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+[
+    {
+        "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\u2011year\u2011old woman who developed dilated cardiomyopathy at age 17, likely on the background of infectious myocarditis after a throat infection. She was hospitalized for 10 months and 10 days with severe heart failure and a very low ejection fraction while being evaluated for heart transplantation. There was no clearly dangerous arrhythmia. Treatment focused on heart failure care and on preventing arrhythmias and blood clots.\nHer heart function recovered\u2014a remission seen in about 16% of patients\u2014and that improvement lasted 4 years. She then had a two\u2011year worsening, followed by several stable years and a normal first pregnancy. During her second pregnancy, she experienced a flare in the second trimester with postpartum dilated cardiomyopathy that lasted a couple of months, then improved.\nAs of May 2017, she was stable on guideline\u2011based therapy (an ACE inhibitor, a beta\u2011blocker, diuretics, and an If\u2011channel blocker), reported no limitation in physical activity, and was a mother of two and unemployed.",
+        "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": 23,
+        "label": "intermediate_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 presented with cough, shortness of breath, and weight loss. Chest CT showed a poorly defined nodule in the right lung. A trans-thoracic biopsy confirmed a pulmonary lymphoepithelioma-like carcinoma: large polygonal tumor cells arranged in sheets with abundant lymphocytes and plasma cells. Immunohistochemistry supported this diagnosis (cytokeratin 5/6 and p63 positive; Napsin A and TTF-1 negative). PD-L1 expression was very high (about 100%), and the tumor cells were positive for Epstein\u2013Barr virus by EBER in situ hybridization. To confirm the lung as the primary site, a nasopharyngeal exam was negative. Additional testing from the case showed no EGFR, KRAS, ALK, or ROS1 alterations. Imaging later showed a right perihilar lesion with nodal disease. He received platinum-based chemotherapy (gemcitabine/cisplatin) with durvalumab; cisplatin was later changed to carboplatin because of side effects. Despite treatment, the disease progressed, and he died 9 months after diagnosis.",
+        "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": "intermediate_health_literacy",
+        "fulltext": "A 13-year-old male patient was admitted to the Children\u2019s Hospital in Damascus after noticing a palpable enlarged mass in the left inguinal region. His medical history was unremarkable except for a surgical intervention on his spine 6 years ago due to an accident, which resulted in the loss of motor function and sensation in both of his lower extremities.\n\nDue to the long period he had spent in bed, the patient developed decubitus sores on his left foot. The only finding on clinical examination was a mass in the left inguinal area, which was movable on deep structures and so was the overlaying skin on it. The mass was not tender on palpation, and no signs of local inflammation were observed.\n\nLaboratory tests revealed an Elevated ESR (119 mm/h in the first hour). Other Basic Laboratory tests including (Complete Blood Count, Liver function tests, electrolytes, Urea, Creatinine and LDH) were ordered and were within normal ranges for age. Ordering these tests was essential to rule out systemic diseases. Given the absence of indicative physical findings for systemic disorders or immunodeficiencies, additional tests like those for HIV or Direct Antiglobulin were deemed unnecessary.\n\nA CT of the abdomen, chest, and pelvis showed enlarged lymph nodes inferior to the inguinal ligament, with the largest measuring approximately (3.5\u2009\u00d7\u20092.4 cm). Other organs and nodes were within normal limits.\n\nAll of the above-mentioned investigations were essential to rule other high-risk diagnosis including lymphoma and leukemia. However, these were not sufficient to reach the definite diagnosis, so a decision of surgical resection of the nodes was taken.\n\nTo confirm the diagnoses and exclude other potential differentials presenting with enlarged lymph nodes, surgical removal of all of these enlarged nodes was performed under general anesthesia, and biopsies were sent for microscopic study.\n\nThe biopsy showed hyperplastic nodal architecture with proliferation of histiocytes and plasma cells with vascular proliferation, consistent with Plasma cell subtype of Castleman\u2019s Disease.\n\nThe patient was discharged from the hospital after 14-day period after ensuring that there were no remaining enlarged lymph nodes. The only recommendation was oral prednisolone. The patient underwent follow-up using a whole-body CT scan every three months. During each hospital visit, a comprehensive clinical examination and laboratory tests (e.g. Complete Blood Test, ESR, C-reactive protein, liver function tests, renal function tests) were performed in addition to the CT scan. After a 12-month follow-up period, the patient reported no new symptoms or enlarged lymph nodes. Additionally, no abnormalities were observed during clinical examination or in laboratory tests.",
+        "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 \u00d7 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 \u2014 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": 25,
+        "label": "intermediate_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 \u2013 myotonia, warm-up phenomenon, characteristic electromyographic pattern and/or family history \u2013 and/or a molecular diagnosis (mutation in the CLCN1 gene). The clinical signs and symptoms, as well as the results of the complementary explorations and the genetic mutation found, were collected by reviewing the medical record. Demographic variables (age and sex), course of the disease (age of onset, symptoms and signs, time elapsed until diagnosis and clinical evolution), family history and evaluation of the response to treatment were collected.\n\nFive cases with clinical diagnosis of congenital myotonia were identified (three with Becker's disease and two with Thomsen's disease). The incidence in relation to the number of births was estimated at 1:15,000 newborns for cases with Becker's phenotype and 1:21,000 newborns for Thomsen's phenotypes.\n\nMost of our patients were female, and the male was the only one who started before the age of six. The initial clinical presentation included myotonia in the lower limbs in four of the five patients and in the upper limbs in all but one. The age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic diagnosis was performed in all cases approximately two years after onset, and the family of one patient refused to have it performed. All had a worsening with cold, but the warming phenomenon was only in those with the Becker phenotype.\n\nPatients with recessive congenital myotonia showed some progression. As a family history, it is worth noting that patients 2 and 3 were sisters, without the parents showing any clinical signs, and that the mother of patient 1 showed mild clinical signs that were doubtful with the cold. The patient who refused the study had a history of myotonia in the maternal branch.\n\nBlood tests did not show elevated creatine kinase in any of the patients. The electromyogram was abnormal in all patients except the first one at 2.8/12 years of age. The test was not repeated later because it was not considered necessary.\n\nThe most used treatment initially was oxcarbazepine (in patients with recessive form), with a good response in general. In case 2 it lost efficacy with time and mexiletine was initiated. Patient 4 initiated several drugs without success due to loss of efficacy or side effects. Patient 5 rejected treatment due to mild clinical presentation.\n\nPatient 1 had a previously undescribed, likely pathogenic mutation (CLCN1: c.824T>C) inherited from his mother. Cases 1 to 3 had the Becker phenotype with composite heterozygosity mutations, and cases 4 and 5 had the Thomsen phenotype. Case 5 declined genetic testing.\n",
+        "diff_label_texts": "Researchers reviewed pediatric neurology records from a tertiary hospital (2015\u20132020) to study congenital myotonia. Patients were included based on clinical features (myotonia, a warm\u2011up phenomenon, a characteristic EMG pattern, and/or family history) and/or a molecular finding in the CLCN1 gene. They collected demographics (age, sex), details on disease onset and symptoms, time to diagnosis and clinical course, family history, and response to treatment. Five cases were identified: three with the Becker type and two with the Thomsen type. Using local birth numbers, they estimated an incidence of about 1 in 15,000 births for Becker and 1 in 21,000 for Thomsen. They also identified a previously unreported CLCN1 gene variant (c.824T>C) that is likely disease\u2011causing.",
+        "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": 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\u2011medicated. 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\u2011inflammatory 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": "low_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\u2009mmHg), and blood tests revealed anaemia (haemoglobin: 9.6\u2009g/dL), which suggested upper gastrointestinal bleeding.\n\nNon-contrast-enhanced CT was performed immediately because of renal dysfunction. CT revealed that the third part of the duodenum flexed steeply on the right side of the aorta and ran caudally, without crossing anterior to the aorta. The jejunum was located on the patient\u2019s right side. The second part of the duodenum and the stomach were dilated, and there were high-density gastric contents that were considered to indicate a haematoma.\n\nUpper gastrointestinal endoscopy was performed following the CT examination, which revealed a mucosal laceration at the gastric cardia. Bleeding from lacerations of the cardia of the stomach as a result of forceful vomiting was first reported by Mallory and Weiss in 1929.1 In our case, the third part of the duodenum flexed steeply, and the lumen was narrowed, which caused an obstruction. As a result, repeat vomiting was considered to have caused Mallory\u2013Weiss syndrome.\n\nOn the basis of the CT findings showing that the duodenal-jejunal junction was located in the right hemi-abdomen, intestinal malrotation was suspected.2 However, 7\u2009days later, when CT was repeated, spontaneous resolution of the malpositioned jejunum was seen. The patient was then discharged from the hospital. However,\u2009months later, she was rushed to the emergency room for repeat haematemesis. Dynamic CT was performed before upper gastrointestinal endoscopy, on admission, and revealed contrast extravasation in the dilated stomach. Additionally, the third part of the duodenum was flexed on the right side of the aorta, and the duodenal-jejunal junction and jejunum were again located in the right hemi-abdomen. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, as in the previous endoscopy, which was considered Mallory\u2013Weiss syndrome.\n\nTwo months after the second episode of haematemesis, the patient presented to the emergency room with nausea. Non-contrast-enhanced CT revealed no abnormalities in the duodenal positioning, but there was oedematous wall thickening in the second part of the duodenum. If we had not had previous CT images, we would have suspected duodenitis, but on the basis of all of the CT findings, we suspected the possibility of an underlying condition after the right-sided deviation of the small intestine had resolved spontaneously.\n\nIn summary, CT was performed 4 times over 5\u2009months. The third and fourth parts of the duodenum and the jejunum deviated repeatedly, but this resolved spontaneously, which is not indicative of intestinal malrotation. Therefore, we diagnosed dysplasia of the ligament of Treitz.\n\nClinical outcomes\nThe patient underwent laparotomy, which revealed no abnormalities in the relative position of the duodenum to the jejunum. Additionally, the jejunum was located on the patient\u2019s left side, and there was no intestinal malrotation. The ligament of Treitz was formed; however, its fixation in the upper jejunum was incomplete as it was attached only to the duodenum. The duodenal-jejunal junction was not fixed to the retroperitoneum, and the jejunum folded easily with the ligament of Treitz as a fulcrum. Surgically, the upper jejunum was fixed with 4 sutures to the retroperitoneum on the patient\u2019s left side. The postoperative course was good, and the patient has remained symptom-free.",
+        "diff_label_texts": "A 77-year-old woman came to the hospital because she threw up blood. A belly scan (CT) was done. It showed the first part of her small intestine bent sharply on the right side of the body\u2019s main artery and went downward. It did not cross in front of that artery. The meeting point between the first and middle parts of the small intestine was on her right side. The middle part of the small intestine was also on her right side. A camera test of her stomach showed a tear at the top of the stomach where it meets the food pipe. This is called a Mallory\u2013Weiss tear. A week later, another CT showed the intestines moved back to a normal spot by themselves. Two months later, she threw up blood again. The CT again showed that the meeting point and the middle small intestine had slid to the right. The camera test again showed a tear in the same spot. At first, doctors thought she might have been born with her intestines in the wrong place. But because the intestines kept sliding to the right and then moving back on their own, the problem was a weak support band called the ligament of Treitz. Surgery showed the band was there but not firmly attached to the upper small intestine. The scan also showed a nearby tissue space was loose and could move. These issues likely let the small intestine slide to the right.",
+        "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": 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\u2009mmHg), and blood tests revealed anaemia (haemoglobin: 9.6\u2009g/dL), which suggested upper gastrointestinal bleeding.\n\nNon-contrast-enhanced CT was performed immediately because of renal dysfunction. CT revealed that the third part of the duodenum flexed steeply on the right side of the aorta and ran caudally, without crossing anterior to the aorta. The jejunum was located on the patient\u2019s right side. The second part of the duodenum and the stomach were dilated, and there were high-density gastric contents that were considered to indicate a haematoma.\n\nUpper gastrointestinal endoscopy was performed following the CT examination, which revealed a mucosal laceration at the gastric cardia. Bleeding from lacerations of the cardia of the stomach as a result of forceful vomiting was first reported by Mallory and Weiss in 1929.1 In our case, the third part of the duodenum flexed steeply, and the lumen was narrowed, which caused an obstruction. As a result, repeat vomiting was considered to have caused Mallory\u2013Weiss syndrome.\n\nOn the basis of the CT findings showing that the duodenal-jejunal junction was located in the right hemi-abdomen, intestinal malrotation was suspected.2 However, 7\u2009days later, when CT was repeated, spontaneous resolution of the malpositioned jejunum was seen. The patient was then discharged from the hospital. However,\u2009months later, she was rushed to the emergency room for repeat haematemesis. Dynamic CT was performed before upper gastrointestinal endoscopy, on admission, and revealed contrast extravasation in the dilated stomach. Additionally, the third part of the duodenum was flexed on the right side of the aorta, and the duodenal-jejunal junction and jejunum were again located in the right hemi-abdomen. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, as in the previous endoscopy, which was considered Mallory\u2013Weiss syndrome.\n\nTwo months after the second episode of haematemesis, the patient presented to the emergency room with nausea. Non-contrast-enhanced CT revealed no abnormalities in the duodenal positioning, but there was oedematous wall thickening in the second part of the duodenum. If we had not had previous CT images, we would have suspected duodenitis, but on the basis of all of the CT findings, we suspected the possibility of an underlying condition after the right-sided deviation of the small intestine had resolved spontaneously.\n\nIn summary, CT was performed 4 times over 5\u2009months. The third and fourth parts of the duodenum and the jejunum deviated repeatedly, but this resolved spontaneously, which is not indicative of intestinal malrotation. Therefore, we diagnosed dysplasia of the ligament of Treitz.\n\nClinical outcomes\nThe patient underwent laparotomy, which revealed no abnormalities in the relative position of the duodenum to the jejunum. Additionally, the jejunum was located on the patient\u2019s left side, and there was no intestinal malrotation. The ligament of Treitz was formed; however, its fixation in the upper jejunum was incomplete as it was attached only to the duodenum. The duodenal-jejunal junction was not fixed to the retroperitoneum, and the jejunum folded easily with the ligament of Treitz as a fulcrum. Surgically, the upper jejunum was fixed with 4 sutures to the retroperitoneum on the patient\u2019s left side. The postoperative course was good, and the patient has remained symptom-free.",
+        "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\u2013Weiss 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\u2019s mother said that the patient was admitted to the hospital because of weakness in both patient\u2019s hands and feet. The patient had a history of falling down about one year ago. The patient\u2019s mother also had a difficulty in cleaning the patient\u2019s oral cavity regularly.\n\nIn the extraoral examination, the patient had a dysmorphic face. The patient also had a cracking and desquamative condition of the vermillion border of the lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1\u00d70.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. There was dentinal caries on 63 tooth and also the tooth remnants on 55, 62, 74, and 85 teeth. The upper and lower tooth remnants were suggested to be extracted by pediatric dentist. The space of the extracted teeth will be maintained using a space maintainer. The 55 tooth was sharp and caused an occlusion trauma to the right lateral border of the tongue.\n\nLaboratory examination showed a decrease in sodium value (130 mEq/L) and an increase in lymphocyte value (46%). The MRI examination was performed in the Radiology Department to determine the presence of abnormalities in the cervical spine. The results of the MRI examination showed a dislocation of the patient\u2019s cervical spine. The patient\u2019s mother provided informed consent to publish the patient\u2019s case details and any accompanying images.\n\nBased on the history review, the clinical examination, and appropriate investigation, the patient was diagnosed with a chronic traumatic ulcer mimicking OSCC, exfoliative cheilitis, reversible pulpitis of 63 teeth, and radix gangrene on 55, 62, 74, and 85 teeth. The diagnosis of the chronic ulcer was based on clinical examination. There was an indurated margin in the traumatic lesion, which mimicked Oral Squamous Cell Carcinoma clinically. The patient has been hospitalized for 4 days and was given paracetamol 120 mg/5 mL oral suspension and amoxicillin 125 mg/5 mL oral suspension from the Pediatric Department. The patient also was given sodium chloride 0.9% solution, povidone-iodine mouthwash 1%, and petroleum jelly from the Oral Medicine Department. The patient\u2019s mother was instructed to clean the patient\u2019s oral cavity using gauze soaked in sodium chloride 0.9% solution, compress the ulcer using povidone-iodine mouthwashes 1% three times a day as an antiseptic and anti-inflammatory agent to the oral ulcer, and apply petroleum jelly to moisturize the patient\u2019s lips. The patient was also suggested to extract the 55, 62, 74, and 85 teeth.\n\nIn the second visit (3 days follow-up), oral lesions already showed improvement. In the third visit (1-week follow-up), the size of the oral ulcer at the lateral border of the tongue was getting smaller and the lesion of the lips had some improvement.\n\nIn the fourth visit (10 days follow-up), the size of the oral ulcer at the lateral border of the tongue already had significant improvement. Two days after the fourth visit, the patient underwent neurosurgery. The patient was observed in the Pediatric Intensive Care Unit postoperatively. After two weeks of observation in the Pediatric Intensive Care Unit, the experienced respiratory failure and was declared dead.",
