{
    "proficient_health_literacy": "An 18-day-old female was admitted to the paediatric intensive care unit (PICU) due to a heart murmur and diminished femoral pulses. The patient was clinically stable, with spontaneous breathing on room air and normal vital signs, except for a significant blood pressure gradient of 30 mmHg between the upper and lower extremities, indicative of obstructive flow in the aortic arch. Transthoracic two-dimensional echocardiography confirmed the diagnosis of aortic coarctation, demonstrating a systolic pressure gradient of 30 mmHg and a closed arterial duct, consistent with a congenital narrowing of the aortic lumen proximal to the origin of the descending aorta. Additionally, the imaging revealed a total retrograde perfusion of the left circumflex coronary artery (LCX), with no visible ostial blood flow from the left aortic sinus, suggesting an abnormal coronary arterial supply pattern. The left ventricular function was preserved, with a normal ejection fraction, absent regional wall motion abnormalities, and no evidence of mitral valve regurgitation. Given the atypical coronary anatomy, coronary angiography was performed, which revealed the absence of a left main coronary artery and instead demonstrated a single right coronary artery (RCA) arising normally from the aortic wall. The LCX was perfused retrogradely via collateral vessels derived from the normal right posterior descending artery (RPD), coursing along the lateral wall of the ascending aorta without entering the aortic lumen, instead draining into the right pulmonary artery (RPA). Small, rudimentary branches of a left anterior descending (LAD) artery were observed arising from the LCX, indicating partial embryological persistence of coronary arterial development. Pulmonary artery pressure remained within normal limits, confirming no significant pulmonary hypertension. At 23 days of age, the patient underwent surgical correction involving resection of the aortic coarctation, end-to-end anastomosis of the aortic segments, and reimplantation of the left coronary artery (LCA) into the posterior aortic sinus using a button technique that avoided stretching or torsion of the coronary artery, thereby preserving coronary artery integrity and preventing ischemic injury. The defect in the right pulmonary artery was closed with a xenopericardial patch. Post-operatively, on day 4, the patient developed recurrent episodes of supraventricular tachycardia (SVT), which were effectively managed


A 36-year-old woman who was overweight since she was 6 years old had type 1 diabetes. She weighed 106.7 kg and was very heavy (BMI 42.2), needing 75 units of insulin every day. Her blood sugar was not well controlled, and her HbA1c was 9.0%. She had surgery called laparoscopic sleeve gastrectomy to lose weight. After the surgery, her weight went down to 81.0 kg (BMI 32.2), which is healthier. She now needs only 24 units of insulin a day, and her blood sugar improved to 7.7%. This means she’s doing better and her body fat, especially the dangerous belly fat, has gone down a lot. The surgery helped her lose weight and control her diabetes better.


A 36-year-old woman with severe obesity and type 1 diabetes mellitus (T1DM), diagnosed at age 6, was admitted for bariatric surgery. At her first visit, she weighed 106.7 kg and had a body mass index (BMI) of 42.2, which is very high. Her HbA1c was 9.0%, showing poor blood sugar control, and she needed 75 units of insulin daily. She had surgery called laparoscopic sleeve gastrectomy, which removes part of her stomach to help with weight loss. Before surgery, her blood sugar was carefully managed, and her weight was reduced to 101.1 kg. One year after surgery, her weight dropped to 81.0 kg, and her BMI improved to 32.2. Her insulin needs decreased to 24 units per day, and her HbA1c improved to 7.7%, meaning her blood sugar control got better. Her body fat, especially around the abdomen, also decreased significantly. There were no serious complications after the surgery.


{
    "proficient_health_literacy": "A 36-year-old Japanese female with morbid obesity and type 1 diabetes mellitus (T1DM), diagnosed at age 6, was referred for bariatric surgery due to progressive weight gain and poor glycemic control. T1DM was managed with multiple daily insulin injections, with insulin requirements escalating in parallel with body weight. By age 20, her body weight was 70 kg, increasing to >100 kg by age 34. At initial assessment, she required 45 units of insulin aspart and 30 units of insulin glargine daily, reflecting a high insulin demand consistent with insulin-dependent diabetes. Preoperative laboratory evaluation revealed an HbA1c of 9.0%, indicating chronic hyperglycemia, and undetectable C-peptide levels (<0.01 ng/mL), confirming complete absence of endogenous insulin secretion, a hallmark of advanced T1DM. Her blood lipid profile remained within normal limits, suggesting no significant dyslipidemia. Abdominal computed tomography (CT) demonstrated a visceral fat area of 162.6 cm² and a subcutaneous fat area of 527.9 cm² at the umbilical level, reflecting substantial adiposity, particularly in the visceral compartment, which is strongly associated with insulin resistance and metabolic complications. Upper gastrointestinal endoscopy showed no structural abnormalities in the esophagus, stomach, or duodenum, ruling out gastrointestinal pathology as a contraindication to surgery. To mitigate the risk of postoperative hypoglycemia due to rapid insulin sensitivity improvement, she was admitted 2 weeks prior to surgery for intensive glycemic control, dietary restriction, and structured exercise therapy. This preoperative intervention achieved a reduction in HbA1c to 7.8% and a transient weight reduction to 101.1 kg. The procedure performed was a laparoscopic sleeve gastrectomy (LSG) using a five-port approach. The greater curvature of the stomach was resected from 4 cm proximal to the pylorus to the His angle, using a linear stapler, with the staple line reinforced by continuous seromuscular sutures with non-absorbable material to ensure anatomical integrity and reduce leakage risk. Postoperatively, insulin therapy was initiated with a sliding-scale regimen: a unit of insulin aspart was mixed with 5 g of glucose in the infusion solution,


The patient had long-lasting pain in her knees and hips, plus bone weakness. Tests showed her phosphate levels were very low, and her bones were thin and damaged. A tumor was found in the left lower leg using a special scan, and the doctor removed it with surgery. The tumor was checked under a microscope and found to be a type called phosphaturia stromal tumor (PMT), which shows a certain protein (Vim) that helps confirm the type. After the surgery, her phosphate levels went back to normal fast, and her pain got much better. Now she walks easier and feels much better.


The patient had long-standing joint pain, especially in her knees, along with groin and back pain that worsened over time. She also had low bone density and very low phosphate levels in her blood, which are signs of a bone disorder. Tests showed increased activity of a protein called somatostatin receptors in her left tibia, leading doctors to suspect a rare condition called TIO (tumor-induced osteomalacia). A PET/CT scan successfully found a tumor in the left tibia, and the tumor was surgically removed. Pathology confirmed it was a phosphaturia stromal tumor (PMT), a type of tumor that causes the body to lose too much phosphate. The tumor showed positive staining for a protein called Vim, which helps confirm the diagnosis. After surgery, her phosphate levels quickly returned to normal, and her pain and symptoms greatly improved.


{
    "proficient_health_literacy": "A 22-year-old female presented with a 10-year history of bilateral knee pain, progressively worsening over the past two months, accompanied by groin pain and right 12th rib pain following a fall. The pain was characterized by recurrent episodes without clear precipitating factors, including knee valgus and dislocation. Prior to the current exacerbation, she had developed low back pain two years earlier, which was transient and relieved with rest, but later progressed to severe pain and loss of mobility, requiring assistance with ambulation and stair climbing. Imaging revealed bone marrow edema in the right intertrochanteric region, femoral neck, lower left femur, and tibial intercondylar crest. Two weeks prior to admission, she experienced widespread joint pain, difficulty walking, and increased pain with weight bearing. Laboratory evaluation demonstrated hypophosphatemia (0.47 mmol/L), elevated serum alkaline phosphatase (257 IU/L), low 25-hydroxyvitamin D (41.1 nmol/L), and reduced bone mineral density as confirmed by dual-energy X-ray absorptiometry (DXA). Physical examination revealed scoliosis, unequal lower limb lengths (right 68 cm, left 67 cm; relative length ratio 77.5:76), reduced thigh and calf circumferences, bilateral knee pain, limited range of motion, left knee evagination, and an 'X'-shaped leg deformity. No joint swelling, tenderness, dislocation, or muscle atrophy was observed. Lower limb length discrepancy and skeletal deformities were consistent with chronic osteomalacia. Radiographic findings included multiple old rib fractures, bone islands in the left ilium and left sacrum, and an elliptical high-signal lesion (1.6 × 0.7 cm) at the posterior cortical edge of the left middle tibia, along with a small vertical nodular abnormal signal (1.5 cm) outside the bone. Quantitative T2-weighted MRI measurements showed T2 signal abnormalities at L1–L2, L1–L3, L1–L4, L2–L3, L2–L4, L3–L4, neck, Wards triangle, and great trochanter, with values ranging from −2.3 to −2.9, indicating generalized bone marrow edema and osteomalacic changes. Pathological evaluation


A 55-year-old man had infections in his surgery scars for over a year. The scars were red, swollen, painful, and kept draining pus. Tests for common infections didn’t find anything wrong. A special test called mNGS found a tiny germ called M. senegalense in the scar tissue. This germ was confirmed with two other simple tests. The man took four antibiotics together for 60 days: clarithromycin, moxifloxacin, rifampicin, and oxycycline. After that, the scars healed and didn’t come back.


A 55-year-old man had repeated infections at surgical incision sites for over a year after having gallbladder surgery. The wounds were red, swollen, painful, and kept draining pus, but standard blood tests and bacterial cultures came back normal. Imaging showed a sinus tract under his chest bone, and surgery was done to remove the infected area and drain the abscess. He was treated with antibiotics, but the infection kept coming back. Tests for tuberculosis were negative, so doctors used a more advanced test called metagenomic next-generation sequencing (mNGS) to find the cause. This test found DNA from a rare bacterium called M. senegalense in the wound tissue. The result was confirmed using two other lab methods: PCR and capillary electrophoresis. The patient was then given a four-drug antibiotic therapy—clarithromycin, moxifloxacin, rifampicin, and oxycycline—for 60 days. After this treatment, his wounds healed completely and no new infections occurred.


