A 37-year-old woman came to our hospital complaining of weakness in both hands. Five years ago, she first noticed mild weakness in her left hand, which slowly got worse. Two years later, her right hand also started to weaken. The weakness gradually progressed, making it hard for her to write, use chopsticks, or make a fist. She visited local clinics but wasn't properly evaluated. When she came to our hospital, her hands were severely weak and had noticeable muscle shrinkage, but she had no numbness or pain. Her mental abilities and brain function were normal, and there were no signs of problems in her face, eyes, or neck.

Neurological tests showed severe weakness in the muscles of her hands, especially in the fingers and wrist areas, with poor muscle strength and visible muscle wasting. Her legs were not affected. Her reflexes in her arms were reduced, but her sense of touch and other sensory functions were normal.

Lab tests showed that her thyroid function (levels of hormones) was normal, but her immune system was active against the thyroid, which led to a diagnosis of Hashimoto's thyroiditis — a common autoimmune condition where the body attacks its own thyroid gland.

Electrical tests of her nerves (nerve conduction studies) showed a specific pattern of weakness in the nerves that control hand movement, particularly in the median, ulnar, and radial nerves. This pattern is typical of a condition called Miller-Fisher-like neuropathy (MMN), which affects motor nerves without affecting sensation. Even though she didn’t have antibodies to certain nerve-related proteins, the clinical signs and test results clearly supported the diagnosis of MMN.

A thyroid biopsy confirmed the presence of Hashimoto's thyroiditis. She was treated with high-dose intravenous immunoglobulin for five days, and one month later, her hand weakness and muscle deformities had improved significantly, with better nerve function. She is now being followed up regularly at our outpatient clinic.


{
    "proficient_health_literacy": "A 37-year-old woman presented with progressive distal upper-limb weakness, initially noted in the left hand five years prior with insidious onset, followed by symmetric progression to the right hand two years later. The weakness evolved gradually, impairing fine motor functions such as writing, chopstick handling, and fist formation. Clinical evaluation revealed severe motor weakness in both hands, with Medical Research Council (MRC) grades ranging from 2/5 to 3/5 across multiple intrinsic hand muscles, including flexor digitorum profundus and sublimis, flexor pollicis longus, extensor digitorum communis, and abductor digiti minimi, with notable muscle atrophy and distal deformities. Motor function in the lower extremities was preserved, and deep tendon reflexes were reduced in the upper limbs. Sensory examination was intact, with normal cortical sensation, cranial nerve function, cerebellar signs, and no evidence of sensory neuropathy. Neurological examination confirmed alertness, intact orientation, and absence of cognitive impairment. No abnormal findings were observed in the cervical spine on magnetic resonance imaging (MRI), which showed only mild disc protrusions at C5-6 and C6-7 levels.\n\nLaboratory investigations revealed normal hemogram, electrolytes, renal function, cerebrospinal fluid, and autoimmune markers for systemic vasculitides including rheumatoid factor, anti-dsDNA, lupus anticoagulant, anticardiolipin, antithrombin III, ANCA, anti-SSA/SSB, complement 3/4, anti-Jo-1, cryoglobulin, immunofixation, and anti-GM1/GD1b antibodies. A mildly elevated fluorescent antinuclear antibody titer (1:40) was detected, but no evidence of systemic autoimmune disease was found. Tumor markers (alpha-fetoprotein, carcinoembryonic antigen, CA-19-9, CA-125) and enzymatic markers (hexosaminidases A and B, creatine kinase) were within normal limits. Notably, thyroid function tests showed normal levels of T3, free T4, and TSH, but significantly elevated antithyroglobulin antibody (794 U/mL; normal: 0–100 U/mL) and antimicrosomal antibody (26,030 U/mL


A man in his 60s got serious burns over 35% of his body after setting himself on fire. The burns were on his chest, arms, neck, and face. He also had smoke in his nose and throat, which meant his airway was burned. He got a bad infection in his blood, called bacteremia, and needed antibiotics to fight it. While on antibiotics, a red rash started on his chest and arms and spread fast to his hands and legs. This rash wasn’t on the burned areas, which means it didn’t start where the burns were. Doctors thought it was a reaction to the medicine, called TEN. They stopped the antibiotics and gave him a strong steroid medicine for 3 days. The rash got better after that. After a few days, the redness faded and he started feeling better. He didn’t get any new infections and was finally able to go home after 41 days in the hospital.


A 68-year-old man suffered severe burns covering 35% of his body after setting himself on fire while trying to commit suicide. He had second- and third-degree burns, and his burns were so severe that he needed hospitalization. During treatment, he developed a blood infection (bacteremia) caused by a resistant bacteria, leading to antibiotic use. However, after stopping the antibiotics, a rash appeared on his trunk and arms and quickly spread to his limbs. This rash was later diagnosed as TEN (toxic epidermal necrolysis), a serious skin reaction that usually occurs outside of burn areas. The rash improved after stopping the antibiotics and starting a short course of high-dose steroid medication (methylprednisolone, 1,000 mg per day for 3 days). The skin reaction was only on non-burned parts, which suggests that TEN did not start at the burn sites. After recovery, he received several skin grafts over time and was eventually discharged from the ICU on day 41. No specific cause for the TEN was found, but the treatment was successful and he fully recovered.