+        "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 \u00d7 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\u00d70.7 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 \u00d7 109 leukocytes/L (6.0-17.5), 18.4 \u00d7 109 neutrophils/L (1.0-8.5), 7.0 \u00d7 109 lymphocytes/L (4.0-13.5), 3.5 \u00d7 109 monocytes/L, 459 \u00d7 109 platelets/L (150-350), and C-reactive protein of 16 mg/L (< 3.0). The first thoracoabdominal tomography showed an abscess in the left axilla, lytic lesions in ribs 3-6, left apical pneumonia, pulmonary nodules in both lungs, and enlarged cervical and mediastinal lymph nodes. The biopsy of the left axilla abscess reported myositis and suppurative panniculitis. Only the culture for bacteria from the bronchoalveolar liquid was negative, and the PCR for the Mycobacterium tuberculosis complex was negative. After 41 days of hospitalization and receiving two antimicrobial regimens of ceftriaxone-clindamycin and cefepime-vancomycin, the patient was discharged.\n\nTwo months later, at eight months of age, he was readmitted to hospital with a fever, irritability and a suppurating abscess in the left scapula. The blood count showed haemoglobin of 10.8 g/dl (10.5-12), 21.2 \u00d7 109 leukocytes/L (6-17), 12.2 \u00d7 109 neutrophils/L (1.5-8.5), 7.5 \u00d7 109 lymphocytes/L (4-10.5), 1.2 \u00d7 109 monocytes/L (600), and 583 \u00d7 109 platelets/L (150-350); the serum test for HIV was negative. A left apical consolidation, bronchiectasis, lytic lesions in ribs 2-7 and dorsal vertebrae 2-7, and a multilocular fluid collection were observed on a chest scan; ultrasound showed a fistula associated with the scapular abscess. The patient received piperacillin-tazobactam, which was later replaced with voriconazole after Aspergillus fumigatus was detected in the secretion sample culture. Given the recurrence and severity of the infection, an innate immunity defect was suspected. The dihydrorhodamine test showed no production of reactive oxygen species and the gp91phox expression in neutrophils was absent, establishing a diagnosis of X-linked chronic granulomatous disease. The pathogenic variant detected by next-generation sequencing was c.80_83del/Y (p.Val27Glyfs*33) in CYBB. The mother was a carrier of the variant (c.80_83del/WT). The two older male siblings, who were apparently healthy, could not be genetically tested. The patient was discharged after 65 days of hospitalisation and 28 days of voriconazole treatment. Daily antibiotic prophylaxis with trimethoprim-sulfamethoxazole and antifungal prophylaxis with fluconazole twice a week were initiated. Two months later, at one year of age, the infant was readmitted due to multifocal pneumonia, for which mechanical respiratory assistance was required. The galactomannan antigen was detected in the serum and A. fumigatus was detected in the culture of the lavage fluid, so treatment with voriconazole was initiated again. The patient suffered a multiple organ failure and died one month after admission.\n",
+        "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": 35,
+        "label": "intermediate_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 \u00d7 109 leukocytes/L (6.0-17.5), 18.4 \u00d7 109 neutrophils/L (1.0-8.5), 7.0 \u00d7 109 lymphocytes/L (4.0-13.5), 3.5 \u00d7 109 monocytes/L, 459 \u00d7 109 platelets/L (150-350), and C-reactive protein of 16 mg/L (< 3.0). The first thoracoabdominal tomography showed an abscess in the left axilla, lytic lesions in ribs 3-6, left apical pneumonia, pulmonary nodules in both lungs, and enlarged cervical and mediastinal lymph nodes. The biopsy of the left axilla abscess reported myositis and suppurative panniculitis. Only the culture for bacteria from the bronchoalveolar liquid was negative, and the PCR for the Mycobacterium tuberculosis complex was negative. After 41 days of hospitalization and receiving two antimicrobial regimens of ceftriaxone-clindamycin and cefepime-vancomycin, the patient was discharged.\n\nTwo months later, at eight months of age, he was readmitted to hospital with a fever, irritability and a suppurating abscess in the left scapula. The blood count showed haemoglobin of 10.8 g/dl (10.5-12), 21.2 \u00d7 109 leukocytes/L (6-17), 12.2 \u00d7 109 neutrophils/L (1.5-8.5), 7.5 \u00d7 109 lymphocytes/L (4-10.5), 1.2 \u00d7 109 monocytes/L (600), and 583 \u00d7 109 platelets/L (150-350); the serum test for HIV was negative. A left apical consolidation, bronchiectasis, lytic lesions in ribs 2-7 and dorsal vertebrae 2-7, and a multilocular fluid collection were observed on a chest scan; ultrasound showed a fistula associated with the scapular abscess. The patient received piperacillin-tazobactam, which was later replaced with voriconazole after Aspergillus fumigatus was detected in the secretion sample culture. Given the recurrence and severity of the infection, an innate immunity defect was suspected. The dihydrorhodamine test showed no production of reactive oxygen species and the gp91phox expression in neutrophils was absent, establishing a diagnosis of X-linked chronic granulomatous disease. The pathogenic variant detected by next-generation sequencing was c.80_83del/Y (p.Val27Glyfs*33) in CYBB. The mother was a carrier of the variant (c.80_83del/WT). The two older male siblings, who were apparently healthy, could not be genetically tested. The patient was discharged after 65 days of hospitalisation and 28 days of voriconazole treatment. Daily antibiotic prophylaxis with trimethoprim-sulfamethoxazole and antifungal prophylaxis with fluconazole twice a week were initiated. Two months later, at one year of age, the infant was readmitted due to multifocal pneumonia, for which mechanical respiratory assistance was required. The galactomannan antigen was detected in the serum and A. fumigatus was detected in the culture of the lavage fluid, so treatment with voriconazole was initiated again. The patient suffered a multiple organ failure and died one month after admission.\n",
+        "diff_label_texts": "This case describes a 4\u2011month\u2011old boy who lived with his mother in a crowded prison cell and developed a painful mass in his left armpit. Initial imaging raised concern for rib fractures, so he was hospitalized for possible child abuse. Imaging also showed an axillary abscess, rib damage, pneumonia, and small nodules in both lungs. He received broad\u2011spectrum antibiotics and was discharged. At 8 months, he returned with fever and an enlarging, pus\u2011draining abscess extending toward the left shoulder. Imaging showed progression. Culture of the abscess grew Aspergillus fumigatus, confirming invasive aspergillosis, and he was treated with 28 days of voriconazole. Because the infection was severe and recurrent, doctors tested his innate immune function. A dihydrorhodamine assay showed a defect consistent with chronic granulomatous disease (CGD). Genetic testing identified an X\u2011linked CYBB pathogenic variant (c.80_83del/Y); his mother was a carrier (c.80_83del/WT). At 12 months, he was readmitted with recurrent invasive aspergillosis that did not respond to treatment and he died.",
+        "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\u00d71 x 0.5 cm in size was seen in the midline of the hard palate. Several teeth were found in caries, radix, and edentulous conditions in all regions. The oral hygiene was poor.\n\nExamination of psychological conditions was evaluated using the DASS-21 questionnaire and showed normal depression level (score 0), normal anxiety level (score 6), and normal stress level (score 6). Based on history and clinical examination, the working diagnosis was suspected HAEM, accompanied by the coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis of tooth 18, irreversible pulpitis of tooth 47, chronic apical periodontitis et causa radix of tooth 15, and edentulous teeth 28, 37, 36, and 46. The differential diagnosis of suspected HAEM lesions on the lips was exfoliative cheilitis. However, exfoliative cheilitis did not have herpes virus involvement. The patient was indicated for serological testing (IgG anti-HSV-1) to confirm the diagnosis. Oral health-related quality of life was measured, and the results of the OHIP-14 examination at the first visit were 35 (moderate OHRQol).\n\nThe non-pharmacological therapy included instruction to maintain oral hygiene by brushing the teeth and tongue using a soft-bristled toothbrush two times a day and using non-detergent toothpaste. Education was given such as increasing the intake of water by at least two liters per day, consuming a balanced nutritional diet, avoiding acidic, spicy, hard, and monosodium glutamate-containing foods, and stopping the bad habit of licking and peeling the skin of the lips. The pharmacological therapy included topical and systemic medications. The topical medications included instructions to compress the lips with gauze moistened with 0.9% NaCl solution at least three times a day and to apply a thin layer of triamcinolone acetonide 0.1% in orabase to the lips three times a day. The systemic medications included instruction to take a multivitamin once a day.\n\nThe progress of improvement was visible in the first follow-up, two days after the initial visit. The pain in the lips was reduced, but the canker sores have not healed. Extra-oral examination revealed serosanguinous crusts on the lips which were still painful and bled easily. The serological test result (IgG anti-HSV-1) was positive with a ratio of: 6.32 (positive: ratio > 1.1). The definitive diagnosis was established based on the history, clinical examination, and serological tests as HAEM. The non-pharmacological and pharmacological therapy was continued, and systemic medication was added in the form of instructions to consume acyclovir 200 mg tablets five times a day for one week.\n\nSignificant improvement was visible in the second follow-up, five days after the previous visit, showing excellent healing in all of the patient\u2019s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient\u2019s physical, psychological, and social conditions showed improvement and returned to normal after 7 days of treatment. Patient was referred to continue dental and oral care in the periodontics, dental conservation, oral surgery, and prosthodontics departments. The patient has approved and written informed consent for the case details to be published included publication of the images, and the institution has also approved for publication. This case had complied with the Declaration of Helsinki.",
+        "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\u00d71 x 0.5 cm in size was seen in the midline of the hard palate. Several teeth were found in caries, radix, and edentulous conditions in all regions. The oral hygiene was poor.\n\nExamination of psychological conditions was evaluated using the DASS-21 questionnaire and showed normal depression level (score 0), normal anxiety level (score 6), and normal stress level (score 6). Based on history and clinical examination, the working diagnosis was suspected HAEM, accompanied by the coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis of tooth 18, irreversible pulpitis of tooth 47, chronic apical periodontitis et causa radix of tooth 15, and edentulous teeth 28, 37, 36, and 46. The differential diagnosis of suspected HAEM lesions on the lips was exfoliative cheilitis. However, exfoliative cheilitis did not have herpes virus involvement. The patient was indicated for serological testing (IgG anti-HSV-1) to confirm the diagnosis. Oral health-related quality of life was measured, and the results of the OHIP-14 examination at the first visit were 35 (moderate OHRQol).\n\nThe non-pharmacological therapy included instruction to maintain oral hygiene by brushing the teeth and tongue using a soft-bristled toothbrush two times a day and using non-detergent toothpaste. Education was given such as increasing the intake of water by at least two liters per day, consuming a balanced nutritional diet, avoiding acidic, spicy, hard, and monosodium glutamate-containing foods, and stopping the bad habit of licking and peeling the skin of the lips. The pharmacological therapy included topical and systemic medications. The topical medications included instructions to compress the lips with gauze moistened with 0.9% NaCl solution at least three times a day and to apply a thin layer of triamcinolone acetonide 0.1% in orabase to the lips three times a day. The systemic medications included instruction to take a multivitamin once a day.\n\nThe progress of improvement was visible in the first follow-up, two days after the initial visit. The pain in the lips was reduced, but the canker sores have not healed. Extra-oral examination revealed serosanguinous crusts on the lips which were still painful and bled easily. The serological test result (IgG anti-HSV-1) was positive with a ratio of: 6.32 (positive: ratio > 1.1). The definitive diagnosis was established based on the history, clinical examination, and serological tests as HAEM. The non-pharmacological and pharmacological therapy was continued, and systemic medication was added in the form of instructions to consume acyclovir 200 mg tablets five times a day for one week.\n\nSignificant improvement was visible in the second follow-up, five days after the previous visit, showing excellent healing in all of the patient\u2019s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient\u2019s physical, psychological, and social conditions showed improvement and returned to normal after 7 days of treatment. Patient was referred to continue dental and oral care in the periodontics, dental conservation, oral surgery, and prosthodontics departments. The patient has approved and written informed consent for the case details to be published included publication of the images, and the institution has also approved for publication. This case had complied with the Declaration of Helsinki.",
+        "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\u2011detergent 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\u2013related 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/\u03bcL). Of note, it was unclear when the patient first started showing HIV symptoms. However, she was diagnosed with HIV about a year prior to presentation. Physical examination revealed a large mass on the cervix measuring 8 \u00d7 8 cm extending to the parametrium and to the pelvic side walls bilaterally. There was bleeding on contact and foul-smelling vaginal discharge. Ultrasonography detected a bulky cervix and bilateral hydronephrosis. The patient was clinically diagnosed with cervical malignancy stage 3B. She was recommenced on antiretroviral therapy with a treatment change from TLD (Tenofovir-Lamivudine-Dolutegravir combination) to a preferable renal friendly regimen (Lamivudine-Abacavir-Dolutegravir combination). A punch biopsy of the cervix was performed, and the histopathological report revealed the diagnosis of an extra-nodal BL. The immunohistochemical and in situ hybridization confirmed the diagnosis, with CD20, CD75a, CD10, PAX5 and Bcl-6 positive. In addition, the CD44 and c-Myc were positive, with the EBER-ISH demonstrating focal positivity. The Ki67 demonstrated a proliferation index of almost 100% and PAX5 moderately positive BCL6. She had white cell count of 2.67 x109/L, haemoglobin of 5.7g/dl and platelet count of 71 \u00d7 109/L. Results of other investigations were serum creatinine 187 mmol/L, urea 11.1 mmol/l, albumin 21 g/l, aspartate transaminase 41 U/l and alkaline phosphatase 100 U/l.\n\nFollowing histological confirmation of the diagnosis and review at an oncology multidisciplinary meeting, she spent 43 days waiting to start treatment at oncology unit. The delay was due to long waiting list. This delay exceeded the 48 hours waiting period during which oncological treatment for BL should commence following diagnosis. The treatment plan was chemo-radiation therapy, and the patient gave written informed consent for the case to be published. However, she demised in the gynaecological ward on the 43rd day while waiting to start the treatment. During the 43 days, further imaging could not be performed due to poor functionality of the available CT and MRI machines. In addition to antiretroviral therapy, the patient received other supportive care such as blood transfusion and analgesia. Again, the number of days between the diagnosis of the BL and her death was 43 days. Histopathological postmortem was not performed as the diagnoses (BL and retroviral disease) were known. We reckon that the main primary cause of death is challenging to assign because of the multiple principal diagnoses. Because BL has rapid progression and high mortality rate in persons living with HIV particularly with high viral load, the attending physician certifying the death assigned BL as the most likely cause of death. However, the secondary cause of death was multiple organ failure (renal and haematological inclusive).",
+        "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/\u03bcL. 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": 37,
+        "label": "intermediate_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/\u03bcL). Of note, it was unclear when the patient first started showing HIV symptoms. However, she was diagnosed with HIV about a year prior to presentation. Physical examination revealed a large mass on the cervix measuring 8 \u00d7 8 cm extending to the parametrium and to the pelvic side walls bilaterally. There was bleeding on contact and foul-smelling vaginal discharge. Ultrasonography detected a bulky cervix and bilateral hydronephrosis. The patient was clinically diagnosed with cervical malignancy stage 3B. She was recommenced on antiretroviral therapy with a treatment change from TLD (Tenofovir-Lamivudine-Dolutegravir combination) to a preferable renal friendly regimen (Lamivudine-Abacavir-Dolutegravir combination). A punch biopsy of the cervix was performed, and the histopathological report revealed the diagnosis of an extra-nodal BL. The immunohistochemical and in situ hybridization confirmed the diagnosis, with CD20, CD75a, CD10, PAX5 and Bcl-6 positive. In addition, the CD44 and c-Myc were positive, with the EBER-ISH demonstrating focal positivity. The Ki67 demonstrated a proliferation index of almost 100% and PAX5 moderately positive BCL6. She had white cell count of 2.67 x109/L, haemoglobin of 5.7g/dl and platelet count of 71 \u00d7 109/L. Results of other investigations were serum creatinine 187 mmol/L, urea 11.1 mmol/l, albumin 21 g/l, aspartate transaminase 41 U/l and alkaline phosphatase 100 U/l.\n\nFollowing histological confirmation of the diagnosis and review at an oncology multidisciplinary meeting, she spent 43 days waiting to start treatment at oncology unit. The delay was due to long waiting list. This delay exceeded the 48 hours waiting period during which oncological treatment for BL should commence following diagnosis. The treatment plan was chemo-radiation therapy, and the patient gave written informed consent for the case to be published. However, she demised in the gynaecological ward on the 43rd day while waiting to start the treatment. During the 43 days, further imaging could not be performed due to poor functionality of the available CT and MRI machines. In addition to antiretroviral therapy, the patient received other supportive care such as blood transfusion and analgesia. Again, the number of days between the diagnosis of the BL and her death was 43 days. Histopathological postmortem was not performed as the diagnoses (BL and retroviral disease) were known. We reckon that the main primary cause of death is challenging to assign because of the multiple principal diagnoses. Because BL has rapid progression and high mortality rate in persons living with HIV particularly with high viral load, the attending physician certifying the death assigned BL as the most likely cause of death. However, the secondary cause of death was multiple organ failure (renal and haematological inclusive).",
+        "diff_label_texts": "A 29-year-old woman (Para 1) with HIV presented with one month of abnormal vaginal bleeding. She had defaulted antiretroviral therapy before this illness and on presentation had a very low CD4 count (26 cells/\u00b5L) and a high viral load. Examination and ultrasound found an 8 \u00d7 8 cm cervical mass with pelvic side wall involvement and bilateral hydronephrosis, and she was clinically staged as FIGO 3B. A cervical punch biopsy confirmed an extranodal Burkitt lymphoma (BL); immunohistochemistry showed B\u2011cell markers and a very high tumor proliferation rate, with focal Epstein\u2013Barr virus (EBV) positivity. Blood tests showed severe anemia (hemoglobin 5.7 g/dL), low platelets (71 \u00d710^9/L), low white cell count (2.67 \u00d710^9/L), and impaired kidney function. The oncology multidisciplinary team recommended chemoradiation, and she was restarted on antiretroviral therapy with a renal\u2011friendly regimen and given supportive care (blood transfusion, pain relief). There was a long delay to start oncologic treatment because of a waiting list and limited imaging availability; she died in the ward 43 days after diagnosis without receiving the planned chemoradiation. The treating physician attributed the most likely primary cause of death to rapidly progressive BL, with multiple organ failure (including kidney and blood\u2011related failure) as contributing causes.",
