A 35-year-old woman had a lump on the side of her face, on the left side, that grew over 2 years. At first, it looked like a harmless gland tumor, but later it got bigger and caused her face to droop. Doctors saw a hard, fixed lump that had spread into nearby muscles. An MRI showed the lump was growing inside the gland and had spread to muscles around it. She had surgery to remove the whole lump and nearby lymph nodes, and her facial nerve was kept safe. The test results showed this was a rare cancer called PNET, which starts in nerve tissue, and it had a special genetic change found in 60% of the cancer cells. After surgery, she got chemotherapy with four cycles of drugs (vincristine, doxorubicin, cyclophosphamide, ifosfamide, and etoposide), followed by radiation to the area. The treatment worked well, with only mild side effects like sore mouth and mild skin issues. She’s been checked every 3 months, and so far, no signs of cancer have come back.


A 35-year-old woman developed a tumor in her left parotid gland, a small gland near the jaw, two years prior. Initially, a small tumor was found, and a biopsy showed it was not cancerous. She had surgery to remove it, and the margins were clear, meaning no cancer was found at the edges. Six months later, a new, firm, painful lump appeared near the surgical site, and she began to lose movement on her left side—this is called facial paralysis. An MRI scan showed a larger tumor, measuring 42 mm, that had spread into nearby muscles and was not well-defined. The tumor was confirmed as a rare type of cancer called extra-skeletal Ewing’s sarcoma, a primary peripheral neuroectodermal tumor (PNET), which is known for spreading quickly. Pathology tests showed the tumor had a specific genetic change (EWING/PNET-type translocation) in 60% of its cells. She had surgery to remove the entire left parotid gland and nearby lymph nodes, with care taken to preserve the facial nerve. After surgery, she received chemotherapy with four cycles of vincristine, doxorubicin, cyclophosphamide, alternating with ifosfamide and etoposide, followed by external radiation therapy. The treatment was well-tolerated, with only mild side effects like mouth sores and mild skin irritation. She has been followed every three months with MRI scans, and at 10 months, there has been no sign of the cancer coming back locally or in distant parts of the body.


{
    "proficient_health_literacy": "A 35-year-old female with no significant past medical history presented with a left parotid tumefaction that had been progressing over the previous two years. Initial biopsy revealed a mixed salivary gland tumor measuring 28 mm, which was histologically non-malignant, and she underwent a large resection with negative surgical margins. Six months later, she developed a new, firm, fixed, 6 cm nodule at the subangulomandibular level, palpable and painful, without signs of inflammation, accompanied by left peripheral facial paralysis. Lymph node examination was unremarkable. Magnetic resonance imaging (MRI) of the parotid region demonstrated an expansive, poorly defined process measuring 42 mm, showing moderate infiltration of the masseter and pterygoid muscles, heterogeneous spontaneous signal intensity, dynamic enhancement consistent with a type C curve, and a very low apparent diffusion coefficient (ADC), indicative of restricted water diffusion and high cellular density. Imaging studies of the thoraco-abdomino-pelvic region and bone scintigraphy, performed due to bone pain, were unremarkable. The patient underwent excision of the lesion, followed by a wide left parotidectomy with ipsilateral triangular lymph node dissection and preservation of the left facial nerve. Definitive pathological evaluation revealed an undifferentiated malignant tumor proliferation. Immunohistochemical staining demonstrated positive expression for cytokeratin (CK) and CD99, while synaptophysin, epithelial membrane antigen (EMA), neuronal-specific enolase (NSE), chromogranin, and vimentin were negative, supporting a diagnosis of a primary peripheral neuroectodermal tumor (PNET). Fluorescence in situ hybridization (FISH) analysis confirmed the presence of a specific EWING/PNET-type translocation in 60% of tumor cells, leading to the definitive diagnosis of extra-skeletal Ewing’s sarcoma. The patient received adjuvant chemotherapy with a VDC/IE regimen consisting of four cycles of vincristine, doxorubicin, and cyclophosphamide alternating with ifosfamide and etoposide. Following chemotherapy, she received external beam radiotherapy delivered at a total dose of 54 Gy using standard fractionation (1.8 Gy per session, five sessions per week) to the clinical target volume (CTV) with a 1.5 cm margin and planning target volume (PTV)


A woman who was pregnant for the first time had a serious blockage in both kidneys at 29 weeks. She had a surgery when she was 3 years old to fix a problem with her urine tubes (ureters), and it worked well back then. When she came in, she had back pain and her kidneys were swollen. Her body couldn’t filter waste properly, so she was admitted right away. Doctors placed small tubes (stents) into her urine tubes to unblock them. After that, she started urinating a lot, which helped her kidneys heal. A catheter was used to help her stay hydrated. After 7 days, the catheter was removed, but then she got a bad infection in her kidneys with fever and pain. Doctors treated it with antibiotics and put in a new catheter. When the infection went away, she was discharged at 33 weeks. She had no signs of early labor. At 39 weeks, she had high blood pressure and had her baby, a healthy boy, born naturally. After delivery, both stents moved into her urine opening (urethra) and caused pain and fever. Doctors put new stents in under anesthesia to fix the pain. Six months later, the stents were removed, but the right urine tube was still blocked. She will have another surgery to fix both tubes in the future.


A 24-year-old woman who was pregnant for the first time was referred to us at 29 weeks of gestation. She had a surgical procedure called bilateral Politano-Leadbetter ureteral reimplantation when she was 3 years old to fix a problem with urine flow from her kidneys. Since then, she had been doing well. But at this visit, she had back pain and an ultrasound showed severe swelling in both kidneys (hydronephrosis). Her kidney function was poor, so she was hospitalized right away. A stent was placed in each ureter to help drain urine and relieve pressure. After the stent was put in, her urine output increased greatly, and her kidney function improved quickly. A catheter was used to help prevent dehydration, and it was removed after 7 days. A week later, she developed a urinary tract infection, which was treated with antibiotics and a new catheter. Her symptoms went away, and she was discharged at 33 weeks. She did not have signs of preterm labor during her stay.

At 39 weeks, she was re-admitted due to high blood pressure. She delivered a healthy male baby weighing 3.14 kg, who had a good start at birth (Apgar scores of 9 and 10). After delivery, she started having back pain and fever. It was found that both stents had moved into her urethra. The stents were reinserted under spinal anesthesia, and her symptoms improved. She was discharged two weeks later. At 6 months post-delivery, the stents were removed, but a blockage was still present in the right ureter. A new stent was placed there, and she is now scheduled for a repeat surgery to fix both ureters.


{
    "proficient_health_literacy": "A 24-year-old primigravida presented at 29 weeks of gestation with mild back pain and severe bilateral hydronephrosis, as detected by abdominal ultrasound. She had a history of bilateral Politano-Leadbetter ureteral reimplantation performed at age 3 years for vesicoureteral reflux (VUR), with an uneventful postoperative course. Her baseline blood pressure was 120/80 mmHg, but serum creatinine was elevated to 3.57 mg/dL, indicating acute postrenal failure due to obstructive uropathy. She was hospitalized immediately and underwent bilateral double-pigtail ureteral stenting (4.7 French) under ultrasound guidance without fluoroscopy. Post-stent placement, daily urine output exceeded 6 L, triggering post-obstructive diuresis; to prevent dehydration, an indwelling urethral catheter was inserted and intravenous saline infusion was initiated. Serum creatinine rapidly normalized to 1.1 mg/dL, and hydronephrosis significantly improved, allowing catheter removal after 7 days. However, within a week, the patient developed high fever and severe back pain, with laboratory findings consistent with pyelonephritis: white blood cell count of 13.1 × 10³/μL and C-reactive protein of 11.34 mg/dL. Urine culture isolated Streptococcus agalactiae, confirming bacterial infection. A second urethral catheter was placed and intravenous ceftriaxone sodium (2 g/day) was administered for 6 days, leading to clinical and laboratory resolution of infection. The catheter was removed when urine output declined, and she was discharged at 33 weeks of gestation without evidence of preterm labor (no cervical shortening or frequent uterine contractions). At 39 weeks, she was re-admitted for gestational hypertension, defined by persistently elevated systolic blood pressure (>140 mmHg) without proteinuria. She underwent labor induction and delivered a healthy male infant weighing 3140 g, with Apgar scores of 9 at 1 minute and 10 at 5 minutes. Postpartum, she developed acute back pain and fever on day 1 after delivery, which was attributed to spontaneous migration of both ureteral stents into the ure


A 10-year-old girl from a Hindu family in Sindh, Pakistan, was healthy until she started having severe pain in her side, blood in her urine, vomiting, and fever for a week. She was very anxious and had high blood pressure. The doctor found her right kidney was swollen and painful, and a blood clot was blocking the blood vessel that supplies it — the right renal vein — and it went all the way into the main vein in her body. Tests showed no infections or other problems, but blood tests found she had a clotting issue linked to a condition called lupus. This is a known problem in people with lupus, called antiphospholipid syndrome.

She was given medicine to prevent clots — first enoxaparin, then warfarin — and later switched to rivaroxaban so she didn’t need frequent blood tests. Her high blood pressure was treated with medicine, and she started taking hydroxychloroquine to help with the lupus. Over time, her symptoms got better. Her blood pressure stayed normal, her kidneys kept working well, and she didn’t have any more clots or flare-ups of lupus.

The right kidney stopped working and was found to be non-functioning. Doctors said it might be removed, but her parents chose not to. Her kidney got smaller over time, and the left kidney grew bigger to help. She stayed healthy for 4 years, grew normally, and had no serious problems. She still takes medicine every day to prevent clots and protect her kidneys. Her mother later got lupus too. Her latest check-up showed normal blood pressure, normal kidney function, and no signs of active disease. She just has a bit of anemia from her periods, which is being managed.