{
    "proficient_health_literacy": "A 68-year-old male presented with extensive thermal burns resulting from a self-inflicted fire incident involving the application of 10 liters of gasoline to his head and body, followed by ignition on a riverbed. He had a history of insomnia and anxiety but no known allergies or smoking history. On admission, his Glasgow Coma Scale was 15, body temperature 35.8°C, heart rate 98 bpm, blood pressure 170/85 mm Hg, respiratory rate 20 bpm, and oxygen saturation 100% on 10-liter mask. Clinical examination revealed erythema and bullae involving the auricular to mandibular neck, thorax, abdomen, occiput, right upper arm, right dorsal hand, and left forearm. The anterior chest and posterior neck were covered with soot, with corresponding grayish-white skin discoloration, indicating deep dermal and epidermal destruction. Soot was also present in the nasal cavity, pharynx, and larynx, confirming upper airway burn injury. Bronchoscopy demonstrated soot adhesion, peripheral edema, and mucosal erythema from the vocal cords to the pharynx, consistent with thermal injury to the upper respiratory tract. Total body surface area (TBSA) burned was 35%, comprising 20% second-degree and 15% third-degree burns, with a revised BAUX score of 120, indicating severe burn severity. Initial wound management included daily washing with warm water, application of dimethyl isopropylazulene and gentamicin sulfate ointment, and coverage with moist wound care pads. Due to lack of guarantor consent, aggressive initial interventions such as surgical debridement and skin grafting were withheld.\n\nOn day 8, the patient developed a high fever (38–40°C) with a marked systemic inflammatory response, and blood culture identified methicillin-resistant *Staphylococcus aureus* (MRSA). Empirical therapy with vancomycin and ampicillin/sulbactam was initiated to manage the burn-associated infection. Once infection control was achieved, first split-thickness skin grafts (STSG) were performed on day 17 using a 0.01-inch graft harvested from both thighs via electric dermatome, meshed at a 1:3 expansion ratio. Following this,


A 50-year-old man had pain in his right eye, blurry vision, headaches, and trouble walking because he was unbalanced. Doctors found a fluid-filled sac inside his brain stem that was pressing on important parts of his brain. This sac was causing the symptoms. He had surgery to fix it. A small hole was made in his skull, and a tiny camera was used to drain the fluid from the sac and create a new path for brain fluid to flow. After the surgery, the fluid-filled sac got smaller, the brain’s fluid spaces shrank, and the fluid could now move freely through the brain’s tunnels. His walking, eye problems, and headaches all got better over time. Now he walks normally and feels much better.


A 50-year-old man came in with pain in his right eye, blurry vision, headaches, and trouble walking due to balance issues. He had no numbness or weakness in his arms or legs. He also had a history of diabetes, high blood pressure, and high cholesterol.

On exam, he was alert and his mental status was normal. His right eye had reduced vision and he had double vision when looking to the sides. He showed slight eye shaking (nystagmus) but other brain nerve functions were normal. His strength and sensation were normal, and although his gait was slightly unsteady, he didn’t have a Romberg sign, which means his balance wasn't due to loss of coordination.

MRI scans showed three cysts in the right part of his midbrain, totaling about 2.2 cm in size, with one large cyst measuring up to 1.7 cm. This cyst was pressing on the narrow passage (aqueduct) that carries cerebrospinal fluid, causing mild buildup of fluid in the brain ventricles (hydrocephalus).

He had surgery to relieve the pressure. Under general anesthesia, two small holes (burr holes) were made in his skull. One was in the right front part of the skull to access the third ventricle and create a new opening (endoscopic third ventriculostomy or ETV) to let fluid flow properly. The second hole was used to reach the brainstem cyst. Using a small camera (endoscope), the surgeon opened the cyst (fenestration) and drained its fluid, which was found to be pure cerebrospinal fluid. An external drain was placed to monitor pressure after surgery.

After the procedure, the patient recovered well. His intracranial pressure stayed normal, and the drain was removed the next day. He could walk without help and perform daily tasks independently. His thinking and memory were unchanged.

Follow-up scans showed that the brain ventricles had shrunk and fluid was now flowing through the aqueduct and the new opening. The brainstem cysts also decreased in size. By one month, his balance and double vision had improved. By five months, his headaches and double vision had almost completely gone, and imaging showed the cysts and ventricles were well decompressed.


{
    "proficient_health_literacy": "A 50-year-old male presented to the inpatient neurosurgical service with a progressive neurological syndrome characterized by right eye pain, blurred vision, occasional diplopia, headache, and gait imbalance with frequent falls. He denied peripheral sensory deficits or motor weakness. His medical history included type II diabetes mellitus, hypertension, and hyperlipidemia, all of which may contribute to cerebrovascular and neurodegenerative risk factors. On neurological examination, he was alert and oriented to person, place, and time. He exhibited decreased visual acuity in the right eye and diplopia on extreme lateral gaze, with subtle horizontal nystagmus. Cranial nerve examination beyond the ocular motor nerves was grossly intact, and all four extremities demonstrated normal strength and sensation. The Romberg sign was negative, though his gait was mildly ataxic, consistent with cerebellar or brainstem dysfunction.\n\nMagnetic resonance imaging (MRI) without contrast revealed a stable cluster of three cystic lesions localized within the tegmentum of the right midbrain, measuring 2.2 cm × 1.4 cm × 1.4 cm in aggregate. The largest cyst, located dorsomedially, reached a maximum dimension of 1.7 cm and demonstrated significant compression of the adjacent cerebral aqueduct. This compression was associated with mild hydrocephalus, evidenced by distention of both the lateral and third ventricles, indicating impaired cerebrospinal fluid (CSF) dynamics and impaired flow through the aqueduct.\n\nThe patient underwent an endoscopic third ventriculostomy (ETV) with cyst fenestration under general anesthesia. He was secured in a Mayfield head holder and stereotactic navigation was used to guide instrument placement. Two burr holes were created: a posterior burr hole in the right frontal region near the coronal suture for ETV access, and an anterior burr hole positioned anterior to the first to provide access to the brainstem cyst and posterior third ventricle. The endoscope was introduced via the posterior burr hole into the lateral ventricle and advanced through the foramen of Monro into the third ventricle. A conventional ETV was performed in the floor of the third ventricle, anterior to the mammillary bodies, establishing a new pathway for CSF flow.\n\nSubsequently, the endoscope was repositioned through the anterior burr hole and advanced posterior