+        "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/\u03bcL. 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": "low_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\u2019s syndrome complicated with interstitial lung disease (ILD) and PAH (Table I). Her chest X-ray at that time showed vascular markings with interstitial thickening, costophrenic (CP) angle blunting and cardiomegaly. An echocardiogram revealed a pulmonary arterial (PA) systolic pressure of 99 mmHg, enlargement of the right atrium and ventricle, D-shaped left ventricle (LV), and severe tricuspid regurgitation. Chest CNYCT showed no filling defects, excluding pulmonary embolism; it also displayed an enlarged pulmonary trunk, right atrium (RA), and right ventricle (RV), further evidencing pulmonary hypertension. Symptoms of dry mouth, dry eyes, and cracked tongue mucosa, with a Schirmer\u2019s test showing <5 cm, oculus uterque (OU). A positive minor salivary gland biopsy, nuclear medicine scan showing impaired salivary gland function, and a positive anti-Ro test, confirmed Sjogren\u2019s syndrome. She started on Revatio (Sildenafil) 20 mg three times a day (TID) for pulmonary hypertension control, adding Tracleer (Bosentan) in 2016 due to disease progression. A right heart catheterization (RHC) revealed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) nearly 15 Woods, and a wedge pressure of 4, indicating pre-capillary type, group I, CTD-related PAH in 2017. The right heart catheterization (RHC) report allowed for insurance coverage of Opsumit (Macitentan) 10 mg once a day (QD), replacing Tracleer (Bosentan) in 2017. From 2017 to 2020, she was hospitalized multiple times for steroid treatments to manage her underlying Sjogren\u2019s syndrome.\n\nPulmonary hypertension treatment is risk-based, and until 2017, the patient was considered low to intermediate risk, controlled with two medications (Sildenafil + Macitentan). Her condition remained stable until October 2020, when she experienced worsened dyspnea accompanied by cough and expectoration of white sputum, suggestive of infection. On November 10, 2020, the patient experienced severe dyspnea, cold sweats, and cyanosis, with SpO2 dropping to 70%, necessitating 100% O2 via face tent. Blood gas and lab tests revealed a lactate level of 5.2 mmol/l and brain natriuretic peptide (BNP) over 10,000 pg/ml, strongly suggesting cardiogenic shock. She was prepped for intensive care unit (ICU) admission, intubated, and initiated on four pulmonary hypertension medications. Her condition stabilized and showed improvement, preventing further deterioration. On November 12, 2020, evaluation for heart-lung transplantation began. Her condition continued to improve with off vasopressors on November 13, 2020, and extubating on November 14, 2020, and transferred to a general ward on November 21, 2020, with O2 tapered to nasal cannula 2l/min. A follow-up RHC continued to show elevated pulmonary artery pressure, likely attributed to chronic hypertension leading to right heart strain and eventual failure. After intensive care unit (ICU) treatment, she was referred to National Taiwan University Hospital for evaluation for heart-lung transplant.\n\nReviewing the records since the onset of her illness, it was evident that pulmonary artery pressure had steadily increased, and the distance covered in the 6-minute walk test was progressively shortened. Currently, the patient is classified as high risk. She continues regular hospitalizations for control. Despite the relatively stable condition, her chief complaint during the admission is still dyspnea. The physical examination revealed mild rhonchi ILD and a pansystolic murmur indicative of severe valvular heart disease, with no other significant findings. Ventavis (Iloprost) 10 mcg/ml 2 ml was added in 2020. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023. Hydrogen capsules (PURE HYDROGEN) were purchased from HoHo Biotech Co., Ltd. (Taipei, Taiwan, ROC). Each capsule contained 170 mg of hydrogen-rich coral calcium containing 1.7\u00d71,021 molecules of hydrogen, which is equivalent to 24 cups of water with 1,200 ppb of hydrogen or 0.6 mM of hydrogen per 200 ml of water. Adjuvant therapy with hydrogen capsules resulted in increased CD127 + Treg, decreased anti-Ro antibody, decreased B cell subsets, and stabilization of clinical symptoms and signs was observed following the addition of hydrogen therapy in this patient. No adverse reactions or events were observed following the administration of hydrogen capsules. Flow cytometry and serological examination were employed for whole-blood analysis to assess changes in immune cells and autoantibody before and after hydrogen therapy. For subsequent whole-blood analysis via flow cytometry, blood samples were prepared using standard fluorescent dye preparation methods and fluorescent antibody reagent kits with dried reagents (Beckman Coulter, Brea, CA, USA). The methods, steps, immunophenotypic analysis, and cell gating were conducted following previously described procedures. Our analysis of immunophenotypic markers before and after hydrogen therapy revealed increased CD127 + Treg and decreased B cell subsets after treatment. Moreover, this study adheres to the CARE reporting guidelines (2013 CARE Checklist).",
+        "diff_label_texts": "This report is about a 56-year-old woman with Sjogren\u2019s syndrome. It caused lung scarring and high blood pressure in the lungs. Doctors found this in 2013. She took medicines for lung pressure and for her immune disease: sildenafil, bosentan, macitentan, iloprost, and steroids. Even with treatment, she got worse. In 2020, she had very hard breathing and went into heart-related shock. In May 2023, her care team added daily hydrogen capsules to help. After starting the hydrogen capsules, tests showed more immune cells that calm the body (CD127+ Tregs). A Sjogren\u2019s antibody called anti-Ro went down. Some B cells, another kind of immune cell, also went down. Her symptoms became stable. She had no side effects.",
+        "summary": "We present the case of a 56-year-old female with CTD-PAH, diagnosed in 2013 with Sjogren\u2019s 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": 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\u2019s syndrome complicated with interstitial lung disease (ILD) and PAH (Table I). Her chest X-ray at that time showed vascular markings with interstitial thickening, costophrenic (CP) angle blunting and cardiomegaly. An echocardiogram revealed a pulmonary arterial (PA) systolic pressure of 99 mmHg, enlargement of the right atrium and ventricle, D-shaped left ventricle (LV), and severe tricuspid regurgitation. Chest CNYCT showed no filling defects, excluding pulmonary embolism; it also displayed an enlarged pulmonary trunk, right atrium (RA), and right ventricle (RV), further evidencing pulmonary hypertension. Symptoms of dry mouth, dry eyes, and cracked tongue mucosa, with a Schirmer\u2019s test showing <5 cm, oculus uterque (OU). A positive minor salivary gland biopsy, nuclear medicine scan showing impaired salivary gland function, and a positive anti-Ro test, confirmed Sjogren\u2019s syndrome. She started on Revatio (Sildenafil) 20 mg three times a day (TID) for pulmonary hypertension control, adding Tracleer (Bosentan) in 2016 due to disease progression. A right heart catheterization (RHC) revealed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) nearly 15 Woods, and a wedge pressure of 4, indicating pre-capillary type, group I, CTD-related PAH in 2017. The right heart catheterization (RHC) report allowed for insurance coverage of Opsumit (Macitentan) 10 mg once a day (QD), replacing Tracleer (Bosentan) in 2017. From 2017 to 2020, she was hospitalized multiple times for steroid treatments to manage her underlying Sjogren\u2019s syndrome.\n\nPulmonary hypertension treatment is risk-based, and until 2017, the patient was considered low to intermediate risk, controlled with two medications (Sildenafil + Macitentan). Her condition remained stable until October 2020, when she experienced worsened dyspnea accompanied by cough and expectoration of white sputum, suggestive of infection. On November 10, 2020, the patient experienced severe dyspnea, cold sweats, and cyanosis, with SpO2 dropping to 70%, necessitating 100% O2 via face tent. Blood gas and lab tests revealed a lactate level of 5.2 mmol/l and brain natriuretic peptide (BNP) over 10,000 pg/ml, strongly suggesting cardiogenic shock. She was prepped for intensive care unit (ICU) admission, intubated, and initiated on four pulmonary hypertension medications. Her condition stabilized and showed improvement, preventing further deterioration. On November 12, 2020, evaluation for heart-lung transplantation began. Her condition continued to improve with off vasopressors on November 13, 2020, and extubating on November 14, 2020, and transferred to a general ward on November 21, 2020, with O2 tapered to nasal cannula 2l/min. A follow-up RHC continued to show elevated pulmonary artery pressure, likely attributed to chronic hypertension leading to right heart strain and eventual failure. After intensive care unit (ICU) treatment, she was referred to National Taiwan University Hospital for evaluation for heart-lung transplant.\n\nReviewing the records since the onset of her illness, it was evident that pulmonary artery pressure had steadily increased, and the distance covered in the 6-minute walk test was progressively shortened. Currently, the patient is classified as high risk. She continues regular hospitalizations for control. Despite the relatively stable condition, her chief complaint during the admission is still dyspnea. The physical examination revealed mild rhonchi ILD and a pansystolic murmur indicative of severe valvular heart disease, with no other significant findings. Ventavis (Iloprost) 10 mcg/ml 2 ml was added in 2020. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023. Hydrogen capsules (PURE HYDROGEN) were purchased from HoHo Biotech Co., Ltd. (Taipei, Taiwan, ROC). Each capsule contained 170 mg of hydrogen-rich coral calcium containing 1.7\u00d71,021 molecules of hydrogen, which is equivalent to 24 cups of water with 1,200 ppb of hydrogen or 0.6 mM of hydrogen per 200 ml of water. Adjuvant therapy with hydrogen capsules resulted in increased CD127 + Treg, decreased anti-Ro antibody, decreased B cell subsets, and stabilization of clinical symptoms and signs was observed following the addition of hydrogen therapy in this patient. No adverse reactions or events were observed following the administration of hydrogen capsules. Flow cytometry and serological examination were employed for whole-blood analysis to assess changes in immune cells and autoantibody before and after hydrogen therapy. For subsequent whole-blood analysis via flow cytometry, blood samples were prepared using standard fluorescent dye preparation methods and fluorescent antibody reagent kits with dried reagents (Beckman Coulter, Brea, CA, USA). The methods, steps, immunophenotypic analysis, and cell gating were conducted following previously described procedures. Our analysis of immunophenotypic markers before and after hydrogen therapy revealed increased CD127 + Treg and decreased B cell subsets after treatment. Moreover, this study adheres to the CARE reporting guidelines (2013 CARE Checklist).",
+        "diff_label_texts": "A 56-year-old woman was diagnosed in 2013 with Sjogren\u2019s 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\u2019s syndrome. The tests showed fewer B cells, which are the immune system\u2019s 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\u2019s 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": 41,
+        "label": "intermediate_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\u2009\u00d7\u2009106\u2009\u00b5/L; haemoglobin 11.4\u2009g/gL; activated partial thromboplastin time (APTT) 93\u2009seconds and international normalised ratio (INR) 1.08.\n\nIntravenous thrombolytic treatment was contraindicated due to double antiplatelet and anticoagulant treatment at full dose with heparin, so an intra-arterial thrombectomy was performed. Although the patient was 23 months old, he was in the third percentile of the weight curve (10\u2009kg). Under general anaesthesia, the right femoral artery was punctured and an 11\u2009cm long 4F sheath (Cordis, Ireland) was placed. A 4F vertebral Radiofocus catheter (Glidecath of Terumo, Belgium) was used to confirm the occlusion of the M1 segment of the left MCA. The artery was recanalised by mechanical thrombectomy with a stentriever using the 4F vertebral catheter as a tutor, positioning it in the petrous segment of the carotid artery. A 3\u2009mm\u2009\u00d7\u200920\u2009mm Trevo XP Pro Vue device (Stryker, The Netherlands) was used, with a straight Rapid Transit microcatheter (Codman Neurovascular, UK), opening the artery in one pass. The whole system was removed (tutor catheter, microcatheter and stentriever) simultaneously. In the control run, an iatrogenic dissection of the left internal carotid artery was detected, which had no clinical significance, however, as the left hemisphere was irrigated through the anterior communicant artery.\n\nOne month later, his heart transplant was carried out successfully. Neurologically, the only long-term sequel that came as a result of the stroke was a right upper limb spasticity.",
+        "diff_label_texts": "A 16-month-old boy with restrictive cardiomyopathy (and a history of hypoxic\u2011ischaemic encephalopathy at birth but normal psychomotor development) was listed for heart transplant. At 20 months he required implantation of an external biventricular assist device (Berlin Heart) and was started on antiplatelet drugs plus full\u2011dose heparin to prevent clots. At 23 months he presented with reduced consciousness and right\u2011sided weakness; CT scan showed an occlusion of the left middle cerebral artery. Because he was on combined antiplatelet and anticoagulant therapy, intravenous thrombolysis was contraindicated, so an urgent intra\u2011arterial mechanical thrombectomy with a stent\u2011retriever was performed and the artery was reopened in a single pass with good clinical result. Angiography detected a small procedure\u2011related dissection of the left internal carotid artery that had no clinical impact because the left hemisphere was perfused through the anterior communicating artery. One month later he underwent a successful heart transplant; the only lasting neurological deficit was spasticity of the right upper limb.",
+        "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": 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/m\u00b2. Ophthalmologic examination yielded expected results, with no visual impairments detected and normal optical coherence tomography (OCT) findings.\n\nThe biological assessment revealed DI, with a serum sodium level of 140 mEq/l and plasma osmolality of 287 mosm/kg, while the urine osmolality was significantly low at 179 mosm/kg. Furthermore, his serum levels of insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were all within the normal range.\n\nMRI scans with and without contrast highlighted apoplexy in an RCC, showing a spontaneous hyperintensity on T1 and T2 sequences measuring 15x6x11 mm. The anterior pituitary gland displayed homogeneous contrast uptake. However, we observed a loss of the typical hyperintensity of the posterior pituitary gland, with no radiological indications of a craniopharyngioma. Therefore, during the initial hormonal evaluation, the only hormone deficiency identified in our case was DI, which showed significant improvement under vasopressin treatment. The case was reviewed in a multidisciplinary meeting, including an endocrinologist, neurosurgeon, and radiologist. Given the absence of clinical or biological signs other than DI and the stability of the RCC apoplexy over nine months of MRI monitoring\u2014with measurements of 12 \u00d7 11 \u00d7 10 mm\u2014a conservative management approach with regular follow-ups was chosen.\n\nThe child was monitored for three years, during which he displayed normal puberty development and maintained a stable hormonal profile (Table 1). Visual evaluations revealed no abnormalities. However, a decrease in growth velocity was noted, dropping from -0.8 SD to -1.1 SD. This necessitated an investigation for acquired growth hormone (GH) deficiency. At the age of 14 years and nine months, the child was readmitted to undergo two GH stimulation tests: A propranolol-glucagon test and an Insulin Tolerance Test, which indicated a partial GH deficiency with peaks of 19.3 \u00b5UI/ml and 10.0 \u00b5UI/ml, respectively. After receiving GH treatment, the patient experienced a notable increase in growth velocity, improving from -1.1 SD to 0.2 SD over one year.\n\nSubsequently, MRI monitoring showed a stable appearance of the RCC apoplexy after two years (11 \u00d7 12 \u00d7 11 mm), with a slight decrease in size observed at the three-year follow-up, measuring 7 \u00d7 10 \u00d7 6 mm. It is important to note that the radiological follow-up was consistently conducted at the same MRI center, with the same radiologist interpreting both recent and previous MRI findings during multidisciplinary meetings that included an endocrinologist and a neurosurgeon.",
+        "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 \u00d7 6 \u00d7 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 \u00d7 11 \u00d7 10 mm at nine months, 11 \u00d7 12 \u00d7 11 mm at two years, and 7 \u00d7 10 \u00d7 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": "low_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": "This report is about a 67-year-old person with no major past illnesses. Their overall health got worse over time. They developed a hoarse voice and trouble swallowing. A large lump showed up in the neck/throat area. A small tissue test (biopsy) showed a slow-growing type of lymphoma (non-Hodgkin), grade 1\u20132. A special X\u2011ray scan found a lump behind the nose about 7 cm by 4 cm, reaching about 6 cm in length. Tests on the soft center of the bones (bone marrow) were normal. The checkup before treatment was also normal. The person had four rounds of a chemo mix called rituximab plus CHOP, but it did not work. Then they had three rounds of rituximab plus DHAOX, and the lump stayed. A new biopsy showed the B\u2011cells were gone, and there was a build\u2011up of an abnormal protein called AL amyloid. A blood test found a protein called immunoglobulin M (IgM). A PET scan showed an active spot in the area behind the nose. The person is now on treatment with bortezomib, prednisone, and bendamustine.",
+        "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": 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\u20132 follicular non-Hodgkin lymphoma. CT of the neck, chest, abdomen, and pelvis found a nasopharyngeal mass measuring about 70 \u00d7 40 mm with extension to 60 mm. Bone marrow biopsy and the pre-treatment evaluation were normal. The patient received four cycles of rituximab plus CHOP without response, followed by three cycles of rituximab plus DHAOX, with persistence of the mass. Repeat biopsy then showed loss of B\u2011cell infiltration and the presence of AL amyloid deposits. Serum protein immunoelectrophoresis detected immunoglobulin M. PET imaging demonstrated a hypermetabolic nasopharyngeal process. The patient is currently being treated with bortezomib, prednisone, and bendamustine.",
+        "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 \u00d7 8.0 cm interspersed with hypochromic areas in the lower lateral part of the left thigh. Telangiectatic vessels overlap the lesion peripherally, with visible veins close to it. The plaque was present from birth, but was initially violaceous. It evolved with the passing of the years, with lightening and depression. There is no discrepancy in the length of the lower limbs.\n\nAngioresonance showed vascular malformations in the skin and subcutaneous tissue supplied by intermuscular branches of the popliteal artery. Early venous filling was found in both the region and the malformations, suggesting early venous shunting. Dilated draining veins were not documented, except for a superficial draining vein running along the subcutaneous cellular tissue of the anterior thigh. In addition, thinning of the subcutaneous tissue was noted in the topography of the vascular alteration, but without intramuscular or bone extension.\n",