{
    "intermediate_health_literacy": "A 10-year-old girl from a Hindu family in Sindh, Pakistan, who had been healthy until 2020, came in with a week-long history of severe abdominal pain, blood in her urine (gross hematuria), vomiting, and fever. She was anxious, had a high fever, and her blood pressure was very high. On exam, her right kidney was enlarged and tender. Other body systems were normal.\n\nLab tests showed low platelets, blood in the urine, and mild protein in the urine. Her kidney and liver functions were normal, and her blood clotting tests were normal. An ultrasound found that her right kidney was enlarged and had areas of abnormal tissue, and a color Doppler scan showed a large blood clot in the right renal vein that blocked blood flow and extended into the inferior vena cava. A CT scan confirmed the clot was fully blocking the vein.\n\nNo known risk factors for blood clots were found, and blood tests for inherited clotting disorders were negative. However, tests for lupus and antiphospholipid antibodies were positive, confirming a secondary antiphospholipid syndrome linked to lupus.\n\nShe was treated with anticoagulant medications (first enoxaparin, then warfarin), and her blood pressure was managed with captopril and later losartan. She improved over 10–12 days and was discharged. Her blood pressure and kidney function have remained stable over the next 4 years. The right kidney stopped working, and a scan showed it was nonfunctioning. Nephrectomy (removal of the kidney) was recommended, but her parents chose not to do it.\n\nHer anticoagulation was later switched to rivaroxaban to avoid frequent blood tests. She continues to take anticoagulants, antiplatelet medicine, blood pressure medication, and hydroxychloroquine to prevent flares and clots. Her growth and kidney function have been stable. Recent tests show normal kidney function, no protein in urine, and normal blood pressure (off blood pressure meds). She had a mild drop in red blood cells due to heavy periods, which was managed with medication. Her lupus markers are now normal, and there have been no new blood clots or flare-ups. Her mother later developed lupus as well.\n\nShe is still on long-term treatment and will likely need it for life,


{
    "proficient_health_literacy": "A 10-year-old female from a Hindu family in Sindh, Pakistan, with a low socioeconomic status, presented in 2020 with a 1-week history of severe right lumbar pain, gross hematuria, vomiting, and fever. The pain was refractory to analgesia and necessitated three emergency department visits prior to hospital admission. She denied dysuria, urinary retention, incontinence, or systemic manifestations such as joint pain, rash, mouth ulcers, or alopecia. Her medical history was unremarkable, including no prior renal disease, immunodeficiency, or family history of thrombotic or autoimmune disorders. She was born via cesarean section to unrelated parents, fully immunized, and developmentally normal, currently enrolled in the 8th grade.\n\nOn physical examination, she was febrile (101°F), hypertensive (systolic/diastolic blood pressure 130/96 mmHg, above the 95th percentile for age and height), anxious, and mildly anemic. Anthropometric parameters included weight 36.4 kg (50th percentile), height 141 cm (above 50th percentile), and body surface area (BSA) 1.2 m². No lymphadenopathy, jaundice, or skin rashes were observed. Abdominal examination revealed localized tenderness in the right lumbar region without splenomegaly. Systemic examinations of respiratory, cardiovascular, locomotor, and nervous systems were unremarkable.\n\nInitial laboratory investigations revealed a white blood cell count of 14.98 × 10⁹/L, platelet count of 75 × 10⁹/L (indicating thrombocytopenia), hemoglobin of 12.4 g/dL, and elevated C-reactive protein (48 mg/dL), lactate dehydrogenase (696 U/L), and D-dimer (19.8 mg/L), consistent with active inflammation and thrombotic processes. Urinalysis demonstrated hazy, reddish appearance with 3+ hematuria, 150 mg/dL proteinuria, numerous red blood cells (RBCs), and 15–20 white blood cells per high-power field (WBCs); leukocyte esterase and nitrites were negative. Spot


A 61-year-old woman had a close call with her heart stopping suddenly. Doctors found a problem in her heart valve called mitral valve prolapse, where the valve leaks badly. This leak, along with other signs from heart tests, showed she was at risk for a sudden heart stop. To keep her safe, they put in a small device called an ICD that can shock her heart if it starts to beat wrong. They also plan to fix the leaking valve with a small surgery in three months. After the device was placed, she got better and was able to move around again. A few weeks later, her heart stayed stable, and after the surgery, a small fast heartbeat happened but was quickly fixed.


A 61-year-old woman had a near-fatal heart event and was saved with intensive care. She was found to have a condition called arrhythmogenic mitral valve prolapse, where the mitral valve in her heart doesn't close properly, leading to severe leakage. This condition, along with other signs seen on heart tests, increased her risk for sudden cardiac death. Tests showed abnormal electrical activity in her heart, including frequent ventricular arrhythmias and brief episodes of atrial fibrillation, which required anticoagulation therapy. An imaging test (CMR) revealed scar tissue in parts of the heart, which is a known risk factor for sudden cardiac death. The patient was given an internal automatic defibrillator (ICD) to monitor and prevent dangerous heart rhythms as a protective measure. She also underwent surgery three months later to repair the damaged mitral valve. After the procedure, she recovered well, regained mobility, and had no further serious heart rhythm issues during follow-up. The ICD successfully prevented any further life-threatening arrhythmias.


{
    "proficient_health_literacy": "A 61-year-old female with a history of obesity (BMI 30.1 kg/m²) presented with an aborted sudden cardiac death. On admission, vital signs were stable: pulse 60/min, blood pressure 120/80 mmHg, temperature 36°C, and oxygen saturation 94% under mechanical ventilation. Physical examination revealed no abnormalities in heart, lungs, or abdomen. Laboratory studies were unremarkable, including complete blood count, coagulation profile (normal D-dimers), and clinical chemistry (C-reactive protein 6 mg/L, within normal limits of 5 mg/L). Electrocardiography (ECG) showed sinus rhythm with a heart rate of 60/min, no atrioventricular block, no QT interval prolongation, and inverted T-waves in inferior leads (III, aVF), suggestive of regional myocardial ischemia or early repolarization abnormalities. Fast echocardiography demonstrated preserved systolic function in both left and right ventricles, with severe mitral regurgitation and no pericardial effusion. Chest X-ray revealed normal cardiac size with pulmonary venous congestion, indicating left-sided volume overload.\n\nIntensive care management led to clinical stabilization; mechanical ventilation was discontinued on day 4. A hypoactive delirium was managed with neuroleptikum and resolved without persistent neurological deficits. The 12-lead ECG did not demonstrate typical electrocardiographic markers of channelopathies (e.g., Brugada syndrome, ARVC, long-QT or short-QT syndromes), ruling out common inherited arrhythmogenic disorders. However, recurrent ventricular arrhythmias (ventricular tachycardia, VT) were observed during continuous monitoring, and a transient atrial fibrillation with spontaneous termination was documented, prompting initiation of oral anticoagulation therapy.\n\nFollow-up echocardiography confirmed persistent severe mitral valve insufficiency with preserved left ventricular ejection fraction. The left ventricle exhibited mild end-systolic and end-diastolic dilation. A markedly enlarged left atrium (area 45 cm²) was identified, consistent with chronic volume overload. Doppler tissue imaging revealed a peak systolic lateral mitral annular velocity of 18 cm/s, indicating reduced annular contractility. Transesophageal echocardiography revealed a high-grade eccentric mitral


A 45-year-old man working at a chemical plant got hurt on his right foot after stepping on a wet shoe that had ethylene oxide (EO) inside. He didn’t wear protective shoes or clothes and didn’t clean the shoe for 5 hours. The liquid soaked through his shoe and didn’t cause pain right away. It took more than 12 hours before he started feeling burning, redness, and oozing. When he finally went to the hospital, his foot was red, blistered, and had skin falling off. Doctors washed the area with salt water, covered it with a wet bandage, and applied medicine to prevent infection. He came back to the clinic every week for 4 weeks. After 9 months, his skin healed, but he still felt less sensation in his foot. He was checked by doctors for other problems, and everything was normal. No serious damage was found.


A 45-year-old man developed painful, red, oozing skin lesions on his right foot after working with ethylene oxide (EO) in a chemical plant. He was replacing a flowmeter connected to the EO tank and did not wear proper protective gear. A large amount of EO solution mixed with water spilled into his shoe, and he wore it for about 5 hours before showering. He didn’t feel any symptoms right away, but by the next morning, he had severe burning, pain, redness, and skin breakdown. The lesions were treated in the emergency department with saline irrigation, wet dressings, and topical antibiotics. He was followed up for 4 weeks at an outpatient clinic, and his skin healed completely with only slight darkening remaining. Nine months later, he reported reduced sensation in his foot, but tests showed no serious damage to his blood, lungs, or nerves. The case highlights the risk of delayed symptoms from chemical exposure and the importance of using proper protective equipment.


{
    "proficient_health_literacy": "A 45-year-old male with no significant past medical history presented with painful, exudative lesions on the right foot following occupational exposure to ethylene oxide (EO). The patient worked in a chemical plant where he was responsible for replacing a worn-out flowmeter connected to the EO supply tank. He was not wearing personal protective equipment (PPE), including chemical-resistant clothing or footwear. EO is typically delivered via an automated isolation line, minimizing routine exposure; however, exposure can occur during maintenance procedures such as indicator system replacement, which involves manual handling of EO-containing lines.\n\nAt approximately 2:00 PM, a significant volume of EO solution mixed with water spilled onto the patient’s right shoe. The patient experienced no immediate symptoms and continued working with the contaminated footwear until approximately 5:30 PM, approximately 5 hours after initial exposure. He returned home and took a shower, which effectively decontaminated the affected area. Clinical symptoms, including a severe burning sensation, pain, erythema, and progressive desquamation, developed approximately 12–14 hours post-exposure, beginning with the dorsum of the right foot and extending to the proximal regions of the second and third digits and the hallux.\n\nOn presentation to the emergency department, the patient exhibited acute dermatological injury with subcutaneous tissue damage, characterized by severe erythema, dark pink dermal appearance, serosanguineous exudate, blister formation, and epidermal desquamation. The total burn surface area was assessed at 3.5% of the total body surface area (TBSA). Vital signs were stable, with normal hemodynamics and alert mental status. No respiratory distress or dyspnea was noted, and pulmonary examination revealed clear breath sounds.\n\nLaboratory investigations—including complete blood count (CBC), blood chemistry panel, urinalysis, and plain chest radiograph—were all within normal limits, indicating no systemic toxicity or organ involvement. The affected skin was irrigated with saline solution and treated with topical silver sulfadiazine to prevent infection in the open wounds. The patient was managed in an outpatient follow-up setting for a duration of 4 weeks, during which complete epidermal regeneration occurred without scarring or structural defects. At a 9-month follow-up, residual hyperpigmentation was observed, but no other abnormalities were detected.\n\nA comprehensive health assessment conducted 9 months post-exposure revealed reduced sensory


A 69-year-old woman had a firm lump on her left thigh that grew over 6 years and caused pain. Doctors first removed the lump with surgery, and tests confirmed it was a type of cancer called soft tissue sarcoma. She had more surgeries and treatment with radioactive seeds, but the cancer came back. After that, she got a new treatment called HIFU — it uses focused sound waves to destroy the cancer. The treatment worked well, and the cancer was completely gone, with no major side effects except for some damage to the bone at the spot. About four months later, the lump came back again, but doctors found it was small and treated it with more surgery. Now she is stable, feels good, and lives a normal life.


