{
    "proficient_health_literacy": "A 76-year-old Asian female presented with a 5-year history of a slowly enlarging lesion on the left breast, with recent acceleration in growth. She reported no pain, pruritus, or systemic symptoms. Medical history was notable for hyperlipidemia, with no comorbidities including hypertension, cardiovascular disease, diabetes, hepatitis, tuberculosis, immunosuppression, or arsenic exposure. There was no personal or familial history of skin or breast cancer, and no significant history of solar or ionizing radiation exposure.\n\nPhysical examination revealed a stable, otherwise well-appearing elderly patient without distress. The left breast demonstrated a 10 mm × 8 mm pigmented plaque with superficial erosion; surrounding skin was intact and unremarkable. No other abnormalities were detected.\n\nImaging modalities including breast ultrasound, chest computed tomography (CT), SPECT-CT, and axillary lymph node ultrasound were performed to assess for metastatic disease, all of which returned negative results, indicating no evidence of distant spread.\n\nDermoscopic evaluation of the lesion revealed characteristic features including multiple blue-gray globules, spoke-wheel patterns, leaf-like structures, and areas of erosion—findings consistent with pigmented basal cell carcinoma (BCC). Histopathological examination confirmed the presence of tumor nests originating from the superficial epidermis, exhibiting a palisading pattern of tumor cells with a narrow, pigmented cleft surrounding the nests—pathognomonic for pigmented superficial basal cell carcinoma.\n\nGiven the patient’s age, the absence of metastatic disease, and the benign clinical course, standard surgical excision was selected after shared decision-making with the patient and her family. The procedure involved complete removal of the nipple and areola with a 10 mm circumferential margin, followed by primary closure. The excised specimen measured 2.0 × 1.8 cm and extended into the subcutaneous adipose tissue layer. Intraoperative frozen section analysis and subsequent postoperative histopathological evaluation both confirmed clear margins, with no residual tumor cells at the surgical edges.\n\nThe patient was discharged on postoperative day 2. No adjuvant therapy was required due to the absence of microscopic residual disease. At a 3-month follow-up, the patient remained asymptomatic, with no clinical signs of local recurrence or metastatic progression. The lesion is currently considered fully resected with no evidence of disease recurrence in the


A 32-year-old woman had kidney problems and needed dialysis for 3 years. She started having bad shaking in her arms, neck, and legs, which got worse over 5 days. The shaking wasn’t just in one part — it spread to both sides of her body. A brain scan showed spots in the deep part of her brain (the basal ganglia) that were damaged, and these spots were the same on both sides. Doctors found that the shaking was likely caused by two things: bad waste from her kidneys and an overactive thyroid. She was treated with stronger dialysis, oxygen therapy, and medicine to fix her thyroid. After a month, the shaking stopped completely, and she could move her body normally again. Her brain scans showed the spots were mostly gone, and her blood tests showed her kidney and thyroid levels were getting better.


A 32-year-old woman with chronic kidney disease had been on hemodialysis for 3 years. She started experiencing severe involuntary movements in her shoulders and neck about 5 days before being admitted to the hospital, which later spread to her limbs. Brain scans showed symmetric, non-hemorrhagic lesions in both sides of her brain’s basal ganglia, areas involved in movement control. These lesions were linked to a combination of uremic toxins (build-up from kidney failure) and hyperthyroidism (overactive thyroid). After treatment with high-frequency, high-flux dialysis, hyperbaric oxygen therapy, and medication to lower her parathyroid hormone levels, her symptoms improved significantly. Within a month, she regained full control of her movements and was discharged. Follow-up scans showed the brain lesions had mostly disappeared, and her blood tests showed improved levels of toxins and thyroid-related markers. The condition was diagnosed as a movement disorder caused by damage to the basal ganglia from kidney disease and thyroid issues.


{
    "proficient_health_literacy": "A 32-year-old female with non-diabetic chronic kidney disease underwent regular hemodialysis via a right forearm arteriovenous fistula for three years. She was admitted due to a five-day history of progressive involuntary movement, initially manifesting as a resting tremor in the shoulders and neck, which progressively evolved into generalized, uncontrolled limb movements. Vital signs were stable, with no evidence of headache, fever, visual disturbance, or cognitive impairment. Neurological examination revealed normal myodynamic parameters and deep tendon reflexes, with suspiciously positive Babinski signs indicating upper motor neuron involvement. Prior to admission, there was a documented history of significant blood creatinine fluctuations, primarily attributed to suboptimal dialysis, and a concurrent severe hyperthyroid state characterized by intact parathyroid hormone (iPTH) levels of 3200 pg/mL, with no prior history of hypertension, diabetes mellitus, respiratory infection, stroke, hepatic disease, hypoxia, or toxic exposure.\n\nBrain magnetic resonance imaging (MRI) performed five days after symptom onset demonstrated symmetrical hyperintense non-hemorrhagic lesions on T2-weighted imaging (T2WI) and T2/fluid-attenuated inversion recovery (T2FLAIR) sequences in the bilateral basal ganglia, consistent with acute or subacute neurotoxic injury. Additional findings included mild diffusion restriction in the corona radiata, suggestive of early ischemic or cytotoxic edema, while T1-weighted imaging (T1WI) and diffusion-weighted imaging (DWI) remained within normal limits, indicating no acute cytotoxic or hemorrhagic change. These findings are consistent with a neurodegenerative or neurotoxic process affecting the basal ganglia circuitry, particularly the striatum, which is critical for motor control.\n\nInitial blood work upon admission revealed markedly elevated uremic toxin levels: urea nitrogen 25.80 mmol/L, serum creatinine 1206 μmol/L, uric acid 548 μmol/L, phosphorus 1.88 mmol/L, calcium 2.33 mmol/L, and anion gap 23.9 mmol/L—indicative of severe uremic burden and metabolic derangement. Hyperthyroidism was confirmed with iPTH of 2487 pg/mL, suggesting a state of secondary hyperparathyroidism likely secondary to chronic uremia and


A 68-year-old woman had numbness in her left arm and pain in her neck. Doctors found a problem with blood vessels in her neck that were pressing on her nerves and spine. This caused her arm to feel numb and weak, and her shoulder to hurt. Tests showed a strange blood vessel connection (like a leak) between her left neck blood vessel and a vein near the spine, at the C5 level. The doctors fixed it using a small tube and special coils placed through her leg artery. They used a balloon to hold the tube in place and put the coils tightly to stop the leak. After the fix, the pain and numbness went away. The woman fully recovered, with no return of the leak or symptoms, and her nerves were no longer being pressed. Four years later, MRI showed the blood vessel problem was completely gone and her arm and neck were back to normal.


A 68-year-old woman came in with numbness in her left arm and pain in her neck. At first, doctors thought it was a musculoskeletal issue, but her symptoms got worse over time. Imaging tests showed abnormal blood vessels pressing on the nerves and spinal cord in her neck, specifically between the C4 and C6 levels. This was confirmed by MRI and angiography, which found a large blood vessel connection — called a VVAVF — between the left vertebral artery and the vertebral venous plexus at the C5 level. This abnormal connection was causing the nerve compression and pain.

To fix it, the patient underwent a minimally invasive procedure under general anesthesia. A small catheter was inserted through her right femoral artery and guided to the area of the blood vessel connection in her neck. Using a special technique with tiny coils and a balloon to keep the catheter stable, doctors successfully blocked the abnormal blood flow. The procedure was done carefully to avoid damaging nearby blood vessels.

After the treatment, the patient’s pain and numbness improved within a month. Four years later, she is doing well with no return of symptoms. Follow-up MRI scans show that the abnormal blood vessel is gone and the nerves are no longer compressed. The left vertebral artery remains open and healthy, and there has been no leakage or complications. She was able to recover fully and has returned to normal daily life.


{
    "proficient_health_literacy": "A 68-year-old woman with no prior history of trauma or vascular disease presented to the orthopedic surgery department for progressive left upper limb numbness and left neck pain. Noncontrast head CT and cervical spine X-ray were unremarkable, and initial management included analgesics, with no improvement over a 12-month period. Cervical magnetic resonance imaging (MRI) revealed an extramedullary lesion characterized by flow voids and abnormal vascular morphology adjacent to the left neural foramen from C4 to C6, demonstrating compression of spinal nerve roots and the spinal cord. Neurological examination confirmed left C5 radiculopathy, with hyperesthesia in the left arm and scapula, and weakness in the left deltoid and biceps brachii muscles. A vascular murmur was auscultated in the left neck, suggesting a high-flow vascular abnormality.\n\nMR angiography (MRA) identified a left vertebral-vertebral venous arteriovenous fistula (VVAVF) with ectasia of the left vertebral artery (VA), but could not precisely localize the fistulous point. Left vertebral artery digital subtraction angiography (DSA) confirmed a high-flow VVAVF connecting the left VA to the vertebral venous plexus, with a single, well-defined fistulous origin at the C5 level within the V2 segment. The fistula drained into the anterior internal vertebral venous plexus, forming a large venous network. No filling of the fistula was observed from the anterior cerebral circulation, confirming the absence of collateral flow from the anterior circulation. The contralateral vertebrobasilar circulation remained intact, with no evidence of steal phenomenon, indicating that the fistula was isolated to the left side.\n\nThe treatment strategy involved targeted microballoon-assisted coil embolization of the expanded paravertebral venous plexus to achieve complete occlusion of the shunt. Preoperatively, heparin (3000 IU intravenously) was administered to prevent thrombosis. Under general anesthesia, a 10 cm, 7-French femoral short sheath (TERUMO) was inserted into the right common femoral artery. A 90 cm, 7-French Guider Guiding Catheter ST (Stryker Japan) was advanced into the left vertebral artery. A 150 cm,


A 26-year-old man had fever, chills, headache, nausea, vomiting, and diarrhea 5 weeks after getting COVID-19. Tests showed he had been infected before, even though the virus wasn't found in his body anymore. He suddenly got very weak and his heart stopped pumping well — it was in shock. Doctors gave him medicine to help his heart beat and to get rid of extra fluid. They were worried it might be a serious heart infection, so they took a small sample of heart tissue. The test showed the heart was inflamed, but mostly with macrophages (a type of immune cell), not the kind that usually means a serious heart attack. This matched what's seen in some people who had COVID-19 and got a bad heart reaction. They called it MIS-A. He also had blood clots in his lungs, which made him short of breath. He got IVIG, steroids, and blood thinners, and started feeling better. His heart function improved, and by the end, it was working normally again. He can now exercise without limits, but is advised to avoid very intense activity. He’s on heart medicine and going to a cardiac rehab program. A follow-up scan will check how his heart is doing long-term.


