{
    "proficient_health_literacy": "A 6-year-old male presented with a one-week history of nausea, vomiting, and headache, initially managed at outpatient clinics without improvement. Progression of symptoms, including fever, led to emergency department (ED) admission. Family history revealed a prior episode of acute otitis media (AOM) in infancy and a single episode of acute sinusitis approximately two months prior to admission. No history of skull trauma was reported. Physical examination demonstrated lethargy, neck stiffness, and positive meningeal signs (Brudzinski’s and Kerning signs), consistent with meningitis. Laboratory evaluation included complete blood count (CBC) with differential (WBC: 29,190/mm³, with 4% bands), biochemistry, glucose, and blood culture. Lumbar puncture was performed, yielding cerebrospinal fluid (CSF) analysis, bacterial/viral culture, and CSF biochemistry. CSF showed a WBC count of 3,240/uL with 91% neutrophils, glucose of 55 mg/dL, and total protein of 160.5 mg/dL. Gram stain of CSF identified Streptococcus pneumoniae, prompting immediate initiation of vancomycin and cefotaxime. Both CSF and blood cultures confirmed Streptococcus pneumoniae serotype 23F. Antibiotic sensitivity testing indicated vancomycin efficacy against this serotype, leading to continued therapy for 14 days. The patient had previously suffered from bacterial meningitis six months prior, with identical findings: CSF gram stain positive for Streptococcus pneumoniae 23F, and positive CSF and blood cultures. Immunological assessment, including complement levels and immunoglobulin profiles, was performed and revealed no abnormalities, ruling out primary immunodeficiency as a cause. Given the history of recurrent sinusitis and the temporal association with recurrent meningitis, a chronic bony defect secondary to persistent sinus inflammation was hypothesized. Initial sinus CT imaging demonstrated right maxillary sinusitis without bony erosion. A nuclear scan was subsequently performed to evaluate for cerebrospinal fluid (CSF) leakage, which revealed CSF leakage originating from the right petroocciptital region into the middle ear. High-resolution CT (HRCT) of the temporal bones demonstrated focal enlargement of the right facial nerve canal, erosion of the bony canal at the geniculate ganglion and tympanic


A woman had problems with her feet, especially the big toe and second toe, that made walking hard and painful. Her toes were bent wrong, and she had thick, painful calluses on her feet. She tried wearing big, soft shoes for years, but it didn’t help much. She kept falling and felt unbalanced. Her doctor found that her big toe was out of place and her second toe was crossing over it. The second toe was bent inward (varus), and this made walking feel like stepping on a pebble. On one foot, the second toe was much worse than on the other. She had surgery on both feet using a soft tissue method called syndesmosis, which didn’t cut any bone. The surgery fixed the big toe position by tying the first and second metatarsal bones together with a special suture. Surprisingly, after this, the second toe bent inward problem fixed itself — it didn’t need any extra surgery. On both feet, the second toe straightened out on its own. Only the right foot’s second toe still had a small problem, so a little extra work was done to fix it. The surgery looked good and felt good after she walked again. This shows that sometimes, fixing one part of the foot can help fix another part without doing extra work.


A 60-year-old woman had long-standing foot problems, including bilateral hallux valgus (HV) deformities and crossover deformities between her first and second toes. She tried wearing wider, softer shoes for years, but the pain from walking—especially on uneven ground or stairs—got worse. She developed thick, painful calluses on her feet and had trouble balancing, leading to several falls. Her mother had a similar issue but didn’t need surgery and managed it without intervention.

On exam, her feet showed that the first metatarsal bones were unstable and the second toe on her right foot was severely bent inward (varus deformity), crossing over the big toe. This deformity was causing discomfort and affecting her walking. X-rays and pressure studies showed that her weight was shifting to the second and third toes, worsening the calluses and foot pain.

She chose surgery to fix both her HV and crossover issues. Instead of cutting bones (osteotomy), her doctor used a soft tissue procedure called a syndesmosis procedure, which involves using sutures to realign the first and second metatarsal bones without removing any bone.

During surgery, the first and second metatarsals were tied together with dissolvable sutures. To our surprise, once the first metatarsal was properly aligned, the second toe’s varus deformity corrected itself—both on the right and left feet—without any extra surgery. The only remaining issue on the right foot was a mild bend in the second toe, which was fixed with a small soft tissue release.

After surgery, she wore a forefoot cast for three months and returned to normal walking and shoes after six months. She now has good function and appearance in her feet. The case raises an interesting question: why does the second toe deformity correct itself when the first metatarsal is realigned? This may be due to how the bones and soft tissues are connected and how movement affects the toe alignment.


