[
  {
    "doc_id": 20,
    "label": "low_health_literacy",
    "fulltext": "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.",
    "diff_label_texts": "A.P. is a 38‑year‑old 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’s 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’s natural pacemaker. She had no limits in daily activity. She is a mother of two. She did not have a job.",
    "summary": "Patient A.P., female, 38 years old, had symptoms of dilated cardiomyopathy (with possible infectious myocarditis in the background) at age 17. After hospitalization for ten months and ten days, while waiting for heart transplantation (with threatening death outcome), without a clearly pronounced threatening arrhythmia, but with a low ejection fraction and a poor general condition, remission occurred. The therapy focused primarily on the treatment of heart failure, prevention of arrhythmia and thromboembolism. Normalization of the disease by improving the function of the left ventricle (expected in 16% of patients) occurred and lasted for 4 years, followed by an exacerbation of the disease that lasted for two years. In the next few years the patient was stable, had a first child with normal pregnancy. During the second trimester of the second pregnancy, there was an exacerbation (postpartum dilatation cardiomyopathy) lasting for couple of months. At the time of case report (May 2017), the patient is stable on therapy (ACE inhibitor, beta blocker, diuretics, If channel blocker), without limitation of physical capacity, mother of two children, unemployed."
  },
  {
    "doc_id": 21,
    "label": "low_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "We present the case of a 27-year-old male patient who presented to the emergency department with a fracture of the right femur at the base of the neck in pathological ground Garden II Pauwells III AO 31B2.3r, after a low energy mechanism of injury characterized by axial load with rotational component of the right hip. The patient had a history of intralesional resection, application of bone graft and prophylactic fixation with unspecified osteosynthesis material in the pertrochanteric region 20 years ago; the biopsy later showed DF; one year later, the osteosynthesis material was removed. Due to the characteristics of the fracture and as a definitive and curative therapeutic method, it was decided to carry out a wide resection of the proximal femur and total arthroplasty of the hip with a modular prosthesis with placement of cerclage, as well as a excisional biopsy that later corroborated that it was the same DF treated in childhood.\n"
  },
  {
    "doc_id": 21,
    "label": "intermediate_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "We present the case of a 27-year-old male patient who presented to the emergency department with a fracture of the right femur at the base of the neck in pathological ground Garden II Pauwells III AO 31B2.3r, after a low energy mechanism of injury characterized by axial load with rotational component of the right hip. The patient had a history of intralesional resection, application of bone graft and prophylactic fixation with unspecified osteosynthesis material in the pertrochanteric region 20 years ago; the biopsy later showed DF; one year later, the osteosynthesis material was removed. Due to the characteristics of the fracture and as a definitive and curative therapeutic method, it was decided to carry out a wide resection of the proximal femur and total arthroplasty of the hip with a modular prosthesis with placement of cerclage, as well as a excisional biopsy that later corroborated that it was the same DF treated in childhood.\n"
  },
  {
    "doc_id": 22,
    "label": "intermediate_health_literacy",
    "fulltext": "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.",
    "diff_label_texts": "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–cord 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.",
    "summary": "A 4-year-old boy was diagnosed with metastatic neuroblastoma and underwent intensive chemotherapy, autologous HSCT, and allogeneic cord blood transplantation (CBT). He experienced PVOD on day 194 following CBT after displaying upper respiratory symptoms and positive RSV antigen test results approximately one month prior. Pathological examination of a lung biopsy specimen revealed lung injury suspected to be associated with viral infection in addition to PVOD-related findings, suggesting that RSV infection might have contributed to the onset of PVOD."
  },
  {
    "doc_id": 23,
    "label": "low_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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–Barr 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.",
    "summary": "We report the case of a 65-year-old man with a pulmonary lymphoepithelioma-like carcinoma, who presented with cough, dyspnea, and weight loss. A chest CT scan showed a poorly defined nodule located in the right lung. A trans-thoracic biopsy of the lesion was performed, and microscopic examination revealed large polygonal cells arranged in sheets, infiltrated by abundant lymphocytes and plasma cells, around the interstitium. The neoplastic cells were positive for cytokeratin 5/6 and p63, and negative for Napsina A and thyroid transcription factor 1 (TTF-1). PD-L1 expression was positive (approximately 100%) by immunohistochemistry; as was the nucleus of the neoplastic cells by in situ hybridization for Epstein-Barr virus-encoded RNA (EBER-ISH). The patient received six cycles of a combination chemotherapy regimen based on platinum (gemcitabine/cisplatin) plus durvalumab. He progressed and ultimately died 9 months after diagnosis.\n"
  },
  {
    "doc_id": 24,
    "label": "low_health_literacy",
    "fulltext": "A 13-year-old male patient was admitted to the Children’s 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 × 2.4 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’s 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.",
    "diff_label_texts": "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.",
    "summary": "We report a unique case of a 13-year-old boy who presented with a palpable enlarged mass in the left inguinal region without any constitutional symptoms. Surgical removal of this mass was essential to exclude worrying causes. Pathologic examination revealed proliferative changes consistent with Castleman's disease plasma cell type which is one of the rarest forms of the disease in children. To our knowledge, this case is the first reported case of Unicentric Castleman Disease (UCD) in the inguinal area. During a 12-month-period of follow-up, no additional lymph node enlargements or other symptoms were reported."
  },
  {
    "doc_id": 25,
    "label": "proficient_health_literacy",
    "fulltext": "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 – myotonia, warm-up phenomenon, characteristic electromyographic pattern and/or family history – 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",
    "diff_label_texts": "We retrospectively reviewed medical records from a pediatric neurology consultation at a third‑level hospital (2015–2020) for patients with congenital myotonia. Inclusion criteria comprised a clinical diagnosis (myotonia, warm‑up 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’s disease (recessive phenotype) and two with Thomsen’s 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‑provoked, doubtful clinical signs; the patient who declined genetic testing had a maternal‑line 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 1–3 (Becker phenotype) carried composite heterozygosity mutations; cases 4–5 had the Thomsen phenotype, and case 5 declined genetic testing.",
    "summary": "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. 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. Five cases with a clinical diagnosis of congenital myotonia were identified (three with Becker disease and two with Thomsen disease). The incidence in relation to the number of births was estimated at 1:15,000 newborns for cases with a Becker phenotype and 1:21,000 newborns for Thomsen phenotypes. We found a probably pathogenic mutation not previously described (CLCN1: c.824T>C).\n"
  },
  {
    "doc_id": 26,
    "label": "low_health_literacy",
    "fulltext": "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’s 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’s 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–12 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 − 0 vascular risk suture, resulting in a significant improvement in the patient’s 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 (18–20 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.",
    "diff_label_texts": "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.",
    "summary": "We present a case involving a patient with congenital AVMs in the lower limb, who had suffered from prolonged swelling in the left lower limb and recently developed symptoms of heart failure. At the age of 67, the patient was definitively diagnosed with a complex congenital AVMs in the lower limb. This article delves into the practical experiences and limitations encountered in employing an abdominal aortic stent graft, coupled with embolization, to address acute heart failure caused by complex congenital AVMs in the lower limb."
  },
  {
    "doc_id": 26,
    "label": "intermediate_health_literacy",
    "fulltext": "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’s 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’s 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–12 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 − 0 vascular risk suture, resulting in a significant improvement in the patient’s 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 (18–20 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.",
    "diff_label_texts": "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.",
    "summary": "We present a case involving a patient with congenital AVMs in the lower limb, who had suffered from prolonged swelling in the left lower limb and recently developed symptoms of heart failure. At the age of 67, the patient was definitively diagnosed with a complex congenital AVMs in the lower limb. This article delves into the practical experiences and limitations encountered in employing an abdominal aortic stent graft, coupled with embolization, to address acute heart failure caused by complex congenital AVMs in the lower limb."
  },
  {
    "doc_id": 26,
    "label": "proficient_health_literacy",
    "fulltext": "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’s 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’s 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–12 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 − 0 vascular risk suture, resulting in a significant improvement in the patient’s 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 (18–20 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.",
    "diff_label_texts": "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 20–12 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’s 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 µg/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 18–20 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.",
    "summary": "We present a case involving a patient with congenital AVMs in the lower limb, who had suffered from prolonged swelling in the left lower limb and recently developed symptoms of heart failure. At the age of 67, the patient was definitively diagnosed with a complex congenital AVMs in the lower limb. This article delves into the practical experiences and limitations encountered in employing an abdominal aortic stent graft, coupled with embolization, to address acute heart failure caused by complex congenital AVMs in the lower limb."
  },
  {
    "doc_id": 27,
    "label": "low_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "The case of a 28-year-old male patient who presented to the dermatology department with a 48-hour history of two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm, accompanied by a burning sensation and pruritus at the site of the lesions, without accompanying symptoms, is reported. As a background, he stated that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed and, due to the clinical characteristics and the background of travel to a tropical region, the diagnosis was made as dermatitis by Paederus and treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions subsided, leaving a post-inflammatory hyperpigmentation.\n"
  },
  {
    "doc_id": 27,
    "label": "proficient_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "The case of a 28-year-old male patient who presented to the dermatology department with a 48-hour history of two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm, accompanied by a burning sensation and pruritus at the site of the lesions, without accompanying symptoms, is reported. As a background, he stated that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed and, due to the clinical characteristics and the background of travel to a tropical region, the diagnosis was made as dermatitis by Paederus and treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions subsided, leaving a post-inflammatory hyperpigmentation.\n"
  },
  {
    "doc_id": 28,
    "label": "low_health_literacy",
    "fulltext": "Technique\nInformation about the procedure of TFD.\nThe patient receives intravenous photosensitizer (Photogen®, 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/cm², with a power of 70 mW/cm². 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",
    "diff_label_texts": "One day before the treatment, you get a light‑activated 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‑year‑old 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’s 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.",
    "summary": "Patient receives intravenous photosensitizer 24 h before the procedure which begins with regular duodenoscopy. After identification of the main papilla and retrograde cannulation, the digital cholangioscope is introduced into the common bile duct. Then the cholangioscopic examination helps to identify neoplastic stenosis. Under direct visualization, the illumination catheter is advanced through the cholangioscope. Repositioning is done every centimeter. At the end of cholangioscopy, the bile duct is evaluated for immediate outcome and adverse events.\n\nResult: This procedure was performed in an 82-year-old man with obstructive jaundice for the past two months. EUS and ERCP revealed severe dilation of the common bile duct associated with choledocholithiasis. In addition, there was dilation of the hepatic duct to a well-circumscribed hypoechoic solid mass measuring 1.8x2 cm, compressing the common hepatic duct. It was considered inoperable and the patient was referred for palliative treatment with PDT, which remained asymptomatic for three months. He died of complications 15 months after the PDT session.\n"
  },
  {
    "doc_id": 28,
    "label": "proficient_health_literacy",
    "fulltext": "Technique\nInformation about the procedure of TFD.\nThe patient receives intravenous photosensitizer (Photogen®, 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/cm², with a power of 70 mW/cm². 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",
    "diff_label_texts": "Technique (TFD/PDT): The patient receives intravenous photosensitizer (Photogen, 1.5 mg/kg) 24 h pre‑procedure; peak absorption is 630 nm. Under general anesthesia, standard duodenoscopy (Olympus TJF‑180) 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., RD10‑323) is advanced through the cholangioscope. The catheter is a three‑way cannula: port 1 carries a 1‑cm cylindrical light diffuser with two black radiopaque markers denoting its limits; port 2 accommodates a 0.025‑inch guidewire; port 3 is an injection portal. Following cholangioscopic positioning, illumination is delivered at 90 J/cm² with power of 70 mW/cm², with 1‑cm stepwise repositioning to cover the entire stenosed segment. Completion cholangioscopy assesses immediate outcome and adverse events. Post‑procedure 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‑year‑old man presented with a 2‑month 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‑circumscribed hypoechoic solid mass (1.8 × 2 cm) compressing the common hepatic duct, with apparent involvement of the common hepatic artery. Ultrasound‑guided 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‑drainage resolved the acute episode. He then remained asymptomatic for three months—the longest interval since symptom onset. At subsequent recurrence, a self‑expanding 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.",
    "summary": "Patient receives intravenous photosensitizer 24 h before the procedure which begins with regular duodenoscopy. After identification of the main papilla and retrograde cannulation, the digital cholangioscope is introduced into the common bile duct. Then the cholangioscopic examination helps to identify neoplastic stenosis. Under direct visualization, the illumination catheter is advanced through the cholangioscope. Repositioning is done every centimeter. At the end of cholangioscopy, the bile duct is evaluated for immediate outcome and adverse events.\n\nResult: This procedure was performed in an 82-year-old man with obstructive jaundice for the past two months. EUS and ERCP revealed severe dilation of the common bile duct associated with choledocholithiasis. In addition, there was dilation of the hepatic duct to a well-circumscribed hypoechoic solid mass measuring 1.8x2 cm, compressing the common hepatic duct. It was considered inoperable and the patient was referred for palliative treatment with PDT, which remained asymptomatic for three months. He died of complications 15 months after the PDT session.\n"
  },
  {
    "doc_id": 29,
    "label": "proficient_health_literacy",
    "fulltext": "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 mmHg), and blood tests revealed anaemia (haemoglobin: 9.6 g/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’s 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–Weiss 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 days later, when CT was repeated, spontaneous resolution of the malpositioned jejunum was seen. The patient was then discharged from the hospital. However, months 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–Weiss 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 months. 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’s 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’s left side. The postoperative course was good, and the patient has remained symptom-free.",
    "diff_label_texts": "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–Weiss 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.",
    "summary": "A 77-year-old woman underwent CT to evaluate haematemesis. The images showed 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 duodenal-jejunal junction and jejunum were located on the patient's right side. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, and a diagnosis of Mallory-Weiss syndrome was made. Repeat CT 7 days later revealed that the abnormal positioning of the intestinal tract had resolved spontaneously. Two months later, the patient experienced another episode of haematemesis, and CT revealed repeat deviation of the duodenal-jejunal junction and jejunum to her right side. Upper gastrointestinal endoscopy revealed another laceration at the gastric cardia, as in the previous study. On the basis of the initial CT findings showing the duodenal-jejunal junction in the right hemi-abdomen, intestinal malrotation was suspected. However, because the jejunum deviated repeatedly to the right side but resolved spontaneously, we diagnosed dysplasia of the ligament of Treitz. Laparotomy revealed a formed ligament of Treitz; however, fixation in the upper jejunum was incomplete. Additionally, CT revealed that the anterior pararenal space was loosely fixed and mobile. These factors may have caused the right-sided deviation of the small intestine."
  },
  {
    "doc_id": 30,
    "label": "low_health_literacy",
    "fulltext": "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 °C, 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°C, 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",
    "diff_label_texts": "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.",
    "summary": "This clinical case was reported in a young Moroccan, presenting a picture of hepatic colic that had been developing for a month, associated with subtle signs of tuberculous infection. Non-specific hepatic nodular lesions were revealed on the scanner and on the hepatic magnetic resonance imaging (MRI). The diagnosis of focal hepatic tuberculosis was confirmed after pathological analysis of hepatic nodule biopsies obtained after a laparoscopy. After the start of well-conducted anti-bacillary treatment, a good clinical-biological improvement was obtained.\n"
  },
  {
    "doc_id": 30,
    "label": "intermediate_health_literacy",
    "fulltext": "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 °C, 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°C, 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",
    "diff_label_texts": "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.",
    "summary": "This clinical case was reported in a young Moroccan, presenting a picture of hepatic colic that had been developing for a month, associated with subtle signs of tuberculous infection. Non-specific hepatic nodular lesions were revealed on the scanner and on the hepatic magnetic resonance imaging (MRI). The diagnosis of focal hepatic tuberculosis was confirmed after pathological analysis of hepatic nodule biopsies obtained after a laparoscopy. After the start of well-conducted anti-bacillary treatment, a good clinical-biological improvement was obtained.\n"
  },
  {
    "doc_id": 30,
    "label": "proficient_health_literacy",
    "fulltext": "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 °C, 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°C, 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",
    "diff_label_texts": "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 °C, 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 × 16 mm) and segment V (36 × 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 × 22 mm) and segment V (33 × 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.",
    "summary": "This clinical case was reported in a young Moroccan, presenting a picture of hepatic colic that had been developing for a month, associated with subtle signs of tuberculous infection. Non-specific hepatic nodular lesions were revealed on the scanner and on the hepatic magnetic resonance imaging (MRI). The diagnosis of focal hepatic tuberculosis was confirmed after pathological analysis of hepatic nodule biopsies obtained after a laparoscopy. After the start of well-conducted anti-bacillary treatment, a good clinical-biological improvement was obtained.\n"
  },
  {
    "doc_id": 31,
    "label": "low_health_literacy",
    "fulltext": "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’s mother said that the patient was admitted to the hospital because of weakness in both patient’s hands and feet. The patient had a history of falling down about one year ago. The patient’s mother also had a difficulty in cleaning the patient’s 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 1×0.7 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’s cervical spine. The patient’s mother provided informed consent to publish the patient’s 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’s mother was instructed to clean the patient’s 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’s 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.",
    "diff_label_texts": "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.",
    "summary": "A 12-year-old boy with Down Syndrome and motoric disorders was referred to Oral Medicine Department. In the extraoral examination, the patient had a dysmorphic face and dry lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1×0.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. The 55 teeth were sharp and caused an occlusion trauma to the right lateral border of the tongue. The patient was diagnosed with a chronic traumatic ulcer mimicking OSCC based on clinical examination. The medication given to the patient were sodium chloride 0.9%, povidone-iodine mouthwash 1%, and petroleum jelly."
  },
  {
    "doc_id": 31,
    "label": "proficient_health_literacy",
    "fulltext": "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’s mother said that the patient was admitted to the hospital because of weakness in both patient’s hands and feet. The patient had a history of falling down about one year ago. The patient’s mother also had a difficulty in cleaning the patient’s 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 1×0.7 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’s cervical spine. The patient’s mother provided informed consent to publish the patient’s 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’s mother was instructed to clean the patient’s 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’s 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.",
    "diff_label_texts": "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’s 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 1×0.7 cm ulcer with an indurated margin and a white‑yellowish 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‑iodine mouthwash, and petroleum jelly. Caregiver instructions: cleanse the oral cavity with gauze soaked in 0.9% saline; apply 1% povidone‑iodine compresses to the ulcer three times daily as an antiseptic/anti‑inflammatory; 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.",
    "summary": "A 12-year-old boy with Down Syndrome and motoric disorders was referred to Oral Medicine Department. In the extraoral examination, the patient had a dysmorphic face and dry lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1×0.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. The 55 teeth were sharp and caused an occlusion trauma to the right lateral border of the tongue. The patient was diagnosed with a chronic traumatic ulcer mimicking OSCC based on clinical examination. The medication given to the patient were sodium chloride 0.9%, povidone-iodine mouthwash 1%, and petroleum jelly."
  },
  {
    "doc_id": 32,
    "label": "low_health_literacy",
    "fulltext": "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’ 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’s 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 936μm and left central corneal thickness of 1134μm. 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 567μm and a left central corneal thickness of 573μm, 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.",
    "diff_label_texts": "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.",
    "summary": "A 59-year-old woman was referred to the ophthalmology department with a few weeks’ history of bilateral blurring of vision. She is a known case of secondary progressive multiple sclerosis, and she was started on levetiracetam by her neurologist a few weeks prior to referral in view of new seizure activity. Examination revealed bilateral clinically evident corneal edema, which was documented on corneal topography.\n\nResults\nUpon levetiracetam dose reduction, symptoms started to improve and eventually the medication was stopped altogether. The patient’s vision and corneal edema normalized on follow-up."
  },
  {
    "doc_id": 32,
    "label": "intermediate_health_literacy",
    "fulltext": "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’ 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’s 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 936μm and left central corneal thickness of 1134μm. 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 567μm and a left central corneal thickness of 573μm, 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.",
    "diff_label_texts": "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.",
    "summary": "A 59-year-old woman was referred to the ophthalmology department with a few weeks’ history of bilateral blurring of vision. She is a known case of secondary progressive multiple sclerosis, and she was started on levetiracetam by her neurologist a few weeks prior to referral in view of new seizure activity. Examination revealed bilateral clinically evident corneal edema, which was documented on corneal topography.\n\nResults\nUpon levetiracetam dose reduction, symptoms started to improve and eventually the medication was stopped altogether. The patient’s vision and corneal edema normalized on follow-up."
  },
  {
    "doc_id": 32,
    "label": "proficient_health_literacy",
    "fulltext": "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’ 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’s 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 936μm and left central corneal thickness of 1134μm. 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 567μm and a left central corneal thickness of 573μm, 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.",
    "diff_label_texts": "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 μm OD and 1134 μm 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 μm OD and 573 μm 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.",
    "summary": "A 59-year-old woman was referred to the ophthalmology department with a few weeks’ history of bilateral blurring of vision. She is a known case of secondary progressive multiple sclerosis, and she was started on levetiracetam by her neurologist a few weeks prior to referral in view of new seizure activity. Examination revealed bilateral clinically evident corneal edema, which was documented on corneal topography.\n\nResults\nUpon levetiracetam dose reduction, symptoms started to improve and eventually the medication was stopped altogether. The patient’s vision and corneal edema normalized on follow-up."
  },
  {
    "doc_id": 33,
    "label": "low_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "77-year-old patient with a history of moderate cognitive impairment who suffered bilateral central dislocation of the hip in the context of a generalized convulsive seizure. Clinically, upon arrival in the emergency department, the patient presented a shortening of the lower right limb compared to the contralateral limb, external rotation and joint blockage when performing the log roll test in both limbs. Imaging and clinical optimization study was performed prior to surgery. It was performed in two stages: first the left hip on the eighth day of admission and the right hip on the fifteenth. In both surgeries the same procedure was performed by implanting an anti-protrusive ring and prosthesis with double mobility acetabulum with non-cemented femoral stem. In the immediate postoperative period, the patient did not present any complications associated with the surgery. In the 12-month follow-up, the patient performed a full load with a Harris hip score (HHS) of 77 in the right hip and 79 in the left; 12 points in the WOMAC scale. He has not presented any postoperative complications to date.\n"
  },
  {
    "doc_id": 33,
    "label": "proficient_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "A 77-year-old male with a history of moderate cognitive impairment presented after a tonic–clonic 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’s 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–weight 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.",
    "summary": "77-year-old patient with a history of moderate cognitive impairment who suffered bilateral central dislocation of the hip in the context of a generalized convulsive seizure. Clinically, upon arrival in the emergency department, the patient presented a shortening of the lower right limb compared to the contralateral limb, external rotation and joint blockage when performing the log roll test in both limbs. Imaging and clinical optimization study was performed prior to surgery. It was performed in two stages: first the left hip on the eighth day of admission and the right hip on the fifteenth. In both surgeries the same procedure was performed by implanting an anti-protrusive ring and prosthesis with double mobility acetabulum with non-cemented femoral stem. In the immediate postoperative period, the patient did not present any complications associated with the surgery. In the 12-month follow-up, the patient performed a full load with a Harris hip score (HHS) of 77 in the right hip and 79 in the left; 12 points in the WOMAC scale. He has not presented any postoperative complications to date.\n"
  },
  {
    "doc_id": 34,
    "label": "low_health_literacy",
    "fulltext": "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.",
    "diff_label_texts": "A 19‑month‑old 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‑cm almond that was blocking the airway.",
    "summary": "We describe the case of a 19-month-old boy who accessed the emergency room initially for a head trauma. The clinical evaluation, however, revealed an unexplained serious respiratory distress needing tracheal intubation. After our evaluation, we hypothesized that the severe respiratory distress determined an altered state of consciousness with following head trauma. The radiological findings raised the suspicion of foreign body aspiration for the presence of an atelectasis of the entire left lung. The computed tomography showed an abrupt interruption of the main bronchus at 12 mm from the hull. The following bronchoscopy identified an almond of 2 cm."
  },
  {
    "doc_id": 34,
    "label": "proficient_health_literacy",
    "fulltext": "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.",
    "diff_label_texts": "A 19‑month‑old 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‑mask ventilation with supplemental oxygen and pulse oximetry monitoring were initiated; paradoxically, SpO2 fell below 70% with ongoing ventilation. Lung ultrasound demonstrated absent A‑lines and consolidation, visualizing the lung as solid parenchyma. Given the poor clinical condition, orotracheal intubation with a cuffed endotracheal tube was performed. Post‑stabilization 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‑cm 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.",
    "summary": "We describe the case of a 19-month-old boy who accessed the emergency room initially for a head trauma. The clinical evaluation, however, revealed an unexplained serious respiratory distress needing tracheal intubation. After our evaluation, we hypothesized that the severe respiratory distress determined an altered state of consciousness with following head trauma. The radiological findings raised the suspicion of foreign body aspiration for the presence of an atelectasis of the entire left lung. The computed tomography showed an abrupt interruption of the main bronchus at 12 mm from the hull. The following bronchoscopy identified an almond of 2 cm."
  },
  {
    "doc_id": 35,
    "label": "proficient_health_literacy",
    "fulltext": "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 × 109 leukocytes/L (6.0-17.5), 18.4 × 109 neutrophils/L (1.0-8.5), 7.0 × 109 lymphocytes/L (4.0-13.5), 3.5 × 109 monocytes/L, 459 × 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 × 109 leukocytes/L (6-17), 12.2 × 109 neutrophils/L (1.5-8.5), 7.5 × 109 lymphocytes/L (4-10.5), 1.2 × 109 monocytes/L (600), and 583 × 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",
    "diff_label_texts": "A 4‑month‑old 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‑fed, 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 (11.0–12.6), leukocytes 29.3 × 10^9/L (6.0–17.5), neutrophils 18.4 × 10^9/L (1.0–8.5), lymphocytes 7.0 × 10^9/L (4.0–13.5), monocytes 3.5 × 10^9/L, platelets 459 × 10^9/L (150–350), 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 3–6, 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–clindamycin, then cefepime–vancomycin, 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 (10.5–12), leukocytes 21.2 × 10^9/L (6–17), neutrophils 12.2 × 10^9/L (1.5–8.5), lymphocytes 7.5 × 10^9/L (4–10.5), monocytes 1.2 × 10^9/L (~0.6), platelets 583 × 10^9/L (150–350); HIV serology was negative. Chest imaging showed left apical consolidation, bronchiectasis, lytic lesions in ribs 2–7 and thoracic vertebrae T2–T7, and a multilocular fluid collection; ultrasound identified a fistula linked to the scapular abscess. Initial piperacillin–tazobactam 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‑linked chronic granulomatous disease. Next‑generation 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–sulfamethoxazole 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‑initiated. 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‑positive organisms, especially Aspergillus spp. X‑linked CYBB variants frequently present in infancy with invasive aspergillosis and osteolytic lesions; A. fumigatus remains a leading cause of mortality in CGD.",
    "summary": "A case of infant with chronic granulomatous disease and invasive aspergillosis is reported. The infant was a 4-month-old male infant living with his mother in a prison cell. The infant had tumors in the left axillary region and a chest X-ray suggested rib fractures; he was hospitalized on suspicion of child abuse. A chest X-ray showed an axillary abscess, osteolysis of ribs, pneumonia and pulmonary nodules; the patient received broad spectrum antibiotics and was discharged. At 8 months, he was readmitted with fever and extension of the purulent abscess to the left shoulder region; a chest X-ray showed worsening of the condition. Aspergillus fumigatus was isolated from the secretion of the abscess and invasive aspergillosis was diagnosed; voriconazole was initiated for 28 days. A dihydro rhodamine test was performed and a diagnosis of chronic granulomatous disease caused by the pathogenic variant c.80_83del/Y of the CYBB gene, carried by the mother (c.80_83del/WT), was made. At 12 months, the patient was readmitted with invasive aspergillosis, resistant to treatment, with fatal outcome.\n"
  },
  {
    "doc_id": 36,
    "label": "proficient_health_literacy",
    "fulltext": "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 2×1 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’s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient’s 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.",
    "diff_label_texts": "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 × 1 × 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–HSV-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 ≥2 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–HSV-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.",
    "summary": "A 25-year-old male patient came to the Department of Oral Medicine with the chief complaint of painful canker sores on the lips. Extra-oral examination revealed serosanguineous crusts on the lips that were painful and easily bleed. Intra-oral examination showed diffused and painful irregular erythematous lesions on the upper and lower labial mucosa. The anti-HSV1 IgG test was positive. The patient was diagnosed with HAEM.\n\nCase management: Pharmacological therapy included triamcinolone acetonide 0.1% in orabase, acyclovir tablets, multivitamins, and 0.9% NaCl. Non-pharmacological therapy included advice on maintaining good oral hygiene, avoiding spicy and sour foods, and breaking the bad habit of licking the lips."
  },
  {
    "doc_id": 37,
    "label": "proficient_health_literacy",
    "fulltext": "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/μL). 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 × 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 × 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).",
    "diff_label_texts": "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/μL). On exam, there was an 8 × 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–Lamivudine–Dolutegravir) to a renal-friendly regimen (Lamivudine–Abacavir–Dolutegravir). 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 × 10^9/L, hemoglobin 5.7 g/dL, platelets 71 × 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—exceeding the recommended ≤48-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’s 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.",
    "summary": "The patient was a 29-year-old woman, Para 1, with abnormal vaginal bleeding for a month and living with HIV and had a CD4 of 26 cells/μL. The histological examination of the cervical biopsy confirmed an extra-nodal BL. She had International Federation of Gynecology and Obstetrics (FIGO) stage 3B cervical cancer based on presence of hydronephrosis and pelvic wall involvement. The patient was reviewed at the oncology multidisciplinary meeting and required chemoradiation. There was delay in her management due to a long waiting list for chemoradiation at oncology unit in the referral center and the patient demised 43 days after diagnosis and did not receive the treatment."
  },
  {
    "doc_id": 38,
    "label": "proficient_health_literacy",
    "fulltext": "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’s 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’s 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’s 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’s 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 1.7×1,021 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).",
    "diff_label_texts": "A 56-year-old female with CTD-PAH secondary to Sjogren’s 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’s was confirmed by sicca symptoms with Schirmer’s <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’s control. Her risk status was low-to-intermediate on dual therapy until October–November 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–lung 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 1.7×1,021 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).",
    "summary": "We present the case of a 56-year-old female with CTD-PAH, diagnosed in 2013 with Sjogren’s syndrome complicated by interstitial lung disease (ILD) and PAH. Despite treatment with sildenafil, bosentan, macitentan, iloprost, and corticosteroids, her condition deteriorated, resulting in severe dyspnea and cardiogenic shock in 2020. In May 2023, molecular hydrogen therapy was initiated as an adjuvant treatment. The patient received daily hydrogen capsules, which led to increased CD127+ Treg cells, reduced anti-Ro antibodies, and decreased B cell subsets. Her clinical symptoms stabilized without adverse effects."
  },
  {
    "doc_id": 39,
    "label": "low_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "The authors present the clinical case of a 45-year-old man admitted for pneumonia with a positive result for SARS-CoV-2, with no neurological history, who, on the 16th day of admission, presented a sudden change in consciousness accompanied by a conjugate deviation of the gaze to the right and myoclonia of the face and thoracic region to the left, followed by a generalized tonic-clonic convulsive seizure, associated with persistent left hemiparesis. From the study carried out, the existence of RT-PCR for SARS-CoV-2 in the cerebrospinal fluid is highlighted. The patient presented a clinical evolution with gradual improvement, and the outcome was favourable.\n"
  },
  {
    "doc_id": 39,
    "label": "intermediate_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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–clonic 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.",
    "summary": "The authors present the clinical case of a 45-year-old man admitted for pneumonia with a positive result for SARS-CoV-2, with no neurological history, who, on the 16th day of admission, presented a sudden change in consciousness accompanied by a conjugate deviation of the gaze to the right and myoclonia of the face and thoracic region to the left, followed by a generalized tonic-clonic convulsive seizure, associated with persistent left hemiparesis. From the study carried out, the existence of RT-PCR for SARS-CoV-2 in the cerebrospinal fluid is highlighted. The patient presented a clinical evolution with gradual improvement, and the outcome was favourable.\n"
  },
  {
    "doc_id": 39,
    "label": "proficient_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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–clonic 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–alcohol 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–associated 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.",
    "summary": "The authors present the clinical case of a 45-year-old man admitted for pneumonia with a positive result for SARS-CoV-2, with no neurological history, who, on the 16th day of admission, presented a sudden change in consciousness accompanied by a conjugate deviation of the gaze to the right and myoclonia of the face and thoracic region to the left, followed by a generalized tonic-clonic convulsive seizure, associated with persistent left hemiparesis. From the study carried out, the existence of RT-PCR for SARS-CoV-2 in the cerebrospinal fluid is highlighted. The patient presented a clinical evolution with gradual improvement, and the outcome was favourable.\n"
  },
  {
    "doc_id": 40,
    "label": "low_health_literacy",
    "fulltext": "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 artésunate, 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/Dolutégravir 7 months ago, not observed due to denial of his illness.\n\nThe general physical examination found a fever (38.2 °C), 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",
    "diff_label_texts": "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.",
    "summary": "The patient presented with a chronic productive cough, otalgia and a chronic right-sided purulent otorrhea. The search for acid-fast bacilli was positive by direct examination in the gastric tube liquid and the swab of the auricular pus.\n\nAn anti-tuberculosis treatment of 6 months, associated with adjuvants, led to the patient's complete recovery.\n"
  },
  {
    "doc_id": 40,
    "label": "intermediate_health_literacy",
    "fulltext": "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 artésunate, 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/Dolutégravir 7 months ago, not observed due to denial of his illness.\n\nThe general physical examination found a fever (38.2 °C), 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",
    "diff_label_texts": "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.",
    "summary": "The patient presented with a chronic productive cough, otalgia and a chronic right-sided purulent otorrhea. The search for acid-fast bacilli was positive by direct examination in the gastric tube liquid and the swab of the auricular pus.\n\nAn anti-tuberculosis treatment of 6 months, associated with adjuvants, led to the patient's complete recovery.\n"
  },
  {
    "doc_id": 40,
    "label": "proficient_health_literacy",
    "fulltext": "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 artésunate, 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/Dolutégravir 7 months ago, not observed due to denial of his illness.\n\nThe general physical examination found a fever (38.2 °C), 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",
    "diff_label_texts": "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 °C, 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/µl, VL 12,370 copies/ml; at 6 months on ART CD4 193 cells/µl, VL 9,460 copies/ml; at TB diagnosis (month 7) CD4 89 cells/µl, VL 10,230 copies/ml.\nMicrobiology: Ziehl–Neelsen 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–related immunosuppression.\nTreatment: first-line anti-tuberculosis therapy for 6 months—intensive 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.",
    "summary": "The patient presented with a chronic productive cough, otalgia and a chronic right-sided purulent otorrhea. The search for acid-fast bacilli was positive by direct examination in the gastric tube liquid and the swab of the auricular pus.\n\nAn anti-tuberculosis treatment of 6 months, associated with adjuvants, led to the patient's complete recovery.\n"
  },
  {
    "doc_id": 41,
    "label": "low_health_literacy",
    "fulltext": "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 × 106 µ/L; haemoglobin 11.4 g/gL; activated partial thromboplastin time (APTT) 93 seconds 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 kg). Under general anaesthesia, the right femoral artery was punctured and an 11 cm 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 mm × 20 mm 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.",
    "diff_label_texts": "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.",
    "summary": "A 16-month-old boy with restrictive cardiomyopathy who was listed for a cardiac transplant. At 20 months he required an implantation of an external biventricular support device (Berlin Heart) and had a left hemisphere stroke at 23 months. An intra-arterial approach was used and produced good clinical results. One month later, a heart transplant was performed successfully."
  },
  {
    "doc_id": 41,
    "label": "proficient_health_literacy",
    "fulltext": "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 × 106 µ/L; haemoglobin 11.4 g/gL; activated partial thromboplastin time (APTT) 93 seconds 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 kg). Under general anaesthesia, the right femoral artery was punctured and an 11 cm 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 mm × 20 mm 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.",
    "diff_label_texts": "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 × 10^6/µL, 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 × 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.",
    "summary": "A 16-month-old boy with restrictive cardiomyopathy who was listed for a cardiac transplant. At 20 months he required an implantation of an external biventricular support device (Berlin Heart) and had a left hemisphere stroke at 23 months. An intra-arterial approach was used and produced good clinical results. One month later, a heart transplant was performed successfully."
  },
  {
    "doc_id": 42,
    "label": "low_health_literacy",
    "fulltext": "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®) 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",
    "diff_label_texts": "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.",
    "summary": "52-year-old male patient, transferred to a high-complexity center for a tonic-clonic convulsion and a right LFGHP. In the initial study with radiographs, a right shoulder injury was confirmed and a simple posterior glenohumeral dislocation of the left shoulder was diagnosed, which had not been previously detected. The study was complemented with a computed tomography (CT) of both shoulders, showing a bilateral LFGHP, which demonstrated intrahospital aggravation of the injury of the left shoulder. An open reduction and osteosynthesis with a bilateral blocked plate was performed in one time. The left shoulder required two reinterventions, one for osteosynthesis failure and another for joint release. Two years after the procedure, the patient was satisfactorily progressing with a 5% on the Quick DASH scale and a score of 72 and 76 on the Constant scale in the left and right shoulder, respectively.\n"
  },
  {
    "doc_id": 42,
    "label": "intermediate_health_literacy",
    "fulltext": "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®) 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",
    "diff_label_texts": "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.",
    "summary": "52-year-old male patient, transferred to a high-complexity center for a tonic-clonic convulsion and a right LFGHP. In the initial study with radiographs, a right shoulder injury was confirmed and a simple posterior glenohumeral dislocation of the left shoulder was diagnosed, which had not been previously detected. The study was complemented with a computed tomography (CT) of both shoulders, showing a bilateral LFGHP, which demonstrated intrahospital aggravation of the injury of the left shoulder. An open reduction and osteosynthesis with a bilateral blocked plate was performed in one time. The left shoulder required two reinterventions, one for osteosynthesis failure and another for joint release. Two years after the procedure, the patient was satisfactorily progressing with a 5% on the Quick DASH scale and a score of 72 and 76 on the Constant scale in the left and right shoulder, respectively.\n"
  },
  {
    "doc_id": 42,
    "label": "proficient_health_literacy",
    "fulltext": "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®) 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",
    "diff_label_texts": "A 52-year-old male with no prior medical history was transferred from a lower-level facility for a tonic–clonic 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–extension 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).",
    "summary": "52-year-old male patient, transferred to a high-complexity center for a tonic-clonic convulsion and a right LFGHP. In the initial study with radiographs, a right shoulder injury was confirmed and a simple posterior glenohumeral dislocation of the left shoulder was diagnosed, which had not been previously detected. The study was complemented with a computed tomography (CT) of both shoulders, showing a bilateral LFGHP, which demonstrated intrahospital aggravation of the injury of the left shoulder. An open reduction and osteosynthesis with a bilateral blocked plate was performed in one time. The left shoulder required two reinterventions, one for osteosynthesis failure and another for joint release. Two years after the procedure, the patient was satisfactorily progressing with a 5% on the Quick DASH scale and a score of 72 and 76 on the Constant scale in the left and right shoulder, respectively.\n"
  },
  {
    "doc_id": 43,
    "label": "low_health_literacy",
    "fulltext": "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 ß-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 °C, 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® 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 “cusp feelers” 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).",
    "diff_label_texts": "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.",
    "summary": "We report the case of a 70-year-old white man who was treated for severe symptomatic aortic regurgitation using transcatheter aortic valve implantation from the apical approach. Because of recurrent cardiac decompensation 4 weeks after implantation he underwent the implantation of a left ventricular assist device system. A year later echocardiography showed a severe transvalvular central insufficiency. Our heart team decided to choose a valve-in-valve approach while reducing the flow rate of left ventricular assist device to minimum and pacing with a frequency of 140 beats/minute. There was an excellent result and our patient is doing well with no relevant insufficiency of the aortic valve at 12-month follow-up."
  },
  {
    "doc_id": 43,
    "label": "intermediate_health_literacy",
    "fulltext": "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 ß-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 °C, 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® 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 “cusp feelers” 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).",
    "diff_label_texts": "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.",
    "summary": "We report the case of a 70-year-old white man who was treated for severe symptomatic aortic regurgitation using transcatheter aortic valve implantation from the apical approach. Because of recurrent cardiac decompensation 4 weeks after implantation he underwent the implantation of a left ventricular assist device system. A year later echocardiography showed a severe transvalvular central insufficiency. Our heart team decided to choose a valve-in-valve approach while reducing the flow rate of left ventricular assist device to minimum and pacing with a frequency of 140 beats/minute. There was an excellent result and our patient is doing well with no relevant insufficiency of the aortic valve at 12-month follow-up."
  },
  {
    "doc_id": 43,
    "label": "proficient_health_literacy",
    "fulltext": "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 ß-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 °C, 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® 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 “cusp feelers” 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).",
    "diff_label_texts": "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 °C, 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.",
    "summary": "We report the case of a 70-year-old white man who was treated for severe symptomatic aortic regurgitation using transcatheter aortic valve implantation from the apical approach. Because of recurrent cardiac decompensation 4 weeks after implantation he underwent the implantation of a left ventricular assist device system. A year later echocardiography showed a severe transvalvular central insufficiency. Our heart team decided to choose a valve-in-valve approach while reducing the flow rate of left ventricular assist device to minimum and pacing with a frequency of 140 beats/minute. There was an excellent result and our patient is doing well with no relevant insufficiency of the aortic valve at 12-month follow-up."
  },
  {
    "doc_id": 44,
    "label": "low_health_literacy",
    "fulltext": "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/m². 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—with measurements of 12 × 11 × 10 mm—a 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 µUI/ml and 10.0 µUI/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 × 12 × 11 mm), with a slight decrease in size observed at the three-year follow-up, measuring 7 × 10 × 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.",
    "diff_label_texts": "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’s 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.",
    "summary": "We present the case of a 12-year-old boy admitted due to the recent onset of headaches and diabetes insipidus. Magnetic resonance imaging revealed Rathke cleft cyst apoplexy. Given the absence of compressive symptoms in a child at the early stages of puberty and without abnormalities in basic endocrine tests, a conservative strategy was employed, involving regular clinical, biological, and radiological follow-ups. The child experienced normal puberty without any endocrine deficiencies except for a partial growth hormone deficiency."
  },
  {
    "doc_id": 44,
    "label": "proficient_health_literacy",
    "fulltext": "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/m². 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—with measurements of 12 × 11 × 10 mm—a 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 µUI/ml and 10.0 µUI/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 × 12 × 11 mm), with a slight decrease in size observed at the three-year follow-up, measuring 7 × 10 × 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.",
    "diff_label_texts": "A 12-year-old boy presented with one week of acute-onset headache and polyuria–polydipsia. Past history was unremarkable. On first assessment: height 146.5 cm (M), weight 30 kg (−1.4 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/m²/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 × 6 × 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 × 11 × 10 mm), and subsequent surveillance at two years remained stable (11 × 12 × 11 mm) with slight size reduction at three years (7 × 10 × 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 −0.8 SD to −1.1 SD, prompting evaluation for acquired GH deficiency. At 14 years 9 months, two GH stimulation tests demonstrated partial GH deficiency: propranolol–glucagon peak 19.3 µUI/ml and insulin tolerance test peak 10.0 µUI/ml. GH therapy led to improved growth velocity from −1.1 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.",
    "summary": "We present the case of a 12-year-old boy admitted due to the recent onset of headaches and diabetes insipidus. Magnetic resonance imaging revealed Rathke cleft cyst apoplexy. Given the absence of compressive symptoms in a child at the early stages of puberty and without abnormalities in basic endocrine tests, a conservative strategy was employed, involving regular clinical, biological, and radiological follow-ups. The child experienced normal puberty without any endocrine deficiencies except for a partial growth hormone deficiency."
