted circulation was weaned uneventfully. Histopathology of the explanted tissues confirmed DCM and cardiac myxoma.\n\nPostoperative course: On postoperative day (POD) 1, urine output was 1200 mL; hs\u2011troponin T was 796.70 ng/L; NT\u2011proBNP 10,798 pg/mL; WBC 17.15 \u00d7 10^9/L. Echocardiography demonstrated normal ventricular wall thickness and morphology with LVEF 65% (FS 35%). Immunosuppression and anti-infective therapy included IV methylprednisolone sodium succinate 0.25 g, cefoperazone/sulbactam 2 g, supportive nutrition, and hepatoprotective therapy. On POD 3, steroids were transitioned to oral prednisone acetate 25 mg; mycophenolate mofetil 0.5 g PO was initiated for rejection prophylaxis; caspofungin acetate 50 mg IV was added for antifungal prophylaxis. Urine output increased to 2000 mL; hs\u2011troponin T decreased to 390 ng/L; NT\u2011proBNP decreased to 7877 pg/mL; WBC 12.15 \u00d7 10^9/L. On POD 7, tacrolimus 1 mg PO was introduced with therapeutic drug monitoring (blood level 10.90 ng/mL), and prednisone was tapered to 10 mg. Clinical status steadily improved. By late postoperative follow-up (October 20, 2023), echocardiography was unremarkable; hs\u2011troponin T was 85 ng/L; NT\u2011proBNP 210 pg/mL; other labs were within normal limits. The patient was discharged in excellent condition and has remained clinically stable on outpatient follow-up.\n\nInterpretation: This case illustrates CNC with PRKAR1A mutation manifesting as atrial myxoma and end-stage DCM, compounded by atrial fibrillation and severe LV systolic dysfunction (LVEF 23.1%). Orthotopic heart transplantation effectively addressed both the intracardiac tumor and the refractory heart failure, with prompt normalization of graft function and favorable early outcomes under standard triple immunosuppression." }, { "index": 52, "label": "low_health_literacy", "original_text": "2 years 6 months old female pre-schooler with a previous diagnosis of NF1. She consulted due to a 4 week diarrhea with blood streaks (5 to 10 episodes a day). A week after the onset of the diarrhea she consulted the emergency department, where rotavirus (+) was detected, with low inflammatory parameters, negative coproculture and normal abdominal ultrasound. She was hospitalized for 3 days to manage dehydration and was discharged without bleeding, with persistence of semi-liquid stools. 10 days after discharge she presented diarrhea with blood streaks, associated with low intake and weight loss of 1 kg reported by parents. They consulted a pediatric gastroenterologist who requested a polymerase chain reaction (PCR) panel of gastrointestinal pathogens and PCR of Clostridium difficile (which were negative) and indicated hospitalization for study.\n\nOn direct questioning, the parents reported no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions. They did not own pets, and there was no history of travel or recent dietary changes.\n\nThe patient was diagnosed with confirmed NF1 at 8 months of age by genetic testing with the heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28). She has skin involvement (caf\u00e9 con leche spots) and bone involvement. At 18 months she required ankle arthrodesis for tibial curvature. She has no family history of NF1 or inflammatory bowel disease.\n\nOn physical examination, the abdomen was soft and indistinct, with increased air-bubble murmurs, without masses or visceral enlargement. The perianal examination was normal. There were multiple brown-coffee stains on the lower extremities and back. General examinations were performed, including a blood count with moderate microcytic-hypochromic anaemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and discretely elevated inflammatory parameters (CRP 1.37 mg/dL, normal value up to 0.5 mg/dL).\n\nA colonoscopy was performed, the rectum, sigmoid and various segments of the colon were examined up to the cecum, visualizing the ileocecal valve and the appendicular orifice. The last few centimeters of the distal ileum were also inspected. The mucosa from the anal margin to the cecum was observed to be erythematous, with loss of vascular transparency, unlike the cecal mucosa, which appeared normal. No lesions were identified in the anal canal or cecum.\n\nBiopsies of the small intestine (ileon) and large intestine were taken. Microscopic examination showed mucosa of ileal type with preserved villous architecture and adequate epithelial differentiation, with a non-inflamed lamina propria. The mucosa of the large intestine had a mild distortion of architecture and adequate epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate and hyperplasia of lymphoid follicles. Isolated foci of microabscesses were recognized. The biopsy was consistent with mild colitis, with signs suggesting chronicity.\n\nIn addition, a PCR study for cytomegalovirus (CMV) was requested in a colon biopsy, which was positive.\n\nGiven a positive PCR for CMV, CMV IgG and IgM and CMV viral load in blood were requested, resulting in a positive IgG, negative IgM, and CMV viral load of 79.7 IU/ml. Further laboratory studies included PCR for gastrointestinal pathogens and PCR for Clostridium difficile in stool, both of which were negative. In the colon biopsy, Gram stain microbiological studies were requested, which showed +++ leukocytes without bacteria; biopsy culture showed S. gallolyticus/equinus complex in very low amount (interpreted as bacterial flora); acridine orange, Ziehl-Neelsen, Koch culture, and ADV PCR were negative.\n\nEndoscopy and histology suggestive of UC was reported in the context of a patient with moderate symptoms (PUCAI 50) who was started on Mesalazine (70 mg/kg/day three times daily) and a request for a faecal calprotectin was made which was greater than 600 ug/g.\n\nThe immunology team evaluated the patient for suspected immunodeficiency. The parents did not report a history of infections, they reported that they were vaccinated, that they had good weight gain, no family history of immunodeficiencies, auto-immunity or early deaths. A study with lymphocyte subpopulations (normal), immunoglobulins (normal), HIV (negative), memory T lymphocytes (with alterations expected in the context of CMV viremia) and lymphoproliferation test (normal) was requested. In addition, a genetic panel of primary immunodeficiencies (Invitae) was performed, which contains 429 genes, of which 68 make up the panel of monogenic inflammatory intestinal disease. 7 variants of uncertain significance were obtained, none included in the panel of monogenic IBD.\n\nGanciclovir was initiated intravenous for CMV infection and continued for 15 days. The last PCR CMV control prior to discharge reported undetectable load.\n\nThe patient improved during the hospital stay with decreased frequency of stools and increased consistency, no rectal bleeding, no nocturnal stools and no abdominal pain, with PUCAI 0 at discharge.\n\nTwo months later, he presented with a reactivation of IBD with bloody diarrhea (PUCAI 35). A blood count was performed (normal), a panel of gastrointestinal pathogens was performed (\u2013), PCR for Clostridium difficile was performed (+), and CMV load was undetectable. He was treated with oral metronidazole. However, he persisted with diarrhea with blood streaks, so he was hospitalized again.\n\nA colonoscopy was performed, where erythematous mucous was observed in a diffuse form from the rectum to the cecum, with nodularity and loss of vascular transparency in the submucosa, greater in the left and transverse colon segments. No focal lesions were observed. The mucosa of the ileum and anal canal were observed without lesions.\n\nBiopsy of the terminal ileum, right colon and left colon was performed. Microscopic examination of the ileal-type mucosa showed preserved villous architecture and adequate epithelial differentiation. The lamina propria showed no signs of inflammation. There were no aphthous erosions or granulomas. The mucosa of the large intestine showed mild distortion of architecture and epithelial dedifferentiation. The lamina propria was expanded by mixed inflammatory infiltrate, transmucosal distribution. Foci of cryptitis and cryptitic microabscesses and hyperplasia of reactive lymphoid follicles were recognized. No granulomas, viral or parasitic cytopathic changes were observed. All fragments of the left colon sample presented a similar histopathological picture.\n\nShe was given oral treatment with Vancomycin and Prednisone (1 mg/kg/day) with a good response and a favorable evolution. She was discharged with a decrease in the frequency of bowel movements. She persists with mild symptoms (PUCAI 5) in outpatient control, so the dose of corticosteroids is progressively decreased and she remains on treatment with Mesalazina.\n", "generated_summary": "This child is 2 and a half years old and has a condition called NF1. She had diarrhea with blood. Doctors used a small camera to look inside her large intestine. The inner lining looked red and irritated from the bottom (anus) to the start of the large intestine (cecum). The usual fine pattern of tiny blood vessels was hard to see. Small tissue samples showed long-lasting swelling. This fits a disease of the large intestine called ulcerative colitis. A special lab test (PCR) on the tissue found a virus called CMV." }, { "index": 52, "label": "intermediate_health_literacy", "original_text": "2 years 6 months old female pre-schooler with a previous diagnosis of NF1. She consulted due to a 4 week diarrhea with blood streaks (5 to 10 episodes a day). A week after the onset of the diarrhea she consulted the emergency department, where rotavirus (+) was detected, with low inflammatory parameters, negative coproculture and normal abdominal ultrasound. She was hospitalized for 3 days to manage dehydration and was discharged without bleeding, with persistence of semi-liquid stools. 10 days after discharge she presented diarrhea with blood streaks, associated with low intake and weight loss of 1 kg reported by parents. They consulted a pediatric gastroenterologist who requested a polymerase chain reaction (PCR) panel of gastrointestinal pathogens and PCR of Clostridium difficile (which were negative) and indicated hospitalization for study.\n\nOn direct questioning, the parents reported no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions. They did not own pets, and there was no history of travel or recent dietary changes.\n\nThe patient was diagnosed with confirmed NF1 at 8 months of age by genetic testing with the heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28). She has skin involvement (caf\u00e9 con leche spots) and bone involvement. At 18 months she required ankle arthrodesis for tibial curvature. She has no family history of NF1 or inflammatory bowel disease.\n\nOn physical examination, the abdomen was soft and indistinct, with increased air-bubble murmurs, without masses or visceral enlargement. The perianal examination was normal. There were multiple brown-coffee stains on the lower extremities and back. General examinations were performed, including a blood count with moderate microcytic-hypochromic anaemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and discretely elevated inflammatory parameters (CRP 1.37 mg/dL, normal value up to 0.5 mg/dL).\n\nA colonoscopy was performed, the rectum, sigmoid and various segments of the colon were examined up to the cecum, visualizing the ileocecal valve and the appendicular orifice. The last few centimeters of the distal ileum were also inspected. The mucosa from the anal margin to the cecum was observed to be erythematous, with loss of vascular transparency, unlike the cecal mucosa, which appeared normal. No lesions were identified in the anal canal or cecum.\n\nBiopsies of the small intestine (ileon) and large intestine were taken. Microscopic examination showed mucosa of ileal type with preserved villous architecture and adequate epithelial differentiation, with a non-inflamed lamina propria. The mucosa of the large intestine had a mild distortion of architecture and adequate epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate and hyperplasia of lymphoid follicles. Isolated foci of microabscesses were recognized. The biopsy was consistent with mild colitis, with signs suggesting chronicity.\n\nIn addition, a PCR study for cytomegalovirus (CMV) was requested in a colon biopsy, which was positive.\n\nGiven a positive PCR for CMV, CMV IgG and IgM and CMV viral load in blood were requested, resulting in a positive IgG, negative IgM, and CMV viral load of 79.7 IU/ml. Further laboratory studies included PCR for gastrointestinal pathogens and PCR for Clostridium difficile in stool, both of which were negative. In the colon biopsy, Gram stain microbiological studies were requested, which showed +++ leukocytes without bacteria; biopsy culture showed S. gallolyticus/equinus complex in very low amount (interpreted as bacterial flora); acridine orange, Ziehl-Neelsen, Koch culture, and ADV PCR were negative.\n\nEndoscopy and histology suggestive of UC was reported in the context of a patient with moderate symptoms (PUCAI 50) who was started on Mesalazine (70 mg/kg/day three times daily) and a request for a faecal calprotectin was made which was greater than 600 ug/g.\n\nThe immunology team evaluated the patient for suspected immunodeficiency. The parents did not report a history of infections, they reported that they were vaccinated, that they had good weight gain, no family history of immunodeficiencies, auto-immunity or early deaths. A study with lymphocyte subpopulations (normal), immunoglobulins (normal), HIV (negative), memory T lymphocytes (with alterations expected in the context of CMV viremia) and lymphoproliferation test (normal) was requested. In addition, a genetic panel of primary immunodeficiencies (Invitae) was performed, which contains 429 genes, of which 68 make up the panel of monogenic inflammatory intestinal disease. 7 variants of uncertain significance were obtained, none included in the panel of monogenic IBD.\n\nGanciclovir was initiated intravenous for CMV infection and continued for 15 days. The last PCR CMV control prior to discharge reported undetectable load.\n\nThe patient improved during the hospital stay with decreased frequency of stools and increased consistency, no rectal bleeding, no nocturnal stools and no abdominal pain, with PUCAI 0 at discharge.\n\nTwo months later, he presented with a reactivation of IBD with bloody diarrhea (PUCAI 35). A blood count was performed (normal), a panel of gastrointestinal pathogens was performed (\u2013), PCR for Clostridium difficile was performed (+), and CMV load was undetectable. He was treated with oral metronidazole. However, he persisted with diarrhea with blood streaks, so he was hospitalized again.\n\nA colonoscopy was performed, where erythematous mucous was observed in a diffuse form from the rectum to the cecum, with nodularity and loss of vascular transparency in the submucosa, greater in the left and transverse colon segments. No focal lesions were observed. The mucosa of the ileum and anal canal were observed without lesions.\n\nBiopsy of the terminal ileum, right colon and left colon was performed. Microscopic examination of the ileal-type mucosa showed preserved villous architecture and adequate epithelial differentiation. The lamina propria showed no signs of inflammation. There were no aphthous erosions or granulomas. The mucosa of the large intestine showed mild distortion of architecture and epithelial dedifferentiation. The lamina propria was expanded by mixed inflammatory infiltrate, transmucosal distribution. Foci of cryptitis and cryptitic microabscesses and hyperplasia of reactive lymphoid follicles were recognized. No granulomas, viral or parasitic cytopathic changes were observed. All fragments of the left colon sample presented a similar histopathological picture.\n\nShe was given oral treatment with Vancomycin and Prednisone (1 mg/kg/day) with a good response and a favorable evolution. She was discharged with a decrease in the frequency of bowel movements. She persists with mild symptoms (PUCAI 5) in outpatient control, so the dose of corticosteroids is progressively decreased and she remains on treatment with Mesalazina.\n", "generated_summary": "A 2.5-year-old preschooler with known neurofibromatosis type 1 (NF1) presented with several weeks of bloody diarrhea. Colonoscopy showed diffuse inflammation from the anal margin to the cecum with loss of the normal vascular pattern. Colon biopsies demonstrated chronic inflammatory changes consistent with ulcerative colitis. Cytomegalovirus (CMV) infection was confirmed by PCR performed on the colon tissue. Together, these findings support a diagnosis of ulcerative colitis with concurrent CMV infection as the likely cause of the bloody diarrhea." }, { "index": 52, "label": "proficient_health_literacy", "original_text": "2 years 6 months old female pre-schooler with a previous diagnosis of NF1. She consulted due to a 4 week diarrhea with blood streaks (5 to 10 episodes a day). A week after the onset of the diarrhea she consulted the emergency department, where rotavirus (+) was detected, with low inflammatory parameters, negative coproculture and normal abdominal ultrasound. She was hospitalized for 3 days to manage dehydration and was discharged without bleeding, with persistence of semi-liquid stools. 10 days after discharge she presented diarrhea with blood streaks, associated with low intake and weight loss of 1 kg reported by parents. They consulted a pediatric gastroenterologist who requested a polymerase chain reaction (PCR) panel of gastrointestinal pathogens and PCR of Clostridium difficile (which were negative) and indicated hospitalization for study.\n\nOn direct questioning, the parents reported no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions. They did not own pets, and there was no history of travel or recent dietary changes.\n\nThe patient was diagnosed with confirmed NF1 at 8 months of age by genetic testing with the heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28). She has skin involvement (caf\u00e9 con leche spots) and bone involvement. At 18 months she required ankle arthrodesis for tibial curvature. She has no family history of NF1 or inflammatory bowel disease.\n\nOn physical examination, the abdomen was soft and indistinct, with increased air-bubble murmurs, without masses or visceral enlargement. The perianal examination was normal. There were multiple brown-coffee stains on the lower extremities and back. General examinations were performed, including a blood count with moderate microcytic-hypochromic anaemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and discretely elevated inflammatory parameters (CRP 1.37 mg/dL, normal value up to 0.5 mg/dL).\n\nA colonoscopy was performed, the rectum, sigmoid and various segments of the colon were examined up to the cecum, visualizing the ileocecal valve and the appendicular orifice. The last few centimeters of the distal ileum were also inspected. The mucosa from the anal margin to the cecum was observed to be erythematous, with loss of vascular transparency, unlike the cecal mucosa, which appeared normal. No lesions were identified in the anal canal or cecum.\n\nBiopsies of the small intestine (ileon) and large intestine were taken. Microscopic examination showed mucosa of ileal type with preserved villous architecture and adequate epithelial differentiation, with a non-inflamed lamina propria. The mucosa of the large intestine had a mild distortion of architecture and adequate epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate and hyperplasia of lymphoid follicles. Isolated foci of microabscesses were recognized. The biopsy was consistent with mild colitis, with signs suggesting chronicity.\n\nIn addition, a PCR study for cytomegalovirus (CMV) was requested in a colon biopsy, which was positive.\n\nGiven a positive PCR for CMV, CMV IgG and IgM and CMV viral load in blood were requested, resulting in a positive IgG, negative IgM, and CMV viral load of 79.7 IU/ml. Further laboratory studies included PCR for gastrointestinal pathogens and PCR for Clostridium difficile in stool, both of which were negative. In the colon biopsy, Gram stain microbiological studies were requested, which showed +++ leukocytes without bacteria; biopsy culture showed S. gallolyticus/equinus complex in very low amount (interpreted as bacterial flora); acridine orange, Ziehl-Neelsen, Koch culture, and ADV PCR were negative.\n\nEndoscopy and histology suggestive of UC was reported in the context of a patient with moderate symptoms (PUCAI 50) who was started on Mesalazine (70 mg/kg/day three times daily) and a request for a faecal calprotectin was made which was greater than 600 ug/g.\n\nThe immunology team evaluated the patient for suspected immunodeficiency. The parents did not report a history of infections, they reported that they were vaccinated, that they had good weight gain, no family history of immunodeficiencies, auto-immunity or early deaths. A study with lymphocyte subpopulations (normal), immunoglobulins (normal), HIV (negative), memory T lymphocytes (with alterations expected in the context of CMV viremia) and lymphoproliferation test (normal) was requested. In addition, a genetic panel of primary immunodeficiencies (Invitae) was performed, which contains 429 genes, of which 68 make up the panel of monogenic inflammatory intestinal disease. 7 variants of uncertain significance were obtained, none included in the panel of monogenic IBD.\n\nGanciclovir was initiated intravenous for CMV infection and continued for 15 days. The last PCR CMV control prior to discharge reported undetectable load.\n\nThe patient improved during the hospital stay with decreased frequency of stools and increased consistency, no rectal bleeding, no nocturnal stools and no abdominal pain, with PUCAI 0 at discharge.\n\nTwo months later, he presented with a reactivation of IBD with bloody diarrhea (PUCAI 35). A blood count was performed (normal), a panel of gastrointestinal pathogens was performed (\u2013), PCR for Clostridium difficile was performed (+), and CMV load was undetectable. He was treated with oral metronidazole. However, he persisted with diarrhea with blood streaks, so he was hospitalized again.\n\nA colonoscopy was performed, where erythematous mucous was observed in a diffuse form from the rectum to the cecum, with nodularity and loss of vascular transparency in the submucosa, greater in the left and transverse colon segments. No focal lesions were observed. The mucosa of the ileum and anal canal were observed without lesions.\n\nBiopsy of the terminal ileum, right colon and left colon was performed. Microscopic examination of the ileal-type mucosa showed preserved villous architecture and adequate epithelial differentiation. The lamina propria showed no signs of inflammation. There were no aphthous erosions or granulomas. The mucosa of the large intestine showed mild distortion of architecture and epithelial dedifferentiation. The lamina propria was expanded by mixed inflammatory infiltrate, transmucosal distribution. Foci of cryptitis and cryptitic microabscesses and hyperplasia of reactive lymphoid follicles were recognized. No granulomas, viral or parasitic cytopathic changes were observed. All fragments of the left colon sample presented a similar histopathological picture.\n\nShe was given oral treatment with Vancomycin and Prednisone (1 mg/kg/day) with a good response and a favorable evolution. She was discharged with a decrease in the frequency of bowel movements. She persists with mild symptoms (PUCAI 5) in outpatient control, so the dose of corticosteroids is progressively decreased and she remains on treatment with Mesalazina.\n", "generated_summary": "A 2 years 6 months old female with genetically confirmed NF1 (heterozygous pathogenic variant c.5606_5627del [p.Gly1869Valfs*28]) presented with 4 weeks of blood-streaked diarrhea (5\u201310/day). Initial ED evaluation showed rotavirus positive, low inflammatory markers, negative coproculture, and a normal abdominal ultrasound; she was hospitalized 3 days for dehydration and discharged with persistent semi-liquid stools. Ten days later she recurred with blood-streaked diarrhea, decreased intake, and ~1 kg weight loss, prompting admission for further workup after outpatient GI pathogen and C. difficile PCR panels were negative. There was no fever, abdominal pain, vomiting, respiratory/urinary symptoms, arthralgia, pet exposure, travel, or dietary changes. NF1 phenotype included caf\u00e9-au-lait macules and osseous involvement; she underwent ankle arthrodesis at 18 months for tibial bowing; no family history of NF1 or IBD. Exam: soft, non-tender abdomen with increased bowel sounds; perianal exam normal; multiple caf\u00e9-au-lait macules. Labs: microcytic\u2013hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (13,900/\u00b5L), CRP 1.37 mg/dL (ULN 0.5).\n\nIndex colonoscopy evaluated rectum, sigmoid, and colon to cecum; distal ileum was also inspected. The colonic mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency; the cecal mucosa itself appeared normal; no lesions in the anal canal or cecum. Biopsies: ileal mucosa with preserved villous architecture, adequate epithelial differentiation, and non-inflamed lamina propria. Colonic mucosa showed mild architectural distortion, adequate epithelial differentiation, lamina propria edema with a mild mixed inflammatory infiltrate, lymphoid follicular hyperplasia, and isolated crypt microabscesses\u2014consistent with mild colitis with features suggesting chronicity. CMV PCR on colon biopsy was positive. Additional virology: CMV IgG positive, IgM negative; plasma CMV viral load 79.7 IU/mL. Stool GI pathogen panel and C. difficile PCR were negative. Biopsy microbiology: Gram stain +++ leukocytes without bacteria; culture with very low S. gallolyticus/equinus interpreted as flora; acridine orange, Ziehl\u2013Neelsen, Koch culture, and adenovirus PCR were negative. Clinical impression: endoscopy and histology suggestive of ulcerative colitis (UC) in the setting of moderate activity (PUCAI 50). Mesalazine 70 mg/kg/day tid initiated; fecal calprotectin >600 \u00b5g/g. Immunology workup for suspected PID: normal lymphocyte subsets and immunoglobulins; HIV negative; memory T-cell abnormalities attributed to CMV viremia; lymphoproliferation normal. Invitae PID panel (429 genes; 68 monogenic IBD) returned 7 VUS, none in monogenic IBD genes.\n\nTreatment with IV ganciclovir for 15 days led to clinical improvement; CMV PCR was undetectable prior to discharge. She achieved PUCAI 0 at discharge with normalized stool frequency/consistency and no rectal bleeding, nocturnal stools, or abdominal pain. Two months later she had an IBD flare with bloody diarrhea (PUCAI 35); CBC normal, GI pathogen panel negative, C. difficile PCR positive, and CMV load undetectable. She received oral metronidazole but persisted with blood-streaked diarrhea and was re-hospitalized. Repeat colonoscopy showed diffuse erythematous mucosa from rectum to cecum with nodularity and loss of vascular transparency, more prominent in the left and transverse colon; no focal lesions; ileum and anal canal without lesions. Histology (terminal ileum, right and left colon): ileal architecture preserved without inflammation; colon with mild architectural distortion and epithelial dedifferentiation; lamina propria expanded by mixed inflammatory infiltrate with transmucosal distribution; foci of cryptitis and crypt abscesses; reactive lymphoid follicular hyperplasia; no granulomas or viral/parasitic cytopathic changes. She was treated with oral vancomycin and prednisone 1 mg/kg/day with good response and was discharged with reduced stool frequency. At outpatient follow-up she has mild residual symptoms (PUCAI 5); corticosteroids are being tapered and mesalazine maintained.\n\nOverall, this case represents pediatric UC in an NF1 patient with tissue CMV positivity at presentation and low-level viremia, responsive to ganciclovir and 5-ASA, followed by a subsequent flare associated with C. difficile infection that improved with vancomycin and corticosteroids; CMV remained undetectable thereafter." }, { "index": 53, "label": "low_health_literacy", "original_text": "40-year-old HIV-positive man with regular adherence to treatment (viral load 4500/mm3 and CD4 70/mm3 from the previous year), consulted for intermittent fever of two years' evolution that did not respect the standard time and gave way to transient antinflammatory non-steroidal drugs. He added in the last two months diffuse abdominal pain with predominance in the upper right lobe where he acquired a configuration of a tree in bud and bilateral pleural effusion, and at the abdominal level, marked increase of hepato-splenomegaly associated with ascites. After 48 hours of his suspension, he presented fulminant hepatic failure and was transferred to the intensive care unit. Tracheal aspirate was performed and after transfusion support a liver biopsy was obtained by puncture. The patient died a few hours later. The postmortem culture of the tracheal aspirate was positive for Mycobacterium tuberculosis and the liver biopsy was performed with non-necrotizing granulomas and the rest of the parenchyma preserved. This work was carried out in accordance with the principles laid out in the ethical code of the WHO (Helsinki Declaration).\n", "generated_summary": "A 40-year-old man has HIV and takes his medicines regularly. For two years, he had fevers that came and went. In the last two months, he also had spreading belly pain and many swollen glands. Blood tests showed very low blood cells, blood that did not clot well, low blood protein, and strong signs of inflammation. A body scan showed a big liver and spleen and many swollen glands. Many germ tests were done and were negative, except one that found the HHV-8 virus. A gland sample showed a rare illness called Castleman\u2019s disease. Even after restarting his HIV drugs, he got worse. Doctors tried steroids and an antiviral called ganciclovir. A week later, many organs started to fail and he swelled all over, so those drugs had to be stopped. A new chest scan showed small branch-like spots in the right lung and fluid around both lungs. The belly scan showed the liver and spleen got bigger and there was fluid in the belly. He went to intensive care because his liver suddenly failed. He died soon after. After his death, a lung sample grew tuberculosis. A liver sample showed tiny immune lumps called granulomas." }, { "index": 53, "label": "intermediate_health_literacy", "original_text": "40-year-old HIV-positive man with regular adherence to treatment (viral load 4500/mm3 and CD4 70/mm3 from the previous year), consulted for intermittent fever of two years' evolution that did not respect the standard time and gave way to transient antinflammatory non-steroidal drugs. He added in the last two months diffuse abdominal pain with predominance in the upper right lobe where he acquired a configuration of a tree in bud and bilateral pleural effusion, and at the abdominal level, marked increase of hepato-splenomegaly associated with ascites. After 48 hours of his suspension, he presented fulminant hepatic failure and was transferred to the intensive care unit. Tracheal aspirate was performed and after transfusion support a liver biopsy was obtained by puncture. The patient died a few hours later. The postmortem culture of the tracheal aspirate was positive for Mycobacterium tuberculosis and the liver biopsy was performed with non-necrotizing granulomas and the rest of the parenchyma preserved. This work was carried out in accordance with the principles laid out in the ethical code of the WHO (Helsinki Declaration).\n", "generated_summary": "A 40-year-old man with HIV on treatment presented with intermittent fevers for two years. Over the prior two months, he developed progressive, diffuse abdominal pain and generalized lymphadenopathy. Laboratory tests showed pancytopenia, coagulopathy, hypoalbuminemia, and elevated inflammatory markers. CT of the chest, abdomen, and pelvis revealed only hepatosplenomegaly and widespread adenopathy. Broad infectious workup, including mycobacterial cultures from multiple specimens, was negative except for a positive HHV-8 RT-PCR. A left iliac lymph node biopsy was consistent with Castleman\u2019s disease. Despite restarting antiretroviral therapy, his condition worsened, so clinicians initiated corticosteroids and ganciclovir. After one week he developed multiorgan failure with anasarca, making those medications unsafe. Repeat chest CT showed right upper lobe tree-in-bud infiltrates with bilateral pleural effusions; abdominal imaging showed worsening hepatosplenomegaly and new ascites. He was transferred to the ICU 48 hours later for fulminant hepatic failure and died shortly afterward. Postmortem testing grew Mycobacterium tuberculosis from a tracheal aspirate, and liver biopsy showed non-necrotizing granulomas." }, { "index": 53, "label": "proficient_health_literacy", "original_text": "40-year-old HIV-positive man with regular adherence to treatment (viral load 4500/mm3 and CD4 70/mm3 from the previous year), consulted for intermittent fever of two years' evolution that did not respect the standard time and gave way to transient antinflammatory non-steroidal drugs. He added in the last two months diffuse abdominal pain with predominance in the upper right lobe where he acquired a configuration of a tree in bud and bilateral pleural effusion, and at the abdominal level, marked increase of hepato-splenomegaly associated with ascites. After 48 hours of his suspension, he presented fulminant hepatic failure and was transferred to the intensive care unit. Tracheal aspirate was performed and after transfusion support a liver biopsy was obtained by puncture. The patient died a few hours later. The postmortem culture of the tracheal aspirate was positive for Mycobacterium tuberculosis and the liver biopsy was performed with non-necrotizing granulomas and the rest of the parenchyma preserved. This work was carried out in accordance with the principles laid out in the ethical code of the WHO (Helsinki Declaration).\n", "generated_summary": "A 40-year-old HIV-positive man with reported regular ART adherence (prior year viral load 4,500 and CD4 70/mm3) presented with a two-year history of intermittent, noncyclical febrile episodes that transiently responded to NSAIDs. Over the preceding two months, he developed progressive, diffuse abdominal pain and generalized adenomegaly. Laboratory evaluation showed pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute phase reactants. Initial CT of the thorax, abdomen, and pelvis demonstrated hepatosplenomegaly and generalized adenomegaly without additional parenchymal findings. A broad microbiologic workup was undertaken, including mycobacterial cultures from multiple specimen types; all were negative except an RT-PCR positive for HHV-8. Excisional biopsy of a left iliac lymph node showed features consistent with Castleman\u2019s disease. Despite reinitiating antiretroviral therapy, clinical status deteriorated, prompting initiation of corticosteroids and ganciclovir. After approximately one week, the patient developed multiorgan failure with anasarca, rendering the instituted therapies contraindicated and necessitating discontinuation. Repeat chest CT revealed right upper lobe tree-in-bud infiltrates with bilateral pleural effusions. Concurrent abdominal imaging showed progression of hepatosplenomegaly and new-onset ascites. Forty-eight hours later, he developed fulminant hepatic failure and was transferred to the intensive care unit. He expired within hours. Tracheal aspirate culture, finalized postmortem, grew Mycobacterium tuberculosis. A percutaneous liver biopsy performed with transfusion support demonstrated non-necrotizing granulomas with otherwise preserved parenchyma. The case management and reporting adhered to the ethical principles of the WHO/Declaration of Helsinki." }, { "index": 54, "label": "low_health_literacy", "original_text": "4-month-old indigenous lactating mother from the rural area of the interior of Panama, from the town of Urrac\u00e1, 3 hours by canoe from the nearest health center. Her background included being the fourth daughter, born by vaginal delivery at home by a relative, without prenatal controls, her weight, height and Apgar score at birth are unknown. She did not breastfeed and was fed with powdered milk formula with iron for children under 6 months, receiving 3 ounces every 4 hours.\n\nThe nuclear family was composed of 6 people (parents and 4 children) who lived in a house with walls and floor of boards and palm roof, 2 rooms, without electricity, they were illuminated with kerosene lamps, water from a well, excreta in a river and they burned the garbage, their economic income came from subsistence agriculture.\n\nHe had no health care in his first 4 months of life and did not receive the vaccinations included in the national expanded programme of immunizations. According to his parents, his neurodevelopment was normal until his hospitalization.\n\nThe minor consulted in a health center with a history of 4 days of diarrhoea, without mucus or blood associated with vomiting of food content (the mother gave her tea because she could not tolerate milk), afebrile and without respiratory symptoms. Oral fluids and 4 doses of Enterogermina\u00ae (B. clausii: two billion spores/5 mL) were administered. Due to the lack of supplies (they did not have catheters, or intraosseous for the administration of intravenous fluids) she was transferred to a second-level hospital in the provincial capital and then to our institution in Panama City with a diagnosis of acute gastroenteritis and severe dehydration.\n\nHe presented to the emergency department with a consciousness compromise, dehydration characterised by a tearless cry, dry oral mucosa. He had oedema of +++ hands, feet, abdomen and face. He was afebrile and had signs of shock, capillary refill time > 2 seconds, cold extremities, filiform pulse and marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. He weighed 4.7 kg and was 56 cm tall at admission, Z-score height/age -2.52, weight/height and weight/age Z-scores were not quantifiable due to severe dehydration. On segmental examination, there were fine crepitus in both lung bases and erythematous-squamous lesions with desquamation of skin and others with hypopigmentation of trunk and upper limbs (interpreted as pellagroid dermatosis).\n\nLactate Ringer bolus was given at 10 ml/kg in the emergency department, followed by 5% Dextrose in 0.33% Saline 500 ml at an infusion rate of 29 ml/h over 6 hours without KCL until diuresis was obtained. She was started on Ceftriaxone 50 mg/kg/day for suspected sepsis, stabilised and sent to the ward where she continued to receive 500 ml of 5% Dextrose in 0.9% Saline at 20 ml/hr.\n\nAmong the examinations, a blood count revealed leukocytosis at 39.0 x 103/uL, severe anaemia 5.6 g/dL, thrombocytosis 502 x 103/uL, the rest of the results are detailed in. He was transfused with 50 ml of filtered and leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to altered coagulation times. Enteral feeding was initiated by nasogastric tube and infusion was decreased to 15 ml/h of 5% Dextrose in 0.9% Saline 500 cc, and continued with negative water balance.\n\nOn day 2, initial peripheral blood culture was reported as Gram positive cocci in clusters, Oxacillin was added at 200 mg/kg/day, Ceftriaxone was increased to 75-100 mg/kg/day, total fluids to 120 ml/kg/day and calcium was corrected (value received 6.38 mg/dL).\n\nOn her 3rd day she lost venous access, so a central venous catheter (CVC) was placed. She was hypovolemic with subhydrated oral mucosa, increased respiratory work, cold extremities and capillary refill time of 3-4 seconds. Ringer's lactate was given at a load of 20 ml/kg in one hour. Arterial blood gas revealed uncompensated metabolic acidosis with pH 7.26, HCO3 13 mmol/L, PCO2 28.4 mmHg, PO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to the paediatric intensive care unit (PICU) where she was placed on mechanical ventilation.\n\nTotal fluids of 100 cc/kg, infused epinephrine, low-salt albumin, and 10% calcium gluconate were administered, and fentanyl was changed to remifentanil due to elevated liver enzymes.\n\nThe blood culture of admission reported growth of methicillin-resistant Staphylococcus aureus (MRSA), Oxacillin was omitted and Clindamycin was added at 40 mg/kg/day; the blood culture of admission on the second day of admission to the ICU with Gram-negative bacillus smear was positive, and Ceftriaxone was changed to Ceftazidime at 150 mg/kg/day.\n\nOn his first day in the ICU, a substantial increase in serum biomarkers of cardiac damage was documented, the echocardiogram showed mild mitral and tricuspid regurgitation, left ventricular dilatation, left ventricular ejection fraction (LVEF) 58%, no evidence of thrombi, vegetations or pericardial effusion, and he was diagnosed with acute myocarditis. Milrinone was started at 0.4 mcg/kg/min, furosemide and IV immunoglobulin 1 g/kg single dose.\n\nThe second day blood culture the germ was identified as Bacillus clausii, identified by the system (VYTEK 2TM), the susceptibility profile was not performed because the team did not have cut points for this germ, for this reason the antibiotic coverage was adjusted, considering it was not a contaminant, Ceftazidime was changed to Ciprofloxacin at 30 mg/kg/day and Ceftaroline was added at 8 mg/kg every 8 hours along with Clindamycin for MRSA. The 3 subsequent blood cultures with intervals of 48 hours between each were positive in both peripheral blood and CVC for isolation of B. clausii.\n\nOn his 6th day in hospital, the gastrointestinal panel (Maripoc gastro test methodology) performed on the second day detected Clostridiodes difficile toxin A/B, the tests for Campylobacteryeyuni, Norovirus GI, Norovirus GII.4, Adenovirus and Rotavirus were negative. Following these findings, therapy was escalated to IV Vancomycin at a dose of 60 mg/kg/day and metronidazole was added orally. Ceftaroline, clindamycin and ciprofloxacin were omitted, covering both B. clausii and C. difficile and MRSA .\n\nHIV testing, serology for Chagas and SARS-CoV-2 antigen by immunofluorescence (FIA) were negative, immunoglobulins were within normal limits.\n\nOn the seventh day, arterial hypertension was reported and spirinolactone was added to the management.\n\nOn the 8th day, the laboratory tests showed altered coagulation times and increased azotaemia associated with anuria that had lasted for 12 hours. However, due to the patient's condition, a peritoneal catheter was not placed, the vancomycin dose was adjusted and vitamin K was administered. The patient continued to have anuria and anasarca, and she developed sustained hypotension. Noradrenaline was added, but her condition deteriorated with multisystem organ failure and she died twelve days after admission. No autopsy was performed because the mother refused permission for cultural reasons.\n", "generated_summary": "This story is about a 4\u2011month\u2011old baby girl from an Indigenous community in rural Panama. The nearest clinic was three hours away by canoe. She was not getting enough protein and calories. She suddenly had bad diarrhea. She got very dehydrated, like a plant without water. A probiotic medicine called Enterogermina was given at the start. She was moved to a large hospital. She arrived breathing hard. She was in shock, which means her blood was not carrying enough to her organs. A blood test found a hard\u2011to\u2011treat germ called MRSA. A stool test found a germ called C. difficile that can cause diarrhea. Later blood tests from her arm and from a central line found Bacillus clausii. Doctors tried many antibiotics, but the germs did not respond. Her organs began to fail. She died 12 days after she got to the hospital." }, { "index": 54, "label": "intermediate_health_literacy", "original_text": "4-month-old indigenous lactating mother from the rural area of the interior of Panama, from the town of Urrac\u00e1, 3 hours by canoe from the nearest health center. Her background included being the fourth daughter, born by vaginal delivery at home by a relative, without prenatal controls, her weight, height and Apgar score at birth are unknown. She did not breastfeed and was fed with powdered milk formula with iron for children under 6 months, receiving 3 ounces every 4 hours.\n\nThe nuclear family was composed of 6 people (parents and 4 children) who lived in a house with walls and floor of boards and palm roof, 2 rooms, without electricity, they were illuminated with kerosene lamps, water from a well, excreta in a river and they burned the garbage, their economic income came from subsistence agriculture.\n\nHe had no health care in his first 4 months of life and did not receive the vaccinations included in the national expanded programme of immunizations. According to his parents, his neurodevelopment was normal until his hospitalization.\n\nThe minor consulted in a health center with a history of 4 days of diarrhoea, without mucus or blood associated with vomiting of food content (the mother gave her tea because she could not tolerate milk), afebrile and without respiratory symptoms. Oral fluids and 4 doses of Enterogermina\u00ae (B. clausii: two billion spores/5 mL) were administered. Due to the lack of supplies (they did not have catheters, or intraosseous for the administration of intravenous fluids) she was transferred to a second-level hospital in the provincial capital and then to our institution in Panama City with a diagnosis of acute gastroenteritis and severe dehydration.\n\nHe presented to the emergency department with a consciousness compromise, dehydration characterised by a tearless cry, dry oral mucosa. He had oedema of +++ hands, feet, abdomen and face. He was afebrile and had signs of shock, capillary refill time > 2 seconds, cold extremities, filiform pulse and marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. He weighed 4.7 kg and was 56 cm tall at admission, Z-score height/age -2.52, weight/height and weight/age Z-scores were not quantifiable due to severe dehydration. On segmental examination, there were fine crepitus in both lung bases and erythematous-squamous lesions with desquamation of skin and others with hypopigmentation of trunk and upper limbs (interpreted as pellagroid dermatosis).\n\nLactate Ringer bolus was given at 10 ml/kg in the emergency department, followed by 5% Dextrose in 0.33% Saline 500 ml at an infusion rate of 29 ml/h over 6 hours without KCL until diuresis was obtained. She was started on Ceftriaxone 50 mg/kg/day for suspected sepsis, stabilised and sent to the ward where she continued to receive 500 ml of 5% Dextrose in 0.9% Saline at 20 ml/hr.\n\nAmong the examinations, a blood count revealed leukocytosis at 39.0 x 103/uL, severe anaemia 5.6 g/dL, thrombocytosis 502 x 103/uL, the rest of the results are detailed in. He was transfused with 50 ml of filtered and leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to altered coagulation times. Enteral feeding was initiated by nasogastric tube and infusion was decreased to 15 ml/h of 5% Dextrose in 0.9% Saline 500 cc, and continued with negative water balance.\n\nOn day 2, initial peripheral blood culture was reported as Gram positive cocci in clusters, Oxacillin was added at 200 mg/kg/day, Ceftriaxone was increased to 75-100 mg/kg/day, total fluids to 120 ml/kg/day and calcium was corrected (value received 6.38 mg/dL).\n\nOn her 3rd day she lost venous access, so a central venous catheter (CVC) was placed. She was hypovolemic with subhydrated oral mucosa, increased respiratory work, cold extremities and capillary refill time of 3-4 seconds. Ringer's lactate was given at a load of 20 ml/kg in one hour. Arterial blood gas revealed uncompensated metabolic acidosis with pH 7.26, HCO3 13 mmol/L, PCO2 28.4 mmHg, PO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to the paediatric intensive care unit (PICU) where she was placed on mechanical ventilation.\n\nTotal fluids of 100 cc/kg, infused epinephrine, low-salt albumin, and 10% calcium gluconate were administered, and fentanyl was changed to remifentanil due to elevated liver enzymes.\n\nThe blood culture of admission reported growth of methicillin-resistant Staphylococcus aureus (MRSA), Oxacillin was omitted and Clindamycin was added at 40 mg/kg/day; the blood culture of admission on the second day of admission to the ICU with Gram-negative bacillus smear was positive, and Ceftriaxone was changed to Ceftazidime at 150 mg/kg/day.\n\nOn his first day in the ICU, a substantial increase in serum biomarkers of cardiac damage was documented, the echocardiogram showed mild mitral and tricuspid regurgitation, left ventricular dilatation, left ventricular ejection fraction (LVEF) 58%, no evidence of thrombi, vegetations or pericardial effusion, and he was diagnosed with acute myocarditis. Milrinone was started at 0.4 mcg/kg/min, furosemide and IV immunoglobulin 1 g/kg single dose.\n\nThe second day blood culture the germ was identified as Bacillus clausii, identified by the system (VYTEK 2TM), the susceptibility profile was not performed because the team did not have cut points for this germ, for this reason the antibiotic coverage was adjusted, considering it was not a contaminant, Ceftazidime was changed to Ciprofloxacin at 30 mg/kg/day and Ceftaroline was added at 8 mg/kg every 8 hours along with Clindamycin for MRSA. The 3 subsequent blood cultures with intervals of 48 hours between each were positive in both peripheral blood and CVC for isolation of B. clausii.\n\nOn his 6th day in hospital, the gastrointestinal panel (Maripoc gastro test methodology) performed on the second day detected Clostridiodes difficile toxin A/B, the tests for Campylobacteryeyuni, Norovirus GI, Norovirus GII.4, Adenovirus and Rotavirus were negative. Following these findings, therapy was escalated to IV Vancomycin at a dose of 60 mg/kg/day and metronidazole was added orally. Ceftaroline, clindamycin and ciprofloxacin were omitted, covering both B. clausii and C. difficile and MRSA .\n\nHIV testing, serology for Chagas and SARS-CoV-2 antigen by immunofluorescence (FIA) were negative, immunoglobulins were within normal limits.\n\nOn the seventh day, arterial hypertension was reported and spirinolactone was added to the management.\n\nOn the 8th day, the laboratory tests showed altered coagulation times and increased azotaemia associated with anuria that had lasted for 12 hours. However, due to the patient's condition, a peritoneal catheter was not placed, the vancomycin dose was adjusted and vitamin K was administered. The patient continued to have anuria and anasarca, and she developed sustained hypotension. Noradrenaline was added, but her condition deteriorated with multisystem organ failure and she died twelve days after admission. No autopsy was performed because the mother refused permission for cultural reasons.\n", "generated_summary": "A 4\u2011month\u2011old Indigenous infant from rural Panama, living three hours by canoe from the nearest health center, had severe protein\u2011calorie malnutrition and presented with acute diarrhea and dehydration. At the first clinic, she received oral therapy that included Enterogermina (a probiotic containing Bacillus clausii) and was transferred to a tertiary hospital. She arrived with respiratory distress and clinical shock. The initial blood culture grew methicillin\u2011resistant Staphylococcus aureus (MRSA). A gastrointestinal panel was positive for Clostridioides difficile toxin. Subsequent serial blood cultures from both peripheral draws and a central venous catheter repeatedly isolated Bacillus clausii. Despite multiple antibiotic regimens aimed at MRSA, C. difficile, and B. clausii, her condition worsened. She developed multisystem organ failure and died on hospital day 12." }, { "index": 54, "label": "proficient_health_literacy", "original_text": "4-month-old indigenous lactating mother from the rural area of the interior of Panama, from the town of Urrac\u00e1, 3 hours by canoe from the nearest health center. Her background included being the fourth daughter, born by vaginal delivery at home by a relative, without prenatal controls, her weight, height and Apgar score at birth are unknown. She did not breastfeed and was fed with powdered milk formula with iron for children under 6 months, receiving 3 ounces every 4 hours.\n\nThe nuclear family was composed of 6 people (parents and 4 children) who lived in a house with walls and floor of boards and palm roof, 2 rooms, without electricity, they were illuminated with kerosene lamps, water from a well, excreta in a river and they burned the garbage, their economic income came from subsistence agriculture.\n\nHe had no health care in his first 4 months of life and did not receive the vaccinations included in the national expanded programme of immunizations. According to his parents, his neurodevelopment was normal until his hospitalization.\n\nThe minor consulted in a health center with a history of 4 days of diarrhoea, without mucus or blood associated with vomiting of food content (the mother gave her tea because she could not tolerate milk), afebrile and without respiratory symptoms. Oral fluids and 4 doses of Enterogermina\u00ae (B. clausii: two billion spores/5 mL) were administered. Due to the lack of supplies (they did not have catheters, or intraosseous for the administration of intravenous fluids) she was transferred to a second-level hospital in the provincial capital and then to our institution in Panama City with a diagnosis of acute gastroenteritis and severe dehydration.\n\nHe presented to the emergency department with a consciousness compromise, dehydration characterised by a tearless cry, dry oral mucosa. He had oedema of +++ hands, feet, abdomen and face. He was afebrile and had signs of shock, capillary refill time > 2 seconds, cold extremities, filiform pulse and marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. He weighed 4.7 kg and was 56 cm tall at admission, Z-score height/age -2.52, weight/height and weight/age Z-scores were not quantifiable due to severe dehydration. On segmental examination, there were fine crepitus in both lung bases and erythematous-squamous lesions with desquamation of skin and others with hypopigmentation of trunk and upper limbs (interpreted as pellagroid dermatosis).\n\nLactate Ringer bolus was given at 10 ml/kg in the emergency department, followed by 5% Dextrose in 0.33% Saline 500 ml at an infusion rate of 29 ml/h over 6 hours without KCL until diuresis was obtained. She was started on Ceftriaxone 50 mg/kg/day for suspected sepsis, stabilised and sent to the ward where she continued to receive 500 ml of 5% Dextrose in 0.9% Saline at 20 ml/hr.\n\nAmong the examinations, a blood count revealed leukocytosis at 39.0 x 103/uL, severe anaemia 5.6 g/dL, thrombocytosis 502 x 103/uL, the rest of the results are detailed in. He was transfused with 50 ml of filtered and leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to altered coagulation times. Enteral feeding was initiated by nasogastric tube and infusion was decreased to 15 ml/h of 5% Dextrose in 0.9% Saline 500 cc, and continued with negative water balance.\n\nOn day 2, initial peripheral blood culture was reported as Gram positive cocci in clusters, Oxacillin was added at 200 mg/kg/day, Ceftriaxone was increased to 75-100 mg/kg/day, total fluids to 120 ml/kg/day and calcium was corrected (value received 6.38 mg/dL).\n\nOn her 3rd day she lost venous access, so a central venous catheter (CVC) was placed. She was hypovolemic with subhydrated oral mucosa, increased respiratory work, cold extremities and capillary refill time of 3-4 seconds. Ringer's lactate was given at a load of 20 ml/kg in one hour. Arterial blood gas revealed uncompensated metabolic acidosis with pH 7.26, HCO3 13 mmol/L, PCO2 28.4 mmHg, PO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to the paediatric intensive care unit (PICU) where she was placed on mechanical ventilation.\n\nTotal fluids of 100 cc/kg, infused epinephrine, low-salt albumin, and 10% calcium gluconate were administered, and fentanyl was changed to remifentanil due to elevated liver enzymes.\n\nThe blood culture of admission reported growth of methicillin-resistant Staphylococcus aureus (MRSA), Oxacillin was omitted and Clindamycin was added at 40 mg/kg/day; the blood culture of admission on the second day of admission to the ICU with Gram-negative bacillus smear was positive, and Ceftriaxone was changed to Ceftazidime at 150 mg/kg/day.\n\nOn his first day in the ICU, a substantial increase in serum biomarkers of cardiac damage was documented, the echocardiogram showed mild mitral and tricuspid regurgitation, left ventricular dilatation, left ventricular ejection fraction (LVEF) 58%, no evidence of thrombi, vegetations or pericardial effusion, and he was diagnosed with acute myocarditis. Milrinone was started at 0.4 mcg/kg/min, furosemide and IV immunoglobulin 1 g/kg single dose.\n\nThe second day blood culture the germ was identified as Bacillus clausii, identified by the system (VYTEK 2TM), the susceptibility profile was not performed because the team did not have cut points for this germ, for this reason the antibiotic coverage was adjusted, considering it was not a contaminant, Ceftazidime was changed to Ciprofloxacin at 30 mg/kg/day and Ceftaroline was added at 8 mg/kg every 8 hours along with Clindamycin for MRSA. The 3 subsequent blood cultures with intervals of 48 hours between each were positive in both peripheral blood and CVC for isolation of B. clausii.\n\nOn his 6th day in hospital, the gastrointestinal panel (Maripoc gastro test methodology) performed on the second day detected Clostridiodes difficile toxin A/B, the tests for Campylobacteryeyuni, Norovirus GI, Norovirus GII.4, Adenovirus and Rotavirus were negative. Following these findings, therapy was escalated to IV Vancomycin at a dose of 60 mg/kg/day and metronidazole was added orally. Ceftaroline, clindamycin and ciprofloxacin were omitted, covering both B. clausii and C. difficile and MRSA .\n\nHIV testing, serology for Chagas and SARS-CoV-2 antigen by immunofluorescence (FIA) were negative, immunoglobulins were within normal limits.\n\nOn the seventh day, arterial hypertension was reported and spirinolactone was added to the management.\n\nOn the 8th day, the laboratory tests showed altered coagulation times and increased azotaemia associated with anuria that had lasted for 12 hours. However, due to the patient's condition, a peritoneal catheter was not placed, the vancomycin dose was adjusted and vitamin K was administered. The patient continued to have anuria and anasarca, and she developed sustained hypotension. Noradrenaline was added, but her condition deteriorated with multisystem organ failure and she died twelve days after admission. No autopsy was performed because the mother refused permission for cultural reasons.\n", "generated_summary": "A 4\u2011month\u2011old Indigenous infant from Urrac\u00e1, rural Panama (approximately 3 hours by canoe from the nearest health subcenter), with protein\u2011calorie malnutrition and no prior healthcare or vaccinations, presented with 4 days of non\u2011bloody diarrhea and vomiting, progressing to moderate\u2013severe dehydration. At the initial health center she received oral fluids and 4 doses of Enterogermina (Bacillus clausii: two billion spores/5 mL), but due to supply limitations was transferred to a second\u2011level facility and then to a tertiary hospital in Panama City with a working diagnosis of acute gastroenteritis and severe dehydration.\n\nOn arrival to the ED she had altered mental status, signs of shock (tearless cry, dry mucosa, cold extremities, capillary refill >2 s, filiform pulse, mottling), tachycardia 170 bpm, tachypnea 55/min, BP 91/37 mmHg, SpO2 99%, generalized edema (+++) of hands, feet, abdomen, and face, and skin changes suggestive of pellagroid dermatosis. Anthropometrics: weight 4.7 kg, length 56 cm, H/A Z \u22122.52 (W/H and W/A not quantifiable due to severe dehydration). Chest exam had fine basal crackles. Initial management included LR 10 mL/kg bolus, followed by 5% dextrose/0.33% saline then 5% dextrose/0.9% saline; empiric ceftriaxone 50 mg/kg/day for suspected sepsis. CBC showed leukocytosis 39\u00d710^3/\u00b5L, severe anemia Hgb 5.6 g/dL, thrombocytosis 502\u00d710^3/\u00b5L. She received 50 mL filtered, leukoreduced PRBCs and 40 cc FFP for coagulopathy. Enteral feeds were started via NGT; fluids were titrated with ongoing negative balance.\n\nOn hospital day (HD) 2, the initial peripheral blood culture signaled Gram\u2011positive cocci in clusters; oxacillin 200 mg/kg/day was added and ceftriaxone increased to 75\u2013100 mg/kg/day. Hypocalcemia (Ca 6.38 mg/dL) was corrected. On HD3 she lost peripheral access; a central venous catheter (CVC) was placed. She remained hypovolemic with worsening work of breathing; LR 20 mL/kg was given. ABG: pH 7.26, HCO3\u2212 13 mmol/L, pCO2 28.4 mmHg, pO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to PICU for mechanical ventilation. Management included total fluids ~100 mL/kg, epinephrine infusion, low\u2011salt albumin, 10% calcium gluconate; analgesia/sedation was switched from fentanyl to remifentanil due to elevated transaminases.\n\nThe admission blood culture grew methicillin\u2011resistant Staphylococcus aureus (MRSA); oxacillin was discontinued and clindamycin 40 mg/kg/day was added. A subsequent blood culture smear showing Gram\u2011negative bacilli prompted a change from ceftriaxone to ceftazidime 150 mg/kg/day. On PICU day 1 there was a marked rise in cardiac injury biomarkers; echocardiogram showed mild MR/TR, LV dilation, LVEF 58%, without thrombi, vegetations, or pericardial effusion, consistent with acute myocarditis. She received milrinone 0.4 mcg/kg/min, furosemide, and IVIG 1 g/kg once.\n\nBy HD4\u20135, the second\u2011day blood culture identified Bacillus clausii via VITEK 2; no susceptibility profile was generated (no interpretive breakpoints). Considering it was not a contaminant, antimicrobial therapy was adjusted: ceftazidime was changed to ciprofloxacin 30 mg/kg/day and ceftaroline 8 mg/kg q8h was added, with clindamycin continued for MRSA coverage. Three subsequent blood cultures at 48\u2011hour intervals remained positive for B. clausii from both peripheral blood and the CVC. On HD6, a GI panel (Maripoc) detected Clostridioides difficile toxin A/B; tests for Campylobacter jejuni, Norovirus GI/GII.4, Adenovirus, and Rotavirus were negative. Therapy was escalated to IV vancomycin 60 mg/kg/day plus oral metronidazole; ceftaroline, clindamycin, and ciprofloxacin were discontinued to streamline coverage for MRSA, B. clausii, and C. difficile. HIV, Chagas serology, and SARS\u2011CoV\u20112 antigen (FIA) were negative; immunoglobulins were within reference ranges.\n\nOn HD7, arterial hypertension developed and spironolactone was initiated. By HD8, coagulopathy worsened and azotemia with 12 hours of anuria was documented; vancomycin dosing was adjusted and vitamin K administered. Due to clinical instability, peritoneal dialysis catheter placement was deferred. She progressed to anasarca and sustained hypotension; norepinephrine was added. Despite intensive care and multiple antibiotic regimens, she developed refractory septic shock and multisystem organ failure. She died 12 days after admission. No autopsy was performed due to family cultural objections.