{
    "proficient_health_literacy": "A 60-year-old female presented with progressive hallux valgus (HV) and bunion deformities, compounded by a bilateral crossover deformity between the first and second toes. Despite initial management with increasingly accommodating footwear—characterized by a widened forefoot region and soft, roomy toe box—she experienced persistent metatarsalgia, with significant pain localized to the first metatarsal head, described as a constant sensation of walking on a pebble. This led to the development of thick, painful metatarsal calluses bilaterally, particularly under the forefoot, and impaired ambulation, including difficulties with balance on uneven terrain and stair descent. She had experienced multiple falls, reflecting functional compromise. Her mother had a milder HV deformity and managed without surgical intervention, suggesting a familial predisposition. Physical examination revealed bilateral HV deformities with only partial correction possible passively. Passive range of motion at the first metatarsophalangeal joint (MPJ) was 45° in extension and 60° in flexion on the right foot, and 60° and 45° on the left foot, indicating hypermobility. The right second toe exhibited a severe varus deformity, crossing over the hallux without notable clawing, while the left second toe had a milder varus deformity. Manual realignment of the left second toe was complete, whereas the right toe remained resistant to realignment. Both second MPJs were moderately tender and demonstrated reduced passive flexion due to pain. First metatarsals displayed hypermobility in both sagittal and frontal planes, consistent with joint instability. Dorsoplantar standing radiographs revealed a right foot first intermetatarsal angle (IMA) of 17.5° (above the normal upper limit of 9°) and metatarsophalangeal angle (MPA) of 33.7° (exceeding the normal upper limit of 15°), with a left foot IMA of 16.8° and MPA of 27.9°. All first and second MPJs were incongruent, and the right second MPJ showed dorsomedial subluxation. Both tibial and fibular sesamoids were dissociated from the first metatarsal, indicating ligamentous insufficiency and joint instability. Preoperative plantar pressure analysis using F-Scan (Tekscan, USA) demonstrated


A 34-year-old woman fell and hit her head, lost consciousness for a few minutes, then woke up. She didn’t go to the hospital right away. Three days later, she started having a mild headache and went to a clinic. Doctors saw her brain scan and found a blood clot on the side of her head — a big one, but not pressing on her brain yet. Her brain’s spaces were bigger than normal, which means she had a condition called hydrocephalus since birth, but it didn’t cause problems in her growing up. She didn’t have seizures in years, and she’s been doing well in school and work. She didn’t show any signs of brain damage. The headache got worse at first, but by day 5, it was getting better. Doctors decided not to do surgery — just gave her pain medicine and watched her closely. Her headache went away, and she stayed healthy. After 3 weeks, the blood clot got smaller. A year later, she was still fine with no symptoms. This is rare — people with this kind of hydrocephalus can get a brain bleed after a fall, even if they don’t feel sick at first. The hydrocephalus might have helped keep the brain from getting too full, so symptoms came later.


A 34-year-old woman with a history of congenital hydrocephalus (a condition where fluid builds up in the brain) due to a narrow aqueduct, did not have surgery. She had no symptoms from the condition and lived a normal life, going to school, earning a bachelor’s degree, and working full time. After falling in the bathroom, she lost consciousness briefly and regained it quickly. She didn’t seek medical help at first but started having a mild headache three days later. A CT scan showed a large blood clot (epidural hematoma) on the right side of her brain, which was causing slight pressure. Her brain’s ventricles were enlarged, a sign of hydrocephalus, but there was no serious fluid buildup or brain swelling. She had a small fracture in her skull but no other injuries. Despite the injury, she remained asymptomatic except for the headache. Because she had no serious symptoms and the blood clot was stable, doctors chose not to operate and instead treated her with pain relief and close monitoring. Her headache improved over time, and by day 8, she was able to go home. Follow-up scans showed the blood clot was shrinking, and her brain pressure was normal. At 10 months after the injury, she was fully recovered with no symptoms. This case is rare — adults with arrested hydrocephalus (where brain fluid buildup stops or slows) may still develop brain bleeds after head injuries, even without noticeable symptoms. The hydrocephalus may have helped reduce pressure in the brain, delaying the appearance of symptoms.


{
    "proficient_health_literacy": "A 34-year-old female presented with traumatic brain injury following a fall on the bathroom floor, resulting in transient loss of consciousness and subsequent development of an acute right temporal epidural hematoma measuring 41 cc in volume, with a midline shift of 0.4 cm on initial cranial CT. The hematoma was associated with effacement of cerebral sulci and enlargement of the lateral and third ventricles, consistent with increased intracranial volume, but without transependymal effusion. A linear, nondisplaced fracture of the right temporal bone was identified. Despite the presence of a large epidural hematoma, the patient remained asymptomatic except for a mild, intermittent right-sided headache that began on day 3 postinjury. Neurological examination revealed a Glasgow Coma Scale (GCS) of 15, with equal and briskly reactive pupils, normal visual acuity (20/25 bilaterally), and absence of papilledema, sensory, or motor deficits. Head circumference of 59 cm was noted to be in the upper 97th percentile for her height, consistent with chronic macrocephaly, likely secondary to congenital hydrocephalus due to aqueductal stenosis, which had been managed without surgical intervention. The patient had a history of epilepsy controlled with phenobarbital, with the last seizure occurring approximately 15 years prior, and a recent mild COVID-19 infection five months before the injury. She had no developmental delays, completed high school at the top of her class, earned a bachelor’s degree at age 20, and was actively pursuing a master’s degree while maintaining full-time employment. The patient was initially advised to seek neurosurgical evaluation but delayed consultation until day 5 postinjury. Repeat cranial CT on day 5 demonstrated stable hematoma size, with a marked reduction in headache severity. Conservative management was initiated, including analgesic therapy and close clinical monitoring, with resolution of headache by day 8. Follow-up imaging at 3 weeks postinjury showed progressive reduction in hematoma volume and attenuation, indicating resolution of the hematoma without significant intracranial pressure elevation. Transcranial Doppler study revealed normal pulsatility indices across all intracranial arteries, confirming the absence of significant cerebral perfusion abnormalities or increased intracranial pressure. At 10-month follow-up, the patient remained asymptomatic with no neurological deficits