  },
  {
    "doc_id": 45,
    "label": "proficient_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "A 67-year-old patient with no medical history presented with a 6‑month 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 × 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 1–2 follicular B‑cell NHL: CD20+, CD19+, CD79a+, CD10+. Bone marrow biopsy and the pre‑therapeutic work‑up were normal. The patient received 4 cures of R‑CHOP‑21 (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‑DHAOX (rituximab 375 mg/m2 IV D1, high‑dose aracytine 2 g/m2 × 2 IV D2, dexamethasone 40 mg D1–D4, 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‑type 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‑associated localized AL amyloid process emerging in the site of the prior follicular lymphoma, despite systemic evaluations (including marrow and organ assessments) remaining normal.",
    "summary": "We report the case of a 67-year-old patient without pathological CDDs who presented with a deterioration of general condition with progressive dysphonia and dysphagia with a large mass in the neck that was biopsy-proven to be a grade 1 and 2 follicular non-Hodgkin lymphoma. A cervico-thoraco-abdomino-pelvic CT scan showed a 70 mm x 40 mm nasopharyngeal mass extending to 60 mm. Bone marrow biopsy was normal and the pre-therapeutic evaluation was normal. The patient received 4 courses of rituximab plus CHOP (cyclophosphamide, adriamycin, prednisone and oncovin) without response and then 3 courses of rituximab plus DHAOX (dexamethasone, high dose ara-cytin and oxalipatin) with persistence of the mass. The biopsy of the latter showed the disappearance of the B lymphocyte infiltration with presence of the AL amyloid deposits. The immunoelectrophoresis of plasma proteins showed the presence of immunoglobulin M. A positron emission tomography (PET) scan showed a hypermetabolic nasopharyngeal process. The patient is currently receiving a protocol of bortezomib, prednisone and bendamustine.\n"
  },
  {
    "doc_id": 46,
    "label": "low_health_literacy",
    "fulltext": "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°C, 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",
    "diff_label_texts": "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.",
    "summary": "A 46-year-old Haitian man, residing in Chile, presented with warty plaques in the anterior tibial region that had been present for one year. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in the histopathology and dematiaceous colonies in the mycological culture. In addition, conidia compatible with Fonsecaea spp. were observed in direct microscopy. After six months of treatment with systemic antimycotics and cryotherapy, complete remission of the lesions was achieved.\n"
  },
  {
    "doc_id": 46,
    "label": "intermediate_health_literacy",
    "fulltext": "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°C, 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",
    "diff_label_texts": "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.",
    "summary": "A 46-year-old Haitian man, residing in Chile, presented with warty plaques in the anterior tibial region that had been present for one year. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in the histopathology and dematiaceous colonies in the mycological culture. In addition, conidia compatible with Fonsecaea spp. were observed in direct microscopy. After six months of treatment with systemic antimycotics and cryotherapy, complete remission of the lesions was achieved.\n"
  },
  {
    "doc_id": 46,
    "label": "proficient_health_literacy",
    "fulltext": "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°C, 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",
    "diff_label_texts": "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 × 1 cm, 2 × 2 cm, and 3 × 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°C 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 6–8 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.",
    "summary": "A 46-year-old Haitian man, residing in Chile, presented with warty plaques in the anterior tibial region that had been present for one year. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in the histopathology and dematiaceous colonies in the mycological culture. In addition, conidia compatible with Fonsecaea spp. were observed in direct microscopy. After six months of treatment with systemic antimycotics and cryotherapy, complete remission of the lesions was achieved.\n"
  },
  {
    "doc_id": 47,
    "label": "low_health_literacy",
    "fulltext": "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 × 10 mm on the right and 45 × 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",
    "diff_label_texts": "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.",
    "summary": "A 19-year-old man with no significant history was admitted to hospital with a painful left scrotal mass that had been present for 8 months. He had undergone an orchidectomy and the pathological examination was in favour of epididymal tuberculosis. A radiological examination had shown other sites of infection: lymph nodes, lungs, parietal and osteoarticular. An anti-tuberculosis treatment was initiated. However, in the 4th month of treatment, the patient had convulsive seizures. A brain MRI was performed and concluded that there were brain tuberculomas. The anti-tuberculosis treatment was continued in association with an anticonvulsant with good clinical and radiological evolution.\n"
  },
  {
    "doc_id": 47,
    "label": "intermediate_health_literacy",
    "fulltext": "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 × 10 mm on the right and 45 × 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",
    "diff_label_texts": "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.",
    "summary": "A 19-year-old man with no significant history was admitted to hospital with a painful left scrotal mass that had been present for 8 months. He had undergone an orchidectomy and the pathological examination was in favour of epididymal tuberculosis. A radiological examination had shown other sites of infection: lymph nodes, lungs, parietal and osteoarticular. An anti-tuberculosis treatment was initiated. However, in the 4th month of treatment, the patient had convulsive seizures. A brain MRI was performed and concluded that there were brain tuberculomas. The anti-tuberculosis treatment was continued in association with an anticonvulsant with good clinical and radiological evolution.\n"
  },
  {
    "doc_id": 47,
    "label": "proficient_health_literacy",
    "fulltext": "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 × 10 mm on the right and 45 × 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",
    "diff_label_texts": "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 (3–4 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 × 10 mm right, 45 × 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.",
    "summary": "A 19-year-old man with no significant history was admitted to hospital with a painful left scrotal mass that had been present for 8 months. He had undergone an orchidectomy and the pathological examination was in favour of epididymal tuberculosis. A radiological examination had shown other sites of infection: lymph nodes, lungs, parietal and osteoarticular. An anti-tuberculosis treatment was initiated. However, in the 4th month of treatment, the patient had convulsive seizures. A brain MRI was performed and concluded that there were brain tuberculomas. The anti-tuberculosis treatment was continued in association with an anticonvulsant with good clinical and radiological evolution.\n"
  },
  {
    "doc_id": 48,
    "label": "low_health_literacy",
    "fulltext": "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/μL), 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/µL), 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",
    "diff_label_texts": "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.",
    "summary": "We present the case of a 10-year-old boy undergoing chemotherapy for acute lymphoblastic leukaemia. During the induction period he developed a cerebral abscess caused by B. cereus that was diagnosed by imaging tests and direct detection in the cerebrospinal fluid. His evolution was favourable with antibiotic treatment.\n"
  },
  {
    "doc_id": 48,
    "label": "intermediate_health_literacy",
    "fulltext": "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/μL), 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/µL), 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",
    "diff_label_texts": "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.",
    "summary": "We present the case of a 10-year-old boy undergoing chemotherapy for acute lymphoblastic leukaemia. During the induction period he developed a cerebral abscess caused by B. cereus that was diagnosed by imaging tests and direct detection in the cerebrospinal fluid. His evolution was favourable with antibiotic treatment.\n"
  },
  {
    "doc_id": 48,
    "label": "proficient_health_literacy",
    "fulltext": "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/μL), 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/µL), 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",
    "diff_label_texts": "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/µL) 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/µL), 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—an 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.",
    "summary": "We present the case of a 10-year-old boy undergoing chemotherapy for acute lymphoblastic leukaemia. During the induction period he developed a cerebral abscess caused by B. cereus that was diagnosed by imaging tests and direct detection in the cerebrospinal fluid. His evolution was favourable with antibiotic treatment.\n"
  },
  {
    "doc_id": 49,
    "label": "low_health_literacy",
    "fulltext": "Female patient, 16 years old, presenting a depressed gray plaque of 10.5 × 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",
    "diff_label_texts": "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.",
    "summary": "16-year-old girl with a depressed gray plaque on the left thigh, with a vascular malformation affecting the skin and subcutaneous tissue evident by angioresonance.\n"
  },
  {
    "doc_id": 49,
    "label": "proficient_health_literacy",
    "fulltext": "Female patient, 16 years old, presenting a depressed gray plaque of 10.5 × 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",
    "diff_label_texts": "Female patient, 16 years old, with a depressed gray plaque measuring 10.5 × 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.",
    "summary": "16-year-old girl with a depressed gray plaque on the left thigh, with a vascular malformation affecting the skin and subcutaneous tissue evident by angioresonance.\n"
  },
  {
    "doc_id": 50,
    "label": "intermediate_health_literacy",
    "fulltext": "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°C, HR 88 bpm, RR 18 bpm). She had a BMI of 16.6 kg/m² 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, 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal range, 3.9–86.4 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’s 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.",
    "diff_label_texts": "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.",
    "summary": "We present a unique case of a 57-year-old patient with a medical history of asthma and allergic rhinitis who presented recurrent abdominal pain, significant blood eosinophilia, and elevated levels of Immunoglobulin G4. After ruling out hematological and secondary causes of eosinophilia, a biopsy of the colon mucosa revealed an excess of tissue eosinophils, confirming the diagnosis of EoC. The patient responded well to corticosteroids and was subsequently maintained on montelukast, with no recurrence of symptoms over 3 months."
  },
  {
    "doc_id": 50,
    "label": "proficient_health_literacy",
    "fulltext": "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°C, HR 88 bpm, RR 18 bpm). She had a BMI of 16.6 kg/m² 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, 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal range, 3.9–86.4 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’s 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.",
    "diff_label_texts": "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/m²) 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.",
    "summary": "We present a unique case of a 57-year-old patient with a medical history of asthma and allergic rhinitis who presented recurrent abdominal pain, significant blood eosinophilia, and elevated levels of Immunoglobulin G4. After ruling out hematological and secondary causes of eosinophilia, a biopsy of the colon mucosa revealed an excess of tissue eosinophils, confirming the diagnosis of EoC. The patient responded well to corticosteroids and was subsequently maintained on montelukast, with no recurrence of symptoms over 3 months."
  },
  {
    "doc_id": 51,
    "label": "low_health_literacy",
    "fulltext": "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’s 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’s 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 2/6–3/6 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 ×43 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’s 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’s LA and recipient’s 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’s 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’s 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 × 109/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’s 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 × 109/L. On the 7th day post-surgery, tacrolimus capsules were introduced at an oral dose of (1 mg) to minimize the patient’s 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’s 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.",
    "diff_label_texts": "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.",
    "summary": "Herein, we report a case of heart failure due to Carney syndrome that resulted in cardiac myxoma combined with dilated cardiomyopathy. A 35-year-old male was admitted to the hospital three years ago because of sudden chest tightness and shortness of breath. Echocardiography indicated myxoma, and a combination of genetic screening and physical examination confirmed Carney syndrome with cardiac myxoma. Following symptomatic management, he was discharged. Surgical interventions were not considered at the time. However, the patient’s chest tightness and shortness of breath symptoms worsened, and he returned to the hospital. A New York Heart Association grade IV heart function was confirmed, and echocardiography indicated the presence of dilated cardiomyopathy accompanied by cardiac myxoma. Ultimately, the patient’s heart failure was successfully treated with heart transplantation."
  },
  {
    "doc_id": 51,
    "label": "intermediate_health_literacy",
    "fulltext": "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’s 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’s 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 2/6–3/6 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 ×43 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’s 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’s LA and recipient’s 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’s 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’s 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 × 109/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’s 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 × 109/L. On the 7th day post-surgery, tacrolimus capsules were introduced at an oral dose of (1 mg) to minimize the patient’s 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’s 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.",
    "diff_label_texts": "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.",
    "summary": "Herein, we report a case of heart failure due to Carney syndrome that resulted in cardiac myxoma combined with dilated cardiomyopathy. A 35-year-old male was admitted to the hospital three years ago because of sudden chest tightness and shortness of breath. Echocardiography indicated myxoma, and a combination of genetic screening and physical examination confirmed Carney syndrome with cardiac myxoma. Following symptomatic management, he was discharged. Surgical interventions were not considered at the time. However, the patient’s chest tightness and shortness of breath symptoms worsened, and he returned to the hospital. A New York Heart Association grade IV heart function was confirmed, and echocardiography indicated the presence of dilated cardiomyopathy accompanied by cardiac myxoma. Ultimately, the patient’s heart failure was successfully treated with heart transplantation."
  },
  {
    "doc_id": 51,
    "label": "proficient_health_literacy",
    "fulltext": "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’s 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’s 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 2/6–3/6 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 ×43 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’s 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’s LA and recipient’s 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’s 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’s 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 × 109/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’s 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 × 109/L. On the 7th day post-surgery, tacrolimus capsules were introduced at an oral dose of (1 mg) to minimize the patient’s 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’s 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.",
    "diff_label_texts": "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 2/6–3/6 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–V3. 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 × 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‑troponin T was 796.70 ng/L; NT‑proBNP 10,798 pg/mL; WBC 17.15 × 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‑troponin T decreased to 390 ng/L; NT‑proBNP decreased to 7877 pg/mL; WBC 12.15 × 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‑troponin T was 85 ng/L; NT‑proBNP 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.",
    "summary": "Herein, we report a case of heart failure due to Carney syndrome that resulted in cardiac myxoma combined with dilated cardiomyopathy. A 35-year-old male was admitted to the hospital three years ago because of sudden chest tightness and shortness of breath. Echocardiography indicated myxoma, and a combination of genetic screening and physical examination confirmed Carney syndrome with cardiac myxoma. Following symptomatic management, he was discharged. Surgical interventions were not considered at the time. However, the patient’s chest tightness and shortness of breath symptoms worsened, and he returned to the hospital. A New York Heart Association grade IV heart function was confirmed, and echocardiography indicated the presence of dilated cardiomyopathy accompanied by cardiac myxoma. Ultimately, the patient’s heart failure was successfully treated with heart transplantation."
  },
  {
    "doc_id": 52,
    "label": "low_health_literacy",
    "fulltext": "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 (café 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 (–), 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",
    "diff_label_texts": "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.",
    "summary": "2.5-year-old pre-schooler with a history of NF1 presenting with bloody diarrhea. On endoscopic examination, the mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency. Colon mucosal biopsies showed signs of chronic inflammation consistent with a diagnosis of ulcerative colitis and CMV infection was diagnosed by PCR.\n"
  },
  {
    "doc_id": 52,
    "label": "proficient_health_literacy",
    "fulltext": "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 (café 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 (–), 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",
    "diff_label_texts": "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 (5–10/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 café-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 café-au-lait macules. Labs: microcytic–hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (13,900/µL), 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—consistent 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–Neelsen, 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 µg/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.",
    "summary": "2.5-year-old pre-schooler with a history of NF1 presenting with bloody diarrhea. On endoscopic examination, the mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency. Colon mucosal biopsies showed signs of chronic inflammation consistent with a diagnosis of ulcerative colitis and CMV infection was diagnosed by PCR.\n"
  },
  {
    "doc_id": 53,
    "label": "proficient_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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’s 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.",
    "summary": "We present the case of a 40-year-old HIV-positive man with regular adherence to treatment, who consulted for intermittent febrile episodes of two years' evolution, adding in the last two months progressive diffuse abdominal pain and generalized adenomegaly. In the laboratory, he presented pancytopenia, coagulopathy, hypoalbuminemia and increased acute phase reactants. The computed tomography (CT) of the thorax, abdomen and pelvis only showed hepato-splenomegaly and generalized adenomegaly. Multiple microbiological examinations were performed, including cultures for Mycobacterium sp. of different samples, all with negative results, with the exception of RT-PCR for HHV-8. A left iliac ganglion biopsy was performed with findings consistent with Castleman's disease. Despite restarting antiretroviral therapy, the symptomatology progressed, initiating treatment with corticosteroids and ganciclovir. After a week, he developed multiple organ failure and anasarca, which contraindicated the drugs initiated. A new chest CT was performed that showed infiltrates with a tree-like pattern in the upper right lobe associated with bilateral pleural effusion, and at the abdominal level, progression of hepato-splenomegaly and ascites. He passed to the intensive care unit 48 hours later due to fulminant hepatic failure. The patient died within a few hours. A postmortem culture of the tracheal aspirate was received positive for Mycobacterium tuberculosis and a liver biopsy with non-necrotizing granulomas.\n"
  },
  {
    "doc_id": 54,
    "label": "proficient_health_literacy",
    "fulltext": "4-month-old indigenous lactating mother from the rural area of the interior of Panama, from the town of Urracá, 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® (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",
    "diff_label_texts": "A 4‑month‑old Indigenous infant from Urracá, rural Panama (approximately 3 hours by canoe from the nearest health subcenter), with protein‑calorie malnutrition and no prior healthcare or vaccinations, presented with 4 days of non‑bloody diarrhea and vomiting, progressing to moderate–severe 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‑level 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 −2.52 (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 39×10^3/µL, severe anemia Hgb 5.6 g/dL, thrombocytosis 502×10^3/µL. 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‑positive cocci in clusters; oxacillin 200 mg/kg/day was added and ceftriaxone increased to 75–100 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− 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‑salt albumin, 10% calcium gluconate; analgesia/sedation was switched from fentanyl to remifentanil due to elevated transaminases.\n\nThe admission blood culture grew methicillin‑resistant Staphylococcus aureus (MRSA); oxacillin was discontinued and clindamycin 40 mg/kg/day was added. A subsequent blood culture smear showing Gram‑negative 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 HD4–5, the second‑day 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‑hour 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‑CoV‑2 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.",
    "summary": "4-month-old lactating infant, indigenous ethnicity, from the rural interior of Panama, 3 hours by canoe from the nearest health subcenter, with protein-caloric malnutrition, who presented with acute diarrhea and moderate-severe dehydration, receiving Enterogermina as part of the initial treatment. She was transferred to a third-level hospital, where she arrived with respiratory distress and signs of shock. The initial blood culture reported growth of methicillin-resistant Staphylococcus aureus (MRSA), the gastrointestinal panel was positive for Clostridiodes difficile, and later growth was confirmed in serial blood cultures of peripheral blood and central venous catheter, of Bacillus clausii. With a torpid evolution and resistance to multiple antibiotic regimens, she died of multisystem organ failure twelve days after admission.\n"
  },
  {
    "doc_id": 55,
    "label": "low_health_literacy",
    "fulltext": "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 mm in diameter), and pupillary reaction was absent. The remaining anterior segment examination showed no apparent abnormalities. Fundus examination was challenging due to the child’s size. Hertel exophthalmometry readings measured 10.5 mm in the right eye and 18 mm 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’ posterior part, tight adhesion to the optic nerve was observed. Due to the mass’s substantial size and the restricted surgical field, volume reduction was necessary. Approximately 12.5 mL 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’s 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’s 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 mm in the right eye and 8 mm in the left. The remaining anterior segment examination showed no apparent abnormalities.",
    "diff_label_texts": "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.",
    "summary": "Patient concerns: A 2-year-old female child was presented exhibiting proptosis and inward and upward eyeball displacement. Enhanced magnetic resonance imaging revealed a well-circumscribed mass, persisting with hypointense signals on T1-weighted images (T1WI) and hyperintense signals on T2-weighted images (T2WI).\n\nDiagnoses: The diagnosis of teratoma was confirmed finally through histological and immunohistochemical exams.\n\nInterventions: A transconjunctival approach via the inferior fornix, coupled with canthotomy and cantholysis, was performed. However, a month postsurgery, the patient developed enophthalmos, conjunctival hyperemia, and keratitis upon ocular examination. A second operation involved the implantation of allogeneic sclera into the orbit to increase orbital volume, improve the pitting of the fossa, and restore keratitis to normal.\n\nOutcomes: No recurrence and other complications were noted during the 1-year follow-up."
  },
  {
    "doc_id": 55,
    "label": "proficient_health_literacy",
    "fulltext": "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 mm in diameter), and pupillary reaction was absent. The remaining anterior segment examination showed no apparent abnormalities. Fundus examination was challenging due to the child’s size. Hertel exophthalmometry readings measured 10.5 mm in the right eye and 18 mm 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’ posterior part, tight adhesion to the optic nerve was observed. Due to the mass’s substantial size and the restricted surgical field, volume reduction was necessary. Approximately 12.5 mL 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’s 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’s 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 mm in the right eye and 8 mm in the left. The remaining anterior segment examination showed no apparent abnormalities.",
    "diff_label_texts": "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.",
    "summary": "Patient concerns: A 2-year-old female child was presented exhibiting proptosis and inward and upward eyeball displacement. Enhanced magnetic resonance imaging revealed a well-circumscribed mass, persisting with hypointense signals on T1-weighted images (T1WI) and hyperintense signals on T2-weighted images (T2WI).\n\nDiagnoses: The diagnosis of teratoma was confirmed finally through histological and immunohistochemical exams.\n\nInterventions: A transconjunctival approach via the inferior fornix, coupled with canthotomy and cantholysis, was performed. However, a month postsurgery, the patient developed enophthalmos, conjunctival hyperemia, and keratitis upon ocular examination. A second operation involved the implantation of allogeneic sclera into the orbit to increase orbital volume, improve the pitting of the fossa, and restore keratitis to normal.\n\nOutcomes: No recurrence and other complications were noted during the 1-year follow-up."
  },
  {
    "doc_id": 56,
    "label": "low_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "78-year-old patient, taking many medicines and included in the Personalised Medication Dosage System (SPD). When she came to collect her medication, she informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. A review of the medication was carried out, focusing on the dosage of the medicines metabolised or eliminated by the kidneys, depending on the patient's estimated glomerular filtration rate (EGFR). A referral was made to the Primary Care Physician (PCP) by means of a report, in which the reduction of the dose of losartan and manidipine was recommended, depending on the patient's estimated glomerular filtration rate (EGFR). The PCP reduced the dose of the antihypertensive medicines. The case was monitored, which allowed us to observe that the patient no longer presented the symptoms described initially.\n"
  },
  {
    "doc_id": 56,
    "label": "intermediate_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "78-year-old patient, taking many medicines and included in the Personalised Medication Dosage System (SPD). When she came to collect her medication, she informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. A review of the medication was carried out, focusing on the dosage of the medicines metabolised or eliminated by the kidneys, depending on the patient's estimated glomerular filtration rate (EGFR). A referral was made to the Primary Care Physician (PCP) by means of a report, in which the reduction of the dose of losartan and manidipine was recommended, depending on the patient's estimated glomerular filtration rate (EGFR). The PCP reduced the dose of the antihypertensive medicines. The case was monitored, which allowed us to observe that the patient no longer presented the symptoms described initially.\n"
  },
  {
    "doc_id": 56,
    "label": "proficient_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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 50–75% of standard dose for eGFR 30–59 ml/min/1.73 m2 and adjusting manidipine for eGFR 15–30 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 300–900 mg for eGFR 30–60). 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.",
    "summary": "78-year-old patient, taking many medicines and included in the Personalised Medication Dosage System (SPD). When she came to collect her medication, she informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. A review of the medication was carried out, focusing on the dosage of the medicines metabolised or eliminated by the kidneys, depending on the patient's estimated glomerular filtration rate (EGFR). A referral was made to the Primary Care Physician (PCP) by means of a report, in which the reduction of the dose of losartan and manidipine was recommended, depending on the patient's estimated glomerular filtration rate (EGFR). The PCP reduced the dose of the antihypertensive medicines. The case was monitored, which allowed us to observe that the patient no longer presented the symptoms described initially.\n"
  },
  {
    "doc_id": 57,
    "label": "low_health_literacy",
    "fulltext": "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 Consciência Fonológica Instrumento de Avaliação 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 – 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 “d” and “b”) 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",
    "diff_label_texts": "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.",
    "summary": "This study is a case report of the evaluation and intervention process of a 9-year-old child with the paradoxical combination of high abilities associated with dyslexia. The objective was to compare the performance in the tasks of phonological processing, reading and writing before and after phonological remediation. In the first evaluation, the child presented an alphabetic level in reading, a transition phase between the syllabic-alphabetic and alphabetic levels in writing and a performance below the expected level in phonological processing abilities. After the intervention, there was an improvement in phonological processing abilities, consolidation of alphabetic writing and of the orthographic level of reading.\n"
  },
  {
    "doc_id": 57,
    "label": "proficient_health_literacy",
    "fulltext": "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 Consciência Fonológica Instrumento de Avaliação 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 – 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 “d” and “b”) 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",
    "diff_label_texts": "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–English 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—phonological awareness (CONFIAS): performance aligned with the writing hypothesis at each time point. T1 scores: syllabic = 35; phonemic = 14 (consistent with a syllabic–alphabetic 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→29 s), objects (62→59 s), and colors (60→56 s), but worsened for digits (37→41 s). Reduced naming latencies indicate more efficient access to the phonological/visual lexicon, though residual RAN deficits persisted—typical in DD.\nReading: T1 showed an alphabetic level with reliance on sub-vocal decoding, confusions for visually/phonologically similar letters, and very slow rate (≈20 words/min), well below grade expectations. T2 advanced to an orthographic level with oral reading ≈94.4 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–alphabetic 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).",
    "summary": "This study is a case report of the evaluation and intervention process of a 9-year-old child with the paradoxical combination of high abilities associated with dyslexia. The objective was to compare the performance in the tasks of phonological processing, reading and writing before and after phonological remediation. In the first evaluation, the child presented an alphabetic level in reading, a transition phase between the syllabic-alphabetic and alphabetic levels in writing and a performance below the expected level in phonological processing abilities. After the intervention, there was an improvement in phonological processing abilities, consolidation of alphabetic writing and of the orthographic level of reading.\n"
  },
  {
    "doc_id": 58,
    "label": "low_health_literacy",
    "fulltext": "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 × 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 × 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",
    "diff_label_texts": "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.",
    "summary": "We present the case of a 65-year-old woman with a primary mediastinal myelolipoma. Computed tomography of the chest showed an ovoid, well-defined bordered tumor of 6.5 × 4.2 cm, located in the posterior mediastinum. A trans-thoracic biopsy of the lesion was performed and microscopic examination revealed haemopoietic elements and mature adipose tissue.\n"
  },
  {
    "doc_id": 58,
    "label": "intermediate_health_literacy",
    "fulltext": "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 × 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 × 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",
    "diff_label_texts": "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 × 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.",
    "summary": "We present the case of a 65-year-old woman with a primary mediastinal myelolipoma. Computed tomography of the chest showed an ovoid, well-defined bordered tumor of 6.5 × 4.2 cm, located in the posterior mediastinum. A trans-thoracic biopsy of the lesion was performed and microscopic examination revealed haemopoietic elements and mature adipose tissue.\n"
  },
  {
    "doc_id": 58,
    "label": "proficient_health_literacy",
    "fulltext": "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 × 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 × 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",
    "diff_label_texts": "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 × 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 × 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.",
    "summary": "We present the case of a 65-year-old woman with a primary mediastinal myelolipoma. Computed tomography of the chest showed an ovoid, well-defined bordered tumor of 6.5 × 4.2 cm, located in the posterior mediastinum. A trans-thoracic biopsy of the lesion was performed and microscopic examination revealed haemopoietic elements and mature adipose tissue.\n"
  },
  {
    "doc_id": 59,
    "label": "low_health_literacy",
    "fulltext": "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°C for five hours. Upon admission to the local hospital’s emergency department, his core temperature (Tc) was recorded as 40°C. 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’s solution and normal saline at a rate of 2.5mL/kg∙h), 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’s 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·min. 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 3.55×109/L to 3.13×109/L, lymphocytes significantly decreased from 0.25×109/L to 0.1×109/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 °C and 38.5 °C. 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°C), 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 14.94×109/L and NEU increased to 13.77×109/L. The levels of serum total bilirubin rose to 235.2 µmol/L, while creatinine increased to 441µmol/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’s 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’s condition progressively worsened over the next 7 days, ultimately resulting in his demise on day 29. The patients’ inflammatory indicators, cytokines, and coagulation indicators are presented in Table 1.",
    "diff_label_texts": "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.",
    "summary": "We report the first case of heatstroke comorbid with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection in a 52-year-old male. After receiving intravenous antibiotics, organ protection measures, and treatment for coagulation disorders, his fever and coma resolved. However, he developed dyspnea and cerebral hemorrhage after several days. This patient experienced a multi-pathogen pulmonary infection and an intractable coagulopathy that ultimately resulted in MODS and death."
  },
  {
    "doc_id": 59,
    "label": "proficient_health_literacy",
    "fulltext": "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°C for five hours. Upon admission to the local hospital’s emergency department, his core temperature (Tc) was recorded as 40°C. 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’s solution and normal saline at a rate of 2.5mL/kg∙h), 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’s 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·min. 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 3.55×109/L to 3.13×109/L, lymphocytes significantly decreased from 0.25×109/L to 0.1×109/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 °C and 38.5 °C. 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°C), 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 14.94×109/L and NEU increased to 13.77×109/L. The levels of serum total bilirubin rose to 235.2 µmol/L, while creatinine increased to 441µmol/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’s 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’s condition progressively worsened over the next 7 days, ultimately resulting in his demise on day 29. The patients’ inflammatory indicators, cytokines, and coagulation indicators are presented in Table 1.",
    "diff_label_texts": "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°C for 5 h). On ED arrival, core temperature was 40°C 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’s and normal saline at 2.5 mL/kg·h; piperacillin–tazobactam; 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 µg/kg·min. Laboratory data showed severe infection, anemia, thrombocytopenia, DIC, and acute hepatic and renal injury: WBC 3.55→3.13×10^9/L, lymphocytes 0.25→0.1×10^9/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 36–38.5°C. 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°C, necessitating reintubation. Bronchoscopy showed scant sputum. Coma recurred (GCS 3/15). Labs: WBC 14.94×10^9/L, NEU 13.77×10^9/L; total bilirubin 235.2 µmol/L; creatinine 441 µmol/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.",
    "summary": "We report the first case of heatstroke comorbid with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection in a 52-year-old male. After receiving intravenous antibiotics, organ protection measures, and treatment for coagulation disorders, his fever and coma resolved. However, he developed dyspnea and cerebral hemorrhage after several days. This patient experienced a multi-pathogen pulmonary infection and an intractable coagulopathy that ultimately resulted in MODS and death."
  },
  {
    "doc_id": 60,
    "label": "proficient_health_literacy",
    "fulltext": "A 19-year-old female presented to our hospital’s 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°C, 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 14.77×10^9/L and a neutrophil count of 13.55×10^9/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’s symptoms, a chest computed tomography (CT) scan was performed. Incidentally, this scan revealed a left adrenal mass with soft tissue density, measuring 43 mm × 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’s 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 × 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’s 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 × 40 mm × 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.",
    "diff_label_texts": "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°C, BP 189/120 mmHg, HR 148 bpm. Laboratory testing showed WBC 14.77×10^9/L and neutrophils 13.55×10^9/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’s sudden unexplained death.\n\nChest CT incidentally identified a left adrenal soft-tissue mass measuring 43 × 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 × 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 × 40 × 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.",
    "summary": "We report the case of a 19-year-old female who presented with pheochromocytoma without experiencing a crisis, despite having a significant adrenal mass and undergoing high-dose glucocorticoid treatment. Genetic testing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), associated with MEN2A. Further endocrine evaluation identified a thyroid nodule with mildly elevated calcitonin levels, but normal electrolyte and parathyroid hormone levels. 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. Further parathyroid scintigraphy using 99mTc-MIBI was performed, yielding a negative result for parathyroid adenoma."
  },
  {
    "doc_id": 61,
    "label": "low_health_literacy",
    "fulltext": "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 ∗ 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 ∗ 3.1 ∗ 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 – Computed tomography (PET/CT) was done for Head and Neck, Chest, Abdomen, Pelvis and musculoskeletal structures. Only a 29 ∗ 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 ∗ 6.0 ∗ 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.",
    "diff_label_texts": "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.",
    "summary": "A 36-year-old man presented with a tender penoscrotal mass for 5 years. The patient underwent surgical resection of the mass. Histopathology revealed cellular spindle cell tumour arranged into interlacing fascicle, Immunohistochemistry analysis revealed a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). In our case, the patient was aggressively treated with two surgical resections and still progressed and metastasized and continued progressing even after different chemotherapy regimens."
  },
  {
    "doc_id": 61,
    "label": "intermediate_health_literacy",
    "fulltext": "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 ∗ 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 ∗ 3.1 ∗ 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 – Computed tomography (PET/CT) was done for Head and Neck, Chest, Abdomen, Pelvis and musculoskeletal structures. Only a 29 ∗ 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 ∗ 6.0 ∗ 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.",
    "diff_label_texts": "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.",
    "summary": "A 36-year-old man presented with a tender penoscrotal mass for 5 years. The patient underwent surgical resection of the mass. Histopathology revealed cellular spindle cell tumour arranged into interlacing fascicle, Immunohistochemistry analysis revealed a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). In our case, the patient was aggressively treated with two surgical resections and still progressed and metastasized and continued progressing even after different chemotherapy regimens."
  },
  {
    "doc_id": 61,
    "label": "proficient_health_literacy",
    "fulltext": "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 ∗ 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 ∗ 3.1 ∗ 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 – Computed tomography (PET/CT) was done for Head and Neck, Chest, Abdomen, Pelvis and musculoskeletal structures. Only a 29 ∗ 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 ∗ 6.0 ∗ 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.",
    "diff_label_texts": "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 × 20 mm) without skin tethering and not involving the spermatic cord. Doppler ultrasound showed a well-defined hypoechoic mass (2.7 × 3.1 × 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 β-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 × 6.0 × 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 × 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.",
    "summary": "A 36-year-old man presented with a tender penoscrotal mass for 5 years. The patient underwent surgical resection of the mass. Histopathology revealed cellular spindle cell tumour arranged into interlacing fascicle, Immunohistochemistry analysis revealed a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). In our case, the patient was aggressively treated with two surgical resections and still progressed and metastasized and continued progressing even after different chemotherapy regimens."
  },
  {
    "doc_id": 62,
    "label": "low_health_literacy",
    "fulltext": "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 38ºC). 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—canoeing 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’s temperature was 37.8°C 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.",
    "diff_label_texts": "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’s own immune system is likely causing this problem. About 20 months later, he feels well, and his breathing tests are normal.",
    "summary": "We describe the case of a 13-year-old adolescent male who presented to the emergency department with acute pleuritic chest pain not associated with systemic complaints. On examination, he had diminished breath sounds in the lower two thirds of the chest with no other abnormal findings; SpO2 (oxygen saturation) was 98% on room air. Chest radiograph revealed a marked interstitial infiltrate, comparable with the one taken 4 years earlier during an acute illness that was presumptively treated with azithromycin. A computed tomography (CT) scan revealed multiple bilateral areas of ground-glass opacities with areas of crazy paving, involving > 65% of lung parenchyma, suggestive of pulmonary alveolar proteinosis (PAP). Respiratory viral testing, including for coronavirus (SARS-CoV2), was negative. Bronchoalveolar lavage performed in the outpatient setting revealed a milky fluid and positive periodic acid-Schiff staining. Spirometry indicated a mild restrictive pattern (forced vital capacity [FVC] = 77%) and diffusing capacity of the lungs for carbon monoxide (DLCO) showed a moderate decrease at 48.6%. No mutations associated with surfactant dysfunction were found on the genetic panel. Anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibody testing was strongly positive, raising suspicion for autoimmune PAP. At 20 months of follow-up, the patient remains asymptomatic with a normal spirometry."
  },
  {
    "doc_id": 62,
    "label": "proficient_health_literacy",
    "fulltext": "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 38ºC). 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—canoeing 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’s temperature was 37.8°C 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.",
    "diff_label_texts": "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°C). 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°C, 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–clavulanate 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–Schiff 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–GM-CSF antibodies that impair alveolar macrophage–mediated surfactant clearance, producing intra-alveolar lipoproteinaceous material that is PAS-positive and radiographically manifests as diffuse bilateral ground-glass opacities (often with a “crazy paving” pattern). Standard therapies include whole lung lavage and GM-CSF replacement; however, observation is appropriate in stable, minimally symptomatic patients, as in this case.",
    "summary": "We describe the case of a 13-year-old adolescent male who presented to the emergency department with acute pleuritic chest pain not associated with systemic complaints. On examination, he had diminished breath sounds in the lower two thirds of the chest with no other abnormal findings; SpO2 (oxygen saturation) was 98% on room air. Chest radiograph revealed a marked interstitial infiltrate, comparable with the one taken 4 years earlier during an acute illness that was presumptively treated with azithromycin. A computed tomography (CT) scan revealed multiple bilateral areas of ground-glass opacities with areas of crazy paving, involving > 65% of lung parenchyma, suggestive of pulmonary alveolar proteinosis (PAP). Respiratory viral testing, including for coronavirus (SARS-CoV2), was negative. Bronchoalveolar lavage performed in the outpatient setting revealed a milky fluid and positive periodic acid-Schiff staining. Spirometry indicated a mild restrictive pattern (forced vital capacity [FVC] = 77%) and diffusing capacity of the lungs for carbon monoxide (DLCO) showed a moderate decrease at 48.6%. No mutations associated with surfactant dysfunction were found on the genetic panel. Anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibody testing was strongly positive, raising suspicion for autoimmune PAP. At 20 months of follow-up, the patient remains asymptomatic with a normal spirometry."
  },
  {
    "doc_id": 63,
    "label": "low_health_literacy",
    "fulltext": "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 °C 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",
    "diff_label_texts": "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.",
    "summary": "A 27-year-old woman presented with facial oedema and trismus 48 hours after completing treatment with phenoxymethylpenicillin for an odontogenic infection. A head and neck CT scan showed a large thrombus in the internal jugular vein and a chest CT scan showed pulmonary septic embolism. Treatment consisted of early intravenous broad spectrum antibiotics and anticoagulation.\n"
  },
  {
    "doc_id": 63,
    "label": "intermediate_health_literacy",
    "fulltext": "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 °C 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",
    "diff_label_texts": "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.",
    "summary": "A 27-year-old woman presented with facial oedema and trismus 48 hours after completing treatment with phenoxymethylpenicillin for an odontogenic infection. A head and neck CT scan showed a large thrombus in the internal jugular vein and a chest CT scan showed pulmonary septic embolism. Treatment consisted of early intravenous broad spectrum antibiotics and anticoagulation.\n"
  },
  {
    "doc_id": 63,
    "label": "proficient_health_literacy",
    "fulltext": "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 °C 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",
    "diff_label_texts": "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 °C 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–tazobactam 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.",
    "summary": "A 27-year-old woman presented with facial oedema and trismus 48 hours after completing treatment with phenoxymethylpenicillin for an odontogenic infection. A head and neck CT scan showed a large thrombus in the internal jugular vein and a chest CT scan showed pulmonary septic embolism. Treatment consisted of early intravenous broad spectrum antibiotics and anticoagulation.\n"
  },
  {
    "doc_id": 64,
    "label": "low_health_literacy",
    "fulltext": "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°C, 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%–100%. 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’s 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’s clinical condition progressively improved and was discharged home after 10 days but was subsequently lost to follow-up.",
    "diff_label_texts": "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.",
    "summary": "We present the case of a 5-year-old with severe organophosphate poisoning from ingestion of chlorpyrifos, further worsened by aspiration of a charcoal-palm oil mixture. The clinical illness was marked by respiratory failure, shock, coma and type I paralysis. The patient was treated in the emergency department with noninvasive ventilation, multiple episodes of exchange transfusion, intravenous atropine, inotrope infusion, antibiotics and steroids. The patient responded rapidly to treatment, did not develop intermediate syndrome and was discharged after 10 days of admission."
  },
  {
    "doc_id": 64,
    "label": "intermediate_health_literacy",
    "fulltext": "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°C, 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%–100%. 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’s 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’s clinical condition progressively improved and was discharged home after 10 days but was subsequently lost to follow-up.",
    "diff_label_texts": "A 5-year-old developed severe organophosphate poisoning after ingesting chlorpyrifos and then aspirated a charcoal–palm 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.",
    "summary": "We present the case of a 5-year-old with severe organophosphate poisoning from ingestion of chlorpyrifos, further worsened by aspiration of a charcoal-palm oil mixture. The clinical illness was marked by respiratory failure, shock, coma and type I paralysis. The patient was treated in the emergency department with noninvasive ventilation, multiple episodes of exchange transfusion, intravenous atropine, inotrope infusion, antibiotics and steroids. The patient responded rapidly to treatment, did not develop intermediate syndrome and was discharged after 10 days of admission."
  },
  {
    "doc_id": 64,
    "label": "proficient_health_literacy",
    "fulltext": "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°C, 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%–100%. 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’s 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’s clinical condition progressively improved and was discharged home after 10 days but was subsequently lost to follow-up.",
    "diff_label_texts": "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–palm oil mixture. On arrival: T 38.3°C, 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 99–100%. 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 41–259 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.",
    "summary": "We present the case of a 5-year-old with severe organophosphate poisoning from ingestion of chlorpyrifos, further worsened by aspiration of a charcoal-palm oil mixture. The clinical illness was marked by respiratory failure, shock, coma and type I paralysis. The patient was treated in the emergency department with noninvasive ventilation, multiple episodes of exchange transfusion, intravenous atropine, inotrope infusion, antibiotics and steroids. The patient responded rapidly to treatment, did not develop intermediate syndrome and was discharged after 10 days of admission."
  },
  {
    "doc_id": 65,
    "label": "low_health_literacy",
    "fulltext": "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 ng/L, normal values <14 ng/L) and NT-pro BNP (aminoterminal pro B-Type Natriuretic Peptide) levels (2225 pg/mL, normal values <130 pg/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 s, and 0.625 mm slice thickness, with intravenous injection of 70 mL 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.",
    "diff_label_texts": "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.",
    "summary": "A 19-year-old woman presented to the emergency department with arrhythmia and signs of cardiogenic shock. After a 12-lead electrocardiogram ruled out acute myocardial infarction, and cardiac magnetic resonance showed no sign of cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed, displaying ostial atresia of the right coronary artery. She was thus referred to a specialist centre for congenital cardiovascular disease, where an electrophysiological study observed an arrhythmogenic focus on the posteromedial papillary muscle, which was ablated, and she has been asymptomatic since."
  },
  {
    "doc_id": 65,
    "label": "intermediate_health_literacy",
    "fulltext": "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 ng/L, normal values <14 ng/L) and NT-pro BNP (aminoterminal pro B-Type Natriuretic Peptide) levels (2225 pg/mL, normal values <130 pg/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 s, and 0.625 mm slice thickness, with intravenous injection of 70 mL 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.",
    "diff_label_texts": "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—the 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.",
    "summary": "A 19-year-old woman presented to the emergency department with arrhythmia and signs of cardiogenic shock. After a 12-lead electrocardiogram ruled out acute myocardial infarction, and cardiac magnetic resonance showed no sign of cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed, displaying ostial atresia of the right coronary artery. She was thus referred to a specialist centre for congenital cardiovascular disease, where an electrophysiological study observed an arrhythmogenic focus on the posteromedial papillary muscle, which was ablated, and she has been asymptomatic since."
  },
  {
    "doc_id": 65,
    "label": "proficient_health_literacy",
    "fulltext": "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 ng/L, normal values <14 ng/L) and NT-pro BNP (aminoterminal pro B-Type Natriuretic Peptide) levels (2225 pg/mL, normal values <130 pg/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 s, and 0.625 mm slice thickness, with intravenous injection of 70 mL 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.",
    "diff_label_texts": "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.",
    "summary": "A 19-year-old woman presented to the emergency department with arrhythmia and signs of cardiogenic shock. After a 12-lead electrocardiogram ruled out acute myocardial infarction, and cardiac magnetic resonance showed no sign of cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed, displaying ostial atresia of the right coronary artery. She was thus referred to a specialist centre for congenital cardiovascular disease, where an electrophysiological study observed an arrhythmogenic focus on the posteromedial papillary muscle, which was ablated, and she has been asymptomatic since."
  },
  {
    "doc_id": 66,
    "label": "low_health_literacy",
    "fulltext": "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.",
    "diff_label_texts": "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.",
    "summary": "We present the case of a 17-year-old male with an asymptomatic NFB discovered incidentally during routine dental radiography. The patient denied any history of nasal obstruction, epistaxis, or discomfort. Imaging revealed a radiopaque object in the right nasal cavity, later identified as a metallic snap button embedded in the floor of the nasal cavity. The foreign body had likely been retained for over a decade."
  },
  {
    "doc_id": 67,
    "label": "proficient_health_literacy",
    "fulltext": "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 3–4 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%–45%, 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 min. 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 133 000 IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%–15% with previously noted severe LV concentric hypertrophy (1.9 cm septum and 2.2 cm 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%–30%, 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 1×1 inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2–3 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–day 3), etoposide (day 1–day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7–day 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.",
    "diff_label_texts": "An 18-year-old Hispanic male with no prior medical history presented with 3–4 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 40–45%, 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 10–15% 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 1×1 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—pericardial effusion refractory to initial therapy, acute heart failure with concentric hypertrophy, and the new diagnosis of EBV(+) NK/T-cell lymphoma—favoured 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 1–3), etoposide (days 1–5), and dexamethasone; peg-asparaginase was added (days 7–21). 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.",
    "summary": "An 18-year-old male patient presented to the emergency department complaining of new onset chest pain, fever and orthopnoea. Initial workup was remarkable for elevated troponin, diffuse ST-segment elevation on ECG and chest X-ray with enlarged cardiac silhouette. Transthoracic echocardiogram (TTE) demonstrates severe biventricular concentric hypertrophy and pericardial effusion. Also, Coxsackie virus A and B titres were positive, concerning for a classic viral pericarditis. However, despite medical management, the patient became dyspnoeic and hypotensive. Impending cardiac tamponade was observed on repeat TTE, and pericardiocentesis was performed, complicated by pulseless electrical activity cardiac arrest, and ultimately patient requiring venoarterial extracorporeal membrane oxygenation support. Emergent endomyocardial biopsy showed no inflammatory process, and a skin biopsy of a small lesion in the right arm showed unexpected diagnosis of Epstein-Barr virus (+) natural killer/T-cell lymphoma. On initiation of chemotherapy, clinical improvement was observed as evidenced by improving ejection fraction, resolution of pericardial effusion and gradual decrease in myocardial hypertrophy."