\n\nKey microbiologic findings were: (1) initial MRSA bacteremia; (2) GI panel positive for C. difficile toxin; and (3) persistent Bacillus clausii bacteremia documented in serial peripheral and CVC cultures after prior administration of Enterogermina. The clinical course was marked by severe malnutrition, shock, myocarditis, evolving renal failure with anuria, coagulopathy, and ultimate multiorgan failure despite escalated antimicrobial and organ support." }, { "index": 55, "label": "low_health_literacy", "original_text": "A 2-year-old female presented with a 1-year history of painless left progressive proptosis with no reported systemic diseases or family history. Ophthalmologic examination revealed light sensation as the only vision in the left eye, along with proptosis, inward and upward eyeball displacement, and restricted extraocular muscle movements in downward and outward directions. An irregularly shaped, well-defined soft mass was palpable in the inferior aspect of the left orbit, accompanied by left lower eyelid ectropion. The pupil was enlarged (4\u2009mm in diameter), and pupillary reaction was absent. The remaining anterior segment examination showed no apparent abnormalities. Fundus examination was challenging due to the child\u2019s size. Hertel exophthalmometry readings measured 10.5\u2009mm in the right eye and 18\u2009mm in the left. Magnetic resonance imaging (MRI) revealed a well-circumscribed mass, displaying hypointense signals on T1-weighted images and hyperintense signals on T2-weighted images. Contrast-enhanced imaging demonstrated no significant improvement. A transconjunctival approach via the inferior fornix with canthotomy and cantholysis was performed, revealing a grayish-white cystic mass with a distinct boundary from surrounding tissues. During posterior separation to the eyeballs\u2019 posterior part, tight adhesion to the optic nerve was observed. Due to the mass\u2019s substantial size and the restricted surgical field, volume reduction was necessary. Approximately 12.5\u2009mL of the fluid was aspirated, and the mass was completely excised. Histopathological examination disclosed a fibrous capsule wall covered with squamous and glandular epithelium, along with visible brain tissue and a cartilage-like matrix consistent with orbital teratoma. One month postsurgery, the patient exhibited enophthalmos, conjunctival hyperemia, and keratitis on ocular examination. This was attributed to the mass\u2019s prior enlargement of the orbital cavity, resulting in postoperative enophthalmos. The cornea could not adhere to the eyelids, creating a space and causing corneal inflammation. After obtaining the consent of the patient\u2019s guardian, a second operation involved the implantation of an allogeneic sclera into the orbit to increase the orbital volume, alleviate fossa pitting and restore keratitis to normal. No recurrence of the teratomas was noted during the 1-year follow-up. The patient still had minor enophthalmos and outer canthus abnormality. The visual acuity remained consistent with pre-operation levels. Hertel exophthalmometry readings measured 10.5\u2009mm in the right eye and 8\u2009mm in the left. The remaining anterior segment examination showed no apparent abnormalities.", "generated_summary": "A 2-year-old girl had a bulging left eye. The eye was pushed inward and upward. An MRI scan showed a clear lump. It looked dark on one kind of picture and bright on another. Tests on the tissue, including special lab tests, proved it was a teratoma (a type of growth). Doctors removed the lump through the inside of the lower eyelid and made small cuts at the outer corner to make room. One month later, the eye looked sunken. The white part was red. The clear front of the eye was inflamed. Doctors did a second surgery. They put donated eye-white tissue into the eye socket to add space, smooth the hollow, and help the eye surface heal. After one year, the growth did not come back, and there were no other problems." }, { "index": 55, "label": "intermediate_health_literacy", "original_text": "A 2-year-old female presented with a 1-year history of painless left progressive proptosis with no reported systemic diseases or family history. Ophthalmologic examination revealed light sensation as the only vision in the left eye, along with proptosis, inward and upward eyeball displacement, and restricted extraocular muscle movements in downward and outward directions. An irregularly shaped, well-defined soft mass was palpable in the inferior aspect of the left orbit, accompanied by left lower eyelid ectropion. The pupil was enlarged (4\u2009mm in diameter), and pupillary reaction was absent. The remaining anterior segment examination showed no apparent abnormalities. Fundus examination was challenging due to the child\u2019s size. Hertel exophthalmometry readings measured 10.5\u2009mm in the right eye and 18\u2009mm in the left. Magnetic resonance imaging (MRI) revealed a well-circumscribed mass, displaying hypointense signals on T1-weighted images and hyperintense signals on T2-weighted images. Contrast-enhanced imaging demonstrated no significant improvement. A transconjunctival approach via the inferior fornix with canthotomy and cantholysis was performed, revealing a grayish-white cystic mass with a distinct boundary from surrounding tissues. During posterior separation to the eyeballs\u2019 posterior part, tight adhesion to the optic nerve was observed. Due to the mass\u2019s substantial size and the restricted surgical field, volume reduction was necessary. Approximately 12.5\u2009mL of the fluid was aspirated, and the mass was completely excised. Histopathological examination disclosed a fibrous capsule wall covered with squamous and glandular epithelium, along with visible brain tissue and a cartilage-like matrix consistent with orbital teratoma. One month postsurgery, the patient exhibited enophthalmos, conjunctival hyperemia, and keratitis on ocular examination. This was attributed to the mass\u2019s prior enlargement of the orbital cavity, resulting in postoperative enophthalmos. The cornea could not adhere to the eyelids, creating a space and causing corneal inflammation. After obtaining the consent of the patient\u2019s guardian, a second operation involved the implantation of an allogeneic sclera into the orbit to increase the orbital volume, alleviate fossa pitting and restore keratitis to normal. No recurrence of the teratomas was noted during the 1-year follow-up. The patient still had minor enophthalmos and outer canthus abnormality. The visual acuity remained consistent with pre-operation levels. Hertel exophthalmometry readings measured 10.5\u2009mm in the right eye and 8\u2009mm in the left. The remaining anterior segment examination showed no apparent abnormalities.", "generated_summary": "A 2-year-old girl presented with left eye proptosis, with the globe displaced inward and upward. MRI showed a well-circumscribed orbital mass that was hypointense on T1-weighted images and hyperintense on T2-weighted images. Pathology, including histology and immunohistochemistry, confirmed teratoma. The mass was removed through a transconjunctival approach via the inferior fornix with canthotomy and cantholysis. One month after surgery, she developed enophthalmos, conjunctival hyperemia, and keratitis. A second procedure placed an allogeneic scleral implant to increase orbital volume, correct the socket hollowing, and resolve the corneal inflammation. At 1-year follow-up, there was no tumor recurrence and no other complications." }, { "index": 55, "label": "proficient_health_literacy", "original_text": "A 2-year-old female presented with a 1-year history of painless left progressive proptosis with no reported systemic diseases or family history. Ophthalmologic examination revealed light sensation as the only vision in the left eye, along with proptosis, inward and upward eyeball displacement, and restricted extraocular muscle movements in downward and outward directions. An irregularly shaped, well-defined soft mass was palpable in the inferior aspect of the left orbit, accompanied by left lower eyelid ectropion. The pupil was enlarged (4\u2009mm in diameter), and pupillary reaction was absent. The remaining anterior segment examination showed no apparent abnormalities. Fundus examination was challenging due to the child\u2019s size. Hertel exophthalmometry readings measured 10.5\u2009mm in the right eye and 18\u2009mm in the left. Magnetic resonance imaging (MRI) revealed a well-circumscribed mass, displaying hypointense signals on T1-weighted images and hyperintense signals on T2-weighted images. Contrast-enhanced imaging demonstrated no significant improvement. A transconjunctival approach via the inferior fornix with canthotomy and cantholysis was performed, revealing a grayish-white cystic mass with a distinct boundary from surrounding tissues. During posterior separation to the eyeballs\u2019 posterior part, tight adhesion to the optic nerve was observed. Due to the mass\u2019s substantial size and the restricted surgical field, volume reduction was necessary. Approximately 12.5\u2009mL of the fluid was aspirated, and the mass was completely excised. Histopathological examination disclosed a fibrous capsule wall covered with squamous and glandular epithelium, along with visible brain tissue and a cartilage-like matrix consistent with orbital teratoma. One month postsurgery, the patient exhibited enophthalmos, conjunctival hyperemia, and keratitis on ocular examination. This was attributed to the mass\u2019s prior enlargement of the orbital cavity, resulting in postoperative enophthalmos. The cornea could not adhere to the eyelids, creating a space and causing corneal inflammation. After obtaining the consent of the patient\u2019s guardian, a second operation involved the implantation of an allogeneic sclera into the orbit to increase the orbital volume, alleviate fossa pitting and restore keratitis to normal. No recurrence of the teratomas was noted during the 1-year follow-up. The patient still had minor enophthalmos and outer canthus abnormality. The visual acuity remained consistent with pre-operation levels. Hertel exophthalmometry readings measured 10.5\u2009mm in the right eye and 8\u2009mm in the left. The remaining anterior segment examination showed no apparent abnormalities.", "generated_summary": "A 2-year-old female with a 1-year history of painless, progressive left proptosis and no systemic disease or family history presented with light perception only in the left eye. Examination showed proptosis with inward and upward globe displacement; restricted extraocular movements in downward and outward gaze; a palpable, irregular, well-defined soft mass in the inferior orbit; left lower lid ectropion; a 4 mm mydriatic, nonreactive pupil; and otherwise unremarkable anterior segment (fundus view limited by age). Hertel exophthalmometry: OD 10.5 mm, OS 18 mm. MRI demonstrated a well-circumscribed mass, hypointense on T1WI and hyperintense on T2WI; contrast-enhanced imaging demonstrated no significant improvement. The lesion was excised via a transconjunctival approach through the inferior fornix with canthotomy and cantholysis. Intraoperatively, a grayish-white cystic mass with a distinct boundary was identified; posterior dissection revealed tight adhesion to the optic nerve. Due to lesion size and limited exposure, volume reduction was performed with aspiration of approximately 12.5 mL of fluid, followed by complete excision. Histopathology showed a fibrous capsule lined by squamous and glandular epithelium with visible brain tissue and cartilage-like matrix, consistent with orbital teratoma; immunohistochemical examination corroborated the diagnosis. One month postoperatively, the patient developed enophthalmos, conjunctival hyperemia, and keratitis, attributed to prior orbital cavity enlargement by the mass leading to postoperative volume deficit; corneal nonapposition to the lids created a gap and corneal inflammation. After guardian consent, a second operation implanted allogeneic sclera to augment orbital volume, alleviate fossa pitting, and normalize keratitis. At 1-year follow-up, there was no recurrence of the teratoma. Residual findings included minor enophthalmos and outer canthus abnormality; visual acuity remained at preoperative levels. Hertel measurements were OD 10.5 mm and OS 8 mm; the remaining anterior segment examination was unremarkable." }, { "index": 56, "label": "low_health_literacy", "original_text": "A 78-year-old woman, who came to collect her blister pack with her medication reconstituted in a personalised dosage system (PDS) from the community pharmacy, informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. These symptoms were preventing her from leaving her home to walk as often as she normally did. In view of this situation, she was invited to the personalised care area to review the degree of knowledge that the patient had of her medication and the use she made of it, to analyse whether any of her medication could be related to the health problem described.\n\nPharmacological treatment of the patient\n\nMedication Dose Dosage Health issue Start date\nDoxazosin 2 mg/24 h 0-0-1 Hypertension 2014\nLosartan 100 mg/24 h 1-0-0 Hypertension 2014\nManidipine 20 mg/24 h 0-1-0 Hypertension 2014\nSimvastatin 40 mg/24 h 0-0-1 Hypercholesterolemia 2014\nAcetylsalicylic acid 100 mg/24 h 1-0-0 Secondary prophylaxis 2014\nOmeprazole 20 mg/24 h 1-0-0 Prevention of peptic ulcer 2014\nPregabalin 100 mg/12 h 1-0-1 Neuralgia 2019\nTorasemide 10 mg/24 h 1-0-0 Edema 2023\nDulaglutide 1.5 mg/week 1 time/week Diabetes 2014\nInsulin glargine 74 IU/24 h 1-0-0 Diabetes 2014\nInsulin lispro 20 IU/24 h 0-1-0 Diabetes 2014\nBrimonidine 1 drop/12 h 1-0-1 Ocular hypertension 2018\n\nStudy and evaluation\nThe interview revealed that there was no new medication and that it did not appear in the SPD service register. Given the suspicion of a possible hypotension, her blood pressure was measured with an Omron Complete device, with the following values: Systolic Blood Pressure (SBP) 96 mmHg, Diastolic Blood Pressure (DBP) 52 mmHg and Heart Rate (HR) 69 beats per minute. Given these values, it was suggested that her blood pressure be monitored and the influence of her medication on these values and the symptoms described by the patient be analysed.\n\nThe patient's medication doses, starting with antihypertensive medications, are reviewed to adjust to the patient's estimated glomerular filtration rate (eGFR) and to see if hypotension is related to the dosage of these medications. The patient's eGFR value, calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, is 30 ml/min/1.73 m2.\n\nThe guidelines for the revision of the dose according to the value of the eGFR are the product information for the medicinal products and the consensus guidelines for the use of medicinal products in renal impairment of the teaching and research group in the field of practical pharmacy of the Faculty of Pharmacy of the University of Barcelona, which is available on the Internet. This guide has been prepared from the analysis of the most dispensed medicinal products in community pharmacies. They have been organised by therapeutic groups according to the ATC (Anatomical-Therapeutic-Chemical) classification, information on the symptoms of overdose has been included and it has been agreed to categorise the risk to the patient of taking these medicinal products according to their eGFR as low, moderate or high.\n\nAfter the medication review was performed according to the eGFR value of 30 ml/min/1.73 m2, the results were obtained.\n\nFollowing the study of the medication, our intervention focuses on the dosage of the following medicines: losartan, manidipine, torasemide and pregabalin. The antihypertensive medicines, losartan and manidipine, and pregabalin require a dose adjustment depending on the patient's eGFR value, while the diuretic torasemide can influence blood pressure values.\n\nInitially, it was decided to intervene in the dosage of losartan and manidipine. There is the possibility of reducing the dose of pregabalin, but the pharmaceutical team agreed with the patient to assess the influence of this medication after the possible adjustment of the dose of antihypertensive during the evolution and follow-up of the patient.\n\nIntervention\nThe information is used to prepare a report for the doctor (see annex), recommending a reduction in the dose of losartan and manidipine, as the available information recommends a reduction in the dose to 50-75% of losartan for eGFR of 30-59 ml/min/1.73 m2 and adjusting the dose of manidipine for eGFR of 15-30 ml/min/1.73 m2.\n\nThe proposed intervention was explained to the patient and the report was given to the primary care doctor, explaining the possibility of adjusting the dose of losartan and manidipine to improve the patient's condition (table 4). When this information reached the doctor, he opted to reduce the dose of losartan to 50 mg/24 hours and manidipine to 10 mg/24 hours. Pregabalin 100 mg/12 hours was also replaced with gabapentin 300 mg/12 hours.\n\nFollow-up\nFollowing this change in the patient's treatment and after a follow-up of two months, the patient showed an improvement in blood pressure values (table 5) and a remission of the symptoms described. It was reviewed whether the gabapentin dose of 300 mg/12 hours was adequate for the eGFR value of 30 ml/min/1.73 m2, and it was correct (eGFR between 30 and 60, recommended total daily dose 300-900 mg).\n\n", "generated_summary": "You are 78 and take many medicines in a pre-packed pill system (SPD). For months, you felt very tired, weak, dizzy, and confused. We checked your medicines. We looked closely at pills that the kidneys help clear, using your kidney filter number (eGFR). We wrote a note to your family doctor. We asked to lower the dose of two blood pressure pills: losartan and manidipine, based on your eGFR. Your doctor lowered the doses. We kept an eye on you. Your symptoms went away." }, { "index": 56, "label": "intermediate_health_literacy", "original_text": "A 78-year-old woman, who came to collect her blister pack with her medication reconstituted in a personalised dosage system (PDS) from the community pharmacy, informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. These symptoms were preventing her from leaving her home to walk as often as she normally did. In view of this situation, she was invited to the personalised care area to review the degree of knowledge that the patient had of her medication and the use she made of it, to analyse whether any of her medication could be related to the health problem described.\n\nPharmacological treatment of the patient\n\nMedication Dose Dosage Health issue Start date\nDoxazosin 2 mg/24 h 0-0-1 Hypertension 2014\nLosartan 100 mg/24 h 1-0-0 Hypertension 2014\nManidipine 20 mg/24 h 0-1-0 Hypertension 2014\nSimvastatin 40 mg/24 h 0-0-1 Hypercholesterolemia 2014\nAcetylsalicylic acid 100 mg/24 h 1-0-0 Secondary prophylaxis 2014\nOmeprazole 20 mg/24 h 1-0-0 Prevention of peptic ulcer 2014\nPregabalin 100 mg/12 h 1-0-1 Neuralgia 2019\nTorasemide 10 mg/24 h 1-0-0 Edema 2023\nDulaglutide 1.5 mg/week 1 time/week Diabetes 2014\nInsulin glargine 74 IU/24 h 1-0-0 Diabetes 2014\nInsulin lispro 20 IU/24 h 0-1-0 Diabetes 2014\nBrimonidine 1 drop/12 h 1-0-1 Ocular hypertension 2018\n\nStudy and evaluation\nThe interview revealed that there was no new medication and that it did not appear in the SPD service register. Given the suspicion of a possible hypotension, her blood pressure was measured with an Omron Complete device, with the following values: Systolic Blood Pressure (SBP) 96 mmHg, Diastolic Blood Pressure (DBP) 52 mmHg and Heart Rate (HR) 69 beats per minute. Given these values, it was suggested that her blood pressure be monitored and the influence of her medication on these values and the symptoms described by the patient be analysed.\n\nThe patient's medication doses, starting with antihypertensive medications, are reviewed to adjust to the patient's estimated glomerular filtration rate (eGFR) and to see if hypotension is related to the dosage of these medications. The patient's eGFR value, calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, is 30 ml/min/1.73 m2.\n\nThe guidelines for the revision of the dose according to the value of the eGFR are the product information for the medicinal products and the consensus guidelines for the use of medicinal products in renal impairment of the teaching and research group in the field of practical pharmacy of the Faculty of Pharmacy of the University of Barcelona, which is available on the Internet. This guide has been prepared from the analysis of the most dispensed medicinal products in community pharmacies. They have been organised by therapeutic groups according to the ATC (Anatomical-Therapeutic-Chemical) classification, information on the symptoms of overdose has been included and it has been agreed to categorise the risk to the patient of taking these medicinal products according to their eGFR as low, moderate or high.\n\nAfter the medication review was performed according to the eGFR value of 30 ml/min/1.73 m2, the results were obtained.\n\nFollowing the study of the medication, our intervention focuses on the dosage of the following medicines: losartan, manidipine, torasemide and pregabalin. The antihypertensive medicines, losartan and manidipine, and pregabalin require a dose adjustment depending on the patient's eGFR value, while the diuretic torasemide can influence blood pressure values.\n\nInitially, it was decided to intervene in the dosage of losartan and manidipine. There is the possibility of reducing the dose of pregabalin, but the pharmaceutical team agreed with the patient to assess the influence of this medication after the possible adjustment of the dose of antihypertensive during the evolution and follow-up of the patient.\n\nIntervention\nThe information is used to prepare a report for the doctor (see annex), recommending a reduction in the dose of losartan and manidipine, as the available information recommends a reduction in the dose to 50-75% of losartan for eGFR of 30-59 ml/min/1.73 m2 and adjusting the dose of manidipine for eGFR of 15-30 ml/min/1.73 m2.\n\nThe proposed intervention was explained to the patient and the report was given to the primary care doctor, explaining the possibility of adjusting the dose of losartan and manidipine to improve the patient's condition (table 4). When this information reached the doctor, he opted to reduce the dose of losartan to 50 mg/24 hours and manidipine to 10 mg/24 hours. Pregabalin 100 mg/12 hours was also replaced with gabapentin 300 mg/12 hours.\n\nFollow-up\nFollowing this change in the patient's treatment and after a follow-up of two months, the patient showed an improvement in blood pressure values (table 5) and a remission of the symptoms described. It was reviewed whether the gabapentin dose of 300 mg/12 hours was adequate for the eGFR value of 30 ml/min/1.73 m2, and it was correct (eGFR between 30 and 60, recommended total daily dose 300-900 mg).\n\n", "generated_summary": "A 78-year-old woman using a prefilled blister pack service (SPD) reported several months of tiredness, weakness, dizziness, and confusion that limited her usual walks. The pharmacy team suspected medication-related low blood pressure and reviewed her treatment, focusing on drugs cleared by the kidneys and on her blood pressure medicines. Her kidney function (eGFR) was about 30, so doses that depend on kidney clearance needed reassessment. The pharmacist prepared a report for the primary care physician recommending lowering the doses of losartan and manidipine according to renal dosing guidance. The physician reduced the doses of these antihypertensives. With follow-up, her blood pressure improved and the earlier symptoms resolved." }, { "index": 56, "label": "proficient_health_literacy", "original_text": "A 78-year-old woman, who came to collect her blister pack with her medication reconstituted in a personalised dosage system (PDS) from the community pharmacy, informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. These symptoms were preventing her from leaving her home to walk as often as she normally did. In view of this situation, she was invited to the personalised care area to review the degree of knowledge that the patient had of her medication and the use she made of it, to analyse whether any of her medication could be related to the health problem described.\n\nPharmacological treatment of the patient\n\nMedication Dose Dosage Health issue Start date\nDoxazosin 2 mg/24 h 0-0-1 Hypertension 2014\nLosartan 100 mg/24 h 1-0-0 Hypertension 2014\nManidipine 20 mg/24 h 0-1-0 Hypertension 2014\nSimvastatin 40 mg/24 h 0-0-1 Hypercholesterolemia 2014\nAcetylsalicylic acid 100 mg/24 h 1-0-0 Secondary prophylaxis 2014\nOmeprazole 20 mg/24 h 1-0-0 Prevention of peptic ulcer 2014\nPregabalin 100 mg/12 h 1-0-1 Neuralgia 2019\nTorasemide 10 mg/24 h 1-0-0 Edema 2023\nDulaglutide 1.5 mg/week 1 time/week Diabetes 2014\nInsulin glargine 74 IU/24 h 1-0-0 Diabetes 2014\nInsulin lispro 20 IU/24 h 0-1-0 Diabetes 2014\nBrimonidine 1 drop/12 h 1-0-1 Ocular hypertension 2018\n\nStudy and evaluation\nThe interview revealed that there was no new medication and that it did not appear in the SPD service register. Given the suspicion of a possible hypotension, her blood pressure was measured with an Omron Complete device, with the following values: Systolic Blood Pressure (SBP) 96 mmHg, Diastolic Blood Pressure (DBP) 52 mmHg and Heart Rate (HR) 69 beats per minute. Given these values, it was suggested that her blood pressure be monitored and the influence of her medication on these values and the symptoms described by the patient be analysed.\n\nThe patient's medication doses, starting with antihypertensive medications, are reviewed to adjust to the patient's estimated glomerular filtration rate (eGFR) and to see if hypotension is related to the dosage of these medications. The patient's eGFR value, calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, is 30 ml/min/1.73 m2.\n\nThe guidelines for the revision of the dose according to the value of the eGFR are the product information for the medicinal products and the consensus guidelines for the use of medicinal products in renal impairment of the teaching and research group in the field of practical pharmacy of the Faculty of Pharmacy of the University of Barcelona, which is available on the Internet. This guide has been prepared from the analysis of the most dispensed medicinal products in community pharmacies. They have been organised by therapeutic groups according to the ATC (Anatomical-Therapeutic-Chemical) classification, information on the symptoms of overdose has been included and it has been agreed to categorise the risk to the patient of taking these medicinal products according to their eGFR as low, moderate or high.\n\nAfter the medication review was performed according to the eGFR value of 30 ml/min/1.73 m2, the results were obtained.\n\nFollowing the study of the medication, our intervention focuses on the dosage of the following medicines: losartan, manidipine, torasemide and pregabalin. The antihypertensive medicines, losartan and manidipine, and pregabalin require a dose adjustment depending on the patient's eGFR value, while the diuretic torasemide can influence blood pressure values.\n\nInitially, it was decided to intervene in the dosage of losartan and manidipine. There is the possibility of reducing the dose of pregabalin, but the pharmaceutical team agreed with the patient to assess the influence of this medication after the possible adjustment of the dose of antihypertensive during the evolution and follow-up of the patient.\n\nIntervention\nThe information is used to prepare a report for the doctor (see annex), recommending a reduction in the dose of losartan and manidipine, as the available information recommends a reduction in the dose to 50-75% of losartan for eGFR of 30-59 ml/min/1.73 m2 and adjusting the dose of manidipine for eGFR of 15-30 ml/min/1.73 m2.\n\nThe proposed intervention was explained to the patient and the report was given to the primary care doctor, explaining the possibility of adjusting the dose of losartan and manidipine to improve the patient's condition (table 4). When this information reached the doctor, he opted to reduce the dose of losartan to 50 mg/24 hours and manidipine to 10 mg/24 hours. Pregabalin 100 mg/12 hours was also replaced with gabapentin 300 mg/12 hours.\n\nFollow-up\nFollowing this change in the patient's treatment and after a follow-up of two months, the patient showed an improvement in blood pressure values (table 5) and a remission of the symptoms described. It was reviewed whether the gabapentin dose of 300 mg/12 hours was adequate for the eGFR value of 30 ml/min/1.73 m2, and it was correct (eGFR between 30 and 60, recommended total daily dose 300-900 mg).\n\n", "generated_summary": "A 78-year-old woman enrolled in a community pharmacy personalised dosage system (PDS/SPD) presented at medication pickup reporting several months of asthenia, weakness, dizziness, and confusion, limiting her usual ambulation. There were no new medicines in the SPD register. On-site vitals with an Omron Complete device showed SBP 96 mmHg, DBP 52 mmHg, HR 69 bpm, raising concern for symptomatic hypotension possibly related to her regimen. Her active medications and doses were: doxazosin 2 mg q24h (0-0-1) for hypertension; losartan 100 mg q24h (1-0-0) for hypertension; manidipine 20 mg q24h (0-1-0) for hypertension; simvastatin 40 mg q24h (0-0-1) for hypercholesterolemia; acetylsalicylic acid 100 mg q24h (1-0-0) for secondary prophylaxis; omeprazole 20 mg q24h (1-0-0) for ulcer prevention; pregabalin 100 mg q12h (1-0-1) for neuralgia; torasemide 10 mg q24h (1-0-0) for edema; dulaglutide 1.5 mg weekly; insulin glargine 74 IU q24h (1-0-0); insulin lispro 20 IU q24h (0-1-0) for diabetes; brimonidine 1 drop q12h (1-0-1) for ocular hypertension.\n\nRenal function by CKD-EPI yielded eGFR 30 ml/min/1.73 m2. Dose appropriateness was assessed against product information and a consensus guideline for drug use in renal impairment from the University of Barcelona Faculty of Pharmacy practical pharmacy group (ATC-organised, with overdose symptom summaries and risk stratification by eGFR). Based on eGFR 30 ml/min/1.73 m2, antihypertensive agents losartan and manidipine required dose adjustment; pregabalin also warranted renal dosing, and torasemide was recognised as potentially contributing to low BP. The team prioritised adjusting antihypertensives first and proposed deferring changes to pregabalin until after reassessing response.\n\nIntervention: A report to the primary care physician recommended reducing losartan to 50\u201375% of standard dose for eGFR 30\u201359 ml/min/1.73 m2 and adjusting manidipine for eGFR 15\u201330 ml/min/1.73 m2. The PCP implemented losartan 50 mg q24h and manidipine 10 mg q24h. The PCP also substituted pregabalin 100 mg q12h with gabapentin 300 mg q12h.\n\nFollow-up over two months showed improved BP values and resolution of the initial symptoms. Gabapentin 300 mg q12h was verified as appropriate for eGFR ~30 ml/min/1.73 m2 (recommended total daily dose 300\u2013900 mg for eGFR 30\u201360). Overall, the case suggests symptomatic hypotension related to cumulative antihypertensive effect in the setting of stage 3b CKD by eGFR, with clinical improvement after renal dose adjustment of losartan and manidipine and subsequent regimen optimisation." }, { "index": 57, "label": "low_health_literacy", "original_text": "It is a case study, approved by the Research Ethics Committee (CEP) under number 1.012.635. The prior authorization of the relatives and the participant was requested from the signature of the Free and Informed Consent (TCLE) and the Free and Informed Consent (TALE).\n\nThe participant in this study is a female student in the 3rd year of elementary school. In the first evaluation, in 2018, the child was 8 years and 2 months old, while in the second evaluation, in 2019, she was 9 years and 6 months old. The interval between the evaluations occurred due to the fact that it is a public service. Thus, the laboratory was absent from activities during the holidays. In addition, it is important to consider that the appointments were only made once a week and, during that period, the participant was absent, which also prolonged the process. As for her history, she was born at term and presented adequate neuropsychomotor and linguistic development. The child was born and lived in a French-speaking country until the age of 2 years, but had exposure to another language at home, since her parents are Brazilian Portuguese speakers. However, her first words were in French. When she returned to Brazil, she went through two private schools. In the first school, she was unable to communicate, as she only expressed herself in French. After that experience, at the age of 3, she began studying in a French school, still in Brazil. Over the years, she presented difficulty in acquiring reading and writing; for that reason, she repeated the 1st year of elementary school, at the request of her mother. At the age of 6, she began studying in a bilingual Portuguese-English school. At the age of 8 years old, she underwent evaluation by an interdisciplinary team in the areas of speech therapy and neuropsychology, finding the diagnosis of developmental dyslexia (DD) and high abilities/giftedness (AH/S). Soon after, she was referred to the evaluation of reading and writing in the Laboratory of Written Language, Interdisciplinarity and Learning - LEIA/UFRN.\n\nPhases of the study: four assessment sessions for each moment - pre and post intervention (T1 and T2, respectively) - and 20 sessions of phonological remediation, once a week for 60 minutes. The intervention took place in the second semester of 2018, where parents were not very engaged due to work demands.\n\nAssessments were conducted individually over a one-hour period. They included tasks to assess performance in phonological processing - phonological working memory, phonological awareness and mental lexical access - reading and writing.\n\nThe following protocols were used to evaluate the child:\n\nPhonological awareness: to evaluate this ability, the Consci\u00eancia Fonol\u00f3gica Instrumento de Avalia\u00e7\u00e3o Sequencial - CONFIAS (11) was used. This protocol proposes tasks of synthesis, segmentation, rhyme, alliteration, initial and final syllable identification, exclusion and transposition. First, syllabic awareness, formed by nine items, is analyzed, followed by phonemic awareness, formed by seven items. Each hit is equivalent to one point, with 40 for syllabic awareness and 30 for phonemic awareness, totaling 70 points. Its results should be compared with the expected writing hypotheses based on Ferreiro and Teberosky (12). In this way, the following normal values were used: for the syllabic-alphabetic writing hypothesis, 27, 12 and 39 for the syllabic, phonemic and total score, respectively; for the alphabetic writing hypothesis, 31, 15 and 46.\n\nPhonological working memory: The Phonological Working Memory Test was used (13). In the application of this protocol, the assessor should begin with the non-word test, which consists of 40 invented words. The assessor should then say each word in the list, asking the child to repeat it immediately. The child has two attempts to repeat the words correctly. In the first attempt, each correct answer is worth two points, in the second attempt, the child is awarded one point, and in the third attempt, the child is awarded zero points. After this, the assessor should move on to the test of digits in direct and reverse order, which is scored in the same way as the pseudo-words. Depending on the age of the participant at the time of the assessments, the normal values of 69, 13 and 6 were used for pseudo-words, direct and reverse digits, respectively.\n\nAccess to the mental lexicon: the Rapid Automatic Naming Test (RAN)(14) was used in the evaluation and the Automatic Naming Test (TENA)(15) in the re-evaluation. Both tests aim to estimate the individual's ability to name a sequence of stimuli, that is, to measure the speed at which the child can verbalize a visual stimulus quickly. Two protocols were used, since the TENA had not yet been published at the time of the first evaluation. In addition, the TENA is a current and more complete protocol for the verification of normality, as it allows analysis according to age and months. The two tests used have similar application and are divided into four boards, where the child must name colors, objects, letters and digits. The naming must be done with the same movement that is used for reading - from left to right and from top to bottom. For T1, which used the RAN, the normality values correspond to children aged between 8 years and 8 years and 11 months, due to the age of the participant in that period, thus, it should have a score of 28, 29, 52 and 46 seconds for the subtests of digits, letters, objects and colors, respectively. For T2, the normality values of the age of 9 years and 6 months of the protocol (TENA) were used, with an expected score of 35, 32, 50, 53 seconds for the subtests of digits, letters, objects and colors, respectively.\n\nReading: First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated \u2013 LPI(16) was used, in which the child is asked to read aloud words and pseudowords, which are scored. 19 regular words, 20 irregular words and 20 pseudowords are arranged in black Arial font, size 24 and white background. The child may obtain a total of 59 points, since each correct reading is worth one point. After this, the Protocol for the Assessment of Reading of Expository Texts was used(17). This instrument aims to assess reading comprehension through directed questions about texts compatible with the subject's school year. It assesses and times patterns of silent and oral reading. This allows the reading level to be verified and compared. In addition, the number of words read per minute is averaged, allowing the reading speed to be verified and compared.\n\nWriting: To evaluate the writing, the child was asked to produce a text on a topic of their interest. After finishing the story, the professional asked the child to read out loud what was written. Furthermore, the child was asked to write the target words of the LPI(16) on a separate sheet, in order to carry out a dictation of words and pseudo-words. With this, a qualitative investigation of the writing was carried out, based on the orthographic analysis of Zorzi and Ciasca(18).\n\nThe remediation was based on a program used for children with dyslexia(19) and included activities that aimed to improve phonological abilities, such as: identification of graphemes and phonemes, phoneme pairs, syllable pairs, word pairs, addition and subtraction of phonemes, syllabic and phonemic manipulation, rhymes, alliteration, access to mental lexicon, visual working memory, auditory working memory and reading training. In all sessions, these activities were explored in a playful way, mainly directed to the metalinguistic aspects of phonological awareness. In reading training, the child was exposed to children's books from the Mico Maneco collection. This collection has various stories that increase the level of complexity of words, so it is possible to follow the child's progress. The activities performed and the child's evolution were described in his/her medical record at the end of each session.\n\nAnalysing the results found, with regard to performance in phonological awareness, in both assessments the child presented performance consistent with the hypotheses of writing presented in each period. In the first assessment, he received the syllabic-alphabetic writing hypothesis and in the second, the alphabetic one, demonstrating progress. The performance score progressed in both categories of the skill, syllabic (T1 = 35; T2 = 37) and phonemic (T1 = 14; T2 = 20) (Table 1). The progress of 4 successes in the phonemic level is highlighted, which can be explained due to the phonological remediation having been performed with focus on the phonemic level.\n\nThe results of phonological working memory at the time prior to phonological remediation expressed below-expected performance for the pseudo-word category, with 66 points in T1, with expected performance for T1 (ET1) of 69, and for the reverse-order digits category (T1 = 04; ET1 = 06) (Table 1). Despite this, it presented results within the expected range for the reverse-order digits category (T1 = 20; ET1 = 13). In the post-intervention evaluation (T2), the results are adequate for the age. It is also possible to notice advances in this skill in all categories, pseudo-word (T1 = 66; T2 = 69), reverse-order digits (T1 = 04; T2 = 12) (Table 1), which requires aspects of executive functions that assist in the rapid storage of the response, a differential aspect in high abilities.\n\nAs for the automatic rapid naming, it is noted that in T1, the performance is inadequate for the standards of normality in all subtests. It is also possible to say that, in T2, the performance was below the expected for the categories of digits (T2 = 41; ET2 = 35), objects (T2 = 59; ET2 = 50) and colors (T2 = 56; ET2 = 53). Only the category of letters presented results within the expected (T2 = 29; ET2 = 32). On the other hand, the advance in the speed of naming is visible for the subtests of letters (T1 = 37; T2 = 29), objects (T1 = 62; T2 = 59) and colors (T1 = 60; T2 = 56), with the exception of digits (T1 = 37; T2 = 41) (Table 1). With the decrease of the time of naming of the stimuli, it is possible to say that the child becomes more effective to access the mental lexicon at the level of the phonological and visual representation, which is also not usual in isolated dyslexia.\n\nAs for reading, in T1 she presented an alphabetic level and in T2 an orthographic level. In the first test, it was noted that there was difficulty mainly with visually similar letters and phonologically close. In addition, the student used sub-vocal support to decode and had an average reading of 20 words per minute, which demonstrates extremely slow decoding and is far below what is expected for her schooling. In the reassessment, she had an average of 94.4 words per minute in oral reading, which is considered adequate for her schooling. She demonstrated presence of prosody, rhythm, global reading, interest and adequate understanding. Qualitatively, it is observed that the child, even with adequate performance, read with a low intensity of speech, still demonstrating insecurity in carrying out the task.\n\nIn writing, it can be observed that in T1 the child had inadequate pencil grip, imprecise writing, with letter changes, omissions, hyper and hyposegments, repetition of words and low use of cohesive elements. In this period, it was shown with writing in the transition from the syllabic-alphabetic phase to the alphabetic phase. In T2 no significant change was observed, since his writing continued to be imprecise, with little intelligibility of the content, visual similarities between letters (such as \u201cd\u201d and \u201cb\u201d) and lack of punctuation. According to the sample collected, it was shown in the alphabetic phase of writing, although difficulties not expected for his age persisted. Despite this, it is noted that he used a greater repertoire in the use of vocabulary for the lexicon of visual input.\n\nAfter the analysis of the results in their entirety, it can be observed that the written language skills advanced during the interval between the evaluations, despite the persistence of consonant characteristics with dyslexia, as it still presents performance below the expected in the access to the mental lexicon and in writing - with the presence of exchanges between phonemes that are audibly and visually similar in a persistent way, omission of letters and hypersegmentation.\n", "generated_summary": "This report tells the story of one 9-year-old girl. She is very bright and also has dyslexia. The team tested how she handles speech sounds, how she reads, and how she writes. They tested her before and after sound-based help. Before help, she read by sounding out letters. Her writing was between early sound-by-sound writing and full letter-by-letter writing. She had trouble with tasks that use the sounds in words. After help, her sound skills got better. Her writing became steady at the letter-by-letter stage. Her reading moved up to the next stage, where she could recognize whole words and common spelling patterns." }, { "index": 57, "label": "intermediate_health_literacy", "original_text": "It is a case study, approved by the Research Ethics Committee (CEP) under number 1.012.635. The prior authorization of the relatives and the participant was requested from the signature of the Free and Informed Consent (TCLE) and the Free and Informed Consent (TALE).\n\nThe participant in this study is a female student in the 3rd year of elementary school. In the first evaluation, in 2018, the child was 8 years and 2 months old, while in the second evaluation, in 2019, she was 9 years and 6 months old. The interval between the evaluations occurred due to the fact that it is a public service. Thus, the laboratory was absent from activities during the holidays. In addition, it is important to consider that the appointments were only made once a week and, during that period, the participant was absent, which also prolonged the process. As for her history, she was born at term and presented adequate neuropsychomotor and linguistic development. The child was born and lived in a French-speaking country until the age of 2 years, but had exposure to another language at home, since her parents are Brazilian Portuguese speakers. However, her first words were in French. When she returned to Brazil, she went through two private schools. In the first school, she was unable to communicate, as she only expressed herself in French. After that experience, at the age of 3, she began studying in a French school, still in Brazil. Over the years, she presented difficulty in acquiring reading and writing; for that reason, she repeated the 1st year of elementary school, at the request of her mother. At the age of 6, she began studying in a bilingual Portuguese-English school. At the age of 8 years old, she underwent evaluation by an interdisciplinary team in the areas of speech therapy and neuropsychology, finding the diagnosis of developmental dyslexia (DD) and high abilities/giftedness (AH/S). Soon after, she was referred to the evaluation of reading and writing in the Laboratory of Written Language, Interdisciplinarity and Learning - LEIA/UFRN.\n\nPhases of the study: four assessment sessions for each moment - pre and post intervention (T1 and T2, respectively) - and 20 sessions of phonological remediation, once a week for 60 minutes. The intervention took place in the second semester of 2018, where parents were not very engaged due to work demands.\n\nAssessments were conducted individually over a one-hour period. They included tasks to assess performance in phonological processing - phonological working memory, phonological awareness and mental lexical access - reading and writing.\n\nThe following protocols were used to evaluate the child:\n\nPhonological awareness: to evaluate this ability, the Consci\u00eancia Fonol\u00f3gica Instrumento de Avalia\u00e7\u00e3o Sequencial - CONFIAS (11) was used. This protocol proposes tasks of synthesis, segmentation, rhyme, alliteration, initial and final syllable identification, exclusion and transposition. First, syllabic awareness, formed by nine items, is analyzed, followed by phonemic awareness, formed by seven items. Each hit is equivalent to one point, with 40 for syllabic awareness and 30 for phonemic awareness, totaling 70 points. Its results should be compared with the expected writing hypotheses based on Ferreiro and Teberosky (12). In this way, the following normal values were used: for the syllabic-alphabetic writing hypothesis, 27, 12 and 39 for the syllabic, phonemic and total score, respectively; for the alphabetic writing hypothesis, 31, 15 and 46.\n\nPhonological working memory: The Phonological Working Memory Test was used (13). In the application of this protocol, the assessor should begin with the non-word test, which consists of 40 invented words. The assessor should then say each word in the list, asking the child to repeat it immediately. The child has two attempts to repeat the words correctly. In the first attempt, each correct answer is worth two points, in the second attempt, the child is awarded one point, and in the third attempt, the child is awarded zero points. After this, the assessor should move on to the test of digits in direct and reverse order, which is scored in the same way as the pseudo-words. Depending on the age of the participant at the time of the assessments, the normal values of 69, 13 and 6 were used for pseudo-words, direct and reverse digits, respectively.\n\nAccess to the mental lexicon: the Rapid Automatic Naming Test (RAN)(14) was used in the evaluation and the Automatic Naming Test (TENA)(15) in the re-evaluation. Both tests aim to estimate the individual's ability to name a sequence of stimuli, that is, to measure the speed at which the child can verbalize a visual stimulus quickly. Two protocols were used, since the TENA had not yet been published at the time of the first evaluation. In addition, the TENA is a current and more complete protocol for the verification of normality, as it allows analysis according to age and months. The two tests used have similar application and are divided into four boards, where the child must name colors, objects, letters and digits. The naming must be done with the same movement that is used for reading - from left to right and from top to bottom. For T1, which used the RAN, the normality values correspond to children aged between 8 years and 8 years and 11 months, due to the age of the participant in that period, thus, it should have a score of 28, 29, 52 and 46 seconds for the subtests of digits, letters, objects and colors, respectively. For T2, the normality values of the age of 9 years and 6 months of the protocol (TENA) were used, with an expected score of 35, 32, 50, 53 seconds for the subtests of digits, letters, objects and colors, respectively.\n\nReading: First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated \u2013 LPI(16) was used, in which the child is asked to read aloud words and pseudowords, which are scored. 19 regular words, 20 irregular words and 20 pseudowords are arranged in black Arial font, size 24 and white background. The child may obtain a total of 59 points, since each correct reading is worth one point. After this, the Protocol for the Assessment of Reading of Expository Texts was used(17). This instrument aims to assess reading comprehension through directed questions about texts compatible with the subject's school year. It assesses and times patterns of silent and oral reading. This allows the reading level to be verified and compared. In addition, the number of words read per minute is averaged, allowing the reading speed to be verified and compared.\n\nWriting: To evaluate the writing, the child was asked to produce a text on a topic of their interest. After finishing the story, the professional asked the child to read out loud what was written. Furthermore, the child was asked to write the target words of the LPI(16) on a separate sheet, in order to carry out a dictation of words and pseudo-words. With this, a qualitative investigation of the writing was carried out, based on the orthographic analysis of Zorzi and Ciasca(18).\n\nThe remediation was based on a program used for children with dyslexia(19) and included activities that aimed to improve phonological abilities, such as: identification of graphemes and phonemes, phoneme pairs, syllable pairs, word pairs, addition and subtraction of phonemes, syllabic and phonemic manipulation, rhymes, alliteration, access to mental lexicon, visual working memory, auditory working memory and reading training. In all sessions, these activities were explored in a playful way, mainly directed to the metalinguistic aspects of phonological awareness. In reading training, the child was exposed to children's books from the Mico Maneco collection. This collection has various stories that increase the level of complexity of words, so it is possible to follow the child's progress. The activities performed and the child's evolution were described in his/her medical record at the end of each session.\n\nAnalysing the results found, with regard to performance in phonological awareness, in both assessments the child presented performance consistent with the hypotheses of writing presented in each period. In the first assessment, he received the syllabic-alphabetic writing hypothesis and in the second, the alphabetic one, demonstrating progress. The performance score progressed in both categories of the skill, syllabic (T1 = 35; T2 = 37) and phonemic (T1 = 14; T2 = 20) (Table 1). The progress of 4 successes in the phonemic level is highlighted, which can be explained due to the phonological remediation having been performed with focus on the phonemic level.\n\nThe results of phonological working memory at the time prior to phonological remediation expressed below-expected performance for the pseudo-word category, with 66 points in T1, with expected performance for T1 (ET1) of 69, and for the reverse-order digits category (T1 = 04; ET1 = 06) (Table 1). Despite this, it presented results within the expected range for the reverse-order digits category (T1 = 20; ET1 = 13). In the post-intervention evaluation (T2), the results are adequate for the age. It is also possible to notice advances in this skill in all categories, pseudo-word (T1 = 66; T2 = 69), reverse-order digits (T1 = 04; T2 = 12) (Table 1), which requires aspects of executive functions that assist in the rapid storage of the response, a differential aspect in high abilities.\n\nAs for the automatic rapid naming, it is noted that in T1, the performance is inadequate for the standards of normality in all subtests. It is also possible to say that, in T2, the performance was below the expected for the categories of digits (T2 = 41; ET2 = 35), objects (T2 = 59; ET2 = 50) and colors (T2 = 56; ET2 = 53). Only the category of letters presented results within the expected (T2 = 29; ET2 = 32). On the other hand, the advance in the speed of naming is visible for the subtests of letters (T1 = 37; T2 = 29), objects (T1 = 62; T2 = 59) and colors (T1 = 60; T2 = 56), with the exception of digits (T1 = 37; T2 = 41) (Table 1). With the decrease of the time of naming of the stimuli, it is possible to say that the child becomes more effective to access the mental lexicon at the level of the phonological and visual representation, which is also not usual in isolated dyslexia.\n\nAs for reading, in T1 she presented an alphabetic level and in T2 an orthographic level. In the first test, it was noted that there was difficulty mainly with visually similar letters and phonologically close. In addition, the student used sub-vocal support to decode and had an average reading of 20 words per minute, which demonstrates extremely slow decoding and is far below what is expected for her schooling. In the reassessment, she had an average of 94.4 words per minute in oral reading, which is considered adequate for her schooling. She demonstrated presence of prosody, rhythm, global reading, interest and adequate understanding. Qualitatively, it is observed that the child, even with adequate performance, read with a low intensity of speech, still demonstrating insecurity in carrying out the task.\n\nIn writing, it can be observed that in T1 the child had inadequate pencil grip, imprecise writing, with letter changes, omissions, hyper and hyposegments, repetition of words and low use of cohesive elements. In this period, it was shown with writing in the transition from the syllabic-alphabetic phase to the alphabetic phase. In T2 no significant change was observed, since his writing continued to be imprecise, with little intelligibility of the content, visual similarities between letters (such as \u201cd\u201d and \u201cb\u201d) and lack of punctuation. According to the sample collected, it was shown in the alphabetic phase of writing, although difficulties not expected for his age persisted. Despite this, it is noted that he used a greater repertoire in the use of vocabulary for the lexicon of visual input.\n\nAfter the analysis of the results in their entirety, it can be observed that the written language skills advanced during the interval between the evaluations, despite the persistence of consonant characteristics with dyslexia, as it still presents performance below the expected in the access to the mental lexicon and in writing - with the presence of exchanges between phonemes that are audibly and visually similar in a persistent way, omission of letters and hypersegmentation.\n", "generated_summary": "This case report describes a 9-year-old child with the unusual combination of high abilities and dyslexia. The goal was to compare her phonological processing, reading, and writing before and after a structured program focused on phonological skills. At the first assessment, she read at the alphabetic level, her writing was in the transition between syllabic\u2013alphabetic and alphabetic stages, and her phonological processing was below expectations. After phonological remediation, her phonological processing improved, her writing consolidated at the alphabetic stage, and her reading advanced to the orthographic level, indicating more efficient recognition of whole-word patterns and spelling regularities." }, { "index": 57, "label": "proficient_health_literacy", "original_text": "It is a case study, approved by the Research Ethics Committee (CEP) under number 1.012.635. The prior authorization of the relatives and the participant was requested from the signature of the Free and Informed Consent (TCLE) and the Free and Informed Consent (TALE).\n\nThe participant in this study is a female student in the 3rd year of elementary school. In the first evaluation, in 2018, the child was 8 years and 2 months old, while in the second evaluation, in 2019, she was 9 years and 6 months old. The interval between the evaluations occurred due to the fact that it is a public service. Thus, the laboratory was absent from activities during the holidays. In addition, it is important to consider that the appointments were only made once a week and, during that period, the participant was absent, which also prolonged the process. As for her history, she was born at term and presented adequate neuropsychomotor and linguistic development. The child was born and lived in a French-speaking country until the age of 2 years, but had exposure to another language at home, since her parents are Brazilian Portuguese speakers. However, her first words were in French. When she returned to Brazil, she went through two private schools. In the first school, she was unable to communicate, as she only expressed herself in French. After that experience, at the age of 3, she began studying in a French school, still in Brazil. Over the years, she presented difficulty in acquiring reading and writing; for that reason, she repeated the 1st year of elementary school, at the request of her mother. At the age of 6, she began studying in a bilingual Portuguese-English school. At the age of 8 years old, she underwent evaluation by an interdisciplinary team in the areas of speech therapy and neuropsychology, finding the diagnosis of developmental dyslexia (DD) and high abilities/giftedness (AH/S). Soon after, she was referred to the evaluation of reading and writing in the Laboratory of Written Language, Interdisciplinarity and Learning - LEIA/UFRN.\n\nPhases of the study: four assessment sessions for each moment - pre and post intervention (T1 and T2, respectively) - and 20 sessions of phonological remediation, once a week for 60 minutes. The intervention took place in the second semester of 2018, where parents were not very engaged due to work demands.\n\nAssessments were conducted individually over a one-hour period. They included tasks to assess performance in phonological processing - phonological working memory, phonological awareness and mental lexical access - reading and writing.\n\nThe following protocols were used to evaluate the child:\n\nPhonological awareness: to evaluate this ability, the Consci\u00eancia Fonol\u00f3gica Instrumento de Avalia\u00e7\u00e3o Sequencial - CONFIAS (11) was used. This protocol proposes tasks of synthesis, segmentation, rhyme, alliteration, initial and final syllable identification, exclusion and transposition. First, syllabic awareness, formed by nine items, is analyzed, followed by phonemic awareness, formed by seven items. Each hit is equivalent to one point, with 40 for syllabic awareness and 30 for phonemic awareness, totaling 70 points. Its results should be compared with the expected writing hypotheses based on Ferreiro and Teberosky (12). In this way, the following normal values were used: for the syllabic-alphabetic writing hypothesis, 27, 12 and 39 for the syllabic, phonemic and total score, respectively; for the alphabetic writing hypothesis, 31, 15 and 46.\n\nPhonological working memory: The Phonological Working Memory Test was used (13). In the application of this protocol, the assessor should begin with the non-word test, which consists of 40 invented words. The assessor should then say each word in the list, asking the child to repeat it immediately. The child has two attempts to repeat the words correctly. In the first attempt, each correct answer is worth two points, in the second attempt, the child is awarded one point, and in the third attempt, the child is awarded zero points. After this, the assessor should move on to the test of digits in direct and reverse order, which is scored in the same way as the pseudo-words. Depending on the age of the participant at the time of the assessments, the normal values of 69, 13 and 6 were used for pseudo-words, direct and reverse digits, respectively.\n\nAccess to the mental lexicon: the Rapid Automatic Naming Test (RAN)(14) was used in the evaluation and the Automatic Naming Test (TENA)(15) in the re-evaluation. Both tests aim to estimate the individual's ability to name a sequence of stimuli, that is, to measure the speed at which the child can verbalize a visual stimulus quickly. Two protocols were used, since the TENA had not yet been published at the time of the first evaluation. In addition, the TENA is a current and more complete protocol for the verification of normality, as it allows analysis according to age and months. The two tests used have similar application and are divided into four boards, where the child must name colors, objects, letters and digits. The naming must be done with the same movement that is used for reading - from left to right and from top to bottom. For T1, which used the RAN, the normality values correspond to children aged between 8 years and 8 years and 11 months, due to the age of the participant in that period, thus, it should have a score of 28, 29, 52 and 46 seconds for the subtests of digits, letters, objects and colors, respectively. For T2, the normality values of the age of 9 years and 6 months of the protocol (TENA) were used, with an expected score of 35, 32, 50, 53 seconds for the subtests of digits, letters, objects and colors, respectively.\n\nReading: First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated \u2013 LPI(16) was used, in which the child is asked to read aloud words and pseudowords, which are scored. 19 regular words, 20 irregular words and 20 pseudowords are arranged in black Arial font, size 24 and white background. The child may obtain a total of 59 points, since each correct reading is worth one point. After this, the Protocol for the Assessment of Reading of Expository Texts was used(17). This instrument aims to assess reading comprehension through directed questions about texts compatible with the subject's school year. It assesses and times patterns of silent and oral reading. This allows the reading level to be verified and compared. In addition, the number of words read per minute is averaged, allowing the reading speed to be verified and compared.\n\nWriting: To evaluate the writing, the child was asked to produce a text on a topic of their interest. After finishing the story, the professional asked the child to read out loud what was written. Furthermore, the child was asked to write the target words of the LPI(16) on a separate sheet, in order to carry out a dictation of words and pseudo-words. With this, a qualitative investigation of the writing was carried out, based on the orthographic analysis of Zorzi and Ciasca(18).\n\nThe remediation was based on a program used for children with dyslexia(19) and included activities that aimed to improve phonological abilities, such as: identification of graphemes and phonemes, phoneme pairs, syllable pairs, word pairs, addition and subtraction of phonemes, syllabic and phonemic manipulation, rhymes, alliteration, access to mental lexicon, visual working memory, auditory working memory and reading training. In all sessions, these activities were explored in a playful way, mainly directed to the metalinguistic aspects of phonological awareness. In reading training, the child was exposed to children's books from the Mico Maneco collection. This collection has various stories that increase the level of complexity of words, so it is possible to follow the child's progress. The activities performed and the child's evolution were described in his/her medical record at the end of each session.\n\nAnalysing the results found, with regard to performance in phonological awareness, in both assessments the child presented performance consistent with the hypotheses of writing presented in each period. In the first assessment, he received the syllabic-alphabetic writing hypothesis and in the second, the alphabetic one, demonstrating progress. The performance score progressed in both categories of the skill, syllabic (T1 = 35; T2 = 37) and phonemic (T1 = 14; T2 = 20) (Table 1). The progress of 4 successes in the phonemic level is highlighted, which can be explained due to the phonological remediation having been performed with focus on the phonemic level.\n\nThe results of phonological working memory at the time prior to phonological remediation expressed below-expected performance for the pseudo-word category, with 66 points in T1, with expected performance for T1 (ET1) of 69, and for the reverse-order digits category (T1 = 04; ET1 = 06) (Table 1). Despite this, it presented results within the expected range for the reverse-order digits category (T1 = 20; ET1 = 13). In the post-intervention evaluation (T2), the results are adequate for the age. It is also possible to notice advances in this skill in all categories, pseudo-word (T1 = 66; T2 = 69), reverse-order digits (T1 = 04; T2 = 12) (Table 1), which requires aspects of executive functions that assist in the rapid storage of the response, a differential aspect in high abilities.