A 26-year-old man developed high fever, chills, headache, nausea, vomiting, and diarrhea about 5 weeks after recovering from COVID-19. Tests showed he had been infected with the virus in the past, but no active virus was found in his body. He was found to be in severe heart failure, with both sides of his heart not pumping properly, leading to low blood pressure and poor oxygen levels. He needed strong medications like inotropes and diuretics to support his heart function. Doctors were worried he might have had a serious heart inflammation called myocarditis, so they performed a heart tissue biopsy. The results showed mainly inflammation from macrophages (a type of immune cell), with only a few T cells, which is similar to what's seen in some COVID-19 patients. This helped rule out full-blown myocarditis and supported a diagnosis of MIS-A (Multisystem Inflammatory Syndrome in Adults), a rare condition that can occur after a COVID-19 infection. He also had blood clots in his lungs, which were treated with anticoagulation therapy. He received intravenous immunoglobulin (IVIg) and steroids to reduce inflammation, and his condition improved quickly. After recovery, his heart function returned to normal, and he was able to resume normal activities. He is now on long-term heart medications, advised to avoid very intense exercise, and is following a cardiac rehabilitation program. A follow-up heart MRI is planned to better understand the heart damage.


{
    "proficient_health_literacy": "A 26-year-old male presented with a 1-week history of fevers (peak 39.2°C), chills, headache, nausea, vomiting, and diarrhea. On emergency department evaluation, he was hypotensive (75/35 mmHg), tachycardic (126 beats per minute), and had an oxygen saturation of 96% on 6 L nasal cannula. Laboratory findings included leukocytosis (WBC 17.1 × 10⁹/L), lymphopenia (absolute lymphocyte count 0.73 × 10⁹/L), acute kidney injury (serum creatinine 1.9 mg/dL), lactic acidosis (lactate 4.1 mmol/L), and elevated cardiac troponin T (0.218 µg/L, above normal range <0.09 µg/L). SARS-CoV-2 PCR was negative, but SARS-CoV-2 IgG was positive, confirming prior infection. Point-of-care ultrasound revealed severely reduced biventricular function, consistent with cardiogenic shock. The patient was admitted to the cardiac care unit and initiated on intravenous diuresis and inotropes for hemodynamic support.\n\nFurther laboratory evaluation demonstrated elevations in transaminases, procalcitonin, NT-proBNP, ferritin, D-dimer, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP), indicating systemic inflammation and organ stress. Chest x-ray showed right lower lobe and left lower lobe opacities, with a borderline enlarged cardiac silhouette. Electrocardiogram revealed sinus tachycardia and right axis deviation. Echocardiography revealed a left ventricular ejection fraction (LVEF) of 20%, global hypokinesis, mild left ventricular dilation, biatrial enlargement, hypokinetic and dilated right ventricle, moderate to severe mitral regurgitation due to leaflet tethering, severe tricuspid regurgitation, small pericardial effusion, and an estimated pulmonary artery systolic pressure of 53 mmHg with a right atrial pressure of 15 mmHg.\n\nA bedside pulmonary artery catheter was placed on admission, revealing right atrial pressure (RA) of 17 mmHg


A young man from Serbia had a very weak heart and couldn't get enough oxygen, so doctors put in a machine to help his heart work. His heart was failing on both sides, and tests showed his heart muscle was full of iron, which made it weak. This iron buildup was causing his heart to stop working properly. Doctors found a gene problem that causes a rare condition called juvenile hemochromatosis — a condition where the body absorbs too much iron. This iron damage also hurt his pancreas, making him develop diabetes, and his body wasn’t making enough hormones for energy. He got a special heart pump to help his heart, and after a few months, his heart started to get better. The iron was removed with medicine, and his heart function improved so much that the pump was safely taken out after 131 days. His heart is now working well, and his iron levels are back to normal. He still needs insulin and regular blood removal to keep iron low, and he’s doing well and back to work.


A 31-year-old Serbian man with severe heart failure due to iron overload was treated with life-support devices and eventually recovered. He had been diagnosed with iron buildup in his body four months earlier, which caused fatigue and other symptoms. His iron levels were very high — serum ferritin was 2,541 μg/L (normal is 30–500) and transferrin saturation was 90% (normal is 10–45%). Despite normal liver and kidney function, tests showed iron was damaging his heart, leading to very weak heart function with an ejection fraction of only 5–10%. He also developed diabetes due to iron damage to the pancreas, with poor insulin production.

He was admitted to the ICU and started on extracorporeal membrane oxygenation (ECMO) to support his heart and lungs. After a few days, he received biventricular assist devices (BiVAD) to help his heart pump blood. A heart biopsy showed iron deposits in the heart muscle, confirming iron overload as the cause of his heart failure. He began iron chelation therapy with desferrioxamine, which quickly reduced his iron levels. His heart function improved over time, and after 131 days, the BiVAD was successfully removed.

Genetic testing revealed a mutation in the HJV gene (called G320V), which is linked to a rare condition called juvenile hemochromatosis — a form of iron overload that can affect the heart and pancreas, especially in young people. This condition often has no family history, which is what this patient had. He continues to receive insulin for diabetes, testosterone for low hormone levels, and regular blood removals (venesections) to manage iron. After 12 months, his heart function had returned to near normal, and follow-up scans showed no significant iron left in his heart or liver. He has returned to work and is doing well.


{
    "proficient_health_literacy": "A 31-year-old male of Serbian origin presented to a quaternary intensive care unit (ICU) with severe biventricular heart failure refractory to maximal inotropic support, characterized by a cardiac index of 1.3 L/min/m² on noradrenaline and dobutamine infusion. He presented with acute shortness of breath, extreme lethargy, and abdominal pain, with clinical signs of hypotension and sinus tachycardia (HR 105 bpm). Physical examination revealed a hyperdynamic apex beat with heave, jugular venous pulsation of 2–3 cm, and dual heart sounds without murmurs. Neurological status was assessed as Glasgow Coma Score 14 (E3, M5, V6). Abdominal examination showed tenderness in the right upper and lower quadrants without guarding. Notably, he had a tanned skin appearance and no peripheral edema. Laboratory investigations on admission revealed normal hemoglobin, platelets, renal function, and electrolytes, but mild derangement of liver function with elevated alanine aminotransferase (88 U/L), bilirubin (62 μmol/L), and decreased albumin (30 g/L). C-reactive protein (9 mg/L) and neutrophil count (10.27 ×10⁹/L) were mildly elevated, while white blood cell count remained within normal limits. High-sensitivity troponin I was mildly elevated (64 ng/L), suggesting subclinical myocardial injury. Urine and blood cultures were negative. Imaging demonstrated a dilated heart with pleural effusions, ascites, and liver congestion. Transthoracic echocardiography revealed severe global systolic dysfunction with left ventricular ejection fraction (LVEF) of 5–10%, right ventricular dysfunction, and mild to moderate mitral and pulmonary regurgitation, with no evidence of myocarditis or coronary artery disease.\n\nThe patient had a prior diagnosis of iron overload, initially identified 4 months earlier, with serum ferritin of 2541 μg/L (reference range 30–500) and transferrin saturation (TS) of 90% (reference range 10–45%). Liver biopsy showed extensive intrahepatocyte iron accumulation with minimal inflammatory infiltrate and fibrosis (hepatic iron index 1


A 43-year-old Black woman had a painful lump on the outside of her vagina on the left side. Doctors thought it was a common infection called a Bartholin's abscess and cut it out to drain the fluid. While doing that, they found a small, tan-brown bump nearby. That bump turned out to be a harmless growth called hidradenoma papilliferum, which is like a small, slow-growing bump in the skin that can sometimes get confused with an infection. It’s not serious and doesn’t need treatment unless it causes trouble.


A 43-year-old African American woman had a painful lump on her left labia majora. Doctors initially diagnosed it as a Bartholin's abscess, which is a common infection in the glands near the vaginal opening. During surgery to remove and drain the abscess, they found an additional tan-brown lump nearby. This second lump was tested under a microscope and showed features of a condition called hidradenoma papilliferum, which is a type of benign (non-cancerous) growth that can develop in the skin. The findings suggest that the abscess formed inside this existing growth. Both conditions are not serious and were successfully treated.


A 43-year-old African American woman presented with a painful cystic mass on the left labia majora. Preoperative imaging and clinical evaluation led to a diagnosis of Bartholin's abscess, a common benign inflammatory condition resulting from obstruction and infection of the Bartholin's gland ducts, typically involving ductal epithelial proliferation and subsequent suppuration. During surgical excision and drainage of the abscess, an additional dermal nodule measuring 2.0 × 0.8 × 0.8 cm was identified and removed for histopathological assessment. The nodule exhibited a tan-brown color consistent with chronic dermal fibrosis and adipocytic infiltration. Microscopic examination revealed fibro-necrotic foci intermingled with a well-circumscribed papillary neoplasm characterized by cystic dilation of the glandular projections. The papillary architecture was lined by basophilic cuboidal to columnar epithelial cells, with a distinct layer of compressed myoepithelial cells at the basal margin, indicating a differentiated glandular origin. Immunohistochemical staining confirmed apocrine differentiation, evidenced by the presence of foci of active decapitation secretion—where secretory vesicles are cleaved off the apical surface of the epithelial cells—suggesting functional apocrine glandular activity. The presence of these features, particularly the well-defined papillary architecture with apocrine and decapitation secretion, is consistent with Hidradenoma papilliferum, a rare benign adnexal tumor of the eccrine or apocrine sweat glands, often arising in the perineal region. The clinical scenario demonstrates a rare overlap where a Bartholin's abscess develops in the context of a pre-existing hidradenoma papilliferum, suggesting that the underlying dermal lesion may have been a latent neoplasm that became inflamed and infected. This finding underscores the importance of thorough histopathological evaluation in perineal masses, as the presence of a hidradenoma papilliferum may be missed in routine diagnosis and may have implications for long-term monitoring due to its potential for local recurrence or transformation in rare cases. The diagnosis was ultimately established as a Bartholin's abscess arising within a hidradenoma papilliferum, with the histological features supporting both the inflammatory and neoplastic components of the lesion.


A 71-year-old man had heart problems since he was a kid. His heart didn’t work well because of a big hole in the heart and a blocked lung valve, which doctors call unrepaired TOF. He had a small tube (shunt) put in when he was 19 to help blood flow, but never had the full fix. Over the years, he had heart failure three times — at 50, 70, and 71 — but kept playing golf and living a normal life until then. When he came to our hospital, his heart was weak, had high pressure, and was not pumping blood well. Tests showed his heart had a big hole, a thick right ventricle, and a narrow lung valve. His blood was thick and his heart was working hard. Even though he couldn’t have the full surgery because of his other health issues, his doctors fixed his heart rhythm with medicine and a tiny device that shocks the heart if it goes wrong. They also gave him medicine to help his heart pump better. After a month in the hospital, his heart started working much better. One year later, he’s doing great — no more shortness of breath, and he’s still playing golf.