  },
  {
    "doc_id": 68,
    "label": "low_health_literacy",
    "fulltext": "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’ 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 ≤ 0.20±0.03).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.",
    "diff_label_texts": "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.",
    "summary": "Here, we present a rare case of euthyroid single muscular GO in a 50-year-old patient who was a smoker and had dyslipidemia for several years. The patient experienced a very rapid and severe depression of ocular motility of the right eye that caused uncorrectable and constant diplopia, severely affecting his quality of life. He was euthyroid, and TSH-R-Ab plasmatic levels were only slightly elevated. Intravenous corticosteroid pulse therapy was partially effective, and two rounds of wall orbital surgical decompression were necessary. Massive mono-muscular fibrosis was evidenced by biopsy of the right inferior rectus muscle."
  },
  {
    "doc_id": 68,
    "label": "intermediate_health_literacy",
    "fulltext": "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’ 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 ≤ 0.20±0.03).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.",
    "diff_label_texts": "We describe a rare case of euthyroid, single-muscle thyroid eye disease (Graves’ 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.",
    "summary": "Here, we present a rare case of euthyroid single muscular GO in a 50-year-old patient who was a smoker and had dyslipidemia for several years. The patient experienced a very rapid and severe depression of ocular motility of the right eye that caused uncorrectable and constant diplopia, severely affecting his quality of life. He was euthyroid, and TSH-R-Ab plasmatic levels were only slightly elevated. Intravenous corticosteroid pulse therapy was partially effective, and two rounds of wall orbital surgical decompression were necessary. Massive mono-muscular fibrosis was evidenced by biopsy of the right inferior rectus muscle."
  },
  {
    "doc_id": 68,
    "label": "proficient_health_literacy",
    "fulltext": "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’ 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 ≤ 0.20±0.03).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.",
    "diff_label_texts": "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 0–100 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–orbit area ratio OD was 0.25 AutoCAD units (vn ≤ 0.20 ± 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.",
    "summary": "Here, we present a rare case of euthyroid single muscular GO in a 50-year-old patient who was a smoker and had dyslipidemia for several years. The patient experienced a very rapid and severe depression of ocular motility of the right eye that caused uncorrectable and constant diplopia, severely affecting his quality of life. He was euthyroid, and TSH-R-Ab plasmatic levels were only slightly elevated. Intravenous corticosteroid pulse therapy was partially effective, and two rounds of wall orbital surgical decompression were necessary. Massive mono-muscular fibrosis was evidenced by biopsy of the right inferior rectus muscle."
  },
  {
    "doc_id": 69,
    "label": "low_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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’s surgery clinic.",
    "summary": "We present the clinical case of a 15-year-old adolescent male with no previous surgical history, who presented with abdominal pain and vomiting, and whose computed tomography suggested a picture of intestinal obstruction due to internal hernia at the level of the Winslow hiatus. He required surgical intervention by exploratory laparoscopy, converted to a supraumbilical midline laparotomy due to poor visualization, for reduction of the herniated ileal loop. This presented a good appearance and intestinal resection was not necessary. No preventive technique was performed to reduce the risk of recurrence. Postoperatively, the patient presented a pelvic collection managed conservatively with antibiotics. He is currently being monitored in outpatient paediatric surgery.\n"
  },
  {
    "doc_id": 69,
    "label": "intermediate_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "We present the clinical case of a 15-year-old adolescent male with no previous surgical history, who presented with abdominal pain and vomiting, and whose computed tomography suggested a picture of intestinal obstruction due to internal hernia at the level of the Winslow hiatus. He required surgical intervention by exploratory laparoscopy, converted to a supraumbilical midline laparotomy due to poor visualization, for reduction of the herniated ileal loop. This presented a good appearance and intestinal resection was not necessary. No preventive technique was performed to reduce the risk of recurrence. Postoperatively, the patient presented a pelvic collection managed conservatively with antibiotics. He is currently being monitored in outpatient paediatric surgery.\n"
  },
  {
    "doc_id": 69,
    "label": "proficient_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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—compatible 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.",
    "summary": "We present the clinical case of a 15-year-old adolescent male with no previous surgical history, who presented with abdominal pain and vomiting, and whose computed tomography suggested a picture of intestinal obstruction due to internal hernia at the level of the Winslow hiatus. He required surgical intervention by exploratory laparoscopy, converted to a supraumbilical midline laparotomy due to poor visualization, for reduction of the herniated ileal loop. This presented a good appearance and intestinal resection was not necessary. No preventive technique was performed to reduce the risk of recurrence. Postoperatively, the patient presented a pelvic collection managed conservatively with antibiotics. He is currently being monitored in outpatient paediatric surgery.\n"
  },
  {
    "doc_id": 70,
    "label": "low_health_literacy",
    "fulltext": "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°C. 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.",
    "diff_label_texts": "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.",
    "summary": "We present the case of retained Lippes loop IUD for 40 years in a 75-year-old postmenopausal patient from Western Ethiopia. The patient presented to the hospital with postmenopausal pelvic pain. Speculum exam showed part of loop at external cervical os. The loop was easily removed with spongy forceps. The patient was discharged with analgesia and doxycycline twice a day for 3 days."
  },
  {
    "doc_id": 70,
    "label": "intermediate_health_literacy",
    "fulltext": "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°C. 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.",
    "diff_label_texts": "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.",
    "summary": "We present the case of retained Lippes loop IUD for 40 years in a 75-year-old postmenopausal patient from Western Ethiopia. The patient presented to the hospital with postmenopausal pelvic pain. Speculum exam showed part of loop at external cervical os. The loop was easily removed with spongy forceps. The patient was discharged with analgesia and doxycycline twice a day for 3 days."
  },
  {
    "doc_id": 71,
    "label": "low_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "A 71-year-old man with a history of long-standing vitiligo who had experienced visual loss in his right eye six months prior to admission, along with bilateral hearing loss, predominantly in the right ear. During his hospital stay, he presented with chronic headaches, fever, and significant involuntary weight loss. On ophthalmologic examination, the right eye was light sensitive with hyperemic bulbar conjunctiva, while the left eye had a visual acuity of 20/200. The fundus of the right eye had scattered pigmentation, while the left eye had a swollen optic disc and right optic atrophy.\n"
  },
  {
    "doc_id": 71,
    "label": "intermediate_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "A 71-year-old man with a history of long-standing vitiligo who had experienced visual loss in his right eye six months prior to admission, along with bilateral hearing loss, predominantly in the right ear. During his hospital stay, he presented with chronic headaches, fever, and significant involuntary weight loss. On ophthalmologic examination, the right eye was light sensitive with hyperemic bulbar conjunctiva, while the left eye had a visual acuity of 20/200. The fundus of the right eye had scattered pigmentation, while the left eye had a swollen optic disc and right optic atrophy.\n"
  },
  {
    "doc_id": 71,
    "label": "proficient_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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/“raised and thinned” 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–neurologic 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–severe 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.",
    "summary": "A 71-year-old man with a history of long-standing vitiligo who had experienced visual loss in his right eye six months prior to admission, along with bilateral hearing loss, predominantly in the right ear. During his hospital stay, he presented with chronic headaches, fever, and significant involuntary weight loss. On ophthalmologic examination, the right eye was light sensitive with hyperemic bulbar conjunctiva, while the left eye had a visual acuity of 20/200. The fundus of the right eye had scattered pigmentation, while the left eye had a swollen optic disc and right optic atrophy.\n"
  },
  {
    "doc_id": 72,
    "label": "proficient_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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.",
    "summary": "We report a case of BK virus nephropathy in a patient who underwent heart transplantation due to peripartum cardiomyopathy. The renal biopsy reported active chronic tubulointerstitial nephritis associated with late-stage BK virus nephritis and the blood viral load for BK virus was positive (log 4.5). The immunosuppressive treatment was reduced, and after two years of follow-up, the patient had stable renal function with serum creatinine of 2.5 mg/dL (GFR of 23.4 mL/min/1.73m2).\n"
  },
  {
    "doc_id": 73,
    "label": "low_health_literacy",
    "fulltext": "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 “Definitive” RAM for the association of L-asp and Prednisone\n",
    "diff_label_texts": "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.",
    "summary": "A teenager who developed pseudohyponatraemia and hypertriglyceridaemia during treatment for non-Hodgkin lymphoma (NHL) was suspected to have a drug reaction (ADR). This suspicion of ADR was evaluated according to the modified causality algorithm (Karch and Lasagna), resulting in a \"definitive\" ADR for the association of L-asp and corticosteroids. He received treatment with a low-fat diet and lipid-modifying medicines. L-asp and prednisone were not discontinued due to the end of the indication, according to the protocol. The hypertriglyceridaemia recovered without complications after 14 days of treatment.\n"
  },
  {
    "doc_id": 73,
    "label": "intermediate_health_literacy",
    "fulltext": "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 “Definitive” RAM for the association of L-asp and Prednisone\n",
    "diff_label_texts": "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’s 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.",
    "summary": "A teenager who developed pseudohyponatraemia and hypertriglyceridaemia during treatment for non-Hodgkin lymphoma (NHL) was suspected to have a drug reaction (ADR). This suspicion of ADR was evaluated according to the modified causality algorithm (Karch and Lasagna), resulting in a \"definitive\" ADR for the association of L-asp and corticosteroids. He received treatment with a low-fat diet and lipid-modifying medicines. L-asp and prednisone were not discontinued due to the end of the indication, according to the protocol. The hypertriglyceridaemia recovered without complications after 14 days of treatment.\n"
  },
  {
    "doc_id": 73,
    "label": "proficient_health_literacy",
    "fulltext": "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 “Definitive” RAM for the association of L-asp and Prednisone\n",
    "diff_label_texts": "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 ≤300 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.",
    "summary": "A teenager who developed pseudohyponatraemia and hypertriglyceridaemia during treatment for non-Hodgkin lymphoma (NHL) was suspected to have a drug reaction (ADR). This suspicion of ADR was evaluated according to the modified causality algorithm (Karch and Lasagna), resulting in a \"definitive\" ADR for the association of L-asp and corticosteroids. He received treatment with a low-fat diet and lipid-modifying medicines. L-asp and prednisone were not discontinued due to the end of the indication, according to the protocol. The hypertriglyceridaemia recovered without complications after 14 days of treatment.\n"
  },
  {
    "doc_id": 74,
    "label": "proficient_health_literacy",
    "fulltext": "A 56-year-old Italian female patient with β-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 β-thalassemia condition (genotype HBB:c.118C > T/ HBB:c.93-21G > A), diagnosed at the age of 7 years, despite the fact that the first transfusion was carried out at 2 years. As a consequence of β-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’s 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 10–10.5 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 = 4.3); 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–Koga; 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 β-thalassemia, treatment with sirolimus was recommended.",
    "diff_label_texts": "A 56-year-old Italian female with transfusion-dependent β-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 10–10.5 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–Koga 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 β-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 β-thalassemia, as reflected by the patient’s 35% prolongation of the transfusion interval.",
    "summary": "A 56-year-old Italian female patient with β-thalassemia major underwent magnetic resonance imaging to quantify myocardial, hepatic, and pancreatic iron deposition. Her medical history included transfusion-dependent β-thalassemia, splenectomy, and cholecystectomy. At the time of magnetic resonance imaging, she had no significant endocrine, cardiac, or hepatic complications and was on deferasirox, vitamin D, and luspatercept. Magnetic resonance imaging revealed a lobulated mass in the prevascular mediastinum, which showed mild radiotracer uptake on positron emission tomography. Chest computed tomography revealed multiple thin-walled cysts in the lungs, indicating lymphangioleiomyomatosis. Following multidisciplinary evaluation, the patient underwent thoracoscopic thymectomy and lung wedge resection. Histopathology confirmed type B2 thymoma and pulmonary lymphangioleiomyomatosis. Post-surgery, the patient was recommended for adjuvant radiation therapy and sirolimus treatment."
  },
  {
    "doc_id": 75,
    "label": "low_health_literacy",
    "fulltext": "We present a case of a 49-year-old woman with renal and heart failure following a long-term (lasting from 13 years 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 mg/dL and proteinuria of 2 g/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 years. While being on active waiting list for kidney transplantation presented remission of laboratory indices of lupus (complement splits within normal limits: C3–0,93 g/l, C4–0,4 g/l, ANA negative) and persisting circulatory insufficiency with markedly reduced stair-climbing capacity (to one flight of stairs) with elevated BNP 619 pg/ml (n. 0–100). 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 μg/kg/min was continued after surgery for a total of 24 h. The patient’s 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’s 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 g 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 weeks (mostly due to fluid retention). BNP levels raised to 2996 pg/ml and then slowly decreased. The kidney biopsy performed 2 weeks 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 mg/dL and BNP level of 1794 pg/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 − 6) 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 pg/ml and normal kidney function were noted.",
    "diff_label_texts": "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.",
    "summary": "We present a case of a 49-year-old woman with renal and heart failure following a long-term SLE prepared for kidney transplantation. During the SLE course, the function of the heart and kidneys gradually deteriorated. The patient required the initiation of renal replacement therapy and was dialyzed until a kidney transplantation for 4 years. In the preparation of the patient for the surgical procedure, due to the extremely low ejection fraction, it was decided to include cardioprotective treatment with Levosimendan. The postoperative period was not straightforward but successful. In the monthly and five-month follow-up, a continuous improvement of heart function with normal renal function was noted."
  },
  {
    "doc_id": 75,
    "label": "proficient_health_literacy",
    "fulltext": "We present a case of a 49-year-old woman with renal and heart failure following a long-term (lasting from 13 years 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 mg/dL and proteinuria of 2 g/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 years. While being on active waiting list for kidney transplantation presented remission of laboratory indices of lupus (complement splits within normal limits: C3–0,93 g/l, C4–0,4 g/l, ANA negative) and persisting circulatory insufficiency with markedly reduced stair-climbing capacity (to one flight of stairs) with elevated BNP 619 pg/ml (n. 0–100). 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 μg/kg/min was continued after surgery for a total of 24 h. The patient’s 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’s 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 g 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 weeks (mostly due to fluid retention). BNP levels raised to 2996 pg/ml and then slowly decreased. The kidney biopsy performed 2 weeks 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 mg/dL and BNP level of 1794 pg/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 − 6) 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 pg/ml and normal kidney function were noted.",
    "diff_label_texts": "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 0–100). Pre-transplant transthoracic echocardiography demonstrated markedly enlarged LV and LA, severely reduced LV systolic function (LVEF 26%, GLS −3). 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 μg/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 −6). 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.",
    "summary": "We present a case of a 49-year-old woman with renal and heart failure following a long-term SLE prepared for kidney transplantation. During the SLE course, the function of the heart and kidneys gradually deteriorated. The patient required the initiation of renal replacement therapy and was dialyzed until a kidney transplantation for 4 years. In the preparation of the patient for the surgical procedure, due to the extremely low ejection fraction, it was decided to include cardioprotective treatment with Levosimendan. The postoperative period was not straightforward but successful. In the monthly and five-month follow-up, a continuous improvement of heart function with normal renal function was noted."
  },
  {
    "doc_id": 76,
    "label": "low_health_literacy",
    "fulltext": "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™ E6, ultrasonography system with a linear 13–5 MHz probe for unilateral PGONB. The patient’s 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",
    "diff_label_texts": "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.",
    "summary": "Herein, we report that a 42-year-old female patient with PCH who could not use the oral medication because of side effects. When she came to the pain clinic with an attack with intensity of 9/10 , we took her to the local operating room. The ultrasound (US) guided proximal greater occipital nerve block with bupivacaine was performed and the intensity of the attack was reduced to 2/10. The blockage was repeated once a week for a month. After two months, both the intensity of headache and number of attacks decreased and no adverse effect was observed."
  },
  {
    "doc_id": 76,
    "label": "proficient_health_literacy",
    "fulltext": "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™ E6, ultrasonography system with a linear 13–5 MHz probe for unilateral PGONB. The patient’s 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",
    "diff_label_texts": "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 13–5 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 (“two horns” 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.",
    "summary": "Herein, we report that a 42-year-old female patient with PCH who could not use the oral medication because of side effects. When she came to the pain clinic with an attack with intensity of 9/10 , we took her to the local operating room. The ultrasound (US) guided proximal greater occipital nerve block with bupivacaine was performed and the intensity of the attack was reduced to 2/10. The blockage was repeated once a week for a month. After two months, both the intensity of headache and number of attacks decreased and no adverse effect was observed."
  },
  {
    "doc_id": 77,
    "label": "low_health_literacy",
    "fulltext": "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° 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 10–15° compared with 0–130°degrees 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’s 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’s active knee extension improved from 5° to 10° and then to a 15° 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’s 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’s 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.",
    "diff_label_texts": "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.",
    "summary": "A 20-year-old male Arabic martial artist had a history of left hamstring strain for the past 5 weeks. He had undergone pharmacological and physiotherapeutic interventions for his clinical conditions but had not responded favorably. Further clinical assessment had ruled out hamstring syndrome. The patient refrained from all sports activities.\n\nIntervention: The patient was treated using a modified slump mobilization technique with four repetitions for 3 consecutive days, together with postural retraining. Results of the numeric pain rating scale and Knee Society score before and after the interventions were obtained.\n\nResults and discussion: Pre-intervention score of the numeric pain rating scale was 5/10 and 7/10 at rest and with activity, respectively. Assessment on the 3rd consecutive day of intervention, the numeric pain rating scale decreased to 2/10 and 4/10 at rest and with activity, respectively. Similarly, the pre- and post-intervention Knee Society score improved from 22 to 61 in pain and from 30 to 80 in function. At the 2-month follow-up, the patient reported a complete recovery from symptoms and resumed his sports activities without any disruption."
  },
  {
    "doc_id": 77,
    "label": "intermediate_health_literacy",
    "fulltext": "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° 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 10–15° compared with 0–130°degrees 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’s 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’s active knee extension improved from 5° to 10° and then to a 15° 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’s 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’s 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.",
    "diff_label_texts": "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.",
    "summary": "A 20-year-old male Arabic martial artist had a history of left hamstring strain for the past 5 weeks. He had undergone pharmacological and physiotherapeutic interventions for his clinical conditions but had not responded favorably. Further clinical assessment had ruled out hamstring syndrome. The patient refrained from all sports activities.\n\nIntervention: The patient was treated using a modified slump mobilization technique with four repetitions for 3 consecutive days, together with postural retraining. Results of the numeric pain rating scale and Knee Society score before and after the interventions were obtained.\n\nResults and discussion: Pre-intervention score of the numeric pain rating scale was 5/10 and 7/10 at rest and with activity, respectively. Assessment on the 3rd consecutive day of intervention, the numeric pain rating scale decreased to 2/10 and 4/10 at rest and with activity, respectively. Similarly, the pre- and post-intervention Knee Society score improved from 22 to 61 in pain and from 30 to 80 in function. At the 2-month follow-up, the patient reported a complete recovery from symptoms and resumed his sports activities without any disruption."
  },
  {
    "doc_id": 77,
    "label": "proficient_health_literacy",
    "fulltext": "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° 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 10–15° compared with 0–130°degrees 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’s 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’s active knee extension improved from 5° to 10° and then to a 15° 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’s 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’s 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.",
    "diff_label_texts": "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 “pop,” followed by progressive loss of knee flexibility and inability to fully flex or extend the knee; the knee rested in approximately 15° 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 10–15° versus 0–130° 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’s tolerance, followed by active cervical flexion–extension coordinated with ankle dorsiflexion–plantarflexion (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° to 10° and then to a 15°-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→Y→W) 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.",
    "summary": "A 20-year-old male Arabic martial artist had a history of left hamstring strain for the past 5 weeks. He had undergone pharmacological and physiotherapeutic interventions for his clinical conditions but had not responded favorably. Further clinical assessment had ruled out hamstring syndrome. The patient refrained from all sports activities.\n\nIntervention: The patient was treated using a modified slump mobilization technique with four repetitions for 3 consecutive days, together with postural retraining. Results of the numeric pain rating scale and Knee Society score before and after the interventions were obtained.\n\nResults and discussion: Pre-intervention score of the numeric pain rating scale was 5/10 and 7/10 at rest and with activity, respectively. Assessment on the 3rd consecutive day of intervention, the numeric pain rating scale decreased to 2/10 and 4/10 at rest and with activity, respectively. Similarly, the pre- and post-intervention Knee Society score improved from 22 to 61 in pain and from 30 to 80 in function. At the 2-month follow-up, the patient reported a complete recovery from symptoms and resumed his sports activities without any disruption."
  },
  {
    "doc_id": 78,
    "label": "proficient_health_literacy",
    "fulltext": "A male was born via an emergency cesarean section due to fetal distress at 40 weeks 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 weeks 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 g (75 percentile), the length was 56.5 cm (over 90 percentile), and the head circumference was 36 cm (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 mm) (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 ACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24–32). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2 weeks 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.",
    "diff_label_texts": "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 1–3 weeks), cardiomegaly with a cardiothoracic circumference ratio ≥0.5, 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 24–32) 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.",
    "summary": "Patient concerns:\nA newborn with neonatal MFS and severe cardiac involvement. He presented various severe clinical features such as arachnodactyly, camptodactyly, elbow and knee joint contracture, senile facial appearance, and deep settling with down-slanting palpebral fissure, hypoplastic ear cartilage, sagging mouth, brachycephaly, and ectopia lentis.\n\nDiagnosis:\nGenetic analysis revealed a novel mutation at nucleotide 3964 (c.3964 + 1 G > T) in intron 32 of the fibrillin-1 gene. This mutation is identified to be in the so-called neonatal region of fibrillin-1 exon 24 to 32, as reported previously.\n\nInterventions:\nThe patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction, full sedation, and use of diuretic were attempted to improve the oliguria and heart failure.\n\nOutcomes:\nDespite the medical management, aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. Surgical treatment is essential to prolong the patient's life, however, considerations for the grave progression of the disease make families decide to continue palliative care instead of surgical treatment. A few months after birth, he presented with rapidly progressive aortic regurgitation, mitral regurgitation, and congestive heart failure leading to death."
  },
  {
    "doc_id": 79,
    "label": "low_health_literacy",
    "fulltext": "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’s 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 β-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®, 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, β-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.",
    "diff_label_texts": "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.",
    "summary": "A 27-year-old woman, suffering from beta thalassemia major who is undergoing therapy in the form of routine blood transfusions every month and taking anti-chelation drugs but is currently stopping this because she is pregnant, currently 16 weeks pregnant, complains complained of swollen gums, bleeding, and bad breath. Extraoral examination revealed dry, exfoliative lips. Intraoral examination revealed gingival hyperplasia with erythema, soft consistency, dark red rounded gingival margins, bleeding, true pockets and pain throughout the labial, buccal, palatal, and lingual. There was no history of systemic disease in this patient. Patient has never visited a dentist, either before or now, with complaints about her oral cavity. Hematological parameters showed abnormalities, and peripheral blood examination revealed an infection. The oral diagnoses included gingival enlargement and chronic periodontitis associated with pregnancy and β- thalassemia major.\n\nCase Management\nDental management consisted of spooling with 3% hydrogen peroxide (H2O2) spooling, chlorine dioxide spray mouthwash, antibiotics, calculus removal, and oral hygiene instructions. Blood transfusions were administered once a month, and anti-chelation therapy was stopped during pregnancy. After three months of multidisciplinary management, the results were satisfactory."
  },
  {
    "doc_id": 79,
    "label": "intermediate_health_literacy",
    "fulltext": "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’s 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 β-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®, 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, β-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.",
    "diff_label_texts": "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.",
    "summary": "A 27-year-old woman, suffering from beta thalassemia major who is undergoing therapy in the form of routine blood transfusions every month and taking anti-chelation drugs but is currently stopping this because she is pregnant, currently 16 weeks pregnant, complains complained of swollen gums, bleeding, and bad breath. Extraoral examination revealed dry, exfoliative lips. Intraoral examination revealed gingival hyperplasia with erythema, soft consistency, dark red rounded gingival margins, bleeding, true pockets and pain throughout the labial, buccal, palatal, and lingual. There was no history of systemic disease in this patient. Patient has never visited a dentist, either before or now, with complaints about her oral cavity. Hematological parameters showed abnormalities, and peripheral blood examination revealed an infection. The oral diagnoses included gingival enlargement and chronic periodontitis associated with pregnancy and β- thalassemia major.\n\nCase Management\nDental management consisted of spooling with 3% hydrogen peroxide (H2O2) spooling, chlorine dioxide spray mouthwash, antibiotics, calculus removal, and oral hygiene instructions. Blood transfusions were administered once a month, and anti-chelation therapy was stopped during pregnancy. After three months of multidisciplinary management, the results were satisfactory."
  },
  {
    "doc_id": 20,
    "label": "intermediate_health_literacy",
    "fulltext": "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.",
    "diff_label_texts": "A.P. is a 38‑year‑old 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—a remission seen in about 16% of patients—and that improvement lasted 4 years. She then had a two‑year 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‑based therapy (an ACE inhibitor, a beta‑blocker, diuretics, and an If‑channel blocker), reported no limitation in physical activity, and was a mother of two and unemployed.",
    "summary": "Patient A.P., female, 38 years old, had symptoms of dilated cardiomyopathy (with possible infectious myocarditis in the background) at age 17. After hospitalization for ten months and ten days, while waiting for heart transplantation (with threatening death outcome), without a clearly pronounced threatening arrhythmia, but with a low ejection fraction and a poor general condition, remission occurred. The therapy focused primarily on the treatment of heart failure, prevention of arrhythmia and thromboembolism. Normalization of the disease by improving the function of the left ventricle (expected in 16% of patients) occurred and lasted for 4 years, followed by an exacerbation of the disease that lasted for two years. In the next few years the patient was stable, had a first child with normal pregnancy. During the second trimester of the second pregnancy, there was an exacerbation (postpartum dilatation cardiomyopathy) lasting for couple of months. At the time of case report (May 2017), the patient is stable on therapy (ACE inhibitor, beta blocker, diuretics, If channel blocker), without limitation of physical capacity, mother of two children, unemployed."
  },
  {
    "doc_id": 24,
    "label": "intermediate_health_literacy",
    "fulltext": "A 13-year-old male patient was admitted to the Children’s 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 × 2.4 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’s 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.",
    "diff_label_texts": "We report a unique case of a 13-year-old boy who presented with a palpable, painless mass in the left inguinal (groin) area and no other constitutional symptoms. His medical history included prior spinal surgery with resulting immobility and a pressure sore on the left foot, but otherwise he was well. Routine blood tests were normal except for a very high erythrocyte sedimentation rate (ESR 119 mm/h), and CT scans of the chest, abdomen and pelvis showed enlarged lymph nodes below the inguinal ligament, the largest about 3.5 × 2.4 cm. Because imaging and blood tests could not rule out malignancy (for example lymphoma or leukemia), the enlarged nodes were surgically removed for definitive diagnosis. Pathology showed features consistent with unicentric Castleman disease, plasma-cell type — one of the rarest forms in children and, to our knowledge, the first reported unicentric Castleman case in the inguinal area. The patient was discharged after 14 days with a course of oral prednisolone and was followed with clinical exams, laboratory tests and whole-body CT scans every three months. After 12 months of follow-up there were no new symptoms, no new enlarged lymph nodes on exam or imaging, and no abnormal laboratory findings.",
    "summary": "We report a unique case of a 13-year-old boy who presented with a palpable enlarged mass in the left inguinal region without any constitutional symptoms. Surgical removal of this mass was essential to exclude worrying causes. Pathologic examination revealed proliferative changes consistent with Castleman's disease plasma cell type which is one of the rarest forms of the disease in children. To our knowledge, this case is the first reported case of Unicentric Castleman Disease (UCD) in the inguinal area. During a 12-month-period of follow-up, no additional lymph node enlargements or other symptoms were reported."
  },
  {
    "doc_id": 27,
    "label": "intermediate_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "A 28-year-old man presented to dermatology with a 48-hour history of two red patches with central blisters and shallow ulcers on the inner (flexor) side of his right arm and forearm. He described burning and itching at the sites, had no other systemic symptoms, and had not self‑medicated. He reported being on vacation in the coastal region of Ecuador when the lesions appeared. A skin biopsy showed changes consistent with an acute inflammatory reaction, and, together with the clinical picture and recent travel, the diagnosis of Paederus dermatitis (skin injury caused by contact with certain rove beetles) was made. He was treated with oral antihistamines, topical corticosteroids and cold compresses. After 8 days the lesions resolved, leaving post‑inflammatory hyperpigmentation.",
    "summary": "The case of a 28-year-old male patient who presented to the dermatology department with a 48-hour history of two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm, accompanied by a burning sensation and pruritus at the site of the lesions, without accompanying symptoms, is reported. As a background, he stated that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed and, due to the clinical characteristics and the background of travel to a tropical region, the diagnosis was made as dermatitis by Paederus and treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions subsided, leaving a post-inflammatory hyperpigmentation.\n"
  },
  {
    "doc_id": 29,
    "label": "intermediate_health_literacy",
    "fulltext": "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 mmHg), and blood tests revealed anaemia (haemoglobin: 9.6 g/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’s 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–Weiss 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 days later, when CT was repeated, spontaneous resolution of the malpositioned jejunum was seen. The patient was then discharged from the hospital. However, months 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–Weiss 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 months. 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’s 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’s left side. The postoperative course was good, and the patient has remained symptom-free.",
    "diff_label_texts": "A 77-year-old woman was admitted with haematemesis. CT scans showed that the third part of her duodenum bent sharply on the right side of the aorta and ran downward without crossing in front of it; the duodenojejunal junction and much of the jejunum were located on the right side of the abdomen. Upper GI endoscopy found a mucosal tear at the gastric cardia consistent with Mallory–Weiss syndrome. Seven days after the first scan the abnormal right-sided position resolved on CT, but two months later the patient had another episode of haematemesis and the duodenojejunal junction and jejunum had again shifted to the right. Because the small bowel moved back and forth rather than staying in the wrong position, true intestinal malrotation was considered unlikely. The working diagnosis was dysplasia (abnormal development) of the ligament of Treitz, meaning the ligament that normally helps fix the upper small intestine was not holding the jejunum securely. At laparotomy the ligament of Treitz was present but did not fully fix the upper jejunum to the back wall of the abdomen (retroperitoneum); the pararenal area also appeared loosely fixed and mobile on CT. These factors probably allowed the jejunum to fold and deviate to the right. Surgically the upper jejunum was tacked to the left retroperitoneum with sutures, the postoperative course was good, and the patient has remained symptom-free.",
    "summary": "A 77-year-old woman underwent CT to evaluate haematemesis. The images showed 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 duodenal-jejunal junction and jejunum were located on the patient's right side. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, and a diagnosis of Mallory-Weiss syndrome was made. Repeat CT 7 days later revealed that the abnormal positioning of the intestinal tract had resolved spontaneously. Two months later, the patient experienced another episode of haematemesis, and CT revealed repeat deviation of the duodenal-jejunal junction and jejunum to her right side. Upper gastrointestinal endoscopy revealed another laceration at the gastric cardia, as in the previous study. On the basis of the initial CT findings showing the duodenal-jejunal junction in the right hemi-abdomen, intestinal malrotation was suspected. However, because the jejunum deviated repeatedly to the right side but resolved spontaneously, we diagnosed dysplasia of the ligament of Treitz. Laparotomy revealed a formed ligament of Treitz; however, fixation in the upper jejunum was incomplete. Additionally, CT revealed that the anterior pararenal space was loosely fixed and mobile. These factors may have caused the right-sided deviation of the small intestine."
  },
  {
    "doc_id": 31,
    "label": "intermediate_health_literacy",
    "fulltext": "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’s mother said that the patient was admitted to the hospital because of weakness in both patient’s hands and feet. The patient had a history of falling down about one year ago. The patient’s mother also had a difficulty in cleaning the patient’s 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 1×0.7 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’s cervical spine. The patient’s mother provided informed consent to publish the patient’s 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’s mother was instructed to clean the patient’s 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’s 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.",
    "diff_label_texts": "A 12-year-old boy with Down syndrome and motor disorders was referred to the Oral Medicine clinic. On exam he had a dysmorphic face and dry, cracked lips; a cervical collar prevented assessment of his neck lymph nodes. Inside the mouth there was an irregular ulcer on the right lateral border of the tongue measuring about 1 × 0.7 cm, with a firm (indurated) edge and a white-yellow base. A sharp remnant of tooth 55 was causing repeated trauma to that part of the tongue. Based on the history and exam, the team diagnosed a chronic traumatic ulcer that clinically looked like oral squamous cell carcinoma (OSCC). Other dental problems included caries and several tooth remnants (63, 55, 62, 74, 85) that were recommended for extraction and later space maintenance. Blood tests showed low sodium and a mildly raised lymphocyte percentage, and MRI revealed a cervical spine dislocation; the patient later had neurosurgery. Treatment in hospital included paracetamol and amoxicillin, and local oral care from the Oral Medicine team: saline rinses (0.9% sodium chloride), 1% povidone-iodine mouthwash as an antiseptic, and petroleum jelly for the lips. The mother was instructed to clean the mouth with gauze soaked in saline, apply the povidone-iodine compress to the ulcer three times daily, and use petroleum jelly to moisturize the lips. The oral lesions improved over follow-up visits at 3 days, 1 week, and 10 days. After neurosurgery the patient was observed in the pediatric intensive care unit but developed respiratory failure and died.",
    "summary": "A 12-year-old boy with Down Syndrome and motoric disorders was referred to Oral Medicine Department. In the extraoral examination, the patient had a dysmorphic face and dry lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1×0.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. The 55 teeth were sharp and caused an occlusion trauma to the right lateral border of the tongue. The patient was diagnosed with a chronic traumatic ulcer mimicking OSCC based on clinical examination. The medication given to the patient were sodium chloride 0.9%, povidone-iodine mouthwash 1%, and petroleum jelly."
  },
  {
    "doc_id": 34,
    "label": "intermediate_health_literacy",
    "fulltext": "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.",
    "diff_label_texts": "A 19-month-old boy came to the emergency department after falling from a highchair and hitting his head. On exam he had severe, unexplained breathing trouble that required tracheal intubation (a tube placed into the windpipe to help him breathe). The team suspected that the breathing problem had caused an altered state of consciousness and led to the fall and head injury. Imaging of the chest showed complete collapse (atelectasis) of the entire left lung and an abrupt cutoff of the left main bronchus about 12 mm from the lung hilum (the area where the bronchus enters the lung). Rigid bronchoscopy found and removed a 2 cm almond that was stuck in the left main bronchus. Earlier signs included very fast breathing and heart rate, low oxygen levels despite bag-mask ventilation, visible chest retractions, and decreased breath sounds on the left. The mother reported the child had an intense coughing episode a few days earlier that resolved without treatment; the child had never eaten almonds before and likely swallowed this one by accident. After the almond was removed the child improved steadily, was extubated 24 hours later, moved from intensive care to the pediatric ward, and made a full recovery of respiratory function.",
    "summary": "We describe the case of a 19-month-old boy who accessed the emergency room initially for a head trauma. The clinical evaluation, however, revealed an unexplained serious respiratory distress needing tracheal intubation. After our evaluation, we hypothesized that the severe respiratory distress determined an altered state of consciousness with following head trauma. The radiological findings raised the suspicion of foreign body aspiration for the presence of an atelectasis of the entire left lung. The computed tomography showed an abrupt interruption of the main bronchus at 12 mm from the hull. The following bronchoscopy identified an almond of 2 cm."
  },
  {
    "doc_id": 35,
    "label": "low_health_literacy",
    "fulltext": "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 × 109 leukocytes/L (6.0-17.5), 18.4 × 109 neutrophils/L (1.0-8.5), 7.0 × 109 lymphocytes/L (4.0-13.5), 3.5 × 109 monocytes/L, 459 × 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 × 109 leukocytes/L (6-17), 12.2 × 109 neutrophils/L (1.5-8.5), 7.5 × 109 lymphocytes/L (4-10.5), 1.2 × 109 monocytes/L (600), and 583 × 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",
    "diff_label_texts": "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.",
    "summary": "A case of infant with chronic granulomatous disease and invasive aspergillosis is reported. The infant was a 4-month-old male infant living with his mother in a prison cell. The infant had tumors in the left axillary region and a chest X-ray suggested rib fractures; he was hospitalized on suspicion of child abuse. A chest X-ray showed an axillary abscess, osteolysis of ribs, pneumonia and pulmonary nodules; the patient received broad spectrum antibiotics and was discharged. At 8 months, he was readmitted with fever and extension of the purulent abscess to the left shoulder region; a chest X-ray showed worsening of the condition. Aspergillus fumigatus was isolated from the secretion of the abscess and invasive aspergillosis was diagnosed; voriconazole was initiated for 28 days. A dihydro rhodamine test was performed and a diagnosis of chronic granulomatous disease caused by the pathogenic variant c.80_83del/Y of the CYBB gene, carried by the mother (c.80_83del/WT), was made. At 12 months, the patient was readmitted with invasive aspergillosis, resistant to treatment, with fatal outcome.\n"
  },
  {
    "doc_id": 36,
    "label": "low_health_literacy",
    "fulltext": "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 2×1 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’s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient’s 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.",
    "diff_label_texts": "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.",
    "summary": "A 25-year-old male patient came to the Department of Oral Medicine with the chief complaint of painful canker sores on the lips. Extra-oral examination revealed serosanguineous crusts on the lips that were painful and easily bleed. Intra-oral examination showed diffused and painful irregular erythematous lesions on the upper and lower labial mucosa. The anti-HSV1 IgG test was positive. The patient was diagnosed with HAEM.\n\nCase management: Pharmacological therapy included triamcinolone acetonide 0.1% in orabase, acyclovir tablets, multivitamins, and 0.9% NaCl. Non-pharmacological therapy included advice on maintaining good oral hygiene, avoiding spicy and sour foods, and breaking the bad habit of licking the lips."
  },
  {
    "doc_id": 36,
    "label": "intermediate_health_literacy",
    "fulltext": "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 2×1 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’s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient’s 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.",
    "diff_label_texts": "A 25-year-old man came to the oral medicine clinic with painful canker sores on his lips that started in the mouth four days earlier and involved the lips two days later. On exam there were blood-tinged crusts on the lips that bled easily, and diffuse, painful red lesions on the inside of the upper and lower lips. He had reported a fever about a week before the sores appeared, a period of heavy workload and poor diet, and a habit of frequently licking his lips. Initial tests showed a positive anti-HSV-1 IgG (ratio 6.32), supporting herpes virus involvement, and the working diagnosis was HAEM. Exfoliative cheilitis was considered but less likely because it does not involve the herpes virus. Other findings included poor oral hygiene and several unrelated dental problems. Treatment combined topical and systemic care: topical steroid ointment (triamcinolone acetonide 0.1% in orabase), warm compresses with 0.9% saline, oral acyclovir tablets (200 mg, five times daily for one week), and a daily multivitamin. Patients were also advised on non-drug measures: brush teeth and tongue twice daily with a soft brush and non‑detergent toothpaste, drink more water, eat a balanced diet, avoid acidic, spicy or hard foods (and foods with MSG), and stop licking or peeling the lips. Two days after the first visit pain was reduced but lesions remained; after starting acyclovir there was marked healing by the next follow-up and complete clinical recovery after 7 days. Oral-health–related quality of life improved (OHIP-14 score from 35 to 4). The patient was referred for further dental care (periodontics, restorative, oral surgery, and prosthodontics) and gave consent for publication.",
    "summary": "A 25-year-old male patient came to the Department of Oral Medicine with the chief complaint of painful canker sores on the lips. Extra-oral examination revealed serosanguineous crusts on the lips that were painful and easily bleed. Intra-oral examination showed diffused and painful irregular erythematous lesions on the upper and lower labial mucosa. The anti-HSV1 IgG test was positive. The patient was diagnosed with HAEM.\n\nCase management: Pharmacological therapy included triamcinolone acetonide 0.1% in orabase, acyclovir tablets, multivitamins, and 0.9% NaCl. Non-pharmacological therapy included advice on maintaining good oral hygiene, avoiding spicy and sour foods, and breaking the bad habit of licking the lips."
  },
  {
    "doc_id": 37,
    "label": "low_health_literacy",
    "fulltext": "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/μL). 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 × 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 × 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).",
    "diff_label_texts": "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.",
    "summary": "The patient was a 29-year-old woman, Para 1, with abnormal vaginal bleeding for a month and living with HIV and had a CD4 of 26 cells/μL. The histological examination of the cervical biopsy confirmed an extra-nodal BL. She had International Federation of Gynecology and Obstetrics (FIGO) stage 3B cervical cancer based on presence of hydronephrosis and pelvic wall involvement. The patient was reviewed at the oncology multidisciplinary meeting and required chemoradiation. There was delay in her management due to a long waiting list for chemoradiation at oncology unit in the referral center and the patient demised 43 days after diagnosis and did not receive the treatment."
  },
  {
    "doc_id": 38,
    "label": "intermediate_health_literacy",
    "fulltext": "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’s 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’s 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’s 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’s 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 1.7×1,021 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).",
    "diff_label_texts": "A 56-year-old woman was diagnosed in 2013 with Sjogren’s syndrome, an autoimmune disease that also caused scarring in her lungs (interstitial lung disease). She developed pulmonary arterial hypertension, which means high blood pressure in the blood vessels of her lungs. Over the years she took many medicines for her lung pressure and autoimmune disease, including sildenafil, bosentan, macitentan, iloprost, and steroid drugs, but her condition got worse. In 2020 she had very bad shortness of breath and her heart began to fail, a life-threatening problem called cardiogenic shock. In May 2023 she started taking one hydrogen capsule each day as an extra treatment. After she began the hydrogen capsules, tests showed she had more of a calming immune cell called CD127+ regulatory T cells. The tests also showed lower levels of anti-Ro antibodies, which are harmful antibodies linked to Sjogren’s syndrome. The tests showed fewer B cells, which are the immune system’s antibody-making cells. Her symptoms became stable and she did not have any side effects from the hydrogen capsules.",
    "summary": "We present the case of a 56-year-old female with CTD-PAH, diagnosed in 2013 with Sjogren’s syndrome complicated by interstitial lung disease (ILD) and PAH. Despite treatment with sildenafil, bosentan, macitentan, iloprost, and corticosteroids, her condition deteriorated, resulting in severe dyspnea and cardiogenic shock in 2020. In May 2023, molecular hydrogen therapy was initiated as an adjuvant treatment. The patient received daily hydrogen capsules, which led to increased CD127+ Treg cells, reduced anti-Ro antibodies, and decreased B cell subsets. Her clinical symptoms stabilized without adverse effects."
  },
  {
    "doc_id": 44,
    "label": "intermediate_health_literacy",
    "fulltext": "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/m². 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—with measurements of 12 × 11 × 10 mm—a 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 µUI/ml and 10.0 µUI/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 × 12 × 11 mm), with a slight decrease in size observed at the three-year follow-up, measuring 7 × 10 × 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.",
    "diff_label_texts": "A 12-year-old boy was admitted with sudden headaches and a week-long history of excessive urination and thirst. Tests showed central diabetes insipidus (low urine concentration with normal blood sodium and plasma osmolality), and MRI identified apoplexy (bleeding or sudden change) in a Rathke cleft cyst measuring about 15 × 6 × 11 mm; the normal bright signal of the posterior pituitary was lost but the anterior pituitary enhanced normally. He had no visual problems and routine pituitary hormone tests were otherwise normal. Because he was early in puberty, had no compressive symptoms, and basic endocrine tests were normal, a multidisciplinary team chose conservative management: clinical, hormonal and MRI follow-up, and treatment of the diabetes insipidus with vasopressin. Over three years the cyst remained stable then decreased in size (about 12 × 11 × 10 mm at nine months, 11 × 12 × 11 mm at two years, and 7 × 10 × 6 mm at three years), puberty progressed normally, and vision stayed normal. During follow-up his growth slowed, and stimulation tests at age 14 years 9 months showed a partial growth hormone deficiency; after starting growth hormone therapy his growth rate improved markedly. Overall, conservative follow-up was effective: the Rathke cleft cyst apoplexy stabilized and shrank, diabetes insipidus was controlled, and the only long-term endocrine issue was a treatable partial GH deficiency.",
    "summary": "We present the case of a 12-year-old boy admitted due to the recent onset of headaches and diabetes insipidus. Magnetic resonance imaging revealed Rathke cleft cyst apoplexy. Given the absence of compressive symptoms in a child at the early stages of puberty and without abnormalities in basic endocrine tests, a conservative strategy was employed, involving regular clinical, biological, and radiological follow-ups. The child experienced normal puberty without any endocrine deficiencies except for a partial growth hormone deficiency."