\n\nAs for the automatic rapid naming, it is noted that in T1, the performance is inadequate for the standards of normality in all subtests. It is also possible to say that, in T2, the performance was below the expected for the categories of digits (T2 = 41; ET2 = 35), objects (T2 = 59; ET2 = 50) and colors (T2 = 56; ET2 = 53). Only the category of letters presented results within the expected (T2 = 29; ET2 = 32). On the other hand, the advance in the speed of naming is visible for the subtests of letters (T1 = 37; T2 = 29), objects (T1 = 62; T2 = 59) and colors (T1 = 60; T2 = 56), with the exception of digits (T1 = 37; T2 = 41) (Table 1). With the decrease of the time of naming of the stimuli, it is possible to say that the child becomes more effective to access the mental lexicon at the level of the phonological and visual representation, which is also not usual in isolated dyslexia.\n\nAs for reading, in T1 she presented an alphabetic level and in T2 an orthographic level. In the first test, it was noted that there was difficulty mainly with visually similar letters and phonologically close. In addition, the student used sub-vocal support to decode and had an average reading of 20 words per minute, which demonstrates extremely slow decoding and is far below what is expected for her schooling. In the reassessment, she had an average of 94.4 words per minute in oral reading, which is considered adequate for her schooling. She demonstrated presence of prosody, rhythm, global reading, interest and adequate understanding. Qualitatively, it is observed that the child, even with adequate performance, read with a low intensity of speech, still demonstrating insecurity in carrying out the task.\n\nIn writing, it can be observed that in T1 the child had inadequate pencil grip, imprecise writing, with letter changes, omissions, hyper and hyposegments, repetition of words and low use of cohesive elements. In this period, it was shown with writing in the transition from the syllabic-alphabetic phase to the alphabetic phase. In T2 no significant change was observed, since his writing continued to be imprecise, with little intelligibility of the content, visual similarities between letters (such as \u201cd\u201d and \u201cb\u201d) and lack of punctuation. According to the sample collected, it was shown in the alphabetic phase of writing, although difficulties not expected for his age persisted. Despite this, it is noted that he used a greater repertoire in the use of vocabulary for the lexicon of visual input.\n\nAfter the analysis of the results in their entirety, it can be observed that the written language skills advanced during the interval between the evaluations, despite the persistence of consonant characteristics with dyslexia, as it still presents performance below the expected in the access to the mental lexicon and in writing - with the presence of exchanges between phonemes that are audibly and visually similar in a persistent way, omission of letters and hypersegmentation.\n", "generated_summary": "This is a single-case report of a female third-grade student with developmental dyslexia (DD) and high abilities/giftedness (AH/S), evaluated pre- and post-phonological remediation. Ethical approval: CEP 1.012.635; informed consent/assent obtained. The first evaluation (T1) occurred at 8y2m (2018) and the second (T2) at 9y6m (2019). History: term birth; typical neuropsychomotor and language development; early bilingual exposure (French first words; Brazilian Portuguese at home); school transitions including French and later Portuguese\u2013English bilingual schooling; interdisciplinary diagnosis of DD and AH/S at age 8; referral to LEIA/UFRN. Protocol: four assessment sessions at each time point (T1, T2) and 20 weekly 60-minute phonological remediation sessions (2H2018); limited parental engagement due to work. Assessments targeted phonological processing (phonological awareness, phonological working memory, rapid naming), reading, and writing. Measures: CONFIAS for phonological awareness; Phonological Working Memory Test (nonword repetition; digit span direct/reverse); RAN at T1 and TENA at T2 for rapid automatic naming; LPI (isolated word/pseudoword reading) and an expository text protocol (accuracy, oral/silent modes, comprehension, words/minute) for reading; spontaneous text plus dictation of LPI target words with Zorzi & Ciasca orthographic analysis for writing.\nResults\u2014phonological awareness (CONFIAS): performance aligned with the writing hypothesis at each time point. T1 scores: syllabic = 35; phonemic = 14 (consistent with a syllabic\u2013alphabetic writing hypothesis). T2 scores: syllabic = 37; phonemic = 20 (consistent with an alphabetic writing hypothesis). The 4-point gain at the phonemic level likely reflects the remediation focus on phonemic skills.\nPhonological working memory: At T1, nonwords were below expected (66 vs ET1 69) and reverse digits were below expected (4 vs ET1 6); direct-order digits were within/above expected (20 vs ET1 13). At T2, age-appropriate performance was documented with gains across categories: nonwords 69; reverse digits 12. The improvement in reverse span implicates executive mechanisms supporting rapid storage/manipulation, consistent with a strength often observed in high-ability profiles.\nRapid naming: T1 RAN performance was below normal across all subtests. At T2 (TENA), digits (41 vs ET2 35), objects (59 vs ET2 50), and colors (56 vs ET2 53) remained below expected; letters were within expected (29 vs ET2 32). Naming speed improved for letters (37\u219229 s), objects (62\u219259 s), and colors (60\u219256 s), but worsened for digits (37\u219241 s). Reduced naming latencies indicate more efficient access to the phonological/visual lexicon, though residual RAN deficits persisted\u2014typical in DD.\nReading: T1 showed an alphabetic level with reliance on sub-vocal decoding, confusions for visually/phonologically similar letters, and very slow rate (\u224820 words/min), well below grade expectations. T2 advanced to an orthographic level with oral reading \u224894.4 words/min, adequate prosody, rhythm, global reading, interest, and comprehension; low speech intensity suggested residual task-related insecurity.\nWriting: T1 reflected a transition from syllabic\u2013alphabetic to alphabetic, with maladaptive pencil grip, imprecision, letter substitutions/omissions, hyper-/hyposegmentation, word repetition, and limited cohesion. T2 remained qualitatively imprecise with low intelligibility, visual letter confusions (e.g., b/d), and limited punctuation; however, the sample was consistent with an alphabetic phase, with a broader vocabulary repertoire (visual input lexicon). Overall, alphabetic writing consolidated but orthographic accuracy lagged.\nConclusion: After phonological remediation, the child demonstrated gains in phonological processing (awareness and working memory) and progressed from alphabetic to orthographic reading, while consolidating alphabetic writing. Nevertheless, characteristic dyslexic features persisted, particularly reduced efficiency in rapid access to the mental lexicon (RAN) and ongoing orthographic/spelling errors (confusions, omissions, hypersegmentation)." }, { "index": 58, "label": "low_health_literacy", "original_text": "65-year-old woman with no relevant personal or family history. In August 2022, a posterior mediastinal tumour was found in the preoperative assessment for a knee surgery, which was why she was referred for evaluation and treatment. On admission, the physical examination was not relevant and the laboratory studies were within normal parameters. A chest CT scan was performed that showed a tumour located in the posterior right mediastinum measuring 6.5 \u00d7 4.2 cm, with well-defined borders, with a fat and solid density, with no evidence of bone erosion or infiltration of surrounding tissue. A biopsy of the lesion was performed using a 18G \u00d7 250 mm semiautomatic cutting needle, with image guidance, through a posterior approach. In the histopathological study, a benign neoplasm consisting of mature adipose tissue with areas of haemorrhage alternating with haematopoietic elements, predominantly precursors of the red series, was observed, as well as elements of the myeloid series in different stages of maturation and megakaryocytes, which established the diagnosis of MPM. Finally, with the diagnosis established and the characteristics of the lesion, conservative management was decided. The patient evolved satisfactorily and was discharged without complications.\n", "generated_summary": "A 65-year-old woman had a lump in the back part of the space between her lungs. A chest scan showed it was oval like an egg, had smooth edges, and measured about 6.5 by 4.2 centimeters. Doctors took a small sample with a needle through the chest. Under the microscope, it had fat and blood-making cells. This means the lump was a myelolipoma in the area between the lungs." }, { "index": 58, "label": "intermediate_health_literacy", "original_text": "65-year-old woman with no relevant personal or family history. In August 2022, a posterior mediastinal tumour was found in the preoperative assessment for a knee surgery, which was why she was referred for evaluation and treatment. On admission, the physical examination was not relevant and the laboratory studies were within normal parameters. A chest CT scan was performed that showed a tumour located in the posterior right mediastinum measuring 6.5 \u00d7 4.2 cm, with well-defined borders, with a fat and solid density, with no evidence of bone erosion or infiltration of surrounding tissue. A biopsy of the lesion was performed using a 18G \u00d7 250 mm semiautomatic cutting needle, with image guidance, through a posterior approach. In the histopathological study, a benign neoplasm consisting of mature adipose tissue with areas of haemorrhage alternating with haematopoietic elements, predominantly precursors of the red series, was observed, as well as elements of the myeloid series in different stages of maturation and megakaryocytes, which established the diagnosis of MPM. Finally, with the diagnosis established and the characteristics of the lesion, conservative management was decided. The patient evolved satisfactorily and was discharged without complications.\n", "generated_summary": "A 65-year-old woman was found to have an incidental mass in the back part of the chest between the lungs (posterior mediastinum). Chest CT showed an oval, well-defined tumor measuring 6.5 \u00d7 4.2 cm. A transthoracic needle biopsy was performed. Microscopy revealed mature fat and blood-forming tissue, confirming a primary mediastinal myelolipoma. Imaging showed no invasion of nearby structures, and the lesion was managed conservatively with a good outcome." }, { "index": 58, "label": "proficient_health_literacy", "original_text": "65-year-old woman with no relevant personal or family history. In August 2022, a posterior mediastinal tumour was found in the preoperative assessment for a knee surgery, which was why she was referred for evaluation and treatment. On admission, the physical examination was not relevant and the laboratory studies were within normal parameters. A chest CT scan was performed that showed a tumour located in the posterior right mediastinum measuring 6.5 \u00d7 4.2 cm, with well-defined borders, with a fat and solid density, with no evidence of bone erosion or infiltration of surrounding tissue. A biopsy of the lesion was performed using a 18G \u00d7 250 mm semiautomatic cutting needle, with image guidance, through a posterior approach. In the histopathological study, a benign neoplasm consisting of mature adipose tissue with areas of haemorrhage alternating with haematopoietic elements, predominantly precursors of the red series, was observed, as well as elements of the myeloid series in different stages of maturation and megakaryocytes, which established the diagnosis of MPM. Finally, with the diagnosis established and the characteristics of the lesion, conservative management was decided. The patient evolved satisfactorily and was discharged without complications.\n", "generated_summary": "A 65-year-old woman with no relevant personal or family history had a posterior mediastinal tumour detected incidentally during preoperative assessment for knee surgery (August 2022). On admission, physical examination was noncontributory and laboratory studies were within normal parameters. Chest CT demonstrated a tumour in the posterior right mediastinum measuring 6.5 \u00d7 4.2 cm with well-defined borders and mixed fat and solid density, without bone erosion or infiltration of surrounding tissues. An image-guided biopsy was obtained via a posterior approach using an 18G \u00d7 250 mm semiautomatic cutting needle. Histopathology showed a benign neoplasm composed of mature adipose tissue with areas of haemorrhage alternating with haemopoietic elements, predominantly erythroid precursors, along with myeloid elements at varying stages of maturation and megakaryocytes, establishing the diagnosis of primary mediastinal myelolipoma (MPM). Given the diagnosis and lesion characteristics, conservative management was chosen. The patient had an uncomplicated course and was discharged in good condition." }, { "index": 59, "label": "low_health_literacy", "original_text": "The 52-year-old man tested positive for SARS-CoV-2 using a self-test kit after having a cold. He returned to work without fever after resting for two days, but lost consciousness while working outdoors in an ambient temperature of 35\u00b0C for five hours. Upon admission to the local hospital\u2019s emergency department, his core temperature (Tc) was recorded as 40\u00b0C. The patient presented with persistent coma, dyspnea and gastrointestinal hemorrhage. No underlying diseases and relative family history was noted. Based on the characteristic presentation of hyperpyrexia, coma and multiple organ damage, a diagnosis of HS was established. He was admitted to emergency intensive care unit (ICU) of the local hospital and then received mechanical ventilation. The test results indicated the presence of pulmonary infection, hepatic and renal dysfunction, myocardial ischemia and coagulation disorders. The patient received initial management including rehydration (intravenously infused Lactated Ringer\u2019s solution and normal saline at a rate of 2.5mL/kg\u2219h), intravenous administration of Piperacillin Sodium and Tazobactam Sodium, vasoactive medications for blood pressure support, continuous mechanical ventilation, and continuous renal replacement therapy (CRRT) to manage subsequent anuria. The patient received plasma transfusion and was administered Tranexamic acid on day 5. The worsening of his condition led to his admission to the medical ICU of our hospital 7 days after HS.\n\nFollowing admission, Reverse-transcription polymerase chain reaction (RT-PCR) testing of a nasopharyngeal swab yielded positive results for SARS-CoV-2. The patient was diagnosed with HS and severe COVID-19 based on China\u2019s COVID-19 Diagnosis and Treatment Program (trial version 10): 1. real-time fluorescent RT-PCR detection of SARS-CoV-2 nucleic acid is positive; 2. respiratory failure and requires mechanical ventilation; 3. shock; 4. combined with multiple organ failure requiring intensive care. The patient had no contact with COVID-19 diagnosed patients or healthcare workers in the hospital, indicating community-acquired infection. The physical examination showed a Glasgow Coma Scale (GCS) score of 3/15, with scores of 1 for eye-opening, verbal response, and motor response. Additionally, the pupils were symmetrical and non-reactive. The heart rate was recorded at 106 bpm and blood pressure was maintained at 126/77 mmHg by continuously infusing norepinephrine at a rate of 0.4 ug/kg\u00b7min. The laboratory test results indicated a severe infection, along with anemia, thrombocytopenia, disseminated intravascular coagulation (DIC), as well as acute liver and kidney injury. The white blood cell count (WBC) decreased from 3.55\u00d7109/L to 3.13\u00d7109/L, lymphocytes significantly decreased from 0.25\u00d7109/L to 0.1\u00d7109/L, and neutrophil percentage (N%) increased to 85.3%. The Procalcitonin level measured 2.81 ng/mL and C-reactive protein (CRP) level was 32.6 mg/L. Sputum culture testing yielded Stenotrophomonas Maltophilia and Candida lipolytica. The central venous catheter culture test detected Staphylococcus epidermidis, but the continuous blood culture test yielded no positive results. The Computed Tomography (CT) scan revealed bilateral frontal subdural effusion, consolidation and atelectasis in the lower lungs, inflammation in the right upper lobe, bilateral pleural effusion, and a small amount of abdominal fluid.\n\nThe patient received synchronized intermittent mandatory ventilation with a positive end expiratory pressure of 5 mmH2O and an oxygen concentration of 80% and continuous administration of norepinephrine and pituitrin to sustain normal blood pressure. Polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration have been employed for the management of hepatic and renal dysfunction. The antibiotic was substituted with Meropenem and Thymalfasin was administered for 20 days to augment immune function. Mannitol was used to alleviate intracranial pressure for 3 days. To improve coagulation dysfunction, the patient received plasma and cryoprecipitate transfusions, continuous intravenous infusion of heparin sodium at 6000u/day and CRRT with sodium citrate for anticoagulant (8g/day) on day 7. Platelet transfusion was administered after 9 days of HS. His Tc fluctuated between 36 \u00b0C and 38.5 \u00b0C. CRRT was administered without anticoagulant on day 8. The patient had gastrointestinal hemorrhage and fever after 9 days of HS, but electronic gastroenteroscopy showed no signs of active bleeding. He underwent red blood cell suspension transfusion, hemostasis treatment and gastric acid suppression. Teicoplanin was added due to the presence of Methicillin-resistant Staphylococcus aureus isolated from sputum culture. The patient regained consciousness on day 13 with a GCS score of 14/15 and presented with a moderate fever. Gastrointestinal hemorrhage was not observed. Mechanical ventilation was discontinued and the tracheal tube was removed. But the creatinine levels increased following the suspension of CRRT on day 12.\n\nOn day 17, he developed sudden dyspnea with desaturation (oxygen saturation <85%) followed by a high fever (Tc: 39.3\u00b0C), necessitating reintubation and mechanical ventilation. Bronchoscopy revealed less sputum in both lungs and subbranches. He experienced a recurrence of coma, with a GCS score of 3/15. WBC increased to 14.94\u00d7109/L and NEU increased to 13.77\u00d7109/L. The levels of serum total bilirubin rose to 235.2 \u00b5mol/L, while creatinine increased to 441\u00b5mol/L. The brain CT scan revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. The patient underwent cooling therapy using CRRT with ice-cold replacement fluid, along with persistent administration of Meropenem and Teicoplanin for anti-infection treatment. Carpofungin was added on day 18 due to the observed elevation in serum levels of Aspergillus galactomannan, Aspergillus IgG antibody, and Candida mannan. The RT-PCR testing for SARS-CoV-2 returned negative results.\n\nThe patient\u2019s fever and infection improved on day 20, but he subsequently developed cerebral hemorrhage and hernia with bilateral dilated pupils. The dehydration therapy was used to reduce intracranial pressure, as surgery was refused by his family. On day 22, indicators of infection, levels of aspartate aminotransferase and creatinine increased again. Carbapenem-resistant Acinetobacter baumannii and A. fumigatus were cultured in the bronchoalveolar lavage fluid. The combination of Meropenem, Teicoplanin, and Carpofungine was administered for anti-infective therapy. The patient\u2019s condition progressively worsened over the next 7 days, ultimately resulting in his demise on day 29. The patients\u2019 inflammatory indicators, cytokines, and coagulation indicators are presented in Table 1.", "generated_summary": "This is the first known report of heatstroke happening at the same time as infection with the virus that causes COVID-19 in a 52-year-old man. Doctors gave him antibiotics through a vein. They used treatments to protect his organs. They also treated his blood-clotting problems. His fever went down, and he woke up from the coma. A few days later, he had trouble breathing. He also had bleeding in his brain. He got a lung infection from several germs, and his blood did not clot the way it should. Many organs stopped working. He died." }, { "index": 59, "label": "intermediate_health_literacy", "original_text": "The 52-year-old man tested positive for SARS-CoV-2 using a self-test kit after having a cold. He returned to work without fever after resting for two days, but lost consciousness while working outdoors in an ambient temperature of 35\u00b0C for five hours. Upon admission to the local hospital\u2019s emergency department, his core temperature (Tc) was recorded as 40\u00b0C. The patient presented with persistent coma, dyspnea and gastrointestinal hemorrhage. No underlying diseases and relative family history was noted. Based on the characteristic presentation of hyperpyrexia, coma and multiple organ damage, a diagnosis of HS was established. He was admitted to emergency intensive care unit (ICU) of the local hospital and then received mechanical ventilation. The test results indicated the presence of pulmonary infection, hepatic and renal dysfunction, myocardial ischemia and coagulation disorders. The patient received initial management including rehydration (intravenously infused Lactated Ringer\u2019s solution and normal saline at a rate of 2.5mL/kg\u2219h), intravenous administration of Piperacillin Sodium and Tazobactam Sodium, vasoactive medications for blood pressure support, continuous mechanical ventilation, and continuous renal replacement therapy (CRRT) to manage subsequent anuria. The patient received plasma transfusion and was administered Tranexamic acid on day 5. The worsening of his condition led to his admission to the medical ICU of our hospital 7 days after HS.\n\nFollowing admission, Reverse-transcription polymerase chain reaction (RT-PCR) testing of a nasopharyngeal swab yielded positive results for SARS-CoV-2. The patient was diagnosed with HS and severe COVID-19 based on China\u2019s COVID-19 Diagnosis and Treatment Program (trial version 10): 1. real-time fluorescent RT-PCR detection of SARS-CoV-2 nucleic acid is positive; 2. respiratory failure and requires mechanical ventilation; 3. shock; 4. combined with multiple organ failure requiring intensive care. The patient had no contact with COVID-19 diagnosed patients or healthcare workers in the hospital, indicating community-acquired infection. The physical examination showed a Glasgow Coma Scale (GCS) score of 3/15, with scores of 1 for eye-opening, verbal response, and motor response. Additionally, the pupils were symmetrical and non-reactive. The heart rate was recorded at 106 bpm and blood pressure was maintained at 126/77 mmHg by continuously infusing norepinephrine at a rate of 0.4 ug/kg\u00b7min. The laboratory test results indicated a severe infection, along with anemia, thrombocytopenia, disseminated intravascular coagulation (DIC), as well as acute liver and kidney injury. The white blood cell count (WBC) decreased from 3.55\u00d7109/L to 3.13\u00d7109/L, lymphocytes significantly decreased from 0.25\u00d7109/L to 0.1\u00d7109/L, and neutrophil percentage (N%) increased to 85.3%. The Procalcitonin level measured 2.81 ng/mL and C-reactive protein (CRP) level was 32.6 mg/L. Sputum culture testing yielded Stenotrophomonas Maltophilia and Candida lipolytica. The central venous catheter culture test detected Staphylococcus epidermidis, but the continuous blood culture test yielded no positive results. The Computed Tomography (CT) scan revealed bilateral frontal subdural effusion, consolidation and atelectasis in the lower lungs, inflammation in the right upper lobe, bilateral pleural effusion, and a small amount of abdominal fluid.\n\nThe patient received synchronized intermittent mandatory ventilation with a positive end expiratory pressure of 5 mmH2O and an oxygen concentration of 80% and continuous administration of norepinephrine and pituitrin to sustain normal blood pressure. Polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration have been employed for the management of hepatic and renal dysfunction. The antibiotic was substituted with Meropenem and Thymalfasin was administered for 20 days to augment immune function. Mannitol was used to alleviate intracranial pressure for 3 days. To improve coagulation dysfunction, the patient received plasma and cryoprecipitate transfusions, continuous intravenous infusion of heparin sodium at 6000u/day and CRRT with sodium citrate for anticoagulant (8g/day) on day 7. Platelet transfusion was administered after 9 days of HS. His Tc fluctuated between 36 \u00b0C and 38.5 \u00b0C. CRRT was administered without anticoagulant on day 8. The patient had gastrointestinal hemorrhage and fever after 9 days of HS, but electronic gastroenteroscopy showed no signs of active bleeding. He underwent red blood cell suspension transfusion, hemostasis treatment and gastric acid suppression. Teicoplanin was added due to the presence of Methicillin-resistant Staphylococcus aureus isolated from sputum culture. The patient regained consciousness on day 13 with a GCS score of 14/15 and presented with a moderate fever. Gastrointestinal hemorrhage was not observed. Mechanical ventilation was discontinued and the tracheal tube was removed. But the creatinine levels increased following the suspension of CRRT on day 12.\n\nOn day 17, he developed sudden dyspnea with desaturation (oxygen saturation <85%) followed by a high fever (Tc: 39.3\u00b0C), necessitating reintubation and mechanical ventilation. Bronchoscopy revealed less sputum in both lungs and subbranches. He experienced a recurrence of coma, with a GCS score of 3/15. WBC increased to 14.94\u00d7109/L and NEU increased to 13.77\u00d7109/L. The levels of serum total bilirubin rose to 235.2 \u00b5mol/L, while creatinine increased to 441\u00b5mol/L. The brain CT scan revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. The patient underwent cooling therapy using CRRT with ice-cold replacement fluid, along with persistent administration of Meropenem and Teicoplanin for anti-infection treatment. Carpofungin was added on day 18 due to the observed elevation in serum levels of Aspergillus galactomannan, Aspergillus IgG antibody, and Candida mannan. The RT-PCR testing for SARS-CoV-2 returned negative results.\n\nThe patient\u2019s fever and infection improved on day 20, but he subsequently developed cerebral hemorrhage and hernia with bilateral dilated pupils. The dehydration therapy was used to reduce intracranial pressure, as surgery was refused by his family. On day 22, indicators of infection, levels of aspartate aminotransferase and creatinine increased again. Carbapenem-resistant Acinetobacter baumannii and A. fumigatus were cultured in the bronchoalveolar lavage fluid. The combination of Meropenem, Teicoplanin, and Carpofungine was administered for anti-infective therapy. The patient\u2019s condition progressively worsened over the next 7 days, ultimately resulting in his demise on day 29. The patients\u2019 inflammatory indicators, cytokines, and coagulation indicators are presented in Table 1.", "generated_summary": "This is the first reported case of a 52-year-old man with heatstroke occurring alongside infection with SARS-CoV-2 (the virus that causes COVID-19). He was treated with intravenous antibiotics, organ-supportive care, and therapy for a blood-clotting disorder. His fever subsided and his coma resolved. Several days later, he developed severe shortness of breath and a brain hemorrhage. Testing showed a lung infection caused by multiple pathogens, and his coagulopathy was difficult to control. He progressed to multiple organ dysfunction syndrome (MODS) and died despite intensive care." }, { "index": 59, "label": "proficient_health_literacy", "original_text": "The 52-year-old man tested positive for SARS-CoV-2 using a self-test kit after having a cold. He returned to work without fever after resting for two days, but lost consciousness while working outdoors in an ambient temperature of 35\u00b0C for five hours. Upon admission to the local hospital\u2019s emergency department, his core temperature (Tc) was recorded as 40\u00b0C. The patient presented with persistent coma, dyspnea and gastrointestinal hemorrhage. No underlying diseases and relative family history was noted. Based on the characteristic presentation of hyperpyrexia, coma and multiple organ damage, a diagnosis of HS was established. He was admitted to emergency intensive care unit (ICU) of the local hospital and then received mechanical ventilation. The test results indicated the presence of pulmonary infection, hepatic and renal dysfunction, myocardial ischemia and coagulation disorders. The patient received initial management including rehydration (intravenously infused Lactated Ringer\u2019s solution and normal saline at a rate of 2.5mL/kg\u2219h), intravenous administration of Piperacillin Sodium and Tazobactam Sodium, vasoactive medications for blood pressure support, continuous mechanical ventilation, and continuous renal replacement therapy (CRRT) to manage subsequent anuria. The patient received plasma transfusion and was administered Tranexamic acid on day 5. The worsening of his condition led to his admission to the medical ICU of our hospital 7 days after HS.\n\nFollowing admission, Reverse-transcription polymerase chain reaction (RT-PCR) testing of a nasopharyngeal swab yielded positive results for SARS-CoV-2. The patient was diagnosed with HS and severe COVID-19 based on China\u2019s COVID-19 Diagnosis and Treatment Program (trial version 10): 1. real-time fluorescent RT-PCR detection of SARS-CoV-2 nucleic acid is positive; 2. respiratory failure and requires mechanical ventilation; 3. shock; 4. combined with multiple organ failure requiring intensive care. The patient had no contact with COVID-19 diagnosed patients or healthcare workers in the hospital, indicating community-acquired infection. The physical examination showed a Glasgow Coma Scale (GCS) score of 3/15, with scores of 1 for eye-opening, verbal response, and motor response. Additionally, the pupils were symmetrical and non-reactive. The heart rate was recorded at 106 bpm and blood pressure was maintained at 126/77 mmHg by continuously infusing norepinephrine at a rate of 0.4 ug/kg\u00b7min. The laboratory test results indicated a severe infection, along with anemia, thrombocytopenia, disseminated intravascular coagulation (DIC), as well as acute liver and kidney injury. The white blood cell count (WBC) decreased from 3.55\u00d7109/L to 3.13\u00d7109/L, lymphocytes significantly decreased from 0.25\u00d7109/L to 0.1\u00d7109/L, and neutrophil percentage (N%) increased to 85.3%. The Procalcitonin level measured 2.81 ng/mL and C-reactive protein (CRP) level was 32.6 mg/L. Sputum culture testing yielded Stenotrophomonas Maltophilia and Candida lipolytica. The central venous catheter culture test detected Staphylococcus epidermidis, but the continuous blood culture test yielded no positive results. The Computed Tomography (CT) scan revealed bilateral frontal subdural effusion, consolidation and atelectasis in the lower lungs, inflammation in the right upper lobe, bilateral pleural effusion, and a small amount of abdominal fluid.\n\nThe patient received synchronized intermittent mandatory ventilation with a positive end expiratory pressure of 5 mmH2O and an oxygen concentration of 80% and continuous administration of norepinephrine and pituitrin to sustain normal blood pressure. Polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration have been employed for the management of hepatic and renal dysfunction. The antibiotic was substituted with Meropenem and Thymalfasin was administered for 20 days to augment immune function. Mannitol was used to alleviate intracranial pressure for 3 days. To improve coagulation dysfunction, the patient received plasma and cryoprecipitate transfusions, continuous intravenous infusion of heparin sodium at 6000u/day and CRRT with sodium citrate for anticoagulant (8g/day) on day 7. Platelet transfusion was administered after 9 days of HS. His Tc fluctuated between 36 \u00b0C and 38.5 \u00b0C. CRRT was administered without anticoagulant on day 8. The patient had gastrointestinal hemorrhage and fever after 9 days of HS, but electronic gastroenteroscopy showed no signs of active bleeding. He underwent red blood cell suspension transfusion, hemostasis treatment and gastric acid suppression. Teicoplanin was added due to the presence of Methicillin-resistant Staphylococcus aureus isolated from sputum culture. The patient regained consciousness on day 13 with a GCS score of 14/15 and presented with a moderate fever. Gastrointestinal hemorrhage was not observed. Mechanical ventilation was discontinued and the tracheal tube was removed. But the creatinine levels increased following the suspension of CRRT on day 12.\n\nOn day 17, he developed sudden dyspnea with desaturation (oxygen saturation <85%) followed by a high fever (Tc: 39.3\u00b0C), necessitating reintubation and mechanical ventilation. Bronchoscopy revealed less sputum in both lungs and subbranches. He experienced a recurrence of coma, with a GCS score of 3/15. WBC increased to 14.94\u00d7109/L and NEU increased to 13.77\u00d7109/L. The levels of serum total bilirubin rose to 235.2 \u00b5mol/L, while creatinine increased to 441\u00b5mol/L. The brain CT scan revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. The patient underwent cooling therapy using CRRT with ice-cold replacement fluid, along with persistent administration of Meropenem and Teicoplanin for anti-infection treatment. Carpofungin was added on day 18 due to the observed elevation in serum levels of Aspergillus galactomannan, Aspergillus IgG antibody, and Candida mannan. The RT-PCR testing for SARS-CoV-2 returned negative results.\n\nThe patient\u2019s fever and infection improved on day 20, but he subsequently developed cerebral hemorrhage and hernia with bilateral dilated pupils. The dehydration therapy was used to reduce intracranial pressure, as surgery was refused by his family. On day 22, indicators of infection, levels of aspartate aminotransferase and creatinine increased again. Carbapenem-resistant Acinetobacter baumannii and A. fumigatus were cultured in the bronchoalveolar lavage fluid. The combination of Meropenem, Teicoplanin, and Carpofungine was administered for anti-infective therapy. The patient\u2019s condition progressively worsened over the next 7 days, ultimately resulting in his demise on day 29. The patients\u2019 inflammatory indicators, cytokines, and coagulation indicators are presented in Table 1.", "generated_summary": "We report the first case of heatstroke (HS) comorbid with SARS-CoV-2 infection in a 52-year-old male. He self-tested positive for SARS-CoV-2 after a cold, then lost consciousness while working outdoors (ambient 35\u00b0C for 5 h). On ED arrival, core temperature was 40\u00b0C with persistent coma, dyspnea, and gastrointestinal hemorrhage. HS was diagnosed based on hyperpyrexia, coma, and multiorgan injury. Initial management at the local ICU included mechanical ventilation; fluid resuscitation with Lactated Ringer\u2019s and normal saline at 2.5 mL/kg\u00b7h; piperacillin\u2013tazobactam; vasoactive support; and continuous renal replacement therapy (CRRT) for anuria. He received plasma transfusion and tranexamic acid on day 5, but clinical worsening prompted transfer on day 7.\n\nOn admission to our medical ICU, nasopharyngeal RT-PCR was positive for SARS-CoV-2, meeting criteria for severe COVID-19 (respiratory failure requiring mechanical ventilation, shock, and multiorgan failure requiring ICU). He had no in-hospital exposures, consistent with community-acquired infection. Examination: GCS 3/15 with bilaterally nonreactive, symmetric pupils; HR 106 bpm; BP 126/77 mmHg on norepinephrine 0.4 \u00b5g/kg\u00b7min. Laboratory data showed severe infection, anemia, thrombocytopenia, DIC, and acute hepatic and renal injury: WBC 3.55\u21923.13\u00d710^9/L, lymphocytes 0.25\u21920.1\u00d710^9/L, N% 85.3%, procalcitonin 2.81 ng/mL, CRP 32.6 mg/L. Microbiology: sputum grew Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture grew Staphylococcus epidermidis; serial blood cultures were negative. CT demonstrated bilateral frontal subdural effusion; lower-lobe consolidation and atelectasis; right upper lobe inflammation; bilateral pleural effusions; and small-volume ascites.\n\nICU course included SIMV with PEEP 5 mmH2O and FiO2 0.80; continuous norepinephrine and pituitrin for hemodynamic support; hepatic/renal support with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration; antimicrobial escalation to meropenem; Thymalfasin for 20 days; mannitol for 3 days for intracranial pressure; and coagulopathy management with plasma and cryoprecipitate transfusions, continuous IV heparin 6000 U/day, and CRRT with sodium citrate anticoagulation 8 g/day (day 7). Platelet transfusion was given on day 9. Tc fluctuated between 36\u201338.5\u00b0C. CRRT was continued without anticoagulation on day 8. On day 9 he developed GI hemorrhage and fever; EGD showed no active bleeding. He received RBC transfusion, hemostatic therapy, and acid suppression. Teicoplanin was added after MRSA was isolated from sputum. By day 13 he regained consciousness (GCS 14/15) with moderate fever; GI bleeding had ceased; he was extubated. Creatinine rose after CRRT was stopped on day 12.\n\nOn day 17 he acutely deteriorated with dyspnea, SpO2 <85%, and fever to 39.3\u00b0C, necessitating reintubation. Bronchoscopy showed scant sputum. Coma recurred (GCS 3/15). Labs: WBC 14.94\u00d710^9/L, NEU 13.77\u00d710^9/L; total bilirubin 235.2 \u00b5mol/L; creatinine 441 \u00b5mol/L. Brain CT: right frontal ischemic stroke and right occipital hemorrhagic infarction. Cooling was provided via CRRT with ice-cold replacement fluid. Meropenem and teicoplanin were continued. Carpofungin was started on day 18 for elevated serum Aspergillus galactomannan, Aspergillus IgG, and Candida mannan. SARS-CoV-2 RT-PCR subsequently turned negative.\n\nBy day 20, fever and infection indices improved, but he developed cerebral hemorrhage with herniation (bilateral fixed dilated pupils). Dehydration therapy for intracranial hypertension was given; neurosurgery was declined. On day 22, infection markers and AST/creatinine rose again; BALF cultured carbapenem-resistant Acinetobacter baumannii and Aspergillus fumigatus. Combination therapy with meropenem, teicoplanin, and Carpofungine was continued. Despite comprehensive antimicrobial therapy, organ support, and repeated attempts to correct a refractory coagulopathy, he progressed to multi-pathogen pulmonary infection, intractable coagulopathy, MODS, and died on day 29." }, { "index": 60, "label": "low_health_literacy", "original_text": "A 19-year-old female presented to our hospital\u2019s emergency room with a chief complaint of a two-day history of headache, accompanied by recurrent nausea, vomiting, and a one-day fever. On admission, her physical examination revealed a high fever of 39.1\u00b0C, elevated blood pressure at 189/120 mmHg, and a pulse rate of 148 beats per minute. Laboratory results indicated an elevated white blood cell count of 14.77\u00d710^9/L and a neutrophil count of 13.55\u00d710^9/L, suggesting a possible infection or inflammatory response. Initial empirical treatment with antibiotics was administered due to suspected infection, but her symptoms persisted. Given her abnormal vital signs, elevated inflammatory markers, and lack of symptom improvement, the patient was admitted for further diagnostic evaluation and transferred to the intensive care unit for close monitoring. A year prior, the patient had presented with similar symptoms and was diagnosed with myocarditis at a local hospital based on clinical findings at that time. During that hospitalization, she was also diagnosed with hypertension and prescribed antihypertensive medications. However, after discharge, the patient did not adhere to the prescribed antihypertensive therapy and did not regularly monitor her blood pressure. Additionally, it is notable that her father had a history of sudden, unexplained death.\n\nTo investigate the underlying etiology of the patient\u2019s symptoms, a chest computed tomography (CT) scan was performed. Incidentally, this scan revealed a left adrenal mass with soft tissue density, measuring 43 mm \u00d7 36 mm. No pathological findings were observed in the head and chest CT scans. The electrocardiogram demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF. Transthoracic echocardiography did not reveal any significant abnormalities.\n\nOn the second day of admission, the patient exhibited rising levels of brain natriuretic peptide (BNP) and Troponin I (TnI). The cardiologist provisionally diagnosed the patient with myocarditis of uncertain etiology, based on clinical presentation, elevated cardiac biomarkers (BNP and TnI), and supportive electrocardiogram findings. Treatment was initiated with methylprednisolone (0.25 g daily) to address potential myocardial inflammation due to suspected myocarditis. Furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) were administered as diuretics to manage fluid retention and reduce cardiac workload. Perindopril amlodipine (10 mg: 5 mg daily) was prescribed as an angiotensin-converting enzyme inhibitor and calcium channel blocker combination to control blood pressure and reduce afterload. Metoprolol tartrate (25 mg every 12 hours) was used to manage heart rate and decrease myocardial oxygen demand, while esmolol (0.2 g/hour intravenous infusion), a short-acting beta-blocker, was administered for additional acute heart rate control due to sinus tachycardia. Due to concerns about a potential infection, moxifloxacin was added as empiric antibiotic therapy.\n\nGiven the patient\u2019s presentation with an adrenal mass and hypertension, the endocrinologist recommended an evaluation of the aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines along with their metabolites. In the recumbent position, plasma and urinary catecholamine levels were markedly elevated (Table 1), including plasma dopamine at 524.5 pmol/L, norepinephrine at 83975 pmol/L, and epinephrine at 10579.3 pmol/L. Additionally, the 24-hour urinary levels showed free adrenaline at 4368.89 nmol/24 hours, free norepinephrine exceeding 12697.60 nmol/24 hours, normetanephrine at 8312 nmol/24 hours, metanephrines at 4078 nmol/24 hours, and vanillylmandelic acid at 58.1 mg/24 hours. These findings supported a clinical diagnosis of pheochromocytoma. On the fifth day post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was substituted with terazosin for more targeted blood pressure management.\n\nAn enhanced abdominal CT scan further confirmed a left adrenal mass, highly suggestive of pheochromocytoma. Additionally, after obtaining informed consent, whole-exome sequencing was performed, revealing a heterozygous missense mutation, c.1900T > C: p. Cys634Arg, in the RET gene, leading to a substitution of cysteine with arginine at codon 634. This mutation raised suspicion for multiple endocrine neoplasia syndrome, prompting further evaluation of the thyroid and parathyroid glands. Thyroid color Doppler ultrasound identified a hypoechoic mass measuring 6 mm \u00d7 4 mm in the left thyroid lobe, and a mild elevation in calcitonin levels was noted. No additional significant abnormalities were detected.\n\nAs the patient\u2019s condition gradually improved, plasma cortisol and ACTH levels returned to normal. The patient was subsequently discharged with a prescription for metoprolol tartrate (100 mg every 12 hours) and ivabradine hydrochloride (5 mg every 12 hours) for home management. Three months later, after achieving stable clinical status, the patient underwent resection of the left adrenal tumor, which measured 50 mm \u00d7 40 mm \u00d7 30 mm. Immunohistochemical analysis confirmed positive staining for Vim, CD56, Syn, CgA, and NSE, with S-100 positive in Sertoli cells, while CKpan, CD10, MART-1/Melan-A, and Melan-A were negative. The Ki67 index was 1%, leading to a definitive diagnosis of adrenal pheochromocytoma. The patient was discharged without further medications and has since been regularly followed up postoperatively without recurrence of symptoms. Over a 15-month postoperative follow-up, the patient exhibited persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium levels showed a progressive increase (Table 2). Further parathyroid scintigraphy using 99mTc-MIBI was performed, and the conclusion was a negative result for parathyroid adenoma.", "generated_summary": "A 19-year-old woman had a tumor on the gland that sits on top of the kidney that makes stress hormones. She did not have a dangerous attack, even though the tumor was large and she was given high-dose steroid medicine. A DNA test found a change in a gene called RET (c.1900T > C: p.Cys634Arg). This change is linked to a condition called MEN2A. Her thyroid had a small lump. A thyroid hormone called calcitonin was a little high. Her blood salts and the hormone that controls calcium (parathyroid hormone) were normal at first. For 15 months after surgery, calcitonin stayed a little high and the thyroid lump did not grow. Her parathyroid hormone and blood calcium slowly went up. A special scan of the parathyroid glands (99mTc-MIBI) did not show a tumor." }, { "index": 60, "label": "intermediate_health_literacy", "original_text": "A 19-year-old female presented to our hospital\u2019s emergency room with a chief complaint of a two-day history of headache, accompanied by recurrent nausea, vomiting, and a one-day fever. On admission, her physical examination revealed a high fever of 39.1\u00b0C, elevated blood pressure at 189/120 mmHg, and a pulse rate of 148 beats per minute. Laboratory results indicated an elevated white blood cell count of 14.77\u00d710^9/L and a neutrophil count of 13.55\u00d710^9/L, suggesting a possible infection or inflammatory response. Initial empirical treatment with antibiotics was administered due to suspected infection, but her symptoms persisted. Given her abnormal vital signs, elevated inflammatory markers, and lack of symptom improvement, the patient was admitted for further diagnostic evaluation and transferred to the intensive care unit for close monitoring. A year prior, the patient had presented with similar symptoms and was diagnosed with myocarditis at a local hospital based on clinical findings at that time. During that hospitalization, she was also diagnosed with hypertension and prescribed antihypertensive medications. However, after discharge, the patient did not adhere to the prescribed antihypertensive therapy and did not regularly monitor her blood pressure. Additionally, it is notable that her father had a history of sudden, unexplained death.\n\nTo investigate the underlying etiology of the patient\u2019s symptoms, a chest computed tomography (CT) scan was performed. Incidentally, this scan revealed a left adrenal mass with soft tissue density, measuring 43 mm \u00d7 36 mm. No pathological findings were observed in the head and chest CT scans. The electrocardiogram demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF. Transthoracic echocardiography did not reveal any significant abnormalities.\n\nOn the second day of admission, the patient exhibited rising levels of brain natriuretic peptide (BNP) and Troponin I (TnI). The cardiologist provisionally diagnosed the patient with myocarditis of uncertain etiology, based on clinical presentation, elevated cardiac biomarkers (BNP and TnI), and supportive electrocardiogram findings. Treatment was initiated with methylprednisolone (0.25 g daily) to address potential myocardial inflammation due to suspected myocarditis. Furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) were administered as diuretics to manage fluid retention and reduce cardiac workload. Perindopril amlodipine (10 mg: 5 mg daily) was prescribed as an angiotensin-converting enzyme inhibitor and calcium channel blocker combination to control blood pressure and reduce afterload. Metoprolol tartrate (25 mg every 12 hours) was used to manage heart rate and decrease myocardial oxygen demand, while esmolol (0.2 g/hour intravenous infusion), a short-acting beta-blocker, was administered for additional acute heart rate control due to sinus tachycardia. Due to concerns about a potential infection, moxifloxacin was added as empiric antibiotic therapy.\n\nGiven the patient\u2019s presentation with an adrenal mass and hypertension, the endocrinologist recommended an evaluation of the aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines along with their metabolites. In the recumbent position, plasma and urinary catecholamine levels were markedly elevated (Table 1), including plasma dopamine at 524.5 pmol/L, norepinephrine at 83975 pmol/L, and epinephrine at 10579.3 pmol/L. Additionally, the 24-hour urinary levels showed free adrenaline at 4368.89 nmol/24 hours, free norepinephrine exceeding 12697.60 nmol/24 hours, normetanephrine at 8312 nmol/24 hours, metanephrines at 4078 nmol/24 hours, and vanillylmandelic acid at 58.1 mg/24 hours. These findings supported a clinical diagnosis of pheochromocytoma. On the fifth day post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was substituted with terazosin for more targeted blood pressure management.\n\nAn enhanced abdominal CT scan further confirmed a left adrenal mass, highly suggestive of pheochromocytoma. Additionally, after obtaining informed consent, whole-exome sequencing was performed, revealing a heterozygous missense mutation, c.1900T > C: p. Cys634Arg, in the RET gene, leading to a substitution of cysteine with arginine at codon 634. This mutation raised suspicion for multiple endocrine neoplasia syndrome, prompting further evaluation of the thyroid and parathyroid glands. Thyroid color Doppler ultrasound identified a hypoechoic mass measuring 6 mm \u00d7 4 mm in the left thyroid lobe, and a mild elevation in calcitonin levels was noted. No additional significant abnormalities were detected.\n\nAs the patient\u2019s condition gradually improved, plasma cortisol and ACTH levels returned to normal. The patient was subsequently discharged with a prescription for metoprolol tartrate (100 mg every 12 hours) and ivabradine hydrochloride (5 mg every 12 hours) for home management. Three months later, after achieving stable clinical status, the patient underwent resection of the left adrenal tumor, which measured 50 mm \u00d7 40 mm \u00d7 30 mm. Immunohistochemical analysis confirmed positive staining for Vim, CD56, Syn, CgA, and NSE, with S-100 positive in Sertoli cells, while CKpan, CD10, MART-1/Melan-A, and Melan-A were negative. The Ki67 index was 1%, leading to a definitive diagnosis of adrenal pheochromocytoma. The patient was discharged without further medications and has since been regularly followed up postoperatively without recurrence of symptoms. Over a 15-month postoperative follow-up, the patient exhibited persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium levels showed a progressive increase (Table 2). Further parathyroid scintigraphy using 99mTc-MIBI was performed, and the conclusion was a negative result for parathyroid adenoma.", "generated_summary": "A 19-year-old woman was found to have a hormone-secreting adrenal tumor but never developed a pheochromocytoma crisis, even though the adrenal mass was large and she received high-dose glucocorticoids for suspected myocarditis. Biochemical testing confirmed catecholamine excess, and imaging supported a left adrenal pheochromocytoma. She later underwent adrenal tumor removal; pathology confirmed pheochromocytoma with a low Ki-67 index. Germline testing identified a RET mutation (c.1900T > C; p.Cys634Arg), consistent with MEN2A. Thyroid evaluation showed a small nodule with mildly elevated calcitonin; electrolytes and parathyroid hormone were initially normal. Over 15 months after surgery, calcitonin remained mildly elevated and the thyroid nodule size was stable, but parathyroid hormone and serum calcium rose progressively. A 99mTc-MIBI parathyroid scan was negative for an adenoma." }, { "index": 60, "label": "proficient_health_literacy", "original_text": "A 19-year-old female presented to our hospital\u2019s emergency room with a chief complaint of a two-day history of headache, accompanied by recurrent nausea, vomiting, and a one-day fever. On admission, her physical examination revealed a high fever of 39.1\u00b0C, elevated blood pressure at 189/120 mmHg, and a pulse rate of 148 beats per minute. Laboratory results indicated an elevated white blood cell count of 14.77\u00d710^9/L and a neutrophil count of 13.55\u00d710^9/L, suggesting a possible infection or inflammatory response. Initial empirical treatment with antibiotics was administered due to suspected infection, but her symptoms persisted. Given her abnormal vital signs, elevated inflammatory markers, and lack of symptom improvement, the patient was admitted for further diagnostic evaluation and transferred to the intensive care unit for close monitoring. A year prior, the patient had presented with similar symptoms and was diagnosed with myocarditis at a local hospital based on clinical findings at that time. During that hospitalization, she was also diagnosed with hypertension and prescribed antihypertensive medications. However, after discharge, the patient did not adhere to the prescribed antihypertensive therapy and did not regularly monitor her blood pressure. Additionally, it is notable that her father had a history of sudden, unexplained death.\n\nTo investigate the underlying etiology of the patient\u2019s symptoms, a chest computed tomography (CT) scan was performed. Incidentally, this scan revealed a left adrenal mass with soft tissue density, measuring 43 mm \u00d7 36 mm. No pathological findings were observed in the head and chest CT scans. The electrocardiogram demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF. Transthoracic echocardiography did not reveal any significant abnormalities.\n\nOn the second day of admission, the patient exhibited rising levels of brain natriuretic peptide (BNP) and Troponin I (TnI). The cardiologist provisionally diagnosed the patient with myocarditis of uncertain etiology, based on clinical presentation, elevated cardiac biomarkers (BNP and TnI), and supportive electrocardiogram findings. Treatment was initiated with methylprednisolone (0.25 g daily) to address potential myocardial inflammation due to suspected myocarditis. Furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) were administered as diuretics to manage fluid retention and reduce cardiac workload. Perindopril amlodipine (10 mg: 5 mg daily) was prescribed as an angiotensin-converting enzyme inhibitor and calcium channel blocker combination to control blood pressure and reduce afterload. Metoprolol tartrate (25 mg every 12 hours) was used to manage heart rate and decrease myocardial oxygen demand, while esmolol (0.2 g/hour intravenous infusion), a short-acting beta-blocker, was administered for additional acute heart rate control due to sinus tachycardia. Due to concerns about a potential infection, moxifloxacin was added as empiric antibiotic therapy.\n\nGiven the patient\u2019s presentation with an adrenal mass and hypertension, the endocrinologist recommended an evaluation of the aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines along with their metabolites. In the recumbent position, plasma and urinary catecholamine levels were markedly elevated (Table 1), including plasma dopamine at 524.5 pmol/L, norepinephrine at 83975 pmol/L, and epinephrine at 10579.3 pmol/L. Additionally, the 24-hour urinary levels showed free adrenaline at 4368.89 nmol/24 hours, free norepinephrine exceeding 12697.60 nmol/24 hours, normetanephrine at 8312 nmol/24 hours, metanephrines at 4078 nmol/24 hours, and vanillylmandelic acid at 58.1 mg/24 hours. These findings supported a clinical diagnosis of pheochromocytoma. On the fifth day post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was substituted with terazosin for more targeted blood pressure management.\n\nAn enhanced abdominal CT scan further confirmed a left adrenal mass, highly suggestive of pheochromocytoma. Additionally, after obtaining informed consent, whole-exome sequencing was performed, revealing a heterozygous missense mutation, c.1900T > C: p. Cys634Arg, in the RET gene, leading to a substitution of cysteine with arginine at codon 634. This mutation raised suspicion for multiple endocrine neoplasia syndrome, prompting further evaluation of the thyroid and parathyroid glands. Thyroid color Doppler ultrasound identified a hypoechoic mass measuring 6 mm \u00d7 4 mm in the left thyroid lobe, and a mild elevation in calcitonin levels was noted. No additional significant abnormalities were detected.\n\nAs the patient\u2019s condition gradually improved, plasma cortisol and ACTH levels returned to normal. The patient was subsequently discharged with a prescription for metoprolol tartrate (100 mg every 12 hours) and ivabradine hydrochloride (5 mg every 12 hours) for home management. Three months later, after achieving stable clinical status, the patient underwent resection of the left adrenal tumor, which measured 50 mm \u00d7 40 mm \u00d7 30 mm. Immunohistochemical analysis confirmed positive staining for Vim, CD56, Syn, CgA, and NSE, with S-100 positive in Sertoli cells, while CKpan, CD10, MART-1/Melan-A, and Melan-A were negative. The Ki67 index was 1%, leading to a definitive diagnosis of adrenal pheochromocytoma. The patient was discharged without further medications and has since been regularly followed up postoperatively without recurrence of symptoms. Over a 15-month postoperative follow-up, the patient exhibited persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium levels showed a progressive increase (Table 2). Further parathyroid scintigraphy using 99mTc-MIBI was performed, and the conclusion was a negative result for parathyroid adenoma.", "generated_summary": "A 19-year-old female presented with a 2-day history of headache plus recurrent nausea/vomiting and a 1-day fever. On admission: T 39.1\u00b0C, BP 189/120 mmHg, HR 148 bpm. Laboratory testing showed WBC 14.77\u00d710^9/L and neutrophils 13.55\u00d710^9/L. She received empiric antibiotics and was admitted to the ICU. One year prior she had similar symptoms and was diagnosed with myocarditis; hypertension was diagnosed at that time, but she was nonadherent post-discharge. Family history was notable for her father\u2019s sudden unexplained death.\n\nChest CT incidentally identified a left adrenal soft-tissue mass measuring 43 \u00d7 36 mm; head and chest CT had no other pathologies. ECG showed sinus tachycardia with a shortened PR interval and tall, peaked P waves in II, III, and aVF. Transthoracic echocardiography was without significant abnormalities.\n\nOn hospital day 2, BNP and troponin I increased. Cardiology provisionally diagnosed myocarditis of uncertain etiology. She was treated with methylprednisolone 0.25 g daily, furosemide 20 mg q12h, spironolactone 20 mg q12h, perindopril amlodipine (10 mg:5 mg daily), metoprolol tartrate 25 mg q12h, and an esmolol infusion at 0.2 g/h; moxifloxacin was added empirically. Despite high-dose glucocorticoids, she did not develop a catecholamine crisis.\n\nGiven the adrenal mass and hypertension, endocrine testing was pursued. In the recumbent position, plasma catecholamines were markedly elevated: dopamine 524.5 pmol/L, norepinephrine 83,975 pmol/L, epinephrine 10,579.3 pmol/L. Twenty-four-hour urine showed free adrenaline 4,368.89 nmol/24 h, free norepinephrine >12,697.60 nmol/24 h, normetanephrine 8,312 nmol/24 h, metanephrines 4,078 nmol/24 h, and vanillylmandelic acid 58.1 mg/24 h, supporting pheochromocytoma. On day 5, glucocorticoids were discontinued and perindopril/amlodipine was changed to terazosin for targeted blood pressure control. Contrast-enhanced abdominal CT confirmed a left adrenal mass highly suggestive of pheochromocytoma.\n\nWhole-exome sequencing identified a heterozygous missense RET mutation, c.1900T > C: p.Cys634Arg, prompting MEN2 evaluation. Thyroid Doppler ultrasound showed a 6 \u00d7 4 mm hypoechoic nodule in the left lobe with mildly elevated calcitonin; no other significant abnormalities were detected.\n\nAs her condition improved, plasma cortisol and ACTH normalized. She was discharged on metoprolol tartrate 100 mg q12h and ivabradine 5 mg q12h. Three months later, she underwent resection of a 50 \u00d7 40 \u00d7 30 mm left adrenal tumor. Immunohistochemistry was positive for Vim, CD56, Syn, CgA, and NSE; S-100 was positive in Sertoli cells; CKpan, CD10, MART-1/Melan-A, and Melan-A were negative. Ki-67 was 1%. The final diagnosis was adrenal pheochromocytoma. She was discharged without medications and remained asymptomatic on follow-up.\n\nOver 15 months postoperatively, she had persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium progressively increased. 99mTc-MIBI parathyroid scintigraphy was negative for parathyroid adenoma.\n\nContext and implications: Glucocorticoids are recognized precipitants of hypertensive crisis in pheochromocytoma, yet no crisis occurred here despite a significant tumor and high-dose methylprednisolone. The RET c.1900T > C (p.Cys634Arg) variant is classically associated with MEN2A, which confers high penetrance of medullary thyroid carcinoma and pheochromocytoma and variable primary hyperparathyroidism. The rising PTH and serum calcium with a negative MIBI scan are compatible with early or multigland parathyroid disease, which is common in MEN2A and may be scintigraphically occult when glands are small or hyperplastic." }, { "index": 61, "label": "low_health_literacy", "original_text": "February 2020, a 36-year-old with no significant past medical history presented with 5 years history of left sided penoscrotal mass. He has no lower urinary tract symptoms. No History of trauma or infections and he denied any history of weight loss, anorexia or fever. On examination, there is a smooth surface, tender cystic lesion around 20 mm \u2217 20 mm attached to the left side of the bulbar urethra at the penoscrotal junction, it was deep without any skin tethering and not related to the left spermatic cord and it was partially mobile.\n\nDoppler ultrasonography showed a well-defined hypoechoic mass measuring 2.7 \u2217 3.1 \u2217 2.0 cm with significantly increased vascularity at the left of penoscrotal junction. Pelvis Magnetic resonance imaging revealed a mass in the left inferolateral side of the base of the penis with a clear fat plane, which is isointense to the testes in the T2 weighted imaging, T1 weighted imaging and Diffusion-weighted imaging and it was connected to the vas deferens, no lymphadenopathy was noted. Alpha fetoprotein and beta-human chronic gonadotrophin levels were all in the normal range. Given the results of workup and the pain experienced by the patient, a decision was made to proceed with surgical removal of the mass for both diagnostic and therapeutic purposes. During surgery, a mass was seen in the left posterolateral of the scrotum and it was resected completely and sent for histopathology.\n\nHistopathology of the mass showed cellular spindle cell tumour arranged into interlacing fascicle, the cells have spindle to oval vesicular nuclei with evenly dispersed chromatin and inconspicuous nucleoli. The tumour showed high mitotic activity reaching up to 3/High-power field. Immunohistochemistry analysis was consistent with synovial sarcoma, revealing a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). The material was sent for Fluorescence in situ hybridization (FISH) and reported a rearrangement of the SS18 gene at 18q11.2 which has been observed in synovial sarcomas. The mass margins were difficult to be assessed by histopathology as the sample had fragmented margins.\n\nThe patient presented to the clinic after 2 weeks and given the histopathology report, a re-resection with wider margin was discussed with the patient and he agreed. Positron emission tomography \u2013 Computed tomography (PET/CT) was done for Head and Neck, Chest, Abdomen, Pelvis and musculoskeletal structures. Only a 29 \u2217 27 mm thyroid nodule in the lower pole of the left thyroid lobe with moderate hypermetabolism at standardized uptake values (SUVs) of 4.9. Thyroid US showed a solid isoechoic well-defined nodule in the lower pole of the left thyroid lobe with no echogenic foci, Thyroid Imaging Reporting and Data System (TIRADS) was TR3.