{
    "proficient_health_literacy": "A 55-year-old male patient presented to our hospital in August 2021 with recurrent surgical site infections at multiple incision sites, persisting for over 12 months following a laparoscopic cholecystectomy performed for gallstone disease complicated by cholangitis. Clinical examination revealed erythema, swelling, dehiscence, localized tenderness, hyperthermic skin, and minimal purulent exudation at the xiphoid process incisions. The patient experienced an average recurrence interval of approximately 25 days between infection episodes, with no abnormalities detected in routine complete blood count (CBC) parameters. B-mode ultrasonography suggested the presence of a subcutaneous sinus tract originating from the xiphoid region. In September 2021, the patient underwent laparoscopic reoperation and abdominal exploration, during which the sinus tract was excised and an abscess was drained. He was subsequently treated with piperacillin-tazobactam, a broad-spectrum beta-lactam/beta-lactamase inhibitor combination, but this regimen failed to achieve clinical resolution, with persistent wound dehiscence, surrounding skin erythema, swelling, pain, and purulent drainage continuing despite therapy.\n\nDespite normal body temperature and CBC results, conventional microbiological testing—including aerobic and anaerobic bacterial cultures, acid-fast bacilli (AFB) staining, and serological evaluation for tuberculous antigen (TB-Ab) antibodies—remained negative. Chest computed tomography (CT) and other tuberculosis-specific investigations were consistent with the absence of active tuberculosis, thereby excluding a tuberculous etiology. Given the persistent and refractory nature of the infections, and the absence of identifiable pathogens via standard diagnostic methods, metagenomic next-generation sequencing (mNGS) was employed to comprehensively detect microbial nucleic acids from tissue samples obtained from the infected incision sites. The mNGS analysis, conducted using the KingMed Diagnostics platform (Changsha, China), identified 53 out of 113 sequenced reads that mapped to *Mycobacterium senegalense*, representing a 0.09% coverage of the total sequencing depth and accounting for 58.76% of all detected microbial sequences, indicating a dominant pathogenic role.\n\nTo validate the mNGS findings, targeted polymerase chain reaction (PCR) assays were performed using two primer sets: (


A 59-year-old woman who had cancer before, came back with pain and numbness in her left leg, numbness in her vulva, and trouble holding her urine. She had a tumor inside her spine, near the lower back, that was spreading. Doctors removed part of her spine to relieve her pain, but the cancer kept growing. After surgery, her leg symptoms got better, but soon she started having new problems — weakness on her right face, numbness, and blurry vision. Doctors found the cancer had spread to her brain and spinal lining, and she passed away two months later.


A 59-year-old woman with a history of recurring cancer of the uterus (endometrial carcinosarcoma) and previous treatments like chemotherapy and radiation now developed new pain, numbness in her left leg, and trouble with bladder control. She had a tumor found inside her spinal cord, just behind the L1 vertebra, that was growing and causing pressure on nerves. After surgery to remove part of the tumor and relieve pressure on her nerves, her leg symptoms improved. However, the cancer spread to the membranes surrounding her brain and spinal cord (leptomeningeal spread), leading to worsening symptoms including vision problems and facial numbness. Despite the surgery, she passed away within two months due to the advanced spread of her cancer.


A 59-year-old morbidly obese African-American female with a history of Stage IIIc recurrent endometrial carcinosarcoma and para-aortic and pelvic lymph node involvement presented with a 1-month history of left vulvar numbness, progressive left lower extremity pain and numbness, and episodic urinary incontinence. Imaging via thoracic-lumbar magnetic resonance (MR) demonstrated a 1.4 × 1.8 cm enhancing intradural extramedullary mass located inferior to the conus at the L1 and L4-L5 levels, accompanied by abnormal enhancement of the left-sided intradural nerve roots. Additional findings included bilateral perihilar lung metastases. The patient underwent a T12-L2 focal decompressive laminectomy with gross total resection of the L1 intradural/extramedullary lesion, performed primarily to achieve neurological symptom relief. Intraoperatively, diffuse carcinomatosis of the cauda equina was identified, with a large tumor mass located anteroinferior to the conus. The tumor exhibited a vascular architecture and involved multiple swollen, engorged nerve roots. Surgical dissection was discontinued when intraoperative electromyographic (EMG) monitoring indicated significant neural dysfunction, particularly in the gastrocnemius muscle, suggesting tumor infiltration and irreversible nerve root compromise. Permanent pathological examination confirmed a mesenchymal malignant Mullerian mixed tumor (carcinosarcoma) with no epithelial component, consistent with the original primary tumor's histological profile. Postoperatively, the patient showed improvement in left lower extremity pain and sensory deficits. However, two weeks later, she presented with worsening lower extremity symptoms, new-onset right-sided facial weakness, numbness, and blurred vision. Neuroimaging revealed leptomeningeal dissemination of disease, including hydrocephalus and multiple new intracranial metastases. Despite initial neurological stabilization, the patient died from progressive metastatic disease within two months of surgery, consistent with the aggressive biological behavior of carcinosarcoma and its propensity for early leptomeningeal spread, particularly in the context of recurrent, treatment-refractory disease and extensive pre-existing tumor burden.


A four-year-old girl came in with a fever and pain in her left hip. She was walking with a limp, and moving her hip hurt, especially when turning it out. Her blood test showed she was anemic (low red blood cells) and had signs of inflammation. The doctors first thought it might be a common hip infection, but the X-ray and ultrasound didn’t show anything wrong. A CT scan of her belly found a tumor in her adrenal gland and swollen lymph nodes. Even though her bones didn’t seem damaged, the tumor was spreading to her bones. Tests showed this was a type of cancer called neuroblastoma. The cancer was spreading through her blood and bone marrow. She started chemotherapy, which helped a little, but the tumor didn’t go away. Because of side effects on her kidneys, they switched to a different drug combo. After 13 months, the tumor still wasn’t shrinking, so surgery wasn’t safe. Instead, she was given a treatment to replace her damaged bone marrow.


A four-year-old girl came to the emergency room with a fever and a painful limp on her left hip. The pain was especially bad when moving her hip, especially turning it outward, but her range of motion was not severely limited. Blood tests showed anemia (low red blood cells) and signs of inflammation, which raised concerns that something was wrong with her hip. An X-ray of the pelvis didn't show any damage, and an ultrasound of the hip found fluid and swelling, suggesting possible infection or arthritis. A sample was taken and tested, but no bacteria were found. Because the symptoms were unusual, a CT scan of her abdomen and pelvis was done, which revealed a tumor in her left adrenal gland and swollen lymph nodes near major blood vessels. The scan also showed bone changes that suggested the tumor had spread. Further tests, including MRI and bone marrow biopsy, confirmed the presence of neuroblastoma — a type of cancer that starts in nerve cells. The tumor was found in the bone marrow and lymph nodes, and the biopsy showed it was spreading. The child started chemotherapy with a standard protocol, and after six months, the tumor hadn't gone away, though the spread had slightly decreased. Due to side effects from the initial treatment, a different chemotherapy plan (using irinotecan and temozolomide) was started. After 13 months, the tumor still hadn't shrunk enough to allow surgery, so the child was offered stem cell treatment instead. The initial signs of pain and anemia were key clues that something serious was going on, leading to the discovery of the tumor.


{
    "proficient_health_literacy": "A four-year-old girl presented to the emergency department with fever and a painful left hip, accompanied by a limp. There was no prior medical history, and no additional systemic or local symptoms were noted except for cervical lymphadenopathy. Physical examination revealed impaired left hip mobility with pain primarily on external rotation, although joint range of motion was not significantly restricted. Laboratory findings included anemia (hemoglobin 8.7 g/dL), normal white blood cell count, elevated erythrocyte sedimentation rate (ESBR 123 mm), and a reactive C-reactive protein level of 149.7 mg/L, suggesting acute inflammation. Initial pelvic X-ray was unremarkable. Ultrasound of the left hip demonstrated synovial inflammation and a small joint effusion. A guided joint aspiration was performed, and the effusion showed macroscopic features consistent with reactive arthritis; however, bacteriological cultures remained negative. Given the atypical presentation of hip pain and persistent inflammatory markers, a contrast-enhanced CT scan of the abdomen and pelvis was obtained, which revealed a left adrenal mass and retroperitoneal adenopathies involving the celiac trunk and superior mesenteric artery. Notably, the CT scan showed no evidence of bone or joint destruction, and thoracic imaging and peripheral blood smear evaluations were unremarkable. MRI was performed, and direct myelography demonstrated diffuse infiltration consistent with neuroblastoma. Histopathological analysis of cervical lymph node biopsy and bone marrow biopsy confirmed the diagnosis of neuroblastoma, not otherwise specified (NOS). Immunohistochemical staining revealed strong expression of synaptophysin and CD56 (NCAM), with absence of myogenin, supporting a neuronal origin and ruling out myogenic differentiation. Skeletal scintigraphy showed multiple osteoblastic foci, indicative of metastatic disease, and 123I-metaiodobenzylguanidine (MIBG) scintigraphy demonstrated low uptake in the adrenal mass (suggesting low noradrenergic transporter expression) and diffuse bone metastases with high noradrenergic transporter expression. Bone marrow biopsy confirmed extensive metastatic involvement. The patient initiated chemotherapy with eight cycles of the rapid COJEC protocol; after six months, the primary adrenal tumor remained unresectable, and metastatic burden showed partial reduction. Due to chemotherapy-induced renal toxicity, treatment was modified to irinotecan combined with temozolomide (TEMIRI).


A baby boy, seven months old, started having trouble eating, vomiting, and not moving his head or body right. Doctors thought it might be a brain problem called subacute rhombencephalitis, and gave him medicine that helped. After a few days, he got better and could eat again. Later, after a vaccine, he started getting worse — he became irritable, didn’t smile, and his muscles weakened. A new brain scan showed a serious brain condition called leukoencephalopathy with evanescent white matter, which is caused by a gene problem. The doctors found the gene fault in his body, and it was passed down from his parents. Even though his parents and brothers are healthy, they carry the gene. The baby had another fit at 15 months and couldn’t eat or respond to people. He needed help at home, and doctors gave him care for comfort. He passed away at 15 months because the disease kept getting worse. He died peacefully at home, with his family by his side.


A seven-month-old baby boy was admitted to the hospital with severe vomiting, refusal to eat, and signs of neurological problems like weak muscle tone, poor head control, and lack of social interaction. His initial tests showed no serious issues, but a brain MRI revealed signs of subacute rhombencephalitis, a type of brain inflammation. He was treated with steroids and intravenous immune therapy, and his symptoms improved over time. By 10 months, he started showing a return of symptoms after receiving a vaccine — this is called a neurological regression. He became more irritable, lost his social smile, and his muscle weakness worsened. A new brain scan showed damage to the white matter of the brain, specifically in areas involved in movement and coordination, which led to a diagnosis of leukoencephalopathy with evanescent white matter. This is a rare genetic disorder that affects the brain's white matter and is inherited in an autosomal recessive pattern. The baby’s parents and two older brothers were found to be carriers but healthy. At 15 months, he had a seizure and needed further care. His condition continued to worsen, and he eventually stopped responding to stimuli and could no longer eat orally, requiring a feeding tube. He was cared for at home with palliative support and passed away at 15 months due to the progression of his disease.