A 69-year-old woman was diagnosed with an undifferentiated spindle cell soft tissue sarcoma on her left thigh. She first had surgery to remove the tumor, and the results confirmed the diagnosis. Over time, the cancer came back at the same site after multiple surgeries and treatments with radioactive particles. After 16 months, imaging showed the cancer had returned again, and she had three more surgeries and radioactive treatments. Despite this, the cancer still came back, so a new treatment called high-intensity focused ultrasound (HIFU) was used. HIFU is a non-invasive method that uses focused sound waves to destroy the tumor. The treatment was given over five sessions, and MRI scans showed the tumor was completely destroyed, with no signs of cancer cells left. The only side effect was minor bone damage at the treatment site. About four months later, the patient had a small break in the bone at the original tumor location, but further testing showed it was not cancer-related. She then had additional surgery to fix it and is now stable with a good quality of life.


{
    "proficient_health_literacy": "A 69-year-old female patient presented with a 3-cm-diameter firm mass on the left thigh that had progressively increased over a 6-year period, accompanied by localized pain. Initial surgical management consisted of a lumpectomy performed at The Second Affiliated Hospital of Chongqing Medical University. Postoperative histopathological examination confirmed the lesion as an undifferentiated spindle cell soft tissue sarcoma. Immunohistochemical profiling revealed CK(-), EMA(-), Vim(+), S100(-), SMA(±), Act(-), CD34(+), BCL-2(-), CD9(±), Ki-67(+), 50% AB(+), MBP(-), NF(-), and CD68(+), consistent with a spindle cell sarcoma of undifferentiated phenotype, likely with features of sarcomatoid differentiation and active cell proliferation (Ki-67 >50%). The patient underwent an expanded resection to ensure clear margins.\n\nTwo years postoperatively, a firmer, tender mass was identified at the surgical site, prompting a second expanded resection followed by radioactive particle implantation (brachytherapy). Repeat immunohistochemistry demonstrated CK(-), EMA(±), DES(-), S100(-), SMA(-), CD34(+), SDX-10(-), CDK4(-), MDM2(-), CD68(-), CD99(±), BCL-2(+), Vim(+), and Ki-67(+) >50%, indicating persistent tumor cell proliferation and a shift in molecular profile, including upregulation of BCL-2, which may confer resistance to apoptosis and contribute to tumor recurrence.\n\nMagnetic resonance imaging (MRI) at 16 months post-second resection revealed local tumor relapse, leading to three additional lumpectomies and brachytherapy. Five months later, follow-up pathology confirmed a further relapse, indicating persistent disease progression despite multimodal local interventions.\n\nA novel treatment strategy was initiated involving five sessions of high-intensity focused ultrasound (HIFU), administered on March 5, June 11, August 20, October 13, and November 24, 2021, using an integrated circuit-type HIFU tumor treatment system (Chongqing Haifu Medical Technology Co., Ltd., China). The system comprises an ultrasonic generator


A woman in her 50s had been dealing with mood swings and crazy thoughts for 27 years. She was on many medicines, including lithium, which can hurt her kidneys. She came to the hospital because she was sad and had scary thoughts. She had a bladder infection, so she started antibiotics. After 5 days, she got fever and her body started to fail — her kidneys couldn’t work right. Her lithium level was too high (2.34), which damaged her kidneys. The doctors stopped the lithium and switched to safer antibiotics. They gave her fluids to help her kidneys recover. After a few days, she got better. But even after stopping the old medicines, she stayed sad and had worse scary thoughts. So they stopped all her old pills and started new ones: lamotrigine and aripiprazole. These helped a little, but didn’t fix it. Then they added quetiapine to help her sleep and calm down. But after giving her a high dose of quetiapine (400 mg a day), she got a serious problem called NMS — which means her body went into trouble. They gave her amantadine, lorazepam, and bromocriptine to fix it, and she got better. The doctors said the quetiapine was most likely to have caused the problem.


A 51-year-old woman with bipolar disorder, who had been managing her condition for 27 years, was admitted to the hospital because she was feeling very sad and had strange, persistent thoughts—like believing others were out to get her. She had been on several medications, including lithium, fluoxetine, olanzapine, gabapentine, perazine, and biperiden, to control her mood and symptoms. Before this hospital stay, she had a history of depression, mania, and one episode of psychosis in 1990. In the past, she had also had kidney problems from high lithium levels and was treated for hypothyroidism.

She was diagnosed with a urinary tract infection, and started on antibiotics. After five days, she began to feel worse—she developed a fever of 38.4°C and her lithium level became dangerously high at 2.34 mmol/l. This caused acute kidney failure, so her lithium was stopped and the antibiotics were changed to a less harmful type. She received fluids to help her body remove the excess lithium, and her kidney function slowly improved.

Once her body stabilized, her mental symptoms got worse—she became more depressed and her delusions returned. All her previous medications were stopped one by one. Instead, she started on lamotrigine and aripiprazole to help stabilize her mood and reduce the delusions. After six weeks, the aripiprazole wasn’t working well, and she started taking quetiapine to help with sleep and mood. However, increasing the quetiapine dose to 400 mg per day eventually led to a serious condition called neuroleptic malignant syndrome (NMS), which is a rare but dangerous reaction to certain psychiatric medications.

To treat NMS, she was given amantadine, lorazepam, and bromocriptine, and her condition improved. The doctors used a scoring system to evaluate how likely each drug was to have caused the NMS. Quetiapine was found to be the most likely contributor, followed by aripiprazole and lamotrigine.

This case shows that even with long-term treatment, changes in medications can lead to serious side effects, and close monitoring is essential, especially in people with a history of kidney issues or mental illness.


{
    "proficient_health_literacy": "A 51-year-old female with a 27-year history of bipolar disorder was admitted to the psychiatric clinic in September 2017 presenting with depressed mood, ideas of reference, delusions of persecution, and anxiety. Her clinical course began with an acute paranoid psychotic episode in 1990, followed by recurrent hospitalizations for depressive and manic episodes, with a pattern of treatment shifts involving antidepressants (imipramine, venlafaxine), mood stabilizers (lithium, carbamazepine), and antipsychotics (perazine). Following outpatient management from 2000 to 2008, treatment was modified in 2015 due to lithium toxicity (>1.2 mmol/L), resulting in acute renal failure and extrapyramidal symptoms (EPS), necessitating withdrawal of lithium and initiation of gabapentine for EPS. Hypothyroidism was concurrently diagnosed and managed with levothyroxine until 2016. Between 2016 and 2017, the patient received fluoxetine (60 mg/d), perazine (150 mg/d), gabapentine (800 mg/d), and carbamazepine (200 mg/d, up to 800 mg/d), which was later discontinued due to worsening psychotic and depressive symptoms. Lithium was reintroduced at maximum dose (up to 1000 mg/d), along with olanzapine (5 mg/d) for psychosis and biperiden (4 mg/d) for muscle rigidity. No psychiatric comorbidities were identified throughout the disease course, with notable historical events including prior lithium intoxication and renal failure.\n\nAt admission, the patient was alert, oriented to person, place, and time, with stable vital signs: blood pressure 115/70 mmHg, pulse 72 bpm, respiratory rate 16/min, BMI 27.22. Physical examination revealed a regular systolic murmur, clear lung fields, symmetrical abdomen with normal bowel sounds, dry skin, and varicose veins of the lower extremities. Laboratory findings at admission included lithium level of 1.48 mmol/L, glomerular filtration rate (GFR) 35 ml/min, serum creatinine 1.56 mg/dL, and white blood cell count (WBC


A 32-year-old man in Iran found a lump on the back of his left hand and wrist. It had been there for about a month and got bigger over time. The doctor first thought it was a common bump called a ganglion cyst. He tried pain medicine for two months, but the lump kept growing. An MRI scan showed it was a rare type of tumor inside the hand, called synovial sarcoma. The doctor took a small sample of the tumor and tested it. The test showed it was cancer. The man didn’t come back for check-ups for two months. By then, the tumor had grown very large. This is a rare case because most people don’t get this kind of tumor in the hand and don’t follow up after the diagnosis. The doctor said he needed surgery, but the man refused and never came back for treatment.


This study describes a rare case of metacarpal synovial sarcoma in a 32-year-old Iranian man. He first noticed a lump on the back of his left hand and wrist about one month before seeking medical help. The doctor initially thought it was a common ganglion cyst and treated it with pain relief medication for two months. During that time, the lump slowly grew larger. An MRI scan showed a soft tissue mass that was encasing part of the hand bone and pushing on tendons, which raised concern. A biopsy was done, and the results confirmed it was a synovial sarcoma — a rare type of cancer that starts in the connective tissue. The tumor was completely removed surgically. However, the patient had poor follow-up care and did not return to the clinic for two months after the surgery. When he finally came back, the tumor had grown significantly. Because of this late return, the cancer was no longer treatable, and the patient refused further treatment. This case is rare because synovial sarcoma in the hand or wrist is uncommon, and the delay in follow-up made it much harder to manage.


{
    "proficient_health_literacy": "A 32-year-old Iranian male with no significant past medical, family, or social history presented with a slowly progressive lump on the dorsal ulnar side of the right hand and wrist, first noted one month prior. The lesion had been increasing in size over the preceding month, with no history of trauma, constitutional symptoms (such as fever or chills), or systemic illness. Vital signs at admission were within normal limits: pulse rate 75 bpm, blood pressure 118/83 mmHg, temperature 36.7°C, and oxygen saturation 98%. Laboratory evaluations, excluding 25-hydroxyvitamin D3, were unremarkable; the patient was subsequently initiated on daily oral vitamin D3 supplementation (1000 mg) due to low serum 25-hydroxyvitamin D3 levels.\n\nStandard hand-wrist radiography was performed to exclude bony abnormalities or foreign bodies, and no evidence of fracture, cortical disruption, or bone invasion was observed. The initial clinical assessment by the primary care physician attributed the lesion to a ganglion cyst. The patient received conservative management including naproxen 500 mg as needed for pain for a duration of two months. During this period, the lesion progressively enlarged. On physical examination, a 30 × 20 mm mass was identified between the second and third metacarpal bones on the dorsal surface of the left hand, extending proximally toward the metacarpal heads and distally into the proximal aspect of the wrist joint. Neurovascular examination revealed no significant deficits: wrist flexion and extension were intact, deep tendon reflexes were normal, sensory function was preserved, and muscle strength was rated 5 out of 5, indicating full motor function.\n\nMagnetic Resonance Imaging (MRI) was subsequently performed and interpreted by a radiologist. The MRI demonstrated a T2-hypersignal lesion with iso-signal intensity on T1-weighted sequences in the deep soft tissue of the middle and medial regions of the hand, specifically involving the 3rd and 4th metacarpal web spaces. The lesion exhibited cystic characteristics with fine internal septations and heterogeneous signal intensity. Tendon displacement was observed: the flexor tendons were deviated due to mass effect, and the extensor tendons of the 3rd, 4th, and 5th fingers were displaced, indicating local


A 56-year-old woman felt her heart was racing, so she went to the doctor. The doctor saw a small bump on her heart valve, about 8 millimeters big, and it was slightly leaking. At first, they thought it was a tumor, but after surgery, they found it was actually a weak, bulging part of the valve — like a small balloon that had stretched out. It wasn’t a cancer, but a sign of wear and tear from years of use. The doctors removed the bulge and fixed the valve with a ring to help it stay strong. After the surgery, she recovered well and has been feeling fine ever since. Ten months later, her heart valve is still healthy and not leaking at all. This kind of problem happens when the heart valve wears down over time, not because of disease or infection.