+        "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 \u00d7 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\u2014it 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\u00b0C, HR 88 bpm, RR 18 bpm). She had a BMI of 16.6 kg/m\u00b2 and sarcopenia, but no skin rash, lymphadenopathy, or edema. The abdominal exam showed tenderness in the epigastric and umbilical regions without guarding. CBC revealed leukocytosis and significant eosinophilia (20.8 G/L, with a total white blood cell count of 26.8 G/L, comprising 77.8% eosinophils). Peripheral blood film examination showed normal eosinophils. Bone marrow aspiration reveals 48% eosinophils without blasts, atypical cells. Fluorescence in situ hybridization (FISH) for CHIC2 deletion as a surrogate marker for FIP1L1-PDGFRA showed no rearrangements of the PDGFRA gene. Autoimmune and vasculitis screenings (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative. Elevated serum IgG (2760 mg/dL; normal range, 700\u20131600 mg/dL) and IgG4 (1260 mg/dL; normal range, 3.9\u201386.4 mg/dL), slightly elevated IgE (137.5 IU/mL; normal range, <100 IU/mL) and high RF (144.4 IU/mL; normal range, <20 IU/mL) were observed. Other parameters were normal, including aminotransferase, blood urea nitrogen, serum creatinine, complement C3, complement C4, vitamin B12, serum cortisol, and NT-proBNP. ECG and echocardiogram were normal. Chest CT scans showed mild fibrosis and bronchiectasis. Sputum AFB smears and bronchoscopy were negative. The cytology of the bronchoalveolar lavage fluid showed 35% neutrophils, no eosinophils. Spirometry indicated severe obstruction with bronchodilator response. The fractional exhaled nitric oxide (FeNO) level was 15 ppb. Stool samples were tested positive for leukocytes, with no signs of ova or parasites. Serology tests were positive for toxocariasis (positive IgG of Toxocara canis at 54.2 NovaTec-Units) but negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. An abdominal contrast-enhanced computed tomography scan revealed gallbladder stones without acute cholecystitis and showed no gastrointestinal tract abnormalities. The upper gastrointestinal endoscopy showed unremarkable results with a normal appearance. Colonoscopy showed mucosal inflammation in the sigmoid, left, transverse, and right colon with systemic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies revealed significant eosinophilic infiltration (>85 eosinophils/High-power field (HPF) in the left colon, >100 eosinophils/HPF in the transverse and right colon). Given the patient\u2019s nonresponse to toxocariasis treatment and the significant eosinophilic infiltration observed in the colon mucosa biopsy, a diagnosis of eosinophilic colitis was confirmed. The patient was treated with oral methylprednisolone (16 mg) and montelukast (5 mg). Symptoms resolved in two weeks and eosinophil counts normalized (0.3 G/L). The corticosteroid was reduced and discontinued, and the patient was maintained on montelukast for three months without symptom recurrence.",
+        "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 (caf\u00e9 con leche spots) and bone involvement. At 18 months she required ankle arthrodesis for tibial curvature. She has no family history of NF1 or inflammatory bowel disease.\n\nOn physical examination, the abdomen was soft and indistinct, with increased air-bubble murmurs, without masses or visceral enlargement. The perianal examination was normal. There were multiple brown-coffee stains on the lower extremities and back. General examinations were performed, including a blood count with moderate microcytic-hypochromic anaemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and discretely elevated inflammatory parameters (CRP 1.37 mg/dL, normal value up to 0.5 mg/dL).\n\nA colonoscopy was performed, the rectum, sigmoid and various segments of the colon were examined up to the cecum, visualizing the ileocecal valve and the appendicular orifice. The last few centimeters of the distal ileum were also inspected. The mucosa from the anal margin to the cecum was observed to be erythematous, with loss of vascular transparency, unlike the cecal mucosa, which appeared normal. No lesions were identified in the anal canal or cecum.\n\nBiopsies of the small intestine (ileon) and large intestine were taken. Microscopic examination showed mucosa of ileal type with preserved villous architecture and adequate epithelial differentiation, with a non-inflamed lamina propria. The mucosa of the large intestine had a mild distortion of architecture and adequate epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate and hyperplasia of lymphoid follicles. Isolated foci of microabscesses were recognized. The biopsy was consistent with mild colitis, with signs suggesting chronicity.\n\nIn addition, a PCR study for cytomegalovirus (CMV) was requested in a colon biopsy, which was positive.\n\nGiven a positive PCR for CMV, CMV IgG and IgM and CMV viral load in blood were requested, resulting in a positive IgG, negative IgM, and CMV viral load of 79.7 IU/ml. Further laboratory studies included PCR for gastrointestinal pathogens and PCR for Clostridium difficile in stool, both of which were negative. In the colon biopsy, Gram stain microbiological studies were requested, which showed +++ leukocytes without bacteria; biopsy culture showed S. gallolyticus/equinus complex in very low amount (interpreted as bacterial flora); acridine orange, Ziehl-Neelsen, Koch culture, and ADV PCR were negative.\n\nEndoscopy and histology suggestive of UC was reported in the context of a patient with moderate symptoms (PUCAI 50) who was started on Mesalazine (70 mg/kg/day three times daily) and a request for a faecal calprotectin was made which was greater than 600 ug/g.\n\nThe immunology team evaluated the patient for suspected immunodeficiency. The parents did not report a history of infections, they reported that they were vaccinated, that they had good weight gain, no family history of immunodeficiencies, auto-immunity or early deaths. A study with lymphocyte subpopulations (normal), immunoglobulins (normal), HIV (negative), memory T lymphocytes (with alterations expected in the context of CMV viremia) and lymphoproliferation test (normal) was requested. In addition, a genetic panel of primary immunodeficiencies (Invitae) was performed, which contains 429 genes, of which 68 make up the panel of monogenic inflammatory intestinal disease. 7 variants of uncertain significance were obtained, none included in the panel of monogenic IBD.\n\nGanciclovir was initiated intravenous for CMV infection and continued for 15 days. The last PCR CMV control prior to discharge reported undetectable load.\n\nThe patient improved during the hospital stay with decreased frequency of stools and increased consistency, no rectal bleeding, no nocturnal stools and no abdominal pain, with PUCAI 0 at discharge.\n\nTwo months later, he presented with a reactivation of IBD with bloody diarrhea (PUCAI 35). A blood count was performed (normal), a panel of gastrointestinal pathogens was performed (\u2013), PCR for Clostridium difficile was performed (+), and CMV load was undetectable. He was treated with oral metronidazole. However, he persisted with diarrhea with blood streaks, so he was hospitalized again.\n\nA colonoscopy was performed, where erythematous mucous was observed in a diffuse form from the rectum to the cecum, with nodularity and loss of vascular transparency in the submucosa, greater in the left and transverse colon segments. No focal lesions were observed. The mucosa of the ileum and anal canal were observed without lesions.\n\nBiopsy of the terminal ileum, right colon and left colon was performed. Microscopic examination of the ileal-type mucosa showed preserved villous architecture and adequate epithelial differentiation. The lamina propria showed no signs of inflammation. There were no aphthous erosions or granulomas. The mucosa of the large intestine showed mild distortion of architecture and epithelial dedifferentiation. The lamina propria was expanded by mixed inflammatory infiltrate, transmucosal distribution. Foci of cryptitis and cryptitic microabscesses and hyperplasia of reactive lymphoid follicles were recognized. No granulomas, viral or parasitic cytopathic changes were observed. All fragments of the left colon sample presented a similar histopathological picture.\n\nShe was given oral treatment with Vancomycin and Prednisone (1 mg/kg/day) with a good response and a favorable evolution. She was discharged with a decrease in the frequency of bowel movements. She persists with mild symptoms (PUCAI 5) in outpatient control, so the dose of corticosteroids is progressively decreased and she remains on treatment with Mesalazina.\n",
+        "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 \u00b5g/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\u2019s disease. Even after restarting his HIV drugs, he got worse. Doctors tried steroids and an antiviral called ganciclovir. A week later, many organs started to fail and he swelled all over, so those drugs had to be stopped. A new chest scan showed small branch-like spots in the right lung and fluid around both lungs. The belly scan showed the liver and spleen got bigger and there was fluid in the belly. He went to intensive care because his liver suddenly failed. He died soon after. After his death, a lung sample grew tuberculosis. A liver sample showed tiny immune lumps called granulomas.",
+        "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\u2019s disease. Despite restarting antiretroviral therapy, his condition worsened, so clinicians initiated corticosteroids and ganciclovir. After one week he developed multiorgan failure with anasarca, making those medications unsafe. Repeat chest CT showed right upper lobe tree-in-bud infiltrates with bilateral pleural effusions; abdominal imaging showed worsening hepatosplenomegaly and new ascites. He was transferred to the ICU 48 hours later for fulminant hepatic failure and died shortly afterward. Postmortem testing grew Mycobacterium tuberculosis from a tracheal aspirate, and liver biopsy showed non-necrotizing granulomas.",
+        "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 Urrac\u00e1, 3 hours by canoe from the nearest health center. Her background included being the fourth daughter, born by vaginal delivery at home by a relative, without prenatal controls, her weight, height and Apgar score at birth are unknown. She did not breastfeed and was fed with powdered milk formula with iron for children under 6 months, receiving 3 ounces every 4 hours.\n\nThe nuclear family was composed of 6 people (parents and 4 children) who lived in a house with walls and floor of boards and palm roof, 2 rooms, without electricity, they were illuminated with kerosene lamps, water from a well, excreta in a river and they burned the garbage, their economic income came from subsistence agriculture.\n\nHe had no health care in his first 4 months of life and did not receive the vaccinations included in the national expanded programme of immunizations. According to his parents, his neurodevelopment was normal until his hospitalization.\n\nThe minor consulted in a health center with a history of 4 days of diarrhoea, without mucus or blood associated with vomiting of food content (the mother gave her tea because she could not tolerate milk), afebrile and without respiratory symptoms. Oral fluids and 4 doses of Enterogermina\u00ae (B. clausii: two billion spores/5 mL) were administered. Due to the lack of supplies (they did not have catheters, or intraosseous for the administration of intravenous fluids) she was transferred to a second-level hospital in the provincial capital and then to our institution in Panama City with a diagnosis of acute gastroenteritis and severe dehydration.\n\nHe presented to the emergency department with a consciousness compromise, dehydration characterised by a tearless cry, dry oral mucosa. He had oedema of +++ hands, feet, abdomen and face. He was afebrile and had signs of shock, capillary refill time > 2 seconds, cold extremities, filiform pulse and marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. He weighed 4.7 kg and was 56 cm tall at admission, Z-score height/age -2.52, weight/height and weight/age Z-scores were not quantifiable due to severe dehydration. On segmental examination, there were fine crepitus in both lung bases and erythematous-squamous lesions with desquamation of skin and others with hypopigmentation of trunk and upper limbs (interpreted as pellagroid dermatosis).\n\nLactate Ringer bolus was given at 10 ml/kg in the emergency department, followed by 5% Dextrose in 0.33% Saline 500 ml at an infusion rate of 29 ml/h over 6 hours without KCL until diuresis was obtained. She was started on Ceftriaxone 50 mg/kg/day for suspected sepsis, stabilised and sent to the ward where she continued to receive 500 ml of 5% Dextrose in 0.9% Saline at 20 ml/hr.\n\nAmong the examinations, a blood count revealed leukocytosis at 39.0 x 103/uL, severe anaemia 5.6 g/dL, thrombocytosis 502 x 103/uL, the rest of the results are detailed in. He was transfused with 50 ml of filtered and leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to altered coagulation times. Enteral feeding was initiated by nasogastric tube and infusion was decreased to 15 ml/h of 5% Dextrose in 0.9% Saline 500 cc, and continued with negative water balance.\n\nOn day 2, initial peripheral blood culture was reported as Gram positive cocci in clusters, Oxacillin was added at 200 mg/kg/day, Ceftriaxone was increased to 75-100 mg/kg/day, total fluids to 120 ml/kg/day and calcium was corrected (value received 6.38 mg/dL).\n\nOn her 3rd day she lost venous access, so a central venous catheter (CVC) was placed. She was hypovolemic with subhydrated oral mucosa, increased respiratory work, cold extremities and capillary refill time of 3-4 seconds. Ringer's lactate was given at a load of 20 ml/kg in one hour. Arterial blood gas revealed uncompensated metabolic acidosis with pH 7.26, HCO3 13 mmol/L, PCO2 28.4 mmHg, PO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to the paediatric intensive care unit (PICU) where she was placed on mechanical ventilation.\n\nTotal fluids of 100 cc/kg, infused epinephrine, low-salt albumin, and 10% calcium gluconate were administered, and fentanyl was changed to remifentanil due to elevated liver enzymes.\n\nThe blood culture of admission reported growth of methicillin-resistant Staphylococcus aureus (MRSA), Oxacillin was omitted and Clindamycin was added at 40 mg/kg/day; the blood culture of admission on the second day of admission to the ICU with Gram-negative bacillus smear was positive, and Ceftriaxone was changed to Ceftazidime at 150 mg/kg/day.\n\nOn his first day in the ICU, a substantial increase in serum biomarkers of cardiac damage was documented, the echocardiogram showed mild mitral and tricuspid regurgitation, left ventricular dilatation, left ventricular ejection fraction (LVEF) 58%, no evidence of thrombi, vegetations or pericardial effusion, and he was diagnosed with acute myocarditis. Milrinone was started at 0.4 mcg/kg/min, furosemide and IV immunoglobulin 1 g/kg single dose.\n\nThe second day blood culture the germ was identified as Bacillus clausii, identified by the system (VYTEK 2TM), the susceptibility profile was not performed because the team did not have cut points for this germ, for this reason the antibiotic coverage was adjusted, considering it was not a contaminant, Ceftazidime was changed to Ciprofloxacin at 30 mg/kg/day and Ceftaroline was added at 8 mg/kg every 8 hours along with Clindamycin for MRSA. The 3 subsequent blood cultures with intervals of 48 hours between each were positive in both peripheral blood and CVC for isolation of B. clausii.\n\nOn his 6th day in hospital, the gastrointestinal panel (Maripoc gastro test methodology) performed on the second day detected Clostridiodes difficile toxin A/B, the tests for Campylobacteryeyuni, Norovirus GI, Norovirus GII.4, Adenovirus and Rotavirus were negative. Following these findings, therapy was escalated to IV Vancomycin at a dose of 60 mg/kg/day and metronidazole was added orally. Ceftaroline, clindamycin and ciprofloxacin were omitted, covering both B. clausii and C. difficile and MRSA .\n\nHIV testing, serology for Chagas and SARS-CoV-2 antigen by immunofluorescence (FIA) were negative, immunoglobulins were within normal limits.\n\nOn the seventh day, arterial hypertension was reported and spirinolactone was added to the management.\n\nOn the 8th day, the laboratory tests showed altered coagulation times and increased azotaemia associated with anuria that had lasted for 12 hours. However, due to the patient's condition, a peritoneal catheter was not placed, the vancomycin dose was adjusted and vitamin K was administered. The patient continued to have anuria and anasarca, and she developed sustained hypotension. Noradrenaline was added, but her condition deteriorated with multisystem organ failure and she died twelve days after admission. No autopsy was performed because the mother refused permission for cultural reasons.\n",
+        "diff_label_texts": "This story is about a 4\u2011month\u2011old baby girl from an Indigenous community in rural Panama. The nearest clinic was three hours away by canoe. She was not getting enough protein and calories. She suddenly had bad diarrhea. She got very dehydrated, like a plant without water. A probiotic medicine called Enterogermina was given at the start. She was moved to a large hospital. She arrived breathing hard. She was in shock, which means her blood was not carrying enough to her organs. A blood test found a hard\u2011to\u2011treat germ called MRSA. A stool test found a germ called C. difficile that can cause diarrhea. Later blood tests from her arm and from a central line found Bacillus clausii. Doctors tried many antibiotics, but the germs did not respond. Her organs began to fail. She died 12 days after she got to the hospital.",