{
    "proficient_health_literacy": "A 7-month-old male infant presented with a severe, persistent vomiting syndrome, anorexia, and progressive neurological deterioration characterized by axial hypotonia, poor head control, impaired suck-swallow coordination, absence of social smiling, and abnormal oral-motor movements. Osteotendinous reflexes were preserved, and there was no perinatal, personal, or familial history of neurologic disorders or consanguinity. Initial evaluation included a comprehensive panel of laboratory, metabolic, autoimmune, neuroimaging, electroencephalographic, and auditory evoked potential studies, all of which yielded normal results except for the isolation of respiratory syncytial virus (RSV) in a nasopharyngeal aspirate and a brain magnetic resonance imaging (MRI) scan demonstrating bilateral, symmetric diffusion restriction in the anterior bulbo-protuberant junction, consistent with subacute rhombencephalitis. The patient was treated with two doses of intravenous immunoglobulin (2 g/kg total), leading to progressive clinical improvement and oral tolerance, followed by outpatient follow-up in a neuropediatric setting. During this period, the child exhibited modest clinical stabilization, including improved visual tracking, enhanced social contact, and brief periods of stable sitting without support, with intermittent masticatory movements observed only in supine position; osteotendinous reflexes remained intact.\n\nAt 10 months of age, the infant was readmitted following a post-vaccination episode of food rejection, which triggered a significant neurological regression. This included increased irritability, a flat affect, loss of social smiling, progressive worsening of axial hypotonia, proximal muscle weakness, and a striking transformation of the osteotendinous reflexes into hyperactive, equine-type reflexes. Neuroimaging was repeated, revealing generalized bilateral and symmetric abnormalities in the signal intensity of deep and subcortical white matter, involving the U-fibers and globus pallidus, consistent with a neurometabolic disorder suggestive of leukodystrophy. The MRI also showed a mild increase in choline concentration on spectroscopic analysis, with normal N-acetylmethionine (NAA) levels, indicating early disruption of myelin synthesis or integrity without overt neuronal loss. Given these findings, a clinical exome sequencing study targeting early-onset leukodystrophies was performed, which identified a pathogenic, homozygous mutation in the EIF2B5 gene. This mutation is associated with


A man in his 60s went to the hospital feeling weak, having muscle aches, a fever, and belly pain. Doctors did a scan and found a blood clot in a vein called the SMV, which only affected that vein and didn’t spread to other important veins. He also had a fever and body aches that didn’t match the clot, so they tested for flu. The test came back positive for flu B. He didn’t need surgery or any other treatment — just medicine to thin his blood. After a few days, the scan showed the clot was getting better. He was sent home with pills to keep his blood thin and follow up with the doctor.


A 64-year-old man went to the hospital with weakness, muscle aches, fever, and abdominal pain that had started a week before. A CT scan showed a blood clot in the superior mesenteric vein (SMV), which supplies blood to the intestines. The clot was only in the SMV and did not spread to the portal or splenic veins, and the patient was stable overall. However, the fever and muscle pain didn't fit what was expected for SMV thrombosis, so the doctor tested for influenza. The test came back positive for influenza B. The patient was started on anticoagulation therapy (medication to prevent blood clots) without needing surgery. A follow-up CT scan showed the clot was improving, and the patient was discharged with ongoing oral anticoagulant treatment.


{
    "proficient_health_literacy": "A 64-year-old male presented to a local medical center on March 4th with a one-week history of general weakness, myalgia, and abdominal pain. On presentation, his temperature was 37.9 °C, and he reported feeling hot, with associated headache; no cough, sputum, diarrhea, or vomiting were noted. Physical examination revealed mild tenderness in the right upper quadrant and hypoactive bowel sounds, with no rebound tenderness. Laboratory findings showed a white blood cell count of 16,160 /mL, erythrocyte sedimentation rate (ESR) of 86 mm/hr, and high-sensitivity C-reactive protein (HS-CRP) level of 16 mg/dL, indicating systemic inflammation. Abdominal computed tomography (CT) demonstrated a large, segmental thrombus extending from the superior mesenteric vein (SMV) gastrocolic trunk to its distal portion, resulting in complete obstruction of a segment of the SMV. The imaging also showed surrounding fat stranding and bowel wall edema consistent with ascending colon involvement, suggesting ischemic or inflammatory bowel changes secondary to venous obstruction. The patient was subsequently transferred to our hospital for further evaluation. Given the atypical presentation—particularly the presence of systemic fever and widespread myalgia not fully explained by the SMV thrombosis alone—a nasopharyngeal swab was collected for testing. An Influenza A/B rapid antigen test using the BD Veritor™ Plus System for Rapid Detection of Flu A+B was performed, with reported sensitivity of 81.3% (95% CI: 71.1–88.5%) and specificity of 98.2% (95% CI: 95.7–99.3%). The test returned a positive result for influenza B, which likely contributed to the patient’s fever and myalgia. Concurrently, a reverse transcription polymerase chain reaction (RT-PCR) test for SARS-CoV-2 (COVID-19) was performed in light of the ongoing pandemic context, though no positive result was reported. The thrombus was localized exclusively to the SMV, with no extension into the portal or splenic veins, confirming isolated venous occlusion. The patient was clinically stable and managed with anticoagulation therapy without surgical intervention. Follow-up CT imaging demonstrated resolution of the throm


A 9-month-old girl had a bump in her eye socket on the right side, noticed by her mom three months before. Doctors first thought it was just a normal thing, but scans showed bone changes in the eye area, like a tumor was eating away at the bones. A scan of her chest and belly found a big tumor in her adrenal gland, along with swollen lymph nodes and spine changes. This matched a serious cancer called stage-4 neuroblastoma. She started chemo and surgery, and after 10 months, the cancer was gone and she hasn’t had any return.


A 9-month-old girl was diagnosed with isolated right-sided enophthalmos, which means her right eye appeared to be pulled back. Her mother noticed this three months before she visited the doctor, and several specialists initially thought it was just a normal variation. However, imaging tests showed bone changes in the orbit and surrounding areas, including osteolysis (bone loss) and thickening of the bone lining, which raised concern for a tumor. A CT scan of her chest and abdomen found a large mass in the left adrenal gland, along with swollen lymph nodes and bone changes, consistent with stage-4 neuroblastoma. This type of cancer is rare in young children and spreads beyond the original site. The child was referred to oncology, started on chemotherapy, and had surgery to remove remaining tissue. She achieved complete remission and has not had a recurrence at a 10-month follow-up.


A 9-month-old Caucasian female with no significant birth or past medical history presented with isolated right-sided enophthalmos, defined as a posterior displacement of the globe relative to the orbital cavity. The mother first noted the abnormality three months prior to presentation, describing a backward shift of the right eye. Initial evaluations by multiple specialists attributed the finding to a constitutional variant, with no evidence of systemic illness, neurological deficits, abdominal or skeletal abnormalities, or deterioration in general health. Ophthalmological examination confirmed mild right enophthalmos without associated facial flattening or structural deformity. All standard eye function tests—including pupillary size and reactivity to light, direct and consensual accommodation, fixation, following, binocular vision, and eye-hand coordination—were within normal limits. Slit lamp and fundus examinations revealed no signs of intraocular pathology. Prior to definitive imaging, routine laboratory assessments, including serum creatinine, were unremarkable, indicating preserved renal function and no evidence of systemic disease. Orbital computed tomography (CT) demonstrated irregular osteolysis with active periosteal reaction involving the right orbital walls, malar bones, and zygomatic arches, predominantly unilateral and asymmetric, which raised a high index of suspicion for an underlying orbital mass, likely neoplastic in origin. A subsequent thoracic-abdominal CT scan identified a retroperitoneal heterogeneous mass measuring 83 mm × 43 mm × 42 mm, located on the left adrenal gland, which encased adjacent vascular structures and was associated with enlarged left supraclavicular lymph nodes and vertebral body condensations. These imaging findings are characteristic of stage-4 neuroblastoma, a malignant peripheral nerve tumor of early childhood origin, typically arising from sympathoadrenal precursors. The diagnosis was confirmed through histopathological and molecular characterization. The patient was promptly referred to pediatric oncology for multimodal management, including induction chemotherapy and surgical evacuation of residual tumor burden. Treatment resulted in complete clinical remission, with no evidence of disease recurrence at a 10-month follow-up. The clinical course underscores the importance of imaging evaluation in the setting of isolated enophthalmos, particularly when orbital bony changes with periosteal reaction are present, as these findings may signal an occult neuroblastoma, even in the absence of other systemic symptoms or signs.


A 21-year-old girl started feeling short of breath and chest pain six months ago. She was diagnosed with heart failure, but had no history of heart problems. Doctors found a strange connection between a blood vessel in her arm (right subclavian artery) and a vein (superior vena cava) that was causing her heart to work harder. This connection, called a fistula, had a narrow part at the start, which made blood flow too fast. She had the fistula closed using a small device placed through a catheter in her vein. After the procedure, her symptoms got much better by the 3-month check-up.


A 21-year-old woman was diagnosed with new-onset heart failure after six months of worsening shortness of breath and chest pain. She had no prior heart problems, injuries, or surgeries. Examination found a continuous heart murmur heard in the right chest area, and imaging showed an enlarged heart and signs of right heart strain. Tests revealed a rare birth defect called a congenital arteriovenous fistula, where a blood vessel (the right subclavian artery) was abnormally connected to the superior vena cava, causing blood to flow directly from artery to vein without going through the heart. This connection was narrowed at its start, which increased pressure and worsened heart function. The fistula was successfully closed using a minimally invasive procedure called transcatheter occlusion, where a small device was guided through a blood vessel to seal the abnormal connection. After the procedure, the patient’s symptoms improved significantly by the three-month follow-up visit.