A 71-year-old man with a history of heart failure had a sudden heart stoppage (cardiopulmonary arrest) caused by a fast, irregular heart rhythm (ventricular fibrillation). Thanks to quick action by bystanders, he survived without brain damage. His low potassium levels were thought to have triggered the heart rhythm problem. He was referred to our clinic for further care.

He had a heart murmur since childhood and was diagnosed with a serious heart condition called tetralogy of Fallot (TOF) at age 19. At 21, he had a shunt procedure (Blalock-Taussig) to help blood flow, but he never had the full repair surgery, which was recommended. For years, he was able to work and play golf without symptoms, but started having heart failure at ages 50, 70, and 71.

At the clinic, his blood pressure and heart rate were normal, but he had low oxygen levels and signs of poor heart function, like blue lips and clubbing. His heart scan showed a large hole in the heart (ventricular septal defect) with the aorta overriding it, thickened right ventricle, and severe narrowing of the pulmonary valve—all signs of an unrepaired TOF. A shunt from his childhood was still present. His heart was not pumping well, and the right side of the heart was enlarged and weak.

Tests showed he had blocked coronary arteries, which can damage the heart muscle. Because of his many health problems, the full heart surgery was not done. Instead, he received medication to control his heart rhythm and improve blood flow. He had a device implanted to prevent sudden, dangerous heart rhythms. His doctors carefully adjusted his medications, which helped his symptoms improve.

One year after being discharged, he was doing well and was able to play golf again. His heart failure symptoms had improved enough that he could now walk around without severe shortness of breath.


{
    "proficient_health_literacy": "A 71-year-old male with a history of chronic kidney disease, paroxysmal atrial fibrillation (AF), and chronic heart failure experienced cardiopulmonary arrest secondary to unexpected ventricular fibrillation (VF). Bystander-initiated cardiopulmonary resuscitation was promptly initiated, resulting in complete recovery without neurological sequelae. Upon prior admission, serum potassium was found to be hypokalemic at 3.3 mEq/L, leading to the hypothesis that incidental hypokalaemia contributed to the induction of VF. The patient was referred to our institution for comprehensive evaluation of his cardiac and systemic status.\n\nClinical history revealed a lifelong presence of a heart murmur, initially unrecognized and uninvestigated. At age 19, the patient was diagnosed with tetralogy of Fallot (TOF) and underwent palliative Blalock–Taussig shunt placement at age 21. Despite recommendations for radical intracardiac repair, the patient declined further surgical intervention. For several decades, he maintained an active lifestyle, including employment and regular participation in golf, without overt symptoms of heart failure; however, he was hospitalized at ages 50, 70, and 71 due to progressive decompensated heart failure.\n\nOn presentation, vital signs included a blood pressure of 114/58 mmHg, heart rate of 69 beats per minute, and oxygen saturation of 89% in ambient air. Physical examination demonstrated lip cyanosis and clubbing, with no evidence of peripheral edema. Cardiac auscultation revealed a harsh systolic ejection murmur localized to the 2nd to 4th intercostal spaces along the left sternal border. Laboratory findings included polycythaemia (hemoglobin 18.0 g/dL, hematocrit 52.6%), serum creatinine of 1.8 mg/dL, and markedly elevated brain natriuretic peptide (BNP) at 697 pg/mL. Chest radiography showed a characteristic 'boot-shaped' cardiac silhouette with bilateral pleural effusions. Electrocardiography confirmed the presence of atrial fibrillation.\n\nTransthoracic echocardiography demonstrated aortic overriding over a large ventricular septal defect (VSD) measuring 32 mm in diameter, right ventricular (RV) hypertrophy, and severe pulmonary sten


A man took simvastatin for seven years to lower his cholesterol. Over time, he started getting weaker, especially in his arms and legs, and couldn't climb stairs or stand up on his own. He also lost a lot of weight. Tests showed his muscle damage was very bad — his muscle enzyme level was very high, and his body made antibodies against a protein that helps make cholesterol. A muscle biopsy showed dead muscle fibers, some new ones growing, and signs of inflammation. This condition is called SINAM, which happens when a statin drug causes the body’s immune system to attack muscles. The doctor stopped the statin and gave him strong steroids, immune shots, and methotrexate to calm the immune attack. After three months, his muscle strength came back, the enzyme level went back to normal, and he could move around again without help.


A 70-year-old woman had been taking simvastatin for seven years to lower her cholesterol. Over time, she started feeling increasing weakness in her muscles, especially when climbing stairs or getting up from a chair. Her weakness got worse until she could no longer walk without help or do basic tasks like combing her hair or bathing. She also lost 15% of her weight over 10 months and had no fever, rash, or other signs of infection.

Tests showed very high levels of creatine kinase (a marker of muscle damage) at 2,954 U/L, and blood tests found positive antibodies to HMG-CoA reductase, a protein targeted by statins. A muscle biopsy showed signs of muscle damage, including dead muscle fibers, some new growing fibers, and inflammation around the muscle tissue. The muscle also had a higher-than-normal level of a protein called MHC class I, which is linked to immune activity.

After doctors ruled out infections, cancer, and other conditions, they diagnosed her with SINAM — a rare condition where a statin drug causes an autoimmune reaction that attacks the muscles. The simvastatin was stopped immediately. She started treatment with high-dose corticosteroids (a type of anti-inflammatory drug), intravenous immunoglobulin (to calm the immune system), and methotrexate (an immune-suppressing medication).

After three months, her muscle strength improved significantly, and her creatine kinase level dropped back to normal (15 U/L). She is now on a lower dose of steroids and methotrexate, and her symptoms have mostly gone away.


{
    "proficient_health_literacy": "A 70-year-old woman with a history of hypertension, type 2 diabetes mellitus, hyperlipidemia, ischemic heart disease, and degenerative joint disease presented with progressive proximal muscle weakness and myalgia over several months. She had been on simvastatin 20 mg/day for the prior seven years, which was discontinued upon diagnosis. Clinical manifestations included impaired functional mobility—difficulty climbing stairs, rising from a chair, combing hair, and bathing—accompanied by a 15% weight loss over 10 months. She denied systemic symptoms such as fever, rash, oral ulcers, dyspnea, chest pain, dysphagia, or visual disturbances, and there was no family history of neuromuscular disorders.\n\nPhysical examination revealed significant proximal muscle weakness on the Medical Research Council (MRC) scale: shoulder abduction 3/5, elbow flexion 4/5, hip flexion 3/5, knee flexion 4/5 bilaterally. She was unable to rise from a sitting position. Deep tendon reflexes, sensory function, and coordination were preserved. No abnormalities were detected on cardiac, pulmonary, or abdominal examination. Cutaneous signs suggestive of dermatomyositis were absent.\n\nLaboratory findings demonstrated markedly elevated creatine kinase (CK) at 2,954 U/L (reference range: 10–149 U/L), aldolase at 45.6 U/L (reference <7.6 U/L), aspartate transaminase (124 U/L, reference 10–31 U/L), and alanine transaminase (95 U/L, reference 10–31 U/L), indicating muscle damage and hepatocellular involvement. Serologic testing for viral infections—including herpes simplex virus, Epstein-Barr virus, cytomegalovirus, varicella-zoster virus, human immunodeficiency virus, and hepatitis C—was negative. Hepatitis B serology revealed past exposure (HBV DNA negative), and thyroid function tests were within normal limits.\n\nNerve conduction studies and electromyography (EMG) revealed abnormal spontaneous electrical activity in proximal muscles of the upper and lower extremities, consistent with an irritable myopathy. Muscle biopsy of the right deltoid demonstrated deep myopathic pathology characterized by widespread necrotic muscle fibers, scattered regenerating fibers


A Chinese boy had two bad episodes when he was 6 and 8 years old. Each time, he got very sick with vomiting, diarrhea, and belly pain, which made his body not get enough blood. His blood pressure dropped very low, and he was very weak. Doctors gave him fluids to help, but the second time, even after giving lots of fluids, his blood pressure stayed low. His heart was not working well — the walls of his heart were thick and stiff. Tests showed his heart wasn’t pumping properly, and he needed a machine called ECMO to help his heart and lungs breathe. After using the machine, his heart started to work better again. The thick heart walls went back to normal over time. Doctors found that his body had swelling in the heart that went away. All his tests matched a condition called ISCLS. Now, he’s healthy, has no symptoms for over a year, and his heart is fully back to normal. He still has a little nerve problem in his leg, but it’s not hurting him anymore.


A Chinese boy had two serious episodes of hypovolaemic shock, starting at age 6 and again at age 8. The first time, he had symptoms like cold, runny nose, vomiting, and stomach pain, which led to low blood pressure and a fast heart rate. He was treated with fluids and antibiotics, and his condition improved. An echo test showed a thickened heart muscle, but it returned to normal a month later. After being healthy again, he had a second episode at age 8 with similar symptoms, but this time his blood pressure stayed very low despite large fluid doses. His heart function was severely weakened, and he needed emergency treatment with powerful medications and was transferred to a specialized cardiac unit. He received extracorporeal membrane oxygenation (ECMO) support, which helped stabilize his heart and lungs. During recovery, his heart function improved significantly, and follow-up echo tests showed normal heart wall thickness and full recovery of heart function. The medical team found that his symptoms were consistent with a rare condition called ISCLS, which is linked to immune system issues. He now takes montelukast daily and receives regular immunoglobulin infusions to prevent future episodes. While he still has some lingering nerve issues, he has been symptom-free for over a year and his heart function is fully recovered.