\n\nA second resection was made 3 weeks from the first one. The whole specimen was resected from both cords bilaterally which was deepened until reaching the corpus spongiosum which was shaved superiorly up to the urethra. The specimen was sent for histopathology. The resected mass was 6.0 \u2217 6.0 \u2217 3.0 cm in size, and it was negative for any pathology. The patient then went into active surveillance and after 16 months of active surveillance he was found to have metastatic lesions in the sixth liver segment and L1 vertebral body. Oncology team started chemotherapy regimen of Ifosfamide and Doxorubicin for 6 cycles with no improvement in the liver lesion. Surgical resection was made for the Fifth and Sixth liver sections with cholecystectomy. Patient then developed a new lung lesion and was started on Pazopanib and Stereotactic Body Radiation Therapy SBRT. The patient then underwent surveillance for 6 months then developed new liver and lung lesions then chemotherapy regimen of Gemcitabine and Docetaxel combination for 3 cycles and progressed then he was started 2 cycles of Dacarbazine and progressed then 2 cycles of Pembrolizumab and progressed. The patient then was shifted to palliative care, and he stopped following up.", "generated_summary": "A 36-year-old man had a painful lump where the penis meets the scrotum for five years. Doctors took the lump out with surgery. Lab tests on the tissue confirmed it was a tumor. He had a second surgery to remove more tissue. Even with these surgeries, the disease spread to other parts of his body. It kept getting worse even after trying different chemotherapy medicines." }, { "index": 61, "label": "intermediate_health_literacy", "original_text": "February 2020, a 36-year-old with no significant past medical history presented with 5 years history of left sided penoscrotal mass. He has no lower urinary tract symptoms. No History of trauma or infections and he denied any history of weight loss, anorexia or fever. On examination, there is a smooth surface, tender cystic lesion around 20 mm \u2217 20 mm attached to the left side of the bulbar urethra at the penoscrotal junction, it was deep without any skin tethering and not related to the left spermatic cord and it was partially mobile.\n\nDoppler ultrasonography showed a well-defined hypoechoic mass measuring 2.7 \u2217 3.1 \u2217 2.0 cm with significantly increased vascularity at the left of penoscrotal junction. Pelvis Magnetic resonance imaging revealed a mass in the left inferolateral side of the base of the penis with a clear fat plane, which is isointense to the testes in the T2 weighted imaging, T1 weighted imaging and Diffusion-weighted imaging and it was connected to the vas deferens, no lymphadenopathy was noted. Alpha fetoprotein and beta-human chronic gonadotrophin levels were all in the normal range. Given the results of workup and the pain experienced by the patient, a decision was made to proceed with surgical removal of the mass for both diagnostic and therapeutic purposes. During surgery, a mass was seen in the left posterolateral of the scrotum and it was resected completely and sent for histopathology.\n\nHistopathology of the mass showed cellular spindle cell tumour arranged into interlacing fascicle, the cells have spindle to oval vesicular nuclei with evenly dispersed chromatin and inconspicuous nucleoli. The tumour showed high mitotic activity reaching up to 3/High-power field. Immunohistochemistry analysis was consistent with synovial sarcoma, revealing a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). The material was sent for Fluorescence in situ hybridization (FISH) and reported a rearrangement of the SS18 gene at 18q11.2 which has been observed in synovial sarcomas. The mass margins were difficult to be assessed by histopathology as the sample had fragmented margins.\n\nThe patient presented to the clinic after 2 weeks and given the histopathology report, a re-resection with wider margin was discussed with the patient and he agreed. Positron emission tomography \u2013 Computed tomography (PET/CT) was done for Head and Neck, Chest, Abdomen, Pelvis and musculoskeletal structures. Only a 29 \u2217 27 mm thyroid nodule in the lower pole of the left thyroid lobe with moderate hypermetabolism at standardized uptake values (SUVs) of 4.9. Thyroid US showed a solid isoechoic well-defined nodule in the lower pole of the left thyroid lobe with no echogenic foci, Thyroid Imaging Reporting and Data System (TIRADS) was TR3.\n\nA second resection was made 3 weeks from the first one. The whole specimen was resected from both cords bilaterally which was deepened until reaching the corpus spongiosum which was shaved superiorly up to the urethra. The specimen was sent for histopathology. The resected mass was 6.0 \u2217 6.0 \u2217 3.0 cm in size, and it was negative for any pathology. The patient then went into active surveillance and after 16 months of active surveillance he was found to have metastatic lesions in the sixth liver segment and L1 vertebral body. Oncology team started chemotherapy regimen of Ifosfamide and Doxorubicin for 6 cycles with no improvement in the liver lesion. Surgical resection was made for the Fifth and Sixth liver sections with cholecystectomy. Patient then developed a new lung lesion and was started on Pazopanib and Stereotactic Body Radiation Therapy SBRT. The patient then underwent surveillance for 6 months then developed new liver and lung lesions then chemotherapy regimen of Gemcitabine and Docetaxel combination for 3 cycles and progressed then he was started 2 cycles of Dacarbazine and progressed then 2 cycles of Pembrolizumab and progressed. The patient then was shifted to palliative care, and he stopped following up.", "generated_summary": "A 36-year-old man had a tender lump at the junction of the penis and scrotum for five years. Surgeons removed the mass. Under the microscope, it was a spindle cell tumor, and special staining supported a diagnosis consistent with synovial sarcoma. He then had a second, wider surgery. Despite these aggressive steps, the cancer spread to other parts of the body and kept progressing even after multiple chemotherapy treatments." }, { "index": 61, "label": "proficient_health_literacy", "original_text": "February 2020, a 36-year-old with no significant past medical history presented with 5 years history of left sided penoscrotal mass. He has no lower urinary tract symptoms. No History of trauma or infections and he denied any history of weight loss, anorexia or fever. On examination, there is a smooth surface, tender cystic lesion around 20 mm \u2217 20 mm attached to the left side of the bulbar urethra at the penoscrotal junction, it was deep without any skin tethering and not related to the left spermatic cord and it was partially mobile.\n\nDoppler ultrasonography showed a well-defined hypoechoic mass measuring 2.7 \u2217 3.1 \u2217 2.0 cm with significantly increased vascularity at the left of penoscrotal junction. Pelvis Magnetic resonance imaging revealed a mass in the left inferolateral side of the base of the penis with a clear fat plane, which is isointense to the testes in the T2 weighted imaging, T1 weighted imaging and Diffusion-weighted imaging and it was connected to the vas deferens, no lymphadenopathy was noted. Alpha fetoprotein and beta-human chronic gonadotrophin levels were all in the normal range. Given the results of workup and the pain experienced by the patient, a decision was made to proceed with surgical removal of the mass for both diagnostic and therapeutic purposes. During surgery, a mass was seen in the left posterolateral of the scrotum and it was resected completely and sent for histopathology.\n\nHistopathology of the mass showed cellular spindle cell tumour arranged into interlacing fascicle, the cells have spindle to oval vesicular nuclei with evenly dispersed chromatin and inconspicuous nucleoli. The tumour showed high mitotic activity reaching up to 3/High-power field. Immunohistochemistry analysis was consistent with synovial sarcoma, revealing a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). The material was sent for Fluorescence in situ hybridization (FISH) and reported a rearrangement of the SS18 gene at 18q11.2 which has been observed in synovial sarcomas. The mass margins were difficult to be assessed by histopathology as the sample had fragmented margins.\n\nThe patient presented to the clinic after 2 weeks and given the histopathology report, a re-resection with wider margin was discussed with the patient and he agreed. Positron emission tomography \u2013 Computed tomography (PET/CT) was done for Head and Neck, Chest, Abdomen, Pelvis and musculoskeletal structures. Only a 29 \u2217 27 mm thyroid nodule in the lower pole of the left thyroid lobe with moderate hypermetabolism at standardized uptake values (SUVs) of 4.9. Thyroid US showed a solid isoechoic well-defined nodule in the lower pole of the left thyroid lobe with no echogenic foci, Thyroid Imaging Reporting and Data System (TIRADS) was TR3.\n\nA second resection was made 3 weeks from the first one. The whole specimen was resected from both cords bilaterally which was deepened until reaching the corpus spongiosum which was shaved superiorly up to the urethra. The specimen was sent for histopathology. The resected mass was 6.0 \u2217 6.0 \u2217 3.0 cm in size, and it was negative for any pathology. The patient then went into active surveillance and after 16 months of active surveillance he was found to have metastatic lesions in the sixth liver segment and L1 vertebral body. Oncology team started chemotherapy regimen of Ifosfamide and Doxorubicin for 6 cycles with no improvement in the liver lesion. Surgical resection was made for the Fifth and Sixth liver sections with cholecystectomy. Patient then developed a new lung lesion and was started on Pazopanib and Stereotactic Body Radiation Therapy SBRT. The patient then underwent surveillance for 6 months then developed new liver and lung lesions then chemotherapy regimen of Gemcitabine and Docetaxel combination for 3 cycles and progressed then he was started 2 cycles of Dacarbazine and progressed then 2 cycles of Pembrolizumab and progressed. The patient then was shifted to palliative care, and he stopped following up.", "generated_summary": "A 36-year-old man presented with a 5-year history of a tender left penoscrotal mass attached to the left side of the bulbar urethra at the penoscrotal junction; on exam it was a deep, smooth, tender, partially mobile cystic lesion (~20 \u00d7 20 mm) without skin tethering and not involving the spermatic cord. Doppler ultrasound showed a well-defined hypoechoic mass (2.7 \u00d7 3.1 \u00d7 2.0 cm) with marked vascularity. Pelvic MRI demonstrated a mass at the left inferolateral base of the penis with a clear fat plane, isointense to the testes on T1, T2, and diffusion-weighted sequences, connected to the vas deferens, without lymphadenopathy. Serum AFP and \u03b2-hCG were normal. The mass was excised for diagnosis and symptom control. Pathology revealed a cellular spindle cell tumor arranged in interlacing fascicles with spindle-to-oval vesicular nuclei, evenly dispersed chromatin, and inconspicuous nucleoli; mitotic activity reached up to 3/HPF. Immunohistochemistry was positive for TLE-1, CD99, and BCL2 with focal cytokeratin and focal EMA, supporting synovial sarcoma. FISH demonstrated SS18 gene rearrangement at 18q11.2, confirming the diagnosis. Margins were difficult to assess due to specimen fragmentation. Two weeks later, a wider re-resection was performed; the specimen (6.0 \u00d7 6.0 \u00d7 3.0 cm), resected deeply to the corpus spongiosum with shaving up to the urethra, showed no residual tumor. Staging PET/CT was notable only for an incidental left thyroid nodule (29 \u00d7 27 mm, SUV 4.9; TR3 on ultrasound). After 16 months of surveillance, metastatic disease developed in liver segment VI and the L1 vertebral body. Systemic ifosfamide/doxorubicin (6 cycles) produced no response in the liver lesion. He subsequently underwent hepatic resection of segments V and VI with cholecystectomy. New pulmonary lesions later emerged; therapy included pazopanib and stereotactic body radiation therapy, followed by gemcitabine/docetaxel (3 cycles), dacarbazine (2 cycles), and pembrolizumab (2 cycles), with continued progression. He was transitioned to palliative care and was lost to follow-up. Overall, this case represents a primary penoscrotal synovial sarcoma with SS18 rearrangement and an aggressive, treatment-refractory course despite two surgical resections and multiple systemic regimens." }, { "index": 62, "label": "low_health_literacy", "original_text": "A 13-year-old adolescent male, with no significant previous medical history, presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain associated with mild non-productive cough and no dyspnea. Associated with this, he had mild rhinorrhea and a single febrile episode that day (temperature of 38\u00baC). Chest pain was localized to the costal margin region and worsened with cough, without diurnal variation. The patient-reported relief with paracetamol. There were no complaints of joint pain, weight loss, anorexia, fatigue, episodes of syncope or exercise restriction. In fact, he practiced sports regularly\u2014canoeing 2 times a week. No evidence of an infectious exposure or contact with household or environmental fumes, dust, or mineral oils was described. There was no known family history of cardiopulmonary conditions. He had a chest radiograph taken 4 years earlier during an acute illness, which showed a marked interstitial infiltrate that was presumptively treated with azithromycin with no further clinical symptoms and no further follow-up.\n\nOn admission, the patient\u2019s temperature was 37.8\u00b0C with normal peripheral oxygen saturation (99%) in room air. His heart (93 beats per minute) and respiratory rate (15 breaths per minute) were normal and blood pressure was on the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two thirds of the chest with no adventitious sounds. No respiratory distress, finger clubbing, cyanosis, abnormal heart sounds, or other findings were present. Chest radiograph revealed a marked interstitial infiltrate, comparable with his previous examination. A thoracic computed tomography (CT) revealed multiple bilateral areas of ground-glass opacities involving > 65% of lung parenchyma, suggestive of PAP. Respiratory viral testing was negative, and he remained stable throughout his monitoring in the emergency department. He was discharged with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) to cover a potential respiratory infection, with clinical resolution of symptoms and was sent for follow-up at the pediatric respiratory clinic.\n\nUpon further investigation in the outpatient setting, positive antinuclear antibodies (ANAs) at a titer of 1/89 with a fine speckled pattern were detected, while other autoantibodies tested negative and immunoglobulin levels remained within normal limits. Bronchoalveolar lavage revealed fluid with a milky appearance and positive periodic acid-Schiff staining; microbiological examination, including for mycobacteria, returned negative results. Spirometry indicated a mild restrictive pattern with reduced forced vital capacity (FVC) at 2.92 L (77%) and forced expiratory volume in 1 second (FEV1) at 3.21 L (69.9%), alongside a normal FEV1/FVC ratio (109%). In addition, the DLCO single breath (SB) showed a moderate decrease at 13.8 ml/min/mmHg (48.6%). Suspecting PAP, a genetic panel was conducted, which showed no mutations associated with surfactant dysfunction. Subsequently, GM-CSF antibody testing was performed with a positive result, raising suspicion for AI-PAP. At 20 months of follow-up, the patient remains asymptomatic and continues to exercise regularly. He repeated spirometry testing with normal FVC at 4.03 L (81.3%); FEV1 at 3.71 L (87.5%); FEV1/FVC ratio at 91.96% and DLCO SB at 25.54 ml/min/mmHg (83.7%). As the patient remains stable with no respiratory symptoms, we decided to defer treatment and continue monitoring with regular clinic visits.", "generated_summary": "This report is about a 13-year-old boy. He came to the ER with sharp chest pain that hurt more when he took a deep breath. He did not feel sick otherwise. His oxygen level was normal at 98% on room air. The lower parts of his chest sounded quieter when the doctor listened. A chest X-ray looked like one he had 4 years earlier. A CT scan showed many hazy and crisscross areas in both lungs, covering more than half of the lungs. This pointed to a rare lung problem called PAP, where material builds up in the air sacs. Tests for viruses, including COVID-19, were negative. A gentle lung wash showed milky fluid, and a special lab stain was positive. Breathing tests showed his lungs held a little less air than expected and moved oxygen less well. A gene test did not find a known cause. A blood test found strong antibodies that mean the body\u2019s own immune system is likely causing this problem. About 20 months later, he feels well, and his breathing tests are normal." }, { "index": 62, "label": "intermediate_health_literacy", "original_text": "A 13-year-old adolescent male, with no significant previous medical history, presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain associated with mild non-productive cough and no dyspnea. Associated with this, he had mild rhinorrhea and a single febrile episode that day (temperature of 38\u00baC). Chest pain was localized to the costal margin region and worsened with cough, without diurnal variation. The patient-reported relief with paracetamol. There were no complaints of joint pain, weight loss, anorexia, fatigue, episodes of syncope or exercise restriction. In fact, he practiced sports regularly\u2014canoeing 2 times a week. No evidence of an infectious exposure or contact with household or environmental fumes, dust, or mineral oils was described. There was no known family history of cardiopulmonary conditions. He had a chest radiograph taken 4 years earlier during an acute illness, which showed a marked interstitial infiltrate that was presumptively treated with azithromycin with no further clinical symptoms and no further follow-up.\n\nOn admission, the patient\u2019s temperature was 37.8\u00b0C with normal peripheral oxygen saturation (99%) in room air. His heart (93 beats per minute) and respiratory rate (15 breaths per minute) were normal and blood pressure was on the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two thirds of the chest with no adventitious sounds. No respiratory distress, finger clubbing, cyanosis, abnormal heart sounds, or other findings were present. Chest radiograph revealed a marked interstitial infiltrate, comparable with his previous examination. A thoracic computed tomography (CT) revealed multiple bilateral areas of ground-glass opacities involving > 65% of lung parenchyma, suggestive of PAP. Respiratory viral testing was negative, and he remained stable throughout his monitoring in the emergency department. He was discharged with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) to cover a potential respiratory infection, with clinical resolution of symptoms and was sent for follow-up at the pediatric respiratory clinic.\n\nUpon further investigation in the outpatient setting, positive antinuclear antibodies (ANAs) at a titer of 1/89 with a fine speckled pattern were detected, while other autoantibodies tested negative and immunoglobulin levels remained within normal limits. Bronchoalveolar lavage revealed fluid with a milky appearance and positive periodic acid-Schiff staining; microbiological examination, including for mycobacteria, returned negative results. Spirometry indicated a mild restrictive pattern with reduced forced vital capacity (FVC) at 2.92 L (77%) and forced expiratory volume in 1 second (FEV1) at 3.21 L (69.9%), alongside a normal FEV1/FVC ratio (109%). In addition, the DLCO single breath (SB) showed a moderate decrease at 13.8 ml/min/mmHg (48.6%). Suspecting PAP, a genetic panel was conducted, which showed no mutations associated with surfactant dysfunction. Subsequently, GM-CSF antibody testing was performed with a positive result, raising suspicion for AI-PAP. At 20 months of follow-up, the patient remains asymptomatic and continues to exercise regularly. He repeated spirometry testing with normal FVC at 4.03 L (81.3%); FEV1 at 3.71 L (87.5%); FEV1/FVC ratio at 91.96% and DLCO SB at 25.54 ml/min/mmHg (83.7%). As the patient remains stable with no respiratory symptoms, we decided to defer treatment and continue monitoring with regular clinic visits.", "generated_summary": "A 13-year-old boy presented with acute pleuritic chest pain but no other systemic symptoms. On exam, he had diminished breath sounds over the lower two thirds of the chest, and his oxygen saturation was normal (98% on room air). Chest X-ray showed a marked interstitial infiltrate similar to an image taken 4 years earlier during an illness treated presumptively with azithromycin. Chest CT demonstrated multiple bilateral ground-glass opacities with areas of \u201ccrazy paving,\u201d involving more than 65% of the lung, which raised concern for pulmonary alveolar proteinosis (PAP). Respiratory viral testing, including SARS-CoV-2, was negative. Bronchoalveolar lavage yielded milky fluid with positive periodic acid\u2013Schiff staining. Pulmonary function testing showed a mild restrictive pattern (FVC 77%) and a moderately reduced diffusing capacity (DLCO 48.6%). A genetic panel found no mutations linked to surfactant dysfunction. Anti\u2013GM-CSF antibodies were strongly positive, supporting autoimmune PAP. At 20 months, he remains asymptomatic, and spirometry has normalized." }, { "index": 62, "label": "proficient_health_literacy", "original_text": "A 13-year-old adolescent male, with no significant previous medical history, presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain associated with mild non-productive cough and no dyspnea. Associated with this, he had mild rhinorrhea and a single febrile episode that day (temperature of 38\u00baC). Chest pain was localized to the costal margin region and worsened with cough, without diurnal variation. The patient-reported relief with paracetamol. There were no complaints of joint pain, weight loss, anorexia, fatigue, episodes of syncope or exercise restriction. In fact, he practiced sports regularly\u2014canoeing 2 times a week. No evidence of an infectious exposure or contact with household or environmental fumes, dust, or mineral oils was described. There was no known family history of cardiopulmonary conditions. He had a chest radiograph taken 4 years earlier during an acute illness, which showed a marked interstitial infiltrate that was presumptively treated with azithromycin with no further clinical symptoms and no further follow-up.\n\nOn admission, the patient\u2019s temperature was 37.8\u00b0C with normal peripheral oxygen saturation (99%) in room air. His heart (93 beats per minute) and respiratory rate (15 breaths per minute) were normal and blood pressure was on the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two thirds of the chest with no adventitious sounds. No respiratory distress, finger clubbing, cyanosis, abnormal heart sounds, or other findings were present. Chest radiograph revealed a marked interstitial infiltrate, comparable with his previous examination. A thoracic computed tomography (CT) revealed multiple bilateral areas of ground-glass opacities involving > 65% of lung parenchyma, suggestive of PAP. Respiratory viral testing was negative, and he remained stable throughout his monitoring in the emergency department. He was discharged with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) to cover a potential respiratory infection, with clinical resolution of symptoms and was sent for follow-up at the pediatric respiratory clinic.\n\nUpon further investigation in the outpatient setting, positive antinuclear antibodies (ANAs) at a titer of 1/89 with a fine speckled pattern were detected, while other autoantibodies tested negative and immunoglobulin levels remained within normal limits. Bronchoalveolar lavage revealed fluid with a milky appearance and positive periodic acid-Schiff staining; microbiological examination, including for mycobacteria, returned negative results. Spirometry indicated a mild restrictive pattern with reduced forced vital capacity (FVC) at 2.92 L (77%) and forced expiratory volume in 1 second (FEV1) at 3.21 L (69.9%), alongside a normal FEV1/FVC ratio (109%). In addition, the DLCO single breath (SB) showed a moderate decrease at 13.8 ml/min/mmHg (48.6%). Suspecting PAP, a genetic panel was conducted, which showed no mutations associated with surfactant dysfunction. Subsequently, GM-CSF antibody testing was performed with a positive result, raising suspicion for AI-PAP. At 20 months of follow-up, the patient remains asymptomatic and continues to exercise regularly. He repeated spirometry testing with normal FVC at 4.03 L (81.3%); FEV1 at 3.71 L (87.5%); FEV1/FVC ratio at 91.96% and DLCO SB at 25.54 ml/min/mmHg (83.7%). As the patient remains stable with no respiratory symptoms, we decided to defer treatment and continue monitoring with regular clinic visits.", "generated_summary": "A previously healthy 13-year-old male presented with 3 days of acute bilateral pleuritic chest pain, mild non-productive cough, no dyspnea, mild rhinorrhea, and a single febrile episode (38\u00b0C). Pain localized to the costal margins, was worse with cough, and improved with paracetamol. He denied constitutional symptoms, syncope, or exercise limitation and regularly canoed twice weekly. There were no reported infectious exposures, environmental/occupational inhalational exposures, or family history of cardiopulmonary disease. A prior chest radiograph 4 years earlier during an acute illness showed a marked interstitial infiltrate; he was presumptively treated with azithromycin and had no follow-up.\nOn admission, temperature was 37.8\u00b0C, SpO2 99% on room air, HR 93 bpm, RR 15/min, and BP 115/66 mmHg (85th percentile). Exam revealed diminished breath sounds in the lower two thirds of the chest without adventitious sounds; there was no respiratory distress, clubbing, cyanosis, or abnormal heart sounds. Chest radiograph again showed a marked interstitial infiltrate comparable to the prior film. Thoracic CT demonstrated multiple bilateral ground-glass opacities involving >65% of the lung parenchyma, suggestive of pulmonary alveolar proteinosis (PAP). Respiratory viral testing was negative, and he remained clinically stable in the ED. He was discharged on empiric amoxicillin\u2013clavulanate and azithromycin with symptom resolution and referred to a pediatric respiratory clinic.\nOutpatient workup showed positive ANA at 1/89 (fine speckled) with other autoantibodies negative and immunoglobulins within normal limits. Bronchoalveolar lavage returned milky fluid with positive periodic acid\u2013Schiff staining; microbiology including mycobacterial studies was negative. Spirometry demonstrated a mild restrictive ventilatory defect with reduced FVC 2.92 L (77% predicted) and FEV1 3.21 L (69.9% predicted) with a normal FEV1/FVC ratio (109%). DLCO (SB) was moderately reduced at 13.8 ml/min/mmHg (48.6% predicted). A surfactant dysfunction genetic panel identified no pathogenic variants. GM-CSF antibody testing was positive, supporting a diagnosis of autoimmune PAP (AI-PAP). At 20 months, he remains asymptomatic and physically active; repeat testing showed FVC 4.03 L (81.3%), FEV1 3.71 L (87.5%), FEV1/FVC 91.96%, and DLCO (SB) 25.54 ml/min/mmHg (83.7%). Given stable, improving physiology and absence of symptoms, treatment was deferred with ongoing surveillance.\nContext: AI-PAP is mediated by neutralizing anti\u2013GM-CSF antibodies that impair alveolar macrophage\u2013mediated surfactant clearance, producing intra-alveolar lipoproteinaceous material that is PAS-positive and radiographically manifests as diffuse bilateral ground-glass opacities (often with a \u201ccrazy paving\u201d pattern). Standard therapies include whole lung lavage and GM-CSF replacement; however, observation is appropriate in stable, minimally symptomatic patients, as in this case." }, { "index": 63, "label": "low_health_literacy", "original_text": "27-year-old woman with a history of uncontrolled asthma, mild SARS-CoV-2 infection. In March 2021, she consulted a doctor for pain in the left hemicara and trismus. She reported having completed 48 hours before the antibiotic treatment with phenoxymethyl penicillin 1,000,000 IU daily orally for five days for a peritonsillar abscess. She was hemodynamically stable at the physical examination, without the need for supplemental oxygen, and without relevant findings in respiratory symptoms. The head and neck examination showed a soft, painful, cervical adenopathy, palpable and painful, predominantly homolateral and trismus. Complementary studies were performed. The admission laboratory reported leukocytosis, platelopenia, increased acute phase reactants and the rest of the parameters within normal values. An angiotomy of the craniofacial mass was performed, where a large thrombus was found in the internal and external carotid arteries. Studies were completed with a chest tomography and arterial Doppler ultrasound of neck vessels with no relevant findings. Early intravenous antibiotic treatment was initiated with ceftriaxone 1 g every 12 hours, clindamycin 300 mg every 6 hours and anticoagulation with enoxaparin adjusted to body weight and renal function, 60 mg subcutaneously every 12 hours. The patient evolved 72 hours after initiating the directed treatment with a fever of 38.5 \u00b0C and increased leukocytosis, so new complementary studies were performed, including a Doppler ultrasound of the heart without finding cardiac vegetations and a chest tomography where bilateral pulmonary septic emboli were found. With the admission hemocultures negative, a new admission of 3 units, culture of pharyngeal exudate and rotation of ceftriaxone to piperacillin tazobactam 4.5 g every 6 hours intravenous was decided. The patient evolved favorably, without rescue of germs in cultures. After 14 days of initiating the new therapeutic scheme, and with a control chest tomography without pulmonary lesions, it was decided to continue antibiotic treatment with oral clindamycin 300 mg every 6 hours, anticoagulation with acenocumarol adjusted to body weight and hospital discharge.\n", "generated_summary": "A 27-year-old woman got face swelling and a tight jaw two days after finishing penicillin for a tooth infection. A blood clot is like a plug that blocks a pipe. A scan of her neck found a big clot in a neck vein. A scan of her chest showed the infection had sent clots to her lungs. Doctors gave strong antibiotics through a vein right away. They also gave blood thinners to treat the clot." }, { "index": 63, "label": "intermediate_health_literacy", "original_text": "27-year-old woman with a history of uncontrolled asthma, mild SARS-CoV-2 infection. In March 2021, she consulted a doctor for pain in the left hemicara and trismus. She reported having completed 48 hours before the antibiotic treatment with phenoxymethyl penicillin 1,000,000 IU daily orally for five days for a peritonsillar abscess. She was hemodynamically stable at the physical examination, without the need for supplemental oxygen, and without relevant findings in respiratory symptoms. The head and neck examination showed a soft, painful, cervical adenopathy, palpable and painful, predominantly homolateral and trismus. Complementary studies were performed. The admission laboratory reported leukocytosis, platelopenia, increased acute phase reactants and the rest of the parameters within normal values. An angiotomy of the craniofacial mass was performed, where a large thrombus was found in the internal and external carotid arteries. Studies were completed with a chest tomography and arterial Doppler ultrasound of neck vessels with no relevant findings. Early intravenous antibiotic treatment was initiated with ceftriaxone 1 g every 12 hours, clindamycin 300 mg every 6 hours and anticoagulation with enoxaparin adjusted to body weight and renal function, 60 mg subcutaneously every 12 hours. The patient evolved 72 hours after initiating the directed treatment with a fever of 38.5 \u00b0C and increased leukocytosis, so new complementary studies were performed, including a Doppler ultrasound of the heart without finding cardiac vegetations and a chest tomography where bilateral pulmonary septic emboli were found. With the admission hemocultures negative, a new admission of 3 units, culture of pharyngeal exudate and rotation of ceftriaxone to piperacillin tazobactam 4.5 g every 6 hours intravenous was decided. The patient evolved favorably, without rescue of germs in cultures. After 14 days of initiating the new therapeutic scheme, and with a control chest tomography without pulmonary lesions, it was decided to continue antibiotic treatment with oral clindamycin 300 mg every 6 hours, anticoagulation with acenocumarol adjusted to body weight and hospital discharge.\n", "generated_summary": "A 27-year-old woman developed facial swelling and trismus 48 hours after finishing phenoxymethylpenicillin for a dental infection. A head and neck CT showed a large blood clot in the internal jugular vein. A chest CT showed septic emboli in the lungs. She was treated promptly with intravenous broad-spectrum antibiotics and anticoagulation. She improved with care and continued treatment after discharge." }, { "index": 63, "label": "proficient_health_literacy", "original_text": "27-year-old woman with a history of uncontrolled asthma, mild SARS-CoV-2 infection. In March 2021, she consulted a doctor for pain in the left hemicara and trismus. She reported having completed 48 hours before the antibiotic treatment with phenoxymethyl penicillin 1,000,000 IU daily orally for five days for a peritonsillar abscess. She was hemodynamically stable at the physical examination, without the need for supplemental oxygen, and without relevant findings in respiratory symptoms. The head and neck examination showed a soft, painful, cervical adenopathy, palpable and painful, predominantly homolateral and trismus. Complementary studies were performed. The admission laboratory reported leukocytosis, platelopenia, increased acute phase reactants and the rest of the parameters within normal values. An angiotomy of the craniofacial mass was performed, where a large thrombus was found in the internal and external carotid arteries. Studies were completed with a chest tomography and arterial Doppler ultrasound of neck vessels with no relevant findings. Early intravenous antibiotic treatment was initiated with ceftriaxone 1 g every 12 hours, clindamycin 300 mg every 6 hours and anticoagulation with enoxaparin adjusted to body weight and renal function, 60 mg subcutaneously every 12 hours. The patient evolved 72 hours after initiating the directed treatment with a fever of 38.5 \u00b0C and increased leukocytosis, so new complementary studies were performed, including a Doppler ultrasound of the heart without finding cardiac vegetations and a chest tomography where bilateral pulmonary septic emboli were found. With the admission hemocultures negative, a new admission of 3 units, culture of pharyngeal exudate and rotation of ceftriaxone to piperacillin tazobactam 4.5 g every 6 hours intravenous was decided. The patient evolved favorably, without rescue of germs in cultures. After 14 days of initiating the new therapeutic scheme, and with a control chest tomography without pulmonary lesions, it was decided to continue antibiotic treatment with oral clindamycin 300 mg every 6 hours, anticoagulation with acenocumarol adjusted to body weight and hospital discharge.\n", "generated_summary": "A 27-year-old woman with uncontrolled asthma and recent mild SARS-CoV-2 infection presented in March 2021 with left hemifacial pain and trismus 48 hours after completing phenoxymethylpenicillin 1,000,000 IU orally once daily for five days for a peritonsillar/oropharyngeal infection. She was hemodynamically stable, without oxygen requirement. Examination showed tender ipsilateral cervical lymphadenopathy and trismus. Admission labs demonstrated leukocytosis, thrombocytopenia, and elevated acute phase reactants; other parameters were within normal limits. Head and neck CT angiography identified a large thrombus within the internal jugular vein. Initial Doppler assessment of neck vessels did not add further actionable findings. Chest CT demonstrated bilateral septic pulmonary emboli. Management included immediate intravenous broad-spectrum antibiotics (ceftriaxone 1 g every 12 hours plus clindamycin 300 mg every 6 hours initially) and therapeutic anticoagulation with enoxaparin 60 mg subcutaneously every 12 hours, dose-adjusted to body weight and renal function. At 72 hours, she developed fever to 38.5 \u00b0C with rising leukocytosis; transthoracic echocardiography showed no valvular vegetations. Blood cultures remained negative and a pharyngeal exudate culture was obtained. Antibiotics were escalated to piperacillin\u2013tazobactam 4.5 g IV every 6 hours, with subsequent clinical improvement and no organisms isolated. After 14 days of the revised regimen, follow-up chest CT showed resolution of pulmonary lesions. She was transitioned to oral clindamycin 300 mg every 6 hours and oral anticoagulation with acenocoumarol (dose-adjusted to body weight) and discharged. The presentation and imaging were consistent with internal jugular vein thrombosis complicated by septic pulmonary emboli." }, { "index": 64, "label": "low_health_literacy", "original_text": "A 5-year-old presented to the paediatric emergency department (ED) having ingested chlorpyriphos 13 hours prior to presentation, followed by abnormal jerks, fast breathing and difficulty with breathing. The history was also comprised of excessive sweating and urination, mouth secretions and involuntary movement of the limbs. Vomiting followed the ingestion of crushed charcoal and palm oil. The patient had lapsed into coma prior to presentation. The temperature at presentation was 38.3\u00b0C, Glasgow coma score was 3, pupils were pinpoint pupils and there was hypotonia in all limbs. In addition, the patient was severely dyspneic, tachypneic (respiratory rate of 48/minute with intermittent sighing breaths), a saturation of 88% and widespread crackles. The pulse rate was 180/minute, blood pressure 120/80 mmHg, and random blood glucose 14 mg/dl. Serum lactate and cholinesterase tests were not done due to lack of facilities.\n\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. As ICU care was beyond the affordability of the parents, non-invasive ventilation (NIV) was administered using bubble continuous positive airway pressure (b-CPAP) causing his saturation to increase to 99%\u2013100%. Hypoglycemia was corrected with a bolus of dextrose solution and tachycardia was treated with 20 ml/kg of normal saline. Intravenous Dexamethasone, Mannitol and IV Atropine at 0.02 mg/kg/dose were also administered. Empirical intravenous antibiotics were administered for aspiration pneumonitis. Pralidoxime was not given due to unavailability. Within 3 hours of presentation, the patient had fresh-whole-blood exchange-blood-transfusion (FWB-EBT) with 500mls of blood.\n\nThe patient\u2019s GCS appreciated to 9/15 but IV Atropine was discontinued after the first dose due to a rapid increase in the heart rate. The blood glucose fluctuated between 41 to 259 mg/dl in the first 15 hours of admission and subsequently normalized with treatment. By the second day on admission, the patient developed thready pulses and hypotension for which another bolus of normal saline was administered. Dopamine infusion was commenced at 5mcg/kg/min using a peripheral vein and IV Mannitol discontinued. A second aliquot of FWB-EBT was administered with 500mls of blood.\n\nOver the first 30 hours of admission, the consciousness level improved and respiratory distress slowly declined. However, the patient developed rhonchi which was treated with nebulized Salbutamol and Budesonide and was subsequently transited to Oxygen therapy with nasal prongs with clinical improvement. The saturation remained stable at 97%. On Day 2 of admission, a chest radiograph was done which showed bilateral infiltrates in keeping with pneumonia.\n\nThe patient regained full consciousness by the 39th hour of admission. Intravenous Vitamin C and B, as well as oral Vitamin E and Zinc were commenced for their antioxidant effects, and regular diet was recommenced in a graded manner over the subsequent 48 hours. The patient\u2019s clinical condition progressively improved and was discharged home after 10 days but was subsequently lost to follow-up.", "generated_summary": "A 5-year-old drank a farm bug killer called chlorpyrifos. Some charcoal and palm oil were later breathed into the lungs. The child got very sick. Breathing failed. The body went into shock. The child was in a coma. There was an early kind of paralysis (type 1). In the emergency room, a mask machine helped with breathing. Doctors swapped out some blood and put in new blood more than once. They gave atropine through a vein. They used a drip to help the heart and blood pressure. They also gave antibiotics and steroids. The child got better quickly. The child did not get the delayed muscle weakness that can happen later. The child went home after 10 days in the hospital." }, { "index": 64, "label": "intermediate_health_literacy", "original_text": "A 5-year-old presented to the paediatric emergency department (ED) having ingested chlorpyriphos 13 hours prior to presentation, followed by abnormal jerks, fast breathing and difficulty with breathing. The history was also comprised of excessive sweating and urination, mouth secretions and involuntary movement of the limbs. Vomiting followed the ingestion of crushed charcoal and palm oil. The patient had lapsed into coma prior to presentation. The temperature at presentation was 38.3\u00b0C, Glasgow coma score was 3, pupils were pinpoint pupils and there was hypotonia in all limbs. In addition, the patient was severely dyspneic, tachypneic (respiratory rate of 48/minute with intermittent sighing breaths), a saturation of 88% and widespread crackles. The pulse rate was 180/minute, blood pressure 120/80 mmHg, and random blood glucose 14 mg/dl. Serum lactate and cholinesterase tests were not done due to lack of facilities.\n\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. As ICU care was beyond the affordability of the parents, non-invasive ventilation (NIV) was administered using bubble continuous positive airway pressure (b-CPAP) causing his saturation to increase to 99%\u2013100%. Hypoglycemia was corrected with a bolus of dextrose solution and tachycardia was treated with 20 ml/kg of normal saline. Intravenous Dexamethasone, Mannitol and IV Atropine at 0.02 mg/kg/dose were also administered. Empirical intravenous antibiotics were administered for aspiration pneumonitis. Pralidoxime was not given due to unavailability. Within 3 hours of presentation, the patient had fresh-whole-blood exchange-blood-transfusion (FWB-EBT) with 500mls of blood.\n\nThe patient\u2019s GCS appreciated to 9/15 but IV Atropine was discontinued after the first dose due to a rapid increase in the heart rate. The blood glucose fluctuated between 41 to 259 mg/dl in the first 15 hours of admission and subsequently normalized with treatment. By the second day on admission, the patient developed thready pulses and hypotension for which another bolus of normal saline was administered. Dopamine infusion was commenced at 5mcg/kg/min using a peripheral vein and IV Mannitol discontinued. A second aliquot of FWB-EBT was administered with 500mls of blood.\n\nOver the first 30 hours of admission, the consciousness level improved and respiratory distress slowly declined. However, the patient developed rhonchi which was treated with nebulized Salbutamol and Budesonide and was subsequently transited to Oxygen therapy with nasal prongs with clinical improvement. The saturation remained stable at 97%. On Day 2 of admission, a chest radiograph was done which showed bilateral infiltrates in keeping with pneumonia.\n\nThe patient regained full consciousness by the 39th hour of admission. Intravenous Vitamin C and B, as well as oral Vitamin E and Zinc were commenced for their antioxidant effects, and regular diet was recommenced in a graded manner over the subsequent 48 hours. The patient\u2019s clinical condition progressively improved and was discharged home after 10 days but was subsequently lost to follow-up.", "generated_summary": "A 5-year-old developed severe organophosphate poisoning after ingesting chlorpyrifos and then aspirated a charcoal\u2013palm oil mixture. The illness progressed to respiratory failure, shock, coma, and acute (type I) paralysis. In the emergency department, the child received noninvasive ventilation, repeated exchange transfusions, intravenous atropine, and an inotrope infusion to support blood pressure, along with antibiotics and steroids. The child improved rapidly, did not develop intermediate syndrome (the delayed muscle weakness sometimes seen after organophosphate poisoning), and was discharged after a 10-day hospitalization. Additional context: the child arrived about 13 hours after ingestion with heavy secretions, pinpoint pupils, fast breathing, low oxygen, and crackles on chest exam. Pralidoxime was unavailable. Blood sugar was low at first and then fluctuated before stabilizing. A chest X-ray on day 2 showed pneumonia. Consciousness returned by about 39 hours, oxygen was weaned to nasal prongs, and recovery continued to discharge." }, { "index": 64, "label": "proficient_health_literacy", "original_text": "A 5-year-old presented to the paediatric emergency department (ED) having ingested chlorpyriphos 13 hours prior to presentation, followed by abnormal jerks, fast breathing and difficulty with breathing. The history was also comprised of excessive sweating and urination, mouth secretions and involuntary movement of the limbs. Vomiting followed the ingestion of crushed charcoal and palm oil. The patient had lapsed into coma prior to presentation. The temperature at presentation was 38.3\u00b0C, Glasgow coma score was 3, pupils were pinpoint pupils and there was hypotonia in all limbs. In addition, the patient was severely dyspneic, tachypneic (respiratory rate of 48/minute with intermittent sighing breaths), a saturation of 88% and widespread crackles. The pulse rate was 180/minute, blood pressure 120/80 mmHg, and random blood glucose 14 mg/dl. Serum lactate and cholinesterase tests were not done due to lack of facilities.\n\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. As ICU care was beyond the affordability of the parents, non-invasive ventilation (NIV) was administered using bubble continuous positive airway pressure (b-CPAP) causing his saturation to increase to 99%\u2013100%. Hypoglycemia was corrected with a bolus of dextrose solution and tachycardia was treated with 20 ml/kg of normal saline. Intravenous Dexamethasone, Mannitol and IV Atropine at 0.02 mg/kg/dose were also administered. Empirical intravenous antibiotics were administered for aspiration pneumonitis. Pralidoxime was not given due to unavailability. Within 3 hours of presentation, the patient had fresh-whole-blood exchange-blood-transfusion (FWB-EBT) with 500mls of blood.\n\nThe patient\u2019s GCS appreciated to 9/15 but IV Atropine was discontinued after the first dose due to a rapid increase in the heart rate. The blood glucose fluctuated between 41 to 259 mg/dl in the first 15 hours of admission and subsequently normalized with treatment. By the second day on admission, the patient developed thready pulses and hypotension for which another bolus of normal saline was administered. Dopamine infusion was commenced at 5mcg/kg/min using a peripheral vein and IV Mannitol discontinued. A second aliquot of FWB-EBT was administered with 500mls of blood.\n\nOver the first 30 hours of admission, the consciousness level improved and respiratory distress slowly declined. However, the patient developed rhonchi which was treated with nebulized Salbutamol and Budesonide and was subsequently transited to Oxygen therapy with nasal prongs with clinical improvement. The saturation remained stable at 97%. On Day 2 of admission, a chest radiograph was done which showed bilateral infiltrates in keeping with pneumonia.\n\nThe patient regained full consciousness by the 39th hour of admission. Intravenous Vitamin C and B, as well as oral Vitamin E and Zinc were commenced for their antioxidant effects, and regular diet was recommenced in a graded manner over the subsequent 48 hours. The patient\u2019s clinical condition progressively improved and was discharged home after 10 days but was subsequently lost to follow-up.", "generated_summary": "A 5-year-old presented to the pediatric ED 13 hours after ingesting chlorpyrifos with abnormal jerks, severe dyspnea, tachypnea (RR 48/min with intermittent sighs), diaphoresis, salivation, polyuria, vomiting, and subsequent aspiration of a charcoal\u2013palm oil mixture. On arrival: T 38.3\u00b0C, GCS 3/15, pinpoint pupils, generalized hypotonia, SpO2 88% with widespread crackles, HR 180/min, BP 120/80 mmHg, random blood glucose 14 mg/dl. Serum lactate and cholinesterase levels were unavailable. The working diagnoses were severe organophosphate poisoning (cholinergic crisis with type I paralysis), aspiration pneumonitis, respiratory failure, and impending shock. Because ICU care was unaffordable, NIV via bubble CPAP was initiated, improving SpO2 to 99\u2013100%. Hypoglycemia was corrected with a dextrose bolus; 20 ml/kg normal saline was given for tachycardia. The patient received IV dexamethasone, mannitol, and atropine 0.02 mg/kg (discontinued after the first dose due to rapid tachycardia), plus empiric IV antibiotics for aspiration pneumonitis; pralidoxime was unavailable. Within 3 hours, a 500 mL fresh whole blood exchange transfusion (FWB-EBT) was performed, after which GCS improved to 9/15. Blood glucose fluctuated between 41\u2013259 mg/dl during the first 15 hours and subsequently normalized. By hospital day 2, the patient developed thready pulses and hypotension; an additional NS bolus was administered and dopamine was started at 5 mcg/kg/min via a peripheral vein. Mannitol was discontinued. A second 500 mL FWB-EBT was performed. Over the first 30 hours, consciousness and respiratory distress improved, though rhonchi developed and were treated with nebulized salbutamol and budesonide; the patient was transitioned to oxygen via nasal prongs with SpO2 ~97%. A day-2 chest radiograph showed bilateral infiltrates consistent with pneumonia. Full consciousness returned by hour 39. Antioxidants (IV vitamins C and B; oral vitamin E and zinc) were started, and diet was advanced over 48 hours. The patient responded rapidly overall, did not develop intermediate syndrome, and was discharged on hospital day 10; follow-up was lost. Exchange transfusion was utilized as a detoxification strategy in the absence of oximes and may have contributed to clinical stabilization by reducing circulating toxin and replenishing cholinesterase activity, alongside atropinization, ventilatory support, fluids, and inotropic therapy." }, { "index": 65, "label": "low_health_literacy", "original_text": "A 19-year-old woman presented to the emergency department of our institution for acute onset of palpitations. An electrocardiogram (ECG) showed ventricular tachycardia, with right branch bundle block associated to left posterior hemiblock, and T waves inversion in the inferior and precordial leads. Blood test showed elevated troponin (27\u2009ng/L, normal values <14\u2009ng/L) and NT-pro BNP (aminoterminal pro B-Type Natriuretic Peptide) levels (2225\u2009pg/mL, normal values <130\u2009pg/mL). Hence, she was admitted to the coronary care unit.\n\nAbout 5 years before, she had already presented to the emergency department with cardiogenic shock due to fascicular ventricular tachycardia; she was subsequently hospitalized and underwent cardiac magnetic resonance (CMR) and a transoesophageal electrophysiological study, both with inconclusive results. She was discharged with a diagnosis of tachycardiomiopathy, with the prescription of a standard medical therapy (angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonist, and beta blockers), and a follow-up was planned. Her subsequent clinical history was uneventful.\n\nDuring the present hospitalization, no further episodes of hyperkinetic arrhythmias were detected. Basal 12-lead ECG. Echocardiography showed diffuse hypokinesia of both the left and the right ventricles, and CMR was once again inconclusive. Then, the patient was advised to undergo cardiac computed tomography angiography (CCTA) to evaluate the anatomy of the coronary tree, under the suspicion of an undiagnosed congenital cardiac anomaly. CCTA was performed with a GE Lightspeed unit (GE HealthCare, Chicago, United States), with retrospective gating, at 100 kVp and 696 mAs, with a gantry rotation time of 0.35\u2009s, and 0.625\u2009mm slice thickness, with intravenous injection of 70\u2009mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).\n\nDifferential diagnosis\nCardiogenic shock, namely a shock caused by inadequate blood flow, may be caused by different pathologies such as myocardial infarction, arrhythmias, or other cardiomyopathies. Undiagnosed congenital heart disease is a non-negligible cause of cardiogenic shock in otherwise healthy adult patients. Once myocardial infarction is ruled out by a 12-lead ECG, and an underlying cardiomyopathy has been excluded by an inconclusive CMR examination, CCTA is the technique of choice for the differential diagnosis among diverse causes of cardiogenic shock.\n\nInvestigations/imaging findings\nThe CCTA examination showed regular origin of the left main coronary artery, the left anterior descending artery, which presented a wide ramus intermedium, 2 diagonal branches, and the left circumflex artery, which appeared thin and non-dominant. Among all these vessels, there was no evidence of obstructive coronary artery disease. However, the ostium and the proximal portion of the right coronary artery (RCA) were absent, whereas its mid and distal portions were supplied by a wide collateral branch originating from the distal left anterior descending artery, which then surrounded the lateral wall of the right ventricle, ran through the distal part of the atrioventricular groove, finally giving rise to thin posterior interventricular and posterolateral arteries. Furthermore, a thin branch going from the mid left anterior descending artery to the sinoatrial node was observed.\n\nTreatment, outcome, and follow-up\nIn view of the CCTA findings, the patient underwent an echo-stress test, which confirmed the presence of inducible myocardial ischaemia in the inferior wall, in line with the positioning of the arrhythmic focus. After being transferred to a specialized centre for the diagnosis and treatment of congenital heart disease, the patient underwent transcatheter radiofrequency ablation of sustained ventricular tachycardia originating by the posteromedial papillary muscle. Then, she was discharged with medical therapy (Acetylsalicylic acid and Verapamil). At her 6-month follow-up, she has always been asymptomatic, with no further signs of arrhythmias.", "generated_summary": "A 19-year-old woman went to the emergency room. Her heart was beating fast and uneven. Her body showed signs that her heart was not pumping enough blood. A heart tracing test showed she was not having a heart attack. A heart MRI did not show a disease of the heart muscle. A special heart CT scan then looked at her heart arteries. It showed the normal opening to her right heart artery was missing from birth. She was sent to a center that treats heart problems people are born with. Doctors did an electrical test inside her heart. They found a small hot spot on a tiny muscle that helps a heart valve. That spot was starting the bad rhythm, like a faulty spark. The team gently burned that spot to stop it. She has had no symptoms since." }, { "index": 65, "label": "intermediate_health_literacy", "original_text": "A 19-year-old woman presented to the emergency department of our institution for acute onset of palpitations. An electrocardiogram (ECG) showed ventricular tachycardia, with right branch bundle block associated to left posterior hemiblock, and T waves inversion in the inferior and precordial leads. Blood test showed elevated troponin (27\u2009ng/L, normal values <14\u2009ng/L) and NT-pro BNP (aminoterminal pro B-Type Natriuretic Peptide) levels (2225\u2009pg/mL, normal values <130\u2009pg/mL). Hence, she was admitted to the coronary care unit.\n\nAbout 5 years before, she had already presented to the emergency department with cardiogenic shock due to fascicular ventricular tachycardia; she was subsequently hospitalized and underwent cardiac magnetic resonance (CMR) and a transoesophageal electrophysiological study, both with inconclusive results. She was discharged with a diagnosis of tachycardiomiopathy, with the prescription of a standard medical therapy (angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonist, and beta blockers), and a follow-up was planned. Her subsequent clinical history was uneventful.\n\nDuring the present hospitalization, no further episodes of hyperkinetic arrhythmias were detected. Basal 12-lead ECG. Echocardiography showed diffuse hypokinesia of both the left and the right ventricles, and CMR was once again inconclusive. Then, the patient was advised to undergo cardiac computed tomography angiography (CCTA) to evaluate the anatomy of the coronary tree, under the suspicion of an undiagnosed congenital cardiac anomaly. CCTA was performed with a GE Lightspeed unit (GE HealthCare, Chicago, United States), with retrospective gating, at 100 kVp and 696 mAs, with a gantry rotation time of 0.35\u2009s, and 0.625\u2009mm slice thickness, with intravenous injection of 70\u2009mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).\n\nDifferential diagnosis\nCardiogenic shock, namely a shock caused by inadequate blood flow, may be caused by different pathologies such as myocardial infarction, arrhythmias, or other cardiomyopathies. Undiagnosed congenital heart disease is a non-negligible cause of cardiogenic shock in otherwise healthy adult patients. Once myocardial infarction is ruled out by a 12-lead ECG, and an underlying cardiomyopathy has been excluded by an inconclusive CMR examination, CCTA is the technique of choice for the differential diagnosis among diverse causes of cardiogenic shock.\n\nInvestigations/imaging findings\nThe CCTA examination showed regular origin of the left main coronary artery, the left anterior descending artery, which presented a wide ramus intermedium, 2 diagonal branches, and the left circumflex artery, which appeared thin and non-dominant. Among all these vessels, there was no evidence of obstructive coronary artery disease. However, the ostium and the proximal portion of the right coronary artery (RCA) were absent, whereas its mid and distal portions were supplied by a wide collateral branch originating from the distal left anterior descending artery, which then surrounded the lateral wall of the right ventricle, ran through the distal part of the atrioventricular groove, finally giving rise to thin posterior interventricular and posterolateral arteries. Furthermore, a thin branch going from the mid left anterior descending artery to the sinoatrial node was observed.\n\nTreatment, outcome, and follow-up\nIn view of the CCTA findings, the patient underwent an echo-stress test, which confirmed the presence of inducible myocardial ischaemia in the inferior wall, in line with the positioning of the arrhythmic focus. After being transferred to a specialized centre for the diagnosis and treatment of congenital heart disease, the patient underwent transcatheter radiofrequency ablation of sustained ventricular tachycardia originating by the posteromedial papillary muscle. Then, she was discharged with medical therapy (Acetylsalicylic acid and Verapamil). At her 6-month follow-up, she has always been asymptomatic, with no further signs of arrhythmias.", "generated_summary": "A 19-year-old woman came to the emergency department with a dangerous arrhythmia and signs that her heart was failing to pump well (cardiogenic shock). An ECG ruled out an acute heart attack, and cardiac MRI did not show cardiomyopathy. Because a hidden congenital issue was suspected, she underwent cardiac CT angiography. The scan showed ostial atresia of the right coronary artery\u2014the opening of the right coronary artery was absent. She was referred to a specialized congenital heart disease center. An electrophysiology study pinpointed the arrhythmia to the posteromedial papillary muscle, and the focus was treated with catheter ablation. She has remained symptom-free since." }, { "index": 65, "label": "proficient_health_literacy", "original_text": "A 19-year-old woman presented to the emergency department of our institution for acute onset of palpitations. An electrocardiogram (ECG) showed ventricular tachycardia, with right branch bundle block associated to left posterior hemiblock, and T waves inversion in the inferior and precordial leads. Blood test showed elevated troponin (27\u2009ng/L, normal values <14\u2009ng/L) and NT-pro BNP (aminoterminal pro B-Type Natriuretic Peptide) levels (2225\u2009pg/mL, normal values <130\u2009pg/mL). Hence, she was admitted to the coronary care unit.\n\nAbout 5 years before, she had already presented to the emergency department with cardiogenic shock due to fascicular ventricular tachycardia; she was subsequently hospitalized and underwent cardiac magnetic resonance (CMR) and a transoesophageal electrophysiological study, both with inconclusive results. She was discharged with a diagnosis of tachycardiomiopathy, with the prescription of a standard medical therapy (angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonist, and beta blockers), and a follow-up was planned. Her subsequent clinical history was uneventful.\n\nDuring the present hospitalization, no further episodes of hyperkinetic arrhythmias were detected. Basal 12-lead ECG. Echocardiography showed diffuse hypokinesia of both the left and the right ventricles, and CMR was once again inconclusive. Then, the patient was advised to undergo cardiac computed tomography angiography (CCTA) to evaluate the anatomy of the coronary tree, under the suspicion of an undiagnosed congenital cardiac anomaly. CCTA was performed with a GE Lightspeed unit (GE HealthCare, Chicago, United States), with retrospective gating, at 100 kVp and 696 mAs, with a gantry rotation time of 0.35\u2009s, and 0.625\u2009mm slice thickness, with intravenous injection of 70\u2009mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).\n\nDifferential diagnosis\nCardiogenic shock, namely a shock caused by inadequate blood flow, may be caused by different pathologies such as myocardial infarction, arrhythmias, or other cardiomyopathies. Undiagnosed congenital heart disease is a non-negligible cause of cardiogenic shock in otherwise healthy adult patients. Once myocardial infarction is ruled out by a 12-lead ECG, and an underlying cardiomyopathy has been excluded by an inconclusive CMR examination, CCTA is the technique of choice for the differential diagnosis among diverse causes of cardiogenic shock.\n\nInvestigations/imaging findings\nThe CCTA examination showed regular origin of the left main coronary artery, the left anterior descending artery, which presented a wide ramus intermedium, 2 diagonal branches, and the left circumflex artery, which appeared thin and non-dominant. Among all these vessels, there was no evidence of obstructive coronary artery disease. However, the ostium and the proximal portion of the right coronary artery (RCA) were absent, whereas its mid and distal portions were supplied by a wide collateral branch originating from the distal left anterior descending artery, which then surrounded the lateral wall of the right ventricle, ran through the distal part of the atrioventricular groove, finally giving rise to thin posterior interventricular and posterolateral arteries. Furthermore, a thin branch going from the mid left anterior descending artery to the sinoatrial node was observed.