A 69-year-old man had cancer in his left breast back in the 1990s. The tumor was big, over 6 cm, and spread to nearby lymph nodes. He had surgery to remove the breast and the lymph nodes. After surgery, he got chemotherapy, but two months later, cancer spread to his lungs. He then started treatment for the breast cancer, including pills that stop estrogen. Two years later, he started having trouble going to the bathroom often. Tests found he also had prostate cancer — a cancer in the prostate gland — with a high PSA level of 40.5. He got radiation to the prostate, and later took a medicine called Estracyt® that stayed in the prostate and helped lower the PSA. The PSA went back to normal, and he kept taking it for three years. But after five years, he got a blood clot in his leg, which happened because of the cancer medicines. Later, when he stopped breast cancer treatment, the breast cancer came back and spread to his liver. Even though he tried other medicines for the prostate cancer, the breast cancer kept getting worse and he passed away five years after getting prostate cancer. This case shows that men can get breast cancer, and they need special care for both cancers at the same time.


A 69-year-old man was diagnosed with breast cancer in the 1990s. He had a large lump in his left breast, and tests showed it was a serious type of cancer (stage IIIC). He had a mastectomy and surgery to remove lymph nodes in his armpit. After surgery, he received chemotherapy, but two months later, the cancer spread to his lungs. He then started treatment for metastatic breast cancer using anti-estrogen therapy and 5-fluorouracil. Two years later, he started having trouble with urination, and tests found that he also had prostate cancer (stage III) with a high PSA level of 40.5 ng/mL. He received radiation therapy for the prostate cancer and later started using Estracyt® to control it. His PSA levels dropped and stayed normal for a few years. However, after five years, he developed a blood clot in his leg, which was linked to the hormone treatments. When he stopped breast cancer treatment, the breast cancer returned and spread to his liver. He continued prostate cancer treatment with other medications, but he eventually died from breast cancer progression five years after his prostate cancer diagnosis. This case shows that men can get breast cancer, and when they have both breast and prostate cancer, they need careful, ongoing care from a team of specialists.


{
    "proficient_health_literacy": "A 69-year-old male presented to the Department of Breast Surgery at Shiga General Hospital (Moriyama, Shiga, Japan) in the 1990s with a palpable lump in the left breast. Physical examination revealed a mass exceeding 6 cm in the upper-lateral quadrant, without evidence of skin invasion, and associated axillary lymphadenopathy. The patient had a comorbid history of type 2 diabetes mellitus, hypertension, cerebral infarction, and a previously managed brain schwannoma, treated with oral glimepiride 0.5 mg, nifedipine 40 mg, and aspirin 100 mg. No significant family history of cancer was reported.\n\nUltrasonographic evaluation confirmed a solid breast mass and right-sided axillary lymph node enlargement. Core needle biopsy demonstrated a high histological grade invasive ductal carcinoma, characterized by estrogen receptor (ER)-positive, progesterone receptor (PgR)-negative, human epidermal growth factor receptor 2 (HER2)-negative, and androgen receptor (AR)-positive status (detected using anti-AR rabbit monoclonal antibody SP107; Roche Tissue Diagnostics, Ltd.), with a Ki-67 labeling index of 10%, indicating a moderately proliferative tumor. Based on the Union for International Cancer Control (UICC) 8th edition TNM classification, the tumor was staged as cT3N3M0, stage IIIC breast cancer.\n\nDue to the absence of preoperative systemic therapy, the patient underwent mastectomy with axillary lymph node dissection. Final pathological assessment confirmed pt3N3a (36/39) M0, consistent with stage IIIC disease. Postoperative adjuvant chemotherapy was administered with a CEF regimen: epirubicin 40 mg/m², 5-fluorouracil (5-FU) 500 mg/m² every 2 weeks, and oral cyclophosphamide 100 mg daily. Following two cycles of chemotherapy, a computed tomography (CT) scan revealed pleural metastasis in the right lung, indicating early dissemination. The patient was then initiated on first-line endocrine therapy with high-dose toremifene (TOR) 120 mg twice daily and oral 5-FU/5’DFUR (doxif


A 45-year-old woman found a lump in her thyroid during a check-up and also had a blood clot in a vein near her thyroid. She didn’t feel sick or have any symptoms. The doctor saw nothing wrong during the exam. Tests showed her thyroid levels were normal. An ultrasound found a solid lump in her left thyroid and a clot in the middle thyroid vein. A small sample taken from the lump showed some cells that were growing, but it wasn’t clear if it was cancer. The doctor decided to remove part of her thyroid, the middle piece, and the lymph nodes near the neck to be safe. After surgery, the tissue test showed a very small type of thyroid cancer, and the clot was found to be part of the cancer spreading into the vein.