A 67-year-old woman from a area where leishmaniasis is common had a swollen face that lasted two months. The swelling was red, puffy, and had bleeding crusts on her nose. She first got treated for a common facial infection with antibiotics, but it didn’t help. Doctors then guessed it was a type of skin infection called cutaneous leishmaniasis, and checked a small skin sample that showed the tiny parasites causing it. She was given two medicines—metronidazole and clarithromycin—for 30 days, and her symptoms got better.


A 67-year-old woman from a region in Morocco where leishmaniasis is common had swelling on her face and nose that lasted for two months. The swelling was red, swollen, and had crusts, and was initially treated for a bacterial infection called facial erysipelas with antibiotics. However, the symptoms did not improve. Based on her medical history and the appearance of the skin, doctors suspected a type of leishmaniasis known as erysipeloid form. This was confirmed by a skin test that showed the presence of Leishmania parasites. She was then treated with metronidazole and clarithromycin for 30 days, and her condition improved significantly. She had a heart condition called left bundle branch block, so the doctors chose this treatment instead of the usual antimonial drugs.


{
    "proficient_health_literacy": "A 67-year-old female from Chichaoua, Morocco—a known endemic zone for Leishmania tropica—presented with a two-month history of progressive swelling in the centrofacial region, characterized by an erythematous and edematous plaque extending to the eyelids, accompanied by hemorrhagic crusts at the nasal tip. The clinical presentation was initially managed as facial erysipelas with a course of amoxicillin-clavulanic acid and ciprofloxacin for 15 days, which failed to result in clinical improvement. Given the patient's residence in an endemic area for Leishmania tropica and the presence of a family history of leishmaniasis (her grandson having been previously treated for the disease), the differential diagnosis was strongly shifted toward cutaneous leishmaniasis in its erysipeloid form. Confirmation was achieved via skin smear, which demonstrated the presence of Leishmania amastigotes, confirming the diagnosis. The specific species of Leishmania could not be identified at the institutional level. Notably, the patient had a left bundle branch block on electrocardiography, which contraindicated the use of pentavalent antimonial agents due to potential cardiac toxicity. As such, a combination therapy of metronidazole (1.5 g daily) and clarithromycin (15 mg/kg body weight) was selected as a safer alternative, based on its efficacy in treating erysipeloid cutaneous leishmaniasis in patients with cardiac comorbidities. The patient received this regimen for 30 days and demonstrated a good clinical response with progressive resolution of the lesion. The erysipeloid form of cutaneous leishmaniasis is a self-limiting but persistent infection, typically presenting with erythematous, edematous plaques and hemorrhagic crusts, and is caused by Leishmania tropica, which resides in the dermal layers and replicates intracellularly within macrophages as amastigotes. The pathogenesis involves the invasion of dermal macrophages, leading to local inflammation, edema, and tissue damage. Metronidazole and clarithromycin are effective due to their ability to penetrate the macrophage phagolysosome and exert activity against intracellular amastigotes, with clarithromycin showing particularly favorable pharmacokinetic properties in this setting. This case underscores the importance of considering leish


A 57-year-old woman had high potassium levels in her blood for years, always between 5.3 and 5.9. Her doctor checked her closely, but she had no symptoms or problems. Her blood pressure was under control, and her heart test was normal. She was referred to a kidney specialist because the high potassium didn’t go down, even when she followed a low-potassium diet. The doctor checked everything — her blood, urine, and other tests — to find the cause. Nothing was wrong with her kidneys, no signs of blood cell breakdown, no infections, no muscle damage, and no other known causes. Even after testing for possible rare conditions, nothing explained the high levels. The doctors thought it might be a rare issue where the blood sample shows high potassium even when it’s not real — like a trick in the lab. They tested the blood under different conditions to see if the high number was just a mistake. The results showed the high level didn’t happen. So, the cause of the high potassium could not be found. The patient’s body is just doing something unusual, and no treatment is needed right now.