{
    "proficient_health_literacy": "A 21-year-old female presented with a six-month history of progressive dyspnoea and chest pain, ultimately diagnosed with new-onset heart failure in the absence of any prior cardiovascular disease, trauma, or surgical history. Physical examination revealed a grade 3/6 continuous machinery murmur, most prominent between the right second and third intercostal spaces and radiating to the right infraclavicular fossa. Resting oxygen saturation was normal (SpO2 95%) with non-cyanotic skin colour, indicating adequate tissue oxygenation. Chest radiography demonstrated cardiomegaly, consistent with right-sided cardiac volume overload. Electrocardiography revealed sinus rhythm at 95 bpm, complete right bundle branch block, and right ventricular hypertrophy, reflecting chronic pressure overload on the right side of the heart. Pulmonary function tests were within normal limits, ruling out obstructive or restrictive lung disease as a contributing factor.\n\nTransthoracic echocardiography identified a dilated right subclavian artery (RSA) with an 8-mm arteriovenous fistula connecting to the superior vena cava (SVC), accompanied by significant stenosis at the proximal origin of the fistula. The right ventricle and right atrium were markedly dilated, consistent with chronic volume and pressure overload. Mild tricuspid regurgitation was observed. Continuous wave Doppler analysis demonstrated a sustained flow signal of 2.3 m/s from the RSA to the SVC with a pressure gradient of 22 mmHg, indicating a low-resistance shunt. At the site of stenosis, the peak flow velocity reached 3.9 m/s with a pressure gradient of 59 mmHg, reflecting a high-velocity, high-resistance flow pattern consistent with a critical stenotic lesion. Computed tomography angiography (CTA) provided detailed anatomical characterization of the arteriovenous fistula, confirming the direct connection between the RSA and SVC and the proximal stenosis, enabling precise procedural planning.\n\nThe patient underwent transcatheter occlusion of the arteriovenous fistula under local anaesthesia. A 10/12 mm Amplatzer ductal occluder was delivered via a 5-F H1 catheter and deployed from the SVC side using angiographic guidance. An 8F sheath was utilized to facilitate catheter advancement and occluder


A 68-year-old woman came to the hospital because her legs were weak for more than 3 days. She also had neck pain, numbness in her hands and feet, trouble going to the bathroom, and couldn’t feel cold or heat well. She didn’t have fever, cough, or other common illness symptoms. She had high blood pressure but no diabetes or allergies. Tests showed her brain and blood were fine, but her spinal cord was inflamed — especially in the neck area. This is a rare case in China, and it’s different from usual cases of this illness. She was treated with strong medicine and immune therapy and got better. This kind of problem with anti-sulfatide antibodies usually affects nerves, but in her case, it hit the spinal cord, which is unusual.


A 68-year-old woman was admitted to the hospital with weakness in her limbs that had lasted more than 3 days. She also had neck pain, numbness in her hands and feet, trouble controlling her bladder and bowels, and a reduced ability to feel temperature. She was diagnosed with a rare form of Guillain-Barré syndrome (GBS) that is positive for anti-sulfatide antibodies. This case was treated with methylprednisolone and intravenous immunoglobulin therapy. Unlike typical GBS cases, this patient showed signs of spinal cord involvement, which is not commonly seen. No other patients with this specific combination of symptoms have been reported in China before. The patient’s symptoms started gradually and were not linked to a recent infection or illness, and she had no history of diabetes or allergies.


{
    "proficient_health_literacy": "A 68-year-old female was admitted to the hospital with progressive limb weakness lasting over three days, accompanied by posterior neck pain, distal sensory disturbances, and a characteristic electric shock-like paresthesia upon tactile stimulation. Symptoms evolved to include impaired manual dexterity, bilateral lower extremity weakness, inability to ambulate, urinary and fecal retention, and heightened posterior neck pain. Notably, she reported cold-related pain in the upper extremities, which is atypical for common Guillain-Barré syndrome (GBS) presentations. Neurological examination revealed preserved consciousness, normal pupillary response, intact eye movements, and symmetrical frontal lines. Upper limb muscle strength was graded 4, lower limb strength was 3, with hypotonia and bilateral diminished tendon reflexes. The Babinski sign was positive bilaterally, indicating upper motor neuron involvement. Sensory examination demonstrated reduced perception of pain and temperature in the distal extremities, while vibration and joint position sensations remained intact. The two-handed finger-nose test was stable, suggesting preserved cerebellar function, whereas the heel-knee-shin test was unstable, indicating impaired proprioception. Meningeal signs were absent, and there was no evidence of autonomic dysfunction such as dysautonomia or respiratory compromise. Vital signs were stable: temperature 36.8 °C, pulse 76 beats/min, respiratory rate 20 breaths/min, blood pressure 145/78 mmHg. Physical examination revealed no signs of infection, cardiac abnormalities, or abdominal pathology; abdominal examination showed softness, no varices, no rebound or peritoneal tenderness, and only slightly reduced bowel sounds (2–3/min), without evidence of ascites. Laboratory studies, including complete blood count, liver and renal function, coagulation profile, and tumor markers, were within normal limits. Cranial CT and cranial MRI showed no evidence of hemorrhage, ischemia, or structural lesions. Lumbar puncture revealed elevated cerebrospinal fluid (CSF) pressure (116 mmH₂O) and cytoalbuminologic dissociation—characteristic of inflammatory demyelinating processes—without the presence of oligoclonal bands, aquaporin-4 antibodies, or anti-MOG antibodies, ruling out other central nervous system demyelinating disorders. Peripheral neuropathy immunoblotting demonstrated a positive IgG response to sulfatide


A 32-year-old man had trouble breathing and suddenly lost consciousness several times in one week. Each time, he would feel dizzy and lose awareness for 3 to 5 minutes, then wake up fine. The episodes happened when he was active or breathed cold air. He went to the hospital after the fourth episode. Tests showed blood clots in his heart and lungs. One clot was blocking a small hole in his heart (PFO), and clots were also in his lung blood vessels. Doctors placed a filter in his biggest vein to catch clots and used a medicine (alteplase) to break down the clots. Two days later, no clots were found in his heart. He was sent home on a blood thinner called warfarin and had no problems. This treatment helped stop the clots from coming back.


A 32-year-old man had repeated episodes of sudden, brief loss of consciousness (syncope) and shortness of breath over a week. The episodes were triggered by physical activity or breathing cold air, and he had no warning signs before them. He went to the hospital after another episode on February 22, 2019. His initial tests showed high levels of a blood clot marker (D-dimer) and a protein linked to heart strain (NT-proBNP), while his blood pressure and other vital signs were normal. An electrocardiogram showed a fast heart rate, and ultrasound found a blood clot in his right leg vein. Echocardiography revealed a blood clot blocking a small hole between the upper chambers of the heart (patent foramen ovale), along with a large clot in the right atrium and a clot in the left atrium. CT scans confirmed blood clots in both pulmonary arteries, indicating pulmonary embolism. He received treatment with a filter placed in his inferior vena cava to prevent clots from traveling to the lungs and was given alteplase to dissolve the clots. Two days after treatment, follow-up echocardiography showed no clots in the heart chambers. He was discharged home two weeks later on warfarin, a blood thinner, without complications.


{
    "proficient_health_literacy": "A 32-year-old male presented to the emergency department with recurrent syncope and intermittent dyspnea over a 7-day period. The initial episode of chest distress occurred on February 15, 2019, followed by four episodes of transient, self-limited syncope each lasting 3–5 minutes with complete recovery between episodes. Triggers included physical exertion and inhalation of cold air; no prodromal symptoms or associated neurological features were reported. The patient sought medical evaluation on February 22, 2019, following a new episode of syncope. There was no personal or family history of thrombotic disorders, and the patient's sedentary lifestyle, due to employment as a news editor, contributed to reduced physical activity.\n\nVital signs at first presentation were stable: pulse rate 96 beats/min, respiratory rate 20 breaths/min, blood pressure 15.5/10.1 kPa, body mass index 23.1 kg/m². Physical examination revealed symmetric and light-responsive pupils, a prominent P2 component in the cardiac auscultation, symmetrical breath sounds without rales or wheezing, and warm extremities without edema. Neurological examination was unremarkable.\n\nInitial laboratory findings included markedly elevated serum D-dimer at 4150 ng/mL (normal <500 ng/mL), indicating active thrombin generation and fibrin formation. Arterial blood gas analysis under ambient air showed a PaO₂ of 79 mmHg, suggesting mild hypoxemia. N-terminal pro-B-type natriuretic peptide (NT-proBNP) was elevated at 4460 pg/mL (normal <450 pg/mL), reflecting right ventricular strain consistent with pulmonary hypertension. Cardiac enzyme levels were within normal limits, excluding acute myocardial injury.\n\nElectrocardiography demonstrated sinus tachycardia, likely secondary to hypoxemia and sympathetic activation. Transthoracic echocardiography revealed a deep venous thrombus in the right popliteal vein, a thrombus straddling a patent foramen ovale (PFO), a dilated right atrium, and moderate pulmonary hypertension. The thrombus dimensions were 3 mm × 20 mm in the left atrium and 8 mm × 25 mm in the right atrium. Computed tom


We used two small cork-screws to safely remove a stuck hip implant when the hip kept slipping out because the socket was too far out of place. This worked well without hurting the patient, and by the second month, she could walk without help.


A new method has been reported to remove a stable, cemented hip component that is causing recurrent dislocations due to improper positioning of the acetabular part. In this case, a 74-year-old woman had repeated hip dislocations (eight times) because the hip socket (acetabulum) was positioned incorrectly. Doctors used two cork-screws inserted into the rim of the hip socket to push out the plastic liner and create cracks in the cement. This allowed them to easily remove the damaged plastic cup. The cement was then carefully broken up and removed piece by piece. A new, reinforced ring and a new cemented hip socket were placed using standard techniques. The metal ball of the hip was replaced, but the stem was kept. There were no complications during or after the surgery. At two months after the procedure, the patient could walk without needing support.


A 74-year-old female underwent revision total hip arthroplasty for recurrent dislocation of a cemented total hip prosthesis, resulting from acetabular malposition, with a history of eight prior dislocations. The acetabular component was stable and cemented, necessitating a technique to remove the cemented acetabular cup without compromising the integrity of the underlying bone or the femoral stem. The all-polyethylene acetabular liner was drilled with a 4.5 mm drill to create a peripheral breach, followed by the insertion of two cork-screws into the rim of the acetabular component, advanced as far as anatomically feasible, to induce extrusion of the polyethylene liner from the cement mantle and to generate fissures within the cement layer. Application of manual torsional shear forces at the polyethylene-cement interface resulted in complete disruption of the polyethylene liner at the cement-polyethylene boundary, with no technical complications or resistance observed. This mechanical disruption enabled complete removal of the polyethylene cup with minimal effort. Subsequently, cement–splitting osteotomes were employed to remove the cement mantle in a piecemeal fashion, with meticulous curettage of residual cement plugs to ensure complete debridement. A roof reinforcement ring was implanted to stabilize the acetabular component, followed by placement of a cemented UHMW polyethylene cup using standard surgical techniques. The original metallic femoral head was replaced, while the cemented femoral stem was retained to preserve stability and biomechanical continuity. The perioperative course was uncomplicated, with no evidence of intraoperative or postoperative complications. At two months postoperatively, the patient achieved full weight-bearing ambulation without the need for external assistive devices, indicating successful restoration of hip joint stability and function. The described technique demonstrates a feasible, technically sound approach for the removal of a stable cemented acetabular component in the setting of recurrent dislocation due to malposition, leveraging mechanical disruption via cork-screw insertion and torsional shear forces to overcome the cement-liner interface without requiring additional instrumentation or surgical intervention.