A 45-year-old woman was found to have a thyroid mass and a blood clot in the middle thyroid vein during a routine physical exam. She had no symptoms and the exam showed no signs of illness. An ultrasound revealed a solid nodule in her left thyroid and a clot in the middle thyroid vein. A biopsy of the nodule showed an atypical lesion with some cells that were growing (classified as TBSRTC III), and no BRAFV600E mutation was found. Because of these findings, she had surgery, including removal of the left thyroid, part of the middle thyroid (isthmus), and nearby lymph nodes. A procedure was also done to remove the blood clot. After surgery, the pathologist found a small papillary thyroid cancer (microcarcinoma) in the left thyroid, and the clot was confirmed to be a tumor thrombus, meaning it had spread from the thyroid cancer.


{
    "proficient_health_literacy": "A 45-year-old woman presented with a thyroid mass and thrombosis in the middle thyroid vein identified during a routine physical examination. The thyroid mass was detected three months prior to presentation, with no associated symptoms. The patient reported undergoing surgery due to psychological stress related to the discovery, despite having no prior medical history of thyroid disease or familial predisposition to thyroid carcinoma. There was no history of childhood radiation exposure. Physical examination findings were unremarkable, with no signs of thyroid enlargement, neck tenderness, or other systemic abnormalities. Laboratory evaluation of thyroid function—specifically triiodothyronine (T3), free triiodothyronine (FT3), thyroxine (T4), thyroglobulin, and thyroid-stimulating hormone (TSH)—revealed normal values, indicating euthyroidism and ruling out overt thyroid dysfunction. Ultrasound imaging demonstrated a solid nodule in the left thyroid lobe, characterized by a medially echoic lesion, and concurrently revealed a thrombotic occlusion within the middle thyroid vein. Subsequent ultrasonography-guided fine-needle aspiration biopsy yielded a cytological diagnosis of an atypical lesion of ambiguous significance (TBSRTC III), exhibiting the presence of some actively proliferating cells, consistent with a biologically aggressive but non-malignant growth pattern. Notably, the BRAFV600E mutation, a well-established driver mutation commonly associated with papillary thyroid carcinoma, was not detected in the biopsy sample. The patient underwent a left thyroidectomy with isthmus lobectomy and prophylactic central neck lymph node dissection to ensure complete removal of potentially involved tissue. Additionally, thromboembolectomy was performed to remove the tumor thrombus from the middle thyroid vein. Final pathological examination confirmed the presence of a papillary microcarcinoma (pT1a) in the left thyroid, measuring less than 1 cm in greatest dimension, with no evidence of lymph node metastasis or extrathyroidal extension. The thrombus in the middle thyroid vein was histologically confirmed as a tumor-derived thrombus, consistent with extension of the papillary thyroid carcinoma into the venous system, a known phenomenon in certain subtypes of thyroid malignancy, particularly those with high vascularity or invasive growth patterns. This case illustrates the importance of imaging and biopsy in evaluating thyroid nodules with venous involvement, as well as the role of molecular testing in refining the biological characterization of thyroid lesions, even


A 22-year-old woman went to the hospital after having diarrhea for 5 days. She started taking clindamycin to treat an infection from a tooth problem. After that, her diarrhea got worse and turned into a serious condition called toxic megacolon, where her colon became swollen and burst. This led to a dangerous infection in her blood, called sepsis. Doctors found a harmful bacteria in her stool, called C. difficile (type 087), and another bacteria, Klebsiella pneumoniae, in her blood. She was treated with antibiotics like metronidazole and ceftriaxone, but she still got worse. Even with treatment, she died 10 days after coming to the hospital. The doctors found yellow spots in her colon during autopsy, which is a sign of pseudomembranous colitis. This case shows that even young, healthy people can get very serious infections from antibiotics, especially if they don’t get the right treatment fast. The infection spread quickly because the bacteria made a lot of harmful toxins. This strain (087) is common in Hungary but rare elsewhere. The patient had no hospital visits before, but her college life was stopped by this illness. She needed surgery, but it wasn’t done in time. This case warns doctors: young people can get severe colitis, and fast action is key to saving lives.


A 22-year-old female university student was admitted to University Hospital of the West Indies, Jamaica with a 5-day history of diarrhea. The diarrhea started after she took clindamycin for a tooth infection. Despite stopping the antibiotic and starting other treatments, her condition worsened. She developed toxic megacolon, a severe swelling of the colon, which eventually led to a bowel perforation and blood infection (sepsis) caused by Gram-negative bacteria. Tests found that the diarrhea was due to Clostridium difficile (C. difficile) strain NAP1/ribotype 087, and blood cultures showed Klebsiella pneumoniae. She was treated with metronidazole and antibiotics to clear the bacteria, but her condition did not improve. She died 10 days after admission. An autopsy confirmed pseudomembranous colitis (PMC), a serious form of C. difficile infection, and found signs of severe inflammation in her large intestine. The case is unusual because it happened in a young person without prior hospital stays or health care exposure. While such severe complications are more common in older adults, this case shows that young people can also develop life-threatening forms of the infection. The doctors did not use recommended treatments like intracolonic vancomycin or surgery when needed, which may have contributed to the poor outcome. This highlights the importance of early recognition and proper treatment of C. difficile infections, even in younger patients.