  },
  {
    "doc_id": 45,
    "label": "intermediate_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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 1–2 follicular non-Hodgkin lymphoma. CT of the neck, chest, abdomen, and pelvis found a nasopharyngeal mass measuring about 70 × 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‑cell 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.",
    "summary": "We report the case of a 67-year-old patient without pathological CDDs who presented with a deterioration of general condition with progressive dysphonia and dysphagia with a large mass in the neck that was biopsy-proven to be a grade 1 and 2 follicular non-Hodgkin lymphoma. A cervico-thoraco-abdomino-pelvic CT scan showed a 70 mm x 40 mm nasopharyngeal mass extending to 60 mm. Bone marrow biopsy was normal and the pre-therapeutic evaluation was normal. The patient received 4 courses of rituximab plus CHOP (cyclophosphamide, adriamycin, prednisone and oncovin) without response and then 3 courses of rituximab plus DHAOX (dexamethasone, high dose ara-cytin and oxalipatin) with persistence of the mass. The biopsy of the latter showed the disappearance of the B lymphocyte infiltration with presence of the AL amyloid deposits. The immunoelectrophoresis of plasma proteins showed the presence of immunoglobulin M. A positron emission tomography (PET) scan showed a hypermetabolic nasopharyngeal process. The patient is currently receiving a protocol of bortezomib, prednisone and bendamustine.\n"
  },
  {
    "doc_id": 49,
    "label": "intermediate_health_literacy",
    "fulltext": "Female patient, 16 years old, presenting a depressed gray plaque of 10.5 × 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",
    "diff_label_texts": "A 16-year-old girl has a depressed gray plaque on the lower outer (lateral) part of her left thigh, about 10.5 × 8.0 cm. The area includes lighter patches and small dilated surface blood vessels (telangiectasias) around the edges, and some nearby veins are visible. The lesion has been present since birth—it was initially purplish (violaceous) and over the years became lighter and sunken. There is no difference in leg length. Vascular imaging (angioresonance) shows a vascular malformation involving the skin and the fat under the skin in that area, supplied by branches of the popliteal artery. The scan showed early filling of veins, which suggests early venous shunting; no markedly dilated draining veins were found except for a superficial draining vein along the front of the thigh. The subcutaneous tissue beneath the plaque is thinner, and there is no extension into muscle or bone.",
    "summary": "16-year-old girl with a depressed gray plaque on the left thigh, with a vascular malformation affecting the skin and subcutaneous tissue evident by angioresonance.\n"
  },
  {
    "doc_id": 50,
    "label": "low_health_literacy",
    "fulltext": "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°C, HR 88 bpm, RR 18 bpm). She had a BMI of 16.6 kg/m² 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, 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal range, 3.9–86.4 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’s 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.",
    "diff_label_texts": "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.",
    "summary": "We present a unique case of a 57-year-old patient with a medical history of asthma and allergic rhinitis who presented recurrent abdominal pain, significant blood eosinophilia, and elevated levels of Immunoglobulin G4. After ruling out hematological and secondary causes of eosinophilia, a biopsy of the colon mucosa revealed an excess of tissue eosinophils, confirming the diagnosis of EoC. The patient responded well to corticosteroids and was subsequently maintained on montelukast, with no recurrence of symptoms over 3 months."
  },
  {
    "doc_id": 52,
    "label": "intermediate_health_literacy",
    "fulltext": "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 (café 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 (–), 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",
    "diff_label_texts": "A 2.5-year-old girl with a known diagnosis of neurofibromatosis type 1 (NF1) developed four weeks of watery diarrhea that became bloody. She was initially treated for dehydration after a rotavirus infection but continued to have bloody stools and weight loss. Colonoscopy showed red, inflamed mucosa from the anal margin through the colon up to the cecum, with loss of the normal visible blood vessels. Biopsies of the colon showed chronic inflammation with cryptitis and microabscesses, findings consistent with ulcerative colitis (UC). A PCR test on the colon tissue was positive for cytomegalovirus (CMV); blood testing showed past CMV exposure (IgG positive), no IgM, and a low CMV viral load. Blood tests showed mild anemia, a raised white count, and slightly increased CRP; faecal calprotectin was >600 µg/g, supporting active intestinal inflammation. Immunology testing and a broad genetic panel for monogenic immune causes were essentially normal. She was treated with mesalazine and received 15 days of intravenous ganciclovir for CMV, with clinical improvement and undetectable CMV on repeat testing at discharge. Two months later she had a flare with bloody diarrhea; stool testing showed Clostridioides difficile and CMV was undetectable. She was treated with antibiotics and prednisone, improved, and is maintained on mesalazine with only mild ongoing symptoms.",
    "summary": "2.5-year-old pre-schooler with a history of NF1 presenting with bloody diarrhea. On endoscopic examination, the mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency. Colon mucosal biopsies showed signs of chronic inflammation consistent with a diagnosis of ulcerative colitis and CMV infection was diagnosed by PCR.\n"
  },
  {
    "doc_id": 53,
    "label": "low_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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’s 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.",
    "summary": "We present the case of a 40-year-old HIV-positive man with regular adherence to treatment, who consulted for intermittent febrile episodes of two years' evolution, adding in the last two months progressive diffuse abdominal pain and generalized adenomegaly. In the laboratory, he presented pancytopenia, coagulopathy, hypoalbuminemia and increased acute phase reactants. The computed tomography (CT) of the thorax, abdomen and pelvis only showed hepato-splenomegaly and generalized adenomegaly. Multiple microbiological examinations were performed, including cultures for Mycobacterium sp. of different samples, all with negative results, with the exception of RT-PCR for HHV-8. A left iliac ganglion biopsy was performed with findings consistent with Castleman's disease. Despite restarting antiretroviral therapy, the symptomatology progressed, initiating treatment with corticosteroids and ganciclovir. After a week, he developed multiple organ failure and anasarca, which contraindicated the drugs initiated. A new chest CT was performed that showed infiltrates with a tree-like pattern in the upper right lobe associated with bilateral pleural effusion, and at the abdominal level, progression of hepato-splenomegaly and ascites. He passed to the intensive care unit 48 hours later due to fulminant hepatic failure. The patient died within a few hours. A postmortem culture of the tracheal aspirate was received positive for Mycobacterium tuberculosis and a liver biopsy with non-necrotizing granulomas.\n"
  },
  {
    "doc_id": 53,
    "label": "intermediate_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "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’s 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.",
    "summary": "We present the case of a 40-year-old HIV-positive man with regular adherence to treatment, who consulted for intermittent febrile episodes of two years' evolution, adding in the last two months progressive diffuse abdominal pain and generalized adenomegaly. In the laboratory, he presented pancytopenia, coagulopathy, hypoalbuminemia and increased acute phase reactants. The computed tomography (CT) of the thorax, abdomen and pelvis only showed hepato-splenomegaly and generalized adenomegaly. Multiple microbiological examinations were performed, including cultures for Mycobacterium sp. of different samples, all with negative results, with the exception of RT-PCR for HHV-8. A left iliac ganglion biopsy was performed with findings consistent with Castleman's disease. Despite restarting antiretroviral therapy, the symptomatology progressed, initiating treatment with corticosteroids and ganciclovir. After a week, he developed multiple organ failure and anasarca, which contraindicated the drugs initiated. A new chest CT was performed that showed infiltrates with a tree-like pattern in the upper right lobe associated with bilateral pleural effusion, and at the abdominal level, progression of hepato-splenomegaly and ascites. He passed to the intensive care unit 48 hours later due to fulminant hepatic failure. The patient died within a few hours. A postmortem culture of the tracheal aspirate was received positive for Mycobacterium tuberculosis and a liver biopsy with non-necrotizing granulomas.\n"
  },
  {
    "doc_id": 54,
    "label": "low_health_literacy",
    "fulltext": "4-month-old indigenous lactating mother from the rural area of the interior of Panama, from the town of Urracá, 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® (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",
    "diff_label_texts": "This story is about a 4‑month‑old 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‑to‑treat 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.",
    "summary": "4-month-old lactating infant, indigenous ethnicity, from the rural interior of Panama, 3 hours by canoe from the nearest health subcenter, with protein-caloric malnutrition, who presented with acute diarrhea and moderate-severe dehydration, receiving Enterogermina as part of the initial treatment. She was transferred to a third-level hospital, where she arrived with respiratory distress and signs of shock. The initial blood culture reported growth of methicillin-resistant Staphylococcus aureus (MRSA), the gastrointestinal panel was positive for Clostridiodes difficile, and later growth was confirmed in serial blood cultures of peripheral blood and central venous catheter, of Bacillus clausii. With a torpid evolution and resistance to multiple antibiotic regimens, she died of multisystem organ failure twelve days after admission.\n"
  },
  {
    "doc_id": 54,
    "label": "intermediate_health_literacy",
    "fulltext": "4-month-old indigenous lactating mother from the rural area of the interior of Panama, from the town of Urracá, 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® (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",
    "diff_label_texts": "A 4‑month‑old indigenous infant from a remote rural area of Panama (about three hours by canoe from the nearest health subcenter) with protein‑calorie malnutrition presented with acute diarrhea and moderate‑to‑severe dehydration. She had limited prior health care, had not received routine vaccinations, and was initially given Enterogermina (Bacillus clausii spores) and oral rehydration before being transferred to higher‑level hospitals because local facilities lacked supplies. On arrival at a third‑level hospital she had respiratory distress and signs of shock and was admitted to the pediatric intensive care unit, intubated, and treated with fluids, blood products, and multiple antibiotics. Initial blood culture grew methicillin‑resistant Staphylococcus aureus (MRSA); a gastrointestinal panel later detected Clostridioides difficile. Subsequent serial blood cultures from both peripheral blood and the central venous catheter repeatedly grew Bacillus clausii. Despite changes to antibiotic therapy to cover MRSA, C. difficile, and B. clausii, she developed worsening multisystem organ failure, including cardiac and kidney dysfunction, and died twelve days after admission.",
    "summary": "4-month-old lactating infant, indigenous ethnicity, from the rural interior of Panama, 3 hours by canoe from the nearest health subcenter, with protein-caloric malnutrition, who presented with acute diarrhea and moderate-severe dehydration, receiving Enterogermina as part of the initial treatment. She was transferred to a third-level hospital, where she arrived with respiratory distress and signs of shock. The initial blood culture reported growth of methicillin-resistant Staphylococcus aureus (MRSA), the gastrointestinal panel was positive for Clostridiodes difficile, and later growth was confirmed in serial blood cultures of peripheral blood and central venous catheter, of Bacillus clausii. With a torpid evolution and resistance to multiple antibiotic regimens, she died of multisystem organ failure twelve days after admission.\n"
  },
  {
    "doc_id": 55,
    "label": "intermediate_health_literacy",
    "fulltext": "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 mm in diameter), and pupillary reaction was absent. The remaining anterior segment examination showed no apparent abnormalities. Fundus examination was challenging due to the child’s size. Hertel exophthalmometry readings measured 10.5 mm in the right eye and 18 mm 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’ posterior part, tight adhesion to the optic nerve was observed. Due to the mass’s substantial size and the restricted surgical field, volume reduction was necessary. Approximately 12.5 mL 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’s 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’s 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 mm in the right eye and 8 mm in the left. The remaining anterior segment examination showed no apparent abnormalities.",
    "diff_label_texts": "A 2-year-old girl had a 1-year history of painless, progressive protrusion of the left eye with the eye displaced inward and upward; vision in that eye was only light perception. MRI showed a well-defined mass in the orbit that was dark on T1-weighted images and bright on T2-weighted images, with no clear contrast enhancement. The mass was removed through the lower eyelid conjunctiva using a transconjunctival approach with canthotomy and cantholysis to widen the surgical field; the tumor was cystic, gray‑white, and tightly adherent to the optic nerve, so about 12.5 mL of fluid was aspirated to reduce its size before complete excision. Histology and immunohistochemistry confirmed an orbital teratoma, showing squamous and glandular epithelium, brain tissue, and cartilage‑like material. One month after the first surgery the child developed enophthalmos (a sunken eye), conjunctival redness, and keratitis because removal of the large mass left reduced orbital volume and the cornea could not fully close. A second operation implanted donor (allogeneic) scleral tissue into the orbit to increase volume, correct the posterior fossa indentation, and allow the cornea to recover. At 1-year follow-up there was no tumor recurrence; vision remained at the preoperative level and the child had only minor residual enophthalmos and an outer canthus abnormality.",
    "summary": "Patient concerns: A 2-year-old female child was presented exhibiting proptosis and inward and upward eyeball displacement. Enhanced magnetic resonance imaging revealed a well-circumscribed mass, persisting with hypointense signals on T1-weighted images (T1WI) and hyperintense signals on T2-weighted images (T2WI).\n\nDiagnoses: The diagnosis of teratoma was confirmed finally through histological and immunohistochemical exams.\n\nInterventions: A transconjunctival approach via the inferior fornix, coupled with canthotomy and cantholysis, was performed. However, a month postsurgery, the patient developed enophthalmos, conjunctival hyperemia, and keratitis upon ocular examination. A second operation involved the implantation of allogeneic sclera into the orbit to increase orbital volume, improve the pitting of the fossa, and restore keratitis to normal.\n\nOutcomes: No recurrence and other complications were noted during the 1-year follow-up."
  },
  {
    "doc_id": 57,
    "label": "intermediate_health_literacy",
    "fulltext": "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 Consciência Fonológica Instrumento de Avaliação 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 – 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 “d” and “b”) 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",
    "diff_label_texts": "This case report describes a 9-year-old girl who was diagnosed with developmental dyslexia alongside high abilities (giftedness). The team compared her phonological processing, reading and writing before and after a program of 20 weekly phonological remediation sessions. Before intervention (age 8y2m) she showed weak phonological processing, reading at an alphabetic level, and writing in transition between syllabic-alphabetic and alphabetic stages. The remediation targeted phonological awareness, working memory, rapid naming and reading practice. After treatment (age 9y6m) phonological skills improved (notably phonemic awareness), phonological working memory reached age-appropriate levels, and rapid naming times improved for letters, objects and colors (digits stayed below expectation). Her reading advanced from an alphabetic to an orthographic level: oral reading rate rose from about 20 words per minute to about 94 words per minute, with better prosody and comprehension. Writing also showed gains and was classified at the alphabetic phase, but remained imprecise with letter reversals, omissions and segmentation errors that reflect persistent dyslexic features. In summary, phonological remediation produced clear gains in phonology and reading fluency, and helped consolidate alphabetic writing, but some difficulties in lexical access and accurate spelling persisted.",
    "summary": "This study is a case report of the evaluation and intervention process of a 9-year-old child with the paradoxical combination of high abilities associated with dyslexia. The objective was to compare the performance in the tasks of phonological processing, reading and writing before and after phonological remediation. In the first evaluation, the child presented an alphabetic level in reading, a transition phase between the syllabic-alphabetic and alphabetic levels in writing and a performance below the expected level in phonological processing abilities. After the intervention, there was an improvement in phonological processing abilities, consolidation of alphabetic writing and of the orthographic level of reading.\n"
  },
  {
    "doc_id": 59,
    "label": "intermediate_health_literacy",
    "fulltext": "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°C for five hours. Upon admission to the local hospital’s emergency department, his core temperature (Tc) was recorded as 40°C. 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’s solution and normal saline at a rate of 2.5mL/kg∙h), 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’s 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·min. 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 3.55×109/L to 3.13×109/L, lymphocytes significantly decreased from 0.25×109/L to 0.1×109/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 °C and 38.5 °C. 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°C), 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 14.94×109/L and NEU increased to 13.77×109/L. The levels of serum total bilirubin rose to 235.2 µmol/L, while creatinine increased to 441µmol/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’s 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’s condition progressively worsened over the next 7 days, ultimately resulting in his demise on day 29. The patients’ inflammatory indicators, cytokines, and coagulation indicators are presented in Table 1.",
    "diff_label_texts": "This report describes the first known case of heatstroke occurring together with SARS‑CoV‑2 infection in a 52‑year‑old man. He had a recent cold and a positive self-test for COVID‑19, then returned to work and lost consciousness after five hours outdoors in 35°C heat. On arrival at the hospital his core temperature was 40°C and he was comatose with breathing problems and gastrointestinal bleeding; clinicians diagnosed heatstroke. He was admitted to the ICU, placed on a ventilator, given IV fluids, antibiotics, blood‑pressure support, and continuous renal replacement therapy when his kidneys failed. Laboratory tests showed severe infection, low platelets and a severe clotting disorder (disseminated intravascular coagulation), plus liver, kidney and heart injury. Sputum and airway cultures later grew several pathogens (including Stenotrophomonas, Candida, MRSA, Acinetobacter and Aspergillus), and he was treated with broad antibiotics, antifungals, plasma and blood products, and anticoagulation as needed. After these treatments his fever subsided and he regained consciousness by about day 13 and was briefly taken off the ventilator. Several days later he suddenly worsened with respiratory failure, high fever and a return to coma; brain imaging showed an ischemic stroke and a hemorrhagic infarct. Despite further intensive care, he developed a large cerebral hemorrhage with brain herniation; surgery was not performed and his condition progressed to multiple organ dysfunction syndrome (MODS). The combination of multi‑pathogen pulmonary infection and an intractable coagulopathy ultimately led to MODS and death on day 29.",
    "summary": "We report the first case of heatstroke comorbid with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection in a 52-year-old male. After receiving intravenous antibiotics, organ protection measures, and treatment for coagulation disorders, his fever and coma resolved. However, he developed dyspnea and cerebral hemorrhage after several days. This patient experienced a multi-pathogen pulmonary infection and an intractable coagulopathy that ultimately resulted in MODS and death."
  },
  {
    "doc_id": 60,
    "label": "intermediate_health_literacy",
    "fulltext": "A 19-year-old female presented to our hospital’s 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°C, 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 14.77×10^9/L and a neutrophil count of 13.55×10^9/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’s symptoms, a chest computed tomography (CT) scan was performed. Incidentally, this scan revealed a left adrenal mass with soft tissue density, measuring 43 mm × 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’s 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 × 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’s 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 × 40 mm × 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.",
    "diff_label_texts": "A 19-year-old woman came to the emergency room with headache, nausea, vomiting and fever and was found to have very high blood pressure and a fast heart rate. Imaging incidentally showed a large mass on her left adrenal gland, and blood and 24-hour urine tests showed markedly raised catecholamines and their metabolites, confirming a diagnosis of pheochromocytoma. Despite the size of the tumor and receiving high‑dose glucocorticoid treatment early in her stay, she did not develop a hypertensive crisis. She had a past episode a year earlier diagnosed as myocarditis and a family history of sudden unexplained death. Genetic testing identified a pathogenic RET gene mutation (c.1900T>C, p.Cys634Arg) consistent with multiple endocrine neoplasia type 2A (MEN2A), so the thyroid and parathyroid glands were evaluated. Thyroid ultrasound found a small nodule and blood tests showed mildly raised calcitonin, while initial electrolytes and parathyroid hormone (PTH) were within the normal range. Three months later she underwent removal of the left adrenal tumor; pathology confirmed pheochromocytoma, and she recovered without recurrence of symptoms. Over 15 months of follow-up she continued to have mildly elevated calcitonin with a stable thyroid nodule, but PTH and serum calcium levels rose progressively. A 99mTc‑MIBI parathyroid scan did not show a parathyroid adenoma.",
    "summary": "We report the case of a 19-year-old female who presented with pheochromocytoma without experiencing a crisis, despite having a significant adrenal mass and undergoing high-dose glucocorticoid treatment. Genetic testing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), associated with MEN2A. Further endocrine evaluation identified a thyroid nodule with mildly elevated calcitonin levels, but normal electrolyte and parathyroid hormone levels. 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. Further parathyroid scintigraphy using 99mTc-MIBI was performed, yielding a negative result for parathyroid adenoma."
  },
  {
    "doc_id": 62,
    "label": "intermediate_health_literacy",
    "fulltext": "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 38ºC). 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—canoeing 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’s temperature was 37.8°C 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.",
    "diff_label_texts": "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 “crazy paving,” 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–Schiff 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–GM-CSF antibodies were strongly positive, supporting autoimmune PAP. At 20 months, he remains asymptomatic, and spirometry has normalized.",
    "summary": "We describe the case of a 13-year-old adolescent male who presented to the emergency department with acute pleuritic chest pain not associated with systemic complaints. On examination, he had diminished breath sounds in the lower two thirds of the chest with no other abnormal findings; SpO2 (oxygen saturation) was 98% on room air. Chest radiograph revealed a marked interstitial infiltrate, comparable with the one taken 4 years earlier during an acute illness that was presumptively treated with azithromycin. A computed tomography (CT) scan revealed multiple bilateral areas of ground-glass opacities with areas of crazy paving, involving > 65% of lung parenchyma, suggestive of pulmonary alveolar proteinosis (PAP). Respiratory viral testing, including for coronavirus (SARS-CoV2), was negative. Bronchoalveolar lavage performed in the outpatient setting revealed a milky fluid and positive periodic acid-Schiff staining. Spirometry indicated a mild restrictive pattern (forced vital capacity [FVC] = 77%) and diffusing capacity of the lungs for carbon monoxide (DLCO) showed a moderate decrease at 48.6%. No mutations associated with surfactant dysfunction were found on the genetic panel. Anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibody testing was strongly positive, raising suspicion for autoimmune PAP. At 20 months of follow-up, the patient remains asymptomatic with a normal spirometry."
  },
  {
    "doc_id": 66,
    "label": "intermediate_health_literacy",
    "fulltext": "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.",
    "diff_label_texts": "A 17-year-old male had an asymptomatic nasal foreign body (NFB) found incidentally on routine dental x-rays and cone beam CT during orthodontic planning. He denied any nasal blockage, nosebleeds, or discomfort. His parents recalled that at age seven he had put something in his nose; the family had been advised at the time to remove it under sedation but did not follow up, assuming it had fallen out. Endoscopic exam showed a deviated septum and enlargement of the lower nasal turbinate, with mild redness and swelling of the nasal lining. A shiny object was seen stuck to the floor of the right nasal cavity beneath the inferior turbinate and was partly covered with mucus and crust. X-rays and CBCT confirmed a circular radiopaque object consistent with a metallic snap button about 1 cm across, with mild surrounding inflammation but no damage to the nearby bone or sinuses. With parental consent, the button was removed in the clinic under local anesthesia and nasal decongestion while the patient was semi‑upright to reduce the risk of it moving toward the airway; removal with a hook and forceps was uncomplicated, with only minimal bleeding. The retrieved snap button showed corrosion and biological deposits, consistent with being present for many years. The patient was discharged in stable condition, advised to use saline nasal rinses, and was doing well with a normal exam at two-week follow-up.",
    "summary": "We present the case of a 17-year-old male with an asymptomatic NFB discovered incidentally during routine dental radiography. The patient denied any history of nasal obstruction, epistaxis, or discomfort. Imaging revealed a radiopaque object in the right nasal cavity, later identified as a metallic snap button embedded in the floor of the nasal cavity. The foreign body had likely been retained for over a decade."
  },
  {
    "doc_id": 66,
    "label": "proficient_health_literacy",
    "fulltext": "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.",
    "diff_label_texts": "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—likely 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.",
    "summary": "We present the case of a 17-year-old male with an asymptomatic NFB discovered incidentally during routine dental radiography. The patient denied any history of nasal obstruction, epistaxis, or discomfort. Imaging revealed a radiopaque object in the right nasal cavity, later identified as a metallic snap button embedded in the floor of the nasal cavity. The foreign body had likely been retained for over a decade."
  },
  {
    "doc_id": 67,
    "label": "low_health_literacy",
    "fulltext": "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 3–4 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%–45%, 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 min. 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 133 000 IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%–15% with previously noted severe LV concentric hypertrophy (1.9 cm septum and 2.2 cm 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%–30%, 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 1×1 inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2–3 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–day 3), etoposide (day 1–day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7–day 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.",
    "diff_label_texts": "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–Barr 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.",
    "summary": "An 18-year-old male patient presented to the emergency department complaining of new onset chest pain, fever and orthopnoea. Initial workup was remarkable for elevated troponin, diffuse ST-segment elevation on ECG and chest X-ray with enlarged cardiac silhouette. Transthoracic echocardiogram (TTE) demonstrates severe biventricular concentric hypertrophy and pericardial effusion. Also, Coxsackie virus A and B titres were positive, concerning for a classic viral pericarditis. However, despite medical management, the patient became dyspnoeic and hypotensive. Impending cardiac tamponade was observed on repeat TTE, and pericardiocentesis was performed, complicated by pulseless electrical activity cardiac arrest, and ultimately patient requiring venoarterial extracorporeal membrane oxygenation support. Emergent endomyocardial biopsy showed no inflammatory process, and a skin biopsy of a small lesion in the right arm showed unexpected diagnosis of Epstein-Barr virus (+) natural killer/T-cell lymphoma. On initiation of chemotherapy, clinical improvement was observed as evidenced by improving ejection fraction, resolution of pericardial effusion and gradual decrease in myocardial hypertrophy."
  },
  {
    "doc_id": 67,
    "label": "intermediate_health_literacy",
    "fulltext": "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 3–4 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%–45%, 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 min. 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 133 000 IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%–15% with previously noted severe LV concentric hypertrophy (1.9 cm septum and 2.2 cm 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%–30%, 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 1×1 inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2–3 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–day 3), etoposide (day 1–day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7–day 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.",
    "diff_label_texts": "An 18-year-old man came to the emergency department with new chest pain, fever, shortness of breath when lying flat (orthopnoea) and a dry cough for several days. Initial tests showed an elevated troponin, diffuse ST-segment elevations on ECG, and an enlarged heart on chest X-ray. Transthoracic echocardiogram (TTE) showed severe concentric thickening of both ventricles and a pericardial effusion; Coxsackie A and B antibody titres were also positive, so clinicians initially treated him for viral myopericarditis with anti-inflammatory medications. Despite treatment he acutely worsened on day four, becoming hypotensive and short of breath; repeat TTE showed impending cardiac tamponade and he underwent pericardiocentesis. The procedure was complicated by a pulseless electrical activity cardiac arrest, and he required intubation and venoarterial extracorporeal membrane oxygenation (VA-ECMO) for circulatory support. An endomyocardial biopsy did not show inflammation, and blood testing found a very high Epstein–Barr virus (EBV) PCR. A separate biopsy of a small painless mass on his right arm unexpectedly showed EBV-positive natural killer/T‑cell lymphoma. With a working diagnosis of lymphoma involving the heart and pericardium, he was started on systemic chemotherapy (initially an emergency regimen followed by modified lymphoma protocols). After treatment his heart function steadily improved: ejection fraction recovered to normal range, the pericardial effusion resolved, and the abnormal myocardial thickening decreased. He completed most planned chemotherapy cycles and continues follow-up with cardiology and oncology.",
    "summary": "An 18-year-old male patient presented to the emergency department complaining of new onset chest pain, fever and orthopnoea. Initial workup was remarkable for elevated troponin, diffuse ST-segment elevation on ECG and chest X-ray with enlarged cardiac silhouette. Transthoracic echocardiogram (TTE) demonstrates severe biventricular concentric hypertrophy and pericardial effusion. Also, Coxsackie virus A and B titres were positive, concerning for a classic viral pericarditis. However, despite medical management, the patient became dyspnoeic and hypotensive. Impending cardiac tamponade was observed on repeat TTE, and pericardiocentesis was performed, complicated by pulseless electrical activity cardiac arrest, and ultimately patient requiring venoarterial extracorporeal membrane oxygenation support. Emergent endomyocardial biopsy showed no inflammatory process, and a skin biopsy of a small lesion in the right arm showed unexpected diagnosis of Epstein-Barr virus (+) natural killer/T-cell lymphoma. On initiation of chemotherapy, clinical improvement was observed as evidenced by improving ejection fraction, resolution of pericardial effusion and gradual decrease in myocardial hypertrophy."
  },
  {
    "doc_id": 72,
    "label": "low_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "She had a heart transplant because her heart got very weak after pregnancy. Later, her kidneys—the body’s filters—were hurt by a germ called BK virus. A small kidney sample showed long‑lasting 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‑rejection 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.",
    "summary": "We report a case of BK virus nephropathy in a patient who underwent heart transplantation due to peripartum cardiomyopathy. The renal biopsy reported active chronic tubulointerstitial nephritis associated with late-stage BK virus nephritis and the blood viral load for BK virus was positive (log 4.5). The immunosuppressive treatment was reduced, and after two years of follow-up, the patient had stable renal function with serum creatinine of 2.5 mg/dL (GFR of 23.4 mL/min/1.73m2).\n"
  },
  {
    "doc_id": 72,
    "label": "intermediate_health_literacy",
    "fulltext": "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",
    "diff_label_texts": "A 39-year-old woman had a heart transplant in 2014 for peripartum cardiomyopathy and was treated with standard immunosuppression (basiliximab induction, then tacrolimus, everolimus and low‑dose prednisone). She had two treated episodes of rejection in the first year and initially normal kidney function. Routine BK virus monitoring was not done. Over the next two to three years her serum creatinine rose: first to 1.9 mg/dL in 2016 (which improved after lowering tacrolimus), then to 2.69 mg/dL in March 2017, when she was hospitalized. Workup including ultrasound and urine tests was unrevealing, so a kidney biopsy was performed. The biopsy showed chronic tubulointerstitial nephritis with late-stage BK virus nephropathy, and blood BK viral load was positive at about 33,800 copies/mL (log 4.5). Tacrolimus was stopped and her creatinine stabilized between 2.2 and 2.5 mg/dL while the BK viral load fell to undetectable levels. After two years of follow-up she had stable renal function with a creatinine of 2.5 mg/dL (estimated GFR about 23.4 mL/min/1.73 m2) and no further cardiac rejection.",
    "summary": "We report a case of BK virus nephropathy in a patient who underwent heart transplantation due to peripartum cardiomyopathy. The renal biopsy reported active chronic tubulointerstitial nephritis associated with late-stage BK virus nephritis and the blood viral load for BK virus was positive (log 4.5). The immunosuppressive treatment was reduced, and after two years of follow-up, the patient had stable renal function with serum creatinine of 2.5 mg/dL (GFR of 23.4 mL/min/1.73m2).\n"
  },
  {
    "doc_id": 74,
    "label": "intermediate_health_literacy",
    "fulltext": "A 56-year-old Italian female patient with β-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 β-thalassemia condition (genotype HBB:c.118C > T/ HBB:c.93-21G > A), diagnosed at the age of 7 years, despite the fact that the first transfusion was carried out at 2 years. As a consequence of β-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’s 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 10–10.5 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 = 4.3); 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–Koga; 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 β-thalassemia, treatment with sirolimus was recommended.",
    "diff_label_texts": "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.",
    "summary": "A 56-year-old Italian female patient with β-thalassemia major underwent magnetic resonance imaging to quantify myocardial, hepatic, and pancreatic iron deposition. Her medical history included transfusion-dependent β-thalassemia, splenectomy, and cholecystectomy. At the time of magnetic resonance imaging, she had no significant endocrine, cardiac, or hepatic complications and was on deferasirox, vitamin D, and luspatercept. Magnetic resonance imaging revealed a lobulated mass in the prevascular mediastinum, which showed mild radiotracer uptake on positron emission tomography. Chest computed tomography revealed multiple thin-walled cysts in the lungs, indicating lymphangioleiomyomatosis. Following multidisciplinary evaluation, the patient underwent thoracoscopic thymectomy and lung wedge resection. Histopathology confirmed type B2 thymoma and pulmonary lymphangioleiomyomatosis. Post-surgery, the patient was recommended for adjuvant radiation therapy and sirolimus treatment."
  },
  {
    "doc_id": 75,
    "label": "intermediate_health_literacy",
    "fulltext": "We present a case of a 49-year-old woman with renal and heart failure following a long-term (lasting from 13 years 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 mg/dL and proteinuria of 2 g/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 years. While being on active waiting list for kidney transplantation presented remission of laboratory indices of lupus (complement splits within normal limits: C3–0,93 g/l, C4–0,4 g/l, ANA negative) and persisting circulatory insufficiency with markedly reduced stair-climbing capacity (to one flight of stairs) with elevated BNP 619 pg/ml (n. 0–100). 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 μg/kg/min was continued after surgery for a total of 24 h. The patient’s 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’s 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 g 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 weeks (mostly due to fluid retention). BNP levels raised to 2996 pg/ml and then slowly decreased. The kidney biopsy performed 2 weeks 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 mg/dL and BNP level of 1794 pg/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 − 6) 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 pg/ml and normal kidney function were noted.",
    "diff_label_texts": "This report describes a 49-year-old woman with long‑standing systemic lupus erythematosus (SLE) who developed progressive kidney and heart failure and was listed for kidney transplantation after four years on dialysis. Her SLE began in childhood with lupus nephritis and she had prior immunosuppressive treatments; she was also hepatitis B and C positive. She had early heart disease, including a heart attack at age 20, later developed ischemic and dilated cardiomyopathy, received an ICD, and underwent mitral and tricuspid valve repair with left‑ventricle surgery; after that operation her kidney function worsened and dialysis was started. Before transplant she had severe heart dysfunction (LVEF about 26%, high BNP) and signs suggesting possible pulmonary hypertension, so the team added perioperative cardioprotective therapy with levosimendan. Levosimendan infusion (0.1 µg/kg/min) began after a dialysis session when the donor match was confirmed and continued through the first 24 hours after surgery. Anesthesia and postoperative care focused on protecting the new kidney and careful fluid and hemodynamic management; invasive pulmonary artery catheterization was avoided because of her ICD and unstable rhythm history. The postoperative course was complicated: she experienced delayed graft function requiring hemodialysis for roughly six weeks, had a biopsy‑proven acute rejection episode with acute tubular necrosis, and developed leukopenia and cytomegalovirus infection that led to changes in immunosuppression. BNP rose after surgery but then gradually fell; she was discharged on day 67 with serum creatinine 1.4 mg/dL. By one month after transplant there was measurable improvement in heart size and function (EF up to ~30%, better strain measurements), lower pressures suggesting less pulmonary hypertension, and better exercise tolerance (NYHA III/IV to II). At five months she had continued improvement in heart function, BNP down to about 1066 pg/mL, and normal kidney function.",
    "summary": "We present a case of a 49-year-old woman with renal and heart failure following a long-term SLE prepared for kidney transplantation. During the SLE course, the function of the heart and kidneys gradually deteriorated. The patient required the initiation of renal replacement therapy and was dialyzed until a kidney transplantation for 4 years. In the preparation of the patient for the surgical procedure, due to the extremely low ejection fraction, it was decided to include cardioprotective treatment with Levosimendan. The postoperative period was not straightforward but successful. In the monthly and five-month follow-up, a continuous improvement of heart function with normal renal function was noted."
  },
  {
    "doc_id": 76,
    "label": "intermediate_health_literacy",
    "fulltext": "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™ E6, ultrasonography system with a linear 13–5 MHz probe for unilateral PGONB. The patient’s 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",
    "diff_label_texts": "A 42-year-old woman with primary cough headache (PCH) could not tolerate oral preventive medicines because of side effects. She developed more than ten short, severe headache attacks a day after a bout of bronchitis; each attack lasted about 30 minutes, was triggered by coughing, straining or lifting, and reached 9/10 on a pain scale. Neurological exam and brain and neck imaging were normal, and she declined a lumbar puncture. Because she could not keep taking indomethacin and could not use other oral options, we offered an ultrasound-guided proximal greater occipital nerve block (PGONB) using bupivacaine. After a single, unilateral block the pain fell from 9/10 to 2/10 within 20 minutes. The block was repeated once weekly for a month; at two months both the number of attacks and their intensity had declined (about two attacks per month at 4/10), and by six months she reported no attacks. No adverse effects from the nerve blocks were observed, suggesting ultrasound-guided GON blockade can be an effective option when oral drugs are not tolerated.",
    "summary": "Herein, we report that a 42-year-old female patient with PCH who could not use the oral medication because of side effects. When she came to the pain clinic with an attack with intensity of 9/10 , we took her to the local operating room. The ultrasound (US) guided proximal greater occipital nerve block with bupivacaine was performed and the intensity of the attack was reduced to 2/10. The blockage was repeated once a week for a month. After two months, both the intensity of headache and number of attacks decreased and no adverse effect was observed."
  },
  {
    "doc_id": 78,
    "label": "low_health_literacy",
    "fulltext": "A male was born via an emergency cesarean section due to fetal distress at 40 weeks 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 weeks 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 g (75 percentile), the length was 56.5 cm (over 90 percentile), and the head circumference was 36 cm (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 mm) (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 ACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24–32). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2 weeks 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.",
    "diff_label_texts": "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’s 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.",
    "summary": "Patient concerns:\nA newborn with neonatal MFS and severe cardiac involvement. He presented various severe clinical features such as arachnodactyly, camptodactyly, elbow and knee joint contracture, senile facial appearance, and deep settling with down-slanting palpebral fissure, hypoplastic ear cartilage, sagging mouth, brachycephaly, and ectopia lentis.\n\nDiagnosis:\nGenetic analysis revealed a novel mutation at nucleotide 3964 (c.3964 + 1 G > T) in intron 32 of the fibrillin-1 gene. This mutation is identified to be in the so-called neonatal region of fibrillin-1 exon 24 to 32, as reported previously.\n\nInterventions:\nThe patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction, full sedation, and use of diuretic were attempted to improve the oliguria and heart failure.\n\nOutcomes:\nDespite the medical management, aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. Surgical treatment is essential to prolong the patient's life, however, considerations for the grave progression of the disease make families decide to continue palliative care instead of surgical treatment. A few months after birth, he presented with rapidly progressive aortic regurgitation, mitral regurgitation, and congestive heart failure leading to death."
  },
  {
    "doc_id": 78,
    "label": "intermediate_health_literacy",
    "fulltext": "A male was born via an emergency cesarean section due to fetal distress at 40 weeks 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 weeks 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 g (75 percentile), the length was 56.5 cm (over 90 percentile), and the head circumference was 36 cm (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 mm) (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 ACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24–32). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2 weeks 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.",
    "diff_label_texts": "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 24–32). 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.",
    "summary": "Patient concerns:\nA newborn with neonatal MFS and severe cardiac involvement. He presented various severe clinical features such as arachnodactyly, camptodactyly, elbow and knee joint contracture, senile facial appearance, and deep settling with down-slanting palpebral fissure, hypoplastic ear cartilage, sagging mouth, brachycephaly, and ectopia lentis.\n\nDiagnosis:\nGenetic analysis revealed a novel mutation at nucleotide 3964 (c.3964 + 1 G > T) in intron 32 of the fibrillin-1 gene. This mutation is identified to be in the so-called neonatal region of fibrillin-1 exon 24 to 32, as reported previously.\n\nInterventions:\nThe patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction, full sedation, and use of diuretic were attempted to improve the oliguria and heart failure.\n\nOutcomes:\nDespite the medical management, aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. Surgical treatment is essential to prolong the patient's life, however, considerations for the grave progression of the disease make families decide to continue palliative care instead of surgical treatment. A few months after birth, he presented with rapidly progressive aortic regurgitation, mitral regurgitation, and congestive heart failure leading to death."
  },
  {
    "doc_id": 0,
    "label": "intermediate_health_literacy",
    "fulltext": "A 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\n\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/µL. Renal and liver functions were normal.\n\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours.",
    "diff_label_texts": "A 20‑year‑old woman had a 12‑year history of idiopathic nephrotic syndrome that initially presented with extensive cerebral venous thrombosis and pulmonary embolism. She was treated with anticoagulation and oral corticosteroids, then mycophenolate mofetil as a steroid‑sparing agent. A comprehensive thrombophilia work‑up was negative. She experienced multiple relapses controlled with steroids until 2017, then remained in remission; anticoagulation and MMF were discontinued. One year later, she developed sudden diffuse abdominal pain with postprandial vomiting and bilateral leg edema. Laboratory tests confirmed a relapse of nephrotic syndrome. Abdominal CT showed acute superior mesenteric artery thrombosis causing acute mesenteric ischemia. At surgery, there was extensive small‑bowel necrosis not compatible with survival. She died 48 hours later.",
    "summary": "We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours."
  },
  {
    "doc_id": 0,
    "label": "low_health_literacy",
    "fulltext": "A 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\n\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/µL. Renal and liver functions were normal.\n\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours.",
    "diff_label_texts": "This is about a 20-year-old woman. She had a kidney problem since age eight that made protein leak into her urine. The problem first showed up when a big blood clot blocked veins in her brain, and a clot also went to her lungs. She took blood thinners and steroid pills. Later she took a medicine that calms the immune system to help her use fewer steroids. Tests showed no inherited blood-clotting problem. She had several flare-ups of the kidney problem. Steroid pills controlled them until 2017. After that she had no relapses. Her doctors stopped the blood thinner and the immune-calming medicine. One year later she had sudden, very bad belly pain all over. She threw up after eating. Both legs were swollen. Tests showed the kidney problem was back. A special X-ray picture (CT scan) showed a new clot in the main artery that feeds the small intestine. It was like a plug in a pipe that stops water. Blood could not reach the intestines. In surgery, most of her small intestine was dead. Taking out that much bowel would not allow life. She died 48 hours later.",
    "summary": "We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours."
  },
  {
    "doc_id": 0,
    "label": "proficient_health_literacy",
    "fulltext": "A 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\n\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/µL. Renal and liver functions were normal.\n\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours.",
    "diff_label_texts": "A 20‑year‑old woman had been followed since age eight for idiopathic nephrotic syndrome (NS) inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism, without sequelae and without personal or family thrombotic history. Kidney biopsy was deferred because there was no kidney failure, gross hematuria, hypertension, or extra‑renal signs suggestive of secondary NS at presentation. She was treated with an oral vitamin K antagonist and oral corticosteroids with good evolution. Subsequently, she had multiple steroid‑dependent relapses and was started on mycophenolate mofetil (MMF) as background therapy to spare corticosteroids and ensure normal growth. An exhaustive thrombophilia assessment was negative: homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden, JAK‑2, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and anti‑β2‑glycoprotein I antibodies were all normal. Anticoagulation was stopped after nine years. Several relapses occurred but were controlled with oral corticosteroids. NS remission was documented from 2017; MMF was gradually discontinued in 2019, and she remained asymptomatic without relapse.\n\nOne year later, she presented to the emergency department with acute intense diffuse abdominal pain without irradiation, associated with postprandial vomiting and bilateral lower‑limb edema for six hours. Examination showed intense epigastric tenderness with normal vital signs (BP 120/70 mm Hg, HR 83 bpm, SpO2 100% on room air) and no fever or neurological impairment. Urinalysis detected proteinuria. Hemogasanalysis showed metabolic acidosis with respiratory compensation. Labs revealed hypoalbuminemia, hypercholesterolemia, prothrombin time 90%, elevated D‑dimer, LDH, and creatine phosphokinase, with inflammatory markers (CRP 37 mg/L) and leukocytosis (26.4 × 10^3/µL); renal and liver function were normal. Urgent abdominal ultrasound showed a low‑to‑moderate intra‑abdominal effusion. Contrast‑enhanced CT demonstrated acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. She underwent emergency laparotomy: intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost the entire small bowel, rendering resection incompatible with life. She died 48 hours later.\n\nThis case illustrates catastrophic arterial thrombosis in the setting of NS despite a negative thrombophilia work‑up. NS is a hypercoagulable state with multifactorial mechanisms, including urinary loss of anticoagulant proteins (e.g., antithrombin III, protein S), increased fibrinogen, hemoconcentration, dyslipidemia, and systemic inflammation. While venous thromboembolism is more common in NS, superior mesenteric artery thrombosis is rare but often fatal, underscoring the need for high clinical suspicion and rapid imaging when severe acute abdominal pain occurs in patients with active or relapsing NS.",
    "summary": "We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours."