A 56-year-old woman was seen for palpitations. Her heart rhythm and sounds were normal, and initial tests showed no signs of infection or heart problems. An echo scan found an 8-mm mass on the anterior mitral leaflet with only slight valve leakage. Further testing confirmed the same finding. Surgery was planned to remove the mass and prevent a possible blood clot from forming. During surgery, it was discovered that the mass was not a tumor, but a bulge resembling an aneurysm, and there was no stretching of the supporting tissue. The surgeon removed the bulge and repaired the valve with a ring procedure. The patient recovered well and had no complications. Path tests showed signs of degenerative changes in the valve tissue, confirming that the issue was due to wear and tear over time. At 10 months after surgery, her heart function is stable with no further valve problems.


A 56-year-old woman with no history of infection presented for evaluation of palpitations. Her clinical examination revealed a regular sinus rhythm with no audible heart murmur. Standard electrocardiographic assessments, including resting ECG and Holter monitoring, as well as chest X-ray, were within normal limits. Transthoracic echocardiography identified an 8 × 8-mm mass localized to the posterior aspect of the anterior mitral leaflet, associated with minimal mitral valve insufficiency. Left ventricular systolic function, wall motion, and chamber dimensions were preserved, indicating no underlying systolic dysfunction. Transesophageal echocardiography confirmed the same lesion morphology, with no evidence of intracardiac thrombus or systemic embolic events. Computed tomography was negative for systemic emboli, further supporting the absence of a thrombotic source. Given the imaging findings and the clinical suspicion of a valvular tumor, surgical resection was performed with the primary goal of preventing potential embolic complications. Intraoperative inspection revealed that the lesion was not a neoplastic tumor, but rather an aneurysm-like bulge of the anterior mitral leaflet, characterized by absence of chordal elongation, which is a key histopathological and biomechanical feature distinguishing it from true neoplastic growths. The lesion was resected via a triangular resection technique, followed by ring annuloplasty to restore normal valve architecture and reduce the risk of residual regurgitation. Postoperative recovery was uneventful, with no complications reported. Histopathological analysis of the resected tissue demonstrated myxomatous degeneration, interstitial fibrosis, and hyalinization—pathological hallmarks of degenerative mitral valve disease. These findings are consistent with a chronic, progressive process involving extracellular matrix remodeling, likely driven by age-related changes in valve tissue elasticity and collagen turnover. At a 10-month follow-up, the patient remains asymptomatic, with no evidence of mitral regurgitation or valvular dysfunction, confirming successful surgical intervention and resolution of the structural abnormality. The case underscores the importance of accurate preoperative imaging and intraoperative differentiation between benign degenerative lesions and malignant tumors in the mitral valve, as misdiagnosis could lead to inappropriate resection or unnecessary intervention.


A 23-year-old man had a serious illness called Burkitt's lymphoma and was also dealing with a condition where his body attacked its own tissues (GVHD). He got very sick with confusion and trouble breathing, and when checked, had a bleed in his brain and a dead area in his brain from a stroke. Doctors found 12 weak spots in blood vessels in his brain — called aneurysms — that started showing up very fast, even though scans showed no sign of infection in his skull bones. The infection was caused by a rare fungus called Scedosporium. Even with strong medicine and surgery, the patient got worse, had infections in his lungs, and died 6 months later because his heart, lungs, and other organs stopped working. What made this case special was how fast the fungus spread through the blood vessels — new aneurysms appeared in just days, even when the brain scans looked clean.


A 23-year-old man with Burkitt's lymphoma and graft-versus-host disease was admitted to the hospital with confusion, sleepiness, and breathing problems. He had a bleeding stroke in his brain and signs of a prior brain injury. Imaging showed several aneurysms—bulges in blood vessels—that formed quickly, including 12 in the front part of the brain. These aneurysms were caused by a widespread infection from a fungus called Scedosporium, which spread rapidly through the blood vessels. Even though there was no clear sign of infection in the skull bones, new aneurysms appeared within days of imaging. The patient received antibiotics, antifungals, and surgery to remove the aneurysms. Despite these efforts, the infection spread and damaged multiple organs. He developed severe infections, including one caused by a drug-resistant bacteria in his lungs, and died six months later from multiorgan failure. This case shows how fast a fungal infection can spread through blood vessels in a patient with weakened immunity, leading to serious brain bleeding and organ damage.


{
    "proficient_health_literacy": "A 23-year-old male with a history of Burkitt’s lymphoma and graft-versus-host disease (GVHD) requiring high-dose corticosteroid therapy was admitted to the Emergency Department with a two-day history of somnolence, confusion, and progressive respiratory distress necessitating endotracheal intubation. On admission, neurological examination revealed impaired eye opening to painful stimuli and intact command following. Initial non-contrast head CT demonstrated a flame-shaped intracerebral hemorrhage in the left gyrus rectus, suggestive of vascular origin, and a hypodense lesion in the left thalamus consistent with an established infarction. The next-day angiogram identified six fusiform aneurysms: three at the frontopolar branch of the left anterior cerebral artery (ACA), one at the orbitofrontal branch of the left ACA, one at the frontopolar branch of the right ACA, and one at the anterior temporal artery of the left middle cerebral artery (MCA). Body imaging revealed multiple cavitary lung lesions, consistent with pulmonary involvement by a systemic infection. Broad-spectrum antibiotics, antifungals, and antivirals were initiated empirically.\n\nThe hemorrhagic focus localized to the left ACA branch aneurysms, prompting surgical intervention to assess rupture status and obtain tissue for microbiological analysis. On postbleed day 2, a bicoronal craniotomy was performed with parent vessel sacrifice and excision of the three left ACA fusiform aneurysms. Intraoperatively, the aneurysms exhibited friable, thin-walled characteristics with high propensity for rupture. The right ACA aneurysm was managed conservatively. Microbiological analysis confirmed angioinvasive infection by Scedosporium apiospermum, leading to initiation of vericonazole, amphotericin B, and caspofungin, which were continued throughout the clinical course.\n\nOn postbleed day 4, a new left frontal intracerebral hemorrhage and intraventricular hemorrhage (IVH) were detected on CT, prompting placement of an emergency external ventricular drain. A follow-up angiogram revealed interval growth of the left orbitofrontal artery aneurysm. With definitive microbiological identification, endovascular parent vessel occlusion was recommended and successfully performed. A subsequent angiogram on postbleed day 7 demonstrated the emergence of three


A woman with a weak heart valve got very short of breath and sharp chest pain. Her heart valve was badly damaged and caused high pressure in her lungs. Doctors tried a simple balloon procedure to fix the valve, but it broke and caused the valve to leak badly, making lung pressure even higher. Because her heart was too weak to handle surgery, they used medicines and a machine (intra-aortic balloon pump) to help her heart pump better. They also used drugs to open her blood vessels and reduce pressure in her lungs. Even with all this, her body couldn’t keep up, so she and her family chose to focus on comfort and peace instead of more treatment.


A 64-year-old woman with a history of heart valve problems, high blood pressure, and previous stroke was admitted with sudden chest pain and shortness of breath. Tests showed severe narrowing of her mitral valve, which is a key heart valve that helps control blood flow. This narrowing was causing high pressure in her lungs (pulmonary hypertension), and her overall risk for surgery was high due to other health issues. Because of this, doctors decided against open heart surgery and instead performed a less invasive procedure called percutaneous mitral balloon valvuloplasty to open up the valve. However, during the procedure, a critical complication occurred: one of the supporting strings of the valve (chordae tendineae) ruptured, leading to severe leakage (mitral regurgitation) and a dramatic rise in lung pressure, now reaching levels above the systemic blood pressure (supra-systemic pulmonary hypertension). To manage this life-threatening situation, the patient received multiple medications, including vasopressors to support blood pressure, inodilators to reduce lung pressure, and an intra-aortic balloon pump to help improve heart function and reduce valve leakage. She also received lung vasodilators and other drugs to ease pressure in her lungs. Despite these efforts, her condition continued to worsen, and after failing to respond to full medical treatment, her family chose to focus on comfort care and hospice support. The main point is that this patient’s complex heart condition led to a serious complication during a planned valve procedure, and her care shifted from surgical to intensive medical management to stabilize her condition and ensure comfort.


{
    "proficient_health_literacy": "A 64-year-old female presented to the emergency department with acute retrosternal chest pain and progressive dyspnea. She has a history of coronary artery disease, hypertension, atrial fibrillation, rheumatic mitral valve (MV) disease, and prior stroke with residual left-sided hemiplegia. Transesophageal echocardiography (TEE) demonstrated severe mitral stenosis (effective orifice area [EOA] 0.9 cm²; normal >1.0 cm²), mild mitral regurgitation (MR), minimal leaflet motion, pronounced valvular thickening, extensive calcification, and a Wilkins score of 14 indicating severe structural degeneration of the mitral valve apparatus. The sub-valvular apparatus showed minimal thickening, no vegetations, and no thrombus in the left atrial appendage. Left ventricular systolic function remained preserved.\n\nLeft heart catheterization confirmed non-obstructive coronary artery disease. Right heart catheterization (RHC) revealed a mean pulmonary artery pressure (PAP) of 71 mmHg and a pulmonary capillary wedge pressure (PCWP) of 15 mmHg, resulting in a transpulmonary pressure gradient (TPG) of 51 mmHg, consistent with severe pulmonary hypertension (PH) due to pulmonary venous hypertension. Her Society of Thoracic Surgeons (STS) surgical mortality risk was estimated at 31% due to the combination of severe PH and multiple comorbidities. A multidisciplinary team—including advanced heart failure, cardiac surgery, intensive care, and cardiac anesthesia—concluded that the patient was not a suitable candidate for surgical mitral valve replacement (MVR) due to the high risk of perioperative mortality and hemodynamic instability. Consequently, percutaneous mitral balloon valvuloplasty (PMBV) was performed under general anesthesia in the cardiac catheterization laboratory.\n\nPre-procedure, invasive lines (radial arterial line and right internal jugular vein catheter) were successfully placed. Induction of general anesthesia was achieved with endotracheal intubation. Repeat RHC showed a mean PAP of 61 mmHg and left atrial pressure of 30 mmHg. TEE confirmed a severely dilated right ventricle and a mitral EOA of 0.9 cm². Cardiac index


A 12-year-old Asian girl with leukemia had swelling in her gums and chin that got worse over time. Even with proper care, the infection didn’t go away and eventually caused a big hole in her face and jaw. Her teeth fell out on their own, and part of her jaw bone also came loose. Because of this, she couldn’t eat properly and kept drooling. After she got better, a simple surgery was done to fix her lips so she could eat again and stop drooling.