\n\nTreatment, outcome, and follow-up\nIn view of the CCTA findings, the patient underwent an echo-stress test, which confirmed the presence of inducible myocardial ischaemia in the inferior wall, in line with the positioning of the arrhythmic focus. After being transferred to a specialized centre for the diagnosis and treatment of congenital heart disease, the patient underwent transcatheter radiofrequency ablation of sustained ventricular tachycardia originating by the posteromedial papillary muscle. Then, she was discharged with medical therapy (Acetylsalicylic acid and Verapamil). At her 6-month follow-up, she has always been asymptomatic, with no further signs of arrhythmias.", "generated_summary": "A 19-year-old woman presented with acute palpitations. The initial ECG demonstrated ventricular tachycardia with right bundle branch block morphology associated with left posterior hemiblock, and T-wave inversion in the inferior and precordial leads. Biomarkers were elevated (troponin 27 ng/L, normal <14 ng/L; NT-proBNP 2225 pg/mL, normal <130 pg/mL). She was admitted to the coronary care unit. Five years earlier, she had presented with cardiogenic shock due to fascicular ventricular tachycardia; CMR and a transoesophageal electrophysiological study at that time were inconclusive. She was discharged with a diagnosis of tachycardiomyopathy on ACE inhibitors, a mineralocorticoid receptor antagonist, and beta blockers, with an uneventful interval thereafter.\n\nDuring the current hospitalization, there were no further hyperkinetic arrhythmias. Basal 12-lead ECG was obtained. Echocardiography showed diffuse hypokinesia of both ventricles. CMR was again inconclusive, and an undiagnosed congenital cardiac anomaly was suspected. Cardiac computed tomography angiography (CCTA) was performed (GE Lightspeed, retrospective gating, 100 kVp, 696 mAs, gantry rotation 0.35 s, 0.625 mm slice thickness; 70 mL Iomeron 400 mgI/mL IV). The left main and left anterior descending (with a wide ramus intermedius and two diagonal branches) and a thin, non-dominant left circumflex showed no obstructive coronary artery disease. The right coronary artery ostium and proximal segment were absent (ostial atresia); the mid and distal RCA were supplied by a large collateral from the distal LAD that coursed around the lateral right ventricular wall, traversed the distal atrioventricular groove, and gave rise to thin posterior interventricular and posterolateral branches. A thin branch from the mid LAD to the sinoatrial node was also observed.\n\nIn the differential for cardiogenic shock in otherwise healthy adults, once acute myocardial infarction is ruled out on 12-lead ECG and cardiomyopathy is not demonstrated on CMR, CCTA is the modality of choice to evaluate for congenital coronary anomalies and other causes. In this case, an echo-stress test confirmed inducible ischemia in the inferior wall, concordant with the arrhythmic focus location. The patient was transferred to a specialist congenital heart disease center, where she underwent transcatheter radiofrequency ablation of sustained ventricular tachycardia arising from the posteromedial papillary muscle. She was discharged on acetylsalicylic acid and verapamil. At 6-month follow-up she remained asymptomatic, without recurrent arrhythmias." }, { "index": 66, "label": "low_health_literacy", "original_text": "A 17-year-old male with no significant past medical or family history was referred to our clinic from the dental department following an incidental finding of a NFB during preoperative orthodontic planning, including dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was entirely asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. The patient's parents recalled an event when their son was seven, where he inserted an object into his nose. They sought medical advice, where no imaging was performed and an anterior rhinoscopy was utilized for diagnoses but due to the child's non-cooperation during the examination, the physician recommended the removal of the foreign body under sedation. However, the family did not follow up, and since the child remained asymptomatic, they assumed the foreign body had fallen out on its own. On endoscopic examination of the right nasal cavity, a deviated nasal septum with inferior turbinate hypertrophy was noted. The mucosa appeared erythematous and slightly edematous. A foreign body was visualized, lodged, and adhered to the floor of the nasal cavity beneath the inferior turbinate. The object was partially covered with mucus and possibly some crusted material and had a shiny appearance, indicating a metallic nature. Radiographic evaluation, including lateral and frontal X-rays, revealed a circular radiopaque object consistent with a metallic snap button located along the floor of the nasal cavity. The surrounding bony structures appeared normal. A CBCT confirmed the presence of the foreign body with associated mild inflammation, but no significant bony damage or sinus involvement was observed. With informed consent from the patient's parent, the foreign body was removed under local anesthesia in a semi-sitting position to reduce the risk of dislodgment to the airway. After decongesting the nasal cavity with Xylometazoline 0.1 % and administering Lidocaine spray (10 mg/spray) in the right nostril, a hook was utilized to disengage the foreign body, which was then retrieved using bayonet forceps. The procedure was uncomplicated, with minimal bleeding, easily controlled with saline irrigation. Post-removal examination showed no significant tissue damage. The retrieved object, a metallic snap button measuring 1 cm in diameter, exhibited signs of long-term exposure, including substantial corrosion and biological deposits. The patient was discharged in stable condition and prescribed nasal rinses with a sodium chloride irrigation solution (0.9 %). The patient was doing well at his two-week follow-up with an unremarkable examination.", "generated_summary": "A 17-year-old boy felt fine. A routine dental x-ray found something in his right nose by accident. He did not have a stuffy nose, nosebleeds, or pain. The pictures showed a bright spot in his right nose. It was a small metal snap button, like one on clothing. It was stuck low on the floor of the right side of his nose. It had probably been there for more than 10 years." }, { "index": 66, "label": "intermediate_health_literacy", "original_text": "A 17-year-old male with no significant past medical or family history was referred to our clinic from the dental department following an incidental finding of a NFB during preoperative orthodontic planning, including dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was entirely asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. The patient's parents recalled an event when their son was seven, where he inserted an object into his nose. They sought medical advice, where no imaging was performed and an anterior rhinoscopy was utilized for diagnoses but due to the child's non-cooperation during the examination, the physician recommended the removal of the foreign body under sedation. However, the family did not follow up, and since the child remained asymptomatic, they assumed the foreign body had fallen out on its own. On endoscopic examination of the right nasal cavity, a deviated nasal septum with inferior turbinate hypertrophy was noted. The mucosa appeared erythematous and slightly edematous. A foreign body was visualized, lodged, and adhered to the floor of the nasal cavity beneath the inferior turbinate. The object was partially covered with mucus and possibly some crusted material and had a shiny appearance, indicating a metallic nature. Radiographic evaluation, including lateral and frontal X-rays, revealed a circular radiopaque object consistent with a metallic snap button located along the floor of the nasal cavity. The surrounding bony structures appeared normal. A CBCT confirmed the presence of the foreign body with associated mild inflammation, but no significant bony damage or sinus involvement was observed. With informed consent from the patient's parent, the foreign body was removed under local anesthesia in a semi-sitting position to reduce the risk of dislodgment to the airway. After decongesting the nasal cavity with Xylometazoline 0.1 % and administering Lidocaine spray (10 mg/spray) in the right nostril, a hook was utilized to disengage the foreign body, which was then retrieved using bayonet forceps. The procedure was uncomplicated, with minimal bleeding, easily controlled with saline irrigation. Post-removal examination showed no significant tissue damage. The retrieved object, a metallic snap button measuring 1 cm in diameter, exhibited signs of long-term exposure, including substantial corrosion and biological deposits. The patient was discharged in stable condition and prescribed nasal rinses with a sodium chloride irrigation solution (0.9 %). The patient was doing well at his two-week follow-up with an unremarkable examination.", "generated_summary": "A 17-year-old male had a nasal foreign body found by chance during routine dental imaging for orthodontic planning. He had no symptoms\u2014no nasal blockage, nosebleeds, or discomfort. The imaging showed a round object that stood out on x-ray along the floor of the right nasal cavity. It was later identified as a metallic snap button embedded low in the right nasal passage. His family history suggested he likely put it there as a child, so it had probably been present for over a decade. There was no damage to nearby bone or the sinuses on imaging. The object was removed under local anesthesia without complications, and follow-up was unremarkable." }, { "index": 66, "label": "proficient_health_literacy", "original_text": "A 17-year-old male with no significant past medical or family history was referred to our clinic from the dental department following an incidental finding of a NFB during preoperative orthodontic planning, including dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was entirely asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. The patient's parents recalled an event when their son was seven, where he inserted an object into his nose. They sought medical advice, where no imaging was performed and an anterior rhinoscopy was utilized for diagnoses but due to the child's non-cooperation during the examination, the physician recommended the removal of the foreign body under sedation. However, the family did not follow up, and since the child remained asymptomatic, they assumed the foreign body had fallen out on its own. On endoscopic examination of the right nasal cavity, a deviated nasal septum with inferior turbinate hypertrophy was noted. The mucosa appeared erythematous and slightly edematous. A foreign body was visualized, lodged, and adhered to the floor of the nasal cavity beneath the inferior turbinate. The object was partially covered with mucus and possibly some crusted material and had a shiny appearance, indicating a metallic nature. Radiographic evaluation, including lateral and frontal X-rays, revealed a circular radiopaque object consistent with a metallic snap button located along the floor of the nasal cavity. The surrounding bony structures appeared normal. A CBCT confirmed the presence of the foreign body with associated mild inflammation, but no significant bony damage or sinus involvement was observed. With informed consent from the patient's parent, the foreign body was removed under local anesthesia in a semi-sitting position to reduce the risk of dislodgment to the airway. After decongesting the nasal cavity with Xylometazoline 0.1 % and administering Lidocaine spray (10 mg/spray) in the right nostril, a hook was utilized to disengage the foreign body, which was then retrieved using bayonet forceps. The procedure was uncomplicated, with minimal bleeding, easily controlled with saline irrigation. Post-removal examination showed no significant tissue damage. The retrieved object, a metallic snap button measuring 1 cm in diameter, exhibited signs of long-term exposure, including substantial corrosion and biological deposits. The patient was discharged in stable condition and prescribed nasal rinses with a sodium chloride irrigation solution (0.9 %). The patient was doing well at his two-week follow-up with an unremarkable examination.", "generated_summary": "A 17-year-old male with no significant past medical or family history was referred from Dentistry after an incidental nasal foreign body (NFB) was detected during preoperative orthodontic planning with dental radiographs and cone beam computed tomography (CBCT) without contrast. He was entirely asymptomatic, denying nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. The parents recalled a prior event at age seven when he inserted an object into his nose; an anterior rhinoscopy was attempted at that time, and removal under sedation was recommended, but the family did not follow up and assumed spontaneous expulsion given the absence of symptoms. Nasal endoscopy of the right cavity showed a deviated nasal septum with inferior turbinate hypertrophy; the mucosa was erythematous and mildly edematous. A foreign body was visualized, lodged and adherent to the floor of the nasal cavity beneath the inferior turbinate, partially covered with mucus/crust, with a shiny surface suggesting a metallic nature. Lateral and frontal radiographs demonstrated a circular radiopaque object along the nasal floor consistent with a metallic snap button; adjacent bony structures were normal. CBCT confirmed the foreign body and mild surrounding inflammation, without significant bony erosion or sinus involvement. With informed consent, removal was performed under local anesthesia in a semi-sitting position to mitigate the risk of airway dislodgment. After decongestion with xylometazoline 0.1% and topical anesthesia with lidocaine spray (10 mg/spray) in the right nostril, a hook was used to disengage the foreign body, which was then extracted with bayonet forceps. The procedure was uncomplicated with minimal bleeding controlled by saline irrigation, and post-removal inspection showed no significant tissue injury. The retrieved object was a metallic snap button (1 cm diameter) with substantial corrosion and biological deposits, consistent with long-term retention\u2014likely over a decade. The patient was discharged in stable condition with 0.9% sodium chloride nasal irrigations and had an unremarkable two-week follow-up." }, { "index": 67, "label": "low_health_literacy", "original_text": "An 18-year-old hispanic male patient with no significant medical history presents to the emergency department (ED) complaining of substernal, non-radiated chest pain, orthopnoea, dry and non-productive cough, and subjective fevers at home, for the last 3\u20134 days. Family history remarkable for paternal grandfather diagnosed with non-ischaemic cardiomyopathy and a pacemaker at age 86 years old. Patient lives with both parents and denies any smoking, ethanol consumption, recreational drug use, abuse or neglect at home. He worked at auto-part shop and planned to start college soon.\n\n\nInvestigations\n\n\nIn the ED, serum troponin I levels were found to be elevated and ECG showed diffuse ST-segment elevation. He was admitted to the local hospital and initial workup was remarkable for an enlarged cardiac silhouette and mild pulmonary oedema observed on chest X-ray, a transthoracic echocardiogram (TTE) demonstrating left ventricular ejection fraction (LVEF) of 40%, with severe left ventricular (LV) concentric hypertrophy and mild posterior pericardial effusion. Additionally, the patient was found to have elevated titres for Coxsackie virus A and B. His symptoms initially improved with the initiation of ibuprofen and colchicine. Cardiac catheterisation was performed, which revealed no evidence of coronary artery disease. Repeat TTE showed an LVEF of 40%\u201345%, hypokinesis of anteroapical and inferolateral wall, with an elevated LV end-diastolic pressure, consistent with diastolic dysfunction. Chest CT angiogram showed evidence of pneumonitis and a pericardial effusion. And at this point, the constellation of symptoms was thought to be secondary to Coxsackie myopericarditis, for which he continued to receive medical treatment as previously mentioned.\n\nOn the fourth day of admission, the patient became diaphoretic, tachycardic and hypotensive with an undetectable blood pressure. Emergent TTE showed large pericardial effusion with impending cardiac tamponade features, and pericardiocentesis was performed. During the procedure, the patient developed pulseless electrical activity (PEA) cardiac arrest and received advanced cardiovascular support for 30\u2009min. Ultimately patient was intubated, placed on venous-arterial extracorporeal membrane oxygenation (VA ECMO) and started on vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min), with numerous transfusions (9 packed red bloodcells, 10 units of platelets, 10 units of cryoprecipitate and 4 units of fresh frozen plasma) due to significant oozing of blood from the ECMO cannula. He was transferred to our hospital where endomyocardial biopsy (EMB) was then obtained due to concern of fulminant myocarditis and to test for other infiltrative cardiomyopathies. Pathology reports showed no signs suggestive of inflammatory or infiltrative process in the endomyocardium. Coxsackie Abs were repeated and were positive for Cox A type 9, Coxsackie B2 and Coxsackie B6, and an elevated Epstein-Barr virus (EBV) DNA quantitative PCR at 133\u2009000\u2009IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%\u201315% with previously noted severe LV concentric hypertrophy (1.9\u2009cm septum and 2.2\u2009cm in the inferolateral wall).\n\nThe patient was started on intravenous immunoglobulin (IVIG) for treatment of Coxsackie myocarditis, and broad-spectrum antibiotics due to worsening leucocytosis, but with no identified infectious focus. Colchicine was discontinued due to concern for rhabdomyolysis, with elevation of serum creatine kinase level to 2874 unit/L. Vasopressors were then discontinued and the patient was extubated. He also developed episode of flushing, fever, dyspnoea and decreasing oxygen saturation, with chest X-ray showing congested lung parenchyma with concerns for ARDS, therefore, IVIG was stopped.\n\nGiven improvement of cardiac function in another TTE with LVEF of 25%\u201330%, it was decided to attempt to remove the ECMO, which was unsuccessful. The patient remained on ECMO support and emergent discussion with heart failure team took place to determine best approach. The patient was evaluated for possible left ventricle assist device, however, deemed not a candidate due to significant global concentric LV hypertrophy, and the multidisciplinary team agreed to facilitate emergency listing for heart transplantation, with consideration to transition to another cardiovascular support such as intra-aortic balloon pump, with potential inotrope support.\n\nDuring further evaluation for possible heart transplant, an incisional biopsy of a 1\u00d71\u2009inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2\u20133 months before presenting to the ED. Pathology report of the right upper extremity mass showed aggressive EBV (+) NK/T-cell lymphoma with a cytotoxic immunophenotype (positive for CD 2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1 and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybridisation), and a modified SMILE (Steroids, Methotrexate with leucovorin, Ifosfamide with mesna, L-asparaginase and Etoposide) chemotherapy regimen was started. In situ hybridisation of the EMB previously obtained were negative for EBV-RNA.\n\nCardiac MRI was obtained, which revealed hypokinesis of the inferolateral and anterolateral wall, as previously described by TTE, delayed enhancement in the subendocardial and transmural distribution in these regions, with relative sparing of the septum. Additionally, avid enhancement and thickening of the pericardium, without a mass identified, and a pocket of pericardial fluid with septations, concerning for loculations, were also noted.\n\n\nDifferential diagnosis\n\nThe constellation of symptoms (shortness of breath, orthopnoea, hypotension and subjective fevers), with findings such as diffuse ST-segment elevation on ECG, leakages of cardiac markers (troponin), elevated Coxsackie virus titres (both of serotype A and B), as well as echocardiographic findings of pericardial effusion; all seemed to correlate with a classic presentation of viral pericarditis clinical due to Coxackie virus. However, despite medical treatment with colchicine, the patient continued to decompensate and eventually required pericardiocentesis due to cardiac tamponade, then developed cardiac arrest and ultimately requires ECMO support, for what seems acute onset heart failure. In this setting, fulminant myocarditis secondary to Coxsackie virus was considered. Cardiotropic RNA virus, such as Coxackie viruses, induce receptor-mediated endocytosis, with viral replication contributing to cellular dysfunction and ultimately apoptosis of the cell.1 When susceptible individuals are infected with highly virulent viral strains, maladaptive immunologic activity can occur, leading to persistent activation of T cells and continued antibody-mediated myocyte destruction, which can ultimately lead to fulminant myocarditis. EBV myocarditis could also explain the rapid deterioration in the setting of a positive EBV PCR, which is a more sensitivity test than traditional serologies for detection of acute infection.2 However, in situ hybridisation was negative for EBV-RNA.\n\nNevertheless, the significant concentric hypertrophy observed on the initial TTEs and the atypical delayed enhancement observed on the cardiac MRI are not explained by this diagnosis. Additionally, the EMB did not show an inflammatory process.\n\nFortuitous finding of EBV (+) NK/T-cell lymphoma by incisional biopsy of the right upper extremity allowed for a more fitting diagnosis for this case. The pericardial effusion, unresponsive to initial medical treatment and new acute heart failure with concentric hypertrophic cardiomyopathy, in the setting of newly diagnosed NK/T-cell lymphoma, raises the possibility of NK/T-cell lymphoma with involvement of the myocardium and pericardium as the most adequate diagnosis in this scenario, which englobes all the features previously mentioned in this case.\n\nOther differentials taken into consideration include infiltrative cardiomyopathy such as amyloidosis. However, Congo red staining of the EMB samples failed to demonstrate deposition of amyloid.\n\n\nTreatment\n\nGiven the diagnosis of extranodal NK/T-cell lymphoma (ENKTCL) with suspected pericardial involvement and no bone marrow involvement, modified SMILE regimen was desired as the first-line chemotherapy regimen. This regimen includes dexamethasone, ifosfamide, mesna and etoposide, and excluded methotrexate, due to evidence of third-spacing and effusions, which could lead to delayed excretion and increased risk of toxicity.\n\nHowever, due to his compromised cardiac function, it was believed that the patient would not tolerate cytotoxic chemotherapy which requires aggressive intravenous, and alternatively, emergent chemotherapy regimen was instituted: carboplatin (day 1\u2013day 3), etoposide (day 1\u2013day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7\u2013day 21). This regimen proved effective, as evidenced by rapid recovery of the LV function and overall haemodynamic stability, and decision was made to incorporate a modified SMILE chemotherapy regimen, of which he received two cycles. Then chemotherapy regimen was changed to dexamethasone, gemcitabine, carboplatin and peg-asparaginase (DDGP). The patient received two cycles of DDGP. A full body positron emission tomography (PET) scan was negative for lymphoma. The plan is to continue two more cycles of chemotherapy (to complete six total cycles of chemotherapy). Currently, the patient is considering radiation therapy and possible stem cell transplant, after completion of the chemotherapy regimen. Additionally, the patient is currently on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation.\n\n\nOutcome and follow-up\n\nThe patient has completed five out of six chemotherapy sessions with the previously mentioned regimens. After initiation of chemotherapy and optimal medical treatment for heart failure, the patient has recovered much of his cardiac function, as evidenced by an LVEF of 55%, no wall motion abnormalities and normal myocardial wall thickness on his most recent TTE. He continues to be followed by heart failure/cardiology team and oncology team in clinic.", "generated_summary": "An 18-year-old man came to the emergency room with new chest pain, fever, and trouble breathing when he lay down. A blood test showed strain on his heart. His heart tracing had changes that can happen when the heart is irritated. His chest X-ray made the heart look bigger than normal. An ultrasound showed the heart muscle was very thick on both sides. It also showed fluid around the heart. Blood tests pointed to a common virus called Coxsackie, which can inflame the sac around the heart. Doctors treated him, but he got worse with shortness of breath and very low blood pressure. A new heart ultrasound showed the fluid was starting to squeeze his heart, like a tight jacket. Doctors drained the fluid, but his heart stopped, and he needed a heart-lung machine to stay alive. A small piece of heart tissue did not show infection. A small skin lump on his right arm was tested. It showed a rare blood cancer linked to the Epstein\u2013Barr virus. He started cancer medicines. His heart pumping got better. The fluid around his heart went away. The thick heart muscle slowly went back toward normal." }, { "index": 67, "label": "intermediate_health_literacy", "original_text": "An 18-year-old hispanic male patient with no significant medical history presents to the emergency department (ED) complaining of substernal, non-radiated chest pain, orthopnoea, dry and non-productive cough, and subjective fevers at home, for the last 3\u20134 days. Family history remarkable for paternal grandfather diagnosed with non-ischaemic cardiomyopathy and a pacemaker at age 86 years old. Patient lives with both parents and denies any smoking, ethanol consumption, recreational drug use, abuse or neglect at home. He worked at auto-part shop and planned to start college soon.\n\n\nInvestigations\n\n\nIn the ED, serum troponin I levels were found to be elevated and ECG showed diffuse ST-segment elevation. He was admitted to the local hospital and initial workup was remarkable for an enlarged cardiac silhouette and mild pulmonary oedema observed on chest X-ray, a transthoracic echocardiogram (TTE) demonstrating left ventricular ejection fraction (LVEF) of 40%, with severe left ventricular (LV) concentric hypertrophy and mild posterior pericardial effusion. Additionally, the patient was found to have elevated titres for Coxsackie virus A and B. His symptoms initially improved with the initiation of ibuprofen and colchicine. Cardiac catheterisation was performed, which revealed no evidence of coronary artery disease. Repeat TTE showed an LVEF of 40%\u201345%, hypokinesis of anteroapical and inferolateral wall, with an elevated LV end-diastolic pressure, consistent with diastolic dysfunction. Chest CT angiogram showed evidence of pneumonitis and a pericardial effusion. And at this point, the constellation of symptoms was thought to be secondary to Coxsackie myopericarditis, for which he continued to receive medical treatment as previously mentioned.\n\nOn the fourth day of admission, the patient became diaphoretic, tachycardic and hypotensive with an undetectable blood pressure. Emergent TTE showed large pericardial effusion with impending cardiac tamponade features, and pericardiocentesis was performed. During the procedure, the patient developed pulseless electrical activity (PEA) cardiac arrest and received advanced cardiovascular support for 30\u2009min. Ultimately patient was intubated, placed on venous-arterial extracorporeal membrane oxygenation (VA ECMO) and started on vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min), with numerous transfusions (9 packed red bloodcells, 10 units of platelets, 10 units of cryoprecipitate and 4 units of fresh frozen plasma) due to significant oozing of blood from the ECMO cannula. He was transferred to our hospital where endomyocardial biopsy (EMB) was then obtained due to concern of fulminant myocarditis and to test for other infiltrative cardiomyopathies. Pathology reports showed no signs suggestive of inflammatory or infiltrative process in the endomyocardium. Coxsackie Abs were repeated and were positive for Cox A type 9, Coxsackie B2 and Coxsackie B6, and an elevated Epstein-Barr virus (EBV) DNA quantitative PCR at 133\u2009000\u2009IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%\u201315% with previously noted severe LV concentric hypertrophy (1.9\u2009cm septum and 2.2\u2009cm in the inferolateral wall).\n\nThe patient was started on intravenous immunoglobulin (IVIG) for treatment of Coxsackie myocarditis, and broad-spectrum antibiotics due to worsening leucocytosis, but with no identified infectious focus. Colchicine was discontinued due to concern for rhabdomyolysis, with elevation of serum creatine kinase level to 2874 unit/L. Vasopressors were then discontinued and the patient was extubated. He also developed episode of flushing, fever, dyspnoea and decreasing oxygen saturation, with chest X-ray showing congested lung parenchyma with concerns for ARDS, therefore, IVIG was stopped.\n\nGiven improvement of cardiac function in another TTE with LVEF of 25%\u201330%, it was decided to attempt to remove the ECMO, which was unsuccessful. The patient remained on ECMO support and emergent discussion with heart failure team took place to determine best approach. The patient was evaluated for possible left ventricle assist device, however, deemed not a candidate due to significant global concentric LV hypertrophy, and the multidisciplinary team agreed to facilitate emergency listing for heart transplantation, with consideration to transition to another cardiovascular support such as intra-aortic balloon pump, with potential inotrope support.\n\nDuring further evaluation for possible heart transplant, an incisional biopsy of a 1\u00d71\u2009inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2\u20133 months before presenting to the ED. Pathology report of the right upper extremity mass showed aggressive EBV (+) NK/T-cell lymphoma with a cytotoxic immunophenotype (positive for CD 2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1 and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybridisation), and a modified SMILE (Steroids, Methotrexate with leucovorin, Ifosfamide with mesna, L-asparaginase and Etoposide) chemotherapy regimen was started. In situ hybridisation of the EMB previously obtained were negative for EBV-RNA.\n\nCardiac MRI was obtained, which revealed hypokinesis of the inferolateral and anterolateral wall, as previously described by TTE, delayed enhancement in the subendocardial and transmural distribution in these regions, with relative sparing of the septum. Additionally, avid enhancement and thickening of the pericardium, without a mass identified, and a pocket of pericardial fluid with septations, concerning for loculations, were also noted.\n\n\nDifferential diagnosis\n\nThe constellation of symptoms (shortness of breath, orthopnoea, hypotension and subjective fevers), with findings such as diffuse ST-segment elevation on ECG, leakages of cardiac markers (troponin), elevated Coxsackie virus titres (both of serotype A and B), as well as echocardiographic findings of pericardial effusion; all seemed to correlate with a classic presentation of viral pericarditis clinical due to Coxackie virus. However, despite medical treatment with colchicine, the patient continued to decompensate and eventually required pericardiocentesis due to cardiac tamponade, then developed cardiac arrest and ultimately requires ECMO support, for what seems acute onset heart failure. In this setting, fulminant myocarditis secondary to Coxsackie virus was considered. Cardiotropic RNA virus, such as Coxackie viruses, induce receptor-mediated endocytosis, with viral replication contributing to cellular dysfunction and ultimately apoptosis of the cell.1 When susceptible individuals are infected with highly virulent viral strains, maladaptive immunologic activity can occur, leading to persistent activation of T cells and continued antibody-mediated myocyte destruction, which can ultimately lead to fulminant myocarditis. EBV myocarditis could also explain the rapid deterioration in the setting of a positive EBV PCR, which is a more sensitivity test than traditional serologies for detection of acute infection.2 However, in situ hybridisation was negative for EBV-RNA.\n\nNevertheless, the significant concentric hypertrophy observed on the initial TTEs and the atypical delayed enhancement observed on the cardiac MRI are not explained by this diagnosis. Additionally, the EMB did not show an inflammatory process.\n\nFortuitous finding of EBV (+) NK/T-cell lymphoma by incisional biopsy of the right upper extremity allowed for a more fitting diagnosis for this case. The pericardial effusion, unresponsive to initial medical treatment and new acute heart failure with concentric hypertrophic cardiomyopathy, in the setting of newly diagnosed NK/T-cell lymphoma, raises the possibility of NK/T-cell lymphoma with involvement of the myocardium and pericardium as the most adequate diagnosis in this scenario, which englobes all the features previously mentioned in this case.\n\nOther differentials taken into consideration include infiltrative cardiomyopathy such as amyloidosis. However, Congo red staining of the EMB samples failed to demonstrate deposition of amyloid.\n\n\nTreatment\n\nGiven the diagnosis of extranodal NK/T-cell lymphoma (ENKTCL) with suspected pericardial involvement and no bone marrow involvement, modified SMILE regimen was desired as the first-line chemotherapy regimen. This regimen includes dexamethasone, ifosfamide, mesna and etoposide, and excluded methotrexate, due to evidence of third-spacing and effusions, which could lead to delayed excretion and increased risk of toxicity.\n\nHowever, due to his compromised cardiac function, it was believed that the patient would not tolerate cytotoxic chemotherapy which requires aggressive intravenous, and alternatively, emergent chemotherapy regimen was instituted: carboplatin (day 1\u2013day 3), etoposide (day 1\u2013day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7\u2013day 21). This regimen proved effective, as evidenced by rapid recovery of the LV function and overall haemodynamic stability, and decision was made to incorporate a modified SMILE chemotherapy regimen, of which he received two cycles. Then chemotherapy regimen was changed to dexamethasone, gemcitabine, carboplatin and peg-asparaginase (DDGP). The patient received two cycles of DDGP. A full body positron emission tomography (PET) scan was negative for lymphoma. The plan is to continue two more cycles of chemotherapy (to complete six total cycles of chemotherapy). Currently, the patient is considering radiation therapy and possible stem cell transplant, after completion of the chemotherapy regimen. Additionally, the patient is currently on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation.\n\n\nOutcome and follow-up\n\nThe patient has completed five out of six chemotherapy sessions with the previously mentioned regimens. After initiation of chemotherapy and optimal medical treatment for heart failure, the patient has recovered much of his cardiac function, as evidenced by an LVEF of 55%, no wall motion abnormalities and normal myocardial wall thickness on his most recent TTE. He continues to be followed by heart failure/cardiology team and oncology team in clinic.", "generated_summary": "An 18-year-old man presented with new chest pain, fever, and shortness of breath when lying flat. Testing showed elevated troponin, diffuse ST-segment elevation on ECG, and an enlarged heart silhouette on chest X-ray. Transthoracic echocardiography revealed markedly thickened heart muscle in both ventricles and a pericardial effusion. Blood tests were positive for Coxsackie A and B, so he was treated for presumed viral pericarditis. Despite this, he became short of breath and hypotensive. Repeat echocardiography showed impending cardiac tamponade. Pericardiocentesis was performed but was complicated by a pulseless electrical activity arrest, and he required venoarterial ECMO. An urgent endomyocardial biopsy did not show inflammation. A biopsy of a small right arm skin lesion unexpectedly diagnosed Epstein\u2013Barr virus\u2013positive NK/T-cell lymphoma. After starting chemotherapy, he improved: his ejection fraction rose, the pericardial effusion resolved, and the previously thickened myocardium gradually regressed." }, { "index": 67, "label": "proficient_health_literacy", "original_text": "An 18-year-old hispanic male patient with no significant medical history presents to the emergency department (ED) complaining of substernal, non-radiated chest pain, orthopnoea, dry and non-productive cough, and subjective fevers at home, for the last 3\u20134 days. Family history remarkable for paternal grandfather diagnosed with non-ischaemic cardiomyopathy and a pacemaker at age 86 years old. Patient lives with both parents and denies any smoking, ethanol consumption, recreational drug use, abuse or neglect at home. He worked at auto-part shop and planned to start college soon.\n\n\nInvestigations\n\n\nIn the ED, serum troponin I levels were found to be elevated and ECG showed diffuse ST-segment elevation. He was admitted to the local hospital and initial workup was remarkable for an enlarged cardiac silhouette and mild pulmonary oedema observed on chest X-ray, a transthoracic echocardiogram (TTE) demonstrating left ventricular ejection fraction (LVEF) of 40%, with severe left ventricular (LV) concentric hypertrophy and mild posterior pericardial effusion. Additionally, the patient was found to have elevated titres for Coxsackie virus A and B. His symptoms initially improved with the initiation of ibuprofen and colchicine. Cardiac catheterisation was performed, which revealed no evidence of coronary artery disease. Repeat TTE showed an LVEF of 40%\u201345%, hypokinesis of anteroapical and inferolateral wall, with an elevated LV end-diastolic pressure, consistent with diastolic dysfunction. Chest CT angiogram showed evidence of pneumonitis and a pericardial effusion. And at this point, the constellation of symptoms was thought to be secondary to Coxsackie myopericarditis, for which he continued to receive medical treatment as previously mentioned.\n\nOn the fourth day of admission, the patient became diaphoretic, tachycardic and hypotensive with an undetectable blood pressure. Emergent TTE showed large pericardial effusion with impending cardiac tamponade features, and pericardiocentesis was performed. During the procedure, the patient developed pulseless electrical activity (PEA) cardiac arrest and received advanced cardiovascular support for 30\u2009min. Ultimately patient was intubated, placed on venous-arterial extracorporeal membrane oxygenation (VA ECMO) and started on vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min), with numerous transfusions (9 packed red bloodcells, 10 units of platelets, 10 units of cryoprecipitate and 4 units of fresh frozen plasma) due to significant oozing of blood from the ECMO cannula. He was transferred to our hospital where endomyocardial biopsy (EMB) was then obtained due to concern of fulminant myocarditis and to test for other infiltrative cardiomyopathies. Pathology reports showed no signs suggestive of inflammatory or infiltrative process in the endomyocardium. Coxsackie Abs were repeated and were positive for Cox A type 9, Coxsackie B2 and Coxsackie B6, and an elevated Epstein-Barr virus (EBV) DNA quantitative PCR at 133\u2009000\u2009IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%\u201315% with previously noted severe LV concentric hypertrophy (1.9\u2009cm septum and 2.2\u2009cm in the inferolateral wall).\n\nThe patient was started on intravenous immunoglobulin (IVIG) for treatment of Coxsackie myocarditis, and broad-spectrum antibiotics due to worsening leucocytosis, but with no identified infectious focus. Colchicine was discontinued due to concern for rhabdomyolysis, with elevation of serum creatine kinase level to 2874 unit/L. Vasopressors were then discontinued and the patient was extubated. He also developed episode of flushing, fever, dyspnoea and decreasing oxygen saturation, with chest X-ray showing congested lung parenchyma with concerns for ARDS, therefore, IVIG was stopped.\n\nGiven improvement of cardiac function in another TTE with LVEF of 25%\u201330%, it was decided to attempt to remove the ECMO, which was unsuccessful. The patient remained on ECMO support and emergent discussion with heart failure team took place to determine best approach. The patient was evaluated for possible left ventricle assist device, however, deemed not a candidate due to significant global concentric LV hypertrophy, and the multidisciplinary team agreed to facilitate emergency listing for heart transplantation, with consideration to transition to another cardiovascular support such as intra-aortic balloon pump, with potential inotrope support.\n\nDuring further evaluation for possible heart transplant, an incisional biopsy of a 1\u00d71\u2009inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2\u20133 months before presenting to the ED. Pathology report of the right upper extremity mass showed aggressive EBV (+) NK/T-cell lymphoma with a cytotoxic immunophenotype (positive for CD 2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1 and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybridisation), and a modified SMILE (Steroids, Methotrexate with leucovorin, Ifosfamide with mesna, L-asparaginase and Etoposide) chemotherapy regimen was started. In situ hybridisation of the EMB previously obtained were negative for EBV-RNA.\n\nCardiac MRI was obtained, which revealed hypokinesis of the inferolateral and anterolateral wall, as previously described by TTE, delayed enhancement in the subendocardial and transmural distribution in these regions, with relative sparing of the septum. Additionally, avid enhancement and thickening of the pericardium, without a mass identified, and a pocket of pericardial fluid with septations, concerning for loculations, were also noted.\n\n\nDifferential diagnosis\n\nThe constellation of symptoms (shortness of breath, orthopnoea, hypotension and subjective fevers), with findings such as diffuse ST-segment elevation on ECG, leakages of cardiac markers (troponin), elevated Coxsackie virus titres (both of serotype A and B), as well as echocardiographic findings of pericardial effusion; all seemed to correlate with a classic presentation of viral pericarditis clinical due to Coxackie virus. However, despite medical treatment with colchicine, the patient continued to decompensate and eventually required pericardiocentesis due to cardiac tamponade, then developed cardiac arrest and ultimately requires ECMO support, for what seems acute onset heart failure. In this setting, fulminant myocarditis secondary to Coxsackie virus was considered. Cardiotropic RNA virus, such as Coxackie viruses, induce receptor-mediated endocytosis, with viral replication contributing to cellular dysfunction and ultimately apoptosis of the cell.1 When susceptible individuals are infected with highly virulent viral strains, maladaptive immunologic activity can occur, leading to persistent activation of T cells and continued antibody-mediated myocyte destruction, which can ultimately lead to fulminant myocarditis. EBV myocarditis could also explain the rapid deterioration in the setting of a positive EBV PCR, which is a more sensitivity test than traditional serologies for detection of acute infection.2 However, in situ hybridisation was negative for EBV-RNA.\n\nNevertheless, the significant concentric hypertrophy observed on the initial TTEs and the atypical delayed enhancement observed on the cardiac MRI are not explained by this diagnosis. Additionally, the EMB did not show an inflammatory process.\n\nFortuitous finding of EBV (+) NK/T-cell lymphoma by incisional biopsy of the right upper extremity allowed for a more fitting diagnosis for this case. The pericardial effusion, unresponsive to initial medical treatment and new acute heart failure with concentric hypertrophic cardiomyopathy, in the setting of newly diagnosed NK/T-cell lymphoma, raises the possibility of NK/T-cell lymphoma with involvement of the myocardium and pericardium as the most adequate diagnosis in this scenario, which englobes all the features previously mentioned in this case.\n\nOther differentials taken into consideration include infiltrative cardiomyopathy such as amyloidosis. However, Congo red staining of the EMB samples failed to demonstrate deposition of amyloid.\n\n\nTreatment\n\nGiven the diagnosis of extranodal NK/T-cell lymphoma (ENKTCL) with suspected pericardial involvement and no bone marrow involvement, modified SMILE regimen was desired as the first-line chemotherapy regimen. This regimen includes dexamethasone, ifosfamide, mesna and etoposide, and excluded methotrexate, due to evidence of third-spacing and effusions, which could lead to delayed excretion and increased risk of toxicity.\n\nHowever, due to his compromised cardiac function, it was believed that the patient would not tolerate cytotoxic chemotherapy which requires aggressive intravenous, and alternatively, emergent chemotherapy regimen was instituted: carboplatin (day 1\u2013day 3), etoposide (day 1\u2013day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7\u2013day 21). This regimen proved effective, as evidenced by rapid recovery of the LV function and overall haemodynamic stability, and decision was made to incorporate a modified SMILE chemotherapy regimen, of which he received two cycles. Then chemotherapy regimen was changed to dexamethasone, gemcitabine, carboplatin and peg-asparaginase (DDGP). The patient received two cycles of DDGP. A full body positron emission tomography (PET) scan was negative for lymphoma. The plan is to continue two more cycles of chemotherapy (to complete six total cycles of chemotherapy). Currently, the patient is considering radiation therapy and possible stem cell transplant, after completion of the chemotherapy regimen. Additionally, the patient is currently on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation.\n\n\nOutcome and follow-up\n\nThe patient has completed five out of six chemotherapy sessions with the previously mentioned regimens. After initiation of chemotherapy and optimal medical treatment for heart failure, the patient has recovered much of his cardiac function, as evidenced by an LVEF of 55%, no wall motion abnormalities and normal myocardial wall thickness on his most recent TTE. He continues to be followed by heart failure/cardiology team and oncology team in clinic.", "generated_summary": "An 18-year-old Hispanic male with no prior medical history presented with 3\u20134 days of substernal, nonradiating chest pain, orthopnoea, dry cough, and subjective fevers. Initial ED workup showed elevated troponin I and diffuse ST-segment elevation. Chest X-ray demonstrated an enlarged cardiac silhouette with mild pulmonary oedema. TTE revealed LVEF 40% with severe LV concentric hypertrophy and a mild posterior pericardial effusion. Coxsackie A and B titres were elevated. Symptoms transiently improved on ibuprofen and colchicine. Coronary angiography showed no CAD. Repeat TTE showed LVEF 40\u201345%, anteroapical and inferolateral hypokinesis, and elevated LVEDP consistent with diastolic dysfunction. Chest CT angiography showed pneumonitis and a pericardial effusion. Working diagnosis was Coxsackie myopericarditis. On hospital day 4 he acutely decompensated (diaphoresis, tachycardia, undetectable BP). Emergent TTE showed a large pericardial effusion with impending tamponade; pericardiocentesis was performed but was complicated by PEA arrest requiring ~30 minutes of ACLS. He was intubated, cannulated to VA-ECMO, and started on vasopressors (norepinephrine 5 mcg/min, vasopressin 0.05 units/min) with substantial transfusion requirements (9 PRBC, 10 platelets, 10 cryoprecipitate, 4 FFP) due to cannula site oozing. At the receiving centre, EMB was obtained for suspected fulminant myocarditis/infiltrative disease and was negative for inflammatory or infiltrative pathology. Repeat serology showed Coxsackie A type 9 and Coxsackie B2/B6 positivity and EBV DNA PCR 133,000 IU/mL. TTE now showed EF 10\u201315% with persistent severe LV concentric hypertrophy (septum 1.9 cm, inferolateral wall 2.2 cm). He was started on IVIG for presumed Coxsackie myocarditis and broad-spectrum antibiotics for worsening leucocytosis without a clear source; colchicine was stopped for concern of rhabdomyolysis (CK 2874 U/L). He subsequently developed flushing, fever, dyspnoea, and hypoxaemia with CXR consistent with pulmonary congestion/concern for ARDS, and IVIG was discontinued. Vasopressors were weaned off and he was extubated. Attempted ECMO decannulation failed; due to global concentric LV hypertrophy he was not an LVAD candidate. Emergency heart transplant listing and possible transition to IABP with inotropes were discussed. During transplant evaluation, an incisional biopsy of a 1\u00d71 inch, painless, mobile right arm mass disclosed aggressive EBV(+) NK/T-cell lymphoma with a cytotoxic immunophenotype (CD2+, CD3+, CD56+, BCL2+, granzyme B+, TIA1+, MUM1+, diffuse EBER positivity). In situ hybridisation of the prior EMB was negative for EBV-RNA. Cardiac MRI demonstrated inferolateral and anterolateral hypokinesis with subendocardial to transmural LGE in those territories with relative septal sparing, marked pericardial thickening with avid enhancement, and a loculated pericardial effusion; no discrete mass was identified. Differential included Coxsackie myopericarditis and EBV myocarditis (noting EBV PCR is more sensitive than serology), but the absence of myocardial inflammation on EMB, marked concentric hypertrophy, and atypical LGE pattern argued against primary viral myocarditis. Amyloidosis was considered, but Congo red staining on EMB was negative. The overall picture\u2014pericardial effusion refractory to initial therapy, acute heart failure with concentric hypertrophy, and the new diagnosis of EBV(+) NK/T-cell lymphoma\u2014favoured pericardial/myocardial involvement by ENKTCL. Given ENKTCL without marrow involvement and concern for third spacing, a modified SMILE was planned (excluding methotrexate). Because of haemodynamic instability and concerns about tolerating cytotoxic therapy, induction was initiated with carboplatin (days 1\u20133), etoposide (days 1\u20135), and dexamethasone; peg-asparaginase was added (days 7\u201321). This regimen led to rapid improvement in LV function and haemodynamic stability, after which two cycles of modified SMILE were administered, followed by two cycles of DDGP (dexamethasone, gemcitabine, carboplatin, peg-asparaginase). Whole-body PET was negative. The treatment plan is to complete six total cycles and consider radiotherapy and possible stem cell transplantation. He is on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation. Outcome: after initiation of chemotherapy and optimisation of HF therapy, TTE showed recovery of LVEF to 55%, normal wall motion, and normal myocardial wall thickness, with resolution of the pericardial effusion and regression of hypertrophy. He continues multidisciplinary follow-up with cardiology/heart failure and oncology. Pathophysiologic context: cardiotropic RNA viruses such as Coxsackie can trigger receptor-mediated endocytosis and replication, leading to myocyte dysfunction and apoptosis; in susceptible hosts, maladaptive immune activation (persistent T-cell activation and antibody-mediated myocyte injury) can precipitate fulminant myocarditis. In this case, however, the lack of myocardial inflammation on EMB and the imaging phenotype supported lymphoma-associated cardiac involvement rather than primary viral myocarditis." }, { "index": 68, "label": "low_health_literacy", "original_text": "We report a rare case of euthyroid unilateral GO with early massive mono-muscular fibrosis in a 50-year-old male patient. The patient had a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis but no family or personal history of thyroid autoimmune disease. The patient was a smoker of 20 cigarettes a day from the age of 30 and presented dyslipidemia for several years. Since June 2020, he experienced rapid and progressive swelling of the soft tissues in the right orbit, moderate pain during ocular globe movements, redness of eyelids and diplopia. Visual acuity was normal in both eyes. In October 2020, the patient was evaluated in our outpatient clinic. Moderate right orbit active inflammation was confirmed by Clinical Activity Score 3/7 (CAS),3 and eyelid edema was moderate. The eyelid aperture was 14 mm in the right orbit and 10 mm in the left orbit, and the Hertel measurements were 24 mm and 18 mm in the right and left orbits, respectively. In addition, the patient presented a severe reduction in elevation, persistent depression in the primary position of the right ocular globe and constant diplopia, as scored according to the Gorman score.4 The quality of life evaluated by Graves\u2019 Ophthalmopathy quality of life questionnaire (GO-QOL)5 was reduced in both appearance and functional subscales. However, the functional subscale was reduced with respect to the appearance subscale, as the values were 12.5 and 50, respectively (considering 0 = worse condition and 100 = the best health state). Visual acuity was normal, and color vision by Ishihara tables was 16/17 and 17/17 in the right and left eyes, respectively. Evaluation of extraocular muscles by computer tomography (CT) scan (contiguous 1.25 mm thick slices, 200 mA, 120 kV, pitch 0.5) showed severe enlargement of the lower rectal body to the edge of the insertion tendon in the right orbit. Remarkably, the morphology of the other extraocular muscles in both orbits was normal. The muscle orbit area ratio measured in the right eyes was 0.25 Autocad units (in-house method; vn \u2264 0.20\u00b10.03).6 Thyroid function was normal with a slight increase in TSH-R-Ab: 1.75 mU/l (n.v. < 1.5 mU/l). The amplitude of the p100 wave was slightly reduced by electrophysiology evaluation in the right eye. A thyroid ultrasound scan of the thyroid gland showed a thyroiditis pattern. Biochemical and clinical evaluations were negative for hematological or other systemic diseases. Routine clinical tests were normal, but the total cholesterol levels that were 220 mg/dl, triglyceride levels were 297 mg/dl, and high-density lipoprotein cholesterol (HDL) levels were 38 mg/dl.\n\nThe patient was treated by intravenous corticosteroid pulse therapy (Solumedrol; Pfizer, Karlsruhe, Germany) with a cumulative dose of 4500 mg over 12 weeks, leading to the resolution of inflammatory signs and symptoms. However, GO-QOL, Hertel measurements and diplopia remained unchanged; in contrast, electrophysiology evaluation and visual acuity worsened. Two-wall orbital surgical decompression plus parenteral glucocorticoids was chosen as the second-line treatment for GO. In that context, a biopsy of the right inferior rectus muscle revealed massive fibrosis with adipose tissue infiltration of this extraocular muscle.", "generated_summary": "This is a rare kind of thyroid eye disease that affected just one eye muscle. The person was 50, smoked, and had high blood fats. His thyroid levels were normal. A thyroid antibody in his blood was only a little high. His right eye lost movement very fast and stayed pulled down. He saw double all the time, and glasses could not fix it. This hurt his daily life a lot. Doctors gave strong steroids through a vein. The swelling got better, but the double vision did not. He then needed two surgeries to make more space in the eye socket. A small sample from the tight eye muscle showed a lot of scar-like tissue in the lower right eye muscle." }, { "index": 68, "label": "intermediate_health_literacy", "original_text": "We report a rare case of euthyroid unilateral GO with early massive mono-muscular fibrosis in a 50-year-old male patient. The patient had a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis but no family or personal history of thyroid autoimmune disease. The patient was a smoker of 20 cigarettes a day from the age of 30 and presented dyslipidemia for several years. Since June 2020, he experienced rapid and progressive swelling of the soft tissues in the right orbit, moderate pain during ocular globe movements, redness of eyelids and diplopia. Visual acuity was normal in both eyes. In October 2020, the patient was evaluated in our outpatient clinic. Moderate right orbit active inflammation was confirmed by Clinical Activity Score 3/7 (CAS),3 and eyelid edema was moderate. The eyelid aperture was 14 mm in the right orbit and 10 mm in the left orbit, and the Hertel measurements were 24 mm and 18 mm in the right and left orbits, respectively. In addition, the patient presented a severe reduction in elevation, persistent depression in the primary position of the right ocular globe and constant diplopia, as scored according to the Gorman score.4 The quality of life evaluated by Graves\u2019 Ophthalmopathy quality of life questionnaire (GO-QOL)5 was reduced in both appearance and functional subscales. However, the functional subscale was reduced with respect to the appearance subscale, as the values were 12.5 and 50, respectively (considering 0 = worse condition and 100 = the best health state). Visual acuity was normal, and color vision by Ishihara tables was 16/17 and 17/17 in the right and left eyes, respectively. Evaluation of extraocular muscles by computer tomography (CT) scan (contiguous 1.25 mm thick slices, 200 mA, 120 kV, pitch 0.5) showed severe enlargement of the lower rectal body to the edge of the insertion tendon in the right orbit. Remarkably, the morphology of the other extraocular muscles in both orbits was normal. The muscle orbit area ratio measured in the right eyes was 0.25 Autocad units (in-house method; vn \u2264 0.20\u00b10.03).6 Thyroid function was normal with a slight increase in TSH-R-Ab: 1.75 mU/l (n.v. < 1.5 mU/l). The amplitude of the p100 wave was slightly reduced by electrophysiology evaluation in the right eye. A thyroid ultrasound scan of the thyroid gland showed a thyroiditis pattern. Biochemical and clinical evaluations were negative for hematological or other systemic diseases. Routine clinical tests were normal, but the total cholesterol levels that were 220 mg/dl, triglyceride levels were 297 mg/dl, and high-density lipoprotein cholesterol (HDL) levels were 38 mg/dl.\n\nThe patient was treated by intravenous corticosteroid pulse therapy (Solumedrol; Pfizer, Karlsruhe, Germany) with a cumulative dose of 4500 mg over 12 weeks, leading to the resolution of inflammatory signs and symptoms. However, GO-QOL, Hertel measurements and diplopia remained unchanged; in contrast, electrophysiology evaluation and visual acuity worsened. Two-wall orbital surgical decompression plus parenteral glucocorticoids was chosen as the second-line treatment for GO. In that context, a biopsy of the right inferior rectus muscle revealed massive fibrosis with adipose tissue infiltration of this extraocular muscle.", "generated_summary": "We describe a rare case of euthyroid, single-muscle thyroid eye disease (Graves\u2019 orbitopathy) in a 50-year-old man who smoked and had dyslipidemia. He developed a very rapid and severe loss of upward movement in the right eye, producing constant, uncorrectable double vision and major quality-of-life impact. Thyroid function was normal, and TSH receptor antibodies were only slightly elevated. Imaging showed isolated enlargement of the right inferior rectus muscle; the other eye muscles were normal. Intravenous steroid pulses reduced inflammation but did not improve the diplopia or eye position. He ultimately required two orbital decompression surgeries. A biopsy of the right inferior rectus confirmed massive fibrosis with fat infiltration, consistent with single-muscle involvement." }, { "index": 68, "label": "proficient_health_literacy", "original_text": "We report a rare case of euthyroid unilateral GO with early massive mono-muscular fibrosis in a 50-year-old male patient. The patient had a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis but no family or personal history of thyroid autoimmune disease. The patient was a smoker of 20 cigarettes a day from the age of 30 and presented dyslipidemia for several years. Since June 2020, he experienced rapid and progressive swelling of the soft tissues in the right orbit, moderate pain during ocular globe movements, redness of eyelids and diplopia. Visual acuity was normal in both eyes. In October 2020, the patient was evaluated in our outpatient clinic. Moderate right orbit active inflammation was confirmed by Clinical Activity Score 3/7 (CAS),3 and eyelid edema was moderate. The eyelid aperture was 14 mm in the right orbit and 10 mm in the left orbit, and the Hertel measurements were 24 mm and 18 mm in the right and left orbits, respectively. In addition, the patient presented a severe reduction in elevation, persistent depression in the primary position of the right ocular globe and constant diplopia, as scored according to the Gorman score.4 The quality of life evaluated by Graves\u2019 Ophthalmopathy quality of life questionnaire (GO-QOL)5 was reduced in both appearance and functional subscales. However, the functional subscale was reduced with respect to the appearance subscale, as the values were 12.5 and 50, respectively (considering 0 = worse condition and 100 = the best health state). Visual acuity was normal, and color vision by Ishihara tables was 16/17 and 17/17 in the right and left eyes, respectively. Evaluation of extraocular muscles by computer tomography (CT) scan (contiguous 1.25 mm thick slices, 200 mA, 120 kV, pitch 0.5) showed severe enlargement of the lower rectal body to the edge of the insertion tendon in the right orbit. Remarkably, the morphology of the other extraocular muscles in both orbits was normal. The muscle orbit area ratio measured in the right eyes was 0.25 Autocad units (in-house method; vn \u2264 0.20\u00b10.03).6 Thyroid function was normal with a slight increase in TSH-R-Ab: 1.75 mU/l (n.v. < 1.5 mU/l). The amplitude of the p100 wave was slightly reduced by electrophysiology evaluation in the right eye. A thyroid ultrasound scan of the thyroid gland showed a thyroiditis pattern. Biochemical and clinical evaluations were negative for hematological or other systemic diseases. Routine clinical tests were normal, but the total cholesterol levels that were 220 mg/dl, triglyceride levels were 297 mg/dl, and high-density lipoprotein cholesterol (HDL) levels were 38 mg/dl.\n\nThe patient was treated by intravenous corticosteroid pulse therapy (Solumedrol; Pfizer, Karlsruhe, Germany) with a cumulative dose of 4500 mg over 12 weeks, leading to the resolution of inflammatory signs and symptoms. However, GO-QOL, Hertel measurements and diplopia remained unchanged; in contrast, electrophysiology evaluation and visual acuity worsened. Two-wall orbital surgical decompression plus parenteral glucocorticoids was chosen as the second-line treatment for GO. In that context, a biopsy of the right inferior rectus muscle revealed massive fibrosis with adipose tissue infiltration of this extraocular muscle.", "generated_summary": "We report a rare case of euthyroid unilateral GO with early massive mono-muscular fibrosis in a 50-year-old male. Family history included cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no family or personal history of thyroid autoimmune disease. He smoked 20 cigarettes/day since age 30 and had longstanding dyslipidemia. Beginning June 2020, he developed rapid, progressive right orbital soft-tissue swelling, pain on ocular movements, eyelid redness, and diplopia; visual acuity was initially normal OU. In October 2020, examination showed active right orbital inflammation (CAS 3/7) with moderate eyelid edema. Palpebral fissure height was 14 mm OD and 10 mm OS. Hertel exophthalmometry was 24 mm OD and 18 mm OS. There was severe limitation of elevation, persistent depression in primary position OD, and constant diplopia per the Gorman score. GO-QOL was reduced in both subscales, with a greater decrement in function (12.5) than appearance (50) on a 0\u2013100 scale. Color vision by Ishihara was 16/17 OD and 17/17 OS. CT (contiguous 1.25 mm slices, 200 mA, 120 kV, pitch 0.5) demonstrated severe enlargement of the right inferior rectus to the tendon insertion; all other extraocular muscles were normal OU. The muscle\u2013orbit area ratio OD was 0.25 AutoCAD units (vn \u2264 0.20 \u00b1 0.03). Thyroid function was normal with slightly increased TSH-R-Ab at 1.75 mU/L (n.v. < 1.5 mU/L). Electrophysiology showed a slight reduction in p100 amplitude OD. Thyroid ultrasound displayed a thyroiditis pattern. Hematologic and systemic evaluations were negative. Routine labs were unremarkable aside from dyslipidemia (total cholesterol 220 mg/dl, triglycerides 297 mg/dl, HDL 38 mg/dl).\n\nTreatment with intravenous corticosteroid pulse therapy (methylprednisolone; cumulative 4,500 mg over 12 weeks) resolved inflammatory signs and symptoms; however, GO-QOL, Hertel exophthalmometry, and diplopia remained unchanged, and both visual acuity and electrophysiology worsened. As second-line therapy, two-wall orbital surgical decompression plus parenteral glucocorticoids was performed. Intraoperative biopsy of the right inferior rectus revealed massive fibrosis with adipose tissue infiltration.