{
    "proficient_health_literacy": "A Chinese boy with a history of eczema and obesity presented with two distinct episodes of anasarca and hypovolaemic shock. The first episode occurred at age 6 years, following a two-day course of coryzal symptoms, followed by one day of vomiting, diarrhoea, and generalized abdominal pain. On presentation, his blood pressure was 85/66 mmHg and heart rate was 144 beats per minute. He rapidly progressed to hypovolaemic shock requiring admission to a paediatric intensive care unit for fluid resuscitation. Laboratory findings included haemoconcentration, hypoalbuminemia, renal impairment, and metabolic acidosis. Echocardiography revealed left ventricular wall thickening. Blood culture yielded coagulase-negative staphylococci, interpreted as a skin contaminant. The patient was managed with intravenous fluid resuscitation and a seven-day course of ceftriaxone; renal function normalized following fluid therapy, and he was discharged after one week. A follow-up echocardiogram one month later demonstrated normal ventricular wall thickness, structure, and function.\n\nBetween episodes, the patient remained asymptomatic until age 8 years, when he presented with one-day history of vomiting, diarrhoea, abdominal pain, and low-grade fever. He was admitted again and developed lethargy, hypotension (76/52 mmHg), tachycardia (141 bpm), and signs of poor perfusion. Despite administration of a total of 3500 mL (70 mL/kg) of normal saline boluses over 8 hours, only transient improvements were observed, with persistent hypotension. Laboratory findings mirrored the first episode: haemoconcentration, hypoalbuminemia, impaired renal function, and metabolic acidosis. Echocardiography from the referring hospital showed significant left ventricular wall thickening, with interventricular septum thickness of 11.9 mm (Z-score +13.34) and free wall thickness of 14.2 mm (Z-score +16.22).\n\nHis haemodynamic instability persisted despite additional fluid resuscitation (total 3500 mL over 12 hours) and administration of multiple inotropic agents, including dopamine, dobutamine, noradrenaline, and stress-dose hydrocortisone.


A 66-year-old man came to the hospital because his right leg was swollen and painful. Tests showed a blood clot in the right leg vein. Doctors found a strange connection in his veins: instead of the usual path, the vein on the left side drained into a different vein called the hemiazygos vein, and his liver vein went straight into the heart. This changed how blood flowed in his body, and it was likely caused by a blockage in the main vein behind the spine. His right leg had a clot, and the left leg’s vein was wider and better able to carry blood, which helped compensate. There was no normal vein behind the liver, and the blood from the liver went directly into the heart. This is a rare way blood flows, but it's not dangerous on its own.


A 66-year-old man was admitted to the hospital because of a blood clot in his right leg. Imaging showed that his body’s main vein on the left side (the IVC) had abnormally drained into the hemiazygos vein instead of going to the heart normally. His liver’s vein drained directly into the heart, bypassing the usual path. This unusual connection was likely caused by a previous blockage in the pelvic veins, which led to the left side of his venous system forming a new path. The clot was in the right leg, and the patient had no other symptoms like fever or chest pain. Tests showed elevated levels of a clot marker (D-dimer) and confirmed the clot in the femoral vein. The imaging also revealed that the right common iliac vein was compressed and narrowed, leading to poor blood flow and the development of collateral veins. This condition is rare and affects how blood flows from the legs to the heart, especially on the left side of the body.


{
    "proficient_health_literacy": "A 66-year-old male was admitted to the hospital with a 2-day history of pain and edema in the right lower extremity, without fever, chest pain, or dyspnea. Prior to admission, he had sustained multiple soft tissue injuries from falls 12 days earlier. There was no significant personal or family history of vascular disease or thrombotic events. Physical examination revealed bilateral swelling of the right leg with palpable pitting edema, normal skin temperature, and intact arterial pulsations. Laboratory evaluation showed a D-dimer level of 2789 ng/mL (normal range: 0–500 ng/mL), indicating a high probability of thrombosis. Color Doppler ultrasonography confirmed right iliac-femoral vein thrombosis with markedly reduced distal blood flow velocity. Following thrombolysis, contrast-enhanced computed tomography was performed to evaluate the retroperitoneal venous anatomy and revealed a congenital anomaly of venous drainage: the right common iliac vein was located posterior to the left common iliac artery and exhibited significant compression and stenosis, resulting in collateral vessel formation in the pelvic region. The left iliac vein was markedly wider than the right, suggesting asymmetrical venous development. An abnormal left-sided inferior vena cava (IVC) was identified, formed by the union of the two common iliac veins at the level of the fourth lumbar vertebra. This left IVC ascended vertically to the left of the abdominal aorta, where it received contributions from the left renal vein at the level of the second lumbar vertebra and the right renal vein at the level of the third lumbar vertebra, with the latter crossing posteriorly over the abdominal aorta. The left IVC continued its ascent, intersecting the hemiazygos vein at the level of the second lumbar vertebra, then traversed posterior to the left diaphragmatic crura and entered the thorax. It ascended through the posterior mediastinum, passing posterior to the thoracic aorta and the azygos vein at the level of the eighth thoracic vertebra, arching over the root of the right lung, and ultimately joining the right superior vena cava at the level of the fifth thoracic vertebra. Notably, this patient lacked a retrohepatic IVC or a right-sided IVC, and the hepatic veins drained directly into the right atrium


A 7-month-old baby started having trouble sitting up and her body started shaking, especially in her head, arms, and legs, about 48 hours after getting the second dose of the MenB vaccine. She had a fever and threw up before, but those went away when she came to the hospital. The doctors checked everything — blood tests, brain scans, and tests for infections — and found nothing wrong. No virus, no bacteria, no other cause could explain her symptoms. The doctors looked at past cases of similar problems in children and found that shaking and balance issues after infections or vaccines are very rare in babies under one year old. They studied 1663 cases from the last 30 years to understand this. The baby’s symptoms got better over 8 days, and by one month, she was sitting still without shaking or falling again. The doctors think the vaccine might have started the problem, but it was very rare and not something that happens often.


A 7-month-old girl developed acute ataxia and cerebellitis within 24 hours of receiving the second dose of the MenB vaccine. She had previously been healthy and had no known medical problems. Her symptoms included difficulty sitting steadily, uncontrolled shaking movements in her head, arms, and body, and fever that resolved by the time she was admitted to the hospital. She had received the first dose of the MenB vaccine at 5 months, and the second dose 72 hours before her symptoms started.

Doctors performed a wide range of tests — including blood work, spinal fluid analysis, imaging scans of the brain and spine, and tests for viruses and bacteria — to rule out infections, genetic conditions, or other serious causes. All tests came back normal. No infection or autoimmune cause was found.

Because the symptoms began right after the vaccine, doctors considered a possible link to the vaccine. They reviewed 20 studies from the past 30 years involving 1,663 patients with similar symptoms, and found that ataxia or cerebellitis caused by infections or other conditions is very rare in children under one year old. This case is unusual because it happened so soon after vaccination and in such a young child.

The girl’s condition improved over 8 days, and by one month, she was able to sit steadily without any shaking or balance problems. No long-term effects were found. A report was filed with health authorities to monitor similar cases in the future.


{
    "proficient_health_literacy": "A 7-month-old female presented with acute cerebellar ataxia (ACA) within 24 hours of receiving the second dose of MenB vaccine (Bexsero, Novartis Vaccines and Diagnostics S.r.l., Siena, Italy). The clinical presentation included impaired sitting balance, previously achieved at 3 weeks of age, with new-onset abnormal involuntary and oscillatory movements affecting the head, limbs, and trunk. Postural control while unsupported was severely compromised, with sustained oscillations and falls. Symptoms began approximately 48 hours prior to presentation and were accompanied by fever and vomiting, both of which resolved at admission. The patient had a unremarkable prenatal and perinatal history, including spontaneous vaginal delivery at 39 weeks gestation, birth weight of 3020 g, Apgar score of 9 at 1 minute, and normal neonatal screening for congenital hypothyroidism, phenylketonuria, cystic fibrosis, and 17-hydroxyprogesterone. She was exclusively breastfed, with a transient episode of cyanosis on day two of life, which was managed appropriately. Vital signs and echocardiography were within normal limits; a mild thrombocytopenia at birth resolved by follow-up. Developmental milestones were otherwise age-appropriate.\n\nVaccination history revealed prior administration of the hexavalent vaccine (DTaP-Hib-IPV-HepB) at 3 and 5 months of age, with no adverse events reported. The MenB vaccine was administered at 5 months, coinciding with the onset of symptoms. On physical examination, the patient was alert, without nystagmus or saccadic eye movements, with normal optic fundi and cranial nerve function, and intact tendon reflexes.\n\nTo exclude infectious meningoencephalitis, a comprehensive diagnostic workup was performed, including blood chemistry, leukocyte count, acute phase proteins, electrolytes, and serologies for adenovirus, cytomegalovirus, Epstein-Barr virus, coxsackievirus, herpes simplex virus, human herpesvirus 6, Mycoplasma pneumoniae, and parvovirus B19—all of which were negative. Cerebrospinal fluid (CSF) analysis revealed a white blood cell count of 1/μL, protein level of 17 mg/dL


A 33-year-old woman was in a car crash going fast and didn't wear a seatbelt. She hit hard and broke bones in her right hip, thigh, and lower leg. Her hip was out of place and had a big crack in the back wall of the hip socket and in the top of the thigh bone. The doctors tried to push the hip back into place in the emergency room but couldn't because of the other broken bones. So they took her to the operating room right away. In there, they used a small pin to push the hip back into place, fixed the thigh and lower leg bones with metal rods, and checked the hip while she was under anesthesia to make sure it was stable. After the surgery, she could start walking with just a little weight and was able to walk fully six weeks later. The bones were healing well, and the hip stayed in place. She never came back for a follow-up visit.


A 33-year-old woman arrived at the trauma center after a high-speed car crash where she was not wearing a seatbelt. She had severe injuries to her right hip and leg, including a dislocated hip, a fracture of the femoral head, fractures of the femur and tibia, and an open wound on her lower leg with exposed bone. Initial attempts to realign her hip in the emergency room failed due to the complexity of her fractures. She was then taken to the operating room for surgery. During the procedure, a small pin was inserted to help realign the hip, and the broken femur and tibia were stabilized using metal rods inserted into the center of the bones. A special X-ray exam under anesthesia was done to check if the hip joint was stable and properly aligned. The results showed that the hip was stable and the fracture pieces were in place. After surgery, she could begin walking with minimal weight and was discharged after 16 days. Six weeks later, she returned to the clinic and was able to fully bear weight on her right leg, with X-rays showing that the hip and leg fractures were healing well. However, she did not return for follow-up care after that.