+        "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 Urrac\u00e1, 3 hours by canoe from the nearest health center. Her background included being the fourth daughter, born by vaginal delivery at home by a relative, without prenatal controls, her weight, height and Apgar score at birth are unknown. She did not breastfeed and was fed with powdered milk formula with iron for children under 6 months, receiving 3 ounces every 4 hours.\n\nThe nuclear family was composed of 6 people (parents and 4 children) who lived in a house with walls and floor of boards and palm roof, 2 rooms, without electricity, they were illuminated with kerosene lamps, water from a well, excreta in a river and they burned the garbage, their economic income came from subsistence agriculture.\n\nHe had no health care in his first 4 months of life and did not receive the vaccinations included in the national expanded programme of immunizations. According to his parents, his neurodevelopment was normal until his hospitalization.\n\nThe minor consulted in a health center with a history of 4 days of diarrhoea, without mucus or blood associated with vomiting of food content (the mother gave her tea because she could not tolerate milk), afebrile and without respiratory symptoms. Oral fluids and 4 doses of Enterogermina\u00ae (B. clausii: two billion spores/5 mL) were administered. Due to the lack of supplies (they did not have catheters, or intraosseous for the administration of intravenous fluids) she was transferred to a second-level hospital in the provincial capital and then to our institution in Panama City with a diagnosis of acute gastroenteritis and severe dehydration.\n\nHe presented to the emergency department with a consciousness compromise, dehydration characterised by a tearless cry, dry oral mucosa. He had oedema of +++ hands, feet, abdomen and face. He was afebrile and had signs of shock, capillary refill time > 2 seconds, cold extremities, filiform pulse and marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. He weighed 4.7 kg and was 56 cm tall at admission, Z-score height/age -2.52, weight/height and weight/age Z-scores were not quantifiable due to severe dehydration. On segmental examination, there were fine crepitus in both lung bases and erythematous-squamous lesions with desquamation of skin and others with hypopigmentation of trunk and upper limbs (interpreted as pellagroid dermatosis).\n\nLactate Ringer bolus was given at 10 ml/kg in the emergency department, followed by 5% Dextrose in 0.33% Saline 500 ml at an infusion rate of 29 ml/h over 6 hours without KCL until diuresis was obtained. She was started on Ceftriaxone 50 mg/kg/day for suspected sepsis, stabilised and sent to the ward where she continued to receive 500 ml of 5% Dextrose in 0.9% Saline at 20 ml/hr.\n\nAmong the examinations, a blood count revealed leukocytosis at 39.0 x 103/uL, severe anaemia 5.6 g/dL, thrombocytosis 502 x 103/uL, the rest of the results are detailed in. He was transfused with 50 ml of filtered and leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to altered coagulation times. Enteral feeding was initiated by nasogastric tube and infusion was decreased to 15 ml/h of 5% Dextrose in 0.9% Saline 500 cc, and continued with negative water balance.\n\nOn day 2, initial peripheral blood culture was reported as Gram positive cocci in clusters, Oxacillin was added at 200 mg/kg/day, Ceftriaxone was increased to 75-100 mg/kg/day, total fluids to 120 ml/kg/day and calcium was corrected (value received 6.38 mg/dL).\n\nOn her 3rd day she lost venous access, so a central venous catheter (CVC) was placed. She was hypovolemic with subhydrated oral mucosa, increased respiratory work, cold extremities and capillary refill time of 3-4 seconds. Ringer's lactate was given at a load of 20 ml/kg in one hour. Arterial blood gas revealed uncompensated metabolic acidosis with pH 7.26, HCO3 13 mmol/L, PCO2 28.4 mmHg, PO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to the paediatric intensive care unit (PICU) where she was placed on mechanical ventilation.\n\nTotal fluids of 100 cc/kg, infused epinephrine, low-salt albumin, and 10% calcium gluconate were administered, and fentanyl was changed to remifentanil due to elevated liver enzymes.\n\nThe blood culture of admission reported growth of methicillin-resistant Staphylococcus aureus (MRSA), Oxacillin was omitted and Clindamycin was added at 40 mg/kg/day; the blood culture of admission on the second day of admission to the ICU with Gram-negative bacillus smear was positive, and Ceftriaxone was changed to Ceftazidime at 150 mg/kg/day.\n\nOn his first day in the ICU, a substantial increase in serum biomarkers of cardiac damage was documented, the echocardiogram showed mild mitral and tricuspid regurgitation, left ventricular dilatation, left ventricular ejection fraction (LVEF) 58%, no evidence of thrombi, vegetations or pericardial effusion, and he was diagnosed with acute myocarditis. Milrinone was started at 0.4 mcg/kg/min, furosemide and IV immunoglobulin 1 g/kg single dose.\n\nThe second day blood culture the germ was identified as Bacillus clausii, identified by the system (VYTEK 2TM), the susceptibility profile was not performed because the team did not have cut points for this germ, for this reason the antibiotic coverage was adjusted, considering it was not a contaminant, Ceftazidime was changed to Ciprofloxacin at 30 mg/kg/day and Ceftaroline was added at 8 mg/kg every 8 hours along with Clindamycin for MRSA. The 3 subsequent blood cultures with intervals of 48 hours between each were positive in both peripheral blood and CVC for isolation of B. clausii.\n\nOn his 6th day in hospital, the gastrointestinal panel (Maripoc gastro test methodology) performed on the second day detected Clostridiodes difficile toxin A/B, the tests for Campylobacteryeyuni, Norovirus GI, Norovirus GII.4, Adenovirus and Rotavirus were negative. Following these findings, therapy was escalated to IV Vancomycin at a dose of 60 mg/kg/day and metronidazole was added orally. Ceftaroline, clindamycin and ciprofloxacin were omitted, covering both B. clausii and C. difficile and MRSA .\n\nHIV testing, serology for Chagas and SARS-CoV-2 antigen by immunofluorescence (FIA) were negative, immunoglobulins were within normal limits.\n\nOn the seventh day, arterial hypertension was reported and spirinolactone was added to the management.\n\nOn the 8th day, the laboratory tests showed altered coagulation times and increased azotaemia associated with anuria that had lasted for 12 hours. However, due to the patient's condition, a peritoneal catheter was not placed, the vancomycin dose was adjusted and vitamin K was administered. The patient continued to have anuria and anasarca, and she developed sustained hypotension. Noradrenaline was added, but her condition deteriorated with multisystem organ failure and she died twelve days after admission. No autopsy was performed because the mother refused permission for cultural reasons.\n",
+        "diff_label_texts": "A 4\u2011month\u2011old indigenous infant from a remote rural area of Panama (about three hours by canoe from the nearest health subcenter) with protein\u2011calorie malnutrition presented with acute diarrhea and moderate\u2011to\u2011severe 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\u2011level hospitals because local facilities lacked supplies. On arrival at a third\u2011level 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\u2011resistant 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\u2009mm in diameter), and pupillary reaction was absent. The remaining anterior segment examination showed no apparent abnormalities. Fundus examination was challenging due to the child\u2019s size. Hertel exophthalmometry readings measured 10.5\u2009mm in the right eye and 18\u2009mm in the left. Magnetic resonance imaging (MRI) revealed a well-circumscribed mass, displaying hypointense signals on T1-weighted images and hyperintense signals on T2-weighted images. Contrast-enhanced imaging demonstrated no significant improvement. A transconjunctival approach via the inferior fornix with canthotomy and cantholysis was performed, revealing a grayish-white cystic mass with a distinct boundary from surrounding tissues. During posterior separation to the eyeballs\u2019 posterior part, tight adhesion to the optic nerve was observed. Due to the mass\u2019s substantial size and the restricted surgical field, volume reduction was necessary. Approximately 12.5\u2009mL of the fluid was aspirated, and the mass was completely excised. Histopathological examination disclosed a fibrous capsule wall covered with squamous and glandular epithelium, along with visible brain tissue and a cartilage-like matrix consistent with orbital teratoma. One month postsurgery, the patient exhibited enophthalmos, conjunctival hyperemia, and keratitis on ocular examination. This was attributed to the mass\u2019s prior enlargement of the orbital cavity, resulting in postoperative enophthalmos. The cornea could not adhere to the eyelids, creating a space and causing corneal inflammation. After obtaining the consent of the patient\u2019s guardian, a second operation involved the implantation of an allogeneic sclera into the orbit to increase the orbital volume, alleviate fossa pitting and restore keratitis to normal. No recurrence of the teratomas was noted during the 1-year follow-up. The patient still had minor enophthalmos and outer canthus abnormality. The visual acuity remained consistent with pre-operation levels. Hertel exophthalmometry readings measured 10.5\u2009mm in the right eye and 8\u2009mm in the left. The remaining anterior segment examination showed no apparent abnormalities.",
+        "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\u2011white, 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\u2011like 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 Consci\u00eancia Fonol\u00f3gica Instrumento de Avalia\u00e7\u00e3o Sequencial - CONFIAS (11) was used. This protocol proposes tasks of synthesis, segmentation, rhyme, alliteration, initial and final syllable identification, exclusion and transposition. First, syllabic awareness, formed by nine items, is analyzed, followed by phonemic awareness, formed by seven items. Each hit is equivalent to one point, with 40 for syllabic awareness and 30 for phonemic awareness, totaling 70 points. Its results should be compared with the expected writing hypotheses based on Ferreiro and Teberosky (12). In this way, the following normal values were used: for the syllabic-alphabetic writing hypothesis, 27, 12 and 39 for the syllabic, phonemic and total score, respectively; for the alphabetic writing hypothesis, 31, 15 and 46.\n\nPhonological working memory: The Phonological Working Memory Test was used (13). In the application of this protocol, the assessor should begin with the non-word test, which consists of 40 invented words. The assessor should then say each word in the list, asking the child to repeat it immediately. The child has two attempts to repeat the words correctly. In the first attempt, each correct answer is worth two points, in the second attempt, the child is awarded one point, and in the third attempt, the child is awarded zero points. After this, the assessor should move on to the test of digits in direct and reverse order, which is scored in the same way as the pseudo-words. Depending on the age of the participant at the time of the assessments, the normal values of 69, 13 and 6 were used for pseudo-words, direct and reverse digits, respectively.\n\nAccess to the mental lexicon: the Rapid Automatic Naming Test (RAN)(14) was used in the evaluation and the Automatic Naming Test (TENA)(15) in the re-evaluation. Both tests aim to estimate the individual's ability to name a sequence of stimuli, that is, to measure the speed at which the child can verbalize a visual stimulus quickly. Two protocols were used, since the TENA had not yet been published at the time of the first evaluation. In addition, the TENA is a current and more complete protocol for the verification of normality, as it allows analysis according to age and months. The two tests used have similar application and are divided into four boards, where the child must name colors, objects, letters and digits. The naming must be done with the same movement that is used for reading - from left to right and from top to bottom. For T1, which used the RAN, the normality values correspond to children aged between 8 years and 8 years and 11 months, due to the age of the participant in that period, thus, it should have a score of 28, 29, 52 and 46 seconds for the subtests of digits, letters, objects and colors, respectively. For T2, the normality values of the age of 9 years and 6 months of the protocol (TENA) were used, with an expected score of 35, 32, 50, 53 seconds for the subtests of digits, letters, objects and colors, respectively.\n\nReading: First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated \u2013 LPI(16) was used, in which the child is asked to read aloud words and pseudowords, which are scored. 19 regular words, 20 irregular words and 20 pseudowords are arranged in black Arial font, size 24 and white background. The child may obtain a total of 59 points, since each correct reading is worth one point. After this, the Protocol for the Assessment of Reading of Expository Texts was used(17). This instrument aims to assess reading comprehension through directed questions about texts compatible with the subject's school year. It assesses and times patterns of silent and oral reading. This allows the reading level to be verified and compared. In addition, the number of words read per minute is averaged, allowing the reading speed to be verified and compared.\n\nWriting: To evaluate the writing, the child was asked to produce a text on a topic of their interest. After finishing the story, the professional asked the child to read out loud what was written. Furthermore, the child was asked to write the target words of the LPI(16) on a separate sheet, in order to carry out a dictation of words and pseudo-words. With this, a qualitative investigation of the writing was carried out, based on the orthographic analysis of Zorzi and Ciasca(18).\n\nThe remediation was based on a program used for children with dyslexia(19) and included activities that aimed to improve phonological abilities, such as: identification of graphemes and phonemes, phoneme pairs, syllable pairs, word pairs, addition and subtraction of phonemes, syllabic and phonemic manipulation, rhymes, alliteration, access to mental lexicon, visual working memory, auditory working memory and reading training. In all sessions, these activities were explored in a playful way, mainly directed to the metalinguistic aspects of phonological awareness. In reading training, the child was exposed to children's books from the Mico Maneco collection. This collection has various stories that increase the level of complexity of words, so it is possible to follow the child's progress. The activities performed and the child's evolution were described in his/her medical record at the end of each session.\n\nAnalysing the results found, with regard to performance in phonological awareness, in both assessments the child presented performance consistent with the hypotheses of writing presented in each period. In the first assessment, he received the syllabic-alphabetic writing hypothesis and in the second, the alphabetic one, demonstrating progress. The performance score progressed in both categories of the skill, syllabic (T1 = 35; T2 = 37) and phonemic (T1 = 14; T2 = 20) (Table 1). The progress of 4 successes in the phonemic level is highlighted, which can be explained due to the phonological remediation having been performed with focus on the phonemic level.\n\nThe results of phonological working memory at the time prior to phonological remediation expressed below-expected performance for the pseudo-word category, with 66 points in T1, with expected performance for T1 (ET1) of 69, and for the reverse-order digits category (T1 = 04; ET1 = 06) (Table 1). Despite this, it presented results within the expected range for the reverse-order digits category (T1 = 20; ET1 = 13). In the post-intervention evaluation (T2), the results are adequate for the age. It is also possible to notice advances in this skill in all categories, pseudo-word (T1 = 66; T2 = 69), reverse-order digits (T1 = 04; T2 = 12) (Table 1), which requires aspects of executive functions that assist in the rapid storage of the response, a differential aspect in high abilities.\n\nAs for the automatic rapid naming, it is noted that in T1, the performance is inadequate for the standards of normality in all subtests. It is also possible to say that, in T2, the performance was below the expected for the categories of digits (T2 = 41; ET2 = 35), objects (T2 = 59; ET2 = 50) and colors (T2 = 56; ET2 = 53). Only the category of letters presented results within the expected (T2 = 29; ET2 = 32). On the other hand, the advance in the speed of naming is visible for the subtests of letters (T1 = 37; T2 = 29), objects (T1 = 62; T2 = 59) and colors (T1 = 60; T2 = 56), with the exception of digits (T1 = 37; T2 = 41) (Table 1). With the decrease of the time of naming of the stimuli, it is possible to say that the child becomes more effective to access the mental lexicon at the level of the phonological and visual representation, which is also not usual in isolated dyslexia.\n\nAs for reading, in T1 she presented an alphabetic level and in T2 an orthographic level. In the first test, it was noted that there was difficulty mainly with visually similar letters and phonologically close. In addition, the student used sub-vocal support to decode and had an average reading of 20 words per minute, which demonstrates extremely slow decoding and is far below what is expected for her schooling. In the reassessment, she had an average of 94.4 words per minute in oral reading, which is considered adequate for her schooling. She demonstrated presence of prosody, rhythm, global reading, interest and adequate understanding. Qualitatively, it is observed that the child, even with adequate performance, read with a low intensity of speech, still demonstrating insecurity in carrying out the task.\n\nIn writing, it can be observed that in T1 the child had inadequate pencil grip, imprecise writing, with letter changes, omissions, hyper and hyposegments, repetition of words and low use of cohesive elements. In this period, it was shown with writing in the transition from the syllabic-alphabetic phase to the alphabetic phase. In T2 no significant change was observed, since his writing continued to be imprecise, with little intelligibility of the content, visual similarities between letters (such as \u201cd\u201d and \u201cb\u201d) and lack of punctuation. According to the sample collected, it was shown in the alphabetic phase of writing, although difficulties not expected for his age persisted. Despite this, it is noted that he used a greater repertoire in the use of vocabulary for the lexicon of visual input.\n\nAfter the analysis of the results in their entirety, it can be observed that the written language skills advanced during the interval between the evaluations, despite the persistence of consonant characteristics with dyslexia, as it still presents performance below the expected in the access to the mental lexicon and in writing - with the presence of exchanges between phonemes that are audibly and visually similar in a persistent way, omission of letters and hypersegmentation.\n",
+        "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\u00b0C for five hours. Upon admission to the local hospital\u2019s emergency department, his core temperature (Tc) was recorded as 40\u00b0C. The patient presented with persistent coma, dyspnea and gastrointestinal hemorrhage. No underlying diseases and relative family history was noted. Based on the characteristic presentation of hyperpyrexia, coma and multiple organ damage, a diagnosis of HS was established. He was admitted to emergency intensive care unit (ICU) of the local hospital and then received mechanical ventilation. The test results indicated the presence of pulmonary infection, hepatic and renal dysfunction, myocardial ischemia and coagulation disorders. The patient received initial management including rehydration (intravenously infused Lactated Ringer\u2019s solution and normal saline at a rate of 2.5mL/kg\u2219h), intravenous administration of Piperacillin Sodium and Tazobactam Sodium, vasoactive medications for blood pressure support, continuous mechanical ventilation, and continuous renal replacement therapy (CRRT) to manage subsequent anuria. The patient received plasma transfusion and was administered Tranexamic acid on day 5. The worsening of his condition led to his admission to the medical ICU of our hospital 7 days after HS.\n\nFollowing admission, Reverse-transcription polymerase chain reaction (RT-PCR) testing of a nasopharyngeal swab yielded positive results for SARS-CoV-2. The patient was diagnosed with HS and severe COVID-19 based on China\u2019s COVID-19 Diagnosis and Treatment Program (trial version 10): 1. real-time fluorescent RT-PCR detection of SARS-CoV-2 nucleic acid is positive; 2. respiratory failure and requires mechanical ventilation; 3. shock; 4. combined with multiple organ failure requiring intensive care. The patient had no contact with COVID-19 diagnosed patients or healthcare workers in the hospital, indicating community-acquired infection. The physical examination showed a Glasgow Coma Scale (GCS) score of 3/15, with scores of 1 for eye-opening, verbal response, and motor response. Additionally, the pupils were symmetrical and non-reactive. The heart rate was recorded at 106 bpm and blood pressure was maintained at 126/77 mmHg by continuously infusing norepinephrine at a rate of 0.4 ug/kg\u00b7min. The laboratory test results indicated a severe infection, along with anemia, thrombocytopenia, disseminated intravascular coagulation (DIC), as well as acute liver and kidney injury. The white blood cell count (WBC) decreased from 3.55\u00d7109/L to 3.13\u00d7109/L, lymphocytes significantly decreased from 0.25\u00d7109/L to 0.1\u00d7109/L, and neutrophil percentage (N%) increased to 85.3%. The Procalcitonin level measured 2.81 ng/mL and C-reactive protein (CRP) level was 32.6 mg/L. Sputum culture testing yielded Stenotrophomonas Maltophilia and Candida lipolytica. The central venous catheter culture test detected Staphylococcus epidermidis, but the continuous blood culture test yielded no positive results. The Computed Tomography (CT) scan revealed bilateral frontal subdural effusion, consolidation and atelectasis in the lower lungs, inflammation in the right upper lobe, bilateral pleural effusion, and a small amount of abdominal fluid.\n\nThe patient received synchronized intermittent mandatory ventilation with a positive end expiratory pressure of 5 mmH2O and an oxygen concentration of 80% and continuous administration of norepinephrine and pituitrin to sustain normal blood pressure. Polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration have been employed for the management of hepatic and renal dysfunction. The antibiotic was substituted with Meropenem and Thymalfasin was administered for 20 days to augment immune function. Mannitol was used to alleviate intracranial pressure for 3 days. To improve coagulation dysfunction, the patient received plasma and cryoprecipitate transfusions, continuous intravenous infusion of heparin sodium at 6000u/day and CRRT with sodium citrate for anticoagulant (8g/day) on day 7. Platelet transfusion was administered after 9 days of HS. His Tc fluctuated between 36 \u00b0C and 38.5 \u00b0C. CRRT was administered without anticoagulant on day 8. The patient had gastrointestinal hemorrhage and fever after 9 days of HS, but electronic gastroenteroscopy showed no signs of active bleeding. He underwent red blood cell suspension transfusion, hemostasis treatment and gastric acid suppression. Teicoplanin was added due to the presence of Methicillin-resistant Staphylococcus aureus isolated from sputum culture. The patient regained consciousness on day 13 with a GCS score of 14/15 and presented with a moderate fever. Gastrointestinal hemorrhage was not observed. Mechanical ventilation was discontinued and the tracheal tube was removed. But the creatinine levels increased following the suspension of CRRT on day 12.\n\nOn day 17, he developed sudden dyspnea with desaturation (oxygen saturation <85%) followed by a high fever (Tc: 39.3\u00b0C), necessitating reintubation and mechanical ventilation. Bronchoscopy revealed less sputum in both lungs and subbranches. He experienced a recurrence of coma, with a GCS score of 3/15. WBC increased to 14.94\u00d7109/L and NEU increased to 13.77\u00d7109/L. The levels of serum total bilirubin rose to 235.2 \u00b5mol/L, while creatinine increased to 441\u00b5mol/L. The brain CT scan revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. The patient underwent cooling therapy using CRRT with ice-cold replacement fluid, along with persistent administration of Meropenem and Teicoplanin for anti-infection treatment. Carpofungin was added on day 18 due to the observed elevation in serum levels of Aspergillus galactomannan, Aspergillus IgG antibody, and Candida mannan. The RT-PCR testing for SARS-CoV-2 returned negative results.\n\nThe patient\u2019s fever and infection improved on day 20, but he subsequently developed cerebral hemorrhage and hernia with bilateral dilated pupils. The dehydration therapy was used to reduce intracranial pressure, as surgery was refused by his family. On day 22, indicators of infection, levels of aspartate aminotransferase and creatinine increased again. Carbapenem-resistant Acinetobacter baumannii and A. fumigatus were cultured in the bronchoalveolar lavage fluid. The combination of Meropenem, Teicoplanin, and Carpofungine was administered for anti-infective therapy. The patient\u2019s condition progressively worsened over the next 7 days, ultimately resulting in his demise on day 29. The patients\u2019 inflammatory indicators, cytokines, and coagulation indicators are presented in Table 1.",