A 57-year-old woman had high potassium levels in her blood for four years, ranging from 5.3 to 5.9 mmol/L (normal is 3.5–5.1 mmol/L). She had no symptoms or signs of illness, and her heart tests were normal. She was on medication for high blood pressure, which was well controlled. After being referred to a nephrology specialist, doctors checked for possible causes like kidney problems, broken cells, or acidosis. All tests came back normal, including blood cell counts, kidney function, and urine tests. A diet low in potassium was recommended, but it didn’t lower her potassium levels. Even after checking for conditions like blood disorders or tissue damage, no cause was found. The doctors considered a rare condition called familial pseudohyperkalemia, where blood samples might show falsely high potassium due to how they’re stored or transported. They tested the blood under different conditions (cold, room temperature, body temperature) and found that the high potassium level only appeared when the sample was left uncentrifuged and exposed to certain conditions. When the sample was properly processed, the potassium level returned to normal. This suggests the high reading was not real, and the cause of the elevated levels could not be confirmed.


{
    "proficient_health_literacy": "We present a case of a 57-year-old female with a four-year history of persistent mild hyperkalemia, defined by serum potassium levels ranging from 5.3 to 5.9 mmol/L (reference range: 3.5–5.1 mmol/L), without associated clinical manifestations such as muscle weakness, cardiac arrhythmias, or hemolysis. Spectrophotometric hemolysis index remained below 6 mg/dL across all laboratory reports, excluding intravascular hemolysis as a contributing factor. Electrocardiographic monitoring was normal, with no evidence of electrolyte-induced conduction abnormalities. The patient's medical history included chronic arterial hypertension, which was well-controlled with angiotensin-converting enzyme (ACE) inhibitor therapy. No significant findings were noted during physical examination or anamnesis. She was receiving amlodipine for blood pressure control, with stable clinical outcomes.\n\nThe patient was referred to the Nephrology Unit for further evaluation due to the persistent elevation of serum potassium despite the absence of identifiable clinical or laboratory triggers. Initial management included a potassium-restricted diet, which was implemented for a three-month period. At the three-month follow-up, a serum sample was collected and analyzed; the sample was non-hemolyzed (hemolysis index <6 mg/dL) and revealed a potassium concentration of 5.5 mmol/L, confirming the continued presence of hyperkalemia.\n\nA comprehensive differential diagnosis was conducted to exclude common etiologies of hyperkalemia, including: (1) renal insufficiency, (2) intravascular hemolysis, (3) metabolic acidosis, (4) tissue breakdown (e.g., rhabdomyolysis), and (5) pseudohyperkalemia secondary to oncohematologic conditions such as essential thrombocytosis or acute or chronic leukemia. Laboratory workup included a hemogram with reticulocyte count and blood smear, general biochemistry (including ions, hemolysis index, hepatic enzymes—GOT, GPT, GGT, LDH, ALP, renal function—creatinine, urea, and estimated glomerular filtration rate via CKD-EPI equation), creatine kinase (CK), haptoglobin, phosphocalcic parameters, and iron metabolism (iron, transferrin saturation, transferrin, ferritin),


A family has a rare condition called Noonan syndrome. The girl, her sister, mother, maternal aunt, grandmother, and one female cousin all have signs of this condition. Three of them had genetic testing, and it showed that the girl and her sister both got the same change in a gene called LZTR1 from their mom. The girl also has a problem with growth hormone, which makes her grow slower than others. She has some typical features like wide-set eyes, a short nose, low ears, and a curved spine. She also has a weak heart rhythm and a small jaw. Her growth hormone level is low, and her bones are not growing as fast as they should. Doctors said she has Noonan syndrome with growth hormone deficiency, and because of her spine problems, they don’t recommend giving her growth hormone treatment right now.


A family has been studied where multiple members have Noonan syndrome, a genetic condition that can cause physical and developmental differences. The proband, a 6.6-year-old girl, along with her sister, mother, maternal aunt, grandmother, and a female cousin, showed signs of Noonan syndrome, either typical or atypical. Only three family members had genetic testing, and the results showed that both the proband and her sister inherited the same genetic change in the LZTR1 gene (c.1149+1G>T) from their mother. This gene mutation is linked to the condition. The girl also had growth hormone deficiency, which means her body doesn't produce enough growth hormone, and she did not have any other genetic changes. She had short stature, delayed development, and physical features common in Noonan syndrome, such as widely spaced eyes, a short nose, low-set ears, and a webbed appearance of the upper lip. She also had scoliosis and a bone deformity in her spine. Her growth hormone levels were low, and her bone age was younger than her actual age. Her heart, liver, kidneys, and brain were normal. Because of her severe spinal issues, treatment with growth hormone was not recommended.