{
    "proficient_health_literacy": "A 22-year-old female university student was admitted to the University Hospital of the West Indies, Jamaica with a presumptive diagnosis of pseudomembranous colitis (PMC) following a 5-day history of diarrhoea and fever that began 5 days after initiation of clindamycin therapy for a dental abscess requiring tooth extraction. Despite discontinuation of clindamycin and initiation of empiric therapy with chloramphenicol and metronidazole, her diarrhoea and fever persisted. Physical examination revealed a febrile patient with severe cardiopulmonary distress, tachycardia (heart rate 150 beats/min), and hypertension (blood pressure 150/100 mmHg). Laboratory findings included haemoglobin 10.4 g/dL, leukopenia (white cell count 2.1 × 10⁹/L), and platelet count 182 × 10⁹/L. Clinical deterioration progressed to toxic megacolon, bowel perforation, and Gram-negative sepsis. Blood cultures collected in brain heart infusion and thioglycollate broths grown from all four bottles after 24-hour incubation at 37°C yielded Klebsiella pneumoniae. Stool specimens collected the day after admission tested positive for Clostridium difficile toxin A and B using ELISA (Alexon Inc., Sunnyvale, CA), and the organism was isolated on cycloserine, cefoxitin, fructose agar (CCFA).  \n\nSusceptibility testing of K. pneumoniae via Kirby Bauer disc diffusion demonstrated susceptibility to ceftriaxone, co-trimoxazole, ceporin, amikacin, gentamicin, ceftazidine, and augmentin, with resistance to chloramphenicol, piperacillin, and ampicillin. The patient received intravenous metronidazole, followed by ceftriaxone and gentamicin, which resulted in fever resolution and sterile blood cultures. However, persistent hypotension, pulmonary oedema, leucopenia, and thrombocytopenia required intensive care management, and the patient died 10 days after admission. Autopsy revealed florid pseudomembranous colitis with multiple discrete yellowish exudative plaques throughout the large bowel mucosa, confirming PMC. Additional pathologic findings included markedly


A 58-year-old woman had a brain tumor before, called a meningioma, and had surgery for it when she was 31. She had more surgeries later, 16 and 26 years later. While treating a broken bone, doctors found a big lump in the back part of her pancreas. This lump looked scary, so they did scans and found it had blood vessels and was not normal. At first, they thought it might be a type of cancer or a rare tumor, but the test results showed it was actually a type of tumor called SFT, which started in her brain tumor. The doctors removed the pancreas part with the tumor safely, and she recovered well. Later, 4 years after surgery, the tumor came back in her brain, but no new tumors have come back in her belly. She is now being treated for the brain problem.


A 58-year-old woman with a history of brain tumors (diagnosed as meningioma) was seen for a cystic tumor in the tail of her pancreas. The tumor was found during a CT scan done for a bone fracture. Imaging showed a complex, blood-rich mass that could have been a type of pancreatic cancer or a rare tumor like a neuroendocrine neoplasm or solid pseudopapillary neoplasm. However, after surgery, the pathologist found it was a malignant hemangiopericytoma (SFT) of the pancreas, a type of tumor that originates from connective tissue. Importantly, the brain tumor she had before was found to be the same type as this pancreatic tumor, meaning the pancreatic tumor likely came from the brain lesion. The surgery was successful with no complications, and she recovered well. Four years after the surgery, she developed a recurrence of brain disease, but no new tumors have appeared in her abdomen. She is currently being treated for the brain recurrence.


{
    "proficient_health_literacy": "A 58-year-old woman with a history of recurrent meningioma, initially resected at age 31 and subsequently reoperated at ages 16 and 26 years post-initial resection, was referred for evaluation of a cystic lesion in the pancreas tail. During admission for femoral fracture management, incidental detection via computed tomography (CT) revealed a 5.5-cm cystic mass in the pancreatic tail. Laboratory findings at presentation included a slightly elevated serum lipase (56 IU/L; normal range: 13–55 IU/L) and gamma-glutamyl transpeptidase (47 IU/L; normal range: 9–32 IU/L), with all tumor markers—carcinoembryonic antigen, carbohydrate antigen 19-9, and DUPAN-2—within normal limits. Endoscopic ultrasonography (EUS) demonstrated a well-encapsulated, circumscribed cystic mass with prominent intratumoral vascularity, including a hypervascular region resembling collateral vessels. Dynamic contrast-enhanced CT revealed a heterogeneously enhancing mass adjacent to the splenic hilum, characterized by strong arterial-to-portal phase enhancement of the solid components' rim and edge, with a large central non-enhancing area. During the portal to delayed phase, the solid components gradually isoattenuated relative to surrounding pancreatic parenchyma, with the non-enhancing region remaining distinct. Magnetic resonance imaging (MRI) confirmed low signal intensity on T1-weighted sequences and slightly higher signal intensity on T2-weighted sequences compared to normal pancreatic tissue, consistent with the presence of solid components. The large non-enhancing region on CT corresponded to a hyperintense signal on T2-weighted MRI, indicating cystic or necrotic transformation. Differential diagnoses included pancreatic neuroendocrine neoplasm, solid pseudopapillary neoplasm, hemangioma, and mucinous cystic neoplasm (due to patient sex and anatomical location), with invasive pancreatic carcinoma excluded based on imaging features. EUS-guided fine-needle aspiration was avoided due to the risk of cystic rupture and hemorrhage. The patient underwent distal pancreatectomy with regional lymph node dissection, with resection extending above the left edge of the superior mesenteric artery. The pancreatic stump was free of residual disease, with a margin of approximately 3 cm including stap


A 70-year-old woman had trouble moving her right side, which started 4 months ago. Doctors used a brain scan and a blood vessel test to check her brain. They found a small, old damage in her brain that could explain the weakness. They also found a strange blood vessel problem under the brain’s cover, called a TDAVF. This problem was feeding from two small blood vessels on the back of the brain and was sending blood backward (like water going uphill), which is dangerous. To fix it, doctors used a special glue to block the main leaky spot. After that, a small new leak appeared — it wasn’t seen before and came from a hidden blood vessel. But one week later, this new leak went away on its own. The patient had no more problems, no more weakness, and no signs of the leak coming back. She’s back to normal and doing fine.