+        "diff_label_texts": "This report describes the first known case of heatstroke occurring together with SARS\u2011CoV\u20112 infection in a 52\u2011year\u2011old man. He had a recent cold and a positive self-test for COVID\u201119, then returned to work and lost consciousness after five hours outdoors in 35\u00b0C heat. On arrival at the hospital his core temperature was 40\u00b0C 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\u2011pressure 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\u2011pathogen 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": "low_health_literacy",
+        "fulltext": "A 19-year-old female presented to our hospital\u2019s emergency room with a chief complaint of a two-day history of headache, accompanied by recurrent nausea, vomiting, and a one-day fever. On admission, her physical examination revealed a high fever of 39.1\u00b0C, elevated blood pressure at 189/120 mmHg, and a pulse rate of 148 beats per minute. Laboratory results indicated an elevated white blood cell count of 14.77\u00d710^9/L and a neutrophil count of 13.55\u00d710^9/L, suggesting a possible infection or inflammatory response. Initial empirical treatment with antibiotics was administered due to suspected infection, but her symptoms persisted. Given her abnormal vital signs, elevated inflammatory markers, and lack of symptom improvement, the patient was admitted for further diagnostic evaluation and transferred to the intensive care unit for close monitoring. A year prior, the patient had presented with similar symptoms and was diagnosed with myocarditis at a local hospital based on clinical findings at that time. During that hospitalization, she was also diagnosed with hypertension and prescribed antihypertensive medications. However, after discharge, the patient did not adhere to the prescribed antihypertensive therapy and did not regularly monitor her blood pressure. Additionally, it is notable that her father had a history of sudden, unexplained death.\n\nTo investigate the underlying etiology of the patient\u2019s symptoms, a chest computed tomography (CT) scan was performed. Incidentally, this scan revealed a left adrenal mass with soft tissue density, measuring 43 mm \u00d7 36 mm. No pathological findings were observed in the head and chest CT scans. The electrocardiogram demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF. Transthoracic echocardiography did not reveal any significant abnormalities.\n\nOn the second day of admission, the patient exhibited rising levels of brain natriuretic peptide (BNP) and Troponin I (TnI). The cardiologist provisionally diagnosed the patient with myocarditis of uncertain etiology, based on clinical presentation, elevated cardiac biomarkers (BNP and TnI), and supportive electrocardiogram findings. Treatment was initiated with methylprednisolone (0.25 g daily) to address potential myocardial inflammation due to suspected myocarditis. Furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) were administered as diuretics to manage fluid retention and reduce cardiac workload. Perindopril amlodipine (10 mg: 5 mg daily) was prescribed as an angiotensin-converting enzyme inhibitor and calcium channel blocker combination to control blood pressure and reduce afterload. Metoprolol tartrate (25 mg every 12 hours) was used to manage heart rate and decrease myocardial oxygen demand, while esmolol (0.2 g/hour intravenous infusion), a short-acting beta-blocker, was administered for additional acute heart rate control due to sinus tachycardia. Due to concerns about a potential infection, moxifloxacin was added as empiric antibiotic therapy.\n\nGiven the patient\u2019s presentation with an adrenal mass and hypertension, the endocrinologist recommended an evaluation of the aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines along with their metabolites. In the recumbent position, plasma and urinary catecholamine levels were markedly elevated (Table 1), including plasma dopamine at 524.5 pmol/L, norepinephrine at 83975 pmol/L, and epinephrine at 10579.3 pmol/L. Additionally, the 24-hour urinary levels showed free adrenaline at 4368.89 nmol/24 hours, free norepinephrine exceeding 12697.60 nmol/24 hours, normetanephrine at 8312 nmol/24 hours, metanephrines at 4078 nmol/24 hours, and vanillylmandelic acid at 58.1 mg/24 hours. These findings supported a clinical diagnosis of pheochromocytoma. On the fifth day post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was substituted with terazosin for more targeted blood pressure management.\n\nAn enhanced abdominal CT scan further confirmed a left adrenal mass, highly suggestive of pheochromocytoma. Additionally, after obtaining informed consent, whole-exome sequencing was performed, revealing a heterozygous missense mutation, c.1900T > C: p. Cys634Arg, in the RET gene, leading to a substitution of cysteine with arginine at codon 634. This mutation raised suspicion for multiple endocrine neoplasia syndrome, prompting further evaluation of the thyroid and parathyroid glands. Thyroid color Doppler ultrasound identified a hypoechoic mass measuring 6 mm \u00d7 4 mm in the left thyroid lobe, and a mild elevation in calcitonin levels was noted. No additional significant abnormalities were detected.\n\nAs the patient\u2019s condition gradually improved, plasma cortisol and ACTH levels returned to normal. The patient was subsequently discharged with a prescription for metoprolol tartrate (100 mg every 12 hours) and ivabradine hydrochloride (5 mg every 12 hours) for home management. Three months later, after achieving stable clinical status, the patient underwent resection of the left adrenal tumor, which measured 50 mm \u00d7 40 mm \u00d7 30 mm. Immunohistochemical analysis confirmed positive staining for Vim, CD56, Syn, CgA, and NSE, with S-100 positive in Sertoli cells, while CKpan, CD10, MART-1/Melan-A, and Melan-A were negative. The Ki67 index was 1%, leading to a definitive diagnosis of adrenal pheochromocytoma. The patient was discharged without further medications and has since been regularly followed up postoperatively without recurrence of symptoms. Over a 15-month postoperative follow-up, the patient exhibited persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium levels showed a progressive increase (Table 2). Further parathyroid scintigraphy using 99mTc-MIBI was performed, and the conclusion was a negative result for parathyroid adenoma.",
+        "diff_label_texts": "A 19-year-old woman had a tumor on the gland that sits on top of the kidney that makes stress hormones. She did not have a dangerous attack, even though the tumor was large and she was given high-dose steroid medicine. A DNA test found a change in a gene called RET (c.1900T > C: p.Cys634Arg). This change is linked to a condition called MEN2A. Her thyroid had a small lump. A thyroid hormone called calcitonin was a little high. Her blood salts and the hormone that controls calcium (parathyroid hormone) were normal at first. For 15 months after surgery, calcitonin stayed a little high and the thyroid lump did not grow. Her parathyroid hormone and blood calcium slowly went up. A special scan of the parathyroid glands (99mTc-MIBI) did not show a tumor.",
+        "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": 60,
+        "label": "intermediate_health_literacy",
+        "fulltext": "A 19-year-old female presented to our hospital\u2019s emergency room with a chief complaint of a two-day history of headache, accompanied by recurrent nausea, vomiting, and a one-day fever. On admission, her physical examination revealed a high fever of 39.1\u00b0C, elevated blood pressure at 189/120 mmHg, and a pulse rate of 148 beats per minute. Laboratory results indicated an elevated white blood cell count of 14.77\u00d710^9/L and a neutrophil count of 13.55\u00d710^9/L, suggesting a possible infection or inflammatory response. Initial empirical treatment with antibiotics was administered due to suspected infection, but her symptoms persisted. Given her abnormal vital signs, elevated inflammatory markers, and lack of symptom improvement, the patient was admitted for further diagnostic evaluation and transferred to the intensive care unit for close monitoring. A year prior, the patient had presented with similar symptoms and was diagnosed with myocarditis at a local hospital based on clinical findings at that time. During that hospitalization, she was also diagnosed with hypertension and prescribed antihypertensive medications. However, after discharge, the patient did not adhere to the prescribed antihypertensive therapy and did not regularly monitor her blood pressure. Additionally, it is notable that her father had a history of sudden, unexplained death.\n\nTo investigate the underlying etiology of the patient\u2019s symptoms, a chest computed tomography (CT) scan was performed. Incidentally, this scan revealed a left adrenal mass with soft tissue density, measuring 43 mm \u00d7 36 mm. No pathological findings were observed in the head and chest CT scans. The electrocardiogram demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF. Transthoracic echocardiography did not reveal any significant abnormalities.\n\nOn the second day of admission, the patient exhibited rising levels of brain natriuretic peptide (BNP) and Troponin I (TnI). The cardiologist provisionally diagnosed the patient with myocarditis of uncertain etiology, based on clinical presentation, elevated cardiac biomarkers (BNP and TnI), and supportive electrocardiogram findings. Treatment was initiated with methylprednisolone (0.25 g daily) to address potential myocardial inflammation due to suspected myocarditis. Furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) were administered as diuretics to manage fluid retention and reduce cardiac workload. Perindopril amlodipine (10 mg: 5 mg daily) was prescribed as an angiotensin-converting enzyme inhibitor and calcium channel blocker combination to control blood pressure and reduce afterload. Metoprolol tartrate (25 mg every 12 hours) was used to manage heart rate and decrease myocardial oxygen demand, while esmolol (0.2 g/hour intravenous infusion), a short-acting beta-blocker, was administered for additional acute heart rate control due to sinus tachycardia. Due to concerns about a potential infection, moxifloxacin was added as empiric antibiotic therapy.\n\nGiven the patient\u2019s presentation with an adrenal mass and hypertension, the endocrinologist recommended an evaluation of the aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines along with their metabolites. In the recumbent position, plasma and urinary catecholamine levels were markedly elevated (Table 1), including plasma dopamine at 524.5 pmol/L, norepinephrine at 83975 pmol/L, and epinephrine at 10579.3 pmol/L. Additionally, the 24-hour urinary levels showed free adrenaline at 4368.89 nmol/24 hours, free norepinephrine exceeding 12697.60 nmol/24 hours, normetanephrine at 8312 nmol/24 hours, metanephrines at 4078 nmol/24 hours, and vanillylmandelic acid at 58.1 mg/24 hours. These findings supported a clinical diagnosis of pheochromocytoma. On the fifth day post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was substituted with terazosin for more targeted blood pressure management.\n\nAn enhanced abdominal CT scan further confirmed a left adrenal mass, highly suggestive of pheochromocytoma. Additionally, after obtaining informed consent, whole-exome sequencing was performed, revealing a heterozygous missense mutation, c.1900T > C: p. Cys634Arg, in the RET gene, leading to a substitution of cysteine with arginine at codon 634. This mutation raised suspicion for multiple endocrine neoplasia syndrome, prompting further evaluation of the thyroid and parathyroid glands. Thyroid color Doppler ultrasound identified a hypoechoic mass measuring 6 mm \u00d7 4 mm in the left thyroid lobe, and a mild elevation in calcitonin levels was noted. No additional significant abnormalities were detected.\n\nAs the patient\u2019s condition gradually improved, plasma cortisol and ACTH levels returned to normal. The patient was subsequently discharged with a prescription for metoprolol tartrate (100 mg every 12 hours) and ivabradine hydrochloride (5 mg every 12 hours) for home management. Three months later, after achieving stable clinical status, the patient underwent resection of the left adrenal tumor, which measured 50 mm \u00d7 40 mm \u00d7 30 mm. Immunohistochemical analysis confirmed positive staining for Vim, CD56, Syn, CgA, and NSE, with S-100 positive in Sertoli cells, while CKpan, CD10, MART-1/Melan-A, and Melan-A were negative. The Ki67 index was 1%, leading to a definitive diagnosis of adrenal pheochromocytoma. The patient was discharged without further medications and has since been regularly followed up postoperatively without recurrence of symptoms. Over a 15-month postoperative follow-up, the patient exhibited persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium levels showed a progressive increase (Table 2). Further parathyroid scintigraphy using 99mTc-MIBI was performed, and the conclusion was a negative result for parathyroid adenoma.",
+        "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\u2011dose 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\u2011MIBI 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 38\u00baC). Chest pain was localized to the costal margin region and worsened with cough, without diurnal variation. The patient-reported relief with paracetamol. There were no complaints of joint pain, weight loss, anorexia, fatigue, episodes of syncope or exercise restriction. In fact, he practiced sports regularly\u2014canoeing 2 times a week. No evidence of an infectious exposure or contact with household or environmental fumes, dust, or mineral oils was described. There was no known family history of cardiopulmonary conditions. He had a chest radiograph taken 4 years earlier during an acute illness, which showed a marked interstitial infiltrate that was presumptively treated with azithromycin with no further clinical symptoms and no further follow-up.\n\nOn admission, the patient\u2019s temperature was 37.8\u00b0C with normal peripheral oxygen saturation (99%) in room air. His heart (93 beats per minute) and respiratory rate (15 breaths per minute) were normal and blood pressure was on the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two thirds of the chest with no adventitious sounds. No respiratory distress, finger clubbing, cyanosis, abnormal heart sounds, or other findings were present. Chest radiograph revealed a marked interstitial infiltrate, comparable with his previous examination. A thoracic computed tomography (CT) revealed multiple bilateral areas of ground-glass opacities involving > 65% of lung parenchyma, suggestive of PAP. Respiratory viral testing was negative, and he remained stable throughout his monitoring in the emergency department. He was discharged with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) to cover a potential respiratory infection, with clinical resolution of symptoms and was sent for follow-up at the pediatric respiratory clinic.\n\nUpon further investigation in the outpatient setting, positive antinuclear antibodies (ANAs) at a titer of 1/89 with a fine speckled pattern were detected, while other autoantibodies tested negative and immunoglobulin levels remained within normal limits. Bronchoalveolar lavage revealed fluid with a milky appearance and positive periodic acid-Schiff staining; microbiological examination, including for mycobacteria, returned negative results. Spirometry indicated a mild restrictive pattern with reduced forced vital capacity (FVC) at 2.92 L (77%) and forced expiratory volume in 1 second (FEV1) at 3.21 L (69.9%), alongside a normal FEV1/FVC ratio (109%). In addition, the DLCO single breath (SB) showed a moderate decrease at 13.8 ml/min/mmHg (48.6%). Suspecting PAP, a genetic panel was conducted, which showed no mutations associated with surfactant dysfunction. Subsequently, GM-CSF antibody testing was performed with a positive result, raising suspicion for AI-PAP. At 20 months of follow-up, the patient remains asymptomatic and continues to exercise regularly. He repeated spirometry testing with normal FVC at 4.03 L (81.3%); FEV1 at 3.71 L (87.5%); FEV1/FVC ratio at 91.96% and DLCO SB at 25.54 ml/min/mmHg (83.7%). As the patient remains stable with no respiratory symptoms, we decided to defer treatment and continue monitoring with regular clinic visits.",
+        "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 \u201ccrazy paving,\u201d involving more than 65% of the lung, which raised concern for pulmonary alveolar proteinosis (PAP). Respiratory viral testing, including SARS-CoV-2, was negative. Bronchoalveolar lavage yielded milky fluid with positive periodic acid\u2013Schiff staining. Pulmonary function testing showed a mild restrictive pattern (FVC 77%) and a moderately reduced diffusing capacity (DLCO 48.6%). A genetic panel found no mutations linked to surfactant dysfunction. Anti\u2013GM-CSF antibodies were strongly positive, supporting autoimmune PAP. At 20 months, he remains asymptomatic, and spirometry has normalized.",
+        "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\u2011upright 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\u2014likely over a decade. The patient was discharged in stable condition with 0.9% sodium chloride nasal irrigations and had an unremarkable two-week follow-up.",