\n\nThis case exemplifies euthyroid unilateral GO with isolated inferior rectus involvement and early fibrotic transformation despite only mildly elevated TSH-R-Ab, producing a profound motility deficit and constant diplopia that was refractory to IV steroids and required bony decompression." }, { "index": 69, "label": "low_health_literacy", "original_text": "We present the clinical case of a 15-year-old male with no medical history or previous interventions, who presented to the paediatric emergency department with a history of vomiting and epigastric abdominal pain of four days' duration, remaining afebrile during the course of the illness.\n\nInitially treated as gastroenteritis, but with no improvement, and with persistence of epigastric abdominal pain and biliary vomiting, he was admitted to the emergency department for further evaluation.\n\nOn physical examination, the patient was in acceptable general condition, afebrile, with mild signs of dehydration. The abdomen was distended, without signs of peritonism and with decreased hydroaerolic sounds. The laboratory tests did not present significant findings, and an abdominal radiograph was performed with findings suggestive of intestinal obstruction.\n\nGiven the evolution, an urgent computed tomography was performed, which showed the presence of ascites and significant dilation of small intestine loops, suggesting the interposition of a small intestine loop at the beginning of the transcavity of the epiplons, with a change in caliber at the level of the hiatus of Winslow.\n\nUrgent surgical intervention was performed, initially by exploratory laparoscopy. Dilated loops of small intestine and terminal ileum, cecum and ascending colon of normal calibre but located in the right hypochondrium, with the cecum very mobile and without presenting adhesions to the right parietocolic space, were observed. Following the terminal ileum proximally, loops of small intestine of different calibre were observed from the depth of the theoretical location of the hiatus of Winslow. It was possible to pull the cecum and terminal ileum until they were displaced to the right iliac fossa, but without correctly identifying the point of change of calibre, since the interposition of the lower edge of the liver and the distension of loops of small intestine hampered the technique. An attempt was made to improve visualization by percutaneous puncture of a dilated loop to empty the gas, without improvement. To ensure the resolution of the obstructive picture, a supraumbilical mid-laparotomy was decided. When accessing the cavity, the change of calibre in the ileum was evident, about 40 centimetres from the ileocecal valve, with signs compatible with hernia of a section of about five centimetres of the ileum through the hiatus of Winslow. In both ends of the herniated loop, we observed the congestive imprint of the hiatus on the loop (Fig. 3). The normal calibre of the hiatus of Winslow was identified, so no preventive technique was performed to reduce the risk of recurrence.\n\nDuring the first days of the postoperative period, the patient presented a paralytic ileus, and the nasogastric tube could be removed five days after surgery and oral tolerance was initiated with a good response. Simultaneously, he developed a pelvic collection that was managed conservatively with antibiotics, with a good evolution. Finally, the patient was discharged ten days after the intervention, with preserved transit, remaining afebrile and with a good general state.\n\nThe patient is currently being followed up in the outpatient department of paediatric surgery.\n", "generated_summary": "A 15-year-old boy had bad belly pain and was throwing up. A CT scan showed his small intestine was blocked because a loop slipped through a small opening deep in the upper belly. Doctors first tried surgery with a small camera. They could not see well. They changed to a bigger cut down the middle above his belly button. They moved the trapped intestine back where it belongs. The intestine looked healthy, so nothing had to be removed. They did not do an extra step to try to stop this from happening again. After surgery, he got a pocket of fluid in the lower belly. It was treated with antibiotics. He is going to follow-up visits in the children\u2019s surgery clinic." }, { "index": 69, "label": "intermediate_health_literacy", "original_text": "We present the clinical case of a 15-year-old male with no medical history or previous interventions, who presented to the paediatric emergency department with a history of vomiting and epigastric abdominal pain of four days' duration, remaining afebrile during the course of the illness.\n\nInitially treated as gastroenteritis, but with no improvement, and with persistence of epigastric abdominal pain and biliary vomiting, he was admitted to the emergency department for further evaluation.\n\nOn physical examination, the patient was in acceptable general condition, afebrile, with mild signs of dehydration. The abdomen was distended, without signs of peritonism and with decreased hydroaerolic sounds. The laboratory tests did not present significant findings, and an abdominal radiograph was performed with findings suggestive of intestinal obstruction.\n\nGiven the evolution, an urgent computed tomography was performed, which showed the presence of ascites and significant dilation of small intestine loops, suggesting the interposition of a small intestine loop at the beginning of the transcavity of the epiplons, with a change in caliber at the level of the hiatus of Winslow.\n\nUrgent surgical intervention was performed, initially by exploratory laparoscopy. Dilated loops of small intestine and terminal ileum, cecum and ascending colon of normal calibre but located in the right hypochondrium, with the cecum very mobile and without presenting adhesions to the right parietocolic space, were observed. Following the terminal ileum proximally, loops of small intestine of different calibre were observed from the depth of the theoretical location of the hiatus of Winslow. It was possible to pull the cecum and terminal ileum until they were displaced to the right iliac fossa, but without correctly identifying the point of change of calibre, since the interposition of the lower edge of the liver and the distension of loops of small intestine hampered the technique. An attempt was made to improve visualization by percutaneous puncture of a dilated loop to empty the gas, without improvement. To ensure the resolution of the obstructive picture, a supraumbilical mid-laparotomy was decided. When accessing the cavity, the change of calibre in the ileum was evident, about 40 centimetres from the ileocecal valve, with signs compatible with hernia of a section of about five centimetres of the ileum through the hiatus of Winslow. In both ends of the herniated loop, we observed the congestive imprint of the hiatus on the loop (Fig. 3). The normal calibre of the hiatus of Winslow was identified, so no preventive technique was performed to reduce the risk of recurrence.\n\nDuring the first days of the postoperative period, the patient presented a paralytic ileus, and the nasogastric tube could be removed five days after surgery and oral tolerance was initiated with a good response. Simultaneously, he developed a pelvic collection that was managed conservatively with antibiotics, with a good evolution. Finally, the patient was discharged ten days after the intervention, with preserved transit, remaining afebrile and with a good general state.\n\nThe patient is currently being followed up in the outpatient department of paediatric surgery.\n", "generated_summary": "A 15-year-old male with no prior surgeries developed four days of abdominal pain and vomiting. CT suggested a small-bowel obstruction from an internal hernia through the foramen (hiatus) of Winslow, an opening behind the stomach. He underwent urgent surgery that began as a diagnostic laparoscopy but was converted to a supraumbilical midline laparotomy because the view was poor. The surgeons reduced a herniated ileal loop; the bowel looked viable, so no resection was needed. They did not perform a preventive maneuver to lower the risk of recurrence. After surgery, he developed a pelvic fluid collection that was managed with antibiotics alone. He is currently followed in the outpatient pediatric surgery clinic." }, { "index": 69, "label": "proficient_health_literacy", "original_text": "We present the clinical case of a 15-year-old male with no medical history or previous interventions, who presented to the paediatric emergency department with a history of vomiting and epigastric abdominal pain of four days' duration, remaining afebrile during the course of the illness.\n\nInitially treated as gastroenteritis, but with no improvement, and with persistence of epigastric abdominal pain and biliary vomiting, he was admitted to the emergency department for further evaluation.\n\nOn physical examination, the patient was in acceptable general condition, afebrile, with mild signs of dehydration. The abdomen was distended, without signs of peritonism and with decreased hydroaerolic sounds. The laboratory tests did not present significant findings, and an abdominal radiograph was performed with findings suggestive of intestinal obstruction.\n\nGiven the evolution, an urgent computed tomography was performed, which showed the presence of ascites and significant dilation of small intestine loops, suggesting the interposition of a small intestine loop at the beginning of the transcavity of the epiplons, with a change in caliber at the level of the hiatus of Winslow.\n\nUrgent surgical intervention was performed, initially by exploratory laparoscopy. Dilated loops of small intestine and terminal ileum, cecum and ascending colon of normal calibre but located in the right hypochondrium, with the cecum very mobile and without presenting adhesions to the right parietocolic space, were observed. Following the terminal ileum proximally, loops of small intestine of different calibre were observed from the depth of the theoretical location of the hiatus of Winslow. It was possible to pull the cecum and terminal ileum until they were displaced to the right iliac fossa, but without correctly identifying the point of change of calibre, since the interposition of the lower edge of the liver and the distension of loops of small intestine hampered the technique. An attempt was made to improve visualization by percutaneous puncture of a dilated loop to empty the gas, without improvement. To ensure the resolution of the obstructive picture, a supraumbilical mid-laparotomy was decided. When accessing the cavity, the change of calibre in the ileum was evident, about 40 centimetres from the ileocecal valve, with signs compatible with hernia of a section of about five centimetres of the ileum through the hiatus of Winslow. In both ends of the herniated loop, we observed the congestive imprint of the hiatus on the loop (Fig. 3). The normal calibre of the hiatus of Winslow was identified, so no preventive technique was performed to reduce the risk of recurrence.\n\nDuring the first days of the postoperative period, the patient presented a paralytic ileus, and the nasogastric tube could be removed five days after surgery and oral tolerance was initiated with a good response. Simultaneously, he developed a pelvic collection that was managed conservatively with antibiotics, with a good evolution. Finally, the patient was discharged ten days after the intervention, with preserved transit, remaining afebrile and with a good general state.\n\nThe patient is currently being followed up in the outpatient department of paediatric surgery.\n", "generated_summary": "A 15-year-old male with no medical history or prior interventions presented to the pediatric emergency department with 4 days of epigastric abdominal pain and bilious vomiting; he remained afebrile. Examination showed mild dehydration, abdominal distension without peritonism, and decreased hydroaeric sounds. Laboratory tests were unremarkable. An abdominal radiograph was suggestive of intestinal obstruction. Urgent CT demonstrated ascites and marked dilation of small-intestinal loops, with interposition of a small-intestinal loop at the entrance to the transcavity of the epiplons and a caliber change at the level of the hiatus (foramen) of Winslow\u2014compatible with small-bowel obstruction due to an internal hernia.\n\nUrgent exploratory laparoscopy was performed. Intraoperatively, dilated small-bowel loops were seen; the terminal ileum, cecum, and ascending colon were of normal caliber but located in the right hypochondrium, with a very mobile cecum and no adhesions to the right parietocolic space. Following the terminal ileum proximally revealed small-bowel loops of differing caliber arising from the depth of the theoretical location of the hiatus of Winslow. Traction on the cecum and terminal ileum allowed displacement toward the right iliac fossa, but the point of caliber change could not be identified due to the interposition of the inferior hepatic edge and small-bowel distension. Percutaneous puncture of a dilated loop for gas decompression did not improve visualization. To ensure definitive management, conversion to a supraumbilical midline laparotomy was undertaken. On entering the cavity, a caliber change in the ileum was evident ~40 cm from the ileocecal valve, with findings consistent with herniation of an approximately 5-cm ileal segment through the hiatus of Winslow; both ends of the herniated loop bore a congestive imprint from the hiatus. The hiatus of Winslow was of normal caliber; no preventive technique (e.g., narrowing or closure) was performed to reduce recurrence risk. The herniated loop was reduced; it appeared viable, and intestinal resection was not necessary.\n\nPostoperatively, the patient developed a paralytic ileus; the nasogastric tube was removed on postoperative day 5, and oral intake was initiated with good tolerance. A pelvic collection occurred and was managed conservatively with antibiotics, with favorable evolution. He was discharged on postoperative day 10 with preserved transit, afebrile, and in good general condition. He is being followed in the outpatient pediatric surgery clinic.\n\nContext: Internal herniation through the foramen of Winslow is an uncommon cause of small-bowel obstruction; CT identification of a transition at the foramen supports prompt operative reduction, and bowel viability often permits avoidance of resection." }, { "index": 70, "label": "low_health_literacy", "original_text": "This is a 75-year-old para 6 patient from Western Ethiopia who saw her last menses 25 years back. Her age at giving birth to her 1st child and menopause were 18 and 50 years, respectively. She had occasional pelvic pain for the last 3 years for which she was visiting different health facilities. Currently, she presented to Nekemte Specialized Hospital with exacerbation of lower abdominal pain for 3 weeks. She feels discomfort in her vagina but no protrusion of mass through her vagina. She has no history of fever, abdominal swelling, vaginal discharge, or bleeding. All her previous deliveries were normal vaginal deliveries. Upon enquiring about the history of family planning utilization, she reported that the intrauterine device was inserted 40 years back at a public hospital. Since then, she had no history of gynecologic evaluation for a checkup. She had no history of gynecologic procedures, pelvic or abdominal surgery. The patient has no history of medical problems like diabetes mellitus, hypertension, cardiac or renal problems.\n\nOn examination, she was acutely sick-looking. Her vital signs were blood pressure (BP) = 120/80mmHg, pulse rate (PR) = 82 beats per minute, respiratory rate (RR) = 18 breaths per minute, and temperature of 37.1\u00b0C. She had pink conjunctivae. Lymph glandular system, chest, and cardiovascular system were normal. On abdominal examination, there was no mass, organomegaly, area of tenderness, or signs of fluid collection. Inspection of external genitalia showed no vulvar mass or lesion. On speculum examination, there is a foreign body at the external cervical os. However, there is no other cervical mass or lesion. On bimanual examination, the uterus was not enlarged and there was no adnexal mass or tenderness. On the integumentary system, she had no palmar pallor. On neurologic examination, she was oriented to time, person, and place. She had normal reflexes and no neurologic deficits.\n\nOn laboratory investigation, an ultrasound examination was done by a radiologist and showed unremarkable pelvic findings. Urinalysis, complete blood count, and serum blood glucose level were normal. With the final diagnosis of postmenopausal pelvic pain secondary to the retained intrauterine device, the patient was prepared and taken to the gynecology procedure room. In the lithotomy position, the speculum was inserted and the intrauterine device was easily removed with spongy forceps. The mother was observed for 4 hours and discharged with analgesia and doxycycline 100 mg PO twice a day for three days. Upon follow-up, the pelvic pain was resolved.", "generated_summary": "A 75-year-old woman in Western Ethiopia had a birth control loop in her womb for 40 years. She had lower belly pain after her periods had stopped. Doctors looked inside the vagina with a small tool. They saw part of the loop at the opening of the womb. They gently pulled it out with a soft clamp. She went home with pain medicine. She also took an antibiotic called doxycycline two times a day for 3 days." }, { "index": 70, "label": "intermediate_health_literacy", "original_text": "This is a 75-year-old para 6 patient from Western Ethiopia who saw her last menses 25 years back. Her age at giving birth to her 1st child and menopause were 18 and 50 years, respectively. She had occasional pelvic pain for the last 3 years for which she was visiting different health facilities. Currently, she presented to Nekemte Specialized Hospital with exacerbation of lower abdominal pain for 3 weeks. She feels discomfort in her vagina but no protrusion of mass through her vagina. She has no history of fever, abdominal swelling, vaginal discharge, or bleeding. All her previous deliveries were normal vaginal deliveries. Upon enquiring about the history of family planning utilization, she reported that the intrauterine device was inserted 40 years back at a public hospital. Since then, she had no history of gynecologic evaluation for a checkup. She had no history of gynecologic procedures, pelvic or abdominal surgery. The patient has no history of medical problems like diabetes mellitus, hypertension, cardiac or renal problems.\n\nOn examination, she was acutely sick-looking. Her vital signs were blood pressure (BP) = 120/80mmHg, pulse rate (PR) = 82 beats per minute, respiratory rate (RR) = 18 breaths per minute, and temperature of 37.1\u00b0C. She had pink conjunctivae. Lymph glandular system, chest, and cardiovascular system were normal. On abdominal examination, there was no mass, organomegaly, area of tenderness, or signs of fluid collection. Inspection of external genitalia showed no vulvar mass or lesion. On speculum examination, there is a foreign body at the external cervical os. However, there is no other cervical mass or lesion. On bimanual examination, the uterus was not enlarged and there was no adnexal mass or tenderness. On the integumentary system, she had no palmar pallor. On neurologic examination, she was oriented to time, person, and place. She had normal reflexes and no neurologic deficits.\n\nOn laboratory investigation, an ultrasound examination was done by a radiologist and showed unremarkable pelvic findings. Urinalysis, complete blood count, and serum blood glucose level were normal. With the final diagnosis of postmenopausal pelvic pain secondary to the retained intrauterine device, the patient was prepared and taken to the gynecology procedure room. In the lithotomy position, the speculum was inserted and the intrauterine device was easily removed with spongy forceps. The mother was observed for 4 hours and discharged with analgesia and doxycycline 100 mg PO twice a day for three days. Upon follow-up, the pelvic pain was resolved.", "generated_summary": "A 75-year-old postmenopausal woman from Western Ethiopia had a Lippes loop IUD retained for 40 years and came in with pelvic pain. On speculum exam, part of the loop was seen at the external opening of the cervix. The device was removed easily with spongy forceps. She was discharged with pain medication and doxycycline twice a day for 3 days. Additional context: She reported no fever, bleeding, or vaginal discharge; her exam and pelvic ultrasound were otherwise unremarkable. She was observed for a few hours after removal, then sent home. On follow-up, her pelvic pain resolved." }, { "index": 70, "label": "proficient_health_literacy", "original_text": "This is a 75-year-old para 6 patient from Western Ethiopia who saw her last menses 25 years back. Her age at giving birth to her 1st child and menopause were 18 and 50 years, respectively. She had occasional pelvic pain for the last 3 years for which she was visiting different health facilities. Currently, she presented to Nekemte Specialized Hospital with exacerbation of lower abdominal pain for 3 weeks. She feels discomfort in her vagina but no protrusion of mass through her vagina. She has no history of fever, abdominal swelling, vaginal discharge, or bleeding. All her previous deliveries were normal vaginal deliveries. Upon enquiring about the history of family planning utilization, she reported that the intrauterine device was inserted 40 years back at a public hospital. Since then, she had no history of gynecologic evaluation for a checkup. She had no history of gynecologic procedures, pelvic or abdominal surgery. The patient has no history of medical problems like diabetes mellitus, hypertension, cardiac or renal problems.\n\nOn examination, she was acutely sick-looking. Her vital signs were blood pressure (BP) = 120/80mmHg, pulse rate (PR) = 82 beats per minute, respiratory rate (RR) = 18 breaths per minute, and temperature of 37.1\u00b0C. She had pink conjunctivae. Lymph glandular system, chest, and cardiovascular system were normal. On abdominal examination, there was no mass, organomegaly, area of tenderness, or signs of fluid collection. Inspection of external genitalia showed no vulvar mass or lesion. On speculum examination, there is a foreign body at the external cervical os. However, there is no other cervical mass or lesion. On bimanual examination, the uterus was not enlarged and there was no adnexal mass or tenderness. On the integumentary system, she had no palmar pallor. On neurologic examination, she was oriented to time, person, and place. She had normal reflexes and no neurologic deficits.\n\nOn laboratory investigation, an ultrasound examination was done by a radiologist and showed unremarkable pelvic findings. Urinalysis, complete blood count, and serum blood glucose level were normal. With the final diagnosis of postmenopausal pelvic pain secondary to the retained intrauterine device, the patient was prepared and taken to the gynecology procedure room. In the lithotomy position, the speculum was inserted and the intrauterine device was easily removed with spongy forceps. The mother was observed for 4 hours and discharged with analgesia and doxycycline 100 mg PO twice a day for three days. Upon follow-up, the pelvic pain was resolved.", "generated_summary": "A 75-year-old para 6, postmenopausal woman from Western Ethiopia (last menses 25 years prior; age at first birth 18 years; menopause at 50 years) presented to Nekemte Specialized Hospital with a 3-week exacerbation of chronic pelvic pain present for 3 years. She described vaginal discomfort without a protruding mass and denied fever, abdominal distension, vaginal discharge, or bleeding. She reported an intrauterine device inserted 40 years earlier at a public hospital and no subsequent gynecologic follow-up; there was no history of gynecologic procedures, pelvic/abdominal surgery, or chronic medical illness (no diabetes mellitus, hypertension, cardiac, or renal disease). On examination, she was acutely sick-appearing but hemodynamically stable: BP 120/80 mmHg, PR 82 bpm, RR 18 breaths/min, Temp 37.1\u00b0C. Conjunctivae were pink; lymphatic, chest, and cardiovascular exams were normal. Abdomen: no masses, organomegaly, tenderness, or fluid wave. External genitalia were normal. Speculum exam revealed a foreign body consistent with a retained Lippes loop IUD visible at the external cervical os; no other cervical lesions were noted. Bimanual exam: uterus not enlarged; no adnexal mass or tenderness. Skin showed no palmar pallor. Neurologic exam: oriented with normal reflexes and no focal deficits. Investigations included a pelvic ultrasound read as unremarkable; urinalysis, CBC, and serum glucose were normal. Working diagnosis was postmenopausal pelvic pain secondary to retained intrauterine device. In the lithotomy position, a speculum was placed and the IUD was easily removed with spongy forceps. She was observed for 4 hours and discharged on analgesia and doxycycline 100 mg PO twice daily for 3 days. At follow-up, pelvic pain had resolved. Context: The Lippes loop is an older inert plastic IUD; prolonged retention can present with pelvic pain, but in this case there was no evidence of perforation, infection, or adnexal pathology on exam or ultrasound." }, { "index": 71, "label": "low_health_literacy", "original_text": "A 71-year-old patient with a history of untreated vitiligo presented with visual loss in the right eye 6 months prior to admission accompanied by bilateral hearing loss with a predominance in the right ear. Chronic headaches and intermittent fever were also reported, although the patient denied a history of drug use or prior infections. He was evaluated by our department due to the presence of significant and unintentional weight loss, generalized weakness and thickening of the skin. On initial ophthalmologic examination, visual acuity in the right eye (RO) was reduced to light perception and color discrimination, and visual acuity in the left eye (LO) was 20/200 with afferent pupillary defect in both eyes with hyperemic margins of the eyelid. On examination of the RO, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, aqueous anterior chamber (AAC) without cellularity, normal iris and lens with nuclear opacities. On examination of the left eye, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, AAC, aqueous without cellularity, normal iris and lens with nuclear opacities. On examination of the right fundus, a round, pale ++ papilla was found with a 50% excavation, slightly blunt nasal border, with a raised and thinned vascular pattern, with macular area and scattered pigment. On the left fundus, a vitreous haze 2+ was found with edematous papilla, blurred borders, hyperemic, peripapillary, streaked hemorrhages, and an unevaluable excavation with a thinned vascular pattern and macular area with scattered pigment, with right optic atrophy and left anterior optic neuritis.\n\nDue to ocular involvement, weight loss and neurological symptoms, additional testing was performed to rule out causes such as tuberculosis, herpes, ANCA and non-ANCA vasculitis, and sarcoidosis. As for the management of the neurological condition, a lumbar puncture was performed and an opening pressure within normal limits and a proteinocracy of 54 mg/dL was found. Due to distal symmetric polyneuropathy, nerve conduction velocities (NCV) were performed, which showed a pattern of polyradiculoneuropathy with moderate to severe axonal degeneration, involving all 4 extremities with a predominance of the lower extremities; the contrasted magnetic resonance imaging (MRI) of the skull and orbit did not show enhancement of the optic nerve or brain tumors; however, it did show sinusitis and meningeal enhancement. Within the management, sarcoidosis was ruled out, with angiotensin converting enzyme (ACE) within normal parameters, as well as a whole body gamma scan, without enhancement or boosting. After all the study and clinical evaluation of the patient, a second ophthalmological assessment was performed in which persistence and progression of the ocular condition was found, with optic atrophy in the right eye and anterior optic neuritis in the left eye. Because of this, high dose pulse steroid treatment was initiated, followed by a gradual reduction of the dose and the patient was referred for follow-up in the Outpatient Department. A clinical and functional improvement was observed, mainly at the neurological and ophthalmological level.\n", "generated_summary": "A 71-year-old man had vitiligo for many years. He lost vision in his right eye about six months before he came to the hospital. He also had hearing loss in both ears, worse on the right. While in the hospital, he had ongoing headaches. He had fevers. He lost a lot of weight without trying. The eye exam showed the right eye could only sense light. The white part of the right eye looked very red. The left eye could see at 20/200, which is very blurry. The back of the right eye had small specks of color. The back of the left eye showed a swollen nerve. The nerve of the right eye looked damaged." }, { "index": 71, "label": "intermediate_health_literacy", "original_text": "A 71-year-old patient with a history of untreated vitiligo presented with visual loss in the right eye 6 months prior to admission accompanied by bilateral hearing loss with a predominance in the right ear. Chronic headaches and intermittent fever were also reported, although the patient denied a history of drug use or prior infections. He was evaluated by our department due to the presence of significant and unintentional weight loss, generalized weakness and thickening of the skin. On initial ophthalmologic examination, visual acuity in the right eye (RO) was reduced to light perception and color discrimination, and visual acuity in the left eye (LO) was 20/200 with afferent pupillary defect in both eyes with hyperemic margins of the eyelid. On examination of the RO, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, aqueous anterior chamber (AAC) without cellularity, normal iris and lens with nuclear opacities. On examination of the left eye, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, AAC, aqueous without cellularity, normal iris and lens with nuclear opacities. On examination of the right fundus, a round, pale ++ papilla was found with a 50% excavation, slightly blunt nasal border, with a raised and thinned vascular pattern, with macular area and scattered pigment. On the left fundus, a vitreous haze 2+ was found with edematous papilla, blurred borders, hyperemic, peripapillary, streaked hemorrhages, and an unevaluable excavation with a thinned vascular pattern and macular area with scattered pigment, with right optic atrophy and left anterior optic neuritis.\n\nDue to ocular involvement, weight loss and neurological symptoms, additional testing was performed to rule out causes such as tuberculosis, herpes, ANCA and non-ANCA vasculitis, and sarcoidosis. As for the management of the neurological condition, a lumbar puncture was performed and an opening pressure within normal limits and a proteinocracy of 54 mg/dL was found. Due to distal symmetric polyneuropathy, nerve conduction velocities (NCV) were performed, which showed a pattern of polyradiculoneuropathy with moderate to severe axonal degeneration, involving all 4 extremities with a predominance of the lower extremities; the contrasted magnetic resonance imaging (MRI) of the skull and orbit did not show enhancement of the optic nerve or brain tumors; however, it did show sinusitis and meningeal enhancement. Within the management, sarcoidosis was ruled out, with angiotensin converting enzyme (ACE) within normal parameters, as well as a whole body gamma scan, without enhancement or boosting. After all the study and clinical evaluation of the patient, a second ophthalmological assessment was performed in which persistence and progression of the ocular condition was found, with optic atrophy in the right eye and anterior optic neuritis in the left eye. Because of this, high dose pulse steroid treatment was initiated, followed by a gradual reduction of the dose and the patient was referred for follow-up in the Outpatient Department. A clinical and functional improvement was observed, mainly at the neurological and ophthalmological level.\n", "generated_summary": "A 71-year-old man with long-standing vitiligo reported six months of visual loss in the right eye and hearing loss in both ears, worse on the right. During hospitalization, he had chronic headaches, fever, and marked unintentional weight loss. On eye exam, the right eye was reduced to light perception and the white of the eye was notably red; the left eye had a visual acuity of 20/200. Fundus findings showed scattered pigmentation in the right eye, a swollen optic disc in the left eye, and evidence of optic atrophy on the right." }, { "index": 71, "label": "proficient_health_literacy", "original_text": "A 71-year-old patient with a history of untreated vitiligo presented with visual loss in the right eye 6 months prior to admission accompanied by bilateral hearing loss with a predominance in the right ear. Chronic headaches and intermittent fever were also reported, although the patient denied a history of drug use or prior infections. He was evaluated by our department due to the presence of significant and unintentional weight loss, generalized weakness and thickening of the skin. On initial ophthalmologic examination, visual acuity in the right eye (RO) was reduced to light perception and color discrimination, and visual acuity in the left eye (LO) was 20/200 with afferent pupillary defect in both eyes with hyperemic margins of the eyelid. On examination of the RO, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, aqueous anterior chamber (AAC) without cellularity, normal iris and lens with nuclear opacities. On examination of the left eye, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, AAC, aqueous without cellularity, normal iris and lens with nuclear opacities. On examination of the right fundus, a round, pale ++ papilla was found with a 50% excavation, slightly blunt nasal border, with a raised and thinned vascular pattern, with macular area and scattered pigment. On the left fundus, a vitreous haze 2+ was found with edematous papilla, blurred borders, hyperemic, peripapillary, streaked hemorrhages, and an unevaluable excavation with a thinned vascular pattern and macular area with scattered pigment, with right optic atrophy and left anterior optic neuritis.\n\nDue to ocular involvement, weight loss and neurological symptoms, additional testing was performed to rule out causes such as tuberculosis, herpes, ANCA and non-ANCA vasculitis, and sarcoidosis. As for the management of the neurological condition, a lumbar puncture was performed and an opening pressure within normal limits and a proteinocracy of 54 mg/dL was found. Due to distal symmetric polyneuropathy, nerve conduction velocities (NCV) were performed, which showed a pattern of polyradiculoneuropathy with moderate to severe axonal degeneration, involving all 4 extremities with a predominance of the lower extremities; the contrasted magnetic resonance imaging (MRI) of the skull and orbit did not show enhancement of the optic nerve or brain tumors; however, it did show sinusitis and meningeal enhancement. Within the management, sarcoidosis was ruled out, with angiotensin converting enzyme (ACE) within normal parameters, as well as a whole body gamma scan, without enhancement or boosting. After all the study and clinical evaluation of the patient, a second ophthalmological assessment was performed in which persistence and progression of the ocular condition was found, with optic atrophy in the right eye and anterior optic neuritis in the left eye. Because of this, high dose pulse steroid treatment was initiated, followed by a gradual reduction of the dose and the patient was referred for follow-up in the Outpatient Department. A clinical and functional improvement was observed, mainly at the neurological and ophthalmological level.\n", "generated_summary": "A 71-year-old patient with untreated, long-standing vitiligo presented with a 6-month history of right-eye visual loss and bilateral hearing loss, right-predominant. During admission he endorsed chronic headaches, intermittent fever, significant unintentional weight loss, generalized asthenia, and skin thickening. Initial ophthalmologic assessment: RO visual acuity reduced to light perception with impaired color discrimination; LO visual acuity 20/200. There was an afferent pupillary defect in both eyes and hyperemic eyelid margins. Anterior segment (both eyes): hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral nummular subepithelial infiltrates, aqueous anterior chamber without cellularity, normal iris, and lenses with nuclear opacities. Fundus, RO: pale (++) optic disc with approximately 50% excavation, slightly blunted nasal margin, attenuated/\u201craised and thinned\u201d vasculature, macular area with scattered pigment. Fundus, LO: 2+ vitreous haze; edematous, hyperemic optic disc with blurred margins; peripapillary streaked hemorrhages; excavation not assessable; thinned vasculature; macular area with scattered pigment. Impression at that time documented right optic atrophy and left anterior optic neuritis. Workup for ocular\u2013neurologic disease included evaluation to exclude tuberculosis, herpes, ANCA and non-ANCA vasculitides, and sarcoidosis. Lumbar puncture: opening pressure within normal limits; CSF protein 54 mg/dL. Nerve conduction velocities showed a polyradiculoneuropathy with moderate\u2013severe axonal degeneration involving all four extremities, greater in the lower limbs. Contrast-enhanced MRI of the brain and orbits showed no optic nerve enhancement and no intracranial masses, but did reveal sinusitis and meningeal enhancement. Sarcoidosis was further disfavored by a normal ACE level and a whole-body gamma scan without hypermetabolic foci. On repeat ophthalmologic evaluation, there was progression with persistent right optic atrophy and left anterior optic neuritis. High-dose pulse corticosteroids were initiated, followed by a taper. The patient experienced clinical and functional improvement, particularly in neurologic and ophthalmologic parameters." }, { "index": 72, "label": "low_health_literacy", "original_text": "A 39-year-old woman with a diagnosis of peripartum cardiomyopathy who received a heart transplant in October 2014. She received induction with Basiliximab and methylprednisolone. She also received maintenance treatment with tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. She had two episodes of acute rejection during the first year post-transplant, and was controlled with methylprednisolone pulse therapy with good results. There was no history of renal disease and her renal function was stable with creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m2 during the first year post-transplant. Follow-up was done exclusively by the heart transplant group and routine polyomavirus viral load BK or urinary cytology was not performed. In 2016, she presented a creatinine serum elevation of up to 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m2. At that time, the minimum tacrolimus level was 7.2 ng/mL and everolimus, 5.2 ng/mL. Anticalcineurin toxicity was suspected; therefore, tacrolimus was reduced to 4 mg daily and creatinine returned to near baseline (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m2); no renal biopsy was performed. In March 2017, creatinine increased to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2, for which she was hospitalized. The patient stated that she did not have any symptoms. During physical examination, she was in good general condition, heart rate of 80 beats per minute, blood pressure of 130/90 mmHg, respiratory rate of 15 per minute, afebrile. Further studies were performed: renal tract ultrasound showed normal renal size but increased echogenicity; urinalysis and urine cultures were negative, without haematuria, pyuria or casts; echocardiogram with adequate cardiac function; HIV, syphilis, hepatitis B and C serologic tests were negative; minimum tacrolimus level of 5.2 ng/mL, and everolimus of 5.98 ng/mL. Control was initiated with intravenous hydration, and tacrolimus XL dose was reduced to 2 mg daily, but there was no improvement in renal function; a renal biopsy was planned.\n\nRenal biopsy revealed active chronic interstitial nephritis associated with advanced poliomyelitis virus nephritis. BK virus PCR was performed and was positive at 33,800 copies/mL in blood (log 4.5). Tacrolimus was discontinued; creatinine levels stabilized between 2.2 and 2.4 mg/dL, with no further elevation in post-discharge controls. Her viral load began to decline to undetectable levels. The patient did not have episodes of cardiac rejection in 3 years of follow-up; the last creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m2.\n", "generated_summary": "She had a heart transplant because her heart got very weak after pregnancy. Later, her kidneys\u2014the body\u2019s filters\u2014were hurt by a germ called BK virus. A small kidney sample showed long\u2011lasting irritation and damage from this virus. A blood test also showed a high amount of BK virus (log 4.5). Her doctors turned down her anti\u2011rejection medicines to help. After about two years, her kidney numbers stayed steady. Her creatinine was 2.5 mg/dL and her GFR was 23.4 mL/min/1.73m2." }, { "index": 72, "label": "intermediate_health_literacy", "original_text": "A 39-year-old woman with a diagnosis of peripartum cardiomyopathy who received a heart transplant in October 2014. She received induction with Basiliximab and methylprednisolone. She also received maintenance treatment with tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. She had two episodes of acute rejection during the first year post-transplant, and was controlled with methylprednisolone pulse therapy with good results. There was no history of renal disease and her renal function was stable with creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m2 during the first year post-transplant. Follow-up was done exclusively by the heart transplant group and routine polyomavirus viral load BK or urinary cytology was not performed. In 2016, she presented a creatinine serum elevation of up to 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m2. At that time, the minimum tacrolimus level was 7.2 ng/mL and everolimus, 5.2 ng/mL. Anticalcineurin toxicity was suspected; therefore, tacrolimus was reduced to 4 mg daily and creatinine returned to near baseline (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m2); no renal biopsy was performed. In March 2017, creatinine increased to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2, for which she was hospitalized. The patient stated that she did not have any symptoms. During physical examination, she was in good general condition, heart rate of 80 beats per minute, blood pressure of 130/90 mmHg, respiratory rate of 15 per minute, afebrile. Further studies were performed: renal tract ultrasound showed normal renal size but increased echogenicity; urinalysis and urine cultures were negative, without haematuria, pyuria or casts; echocardiogram with adequate cardiac function; HIV, syphilis, hepatitis B and C serologic tests were negative; minimum tacrolimus level of 5.2 ng/mL, and everolimus of 5.98 ng/mL. Control was initiated with intravenous hydration, and tacrolimus XL dose was reduced to 2 mg daily, but there was no improvement in renal function; a renal biopsy was planned.\n\nRenal biopsy revealed active chronic interstitial nephritis associated with advanced poliomyelitis virus nephritis. BK virus PCR was performed and was positive at 33,800 copies/mL in blood (log 4.5). Tacrolimus was discontinued; creatinine levels stabilized between 2.2 and 2.4 mg/dL, with no further elevation in post-discharge controls. Her viral load began to decline to undetectable levels. The patient did not have episodes of cardiac rejection in 3 years of follow-up; the last creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m2.\n", "generated_summary": "A woman with peripartum cardiomyopathy underwent a heart transplant and later developed kidney problems due to BK virus. A kidney biopsy showed active, chronic tubulointerstitial nephritis consistent with late-stage BK virus nephropathy. Blood testing confirmed BK viremia with a viral load of log 4.5. Her immunosuppressive therapy was reduced. Over the next two years, her kidney function stabilized, with a serum creatinine of 2.5 mg/dL and an estimated GFR of 23.4 mL/min/1.73m2." }, { "index": 72, "label": "proficient_health_literacy", "original_text": "A 39-year-old woman with a diagnosis of peripartum cardiomyopathy who received a heart transplant in October 2014. She received induction with Basiliximab and methylprednisolone. She also received maintenance treatment with tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. She had two episodes of acute rejection during the first year post-transplant, and was controlled with methylprednisolone pulse therapy with good results. There was no history of renal disease and her renal function was stable with creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m2 during the first year post-transplant. Follow-up was done exclusively by the heart transplant group and routine polyomavirus viral load BK or urinary cytology was not performed. In 2016, she presented a creatinine serum elevation of up to 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m2. At that time, the minimum tacrolimus level was 7.2 ng/mL and everolimus, 5.2 ng/mL. Anticalcineurin toxicity was suspected; therefore, tacrolimus was reduced to 4 mg daily and creatinine returned to near baseline (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m2); no renal biopsy was performed. In March 2017, creatinine increased to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2, for which she was hospitalized. The patient stated that she did not have any symptoms. During physical examination, she was in good general condition, heart rate of 80 beats per minute, blood pressure of 130/90 mmHg, respiratory rate of 15 per minute, afebrile. Further studies were performed: renal tract ultrasound showed normal renal size but increased echogenicity; urinalysis and urine cultures were negative, without haematuria, pyuria or casts; echocardiogram with adequate cardiac function; HIV, syphilis, hepatitis B and C serologic tests were negative; minimum tacrolimus level of 5.2 ng/mL, and everolimus of 5.98 ng/mL. Control was initiated with intravenous hydration, and tacrolimus XL dose was reduced to 2 mg daily, but there was no improvement in renal function; a renal biopsy was planned.\n\nRenal biopsy revealed active chronic interstitial nephritis associated with advanced poliomyelitis virus nephritis. BK virus PCR was performed and was positive at 33,800 copies/mL in blood (log 4.5). Tacrolimus was discontinued; creatinine levels stabilized between 2.2 and 2.4 mg/dL, with no further elevation in post-discharge controls. Her viral load began to decline to undetectable levels. The patient did not have episodes of cardiac rejection in 3 years of follow-up; the last creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m2.\n", "generated_summary": "A 39-year-old woman with peripartum cardiomyopathy underwent orthotopic heart transplantation in October 2014. Induction was basiliximab plus methylprednisolone. Maintenance immunosuppression included tacrolimus XL 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. She had two episodes of acute rejection in the first post-transplant year, managed with methylprednisolone pulse therapy. Baseline renal function during year one was normal (creatinine 0.88 mg/dL; eGFR 102 mL/min/1.73m2). Follow-up was by the heart transplant team; routine BK polyomavirus screening (plasma PCR or urine cytology) was not performed.\n\nIn 2016, creatinine rose to 1.9 mg/dL (eGFR 32.6), with tacrolimus trough 7.2 ng/mL and everolimus 5.2 ng/mL. Calcineurin inhibitor toxicity was suspected; tacrolimus was reduced to 4 mg daily, and creatinine improved to 1.25 mg/dL (eGFR 54.1); no biopsy was obtained. In March 2017, creatinine increased to 2.69 mg/dL (eGFR 21.4) without symptoms. Vitals and exam were unremarkable; renal ultrasound showed normal size with increased echogenicity; urinalysis/culture were negative (no hematuria, pyuria, or casts); echocardiogram showed adequate cardiac function; HIV, syphilis, HBV, and HCV serologies were negative. Tacrolimus and everolimus troughs were 5.2 ng/mL and 5.98 ng/mL, respectively. Despite IV hydration and reducing tacrolimus XL to 2 mg daily, renal function did not improve, prompting biopsy.\n\nRenal biopsy demonstrated active chronic interstitial (tubulointerstitial) nephritis associated with advanced polyomavirus nephritis. Plasma BK virus PCR was positive at 33,800 copies/mL (log 4.5). Tacrolimus was discontinued; creatinine stabilized between 2.2 and 2.4 mg/dL with declining BK viremia to undetectable. Over three years, there were no further cardiac rejection episodes. At two years of follow-up from diagnosis of BKVN, renal function was stable with creatinine 2.5 mg/dL (eGFR 23.4 mL/min/1.73m2).\n\nContext: BK polyomavirus nephropathy, while classically described in kidney transplant recipients, can occur in non-renal solid organ transplant recipients under potent immunosuppression. Management centers on reduction of immunosuppression; maintaining an mTOR inhibitor (everolimus) while withdrawing the calcineurin inhibitor can aid viral clearance, at the potential cost of rejection risk, which was not observed here. Plasma BK viral load (log 4.5) plus biopsy-proven late-stage BKVN established the diagnosis and guided therapy." }, { "index": 73, "label": "low_health_literacy", "original_text": "14-year-old previously healthy adolescent who presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of a predominantly nocturnal irritative cough. Symptomatic treatment was indicated, evolving with dyspnoea and orthopnoea. He presented to the Emergency Department of the Osorno Base Hospital (OBH), with severe respiratory distress, intolerance to supine position, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU), tachycardic, hypertensive, polypneic, oxygen saturation 96% with FiO2 35%, rosy, hydrated and well perfused, with flat jugular veins, small bilateral supraclavicular lymphadenopathies. The thorax was without retraction of soft tissue, maintained in a genupectoral position, with decreased pulmonary murmurs in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The soft abdomen was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and\n\nA nephrological evaluation was performed, which confirmed renal failure secondary to tumor lysis syndrome, without dialysis urgency and tendency to hypertension, with creatinine 1.54 mg/dL, phosphemia 11 mg/dL, without hypernatremia. It continued with hyperhydration, diuretic (furosemide) and antihypertensive (amlodipine). From the respiratory point of view, it presented oxygen requirement, with FIO2 35% by mask of Venturi, suspending this supply on the third day of admission. It evolved with episodes of psychomotor agitation, associated to the diagnosis in process, which was treated according to the institutional protocol of psychomotor agitation, with psychological and psychiatric support, with satisfactory evolution. On the third day of admission and treatment a CT scan of the thorax, abdomen and pelvis was performed with contrast, observing an increase in the size of the thymus, of homogeneous aspect, probably in the context of a lymphoproliferative process and findings suggestive of pulmonary thromboembolism. The angioCT of the thorax showed thrombosis of the jugular vein, extensive bilateral pleural effusion associated to atelectatic phenomena in both bases, with signs of medical bilateral nephrosis. Anticoagulation with enoxaparin (1 mg/kg dose, every 12 hours) was indicated for twenty days. Then the angioCT of control showed resolution of the thrombosis.On the fourth day of admission and treatment, a diagnostic and extension study was performed, which included, among others, a complete biochemical profile including lipid profile, granulopoietic hyperplasia of the bone marrow (myelogram), flow cytometry (bone marrow) in which no cells with a predominant clonal or neoplastic immunophenotype of haemological lineage were observed, flow cytometry in peripheral blood negative for neoplastic cells, cytological of pleural fluid negative for neoplastic cells, flow cytometry of pleural fluid without evidence of haemological neoplasia. It was presented to the paediatric oncological committee, highlighting that it was not possible to take a biopsy of the tumour given that the mediastinal mass disappeared with the cytoreductive treatment, assuming the diagnosis of lymphoblastic lymphoma by the clinical picture and the response to treatment, according to the PINDA 0516 protocol. This protocol contemplates in Induction IA eight doses of Lasp E. coli of 10,000 IU/m2. Having received seven doses of L-asp and with a cumulative dose of ninety thousand international units plus glucocorticoid (prednisone), presented a picture of decline, vomiting, abdominal pain and mild dehydration. There was suspicion of pancreatitis, which was ruled out by normal amylase/lipase values and normal hepatic tests. At that time it had plasma electrolyte profile with hyponatraemia of 126 mOsm/kg and urinary osmolality of 510 mOsm/kg, both normal values. With hyponatraemia and hypertriglyceridaemia, there was suspicion of RAM of pseudohyponatraemia secondary to hypertriglyceridaemia associated to L-asp. It was evaluated by Gastroenterology and Endocrinology, indicating a diet low in refined sugars and rich in fiber, fibrates (ciprofibrato 100 mg oral daily) and omega 3 (4 g oral daily), until triglyceride values of 300 mg/dL were achieved. Two weeks later the triglycerides had a value of 79 mg/dL. Ciprofibrato and omega3 were suspended, indicating prophylactic use associated to corticoid and L-asp treatment. A total of twelve doses of L-asp were completed with a cumulative dose of one hundred and eighty four thousand international units corresponding to the induction protocol. The suspicion of RAM was subjected to causality evaluation, with the modified Karch and Lasagna algorithm by WHO5, which resulted in \u201cDefinitive\u201d RAM for the association of L-asp and Prednisone\n", "generated_summary": "A teenager was getting treatment for a blood cancer called non-Hodgkin lymphoma. He developed very high blood fats (triglycerides). This made a lab test say his sodium was low, even though his body sodium was okay. Think of it like the blood looked milky with fat, which can trick the test. Doctors thought this was a side effect from two cancer medicines: asparaginase and a steroid (prednisone). They used a standard checklist and decided the side effect was definitely from those medicines. He was treated with a low-fat eating plan and medicines that lower blood fats. The cancer drugs were not stopped because that part of his treatment had already reached its planned end. His blood fats went back to normal in about two weeks, and he had no problems." }, { "index": 73, "label": "intermediate_health_literacy", "original_text": "14-year-old previously healthy adolescent who presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of a predominantly nocturnal irritative cough. Symptomatic treatment was indicated, evolving with dyspnoea and orthopnoea. He presented to the Emergency Department of the Osorno Base Hospital (OBH), with severe respiratory distress, intolerance to supine position, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU), tachycardic, hypertensive, polypneic, oxygen saturation 96% with FiO2 35%, rosy, hydrated and well perfused, with flat jugular veins, small bilateral supraclavicular lymphadenopathies. The thorax was without retraction of soft tissue, maintained in a genupectoral position, with decreased pulmonary murmurs in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The soft abdomen was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and\n\nA nephrological evaluation was performed, which confirmed renal failure secondary to tumor lysis syndrome, without dialysis urgency and tendency to hypertension, with creatinine 1.54 mg/dL, phosphemia 11 mg/dL, without hypernatremia. It continued with hyperhydration, diuretic (furosemide) and antihypertensive (amlodipine). From the respiratory point of view, it presented oxygen requirement, with FIO2 35% by mask of Venturi, suspending this supply on the third day of admission. It evolved with episodes of psychomotor agitation, associated to the diagnosis in process, which was treated according to the institutional protocol of psychomotor agitation, with psychological and psychiatric support, with satisfactory evolution. On the third day of admission and treatment a CT scan of the thorax, abdomen and pelvis was performed with contrast, observing an increase in the size of the thymus, of homogeneous aspect, probably in the context of a lymphoproliferative process and findings suggestive of pulmonary thromboembolism. The angioCT of the thorax showed thrombosis of the jugular vein, extensive bilateral pleural effusion associated to atelectatic phenomena in both bases, with signs of medical bilateral nephrosis. Anticoagulation with enoxaparin (1 mg/kg dose, every 12 hours) was indicated for twenty days. Then the angioCT of control showed resolution of the thrombosis.On the fourth day of admission and treatment, a diagnostic and extension study was performed, which included, among others, a complete biochemical profile including lipid profile, granulopoietic hyperplasia of the bone marrow (myelogram), flow cytometry (bone marrow) in which no cells with a predominant clonal or neoplastic immunophenotype of haemological lineage were observed, flow cytometry in peripheral blood negative for neoplastic cells, cytological of pleural fluid negative for neoplastic cells, flow cytometry of pleural fluid without evidence of haemological neoplasia. It was presented to the paediatric oncological committee, highlighting that it was not possible to take a biopsy of the tumour given that the mediastinal mass disappeared with the cytoreductive treatment, assuming the diagnosis of lymphoblastic lymphoma by the clinical picture and the response to treatment, according to the PINDA 0516 protocol. This protocol contemplates in Induction IA eight doses of Lasp E. coli of 10,000 IU/m2. Having received seven doses of L-asp and with a cumulative dose of ninety thousand international units plus glucocorticoid (prednisone), presented a picture of decline, vomiting, abdominal pain and mild dehydration. There was suspicion of pancreatitis, which was ruled out by normal amylase/lipase values and normal hepatic tests. At that time it had plasma electrolyte profile with hyponatraemia of 126 mOsm/kg and urinary osmolality of 510 mOsm/kg, both normal values. With hyponatraemia and hypertriglyceridaemia, there was suspicion of RAM of pseudohyponatraemia secondary to hypertriglyceridaemia associated to L-asp. It was evaluated by Gastroenterology and Endocrinology, indicating a diet low in refined sugars and rich in fiber, fibrates (ciprofibrato 100 mg oral daily) and omega 3 (4 g oral daily), until triglyceride values of 300 mg/dL were achieved. Two weeks later the triglycerides had a value of 79 mg/dL. Ciprofibrato and omega3 were suspended, indicating prophylactic use associated to corticoid and L-asp treatment. A total of twelve doses of L-asp were completed with a cumulative dose of one hundred and eighty four thousand international units corresponding to the induction protocol. The suspicion of RAM was subjected to causality evaluation, with the modified Karch and Lasagna algorithm by WHO5, which resulted in \u201cDefinitive\u201d RAM for the association of L-asp and Prednisone\n", "generated_summary": "A 14-year-old treated for non-Hodgkin lymphoma developed hypertriglyceridaemia and pseudohyponatraemia after multiple doses of L-asparaginase with prednisone. Pseudohyponatraemia means the sodium result looks low because very high blood lipids interfere with the lab method; the body\u2019s actual sodium status is not truly low. Clinicians suspected an adverse drug reaction and, using the modified Karch and Lasagna causality algorithm, classified the reaction as definitive for the combination of L-asparaginase and corticosteroids. Management included diet changes (low fat/low refined sugars, high fiber) and lipid-lowering therapy with a fibrate (ciprofibrate 100 mg daily) plus omega-3 fatty acids (4 g daily). Per protocol, L-asparaginase and prednisone were not discontinued because the indicated treatment phase had reached its end; the patient completed the planned doses. Triglycerides fell to 79 mg/dL within 14 days, and the episode resolved without complications." }, { "index": 73, "label": "proficient_health_literacy", "original_text": "14-year-old previously healthy adolescent who presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of a predominantly nocturnal irritative cough. Symptomatic treatment was indicated, evolving with dyspnoea and orthopnoea. He presented to the Emergency Department of the Osorno Base Hospital (OBH), with severe respiratory distress, intolerance to supine position, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU), tachycardic, hypertensive, polypneic, oxygen saturation 96% with FiO2 35%, rosy, hydrated and well perfused, with flat jugular veins, small bilateral supraclavicular lymphadenopathies. The thorax was without retraction of soft tissue, maintained in a genupectoral position, with decreased pulmonary murmurs in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The soft abdomen was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and\n\nA nephrological evaluation was performed, which confirmed renal failure secondary to tumor lysis syndrome, without dialysis urgency and tendency to hypertension, with creatinine 1.54 mg/dL, phosphemia 11 mg/dL, without hypernatremia. It continued with hyperhydration, diuretic (furosemide) and antihypertensive (amlodipine). From the respiratory point of view, it presented oxygen requirement, with FIO2 35% by mask of Venturi, suspending this supply on the third day of admission. It evolved with episodes of psychomotor agitation, associated to the diagnosis in process, which was treated according to the institutional protocol of psychomotor agitation, with psychological and psychiatric support, with satisfactory evolution. On the third day of admission and treatment a CT scan of the thorax, abdomen and pelvis was performed with contrast, observing an increase in the size of the thymus, of homogeneous aspect, probably in the context of a lymphoproliferative process and findings suggestive of pulmonary thromboembolism. The angioCT of the thorax showed thrombosis of the jugular vein, extensive bilateral pleural effusion associated to atelectatic phenomena in both bases, with signs of medical bilateral nephrosis. Anticoagulation with enoxaparin (1 mg/kg dose, every 12 hours) was indicated for twenty days. Then the angioCT of control showed resolution of the thrombosis.On the fourth day of admission and treatment, a diagnostic and extension study was performed, which included, among others, a complete biochemical profile including lipid profile, granulopoietic hyperplasia of the bone marrow (myelogram), flow cytometry (bone marrow) in which no cells with a predominant clonal or neoplastic immunophenotype of haemological lineage were observed, flow cytometry in peripheral blood negative for neoplastic cells, cytological of pleural fluid negative for neoplastic cells, flow cytometry of pleural fluid without evidence of haemological neoplasia. It was presented to the paediatric oncological committee, highlighting that it was not possible to take a biopsy of the tumour given that the mediastinal mass disappeared with the cytoreductive treatment, assuming the diagnosis of lymphoblastic lymphoma by the clinical picture and the response to treatment, according to the PINDA 0516 protocol. This protocol contemplates in Induction IA eight doses of Lasp E. coli of 10,000 IU/m2. Having received seven doses of L-asp and with a cumulative dose of ninety thousand international units plus glucocorticoid (prednisone), presented a picture of decline, vomiting, abdominal pain and mild dehydration. There was suspicion of pancreatitis, which was ruled out by normal amylase/lipase values and normal hepatic tests. At that time it had plasma electrolyte profile with hyponatraemia of 126 mOsm/kg and urinary osmolality of 510 mOsm/kg, both normal values. With hyponatraemia and hypertriglyceridaemia, there was suspicion of RAM of pseudohyponatraemia secondary to hypertriglyceridaemia associated to L-asp. It was evaluated by Gastroenterology and Endocrinology, indicating a diet low in refined sugars and rich in fiber, fibrates (ciprofibrato 100 mg oral daily) and omega 3 (4 g oral daily), until triglyceride values of 300 mg/dL were achieved. Two weeks later the triglycerides had a value of 79 mg/dL. Ciprofibrato and omega3 were suspended, indicating prophylactic use associated to corticoid and L-asp treatment. A total of twelve doses of L-asp were completed with a cumulative dose of one hundred and eighty four thousand international units corresponding to the induction protocol. The suspicion of RAM was subjected to causality evaluation, with the modified Karch and Lasagna algorithm by WHO5, which resulted in \u201cDefinitive\u201d RAM for the association of L-asp and Prednisone\n", "generated_summary": "A 14-year-old with suspected lymphoblastic non-Hodgkin lymphoma on protocolized induction (PINDA 0516) received L-asp E. coli 10,000 IU/m2 plus a glucocorticoid (prednisone). After seven doses of L-asp (cumulative ~90,000 IU) he developed clinical decline with vomiting, abdominal pain, and mild dehydration. Pancreatitis was suspected but excluded (amylase/lipase normal; liver tests normal). Laboratory assessment showed hyponatraemia (reported as 126 mOsm/kg) with urinary osmolality 510 mOsm/kg and concurrent hypertriglyceridaemia, prompting the diagnosis of pseudohyponatraemia secondary to hypertriglyceridaemia associated with L-asp plus corticosteroids. He was managed by Gastroenterology and Endocrinology with a diet low in refined sugars and rich in fiber, fibrates (ciprofibrato/ciprofibrate 100 mg PO daily), and omega-3 fatty acids (4 g PO daily), targeting triglycerides \u2264300 mg/dL. Two weeks later triglycerides were 79 mg/dL; ciprofibrato and omega-3 were discontinued with advice for prophylactic use during subsequent corticosteroid/L-asp exposure. The patient ultimately completed 12 total doses of L-asp (cumulative 184,000 IU) for induction; L-asp and prednisone were not discontinued due to the end of indication per protocol. Causality assessment for the adverse drug reaction (ADR) using the modified Karch and Lasagna algorithm (WHO) was Definitive for the association of L-asp plus prednisone. No complications occurred, and the hypertriglyceridaemia resolved within 14 days. Mechanistically, L-asparaginase can reduce lipoprotein lipase activity and increase VLDL, while corticosteroids augment hepatic VLDL production; marked lipaemia then produces pseudohyponatraemia via indirect ion-selective electrode dilutional error, with normalization as triglycerides fall." }, { "index": 74, "label": "low_health_literacy", "original_text": "A 56-year-old Italian female patient with \u03b2-thalassemia major presented to the radiology department to undergo MRI to quantify myocardial, hepatic, and pancreatic iron deposition. The clinical history of the patient included a transfusion-dependent \u03b2-thalassemia condition (genotype HBB:c.118C\u2009>\u2009T/ HBB:c.93-21G\u2009>\u2009A), diagnosed at the age of 7 years, despite the fact that the first transfusion was carried out at 2 years. As a consequence of \u03b2-thalassemia, the patient underwent splenectomy and cholecystectomy.