{
    "proficient_health_literacy": "We herein describe a family with LZTR1-related Noonan syndrome. The proband, a 6.6-year-old female, was referred for evaluation of short stature as the first child of nonconsanguineous parents, born at 41 weeks of gestation via vaginal delivery with a birth weight of 1800 g (<P3rd) and length of 47 cm (<P3rd). She exhibited significant prenatal and postnatal growth retardation, with current height of 90.5 cm (−6.3 SD), weight of 11 kg (−4.9 SD), and BMI of 13.4 kg/m² (P10–25th). Her arm span/height ratio was 0.92 (−2 SD) and sitting height/height ratio was 0.58 (+3 SD), both deviating from standard reference values. Psychomotor development was mildly delayed. Clinical examination revealed typical Noonan syndrome features including hypertelorism, downslanting palpebral fissures, epicanthal folds, low-set oval posteriorly rotated ears with thick helix, short broad nose with depressed root and full tip, deeply grooved long philtrum, high and wide vermilion peaks, highly arched palate, micrognathia, short neck, cubitus valgus, scoliosis, café au lait spots, and mild hypertrichosis. Additional findings included squinting, refractive errors, and nystagmus. Laboratory investigations showed IGF-1 level of 61 μg/L (−1.9 SD), and growth hormone (GH) stimulation testing (insulin and levodopa protocols) demonstrated a GH peak of 5.54 ng/mL, below the cut-off value of 7 ng/mL, confirming growth hormone deficiency. Electrocardiography revealed frequent premature ventricular beats (second and third rhythms). Imaging studies, including X-ray and MRI of the spine, identified a hemivertebral deformity of the third thoracic vertebra and scoliosis with a Cobb’s angle of 28°; bone age was assessed at 5.5 years. Hormonal evaluations of the adrenal, thyroid, and gonadal axes were within normal limits, and tumor markers (AFP, HCG, CEA) were negative. No structural abnormalities were detected on cardiac, hepatic, renal, gynecological,


An 82-year-old man had surgery to remove his bladder and prostate because of cancer. Four days after surgery, he suddenly lost movement in all four limbs — his arms and legs — but didn’t feel pain or have trouble speaking. Doctors thought it might be a problem in his spine, but scans showed no blockage or bleeding in the spine. Instead, the problem was found in his brain: two small strokes happened at the same time on both sides, in areas that control movement. These strokes were caused by a lack of blood flow, likely because of a blood clot that came from his heart, maybe linked to his cancer. Since there was no clear reason found, doctors started giving him medicine to prevent more clots. His arms got better over time, but his legs stayed weak. This case shows that even after major surgery, a stroke can happen due to blood clots, and early treatment helps prevent more problems.


An 82-year-old man had surgery to remove his bladder and prostate due to cancer. Four days after the surgery, he suddenly developed severe weakness in all four limbs — arms and legs — without pain or loss of sensation. His brain scans showed acute bilateral strokes in the areas of the brain that control movement (precentral gyri), which explains the weakness. These strokes were caused by a sudden blockage of blood flow, likely due to a blood clot that traveled from his heart. Although the spinal cord was checked and found normal, the brain imaging revealed the strokes. The patient had no history of falls or trauma, and his blood clotting tests were normal, making the cause harder to find. Because of the surgery and anesthesia, doctors suspected a clot from the heart. He was started on anticoagulant medication to prevent future clots. After recovery, he began taking aspirin for long-term prevention. The key point is that this rare case shows that strokes can happen after major surgery, even without obvious risk factors, and brain imaging is essential for diagnosis.


{
    "proficient_health_literacy": "An 82-year-old Caucasian male was admitted to the urology department for radical cystoprostatectomy due to localized prostate adenocarcinoma. On the fourth postoperative day, he abruptly developed severe painless tetraparesis, characterized by Medical Research Council (MRC) grade 2/5 muscle strength in proximal upper limb muscles bilaterally and 0/5 in both lower limbs, with no involvement of cranial nerves, impaired consciousness, or sensory deficits. There were no cerebellar signs. Neurological examination revealed brisk tendon reflexes and positive pyramidal signs bilaterally, strongly suggesting a lesion affecting the central nervous system, such as acute spinal cord compression, subdural hemorrhage, or ischemia. No recent trauma or fall was reported prior to symptom onset. A peridural catheter had been placed for analgesia postoperatively and was removed the previous day without complications.\n\nAn emergency magnetic resonance imaging (MRI) study was performed, requiring the removal of metal brackets from subcutaneous tissue due to surgical implants. Spinal MRI did not demonstrate any evidence of spinal cord compression, subarachnoid hemorrhage, or ischemic changes (Figure A), thereby excluding a primary spinal cord pathology. In contrast, cranial MRI revealed acute bilateral ischemic infarctions localized to the precentral gyri—specifically, the median portion of the precentral gyrus on both sides (Figure B and C; arrows)—with no involvement of the internal capsule (Figure D). T2-weighted imaging at the level of the primary motor cortex showed no abnormal signal intensity at the time of presentation, which is consistent with acute ischemia and supports a time-dependent pathophysiological mechanism (Figure E). The precentral gyrus is supplied by the anterior cerebral artery (supplying the medial one-third) and the middle cerebral artery (supplying the lateral two-thirds) bilaterally.\n\nOver the subsequent days, upper extremity weakness gradually resolved, while lower limb paralysis persisted, indicating a regionally selective motor cortex infarction. Comprehensive diagnostic evaluation, including carotid duplex sonography, 24-hour electrocardiography (ECG), and transesophageal echocardiography, failed to identify any structural vascular disease, cardiac thrombus, or paroxysmal atrial fibrillation. While hypercoagulability associated with prostate cancer may have contributed to the cerebral ischemia,