A 25-year-old woman had a planned C-section at 39 weeks because she wanted to. After the surgery, she suddenly got a very high fever and her blood pressure dropped sharply. A few days later, doctors found a bad germ in her blood called Ralstonia mannitolilytica. This meant she had a serious infection that caused her body to go into shock. Doctors gave her lots of fluids, blood transfusions, medicines to raise her blood pressure, and strong antibiotics like imipenem and cefoperazone. She stayed in the hospital for a few days in a serious care unit, and after treatment, she got better. She was finally able to go home without any problems, and six months later, everything was normal.


A 25-year-old woman had a planned cesarean section at 39 weeks of pregnancy. After the surgery, she suddenly developed a high fever and low blood pressure, which are signs of a serious infection called sepsis. Five days later, a bacteria named Ralstonia mannitolilytica was found in her blood. This infection led to septic shock, so she received strong fluids, blood transfusions, and medicines to support her body. She was treated in the intensive care unit and recovered without major complications. She was discharged on day 15 and had no issues during a six-month follow-up.


{
    "proficient_health_literacy": "A 25-year-old woman, gravida 1 para 0, with no history of chronic medical conditions, was admitted for an elective cesarean delivery at 39+1 weeks of gestation by maternal request. Combined spinal-epidural anesthesia was administered: 15 mg of 0.5% ropivacaine hydrochloride (AstraZeneca AB, Sweden) was injected into the subarachnoid space, and 5 mL of 2% lidocaine (Shanxi Shiyao Yinhu, China) was administered epidurally. Prophylactic intravenous cefathiamidine (1.0 g, Shandong Luoxin, China) was initiated preoperatively. During surgery, the patient developed shivering, but vital signs remained stable, and the procedure was completed successfully. Postoperatively, she was transferred to the anesthetic resuscitation room where she continued to shiver, reported generalized numbness and dyspnea, and developed a high fever of 40.7 °C. Her blood pressure dropped to 78/44 mmHg, with tachycardia reaching a maximum of 177 bpm, and intermittent vaginal bleeding was noted; oxygen saturation remained at 98%. Septic shock was clinically suspected, though anaphylactic shock could not be excluded. Immediate resuscitation was initiated with massive fluid resuscitation, intravenous dexamethasone (Sinopharm, China), and intramuscular carboprost tromethamine (250 μg, Pharmacia and Upjohn Company, USA) as a uterotonic agent. A Bakri postpartum balloon (Cook, USA) was placed to manage postpartum hemorrhage. Despite interventions, blood pressure remained critically low (<90/60 mmHg). Laboratory findings revealed severe metabolic acidosis (pH 7.252 [normal 7.35–7.45], serum lactate 6.52 mmol/L [normal 0.36–1.25]), markedly elevated procalcitonin (94.5 ng/mL [normal 0.0–0.5]), leukocytosis (WBC 15 × 10⁹/L [normal 4–10 × 10⁹/L]), neutrophilic predominance (


A 71-year-old woman had early breast cancer in her right breast. She had surgery to remove the tumor, then took chemo, radiation, and hormone pills to fight it. She stayed healthy for years until 2015, when she started coughing. Doctors found the cancer had spread to her lungs and bones, like in the shoulder, hip, and back. She started taking two medicines to stop the cancer from growing — ribociclib and letrozole — which helped for a while. But she still had low blood cell counts, so her dose was cut in half. A few months later, she noticed white spots on her hands, feet, and face — like patches of skin losing color. These spots grew slowly and were not from an autoimmune problem. Her doctor tried creams, but they didn’t help much. This is a known side effect of the cancer medicines she’s taking.


A 71-year-old woman was first diagnosed with early-stage right breast cancer in 1999. The cancer was hormone-sensitive (HR+/HER2-) and small, less than 2 cm, with no spread to lymph nodes. She had breast-conserving surgery, followed by chemotherapy, radiation, and hormonal therapy with tamoxifen for 5 years. She stayed in good health and followed up regularly until 2015, when she started having a persistent cough. Imaging showed the cancer had spread to the lymph nodes near the lungs and to several bones, including the left shoulder, scapula, pelvis, and spine. A biopsy confirmed it was breast cancer that had spread. Her cancer remained hormone-sensitive, so she was treated with endocrine therapy, first with fulvestrant, then with exemestane and everolimus, but she had to stop due to lung and kidney side effects. She later joined a clinical trial testing a new drug class called CDK4/6 inhibitors, but stopped when her cancer progressed. After the FDA approved these drugs, she started taking ribociclib and letrozole, which worked well overall, though her blood counts were low, so her ribociclib dose was reduced. About 20 weeks into treatment, she noticed white, patchy spots on her hands, feet, and face that looked like vitiligo. These lesions spread slowly and were not linked to any family or personal history of autoimmune conditions. She saw a dermatologist, tried topical treatments, and was given steroids, but the spots did not improve significantly.


{
    "proficient_health_literacy": "A 71-year-old female with a history of thalassemia minor and hypertension was diagnosed in 1999 with early-stage right breast cancer, specifically invasive ductal carcinoma measuring less than 2 cm, node-negative, with hormone receptor (HR) positivity (ER 90%, PR 30%) and HER2 negativity. She underwent breast-conserving surgery with axillary dissection, followed by adjuvant chemotherapy consisting of cyclophosphamide, methotrexate, and 5-fluorouracil (CMF), subsequent radiotherapy, and five years of tamoxifen therapy. The patient maintained excellent clinical and mammographic follow-up until 2015, when she presented with an intractable cough. Imaging revealed a left hilar lesion and multiple osteolytic bone metastases involving the left scapula, left shoulder, left iliac bone, and the fourth and seventh dorsal vertebrae. Fine needle aspiration via endobronchial ultrasound confirmed metastatic breast cancer with preservation of the same molecular phenotype: HR-positive, HER2-negative. Initial endocrine therapy with fulvestrant resulted in a progression-free survival of 2 years; she was subsequently switched to exemestane and everolimus, which was discontinued due to grade II pneumonitis and proteinuria consistent with prenephrotic range. During this period, she was enrolled in a double-blind, randomized clinical trial evaluating the addition of CDK4/6 inhibitors to aromatase inhibitor therapy. Due to disease progression, she was withdrawn from the trial and found to be on the placebo arm. Following FDA approval of CDK4/6 inhibitors, she was initiated on ribociclib and letrozole, which she tolerated with moderate neutropenia necessitating dose reduction to 400 mg daily on days 1–21 of a 28-day cycle. Approximately 20 weeks after starting this regimen, she developed small, rounded, well-demarcated hypopigmented lesions initially on both hands, which expanded to the midforearms. Three weeks later, similar lesions appeared on the face and feet. These lesions were clinically consistent with vitiligo-like depigmentation, and the patient had no personal or family history of autoimmune disorders. Dermatological evaluation was performed, and topical immunomodulators (calcineurin inhibitors) were offered but declined; she was managed with topical corticosteroids


An 81-year-old woman came to the hospital because she was bleeding from her stomach and had black stools. She had a history of a cancer in her stomach area (GIST) that spread to her liver and belly, and she had been treated with medicine (sunitinib) for it. Four years earlier, she had surgery to fix her stomach and used a part of her small intestine (jejunum) to connect the stomach to the esophagus (Merendino procedure). During an emergency exam, doctors found a bleeding spot in the small intestine where the connection was made. They stopped the bleeding with medicine and a special powder, and gave her blood transfusions. But her blood count kept dropping, and they thought she had a reaction to the blood. She got fever, started passing blood in her urine, and her breathing got worse. Tests showed she had a serious infection caused by a type of bacteria called Clostridium perfringens, which spread to many of her organs. Even though the blood she got was checked, it wasn’t infected. She died three days after being admitted because of the severe infection. The infection had spread all over her body and damaged her tissues.


An 81-year-old woman was admitted to the hospital suddenly because she was bleeding from her stomach and had black, tarry stools (melena). She had a history of a cancer in the stomach area called a gastrointestinal stromal tumor (GIST), which had spread to her liver and abdomen. She had been treated with medication (sunitinib) for this advanced cancer and had undergone a surgery four years earlier called a Merendino procedure, where part of her small intestine was used to reconstruct her stomach and esophagus. During an emergency endoscopy, doctors found a bleeding ulcer in the reconstructed part of her small intestine. The bleeding was stopped right away, and she received blood transfusions. However, her blood levels continued to drop, and doctors suspected a reaction to the transfused blood. She was given treatment for a possible hemolytic transfusion reaction, but her condition worsened. Three days after admission, she died. Blood tests later showed that she had a severe infection caused by Clostridium perfringens, a type of bacteria that spreads widely in her organs. The autopsy confirmed that the bacteria had spread throughout her body, causing tissue damage and septic shock. The infection was not caused by contaminated blood products, and the bleeding ulcer was not the direct cause of death.


{
    "proficient_health_literacy": "An 81-year-old female presented to the emergency department with acute hematemesis and melena, exhibiting poor general condition and hemodynamic instability. Initial laboratory findings showed a hemoglobin level of 7.7 mg/dL, with no leukocytosis or elevation in C-reactive protein (CRP), suggesting a non-infectious or non-inflammatory etiology at presentation. The patient had a history of a 6.5 cm gastrointestinal stromal tumor (GIST) originating in the cardia, initially treated with imatinib 400 mg/day for downsizing, followed by surgical resection of the gastroesophageal junction and reconstruction via a jejunal interposition (Merendino procedure) four years prior. Histopathological analysis of the primary tumor revealed a T3-stage lesion with a positive c-Kit mutation in exon 11 and a Ki-67 proliferation index of 15%, indicating a high proliferative activity. According to Miettinen's prognostic criteria, the tumor was classified as high-risk due to size (>5 cm) and mitotic rate (>5 mitoses per high-power field), leading to initiation of first-line adjuvant imatinib therapy at 400 mg/day. After two years of first-line therapy, the patient developed hepatic and peritoneal metastases, prompting transition to sunitinib as second-line therapy for metastatic disease. Proton pump inhibitor (PPI) use was discontinued for an unspecified duration prior to admission, which may have contributed to mucosal vulnerability and ulceration. Emergency gastroscopy revealed active bleeding from a vessel stump in the jejunal interposition, consistent with Forrest stage I b upper gastrointestinal bleeding. Endoscopic hemostasis was achieved through local adrenaline injection and polymer powder application. A thoracoabdominal CT scan demonstrated no active hemorrhage or free intraperitoneal fluid, with hepatic and peritoneal metastases remaining stable in size but increasingly necrotic compared to prior imaging. A subsequent decline in hemoglobin prompted repeat gastroscopy, which identified diffuse, non-localized bleeding, necessitating aggressive coagulopathy management. The patient received 9 units of packed red blood cells (pRBCs), 6 units of fresh frozen plasma (FFPs), 6 units of platelet concentrates, 3 g of fibrinogen, and 4000 IU of PPSB® (a prothrom


A 67-year-old man started having problems with his legs, like numbness and pain, that went away on their own. Later, at age 73, he had eye problems and was told he had multiple sclerosis. His condition got worse over time, with more nerve issues in his spine and eyes. He tried medicines like interferon and steroids, but they didn’t help. He also tried natalizumab, but still had relapses — his eyes and legs got worse each time. After stopping natalizumab, he had plasma exchange treatments and started rituxan, which helped his symptoms stop worsening. But later, he had another serious back nerve attack. So, he started cyclophosphamide, and after that, he didn’t have any more attacks for 24 months. Tests later showed he had a specific antibody called anti-aquaporin-4, which explains his condition. This is a rare disease called neuromyelitis optica, not multiple sclerosis.