\n\nAt the moment of MRI, she had a negative HCV-RNA (Hepatitis C virus-Ribonucleic acid) test, no osteoporosis or other endocrine, cardiac, or hepatic complications, and good iron levels. The patient\u2019s therapy included iron chelation with deferasirox, vitamin D, and luspatercept, an erythropoiesis modulator started 2 years before the MRI examination (good response, with an increase of about 35% of transfusion interval duration). Transfusion therapy included two units of concentrated and filtered red blood cells every 25 days with pre-transfusion hemoglobin values of 10\u201310.5 g/dl.\n\nOn MRI, a solid mass with lobulated and regular contours was incidentally identified within the prevascular compartment of the mediastinum.\n\nThe lesion was mildly hyperintense on T2-weighted images (T2-wi) and isointense on T1-wi. The mediastinal mass in question was discernible in a prior MRI examination conducted for the same purpose in 2020 before starting luspatercept therapy, albeit with a marginal enlargement.\n\nThere were no other apparent abnormalities observed in the remaining mediastinal compartments. No pleural or pericardial effusions were present.\n\nThe neurological examination was unremarkable, and in the preceding months, the patient exhibited no symptoms of mediastinal syndrome associated with compression of the adjacent neurovascular structures. Moreover, she did not exhibit any fever or experience any weight loss.\n\nFor further evaluation, the patient underwent 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) and chest CT with contrast media. On PET-CT, the mediastinal mass showed only mild FDG uptake (SUVmax\u2009=\u20094.3); no other sites of abnormal radiotracer uptake were reported in the neck, chest, abdomen, and skeleton. On CT images, the lesion presented regular margins, solid density, and mild contrast enhancement. The adjacent structures did not exhibit any signs of invasion, and lymphadenopathies or extra-thoracic disease were not present. Such radiological features, the indolent behaviour over time, the absence of systemic symptoms, and the lack of avid FDG uptake on PET-CT scan made the diagnosis of thymoma probable.\n\nHowever, on lung window visualization, multiple rounded areas of parenchymal lucency, consistent with thin-walled cysts distributed symmetrically throughout both lungs, with normal intervening parenchyma, were evident.\n\nNo nodules or other interstitial abnormalities were associated with the cysts. No pneumothorax was detected. Coherently with thalassemic bone disease, the ribs appeared widened, and the spine displayed mild platyspondyly. The remaining portion of the chest and visible upper abdomen were unremarkable. The radiological findings were consistent with cystic lung disease, most likely LAM.\n\nThe patient was then referred to the pulmonary clinic for further evaluation. She was a never-smoker and did not report any respiratory symptoms. In particular, she denied a history of chronic cough, recurrent respiratory infections, or pneumothorax. No cutaneous lesions, notably facial fibrofolliculomas, were evident. On chest examination, the lung fields were clear. Peripheral capillary oxygen saturation was normal (98%), with a heart rate of 75 beats per minute. Pulmonary function tests revealed a substantial reduction in diffusing capacity of the lungs for carbon monoxide (DLCO; 42% of the predicted value), partly imputable to the condition of anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of the predicted value. After discussion in a multidisciplinary tumor board setting, including a pulmonologist, the patient underwent left thoracoscopic thymectomy and concomitant lingual segment wedge resection. The histopathological report revealed a morphological finding and immunohistochemical pattern referable to type B2 thymoma with focal infiltration of the capsule. Extracapsular extension was not evident. However, the lesion was present at the resection margin (stage IIa according to Masaoka\u2013Koga; stage 1a according to the tumor, node, metastasis [TNM] classification).\n\nRegarding the lung parenchyma, histopathologic analysis described lung parenchyma with cysts of variable size lined by spindle cells in myoid habit with immunohistochemical reactivity for actin, estrogen, progesterone receptors, and HMB45 (focal positivity). Modest chronic interstitial inflammation, vascular congestion, and recent blood extravasation were evident. These morphological findings were compatible with pulmonary LAM.\n\nA final histological diagnosis of thymoma and pulmonary LAM was made. For the neoplastic condition, the patient was a candidate for adjuvant radiation therapy due to the microscopically incomplete resection (R1). For LAM with concomitant \u03b2-thalassemia, treatment with sirolimus was recommended.", "generated_summary": "A 56-year-old Italian woman has a serious inherited blood problem that needs regular transfusions. She had an MRI to check iron in her heart, liver, and pancreas. At that time, her heart, liver, and hormone health were okay. She was taking an iron-removing medicine, vitamin D, and a medicine that helps her body make red blood cells. The MRI also spotted a lump in the middle of her chest, in front of the heart, where the thymus sits. A PET scan showed the lump was only a little active. A chest CT showed many thin-walled air pockets like bubbles in both lungs. This pattern fits a rare lung disease called LAM. A team of doctors reviewed her case. She had keyhole surgery to remove the thymus lump and a small wedge of lung. Lab tests showed the chest lump was a thymus tumor called thymoma. The lung tissue showed LAM. After surgery, her doctors advised radiation to the chest area and a medicine called sirolimus for LAM." }, { "index": 74, "label": "intermediate_health_literacy", "original_text": "A 56-year-old Italian female patient with \u03b2-thalassemia major presented to the radiology department to undergo MRI to quantify myocardial, hepatic, and pancreatic iron deposition. The clinical history of the patient included a transfusion-dependent \u03b2-thalassemia condition (genotype HBB:c.118C\u2009>\u2009T/ HBB:c.93-21G\u2009>\u2009A), diagnosed at the age of 7 years, despite the fact that the first transfusion was carried out at 2 years. As a consequence of \u03b2-thalassemia, the patient underwent splenectomy and cholecystectomy.\n\nAt the moment of MRI, she had a negative HCV-RNA (Hepatitis C virus-Ribonucleic acid) test, no osteoporosis or other endocrine, cardiac, or hepatic complications, and good iron levels. The patient\u2019s therapy included iron chelation with deferasirox, vitamin D, and luspatercept, an erythropoiesis modulator started 2 years before the MRI examination (good response, with an increase of about 35% of transfusion interval duration). Transfusion therapy included two units of concentrated and filtered red blood cells every 25 days with pre-transfusion hemoglobin values of 10\u201310.5 g/dl.\n\nOn MRI, a solid mass with lobulated and regular contours was incidentally identified within the prevascular compartment of the mediastinum.\n\nThe lesion was mildly hyperintense on T2-weighted images (T2-wi) and isointense on T1-wi. The mediastinal mass in question was discernible in a prior MRI examination conducted for the same purpose in 2020 before starting luspatercept therapy, albeit with a marginal enlargement.\n\nThere were no other apparent abnormalities observed in the remaining mediastinal compartments. No pleural or pericardial effusions were present.\n\nThe neurological examination was unremarkable, and in the preceding months, the patient exhibited no symptoms of mediastinal syndrome associated with compression of the adjacent neurovascular structures. Moreover, she did not exhibit any fever or experience any weight loss.\n\nFor further evaluation, the patient underwent 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) and chest CT with contrast media. On PET-CT, the mediastinal mass showed only mild FDG uptake (SUVmax\u2009=\u20094.3); no other sites of abnormal radiotracer uptake were reported in the neck, chest, abdomen, and skeleton. On CT images, the lesion presented regular margins, solid density, and mild contrast enhancement. The adjacent structures did not exhibit any signs of invasion, and lymphadenopathies or extra-thoracic disease were not present. Such radiological features, the indolent behaviour over time, the absence of systemic symptoms, and the lack of avid FDG uptake on PET-CT scan made the diagnosis of thymoma probable.\n\nHowever, on lung window visualization, multiple rounded areas of parenchymal lucency, consistent with thin-walled cysts distributed symmetrically throughout both lungs, with normal intervening parenchyma, were evident.\n\nNo nodules or other interstitial abnormalities were associated with the cysts. No pneumothorax was detected. Coherently with thalassemic bone disease, the ribs appeared widened, and the spine displayed mild platyspondyly. The remaining portion of the chest and visible upper abdomen were unremarkable. The radiological findings were consistent with cystic lung disease, most likely LAM.\n\nThe patient was then referred to the pulmonary clinic for further evaluation. She was a never-smoker and did not report any respiratory symptoms. In particular, she denied a history of chronic cough, recurrent respiratory infections, or pneumothorax. No cutaneous lesions, notably facial fibrofolliculomas, were evident. On chest examination, the lung fields were clear. Peripheral capillary oxygen saturation was normal (98%), with a heart rate of 75 beats per minute. Pulmonary function tests revealed a substantial reduction in diffusing capacity of the lungs for carbon monoxide (DLCO; 42% of the predicted value), partly imputable to the condition of anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of the predicted value. After discussion in a multidisciplinary tumor board setting, including a pulmonologist, the patient underwent left thoracoscopic thymectomy and concomitant lingual segment wedge resection. The histopathological report revealed a morphological finding and immunohistochemical pattern referable to type B2 thymoma with focal infiltration of the capsule. Extracapsular extension was not evident. However, the lesion was present at the resection margin (stage IIa according to Masaoka\u2013Koga; stage 1a according to the tumor, node, metastasis [TNM] classification).\n\nRegarding the lung parenchyma, histopathologic analysis described lung parenchyma with cysts of variable size lined by spindle cells in myoid habit with immunohistochemical reactivity for actin, estrogen, progesterone receptors, and HMB45 (focal positivity). Modest chronic interstitial inflammation, vascular congestion, and recent blood extravasation were evident. These morphological findings were compatible with pulmonary LAM.\n\nA final histological diagnosis of thymoma and pulmonary LAM was made. For the neoplastic condition, the patient was a candidate for adjuvant radiation therapy due to the microscopically incomplete resection (R1). For LAM with concomitant \u03b2-thalassemia, treatment with sirolimus was recommended.", "generated_summary": "A 56-year-old Italian woman with transfusion-dependent beta-thalassemia major (with prior splenectomy and cholecystectomy) underwent MRI to measure iron in the heart, liver, and pancreas. At the time of imaging, she had no significant endocrine, cardiac, or hepatic complications and was taking deferasirox, vitamin D, and luspatercept. The MRI incidentally revealed a lobulated mass in the prevascular mediastinum. PET showed only mild FDG uptake, and chest CT identified multiple thin-walled cysts throughout both lungs, a pattern consistent with lymphangioleiomyomatosis (LAM). After multidisciplinary review, she had thoracoscopic thymectomy and a lung wedge resection. Pathology confirmed type B2 thymoma and pulmonary LAM. Based on these findings, adjuvant radiation therapy was recommended for the thymoma, and sirolimus was advised for LAM." }, { "index": 74, "label": "proficient_health_literacy", "original_text": "A 56-year-old Italian female patient with \u03b2-thalassemia major presented to the radiology department to undergo MRI to quantify myocardial, hepatic, and pancreatic iron deposition. The clinical history of the patient included a transfusion-dependent \u03b2-thalassemia condition (genotype HBB:c.118C\u2009>\u2009T/ HBB:c.93-21G\u2009>\u2009A), diagnosed at the age of 7 years, despite the fact that the first transfusion was carried out at 2 years. As a consequence of \u03b2-thalassemia, the patient underwent splenectomy and cholecystectomy.\n\nAt the moment of MRI, she had a negative HCV-RNA (Hepatitis C virus-Ribonucleic acid) test, no osteoporosis or other endocrine, cardiac, or hepatic complications, and good iron levels. The patient\u2019s therapy included iron chelation with deferasirox, vitamin D, and luspatercept, an erythropoiesis modulator started 2 years before the MRI examination (good response, with an increase of about 35% of transfusion interval duration). Transfusion therapy included two units of concentrated and filtered red blood cells every 25 days with pre-transfusion hemoglobin values of 10\u201310.5 g/dl.\n\nOn MRI, a solid mass with lobulated and regular contours was incidentally identified within the prevascular compartment of the mediastinum.\n\nThe lesion was mildly hyperintense on T2-weighted images (T2-wi) and isointense on T1-wi. The mediastinal mass in question was discernible in a prior MRI examination conducted for the same purpose in 2020 before starting luspatercept therapy, albeit with a marginal enlargement.\n\nThere were no other apparent abnormalities observed in the remaining mediastinal compartments. No pleural or pericardial effusions were present.\n\nThe neurological examination was unremarkable, and in the preceding months, the patient exhibited no symptoms of mediastinal syndrome associated with compression of the adjacent neurovascular structures. Moreover, she did not exhibit any fever or experience any weight loss.\n\nFor further evaluation, the patient underwent 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) and chest CT with contrast media. On PET-CT, the mediastinal mass showed only mild FDG uptake (SUVmax\u2009=\u20094.3); no other sites of abnormal radiotracer uptake were reported in the neck, chest, abdomen, and skeleton. On CT images, the lesion presented regular margins, solid density, and mild contrast enhancement. The adjacent structures did not exhibit any signs of invasion, and lymphadenopathies or extra-thoracic disease were not present. Such radiological features, the indolent behaviour over time, the absence of systemic symptoms, and the lack of avid FDG uptake on PET-CT scan made the diagnosis of thymoma probable.\n\nHowever, on lung window visualization, multiple rounded areas of parenchymal lucency, consistent with thin-walled cysts distributed symmetrically throughout both lungs, with normal intervening parenchyma, were evident.\n\nNo nodules or other interstitial abnormalities were associated with the cysts. No pneumothorax was detected. Coherently with thalassemic bone disease, the ribs appeared widened, and the spine displayed mild platyspondyly. The remaining portion of the chest and visible upper abdomen were unremarkable. The radiological findings were consistent with cystic lung disease, most likely LAM.\n\nThe patient was then referred to the pulmonary clinic for further evaluation. She was a never-smoker and did not report any respiratory symptoms. In particular, she denied a history of chronic cough, recurrent respiratory infections, or pneumothorax. No cutaneous lesions, notably facial fibrofolliculomas, were evident. On chest examination, the lung fields were clear. Peripheral capillary oxygen saturation was normal (98%), with a heart rate of 75 beats per minute. Pulmonary function tests revealed a substantial reduction in diffusing capacity of the lungs for carbon monoxide (DLCO; 42% of the predicted value), partly imputable to the condition of anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of the predicted value. After discussion in a multidisciplinary tumor board setting, including a pulmonologist, the patient underwent left thoracoscopic thymectomy and concomitant lingual segment wedge resection. The histopathological report revealed a morphological finding and immunohistochemical pattern referable to type B2 thymoma with focal infiltration of the capsule. Extracapsular extension was not evident. However, the lesion was present at the resection margin (stage IIa according to Masaoka\u2013Koga; stage 1a according to the tumor, node, metastasis [TNM] classification).\n\nRegarding the lung parenchyma, histopathologic analysis described lung parenchyma with cysts of variable size lined by spindle cells in myoid habit with immunohistochemical reactivity for actin, estrogen, progesterone receptors, and HMB45 (focal positivity). Modest chronic interstitial inflammation, vascular congestion, and recent blood extravasation were evident. These morphological findings were compatible with pulmonary LAM.\n\nA final histological diagnosis of thymoma and pulmonary LAM was made. For the neoplastic condition, the patient was a candidate for adjuvant radiation therapy due to the microscopically incomplete resection (R1). For LAM with concomitant \u03b2-thalassemia, treatment with sirolimus was recommended.", "generated_summary": "A 56-year-old Italian female with transfusion-dependent \u03b2-thalassemia major (genotype HBB:c.118C > T/HBB:c.93-21G > A), diagnosed at age 7 years with first transfusion at age 2, presented for MRI quantification of myocardial, hepatic, and pancreatic iron. Past history included splenectomy and cholecystectomy. At the time of MRI, HCV-RNA was negative; there were no osteoporosis or other endocrine, cardiac, or hepatic complications; and iron levels were good. Ongoing therapy included deferasirox, vitamin D, and luspatercept started 2 years prior with a good response (approximately 35% increase in transfusion interval). Transfusion regimen was two units of concentrated, filtered RBCs every 25 days with pre-transfusion hemoglobin 10\u201310.5 g/dL.\nOn MRI, an incidental solid mass with lobulated, regular contours was identified in the prevascular mediastinum. The lesion was mildly hyperintense on T2-weighted imaging and isointense on T1-weighted imaging. It had been visible on a prior MRI in 2020 (before luspatercept) with marginal enlargement over time. No other mediastinal abnormalities and no pleural or pericardial effusions were present. Neurological examination was unremarkable, and there were no symptoms of mediastinal compression, fever, or weight loss.\nFurther evaluation with 18F-FDG PET-CT and contrast-enhanced chest CT showed mild FDG uptake of the mediastinal mass (SUVmax 4.3) with no other abnormal uptake in the neck, chest, abdomen, or skeleton. On CT, the mass had regular margins, solid density, mild contrast enhancement, no invasion of adjacent structures, and no lymphadenopathies or extra-thoracic disease. Lung window images revealed multiple, symmetrically distributed, thin-walled cysts with normal intervening parenchyma, without nodules, additional interstitial abnormalities, or pneumothorax. Skeletal findings coherent with thalassemic bone disease included widened ribs and mild platyspondyly. Overall, these findings were consistent with cystic lung disease, most likely lymphangioleiomyomatosis (LAM).\nPulmonary evaluation noted a never-smoker with no respiratory symptoms, no history of chronic cough, recurrent infections, or pneumothorax, and no cutaneous lesions such as facial fibrofolliculomas. Lung fields were clear on exam; SpO2 was 98% and heart rate 75 bpm. Pulmonary function testing showed reduced DLCO at 42% predicted, partially attributable to anemia, with KCO at 73% predicted.\nAfter multidisciplinary tumor board discussion (including a pulmonologist), the patient underwent left thoracoscopic thymectomy with concomitant lingual segment wedge resection. Histopathology demonstrated a type B2 thymoma with focal capsular infiltration, no extracapsular extension, but tumor at the resection margin (R1), corresponding to Masaoka\u2013Koga stage IIa and TNM stage 1a. Lung parenchyma showed cysts of variable size lined by spindle cells with myoid habit and immunohistochemical reactivity for actin, estrogen and progesterone receptors, and focal HMB45 positivity, with modest chronic interstitial inflammation, vascular congestion, and recent blood extravasation, consistent with pulmonary LAM.\nFinal diagnosis: type B2 thymoma and pulmonary LAM. Management recommendations included adjuvant radiation therapy for the microscopically incomplete thymoma resection (R1) and sirolimus for LAM in the context of concomitant \u03b2-thalassemia.\nContextual considerations: B2 thymoma with R1 margins is generally managed with adjuvant radiotherapy to reduce local recurrence risk. LAM is a cystic lung disease characterized by aberrant smooth muscle-like cell proliferation with mTOR pathway activation; sirolimus (an mTOR inhibitor) is standard therapy to stabilize lung function and reduce disease progression. Luspatercept, an erythroid maturation agent, can reduce transfusion burden in transfusion-dependent \u03b2-thalassemia, as reflected by the patient\u2019s 35% prolongation of the transfusion interval." }, { "index": 75, "label": "low_health_literacy", "original_text": "We present a case of a 49-year-old woman with renal and heart failure following a long-term (lasting from 13\u2009years of age) SLE prepared for kidney transplantation. Due to LN (class III, then IV), starting at childhood, she was treated with steroids, together with cyclophosphamide, replaced later by methotrexate and then azathioprine. Hence, the partial remission of nephrotic syndrome was achieved and from 2002 the patient did not receive any immunosuppressive therapy. She was also HBV and HCV positive. SLE involvement of circulatory system presented with early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at the age of 20. In 2007, because of deterioration of kidney function with a serum creatinine concentration of 2.2\u2009mg/dL and proteinuria of 2\u2009g/day, the kidney biopsy was performed. The biopsy showed active and sclerotic focal proliferative lupus nephritis nevertheless immunosuppressive therapy was not introduced for the reason of active replication of HCV. The kidney function was gradually deteriorating over time. Despite cardiac intervention (PCI RCA), the patient developed severe post-infarction and dilated cardiomyopathy and required ICD implantation in primary prevention in 2009. Later, on lupus and secondary cardiomyopathic background, the patient developed severe MV and TV regurgitation. For this reason, the patient underwent mitral and tricuspid valve repair and left ventricle volume reduction surgery complicated by low cardiac output syndrome with a need for intra-aortic balloon pump use (2014). In the postoperative period, the kidney function deteriorated, requiring the initiation of renal replacement therapy. The patient has been on dialysis for 4\u2009years. While being on active waiting list for kidney transplantation presented remission of laboratory indices of lupus (complement splits within normal limits: C3\u20130,93\u2009g/l, C4\u20130,4\u2009g/l, ANA negative) and persisting circulatory insufficiency with markedly reduced stair-climbing capacity (to one flight of stairs) with elevated BNP 619\u2009pg/ml (n. 0\u2013100). In transthoracic echocardiography, performed before renal transplantation, the left ventricle and the left atrium were significantly enlarged and the left ventricular systolic function was significantly reduced with LVEF 26% and GLS -3. Due to the implantation of the mitral ring, it was not possible to assess the left ventricular diastolic function. The high tricuspid regurgitant flow gradient with widened and poorly respiratory mobile inferior vena cava indicated a high probability of pulmonary hypertension. Furthermore, while preparing the patient for the surgical procedure, it was decided to include cardioprotective therapy with Levosimendan. Due to the time frame associated with the transplantation procedure, the drug infusion was started as soon as possible after cross-match results were known, immediately after the dialysis session. The infusion at a dose of 0.1\u2009\u03bcg/kg/min was continued after surgery for a total of 24\u2009h. The patient\u2019s anesthesia for kidney transplantation and perioperative care included the aspect of optimizing transplanted kidney perfusion, avoiding the use of renal toxic drugs and those excreted by properly functioning kidneys, as well as the use of nephroprotective agents. Because of the patient\u2019s cardiological burden, including recurrent episodes of extrasystole proceeding with decompensation of the circulatory system, together with the need of ICD turning off for the transplantation period, the Swan-Ganz catheter for hemodynamic assessment was not used. Anesthesia monitoring was limited the to ECG, central catheter with CVP assessment, direct blood pressure measurement from the cannula inserted into the radial artery, and cardiac ultrasound. In the perioperative period the CVP parameter was used to assess the volatility, and in the postoperative period, a cardiac ultrasound was used along with the assessment of VCI respiratory fill and motility. The therapy was aimed at the standard of fluid therapy called Goal Directed Therapy (GDT). During general anesthesia, fentanyl, triacrium, propofol, desflurane, antibiotic therapy, and standard immunosuppressive treatment were used as well as 25\u2009g of mannitol infusion was administered as a nephroprotective treatment and 0.9% NaCl as a fluid therapy. In the course of postoperative immunosuppression, she received steroids, tacrolimus with mycophenolate mofetil which was stopped due to persistent leukopenia and cytomegalovirus infection. Furthermore delayed graft function was observed with a need for hemodialysis for almost 6\u2009weeks (mostly due to fluid retention). BNP levels raised to 2996\u2009pg/ml and then slowly decreased. The kidney biopsy performed 2\u2009weeks after transplantation revealed acute rejection (AR II B Banff 2015) with ATN. Finally, the patient was discharged from the hospital on the 67th POD with the serum creatinine concentration of 1.4\u2009mg/dL and BNP level of 1794\u2009pg/ml. One month after kidney transplantation, there was a reduction in left ventricular dimensions, improved systolic function in the EF (increase to 30%) and GLS (decrease to \u2212\u20096) assessment. In addition, there was a decrease in the tricuspid regurgitant flow gradient with normal width and respiratory motility of the IVC, which indicates a low probability of pulmonary hypertension. The improvement of echocardiographic parameters also reflected the simultaneous improvement of exercise capacity in the recipient from NYHA III/IV to NYHA II. In the 5-month observation, further improvement of heart function with a drop of BNP to 1066\u2009pg/ml and normal kidney function were noted.", "generated_summary": "This story is about a 49-year-old woman who had lupus for many years. Over time, her kidneys and her heart got weaker. She needed dialysis to do the work of her kidneys for 4 years until she could get a kidney transplant. Her heart pump was very weak before surgery. To help her heart get through the operation, doctors gave her a heart-helping medicine called levosimendan. The time after surgery had some ups and downs. But she got through it. At about one month after surgery, her heart started to work better, and her new kidney worked normally. At about five months, her heart kept improving, and her kidney function stayed normal." }, { "index": 75, "label": "intermediate_health_literacy", "original_text": "We present a case of a 49-year-old woman with renal and heart failure following a long-term (lasting from 13\u2009years of age) SLE prepared for kidney transplantation. Due to LN (class III, then IV), starting at childhood, she was treated with steroids, together with cyclophosphamide, replaced later by methotrexate and then azathioprine. Hence, the partial remission of nephrotic syndrome was achieved and from 2002 the patient did not receive any immunosuppressive therapy. She was also HBV and HCV positive. SLE involvement of circulatory system presented with early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at the age of 20. In 2007, because of deterioration of kidney function with a serum creatinine concentration of 2.2\u2009mg/dL and proteinuria of 2\u2009g/day, the kidney biopsy was performed. The biopsy showed active and sclerotic focal proliferative lupus nephritis nevertheless immunosuppressive therapy was not introduced for the reason of active replication of HCV. The kidney function was gradually deteriorating over time. Despite cardiac intervention (PCI RCA), the patient developed severe post-infarction and dilated cardiomyopathy and required ICD implantation in primary prevention in 2009. Later, on lupus and secondary cardiomyopathic background, the patient developed severe MV and TV regurgitation. For this reason, the patient underwent mitral and tricuspid valve repair and left ventricle volume reduction surgery complicated by low cardiac output syndrome with a need for intra-aortic balloon pump use (2014). In the postoperative period, the kidney function deteriorated, requiring the initiation of renal replacement therapy. The patient has been on dialysis for 4\u2009years. While being on active waiting list for kidney transplantation presented remission of laboratory indices of lupus (complement splits within normal limits: C3\u20130,93\u2009g/l, C4\u20130,4\u2009g/l, ANA negative) and persisting circulatory insufficiency with markedly reduced stair-climbing capacity (to one flight of stairs) with elevated BNP 619\u2009pg/ml (n. 0\u2013100). In transthoracic echocardiography, performed before renal transplantation, the left ventricle and the left atrium were significantly enlarged and the left ventricular systolic function was significantly reduced with LVEF 26% and GLS -3. Due to the implantation of the mitral ring, it was not possible to assess the left ventricular diastolic function. The high tricuspid regurgitant flow gradient with widened and poorly respiratory mobile inferior vena cava indicated a high probability of pulmonary hypertension. Furthermore, while preparing the patient for the surgical procedure, it was decided to include cardioprotective therapy with Levosimendan. Due to the time frame associated with the transplantation procedure, the drug infusion was started as soon as possible after cross-match results were known, immediately after the dialysis session. The infusion at a dose of 0.1\u2009\u03bcg/kg/min was continued after surgery for a total of 24\u2009h. The patient\u2019s anesthesia for kidney transplantation and perioperative care included the aspect of optimizing transplanted kidney perfusion, avoiding the use of renal toxic drugs and those excreted by properly functioning kidneys, as well as the use of nephroprotective agents. Because of the patient\u2019s cardiological burden, including recurrent episodes of extrasystole proceeding with decompensation of the circulatory system, together with the need of ICD turning off for the transplantation period, the Swan-Ganz catheter for hemodynamic assessment was not used. Anesthesia monitoring was limited the to ECG, central catheter with CVP assessment, direct blood pressure measurement from the cannula inserted into the radial artery, and cardiac ultrasound. In the perioperative period the CVP parameter was used to assess the volatility, and in the postoperative period, a cardiac ultrasound was used along with the assessment of VCI respiratory fill and motility. The therapy was aimed at the standard of fluid therapy called Goal Directed Therapy (GDT). During general anesthesia, fentanyl, triacrium, propofol, desflurane, antibiotic therapy, and standard immunosuppressive treatment were used as well as 25\u2009g of mannitol infusion was administered as a nephroprotective treatment and 0.9% NaCl as a fluid therapy. In the course of postoperative immunosuppression, she received steroids, tacrolimus with mycophenolate mofetil which was stopped due to persistent leukopenia and cytomegalovirus infection. Furthermore delayed graft function was observed with a need for hemodialysis for almost 6\u2009weeks (mostly due to fluid retention). BNP levels raised to 2996\u2009pg/ml and then slowly decreased. The kidney biopsy performed 2\u2009weeks after transplantation revealed acute rejection (AR II B Banff 2015) with ATN. Finally, the patient was discharged from the hospital on the 67th POD with the serum creatinine concentration of 1.4\u2009mg/dL and BNP level of 1794\u2009pg/ml. One month after kidney transplantation, there was a reduction in left ventricular dimensions, improved systolic function in the EF (increase to 30%) and GLS (decrease to \u2212\u20096) assessment. In addition, there was a decrease in the tricuspid regurgitant flow gradient with normal width and respiratory motility of the IVC, which indicates a low probability of pulmonary hypertension. The improvement of echocardiographic parameters also reflected the simultaneous improvement of exercise capacity in the recipient from NYHA III/IV to NYHA II. In the 5-month observation, further improvement of heart function with a drop of BNP to 1066\u2009pg/ml and normal kidney function were noted.", "generated_summary": "A 49-year-old woman had long-standing lupus that gradually led to kidney failure and heart failure. She was on dialysis for four years while waiting for a kidney transplant. Because her heart\u2019s pumping ability was extremely weak before surgery, the team used levosimendan to support her heart around the time of the transplant.\n\nRecovery was difficult but ultimately successful. Early on, she needed extra support, yet by about one month after transplant her heart function had begun to improve, and her kidney function was normal. At five months, her heart function continued to improve, and her kidney function remained normal." }, { "index": 75, "label": "proficient_health_literacy", "original_text": "We present a case of a 49-year-old woman with renal and heart failure following a long-term (lasting from 13\u2009years of age) SLE prepared for kidney transplantation. Due to LN (class III, then IV), starting at childhood, she was treated with steroids, together with cyclophosphamide, replaced later by methotrexate and then azathioprine. Hence, the partial remission of nephrotic syndrome was achieved and from 2002 the patient did not receive any immunosuppressive therapy. She was also HBV and HCV positive. SLE involvement of circulatory system presented with early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at the age of 20. In 2007, because of deterioration of kidney function with a serum creatinine concentration of 2.2\u2009mg/dL and proteinuria of 2\u2009g/day, the kidney biopsy was performed. The biopsy showed active and sclerotic focal proliferative lupus nephritis nevertheless immunosuppressive therapy was not introduced for the reason of active replication of HCV. The kidney function was gradually deteriorating over time. Despite cardiac intervention (PCI RCA), the patient developed severe post-infarction and dilated cardiomyopathy and required ICD implantation in primary prevention in 2009. Later, on lupus and secondary cardiomyopathic background, the patient developed severe MV and TV regurgitation. For this reason, the patient underwent mitral and tricuspid valve repair and left ventricle volume reduction surgery complicated by low cardiac output syndrome with a need for intra-aortic balloon pump use (2014). In the postoperative period, the kidney function deteriorated, requiring the initiation of renal replacement therapy. The patient has been on dialysis for 4\u2009years. While being on active waiting list for kidney transplantation presented remission of laboratory indices of lupus (complement splits within normal limits: C3\u20130,93\u2009g/l, C4\u20130,4\u2009g/l, ANA negative) and persisting circulatory insufficiency with markedly reduced stair-climbing capacity (to one flight of stairs) with elevated BNP 619\u2009pg/ml (n. 0\u2013100). In transthoracic echocardiography, performed before renal transplantation, the left ventricle and the left atrium were significantly enlarged and the left ventricular systolic function was significantly reduced with LVEF 26% and GLS -3. Due to the implantation of the mitral ring, it was not possible to assess the left ventricular diastolic function. The high tricuspid regurgitant flow gradient with widened and poorly respiratory mobile inferior vena cava indicated a high probability of pulmonary hypertension. Furthermore, while preparing the patient for the surgical procedure, it was decided to include cardioprotective therapy with Levosimendan. Due to the time frame associated with the transplantation procedure, the drug infusion was started as soon as possible after cross-match results were known, immediately after the dialysis session. The infusion at a dose of 0.1\u2009\u03bcg/kg/min was continued after surgery for a total of 24\u2009h. The patient\u2019s anesthesia for kidney transplantation and perioperative care included the aspect of optimizing transplanted kidney perfusion, avoiding the use of renal toxic drugs and those excreted by properly functioning kidneys, as well as the use of nephroprotective agents. Because of the patient\u2019s cardiological burden, including recurrent episodes of extrasystole proceeding with decompensation of the circulatory system, together with the need of ICD turning off for the transplantation period, the Swan-Ganz catheter for hemodynamic assessment was not used. Anesthesia monitoring was limited the to ECG, central catheter with CVP assessment, direct blood pressure measurement from the cannula inserted into the radial artery, and cardiac ultrasound. In the perioperative period the CVP parameter was used to assess the volatility, and in the postoperative period, a cardiac ultrasound was used along with the assessment of VCI respiratory fill and motility. The therapy was aimed at the standard of fluid therapy called Goal Directed Therapy (GDT). During general anesthesia, fentanyl, triacrium, propofol, desflurane, antibiotic therapy, and standard immunosuppressive treatment were used as well as 25\u2009g of mannitol infusion was administered as a nephroprotective treatment and 0.9% NaCl as a fluid therapy. In the course of postoperative immunosuppression, she received steroids, tacrolimus with mycophenolate mofetil which was stopped due to persistent leukopenia and cytomegalovirus infection. Furthermore delayed graft function was observed with a need for hemodialysis for almost 6\u2009weeks (mostly due to fluid retention). BNP levels raised to 2996\u2009pg/ml and then slowly decreased. The kidney biopsy performed 2\u2009weeks after transplantation revealed acute rejection (AR II B Banff 2015) with ATN. Finally, the patient was discharged from the hospital on the 67th POD with the serum creatinine concentration of 1.4\u2009mg/dL and BNP level of 1794\u2009pg/ml. One month after kidney transplantation, there was a reduction in left ventricular dimensions, improved systolic function in the EF (increase to 30%) and GLS (decrease to \u2212\u20096) assessment. In addition, there was a decrease in the tricuspid regurgitant flow gradient with normal width and respiratory motility of the IVC, which indicates a low probability of pulmonary hypertension. The improvement of echocardiographic parameters also reflected the simultaneous improvement of exercise capacity in the recipient from NYHA III/IV to NYHA II. In the 5-month observation, further improvement of heart function with a drop of BNP to 1066\u2009pg/ml and normal kidney function were noted.", "generated_summary": "We report a 49-year-old woman with end-stage renal disease and advanced heart failure secondary to long-standing systemic lupus erythematosus (SLE, onset at age 13) and lupus nephritis (LN class III, then IV). Childhood LN was treated with steroids plus cyclophosphamide, later transitioned to methotrexate and then azathioprine, achieving partial remission of nephrotic syndrome; she had no immunosuppression after 2002. She was HBV- and HCV-positive. Cardiovascular SLE involvement included early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at age 20. In 2007, with creatinine 2.2 mg/dL and proteinuria 2 g/day, kidney biopsy showed active and sclerotic focal proliferative LN; immunosuppression was withheld due to active HCV replication. Renal function progressively declined. Despite PCI to the RCA, she developed severe post-infarction and dilated cardiomyopathy, requiring primary-prevention ICD implantation in 2009. On a lupus and secondary cardiomyopathic background, she developed severe mitral and tricuspid regurgitation. In 2014 she underwent mitral and tricuspid valve repair and left ventricular volume reduction surgery, complicated by low cardiac output syndrome necessitating intra-aortic balloon pump support. Postoperatively, renal function worsened, prompting initiation of renal replacement therapy; she remained on dialysis for four years.\n\nWhile listed for kidney transplantation, laboratory indices indicated lupus remission (C3 0.93 g/L, C4 0.4 g/L, ANA negative) but persistent circulatory insufficiency with markedly reduced functional capacity (limited to one flight of stairs) and elevated BNP 619 pg/mL (n 0\u2013100). Pre-transplant transthoracic echocardiography demonstrated markedly enlarged LV and LA, severely reduced LV systolic function (LVEF 26%, GLS \u22123). Mitral ring precluded diastolic assessment. High tricuspid regurgitant flow gradient with a dilated, poorly respiratory mobile IVC suggested high probability of pulmonary hypertension.\n\nGiven the extremely low ejection fraction, cardioprotective therapy with levosimendan (a calcium sensitizer/inodilator) was instituted perioperatively. Due to transplant timing constraints, infusion (0.1 \u03bcg/kg/min) began as soon as crossmatch results were available, immediately post-dialysis, and was continued through the operation for a total of 24 h. Anesthetic management prioritized optimization of allograft perfusion, avoidance of nephrotoxins and renally excreted agents, and use of nephroprotective measures. Because of recurrent extrasystoles with prior decompensation and the need to deactivate the ICD during transplantation, a Swan-Ganz catheter was not placed. Monitoring included ECG, central venous catheter with CVP, invasive arterial blood pressure via radial arterial cannula, and cardiac ultrasound. CVP guided intravascular volume during anesthesia, and postoperative assessments incorporated focused cardiac ultrasound with IVC diameter and respirophasic variability. Fluid management followed a Goal Directed Therapy paradigm. Agents included fentanyl, triacrium, propofol, desflurane, antibiotic prophylaxis, standard immunosuppression, mannitol 25 g for nephroprotection, and 0.9% NaCl for fluid therapy.\n\nPostoperatively, immunosuppression comprised steroids and tacrolimus; mycophenolate mofetil was discontinued due to persistent leukopenia and cytomegalovirus infection. Delayed graft function occurred, necessitating hemodialysis for almost six weeks (largely due to fluid retention). BNP rose to 2996 pg/mL and then gradually declined. Allograft biopsy at postoperative week two revealed acute rejection (AR II B, Banff 2015) with acute tubular necrosis. She was discharged on postoperative day 67 with serum creatinine 1.4 mg/dL and BNP 1794 pg/mL.\n\nAt one month post-transplant, echocardiography showed reduced LV dimensions and improved systolic performance (EF increased to 30%, GLS to \u22126). Tricuspid regurgitant gradient decreased, and IVC caliber and respirophasic motion normalized, indicating low probability of pulmonary hypertension. Functional status improved from NYHA III/IV to NYHA II. At five months, there was continued cardiac improvement with BNP down to 1066 pg/mL and normalization of renal function. Overall, despite a nontrivial postoperative course, perioperative levosimendan support and tailored hemodynamic and nephroprotective strategies were associated with successful kidney transplantation, progressive recovery of LV function, and stable, normal allograft function at short-term follow-up." }, { "index": 76, "label": "low_health_literacy", "original_text": "The patient was a 42-year-old woman with a history of menstrual migraine, Hashimoto Thyroiditis, Familial Mediterian Fever (FMF), and dyspepsia. She was taking 75 mg of levothyroxine, 30 mg of lansoprazole, and 1.5 mg of colchicine daily. In February of 2023, she was diagnosed with acute bronchitis, which was treated with antibiotics and bronchodilators. She developed a daily headache after two weeks, manifesting as more than ten short-lasting attacks per day provoked by coughing, straining, and lifting. The duration of each attack was 30 minutes, and the pain was bilaterally distributed from the neck to the top of the head. The headache was sharp and severe. She described the attack as a sensation of storm-like fluid movement in the head. She did not suffer any of the symptoms associated with previous migraine attacks, such as phonophobia, photophobia, vomiting, or throbbing. The severity of the attack was determined using a numeric rating scale (NRS) with a score of 9 out of 10. These attacks typically necessitated a visit to the emergency room. The results of her physical and neurological exams were unremarkable. The laboratory tests, including those for thyroid hormones, electrolytes, liver and kidney function, and serology, were negative. Brain and cervical spinal magnetic resonance imaging (MRI) with and without contrast, magnetic resonance venography (MRV), and angiography (MRA) were all normal. She did not give consent for a lumbar puncture. When we first encountered her in the clinic, she was taking 25 mg of indomethacin per day. Her attacks stopped after putting her on 60 mg of lansoprazole and increasing her daily dose of indomethacin to 150 mg. However, she encountered gastrointestinal side effects, so the indomethacin was discontinued on day three. Due to the adverse effects, she was unable to take topiramate and propranolol.\n\nShe came to the clinic 15 days after her initial visit with an NRS score of 9/10. She was taken to the local operating room. We used a GE Healthcare, Voluson\u2122 E6, ultrasonography system with a linear 13\u20135 MHz probe for unilateral PGONB. The patient\u2019s neck was prone to flexion. The linear probe was initially transversely positioned on the occipital protuberance and then advanced caudally, demonstrating that the C2 spinous process resembled the two horns. Through lateral probe movement, the inferior muscles of the obliquus capitis and semispinalis capitis were located. Here, the superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle were identified to be the greater occipital neuron (GON). From this location, a 22-gauge spinal needle and 3 ccs of bupivacaine at a concentration of 0.5% were used to perform GON blocking. The intensity of her attack decreased from 9/10 to 2/10 after the first 20 minutes of the block. Throughout a month, the blocks were repeated once a week. In the second month, the frequency of her attacks decreased to two per month, with an intensity of 4/10. She did not encounter any attacks in the sixth month.\n\n", "generated_summary": "A 42-year-old woman had a hard-to-treat headache condition. Headache pills made her feel sick, so she could not take them. She came to the clinic with very strong pain, 9 out of 10. We took her to a small operating room. We used ultrasound, like a live picture, to guide a numbing shot to a nerve at the back of her head. The numbing medicine made her pain drop to 2 out of 10 within minutes. We repeated the same shot once a week for four weeks. After two months, her headaches happened less often and hurt less. She had no side effects." }, { "index": 76, "label": "intermediate_health_literacy", "original_text": "The patient was a 42-year-old woman with a history of menstrual migraine, Hashimoto Thyroiditis, Familial Mediterian Fever (FMF), and dyspepsia. She was taking 75 mg of levothyroxine, 30 mg of lansoprazole, and 1.5 mg of colchicine daily. In February of 2023, she was diagnosed with acute bronchitis, which was treated with antibiotics and bronchodilators. She developed a daily headache after two weeks, manifesting as more than ten short-lasting attacks per day provoked by coughing, straining, and lifting. The duration of each attack was 30 minutes, and the pain was bilaterally distributed from the neck to the top of the head. The headache was sharp and severe. She described the attack as a sensation of storm-like fluid movement in the head. She did not suffer any of the symptoms associated with previous migraine attacks, such as phonophobia, photophobia, vomiting, or throbbing. The severity of the attack was determined using a numeric rating scale (NRS) with a score of 9 out of 10. These attacks typically necessitated a visit to the emergency room. The results of her physical and neurological exams were unremarkable. The laboratory tests, including those for thyroid hormones, electrolytes, liver and kidney function, and serology, were negative. Brain and cervical spinal magnetic resonance imaging (MRI) with and without contrast, magnetic resonance venography (MRV), and angiography (MRA) were all normal. She did not give consent for a lumbar puncture. When we first encountered her in the clinic, she was taking 25 mg of indomethacin per day. Her attacks stopped after putting her on 60 mg of lansoprazole and increasing her daily dose of indomethacin to 150 mg. However, she encountered gastrointestinal side effects, so the indomethacin was discontinued on day three. Due to the adverse effects, she was unable to take topiramate and propranolol.\n\nShe came to the clinic 15 days after her initial visit with an NRS score of 9/10. She was taken to the local operating room. We used a GE Healthcare, Voluson\u2122 E6, ultrasonography system with a linear 13\u20135 MHz probe for unilateral PGONB. The patient\u2019s neck was prone to flexion. The linear probe was initially transversely positioned on the occipital protuberance and then advanced caudally, demonstrating that the C2 spinous process resembled the two horns. Through lateral probe movement, the inferior muscles of the obliquus capitis and semispinalis capitis were located. Here, the superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle were identified to be the greater occipital neuron (GON). From this location, a 22-gauge spinal needle and 3 ccs of bupivacaine at a concentration of 0.5% were used to perform GON blocking. The intensity of her attack decreased from 9/10 to 2/10 after the first 20 minutes of the block. Throughout a month, the blocks were repeated once a week. In the second month, the frequency of her attacks decreased to two per month, with an intensity of 4/10. She did not encounter any attacks in the sixth month.\n\n", "generated_summary": "A 42-year-old woman with primary cough headache could not tolerate oral medications because of side effects. She presented in an acute attack with pain rated 9/10 and was taken to a local operating room. An ultrasound-guided proximal greater occipital nerve block was performed using a local anesthetic. Her pain fell to 2/10 shortly after the injection. The block was repeated once weekly for one month. At two months, both the frequency and intensity of her headaches had decreased, and no adverse effects were observed." }, { "index": 76, "label": "proficient_health_literacy", "original_text": "The patient was a 42-year-old woman with a history of menstrual migraine, Hashimoto Thyroiditis, Familial Mediterian Fever (FMF), and dyspepsia. She was taking 75 mg of levothyroxine, 30 mg of lansoprazole, and 1.5 mg of colchicine daily. In February of 2023, she was diagnosed with acute bronchitis, which was treated with antibiotics and bronchodilators. She developed a daily headache after two weeks, manifesting as more than ten short-lasting attacks per day provoked by coughing, straining, and lifting. The duration of each attack was 30 minutes, and the pain was bilaterally distributed from the neck to the top of the head. The headache was sharp and severe. She described the attack as a sensation of storm-like fluid movement in the head. She did not suffer any of the symptoms associated with previous migraine attacks, such as phonophobia, photophobia, vomiting, or throbbing. The severity of the attack was determined using a numeric rating scale (NRS) with a score of 9 out of 10. These attacks typically necessitated a visit to the emergency room. The results of her physical and neurological exams were unremarkable. The laboratory tests, including those for thyroid hormones, electrolytes, liver and kidney function, and serology, were negative. Brain and cervical spinal magnetic resonance imaging (MRI) with and without contrast, magnetic resonance venography (MRV), and angiography (MRA) were all normal. She did not give consent for a lumbar puncture. When we first encountered her in the clinic, she was taking 25 mg of indomethacin per day. Her attacks stopped after putting her on 60 mg of lansoprazole and increasing her daily dose of indomethacin to 150 mg. However, she encountered gastrointestinal side effects, so the indomethacin was discontinued on day three. Due to the adverse effects, she was unable to take topiramate and propranolol.\n\nShe came to the clinic 15 days after her initial visit with an NRS score of 9/10. She was taken to the local operating room. We used a GE Healthcare, Voluson\u2122 E6, ultrasonography system with a linear 13\u20135 MHz probe for unilateral PGONB. The patient\u2019s neck was prone to flexion. The linear probe was initially transversely positioned on the occipital protuberance and then advanced caudally, demonstrating that the C2 spinous process resembled the two horns. Through lateral probe movement, the inferior muscles of the obliquus capitis and semispinalis capitis were located. Here, the superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle were identified to be the greater occipital neuron (GON). From this location, a 22-gauge spinal needle and 3 ccs of bupivacaine at a concentration of 0.5% were used to perform GON blocking. The intensity of her attack decreased from 9/10 to 2/10 after the first 20 minutes of the block. Throughout a month, the blocks were repeated once a week. In the second month, the frequency of her attacks decreased to two per month, with an intensity of 4/10. She did not encounter any attacks in the sixth month.\n\n", "generated_summary": "A 42-year-old woman with a history of menstrual migraine, Hashimoto thyroiditis, familial Mediterranean fever, and dyspepsia developed daily, short-lasting headache attacks approximately two weeks after an episode of acute bronchitis treated with antibiotics and bronchodilators. Attacks were provoked by coughing, straining, and lifting; occurred more than ten times per day; lasted about 30 minutes; were bilaterally distributed from the neck to the vertex; and were described as sharp, severe, with a sensation of storm-like fluid movement. She denied prior migraine-associated symptoms (no phonophobia, photophobia, vomiting, or throbbing). Neurological examination and laboratory studies (thyroid hormones, electrolytes, liver/kidney function, serologies) were unremarkable. Brain and cervical spine MRI with and without contrast, MRV, and MRA were normal. She declined lumbar puncture. At initial clinic contact, she was taking indomethacin 25 mg/day; increasing indomethacin to 150 mg/day with lansoprazole 60 mg/day aborted attacks, but gastrointestinal adverse effects led to discontinuation on day 3. She was unable to take topiramate and propranolol due to adverse effects. Fifteen days later she returned with an NRS 9/10 attack and was brought to the local operating room for an ultrasound-guided proximal greater occipital nerve block (PGONB). Using a GE Healthcare Voluson E6 system with a 13\u20135 MHz linear probe, the patient was positioned prone with neck flexed. The probe was placed transversely at the external occipital protuberance and moved caudally to identify the C2 spinous process (\u201ctwo horns\u201d appearance). Via lateral probe movement, the obliquus capitis inferior and semispinalis capitis were visualized; the greater occipital nerve was identified superior to the obliquus capitis inferior and beneath the semispinalis capitis. A 22-gauge spinal needle was advanced, and 3 mL of 0.5% bupivacaine was injected for GON blockade. Pain intensity decreased from 9/10 to 2/10 within 20 minutes. The block was repeated weekly for one month. By the second month, attack frequency decreased to two per month with intensity 4/10; no adverse effects were observed. At month six, she reported no further attacks." }, { "index": 77, "label": "low_health_literacy", "original_text": "Patient information\nA 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, and body mas index (BMI) 28.24) presented with pain in the back of the left thigh for the past 5 weeks and underwent pharmacological and physiotherapeutic intervention; however, he did not responded well to symptomatic treatment. He reported that the symptoms first appeared during a short sprint while playing soccer and heard a pop in the back of his thigh. The pain was so bad that he withdrew from the game soon after his injury and noted no bruising on the back of his thigh or significant swelling in that area. However, he reported progressive loss of flexibility in the left knee and inability to flex and extend the knee joint while the knee remained flexed at a 15\u00b0 angle, whether standing or having the leg in the air. He denied any previous history of lower back pain but could barely support the weight of the affected limb. There was no history of alcohol, smoking, diabetes, high blood pressure, or other serious genetic diseases.\n\nClinical findings and diagnostic assessment\nThe patient reported having received icing and elevation of the affected leg while lying down following the injury as therapeutic interventions. He had a crepe bandage applied to his affected thigh to support him while standing and walking. He used crutches for ambulation and to go for a little longer distance. To climb the stairs, he had to use one step at a time, relying on his right lower extremity. He also reported adopting a sitting position at the edge of the chair as direct pressure on the thigh from the chair caused him discomfort. He denied ever hurting his legs or back in sports. As a result, the patient withdrew from all activities, such as playing sports, owing to the pain, and his knee was mildly bent most of the time. Despite taking medication (nonsteroidal antiinflammatory drugs (NSAIDs)), the pain worsened over time. Since the patient did not respond well to cryotherapy, compression bandages, and medications, he decided to see a doctor for further diagnosis and treatment before meeting with us.\n\nOn further evaluation, he presented with limited knee extension and flexion and exhibited an analgesic gait with a reduced heel strike phase. Active range of motion (AROM) of the left knee was 10\u201315\u00b0 compared with 0\u2013130\u00b0degrees in the right knee. Palpation revealed tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles.\n\nManual muscle testing and isometrics could not be performed owing to persistent discomfort. The patient reported pain at rest, rated 5/10, and during activity it was rated 7/10. Further, clinical evaluation rule out lumbar disc involvement or gluteal and ischial tunnel syndrome [4, 6].\n\nThe best way to screen nerve tension for peripheral pain in the lower extremities is with a slump test [17]. However, the result of the slump test in this patient was negative.\n\nTherapeutic interventions\nDespite the patient\u2019s current clinical presentation, which was suggestive of HSI, the authors decided to treat him with neural glide technique on the basis of the structural and functional proximity of nerve to the lower limb flexibility through a novel neurodynamic tension technique [18, 19]. The scientific rationale for this neural approach was detailed to the patient and consent was obtained.\n\nThe patient was directed to sit with arms folded behind his back and knees and ankles held in extension and dorsiflexion, respectively, while a therapist guided the patient to flex his thoracic and cervical spine and extend his knee joint to the maximum tolerable limit. Next, the patient was instructed to move his neck forward and backward as much as possible while also moving his ankle up and down 15 times to help with nerve glide.\n\nThis was done in three sets each day. The therapist then helped the patient bend their middle and upper back as much as possible until the patient felt pain in the knee area. Then, the process was repeated. By the 3rd day, the patient\u2019s active knee extension improved from 5\u00b0 to 10\u00b0 and then to a 15\u00b0 degree bent position. In addition, the standing posture also got better.\n\nSubsequently, the patient was instructed in executing a set of posture re-education workouts, which involved doing active chin flexion, engaging in passive stretching of the cervical extensors while lying down in prone, and building up the shoulder retractors, arm from positions T to Y, then from Y to W with the limb\u2019s weight while lying down.\n\nTo address the kyphotic posture, active chest stretches were taught at wall corners. The patient was instructed to increase the duration of the exercises from 5 to 10 seconds, doing 10 reps and 3 sets daily.