{
    "proficient_health_literacy": "A 33-year-old female with a history of schizophrenia and bipolar disorder presented to the trauma center following a high-impact motor vehicle collision at approximately 50 miles per hour, during which she was an unrestrained driver. The mechanism of injury resulted in significant blunt force trauma to the pelvis and lower extremity. Upon arrival in the trauma bay, she reported acute pain in the right hip and leg, with physical examination revealing shortening and deformity of the right lower extremity. A 2 cm × 1 cm open laceration was observed over the distal tibia with exposed bone fragments, indicating a comminuted open tibial fracture. The patient was intubated for airway protection due to potential respiratory compromise from pain and shock. Initial radiographic evaluation of the right hip, femur, and tibia revealed a right hip dislocation with associated fractures of the femoral shaft and tibial shaft. Computed tomography (CT) of the pelvis confirmed a posterosuperior acetabular hip dislocation with specific involvement of the posterior wall of the acetabulum and an inferior infrafoveal femoral head impaction fracture, consistent with a posterior wall fracture dislocation. The presence of these fractures raises concerns for avascular necrosis (AVN) of the femoral head due to disruption of the vascular supply from the femoral neck. Attempts at closed reduction of the hip dislocation in the emergency department were unsuccessful, primarily due to the presence of concomitant femoral and tibial shaft fractures, which limited the feasibility of manual reduction and introduced biomechanical instability. Given the severity of the injuries and the risk of AVN, the patient was transferred urgently to the operating room for surgical intervention. In the operating room, she was placed in supine position on a radiolucent table with a small elevation under the right buttock to facilitate optimal pelvic alignment. A 5 mm Schanz pin was inserted percutaneously along the anatomical axis of the femoral neck to provide temporary stabilization and serve as a guide for reduction. Traction and controlled rotational forces were applied to achieve reduction of the femoral head into the acetabulum, confirming the presence of an inferior infrafoveal impaction fracture. The open tibial fracture was debrided to remove contaminated bone fragments and soft tissue debris, followed by primary closure. Both the femoral and tibial shaft fractures were stabilized using intramedullary nailing


A 50-year-old woman was bleeding from her vagina for 4 months, had lower belly pain, and trouble with sex. Doctors found her uterus was big and hard, and a sample from inside it showed a rare type of cancer called uterine carcinosarcoma (MMT). At the same time, they saw a lump in her left kidney that looked like kidney cancer (RCC) on scans. They tried to check the kidney lump with a tiny needle, but it only came back with blood. So they did surgery to check both the uterus and the kidney. The uterus cancer was confirmed, and the kidney lump was not cancer — it was a very rare, harmless tumor called RH. The woman had surgery to remove the uterus and both ovaries, and also the kidney. She recovered well and is now on chemo for the uterine cancer. The kidney tumor was not dangerous, and no family history of cancer was found. She’s doing fine and is being followed up regularly.


A 50-year-old woman came in with vaginal bleeding that had been going on for 4 months, along with lower abdominal pain and discomfort during sex. She had regular periods before this, but now her bleeding was heavy, with clots and pain. She had two children from normal deliveries and had no history of family cancer. She was also diagnosed with hypothyroidism a few years ago, which she manages with medication.

On exam, her abdomen was normal, but her cervix was enlarged and firm. Her uterus was bulky and firm. A sample of the uterine lining (endometrial sampling) showed a rare type of cancer called uterine carcinosarcoma (MMT), which is a serious but uncommon cancer. Blood tests were normal, and her thyroid and other liver/kidney levels were within range.

Imaging scans showed a large, abnormal uterus and a mass in the left kidney. The kidney mass looked very vascular (full of blood) and was initially thought to be renal cell carcinoma (RCC), a common kidney cancer. A needle biopsy (FNAC) of the kidney mass was done twice, but it only showed blood — no cancer cells were found.

The patient had surgery to remove the uterus and both ovaries and fallopian tubes (staging laparotomy), and a frozen section of the kidney mass was checked. The results were unclear, with only a few unusual cells seen. Because of this uncertainty, a full kidney removal (radical nephrectomy) was done.

After surgery, the tissue samples were examined under a microscope. The uterine tumor was confirmed as MMT — a rare cancer with both glandular and connective tissue parts. The kidney tumor was found to be a very rare benign tumor called renal hemangioma (RH), not cancer. This tumor is not aggressive and does not spread.

The patient recovered well and was discharged after 6 days. Tests for a genetic condition linked to such tumors (VHL) were normal. She started chemotherapy for her uterine cancer using paclitaxel and carboplatin, and she is now doing well with regular follow-up for 15 months.


{
    "proficient_health_literacy": "A 50-year-old female presented to the Gynecology Outpatient Department with a four-month history of abnormal vaginal bleeding, including passage of clots, accompanied by lower abdominal pain and dyspareunia for two months. Her menstrual cycles had previously been regular, lasting six days every 28 days, until four months prior when bleeding commenced. She reported no use of oral contraceptives or other forms of contraception. She has two term deliveries via vaginal birth, with the most recent delivery occurring 17 years ago. She was diagnosed with hypothyroidism two years prior and is currently maintained on thyroxine 50 μg daily with euthyroid status. There is no family history of genital, colonic, or renal malignancies.\n\nOn physical examination, she was afebrile, with a pulse of 76 beats per minute, blood pressure of 110/74 mmHg, and mild pallor. Abdominal examination was unremarkable, with no palpable mass. Speculum examination revealed a hypertrophied cervix with active bleeding at the external os. Vaginal examination demonstrated a firm cervix and a bulky, firm uterus with normal mobility and no palpable adnexal mass. Rectal examination showed normal rectal mucosa and soft parametrium.\n\nEndometrial sampling revealed a high-grade endometrial adenocarcinoma, specifically the villonodular subtype. Hemoglobin was 8.9 g/dL, and all liver and renal function tests were within normal limits. Serum TSH was 2.6 uIU/mL, and CA-125 was elevated at 165 IU/L. Pap smear was negative for intraepithelial lesions or malignancy. Pelvic ultrasonography showed a bulky uterus with increased endometrial thickness and an intracavitary lesion. Contrast-enhanced computed tomography (CT) demonstrated a heterogeneous, centrally enhancing mass in the lower pole of the left kidney, suggestive of a highly vascular lesion with mitotic activity, most likely renal cell carcinoma (RCC). MRI of the abdomen and pelvis further revealed a lobulated, ill-defined myometrial-based endometrial mass measuring 2.4 × 1.1 × 2.0 cm, extending into the endometrium and distorting the endometrial cavity, consistent with adenomyosis. A heterogeneously enhancing renal lesion measuring


A 20-year-old man had a lump on the back of his right hand for 5 years. It started small and got bigger over time, now measuring about 4 cm long. The lump was hard, stayed in one place, and didn’t move when he moved his hand. It didn’t hurt much, only when he did heavy work, and it didn’t bother him at night or stop him from doing daily tasks. Doctors saw the lump and used X-rays and MRI to check it. The MRI showed a bony growth coming from the hand bone, with a soft part on top, which matched a condition called osteochondroma. The lump was removed in surgery, and the tissue was tested. The test confirmed it was an osteochondroma. After surgery, the man had no pain, could move his hand freely, and at one year later, the doctors said he was doing well with no signs of the lump coming back.


A 20-year-old man had a swelling on the right hand for 5 years that slowly got bigger, reaching 4 cm × 3 cm × 2 cm. The swelling was on the palm side, near the inside of the hand, and felt hard with no pain except when doing heavy activities. It didn’t cause night pain or limit daily tasks. On exam, it was fixed to the bone and couldn’t move. X-rays showed a bony growth coming from the end of the fifth metacarpal bone. MRI confirmed the growth, showing it was made of bone and cartilage, and it was pushing on nearby tendons and muscles. A diagnosis of osteochondroma was made. The swelling was surgically removed under general anesthesia through a small incision on the back and inside of the hand. The removed tissue was tested under a microscope and confirmed to be an osteochondroma — a benign bone and cartilage growth. The surgery went smoothly, with no complications. The patient recovered well, had no pain, and could move his hand normally. At one-year follow-up, the results were good with no signs of recurrence.


{
    "proficient_health_literacy": "A 20-year-old male presented in January 2021 with a progressive, insidious-onset swelling of the right hand, localized to the palmar medial border, lasting for five years. The lesion gradually increased in size, reaching dimensions of 4 cm × 3 cm × 2 cm, and was characterized clinically as bony, hard, with an irregular surface, adherent to the underlying bone, and fixed in both coronal and sagittal planes. Palpation revealed no fluctuance, local warmth, or signs of inflammation, and there was no associated fever, regional lymphadenopathy, skin changes, sinuses, dilated veins, or systemic symptoms. The swelling was not present elsewhere in the body and was not associated with nocturnal pain or functional limitation during daily activities, though it was aggravated by excessive mechanical loading and relieved with rest.\n\nClinical examination confirmed the lesion's fixed, bony nature and its position on the ulnar aspect of the hand. Radiographic evaluation (X-ray) demonstrated a pedunculated bony lesion originating from the distal metaphyseal region of the fifth metacarpal bone, consistent with an exophytic bony outgrowth. Magnetic resonance imaging (MRI) further characterized the lesion as measuring 2 × 2.5 × 3 cm (anteroposterior × transverse × sagittal), arising from the distal metaphysis of the fifth metacarpal and exhibiting continuity with the medullary cavity, extending away from the epiphysis. The MRI also revealed displacement of the fifth flexor digitorum profundus tendon laterally and compression of the flexor digiti minimi and abductor digiti minimi muscles. Additionally, a bursa with inflammatory fluid accumulation was identified within the soft tissue compartment adjacent to the lesion. Based on these imaging and clinical findings, a provisional diagnosis of osteochondroma was established.\n\nThe lesion was surgically excised under general anesthesia with tourniquet control via a posteromedial incision. The excision was performed at the base of the pedicle, removing a tumor mass of approximately 3 × 2 cm. The resected specimen was sent for histopathological evaluation. Histopathology confirmed the presence of a cartilaginous cap overlying a bony component, with well-organized bony trabeculae. The cartilaginous layer was lined by perichondrium and


A 68-year-old man who had never had any heart problems before suddenly became confused and stopped breathing normally. His wife called emergency services when she found him not responding. When doctors arrived, he was unresponsive and had a heart stoppage. They revived him with life-saving steps, including shock and breathing support. An electrical test of his heart showed signs that match a rare heart condition called Brugada syndrome. This condition can cause the heart to stop suddenly, even without any blockage or heart attack. Doctors found no heart damage, and his heart’s blood flow was normal. He was given medicine for a slow thyroid and later agreed to get a small device in his chest to prevent future heart problems. The doctors confirmed the diagnosis based on the heart test results and his history of no symptoms before this event.


A 68-year-old Hispanic man was brought to the emergency department after his wife found him breathing badly and unresponsive. When doctors arrived, he was confused and had a sudden heart rhythm problem that led to cardiac arrest. He was revived with emergency treatment, including defibrillation and CPR. An electrocardiogram (ECG) taken during this event showed abnormal heart patterns, specifically ST-segment elevations in the chest leads V1 to V3 and unusual repolarization changes in V1 and V2 — findings that are typical of Brugada syndrome. Other ECG results showed a slow heart signal (first-degree AV block) and a normal QRS duration. Blood tests revealed low levels of sodium, potassium, magnesium, and thyroid hormone, indicating severe hypothyroidism, which was treated with hormone replacement. No blockages were found in the heart arteries during catheterization. After recovery, the patient was found to have small brain injuries from previous events, but no major heart problems were present. He was discharged with medications for heart and brain health. Later testing confirmed that his heart rhythm abnormalities matched the pattern of Brugada syndrome, a condition that can cause sudden cardiac death. The doctors recommended he get an implantable cardioverter defibrillator (ICD) to help prevent future heart problems.