  },
  {
    "doc_id": 1,
    "label": "low_health_literacy",
    "fulltext": "We present the case of a 34-year-old woman, eight weeks pregnant with no other personal history of interest, who presents to the emergency department with generalized convulsions with dysarthria in the postcritical period, which resolve progressively in less than two hours. On physical examination, she is conscious, oriented, with no language or motor or sensory deficits. Only signs of a right lateral tongue bite are observed.\n\nThe complementary tests, such as blood tests or the electrocardiogram, are normal. Given that the episode corresponds with a first epileptic seizure and the patient is pregnant, an urgent magnetic resonance of the skull is requested.\n\nThe usual protocol was performed and 3D T1 sequences without and with intravenous contrast were obtained in axial, coronal and sagital planes, axial FLAIR, axial T2, VEN BOLD and magnetic susceptibility sequences, as well as axial diffusion and apparent diffusion coefficient map. The MRI identified multiple venous cortico-medullary vascular structures converging centripetally to a large central venous structure draining through the inferior anastomotic vein into the left transverse sinus, forming the classic ‘Medusa head’ sign. In the T1 sequences, the drainage vein was seen to be increased in signal with central hyphocaptation after contrast administration, suggesting partial thrombosis versus slow flow. In addition, in T2 and FLAIR sequences, the brain tissue surrounding the drainage vein was seen to be hyperintense, without diffusion restriction and compatible with edema.\n\nThese findings are suggestive of a venous anomaly of development with signs of partial peripheral thrombosis and slow flow more proximal, which cause edema of the surrounding tissue. She is started on clexane 60 mg/12 hours and levetiracetam 500 mg/12 hours and the patient shows improvement and symptomatic stability after one week.\n",
    "diff_label_texts": "She is 34 years old and pregnant. She had a seizure and trouble speaking clearly. She was sent right away for a head MRI scan. The scan showed a pattern doctors call the “Medusa head.” This means the veins in her brain are arranged in an unusual way that she was born with. There is a small blood clot at the outer part of this vein pattern. The blood is also moving slowly closer to the main vein.",
    "summary": "A 34-year-old pregnant woman presents with seizures and dysarthria and is urgently referred for a cranial MRI. The classic ‘Medusa head’ sign is seen and the diagnosis is made as a venous anomaly of development with peripheral partial thrombosis and proximal slow flow.\n"
  },
  {
    "doc_id": 2,
    "label": "intermediate_health_literacy",
    "fulltext": "A 22-year-old woman came to the Department of Oral Medicine with complaints of mouth ulcers causing pain and eating and drinking difficulty persisting for a duration of one month. This condition begins with a fever and appears like pimples on the lips. Based on the anamnesis, it was discovered that she had been using pod-type vapes for about a year but had never experienced complaints like when she came for treatment. She had never smoked traditional cigarettes before starting to vape. She said the reason for trying vaping was out of curiosity, and she quite often tried different types of e-liquid with different flavors. Before her complaint, she had simply changed the type of e-liquid to a different flavor without mentioning the brand. She vapes almost every day, but not all day, only in her free time or with friends. She was a healthy individual, and before this condition appeared, she had no history of taking medications, including antibiotics, analgesics, anticonvulsants, non-steroidal anti-inflammatory drugs, and antifungals. She also had no history of drug or food allergies, but the patient has unhealthy eating habits (eating irregularly and not consuming vegetables and fruit). Extraoral examination showed no lesions on other parts of the body, while the lips of the patient had serosanguineous crusts and an erosive area at the corner of the mouth, and tended to bleed. Intraoral examination revealed white ulcers with yellowish edges, irregular, varying sizes, and pain on the labial, buccal, lateral, and ventral mucosa of the tongue and floor of the mouth.\n\nBased on the medical history of the patient and physical examination, which revealed oral mucosal involvement but no symptoms elsewhere in the body, as well as the non-reactive anti-HSV1 IgG results, the diagnosis of vaping-related oral erythema multiforme was established. The medical condition has been classified as minor erythema multiforme. The oral conditions were treated with 0.9% NaCl, which was moistened in gauze and placed on the lips three times a day. The patient was instructed to gargle 1 mg of dexamethasone in 10 mL of hyaluronic acid three times a day and avoid eating or drinking for at least 30 minutes after gargling. She was also given 2% miconazole cream applied to the wound in the right corner of the mouth twice a day, as well as vaseline album cream for dry lips. To maintain good oral hygiene, she was advised to brush her teeth and tongue twice a day, after breakfast and before bed. She was also instructed to stop vaping and avoid foods containing monosodium glutamate (MSG). The control was carried out after a week following therapy and showed that oral condition had improved. Written informed consent for the publication of details was obtained from the patient. This case report conformed with the Helsinki Declaration. The publication of this case report has also been approved by the institution.",
    "diff_label_texts": "A 22-year-old woman presented with a month of painful stomatitis that made eating and drinking difficult. The illness began with a fever and pimple-like lesions on the lips. She had been vaping regularly for about one year. Examination showed no skin lesions elsewhere. The lips had serosanguineous crusts and erosions at the labial commissures that tended to bleed. Intraorally, there were multiple irregular white ulcers with yellowish borders on several sites of the oral mucosa. Anti–HSV-1 IgG was non-reactive. The diagnosis was oral erythema multiforme, likely related to vaping. Management included normal saline compresses to the lips, a dexamethasone mouth rinse mixed with hyaluronic acid, 2% miconazole cream applied to the lip corner, petroleum jelly for dry lips, and stopping vaping. Her oral condition improved within one week.",
    "summary": "A 22-year-old woman came to the Oral Medicine Department with complaints of stomatitis causing pain, eating, and drinking difficulty, which started with fever and pimple-like on the lips. She was an active vape user for one year. Extraoral examination revealed no lesions on other body parts. The serosanguinolent crusts on the lips, an erosive area on the labial commissures and tended to bleed. Intraoral examination revealed white ulcers with yellowish edges and irregular, varying sizes in several parts of the oral mucosa. The anti-HSV-1 IgG laboratory results showed non-reactive, leading to a diagnosis of oral erythema multiforme. Management of oral conditions using 0.9% NaCl compress, dexamethasone mouthwash, and hyaluronic acid, applying 2% miconazole cream on labial commissures and vaseline album cream on the dry lips, and stopping vaping. Oral condition improved in a week of therapy."
  },
  {
    "doc_id": 3,
    "label": "low_health_literacy",
    "fulltext": "A 29-year-old gravida V par IV (all alive, 3 spontaneous vaginal deliveries, and the last child was delivered by cesarean section for the indication of a failed induction 4 years prior to the current pregnancy) came for ANC follow-up at a gestational age of 32 weeks from her LNMP.\n\nAfter taking a medical history, it was discovered that all four of her children are healthy, doing well in school, and have no known history of genetic or seizure disorders. She was investigated with the Venereal Disease Research Laboratory (VDRL), Hepatitis B surface antigen (HBSag), and urine analysis, all of which were negative. All cell lines in the CBC were normal, her blood group is A, and Rh is positive, according to the Complete Blood Count (CBC), blood group, and RH. Obstetric ultrasound was also performed showing normal anatomical scan of the all body parts of the fetus except the heart. Detailed fetal echocardiography evaluation was done with findings of: both atria have comparable size and normal situs. Both atrioventricular and semilunar valves are normally positioned with normal opening and closure. Both ventricles are comparable in size and contractility; in both 2D and color flow, the left ventricle forms the apex of the heart without any ventricular septal defect. But on the papillary muscles of the left ventricle there were two circumscribed, round, echogenic mass measuring 18.2 mm by 8.3mm and 13.5mm by 8.3 mm. Upon evaluation of the outflow tract, both the LVOT (left ventricular outflow tract) and RVOT (right ventricular outflow tract) have normal anatomy and function using 2D and CF ultrasound evaluation. According to the fetal echo finding, a diagnosis of cardiac rhabdomyoma was made. Since there is a high chance of tuberous sclerosis in cardiac rhabdomyoma, detailed neurosonography and other system exams were done to look for other signs of tuberous sclerosis. Despite searching for the other features of tuberous sclerosis, no other sign of it was found other than the tumor. She had regular ANC follow-up from 32 weeks of gestation up to 39 weeks without any complications.\n\nAt gestational age of 39 weeks plus 1 day, she underwent a cesarean section for the indication of full-term pregnancy plus a request for a repeat cesarean section, with the outcome of a 3200-gram female with an APGAR score of 10 and 10 at the 1st and 5th minutes. Both the mother and the neonate had a smooth post-operative period and were discharged on the third day.\n\nAfter delivery, the neonate was evaluated on the 1st, 7th, and 30th days for any regression or increment of the mass, emergence of skin lesions, or seizure. All physical examination results were normal, and the mass size was similar to the antepartal evaluation.\n\nAt her 7th month, the child was evaluated again, and upon history inquiries, the infant was doing great developmentally for her age group. The infant was examined for neurodevelopmental delay, and the child was growing appropriately for her age. An echocardiography study by a pediatric cardiologist revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles, each measuring 21.8 mm by 9.2 mm and 14.7 mm by 8.5 mm and creating no left ventricular inflow obstruction.\n\nA history from the family was obtained, and a physical examination with anthropometric measurements was performed to assess her developmental condition during her first-year evaluation. The child was developing normally, as other children her age were. Except for the heart, all of the systems examined were unremarkable. An echocardiography study has revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles with no size increment and creating no left ventricular inflow obstruction.",
    "diff_label_texts": "At 32 weeks of pregnancy, a routine scan found one small lump inside the baby’s heart. It caused no symptoms. This was the only problem seen. Doctors watched it with clinic visits until 39 weeks plus 1 day. Then the baby was delivered by C-section (a surgery to deliver the baby). After birth, the child had checkups on day 1, day 7, day 30, month 7, and month 12. At each visit, the child’s growth and behavior were healthy for age. The heart lump stayed the same size; it did not grow or shrink. By 1 year old, there were no signs of a related condition called tuberous sclerosis complex.",
    "summary": "We are reporting an isolated, asymptomatic fetal intra-cardiac mass (rhabdomyoma) that was discovered at 32 weeks of gestation and was followed as an outpatient until 39 weeks plus one day, at which point a cesarean section was performed. After delivery, the child underwent evaluations at the 1st day, 7th day, 30th day, 7th month, and 12th month of age. Following a checkup, the child's anthropometric and neurobehavioral growth were both healthy. Except for the tumor, which was neither growing nor shrinking in size, none of the clinical diagnostic criteria for tuberous sclerosis complex were met for this child up to the age of one year."
  },
  {
    "doc_id": 3,
    "label": "proficient_health_literacy",
    "fulltext": "A 29-year-old gravida V par IV (all alive, 3 spontaneous vaginal deliveries, and the last child was delivered by cesarean section for the indication of a failed induction 4 years prior to the current pregnancy) came for ANC follow-up at a gestational age of 32 weeks from her LNMP.\n\nAfter taking a medical history, it was discovered that all four of her children are healthy, doing well in school, and have no known history of genetic or seizure disorders. She was investigated with the Venereal Disease Research Laboratory (VDRL), Hepatitis B surface antigen (HBSag), and urine analysis, all of which were negative. All cell lines in the CBC were normal, her blood group is A, and Rh is positive, according to the Complete Blood Count (CBC), blood group, and RH. Obstetric ultrasound was also performed showing normal anatomical scan of the all body parts of the fetus except the heart. Detailed fetal echocardiography evaluation was done with findings of: both atria have comparable size and normal situs. Both atrioventricular and semilunar valves are normally positioned with normal opening and closure. Both ventricles are comparable in size and contractility; in both 2D and color flow, the left ventricle forms the apex of the heart without any ventricular septal defect. But on the papillary muscles of the left ventricle there were two circumscribed, round, echogenic mass measuring 18.2 mm by 8.3mm and 13.5mm by 8.3 mm. Upon evaluation of the outflow tract, both the LVOT (left ventricular outflow tract) and RVOT (right ventricular outflow tract) have normal anatomy and function using 2D and CF ultrasound evaluation. According to the fetal echo finding, a diagnosis of cardiac rhabdomyoma was made. Since there is a high chance of tuberous sclerosis in cardiac rhabdomyoma, detailed neurosonography and other system exams were done to look for other signs of tuberous sclerosis. Despite searching for the other features of tuberous sclerosis, no other sign of it was found other than the tumor. She had regular ANC follow-up from 32 weeks of gestation up to 39 weeks without any complications.\n\nAt gestational age of 39 weeks plus 1 day, she underwent a cesarean section for the indication of full-term pregnancy plus a request for a repeat cesarean section, with the outcome of a 3200-gram female with an APGAR score of 10 and 10 at the 1st and 5th minutes. Both the mother and the neonate had a smooth post-operative period and were discharged on the third day.\n\nAfter delivery, the neonate was evaluated on the 1st, 7th, and 30th days for any regression or increment of the mass, emergence of skin lesions, or seizure. All physical examination results were normal, and the mass size was similar to the antepartal evaluation.\n\nAt her 7th month, the child was evaluated again, and upon history inquiries, the infant was doing great developmentally for her age group. The infant was examined for neurodevelopmental delay, and the child was growing appropriately for her age. An echocardiography study by a pediatric cardiologist revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles, each measuring 21.8 mm by 9.2 mm and 14.7 mm by 8.5 mm and creating no left ventricular inflow obstruction.\n\nA history from the family was obtained, and a physical examination with anthropometric measurements was performed to assess her developmental condition during her first-year evaluation. The child was developing normally, as other children her age were. Except for the heart, all of the systems examined were unremarkable. An echocardiography study has revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles with no size increment and creating no left ventricular inflow obstruction.",
    "diff_label_texts": "A 29-year-old gravida V para IV (3 spontaneous vaginal deliveries, prior cesarean for failed induction 4 years earlier) presented for ANC at 32 weeks by LNMP. Maternal labs: VDRL, HBsAg, and urinalysis negative; CBC within normal limits; blood group A Rh-positive. Obstetric ultrasound revealed normal fetal anatomy except the heart. Fetal echocardiography showed normal situs; atria of comparable size; normally positioned atrioventricular and semilunar valves with normal motion; ventricles comparable in size and contractility; left ventricle forming the apex; no ventricular septal defect. Two circumscribed, round, echogenic masses were noted on the left ventricular papillary muscles, measuring 18.2 × 8.3 mm and 13.5 × 8.3 mm. LVOT and RVOT anatomy and function were normal on 2D and color flow. Impression: cardiac rhabdomyoma. Given the association with tuberous sclerosis complex (TSC), detailed neurosonography and systemic evaluation were performed and were unremarkable. She continued routine ANC without complications to 39 weeks. At 39 weeks + 1 day, a cesarean section (repeat on request at term) delivered a 3200 g female, Apgar 10 and 10 at 1 and 5 minutes. Postoperative courses for mother and neonate were uneventful; discharge occurred on postoperative day 3. The neonate was evaluated on days 1, 7, and 30: physical examinations were normal; no seizure activity or new cutaneous lesions; mass dimensions were similar to the antenatal findings. At 7 months, development was age-appropriate; pediatric echocardiography showed well-circumscribed hyperechoic masses on both left ventricular papillary muscles measuring 21.8 × 9.2 mm and 14.7 × 8.5 mm, without left ventricular inflow obstruction. At 12 months, anthropometric and neurobehavioral development remained normal. Echocardiography again demonstrated well-circumscribed hyperechoic masses on both left ventricular papillary muscles with no size increment and no left ventricular inflow obstruction. Up to one year of age, apart from the persistent intracardiac rhabdomyomas, the child met none of the clinical diagnostic criteria for TSC. Notably, while cardiac rhabdomyomas often regress spontaneously in infancy, these lesions were stable through 12 months.",
    "summary": "We are reporting an isolated, asymptomatic fetal intra-cardiac mass (rhabdomyoma) that was discovered at 32 weeks of gestation and was followed as an outpatient until 39 weeks plus one day, at which point a cesarean section was performed. After delivery, the child underwent evaluations at the 1st day, 7th day, 30th day, 7th month, and 12th month of age. Following a checkup, the child's anthropometric and neurobehavioral growth were both healthy. Except for the tumor, which was neither growing nor shrinking in size, none of the clinical diagnostic criteria for tuberous sclerosis complex were met for this child up to the age of one year."
  },
  {
    "doc_id": 4,
    "label": "low_health_literacy",
    "fulltext": "13-year-old boy from Cusco with a history of laryngeal papillomatosis since the age of two (at the age of three he required a tracheostomy) and a mother with a history of genital papilloma. The patient was admitted to the San Borja National Institute of Child Health in Lima, after a 16-day illness characterised by respiratory difficulties predominantly at night, inspiratory laryngeal stridor and moderate dysphonia; he previously received azithromycin and oxygen support, without improvement.\n\nThe physical examination revealed mild subcostal retraction, decreased vesicular murmurs in the left hemithorax and scanty wheezy breath sounds with predominance in the right hemithorax, which required oxygen support with a binasal cannula at 4 liters. The rest of the evaluation had no relevant findings. At the laboratory level, leukocytes were found at 8.03 × 103/u, platelets 209 × 103/u, hemoglobin 13.2 g/dL, C-reactive protein at 36.6 mg/L. As part of the imaging studies, a chest radiograph and a head and neck tomography were performed.\n\n48 hours after admission, she presented with increased stridor and respiratory difficulty, so admission to the emergency operating room for tracheostomy, microsurgery and excision of papillomatosis lesions was decided. An appendicular tumour of papillomatose appearance with ventricular bands in the epiglottis, glottic face, vocal cords, subglottis and trachea up to ring 5 was evident. The anatomopathological report reported coilocitic atypia due to HPV and mild focal dysplasia.\n\nIn the immediate postoperative period, he was transferred to the paediatric intensive care unit for respiratory monitoring, with weaning from oxygen at 48 hours. He received a single dose of bevacizumab 400 mg intravenous and subsequently improved clinically. The patient remained hospitalised for seven days, achieving clinical stability through normalisation of oxygen saturation levels and progressive weaning from oxygen, and was subsequently referred to the hospital in Breña to continue his management. Telemonitoring was carried out after eight months and the family indicated that there was no evidence of relapse or other intercurrences.\n",
    "diff_label_texts": "This is about a 13-year-old boy. He has had small growths in his throat since he was two years old. The growths were in his voice box and windpipe. They narrowed his breathing tube, so he had trouble breathing. It was like trying to breathe through a pinched straw. A chest scan showed several small cysts in his lungs. Doctors removed the throat growths. They also placed a breathing tube through a small hole in his neck to help him breathe. He got one dose of a medicine called bevacizumab (400 mg) through a vein. He also had breathing therapy. He got better. The problem has not come back during follow-up.",
    "summary": "A 13-year-old boy with a history of laryngeal papillomatosis since the age of two years was presented. The patient presented respiratory distress and multiple stenosing nodules in the larynx and trachea, and several pulmonary cysts were visualized on a chest tomography. The patient underwent exeresis of the papillomatosis lesions and tracheostomy. He received a single dose of 400 mg bevacizumab intravenous and respiratory therapy with a favorable evolution, without recurrence in the follow-up.\n"
  },
  {
    "doc_id": 4,
    "label": "proficient_health_literacy",
    "fulltext": "13-year-old boy from Cusco with a history of laryngeal papillomatosis since the age of two (at the age of three he required a tracheostomy) and a mother with a history of genital papilloma. The patient was admitted to the San Borja National Institute of Child Health in Lima, after a 16-day illness characterised by respiratory difficulties predominantly at night, inspiratory laryngeal stridor and moderate dysphonia; he previously received azithromycin and oxygen support, without improvement.\n\nThe physical examination revealed mild subcostal retraction, decreased vesicular murmurs in the left hemithorax and scanty wheezy breath sounds with predominance in the right hemithorax, which required oxygen support with a binasal cannula at 4 liters. The rest of the evaluation had no relevant findings. At the laboratory level, leukocytes were found at 8.03 × 103/u, platelets 209 × 103/u, hemoglobin 13.2 g/dL, C-reactive protein at 36.6 mg/L. As part of the imaging studies, a chest radiograph and a head and neck tomography were performed.\n\n48 hours after admission, she presented with increased stridor and respiratory difficulty, so admission to the emergency operating room for tracheostomy, microsurgery and excision of papillomatosis lesions was decided. An appendicular tumour of papillomatose appearance with ventricular bands in the epiglottis, glottic face, vocal cords, subglottis and trachea up to ring 5 was evident. The anatomopathological report reported coilocitic atypia due to HPV and mild focal dysplasia.\n\nIn the immediate postoperative period, he was transferred to the paediatric intensive care unit for respiratory monitoring, with weaning from oxygen at 48 hours. He received a single dose of bevacizumab 400 mg intravenous and subsequently improved clinically. The patient remained hospitalised for seven days, achieving clinical stability through normalisation of oxygen saturation levels and progressive weaning from oxygen, and was subsequently referred to the hospital in Breña to continue his management. Telemonitoring was carried out after eight months and the family indicated that there was no evidence of relapse or other intercurrences.\n",
    "diff_label_texts": "A 13-year-old male from Cusco with recurrent respiratory papillomatosis (RRP) since age two (tracheostomy at age three) and a maternal history of genital papilloma presented after 16 days of predominantly nocturnal respiratory difficulty, inspiratory laryngeal stridor, and moderate dysphonia. He had previously received azithromycin and supplemental oxygen without improvement. On exam, there was mild subcostal retraction, decreased vesicular breath sounds over the left hemithorax, and scant wheezes predominating on the right; he required 4 L/min oxygen via binasal cannula. Laboratory studies showed WBC 8.03 × 10^3/μL, platelets 209 × 10^3/μL, hemoglobin 13.2 g/dL, and CRP 36.6 mg/L. Imaging included a chest study and head and neck tomography; chest tomography visualized several pulmonary cysts. Forty-eight hours after admission, he developed worsening stridor and respiratory distress, prompting emergent OR transfer for tracheostomy, microlaryngoscopy, and excision of papillomatous lesions. Intraoperative findings demonstrated extensive papillomatous disease with appendicular tumor-like lesions and ventricular bands involving the epiglottis, glottic surface, vocal cords, subglottis, and trachea to ring 5. Histopathology showed koilocytotic atypia consistent with HPV and mild focal dysplasia. Postoperatively, he was managed in the PICU with respiratory monitoring and was weaned off oxygen within 48 hours. He received a single intravenous dose of bevacizumab 400 mg and showed prompt clinical improvement. He completed a seven-day hospitalization with normalization of oxygen saturation and progressive oxygen weaning, then was transferred for ongoing care. He also received respiratory therapy. On telemonitoring at eight months, there was no evidence of recurrence or intercurrent events. Clinical context: RRP is typically HPV-related (often low-risk types) and can cause multifocal papillomas leading to airway stenosis; anti-VEGF therapy such as bevacizumab is used off-label to reduce angiogenesis and disease recurrence, and in this case was associated with a favorable short- to mid-term outcome.",
    "summary": "A 13-year-old boy with a history of laryngeal papillomatosis since the age of two years was presented. The patient presented respiratory distress and multiple stenosing nodules in the larynx and trachea, and several pulmonary cysts were visualized on a chest tomography. The patient underwent exeresis of the papillomatosis lesions and tracheostomy. He received a single dose of 400 mg bevacizumab intravenous and respiratory therapy with a favorable evolution, without recurrence in the follow-up.\n"
  },
  {
    "doc_id": 5,
    "label": "low_health_literacy",
    "fulltext": "A 54-year-old male who had a medical history of membranous nephropathy II with nephrotic syndrome was administered with long-term oral glucocorticoids and immunosuppressants. The patient had a 20 pack-year history of smoking, and denied a family history of hereditary diseases. Chest x-ray demonstrated normal findings at one month before admission. On August 8, 2016, the patient was hospitalized for fever accompanied by progressive dyspnea, cough, and expectoration for 5 days. On admission, the BMI of the patient was 24.5 kg/m2, and his body temperature was 39.0°C. Furthermore, the patient had symptoms of tachypnea (35 bpm) and severe hypoxemia (SaO2 86%). On auscultation, the patient had good air entrance bilaterally with scattered diffuse crackles and rhonchi. Furthermore, the chest CT scan revealed multiple ground-glass opacities, and laboratory tests revealed normal white blood cell (WBC) count, but with elevated neutrophil count, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and (1→3)-β-D-glucan. The patient was diagnosed as RSV infection on the fourth day of hospitalization when positive RSV-Ab was detected.\n\nOn admission, the patient was immediately given respiratory monitoring and supplemental oxygen to improve the low oxygen saturation, as well as antibiotics (moxifloxacin for 4 days, followed by cefminoxine for 8 days), and antifungal therapy (voriconazole for 10 days). The dose of the glucocorticoids and immunosuppressants remained largely unchanged. After 10 days of treatment, the patient's condition became worse. Chest CT revealed the progression of the disease, and oxygen partial pressure was further decreased. The patient was transferred to the Emergency Intensive Care Unit, where the patient was intensively treated, including noninvasive mechanical ventilation, broad-spectrum antibiotics (i.v. meropenem, oral moxifloxacin, and cotrimoxazole), antifungal therapy (micafungin), corticosteroids (methylprednisolone 40 mg bid iv) to relieve the inflammation, and other supportive treatment. Ganciclovir was also prescribed due to a possibility of viral infection, such as cytomegalovirus. Five days later, the patient's condition was further aggravated based on the chest x-ray evaluation. Despite receiving another round of treatments, including invasive ventilator-assisted ventilation therapy, methylprednisolone (80 mg bid), antibacterial agents (cefoperazone sulbactam, tigecycline, and cotrimoxazole) and antifungal (micafungin) therapy, the patient eventually died after 2 days.",
    "diff_label_texts": "This 54-year-old man had long-term kidney disease. He took steroids and other medicines that weaken the body’s defenses for a long time. He came to the lung department with fever, cough with mucus, and trouble breathing. A scan showed many cloudy spots in both lungs, like frosted glass. Blood tests showed a lot of inflammation. This suggested an infection from germs such as bacteria, a virus, or a fungus. A blood test was positive for RSV antibodies. Tests for other germs were not positive. His immune system was weak. His antibody level (IgG) was low. His infection-fighting T cells (CD4 and CD8) were also low. Doctors gave strong medicines for infection and support to help his breathing. His illness got worse quickly. He died from breathing failure.",
    "summary": "Patient concerns:\nA 54-year-old male patient with chronic nephropathy, who received long-term immunosuppressants, was admitted to the Department of Respiratory Medicine due to the symptoms of fever, cough, expectoration, and dyspnea.\n\nDiagnoses:\nPulmonary radiology revealed multiple bilateral ground-glass opacity. Laboratory tests revealed elevated inflammation indicators, implying infection with bacteria, viruses, and/or fungi. Furthermore, the patient was positive for RSV antibodies, without positive results for other pathogens. Moreover, the patient was immunocompromised due to the long-term use of corticosteroids and immunosuppressants, as evidenced by decreased total IgG levels and reduced CD4 and CD8 T-lymphocyte counts.\n\nInterventions and outcome:\nDespite the intensive anti-infection treatment and respiratory support, the patient developed rapid progression, and subsequently died of respiratory failure."
  },
  {
    "doc_id": 6,
    "label": "low_health_literacy",
    "fulltext": "A 34-year-old patient with a disease duration of four weeks. Two months earlier, she had a cesarean section in the 37th week of pregnancy and had persistent bleeding from the surgical wound. She denied a history of bleeding in childhood or adolescence. Three years earlier, she had given birth to her first child (also by cesarean section), who died due to a chromosome disorder (referred to by the patient). She also stated that she was allergic to tramadol.\n\nThe clinical picture began with lower back pain due to bilateral renal lithiasis. Subsequently, he managed to expel a stone and after that he presented haematuria for three days, for which he received tranexamic acid c/12 h. Three weeks later, he presented pain in the lower region of the left thigh that increased in intensity, with hardening of the area. Due to persistence of the symptoms, he was given diclofenac intramuscularly, which caused ecchymosis and bleeding in the gluteal area and persists despite the compression with gauze.\n\nThe patient underwent a particular Doppler ultrasound that revealed deep venous thrombosis of the left lower limb, and went to the hospital in her locality with these results. She was given anticoagulation with enoxaparin 30 mg/24 h subcutaneously, in addition to morphine for pain management and was hospitalized. The next day, she presented epigastralgia, blurred vision, heart rate of 117 beats/min, blood pressure of 113/85 mmHg and saturation of 93%. It was decided to discontinue enoxaparin. The blood count revealed a hemoglobin of 6.4 g/dl, which represented a difference of 4 g/dl from the result one day before admission, which was 10.4 g/dl. Because of the above, two blood transfusions were given. Due to the suspicion of vasculitis, methylprednisolone was indicated and she was referred to our hospital for further study.\n\nOn admission, the physical examination revealed severe pallor, extensive ecchymosis on the left thigh and lateral knee, and a haematoma on the right thigh. The haemogram showed moderate anaemia (Hb = 9.8 g/dl), normocytic and normochromic. The biochemical examination showed glucose values of 160 mg/dl. The liver enzymes AST and ALT were at 52 U/L and 86 U/L, respectively. The coagulation profile showed a prolonged activated partial thromboplastin time (APTT) of 91.2 s. The rest of the haemogram, biochemical, electrolyte, liver profile and coagulation profile were normal. The ultrasound of soft parts of the right gluteal region revealed a collection at the level of the subcutaneous cellular tissue (TCSC) and oedema up to the upper third of the thigh. The Doppler ultrasound in the left lower limb showed adequate flowometry without signs of thrombosis in the common femoral vein, superficial and deep.\n\nSymptomatic treatment was initiated and blood and urine cultures were requested and were negative. Antinuclear antibody (ANA) values, complement C3 and C4 and ferritin were within the reference range.\n\nIn the face of suspected acquired haemophilia, studies were requested for confirmation, where a partial correction of aPTT was found in the mixing test. Factor VIII was measured and its activity was found to be decreased (<1.0 U/dl) and the presence of a factor VIII inhibitor was demonstrated: 8.64 Bethesda units/ml. The above allowed the diagnosis of acquired haemophilia to be confirmed, which was related to the postpartum period due to the onset of symptoms.\n\nPrednisone 50 mg orally at breakfast and 10 mg orally at lunch, cyclophosphamide 50 mg 2 tablets orally every 24 hours and anti-inhibitor coagulant complex for haemophilia (FEIBA) were initiated. Five days later, the latter was discontinued due to chest tightness, dyspnoea and nausea (possible adverse drug reaction) and replaced with activated recombinant factor VII (NovoSeven).\n\nThe patient's clinical evolution was favorable, with a decrease in ecchymosis and no other symptoms, so she was discharged from the hospital.\n",
    "diff_label_texts": "A 34-year-old woman had new lower back pain. She saw blood in her urine. She also had a big bruise under the skin on her right buttock. She had never had bleeding problems before. Because these bleeding signs were serious, she was sent to the emergency room. Doctors did blood-clotting tests. One test mixed her blood with normal blood to see how it clotted. Another test looked for a blocker against a clotting protein called factor eight. These tests confirmed the diagnosis.",
    "summary": "A 34-year-old female patient presented with lower back pain, haematuria and a haematoma in the right gluteal region, with no previous history of bleeding. Due to the extent of the haemorrhagic manifestations, she was transferred to the emergency department. The coagulation profile, mixing test and measurement of the factor VIII inhibitor titres confirmed the diagnosis.\n"
  },
  {
    "doc_id": 7,
    "label": "intermediate_health_literacy",
    "fulltext": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. He was kept in the nursery for one day. The examining doctor referred them for urgent surgical care, but it took them one day to arrive at our hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in the right but positive in the contralateral testis. Both hernial orifices were normal. All the laboratory investigations were performed with an urgent Doppler ultrasound of the inguinoscrotal area. The ultrasound examination found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color Doppler analysis. Left testis appeared normal in size, shape and echotexture with minimal hydrocele. An urgent scrotal exploration was undertaken. Intra-operatively, there was frank necrotic right testis with intravaginal torsion of the testis with minimal hydrocele. A right orchidectomy and contralateral orchidopexy was then performed.",
    "diff_label_texts": "A full‑term male newborn, 2 days old and delivered by cesarean section, presented with a congenital right scrotal swelling. On arrival he appeared well perfused and stable. Examination showed the right testis was enlarged, tense, non‑tender, and visibly reddish with excoriated overlying skin. Transillumination was negative on the right and positive on the left; both hernia openings were normal. Doppler ultrasound showed the right testis was enlarged with a heterogeneous, darker appearance and no detectable blood flow; the left testis looked normal, with only a small amount of fluid. He was taken urgently to surgery. Intra‑operatively, the right testis was frankly nonviable due to intravaginal torsion, with minimal hydrocele. Surgeons removed the right testis (orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to reduce the risk of future twisting.",
    "summary": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in right but positive in the contralateral testis. Both hernial orifices were normal. Doppler ultrasound of the inguinoscrotal area found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color doppler analysis. An urgent scrotal exploration was undertaken. Intra-operatively there was frank necrotic right testis with intravaginal torsion of the testis and minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed."
  },
  {
    "doc_id": 7,
    "label": "low_health_literacy",
    "fulltext": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. He was kept in the nursery for one day. The examining doctor referred them for urgent surgical care, but it took them one day to arrive at our hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in the right but positive in the contralateral testis. Both hernial orifices were normal. All the laboratory investigations were performed with an urgent Doppler ultrasound of the inguinoscrotal area. The ultrasound examination found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color Doppler analysis. Left testis appeared normal in size, shape and echotexture with minimal hydrocele. An urgent scrotal exploration was undertaken. Intra-operatively, there was frank necrotic right testis with intravaginal torsion of the testis with minimal hydrocele. A right orchidectomy and contralateral orchidopexy was then performed.",
    "diff_label_texts": "This is about a 2-day-old newborn boy. He was born at full term by C-section at a private hospital. He came to the children’s hospital because the right side of his scrotum (the sack that holds the testicles) was swollen since birth. In the emergency room, he looked well. His skin was pink and warm. His blood flow looked good. On exam, the right testicle was big and tight. It was not sore when touched. The skin was red and looked rubbed. A light test did not shine through the right side. The light did shine through the left side. There were no signs of a hernia. An urgent ultrasound scan was done. The scan showed the right testicle was larger and looked uneven inside. No blood was flowing to it. The doctors took him quickly to surgery to look inside the scrotum. In surgery, the right testicle was dead because it had twisted, like a kinked hose that stops flow. There was a small amount of fluid. They removed the right testicle. They fixed the left testicle in place to help prevent twisting.",
    "summary": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in right but positive in the contralateral testis. Both hernial orifices were normal. Doppler ultrasound of the inguinoscrotal area found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color doppler analysis. An urgent scrotal exploration was undertaken. Intra-operatively there was frank necrotic right testis with intravaginal torsion of the testis and minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed."
  },
  {
    "doc_id": 7,
    "label": "proficient_health_literacy",
    "fulltext": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. He was kept in the nursery for one day. The examining doctor referred them for urgent surgical care, but it took them one day to arrive at our hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in the right but positive in the contralateral testis. Both hernial orifices were normal. All the laboratory investigations were performed with an urgent Doppler ultrasound of the inguinoscrotal area. The ultrasound examination found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color Doppler analysis. Left testis appeared normal in size, shape and echotexture with minimal hydrocele. An urgent scrotal exploration was undertaken. Intra-operatively, there was frank necrotic right testis with intravaginal torsion of the testis with minimal hydrocele. A right orchidectomy and contralateral orchidopexy was then performed.",
    "diff_label_texts": "A 2‑day‑old term male neonate, delivered by cesarean section at a private hospital, was referred for a congenital right scrotal swelling and presented to our children’s hospital one day later. On ED arrival he was well hydrated, pink on room air with good perfusion. Physical exam: right hemiscrotum with an enlarged, tense, non‑tender, visibly reddish testis and overlying skin excoriation; transillumination negative on the right and positive contralaterally; both hernial orifices normal. Laboratory studies were obtained, and urgent inguinoscrotal Doppler ultrasonography demonstrated an enlarged right testis measuring 15.6 × 9.4 mm with heterogeneous hypoechoic echotexture, prominent rete testis, and absent intratesticular color Doppler flow. The left testis was normal in size, shape, and echotexture; there was minimal hydrocele. The patient underwent urgent scrotal exploration. Intra‑operatively there was frank necrosis of the right testis secondary to intravaginal testicular torsion, with minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed. Contextually, perinatal testicular torsion often presents at or shortly after birth and Doppler evidence of absent flow with heterogeneous hypoechoic parenchyma correlates with nonviability; salvage rates are low when presentation is delayed. Contralateral orchidopexy is commonly performed to mitigate future torsion risk.",
    "summary": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in right but positive in the contralateral testis. Both hernial orifices were normal. Doppler ultrasound of the inguinoscrotal area found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color doppler analysis. An urgent scrotal exploration was undertaken. Intra-operatively there was frank necrotic right testis with intravaginal torsion of the testis and minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed."