A 60-year-old man had cancer in the back part of his pancreas. He didn’t have diabetes at first, and his blood sugar was normal. Doctors found the cancer with a blood test and imaging. They removed the cancer with surgery and gave him chemo to help fight it. Two years later, the cancer came back in one spot in his liver. The blood test for sugar started going up fast, and his blood sugar got worse as the cancer grew. So, doctors started giving him insulin to control his blood sugar. Even though the liver cancer didn’t respond well to chemo, it was only one spot, so they did surgery to remove it. After that surgery, his blood sugar got better right away and he stopped needing insulin. Now, two years later, he’s still alive and the cancer hasn’t come back.


A 60-year-old man was diagnosed with cancer in the tail of the pancreas, and his blood sugar levels were normal at the time of diagnosis. He had no history of diabetes or family history of pancreatic cancer. After surgery to remove the tumor (distal pancreatectomy) with lymph node removal, he received chemotherapy (S-1) to reduce the risk of the cancer coming back. Two years later, a single tumor was found in his liver, which was treated with two rounds of chemotherapy—first gemcitabine/nab-paclitaxel, then modified FOLFIRINOX. However, his blood sugar control worsened over time, rising from 5.6% to over 10%, and matched the growth of the tumor. Because of this, insulin therapy was started to manage his high blood sugar. Despite the liver tumor not responding well to chemotherapy, it was completely removed with a left hepatectomy since only one tumor was present. After the surgery, his blood sugar improved right away, and insulin was stopped. Two years after the second surgery, the patient is still alive and has not had any signs of cancer coming back.


{
    "proficient_health_literacy": "A 60-year-old male with a history of past smoking (Brinkman Index: 800) and chronic alcohol consumption (20 g/day for 20 years) was referred for evaluation of suspected pancreatic tail adenocarcinoma based on an elevated carbohydrate antigen 19-9 (CA19-9) concentration of 286.8 U/mL during a routine medical screening. He had no prior history of diabetes, significant comorbidities, or familial predisposition to pancreatic cancer. His body mass index was 20.8 kg/m², and he reported no weight loss. Dynamic contrast-enhanced computed tomography (dCECT) demonstrated a hypovascular lesion in the pancreatic tail, consistent with a resectable tumor. Endoscopic ultrasonographic fine-needle aspiration confirmed the diagnosis of adenocarcinoma. Positron emission tomography (PET) revealed a high standardized uptake value (SUVmax = 6.6), supporting malignant activity. Magnetic resonance imaging with gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA) showed no synchronous liver metastases, and the tumor was deemed anatomically resectable. The patient underwent a curative-intent distal pancreatectomy with regional lymph node dissection via radical antegrade modular pancreatosplenectomy. The pancreatic parenchyma was resected just above the superior mesenteric vein using tri-stapler technology, resulting in an operative time of 251 minutes and extraoperative blood loss of 720 mL. A clinically significant postoperative pancreatic fistula developed but resolved spontaneously without intervention, and the patient was discharged on postoperative day 40. Pathological examination revealed a 36 × 18 × 17-mm moderately differentiated tubular adenocarcinoma with no lymph node metastasis (0/27), absence of microscopic lymphatic invasion, but presence of microscopic venous invasion. The tumor margin was negative for extrapancreatic extension, and the resection margins were clear. The postoperative stage was classified as IB (T2N0M0) according to the Union for International Cancer Control 8th edition. Adjuvant S-1 chemotherapy (120 mg/m²/day) was administered for six months postoperatively.\n\nTwo years following the initial pan


A 61-year-old man had high blood pressure and a small cancer in his kidney called chromophobe renal cell carcinoma. Later, a tumor was found in his seminal vesicle (a part of the male reproductive system). Doctors thought it might be a spread from the kidney cancer, but tests showed it was actually a separate tumor called a primary paraganglioma. This new tumor did not spread to other parts of the body and was not made from cancer cells. It had features that match a normal type of tumor in that area. The tumor cells showed signs of a specific protein (synaptophysin and chromogranin), and some surrounding cells had S100 protein. Tests for genetic changes found nothing in either tumor, which supports it being a new, original tumor. The man had surgery to remove the tumor, and his blood pressure is now under control. He is still alive after 14 months.