{
    "proficient_health_literacy": "A 68-year-old Hispanic male with no significant past medical history was evaluated in the emergency department (ED) following an acute episode of confusion and altered mental status. Emergency medical services (EMS) were dispatched by the patient's wife after she observed erratic breathing and inability to rouse him. Upon ED arrival, the patient was obtunded and experienced in-hospital cardiac arrest due to ventricular fibrillation. Immediate advanced cardiac life support (ACLS) was initiated, including endotracheal intubation, cardiopulmonary resuscitation (CPR), and defibrillation, resulting in return of spontaneous circulation (ROSC). An electrocardiogram (ECG) obtained during the cardiac arrest event revealed ST-segment elevations in leads V1–V3, consistent with a type 1 Brugada pattern, along with prominent repolarization abnormalities in V1 and V2. Additional ECG findings included first-degree atrioventricular (AV) block with a PR interval of 220 milliseconds (normal range: 120–200 ms), and a QRS duration of 0.11 seconds (normal: 0.08–0.12 s), both of which are non-specific but support the presence of underlying conduction system abnormalities.\n\nInitial laboratory values demonstrated hyponatremia (sodium: 132 meq/L; normal: 136–145 meq/L), hypokalemia (potassium: 3.3 meq/L; normal: 3.5–5.0 meq/L), hypomagnesemia (magnesium: 3.3 mg/dL; normal: 1.5–2.4 mg/dL), hyperglycemia (glucose: 197 mg/dL), normal troponin (<0.02 ng/mL), mild elevation of brain natriuretic peptide (BNP: 65 pg/mL), prolonged prothrombin time (PT: 13.6 s; normal: 11–13 s) and international normalized ratio (INR: 1.3), and severe primary hypothyroidism (thyroid-stimulating hormone [TSH]: 59.4 mU/L; normal: 0.5–5.0 mU/L). These abnormalities were not attributable to acute ischemia


A 52-year-old woman had dry eyes and dry mouth for years, and finally got checked. Doctors found she had Sjögren’s syndrome — a condition where her body stops making enough saliva and tears. This was confirmed by blood tests showing antibodies to Ro (SS-A), a biopsy of her salivary glands, and a scan that showed no saliva flow. She also had kidney damage, called membranous glomerulonephritis, which was seen in a kidney biopsy. Three months later, she had a serious stomach problem — a hole in her small intestine that let air in (pneumoperitoneum), and the tissue sample showed a cancer called Epstein-Barr virus-positive diffuse large B-cell lymphoma (DLBCL). She didn’t get chemotherapy because she was too weak, poor, and didn’t want to. But she was taking low-dose steroids and hydroxychloroquine for her Sjögren’s, and after one year, her dry symptoms and protein in her urine got better. A scan showed the cancer wasn’t getting worse.


A 52-year-old woman was diagnosed with primary Sjögren's syndrome, a condition that causes dry eyes and dry mouth, based on her symptoms, blood tests, salivary gland biopsy, and imaging. She had positive results for anti-nuclear antibody (ANA) and anti-Ro (SS-A) antibodies, and her salivary glands showed signs of inflammation. A kidney biopsy later confirmed she had membranous glomerulonephritis, a type of kidney disease that causes protein in the urine. Three months after her diagnosis, she developed a serious abdominal complication: a perforation in her small bowel, which led to infection. A biopsy of the bowel tissue showed Epstein-Barr virus-positive diffuse large B-cell lymphoma (DLBCL), a type of aggressive cancer. Despite being diagnosed with both Sjögren's syndrome and lymphoma, she did not receive chemotherapy due to poor health, low motivation, and financial hardship. However, over the course of one year, her proteinuria improved and her dry eye and dry mouth symptoms got better. A follow-up scan showed that the lymphoma was stable, meaning it did not get worse.


{
    "proficient_health_literacy": "A 52-year-old woman presented with intermittent abdominal tenderness, chronic dry eyes, and dry mouth, which had persisted for several years without prior medical evaluation. She had a history of dilated cardiomyopathy and left-eye glaucoma, managed with loop diuretics, proton pump inhibitors, and anthocyanosides. Physical examination revealed lower extremity edema, with normal body temperature (36.5°C) and blood pressure. Laboratory findings included a white blood cell count of 8,600/mm³ (neutrophilic predominance, 73.4%), sodium 141 mEq/L, chloride 108 mEq/L, blood urea nitrogen 15.7 mg/dL, and creatinine 0.6 mg/dL. Serum total protein was 5.5 g/dL, albumin 1.5 g/dL, and total cholesterol 257 mg/dL. Urinalysis demonstrated significant proteinuria (6.3 g/day), 30–49 red blood cells per high-power field, and no casts. Serologic testing revealed a positive anti-nuclear antibody (ANA; 1:80, homogeneous and speckled pattern), rheumatoid factor (390 IU/mL), and anti-Ro (SS-A) autoantibody (>200 U/mL). Notably, antibodies against double-stranded DNA, La (SS-B), Sm, ribonucleoproteins, antineutrophil cytoplasmic antibodies, lupus anticoagulant, IgG/IgM anti-cardiolipin, and IgG β2-glycoprotein-1 were absent. Complement levels showed a marked reduction in C3 (38 mg/dL; normal range 90–180 mg/dL), while C4 (16 mg/dL; normal 10–40 mg/dL) and complement component 50 (33.1 U/mL; normal 23–46 U/mL) remained within normal limits. Hepatitis B surface antigen, hepatitis C antibodies, cryoglobulins, and human immunodeficiency virus were all negative. Minor salivary gland biopsy demonstrated diffuse lymphocytic infiltrates with a focus score of 3, consistent with lymphoid infiltration in the exocrine glands. Salivary scintigraphy showed non-visualization


A 47-year-old woman had numbness in her toes and trouble urinating for a year. Tests showed her spine's end part was stuck low, like a string tied to the bottom of the spine. The doctors fixed it by cutting part of her spine at the L2 level to free it up. They used screws at L1 and L3 to hold the spine in place, and made sure they were straight and lined up right. They removed part of the bone on the top and sides of L2, and took out the disc between L1 and L2. Then they removed the top part of the L2 bone. A metal rod was attached to the screws and pressed in to hold the spine together. Two soft tapes were placed on the spine to keep it stable. After surgery, her leg numbness got better right away, and her bladder problems improved after one year. The bone healed fully, and the metal parts were taken out after a year. She hasn’t had any problems since then.


A 47-year-old Asian woman was admitted to the hospital with a 1-year history of leg numbness and trouble with urination. She had first noticed numbness in her third and fourth toes five years ago, and over time, her entire toes became numb. She also started having frequent urination. After imaging tests, doctors found that her spinal cord was low in position, extending to the S2 level and surrounded by fat, which led to the diagnosis of adult tethered cord syndrome. To fix this, surgeons performed a spine-shortening procedure at the L2 level.

The surgery involved making a cut from T11 to L4, placing screws at L1 and L3 to help stabilize the spine. The screws were inserted carefully, parallel to the top surfaces of the vertebrae, to make sure the bones aligned properly. The upper part of the L2 lamina (the back part of the bone) and part of the L2 pedicle were removed. The disc between L1 and L2 was also removed. Then, the top part of the L2 vertebra was taken out using a drill. After removing the vertebra, a straight rod was attached to the screws and used to press the bones together. Two polyethylene tapes were placed to support the spine.

The surgery took 5 hours and 13 minutes, with only 108 ml of blood loss. The patient’s leg numbness improved right after the surgery, and her urinary problems improved one year later. A year after surgery, CT scans showed the bones had fully healed, and the hardware was removed. No symptoms returned after two years. This procedure helps free the spinal cord and improve nerve function in patients with tethered cord syndrome.


{
    "proficient_health_literacy": "A 47-year-old Asian woman presented with a 1-year history of progressive bilateral leg numbness, initially affecting the third and fourth toes for 5 years, and subsequent involvement of all toes, along with a 1-year history of urinary frequency. Physical examination revealed intact motor function and normal deep tendon reflexes; sensory disturbance was localized to the anal region. Her finger-to-floor distance was 10 cm, and straight leg raise testing yielded 80 degrees, indicating no significant hamstring tightness. Magnetic resonance imaging (MRI) demonstrated a low-lying conus medullaris extending to the S2 level, surrounded by fat tissue, with no other structural abnormalities identified. This finding was consistent with adult tethered cord syndrome (ATCS), a condition characterized by a fixed, low-lying conus medullaris that is tethered to the spinal column, leading to chronic neurologic compression and progressive sensory and motor deficits. Given the clinical and imaging findings, a spine-shortening vertebral osteotomy was planned at the L2 level to decompress the conus medullaris by reducing spinal length and relieving tethering forces.\n\nAfter obtaining informed consent, the patient underwent surgical intervention under general anesthesia, positioned on a Jackson Spinal Table (Mizuho Co. Ltd., Tokyo, Japan). Neurophysiological monitoring using motor evoked potentials was performed to assess real-time spinal cord function during the procedure. A midline incision was extended from the T11 to L4 spinous process level, allowing extensive exposure of the L2 vertebral segment, including posterior elements and transverse processes bilaterally. Bilateral pedicle screws were placed at L1 and L3 using an anterior-posterior image intensifier. Critical to surgical precision, monoaxial screws were inserted parallel to the rostral endplates of each vertebral body to ensure optimal alignment between the L1 caudal endplate and the L2 osteotomy surface, minimizing the risk of postoperative spinal misalignment and neurological compromise.\n\nThe osteotomy procedure commenced after screw placement. Initial resections included the lower half of the L1 lamina, bilateral inferior articular processes of L1, and bilateral superior articular processes of L2. Subsequently, the upper one-third of the L2 lamina was resected, and the bilateral two-thirds of the L2 pedicle were removed using a surgical air drill. This lamina resection is clinically significant because complete preservation


A 60-year-old man had a tumor in his bladder that wasn't painful or linked to other health problems. After tests, doctors found it was a serious type of cancer called small cell bladder cancer. They removed the tumor first, then gave him chemotherapy and radiation to kill any leftover cancer cells. He also had surgery to remove his bladder and part of his prostate, and replaced it with a new bladder made from part of his intestine. The surgery and treatment worked well — no cancer came back even 33 months later. He’s now healthy and being checked every 6 months to make sure everything stays clear.