  },
  {
    "doc_id": 8,
    "label": "low_health_literacy",
    "fulltext": "4-year-old male patient with a history of nasal impetigo two weeks before admission (treated with topical mupirocin and oral cefadroxil; dose, duration and adherence to treatment unknown), with no other morbid history, who presented macroscopic glomerular haematuria associated with oedema of the lower extremities of 5 days' evolution, with the last 12 hours prior to the consultation adding headaches, nausea and vomiting. He went to the emergency department (ED) in convulsive status, after 20 minutes of generalised tonic-clonic convulsions.\n\nOn admission to the ED, the patient was afebrile, with non-evaluable blood pressure, with quantitative consciousness impairment associated with generalized hypertonia and bilateral and pretibial oedema. Endotracheal intubation was decided and phenobarbital (10 mg/kg) was administered to manage the convulsive status.\n\nOn physical examination in the intensive care unit (ICU), blood pressure was 134/94 mmHg (BP 110 mmHg) (p95 for patient 108/66 mmHg, p95+12 120/78 mmHg).\n\nInitial laboratory parameters included: complete urine with haematuria (> 100 erythrocytes per field), proteinuria 3+ and leucocyturia 10-25 per field, creatinemia 0.3 mg/dL, anaemia with haematocrit (HTO) 21%, haemoglobin (Hb) 7 g/dL, with normal mean corpuscular volume (VCM) and mean corpuscular haemoglobin concentration (CHCM), leukocytosis of 23,900 cells/mm3, thrombocytosis of 756,000/mm3, without elevation of acute phase reactants, hypocomplementemia with complement C3 level at 25 mg/dL (normal value, VN: 80-150 mg/dL) and normal C4. The rapid antigen test for Streptococcus beta-haemolytic group A (Streptococcus pyogenes) in pharynx was positive and the Anti-streptolysin O (ASO) was (+). The non-contrast brain computed tomography showed no acute changes. The renal ultrasound concluded bilateral nephromegaly with increased cortical echogenicity and decreased corticomedullar differentiation.\n\nThe patient was diagnosed with nephritic syndrome due to complicated GNAPE with hypertensive emergency - convulsive status.\n\nWithin the first 24 hours of his ICU stay, the patient required mechanical ventilation (MV) and anticonvulsant therapy with phenobarbital. He progressed without seizures, with a normal electroencephalogram (EEG) (on the day following admission) and a normal cerebrospinal fluid study. Antibiotic therapy was initiated for eradication of Streptococcus pyogenes with cefotaxime and diuretic therapy with furosemide.\n\nThe next day, he developed renal impairment with creatinine elevation to 0.99 mg/dL, hypertension and 24 hour proteinuria of 36.6 mg/m2/h, without oliguria. He initiated antihypertensive therapy with amlodipine and intravenous labetalol, with good initial control.\n\nWith favorable evolution, extubation was performed at 48 hours, which was well tolerated from the ventilatory point of view. However, after 24 hours of extubation, the patient's consciousness deteriorated, with both ocular opening and withdrawal of limb only in response to painful stimulus and poor verbal response (Glasgow Coma Scale 8), and developed blood pressure figures > p95+12 despite receiving therapy with labetalol in continuous infusion (up to 3 mg/kg/h), amlodipine (10 mg/day) and furosemide, which required the reintroduction of mechanical ventilation and infusion of sodium nitroprusside (up to 3 mcg/kg/min), with the aim of achieving gradual reduction of blood pressure figures (25% daily) to prevent secondary neurological damage. Given the presence of acute neurological symptomatology associated with HTA in a patient with glomerulonephritis, the diagnosis of PRES was suspected, which was confirmed by magnetic resonance imaging (MRI) of the brain (day 5), which showed an increase in the subcortical signal in bilateral and symmetric occipital region, without restriction in diffusion, which was compatible with vasogenic edema (PRES). Ophthalmological evaluation was normal and a new EEG evidenced occasional episodes of generalized voltage depression.\n\nAdding enalapril to the treatment. Finally, after 10 days with a slow pharmacological weaning, normalization of blood pressure was achieved. The control MRI (day 12) revealed regression of the previously described findings. Successful extubation was achieved after 5 days.\n\nDuring his stay in the ICU, the hemoglobin level dropped to 5 g/dL, with normal mean corpuscular volume and mean corpuscular hemoglobin concentration, without plateletopenia, so hemolytic anemia was suspected given a positive direct Coombs test and hemoglobinuria. He required red blood cell transfusions twice. Steroid therapy with methylprednisolone (1 mg/kg/d) was initiated for 72 hours. The coproculture was negative, as was the urinary antigen for Streptococcus pneumoniae. Epstein-Barr virus and Parvovirus B19 serology, extractable nuclear antigen (ENA) profile, anti-neutrophil cytoplasmic antibodies (ANCA), anti-DNA antibodies, anti-B2 glycoprotein 1 antibodies, anti-cardiolipin antibodies and lupus anticoagulant were all negative. All cultures were negative (blood cultures, urine cultures, cultures of endotracheal aspirate and pharyngeal cultures). ANA (antinuclear antibodies) was positive 1/160.\n\nThe patient improved with blood pressure normalization, increased complement levels, and a urine test without proteinuria or hematuria. The direct Coombs test remained positive on the 9th day of hospitalization.\n\nOn day 31, the patient was discharged normotensive, without anaemia, with preserved renal function, without proteinuria or haematuria, with normalisation of C3 levels and asymptomatic from the neurological point of view. He was discharged with pharmacological therapy with prednisone, amlodipine, enalapril and folic acid. The patient did not present recurrence and remained asymptomatic 6 months after discharge.\n",
    "diff_label_texts": "A 4-year-old boy had blood in his pee and swelling for 5 days. He then had headaches, nausea, and vomiting. He came to the hospital with seizures and very high blood pressure. Blood tests showed a low level of a protein called C3 and signs of a recent strep infection. This meant his kidney filters were inflamed after strep. His brain was affected by the very high blood pressure. Doctors suspected a problem called PRES, which is brain swelling from high pressure. A brain MRI confirmed this. His immune system also attacked his red blood cells. This made his blood level drop very low, to 5 g/dL. He was treated with medicines to lower his blood pressure, steps to protect his brain, and steroid medicines. He left the hospital after 31 days. Six months later, he had no symptoms.",
    "summary": "4-year-old male patient with a history of 5 days of haematuria and oedema, with additional headaches, nausea and vomiting, who entered a convulsive state and hypertensive crisis. Laboratory tests showed hypocomplementemia C3 and elevated Anti-Streptolysin O titers, which was interpreted as GNAPE. He developed encephalopathy, which led to suspicion of secondary PRES due to hypertensive emergency, which was finally confirmed by magnetic resonance of the brain. He also developed autoimmune haemolytic anaemia with haemoglobin up to 5 g/dL. His treatment was based on antihypertensive therapy, neuroprotection measures and steroid treatment. He was discharged after 31 days of hospitalisation, asymptomatic 6 months after discharge.\n"
  },
  {
    "doc_id": 8,
    "label": "proficient_health_literacy",
    "fulltext": "4-year-old male patient with a history of nasal impetigo two weeks before admission (treated with topical mupirocin and oral cefadroxil; dose, duration and adherence to treatment unknown), with no other morbid history, who presented macroscopic glomerular haematuria associated with oedema of the lower extremities of 5 days' evolution, with the last 12 hours prior to the consultation adding headaches, nausea and vomiting. He went to the emergency department (ED) in convulsive status, after 20 minutes of generalised tonic-clonic convulsions.\n\nOn admission to the ED, the patient was afebrile, with non-evaluable blood pressure, with quantitative consciousness impairment associated with generalized hypertonia and bilateral and pretibial oedema. Endotracheal intubation was decided and phenobarbital (10 mg/kg) was administered to manage the convulsive status.\n\nOn physical examination in the intensive care unit (ICU), blood pressure was 134/94 mmHg (BP 110 mmHg) (p95 for patient 108/66 mmHg, p95+12 120/78 mmHg).\n\nInitial laboratory parameters included: complete urine with haematuria (> 100 erythrocytes per field), proteinuria 3+ and leucocyturia 10-25 per field, creatinemia 0.3 mg/dL, anaemia with haematocrit (HTO) 21%, haemoglobin (Hb) 7 g/dL, with normal mean corpuscular volume (VCM) and mean corpuscular haemoglobin concentration (CHCM), leukocytosis of 23,900 cells/mm3, thrombocytosis of 756,000/mm3, without elevation of acute phase reactants, hypocomplementemia with complement C3 level at 25 mg/dL (normal value, VN: 80-150 mg/dL) and normal C4. The rapid antigen test for Streptococcus beta-haemolytic group A (Streptococcus pyogenes) in pharynx was positive and the Anti-streptolysin O (ASO) was (+). The non-contrast brain computed tomography showed no acute changes. The renal ultrasound concluded bilateral nephromegaly with increased cortical echogenicity and decreased corticomedullar differentiation.\n\nThe patient was diagnosed with nephritic syndrome due to complicated GNAPE with hypertensive emergency - convulsive status.\n\nWithin the first 24 hours of his ICU stay, the patient required mechanical ventilation (MV) and anticonvulsant therapy with phenobarbital. He progressed without seizures, with a normal electroencephalogram (EEG) (on the day following admission) and a normal cerebrospinal fluid study. Antibiotic therapy was initiated for eradication of Streptococcus pyogenes with cefotaxime and diuretic therapy with furosemide.\n\nThe next day, he developed renal impairment with creatinine elevation to 0.99 mg/dL, hypertension and 24 hour proteinuria of 36.6 mg/m2/h, without oliguria. He initiated antihypertensive therapy with amlodipine and intravenous labetalol, with good initial control.\n\nWith favorable evolution, extubation was performed at 48 hours, which was well tolerated from the ventilatory point of view. However, after 24 hours of extubation, the patient's consciousness deteriorated, with both ocular opening and withdrawal of limb only in response to painful stimulus and poor verbal response (Glasgow Coma Scale 8), and developed blood pressure figures > p95+12 despite receiving therapy with labetalol in continuous infusion (up to 3 mg/kg/h), amlodipine (10 mg/day) and furosemide, which required the reintroduction of mechanical ventilation and infusion of sodium nitroprusside (up to 3 mcg/kg/min), with the aim of achieving gradual reduction of blood pressure figures (25% daily) to prevent secondary neurological damage. Given the presence of acute neurological symptomatology associated with HTA in a patient with glomerulonephritis, the diagnosis of PRES was suspected, which was confirmed by magnetic resonance imaging (MRI) of the brain (day 5), which showed an increase in the subcortical signal in bilateral and symmetric occipital region, without restriction in diffusion, which was compatible with vasogenic edema (PRES). Ophthalmological evaluation was normal and a new EEG evidenced occasional episodes of generalized voltage depression.\n\nAdding enalapril to the treatment. Finally, after 10 days with a slow pharmacological weaning, normalization of blood pressure was achieved. The control MRI (day 12) revealed regression of the previously described findings. Successful extubation was achieved after 5 days.\n\nDuring his stay in the ICU, the hemoglobin level dropped to 5 g/dL, with normal mean corpuscular volume and mean corpuscular hemoglobin concentration, without plateletopenia, so hemolytic anemia was suspected given a positive direct Coombs test and hemoglobinuria. He required red blood cell transfusions twice. Steroid therapy with methylprednisolone (1 mg/kg/d) was initiated for 72 hours. The coproculture was negative, as was the urinary antigen for Streptococcus pneumoniae. Epstein-Barr virus and Parvovirus B19 serology, extractable nuclear antigen (ENA) profile, anti-neutrophil cytoplasmic antibodies (ANCA), anti-DNA antibodies, anti-B2 glycoprotein 1 antibodies, anti-cardiolipin antibodies and lupus anticoagulant were all negative. All cultures were negative (blood cultures, urine cultures, cultures of endotracheal aspirate and pharyngeal cultures). ANA (antinuclear antibodies) was positive 1/160.\n\nThe patient improved with blood pressure normalization, increased complement levels, and a urine test without proteinuria or hematuria. The direct Coombs test remained positive on the 9th day of hospitalization.\n\nOn day 31, the patient was discharged normotensive, without anaemia, with preserved renal function, without proteinuria or haematuria, with normalisation of C3 levels and asymptomatic from the neurological point of view. He was discharged with pharmacological therapy with prednisone, amlodipine, enalapril and folic acid. The patient did not present recurrence and remained asymptomatic 6 months after discharge.\n",
    "diff_label_texts": "A 4-year-old male, two weeks post nasal impetigo treated with topical mupirocin and oral cefadroxil (dose/duration/adherence unknown), presented with 5 days of macroscopic glomerular haematuria and lower-extremity oedema, followed by 12 hours of headache, nausea, and vomiting, and arrived to the ED in convulsive status after 20 minutes of generalized tonic–clonic seizures. On ED arrival he was afebrile, with non-evaluable BP, depressed consciousness, generalized hypertonia, and bilateral pretibial oedema. He was intubated and loaded with phenobarbital 10 mg/kg. In the ICU, BP was 134/94 mmHg (p95 for age 108/66; p95+12 120/78), consistent with hypertensive emergency. Initial labs: urinalysis with haematuria (>100 RBC/hpf), proteinuria 3+, leucocyturia 10–25/hpf; creatinine 0.3 mg/dL; anaemia Hct 21%, Hb 7 g/dL with normocytic, normochromic indices; leukocytosis 23,900/mm3; thrombocytosis 756,000/mm3; no elevation of acute-phase reactants; hypocomplementemia with C3 25 mg/dL (VN 80–150) and normal C4. Throat rapid antigen for group A Streptococcus was positive and ASO positive. Non-contrast head CT was unremarkable. Renal ultrasound showed bilateral nephromegaly with increased cortical echogenicity and decreased corticomedullary differentiation. The working diagnosis was nephritic syndrome due to complicated GNAPE with hypertensive emergency and status epilepticus. He required mechanical ventilation and phenobarbital; EEG the next day was normal; CSF was normal. Cefotaxime was started for Streptococcus pyogenes eradication and furosemide for diuresis. By day 2 he developed AKI (creatinine 0.99 mg/dL), hypertension, and 24-hour proteinuria 36.6 mg/m2/h without oliguria. Antihypertensive therapy included amlodipine and IV labetalol with initial control. After extubation at 48 hours, he deteriorated neurologically within 24 hours (GCS 8) with BP > p95+12 despite labetalol infusion up to 3 mg/kg/h, amlodipine 10 mg/day, and furosemide, necessitating reintubation and sodium nitroprusside infusion up to 3 mcg/kg/min with a planned gradual BP reduction of 25% per day to mitigate secondary neurologic injury. Given acute neurologic deficits with severe HTN in GN, PRES was suspected and confirmed by brain MRI on day 5 showing increased subcortical T2/FLAIR signal in bilateral symmetric occipital regions without diffusion restriction, consistent with vasogenic edema. Ophthalmologic exam was normal; repeat EEG showed occasional generalized voltage depression. Enalapril was added. Over 10 days, BP normalized with slow pharmacologic weaning; follow-up MRI on day 12 showed radiologic regression, and he was successfully extubated after 5 days. During the ICU course, Hb fell to 5 g/dL with normocytic, normochromic indices and no thrombocytopenia; hemolytic anemia was diagnosed given a positive direct Coombs test and hemoglobinuria. He required two packed RBC transfusions. Methylprednisolone 1 mg/kg/day was given for 72 hours. Stool culture and urinary antigen for Streptococcus pneumoniae were negative. Serologies for EBV and Parvovirus B19, ENA profile, ANCA, anti-dsDNA, anti-β2 glycoprotein I, anticardiolipin, and lupus anticoagulant were all negative; all cultures (blood, urine, endotracheal aspirate, pharyngeal) were negative. ANA was positive at 1:160. Clinical status improved with BP control, rising complement levels, and resolution of proteinuria and haematuria; the direct Coombs remained positive on hospital day 9. He was discharged on day 31 normotensive, non-anaemic, with preserved renal function, no proteinuria or haematuria, normalized C3, and asymptomatic neurologically. Discharge medications: prednisone, amlodipine, enalapril, and folic acid. He remained asymptomatic with no recurrence at 6 months. Overall, the case represents GNAPE with hypocomplementemia (low C3) and elevated ASO complicated by hypertensive emergency causing encephalopathy and secondary PRES, plus autoimmune hemolytic anemia with Hb nadir 5 g/dL, successfully managed with antihypertensives, neuroprotective measures, and corticosteroids, with full clinical and radiologic recovery.",
    "summary": "4-year-old male patient with a history of 5 days of haematuria and oedema, with additional headaches, nausea and vomiting, who entered a convulsive state and hypertensive crisis. Laboratory tests showed hypocomplementemia C3 and elevated Anti-Streptolysin O titers, which was interpreted as GNAPE. He developed encephalopathy, which led to suspicion of secondary PRES due to hypertensive emergency, which was finally confirmed by magnetic resonance of the brain. He also developed autoimmune haemolytic anaemia with haemoglobin up to 5 g/dL. His treatment was based on antihypertensive therapy, neuroprotection measures and steroid treatment. He was discharged after 31 days of hospitalisation, asymptomatic 6 months after discharge.\n"
  },
  {
    "doc_id": 9,
    "label": "intermediate_health_literacy",
    "fulltext": "A 69-year-old male with prior history of CABG presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration was admitted in our center. The electrocardiogram showed ST depression in leads II, III, aVF, and V4-6, and blood examination revealed elevation of plasma N-terminal pro-B-type natriuretic peptide levels (2640 pg/mL). Echocardiogram showed left ventricular systolic dysfunction and low left ventricular ejection fraction (30%). The patient had inferior ST-segment-elevation myocardial infarction in 2009, when he was 59 years old, with angiographic evidence of severe 3 vessels disease (coronary angiography showed CTO in proximal left anterior descending artery (LAD), 90% stenosis in mid and distal left circumflex artery, and 95% stenosis in mid RCA. The patient underwent CABG with left internal mammary artery (LIMA) to LAD, and sequential SVG to 1st obtuse marginal branch (OM1), 2nd obtuse marginal branch (OM2), and posterolateral branch (PL) in 2009.\n\nCoronary angiography was performed via 6 French (Fr) left radial artery access and demonstrated patency of LIMA to LAD and SVG to OM1, OM2 conduits, but a complete occlusion of sequential SVG to PL conduit. Native left main coronary artery was occluded in ostium and native RCA was occluded in the mid portion with bridging collaterals. We decided to treat the native RCA CTO. Dual arterial access was achieved with another 6 Fr sheath in right femoral artery. The left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic; USA) and 6 Fr EBU 3.5 (Launcher; Medtronic; USA) guide catheters, respectively. An antegrade approach via left radial artery was attempted; however, neither Fielder XTR wire (Asahi Intec, Japan) nor Gaia 3 wire (Asahi Intec, Japan) with Finecross microcatheter (Terumo, Japan) reached the true lumen in distal RCA. Then, parallel wire technique with Crusade microcatheter (Kaneka, Japan) and two Gaia 3 wires (Asahi Intec, Japan) were attempted, but also failed. We therefore switched to the retrograde approach using septal channel from LAD through occluded left coronary artery. Gaia 3 wire (Asahi Intec, Japan) crossed occluded left main (LM) and LAD, and finally reached true lumen in distal LAD. Sion wire was exchanged by Finecross microcatheter (Terumo, Japan) into dital LAD, and dilation of LM and proximal LAD with a 2.0 × 15 mm balloon was performed. Then, septal surfing technique (SST) was used for septal crossing. We tried different septal channels originating from proximal to distal LAD, and delivered Sion wire (Asahi Intec, Japan) retrogradely through distal septal branch into distal RCA supported by a 150-cm Finecross microcatheter (Terumo, Japan). Gaia 3 wire (Asahi Intec, Japan) crossed CTO lesion retrogradely into the true lumen in proximal RCA, and was advanced into Guidezilla guide extension catheter (Boston Scientific, USA) positioned in the antegrade guiding catheter. The Finecross microcatheter (Terumo, Japan) was delivered to the antegrade catheter and a RG3 wire (Asahi Intec, Japan) was externalized. The CTO was then predilated by a 2.0 × 15 mm balloon and stented with 2 overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm) with excellent angiographic result and TIMI3 flow in all distal branches.\n\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea.",
    "diff_label_texts": "A 69-year-old man with prior coronary bypass surgery presented with two months of severe shortness of breath with mild activity (NYHA class III). He was diagnosed with heart failure due to ischemia after failure of a saphenous vein graft to the right coronary artery. This was supported by an abnormal ECG, elevated NT-proBNP, and a coronary angiogram; echocardiography also showed reduced pumping function. The team reopened a chronic total occlusion in the native right coronary artery using a retrograde approach through septal channels (septal surfing). To enable that route, they first re-opened the totally occluded left coronary artery. After the procedure, his dyspnea improved before discharge, and at 6 months he had no recurrence of shortness of breath.",
    "summary": "Patient concerns:\nThis is a 69-year-old male with prior history of coronary artery bypass grafting presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration.\n\nDiagnosis:\nThe patient was diagnosed as heart failure caused by ischemia after SVG failure (SVG to right coronary artery) according to electrocardiogram, plasma N-terminal pro-B-type natriuretic peptide levels, and coronary angiogram.\n\nInterventions:\nWe recanalized native right coronary artery CTO by retrograde approach using septal collaterals by surfing technique after recanalization of totally occluded left coronary artery.\n\nOutcomes:\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea."
  },
  {
    "doc_id": 9,
    "label": "low_health_literacy",
    "fulltext": "A 69-year-old male with prior history of CABG presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration was admitted in our center. The electrocardiogram showed ST depression in leads II, III, aVF, and V4-6, and blood examination revealed elevation of plasma N-terminal pro-B-type natriuretic peptide levels (2640 pg/mL). Echocardiogram showed left ventricular systolic dysfunction and low left ventricular ejection fraction (30%). The patient had inferior ST-segment-elevation myocardial infarction in 2009, when he was 59 years old, with angiographic evidence of severe 3 vessels disease (coronary angiography showed CTO in proximal left anterior descending artery (LAD), 90% stenosis in mid and distal left circumflex artery, and 95% stenosis in mid RCA. The patient underwent CABG with left internal mammary artery (LIMA) to LAD, and sequential SVG to 1st obtuse marginal branch (OM1), 2nd obtuse marginal branch (OM2), and posterolateral branch (PL) in 2009.\n\nCoronary angiography was performed via 6 French (Fr) left radial artery access and demonstrated patency of LIMA to LAD and SVG to OM1, OM2 conduits, but a complete occlusion of sequential SVG to PL conduit. Native left main coronary artery was occluded in ostium and native RCA was occluded in the mid portion with bridging collaterals. We decided to treat the native RCA CTO. Dual arterial access was achieved with another 6 Fr sheath in right femoral artery. The left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic; USA) and 6 Fr EBU 3.5 (Launcher; Medtronic; USA) guide catheters, respectively. An antegrade approach via left radial artery was attempted; however, neither Fielder XTR wire (Asahi Intec, Japan) nor Gaia 3 wire (Asahi Intec, Japan) with Finecross microcatheter (Terumo, Japan) reached the true lumen in distal RCA. Then, parallel wire technique with Crusade microcatheter (Kaneka, Japan) and two Gaia 3 wires (Asahi Intec, Japan) were attempted, but also failed. We therefore switched to the retrograde approach using septal channel from LAD through occluded left coronary artery. Gaia 3 wire (Asahi Intec, Japan) crossed occluded left main (LM) and LAD, and finally reached true lumen in distal LAD. Sion wire was exchanged by Finecross microcatheter (Terumo, Japan) into dital LAD, and dilation of LM and proximal LAD with a 2.0 × 15 mm balloon was performed. Then, septal surfing technique (SST) was used for septal crossing. We tried different septal channels originating from proximal to distal LAD, and delivered Sion wire (Asahi Intec, Japan) retrogradely through distal septal branch into distal RCA supported by a 150-cm Finecross microcatheter (Terumo, Japan). Gaia 3 wire (Asahi Intec, Japan) crossed CTO lesion retrogradely into the true lumen in proximal RCA, and was advanced into Guidezilla guide extension catheter (Boston Scientific, USA) positioned in the antegrade guiding catheter. The Finecross microcatheter (Terumo, Japan) was delivered to the antegrade catheter and a RG3 wire (Asahi Intec, Japan) was externalized. The CTO was then predilated by a 2.0 × 15 mm balloon and stented with 2 overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm) with excellent angiographic result and TIMI3 flow in all distal branches.\n\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea.",
    "diff_label_texts": "This 69-year-old man had heart bypass surgery in the past. For 2 months, he got very short of breath with light activity. Tests—a heart tracing, a blood test, and an X-ray movie with dye of the heart arteries—showed heart failure from poor blood flow after a bypass vein to the right heart artery failed. Doctors first opened a totally blocked artery on the left side of his heart. Then they used tiny natural detours between heart arteries to reach the right heart artery from the far end and open it. His breathing was better when he left the hospital. Six months later, his shortness of breath had not come back.",
    "summary": "Patient concerns:\nThis is a 69-year-old male with prior history of coronary artery bypass grafting presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration.\n\nDiagnosis:\nThe patient was diagnosed as heart failure caused by ischemia after SVG failure (SVG to right coronary artery) according to electrocardiogram, plasma N-terminal pro-B-type natriuretic peptide levels, and coronary angiogram.\n\nInterventions:\nWe recanalized native right coronary artery CTO by retrograde approach using septal collaterals by surfing technique after recanalization of totally occluded left coronary artery.\n\nOutcomes:\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea."
  },
  {
    "doc_id": 9,
    "label": "proficient_health_literacy",
    "fulltext": "A 69-year-old male with prior history of CABG presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration was admitted in our center. The electrocardiogram showed ST depression in leads II, III, aVF, and V4-6, and blood examination revealed elevation of plasma N-terminal pro-B-type natriuretic peptide levels (2640 pg/mL). Echocardiogram showed left ventricular systolic dysfunction and low left ventricular ejection fraction (30%). The patient had inferior ST-segment-elevation myocardial infarction in 2009, when he was 59 years old, with angiographic evidence of severe 3 vessels disease (coronary angiography showed CTO in proximal left anterior descending artery (LAD), 90% stenosis in mid and distal left circumflex artery, and 95% stenosis in mid RCA. The patient underwent CABG with left internal mammary artery (LIMA) to LAD, and sequential SVG to 1st obtuse marginal branch (OM1), 2nd obtuse marginal branch (OM2), and posterolateral branch (PL) in 2009.\n\nCoronary angiography was performed via 6 French (Fr) left radial artery access and demonstrated patency of LIMA to LAD and SVG to OM1, OM2 conduits, but a complete occlusion of sequential SVG to PL conduit. Native left main coronary artery was occluded in ostium and native RCA was occluded in the mid portion with bridging collaterals. We decided to treat the native RCA CTO. Dual arterial access was achieved with another 6 Fr sheath in right femoral artery. The left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic; USA) and 6 Fr EBU 3.5 (Launcher; Medtronic; USA) guide catheters, respectively. An antegrade approach via left radial artery was attempted; however, neither Fielder XTR wire (Asahi Intec, Japan) nor Gaia 3 wire (Asahi Intec, Japan) with Finecross microcatheter (Terumo, Japan) reached the true lumen in distal RCA. Then, parallel wire technique with Crusade microcatheter (Kaneka, Japan) and two Gaia 3 wires (Asahi Intec, Japan) were attempted, but also failed. We therefore switched to the retrograde approach using septal channel from LAD through occluded left coronary artery. Gaia 3 wire (Asahi Intec, Japan) crossed occluded left main (LM) and LAD, and finally reached true lumen in distal LAD. Sion wire was exchanged by Finecross microcatheter (Terumo, Japan) into dital LAD, and dilation of LM and proximal LAD with a 2.0 × 15 mm balloon was performed. Then, septal surfing technique (SST) was used for septal crossing. We tried different septal channels originating from proximal to distal LAD, and delivered Sion wire (Asahi Intec, Japan) retrogradely through distal septal branch into distal RCA supported by a 150-cm Finecross microcatheter (Terumo, Japan). Gaia 3 wire (Asahi Intec, Japan) crossed CTO lesion retrogradely into the true lumen in proximal RCA, and was advanced into Guidezilla guide extension catheter (Boston Scientific, USA) positioned in the antegrade guiding catheter. The Finecross microcatheter (Terumo, Japan) was delivered to the antegrade catheter and a RG3 wire (Asahi Intec, Japan) was externalized. The CTO was then predilated by a 2.0 × 15 mm balloon and stented with 2 overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm) with excellent angiographic result and TIMI3 flow in all distal branches.\n\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea.",
    "diff_label_texts": "A 69-year-old male with prior CABG presented with 2 months of severe dyspnea on mild exertion (NYHA III). ECG showed ST depression in II, III, aVF, and V4–6; NT-proBNP was 2640 pg/mL. Echocardiography demonstrated LV systolic dysfunction with LVEF 30%. His history included an inferior STEMI in 2009 with severe 3-vessel disease (proximal LAD CTO, 90% mid/distal LCx stenoses, 95% mid RCA stenosis) treated with CABG (LIMA–LAD; sequential SVG to OM1, OM2, and PL). Current angiography via 6 Fr left radial access showed patent LIMA–LAD and SVG–OM1/OM2, but complete occlusion of the sequential SVG to PL. The native LM was occluded at the ostium and the native RCA was occluded in the mid segment with bridging collaterals. The strategy was to treat the native RCA CTO. Dual arterial access was obtained with an additional 6 Fr right femoral sheath. The right and left coronaries were engaged with 6 Fr AL 0.75 (Launcher; Medtronic) and 6 Fr EBU 3.5 (Launcher; Medtronic) guide catheters, respectively. An antegrade approach from the left radial artery failed: neither a Fielder XTR nor a Gaia 3 with a Finecross microcatheter could enter the distal true lumen. A parallel wire technique with a Crusade microcatheter and two Gaia 3 wires also failed. The team then switched to a retrograde approach via septal channels from the LAD through the occluded left coronary system. A Gaia 3 crossed the occluded LM and LAD to reach the distal LAD true lumen. A Sion wire was exchanged via a Finecross into the distal LAD, followed by dilation of the LM and proximal LAD with a 2.0 × 15 mm balloon. Septal surfing technique (SST) was then used to identify a viable septal channel. A Sion wire, supported by a 150-cm Finecross, was advanced retrogradely through a distal septal branch into the distal RCA. A Gaia 3 traversed the RCA CTO retrogradely into the proximal RCA true lumen and was advanced into a Guidezilla guide extension catheter positioned in the antegrade guide. The Finecross was delivered to the antegrade guide and an RG3 wire was externalized. The CTO segment was predilated with a 2.0 × 15 mm balloon and stented with two overlapping DES (2.5 × 38 mm and 3.0 × 38 mm), achieving an excellent angiographic result with TIMI 3 flow in all distal branches. Dyspnea was relieved at discharge, and at 6-month follow-up there was no recurrence of dyspnea.",
    "summary": "Patient concerns:\nThis is a 69-year-old male with prior history of coronary artery bypass grafting presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration.\n\nDiagnosis:\nThe patient was diagnosed as heart failure caused by ischemia after SVG failure (SVG to right coronary artery) according to electrocardiogram, plasma N-terminal pro-B-type natriuretic peptide levels, and coronary angiogram.\n\nInterventions:\nWe recanalized native right coronary artery CTO by retrograde approach using septal collaterals by surfing technique after recanalization of totally occluded left coronary artery.\n\nOutcomes:\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea."
  },
  {
    "doc_id": 10,
    "label": "intermediate_health_literacy",
    "fulltext": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20, and hand motion (HM) detection for the right eye (RE) and LE, respectively. The ocular movement was normal in both eyes. Anterior segment examination was unremarkable for both eyes. The LE fundus examination showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Fundus examination of the RE was unremarkable.\n\nWe used multimodal imaging including Optical coherence tomography (OCT) (OptoVue, Inc., Fremont, CA, USA, software version: 2018,0,0,18), fundus blue-autofluorescence (BAF), fluorescein angiography (FA) (Heidelberg Eye Explorer version 1.9.13.0, Spectralis Viewing Module 6.5.2.0; Heidelberg Engineering), Indocyanin green angiography (ICGA), and B-scan ultrasonography for further evaluation. Besides, orbital and brain MRIs with gadolinium enhancement were ordered. The OCT image revealed a mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid accumulation, and mild retinal thickening. A geographic area of macular hypocyanescence was apparent in the ICGA image of the left eye. BAF showed a geographic area with a speckled autofluorescence pattern at the macula. Optic nerve enlargement was found in the B-scan ultrasonography. In FA images, vascular leakage was apparent at the ONH (hot disc). Besides, a geographic patchy hypofluorescent area with speckled hyperfluorescent margins with a size of three disc diameters (DD) was detected. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the junction of the optic nerve and sclera. An oncology consultation was done with no remarkable finding.\n\nConsidering the suspicion of malignancy and the presence of an enhancing nodular mass in the orbit, the patient underwent transconjunctival lateral orbitotomy one week after the presentation. A pink localized scleral nodule with edematous tenon was found. Sub-tenon triamcinolone acetonide was injected with the clinical diagnosis of nodular posterior scleritis. The patient refused admission and intravenous corticosteroid injection as the treatment order. Oral prednisolone 50 mg/Kg was started. Rheumatology consultation and screening lab results, including PPD test (tuberculosis), chest X-ray, serum ACE level (sarcoidosis), and C-ANCA level (Wegner granulomatosis), were unremarkable. At the last follow-up examination (one week after the surgery), the patient’s BCDVA was 20/20, and counting fingers at 2 meters for the RE and LE, respectively. Furthermore, SRF was absorbed, and the macula became atrophic. Oral prednisolone was tapered off slowly for three months.",
    "diff_label_texts": "A 51-year-old man presented with 3 days of sudden, painful vision loss in the left eye. Visual acuity was 20/20 in the right eye and hand motion in the left eye. Left fundus findings included optic nerve head swelling, choroidal bulging, multiple areas of subretinal fluid, and RPE corrugations. Orbital/brain MRI with gadolinium showed a retrobulbar nodular mass enhancing at the junction of the optic nerve and sclera. Oncology and rheumatology evaluations were unremarkable. The clinical diagnosis was nodular posterior scleritis, and oral prednisolone was started.",
    "summary": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20 and hand motion (HM) for the right eye (RE) and LE, respectively. Fundus examination of the LE showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the optic nerve and sclera junction. Oncology and rheumatology work-ups were unremarkable. With the clinical diagnosis of nodular posterior scleritis oral prednisolone 50 mg/Kg was started."
  },
  {
    "doc_id": 10,
    "label": "low_health_literacy",
    "fulltext": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20, and hand motion (HM) detection for the right eye (RE) and LE, respectively. The ocular movement was normal in both eyes. Anterior segment examination was unremarkable for both eyes. The LE fundus examination showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Fundus examination of the RE was unremarkable.\n\nWe used multimodal imaging including Optical coherence tomography (OCT) (OptoVue, Inc., Fremont, CA, USA, software version: 2018,0,0,18), fundus blue-autofluorescence (BAF), fluorescein angiography (FA) (Heidelberg Eye Explorer version 1.9.13.0, Spectralis Viewing Module 6.5.2.0; Heidelberg Engineering), Indocyanin green angiography (ICGA), and B-scan ultrasonography for further evaluation. Besides, orbital and brain MRIs with gadolinium enhancement were ordered. The OCT image revealed a mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid accumulation, and mild retinal thickening. A geographic area of macular hypocyanescence was apparent in the ICGA image of the left eye. BAF showed a geographic area with a speckled autofluorescence pattern at the macula. Optic nerve enlargement was found in the B-scan ultrasonography. In FA images, vascular leakage was apparent at the ONH (hot disc). Besides, a geographic patchy hypofluorescent area with speckled hyperfluorescent margins with a size of three disc diameters (DD) was detected. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the junction of the optic nerve and sclera. An oncology consultation was done with no remarkable finding.\n\nConsidering the suspicion of malignancy and the presence of an enhancing nodular mass in the orbit, the patient underwent transconjunctival lateral orbitotomy one week after the presentation. A pink localized scleral nodule with edematous tenon was found. Sub-tenon triamcinolone acetonide was injected with the clinical diagnosis of nodular posterior scleritis. The patient refused admission and intravenous corticosteroid injection as the treatment order. Oral prednisolone 50 mg/Kg was started. Rheumatology consultation and screening lab results, including PPD test (tuberculosis), chest X-ray, serum ACE level (sarcoidosis), and C-ANCA level (Wegner granulomatosis), were unremarkable. At the last follow-up examination (one week after the surgery), the patient’s BCDVA was 20/20, and counting fingers at 2 meters for the RE and LE, respectively. Furthermore, SRF was absorbed, and the macula became atrophic. Oral prednisolone was tapered off slowly for three months.",
    "diff_label_texts": "A 51-year-old man came to us with sudden, painful vision loss in his left eye for three days. His right eye could see clearly (20/20). His left eye could only see hand movements. The back of his left eye showed swelling of the seeing nerve, a bulge in the layer under the retina, several patches of fluid under the retina, and wrinkles in the thin lining there. An MRI scan with contrast dye of the eyes and brain showed a small lump behind the eye where the eye nerve meets the white part of the eye. Tests for cancer and immune diseases were normal. The doctors diagnosed inflammation in the back part of the eye’s white coat that forms a small lump (nodular posterior scleritis). They started high-dose steroid pills by mouth (prednisolone).",
    "summary": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20 and hand motion (HM) for the right eye (RE) and LE, respectively. Fundus examination of the LE showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the optic nerve and sclera junction. Oncology and rheumatology work-ups were unremarkable. With the clinical diagnosis of nodular posterior scleritis oral prednisolone 50 mg/Kg was started."
  },
  {
    "doc_id": 10,
    "label": "proficient_health_literacy",
    "fulltext": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20, and hand motion (HM) detection for the right eye (RE) and LE, respectively. The ocular movement was normal in both eyes. Anterior segment examination was unremarkable for both eyes. The LE fundus examination showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Fundus examination of the RE was unremarkable.\n\nWe used multimodal imaging including Optical coherence tomography (OCT) (OptoVue, Inc., Fremont, CA, USA, software version: 2018,0,0,18), fundus blue-autofluorescence (BAF), fluorescein angiography (FA) (Heidelberg Eye Explorer version 1.9.13.0, Spectralis Viewing Module 6.5.2.0; Heidelberg Engineering), Indocyanin green angiography (ICGA), and B-scan ultrasonography for further evaluation. Besides, orbital and brain MRIs with gadolinium enhancement were ordered. The OCT image revealed a mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid accumulation, and mild retinal thickening. A geographic area of macular hypocyanescence was apparent in the ICGA image of the left eye. BAF showed a geographic area with a speckled autofluorescence pattern at the macula. Optic nerve enlargement was found in the B-scan ultrasonography. In FA images, vascular leakage was apparent at the ONH (hot disc). Besides, a geographic patchy hypofluorescent area with speckled hyperfluorescent margins with a size of three disc diameters (DD) was detected. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the junction of the optic nerve and sclera. An oncology consultation was done with no remarkable finding.\n\nConsidering the suspicion of malignancy and the presence of an enhancing nodular mass in the orbit, the patient underwent transconjunctival lateral orbitotomy one week after the presentation. A pink localized scleral nodule with edematous tenon was found. Sub-tenon triamcinolone acetonide was injected with the clinical diagnosis of nodular posterior scleritis. The patient refused admission and intravenous corticosteroid injection as the treatment order. Oral prednisolone 50 mg/Kg was started. Rheumatology consultation and screening lab results, including PPD test (tuberculosis), chest X-ray, serum ACE level (sarcoidosis), and C-ANCA level (Wegner granulomatosis), were unremarkable. At the last follow-up examination (one week after the surgery), the patient’s BCDVA was 20/20, and counting fingers at 2 meters for the RE and LE, respectively. Furthermore, SRF was absorbed, and the macula became atrophic. Oral prednisolone was tapered off slowly for three months.",
    "diff_label_texts": "A 51-year-old male presented with acute, painful visual loss of the left eye (LE) for 3 days. Best-corrected distance visual acuity (BCDVA) was 20/20 OD and hand motion (HM) OS. Ocular motility and anterior segment were unremarkable OU. Fundus OS showed optic nerve head (ONH) swelling, choroidal bulging, multiple patches of subretinal fluid (SRF), and retinal pigment epithelial (RPE) corrugations; OD fundus was unremarkable.\n\nMultimodal imaging was obtained: OCT (OptoVue, Inc., Fremont, CA, USA; software version 2018.0.0.18) demonstrated mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid, and mild retinal thickening. Indocyanine green angiography (ICGA) showed a geographic macular hypocyanescent area OS. Blue-autofluorescence (BAF) revealed a geographic macular area with speckled autofluorescence. B-scan ultrasonography showed optic nerve enlargement. Fluorescein angiography (FA) demonstrated vascular leakage at the ONH (hot disc) and a geographic patchy hypofluorescent area with speckled hyperfluorescent margins measuring approximately three disc diameters. Orbital and brain MRI with gadolinium revealed a retrobulbar nodular enhancing mass at the optic nerve–sclera junction. Oncology consultation was unremarkable.\n\nGiven concern for malignancy and the enhancing orbital nodule, the patient underwent transconjunctival lateral orbitotomy one week after presentation. Intraoperatively, a pink localized scleral nodule with edematous Tenon was identified. With a clinical diagnosis of nodular posterior scleritis, sub-Tenon triamcinolone acetonide was administered. The patient declined admission and intravenous corticosteroids; oral prednisolone 50 mg/Kg was initiated. Rheumatologic and infectious work-up, including PPD (tuberculosis), chest X-ray, serum ACE (sarcoidosis), and C-ANCA (Wegener granulomatosis), was unremarkable.\n\nAt the one-week postoperative follow-up, BCDVA was 20/20 OD and counting fingers at 2 meters OS. SRF had resolved, and the macula was atrophic. Oral prednisolone was tapered over three months.",
    "summary": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20 and hand motion (HM) for the right eye (RE) and LE, respectively. Fundus examination of the LE showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the optic nerve and sclera junction. Oncology and rheumatology work-ups were unremarkable. With the clinical diagnosis of nodular posterior scleritis oral prednisolone 50 mg/Kg was started."
  },
  {
    "doc_id": 11,
    "label": "intermediate_health_literacy",
    "fulltext": "An elderly 78-year-old patient from the Amhara region of Ethiopia, who has had a permanent cardiac pacemaker for 7 years, was scheduled for retropubic prostatectomy due to benign prostatic hyperplasia (BPH). This condition developed following a previous transurethral resection of the prostate 3 months earlier. The patient in the preoperative anesthesia evaluation was fully evaluated, and all the routine investigations required for the proposed surgery, which were within normal limits, were investigated. The patient presented with a history of frequency, urgency, nocturia, and dribbling for the past 2 months. Additionally, the patient had been known to have hypertension for the past 16 years and was taking amlodipine 5 mg orally daily, enalapril 10 mg orally twice daily (BID), and atorvastatin 10 mg orally daily. He had also been known to have type II diabetes mellitus for the past 25 years and was on metformin 500 mg orally BID and neutral protamine Hagedorn (NPH) 20 IU and 10 IU. He was admitted to a hospital for further evaluation, and complete bundle branch block (BBB) was detected via electrocardiogram (ECG). In an electrophysiology study, the patient was diagnosed with left ventricular hypertrophy secondary to hypertensive heart disease, mild diastolic dysfunction, and an ejection fraction of 62%. Abdominal ultrasound revealed an enlarged prostate size of 82 ml; anterior–posterior (AP) chest X-ray revealed a normal chest region with a left-side pacemaker in situ, and all the other blood parameters, including electrolytes and serum troponin levels, were within normal limits.\n\nA cardiologist was involved preoperatively as a multidisciplinary approach and risk determination tool for cardiac risk assessment. The patient had a frailty score of 5.5 with a poor functional cardiopulmonary reserve of metabolic equivalent (MET) = 3.4 and Revised Cardiac Risk Index (RCRI) class III, which accounts for 10.1% of major cardiac adverse events (myocardial infarction [MI], cardiac arrest, or death) within 30 days of the postoperative period, and intermediate risk on the basis of surgery type and patient risk factors. After preoperative evaluation and risk disclosure regarding the un-reprogrammed pacemaker and the associated complications during anesthesia and surgery, the patient was unable to afford the necessary health coverage for pacemaker reprogramming. This is because the cardiac surgery was performed in Addis Ababa, Ethiopia, which has a long waiting list with few cardiac surgeons for millions of people and is a considerable distance from the patient’s home institution, and there is a period of monitoring after pacemaker reprogramming for considerable post-reprogramming complication. As a result, the patient chose to proceed with the surgery, accepting the potential risks and harm associated with the situation. Continuous cardiac monitoring during the intraoperative period is highly advocated. Despite these factors, the patient did not experience cardiorespiratory failure, and he was stable. The patient continued on medication until the day of surgery, which included amlodipine, enalapril, atorvastatin, and a morning lower dose of two-thirds of the NPH. He also took 5 mg of diazepam orally for anxiolytics at midnight before the day of surgery.\n\nOn the day of surgery, the patient’s random blood sugar (RBS) was measured, and sliding scale glycemic control was implemented. Communication among the anesthetist, surgeon, and nurses was emphasized, ensuring that the cautery pad was placed away from the pacemaker, and that emergency drugs and a defibrillator were ready. The patient was premedicated with dexamethasone for nausea prophylaxis and paracetamol for pain relief as preemptive analgesia. American Society of Anesthesiology (ASA) standard monitoring was applied, and baseline parameters were recorded. Combined epidural–spinal anesthesia was administered via 0.5% isobaric bupivacaine (12.5 mg) and 50 µg fentanyl at the L3–L4 interspace. The block achieved anesthesia up to the umbilicus, and the sensory block was performed at T7. The surgery involved a midline incision below the umbilicus, with monopolar cautery used at low voltage (20 mA). Hemostasis was achieved through bipolar low-voltage cautery. Throughout the procedure, the patient’s vital signs remained stable. The patient’s vital signs did not change by more than 10% from the baseline vital signs. The intravenous fluid was resuscitated intraoperatively. During the postoperative period, the patient was transferred to the postanesthesia care unit (PACU) with vigilant monitoring, and 10 ml of 0.125% epidural top-up analgesia was given. Postop investigations were within normal limits. The patient was observed in the PACU for 12 hours and later transferred to the ward in stable condition with regular follow-up with the cardiology team. After 88th day of postsurgery the patient was discharged and advised to have regular checkups for pacemaker’s in situ status.",
    "diff_label_texts": "A 78-year-old man from the Amhara region, Ethiopia, with a permanent pacemaker placed for complete heart block was scheduled for retropubic prostatectomy. The anesthesia and cardiology teams recommended switching his dual-chamber, rate‑modulated pacemaker to an asynchronous mode perioperatively to reduce the risk of electromagnetic interference during surgery. He could not afford reprogramming and chose to proceed with the existing plan after informed consent; permission to publish the case was obtained after the operation. He received combined spinal–epidural anesthesia at L3–L4 using 0.5% isobaric bupivacaine 2.5 ml (12.5 mg) plus fentanyl 50 µg. Standard ASA monitoring was applied with special attention to cardiac stability. Intraoperatively, he remained stable with minimal changes in vital signs; blood pressure was supported with isotonic saline as needed. Postoperatively, he was monitored in the PACU, received analgesia at 4 hours with an epidural top‑up, and was transferred to the ward about 6 hours after surgery in stable condition. Epidural analgesia was continued for 72 hours. He was discharged at the 88th postoperative hour in good condition.",
    "summary": "A 78-year-old male from the Amhara region, Ethiopia, with a permanent pacemaker for complete heart block was scheduled for retropubic prostatectomy. Preoperative assessments by the anesthetist and cardiologist recommended reprogramming the pacemaker to asynchronous mode to reduce risks related to its dual-chamber, rate-modulated mode setting. However, the patient could not afford reprogramming and opted to proceed with the existing perioperative plan. Informed consent was obtained, and case report publication permission was obtained after operation. The patient received combined epidural-spinal anesthesia with 2.50 ml of 0.5% isobaric bupivacaine and 50 µg fentanyl at the L3-L4 interspace. Standard American Society of Anesthesiology monitoring was applied, with a focus on cardiac stability. The patient remained stable with minimal vital sign fluctuations and maintained adequate blood pressure using isotonic saline. Postoperatively, the patient was transferred to the postanesthesia care unit, receiving analgesia after 4 hours and an epidural top-up. After 6 hours, he was transferred to the ward in stable condition. Epidural analgesia was continued for 72 hours, and the patient was discharged on the 88th postoperative hour in stable condition."
  },
  {
    "doc_id": 11,
    "label": "low_health_literacy",
    "fulltext": "An elderly 78-year-old patient from the Amhara region of Ethiopia, who has had a permanent cardiac pacemaker for 7 years, was scheduled for retropubic prostatectomy due to benign prostatic hyperplasia (BPH). This condition developed following a previous transurethral resection of the prostate 3 months earlier. The patient in the preoperative anesthesia evaluation was fully evaluated, and all the routine investigations required for the proposed surgery, which were within normal limits, were investigated. The patient presented with a history of frequency, urgency, nocturia, and dribbling for the past 2 months. Additionally, the patient had been known to have hypertension for the past 16 years and was taking amlodipine 5 mg orally daily, enalapril 10 mg orally twice daily (BID), and atorvastatin 10 mg orally daily. He had also been known to have type II diabetes mellitus for the past 25 years and was on metformin 500 mg orally BID and neutral protamine Hagedorn (NPH) 20 IU and 10 IU. He was admitted to a hospital for further evaluation, and complete bundle branch block (BBB) was detected via electrocardiogram (ECG). In an electrophysiology study, the patient was diagnosed with left ventricular hypertrophy secondary to hypertensive heart disease, mild diastolic dysfunction, and an ejection fraction of 62%. Abdominal ultrasound revealed an enlarged prostate size of 82 ml; anterior–posterior (AP) chest X-ray revealed a normal chest region with a left-side pacemaker in situ, and all the other blood parameters, including electrolytes and serum troponin levels, were within normal limits.\n\nA cardiologist was involved preoperatively as a multidisciplinary approach and risk determination tool for cardiac risk assessment. The patient had a frailty score of 5.5 with a poor functional cardiopulmonary reserve of metabolic equivalent (MET) = 3.4 and Revised Cardiac Risk Index (RCRI) class III, which accounts for 10.1% of major cardiac adverse events (myocardial infarction [MI], cardiac arrest, or death) within 30 days of the postoperative period, and intermediate risk on the basis of surgery type and patient risk factors. After preoperative evaluation and risk disclosure regarding the un-reprogrammed pacemaker and the associated complications during anesthesia and surgery, the patient was unable to afford the necessary health coverage for pacemaker reprogramming. This is because the cardiac surgery was performed in Addis Ababa, Ethiopia, which has a long waiting list with few cardiac surgeons for millions of people and is a considerable distance from the patient’s home institution, and there is a period of monitoring after pacemaker reprogramming for considerable post-reprogramming complication. As a result, the patient chose to proceed with the surgery, accepting the potential risks and harm associated with the situation. Continuous cardiac monitoring during the intraoperative period is highly advocated. Despite these factors, the patient did not experience cardiorespiratory failure, and he was stable. The patient continued on medication until the day of surgery, which included amlodipine, enalapril, atorvastatin, and a morning lower dose of two-thirds of the NPH. He also took 5 mg of diazepam orally for anxiolytics at midnight before the day of surgery.\n\nOn the day of surgery, the patient’s random blood sugar (RBS) was measured, and sliding scale glycemic control was implemented. Communication among the anesthetist, surgeon, and nurses was emphasized, ensuring that the cautery pad was placed away from the pacemaker, and that emergency drugs and a defibrillator were ready. The patient was premedicated with dexamethasone for nausea prophylaxis and paracetamol for pain relief as preemptive analgesia. American Society of Anesthesiology (ASA) standard monitoring was applied, and baseline parameters were recorded. Combined epidural–spinal anesthesia was administered via 0.5% isobaric bupivacaine (12.5 mg) and 50 µg fentanyl at the L3–L4 interspace. The block achieved anesthesia up to the umbilicus, and the sensory block was performed at T7. The surgery involved a midline incision below the umbilicus, with monopolar cautery used at low voltage (20 mA). Hemostasis was achieved through bipolar low-voltage cautery. Throughout the procedure, the patient’s vital signs remained stable. The patient’s vital signs did not change by more than 10% from the baseline vital signs. The intravenous fluid was resuscitated intraoperatively. During the postoperative period, the patient was transferred to the postanesthesia care unit (PACU) with vigilant monitoring, and 10 ml of 0.125% epidural top-up analgesia was given. Postop investigations were within normal limits. The patient was observed in the PACU for 12 hours and later transferred to the ward in stable condition with regular follow-up with the cardiology team. After 88th day of postsurgery the patient was discharged and advised to have regular checkups for pacemaker’s in situ status.",
    "diff_label_texts": "A 78-year-old man from the Amhara region of Ethiopia had a permanent heart pacemaker because of a complete heart block. He was scheduled for prostate surgery. Before surgery, the anesthesia and heart doctors advised switching his pacemaker to a steady, fixed beat to lower the chance of problems. He could not afford that change. He chose to go ahead with the operation. He signed consent for the plan. After surgery, he also gave permission to share his case. For anesthesia, he got a numbing injection in the lower back (a combined spinal–epidural). The team used 2.5 ml of strong numbing medicine (0.5% bupivacaine) and a tiny dose of fentanyl (50 micrograms). Standard monitors were used, and his heart was watched closely. His vital signs stayed steady, with only small changes. His blood pressure stayed good with IV salt water. After surgery, he went to the recovery room. He got pain medicine after 4 hours and an extra dose through the epidural. Six hours after surgery, he moved to the ward in stable condition. The epidural pain control continued for 72 hours. He went home in stable condition about 88 hours after surgery.",
    "summary": "A 78-year-old male from the Amhara region, Ethiopia, with a permanent pacemaker for complete heart block was scheduled for retropubic prostatectomy. Preoperative assessments by the anesthetist and cardiologist recommended reprogramming the pacemaker to asynchronous mode to reduce risks related to its dual-chamber, rate-modulated mode setting. However, the patient could not afford reprogramming and opted to proceed with the existing perioperative plan. Informed consent was obtained, and case report publication permission was obtained after operation. The patient received combined epidural-spinal anesthesia with 2.50 ml of 0.5% isobaric bupivacaine and 50 µg fentanyl at the L3-L4 interspace. Standard American Society of Anesthesiology monitoring was applied, with a focus on cardiac stability. The patient remained stable with minimal vital sign fluctuations and maintained adequate blood pressure using isotonic saline. Postoperatively, the patient was transferred to the postanesthesia care unit, receiving analgesia after 4 hours and an epidural top-up. After 6 hours, he was transferred to the ward in stable condition. Epidural analgesia was continued for 72 hours, and the patient was discharged on the 88th postoperative hour in stable condition."