A 70-year-old woman had right-side weakness that had been present for 4 months. MRI showed a small area of damage (chronic infarction) in the left corona radiata, which likely caused her weakness. During the imaging, a vascular abnormality was found beneath the cerebellar tentorium. This abnormality was an arteriovenous fistula (TDAVF) supplied by the bilateral posterior meningeal arteries. It had a shunting point under the tentorium with blood flowing backward (retrograde flow), which is a type known as Borden III and Cognard III. This kind of abnormality can lead to bleeding, so it was treated with endovascular embolization using a special glue called n-butyl-2-cyanoacrylate (NBCA) to block the shunting point. After the procedure, the main shunt disappeared, but a small, new shunt was found that was not seen before. This new shunt was supplied by a blood vessel called the AWW, which was not visible on the preoperative scans. One week later, follow-up imaging showed that this residual shunt disappeared on its own. The patient had no further issues, no neurological problems, and no recurrence of the fistula after 6 months of follow-up. The treatment was successful in preventing complications.


{
    "proficient_health_literacy": "A 70-year-old woman presented with a 4-month history of right hemispheric motor weakness, which was evaluated with magnetic resonance imaging (MRI). Fluid-attenuated inversion recovery (FLAIR) sequences revealed chronic lacunar infarction in the left corona radiata, consistent with a contributing pathophysiological mechanism for her right-sided motor deficit. No edema or acute infarct was observed in either supratentorial or infratentorial regions. MRI angiography (MRA) identified a vascular lesion located beneath the cerebellar tentorium on constructive interference in steady-state (CISS) images, suggesting an arteriovenous shunt. Cerebral angiography confirmed the presence of a dural arteriovenous fistula (TDAVF) supplied by the bilateral posterior meningeal arteries (PMAs), with no other identifiable feeders detected. The shunting point was situated on the inferior surface of the cerebellar tentorium, exhibiting retrograde venous flow into the tentorial sinus and ultimately the transverse sinus, consistent with Borden type III and Cognard type III classification. The left vertebral angiogram demonstrated venous congestion with no retrograde flow in the basal vein of Rosenthal, while the internal carotid and bilateral posterior cerebral arteries exhibited fetal-type vasculature. The straight sinus demonstrated anterograde flow, and no arterial feeders were observed in the internal carotid or vertebral systems. The arteriovenous shunt was primarily fed by the PMAs, with drainage via the superior vermian vein to the petrosal vein and superior petrosal sinus, and alternatively through the inferior hemispheric vein, inferior hemispheric vein, and tentorial sinus. A selective angiogram of the mastoid branch of the occipital artery confirmed the PMA as the primary arterial supply, with bilateral involvement observed in both left and right occipital territories. The shunting point was precisely localized beneath the cerebellar tentorium on maximum intensity projection (MIP) images, with venous drainage converging into the transverse sinus. Transarterial endovascular embolization was performed under general anesthesia using two Envoy 5F 90 cm microcatheters (MPD, Codman Neuro) introduced into the bilateral occipital arteries. A Masters HF 2.8-Fr/3.2-Fr 125 cm


A 11-year-old girl had a serious bone cancer in her leg. Doctors removed the cancer and put in a fake joint (prosthesis) to replace the broken part. Six months later, the joint got infected, so they had to take it out and clean the area deeply. They used a temporary spacer with medicine to fight the infection. After healing, the girl broke a small bone in her thigh because she started walking too soon. This stopped her leg from growing longer. Her leg was now 5 cm shorter than the other. To fix this, they used a special growing prosthesis that can stretch over time. This device added 8 cm of bone length, helping her leg grow to the right size. The girl now walks without pain, carries her full weight, and plays sports again. There’s no sign of infection or cancer coming back. The leg is almost the same length now, and she’s doing well after all the surgeries.


This report shares a case of a 11-year-old girl who had a serious bone cancer in her left leg, called high-grade osteosarcoma, which required surgery to remove the affected part of her femur. After the initial surgery, she developed a deep infection six months later, which required a two-stage revision. In the first stage, the infected implant was removed, the infection was treated with antibiotics, and the area was cleaned thoroughly. During recovery, she accidentally broke a bone in her tibia (the shin bone) because she started walking too early, which stopped her leg from growing properly. This caused a 5 cm difference in leg length.

Because the infection had already damaged the bone and growth plates, doctors chose a special bio-expandable prosthesis called MUTARS® BioXpand to fix the leg length. This device can grow longer over time by using a motorized nail that gently stretches the bone. It was designed to add 8 cm of bone length without needing to remove more bone or use a large implant. The prosthesis was placed, and the leg was gradually lengthened over several months. However, the family did not follow the required care schedule, which led to a small bony bridge forming at the break site. After adjusting the care plan, the lengthening was resumed safely.