+        "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\u20134 days. Family history remarkable for paternal grandfather diagnosed with non-ischaemic cardiomyopathy and a pacemaker at age 86 years old. Patient lives with both parents and denies any smoking, ethanol consumption, recreational drug use, abuse or neglect at home. He worked at auto-part shop and planned to start college soon.\n\n\nInvestigations\n\n\nIn the ED, serum troponin I levels were found to be elevated and ECG showed diffuse ST-segment elevation. He was admitted to the local hospital and initial workup was remarkable for an enlarged cardiac silhouette and mild pulmonary oedema observed on chest X-ray, a transthoracic echocardiogram (TTE) demonstrating left ventricular ejection fraction (LVEF) of 40%, with severe left ventricular (LV) concentric hypertrophy and mild posterior pericardial effusion. Additionally, the patient was found to have elevated titres for Coxsackie virus A and B. His symptoms initially improved with the initiation of ibuprofen and colchicine. Cardiac catheterisation was performed, which revealed no evidence of coronary artery disease. Repeat TTE showed an LVEF of 40%\u201345%, hypokinesis of anteroapical and inferolateral wall, with an elevated LV end-diastolic pressure, consistent with diastolic dysfunction. Chest CT angiogram showed evidence of pneumonitis and a pericardial effusion. And at this point, the constellation of symptoms was thought to be secondary to Coxsackie myopericarditis, for which he continued to receive medical treatment as previously mentioned.\n\nOn the fourth day of admission, the patient became diaphoretic, tachycardic and hypotensive with an undetectable blood pressure. Emergent TTE showed large pericardial effusion with impending cardiac tamponade features, and pericardiocentesis was performed. During the procedure, the patient developed pulseless electrical activity (PEA) cardiac arrest and received advanced cardiovascular support for 30\u2009min. Ultimately patient was intubated, placed on venous-arterial extracorporeal membrane oxygenation (VA ECMO) and started on vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min), with numerous transfusions (9 packed red bloodcells, 10 units of platelets, 10 units of cryoprecipitate and 4 units of fresh frozen plasma) due to significant oozing of blood from the ECMO cannula. He was transferred to our hospital where endomyocardial biopsy (EMB) was then obtained due to concern of fulminant myocarditis and to test for other infiltrative cardiomyopathies. Pathology reports showed no signs suggestive of inflammatory or infiltrative process in the endomyocardium. Coxsackie Abs were repeated and were positive for Cox A type 9, Coxsackie B2 and Coxsackie B6, and an elevated Epstein-Barr virus (EBV) DNA quantitative PCR at 133\u2009000\u2009IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%\u201315% with previously noted severe LV concentric hypertrophy (1.9\u2009cm septum and 2.2\u2009cm in the inferolateral wall).\n\nThe patient was started on intravenous immunoglobulin (IVIG) for treatment of Coxsackie myocarditis, and broad-spectrum antibiotics due to worsening leucocytosis, but with no identified infectious focus. Colchicine was discontinued due to concern for rhabdomyolysis, with elevation of serum creatine kinase level to 2874 unit/L. Vasopressors were then discontinued and the patient was extubated. He also developed episode of flushing, fever, dyspnoea and decreasing oxygen saturation, with chest X-ray showing congested lung parenchyma with concerns for ARDS, therefore, IVIG was stopped.\n\nGiven improvement of cardiac function in another TTE with LVEF of 25%\u201330%, it was decided to attempt to remove the ECMO, which was unsuccessful. The patient remained on ECMO support and emergent discussion with heart failure team took place to determine best approach. The patient was evaluated for possible left ventricle assist device, however, deemed not a candidate due to significant global concentric LV hypertrophy, and the multidisciplinary team agreed to facilitate emergency listing for heart transplantation, with consideration to transition to another cardiovascular support such as intra-aortic balloon pump, with potential inotrope support.\n\nDuring further evaluation for possible heart transplant, an incisional biopsy of a 1\u00d71\u2009inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2\u20133 months before presenting to the ED. Pathology report of the right upper extremity mass showed aggressive EBV (+) NK/T-cell lymphoma with a cytotoxic immunophenotype (positive for CD 2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1 and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybridisation), and a modified SMILE (Steroids, Methotrexate with leucovorin, Ifosfamide with mesna, L-asparaginase and Etoposide) chemotherapy regimen was started. In situ hybridisation of the EMB previously obtained were negative for EBV-RNA.\n\nCardiac MRI was obtained, which revealed hypokinesis of the inferolateral and anterolateral wall, as previously described by TTE, delayed enhancement in the subendocardial and transmural distribution in these regions, with relative sparing of the septum. Additionally, avid enhancement and thickening of the pericardium, without a mass identified, and a pocket of pericardial fluid with septations, concerning for loculations, were also noted.\n\n\nDifferential diagnosis\n\nThe constellation of symptoms (shortness of breath, orthopnoea, hypotension and subjective fevers), with findings such as diffuse ST-segment elevation on ECG, leakages of cardiac markers (troponin), elevated Coxsackie virus titres (both of serotype A and B), as well as echocardiographic findings of pericardial effusion; all seemed to correlate with a classic presentation of viral pericarditis clinical due to Coxackie virus. However, despite medical treatment with colchicine, the patient continued to decompensate and eventually required pericardiocentesis due to cardiac tamponade, then developed cardiac arrest and ultimately requires ECMO support, for what seems acute onset heart failure. In this setting, fulminant myocarditis secondary to Coxsackie virus was considered. Cardiotropic RNA virus, such as Coxackie viruses, induce receptor-mediated endocytosis, with viral replication contributing to cellular dysfunction and ultimately apoptosis of the cell.1 When susceptible individuals are infected with highly virulent viral strains, maladaptive immunologic activity can occur, leading to persistent activation of T cells and continued antibody-mediated myocyte destruction, which can ultimately lead to fulminant myocarditis. EBV myocarditis could also explain the rapid deterioration in the setting of a positive EBV PCR, which is a more sensitivity test than traditional serologies for detection of acute infection.2 However, in situ hybridisation was negative for EBV-RNA.\n\nNevertheless, the significant concentric hypertrophy observed on the initial TTEs and the atypical delayed enhancement observed on the cardiac MRI are not explained by this diagnosis. Additionally, the EMB did not show an inflammatory process.\n\nFortuitous finding of EBV (+) NK/T-cell lymphoma by incisional biopsy of the right upper extremity allowed for a more fitting diagnosis for this case. The pericardial effusion, unresponsive to initial medical treatment and new acute heart failure with concentric hypertrophic cardiomyopathy, in the setting of newly diagnosed NK/T-cell lymphoma, raises the possibility of NK/T-cell lymphoma with involvement of the myocardium and pericardium as the most adequate diagnosis in this scenario, which englobes all the features previously mentioned in this case.\n\nOther differentials taken into consideration include infiltrative cardiomyopathy such as amyloidosis. However, Congo red staining of the EMB samples failed to demonstrate deposition of amyloid.\n\n\nTreatment\n\nGiven the diagnosis of extranodal NK/T-cell lymphoma (ENKTCL) with suspected pericardial involvement and no bone marrow involvement, modified SMILE regimen was desired as the first-line chemotherapy regimen. This regimen includes dexamethasone, ifosfamide, mesna and etoposide, and excluded methotrexate, due to evidence of third-spacing and effusions, which could lead to delayed excretion and increased risk of toxicity.\n\nHowever, due to his compromised cardiac function, it was believed that the patient would not tolerate cytotoxic chemotherapy which requires aggressive intravenous, and alternatively, emergent chemotherapy regimen was instituted: carboplatin (day 1\u2013day 3), etoposide (day 1\u2013day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7\u2013day 21). This regimen proved effective, as evidenced by rapid recovery of the LV function and overall haemodynamic stability, and decision was made to incorporate a modified SMILE chemotherapy regimen, of which he received two cycles. Then chemotherapy regimen was changed to dexamethasone, gemcitabine, carboplatin and peg-asparaginase (DDGP). The patient received two cycles of DDGP. A full body positron emission tomography (PET) scan was negative for lymphoma. The plan is to continue two more cycles of chemotherapy (to complete six total cycles of chemotherapy). Currently, the patient is considering radiation therapy and possible stem cell transplant, after completion of the chemotherapy regimen. Additionally, the patient is currently on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation.\n\n\nOutcome and follow-up\n\nThe patient has completed five out of six chemotherapy sessions with the previously mentioned regimens. After initiation of chemotherapy and optimal medical treatment for heart failure, the patient has recovered much of his cardiac function, as evidenced by an LVEF of 55%, no wall motion abnormalities and normal myocardial wall thickness on his most recent TTE. He continues to be followed by heart failure/cardiology team and oncology team in clinic.",
+        "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\u2013Barr virus. He started cancer medicines. His heart pumping got better. The fluid around his heart went away. The thick heart muscle slowly went back toward normal.",
+        "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\u20134 days. Family history remarkable for paternal grandfather diagnosed with non-ischaemic cardiomyopathy and a pacemaker at age 86 years old. Patient lives with both parents and denies any smoking, ethanol consumption, recreational drug use, abuse or neglect at home. He worked at auto-part shop and planned to start college soon.\n\n\nInvestigations\n\n\nIn the ED, serum troponin I levels were found to be elevated and ECG showed diffuse ST-segment elevation. He was admitted to the local hospital and initial workup was remarkable for an enlarged cardiac silhouette and mild pulmonary oedema observed on chest X-ray, a transthoracic echocardiogram (TTE) demonstrating left ventricular ejection fraction (LVEF) of 40%, with severe left ventricular (LV) concentric hypertrophy and mild posterior pericardial effusion. Additionally, the patient was found to have elevated titres for Coxsackie virus A and B. His symptoms initially improved with the initiation of ibuprofen and colchicine. Cardiac catheterisation was performed, which revealed no evidence of coronary artery disease. Repeat TTE showed an LVEF of 40%\u201345%, hypokinesis of anteroapical and inferolateral wall, with an elevated LV end-diastolic pressure, consistent with diastolic dysfunction. Chest CT angiogram showed evidence of pneumonitis and a pericardial effusion. And at this point, the constellation of symptoms was thought to be secondary to Coxsackie myopericarditis, for which he continued to receive medical treatment as previously mentioned.\n\nOn the fourth day of admission, the patient became diaphoretic, tachycardic and hypotensive with an undetectable blood pressure. Emergent TTE showed large pericardial effusion with impending cardiac tamponade features, and pericardiocentesis was performed. During the procedure, the patient developed pulseless electrical activity (PEA) cardiac arrest and received advanced cardiovascular support for 30\u2009min. Ultimately patient was intubated, placed on venous-arterial extracorporeal membrane oxygenation (VA ECMO) and started on vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min), with numerous transfusions (9 packed red bloodcells, 10 units of platelets, 10 units of cryoprecipitate and 4 units of fresh frozen plasma) due to significant oozing of blood from the ECMO cannula. He was transferred to our hospital where endomyocardial biopsy (EMB) was then obtained due to concern of fulminant myocarditis and to test for other infiltrative cardiomyopathies. Pathology reports showed no signs suggestive of inflammatory or infiltrative process in the endomyocardium. Coxsackie Abs were repeated and were positive for Cox A type 9, Coxsackie B2 and Coxsackie B6, and an elevated Epstein-Barr virus (EBV) DNA quantitative PCR at 133\u2009000\u2009IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%\u201315% with previously noted severe LV concentric hypertrophy (1.9\u2009cm septum and 2.2\u2009cm in the inferolateral wall).\n\nThe patient was started on intravenous immunoglobulin (IVIG) for treatment of Coxsackie myocarditis, and broad-spectrum antibiotics due to worsening leucocytosis, but with no identified infectious focus. Colchicine was discontinued due to concern for rhabdomyolysis, with elevation of serum creatine kinase level to 2874 unit/L. Vasopressors were then discontinued and the patient was extubated. He also developed episode of flushing, fever, dyspnoea and decreasing oxygen saturation, with chest X-ray showing congested lung parenchyma with concerns for ARDS, therefore, IVIG was stopped.\n\nGiven improvement of cardiac function in another TTE with LVEF of 25%\u201330%, it was decided to attempt to remove the ECMO, which was unsuccessful. The patient remained on ECMO support and emergent discussion with heart failure team took place to determine best approach. The patient was evaluated for possible left ventricle assist device, however, deemed not a candidate due to significant global concentric LV hypertrophy, and the multidisciplinary team agreed to facilitate emergency listing for heart transplantation, with consideration to transition to another cardiovascular support such as intra-aortic balloon pump, with potential inotrope support.\n\nDuring further evaluation for possible heart transplant, an incisional biopsy of a 1\u00d71\u2009inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2\u20133 months before presenting to the ED. Pathology report of the right upper extremity mass showed aggressive EBV (+) NK/T-cell lymphoma with a cytotoxic immunophenotype (positive for CD 2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1 and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybridisation), and a modified SMILE (Steroids, Methotrexate with leucovorin, Ifosfamide with mesna, L-asparaginase and Etoposide) chemotherapy regimen was started. In situ hybridisation of the EMB previously obtained were negative for EBV-RNA.\n\nCardiac MRI was obtained, which revealed hypokinesis of the inferolateral and anterolateral wall, as previously described by TTE, delayed enhancement in the subendocardial and transmural distribution in these regions, with relative sparing of the septum. Additionally, avid enhancement and thickening of the pericardium, without a mass identified, and a pocket of pericardial fluid with septations, concerning for loculations, were also noted.\n\n\nDifferential diagnosis\n\nThe constellation of symptoms (shortness of breath, orthopnoea, hypotension and subjective fevers), with findings such as diffuse ST-segment elevation on ECG, leakages of cardiac markers (troponin), elevated Coxsackie virus titres (both of serotype A and B), as well as echocardiographic findings of pericardial effusion; all seemed to correlate with a classic presentation of viral pericarditis clinical due to Coxackie virus. However, despite medical treatment with colchicine, the patient continued to decompensate and eventually required pericardiocentesis due to cardiac tamponade, then developed cardiac arrest and ultimately requires ECMO support, for what seems acute onset heart failure. In this setting, fulminant myocarditis secondary to Coxsackie virus was considered. Cardiotropic RNA virus, such as Coxackie viruses, induce receptor-mediated endocytosis, with viral replication contributing to cellular dysfunction and ultimately apoptosis of the cell.1 When susceptible individuals are infected with highly virulent viral strains, maladaptive immunologic activity can occur, leading to persistent activation of T cells and continued antibody-mediated myocyte destruction, which can ultimately lead to fulminant myocarditis. EBV myocarditis could also explain the rapid deterioration in the setting of a positive EBV PCR, which is a more sensitivity test than traditional serologies for detection of acute infection.2 However, in situ hybridisation was negative for EBV-RNA.\n\nNevertheless, the significant concentric hypertrophy observed on the initial TTEs and the atypical delayed enhancement observed on the cardiac MRI are not explained by this diagnosis. Additionally, the EMB did not show an inflammatory process.\n\nFortuitous finding of EBV (+) NK/T-cell lymphoma by incisional biopsy of the right upper extremity allowed for a more fitting diagnosis for this case. The pericardial effusion, unresponsive to initial medical treatment and new acute heart failure with concentric hypertrophic cardiomyopathy, in the setting of newly diagnosed NK/T-cell lymphoma, raises the possibility of NK/T-cell lymphoma with involvement of the myocardium and pericardium as the most adequate diagnosis in this scenario, which englobes all the features previously mentioned in this case.\n\nOther differentials taken into consideration include infiltrative cardiomyopathy such as amyloidosis. However, Congo red staining of the EMB samples failed to demonstrate deposition of amyloid.\n\n\nTreatment\n\nGiven the diagnosis of extranodal NK/T-cell lymphoma (ENKTCL) with suspected pericardial involvement and no bone marrow involvement, modified SMILE regimen was desired as the first-line chemotherapy regimen. This regimen includes dexamethasone, ifosfamide, mesna and etoposide, and excluded methotrexate, due to evidence of third-spacing and effusions, which could lead to delayed excretion and increased risk of toxicity.\n\nHowever, due to his compromised cardiac function, it was believed that the patient would not tolerate cytotoxic chemotherapy which requires aggressive intravenous, and alternatively, emergent chemotherapy regimen was instituted: carboplatin (day 1\u2013day 3), etoposide (day 1\u2013day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7\u2013day 21). This regimen proved effective, as evidenced by rapid recovery of the LV function and overall haemodynamic stability, and decision was made to incorporate a modified SMILE chemotherapy regimen, of which he received two cycles. Then chemotherapy regimen was changed to dexamethasone, gemcitabine, carboplatin and peg-asparaginase (DDGP). The patient received two cycles of DDGP. A full body positron emission tomography (PET) scan was negative for lymphoma. The plan is to continue two more cycles of chemotherapy (to complete six total cycles of chemotherapy). Currently, the patient is considering radiation therapy and possible stem cell transplant, after completion of the chemotherapy regimen. Additionally, the patient is currently on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation.\n\n\nOutcome and follow-up\n\nThe patient has completed five out of six chemotherapy sessions with the previously mentioned regimens. After initiation of chemotherapy and optimal medical treatment for heart failure, the patient has recovered much of his cardiac function, as evidenced by an LVEF of 55%, no wall motion abnormalities and normal myocardial wall thickness on his most recent TTE. He continues to be followed by heart failure/cardiology team and oncology team in clinic.",
+        "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\u2013Barr virus (EBV) PCR. A separate biopsy of a small painless mass on his right arm unexpectedly showed EBV-positive natural killer/T\u2011cell 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\u2014the body\u2019s filters\u2014were hurt by a germ called BK virus. A small kidney sample showed long\u2011lasting irritation and damage from this virus. A blood test also showed a high amount of BK virus (log 4.5). Her doctors turned down her anti\u2011rejection medicines to help. After about two years, her kidney numbers stayed steady. Her creatinine was 2.5 mg/dL and her GFR was 23.4 mL/min/1.73m2.",