  },
  {
    "doc_id": 12,
    "label": "low_health_literacy",
    "fulltext": "A 52-year-old woman referred to the urology clinic with urinary complaints. Her symptoms began three years ago with frequency, dysuria and dribbling. She also mentioned the frequent passage of red and black thread-like substances in her urine. Moreover, during these discharges, she had headache, fever and chills. Intermittent periurethral and genital itching was another complaint of hers. She had been treated by several specialists with the diagnosis of recurrent urinary tract infections, with no clinical improvement. The patient denied recent travel, camping, hiking, farming, swimming and insect bites. She had positive history of pilonidal sinus surgery and hysterectomy, 8 and 7 years earlier, respectively. Two years prior to the current visit, she had been hospitalized for assessment. On physical examination, she was well-appearing with normal vital signs. All her laboratory tests, including cell blood count, urine analysis and biochemistries were in normal ranges. Abdominopelvic computed tomography (CT) scan revealed no abnormalities. Hence, she underwent cystoscopy, which demonstrated erythema and hyperemia of the bladder mucosa, suspended debris, and dilation of the left ureteral orifice. During consultation with an infectious diseases’ specialist, schistosomiasis was suspected, Therefore, she was treated with Praziquantel with the appropriate dose and duration and was discharged from the hospital.\n\nHowever, her symptoms did not subside. She was revisited by another infectious disease specialist, who prescribed her ivermectin due to suspicion to urinary myiasis. Nevertheless, no improvement was observed. She was readmitted to undergo bladder irrigation with polyethylene glycol, but the bladder washfluid did not contain any visible larvae. This procedure was followed by a two-day hematuria with spontaneous cessation. She was discharged home and advised to repeat the urine analysis one months later. Her random urine analysis was normal, so she collected her 24-h urine and sent it to the laboratory for analysis, in which a live larva was demonstrated under light microscope by the pathologist. The larva was isolated and sent to an entomologist to be identified morphologically. Finally, it was determined that the larva belonged to the species Sarcophaga. The patient was advised to take personal hygiene and consume at least 3 L of water daily.",
    "diff_label_texts": "A 52-year-old woman had burning when she peed and had to pee very often for a long time. She tried many treatments for bladder infections, but the problem did not go away. Regular scans and lab tests looked normal. A camera test that looked inside her bladder showed the lining was red and irritated, with tiny bits floating in the urine. Later, the lab saw a live larva (a baby insect) in her urine under the microscope. That finding explained her symptoms. She was told to keep very clean. She was also told to drink plenty of water every day.",
    "summary": "We report a 52-year-old woman with persistent dysuria, frequency despite multiple treatments for suspected infections. Cystoscopy revealed erythema and debris, but imaging and laboratory tests were unremarkable. A live larva was identified in urine analysis, confirming the diagnosis. Treatment involved improved hygiene and hydration."
  },
  {
    "doc_id": 13,
    "label": "intermediate_health_literacy",
    "fulltext": "A 36-year-old female patient with a history of ulcerative colitis and good disease control on sulfasalazine, ferrous fumarate and intermittent prednisone for flare-ups is presented.\n\nHe was admitted to the emergency unit with a 1 week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, an electrocardiogram was performed in sinus rhythm, with finding of supradesnivel of the ST segment in the lower wall.\n\nThe patient reported a 6-month history of general disorders, fatigue and night sweats. She had previously presented episodes of precordial pain in relation to effort that progressed to rest. The physical examination was without murmurs or alterations of the peripheral pulses.\n\nAn emergency coronary angiography was performed, which revealed severe 2-vessel disease: severe ostial lesion 90% in the left coronary trunk and severe subocclusive lesion 99-100% at the ostial level in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful installation of a medicated stent. The hemodynamicist was impressed by a possible aortitis due to involvement of the arch and friability of the vessels when the balloon was advanced, so he suggested an etiological study oriented to inflammatory disease, prior to surgical resolution of the lesion of the left coronary trunk.\n\nLaboratory tests showed mild anaemia (haemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated erythrocyte sedimentation rate (ESR): 42 mm/h and C-reactive protein (CRP): 4.9 mg/L (normal value <1) and elevated ultrasensitive troponin. From the autoimmunity study, normal levels of complement C3 and C4, negative anti-nuclear antibodies (ANA), anti-DNA, negative extracellular nuclear antigen (ENA) profile and non-reactive VDRL were rescued.\n\nCardiac magnetic resonance (MRI) with contrast was completed with findings of acute infarction of the left ventricular inferior wall non-transmural myocardium and subendocardial ischemia in the anteroseptoapical resting of the left ventricle. Mild aortic and mitral insufficiency. Preserved biventricular systolic function.\n\nComputed tomography angiography (CTA) of the chest, abdomen and pelvis showed periaortic fibrotic wall thickening involving the root, aortic arch and abdominal aorta with severe left coronary trunk stenosis and mild left subclavian, left vertebral artery stenosis and severe lower mesenteric artery stenosis. Immune globulin G (IgG) 4 deposition disease or Takayasu's arteritis was suggested.\n\nWithin the differential diagnosis study, IgG levels were performed at 1,600 mg/dl (reference values: 700-1,600), and its subclasses: IgG1: 1024 mg/dl (elevated), and the rest in normal range (IgG2: 456 mg/dl; IgG3: 98.8 mg/dl and IgG4: 13.6 mg/dl).\n\nTakayasu arteritis was diagnosed clinically and by imaging and treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by injection and folic acid 1 mg daily. After 3 weeks of treatment she underwent myocardial revascularisation surgery with use of the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and aortocoronary bypass to circumflex artery. It was noted intraoperatively that the root of the aorta and the ascending aorta presented a healthy appearance. The patient is currently at home in good general condition and under ambulatory follow-up.\n",
    "diff_label_texts": "A 36-year-old woman with ulcerative colitis developed a week of worsening chest pressure with autonomic symptoms (such as sweating and nausea). Her electrocardiogram showed ST-segment elevation in the inferior leads, consistent with an inferior-wall heart attack. She also reported several months of fatigue and night sweats.\n\nUrgent coronary angiography found severe two-vessel coronary artery disease. The right coronary artery was the culprit lesion and was opened successfully with a stent. Because the interventional team suspected inflammation of the aorta (aortitis), additional workup was done. Inflammatory markers were mildly elevated, and CT angiography showed fibrotic thickening around the aorta with significant narrowing in multiple arteries, pointing to Takayasu arteritis.\n\nShe started treatment with prednisone and methotrexate. After stabilization, she underwent delayed coronary bypass surgery and did well.",
    "summary": "A 36-year-old woman with ulcerative colitis presented with progressive precordial pain and neurovegetative symptoms. The electrocardiogram showed a ST segment elevation in the inferior wall. The patient had a history of fatigue and night sweats. She underwent a coronary angiography that revealed severe disease in two coronary arteries, with successful primary angioplasty of the culprit artery. Aortitis was suspected, which led to additional studies, including a mild elevation of inflammatory activity indices and a computed tomographic angiography with periaortic fibrotic thickening and significant stenosis in multiple arteries, suggesting Takayasu arteritis. She was treated with prednisone, methotrexate, and underwent delayed myocardial revascularization surgery with good results.\n"
  },
  {
    "doc_id": 13,
    "label": "low_health_literacy",
    "fulltext": "A 36-year-old female patient with a history of ulcerative colitis and good disease control on sulfasalazine, ferrous fumarate and intermittent prednisone for flare-ups is presented.\n\nHe was admitted to the emergency unit with a 1 week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, an electrocardiogram was performed in sinus rhythm, with finding of supradesnivel of the ST segment in the lower wall.\n\nThe patient reported a 6-month history of general disorders, fatigue and night sweats. She had previously presented episodes of precordial pain in relation to effort that progressed to rest. The physical examination was without murmurs or alterations of the peripheral pulses.\n\nAn emergency coronary angiography was performed, which revealed severe 2-vessel disease: severe ostial lesion 90% in the left coronary trunk and severe subocclusive lesion 99-100% at the ostial level in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful installation of a medicated stent. The hemodynamicist was impressed by a possible aortitis due to involvement of the arch and friability of the vessels when the balloon was advanced, so he suggested an etiological study oriented to inflammatory disease, prior to surgical resolution of the lesion of the left coronary trunk.\n\nLaboratory tests showed mild anaemia (haemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated erythrocyte sedimentation rate (ESR): 42 mm/h and C-reactive protein (CRP): 4.9 mg/L (normal value <1) and elevated ultrasensitive troponin. From the autoimmunity study, normal levels of complement C3 and C4, negative anti-nuclear antibodies (ANA), anti-DNA, negative extracellular nuclear antigen (ENA) profile and non-reactive VDRL were rescued.\n\nCardiac magnetic resonance (MRI) with contrast was completed with findings of acute infarction of the left ventricular inferior wall non-transmural myocardium and subendocardial ischemia in the anteroseptoapical resting of the left ventricle. Mild aortic and mitral insufficiency. Preserved biventricular systolic function.\n\nComputed tomography angiography (CTA) of the chest, abdomen and pelvis showed periaortic fibrotic wall thickening involving the root, aortic arch and abdominal aorta with severe left coronary trunk stenosis and mild left subclavian, left vertebral artery stenosis and severe lower mesenteric artery stenosis. Immune globulin G (IgG) 4 deposition disease or Takayasu's arteritis was suggested.\n\nWithin the differential diagnosis study, IgG levels were performed at 1,600 mg/dl (reference values: 700-1,600), and its subclasses: IgG1: 1024 mg/dl (elevated), and the rest in normal range (IgG2: 456 mg/dl; IgG3: 98.8 mg/dl and IgG4: 13.6 mg/dl).\n\nTakayasu arteritis was diagnosed clinically and by imaging and treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by injection and folic acid 1 mg daily. After 3 weeks of treatment she underwent myocardial revascularisation surgery with use of the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and aortocoronary bypass to circumflex artery. It was noted intraoperatively that the root of the aorta and the ascending aorta presented a healthy appearance. The patient is currently at home in good general condition and under ambulatory follow-up.\n",
    "diff_label_texts": "A 36-year-old woman had a long-term bowel disease (ulcerative colitis). She came in with chest pain that kept getting worse. She also had shortness of breath, sweating, and felt sick to her stomach. For months she had felt very tired and had night sweats. Her heart test (EKG) showed signs of a heart attack in the lower part of the heart. Doctors did a dye X-ray to look at the heart arteries. It showed bad blockages in two heart pipes. They opened the most blocked pipe right away with a balloon and a tiny mesh tube (stent). While looking, the team worried the main body artery (aorta) was swollen. Blood tests showed mild inflammation. A special CT scan showed the aorta wall looked thick and scarred, with tight narrow spots in several arteries. This pointed to a rare illness that causes swollen big arteries, called Takayasu arteritis. She started strong anti-inflammatory and immune medicines (prednisone and methotrexate). Later she had heart bypass surgery to improve blood flow. She did well after treatment.",
    "summary": "A 36-year-old woman with ulcerative colitis presented with progressive precordial pain and neurovegetative symptoms. The electrocardiogram showed a ST segment elevation in the inferior wall. The patient had a history of fatigue and night sweats. She underwent a coronary angiography that revealed severe disease in two coronary arteries, with successful primary angioplasty of the culprit artery. Aortitis was suspected, which led to additional studies, including a mild elevation of inflammatory activity indices and a computed tomographic angiography with periaortic fibrotic thickening and significant stenosis in multiple arteries, suggesting Takayasu arteritis. She was treated with prednisone, methotrexate, and underwent delayed myocardial revascularization surgery with good results.\n"
  },
  {
    "doc_id": 13,
    "label": "proficient_health_literacy",
    "fulltext": "A 36-year-old female patient with a history of ulcerative colitis and good disease control on sulfasalazine, ferrous fumarate and intermittent prednisone for flare-ups is presented.\n\nHe was admitted to the emergency unit with a 1 week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, an electrocardiogram was performed in sinus rhythm, with finding of supradesnivel of the ST segment in the lower wall.\n\nThe patient reported a 6-month history of general disorders, fatigue and night sweats. She had previously presented episodes of precordial pain in relation to effort that progressed to rest. The physical examination was without murmurs or alterations of the peripheral pulses.\n\nAn emergency coronary angiography was performed, which revealed severe 2-vessel disease: severe ostial lesion 90% in the left coronary trunk and severe subocclusive lesion 99-100% at the ostial level in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful installation of a medicated stent. The hemodynamicist was impressed by a possible aortitis due to involvement of the arch and friability of the vessels when the balloon was advanced, so he suggested an etiological study oriented to inflammatory disease, prior to surgical resolution of the lesion of the left coronary trunk.\n\nLaboratory tests showed mild anaemia (haemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated erythrocyte sedimentation rate (ESR): 42 mm/h and C-reactive protein (CRP): 4.9 mg/L (normal value <1) and elevated ultrasensitive troponin. From the autoimmunity study, normal levels of complement C3 and C4, negative anti-nuclear antibodies (ANA), anti-DNA, negative extracellular nuclear antigen (ENA) profile and non-reactive VDRL were rescued.\n\nCardiac magnetic resonance (MRI) with contrast was completed with findings of acute infarction of the left ventricular inferior wall non-transmural myocardium and subendocardial ischemia in the anteroseptoapical resting of the left ventricle. Mild aortic and mitral insufficiency. Preserved biventricular systolic function.\n\nComputed tomography angiography (CTA) of the chest, abdomen and pelvis showed periaortic fibrotic wall thickening involving the root, aortic arch and abdominal aorta with severe left coronary trunk stenosis and mild left subclavian, left vertebral artery stenosis and severe lower mesenteric artery stenosis. Immune globulin G (IgG) 4 deposition disease or Takayasu's arteritis was suggested.\n\nWithin the differential diagnosis study, IgG levels were performed at 1,600 mg/dl (reference values: 700-1,600), and its subclasses: IgG1: 1024 mg/dl (elevated), and the rest in normal range (IgG2: 456 mg/dl; IgG3: 98.8 mg/dl and IgG4: 13.6 mg/dl).\n\nTakayasu arteritis was diagnosed clinically and by imaging and treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by injection and folic acid 1 mg daily. After 3 weeks of treatment she underwent myocardial revascularisation surgery with use of the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and aortocoronary bypass to circumflex artery. It was noted intraoperatively that the root of the aorta and the ascending aorta presented a healthy appearance. The patient is currently at home in good general condition and under ambulatory follow-up.\n",
    "diff_label_texts": "A 36-year-old female with ulcerative colitis (well controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares) presented with 1 week of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, the ECG was in sinus rhythm with ST-segment elevation in the inferior wall. She endorsed a 6-month history of general malaise, fatigue, and night sweats, and had experienced exertional precordial pain that progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.\n\nEmergency coronary angiography demonstrated severe 2-vessel coronary disease: a severe 90% ostial lesion in the left coronary trunk (left main) and a severe 99–100% subocclusive ostial lesion in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful placement of a drug-eluting stent. The hemodynamicist noted possible aortitis given arch involvement and vessel friability during balloon advancement and recommended an inflammatory/etiologic evaluation prior to definitive management of the left main lesion.\n\nLaboratory testing showed mild anemia (hemoglobin 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated ESR 42 mm/h, CRP 4.9 mg/L (normal <1), and elevated high-sensitivity troponin. Autoimmunity panel: normal complement C3/C4, negative ANA, anti-DNA, and ENA profile; non-reactive VDRL. Cardiac MRI with contrast demonstrated acute non-transmural infarction of the left ventricular inferior wall and subendocardial ischemia in the anteroseptoapical region at rest, with mild aortic and mitral insufficiency and preserved biventricular systolic function.\n\nComputed tomographic angiography of the chest/abdomen/pelvis showed periaortic fibrotic wall thickening involving the aortic root, arch, and abdominal aorta, with severe left coronary trunk stenosis, mild left subclavian and left vertebral artery stenoses, and severe inferior mesenteric artery stenosis. The differential included IgG4-related disease versus Takayasu arteritis. Total IgG was 1,600 mg/dL (ref 700–1,600) with IgG1 1,024 mg/dL (elevated) and normal IgG2 456 mg/dL, IgG3 98.8 mg/dL, and IgG4 13.6 mg/dL, findings not supportive of IgG4-related aortitis. Takayasu arteritis was diagnosed clinically and by imaging.\n\nImmunosuppression was initiated with prednisone 60 mg daily and methotrexate 20 mg weekly (parenteral) with folic acid 1 mg daily. After 3 weeks of therapy, she underwent myocardial revascularization surgery using the left internal mammary artery graft to the descending anterior artery (LAD) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta appeared healthy. She was discharged home in good general condition and remains under ambulatory follow-up.\n\nContext: Takayasu arteritis is a large-vessel granulomatous vasculitis affecting the aorta and its major branches that can produce aorto-ostial coronary lesions (as in this case, involving the left main and right coronary ostia), leading to myocardial ischemia/infarction. The mildly elevated inflammatory indices, periaortic fibrotic thickening, and multifocal arterial stenoses on CTA are characteristic, and the lack of IgG4 elevation argues against IgG4-related aortitis. The staged approach—urgent culprit-vessel PCI followed by immunosuppression and delayed CABG—is consistent with management principles aiming to control vascular inflammation before definitive surgical revascularization.",
    "summary": "A 36-year-old woman with ulcerative colitis presented with progressive precordial pain and neurovegetative symptoms. The electrocardiogram showed a ST segment elevation in the inferior wall. The patient had a history of fatigue and night sweats. She underwent a coronary angiography that revealed severe disease in two coronary arteries, with successful primary angioplasty of the culprit artery. Aortitis was suspected, which led to additional studies, including a mild elevation of inflammatory activity indices and a computed tomographic angiography with periaortic fibrotic thickening and significant stenosis in multiple arteries, suggesting Takayasu arteritis. She was treated with prednisone, methotrexate, and underwent delayed myocardial revascularization surgery with good results.\n"
  },
  {
    "doc_id": 14,
    "label": "intermediate_health_literacy",
    "fulltext": "A 36-year-old female patient complained of dysphagia with longstanding cervical and upper thoracic pain. She also had a multinodular goiter with no other significant history. Esophagogastroduodenal transit was performed. It showed a posterior and lateral right impression of the proximal esophagus after ingestion of baryte, extending 3.5 cm cephalocaudal. A maximum esophageal stenosis of 60% was estimated. A cervical and thoracic CT scan revealed a congenital anomaly of the aortic arch: a mirror image of the right aortic arch. The aortic arch originates from the root of the aorta and runs above the right stem bronchus, giving rise to the three supra-aortic trunks as follows: the first is the left brachiocephalic artery (which gives rise to the left common carotid artery and the left subclavian artery); the second is the right common carotid artery; and the third is the right subclavian artery. The aortic arch then enters posteriorly to the esophagus and gives rise to a small anterior saccule of 1.3 cm, known as the Kommerell diverticulum. This configuration forms a ring around the tracheo-esophageal pair, whose edges are formed posterior-lateral to the right by the aortic arch, posterior-lateral to the left by the Kommerell diverticulum, lateral to the left by the arteriosum ligamentum (or arterial ligament), and anteriorly by the left brachiocephalic artery. A gastroscopy confirmed the endoluminal impact of extrinsic compression. In view of minimal clinical repercussions and the absence of nutritional disorders, no surgical cure was ultimately performed. The evolution was favorable with, according to the patient, a spontaneous amelioration of symptoms.\n",
    "diff_label_texts": "A 36-year-old woman had dysphagia due to a congenital right aortic arch with mirror-image branching.\nIn this rare pattern, the aorta runs to the right, wraps around the right main bronchus, and the head-and-arm arteries branch in the reverse order of normal.\nMost people have no symptoms unless the aorta or an associated bulge compresses the esophagus or trachea.\nSurgery is considered for major airway or esophageal compression, aneurysmal disease, thoracic aortic dissection, or a Kommerell diverticulum larger than 2 cm.\nThere is no standard operation; treatment is tailored to the person’s anatomy and symptoms.\nIn this case, imaging showed external compression of the upper esophagus with a small Kommerell diverticulum (about 1.3 cm), so no intervention was performed and her symptoms improved.",
    "summary": "We report the case of a 36-year-old female patient whose dysphagia presented a congenital anomaly of the thoracic aorta: the right aortic arch with mirror image. This is a rare anomaly of embryonic development where the aorta winds around the right stem bronchus and the supra-aortic trunks emerge from the crown in the reverse and opposite order to normal. The vast majority of patients are asymptomatic unless there is a compression of the mediastinal structures. Major compression of the esophagus or trachea, aneurysmal disease, thoracic aortic dissection or the presence of a Kommerell diverticulum of more than 2 cm may warrant surgical intervention. There is no standard treatment and it must be adapted to the clinical presentation and anatomical configuration of the patient. Our patient did not receive any treatment for her condition.\n"
  },
  {
    "doc_id": 14,
    "label": "low_health_literacy",
    "fulltext": "A 36-year-old female patient complained of dysphagia with longstanding cervical and upper thoracic pain. She also had a multinodular goiter with no other significant history. Esophagogastroduodenal transit was performed. It showed a posterior and lateral right impression of the proximal esophagus after ingestion of baryte, extending 3.5 cm cephalocaudal. A maximum esophageal stenosis of 60% was estimated. A cervical and thoracic CT scan revealed a congenital anomaly of the aortic arch: a mirror image of the right aortic arch. The aortic arch originates from the root of the aorta and runs above the right stem bronchus, giving rise to the three supra-aortic trunks as follows: the first is the left brachiocephalic artery (which gives rise to the left common carotid artery and the left subclavian artery); the second is the right common carotid artery; and the third is the right subclavian artery. The aortic arch then enters posteriorly to the esophagus and gives rise to a small anterior saccule of 1.3 cm, known as the Kommerell diverticulum. This configuration forms a ring around the tracheo-esophageal pair, whose edges are formed posterior-lateral to the right by the aortic arch, posterior-lateral to the left by the Kommerell diverticulum, lateral to the left by the arteriosum ligamentum (or arterial ligament), and anteriorly by the left brachiocephalic artery. A gastroscopy confirmed the endoluminal impact of extrinsic compression. In view of minimal clinical repercussions and the absence of nutritional disorders, no surgical cure was ultimately performed. The evolution was favorable with, according to the patient, a spontaneous amelioration of symptoms.\n",
    "diff_label_texts": "A 36-year-old woman had trouble swallowing. Tests found she was born with an unusual shape of the main body artery in her chest. The artery curves to the right in a mirror-image pattern. It wraps around a main branch of the airway. The side branches of the artery come off in the reverse order from normal. Most people with this have no symptoms. Problems happen only if the artery squeezes the space in the middle of the chest. This can press on the food pipe or the windpipe. Surgery may be needed if there is strong pressure on these tubes, a bulge or a tear in the chest artery, or a pouch on the artery bigger than 2 cm. There is no one-size-fits-all treatment. Care is tailored to the person’s symptoms and body anatomy. This patient did not receive any treatment.",
    "summary": "We report the case of a 36-year-old female patient whose dysphagia presented a congenital anomaly of the thoracic aorta: the right aortic arch with mirror image. This is a rare anomaly of embryonic development where the aorta winds around the right stem bronchus and the supra-aortic trunks emerge from the crown in the reverse and opposite order to normal. The vast majority of patients are asymptomatic unless there is a compression of the mediastinal structures. Major compression of the esophagus or trachea, aneurysmal disease, thoracic aortic dissection or the presence of a Kommerell diverticulum of more than 2 cm may warrant surgical intervention. There is no standard treatment and it must be adapted to the clinical presentation and anatomical configuration of the patient. Our patient did not receive any treatment for her condition.\n"
  },
  {
    "doc_id": 15,
    "label": "intermediate_health_literacy",
    "fulltext": "A 62-year-old Tunisian Arab postmenopausal female diagnosed with Von Hippel–Lindau disease in 2021 presented with various manifestations related to the disease. She had a history of multiple surgeries, primarily for renal, adrenal, and pancreatic tumors, with incidental findings of ovarian masses.\n\nThe patient was asymptomatic from a gynecological standpoint, but primarily complained of headaches before undergoing brain surgery. She had no significant family or psychosocial history.\n\nHer surgical history included\n2021: A non-operable tumor (6 cm) of the left petrous bone endolymphatic sac, managed with radiotherapy.\n\n2021: Left adrenalectomy for a 6 cm pheochromocytoma. Pathological examination revealed pheochromocytoma.\n\n2021: Left nephrectomy for a ruptured left renal tumor. Microscopy showed multifocal clear-cell renal carcinoma of nuclear grade 2.\n\n2022: Cephalic duodenopancreatectomy for a mass in the pancreas. Histological examination confirmed three serous cystadenomas and two well-differentiated neuroendocrine tumors.\n\nIn January 2021, during postoperative surveillance with an abdominal–pelvic computed tomography (CT) scan, a 4 cm solid cystic left adnexal mass was incidentally discovered, which raised suspicion of malignancy. The mass was confirmed by transvaginal ultrasound and pelvic MRI, classified as Ovarian-Adnexal Reporting and Data System (O-RADS) 5 (high suspicion for malignancy).\n\nGynecological examination and surgical history\nPhysical examination: No abdominal–pelvic mass detected.\n\nSpeculum examination: Healthy cervix observed.\n\nSurgical scars from previous left nephrectomy and cephalic duodenopancreatectomy were noted.\n\nA multidisciplinary staff meeting concluded that surgery was necessary. A laparotomy was performed via a midline incision below the umbilicus, revealing a well-defined solid cystic mass in the left adnexa. No ascites or signs of peritoneal carcinomatosis were present, and the right adnexa appeared normal, with no macroscopic signs of malignancy observed intraoperatively, including the absence of exocystic vegetations.\n\nCytology was performed along with left adnexectomy, and the specimen was sent for frozen section examination. The results were inconclusive, raising the possibility of borderline tumors or tumors specific to Von Hippel–Lindau syndrome. Considering the patient’s postmenopausal status, a right adnexectomy and total hysterectomy were performed.\n\nHistological examination later revealed bilateral clear-cell papillary cystadenomas of the Fallopian Tubes and broad ligament, characteristic of Von Hippel–Lindau disease (0.5 cm on the right side and 4 cm on the left side).The tumors consisted of tightly packed papillae with fibrous cores, covered by monolayered epithelium.\n\nThe immediate postoperative period was uneventful, and at the 1-month follow-up, no abnormalities were detected. The patient has since been followed up with every 4 months with normal pelvic ultrasounds. During these 2 years of follow-up, no complications have arisen, but the patient was recently readmitted to the neurosurgery department for recurrence of a brain tumor.",
    "diff_label_texts": "A 62-year-old white North African woman with Von Hippel–Lindau (VHL) disease diagnosed in 2021 developed several VHL-related tumors: a left petrous bone tumor, a left pheochromocytoma, left renal cell carcinoma, a multicystic right kidney, and pancreatic masses. She was treated with radiotherapy to the petrous bone lesion, left adrenalectomy, left nephrectomy, and cephalic duodenopancreatectomy for the pancreatic tumors. During surveillance, ultrasound and MRI showed a solid–cystic mass in the left adnexal (ovary/tube) region. Laparoscopy then identified cystic tumors in the mesosalpinx on both the right and left sides. She underwent hysterectomy with removal of both adnexa. Pathology confirmed bilateral clear-cell papillary cystadenomas of the mesosalpinx and broad ligament, a pattern consistent with VHL.",
    "summary": "A 62-year-old white North African woman diagnosed with Von Hippel-Lindau disease in 2021 presented with multiple manifestations, including a left petrous bone tumor, left pheochromocytoma, left renal cell carcinoma, multi-cystic right kidney, and pancreatic masses. She underwent various treatments, including radiotherapy, adrenalectomy, nephrectomy, and cephalic duodenopancreatectomy. Ultrasonographic and magnetic resonance imaging examinations revealed a solid cystic mass in the left adnexal region. Laparoscopy identified cystic tumors in the right and left mesosalpinx. Following a hysterectomy with bilateral adnexectomy, histological examination revealed bilateral clear-cell papillary cystadenomas of the mesosalpinx and broad ligament, consistent with Von Hippel-Lindau disease."
  },
  {
    "doc_id": 15,
    "label": "low_health_literacy",
    "fulltext": "A 62-year-old Tunisian Arab postmenopausal female diagnosed with Von Hippel–Lindau disease in 2021 presented with various manifestations related to the disease. She had a history of multiple surgeries, primarily for renal, adrenal, and pancreatic tumors, with incidental findings of ovarian masses.\n\nThe patient was asymptomatic from a gynecological standpoint, but primarily complained of headaches before undergoing brain surgery. She had no significant family or psychosocial history.\n\nHer surgical history included\n2021: A non-operable tumor (6 cm) of the left petrous bone endolymphatic sac, managed with radiotherapy.\n\n2021: Left adrenalectomy for a 6 cm pheochromocytoma. Pathological examination revealed pheochromocytoma.\n\n2021: Left nephrectomy for a ruptured left renal tumor. Microscopy showed multifocal clear-cell renal carcinoma of nuclear grade 2.\n\n2022: Cephalic duodenopancreatectomy for a mass in the pancreas. Histological examination confirmed three serous cystadenomas and two well-differentiated neuroendocrine tumors.\n\nIn January 2021, during postoperative surveillance with an abdominal–pelvic computed tomography (CT) scan, a 4 cm solid cystic left adnexal mass was incidentally discovered, which raised suspicion of malignancy. The mass was confirmed by transvaginal ultrasound and pelvic MRI, classified as Ovarian-Adnexal Reporting and Data System (O-RADS) 5 (high suspicion for malignancy).\n\nGynecological examination and surgical history\nPhysical examination: No abdominal–pelvic mass detected.\n\nSpeculum examination: Healthy cervix observed.\n\nSurgical scars from previous left nephrectomy and cephalic duodenopancreatectomy were noted.\n\nA multidisciplinary staff meeting concluded that surgery was necessary. A laparotomy was performed via a midline incision below the umbilicus, revealing a well-defined solid cystic mass in the left adnexa. No ascites or signs of peritoneal carcinomatosis were present, and the right adnexa appeared normal, with no macroscopic signs of malignancy observed intraoperatively, including the absence of exocystic vegetations.\n\nCytology was performed along with left adnexectomy, and the specimen was sent for frozen section examination. The results were inconclusive, raising the possibility of borderline tumors or tumors specific to Von Hippel–Lindau syndrome. Considering the patient’s postmenopausal status, a right adnexectomy and total hysterectomy were performed.\n\nHistological examination later revealed bilateral clear-cell papillary cystadenomas of the Fallopian Tubes and broad ligament, characteristic of Von Hippel–Lindau disease (0.5 cm on the right side and 4 cm on the left side).The tumors consisted of tightly packed papillae with fibrous cores, covered by monolayered epithelium.\n\nThe immediate postoperative period was uneventful, and at the 1-month follow-up, no abnormalities were detected. The patient has since been followed up with every 4 months with normal pelvic ultrasounds. During these 2 years of follow-up, no complications have arisen, but the patient was recently readmitted to the neurosurgery department for recurrence of a brain tumor.",
    "diff_label_texts": "This story is about a 62-year-old white North African woman. She was diagnosed in 2021 with a rare condition called Von Hippel–Lindau disease. This condition caused growths in several parts of her body. She had a tumor in a bone near her left ear. She had a tumor in the left adrenal gland, which sits above the kidney. She had cancer in her left kidney. Her right kidney had many cysts. She also had growths in her pancreas. She received several treatments. She had radiation treatment. She had surgery to remove the left adrenal gland. She had surgery to remove the left kidney. She had major surgery on the pancreas and nearby small intestine. Later, ultrasound and MRI scans showed a lump with both fluid and solid parts near the left ovary and tube. Keyhole surgery looked inside the pelvis. It found cyst-type tumors in the thin support tissue next to both fallopian tubes. Doctors then removed the uterus and both ovaries and tubes. The lab checked the tissue. It showed tumors of the same type on both sides in the thin support tissue around the tubes and the uterus. These findings fit with Von Hippel–Lindau disease.",
    "summary": "A 62-year-old white North African woman diagnosed with Von Hippel-Lindau disease in 2021 presented with multiple manifestations, including a left petrous bone tumor, left pheochromocytoma, left renal cell carcinoma, multi-cystic right kidney, and pancreatic masses. She underwent various treatments, including radiotherapy, adrenalectomy, nephrectomy, and cephalic duodenopancreatectomy. Ultrasonographic and magnetic resonance imaging examinations revealed a solid cystic mass in the left adnexal region. Laparoscopy identified cystic tumors in the right and left mesosalpinx. Following a hysterectomy with bilateral adnexectomy, histological examination revealed bilateral clear-cell papillary cystadenomas of the mesosalpinx and broad ligament, consistent with Von Hippel-Lindau disease."