Once the leg reached its full length, the temporary prosthesis was replaced with a permanent one. The new implant was stable and well-integrated. At the final follow-up, the girl was pain-free, walking without any support, and able to do all her normal activities, including sports. There was no sign of infection or cancer coming back. Although her knee joint is now slightly uneven due to the growth stoppage, she has excellent movement and function. Her outcomes were rated very well by medical scoring systems, showing a full return to daily life.


{
    "proficient_health_literacy": "An 11-year-old female presented with high-grade osteosarcoma of the left distal femur, undergoing wide resection followed by initial prosthetic reconstruction with a conventional endoprosthesis. Six months postoperatively, during the final cycle of adjuvant chemotherapy, she developed septic shock secondary to acute deep infection characterized by extensive pus formation and skin necrosis on the anteromedial knee, exposing the implant. Microbiological analysis revealed polymicrobial flora including Staphylococcus epidermidis, Neisseria mucosa, Cutibacterium acnes, and Bacillus sp., with no detectable genetic markers of antibiotic resistance; sensitivity testing confirmed standard susceptibility to empiric agents.\n\nFirst-stage revision involved explantation of the infected endoprosthesis, followed by thorough debridement of soft tissues and intramedullary canals using high-pressure lavage irrigation. A reinforced temporary antibiotic cement spacer (containing Vancomycin-loaded calcium phosphate beads, STIMULAN®) was implanted to maintain joint space and deliver localized antimicrobial therapy. The surgical site was covered with a vacuum-assisted closure device. Empiric therapy with ciprofloxacin and metronidazole was initiated, subsequently switched to linezolid and cefixime upon culture confirmation. Clinical improvement was observed with wound healing and normalization of inflammatory markers.\n\nDespite infection control, the patient independently transitioned to full weight-bearing, resulting in a Salter-Harris type V-like fracture of the proximal tibia physis. This fracture formed a bony bridge across the lateral half of the physis, resulting in irreversible loss of growth potential in the proximal tibia. The combined resection of the distal femur and proximal tibia physeal structures resulted in a 5 cm leg length discrepancy at the time of planned second-stage reconstruction. The initial cement spacer measured 10 cm, which is insufficient for an expandable prosthesis due to the minimum required implant length of 18 cm for distal femoral endoprostheses.\n\nGiven the anticipated end-growth discrepancy of 10 cm, which would be unmanageable without a lengthening implant, and considering the prior deep infection and compromised bone quality, a bioexpandable MUTARS® BioXpand endoprosthesis (Implantcast, Germany) was selected. This system comprises a 10 cm-long femoral component


A man in his 60s had trouble remembering things, had poor brain function, and had problems with his nerves and eyes. He had diabetes, but his blood sugar was well controlled. He also had trouble with his bladder, blood pressure, and hearing. Doctors thought it might be a rare nerve or brain problem, so they checked his genes. They found a gene mutation in WFS1 that has been seen before in a person with Wolfram syndrome — a rare condition that causes memory loss, eye problems, and nerve issues. The test also found missing pieces in his energy-producing parts of the cells, which supports this diagnosis. Even though he had a normal diet, he was missing thiamine (a vitamin), which likely hurt his brain and nerves. Treatment for the vitamin didn’t help much. The doctors now believe he has Wolfram syndrome, and this explains most of his problems.


A 61-year-old man with diabetes, memory problems, brain and nerve damage, and vision issues was initially diagnosed with a condition called multiple system atrophy. However, further testing showed that he had multiple problems in his mitochondria — the energy-producing parts of cells — and a severe lack of thiamine (a vitamin needed for brain function), even though he had a normal diet and no alcohol use. Tests found several mutations in his mitochondrial DNA, and while some genetic tests were negative, targeted exome sequencing revealed a specific mutation in the WFS1 gene. This mutation has been seen before in people with Wolfram syndrome, a rare disorder that affects the brain, eyes, pancreas, and nerves. The patient’s symptoms — including memory loss, vision problems, nerve damage, and diabetes — match what is seen in Wolfram syndrome. Although thiamine treatment had little effect, the genetic finding confirms the diagnosis. The patient now has a clear explanation for his condition and is being managed accordingly.


{
    "proficient_health_literacy": "A 61-year-old man with a history of diabetes mellitus (DM), autonomic neuropathy, diffuse brain atrophy, optic nerve atrophy (OA), and severe amnestic syndrome was referred for neurologic evaluation. Initially diagnosed with multiple system atrophy-cerebellar type (MSAc) based on MRI findings of severe cerebellar and brainstem atrophy, the clinical picture raised significant diagnostic concerns due to the absence of cerebellar motor signs and the prominent, progressive anterograde amnesia. The patient's early history included childhood bedwetting and urinary urgency in early adulthood, followed by bladder dysfunction requiring intermittent catheterization and erectile dysfunction in his 20s. At age 33, he was diagnosed with type 1 diabetes, with a random C-peptide level of 0.6 ng/mL (reference range 0.9–4.3 ng/mL) at a blood glucose of 83 mg/dL, indicating significant insulin deficiency. Despite good long-term glycemic control (HbA1c 6.5–7.2%), he had no evidence of microvascular or macrovascular complications, and polyuria/polydipsia resolved with insulin therapy.\n\nIn his 30s, he began wearing unusual clothing, later diagnosed with color blindness. At age 53, ophthalmologic examination revealed bilateral optic atrophy with preserved vision, and brain MRI demonstrated severe atrophy of the cerebellar hemispheres, vermis, pons, and middle cerebellar peduncles, along with moderate cerebral atrophy—findings that worsened at age 61 with more pronounced cerebral atrophy. Notably, he reported no gait instability or upper extremity incoordination, which is inconsistent with typical cerebellar atrophy.\n\nNeuropsychological assessment revealed profound anterograde amnesia, with additional deficits in cognitive flexibility, executive function, naming, and high-order visual processing. Attention, mental tracking, verbal abstract reasoning, complex auditory instructions, and visual spatial functions remained intact. Psychiatric evaluation identified depression, which responded to sertraline. Concurrently, progressive autonomic neuropathy developed, manifesting as gastroparesis and severe postural hypotension—exceeding the expected severity given his well-controlled diabetes and absence of diabetic complications. Bladder dysfunction progressed to the need for suprapubic catheterization at age 6