+        "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\u2011dose 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 \u03b2-thalassemia major presented to the radiology department to undergo MRI to quantify myocardial, hepatic, and pancreatic iron deposition. The clinical history of the patient included a transfusion-dependent \u03b2-thalassemia condition (genotype HBB:c.118C\u2009>\u2009T/ HBB:c.93-21G\u2009>\u2009A), diagnosed at the age of 7 years, despite the fact that the first transfusion was carried out at 2 years. As a consequence of \u03b2-thalassemia, the patient underwent splenectomy and cholecystectomy.\n\nAt the moment of MRI, she had a negative HCV-RNA (Hepatitis C virus-Ribonucleic acid) test, no osteoporosis or other endocrine, cardiac, or hepatic complications, and good iron levels. The patient\u2019s therapy included iron chelation with deferasirox, vitamin D, and luspatercept, an erythropoiesis modulator started 2 years before the MRI examination (good response, with an increase of about 35% of transfusion interval duration). Transfusion therapy included two units of concentrated and filtered red blood cells every 25 days with pre-transfusion hemoglobin values of 10\u201310.5 g/dl.\n\nOn MRI, a solid mass with lobulated and regular contours was incidentally identified within the prevascular compartment of the mediastinum.\n\nThe lesion was mildly hyperintense on T2-weighted images (T2-wi) and isointense on T1-wi. The mediastinal mass in question was discernible in a prior MRI examination conducted for the same purpose in 2020 before starting luspatercept therapy, albeit with a marginal enlargement.\n\nThere were no other apparent abnormalities observed in the remaining mediastinal compartments. No pleural or pericardial effusions were present.\n\nThe neurological examination was unremarkable, and in the preceding months, the patient exhibited no symptoms of mediastinal syndrome associated with compression of the adjacent neurovascular structures. Moreover, she did not exhibit any fever or experience any weight loss.\n\nFor further evaluation, the patient underwent 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) and chest CT with contrast media. On PET-CT, the mediastinal mass showed only mild FDG uptake (SUVmax\u2009=\u20094.3); no other sites of abnormal radiotracer uptake were reported in the neck, chest, abdomen, and skeleton. On CT images, the lesion presented regular margins, solid density, and mild contrast enhancement. The adjacent structures did not exhibit any signs of invasion, and lymphadenopathies or extra-thoracic disease were not present. Such radiological features, the indolent behaviour over time, the absence of systemic symptoms, and the lack of avid FDG uptake on PET-CT scan made the diagnosis of thymoma probable.\n\nHowever, on lung window visualization, multiple rounded areas of parenchymal lucency, consistent with thin-walled cysts distributed symmetrically throughout both lungs, with normal intervening parenchyma, were evident.\n\nNo nodules or other interstitial abnormalities were associated with the cysts. No pneumothorax was detected. Coherently with thalassemic bone disease, the ribs appeared widened, and the spine displayed mild platyspondyly. The remaining portion of the chest and visible upper abdomen were unremarkable. The radiological findings were consistent with cystic lung disease, most likely LAM.\n\nThe patient was then referred to the pulmonary clinic for further evaluation. She was a never-smoker and did not report any respiratory symptoms. In particular, she denied a history of chronic cough, recurrent respiratory infections, or pneumothorax. No cutaneous lesions, notably facial fibrofolliculomas, were evident. On chest examination, the lung fields were clear. Peripheral capillary oxygen saturation was normal (98%), with a heart rate of 75 beats per minute. Pulmonary function tests revealed a substantial reduction in diffusing capacity of the lungs for carbon monoxide (DLCO; 42% of the predicted value), partly imputable to the condition of anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of the predicted value. After discussion in a multidisciplinary tumor board setting, including a pulmonologist, the patient underwent left thoracoscopic thymectomy and concomitant lingual segment wedge resection. The histopathological report revealed a morphological finding and immunohistochemical pattern referable to type B2 thymoma with focal infiltration of the capsule. Extracapsular extension was not evident. However, the lesion was present at the resection margin (stage IIa according to Masaoka\u2013Koga; stage 1a according to the tumor, node, metastasis [TNM] classification).\n\nRegarding the lung parenchyma, histopathologic analysis described lung parenchyma with cysts of variable size lined by spindle cells in myoid habit with immunohistochemical reactivity for actin, estrogen, progesterone receptors, and HMB45 (focal positivity). Modest chronic interstitial inflammation, vascular congestion, and recent blood extravasation were evident. These morphological findings were compatible with pulmonary LAM.\n\nA final histological diagnosis of thymoma and pulmonary LAM was made. For the neoplastic condition, the patient was a candidate for adjuvant radiation therapy due to the microscopically incomplete resection (R1). For LAM with concomitant \u03b2-thalassemia, treatment with sirolimus was recommended.",
+        "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 \u03b2-thalassemia major underwent magnetic resonance imaging to quantify myocardial, hepatic, and pancreatic iron deposition. Her medical history included transfusion-dependent \u03b2-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\u2009years of age) SLE prepared for kidney transplantation. Due to LN (class III, then IV), starting at childhood, she was treated with steroids, together with cyclophosphamide, replaced later by methotrexate and then azathioprine. Hence, the partial remission of nephrotic syndrome was achieved and from 2002 the patient did not receive any immunosuppressive therapy. She was also HBV and HCV positive. SLE involvement of circulatory system presented with early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at the age of 20. In 2007, because of deterioration of kidney function with a serum creatinine concentration of 2.2\u2009mg/dL and proteinuria of 2\u2009g/day, the kidney biopsy was performed. The biopsy showed active and sclerotic focal proliferative lupus nephritis nevertheless immunosuppressive therapy was not introduced for the reason of active replication of HCV. The kidney function was gradually deteriorating over time. Despite cardiac intervention (PCI RCA), the patient developed severe post-infarction and dilated cardiomyopathy and required ICD implantation in primary prevention in 2009. Later, on lupus and secondary cardiomyopathic background, the patient developed severe MV and TV regurgitation. For this reason, the patient underwent mitral and tricuspid valve repair and left ventricle volume reduction surgery complicated by low cardiac output syndrome with a need for intra-aortic balloon pump use (2014). In the postoperative period, the kidney function deteriorated, requiring the initiation of renal replacement therapy. The patient has been on dialysis for 4\u2009years. While being on active waiting list for kidney transplantation presented remission of laboratory indices of lupus (complement splits within normal limits: C3\u20130,93\u2009g/l, C4\u20130,4\u2009g/l, ANA negative) and persisting circulatory insufficiency with markedly reduced stair-climbing capacity (to one flight of stairs) with elevated BNP 619\u2009pg/ml (n. 0\u2013100). In transthoracic echocardiography, performed before renal transplantation, the left ventricle and the left atrium were significantly enlarged and the left ventricular systolic function was significantly reduced with LVEF 26% and GLS -3. Due to the implantation of the mitral ring, it was not possible to assess the left ventricular diastolic function. The high tricuspid regurgitant flow gradient with widened and poorly respiratory mobile inferior vena cava indicated a high probability of pulmonary hypertension. Furthermore, while preparing the patient for the surgical procedure, it was decided to include cardioprotective therapy with Levosimendan. Due to the time frame associated with the transplantation procedure, the drug infusion was started as soon as possible after cross-match results were known, immediately after the dialysis session. The infusion at a dose of 0.1\u2009\u03bcg/kg/min was continued after surgery for a total of 24\u2009h. The patient\u2019s anesthesia for kidney transplantation and perioperative care included the aspect of optimizing transplanted kidney perfusion, avoiding the use of renal toxic drugs and those excreted by properly functioning kidneys, as well as the use of nephroprotective agents. Because of the patient\u2019s cardiological burden, including recurrent episodes of extrasystole proceeding with decompensation of the circulatory system, together with the need of ICD turning off for the transplantation period, the Swan-Ganz catheter for hemodynamic assessment was not used. Anesthesia monitoring was limited the to ECG, central catheter with CVP assessment, direct blood pressure measurement from the cannula inserted into the radial artery, and cardiac ultrasound. In the perioperative period the CVP parameter was used to assess the volatility, and in the postoperative period, a cardiac ultrasound was used along with the assessment of VCI respiratory fill and motility. The therapy was aimed at the standard of fluid therapy called Goal Directed Therapy (GDT). During general anesthesia, fentanyl, triacrium, propofol, desflurane, antibiotic therapy, and standard immunosuppressive treatment were used as well as 25\u2009g of mannitol infusion was administered as a nephroprotective treatment and 0.9% NaCl as a fluid therapy. In the course of postoperative immunosuppression, she received steroids, tacrolimus with mycophenolate mofetil which was stopped due to persistent leukopenia and cytomegalovirus infection. Furthermore delayed graft function was observed with a need for hemodialysis for almost 6\u2009weeks (mostly due to fluid retention). BNP levels raised to 2996\u2009pg/ml and then slowly decreased. The kidney biopsy performed 2\u2009weeks after transplantation revealed acute rejection (AR II B Banff 2015) with ATN. Finally, the patient was discharged from the hospital on the 67th POD with the serum creatinine concentration of 1.4\u2009mg/dL and BNP level of 1794\u2009pg/ml. One month after kidney transplantation, there was a reduction in left ventricular dimensions, improved systolic function in the EF (increase to 30%) and GLS (decrease to \u2212\u20096) assessment. In addition, there was a decrease in the tricuspid regurgitant flow gradient with normal width and respiratory motility of the IVC, which indicates a low probability of pulmonary hypertension. The improvement of echocardiographic parameters also reflected the simultaneous improvement of exercise capacity in the recipient from NYHA III/IV to NYHA II. In the 5-month observation, further improvement of heart function with a drop of BNP to 1066\u2009pg/ml and normal kidney function were noted.",
+        "diff_label_texts": "This report describes a 49-year-old woman with long\u2011standing 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\u2011ventricle 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 \u00b5g/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\u2011proven 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\u2009years. 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\u2122 E6, ultrasonography system with a linear 13\u20135 MHz probe for unilateral PGONB. The patient\u2019s neck was prone to flexion. The linear probe was initially transversely positioned on the occipital protuberance and then advanced caudally, demonstrating that the C2 spinous process resembled the two horns. Through lateral probe movement, the inferior muscles of the obliquus capitis and semispinalis capitis were located. Here, the superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle were identified to be the greater occipital neuron (GON). From this location, a 22-gauge spinal needle and 3 ccs of bupivacaine at a concentration of 0.5% were used to perform GON blocking. The intensity of her attack decreased from 9/10 to 2/10 after the first 20 minutes of the block. Throughout a month, the blocks were repeated once a week. In the second month, the frequency of her attacks decreased to two per month, with an intensity of 4/10. She did not encounter any attacks in the sixth month.\n\n",
+        "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\u200aweeks of gestational age. The mother's age was 33 years, with gravida 1 and para 1 parity. Both the parents and brother had no family history of congenital anomalies, aortic-related diseases, or sudden death. Based on the results of the prenatal ultrasonography at the end of the second trimester, the femur length of the fetus was found to be 1 to 3\u200aweeks longer than the supposed length of the actual gestational age. Fetal echocardiography showed cardiomegaly with a fetal cardiothoracic circumference ratio of 0.5 or higher based on the baby's term. Moreover, the size of the foramen ovale was larger than normal, and left aortic constriction was seen next to the subclavian artery basin. Furthermore, no other abnormalities were found on prenatal ultrasound.\n\nAt birth, the weight was 3560\u200ag (75 percentile), the length was 56.5\u200acm (over 90 percentile), and the head circumference was 36\u200acm (over 90 percentile). Apgar scores at 1 and 5 minutes were 4 and 6 points, respectively. In the delivery room, the patient had no spontaneous breathing and had bradycardia and cyanosis. After being admitted to the neonatal intensive care unit, various musculoskeletal malformations were confirmed via physical examination. Severe arachnodactyly and camptodactyly were observed in both hands and feet, and the soles of the feet were flat. The elbow and knee joints were not fully extended. The face had malar hypoplasia with senile facial appearance. The eye was deeply settled with a down-slanting palpebral fissure, and the ear with hypoplastic cartilage was poorly settled and crumpled. The patient presented with a sagging mouth, prominent coronal suture, and brachycephaly. A grade V/VI systolic murmur was heard at both the upper sternal border and left lower sternal border with grade III parasternal heave. Echocardiography showed poor cardiac contractility, severe pulmonary hypertension, dilated aortic sinus (20.2\u200amm) (Z-score; 8.08 by Boston, 6.37 by Detroit, or 5.97 by Halifax), and multiple intracardiac valvular dysfunction with valve prolapses (moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation). And the ophthalmologic examination results showed ectopia lentis in both eyes as well as lens subluxation. Liver herniation was confirmed using abdominal X-ray and ultrasound. The systemic score of the musculoskeletal manifestation was 11 points, according to the Ghent criteria (international diagnostic criteria for MFS).\n\nFor genetic diagnosis, Sanger sequencing and polymerase chain reaction were performed on the nucleotide sequence as reference for the FBN1 gene. As a result, a mutation in which G, the first base of the 32nd intron in the form of a heterogeneous mutation, was substituted with T (c.3964 + 1G > T). This was confirmed as the likely pathogen variant based on the 2015\u200aACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24\u201332). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2\u200aweeks of life.\n\nOn the first day of life, differential cyanosis was found to show refractory hypoxemia despite more than 60% oxygen supply and signs of low cardiac output. The patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction including milrinone continuous infusion, full sedation using fentanyl continuous infusion, and use of diuretic were attempt to improve the oliguria and heart failure. Despite the medical management, the patient presented with respiratory failure, heart failure, and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. After several consultations with the patient's family and medical staff about the treatment plan, palliative care was continued instead of surgical treatment. As a result, hepatic and pulmonary congestion accompanied by pulmonary hemorrhage had progressed as well. Eventually, it had progressed to multiple organ dysfunction syndrome, and the patient died 32 days after the birth.",
+        "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\u2019s workload, kept him deeply sedated to reduce strain, and gave water pills to help him pee and move extra fluid. Even with this care, the heart valve leaks and high pressure in the lungs got worse, and the heart grew weaker. Surgery would have been needed to help him live longer. Because the disease was getting worse very fast, the family chose comfort care. A few months after birth, his heart failure worsened and he died.",
+        "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\u200aG > 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\u200aweeks of gestational age. The mother's age was 33 years, with gravida 1 and para 1 parity. Both the parents and brother had no family history of congenital anomalies, aortic-related diseases, or sudden death. Based on the results of the prenatal ultrasonography at the end of the second trimester, the femur length of the fetus was found to be 1 to 3\u200aweeks longer than the supposed length of the actual gestational age. Fetal echocardiography showed cardiomegaly with a fetal cardiothoracic circumference ratio of 0.5 or higher based on the baby's term. Moreover, the size of the foramen ovale was larger than normal, and left aortic constriction was seen next to the subclavian artery basin. Furthermore, no other abnormalities were found on prenatal ultrasound.\n\nAt birth, the weight was 3560\u200ag (75 percentile), the length was 56.5\u200acm (over 90 percentile), and the head circumference was 36\u200acm (over 90 percentile). Apgar scores at 1 and 5 minutes were 4 and 6 points, respectively. In the delivery room, the patient had no spontaneous breathing and had bradycardia and cyanosis. After being admitted to the neonatal intensive care unit, various musculoskeletal malformations were confirmed via physical examination. Severe arachnodactyly and camptodactyly were observed in both hands and feet, and the soles of the feet were flat. The elbow and knee joints were not fully extended. The face had malar hypoplasia with senile facial appearance. The eye was deeply settled with a down-slanting palpebral fissure, and the ear with hypoplastic cartilage was poorly settled and crumpled. The patient presented with a sagging mouth, prominent coronal suture, and brachycephaly. A grade V/VI systolic murmur was heard at both the upper sternal border and left lower sternal border with grade III parasternal heave. Echocardiography showed poor cardiac contractility, severe pulmonary hypertension, dilated aortic sinus (20.2\u200amm) (Z-score; 8.08 by Boston, 6.37 by Detroit, or 5.97 by Halifax), and multiple intracardiac valvular dysfunction with valve prolapses (moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation). And the ophthalmologic examination results showed ectopia lentis in both eyes as well as lens subluxation. Liver herniation was confirmed using abdominal X-ray and ultrasound. The systemic score of the musculoskeletal manifestation was 11 points, according to the Ghent criteria (international diagnostic criteria for MFS).\n\nFor genetic diagnosis, Sanger sequencing and polymerase chain reaction were performed on the nucleotide sequence as reference for the FBN1 gene. As a result, a mutation in which G, the first base of the 32nd intron in the form of a heterogeneous mutation, was substituted with T (c.3964 + 1G > T). This was confirmed as the likely pathogen variant based on the 2015\u200aACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24\u201332). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2\u200aweeks of life.\n\nOn the first day of life, differential cyanosis was found to show refractory hypoxemia despite more than 60% oxygen supply and signs of low cardiac output. The patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction including milrinone continuous infusion, full sedation using fentanyl continuous infusion, and use of diuretic were attempt to improve the oliguria and heart failure. Despite the medical management, the patient presented with respiratory failure, heart failure, and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. After several consultations with the patient's family and medical staff about the treatment plan, palliative care was continued instead of surgical treatment. As a result, hepatic and pulmonary congestion accompanied by pulmonary hemorrhage had progressed as well. Eventually, it had progressed to multiple organ dysfunction syndrome, and the patient died 32 days after the birth.",
+        "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\u201332). He developed low cardiac output due to severe mitral and aortic regurgitation and also had pulmonary hypertension. Medical management focused on afterload reduction, deep sedation to lessen cardiac work, and diuretics to treat fluid overload and low urine output. Despite treatment, the valve regurgitation, pulmonary hypertension, and poor heart pumping worsened. Surgery would likely have been required to extend survival, but given the rapid and grave progression, the family chose palliative care. Within a few months after birth, he experienced rapidly progressive heart failure and died.",
+        "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\u200aG > 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."
+    }
+]
\ No newline at end of file