A 12-year-old Asian girl with acute myeloid leukemia (AML) developed worsening gingivitis, which started as swollen gums and chin. She had already received chemotherapy for her leukemia and was hospitalized for a high fever, which was treated with multiple antibiotics, antifungals, and antivirals. Her white blood cell count was very low, and her neutrophils were absent, making it hard to fight infections. Despite proper treatment, her oral condition got worse. Six days after the start, she had a cardiac arrest due to uncontrolled fever, but she recovered. Over time, the swelling turned into a full-thickness tissue loss in her mouth and face, causing the gums and underlying bone to separate and the teeth to fall out. After recovering from the illness, she had serious problems with her lips, making it hard to eat or control drooling. Because of her weakened blood counts, surgery was done simply to repair the lip and restore the ability to eat, using a local flap to reconnect the muscle that controls the lips.


{
    "proficient_health_literacy": "A 12-year-old Asian female patient with acute myeloid leukemia (AML) was referred for evaluation and management of progressive gingival swelling and chin involvement. The patient had a history of patent ductus arteriosus (PDA) closure at age 6 and had undergone four cycles of induction chemotherapy for AML, diagnosed one year prior. She was admitted for neutropenic fever exceeding 39°C, managed with a broad-spectrum regimen including linezolid, meropenem, sulfamethoxazole, metronidazole, teicoplanin, cefpiramide, and amikacin, along with antifungals (fluconazole, nystatin, amphotericin B, voriconazole, caspofungin) and antiviral therapy (acyclovir), consistent with suspected vancomycin-resistant enterococci (VRE) sepsis. Laboratory findings revealed a white blood cell (WBC) count of 40/μL, platelet count of 8000/μL, and an absolute neutrophil count of 0/μL, confirming profound neutropenia and pancytopenia. Given the absence of viable neutrophils and the patient's unstable hematologic status, surgical intervention was contraindicated. Over the course of six days, the patient developed uncontrolled fever leading to cardiac arrest; return of spontaneous circulation (ROSC) was achieved through resuscitation, followed by gradual clinical improvement. The oral and facial lesions progressed to full-thickness necrotic gangrene, with complete separation of the necrotic alveolar bone from the surrounding mandibular bone. Teeth in the affected segment spontaneously exfoliated, and the necrotic bone segment also detached independently. Following resolution of fever and recovery of systemic stability, the patient faced persistent functional deficits, including lip incompetence and drooling due to loss of oral closure, rendering oral intake impossible. In the context of her pancytopenia and high surgical risk, a minimally invasive local flap procedure was performed to restore continuity of the orbicularis oris muscle, thereby achieving functional lip competency and enabling safe oral intake. The case illustrates the severe mucosal and skeletal complications of prolonged neutropenia in pediatric leukemia, particularly involving the maxillofacial region, with gingivitis progressing to full-thickness tissue and bone necrosis due to impaired host defense mechanisms, disrupted tissue perf


A 48-year-old man had eye inflammation in his left eye that didn’t go away. His doctor tried a steroid called prednisolone, which helped a little, but when the dose was lowered, the eye swelling came back. He was referred to a better eye hospital because the problem kept returning. At first, his vision was okay, but his eye had signs of swelling and inflammation. Tests showed his eye had a type of blood vessel problem that matches a condition called Bechet’s disease. He also had mouth sores and red bumps on his legs, and a test showed a specific gene (HLA-A26) was present. He started a drug called adalimumab to reduce the need for steroids. It worked — his eye swelling got better and he could slowly cut down on the steroid. But after 8 months, he started feeling sick and tests found signs of tuberculosis (TB) in his lungs. He was diagnosed with miliary TB, a serious form of TB. His steroid and adalimumab were stopped right away, and he started TB treatment for 6 months. Even after that, the TB test stayed positive. During this time, his eye problem got worse, and his vision dropped. So, they restarted a different drug called infliximab, along with isoniazid to fight TB. After starting this, his eye swelling and vision improved again. No TB came back after 3 years of treatment. The key point: his eye problem needed special medicine, and TB was a serious side risk, but it was managed with the right steps.


A 48-year-old Japanese man was treated for eye inflammation (uveitis) in his left eye, which had developed into macula edema (swelling in the central part of the retina). His doctor first tried prednisolone, a steroid, which helped temporarily, but when the dose was reduced, the swelling returned. Because the condition didn't improve, he was referred to a specialized eye hospital in Tokyo. At the hospital, doctors found signs of Bechet’s disease — a rare condition that causes inflammation in blood vessels — through eye exams, blood tests, and imaging. Key signs included swollen blood vessels in the retina, recurring mouth sores, a rash on his legs, and a specific genetic marker (HLA-A26). He started treatment with adalimumab (ADA), a drug that reduces inflammation and helps lower steroid use. Over time, his eye swelling improved and he was able to reduce his steroid dose. However, eight months later, he developed symptoms of tuberculosis (TB), including fatigue and lung shadows on imaging. He was diagnosed with miliary TB, a serious form of TB. His steroid and ADA treatments were stopped immediately, and he began a six-month course of TB medication. Even after recovery, his TB test remained positive. During this time, his eye condition worsened, with increased swelling and vision loss. After stopping ADA, he used eye drops and injections to control the eye inflammation, but these only provided limited relief and caused some side effects like higher eye pressure. Eventually, he restarted treatment with infliximab (IFX), combined with isoniazid for TB prevention. After starting IFX, his eye swelling and vision improved, and his TB did not return during the next three years. This case shows that while treatments for Bechet’s disease can help control eye symptoms, patients need careful monitoring for infections like TB, especially when using anti-inflammatory drugs.


{
    "proficient_health_literacy": "A 48-year-old Japanese male presented with uveitis of unknown origin in the left eye, initially managed at a general ophthalmology clinic. Macula oedema (ME) was identified, and prednisolone (PSL) 40 mg/day was initiated. Although ME showed transient improvement, tapering PSL to 20 mg/day resulted in relapse of ME, prompting referral to the Department of Ophthalmology, Tokyo Medical University Hospital due to persistent intraocular inflammation and worsening visual function. At presentation, best-corrected visual acuity (BCVA) was 20/12.5 in the right and 24/20 in the left eye, with normal intraocular pressure. Slit-lamp examination revealed 1+ anterior chamber cells; fundus photography demonstrated diffuse vitreous haze and mild peripheral retinal exudates; fluorescein angiography revealed diffuse retinal vasculitis involving the posterior pole and peripheral retina, consistent with Bechet’s disease (BD); optical coherence tomography (OCT) confirmed the presence of macula oedema. Peripheral blood tests showed elevated white blood cell count, increased neutrophil percentage, elevated lactate dehydrogenase (LDH), HLA-A26 positivity, negative HLA-B51, and negative results for both tuberculin skin test (TST) and T-SPOT.TB. Based on the clinical presentation—recurrent oral aphthous ulcers, erythema nodosum-like cutaneous rash, HLA-A26 positivity, and characteristic retinal vasculitis—the diagnosis of incomplete Bechet’s disease was established. Adalimumab (ADA), a tumor necrosis factor (TNF) inhibitor, was initiated as steroid-sparing therapy following screening for latent or active infection. Following ADA initiation, ME gradually improved, allowing successful tapering of PSL to 2 mg/day, resulting in sustained clinical remission of ocular inflammation.\n\nEight months after ADA initiation, the patient developed systemic symptoms of general malaise. Repeat peripheral blood testing revealed a positive T-SPOT.TB result. Chest X-ray and computed tomography (CT) demonstrated bilateral pulmonary granular shadows, leading to a diagnosis of miliary tuberculosis (TB). ADA and PSL were immediately discontinued due to the risk of exacerbating TB. A standard 4-drug regimen for miliary TB was commenced: isonia


A 70-year-old Japanese woman had sudden, very bad neck pain that made her unable to move her neck at all. She had a fever of about 37.5°C and couldn’t turn her head. X-rays and scans showed a hard, yellow substance in her neck, like a small piece of old stone, between two bones (C5 and C6). The scan showed fluid inside this yellow part, and it looked like thick, yellow goo. Doctors found tiny crystals in the fluid that are linked to a condition called pseudogout, which affects the yellow ligament. This caused the pain and the swelling. She had surgery to remove the bad part and the fluid. After the surgery, her pain went away, and she never had another bad neck pain again. Now, 7 years later, she’s completely pain-free and has no nerve problems.


A 70-year-old Japanese woman developed sudden, severe neck pain that made it impossible for her to move her neck. She had a mild fever (37.5°C) and was experiencing intense pain, with her pain level rated at 100 out of 100. X-rays showed calcification between the C5 and C6 vertebrae, and MRI scans revealed a yellow fluid collection in the yellow ligament — a band of tissue in the neck. The fluid was cloudy and yellow, and under a microscope, it was found to contain calcium pyrophosphate dihydrate crystals, which are linked to a condition called pseudogout. This condition causes inflammation in the ligament, leading to severe pain and neck stiffness. The MRI also showed compression of the spinal cord, which is why surgery was needed. She underwent surgery to remove the affected yellow ligament and relieve pressure on the spinal cord. After the procedure, her pain improved, lab tests returned to normal, and she eventually had full relief of neck pain with no further issues, even 7 years later.