A 60-year-old man was diagnosed with a rare type of bladder cancer called small cell bladder cancer (SCBC) two and a half years ago. He had no risk factors like smoking or family history, and his symptoms were mild—just painless blood in his urine. After tests, a 6 cm tumor was found on the bladder wall, and initial tests showed no signs of spread. The tumor was removed, and further testing confirmed it was muscle-invasive and aggressive, with a very high growth rate.

Because this type of cancer can spread quickly, the patient received four cycles of chemotherapy using cisplatin and etoposide, followed by radiation to the brain to prevent spread. He then had surgery to remove his bladder and prostate, along with nearby lymph nodes. The surgery was successful, and final tests showed no cancer cells left in the tissue or lymph nodes.

Since the treatment, the patient has remained free of cancer for 33 months. He now has regular check-ups every six months, including urine tests and imaging, and no signs of recurrence have been found. This case shows an unusually long period of disease-free survival for someone with this type of cancer.


{
    "proficient_health_literacy": "A 60-year-old male presented with painless gross hematuria, with no identifiable risk factors including smoking, prior radiation exposure, occupational hazards, or hereditary predisposition. No systemic symptoms such as weight loss, night sweats, or B-symptoms were present, and no neurological deficits were reported. Urinary infection was excluded by appropriate laboratory and microbiological workup. Cystoscopy revealed a 6 cm solid tumor on the right bladder wall, which was completely resected via transurethral resection of the bladder tumor (TURBT). Primary histopathological evaluation confirmed a muscle-invasive small cell neuroendocrine carcinoma (SCBC) with pT2a GIII classification. Immunohistochemical staining demonstrated strong positivity for synaptophysin and AE1/AE3, consistent with neuroendocrine differentiation, while chromogranin A, CD56, CD3, CD20, TdT, S-100, and HMB45 were negative, supporting the diagnosis of small cell carcinoma without features of other neuroendocrine or epithelial tumors. The tumor exhibited a high proliferative index, with a KI-67 labeling index of 95%, indicating aggressive cellular turnover. An 18F-FDG PET/CT scan at initial diagnosis showed no evidence of lymph node or visceral metastasis, and cranial magnetic resonance tomography (MRT) confirmed absence of brain infiltration, supporting a localized disease at presentation. Given the established evidence in the literature that neoadjuvant chemotherapy improves outcomes in SCBC, the patient received four cycles of cisplatin (25 mg/m²) and etoposide (100 mg/m²), administered every 21 days (days 1–3 per cycle), with no treatment-related adverse events. Concurrently, prophylactic whole-brain radiotherapy (WBRT) was delivered at a total dose of 26 Gray to mitigate the risk of central nervous system relapse, a known site of early dissemination in SCBC. Following chemotherapy, the patient underwent radical cystoprostatectomy with ileal neobladder reconstruction and bilateral extended pelvic lymphadenectomy, including the resection of 32 lymph nodes, all of which were tumor-free. Final pathological assessment confirmed a complete pathological response (ypT0, N0, L0, V0, Pn0), indicating absence of viable small cell carcinoma in the


A 72-year-old man who had been sick with a type of cancer called chronic lymphocytic leukemia (CLL) for years started getting worse symptoms two weeks before he was admitted to the hospital. He had a fever, chills, night sweats, tiredness, trouble swallowing, and fast-growing swollen lymph nodes in his neck. Tests showed his cancer had changed into a more serious form called diffuse large B-cell lymphoma. He began chemotherapy called DA-R-EPOCH, which helped shrink the swollen nodes but also caused serious side effects. Soon after, he had trouble breathing because the swollen neck nodes blocked his airway, so doctors had to put a tube in his throat to keep his airway open. After a few days, the swelling went down, but he stayed unconscious and started having severe, hard-to-stop seizures. Brain scans showed swelling in the back part of his brain, which is a condition called PRES. This swelling was likely caused by the chemotherapy, his damaged kidneys, and a serious infection. Even with treatment, he did not get better and eventually had a heart stop. His brain problem was caused by a mix of these factors.


A 72-year-old man with a history of chronic lymphocytic leukemia (CLL) that had changed to a more aggressive form of lymphoma called diffuse large B-cell lymphoma (DLBCL) presented with a two-week history of low-grade fever, chills, night sweats, fatigue, difficulty swallowing, and fast-growing swollen lymph nodes in his neck. Tests showed his lymphocyte count had risen and his platelet count had dropped, and a scan revealed widespread swelling in his neck, chest, abdomen, and pelvis. A biopsy confirmed the lymphoma had transformed from his original CLL, a condition known as Richter syndrome. He began treatment with DA-R-EPOCH chemotherapy, but soon developed complications including tumor lysis syndrome, kidney damage, and a bacterial infection caused by Pseudomonas aeruginosa. A few days later, his neck swelling became so severe that he needed emergency intubation to protect his airway. Although the swelling improved, he did not regain consciousness and started having severe, uncontrolled seizures. Brain imaging showed swelling in the back part of his brain, specifically in the occipital and inferior temporal lobes, which is consistent with posterior reversible encephalopathy syndrome (PRES). His seizures were hard to control with standard medications but responded to midazolam and propofol. Additional infections were found, and antibiotics were adjusted, but due to his poor outlook, care was not escalated. His condition eventually worsened, and he suffered a cardiac arrest. Experts believe his PRES was caused by a combination of the new chemotherapy, kidney injury, and sepsis.


{
    "proficient_health_literacy": "A 72-year-old White man with an 8-year history of chronic lymphocytic leukemia (CLL), previously treated with four cycles of fludarabine, cyclophosphamide, and rituximab in 2012, and subsequent maintenance therapy with ibrutinib since 2014, presented to the oncology clinic with a 2-week history of low-grade fever, chills, night sweats, fatigue, dysphagia, and rapidly progressive cervical lymphadenopathy. Laboratory evaluation revealed a significant increase in lymphocyte percentage (61% at presentation versus 40.2% at 6 months prior), along with thrombocytopenia (42 vs. 92 K/mm³). Positron emission tomography (PET) imaging demonstrated extensive, confluent hypermetabolic lymphadenopathy involving bilateral neck, chest, abdomen, and pelvis, suggestive of disease progression. Lymph node biopsy confirmed transformation of CLL to high-grade diffuse large B-cell lymphoma (DLBCL), consistent with Richter syndrome. The patient was initiated on dose-adjusted rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-R-EPOCH) chemotherapy. Concurrently, he developed tumor lysis syndrome, acute kidney injury, and neutropenic fever with Pseudomonas aeruginosa bacteremia, requiring broad-spectrum antibacterial and antifungal therapy, as well as granulocyte colony-stimulating factor (G-CSF) support. On day 9 of hospitalization, the patient experienced severe airway obstruction due to extensive cervical lymphadenopathy, necessitating emergency endotracheal intubation and transfer to the intensive care unit (ICU). Neck magnetic resonance imaging (MRI) revealed marked soft-tissue edema, which was treated with high-dose hydrocortisone without clinical improvement. On day 10, after sedation was withdrawn, the patient remained unresponsive and developed two episodes of generalized, refractory seizures. Head computed tomography (CT) showed no acute structural abnormalities; electroencephalography (EEG) failed to detect focal or generalized epileptiform activity. Brain MRI revealed bilateral occipital and inferior temporal lobe edema involving cortical gray matter and subcortical white matter, consistent with posterior reversible encephalopathy syndrome


An 84-year-old man had eye pressure problems from glaucoma. His doctor tried medicines for years, but the pressure stayed high and his vision got worse, especially in his right eye. So, they did a small surgery in his right eye to help lower the pressure using a tiny device called XEN45. Right after, his eye pressure dropped too low, and a small part of the eye (the choroid) detached, but doctors fixed it with eye drops and steroids. Eight months later, they did the same surgery in his left eye. After that, the same problem happened — the choroid detached again — so they did a second surgery to fix it. Both eyes now have normal eye pressure and the problem is gone. The man also had cloudy lenses in both eyes, which made it hard to see clearly, so they did cataract surgery in both eyes. After that, his vision improved a little, but some parts of his eye still have changes from aging, and that doesn’t hurt his daily vision much.


An 84-year-old man with glaucoma had surgery to lower pressure in his eyes using the XEN45 device. The procedure was done in his right eye first in July 2020 and went smoothly. After surgery, his eye pressure dropped very low (to 10 mmHg), which caused a temporary condition called hypotony and a type of detachment in the choroid (a layer behind the retina). This was treated with steroid eye drops and eye drops that reduce muscle activity (cycloplegic drops), and it improved over time. By month eight, the left eye had the same surgery, and again, choroidal detachment occurred. This time, a small surgical procedure was needed to drain the fluid and fix the problem. After that, pressure stabilized between 10 and 12 mmHg, and the detachment fully resolved. Both eyes now have the XEN45 device in place and the pressure is well controlled. The patient also had cataract surgery in both eyes later in 2022. After the surgery, his vision improved in the right eye to 10/10, and in the left eye to 6/10. Although there were some eye conditions like lens clouding and age-related changes in the back of the eye, these did not significantly affect his daily vision.


{
    "proficient_health_literacy": "An 84-year-old male with primary open-angle glaucoma (POAG) presented with decompensated intraocular pressure (IOP) in the right eye, despite maximal medical therapy. His preoperative topical regimen included tafluprost (15 µg/mL once daily), brinzolamide (twice daily), and timolol (twice daily), with addition of oral acetazolamide (250 mg twice daily) in the prior year. Preoperative best-corrected visual acuity (BCVA) was 6/10 in the right eye and 4/10 in the left eye (Snellen chart). Slit-lamp examination revealed transparent corneas, normal anterior chambers, and nuclear cataract opacities in both eyes, with no other anterior segment abnormalities. Preoperative IOP was 24 mmHg in the right eye and 20 mmHg in the left eye. Fundus examination demonstrated a large cup-to-disc ratio (CDR = 0.9) and neuroretinal rim narrowing in all disc sectors bilaterally. Despite optimization of both oral and topical glaucoma medications, a progressive bilateral visual field defect was documented in June 2020, with the most significant decline observed in the right eye.\n\nGiven the patient’s age, bilateral glaucomatous optic nerve damage, and failure of medical therapy to achieve target IOP (ideally <21 mmHg in this population), ab interno XEN45 glaucoma drainage device implantation was selected as the most appropriate surgical intervention. In July 2020, a subconjunctival injection of mitomycin C (0.2 mg/mL) was administered during the right eye XEN45 implantation, which proceeded without intraoperative complications. Postoperatively, IOP dropped to 10 mmHg on day 1, with a diffusely distributed filtration bleb and flat anterior chamber. Fundus examination revealed serous nasal and temporal choroidal detachments, confirmed by eco-B scan as serous choroidal detachments (SCDs), consistent with hypotonic stress-induced fluid accumulation due to excessive outflow and reduced intraocular pressure.\n\nTo mitigate postoperative inflammation and prevent further complications associated with hypotony, a combination of topical dexamethasone (2 mg/mL, three times daily), atropine


A 22-year-old man had a big, soft lump in his belly that made him feel full and sick. Years ago, he had a tube (VPS) put in to drain fluid from his brain, because of a birth condition called spina bifida. The tube had been in place for 21 years, and no other surgeries were done. Doctors found a fluid-filled bag near the tube’s end, which was blocking his stomach. This bag, called a pseudocyst, was filled with cerebrospinal fluid — the same fluid that flows in the brain. The fluid looked like brain fluid, and tests showed no infection. The bag was in the upper left part of his belly, between his stomach and colon. Surgeons opened it, drained 1500 ml of clear fluid, and moved the tube out of the bag. The problem was confirmed as a rare complication of the brain drain tube. This kind of cyst can happen years after the tube is placed, even after 20 years. It causes belly swelling and a lump, and if not treated, can be dangerous. The only way to fix it is to remove the bag and move the tube safely. In this case, surgery was needed because the belly had too much scar tissue to do it with small tools.