This report describes a rare case of a primary paraganglioma in the seminal vesicle of a 61-year-old man. He had been dealing with high blood pressure and previously had a tumor in his kidney, diagnosed as chromophobe renal cell carcinoma. When a new tumor appeared in his left seminal vesicle, doctors considered it a possible spread (metastasis) from the kidney cancer. However, tests showed that the seminal vesicle tumor was not made of cancer cells and did not match the kidney tumor's characteristics. Instead, it showed markers typical of a paraganglioma — a type of tumor that arises from nerve tissue. The tumor cells expressed synaptophysin and chromogranin, and the surrounding cells showed S100 protein, which is common in such tumors. Both the kidney tumor and the seminal vesicle tumor had normal levels of SDHA and SDHB proteins, and no gene mutations were found in these genes. Imaging confirmed no other tumors were present, supporting the diagnosis that this was a primary tumor in the seminal vesicle, not a spread from the kidney. The patient recovered well and remains alive with controlled blood pressure after 14 months of follow-up.


{
    "proficient_health_literacy": "A 61-year-old obese male presented with persistent arterial hypertension and was evaluated for an incidental renal tumor discovered during imaging for hypertension. Laparoscopic partial nephrectomy revealed a chromophobe renal cell carcinoma (cRCC), a rare subtype of clear cell carcinoma characterized by minimal cytoplasmic visibility and low mitochondrial content, typically associated with intact von Hippel-Lindau (VHL) pathway function. Following one year of surveillance, a new lesion was identified in the left seminal vesicle. Magnetic resonance imaging (MRI) demonstrated a well-circumscribed, heterogeneous solid tumor measuring 32 mm in maximum dimension, with clear anatomical separation from the rectal and bladder walls, suggesting a benign or low-aggressiveness growth pattern. The patient underwent laparoscopic excision of the left seminal vesicle.\n\nGross examination revealed a seminal vesicle measuring 6 × 3 × 2 cm, with a solid, smooth, brownish nodule of 30 mm in greatest diameter. Surgical margins were negative for residual tumor, indicating complete resection. Microscopic evaluation showed well-defined nests of cuboidal tumor cells separated by vascular fibrous septa, with no evidence of vascular invasion, mitotic activity, or necrosis. Focal glandular structures were observed, and individual tumor cells exhibited a large central nucleus with small to medium-sized nucleoli and granular eosinophilic cytoplasm, consistent with neuroendocrine differentiation.\n\nDifferential diagnoses included metastatic chromophobe renal cell carcinoma, primary adenocarcinoma of the seminal vesicle, and paraganglioma. Immunohistochemical analysis was performed to discriminate between these entities. Tumor cells demonstrated strong positive immunoreactivity for synaptophysin and chromogranin, markers of neuroendocrine differentiation, supporting a neuroendocrine origin. Peripheral S100 protein-positive cells, likely corresponding to sustentacular cells, were identified at the tumor nest margins, further supporting a paraganglioma phenotype. Absence of keratin expression (AE1/AE3, CK7, CK8/18) excluded both primary and metastatic adenocarcinoma, reinforcing the diagnosis of a primary paraganglioma of the seminal vesicle. The Ki-67 labeling index was less than 2%, indicating a very low proliferative rate and favorable biological behavior.\n\nGenomic analysis was conducted on paraffin-


A 32-year-old Chinese woman had pain in her upper belly for 6 months. A scan found a small spot in her left liver, about 1.1 x 1.3 cm in size. The spot looked different on the scan — dark on one setting and bright on another — which made doctors think it might be cancer. After checking the tissue from the surgery, they found it was a rare type of liver cancer called LEL-ICC. She had the surgery using a small camera (laparoscopic) and recovered well, going home after 5 days. No signs of cancer were found after 28 months of follow-up. She still checks in every 3 months for blood tests and scans to stay safe.


A 32-year-old Chinese woman had been experiencing upper abdominal pain for six months. An MRI scan found a 1.1×1.3 cm lesion in the left part of her liver. The lesion looked different on the scan — it appeared dark on T1-weighted images and bright on T2-weighted images — which made doctors think it could be liver cancer. However, after surgery, the tissue was examined closely. The results showed it was a rare type of liver cancer called LEL-ICC. This type of cancer is linked to Epstein-Barr virus (EBV) and has specific markers that helped confirm the diagnosis. The patient had hepatitis B for six years, but her virus was inactive and not actively causing harm. Her other cancer markers were within normal ranges. She had a laparoscopic surgery to remove the part of the liver, and she recovered well, being discharged on postoperative day 5. After surgery, she had regular check-ups every three months for the first two years, then every six months. All tests remained normal, and she has not had any signs of cancer recurrence even after 28 months of follow-up. She is currently healthy and doing well.