{
    "proficient_health_literacy": "A 70-year-old Japanese woman presented with a 14-day history of progressive neck pain prior to hospital admission. She had no history of tuberculosis, recent head or neck trauma, or diabetes mellitus. Initial physical examination revealed mild limitation of neck motion without neurological deficits, including preserved motor strength, sensory function, and normal deep tendon reflexes. Plain lateral radiography demonstrated calcification within the interlaminar space at the C5-C6 level, consistent with yellow ligament calcification. Magnetic resonance imaging (MRI) revealed a low-signal lesion on both T1-weighted and T2-weighted sequences, with surrounding intermediate signal intensity on T1WI and high signal intensity on T2WI, accompanied by cord compression—findings suggestive of either a pseudogout attack or an epidural abscess. Her neck pain was initially managed with nonsteroidal anti-inflammatory drugs (NSAIDs), resulting in gradual improvement. However, two months later, her symptoms recurred with a moderately elevated fever (37.5 °C), severe neck pain preventing any range of motion, and a visual analog scale (VAS) pain score of 100 mm. Laboratory investigations showed a white blood cell count of 7800/mm³ (within normal range: 3500–9300/mm³) and markedly elevated C-reactive protein (5.13 mg/dL, normal: 0–0.3 mg/dL), indicating acute inflammation. Computed tomography (CT) confirmed a high-density area between the C5 and C6 laminae, consistent with calcification of the yellow ligament. Repeat MRI demonstrated persistent T1- and T2-low signal central region with surrounding intermediate and high signal intensity, confirming ongoing inflammatory or crystalline process with spinal cord compression. Despite continued NSAID therapy, pain remained uncontrolled. Surgical intervention was performed two weeks after the second admission, consisting of C6 laminectomy and resection of the C5-C6 yellow ligament. Intraoperative findings included a turbid, yellow fluid collection within the yellow ligament, visible calcifications, and dural adhesions to the ligament. Histopathological analysis of the fluid revealed calcium pyrophosphate dihydrate (CPPD) crystals, confirming the diagnosis of pseudogout (calcium pyrophosphate deposition disease) involving the yellow ligament. Postoperatively, her clinical course was uneventful; pain


A 68-year-old woman had heart problems for a long time. Her heart couldn’t pump blood well, and doctors found a buildup of protein in her heart muscle called amyloidosis. After 3 years, she got a small device in her chest to help her heart beat better. For 7 years, she stayed quiet, but then at age 78, she started having shortness of breath and her heart was much bigger than normal. A scan showed a big lump in her liver and a tumor that had spread from the liver through blood vessels all the way to her heart’s upper chamber. This tumor was diagnosed as liver cancer (hepatocellular carcinoma). Her blood test showed very high levels of a cancer marker. Even though she was on medicine to prevent blood clots, her body still had clots for months. The cancer in her liver and the blood clot were likely what made her heart problems worse. Her symptoms got better with medicine that helps remove extra fluid from her body.


A 68-year-old woman was first admitted to the hospital with heart failure caused by a type of protein buildup in her heart called AL type primary cardiac amyloidosis. After three years, she had a device implanted to help her heart beat more effectively — this is called cardiac resynchronization therapy (CRT). The device was used because her heart was not pumping well, with a left ventricular ejection fraction of only 34%, and she had severe heart failure symptoms (NYHA class III). She remained stable for seven years after the device was implanted. At age 78, she returned with worsening heart failure symptoms, including shortness of breath and an enlarged heart seen on chest X-ray. An ultrasound and CT scan revealed a large tumor in her liver — specifically, hepatocellular carcinoma (HCC) — and a tumor that had spread from the liver through blood vessels into her heart, filling the right atrium. The tumor was confirmed with a contrast CT, and her alpha-fetoprotein level was extremely high, which is a sign of liver cancer. Even though she was on blood-thinning medication, her blood had been abnormally clotting for more than six months before her symptoms returned. Her heart failure symptoms improved with standard diuretics. Doctors believe the tumor and its spread caused the heart problems in this case. The patient’s specialty care was in cardiology.


{
    "proficient_health_literacy": "A 68-year-old female was initially admitted to the hospital due to symptomatic heart failure, which was ultimately diagnosed as AL type primary cardiac amyloidosis, confirmed by endomyocardial biopsy. Following a 3-year period of clinical follow-up, she underwent implantation of a cardiac resynchronization therapy (CRT) device for biventricular pacing, due to recurrent heart failure episodes (New York Heart Association class III), a left ventricular ejection fraction of 34%, and a wide QRS complex of 143 ms indicative of complete left bundle branch block. She remained clinically stable for seven years post-implantation. At age 78, she presented with a recurrence of heart failure symptoms, including progressive shortness of breath, physical examination findings consistent with decompensated heart failure, and significant cardiomegaly evidenced by an extended cardiothoracic ratio of 74% on chest radiography. Echocardiographic evaluation revealed a large echogenic mass occupying the right atrium. Sixty-four multi-detector computed tomography (CT) imaging demonstrated a lobulated, heterogeneously enhancing mass in the right upper lobe of the liver, consistent with hepatocellular carcinoma (HCC), and a continuous tumor thrombus extending from the portal vein and hepatic vein through the inferior vena cava to the right atrium. Alpha-fetoprotein levels were markedly elevated at >20,000 ng/mL (reference range: 0.0–10.0 ng/mL), supporting the diagnosis of HCC. The presence of persistent hypercoagulability was documented for more than six months prior to the clinical deterioration, despite concomitant anticoagulant therapy, suggesting a prothrombotic state that likely contributed to the formation and propagation of the tumor thrombus. The extensive tumor thrombus was deemed the primary hemodynamic contributor to the decompensated heart failure, leading to impaired cardiac filling and outflow. The patient's symptoms were initially managed with standard diuretic therapy, which provided partial relief. This case illustrates a rare and severe complication in which advanced hepatocellular carcinoma with portal and hepatic venous invasion leads to systemic venous obstruction and right-sided heart dysfunction, likely mediated by both tumor-induced thrombosis and chronic hemodynamic stress in the context of pre-existing cardiac amyloidosis and CRT device use. The interplay between cardiac amyloidosis, chronic left


An 80-year-old woman had a liver problem from hepatitis C, which caused scar tissue in her liver and a cancer in her liver (HCC). She had a small tumor treated with a procedure called RFA in two sessions, one 25 months ago and another 3 months later. A year before she got sick, a scan showed no signs of cancer or a hole in her diaphragm. Then, suddenly, she had a sharp pain in her belly. A chest X-ray showed part of her small intestine stuck in her chest. Doctors found that the intestine was trapped and not getting enough blood — this is called a strangulated diaphragmatic hernia. The hole where the intestine slipped through was about 2 cm wide. The doctors did emergency surgery to push the intestine back, cut out the damaged part, and fixed the hole with strong, dissolvable stitches. She recovered well and was out of the hospital in 10 days. Five months after surgery, no signs of the hole coming back were found.


An 80-year-old woman with liver damage from hepatitis C and a history of liver cancer (HCC) was admitted to the hospital with sudden, severe pain in her upper abdomen. She had previously received radiofrequency ablation (RFA) treatment for HCC in segments 6 and 7 of her liver, a procedure that uses heat to destroy cancer cells. Twenty-two months before her admission, she had a second RFA session. A follow-up CT scan done a month before admission showed no signs of cancer or a diaphragmatic hernia (DH). However, on the day of admission, she developed intense abdominal pain, and a chest X-ray showed gas in the chest area, suggesting the small intestine had pushed through the diaphragm into the chest. Emergency laparoscopic surgery was performed. The surgery found that the small intestine had herniated through a hole in the diaphragm, and part of it was damaged due to lack of blood supply (ischaemic). The damaged section was removed, and the hole was closed with absorbable stitches. The patient recovered well and was discharged on day 10. At her 15-month follow-up, no signs of hernia recurrence were found.


{
    "proficient_health_literacy": "An 80-year-old woman with a history of hepatitis C-induced liver cirrhosis and hepatocellular carcinoma (HCC) involving segment 6 of the liver was admitted due to acute, sudden-onset epigastric pain. Prior to admission, she had undergone two ultrasonography-guided percutaneous radiofrequency ablation (RFA) procedures using the LeVeen Super Slim 3.0 device (Boston Scientific, Marlborough, Massachusetts, US). The first RFA session, performed 25 months earlier, targeted HCC in segment 6 and lasted 114 minutes, without the use of artificial pleural effusion or ascites. Three months later, a second RFA procedure was conducted for recurrent HCC in segment 6/7, again using the same device, this time with artificial pleural effusion, and lasted 125 minutes. A follow-up contrast-enhanced computed tomography (CT) scan performed one month prior to admission (21 months after the second RFA) showed no evidence of HCC recurrence or diaphragmatic hernia (DH). No history of trauma was present. On the day of presentation, she experienced acute, severe epigastric pain and was evaluated by her family physician. Chest radiography revealed a massive accumulation of intestinal gas above the right lobe of the liver, suggestive of intestinal herniation. She was transferred to our institution for further assessment. Vital signs at admission were stable: blood pressure 100/70 mmHg, pulse 80 beats per minute, and oxygen saturation 94% on room air. Physical examination revealed mild umbilical tenderness without signs of peritoneal irritation or trauma. Laboratory studies, including white blood cell count and C-reactive protein, were within normal limits. Hepatic function was impaired, with Child–Pugh Class B classification, mild hypoalbuminemia (3.2 g/dL), and a significantly prolonged prothrombin time (63% increase above baseline). Contrast-enhanced CT imaging demonstrated herniation of the small intestine into the right thoracic cavity, with congestion and haziness of the surrounding mesenteric fat, indicating ischemic changes; however, no evidence of bowel perforation was observed. Emergency laparoscopic surgery was performed under general anesthesia in the supine position using the open Hasson technique. A 12-mm port was placed above the umbilicus, followed


A 41-year-old man had long-term joint pain from rheumatoid arthritis, which he didn’t properly treat for a year. His body started showing signs of damage — red, non-blanching rashes on his legs and fingers, swelling, and lots of protein in his urine. Doctors found a kidney problem called membranous nephropathy, where tiny blood clots formed in the kidney’s filters. Even after stopping pain medicines and arthritis drugs, the protein in his urine stayed high. He also developed blood vessel inflammation (vasculitis) and lung disease (sarcoidosis), both of which improved with steroids. But the kidney problem only got better a little, not fully. He tried a special medicine called Rituximab, which helped at first, but the protein in his urine slowly went back up. His skin and joint issues completely went away after starting strong steroids, but the kidney problem still isn’t fully fixed. His blood tests show he still has cryoglobulins, meaning the problem is ongoing.


A 41-year-old man with chronic rheumatoid arthritis had worsening symptoms, including skin rashes, swelling in his legs, and high protein in his urine, leading to a diagnosis of nephrotic syndrome. A kidney biopsy showed membranous nephropathy with blood clots inside the kidney's tiny blood vessels (intracapillary thrombi), which is linked to his autoimmune condition. Despite stopping his usual arthritis medications like NSAIDs and DMARDs, his proteinuria did not improve. He also developed cryoglobulinemic vasculitis and pulmonary sarcoidosis, both of which improved with high-dose steroids. Rituximab, a drug used to reduce immune system activity, helped reduce proteinuria initially, but only partially. After restarting the treatment, proteinuria gradually returned to higher levels, showing only partial response. His skin and joint symptoms fully resolved with treatment, but the underlying kidney issue remained difficult to fully control. His cryoglobulin levels stayed positive, suggesting ongoing immune system problems.