A 67-year-old man with no prior health issues first developed symptoms in his legs, including numbness and reduced pain sensation, which went away on their own. Later, at age 73, he had vision problems in both eyes (optic neuritis) and was initially diagnosed with multiple sclerosis (MS). His condition worsened over time, with MRI scans showing damage to his spinal cord and brain. He was treated with interferon and corticosteroids, but these did not stop the relapses. He then started natalizumab, which also failed—he had three more relapses, each affecting his vision and movement, leading to severe weakness and a significant drop in his disability score. After stopping natalizumab and undergoing repeated plasma exchanges, his symptoms began to stabilize. He started treatment with rituxan, which depleted his B cells, but later had another serious spinal relapse. This led to starting cyclophosphamide, an immune-suppressing drug, which successfully prevented any further relapses over the next 24 months. Testing later confirmed the presence of anti-aquaporin-4 antibodies, which are linked to neuromyelitis optica (NMO), a different condition from MS. This case shows that early diagnosis and appropriate treatment are key in managing such rare and serious autoimmune diseases.


{
    "proficient_health_literacy": "A 67-year-old Caucasian male with no significant prior medical history presented with acute spinal symptoms characterized by transient hypesthesia and hypoalgesia in both lower extremities, which spontaneously resolved without a definitive diagnosis. At age 73, he developed bilateral optic neuritis, leading to a diagnosis of multiple sclerosis (MS) at an external healthcare facility. At that time, his expanded disability status scale (EDSS) score was 2.5. Magnetic resonance imaging (MRI) of the spinal cord revealed diffuse cord swelling and longitudinally extensive T2-hypertensive lesions spanning from C2 to T3, consistent with longitudinal myelitis. Cranial MRI demonstrated sparse periventricular and cerebellar lesions without contrast enhancement and did not meet the Barkhof criteria for MS. Cerebrospinal fluid (CSF) analysis revealed oligoclonal bands, a hallmark of MS, although anti-aquaporin-4 (AQP-4) antibody testing was not performed at the time. Initial therapy consisted of interferon beta-1a for six months, subsequently switched to interferon beta-1b by the treating neurologist. During this period, the patient experienced two additional spinal relapses, each managed with corticosteroid pulses without clinical benefit, resulting in a progressive worsening of disability, with EDSS increasing from 2.5 to 4.0. Subsequent initiation of natalizumab at an external clinic was associated with three relapses: the first occurring at four months, the second at six months, and the third at eight months post-initiation. Each relapse involved bilateral optic nerve involvement and spinal cord pathology, leading to progressive visual and motor deficits, culminating in high-grade spastic tetraparesis and bilateral visual acuity impairment, with EDSS progression to 8.0. Given the clinical pattern and persistence of relapses despite immunomodulatory therapy, neuromyelitis optica (NMO) was considered upon referral to our institution. Natalizumab was discontinued after nine courses. Following repeated cycles of plasma exchange, the disease course stabilized, and therapy with rituximab (anti-CD20 monoclonal antibody) was initiated. Despite complete B-cell depletion as confirmed by flow cytometry, a severe myelitis relapse occurred three months later. This prompted the initiation of additional immunosuppressive therapy with cyclophosphamide at a dose of


A 22-year-old woman had a serious stomach problem called ulcerative colitis, which caused her to have diarrhea with blood, severe belly pain, vomiting, and a swollen belly. Tests found she had a harmful bacteria called C. difficile and her colon was too big and stretched (megacolon), which made things worse. She was given medicine by mouth to fight the bacteria and medicine by IV to calm down the inflammation, and her swollen belly went away. Even after that, her colitis kept getting bad, so she started a special medicine called infliximab, given by IV every few weeks. The doctors checked how much medicine was in her blood and how much inflammation was in her stool, and both showed the treatment was working. After 6 months, her symptoms got better, and she didn’t need surgery to remove her colon.


A 22-year-old woman was diagnosed with ulcerative colitis three months earlier, experiencing bloody diarrhea, abdominal pain, and weight loss. She stopped taking mesalamine because it caused stomach upset. Before hospitalization, her colonoscopy showed moderate inflammation. She was admitted due to worsening symptoms, including frequent bloody stools, severe abdominal pain, nausea, vomiting, and a 10-kilogram weight loss, with no improvement from previous antibiotics.

At admission, she was dehydrated, had a fast heart rate, low blood pressure, and a fever. Her abdomen was swollen and painful. Lab tests showed high inflammation and anemia. An X-ray showed her colon was dilated to 7 cm, indicating megacolon, a serious complication. Tests also found a toxin from Clostridium difficile, so she started oral vancomycin. However, her symptoms worsened, including more diarrhea, bleeding, and fever. A sigmoidoscopy revealed severe inflammation with bleeding in the lower colon, confirming active, severe ulcerative colitis.

She was treated with intravenous hydrocortisone for severe colitis, which helped reduce the swelling in her colon. After initial treatment, she started infliximab, a biologic medication, at a dose of 5 mg/kg. Her treatment was monitored through blood levels (trough level of 8.8 μg/mL) and a stool test (fecal calprotectin of 921 μg/g, which is above the normal limit of 30 μg/g). After one week, her drug level was too low, so she received a second infusion at week 1, following an accelerated treatment schedule (infusions at weeks 0, 1, 2, and 6). After six months of therapy, her symptoms improved both clinically and on endoscopy, and she did not need surgery (colectomy).


{
    "proficient_health_literacy": "A 22-year-old female Caucasian patient with a three-month history of ulcerative colitis (UC) presented with progressive bloody diarrhea, abdominal pain, and significant weight loss (10 kg), leading to discontinuation of mesalamine therapy due to gastric intolerance. Colonoscopy performed two weeks prior to hospital admission demonstrated moderate endoscopic activity of UC, as evidenced by a Mayo endoscopic score of 2. Upon hospital admission, the patient exhibited severe clinical deterioration, including frequent liquid and bloody stools, intense abdominal pain, nausea, vomiting, dehydration, tachycardia (110 beats per minute), hypotension (100/60 mmHg), fever (>37.8 °C), and a diffusely painful, distended abdomen with rebound tenderness. Laboratory findings revealed signs of systemic inflammation (C-reactive protein 20.3 mg/dL) and severe anemia (hematocrit 25.8%, hemoglobin 8.1 g/dL). Abdominal X-ray confirmed colonic dilatation of 7 cm, consistent with megacolon, a complication of severe colonic inflammation and impaired motility. Stool testing for *Clostridium difficile* (C. difficile) revealed a positive toxin assay for both A and B toxins, indicating active pseudomembranous colitis. The patient was initiated on oral vancomycin 250 mg four times daily; however, within days, symptoms worsened, with increased diarrhea (>10 episodes/day), rectal bleeding, abdominal distension, and fever. A flexible sigmoidoscopy performed on day 4 of admission, conducted without insufflation and extended to 25 cm, revealed severe mucosal lesions including ulcers covered by fibrin, mucosal friability, edema, and intense enanthem with spontaneous bleeding in the sigmoid and rectum, consistent with severe UC activity (Mayo endoscopic score 3). Histopathological examination confirmed chronic active colitis with structural mucosal damage, crypt microabscesses, and plasmacytosis, supporting a diagnosis of severe inflammatory activity without evidence of *C. difficile* or cytomegalovirus infection. The patient was managed with intravenous hydrocortisone for severe colitis, which led to clinical and radiological improvement, including resolution of megacolon. Due to persistent severe colitis symptoms despite corticosteroid therapy


A 34-year-old woman started having trouble walking and balance, and later had shaking in her hands and head, trouble speaking, and numbness. She also had dizziness, headaches, and lost weight. Tests showed damage to the parts of her brain that help with movement and balance. A gene test found two changes in a gene called POLR3A, which is linked to a rare brain disease called hypomyelinating leukodystrophy type 7. This disease affects how nerves grow and work in the brain. She was given medicines to help her nerves, like vitamin B12 and acetylglutamine, but after one month, her symptoms didn’t get better — she still had trouble walking and holding things. After leaving the hospital, she kept taking medicines, including herbs, and now she can walk slowly and climb stairs, her shaking is much better, and she can hold things and cook. But her speech is still slower and harder to understand than before.


A 34-year-old woman was seen because she had trouble with balance and coordination, a condition called ataxia. Over the past few years, she had developed walking problems, hand and head tremors, difficulty speaking, numbness in her limbs, and trouble swallowing. She also had dizziness, headaches, and nausea. Tests showed abnormal signals in the white matter of her brain, which are signs of damage to the myelin sheath—the protective covering around nerve fibers. This type of damage is known as demyelinating lesions. Genetic testing found two specific changes in the POLR3A gene: c.4044C > G and c.1186-2A > G. These mutations are linked to a rare disorder called hypomyelinating leukodystrophy type 7 (HLD7), which affects nerve development and function. The patient was treated with vitamin B12, acetylglutamine, and other supportive therapies, including traditional Chinese medicine. However, after one month, her symptoms did not improve and actually worsened. She needed help walking and could not hold objects. After discharge, she continued treatment and has shown some improvement—she can now walk slowly and climb stairs, her tremors have reduced, and she can hold objects and cook on her own. But her speech is still slower and less clear than before.