{
    "proficient_health_literacy": "A 32-year-old Chinese female presented to Sichuan University West China Hospital with a 6-month history of upper abdominal pain. She had no history of radiotherapy, industrial chemical exposure, hormonal therapy, or contraceptive use. She reported one prior pregnancy and delivery of a male child. No personal or family history of hypertension, diabetes, smoking, or alcohol consumption was noted. Physical examination was unremarkable. Laboratory findings included hemoglobin 14.2 g/dL (normal range: 13–17.5 g/dL), white blood cells 7.12×10⁹/L (normal: 3.5–9.5×10⁹/L), platelets 249×10⁹/L (normal: 100–300×10⁹/L), total bilirubin 12.5 μmol/L (normal: 5.0–28 μmol/L), and aspartate aminotransferase (AST) 35 IU/L (normal <50 IU/L). Serological testing revealed carcinoembryonic antigen (CEA) of 5.54 ng/mL (abnormal threshold: ≥3.4 ng/mL), hepatitis B surface antigen (HBsAg) positive, and hepatitis B virus DNA (HBV-DNA) less than 1×10² IU/mL (indicating inactive HBV infection). Tumor markers CA19-9, CA125, and α-fetoprotein were 25.6 U/mL (normal <30 U/mL), 13.3 U/mL (normal <24 U/mL), and 3.37 ng/mL (normal <7 ng/mL), respectively. Abdominal computed tomography (CT) identified a lesion in the left lobe of the liver with no evidence of metastatic disease. Magnetic resonance imaging (MRI) of the upper abdomen revealed a 1.1×1.3 cm lesion in the left hepatic lobe exhibiting low signal intensity on T1-weighted sequences and high signal intensity on T2-weighted sequences, findings consistent with hepatocellular carcinoma (HCC) on initial preoperative evaluation. The patient underwent laparoscopic left lateral sectionectomy. Macroscopic examination revealed a yellowish solid mass measuring 12 mm in diameter. Microscopic analysis demonstrated an undifferentiated


A 66-year-old man suddenly lost movement on his right side and had trouble speaking. Doctors found a blocked blood vessel in his brain, on the left side, that was causing the stroke. They gave him a medicine called alteplase to open the blockage, then used a special tool to remove the clot. The blood vessel didn’t fully open at first, so they used a balloon to stretch it out while keeping blood flowing to other parts of the body. This helped the blood vessel open up again. After 15 minutes, the blockage was fixed and the man’s symptoms went away. He didn’t have any brain damage, and by the next day, he could move and speak normally. The doctors said the treatment worked well and the blockage improved over time. He’s now back to normal, with no problems after a year.


A 66-year-old man suddenly developed weakness on his right side and difficulty speaking. MRI scans showed a blockage in the left middle cerebral artery, which supplies blood to part of the brain. He received alteplase, a clot-dissolving drug, and then underwent a procedure to remove the clot using a catheter (mechanical thrombectomy). The clot was partially removed, but the artery remained narrowed (stenosis), leading to a recurrence of blockage. To fix this, a special balloon catheter was used for a 15-minute angioplasty while keeping blood flow to other parts of the body. This helped reopen the artery and improved blood flow. The patient’s symptoms improved significantly, and by the next day, his neurological score was back to normal. Follow-up scans showed the blockage had improved, and he was able to go home without any lasting brain damage. He was prescribed medications to prevent future clots, and after three months, his artery showed better flow. No major problems occurred for over a year. The treatment used a device not yet officially approved, but it was approved by the hospital after careful review and with the patient’s informed consent.


{
    "proficient_health_literacy": "A 66-year-old male presented with an acute onset of right hemiplegia and dysarthria at 7:30 a.m. while driving, prompting immediate transport to the hospital. Clinical examination revealed right facial paralysis, dysarthria, right upper extremity paralysis, and right upper and lower extremity paresthesia, with an initial National Institutes of Health Stroke Scale (NIHSS) score of 6/42. Magnetic resonance imaging (MRI) diffusion-weighted imaging (DWI) demonstrated hyperintense signals in the left putamen, corona radiata, and partial region of the middle cerebral artery, consistent with acute ischemic infarction. Magnetic resonance angiography (MRA) confirmed a distal occlusion of the left middle cerebral artery (MCA), while T2-weighted imaging showed no visible thrombus within the occluded segment, suggesting a thrombus-free occlusion with possible vasospasm or plaque-induced stenosis. A perfusion-diffusion mismatch was identified, supporting the indication for intravenous alteplase therapy, which was administered at 9:27 a.m. after correction of hypotension with nicardipine. The treatment protocol was guided by current stroke guidelines, with no contraindications identified.\n\nEndovascular recanalization was initiated using a 9 Fr sheath placed in the right femoral artery, with subsequent guidance of a 9 Fr OPTIMO catheter into the left internal carotid artery. Internal carotid arteriography revealed a distal occlusion of the left MCA. In the delayed phase, collateral circulation was observed via anastomosis of the cerebral pia mater, providing anterior-to-middle cerebral artery perfusion. A rebar (Medtronic) was advanced distal to the occlusion using a CHIKAI 14 × 200 cm catheter to secure the distal vessel, and a Trevo XP ProVue Retriever (4.0 × 30 mm, Stryker) was deployed. Post-deployment imaging demonstrated immediate flow restoration, but poor stent dilation was noted in the occluded segment, indicating significant arterial stenosis. The proximal diameter of the stenosis was 2.6 mm, and the distal diameter was 2.1 mm, confirming a moderate to severe stenotic lesion. Following retrieval of the Trevo, a 1