\n\nOutcomes and follow-up\nThe results were assessed using a numeric pain rating scale (NPRS) and Knee Society score (KSS). Substantial enhancement in clinical outcome measures such as pain and function were achieved within 3 successive days of therapy. The use of pain medication was discontinued.\n\nThe patient continued his self-neural glides and postural reduction exercises at home and was advised for a follow-up after 4 weeks or to contact us if symptoms worsened. On the 3rd follow-up day, the patient\u2019s NPRS from 5 at rest and 7 with activity to 2 at rest and 4 with activity. The KSS increased from 22 to 61 and from 30 to 80 in the functional domain. At the end of the 2-week home program, the patient reported to have full active straight leg raise (SLR). The patient had fully recovered from his knee dysfunction and pain at the 2-month follow-up.", "generated_summary": "Who: A 20-year-old Arabic man who practices martial arts. Problem: Pain in the back of his left thigh for 5 weeks. He tried medicines and physical therapy, but they did not help. Doctors said it was not a trapped-nerve problem in the hamstring. He stopped all sports. Treatment: He did a gentle seated nerve-glide exercise four times a day for three days in a row. He also learned better posture. Pain before treatment: 5 out of 10 at rest. 7 out of 10 with activity. Pain after 3 days: 2 out of 10 at rest. 4 out of 10 with activity. Knee scores got better. Pain part went from 22 to 61. Function part went from 30 to 80. After 2 months, he felt fully recovered and returned to sports with no problems." }, { "index": 77, "label": "intermediate_health_literacy", "original_text": "Patient information\nA 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, and body mas index (BMI) 28.24) presented with pain in the back of the left thigh for the past 5 weeks and underwent pharmacological and physiotherapeutic intervention; however, he did not responded well to symptomatic treatment. He reported that the symptoms first appeared during a short sprint while playing soccer and heard a pop in the back of his thigh. The pain was so bad that he withdrew from the game soon after his injury and noted no bruising on the back of his thigh or significant swelling in that area. However, he reported progressive loss of flexibility in the left knee and inability to flex and extend the knee joint while the knee remained flexed at a 15\u00b0 angle, whether standing or having the leg in the air. He denied any previous history of lower back pain but could barely support the weight of the affected limb. There was no history of alcohol, smoking, diabetes, high blood pressure, or other serious genetic diseases.\n\nClinical findings and diagnostic assessment\nThe patient reported having received icing and elevation of the affected leg while lying down following the injury as therapeutic interventions. He had a crepe bandage applied to his affected thigh to support him while standing and walking. He used crutches for ambulation and to go for a little longer distance. To climb the stairs, he had to use one step at a time, relying on his right lower extremity. He also reported adopting a sitting position at the edge of the chair as direct pressure on the thigh from the chair caused him discomfort. He denied ever hurting his legs or back in sports. As a result, the patient withdrew from all activities, such as playing sports, owing to the pain, and his knee was mildly bent most of the time. Despite taking medication (nonsteroidal antiinflammatory drugs (NSAIDs)), the pain worsened over time. Since the patient did not respond well to cryotherapy, compression bandages, and medications, he decided to see a doctor for further diagnosis and treatment before meeting with us.\n\nOn further evaluation, he presented with limited knee extension and flexion and exhibited an analgesic gait with a reduced heel strike phase. Active range of motion (AROM) of the left knee was 10\u201315\u00b0 compared with 0\u2013130\u00b0degrees in the right knee. Palpation revealed tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles.\n\nManual muscle testing and isometrics could not be performed owing to persistent discomfort. The patient reported pain at rest, rated 5/10, and during activity it was rated 7/10. Further, clinical evaluation rule out lumbar disc involvement or gluteal and ischial tunnel syndrome [4, 6].\n\nThe best way to screen nerve tension for peripheral pain in the lower extremities is with a slump test [17]. However, the result of the slump test in this patient was negative.\n\nTherapeutic interventions\nDespite the patient\u2019s current clinical presentation, which was suggestive of HSI, the authors decided to treat him with neural glide technique on the basis of the structural and functional proximity of nerve to the lower limb flexibility through a novel neurodynamic tension technique [18, 19]. The scientific rationale for this neural approach was detailed to the patient and consent was obtained.\n\nThe patient was directed to sit with arms folded behind his back and knees and ankles held in extension and dorsiflexion, respectively, while a therapist guided the patient to flex his thoracic and cervical spine and extend his knee joint to the maximum tolerable limit. Next, the patient was instructed to move his neck forward and backward as much as possible while also moving his ankle up and down 15 times to help with nerve glide.\n\nThis was done in three sets each day. The therapist then helped the patient bend their middle and upper back as much as possible until the patient felt pain in the knee area. Then, the process was repeated. By the 3rd day, the patient\u2019s active knee extension improved from 5\u00b0 to 10\u00b0 and then to a 15\u00b0 degree bent position. In addition, the standing posture also got better.\n\nSubsequently, the patient was instructed in executing a set of posture re-education workouts, which involved doing active chin flexion, engaging in passive stretching of the cervical extensors while lying down in prone, and building up the shoulder retractors, arm from positions T to Y, then from Y to W with the limb\u2019s weight while lying down.\n\nTo address the kyphotic posture, active chest stretches were taught at wall corners. The patient was instructed to increase the duration of the exercises from 5 to 10 seconds, doing 10 reps and 3 sets daily.\n\nOutcomes and follow-up\nThe results were assessed using a numeric pain rating scale (NPRS) and Knee Society score (KSS). Substantial enhancement in clinical outcome measures such as pain and function were achieved within 3 successive days of therapy. The use of pain medication was discontinued.\n\nThe patient continued his self-neural glides and postural reduction exercises at home and was advised for a follow-up after 4 weeks or to contact us if symptoms worsened. On the 3rd follow-up day, the patient\u2019s NPRS from 5 at rest and 7 with activity to 2 at rest and 4 with activity. The KSS increased from 22 to 61 and from 30 to 80 in the functional domain. At the end of the 2-week home program, the patient reported to have full active straight leg raise (SLR). The patient had fully recovered from his knee dysfunction and pain at the 2-month follow-up.", "generated_summary": "A 20-year-old Arabic male martial artist had 5 weeks of left hamstring pain after a sports injury and did not improve with medications or physiotherapy. Hamstring syndrome was ruled out, and he stopped all sports during recovery. Intervention: a modified slump mobilization (a seated nerve-gliding technique) was performed with four repetitions on 3 consecutive days, along with postural retraining. Outcomes: Pain on the numeric pain rating scale improved from 5/10 at rest and 7/10 with activity to 2/10 at rest and 4/10 with activity by day 3. The Knee Society Score also improved: pain from 22 to 61 and function from 30 to 80. At 2 months, he reported complete symptom resolution and returned to sports without limitation." }, { "index": 77, "label": "proficient_health_literacy", "original_text": "Patient information\nA 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, and body mas index (BMI) 28.24) presented with pain in the back of the left thigh for the past 5 weeks and underwent pharmacological and physiotherapeutic intervention; however, he did not responded well to symptomatic treatment. He reported that the symptoms first appeared during a short sprint while playing soccer and heard a pop in the back of his thigh. The pain was so bad that he withdrew from the game soon after his injury and noted no bruising on the back of his thigh or significant swelling in that area. However, he reported progressive loss of flexibility in the left knee and inability to flex and extend the knee joint while the knee remained flexed at a 15\u00b0 angle, whether standing or having the leg in the air. He denied any previous history of lower back pain but could barely support the weight of the affected limb. There was no history of alcohol, smoking, diabetes, high blood pressure, or other serious genetic diseases.\n\nClinical findings and diagnostic assessment\nThe patient reported having received icing and elevation of the affected leg while lying down following the injury as therapeutic interventions. He had a crepe bandage applied to his affected thigh to support him while standing and walking. He used crutches for ambulation and to go for a little longer distance. To climb the stairs, he had to use one step at a time, relying on his right lower extremity. He also reported adopting a sitting position at the edge of the chair as direct pressure on the thigh from the chair caused him discomfort. He denied ever hurting his legs or back in sports. As a result, the patient withdrew from all activities, such as playing sports, owing to the pain, and his knee was mildly bent most of the time. Despite taking medication (nonsteroidal antiinflammatory drugs (NSAIDs)), the pain worsened over time. Since the patient did not respond well to cryotherapy, compression bandages, and medications, he decided to see a doctor for further diagnosis and treatment before meeting with us.\n\nOn further evaluation, he presented with limited knee extension and flexion and exhibited an analgesic gait with a reduced heel strike phase. Active range of motion (AROM) of the left knee was 10\u201315\u00b0 compared with 0\u2013130\u00b0degrees in the right knee. Palpation revealed tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles.\n\nManual muscle testing and isometrics could not be performed owing to persistent discomfort. The patient reported pain at rest, rated 5/10, and during activity it was rated 7/10. Further, clinical evaluation rule out lumbar disc involvement or gluteal and ischial tunnel syndrome [4, 6].\n\nThe best way to screen nerve tension for peripheral pain in the lower extremities is with a slump test [17]. However, the result of the slump test in this patient was negative.\n\nTherapeutic interventions\nDespite the patient\u2019s current clinical presentation, which was suggestive of HSI, the authors decided to treat him with neural glide technique on the basis of the structural and functional proximity of nerve to the lower limb flexibility through a novel neurodynamic tension technique [18, 19]. The scientific rationale for this neural approach was detailed to the patient and consent was obtained.\n\nThe patient was directed to sit with arms folded behind his back and knees and ankles held in extension and dorsiflexion, respectively, while a therapist guided the patient to flex his thoracic and cervical spine and extend his knee joint to the maximum tolerable limit. Next, the patient was instructed to move his neck forward and backward as much as possible while also moving his ankle up and down 15 times to help with nerve glide.\n\nThis was done in three sets each day. The therapist then helped the patient bend their middle and upper back as much as possible until the patient felt pain in the knee area. Then, the process was repeated. By the 3rd day, the patient\u2019s active knee extension improved from 5\u00b0 to 10\u00b0 and then to a 15\u00b0 degree bent position. In addition, the standing posture also got better.\n\nSubsequently, the patient was instructed in executing a set of posture re-education workouts, which involved doing active chin flexion, engaging in passive stretching of the cervical extensors while lying down in prone, and building up the shoulder retractors, arm from positions T to Y, then from Y to W with the limb\u2019s weight while lying down.\n\nTo address the kyphotic posture, active chest stretches were taught at wall corners. The patient was instructed to increase the duration of the exercises from 5 to 10 seconds, doing 10 reps and 3 sets daily.\n\nOutcomes and follow-up\nThe results were assessed using a numeric pain rating scale (NPRS) and Knee Society score (KSS). Substantial enhancement in clinical outcome measures such as pain and function were achieved within 3 successive days of therapy. The use of pain medication was discontinued.\n\nThe patient continued his self-neural glides and postural reduction exercises at home and was advised for a follow-up after 4 weeks or to contact us if symptoms worsened. On the 3rd follow-up day, the patient\u2019s NPRS from 5 at rest and 7 with activity to 2 at rest and 4 with activity. The KSS increased from 22 to 61 and from 30 to 80 in the functional domain. At the end of the 2-week home program, the patient reported to have full active straight leg raise (SLR). The patient had fully recovered from his knee dysfunction and pain at the 2-month follow-up.", "generated_summary": "A 20-year-old Arabic male martial artist (91.5 kg, 180 cm, BMI 28.24) presented with 5 weeks of posterior left thigh pain after a short sprint during soccer, described as an acute \u201cpop,\u201d followed by progressive loss of knee flexibility and inability to fully flex or extend the knee; the knee rested in approximately 15\u00b0 of flexion. He reported no ecchymosis or significant swelling, could barely weight-bear on the affected limb, and withdrew from all sport. Initial self-management included icing, elevation, a crepe bandage, crutches, and step-to stair negotiation; NSAIDs, cryotherapy, and compression provided little relief. He denied prior lumbar symptoms and had no notable medical comorbidities (no alcohol use, smoking, diabetes, hypertension, or hereditary disease). Examination showed an analgesic gait with reduced heel strike; AROM of the left knee was 10\u201315\u00b0 versus 0\u2013130\u00b0 on the right. Palpation identified tenderness and firmness in the middle third of the semimembranosus and semitendinosus. Manual muscle testing and isometrics were deferred due to discomfort. NPRS was 5/10 at rest and 7/10 with activity. Clinical evaluation ruled out lumbar disc involvement and gluteal/ischial tunnel syndromes. Although the slump test is a standard screen for lower-limb neurodynamic mechanosensitivity, it was negative in this patient. Despite a presentation suggestive of hamstring strain injury, the team implemented a neural glide based on neurodynamic principles and the anatomical/functional proximity of peripheral nerve structures to hamstring flexibility. Technique: seated with arms folded behind the back; knees extended and ankles dorsiflexed; therapist-guided thoracic and cervical flexion with knee extension to the patient\u2019s tolerance, followed by active cervical flexion\u2013extension coordinated with ankle dorsiflexion\u2013plantarflexion (15 repetitions) to facilitate nerve gliding. Three sets were performed daily over 3 consecutive days. The therapist also facilitated progressive thoracic/cervical flexion until knee-area pain was provoked and then repeated the sequence. By day 3, active knee extension improved from approximately 5\u00b0 to 10\u00b0 and then to a 15\u00b0-bent position, and standing posture improved. Postural re-education included active chin flexion, prone passive stretching of cervical extensors, and progressive scapular retractor strengthening (arm positions T\u2192Y\u2192W) in prone with limb weight. To address kyphotic posture, active pectoral stretches at wall corners were prescribed, progressing hold time from 5 to 10 seconds, 10 repetitions, 3 sets daily. Outcomes: Measured by NPRS and Knee Society Score (KSS). Within 3 treatment days, substantial improvement was observed; pain medication was discontinued. NPRS decreased from 5/10 (rest) and 7/10 (activity) to 2/10 and 4/10, respectively. KSS improved from 22 to 61 (pain domain) and from 30 to 80 (function). After a 2-week home program, the patient achieved full active straight leg raise. At 2-month follow-up, he reported full recovery of knee function and pain resolution and had returned to sport without disruption. This case suggests that, even with a negative slump test, targeted neurodynamic mobilization combined with postural retraining may rapidly improve pain and function in select hamstring strain presentations; proposed mechanisms include reduced intraneural/extraneural adhesions, improved neural excursion, and modulation of nociceptive input." }, { "index": 78, "label": "low_health_literacy", "original_text": "A male was born via an emergency cesarean section due to fetal distress at 40\u200aweeks of gestational age. The mother's age was 33 years, with gravida 1 and para 1 parity. Both the parents and brother had no family history of congenital anomalies, aortic-related diseases, or sudden death. Based on the results of the prenatal ultrasonography at the end of the second trimester, the femur length of the fetus was found to be 1 to 3\u200aweeks longer than the supposed length of the actual gestational age. Fetal echocardiography showed cardiomegaly with a fetal cardiothoracic circumference ratio of 0.5 or higher based on the baby's term. Moreover, the size of the foramen ovale was larger than normal, and left aortic constriction was seen next to the subclavian artery basin. Furthermore, no other abnormalities were found on prenatal ultrasound.\n\nAt birth, the weight was 3560\u200ag (75 percentile), the length was 56.5\u200acm (over 90 percentile), and the head circumference was 36\u200acm (over 90 percentile). Apgar scores at 1 and 5 minutes were 4 and 6 points, respectively. In the delivery room, the patient had no spontaneous breathing and had bradycardia and cyanosis. After being admitted to the neonatal intensive care unit, various musculoskeletal malformations were confirmed via physical examination. Severe arachnodactyly and camptodactyly were observed in both hands and feet, and the soles of the feet were flat. The elbow and knee joints were not fully extended. The face had malar hypoplasia with senile facial appearance. The eye was deeply settled with a down-slanting palpebral fissure, and the ear with hypoplastic cartilage was poorly settled and crumpled. The patient presented with a sagging mouth, prominent coronal suture, and brachycephaly. A grade V/VI systolic murmur was heard at both the upper sternal border and left lower sternal border with grade III parasternal heave. Echocardiography showed poor cardiac contractility, severe pulmonary hypertension, dilated aortic sinus (20.2\u200amm) (Z-score; 8.08 by Boston, 6.37 by Detroit, or 5.97 by Halifax), and multiple intracardiac valvular dysfunction with valve prolapses (moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation). And the ophthalmologic examination results showed ectopia lentis in both eyes as well as lens subluxation. Liver herniation was confirmed using abdominal X-ray and ultrasound. The systemic score of the musculoskeletal manifestation was 11 points, according to the Ghent criteria (international diagnostic criteria for MFS).\n\nFor genetic diagnosis, Sanger sequencing and polymerase chain reaction were performed on the nucleotide sequence as reference for the FBN1 gene. As a result, a mutation in which G, the first base of the 32nd intron in the form of a heterogeneous mutation, was substituted with T (c.3964 + 1G > T). This was confirmed as the likely pathogen variant based on the 2015\u200aACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24\u201332). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2\u200aweeks of life.\n\nOn the first day of life, differential cyanosis was found to show refractory hypoxemia despite more than 60% oxygen supply and signs of low cardiac output. The patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction including milrinone continuous infusion, full sedation using fentanyl continuous infusion, and use of diuretic were attempt to improve the oliguria and heart failure. Despite the medical management, the patient presented with respiratory failure, heart failure, and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. After several consultations with the patient's family and medical staff about the treatment plan, palliative care was continued instead of surgical treatment. As a result, hepatic and pulmonary congestion accompanied by pulmonary hemorrhage had progressed as well. Eventually, it had progressed to multiple organ dysfunction syndrome, and the patient died 32 days after the birth.", "generated_summary": "This newborn had a very serious genetic condition called neonatal Marfan syndrome. It badly affected his heart. His fingers and toes were very long like spider legs. Some fingers and toes were stuck in a bent position. His elbows and knees could not fully straighten. His face looked old for a baby. His eyes were deep set and tilted downward. His ears were soft and not well formed. His mouth sagged. His head was short and wide. The clear lenses in his eyes were out of place. A DNA test found a new change in the fibrillin-1 gene in a spot linked to the newborn form of this condition. Doctors tried medicines to lower the heart\u2019s workload, kept him deeply sedated to reduce strain, and gave water pills to help him pee and move extra fluid. Even with this care, the heart valve leaks and high pressure in the lungs got worse, and the heart grew weaker. Surgery would have been needed to help him live longer. Because the disease was getting worse very fast, the family chose comfort care. A few months after birth, his heart failure worsened and he died." }, { "index": 78, "label": "intermediate_health_literacy", "original_text": "A male was born via an emergency cesarean section due to fetal distress at 40\u200aweeks of gestational age. The mother's age was 33 years, with gravida 1 and para 1 parity. Both the parents and brother had no family history of congenital anomalies, aortic-related diseases, or sudden death. Based on the results of the prenatal ultrasonography at the end of the second trimester, the femur length of the fetus was found to be 1 to 3\u200aweeks longer than the supposed length of the actual gestational age. Fetal echocardiography showed cardiomegaly with a fetal cardiothoracic circumference ratio of 0.5 or higher based on the baby's term. Moreover, the size of the foramen ovale was larger than normal, and left aortic constriction was seen next to the subclavian artery basin. Furthermore, no other abnormalities were found on prenatal ultrasound.\n\nAt birth, the weight was 3560\u200ag (75 percentile), the length was 56.5\u200acm (over 90 percentile), and the head circumference was 36\u200acm (over 90 percentile). Apgar scores at 1 and 5 minutes were 4 and 6 points, respectively. In the delivery room, the patient had no spontaneous breathing and had bradycardia and cyanosis. After being admitted to the neonatal intensive care unit, various musculoskeletal malformations were confirmed via physical examination. Severe arachnodactyly and camptodactyly were observed in both hands and feet, and the soles of the feet were flat. The elbow and knee joints were not fully extended. The face had malar hypoplasia with senile facial appearance. The eye was deeply settled with a down-slanting palpebral fissure, and the ear with hypoplastic cartilage was poorly settled and crumpled. The patient presented with a sagging mouth, prominent coronal suture, and brachycephaly. A grade V/VI systolic murmur was heard at both the upper sternal border and left lower sternal border with grade III parasternal heave. Echocardiography showed poor cardiac contractility, severe pulmonary hypertension, dilated aortic sinus (20.2\u200amm) (Z-score; 8.08 by Boston, 6.37 by Detroit, or 5.97 by Halifax), and multiple intracardiac valvular dysfunction with valve prolapses (moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation). And the ophthalmologic examination results showed ectopia lentis in both eyes as well as lens subluxation. Liver herniation was confirmed using abdominal X-ray and ultrasound. The systemic score of the musculoskeletal manifestation was 11 points, according to the Ghent criteria (international diagnostic criteria for MFS).\n\nFor genetic diagnosis, Sanger sequencing and polymerase chain reaction were performed on the nucleotide sequence as reference for the FBN1 gene. As a result, a mutation in which G, the first base of the 32nd intron in the form of a heterogeneous mutation, was substituted with T (c.3964 + 1G > T). This was confirmed as the likely pathogen variant based on the 2015\u200aACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24\u201332). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2\u200aweeks of life.\n\nOn the first day of life, differential cyanosis was found to show refractory hypoxemia despite more than 60% oxygen supply and signs of low cardiac output. The patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction including milrinone continuous infusion, full sedation using fentanyl continuous infusion, and use of diuretic were attempt to improve the oliguria and heart failure. Despite the medical management, the patient presented with respiratory failure, heart failure, and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. After several consultations with the patient's family and medical staff about the treatment plan, palliative care was continued instead of surgical treatment. As a result, hepatic and pulmonary congestion accompanied by pulmonary hemorrhage had progressed as well. Eventually, it had progressed to multiple organ dysfunction syndrome, and the patient died 32 days after the birth.", "generated_summary": "A term newborn boy had neonatal Marfan syndrome with severe heart involvement. He showed typical features: very long fingers and toes (arachnodactyly), bent fingers and toes (camptodactyly), elbow and knee contractures, an aged facial appearance, deep-set downward-slanting eyes, underdeveloped ear cartilage with a sagging mouth, a short-wide head shape (brachycephaly), and ectopia lentis (displaced eye lenses). Genetic testing identified a new FBN1 mutation affecting a splice site (c.3964+1G>T in intron 32) within the known neonatal region (exons 24\u201332). He developed low cardiac output due to severe mitral and aortic regurgitation and also had pulmonary hypertension. Medical management focused on afterload reduction, deep sedation to lessen cardiac work, and diuretics to treat fluid overload and low urine output. Despite treatment, the valve regurgitation, pulmonary hypertension, and poor heart pumping worsened. Surgery would likely have been required to extend survival, but given the rapid and grave progression, the family chose palliative care. Within a few months after birth, he experienced rapidly progressive heart failure and died." }, { "index": 78, "label": "proficient_health_literacy", "original_text": "A male was born via an emergency cesarean section due to fetal distress at 40\u200aweeks of gestational age. The mother's age was 33 years, with gravida 1 and para 1 parity. Both the parents and brother had no family history of congenital anomalies, aortic-related diseases, or sudden death. Based on the results of the prenatal ultrasonography at the end of the second trimester, the femur length of the fetus was found to be 1 to 3\u200aweeks longer than the supposed length of the actual gestational age. Fetal echocardiography showed cardiomegaly with a fetal cardiothoracic circumference ratio of 0.5 or higher based on the baby's term. Moreover, the size of the foramen ovale was larger than normal, and left aortic constriction was seen next to the subclavian artery basin. Furthermore, no other abnormalities were found on prenatal ultrasound.\n\nAt birth, the weight was 3560\u200ag (75 percentile), the length was 56.5\u200acm (over 90 percentile), and the head circumference was 36\u200acm (over 90 percentile). Apgar scores at 1 and 5 minutes were 4 and 6 points, respectively. In the delivery room, the patient had no spontaneous breathing and had bradycardia and cyanosis. After being admitted to the neonatal intensive care unit, various musculoskeletal malformations were confirmed via physical examination. Severe arachnodactyly and camptodactyly were observed in both hands and feet, and the soles of the feet were flat. The elbow and knee joints were not fully extended. The face had malar hypoplasia with senile facial appearance. The eye was deeply settled with a down-slanting palpebral fissure, and the ear with hypoplastic cartilage was poorly settled and crumpled. The patient presented with a sagging mouth, prominent coronal suture, and brachycephaly. A grade V/VI systolic murmur was heard at both the upper sternal border and left lower sternal border with grade III parasternal heave. Echocardiography showed poor cardiac contractility, severe pulmonary hypertension, dilated aortic sinus (20.2\u200amm) (Z-score; 8.08 by Boston, 6.37 by Detroit, or 5.97 by Halifax), and multiple intracardiac valvular dysfunction with valve prolapses (moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation). And the ophthalmologic examination results showed ectopia lentis in both eyes as well as lens subluxation. Liver herniation was confirmed using abdominal X-ray and ultrasound. The systemic score of the musculoskeletal manifestation was 11 points, according to the Ghent criteria (international diagnostic criteria for MFS).\n\nFor genetic diagnosis, Sanger sequencing and polymerase chain reaction were performed on the nucleotide sequence as reference for the FBN1 gene. As a result, a mutation in which G, the first base of the 32nd intron in the form of a heterogeneous mutation, was substituted with T (c.3964 + 1G > T). This was confirmed as the likely pathogen variant based on the 2015\u200aACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24\u201332). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2\u200aweeks of life.\n\nOn the first day of life, differential cyanosis was found to show refractory hypoxemia despite more than 60% oxygen supply and signs of low cardiac output. The patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction including milrinone continuous infusion, full sedation using fentanyl continuous infusion, and use of diuretic were attempt to improve the oliguria and heart failure. Despite the medical management, the patient presented with respiratory failure, heart failure, and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. After several consultations with the patient's family and medical staff about the treatment plan, palliative care was continued instead of surgical treatment. As a result, hepatic and pulmonary congestion accompanied by pulmonary hemorrhage had progressed as well. Eventually, it had progressed to multiple organ dysfunction syndrome, and the patient died 32 days after the birth.", "generated_summary": "A male infant was delivered at 40 weeks via emergency cesarean section for fetal distress to a 33-year-old G1P1 mother. Family history was negative for congenital anomalies, aortic disease, or sudden death. Prenatal imaging showed advanced femur length (by 1\u20133 weeks), cardiomegaly with a cardiothoracic circumference ratio \u22650.5, an enlarged foramen ovale, and left aortic constriction near the subclavian artery basin; no other anomalies were noted. Birth measurements: 3560 g (75th percentile), length 56.5 cm (>90th), head circumference 36 cm (>90th). Apgars were 4 and 6 at 1 and 5 minutes. In the delivery room he had no spontaneous respirations, bradycardia, and cyanosis, prompting NICU admission. Physical exam revealed multiple musculoskeletal and craniofacial anomalies: severe arachnodactyly and camptodactyly of all extremities with flat soles; elbow and knee contractures; malar hypoplasia with senile facial appearance; deep-set eyes with down-slanting palpebral fissures; hypoplastic, crumpled auricular cartilage; sagging mouth; prominent coronal suture; and brachycephaly. A grade V/VI systolic murmur was audible at both upper sternal borders and the left lower sternal border with a grade III parasternal heave. The Ghent systemic score for musculoskeletal features was 11. Echocardiography demonstrated poor contractility, severe pulmonary hypertension, a dilated aortic sinus measuring 20.2 mm (Z-score 8.08 Boston, 6.37 Detroit, 5.97 Halifax), and multivalvular prolapse with dysfunction: moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation. Ophthalmology confirmed bilateral ectopia lentis with lens subluxation. Abdominal radiography and ultrasound identified liver herniation.\n\nMolecular testing (Sanger sequencing/PCR) of FBN1 detected a heterozygous donor splice-site variant, c.3964+1G>T in intron 32, classified as likely pathogenic per the 2015 ACMG/AMP guideline. The variant resides within the established neonatal region of FBN1 (exons 24\u201332) associated with the severe neonatal Marfan phenotype. Mechanistically, splice-site variants at this locus are expected to disrupt normal FBN1 splicing, compromising microfibril integrity and driving the aggressive cardiovascular phenotype observed in neonatal MFS (notably early aortic root dilation and severe atrioventricular valve regurgitation).\n\nOn day 1, he exhibited differential cyanosis with refractory hypoxemia despite >60% oxygen and clinical signs of low cardiac output. Medical management targeted afterload reduction (continuous milrinone infusion), full sedation (continuous fentanyl infusion), and diuresis to address oliguria and heart failure. Despite these measures, he progressed to respiratory failure and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic and mitral regurgitation worsened, pulmonary hypertension escalated, and cardiac contractility deteriorated. Given the grave trajectory and the expectation that surgical intervention would be essential to prolong life but with limited prospects in the face of rapid progression, the family elected palliative care after multidisciplinary discussions. He developed hepatic and pulmonary congestion with pulmonary hemorrhage, progressed to multiple organ dysfunction syndrome, and died 32 days after birth.\n\nThis case documents a novel FBN1 c.3964+1G>T splice-site variant in the neonatal region, concordant with the classic neonatal MFS phenotype: severe early valvulopathy, aortic root dilation, ectopia lentis, characteristic skeletal/craniodysmorphic features, and a fulminant cardiorespiratory course with death in early infancy." }, { "index": 79, "label": "low_health_literacy", "original_text": "A 27-year-old woman with beta-thalassemia major since 24 years and 16 weeks of pregnancy was referred from the Internal Medicine Department to the Oral Medicine Department with complaints of swelling, bleeding gums since early pregnancy, and bad breath. The patient was hospitalized with complaints of pain in her knee so he could not move. She was admitted to hospital with complaints of pain in her knees so she could not move and was diagnosed with Arthritis ar Genue Sinistra related to Thalassemia by an internal medicine specialist, sub division of rheumatology. General condition patient was weak, sick, and difficult to move during the approximately two weeks, when she was hospitalized. Patient has never visited a dentist, either before or now, with complaints about her oral cavity. The patient had a splenectomy in 2009. Her beta-thalassemia major was treated with routine blood transfusions once a month and iron anti- chelation drugs (deferoxamine); however, it was stopped due to pregnancy. There was no history of other systemic disease in this patient. A family history of the same disease was ruled out. History of recurrent stomatitis and drug or food allergies was ruled out.\n\nThe patient\u2019s general condition weak, with normal vital signs; however, the patient had fever. Intraoral examination revealed gingival hyperplasia; erythema; soft consistency; a dark red, rounded gingival margin; tendencies to bleed on the labial, buccal, palatal, and lingual areas; and pain. Oral hygiene index-simplified (OHIS) score was poor (5.7) and there were true pockets in all regions. Peripheral blood morphology result: (1) erythrocytes: polychromacy in anisochrome populations (hypochrome, normochrome), anisopoikilocytosis (ovalocytes, target); (2) leukocytes: sufficient quantity, hypersegmentation (+); (3) platelet count: numbers increase, spread out; Interpretation: moderate anemia et causa thalassemia major accompanied by signs of increased erythropoiesis activity with suspected infection. The diagnosis was made based on the history, clinical features, and examination, as well as additional examinations, namely gingival enlargement accompanied by chronic periodontitis associated to pregnancy with \u03b2-thalassemia major and exfoliative cheilitis of the lips. The classification of periodontal disease in this patient is chronic periodontitis with gingival enlargement associated with pregnancy and beta-thalassemia major. The prognosis in this case was good because the patient was cooperative and followed the directions of the Oral Medicine Department. In this case, multidisciplinary therapy was a collaboration between an oral medicine specialist, a periodontist, and an internist. Dental therapy consisted of spooling with 3% hydrogen peroxide (H2O2) solution, chlorine dioxide spray mouthwash (Oxyfresh\u00ae, USA), antibiotics (amoxicillin 500 mg tablet, and metronidazole 300 mg tablet), and scaling/root planning. Spooling of H2O2 3% solution was performed at every visit; chlorine dioxide spray mouthwash was used three times a day after meals, and antibiotics were administered for seven days at third visit. Scaling and root planning were performed by the periodontist after the general condition was controlled and after the gingival hyperplasia and spontaneous bleeding improved. Blood transfusions to remove packed red cell buffy coat (PRC BCR) are also carried out routinely once a month. Non-pharmacological therapy, including oral hygiene instructions, was still given to patients. Oral complaints in this case occurred due to the poor oral hygiene, \u03b2-thalassemia major, and pregnancy, were also informed to the patient as education.\n\nThis patient had eight follow-up visits, consisting of two inpatient and six outpatient visits, with the following details:\n\nFirst Visit\nThe first visit was carried out one day after the initial inpatient visit (day +1). Intraoral bleeding still exists in the lingual-anterior part of the mandible, but bleeding in the anterior part of the maxilla has stopped. The patient still had a fever. Medications previously provided were used accordingly. Pharmacological were continued, including spooling 3% H2O2 on all parts of the gingiva, using chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. A blood transfusion was carried out last night. Oral hygiene instructions are still given to patients.\n\nSecond Visit\nThe second visit was performed two days after the initial visit (day +2). Intraoral bleeding Follow-up visits should be conducted in outpatient settings. Pharmacological therapy including spooling 3% H2O2 on all parts of the gingiva, using chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. A blood transfusion was carried out last night. Oral hygiene instructions are still given to patients.\n\nThird Visit\nNine days after the initial visit (Day+9). First outpatient treatment. Oral symptoms appeared to improve; bad breath was greatly reduced, but the gums were still swollen. The chlorine dioxide spray mouthwash was still being used and had run out. The patient could brush her teeth with a soft toothbrush but still experienced bleeding. Spooling was performed with 3% H2O2. The previous therapy was continued, antibiotics were prescribed 3x/day for seven days, and a blood transfusion was planned as a preparation for scaling the dental calculus. Oral hygiene instructions are still given to patients.\n\nFourth Visit\nOne month after the first visit (Day+30). Oral complaints improved significantly, bad breath was absent, gingiva enlargement decreased, and spontaneous bleeding ceased. The patient did not experience bleeding when brushing her teeth. Transfusions were performed between visits H+9 and H+30. During this visit, laboratory hematology tests and subsequent blood transfusions were performed. Antibiotics were no longer administered, 3% H2O2, chlorine dioxide, petroleum jelly and oral hygiene instructions were continued.\n\nFifth Visit\nOne week after the 4th visit (day +37), the oral complaints improved, but pharmacological and non-pharmacological therapy continued, including spooling 3% H2O2 on all parts of the gingiva, chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. Oral hygiene instructions are still given to patients. Supragingival scaling was planned two weeks later or after routine transfusions were administered.\n\nSixth Visit\nTwo months after the initial visit (day +60), the oral complaints improved. The gingival hyperplasia in some areas was no longer present, although in other areas still present, but they have undergone improvement. The transfusion had already been performed one week previously. Pharmacological therapy was continued, including 3% H2O2 spooling, chlorine dioxide spray mouthwash, and petroleum jelly. Non-pharmacological therapy namely oral hygiene instructions and an interdental toothbrush was suggested. Supra- and subgival scaling were performed.\n\nSeventh Visit\nTwo weeks after the 6th visit (Day+74), all the complaints improved. Gingival hyperplasia mostly resolved after scaling. Pharmacological includes 3% H2O2 spooling, chlorine dioxide spray mouthwash, and petroleum jelly as well as non-pharmacological therapy, consisting of oral hygiene instructions and the use of an interdental toothbrush.\n\nEighth Visit\nThree months after the initial visit (day +90), routine blood transfusions were performed one week before the visit. The patient is no longer presented with any oral complaints. All patients with gingival hyperplasia recovered optimally. The spooling process was stopped with 3% H2O2. Supra- and subgival scaling were performed again in all maxillary and mandibular regions. Instructions for the use of an interdental toothbrush, chlorine dioxide spray mouthwash, and petroleum jelly are still provided.", "generated_summary": "Who: A 27-year-old woman, 16 weeks pregnant. She has a blood problem called beta thalassemia major. She gets a blood transfusion every month. She stopped her iron-removing medicine because she is pregnant.\n\nMain mouth problems: Her gums are swollen, red, soft, and bleed easily. She has bad breath. Her lips are very dry and peeling. There are deep spaces like pockets around her teeth that trap germs and cause pain all around her mouth. She had never seen a dentist before. Her blood test showed anemia and signs of an infection.\n\nWhat the dentists called it: Swollen gums and long-term gum disease linked to pregnancy and her blood problem.\n\nCare plan: Rinse the mouth with 3% hydrogen peroxide. Use a chlorine dioxide spray mouthwash. Take antibiotics. Get a professional teeth cleaning to remove hard buildup. Follow simple daily mouth-care steps at home. Keep getting monthly blood transfusions. Do not take the iron-removing medicine during pregnancy.\n\nResult: After three months of care by a dental and medical team, her mouth got much better." }, { "index": 79, "label": "intermediate_health_literacy", "original_text": "A 27-year-old woman with beta-thalassemia major since 24 years and 16 weeks of pregnancy was referred from the Internal Medicine Department to the Oral Medicine Department with complaints of swelling, bleeding gums since early pregnancy, and bad breath. The patient was hospitalized with complaints of pain in her knee so he could not move. She was admitted to hospital with complaints of pain in her knees so she could not move and was diagnosed with Arthritis ar Genue Sinistra related to Thalassemia by an internal medicine specialist, sub division of rheumatology. General condition patient was weak, sick, and difficult to move during the approximately two weeks, when she was hospitalized. Patient has never visited a dentist, either before or now, with complaints about her oral cavity. The patient had a splenectomy in 2009. Her beta-thalassemia major was treated with routine blood transfusions once a month and iron anti- chelation drugs (deferoxamine); however, it was stopped due to pregnancy. There was no history of other systemic disease in this patient. A family history of the same disease was ruled out. History of recurrent stomatitis and drug or food allergies was ruled out.\n\nThe patient\u2019s general condition weak, with normal vital signs; however, the patient had fever. Intraoral examination revealed gingival hyperplasia; erythema; soft consistency; a dark red, rounded gingival margin; tendencies to bleed on the labial, buccal, palatal, and lingual areas; and pain. Oral hygiene index-simplified (OHIS) score was poor (5.7) and there were true pockets in all regions. Peripheral blood morphology result: (1) erythrocytes: polychromacy in anisochrome populations (hypochrome, normochrome), anisopoikilocytosis (ovalocytes, target); (2) leukocytes: sufficient quantity, hypersegmentation (+); (3) platelet count: numbers increase, spread out; Interpretation: moderate anemia et causa thalassemia major accompanied by signs of increased erythropoiesis activity with suspected infection. The diagnosis was made based on the history, clinical features, and examination, as well as additional examinations, namely gingival enlargement accompanied by chronic periodontitis associated to pregnancy with \u03b2-thalassemia major and exfoliative cheilitis of the lips. The classification of periodontal disease in this patient is chronic periodontitis with gingival enlargement associated with pregnancy and beta-thalassemia major. The prognosis in this case was good because the patient was cooperative and followed the directions of the Oral Medicine Department. In this case, multidisciplinary therapy was a collaboration between an oral medicine specialist, a periodontist, and an internist. Dental therapy consisted of spooling with 3% hydrogen peroxide (H2O2) solution, chlorine dioxide spray mouthwash (Oxyfresh\u00ae, USA), antibiotics (amoxicillin 500 mg tablet, and metronidazole 300 mg tablet), and scaling/root planning. Spooling of H2O2 3% solution was performed at every visit; chlorine dioxide spray mouthwash was used three times a day after meals, and antibiotics were administered for seven days at third visit. Scaling and root planning were performed by the periodontist after the general condition was controlled and after the gingival hyperplasia and spontaneous bleeding improved. Blood transfusions to remove packed red cell buffy coat (PRC BCR) are also carried out routinely once a month. Non-pharmacological therapy, including oral hygiene instructions, was still given to patients. Oral complaints in this case occurred due to the poor oral hygiene, \u03b2-thalassemia major, and pregnancy, were also informed to the patient as education.\n\nThis patient had eight follow-up visits, consisting of two inpatient and six outpatient visits, with the following details:\n\nFirst Visit\nThe first visit was carried out one day after the initial inpatient visit (day +1). Intraoral bleeding still exists in the lingual-anterior part of the mandible, but bleeding in the anterior part of the maxilla has stopped. The patient still had a fever. Medications previously provided were used accordingly. Pharmacological were continued, including spooling 3% H2O2 on all parts of the gingiva, using chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. A blood transfusion was carried out last night. Oral hygiene instructions are still given to patients.\n\nSecond Visit\nThe second visit was performed two days after the initial visit (day +2). Intraoral bleeding Follow-up visits should be conducted in outpatient settings. Pharmacological therapy including spooling 3% H2O2 on all parts of the gingiva, using chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. A blood transfusion was carried out last night. Oral hygiene instructions are still given to patients.\n\nThird Visit\nNine days after the initial visit (Day+9). First outpatient treatment. Oral symptoms appeared to improve; bad breath was greatly reduced, but the gums were still swollen. The chlorine dioxide spray mouthwash was still being used and had run out. The patient could brush her teeth with a soft toothbrush but still experienced bleeding. Spooling was performed with 3% H2O2. The previous therapy was continued, antibiotics were prescribed 3x/day for seven days, and a blood transfusion was planned as a preparation for scaling the dental calculus. Oral hygiene instructions are still given to patients.\n\nFourth Visit\nOne month after the first visit (Day+30). Oral complaints improved significantly, bad breath was absent, gingiva enlargement decreased, and spontaneous bleeding ceased. The patient did not experience bleeding when brushing her teeth. Transfusions were performed between visits H+9 and H+30. During this visit, laboratory hematology tests and subsequent blood transfusions were performed. Antibiotics were no longer administered, 3% H2O2, chlorine dioxide, petroleum jelly and oral hygiene instructions were continued.\n\nFifth Visit\nOne week after the 4th visit (day +37), the oral complaints improved, but pharmacological and non-pharmacological therapy continued, including spooling 3% H2O2 on all parts of the gingiva, chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. Oral hygiene instructions are still given to patients. Supragingival scaling was planned two weeks later or after routine transfusions were administered.\n\nSixth Visit\nTwo months after the initial visit (day +60), the oral complaints improved. The gingival hyperplasia in some areas was no longer present, although in other areas still present, but they have undergone improvement. The transfusion had already been performed one week previously. Pharmacological therapy was continued, including 3% H2O2 spooling, chlorine dioxide spray mouthwash, and petroleum jelly. Non-pharmacological therapy namely oral hygiene instructions and an interdental toothbrush was suggested. Supra- and subgival scaling were performed.\n\nSeventh Visit\nTwo weeks after the 6th visit (Day+74), all the complaints improved. Gingival hyperplasia mostly resolved after scaling. Pharmacological includes 3% H2O2 spooling, chlorine dioxide spray mouthwash, and petroleum jelly as well as non-pharmacological therapy, consisting of oral hygiene instructions and the use of an interdental toothbrush.\n\nEighth Visit\nThree months after the initial visit (day +90), routine blood transfusions were performed one week before the visit. The patient is no longer presented with any oral complaints. All patients with gingival hyperplasia recovered optimally. The spooling process was stopped with 3% H2O2. Supra- and subgival scaling were performed again in all maxillary and mandibular regions. Instructions for the use of an interdental toothbrush, chlorine dioxide spray mouthwash, and petroleum jelly are still provided.", "generated_summary": "Patient: 27-year-old woman, 16 weeks pregnant, with beta thalassemia major on monthly transfusions. Iron chelation was stopped during pregnancy.\n\nPresenting concerns: Since early pregnancy she had swollen, bleeding gums and bad breath. Exam showed dry, exfoliative lips and generalized gingival enlargement with redness, soft tissue, dark red rounded margins, easy bleeding, pain, and true periodontal pockets on the labial, buccal, palatal, and lingual surfaces. She had never seen a dentist for these issues. No other systemic illnesses were reported. Hematology showed anemia with abnormalities and evidence suggesting infection.\n\nAssessment: Gingival enlargement and chronic periodontitis associated with pregnancy and beta thalassemia major.\n\nManagement: Multidisciplinary dental care included 3% hydrogen peroxide rinses, a chlorine dioxide spray mouthwash, a course of antibiotics, professional calculus removal (scaling/root planing), and oral hygiene instructions. Medical care continued monthly transfusions; iron chelation remained on hold during pregnancy.\n\nOutcome: After about three months of coordinated care, symptoms and clinical findings improved satisfactorily." }, { "index": 79, "label": "proficient_health_literacy", "original_text": "A 27-year-old woman with beta-thalassemia major since 24 years and 16 weeks of pregnancy was referred from the Internal Medicine Department to the Oral Medicine Department with complaints of swelling, bleeding gums since early pregnancy, and bad breath. The patient was hospitalized with complaints of pain in her knee so he could not move. She was admitted to hospital with complaints of pain in her knees so she could not move and was diagnosed with Arthritis ar Genue Sinistra related to Thalassemia by an internal medicine specialist, sub division of rheumatology. General condition patient was weak, sick, and difficult to move during the approximately two weeks, when she was hospitalized. Patient has never visited a dentist, either before or now, with complaints about her oral cavity. The patient had a splenectomy in 2009. Her beta-thalassemia major was treated with routine blood transfusions once a month and iron anti- chelation drugs (deferoxamine); however, it was stopped due to pregnancy. There was no history of other systemic disease in this patient. A family history of the same disease was ruled out. History of recurrent stomatitis and drug or food allergies was ruled out.\n\nThe patient\u2019s general condition weak, with normal vital signs; however, the patient had fever. Intraoral examination revealed gingival hyperplasia; erythema; soft consistency; a dark red, rounded gingival margin; tendencies to bleed on the labial, buccal, palatal, and lingual areas; and pain. Oral hygiene index-simplified (OHIS) score was poor (5.7) and there were true pockets in all regions. Peripheral blood morphology result: (1) erythrocytes: polychromacy in anisochrome populations (hypochrome, normochrome), anisopoikilocytosis (ovalocytes, target); (2) leukocytes: sufficient quantity, hypersegmentation (+); (3) platelet count: numbers increase, spread out; Interpretation: moderate anemia et causa thalassemia major accompanied by signs of increased erythropoiesis activity with suspected infection. The diagnosis was made based on the history, clinical features, and examination, as well as additional examinations, namely gingival enlargement accompanied by chronic periodontitis associated to pregnancy with \u03b2-thalassemia major and exfoliative cheilitis of the lips. The classification of periodontal disease in this patient is chronic periodontitis with gingival enlargement associated with pregnancy and beta-thalassemia major. The prognosis in this case was good because the patient was cooperative and followed the directions of the Oral Medicine Department. In this case, multidisciplinary therapy was a collaboration between an oral medicine specialist, a periodontist, and an internist. Dental therapy consisted of spooling with 3% hydrogen peroxide (H2O2) solution, chlorine dioxide spray mouthwash (Oxyfresh\u00ae, USA), antibiotics (amoxicillin 500 mg tablet, and metronidazole 300 mg tablet), and scaling/root planning. Spooling of H2O2 3% solution was performed at every visit; chlorine dioxide spray mouthwash was used three times a day after meals, and antibiotics were administered for seven days at third visit. Scaling and root planning were performed by the periodontist after the general condition was controlled and after the gingival hyperplasia and spontaneous bleeding improved. Blood transfusions to remove packed red cell buffy coat (PRC BCR) are also carried out routinely once a month. Non-pharmacological therapy, including oral hygiene instructions, was still given to patients. Oral complaints in this case occurred due to the poor oral hygiene, \u03b2-thalassemia major, and pregnancy, were also informed to the patient as education.\n\nThis patient had eight follow-up visits, consisting of two inpatient and six outpatient visits, with the following details:\n\nFirst Visit\nThe first visit was carried out one day after the initial inpatient visit (day +1). Intraoral bleeding still exists in the lingual-anterior part of the mandible, but bleeding in the anterior part of the maxilla has stopped. The patient still had a fever. Medications previously provided were used accordingly. Pharmacological were continued, including spooling 3% H2O2 on all parts of the gingiva, using chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. A blood transfusion was carried out last night. Oral hygiene instructions are still given to patients.\n\nSecond Visit\nThe second visit was performed two days after the initial visit (day +2). Intraoral bleeding Follow-up visits should be conducted in outpatient settings. Pharmacological therapy including spooling 3% H2O2 on all parts of the gingiva, using chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. A blood transfusion was carried out last night. Oral hygiene instructions are still given to patients.\n\nThird Visit\nNine days after the initial visit (Day+9). First outpatient treatment. Oral symptoms appeared to improve; bad breath was greatly reduced, but the gums were still swollen. The chlorine dioxide spray mouthwash was still being used and had run out. The patient could brush her teeth with a soft toothbrush but still experienced bleeding. Spooling was performed with 3% H2O2. The previous therapy was continued, antibiotics were prescribed 3x/day for seven days, and a blood transfusion was planned as a preparation for scaling the dental calculus. Oral hygiene instructions are still given to patients.\n\nFourth Visit\nOne month after the first visit (Day+30). Oral complaints improved significantly, bad breath was absent, gingiva enlargement decreased, and spontaneous bleeding ceased. The patient did not experience bleeding when brushing her teeth. Transfusions were performed between visits H+9 and H+30. During this visit, laboratory hematology tests and subsequent blood transfusions were performed. Antibiotics were no longer administered, 3% H2O2, chlorine dioxide, petroleum jelly and oral hygiene instructions were continued.\n\nFifth Visit\nOne week after the 4th visit (day +37), the oral complaints improved, but pharmacological and non-pharmacological therapy continued, including spooling 3% H2O2 on all parts of the gingiva, chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. Oral hygiene instructions are still given to patients. Supragingival scaling was planned two weeks later or after routine transfusions were administered.\n\nSixth Visit\nTwo months after the initial visit (day +60), the oral complaints improved. The gingival hyperplasia in some areas was no longer present, although in other areas still present, but they have undergone improvement. The transfusion had already been performed one week previously. Pharmacological therapy was continued, including 3% H2O2 spooling, chlorine dioxide spray mouthwash, and petroleum jelly. Non-pharmacological therapy namely oral hygiene instructions and an interdental toothbrush was suggested. Supra- and subgival scaling were performed.\n\nSeventh Visit\nTwo weeks after the 6th visit (Day+74), all the complaints improved. Gingival hyperplasia mostly resolved after scaling. Pharmacological includes 3% H2O2 spooling, chlorine dioxide spray mouthwash, and petroleum jelly as well as non-pharmacological therapy, consisting of oral hygiene instructions and the use of an interdental toothbrush.\n\nEighth Visit\nThree months after the initial visit (day +90), routine blood transfusions were performed one week before the visit. The patient is no longer presented with any oral complaints. All patients with gingival hyperplasia recovered optimally. The spooling process was stopped with 3% H2O2. Supra- and subgival scaling were performed again in all maxillary and mandibular regions. Instructions for the use of an interdental toothbrush, chlorine dioxide spray mouthwash, and petroleum jelly are still provided.", "generated_summary": "History: A 27-year-old woman with beta-thalassemia major since childhood (24 years) at 16 weeks\u2019 gestation was referred from Internal Medicine to Oral Medicine for gingival swelling, bleeding since early pregnancy, and halitosis. She was hospitalized ~2 weeks for severe knee pain and was diagnosed by rheumatology with arthritis genu sinistra related to thalassemia. Past history: splenectomy in 2009. Transfusion-dependent (monthly). Iron chelation with deferoxamine had been stopped due to pregnancy. No history of other systemic disease, no family history of thalassemia, and no history of recurrent stomatitis or drug/food allergies. She had never sought dental care for oral complaints.\n\nGeneral and oral findings: General condition weak; vitals normal; febrile. Extraoral: dry, exfoliative lips (exfoliative cheilitis). Intraoral: generalized gingival hyperplasia with erythema, soft consistency, dark red, rounded gingival margins; spontaneous bleeding tendencies with pain on labial, buccal, palatal, and lingual aspects. OHIS was poor (5.7). Periodontal probing revealed true pockets in all regions.\n\nLaboratory data: Peripheral smear\u2014erythrocytes: polychromasia in anisochrome populations (hypochrome, normochrome), anisopoikilocytosis (ovalocytes, target cells). Leukocytes: adequate count, hypersegmentation (+). Platelets: increased numbers, spread out. Interpretation: moderate anemia due to thalassemia major with increased erythropoiesis and suspected infection.\n\nDiagnosis and classification: Gingival enlargement with chronic periodontitis associated with pregnancy and beta-thalassemia major; exfoliative cheilitis. Prognosis: good (patient cooperative and adherent).\n\nMultidisciplinary management: Collaboration among oral medicine, periodontics, and internal medicine. Dental therapy comprised spooling with 3% hydrogen peroxide (H2O2) at each visit; chlorine dioxide spray mouthwash (Oxyfresh, USA) three times daily after meals; petroleum jelly to lips; systemic antibiotics (amoxicillin 500 mg and metronidazole 300 mg, each TID for 7 days, initiated at the third visit); and scaling/root planing once general status and spontaneous bleeding improved. Non-pharmacologic: oral hygiene instructions and interdental brush use. Medical therapy: routine monthly PRC BCR transfusions continued; deferoxamine remained discontinued during pregnancy.\n\nCourse and timeline (8 visits):\n- Day +1 (inpatient): Lingual-anterior mandibular bleeding persisted; maxillary anterior bleeding stopped; patient febrile; continued H2O2 spooling, chlorine dioxide mouthwash, petroleum jelly; transfusion performed the prior night; OHI reinforced.\n- Day +2 (inpatient): Continued intraoral care as above; transfusion the prior night; planned outpatient follow-up.\n- Day +9 (first outpatient): Marked reduction in halitosis; gingival swelling persisted; continued H2O2 spooling and chlorine dioxide; initiated amoxicillin + metronidazole TID \u00d77 days; planned transfusion prior to scaling.\n- Day +30: Significant improvement\u2014no halitosis, reduced enlargement, cessation of spontaneous bleeding; laboratory hematology rechecked; transfusion performed between Day +9 and +30; continued H2O2, chlorine dioxide, petroleum jelly; no further antibiotics.\n- Day +37: Continued improvement; maintained pharmacologic measures; planned supragingival scaling 2 weeks later after routine transfusion.\n- Day +60: Further improvement; some residual hyperplasia; transfusion 1 week earlier; continued H2O2, chlorine dioxide, petroleum jelly; added interdental toothbrush; performed supra- and subgingival scaling.\n- Day +74: Near-complete resolution of gingival hyperplasia post-scaling; continued H2O2, chlorine dioxide, petroleum jelly, OHI, interdental brush.\n- Day +90: One week post-transfusion; no oral complaints; gingival hyperplasia resolved optimally; discontinued H2O2 spooling; repeated supra- and subgingival scaling in all quadrants; continued chlorine dioxide mouthwash, petroleum jelly, and interdental hygiene.\n\nOutcome: After three months of multidisciplinary care with ongoing monthly transfusions and cessation of chelation during pregnancy, gingival enlargement and chronic periodontitis signs resolved or improved substantially, halitosis ceased, bleeding stopped, and overall oral health stabilized." } ], "results": [ { "queue_position": 0, "doc_id": 20, "label": "low_health_literacy", "rating": 2, "timestamp": "2026-01-14 22:37:20" } ], "completed": false }