{
    "proficient_health_literacy": "A 41-year-old Hispanic man with a 2-year history of rheumatoid arthritis (RA) and type 2 diabetes mellitus presented to the emergency department with newly developed bilateral lower extremity purpuric rash and edema following a 1-year period of lost follow-up. RA was initially diagnosed two years prior, characterized by polyarthritis and markedly elevated serum immunologic markers: rheumatoid factor titer of 1220 IU/ml (normal <20 IU/ml) and anti-cyclic citrullinated peptide (anti-CCP) titer of 240.05 U/ml (normal <20 U/ml; strongly positive >60 U/ml). Prior therapy with methotrexate, low-dose prednisone, and sulfasalazine achieved disease control, but the patient discontinued DMARDs and was intermittently managed with ibuprofen 800 mg every 8 hours for joint pain for approximately one month.\n\nOn admission (day 0), physical examination revealed non-tender, non-blanching purpuric macules coalescing into large patches on the left leg, with smaller lesions on the right, in a dependent, flexor-surface distribution. Polyarticular arthritis was present with pain and swelling in the right 2nd and 3rd metacarpophalangeal (MCP) joints and left 3rd MCP joint. Boutonniere deformities were observed bilaterally, with greater severity on the left. Subcutaneous nodules were present at the elbows. Significant pitting edema was noted in the lower extremities. Urinalysis showed 21 red blood cells/high power field (hpf) and 7 white blood cells/hpf. Creatinine was 0.9 mg/dL, with an estimated glomerular filtration rate (eGFR) of 93 mL/min by the MDRD equation. Nephrotic syndrome was diagnosed based on proteinuria of 11 g/gm, hypoalbuminemia (2.2 g/dL), and peripheral edema.\n\nSerologic evaluation revealed low complement levels: C3 (86, normal 88–201), C4 (24, normal 16–47), positive cryoglobulin qualitative test (<1% cryocrit), and negative c-ANCA, p-ANCA,


A 79-year-old woman had a small hole in her heart’s left side that was still letting blood leak after surgery. Doctors used a tiny device (WATCHMAN) to close it. The device fit perfectly, stayed in place, and sealed the hole well. There was just 1.4 mm of tiny leak left, which is very small. After the procedure, she kept taking two pills: aspirin and apixaban. Six weeks later, the leak was still very small (1.49 mm) and there was no blood clot. So, her doctors stopped the apixaban pill and switched her to taking aspirin and another pill called clopidogrel. She hasn’t had any more bleeding, and they plan to stop the clopidogrel in 6 months, but she will keep taking aspirin forever.


A 79-year-old woman had a procedure to close off a small pocket in her left atrium (LAA) using a device called the WATCHMAN™. She had previously had surgery to fix her heart valves and had been on blood thinners because of a high risk of stroke, but she had trouble with bleeding in her stomach due to diverticulosis. Before the procedure, her heart was stable and her kidneys were working well, though she had mild anemia. During the procedure, imaging showed that the LAA was still open, with only 1.4 mm of leak (PDL), and the device was placed successfully, meeting all key safety and placement standards. After the procedure, she continued on apixaban and aspirin. At 6 weeks, a follow-up scan showed the leak had slightly increased to 1.49 mm but no blood clots were found. Her doctors decided to stop apixaban and switch her to aspirin and clopidogrel instead. She has not had any major bleeding since, and her team plans to stop clopidogrel after 6 months, while continuing aspirin forever.


{
    "proficient_health_literacy": "A 79-year-old Black female with a history of mitral regurgitation, tricuspid regurgitation, and persistent atrial fibrillation complicated by recurrent significant gastrointestinal hemorrhage on anticoagulation due to diverticulosis was referred for percutaneous left atrial appendage occlusion (LAAO). Five months prior, she underwent surgical mitral and tricuspid valve repair, along with LAA ligation using a 35 mm AtriClip, driven by a high stroke risk (CHA2DS2-VASc score of 5) and intolerance to oral anticoagulation. Pre-procedural evaluation revealed a hemodynamically stable patient with regular heart rate and irregular rhythm, normal renal function (serum creatinine 0.81 mg/dL), and mild anemia (hemoglobin 10.8 g/dL, reference range 12.0–15.0 g/dL). Intra-procedural transesophageal echocardiography (TEE) confirmed complete closure of the left atrial appendage at the time of surgery. However, 40-day follow-up TEE and cardiac computed tomography (CT) demonstrated a persistent anatomic communication between the left atrium and the left atrial appendage, with no evidence of thrombus formation, indicating incomplete occlusion. Given this finding, a percutaneous LAAO device was considered to achieve definitive occlusion of the residual LAA pouch. Trans-septal puncture was performed under fluoroscopic and TEE guidance, with intracardiac ultrasound confirming mid-septal access. Intra-procedural TEE was utilized for precise LAA sizing, leading to the selection and deployment of a 27 mm WATCHMAN™ device. Deployment was successful, with all P.A.S.S. (Position, Anchor, Size, and Seal) criteria met. The residual patent left atrial appendage (PDL) measured 1.4 mm at the time of device placement. Post-procedural management included apixaban 5 mg twice daily and aspirin 81 mg daily. At 6-week follow-up TEE, a trivial PDL of 1.9 mm was identified along the posterior aspect of the appendage, with no detectable thrombus. The anticoagulation regimen was adjusted to


A man in his 40s had a swollen belly and belly pain for months. His doctor couldn't find the cause at first, even after checking for cancer or liver problems. Tests showed no signs of infection or cancer, but later, his belly fluid had high levels of a substance linked to tuberculosis. When the doctor looked inside his belly with a small camera, they found a thick, fibrous layer wrapping around his small intestine, full of old infection signs. Biopsy samples proved it was tuberculosis, not cancer. After starting medicine to fight the TB, the swelling went down a lot and he started feeling better. He’s been back to normal for years with no more problems.


A 47-year-old man had a 3-month history of abdominal swelling, pain, and nausea. Even though he lost some weight, he didn’t have fever, cough, or night sweats. He had no history of liver disease or abdominal surgery, but had had tuberculous pleurisy about 20 years earlier. Tests showed no signs of cancer, infection, or liver problems, and imaging didn’t show obvious causes. His abdominal fluid was clear and contained no bacteria or cancer cells. After two months, his symptoms worsened, with more fatigue, weight loss, and increased abdominal swelling. New tests showed higher levels of markers linked to infection and inflammation. Imaging revealed a thick membrane covering his small intestine and small nodules in the abdominal lining, which raised concern for either cancer or tuberculosis. A laparoscopy was done and found a dense fibrous membrane wrapping the small bowel, with small nodules that tested positive for tuberculosis. Biopsies confirmed tuberculous infection. The surgery tried to remove the membrane and release the trapped bowel, but it was very difficult due to the thick, fibrous tissue. The patient was then treated with anti-tuberculosis medication for six months. After treatment, his abdominal fluid greatly decreased, his symptoms improved, and he returned to normal function. He has remained symptom-free for six years without needing further surgery.


{
    "proficient_health_literacy": "A 47-year-old male presented with a three-month history of progressive abdominal distension, intermittent abdominal pain, and nausea, despite a 4 kg weight loss. He reported no fever, chronic cough, or night sweats, and had no prior history of abdominal surgery, liver cirrhosis, or chronic hepatitis virus infection. Notably, he had a history of tuberculous pleurisy approximately 20 years earlier. Physical examination revealed gross abdominal distension with ascitic fluid of unknown etiology, but no tenderness. Laboratory evaluation, including serum tumor markers, erythrocyte sedimentation rate (ESR), adenosine deaminase (ADA) activity, and anti-tuberculosis antibody (TB-Ab), was within normal limits. The tuberculin skin test was negative, and HIV serology was negative. Chest radiography showed no evidence of pulmonary tuberculosis. Plain upright abdominal X-ray demonstrated colonic air without air-fluid levels or free intraperitoneal gas, suggesting a non-obstructive fluid collection. Contrast-enhanced computed tomography (CT) of the abdomen revealed duodenal dilatation and congestion of small bowel loops trapped within a large volume of ascitic fluid, surrounded by a dense, fibrous membrane. Gastroscopy excluded gastrointestinal malignancy. Two paracenteses were performed, yielding blood-stained ascitic fluid without detection of malignant cells, acid-fast bacilli (AFB), or tuberculosis organisms. The ascitic fluid was classified as exudative, with ADA levels within the normal range (4–18 U/L), consistent with a non-infectious or non-tuberculous exudate. The patient declined laparoscopy and was discharged without a definitive diagnosis.\n\nTwo months later, the patient returned with worsening symptoms, including increased fatigue, emaciation, and a 10-kg weight loss over the prior two months. Repeat laboratory testing revealed elevated serum ADA (21 U/L, above the normal range of 4–18 U/L), elevated ESR (28 mm/h, normal 0–15 mm/h), and negative TB-Ab. Paracentesis fluid remained negative for bacteria, AFB, and malignant cells, but ascitic ADA increased significantly to 41 U/L, supporting an infectious etiology. Serum CA-125 was markedly elevated (97.39 U/mL, normal <35 U/mL), suggesting per


A 45-year-old man had high blood sugar for six months and was hospitalized. Tests showed a big tumor in his abdomen, but his blood pressure was normal. Doctors found the tumor was benign (not cancer), and they removed it using a small surgery (laparoscopy) with no major problems. After surgery, his hormone levels (which were high before) went back to normal, but his blood sugar stayed high. Tests on the tumor’s genes showed no changes that would mean it was cancerous. He’s doing well now, but his sugar level still needs attention.


A 45-year-old man was hospitalized due to high blood sugar (hyperglycemia). He didn't have symptoms like headaches, high blood pressure, or heart palpitations. Tests showed his blood pressure was normal, but his serum and urine had high levels of catecholamines, which are chemicals linked to certain tumors. An abdominal CT scan found a 7.2 × 6.5 cm mass in the right area near the aorta, and the adrenal glands were normal. This led to a diagnosis of a large paraganglioma (PGL), a type of tumor that can cause high sugar levels. Because of financial reasons and lack of equipment, he didn't get a MIBG scan, which is often used to confirm such tumors. He was then treated with laparoscopic surgery — a minimally invasive procedure — where the tumor was safely removed. During surgery, his blood pressure stayed stable, and the procedure took 120 minutes with only about 50 mL of blood loss. He recovered well and was discharged on day 5. Pathology confirmed the tumor was benign, and DNA tests for SDHB and SDHD genes showed no mutations. Six months after surgery, his catecholamine levels returned to normal, but his blood sugar remained high, suggesting that the cause of his high sugar levels is still not fully explained.