  },
  {
    "doc_id": 16,
    "label": "intermediate_health_literacy",
    "fulltext": "The patient was a 59-year-old Japanese man with a 28-year history of type 1 diabetes. He visited our hospital monthly for management of diabetes with intensive therapy employing multiple-dose insulin injections. His height and body weight were 168 cm and 52 kg (body mass index: 18.4 kg/m2), respectively. He showed depleted insulin secretion (serum C-peptide level was below the limit of detection), such that his blood glucose levels fluctuated severely, and his hemoglobin A1c (HbA1c) level was around 9.0% despite intensive insulin therapy. He had been diagnosed with asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years before the current presentation but had declined follow-up for the AR. He had never undergone surgery nor the implantation of any prosthetic devices.\n\nEight days after his regular hospital visit, he visited an emergency clinic complaining of breathing difficulty and had a fever above 38℃. Until that day, he had not noticed any fever, chills, weakness, or any other symptoms. His blood pressure and pulse rate were 192/82 mmHg and 118/min, respectively. He showed orthopnea, and his oxygen saturation (SpO2) was 80%. He was transported to the emergency department of our hospital. A physical examination revealed a Levine 3/6 systolic murmur, although his cardiac murmur had not been checked at regular hospital visits. No physical findings suggesting IE, such as Osler nodes, Janeway lesions, or conjunctival petechiae, were recognized. His white blood cell (WBC) count was markedly increased to 20,800 /μL, and his C-reactive protein (CRP) was elevated to 6.06 mg/dL. Serum creatine phosphokinase MB was within the normal range, at 6.0 IU/L, and troponin T was negative. Chest X-ray showed pulmonary congestion with cardiac enlargement (cardiothoracic ratio: 55%). Electrocardiography revealed ST elevation on V1-V4, but emergency echocardiography showed no dysfunction of cardiac contractility. He was diagnosed with acute heart failure due to valvular disease, and treatment with non-invasive positive pressure ventilation and nitrates was initiated.\n\nAfter hospital admission, a detailed examination by transthoracic echocardiography showed severe aortic regurgitation, severe mitral regurgitation, and a mobile vegetation on the mitral valve. Transesophageal echocardiography revealed a 16.5×6-mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings raised strong suspicion of NVE. In this case, head computed tomography (CT) and magnetic resonance imaging revealed no cerebral infarction or hemorrhaging, although a mobile vegetation was detected.\n\nOn reviewing the clinical course until hospitalization, we noted that at the visit four months before admission, his WBC count had been slightly elevated. The following month, his albumin (Alb) level decreased to 3.0 g/dL, and his hemoglobin (Hb) level had shown a gradual decline over the 2 months prior to admission. During this period, he had experienced a 4-kg weight loss. Esophagogastroduodenoscopy and whole-body CT were performed, but no abnormalities were detected. One month later, he had regained some weight, and the laboratory findings had nearly normalized, except for a slightly elevated CRP level (0.54 mg/dL). At the last visit (8 days before admission), his WBC count had again risen to 9,300 /μL, while his Hb and Alb levels had again decreased to 13.1 g/dL and 3.0 g/dL, respectively. Furthermore, his CRP level had increased to 4.18 mg/dL. At that time, his diastolic blood pressure has shown an obvious decrease. Thus far, he had not experienced a fever or any symptoms other than weight loss. We suspected diseases of infectious and/or malignant origin and initiated comprehensive examinations to identify the source of his clinical findings.\n\nAfter heart failure treatment had been started, his clinical symptoms showed rapid improvement, and his hemodynamic stability was maintained during the first six hours. He initially received empirical intravenous antibiotic therapy consisting of 12 g/day of ampicillin sulbactam (ABPC/S) and 120 mg/day of gentamycin (GM). Three blood culture sets were obtained on the admission, and all were positive for S. warneri [minimum inhibitory concentration (MIC) to ABPC/S ≤8 μg/mL; MIC to GM ≤1 μg/mL; MIC to cefazolin (CEZ) ≤2 μg/mL]. Thus, IE caused by this organism was diagnosed.\n\nAccording to the clinical guideline established by the Japanese Circulation Society, emergency surgery is generally recommended for heart failure of NYHA III to IV or urgent surgery for NVE mobile vegetation exceeding 10 mm and severe valve dysfunction. In this case, however, his heart failure was successfully improved. Based on the guideline, the risk of embolism was considered to have been reduced by the administration of appropriate antibiotic therapy. In addition, the patient had type 1 diabetes, and his glycemic control was so poor that we were concerned that double-valve surgery would be a high-risk procedure. Therefore, we planned elective surgery after sufficient control of both infection and diabetes.\n\nBased on the blood culture results, the antibiotic regimen was switched to 6 g/day of CEZ. A detailed dental examination revealed no abnormalities, such as periodontitis. After four weeks of antibiotic therapy, he underwent surgical therapy. His aortic valve was found to be bicuspid, and the aortic and mitral annuli were intact without abscess formation. Large vegetations were exenterated, and the mitral and aortic valves were both replaced with mechanical valves. He experienced no postoperative complications and was discharged on the 22nd day after the operation without apparent embolism. He has not had any recurrence in over two years since the operation.",
    "diff_label_texts": "A 59-year-old man with long-standing type 1 diabetes presented with acute heart failure. An echocardiogram showed large vegetations on the mitral and aortic valves. Blood cultures were positive for Staphylococcus warneri, a coagulase‑negative staphylococcus commonly found on the skin. He was diagnosed with native valve endocarditis. After medical stabilization, he ultimately underwent replacement of both the mitral and aortic valves. In retrospect, mild laboratory abnormalities and several months of weight loss beginning about four months earlier were likely early signs of endocarditis. He had no history of immunosuppressive therapy and no implanted medical devices.",
    "summary": "A 59-year-old man with type 1 diabetes presented with heart failure. Echocardiography showed large vegetations on the mitral and aortic valves. Blood bacterial culture was positive for Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS) family member. He was diagnosed with native valve endocarditis (NVE) induced by the resident bacteria and ultimately underwent double valve replacement. Retrospectively, slight laboratory data abnormalities and weight loss beginning four months before may have been signs of NVE. He had no history of immunosuppressive therapies or medical device implantation. "
  },
  {
    "doc_id": 16,
    "label": "low_health_literacy",
    "fulltext": "The patient was a 59-year-old Japanese man with a 28-year history of type 1 diabetes. He visited our hospital monthly for management of diabetes with intensive therapy employing multiple-dose insulin injections. His height and body weight were 168 cm and 52 kg (body mass index: 18.4 kg/m2), respectively. He showed depleted insulin secretion (serum C-peptide level was below the limit of detection), such that his blood glucose levels fluctuated severely, and his hemoglobin A1c (HbA1c) level was around 9.0% despite intensive insulin therapy. He had been diagnosed with asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years before the current presentation but had declined follow-up for the AR. He had never undergone surgery nor the implantation of any prosthetic devices.\n\nEight days after his regular hospital visit, he visited an emergency clinic complaining of breathing difficulty and had a fever above 38℃. Until that day, he had not noticed any fever, chills, weakness, or any other symptoms. His blood pressure and pulse rate were 192/82 mmHg and 118/min, respectively. He showed orthopnea, and his oxygen saturation (SpO2) was 80%. He was transported to the emergency department of our hospital. A physical examination revealed a Levine 3/6 systolic murmur, although his cardiac murmur had not been checked at regular hospital visits. No physical findings suggesting IE, such as Osler nodes, Janeway lesions, or conjunctival petechiae, were recognized. His white blood cell (WBC) count was markedly increased to 20,800 /μL, and his C-reactive protein (CRP) was elevated to 6.06 mg/dL. Serum creatine phosphokinase MB was within the normal range, at 6.0 IU/L, and troponin T was negative. Chest X-ray showed pulmonary congestion with cardiac enlargement (cardiothoracic ratio: 55%). Electrocardiography revealed ST elevation on V1-V4, but emergency echocardiography showed no dysfunction of cardiac contractility. He was diagnosed with acute heart failure due to valvular disease, and treatment with non-invasive positive pressure ventilation and nitrates was initiated.\n\nAfter hospital admission, a detailed examination by transthoracic echocardiography showed severe aortic regurgitation, severe mitral regurgitation, and a mobile vegetation on the mitral valve. Transesophageal echocardiography revealed a 16.5×6-mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings raised strong suspicion of NVE. In this case, head computed tomography (CT) and magnetic resonance imaging revealed no cerebral infarction or hemorrhaging, although a mobile vegetation was detected.\n\nOn reviewing the clinical course until hospitalization, we noted that at the visit four months before admission, his WBC count had been slightly elevated. The following month, his albumin (Alb) level decreased to 3.0 g/dL, and his hemoglobin (Hb) level had shown a gradual decline over the 2 months prior to admission. During this period, he had experienced a 4-kg weight loss. Esophagogastroduodenoscopy and whole-body CT were performed, but no abnormalities were detected. One month later, he had regained some weight, and the laboratory findings had nearly normalized, except for a slightly elevated CRP level (0.54 mg/dL). At the last visit (8 days before admission), his WBC count had again risen to 9,300 /μL, while his Hb and Alb levels had again decreased to 13.1 g/dL and 3.0 g/dL, respectively. Furthermore, his CRP level had increased to 4.18 mg/dL. At that time, his diastolic blood pressure has shown an obvious decrease. Thus far, he had not experienced a fever or any symptoms other than weight loss. We suspected diseases of infectious and/or malignant origin and initiated comprehensive examinations to identify the source of his clinical findings.\n\nAfter heart failure treatment had been started, his clinical symptoms showed rapid improvement, and his hemodynamic stability was maintained during the first six hours. He initially received empirical intravenous antibiotic therapy consisting of 12 g/day of ampicillin sulbactam (ABPC/S) and 120 mg/day of gentamycin (GM). Three blood culture sets were obtained on the admission, and all were positive for S. warneri [minimum inhibitory concentration (MIC) to ABPC/S ≤8 μg/mL; MIC to GM ≤1 μg/mL; MIC to cefazolin (CEZ) ≤2 μg/mL]. Thus, IE caused by this organism was diagnosed.\n\nAccording to the clinical guideline established by the Japanese Circulation Society, emergency surgery is generally recommended for heart failure of NYHA III to IV or urgent surgery for NVE mobile vegetation exceeding 10 mm and severe valve dysfunction. In this case, however, his heart failure was successfully improved. Based on the guideline, the risk of embolism was considered to have been reduced by the administration of appropriate antibiotic therapy. In addition, the patient had type 1 diabetes, and his glycemic control was so poor that we were concerned that double-valve surgery would be a high-risk procedure. Therefore, we planned elective surgery after sufficient control of both infection and diabetes.\n\nBased on the blood culture results, the antibiotic regimen was switched to 6 g/day of CEZ. A detailed dental examination revealed no abnormalities, such as periodontitis. After four weeks of antibiotic therapy, he underwent surgical therapy. His aortic valve was found to be bicuspid, and the aortic and mitral annuli were intact without abscess formation. Large vegetations were exenterated, and the mitral and aortic valves were both replaced with mechanical valves. He experienced no postoperative complications and was discharged on the 22nd day after the operation without apparent embolism. He has not had any recurrence in over two years since the operation.",
    "diff_label_texts": "A 59-year-old man with type 1 diabetes came to the hospital with heart failure. A heart ultrasound showed big clumps of germs stuck to two heart valves, the mitral and the aortic valves. His blood test grew a germ called Staphylococcus warneri. This is a kind of staph that usually lives on the skin and is normally harmless. Doctors found he had an infection on his own heart valves (native valve endocarditis). He later had surgery to replace both the mitral and the aortic valves. Looking back, small lab changes and weight loss that began about four months earlier may have been early warning signs. He had not been on immune-weakening medicines and did not have any implanted medical devices.",
    "summary": "A 59-year-old man with type 1 diabetes presented with heart failure. Echocardiography showed large vegetations on the mitral and aortic valves. Blood bacterial culture was positive for Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS) family member. He was diagnosed with native valve endocarditis (NVE) induced by the resident bacteria and ultimately underwent double valve replacement. Retrospectively, slight laboratory data abnormalities and weight loss beginning four months before may have been signs of NVE. He had no history of immunosuppressive therapies or medical device implantation. "
  },
  {
    "doc_id": 16,
    "label": "proficient_health_literacy",
    "fulltext": "The patient was a 59-year-old Japanese man with a 28-year history of type 1 diabetes. He visited our hospital monthly for management of diabetes with intensive therapy employing multiple-dose insulin injections. His height and body weight were 168 cm and 52 kg (body mass index: 18.4 kg/m2), respectively. He showed depleted insulin secretion (serum C-peptide level was below the limit of detection), such that his blood glucose levels fluctuated severely, and his hemoglobin A1c (HbA1c) level was around 9.0% despite intensive insulin therapy. He had been diagnosed with asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years before the current presentation but had declined follow-up for the AR. He had never undergone surgery nor the implantation of any prosthetic devices.\n\nEight days after his regular hospital visit, he visited an emergency clinic complaining of breathing difficulty and had a fever above 38℃. Until that day, he had not noticed any fever, chills, weakness, or any other symptoms. His blood pressure and pulse rate were 192/82 mmHg and 118/min, respectively. He showed orthopnea, and his oxygen saturation (SpO2) was 80%. He was transported to the emergency department of our hospital. A physical examination revealed a Levine 3/6 systolic murmur, although his cardiac murmur had not been checked at regular hospital visits. No physical findings suggesting IE, such as Osler nodes, Janeway lesions, or conjunctival petechiae, were recognized. His white blood cell (WBC) count was markedly increased to 20,800 /μL, and his C-reactive protein (CRP) was elevated to 6.06 mg/dL. Serum creatine phosphokinase MB was within the normal range, at 6.0 IU/L, and troponin T was negative. Chest X-ray showed pulmonary congestion with cardiac enlargement (cardiothoracic ratio: 55%). Electrocardiography revealed ST elevation on V1-V4, but emergency echocardiography showed no dysfunction of cardiac contractility. He was diagnosed with acute heart failure due to valvular disease, and treatment with non-invasive positive pressure ventilation and nitrates was initiated.\n\nAfter hospital admission, a detailed examination by transthoracic echocardiography showed severe aortic regurgitation, severe mitral regurgitation, and a mobile vegetation on the mitral valve. Transesophageal echocardiography revealed a 16.5×6-mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings raised strong suspicion of NVE. In this case, head computed tomography (CT) and magnetic resonance imaging revealed no cerebral infarction or hemorrhaging, although a mobile vegetation was detected.\n\nOn reviewing the clinical course until hospitalization, we noted that at the visit four months before admission, his WBC count had been slightly elevated. The following month, his albumin (Alb) level decreased to 3.0 g/dL, and his hemoglobin (Hb) level had shown a gradual decline over the 2 months prior to admission. During this period, he had experienced a 4-kg weight loss. Esophagogastroduodenoscopy and whole-body CT were performed, but no abnormalities were detected. One month later, he had regained some weight, and the laboratory findings had nearly normalized, except for a slightly elevated CRP level (0.54 mg/dL). At the last visit (8 days before admission), his WBC count had again risen to 9,300 /μL, while his Hb and Alb levels had again decreased to 13.1 g/dL and 3.0 g/dL, respectively. Furthermore, his CRP level had increased to 4.18 mg/dL. At that time, his diastolic blood pressure has shown an obvious decrease. Thus far, he had not experienced a fever or any symptoms other than weight loss. We suspected diseases of infectious and/or malignant origin and initiated comprehensive examinations to identify the source of his clinical findings.\n\nAfter heart failure treatment had been started, his clinical symptoms showed rapid improvement, and his hemodynamic stability was maintained during the first six hours. He initially received empirical intravenous antibiotic therapy consisting of 12 g/day of ampicillin sulbactam (ABPC/S) and 120 mg/day of gentamycin (GM). Three blood culture sets were obtained on the admission, and all were positive for S. warneri [minimum inhibitory concentration (MIC) to ABPC/S ≤8 μg/mL; MIC to GM ≤1 μg/mL; MIC to cefazolin (CEZ) ≤2 μg/mL]. Thus, IE caused by this organism was diagnosed.\n\nAccording to the clinical guideline established by the Japanese Circulation Society, emergency surgery is generally recommended for heart failure of NYHA III to IV or urgent surgery for NVE mobile vegetation exceeding 10 mm and severe valve dysfunction. In this case, however, his heart failure was successfully improved. Based on the guideline, the risk of embolism was considered to have been reduced by the administration of appropriate antibiotic therapy. In addition, the patient had type 1 diabetes, and his glycemic control was so poor that we were concerned that double-valve surgery would be a high-risk procedure. Therefore, we planned elective surgery after sufficient control of both infection and diabetes.\n\nBased on the blood culture results, the antibiotic regimen was switched to 6 g/day of CEZ. A detailed dental examination revealed no abnormalities, such as periodontitis. After four weeks of antibiotic therapy, he underwent surgical therapy. His aortic valve was found to be bicuspid, and the aortic and mitral annuli were intact without abscess formation. Large vegetations were exenterated, and the mitral and aortic valves were both replaced with mechanical valves. He experienced no postoperative complications and was discharged on the 22nd day after the operation without apparent embolism. He has not had any recurrence in over two years since the operation.",
    "diff_label_texts": "A 59-year-old Japanese man with a 28-year history of type 1 diabetes on intensive multiple-dose insulin therapy (BMI 18.4 kg/m2, undetectable C‑peptide, HbA1c ~9.0%) and remote, asymptomatic chronic severe (grade III) aortic regurgitation (diagnosed 16 years earlier without subsequent follow‑up) presented with acute decompensated heart failure. He had never undergone surgery or prosthetic device implantation and had no history of immunosuppressive therapies.\n\nEight days after a routine visit, he developed dyspnea and fever >38℃. On arrival: BP 192/82 mmHg, HR 118/min, orthopnea, SpO2 80%. Exam: Levine 3/6 systolic murmur; no Osler nodes, Janeway lesions, or conjunctival petechiae. Labs: WBC 20,800/μL, CRP 6.06 mg/dL, CK‑MB 6.0 IU/L, troponin T negative. CXR showed pulmonary congestion with cardiomegaly (CTR 55%). ECG had ST elevation in V1–V4, but emergent echocardiography showed no systolic dysfunction. He was diagnosed with acute heart failure due to valvular disease and treated with non‑invasive positive pressure ventilation and nitrates.\n\nTransthoracic echocardiography demonstrated severe aortic regurgitation and severe mitral regurgitation with a mobile mitral vegetation. Transesophageal echocardiography identified a 16.5×6‑mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5‑mm nonmobile vegetation on the noncoronary cusp of the aortic valve, raising strong suspicion for native valve endocarditis (NVE). Head CT and MRI showed no cerebral infarction or hemorrhage.\n\nRetrospective review revealed subtle abnormalities starting four months pre‑admission: mildly elevated WBC, albumin decreased to 3.0 g/dL the following month, and gradual hemoglobin decline over two months, with a 4‑kg weight loss. EGD and whole‑body CT were unrevealing. He partially regained weight and labs nearly normalized except for a CRP of 0.54 mg/dL. At the last pre‑admission visit (8 days prior), WBC was 9,300/μL, Hb 13.1 g/dL, Alb 3.0 g/dL, CRP 4.18 mg/dL, and diastolic BP had fallen; he remained afebrile and asymptomatic aside from weight loss.\n\nEmpiric antibiotics were initiated with ampicillin–sulbactam 12 g/day plus gentamicin 120 mg/day. Three admission blood culture sets all grew Staphylococcus warneri, a coagulase‑negative staphylococcus (CoNS) and resident skin flora (MICs: ABPC/S ≤8 μg/mL; GM ≤1 μg/mL; CEZ ≤2 μg/mL), confirming S. warneri IE. Per Japanese Circulation Society guidance, emergency surgery is generally recommended for NYHA III–IV heart failure or urgent surgery for NVE with mobile vegetation >10 mm and severe valve dysfunction. Because heart failure improved rapidly and appropriate antibiotics were started (reducing embolic risk), and given poorly controlled type 1 diabetes increasing operative risk, elective surgery was planned after stabilization of infection and glycemia. Antibiotics were narrowed to cefazolin 6 g/day; dental evaluation showed no periodontitis.\n\nAfter four weeks of antibiotics, surgery revealed a bicuspid aortic valve with intact aortic and mitral annuli and no abscess. Large vegetations were exenterated, and both valves were replaced with mechanical prostheses. The postoperative course was uneventful; he was discharged on postoperative day 22 without apparent embolism and has remained recurrence‑free for over two years. This case represents NVE due to the resident CoNS S. warneri in a patient without prosthetic material or immunosuppression, with prodromal laboratory abnormalities and weight loss evident up to four months before presentation.",
    "summary": "A 59-year-old man with type 1 diabetes presented with heart failure. Echocardiography showed large vegetations on the mitral and aortic valves. Blood bacterial culture was positive for Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS) family member. He was diagnosed with native valve endocarditis (NVE) induced by the resident bacteria and ultimately underwent double valve replacement. Retrospectively, slight laboratory data abnormalities and weight loss beginning four months before may have been signs of NVE. He had no history of immunosuppressive therapies or medical device implantation. "
  },
  {
    "doc_id": 17,
    "label": "intermediate_health_literacy",
    "fulltext": "A 27-year-old woman with multiple colorectal cancers on a background of FAP was presented to our department. Notably, a large lesion was detected in the ascending, transverse, and sigmoid colon and the upper rectum, and pathological examination confirmed some of them as adenocarcinoma. Preoperative computed tomography revealed multiple lymph node swellings along the inferior mesenteric artery (IMA) and middle colic artery, without any evidence of distant metastases. After a comprehensive evaluation by a multidisciplinary cancer board, we decided to perform TPC with lymph node dissection of the entire colorectal region, using the Hugo RAS system as a surgical device.\n\nRobot-assisted TPC using the Hugo RAS system was approved by the Evaluating Committee for Highly Difficult New Medical Technologies (approval number H-0051) and the Institutional Review Board at Kyoto University.\n\nUnder general anesthesia, the patient was placed in a lithotomy position with the arms tucked. After a 5-cm vertical skin incision was made at the umbilicus, a wound-protecting device was applied. After pneumoperitoneum, 4 robotic trocars and 2 assistant trocars were placed. The instruments used in robot-assisted TPC with Hugo were a camera, monopolar curved shears for the right hand, bipolar fenestrated forceps for the left hand, and Cadiere/double fenestrated forceps for the reserve arm. Robot-assisted TPC with Hugo consists of 3 distinct steps, followed by transanal specimen extraction, ileal pouch construction through a small laparotomy, and ileal pouch-anus anastomosis (IPAA). Two table positions, Trendelenburg and flat, were required, each with specific docking tilts but the same angles of the arm carts throughout the robotic procedure. The detailed operative procedure is presented in Supplementary Videos.\n\nStep 1: Ascending colon complete mesocolic excision (CME)\n\nThe ascending colon CME from the caudal approach proceeded until the completion of the hepatic flexure mobilization (Supplementary Video S1).\n\nStep 2: Central vessel ligation (CVL) of the IMA, descending colon CME, and total mesorectal excision (TME)\n\nAfter CVL of the IMA, descending colon CME proceeded until the completion of splenic flexure mobilization, followed by TME until the intersphincteric space was fully exposed (Supplementary Video S2).\n\nStep 3: CVL along the superior mesenteric artery (SMA)\n\nAfter undocking all the robotic arms, the patient was placed in a flat position. Then, CVL along the SMA was performed to ligate the ileocolic, right colic, and middle colic vessels (Supplementary Video S3). The final step of this procedure was the ligation of the inferior mesenteric vein (IMV) at its root, which was exposed in Step 2.\n\nTransanal and small laparotomy procedures\nAfter transection of the terminal ileum, we extracted the specimen transanally by excising the rectal mucosa entirely from just below the dentate line because of multiple adenomas in the anal canal. After constructing the ileal pouch through the small umbilical incision and confirming that the ileal pouch could reach the bottom of the anal canal for anastomosis, transanal hand-sewn IPAA was performed. A diverting ileostomy was not performed.\n\nAll 3 steps were completed without conversion to open surgery. After undocking Hugo when we finished Step 3, we performed a laparoscopy to confirm hemostasis, specimen extraction, and appropriate anastomosis. The operative time was 632 min (36 min for Step 1, 160 min for Step 2, 188 min for Step 3, and 248 min for other procedures such as positioning, docking, specimen extraction, and anastomosis), with a minimal intraoperative estimated blood loss of 20 mL. The patient exhibited an uneventful postoperative recovery, with gas passage and initiation of liquid nutrition on postoperative day 1 (POD 1) and a solid diet on POD 3 with a functional ileal pouch and satisfactory anal function. Pathological examination revealed 2 sigmoid colon cancers (S1, Type 0-Ip, 55 × 50 mm, tub1, T1b, ly0, v0; S2, Type 0-Isp, 55 × 50 mm, tub1, Tis, ly0, v0) and 1 rectal cancer (R1, Type 0-Ip, 40 × 35 mm, tub1, Tis, ly0, v0). It also revealed 18 out of 89 positive lymph nodes, all of which belonged to the sigmoid colon and rectosigmoid lesions (stations #241, 242, and 251), resulting in UICC pT1bN2b stage.",
    "diff_label_texts": "A 27-year-old woman with familial adenomatous polyposis and multiple colorectal cancers underwent robot-assisted total proctocolectomy with complete lymph node dissection using the Hugo RAS system. The robotic work was organized into three steps: 1) in Trendelenburg position, ascending colon complete mesocolic excision up to the hepatic flexure; 2) descending colon complete mesocolic excision and total mesorectal excision with D3 lymph node dissection; and 3) in a flat position, central vessel ligation along the superior mesenteric artery. After undocking, the specimen was removed transanally. An ileal pouch was created through a small umbilical incision and then connected to the anus (ileal pouch–anal anastomosis). The operation lasted 632 minutes with minimal blood loss, and the postoperative course was uneventful.",
    "summary": "A 27-year-old woman with multiple colorectal cancers with a background of familial adenomatous polyposis underwent robot-assisted TPC, including lymph node dissection of the entire colorectal region using the Hugo RAS system. The robotic procedure was divided into 3 steps: 1) Trendelenburg position to perform ascending colon complete mesocolic excision (CME) to the hepatic flexure, 2) descending colon CME and total mesorectal excision with D3 lymph node dissection, and 3) flat position to perform central vessel ligation along the superior mesenteric artery. After undocking, the specimen was extracted transanally, and an ileal pouch was constructed from a small laparotomy at the umbilical incision, followed by ileal pouch-anal anastomosis. The operative time was 632 min, and the estimated blood loss was minimal. The postoperative period was uneventful."
  },
  {
    "doc_id": 18,
    "label": "intermediate_health_literacy",
    "fulltext": "A 65-year-old male presented with swelling and boutonniere deformity on the right middle finger for six months after a motorcycle accident on January 1st, 2023. Initially, he managed the injury with painkillers and did not seek medical attention. After six months of persistent symptoms, including an inability to fully extend the finger and noticeable edema, he sought treatment.\n\nClinical findings\nThe inspection of the right hand showed the presence of deformity with edema. The active range of motion (ROM) was impaired in PIP joint in digiti III of the right hand. The active ROM of PIP joint digiti III of the right hand 45–110 degrees. The passive ROM of PIP joint digiti III of the right hand within normal.\n\nDiagnostic assessment\nWe performed X-ray of the right hand AP/Lateral which showed there are no abnormality in the bone and we diagnosed the deformity from soft tissue which is central slip injury.\n\nSurgical technique\nA central slip defect reconstruction utilizing partial ulnar side of flexor digitorum superficial tendon was performed. Under anesthesia, the patient was positioned supine with a tourniquet applied to the upper arm. A midlateral incision was made on the ulnar aspect of the right middle phalanx, centered at the PIP joint. The incision extended dorsally in an oblique manner. A transverse incision was made over the MCP joint flexion crease, just proximal to the A1 pulley. The procedure involves identifying and protecting the ulnar digital neurovascular bundle, exposing the central slip and extensor tendon to the PIPJ, full-thickness dorsal flaps are elevated. Scar tissue and pseudotendinous tissue is identified and excised. The central slip cannot be repaired primarily, so the ulnar slip of the FDS tendon is used for reconstruction. The ulnar neurovascular bundle is mobilized to visualize the periosteal insertion of the A3 pulley.\n\nThe extensor tendon is mobilized and tenolyzed, followed by incision of the dorsal capsule of the PIP joint and removal of interposed tissue. The A3 pulley's periosteal insertion is incised longitudinally, and the PIP joint's volar capsule is incised longitudinally. The ulnar slip of the FDS tendon is identified and a 2–0 non-absorbable, monofilament suture is placed around it. A transverse incision is made at the MCP joint flexion crease, proximal to the A1 pulley revealing the flexor tendon sheath. The tendon sheath and A1 pulley are incised longitudinally. The FDS tendon is identified. The ulnar slip of the FDS tendon is isolated and transected to release the ulnar slip, avoiding entrapment or catching of the radial slip. The 2–0 suture that was placed around the ulnar slip at the level of the PIP joint is used to release distally based FDS tendon slip and deliver the ulnar slip of the FDS tendon distally.\n\nA 2.8-mm drill is used to create a vertically oriented bone tunnel dorsal to volar. An elevator is placed between the flexor digitorum profundus tendon, volar plate, and volar aspect of the base of the middle phalanx protecting the volar anatomic structures. The FDS tendon slip passes through the tunnel while maintaining the PIP joint in extension and reduced position. The FDS tendon slip passed through the intact proximal section of the central slip and extensor tendon. A tendon weaver completes a Pulvertaft weave, confirming the appropriate tension with the PIPJ in the reduced, full extension position. A 3–0 non-absorbable suture secures the pulvertaft weave. The margins of the capsule and central slip reconstruction are approximated across the PIP joint, and adhesions are released and the lateral bands mobilized.\n\nThe overall posture, stability, and motion with tenodesis assessed. All the incisions are copiously irrigated. The tourniquet is deflated and hemostasis is obtained. Capillary refill of all fingers is assessed. The skin is closed using horizontal mattress stiches. A sterile dressing is applied with an appropriately padded PIP joint extension splint to allow for early DIP joint and MCP joint motion.\n\nFollow-up and outcomes\nFirst follow-up was done 4 days after for wound treatment. The patient was given oral meloxicam 7,5 mg twice a day and doxycycline 100 mg twice a day for 3 days. The second follow-up was done 3 days after for wound treatment. After 2 weeks, we remove the back slab, remove the external suture and begin the active and passive ROM exercise. After 3 weeks, the wound was healed, and we found the ROM of PIP joint 0 to 90 degrees. And after a month, the patient came with improved ROM of PIP joint 0 to 100 degrees, and improved functional outcome. After 7 weeks of physical rehabilitation, patients already back to work with improve ROM of PIP joint 0 to 110 degrees. The function of the patient's right hand is evaluated with DASH score, which improves significantly from 50 to 4.2.",
    "diff_label_texts": "A 65-year-old man developed persistent swelling and a boutonniere deformity of the right middle finger after a motorcycle fall six months earlier. He could not fully extend the finger. On exam, the finger showed edema with flexion at the proximal interphalangeal (PIP) joint and hyperextension at the distal interphalangeal (DIP) joint. Active PIP range of motion (ROM) was 45–110 degrees. X‑rays of the right hand (AP/oblique) showed no bone injury, indicating a soft-tissue problem consistent with a central slip injury. The patient underwent reconstruction of the central slip using a partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. A PIP extension splint was used for 2 weeks. Active and passive PIP ROM exercises began after 2 weeks. One month after surgery, PIP ROM improved to 0–90 degrees, and by 2 months it returned to normal. Hand function, measured by the DASH score, improved markedly from 50 to 4.2.",
    "summary": "A 65-year-old male patient presented with swelling and boutonniere deformity on the digiti III of the right hand. The patient had previously fallen from a motorcycle, and the patient's right middle finger got was by a motorcycle six months ago. After the incident, the patient's right middle finger cannot be fully extended. The patient's right hand showed edema with flexion of the interphalangeal (PIP) joint and hyperextension of the distal interphalangeal (DIP) joint. The Range of Motion (ROM) of the PIP joint right middle finger was 45-110 degrees. The X-ray of the right hand AP/oblique showed no bone involvement in the deformity. The patient underwent central slip defect reconstruction utilizing the partial ulnar side of the flexor digitorum superficial tendon. A PIP joint extension splint was applied for 2 weeks. Active and passive exercise of the ROM of the PIP joint began after 2 weeks of PIP extension joint splinting. The patient's ROM of the PIP joint (0-90 degrees) significantly improved 1 month after surgery. The patient's ROM of the PIP joint returned to normal after 2 months after surgery. The function of the patient's right hand is evaluated with the DASH score, which improves significantly from 50 to 4.2."
  },
  {
    "doc_id": 18,
    "label": "proficient_health_literacy",
    "fulltext": "A 65-year-old male presented with swelling and boutonniere deformity on the right middle finger for six months after a motorcycle accident on January 1st, 2023. Initially, he managed the injury with painkillers and did not seek medical attention. After six months of persistent symptoms, including an inability to fully extend the finger and noticeable edema, he sought treatment.\n\nClinical findings\nThe inspection of the right hand showed the presence of deformity with edema. The active range of motion (ROM) was impaired in PIP joint in digiti III of the right hand. The active ROM of PIP joint digiti III of the right hand 45–110 degrees. The passive ROM of PIP joint digiti III of the right hand within normal.\n\nDiagnostic assessment\nWe performed X-ray of the right hand AP/Lateral which showed there are no abnormality in the bone and we diagnosed the deformity from soft tissue which is central slip injury.\n\nSurgical technique\nA central slip defect reconstruction utilizing partial ulnar side of flexor digitorum superficial tendon was performed. Under anesthesia, the patient was positioned supine with a tourniquet applied to the upper arm. A midlateral incision was made on the ulnar aspect of the right middle phalanx, centered at the PIP joint. The incision extended dorsally in an oblique manner. A transverse incision was made over the MCP joint flexion crease, just proximal to the A1 pulley. The procedure involves identifying and protecting the ulnar digital neurovascular bundle, exposing the central slip and extensor tendon to the PIPJ, full-thickness dorsal flaps are elevated. Scar tissue and pseudotendinous tissue is identified and excised. The central slip cannot be repaired primarily, so the ulnar slip of the FDS tendon is used for reconstruction. The ulnar neurovascular bundle is mobilized to visualize the periosteal insertion of the A3 pulley.\n\nThe extensor tendon is mobilized and tenolyzed, followed by incision of the dorsal capsule of the PIP joint and removal of interposed tissue. The A3 pulley's periosteal insertion is incised longitudinally, and the PIP joint's volar capsule is incised longitudinally. The ulnar slip of the FDS tendon is identified and a 2–0 non-absorbable, monofilament suture is placed around it. A transverse incision is made at the MCP joint flexion crease, proximal to the A1 pulley revealing the flexor tendon sheath. The tendon sheath and A1 pulley are incised longitudinally. The FDS tendon is identified. The ulnar slip of the FDS tendon is isolated and transected to release the ulnar slip, avoiding entrapment or catching of the radial slip. The 2–0 suture that was placed around the ulnar slip at the level of the PIP joint is used to release distally based FDS tendon slip and deliver the ulnar slip of the FDS tendon distally.\n\nA 2.8-mm drill is used to create a vertically oriented bone tunnel dorsal to volar. An elevator is placed between the flexor digitorum profundus tendon, volar plate, and volar aspect of the base of the middle phalanx protecting the volar anatomic structures. The FDS tendon slip passes through the tunnel while maintaining the PIP joint in extension and reduced position. The FDS tendon slip passed through the intact proximal section of the central slip and extensor tendon. A tendon weaver completes a Pulvertaft weave, confirming the appropriate tension with the PIPJ in the reduced, full extension position. A 3–0 non-absorbable suture secures the pulvertaft weave. The margins of the capsule and central slip reconstruction are approximated across the PIP joint, and adhesions are released and the lateral bands mobilized.\n\nThe overall posture, stability, and motion with tenodesis assessed. All the incisions are copiously irrigated. The tourniquet is deflated and hemostasis is obtained. Capillary refill of all fingers is assessed. The skin is closed using horizontal mattress stiches. A sterile dressing is applied with an appropriately padded PIP joint extension splint to allow for early DIP joint and MCP joint motion.\n\nFollow-up and outcomes\nFirst follow-up was done 4 days after for wound treatment. The patient was given oral meloxicam 7,5 mg twice a day and doxycycline 100 mg twice a day for 3 days. The second follow-up was done 3 days after for wound treatment. After 2 weeks, we remove the back slab, remove the external suture and begin the active and passive ROM exercise. After 3 weeks, the wound was healed, and we found the ROM of PIP joint 0 to 90 degrees. And after a month, the patient came with improved ROM of PIP joint 0 to 100 degrees, and improved functional outcome. After 7 weeks of physical rehabilitation, patients already back to work with improve ROM of PIP joint 0 to 110 degrees. The function of the patient's right hand is evaluated with DASH score, which improves significantly from 50 to 4.2.",
    "diff_label_texts": "A 65-year-old male presented with six months of swelling and boutonniere deformity of the right digit III following a motorcycle accident on January 1, 2023. He initially self-managed with analgesics and did not seek care. He reported inability to fully extend the right middle finger. Examination demonstrated edema and a boutonniere posture (PIP flexion, DIP hyperextension). Active PIP ROM was 45–110 degrees, with passive PIP ROM within normal limits. Radiographs of the right hand (AP/lateral) revealed no osseous pathology, supporting a soft-tissue etiology consistent with a central slip injury. \n\nSurgical technique: Central slip defect reconstruction was performed using the partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. Under anesthesia and tourniquet control in the supine position, a midlateral incision was made on the ulnar aspect of the middle phalanx centered at the PIP joint with dorsal oblique extension, and a transverse incision was made over the MCP flexion crease proximal to the A1 pulley. The ulnar digital neurovascular bundle was identified and protected. Full-thickness dorsal flaps were elevated to expose the central slip and extensor mechanism to the PIPJ. Scar and pseudotendinous tissue were excised. The central slip was not amenable to primary repair; therefore, the ulnar slip of the FDS was selected for reconstruction. The ulnar neurovascular bundle was mobilized to visualize the periosteal insertion of the A3 pulley. The extensor tendon was mobilized and tenolyzed; the dorsal PIP capsule was incised with removal of interposed tissue. The A3 pulley periosteal insertion and the volar capsule of the PIP joint were incised longitudinally. A 2–0 non-absorbable monofilament suture was placed around the ulnar FDS slip at the PIP level. Through the proximal incision, the flexor sheath and A1 pulley were incised longitudinally to expose the FDS; the ulnar slip was isolated and transected, preserving the radial slip. The previously placed 2–0 suture facilitated delivery of the distally based ulnar FDS slip distally. A 2.8‑mm dorsal-to-volar bone tunnel was drilled at the base of the middle phalanx; an elevator protected the FDP, volar plate, and volar structures. With the PIP reduced in full extension, the FDS slip was passed through the tunnel and routed through the intact proximal segment of the central slip/extensor tendon. A tendon weaver completed a Pulvertaft weave under appropriate tension with the PIP in full extension and reduction, secured with 3–0 non-absorbable suture. The capsule and central slip reconstruction margins were approximated; adhesions were released and lateral bands mobilized. Tenodesis effect, posture, stability, and motion were assessed. Wounds were irrigated, the tourniquet deflated, hemostasis obtained, and capillary refill confirmed. Skin was closed with horizontal mattress sutures. A sterile dressing and a well-padded PIP extension splint were applied to allow early DIP and MCP motion.\n\nPostoperative course: First wound check at postoperative day 4; the patient received meloxicam 7.5 mg PO BID and doxycycline 100 mg PO BID for 3 days. A second wound visit occurred 3 days later. At 2 weeks, the back slab and external sutures were removed, and active and passive PIP ROM exercises were initiated. By 3 weeks, the wound had healed and PIP ROM was 0–90 degrees. At 1 month, PIP ROM improved to 0–100 degrees, with continued functional gains. After 7 weeks of rehabilitation, he returned to work with PIP ROM 0–110 degrees. Overall function improved substantially, with the DASH score decreasing from 50 to 4.2.\n\nInterpretation: Clinical and radiographic findings were concordant with a chronic central slip injury producing boutonniere deformity (PIP flexion, DIP hyperextension due to dorsal apparatus disruption and volar migration of lateral bands). Reconstruction using an ulnar FDS slip via bone tunnel and Pulvertaft weave restored PIP extension and yielded progressive ROM gains and marked functional recovery.",
    "summary": "A 65-year-old male patient presented with swelling and boutonniere deformity on the digiti III of the right hand. The patient had previously fallen from a motorcycle, and the patient's right middle finger got was by a motorcycle six months ago. After the incident, the patient's right middle finger cannot be fully extended. The patient's right hand showed edema with flexion of the interphalangeal (PIP) joint and hyperextension of the distal interphalangeal (DIP) joint. The Range of Motion (ROM) of the PIP joint right middle finger was 45-110 degrees. The X-ray of the right hand AP/oblique showed no bone involvement in the deformity. The patient underwent central slip defect reconstruction utilizing the partial ulnar side of the flexor digitorum superficial tendon. A PIP joint extension splint was applied for 2 weeks. Active and passive exercise of the ROM of the PIP joint began after 2 weeks of PIP extension joint splinting. The patient's ROM of the PIP joint (0-90 degrees) significantly improved 1 month after surgery. The patient's ROM of the PIP joint returned to normal after 2 months after surgery. The function of the patient's right hand is evaluated with the DASH score, which improves significantly from 50 to 4.2."
  },
  {
    "doc_id": 19,
    "label": "intermediate_health_literacy",
    "fulltext": "A 23-year-old male patient presented to the emergency department with a sudden onset of severe frontal headache lasting for 2 h. He experienced associated symptoms of nausea, vomiting, and chest heaviness. He has a unremarkable medical record and denies the use of illicit drugs. However, he is a smoker with a history of 23 pack-years but does not consume alcohol.\n\nOn physical examination, the young male appeared distressed but was fully conscious and oriented to time, place, and person. Chest auscultation revealed normal vesicular breathing sounds, while cardiovascular and abdominal examinations were inconclusive. Neurological examinations demonstrated neck stiffness, dilated pupils reactive to light, normal plantar reflexes, and no focal neurological deficits.\n\nHis vital signs were as follows: blood pressure 178/103 mmHg, respiratory rate 26 breaths/min, temperature 38.9°C, heart rate 87 beats/min, and oxygen saturation of 94%.\n\nEmergency tests were initiated. An ECG revealed ST segment elevation >2 mm in leads V2-V5, consistent with STEMI as the top of our differential diagnosis, requiring confirmation by cardiac markers. With prompt referral to a tertiary cardiac centre implemented, the patient received a 300 mg aspirin load while being transferred to the catheter lab. Troponin levels were significantly elevated at 1.48 mg/dl (normal <0.16 mg/dl).\n\nPercutaneous coronary intervention was performed via the femoral artery, and the result showed normal coronary arteries with thrombolysis in myocardial infarction (TIMI) flow grade of 3.\n\nHis ECG after coronary angiography revealed normal sinus rhythm with left ventricular hypertrophy LVH. An echocardiogram was performed, revealing normal ventricular function with no regional wall motion abnormalities (RWMA).\n\nFollowing coronary intervention, he was admitted to the medical ward for further assessment and investigation. Blood samples were drawn for a complete blood count, random blood sugar, renal function tests, and CRP. The results revealed lymphocytosis and mildly elevated CRP.\n\nWe proceeded further with CT brain to exclude serious cause of headache. His brain CT showed cisternal subarachnoid haemorrhage SAH with extension anterior to the right temporal lobe. Abdominal ultrasound screening was performed to rule out polycystic kidney disease which was negative and cerebral CT angiography was scheduled to exclude cerebral aneurysm Nimodipine 60 mg every 4 h was initiated, with a target blood pressure of 160/100 mmHg.\n\nOn the second day, his condition suddenly deteriorated, culminating with cardiac arrest. Therefore, cardiopulmonary resuscitation (CPR), resulting in a Glasgow Coma Scale score (GCS) of 6. The patient was subsequently, intubated and placed on mechanical ventilation in the Intensive Care Unit (ICU). Due to his unstable condition in the ICU, we could not perform a repeated CT brain scan or the planned cerebral CT angiography.\n\nOver the next 7 days, we diligently monitored him with a strict multidisciplinary team. A nasogastric tube was inserted for feeding and fluid replacement. His medications included intravenous fluids, antibiotics, proton pump inhibitors, and nimodipine.\n\nOn the 8th day, he suddenly developed ventricular fibrillation, and despite CPR with more than five defibrillations, we were unable to revive him and death was the final outcome.39734686",
    "diff_label_texts": "A 23-year-old man came to the emergency department with a sudden severe headache, nausea, vomiting, and chest heaviness. His initial vital signs showed high blood pressure and a fast breathing rate. An emergency ECG showed a heart attack pattern (STEMI), so he was urgently sent for percutaneous coronary intervention; the angiogram revealed normal coronary arteries. Further evaluation with a brain CT identified a cisternal subarachnoid hemorrhage (bleeding around the brain). Despite coordinated care by multiple teams, his condition rapidly worsened, leading to cardiac arrest and death.",
    "summary": "We present a case detailing the diagnostic challenges of a 23-year-old male presenting with a sudden severe headache, nausea, vomiting, and chest heaviness. Initial evaluation showed elevated blood pressure and respiratory rate. An emergency electrocardiogram (ECG) indicated ST-segment elevation myocardial infarction (STEMI), leading to immediate referral for percutaneous coronary intervention, which revealed normal coronary arteries. Further investigations identified a cisternal subarachnoid haemorrhage (SAH) on CT brain imaging. Despite multidisciplinary management, the patient's condition rapidly deteriorated, resulting in cardiac arrest and mortality."
  },
  {
    "doc_id": 19,
    "label": "low_health_literacy",
    "fulltext": "A 23-year-old male patient presented to the emergency department with a sudden onset of severe frontal headache lasting for 2 h. He experienced associated symptoms of nausea, vomiting, and chest heaviness. He has a unremarkable medical record and denies the use of illicit drugs. However, he is a smoker with a history of 23 pack-years but does not consume alcohol.\n\nOn physical examination, the young male appeared distressed but was fully conscious and oriented to time, place, and person. Chest auscultation revealed normal vesicular breathing sounds, while cardiovascular and abdominal examinations were inconclusive. Neurological examinations demonstrated neck stiffness, dilated pupils reactive to light, normal plantar reflexes, and no focal neurological deficits.\n\nHis vital signs were as follows: blood pressure 178/103 mmHg, respiratory rate 26 breaths/min, temperature 38.9°C, heart rate 87 beats/min, and oxygen saturation of 94%.\n\nEmergency tests were initiated. An ECG revealed ST segment elevation >2 mm in leads V2-V5, consistent with STEMI as the top of our differential diagnosis, requiring confirmation by cardiac markers. With prompt referral to a tertiary cardiac centre implemented, the patient received a 300 mg aspirin load while being transferred to the catheter lab. Troponin levels were significantly elevated at 1.48 mg/dl (normal <0.16 mg/dl).\n\nPercutaneous coronary intervention was performed via the femoral artery, and the result showed normal coronary arteries with thrombolysis in myocardial infarction (TIMI) flow grade of 3.\n\nHis ECG after coronary angiography revealed normal sinus rhythm with left ventricular hypertrophy LVH. An echocardiogram was performed, revealing normal ventricular function with no regional wall motion abnormalities (RWMA).\n\nFollowing coronary intervention, he was admitted to the medical ward for further assessment and investigation. Blood samples were drawn for a complete blood count, random blood sugar, renal function tests, and CRP. The results revealed lymphocytosis and mildly elevated CRP.\n\nWe proceeded further with CT brain to exclude serious cause of headache. His brain CT showed cisternal subarachnoid haemorrhage SAH with extension anterior to the right temporal lobe. Abdominal ultrasound screening was performed to rule out polycystic kidney disease which was negative and cerebral CT angiography was scheduled to exclude cerebral aneurysm Nimodipine 60 mg every 4 h was initiated, with a target blood pressure of 160/100 mmHg.\n\nOn the second day, his condition suddenly deteriorated, culminating with cardiac arrest. Therefore, cardiopulmonary resuscitation (CPR), resulting in a Glasgow Coma Scale score (GCS) of 6. The patient was subsequently, intubated and placed on mechanical ventilation in the Intensive Care Unit (ICU). Due to his unstable condition in the ICU, we could not perform a repeated CT brain scan or the planned cerebral CT angiography.\n\nOver the next 7 days, we diligently monitored him with a strict multidisciplinary team. A nasogastric tube was inserted for feeding and fluid replacement. His medications included intravenous fluids, antibiotics, proton pump inhibitors, and nimodipine.\n\nOn the 8th day, he suddenly developed ventricular fibrillation, and despite CPR with more than five defibrillations, we were unable to revive him and death was the final outcome.39734686",
    "diff_label_texts": "A 23-year-old man came to the emergency room with a sudden, very bad headache. He also felt sick, threw up, and felt heavy pressure in his chest. His blood pressure was high and he was breathing fast. A quick heart test looked like a major heart attack. He was rushed for a procedure to check and open the heart arteries. The heart arteries looked normal. A head CT scan then showed bleeding in the space around his brain. A team of specialists cared for him, but he got worse quickly. He went into cardiac arrest and died.",
    "summary": "We present a case detailing the diagnostic challenges of a 23-year-old male presenting with a sudden severe headache, nausea, vomiting, and chest heaviness. Initial evaluation showed elevated blood pressure and respiratory rate. An emergency electrocardiogram (ECG) indicated ST-segment elevation myocardial infarction (STEMI), leading to immediate referral for percutaneous coronary intervention, which revealed normal coronary arteries. Further investigations identified a cisternal subarachnoid haemorrhage (SAH) on CT brain imaging. Despite multidisciplinary management, the patient's condition rapidly deteriorated, resulting in cardiac arrest and mortality."
  },
  {
    "doc_id": 19,
    "label": "proficient_health_literacy",
    "fulltext": "A 23-year-old male patient presented to the emergency department with a sudden onset of severe frontal headache lasting for 2 h. He experienced associated symptoms of nausea, vomiting, and chest heaviness. He has a unremarkable medical record and denies the use of illicit drugs. However, he is a smoker with a history of 23 pack-years but does not consume alcohol.\n\nOn physical examination, the young male appeared distressed but was fully conscious and oriented to time, place, and person. Chest auscultation revealed normal vesicular breathing sounds, while cardiovascular and abdominal examinations were inconclusive. Neurological examinations demonstrated neck stiffness, dilated pupils reactive to light, normal plantar reflexes, and no focal neurological deficits.\n\nHis vital signs were as follows: blood pressure 178/103 mmHg, respiratory rate 26 breaths/min, temperature 38.9°C, heart rate 87 beats/min, and oxygen saturation of 94%.\n\nEmergency tests were initiated. An ECG revealed ST segment elevation >2 mm in leads V2-V5, consistent with STEMI as the top of our differential diagnosis, requiring confirmation by cardiac markers. With prompt referral to a tertiary cardiac centre implemented, the patient received a 300 mg aspirin load while being transferred to the catheter lab. Troponin levels were significantly elevated at 1.48 mg/dl (normal <0.16 mg/dl).\n\nPercutaneous coronary intervention was performed via the femoral artery, and the result showed normal coronary arteries with thrombolysis in myocardial infarction (TIMI) flow grade of 3.\n\nHis ECG after coronary angiography revealed normal sinus rhythm with left ventricular hypertrophy LVH. An echocardiogram was performed, revealing normal ventricular function with no regional wall motion abnormalities (RWMA).\n\nFollowing coronary intervention, he was admitted to the medical ward for further assessment and investigation. Blood samples were drawn for a complete blood count, random blood sugar, renal function tests, and CRP. The results revealed lymphocytosis and mildly elevated CRP.\n\nWe proceeded further with CT brain to exclude serious cause of headache. His brain CT showed cisternal subarachnoid haemorrhage SAH with extension anterior to the right temporal lobe. Abdominal ultrasound screening was performed to rule out polycystic kidney disease which was negative and cerebral CT angiography was scheduled to exclude cerebral aneurysm Nimodipine 60 mg every 4 h was initiated, with a target blood pressure of 160/100 mmHg.\n\nOn the second day, his condition suddenly deteriorated, culminating with cardiac arrest. Therefore, cardiopulmonary resuscitation (CPR), resulting in a Glasgow Coma Scale score (GCS) of 6. The patient was subsequently, intubated and placed on mechanical ventilation in the Intensive Care Unit (ICU). Due to his unstable condition in the ICU, we could not perform a repeated CT brain scan or the planned cerebral CT angiography.\n\nOver the next 7 days, we diligently monitored him with a strict multidisciplinary team. A nasogastric tube was inserted for feeding and fluid replacement. His medications included intravenous fluids, antibiotics, proton pump inhibitors, and nimodipine.\n\nOn the 8th day, he suddenly developed ventricular fibrillation, and despite CPR with more than five defibrillations, we were unable to revive him and death was the final outcome.39734686",
    "diff_label_texts": "A 23-year-old male with a 23 pack-year smoking history, no alcohol use, and no illicit drug use presented with 2 hours of sudden severe frontal headache, nausea, vomiting, and chest heaviness. He was distressed but alert and oriented. Vitals: BP 178/103 mmHg, RR 26/min, T 38.9°C, HR 87/min, SpO2 94%. Exam: normal vesicular breath sounds; cardiovascular and abdominal exams inconclusive; neurological exam notable for neck stiffness, dilated but light-reactive pupils, normal plantar reflexes, and no focal deficits. ECG showed ST-segment elevation >2 mm in V2–V5, consistent with STEMI; he received a 300 mg aspirin load and was urgently transferred for PCI. Troponin was elevated at 1.48 mg/dl (normal <0.16 mg/dl). Femoral-access coronary angiography demonstrated normal coronary arteries with TIMI 3 flow. Post-angiography ECG showed normal sinus rhythm with LVH; echocardiography revealed normal ventricular function without RWMA. Subsequent workup found lymphocytosis and mildly elevated CRP. Non-contrast CT brain demonstrated a cisternal subarachnoid haemorrhage with extension anterior to the right temporal lobe. Abdominal ultrasound was negative for polycystic kidney disease; cerebral CT angiography was planned to exclude aneurysm. Nimodipine 60 mg q4h was initiated with a BP target of 160/100 mmHg. On day 2, he acutely deteriorated with cardiac arrest; after CPR, GCS was 6, and he was intubated and mechanically ventilated in the ICU. Owing to instability, repeat CT brain and planned cerebral CTA were not performed. He received multidisciplinary ICU care with NG feeding, IV fluids, antibiotics, a proton pump inhibitor, and nimodipine. On day 8, he developed ventricular fibrillation and, despite CPR and more than five defibrillation attempts, could not be resuscitated and died.",
    "summary": "We present a case detailing the diagnostic challenges of a 23-year-old male presenting with a sudden severe headache, nausea, vomiting, and chest heaviness. Initial evaluation showed elevated blood pressure and respiratory rate. An emergency electrocardiogram (ECG) indicated ST-segment elevation myocardial infarction (STEMI), leading to immediate referral for percutaneous coronary intervention, which revealed normal coronary arteries. Further investigations identified a cisternal subarachnoid haemorrhage (SAH) on CT brain imaging. Despite multidisciplinary management, the patient's condition rapidly deteriorated, resulting in cardiac arrest and mortality."
  }
]