{
    "proficient_health_literacy": "A 34-year-old Han female presented with progressive cerebellar ataxia, initially manifesting as a mild gait abnormality 7–8 years prior, which evolved into significant walking instability approximately one year before presentation. Postpartum, she developed worsening gait disturbance, static tremors involving the hands and head, dysarthria, occasional limb numbness, and a water-induced cough. Neurological examination revealed dysarthria, upbeating nystagmus with right gaze-evoked nystagmus, absent limb reflexes, impaired bilateral finger-nose test, instability on calcaneal-tibial testing, positive Romberg sign, and bilateral Babinski and Chaddock signs. The ataxia severity was quantified using a standardized ataxia assessment scale, yielding a total score of 24: gait (5), stance (4), sitting (2), speech (2), finger chase (2), nose–finger test (2), fast alternating hand movement (3), and heel–shin slide (4). Mini-Mental State Examination was within normal limits; Montreal Cognitive Scale was not completed due to severe hand and head tremors. Laboratory investigations, including tumor markers, ceruloplasmin, thyroid function (TSH, free T3, free T4, thyroglobulin antibody, thyroid peroxidase antibody), rheumatological markers (rheumatoid factor, anti-streptolysin O, hs-CRP), immunoglobulins (IgG, IgA, IgM), complement components (C3, C4), antinuclear antibody, anticardiolipin antibody, and anti-neutrophil cytoplasmic antibody (ANCA), were all within normal ranges. Lumbar puncture demonstrated no evidence of inflammatory or infectious pathology. Brain MRI revealed bilateral, speckled, and patchy hyperintense lesions in the corona radiata, paraventricular regions, frontal lobes, and left temporal lobe, appearing hypointense on T1-weighted images and hyperintense on T2 and FLAIR sequences, with no abnormal diffusion signals on DWI or ADC maps, consistent with multiple white matter demyelinating lesions. Color Doppler ultrasound of gynecological, abdominal, cardiac, carotid, and intracranial vessels showed no vascular abnormalities. Whole-exome sequencing identified two pathogenic variants in the POLR3A gene:


A 23-year-old woman took a very large amount of metformin (about 30 grams) after a stressful event. Four hours later, she came to the hospital feeling tired but still alive. She had very low blood sugar several times (down to 6.3 mg/dL, then 38 mg/dL, and again 42 mg/dL), which made her feel weak and sick. Each time her blood sugar dropped, she also had a buildup of acid in her body (lactic acidosis), which made her blood too acidic. Her blood pressure dropped, so doctors gave her fluids and medicine to raise it. She needed a machine that filters her blood (CRRT) for 24 hours to help her body clear the poison and fix her blood. After 24 hours, her blood sugar and body started to get better. She was able to go home on day 5, but she didn’t follow up with her doctors for mental health, kidney, or general care.


A 23-year-old Arabic woman took 30 grams of metformin intentionally after a stressful event. Four hours later, she was brought to the emergency department. She was alert but feeling very tired. Her vital signs were normal at first, though she had low blood sugar and high lactate levels, which showed her body was under stress. She developed severe lactic acidosis and low blood pressure, which required fluid and medication (like norepinephrine) to stabilize. She had three episodes of very low blood sugar — 6.3 mg/dL, 38 mg/dL, and 42 mg/dL — each time requiring a 50% dextrose injection to raise her sugar levels. These low sugar episodes happened at the same time as her severe acidosis. She was treated with continuous renal replacement therapy (CRRT) for 24 hours, which helped her recover. After this, her blood pressure and blood sugar stabilized, and she improved. By day 3, she was able to eat normally and was transferred to a regular ward. A psychiatrist was involved to assess her mental health, and she was discharged on day 5. However, she did not attend any follow-up appointments for medicine, kidney, or mental health care.


{
    "proficient_health_literacy": "A 23-year-old Arabic female with a body mass index of 28 was prescribed metformin for weight management in the context of polycystic ovary syndrome (PCOS). She intentionally ingested approximately 60 tablets of 500 mg metformin (totaling 30 g) following a stressful social event, which was initially recognized as a suicide attempt. Four years prior, she had undergone a living kidney donation to her brother, who had end-stage renal disease of unknown etiology; she has no known comorbidities, including psychiatric disorders, prior suicidal ideation, or substance use (no history of smoking or alcohol intake). She has no family history of diabetes mellitus or mental illness. On presentation to the emergency department (ED) approximately 4 hours after ingestion, she was alert, well-nourished, and generally fatigued, with no signs of pallor, jaundice, or cyanosis. Vital signs included blood pressure of 119/65 mmHg, heart rate of 122 beats/min, respiratory rate of 20 breaths/min, oxygen saturation of 100% on room air, and oral temperature of 36.9 °C. Physical examination revealed dry, cool skin and bilaterally mid-sized, equal, and reactive pupils; no other abnormalities were noted.\n\nInitial point-of-care capillary blood glucose was low, prompting the administration of 50 mL of 50% dextrose (D50) solution. Serum glucose measured 6.3 mg/dL, which transiently rose to 106 mg/dL following D50 infusion. Maintenance infusion with 5% dextrose-water was initiated. Laboratory findings showed a markedly low blood glucose, leukocytosis, hypocalcemia, hyperphosphatemia, and mild elevation in serum creatinine. Initial arterial blood gas analysis revealed a pH of 7.18, PaO2 of 76.9 mmHg, PaCO2 of 40.3 mmHg, and bicarbonate of 14.3 mmol/L, consistent with metabolic acidosis. Baseline lactate was markedly elevated at 8.4 mmol/L, prompting a 1 L bolus of Ringer lactate. Serial blood gas and lactate measurements demonstrated progressive worsening of lactic acidosis, with lact


A 59-year-old woman felt confused, was upset, and had trouble moving her right leg. She had been taking medicine for a type of cancer called chronic lymphocytic leukemia (CLL) and a blood problem called hemolytic anemia for months. Her doctor found that her right leg was very weak, her reflexes were uneven, and there was a sign called Babinski on her right side. She was a little overweight and had a low fever. A brain scan showed a spot in the left front part of her brain that looked like a stroke. Later, she got a fever and signs of infection in her brain. A more detailed brain scan showed a large area of damage in the left front brain and small spots that were active. A spinal fluid test found many white blood cells and red blood cells, which means infection. The test found bacteria called Listeria in her blood and spinal fluid. This kind of infection is rare and wasn’t from eating risky food. She started antibiotics and after two days, her fever went away and her brain symptoms got better. After one week, the spinal fluid test showed no more signs of infection. One month later, she was back to normal and could move her legs without trouble.


A 59-year-old woman was admitted to the hospital because she was confused, agitated, and had weakness in her right leg. She had been treated for chronic lymphocytic leukemia (CLL) with fludarabine for 3 months and for hemolytic anemia with corticosteroids for 2 months. Before admission, she had mild obesity and a slight fever. A neurological exam showed severe weakness in her right leg, abnormal reflexes, and a sign called a Babinski sign on the right side. There were no signs of inflammation in her brain membranes. A brain CT scan showed a small area of damage in the left frontal lobe, which looked like an ischemic stroke. Later, a brain MRI showed a larger area of abnormality in the same region, spreading toward the basal ganglia, and also showed small areas of increased activity after contrast was given. On the second day, she developed a higher fever and signs of meningeal irritation. A spinal fluid test found many white blood cells, red blood cells, and high protein levels, which suggested infection. Cultures from blood and spinal fluid tested positive for Listeria monocytogenes, a type of bacteria that can cause serious brain and spinal infections. She had no recent history of eating high-risk foods like unpasteurized cheeses or deli meats. The diagnosis was Listeria meningoencephalitis. She was started on ampicillin, and within 48 hours, her fever went down and her neurological symptoms improved. After one week of treatment, the spinal fluid showed normal results. One month later, her leg strength and mental status had fully returned to normal.


{
    "proficient_health_literacy": "A 59-year-old hypertensive white female with a history of chronic lymphocytic leukemia (CLL) diagnosed in 2009 presented with a 24-hour history of confusion, agitation, and mild right-lower extremity weakness. She had received fludarabine-based chemotherapy three months prior for CLL and methylprednisolone therapy two months prior for hemolytic anemia secondary to fludarabine-induced immune-mediated destruction of red blood cells. Physical examination revealed grade 1 obesity and subfebrility (99.32 ºF; 37.4 ºC). Neurological examination demonstrated grade 4 right-lower extremity weakness, reflex asymmetry, and a right-sided Babinski sign, with no signs of meningeal irritation at admission. Laboratory findings included a white blood cell (WBC) count of 3.5 × 10³/μL, hemoglobin of 7.1 g/dL, hematocrit of 21.5%, platelets of 109 × 10³/μL, aspartate aminotransferase (AST) of 59 U/L, and alanine transaminase (ALT) of 79 U/L; all other metabolic parameters (serum glucose, urea nitrogen, creatinine, bilirubin, sodium, potassium) were within normal limits. Cerebral computed tomography (CT) revealed a hypodense lesion in the left frontal lobe, consistent with acute ischemic stroke pathology, likely due to small vessel disease or thrombotic occlusion secondary to hypercoagulable states associated with immunosuppression. On day two of hospitalization, the patient developed fever (101.12 ºF; 38.4 ºC) and new signs of meningeal irritation, including a positive Kernig’s sign. Cerebral magnetic resonance imaging (MRI) showed a hyperintense lesion in the left frontal lobe extending into the basal ganglia on T2 and fluid-attenuated inversion recovery (FLAIR) sequences, with small nodular areas of gadolinium enhancement following intravenous administration, suggesting active inflammatory or infectious intracerebral involvement. Lumbar puncture was performed on day two, yielding cerebrospinal fluid (CSF) analysis revealing 24 red blood cells (RBC


An 81-year-old woman felt very tired and weak for 3 days, then got dizzy and had trouble breathing. By November 16, 2021, she fell into a coma. Her oxygen levels dropped to just 70-80%, so she was taken to the ICU. She had long-term lung problems like chronic bronchitis and emphysema, and her lungs were full of infections. Her heart was also not working well, and doctors thought she might have had a heart attack. They did a procedure to check her heart, but found no blockages. She started having belly swelling and constipation, and got a glycerin enema. On day 4, she lost consciousness again, her blood pressure dropped, her belly became swollen and tight, and her bowels stopped working. A scan showed gas in her liver area and dead parts of her intestines. She died on day 5 because her body couldn’t fix the shock from the damage.


An 81-year-old woman came to the hospital with fatigue, lethargy, fever, chills, cough, and shortness of breath over three days. By November 16, 2021, she fell into a coma. Her oxygen levels dropped to 70%-80%, so she was admitted to the intensive care unit (ICU) for treatment. She had a long history of chronic lung disease, including chronic bronchitis and emphysema, and had been on long-term oxygen therapy. She also had heart problems for five years and was taking medication for heart failure.