{
    "proficient_health_literacy": "A 45-year-old male presented with a six-month history of hyperglycemia. He denied symptoms of episodic headache, hypertension, palpitations, or diaphoresis. Initial evaluation included 24-hour electrocardiographic monitoring and serial blood pressure measurements, both of which remained within normal limits. Glycemic control was achieved with insulin therapy, with serum glucose levels returning to baseline. Laboratory investigations were otherwise unremarkable, except for elevated serum and urinary catecholamine levels, suggesting possible pheochromocytoma or paraganglioma (PGL). Abdominal-pelvic computed tomography (CT) with contrast revealed a 7.2 × 6.5 cm inhomogeneous mass in the right para-aortic region, at the level of the inferior mesenteric artery, with no evidence of adrenal parenchymal involvement. This finding supported a diagnosis of paraganglioma, specifically a large para-aortic paraganglioma (POZ). Despite the absence of hypertension or autonomic symptoms, the elevated catecholamines indicated a functional tumor. Preoperative management included intravascular volume expansion and alpha-adrenergic blockade with phenoxybenzamine for two weeks, even in the absence of elevated blood pressure, to mitigate potential intraoperative catecholamine surges. Given the tumor's size, location, and potential for vascular involvement, a comprehensive surgical strategy was implemented, with full contingency planning for conversion to open surgery in the event of acute hemorrhage, limited operative field, malignant tumor invasion, or vascular injury. A laparoscopic approach was adopted, with the patient positioned in 70° left lateral decubitus. Trocars were placed at the umbilicus (10 mm), right costal margin (10 mm), right anterior axillary line (10 mm), and subxiphoid (5 mm). A steep Trendelenburg position was utilized to displace the small bowel and omentum away from the mass. Dissection began with ultrasonic shearing of the hepatic triangular ligament and hepatocolic ligament to mobilize the liver and expose the upper pole of the right kidney. The ascending mesocolon was longitudinally incised and expanded to visualize the right kidney and renal vein, with the descending and horizontal duodenal segments separated to expose the tumor's vascular supply. The tumor was found to be well-encapsulated


A 12-year-old boy from Syria came to the hospital because he was bleeding from his nose, not eating, losing weight, and sweating at night. When doctors checked him, they found swollen lymph nodes in the neck and under the jaw. There was also a lump on the roof of his mouth that pushed his uvula to one side, making it hard for him to swallow and breathe. Blood tests showed high white blood cells and a very high inflammation level. An ultrasound showed a slightly enlarged spleen, and chest X-ray was normal. A CT scan found many swollen lymph nodes on the right side of his neck. A small piece of tissue from a neck lump was taken and tested. At first, doctors thought it was a type of cancer called Classical Hodgkin Lymphoma. But later, tests showed it was actually a different kind of cancer — ALK-negative Anaplastic Large Cell Lymphoma — because the cancer cells had certain markers that matched this type. The boy got chemotherapy, but after 5 months, his condition didn’t improve, so doctors retested. The new test confirmed the cancer type. He got 5 rounds of chemo, but sadly, he passed away six months later.


A 12-year-old Syrian boy was admitted to the hospital with bleeding from the nose (epistaxis), loss of appetite, weight loss, and night sweats. On exam, doctors found enlarged lymph nodes in the neck and under the jaw, with one node about 3 to 5 cm in size. A mass on the hard palate pushed the uvula to the right, causing trouble swallowing and breathing. Blood tests showed high white blood cells and elevated inflammation markers. An ultrasound showed a slightly enlarged spleen, and chest X-ray was normal. A CT scan found multiple enlarged lymph nodes on the right side of the neck. A biopsy of one of the lymph nodes showed abnormal cells that looked like Reed-Sternberg cells, leading to a preliminary diagnosis of Classical Hodgkin Lymphoma. However, because the lab tests needed to confirm the diagnosis were not available at the time, the exact type could not be confirmed. The boy started chemotherapy with the ABVD protocol, but after five months, there was no improvement, so the diagnosis was questioned. Later, immunohistochemistry tests confirmed the presence of CD30 and CD3 positive cells, but no ALK, CD15, or CD20, which led to the final diagnosis of ALK-negative Anaplastic Large Cell Lymphoma (ALCL). He received five cycles of chemotherapy, but unfortunately passed away six months after starting treatment.


{
    "proficient_health_literacy": "A 12-year-old Syrian boy was admitted to our hospital with symptoms of epistaxis, anorexia, weight loss, and night sweats. Medical and family history were unremarkable. Physical examination revealed preauricular, postauricular, and submandibular lymphadenopathy, with the largest node measuring approximately 3 × 5 cm. A hard palate mass was identified, deviating the uvula to the right, resulting in dysphagia and dyspnea. Laboratory findings included a white blood cell count of 35,380/μL, hemoglobin of 10.1 g/dL, platelets of 641 × 10³/μL, and an erythrocyte sedimentation rate (ESR) of 124 mm/hr, indicating systemic inflammation. Abdominal ultrasound demonstrated mild splenomegaly without focal lesions. Chest radiography was normal, with no mediastinal widening. A computed tomography (CT) scan revealed multiple enlarged lymph nodes on the right side of the neck. An excisional biopsy of a cervical lymph node (3 × 4 cm) was performed. Histopathological examination showed complete effacement of lymph node architecture, with proliferation of medium to large-sized anaplastic cells resembling Reed-Sternberg cells located in the interfollicular zones and subcapsular sinuses, admixed with histiocytes, small lymphocytes, and sparse eosinophils. The neoplastic cells exhibited a cohesive growth pattern, abundant cytoplasm, wreath-like or multiple nuclei, multiple nucleoli, and occasional mitotic figures, consistent with a large B-cell lymphoma. Bone marrow aspiration revealed hypercellularity with reactive inflammatory changes, but no evidence of neoplastic infiltration was detected. Based on routine histological staining, the initial diagnosis was Classical Hodgkin Lymphoma (CHL), with a recommendation for immunohistochemical confirmation. At the time, immunohistochemistry was not available at our institution. The patient was initiated on ABVD chemotherapy (doxorubicin, bleomycin, vinblastine, and dacarbazine). Five months later, the patient presented with no clinical improvement, prompting a re-evaluation of the diagnosis. Immunohistochemical analysis confirmed strong CD30 positivity in large Reed-Sternberg-like cells and CD3 positivity, while ALK, CD15, and CD20


A 6-year-old boy was brought to the emergency room because he suddenly couldn’t breathe after eating popcorn. At first, he was okay, but then he started coughing and had trouble breathing. He became very tired and hard to wake up. Doctors saw no blockage in his throat, but one side of his lung wasn’t working. A small bubble of air showed up under his skin on the right neck, which meant something was wrong with his breathing.

He was put to sleep with medicine to help him breathe, and a tube was put into his windpipe. A chest X-ray showed that air was trapped on the left side, and a small piece of popcorn was stuck in the main airway. Doctors knew it had to be removed right away.

They went into the operating room and used a special tool to look inside his airway. They found a piece of popcorn stuck in the trachea, right at the main split of the airway. They also saw a rare extra airway on the right side — it’s not normal, but it’s part of his body now.

The popcorn was safely taken out using a small tool. After that, the airway cleared up, and his breathing improved. He stayed in the hospital for a day, got medicine to help his airway heal, and was able to play and eat normally. He went home the next day feeling fine, with no more breathing problems.


A 6-year-old boy who had no prior medical or surgical issues was brought to the Emergency Department with severe shortness of breath after accidentally swallowing a piece of popcorn. At first, his oxygen levels were okay, but soon he became very distressed and could not breathe properly. He was quickly intubated (a tube placed into his airway) and taken to the operating room for a procedure called direct laryngobronchoscopy, which allows doctors to see the airway and remove a foreign object.

During the procedure, the doctors found a piece of popcorn stuck in the trachea (the main airway), blocking airflow. They successfully removed it using special tools. While doing this, they also discovered that the boy had a rare condition called a tracheal bronchus — a small extra airway that connects the trachea to a bronchus, which can sometimes cause breathing problems.

After the foreign body was removed, the boy’s breathing improved, and his oxygen levels stabilized. He was moved to the pediatric intensive care unit (PICU) and stayed there until he was fully awake and able to breathe on his own. He was given medicine to reduce airway swelling and was able to eat and play normally. He was discharged the next day in good health with no further treatment needed.


{
    "proficient_health_literacy": "A 6-year-old male, medically and surgically free, with a body weight of 22 kg and height of 122 cm, was admitted to the emergency department (ED) by his teacher following sudden onset of severe shortness of breath after ingestion of popcorn. The clinical presentation began with acute respiratory distress, characterized by agitation, drowsiness, and semi-consciousness. Physical examination revealed no overt upper airway obstruction, but auscultation demonstrated absent air entry in the left lung, with subcutaneous emphysema noted on the right neck. Oxygen saturation remained stable with supplemental oxygen.\n\nShortly thereafter, the patient experienced a rapid deterioration in respiratory status and was intubated using a combination of midazolam, ketamine, and succinylcholine. Post-intubation chest radiography revealed proper endotracheal tube (ETT) placement, a hyperlucent left hemithorax, flattening of the left hemidiaphragm, rightward mediastinal shift, and a radiopaque lesion within the left main bronchus. Auscultation post-intubation showed minimal airflow in the left lung, with intermittent desaturation episodes.\n\nOtolaryngology–Head and Neck Surgery was consulted for urgent direct laryngoscopy and bronchoscopy (DLB). After stabilization, the patient was transferred to the operating room for DLB and foreign body removal, with informed consent obtained for potential complications including hemorrhage, infection, failure of foreign body extraction, pneumothorax, and dental injury.\n\nIn the operating room, the patient was intubated via bag-mask ventilation. Bilateral air entry was diminished, with scattered wheezing; significant chest wall expansion was observed on the left side, indicating impaired ventilation. Initial end-tidal CO₂ was 104 mm Hg. Arterial blood gas analysis revealed a pH of 6.87, PaCO₂ of 181 mm Hg (indicating severe respiratory acidosis), and PaO₂ of 231 mm Hg (mild hypoxemia).\n\nGeneral anesthesia was maintained with continuous propofol infusion at 250 mcg/kg/min and dexmedetomidine at 1 mcg/kg/hr. A single dose of dexamethasone (0.5 mg/kg


A 37-year-old woman started feeling weak in her hands about 5 years ago, first in her left hand, then later in her right. The weakness got worse over time, making it hard to write, hold chopsticks, or make a fist. By the time she came to the hospital, her hands were very weak and had shriveled. She didn’t get proper care before this. Tests showed that her hands were weak, but her sense of touch and thinking were normal. The nerves in her arms were damaged, especially the ones that control hand movement, and the damage was seen in the median, ulnar, and radial nerves. There was no damage to her nerves that carry feeling. She also has a condition called Hashimoto’s thyroiditis, which means her body is attacking its own thyroid gland. Even though her thyroid hormones were normal, the antibodies were high, showing the immune system is active. She was treated with medicine that helps calm the immune system, and after a month, her hand strength improved a lot. She will keep coming back for check-ups.