{
    "intermediate_health_literacy": "A 22-year-old man was admitted to the hospital because of a swollen, distended abdomen and nausea. He had a ventriculoperitoneal shunt (VPS) placed 21 years earlier to treat fluid buildup in his brain due to spina bifida. This shunt was originally placed when he was just a few months old, and he had no other abdominal surgeries since then. No history of cancer, liver, or pancreas problems was found.\n\nOn exam, a large, soft mass was felt in his upper abdomen. Blood tests were normal, and imaging showed a fluid-filled collection near the tip of the VPS catheter. This suggested a cyst formed around the shunt, likely filled with cerebrospinal fluid (CSF), a type of fluid that normally flows in the brain and spinal cord.\n\nThe doctors suspected a peritoneal pseudocyst — a rare complication of VPS — and performed emergency surgery. The cyst was located in the left upper abdomen, between the stomach and the colon, in a space called the omental bursa. During surgery, 1500 ml of clear fluid was drained, and the VPS catheter was moved outside the cyst. The cyst wall was removed, and the tissue was found to be fibrous with some inflammation.\n\nThe fluid from the cyst matched cerebrospinal fluid in appearance and had no signs of infection. This confirmed the diagnosis: an abdominal cerebrospinal fluid pseudocyst as a complication of the VPS. This condition is rare but can be serious, especially if it causes blockage or swelling in the abdomen.\n\nThis case is notable because the symptoms appeared 21 years after the initial VPS surgery — the longest time reported in the medical literature for such a complication. In most cases, these cysts form within a few weeks to a decade after shunt placement, but this one developed much later.\n\nSymptoms in adults usually include abdominal pain, bloating, and a noticeable mass. Children more often have symptoms like headaches or nausea due to shunt issues. In this case, the patient had no signs of infection or inflammation, making it unlikely to be an abscess or a pancreatic cyst.\n\nThe treatment involved open surgery to remove the cyst and drain the fluid. While some doctors now use smaller, less invasive procedures like laparoscopy, this patient had severe scar tissue (adhesions


{
    "proficient_health_literacy": "A 22-year-old male presented with progressive abdominal distention and nausea. He had a ventriculoperitoneal shunt (VPS) implanted 21 years earlier to manage hydrocephalus secondary to spina bifida. Shunt revision occurred only at age 10 months, with no subsequent abdominal surgical interventions. No history of malignancy, pancreatic disease, or liver pathology was reported. Physical examination revealed a large, elastic, palpable mass in the upper abdomen, with no neurological deficits. Laboratory findings, including white blood cell count and serum amylase, were within normal limits. Supine abdominal radiography demonstrated the VPS in the left upper quadrant and a soft-tissue mass in the upper abdomen. Unenhanced abdominal computed tomography (CT) revealed a homogeneous low-density fluid collection adjacent to the VPS catheter tip, consistent with a cystic lesion arising in the peritoneal cavity. The mass was anatomically localized between the stomach and the mesentery of the transverse colon, specifically within the omental bursa, and was independent of the pancreas. The fluid collection exhibited characteristics consistent with cerebrospinal fluid (CSF), including negative microbial cultures and absence of detectable bacterial flora, as confirmed by fluid analysis. Histopathological examination of the resected pseudocyst wall revealed fibrous tissue with mild inflammatory cell infiltration, confirming the absence of epithelial lining, which is characteristic of a pseudocyst rather than a true cyst or neoplasm.\n\nEmergency laparotomy was performed to address the obstructive effect of the mass on the gastric outlet. The cystic mass was excised, and 1500 ml of clear fluid was drained. A portion of the pseudocyst wall, comprising the posterior gastric wall and adjacent colonic mesentery, was completely resected to facilitate decompression and prevent recurrence. The distal end of the VPS catheter was repositioned externally to the cystic mass to ensure proper drainage and avoid further complications. Postoperatively, the patient's appetite improved, and he was discharged on postoperative day 8 in stable condition. His recovery has been uneventful over the subsequent 4 months.\n\nAbdominal cerebrospinal fluid pseudocyst is a rare but potentially life-threatening complication of VPS placement, typically manifesting as a thin-walled, fluid-filled cystic mass adjacent to the shunt tip. The


An 8-month-old boy had a fever for 9 days and started with a droopy left eye (ptosis) right from the beginning. His eye also pointed down and out. The pupil reacted normally, and tests showed no measles or virus in his spinal fluid. The fever was mild and not linked to rash, seizures, or brain problems. His muscles and nerves were normal. Tests for infections and blood were normal. Brain and eye scans were clear, and no serious issues were found. The eye problem went away on its own in about 3 weeks without any medicine. This kind of eye problem in young kids is rare, and it often happens after a virus. In this case, the virus was likely the cause, but no specific test could confirm it. The child fully recovered with no long-term effects.


An 8-month-old boy had a fever for 9 days and developed left-sided ptosis (drooping eyelid) from the first day of fever. His eye was also turned down and out, but his pupil reacted normally. There was no rash, seizures, or other neurological problems. The child was otherwise active and healthy. Tests showed normal blood work, no signs of infection like measles or other autoimmune conditions, and normal brain and eye scans. The spinal fluid (CSF) showed mild inflammation (lymphocytic pleocytosis), with normal protein and sugar levels, and no detectable measles antibodies. No steroids were given, and the ptosis and eye deviation improved within 2 weeks, fully resolving after 3 weeks. Oculomotor nerve palsy in children is rare and often linked to trauma, infection, or inflammation. In this case, the fever and short duration of symptoms suggest a viral cause, even though measles antibodies were normal. Since the scans were normal and no other serious conditions were found, this appears to be a rare case of temporary viral nerve damage that fully recovered without treatment.


{
    "proficient_health_literacy": "An 8-month-old boy presented with a 9-day history of moderate, intermittent fever, accompanied from the first day by left-sided ptosis and infero-lateral deviation of the left eye. There was no associated rash, joint pain, convulsions, altered sensorium, or neurologic deficits; the child remained otherwise playful and interactive. On clinical examination, left-sided ptosis was present with downward and outward deviation of the globe, and the pupil exhibited normal reactivity. Inability to elevate the left eyelid was noted, but there were no abnormalities in motor strength, tone, or reflexes in any of the four limbs. Laboratory investigations, including complete blood count, electrolytes, urea, and creatinine, were within normal limits. Autoimmune markers—ANA, ASO titer, pANCA, and cANCA—were all within normal ranges. Magnetic resonance imaging (MRI) of the brain and both orbits, along with MRI angiography, was unremarkable, excluding structural abnormalities, including intracranial aneurysms of the internal carotid artery or posterior communicating artery, which are well-documented causes of pediatric oculomotor nerve (CN-III) palsy. Cerebrospinal fluid (CSF) analysis revealed lymphocytic pleocytosis (10 cells/HPF), with normal protein and glucose levels, consistent with aseptic meningitis. IgM and IgG antimeasles antibody titers in CSF were within normal limits, and CSF norovirus polymerase chain reaction was not performed due to financial constraints. The clinical course was self-limiting: ptosis and eye deviation resolved almost completely within 2 weeks and fully after 3 weeks, without the use of corticosteroids. Pediatric oculomotor nerve palsy is a rare entity, with reported etiologies including trauma, infection, congenital causes, and inflammatory processes. In a series by Keith (n=28), trauma, infection, and idiopathic causes were the most common; in Miller’s series (n=30), congenital or traumatic/inflammatory origins predominated. Schumacher-Feero et al. reported that 47% of patients with partial CN-III palsy achieved full recovery without surgical intervention due to spontaneous resolution or partial functional recovery. Viral infections, particularly measles and norovirus, have been linked to postviral oculomotor nerve


A 6-year-old boy kept getting sick with bacterial meningitis, caused by a type of bacteria called Streptococcus Pneumoniae 23F. He had headaches, vomiting, and fever, and the doctors found this bacteria in his spinal fluid and blood. After treating him with antibiotics for 14 days, he got better and went home. But the infections kept coming back. The doctors looked for a reason and found that fluid from his brain was leaking out through a small hole in his skull, into his middle ear — this happened on the right side. This leak likely let bacteria get into his brain again. Tests showed damage to the bone near his ear and brain, especially around the facial nerve and areas near the ear. The doctors confirmed the leak was coming from the right side of his skull, and that’s why the infections kept coming back. The family didn’t want surgery, so the boy just got vaccinated with Prevenar 7 to help prevent future infections. This vaccine is not part of the regular national vaccine schedule and had to be paid for himself.


A 6-year-old boy had repeated episodes of bacterial meningitis caused by Streptococcus Pneumoniae type 23F. He had been treated before with antibiotics, and after one episode, he was discharged without complications. However, the infections kept coming back. Tests showed his immune system was normal, so the cause was likely a problem in his skull bone related to chronic sinusitis. Initial imaging showed sinus inflammation on the right side, but no bone damage. A nuclear scan found that cerebrospinal fluid (CSF) was leaking from the right petroocipital region into the middle ear. Further high-resolution CT and MRI scans showed damage to the bone around the right side of his skull, including areas near the facial nerve and the carotid and jugular canals. These changes showed that the CSF leak was likely the reason for the repeated meningitis. Doctors recommended surgery to fix the bone defect, but the family chose not to proceed. The boy completed antibiotic treatment with vancomycin for 14 days and was sent home. He later received the Prevenar 7 vaccine for pneumococcal infection, though it was not part of the national vaccination program at that time.