In the ICU, her blood pressure dropped, and she needed medicine (norepinephrine) to keep it stable. Tests showed signs of infection in her lungs, with high white blood cell counts and markers of inflammation. Chest CT scans showed chronic lung disease and multiple lung infections, especially in the lower and middle parts of the right lung. Her abdominal CT scan showed no major issues, but her abdominal blood vessels were heavily calcified.

Her heart tests showed abnormal heart rhythms and signs of heart damage. Her troponin levels went up, which suggests heart muscle injury. The doctors suspected she had a heart attack (ACS) and performed a procedure called PCI through her femoral artery. No major blockages were found in her coronary arteries.

On the second day, she had constipation, which was treated with a glycerin enema. On day 4, she suddenly lost consciousness, had very low blood pressure, and developed swelling in her abdomen with no bowel sounds. An urgent abdominal CT scan showed gas in the liver portal area and severe damage to her bowel walls. The patient died on day 5 from severe, uncontrolled shock due to these complications.


{
    "proficient_health_literacy": "An 81-year-old female presented to a local hospital with a three-day history of fatigue, lethargy, fever, chills, productive cough, and wheezing, without prior intervention. On November 16, 2021, she developed acute coma and was transported to the emergency department. Her oxygen saturation declined to 70%–80%, prompting immediate admission to the intensive care unit (ICU) for respiratory and hemodynamic support. Upon ICU admission, she exhibited a progressive hypotensive state, requiring norepinephrine infusion to maintain a mean arterial pressure above 65 mmHg.\n\nThe patient had a long-standing history of chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema, with over 50 years of documented disease course, and had been on long-term home oxygen therapy. She also had a five-year history of chronic heart failure, managed with oral bisoprolol, with no prior history of abdominal pain or chronic renal insufficiency. There was no history of tobacco or alcohol use, and no relevant family history of cardiovascular or pulmonary disease.\n\nOn initial assessment, vital signs were: temperature 36°C, heart rate 85 beats/min, respiratory rate 18 breaths/min, blood pressure 105/45 mmHg. Physical examination revealed diminished breath sounds bilaterally, with wet rales predominantly at the bases of both lungs. Cardiac and abdominal examinations were unremarkable.\n\nLaboratory findings included an initial troponin level of 0.05 ng/mL, which subsequently increased, indicating myocardial injury. B-type natriuretic peptide (BNP) was elevated at 4164 pg/mL, consistent with volume overload and systolic dysfunction. Arterial blood gas analysis demonstrated a partial pressure of carbon dioxide (PaCO₂) of 58.7 mmHg, oxygen partial pressure (PaO₂) of 86.5 mmHg, and an oxygenation index of 172.97 mmHg—indicating severe hypoxemia. Inflammatory markers were markedly elevated: white blood cell count 8.12 × 10⁹/L, neutrophil percentage 93.2%, C-reactive protein 298.38 mg/L, procalcitonin 6


A man had a serious brain problem caused by a medicine called ganciclovir, which he was taking for a stomach infection. The medicine made him confused, unsteady on his feet, and eventually fell. Doctors thought it was the medicine, not an infection, because tests showed no signs of virus in his brain fluid. The medicine was stopped, and he got dialysis to clean his blood, which helped his brain feel better. He fully recovered after two dialysis sessions. This was the worst case ever reported for this medicine, with the highest amount ever found in his blood.


This case involves a 55-year-old man who had diabetes and kidney failure, leading to a kidney transplant 1.5 years earlier. After the transplant, he developed a severe infection caused by cytomegalovirus (CMV), which required treatment with ganciclovir. Because his infection was serious, he received high doses of the drug without reducing them to standard maintenance levels. Two days after starting the treatment, he began to have balance problems and mild confusion. His condition worsened, leading to delirium and a fall. His brain function declined further, and he could no longer take oral medication. Doctors ruled out other causes of brain inflammation, such as encephalitis, and instead suspected ganciclovir-induced encephalopathy. The drug was stopped, and he received two sessions of therapeutic dialysis, which helped clear the drug from his blood. After the second dialysis, his brain function fully recovered. This patient had the highest known level of ganciclovir in his blood and was the only one in the study with severe symptoms and complete recovery after dialysis.


{
    "proficient_health_literacy": "A 55-year-old male with a history of diabetic renal failure initiated hemodialysis two years prior, followed by renal transplantation 1.5 years earlier, with subsequent initiation of immunosuppressive therapy. Eight months post-transplantation, his serum creatinine rose to 4.4 mg/dL, indicating progressive renal dysfunction. He presented with CMV enteritis, evidenced by occult gastrointestinal bleeding and a significantly elevated CMV pp65 (C7-HRP) antigen level in peripheral blood mononuclear cells, prompting antiviral intervention. Intravenous ganciclovir was administered at a dose of 150 mg/day for 11 days, followed by transition to valganciclovir at 450 mg/day. Due to the severity of enteritis, the antiviral regimen was not reduced to standard maintenance doses (typically half of initial doses), which is atypical and increases systemic exposure. Two days after initiating valganciclovir, the patient developed gait instability, initially ambulating independently, but within 24 hours required assistance. His level of consciousness deteriorated to E3, V5, M6 on the Glasgow Coma Scale (GCS), indicating mild impairment. The next day, he exhibited intermittent delirium. Two days later, he fell and was found on the floor without significant injury; clinical suspicion initially pointed to exhaustion secondary to severe enteritis. Nine days after starting valganciclovir, his neurological status worsened to E3, V3, M5, and he became unable to ingest oral medications, including valganciclovir. Neurological consultation was obtained; encephalitis was ruled out due to the absence of meningeal signs, fever, and a normal cerebrospinal fluid (CSF) cell count (0.33 cells/μL), with only a marginal elevation in protein concentration (54 mg/dL). Polymerase chain reaction (PCR) testing for CMV, herpes simplex virus (HSV), varicella-zoster virus (VZV), and Epstein-Barr virus (EBV) DNA in the CSF remained negative, supporting exclusion of these viral etiologies. Ganciclovir-induced encephalopathy was therefore clinically and virologically suspected, and the drug was immediately discontinued. To mitigate the risk of further falls and to remove ganciclovir from the systemic circulation,


A 59-year-old man had yellow skin and belly pain for over 15 days, and lost 5 pounds. Doctors found a tumor at the opening of the small intestine (duodenal papilla) using a special camera test. The tumor was checked under a microscope and found to be a fast-growing type of cancer called aggressive B-cell lymphoma. Instead of surgery, he started treatment with special medicines that target the cancer cells, along with a standard chemotherapy plan called CHOP.


A 59-year-old man was seen for jaundice and weight loss. Tests showed a blockage in his bile ducts, and imaging found a tumor at the duodenal papilla. A biopsy was taken and examined under a microscope, which showed a type of lymphoma called aggressive B-cell non-Hodgkin's lymphoma. This type of cancer grows quickly and spreads fast. Based on the results, the doctors decided not to do surgery. Instead, he started treatment with chemotherapy (the CHOP regimen) combined with targeted therapy to fight the cancer more effectively.


{
    "proficient_health_literacy": "A 59-year-old male was admitted to the Department of Gastroenterology on June 16, 2020, presenting with a 15-day history of pruritic jaundice affecting the skin and sclera, accompanied by progressive weight loss of approximately 5 kg. He had a prior history of brain stem infarction with residual left lower limb weakness and occasional dysphagia, particularly when drinking water. No history of hepatitis, tuberculosis, or other infectious diseases was reported. Physical examination revealed a chronic illness appearance with marked jaundice, absence of palpable superficial lymphadenopathy, and no significant abdominal signs. Laboratory findings at admission included hemoglobin 101 g/L, alanine aminotransferase (ALT) 158 U/L, aspartate aminotransferase (AST) 150 U/L, total bilirubin 217.3 μmol/L, direct bilirubin 152.4 μmol/L, indirect bilirubin 64.9 μmol/L, high-sensitivity C-reactive protein (hs-CRP) 5.8 mg/L, procalcitonin 0.11 ng/mL, carcinoembryonic antigen (CEA) 6.19 μg/L, and carbohydrate antigen 125 (CA125) 117.1 kU/L. Abdominal ultrasonography on June 17 demonstrated gallbladder enlargement, cholecystitis, cholestasis, and significant dilatation of both intrahepatic and extrahepatic bile ducts. Magnetic resonance cholangiopancreatography (MRCP) and abdominal MRI on June 18 confirmed neoplastic involvement of the duodenal papilla, severe bile duct dilatation, bile stasis in the common bile duct, and a markedly enlarged gallbladder. Endoscopic ultrasound (EUS) on June 19 revealed a 2.5 × 2.5 cm neoplasm at the duodenal papilla with surface ulceration, exudative yellow-white slough, and contact bleeding; three biopsy specimens were obtained. The patient was transferred to the surgical oncology department on June 20. Abdominal enhanced computed tomography (CT) on June 23 showed findings consistent with MRI, supporting the


A 27-year-old man woke up with sudden neck pain, numbness in his arms and legs, and weakness. It had started 4 days before he came to the hospital. He had no injury or past history of similar problems. When doctors checked him, his neck muscles were tender, his arms and legs felt numb, and his muscles were strong. Blood tests showed no signs of infection, clotting issues, or cancer. X-rays and CT scans didn’t show broken bones. MRI showed a big lump pressing on his spine in the neck and upper back area, and a small, harmless growth inside his C7 vertebra. This growth is called a vertebral hemangioma. Doctors removed the lump and the growth. After 6 months, his pain and weakness went away and he hasn’t had a return of symptoms. This condition, called IPEH, is rare and can be confused with other spine problems, but it’s treatable with surgery and recovery is good.


A 27-year-old man came in with sudden neck pain, numbness in his arms and legs, and weakness in his limbs. The symptoms started four days before he visited the hospital, and he had no history of injury or other medical conditions. Earlier, six years ago, he had a similar but brief episode of numbness and weakness. On exam, his neck muscles were tender, and his sensation and muscle strength were reduced, especially in the areas served by the T1 nerve. Blood tests showed no signs of infection, clotting issues, or cancer. X-rays and CT scans didn't show bone damage. MRI scans revealed a large mass pressing on the spinal cord in the C6-T1 region, extending into the C7-T1 area. This mass was bright on T2 images and dark on T1, which is typical for certain types of tumors. Additionally, a small, round mass was found in the C7 vertebra, consistent with a benign vertebral hemangioma (VH). The surgery involved removing the spinal mass through a laminectomy and excising the abnormal tissue. Pathology tests confirmed the presence of abnormal blood vessel growth with blood clots, leading to a diagnosis of intraparenchymal hemangioma of the spine (IPEH). At his six-month follow-up, his symptoms had improved completely, and there was no sign of recurrence. This case highlights the clinical features, imaging signs, possible causes, how it's different from other conditions, and how it's treated.