A 35-year-old housewife had sudden paralysis in her legs and trouble controlling her bladder after giving birth. She had back pain and couldn’t feel her legs properly, even though she was otherwise fine. Doctors found a growth outside her spine (in the middle back) that was pressing on her spinal cord. This growth, called an angiolipoma, was removed with surgery. The surgery worked well, and she recovered fully.


A 35-year-old housewife developed sudden paralysis in her lower limbs and loss of bladder control one month after giving birth. She also had back pain. Upon examination, she had no weakness or reflex issues in her upper body, but her lower limbs showed no muscle strength, stiff muscles, overactive reflexes, and a positive Babinski sign. Sensory tests showed she lost feeling below the umbilicus, and there was tenderness in the middle back. Blood tests were normal. An MRI scan revealed a tumor outside the spinal cord, between the fifth and eighth thoracic vertebrae (D5 to D8), pressing on the spinal cord. The tumor appeared similar to fat on imaging and showed signs of being made of blood vessels and fat (angiolipoma). It was surgically removed through a back approach with no major complications. The surgery was successful, and the patient recovered well. The diagnosis was confirmed through tissue testing after surgery.


{
    "proficient_health_literacy": "A 35-year-old female presented to the emergency department with a sudden onset of bilateral lower limb paralysis lasting one month following vaginal delivery. The onset was acute and was accompanied by severe back pain and complete loss of sphincteric control, including urinary incontinence. On clinical examination, the patient was otherwise generally well with normal vital signs and a Glasgow Coma Scale (GCS) of 15/15. Cranial nerve function was intact, and upper limb motor strength, tone, and reflexes were normal, with preserved sensation to all modalities. In contrast, lower limb motor examination revealed complete paralysis (motor power grade 0), hypertonia, hyperreflexia (grade 4), and a positive Babinski sign, indicating upper motor neuron pathology. Sensory assessment demonstrated impaired vibration and position sense extending to the level of the umbilicus, consistent with a sensory level at T10. Mid-dorsal tenderness was noted, particularly at the D5–D8 region.\n\nHematological investigations were unremarkable, excluding hematologic causes of spinal cord compression. A dorsal lumbar MRI was performed, revealing a T1-weighted extradural hyperintense lesion extending from D5 to D8, posteriorly compressing the spinal cord. On T2-weighted imaging, the lesion exhibited hyperintensity relative to the spinal cord and was nearly isointense with normal adipose tissue, suggesting a lipid-rich composition. The lesion demonstrated characteristic myelopathic changes in the surrounding cord, consistent with acute compressive injury. Contrast-enhanced MRI showed focal, slightly inhomogeneous contrast uptake, indicating partial vascular permeability and possible active angiogenesis within the lesion.\n\nThe diagnosis was confirmed as a thoracic spinal extradural angiolipoma, a rare benign neoplasm composed of adipocytes and blood vessels, typically arising in the extradural space of the spinal column. Surgical intervention was performed via a posterior approach, involving dorsal decompressive laminectomy and complete resection of the lesion. The procedure was uncomplicated, with no intraoperative complications. The resected specimen was sent for histopathological analysis, which confirmed the presence of mature adipocytes, vascular channels, and a well-differentiated angiolipomatous tissue consistent with a benign angiolipoma. Postoperative recovery was excellent, with full restoration of motor and sensory function and resolution of sphincter dysfunction, indicating successful decompression and complete removal of the


A 46-year-old man got very sick with fever, cough, and chest tightness. Doctors tested his lung fluid and did a lung scan to find out if it was COVID-19. The test came back positive. He got medicine to fight the virus, like interferon and ribavirin, and other medicines to calm his body, clear mucus, protect his liver, and stop his lungs from scarring. He used a machine that gives him extra oxygen through his nose and mouth to help breathe easier. His breathing got better over time, his lungs healed, and he was finally able to go home. He fully recovered.


A 46-year-old man was hospitalized with severe symptoms of fever, cough, and chest tightness that had lasted for about 11 days. He had recently traveled to several cities in China and had been in close contact with someone from Wuhan. Tests showed he had severe pneumonia, and although initial tests did not find the virus, a later test on his lung fluid (BALF) confirmed he had SARS-CoV-2 infection. To treat the virus, he received a combination of antiviral medications, including interferonalfa-1b and ribavirin, as well as lopinavir and ritonavir at different stages of his illness. He also got medicines to reduce inflammation, protect his liver, clear mucus, and support healthy gut bacteria. Because he was having trouble breathing, he was given oxygen through a BIPAP machine and later switched to high-flow humidified oxygen. His oxygen levels improved over time, and by early February, his symptoms had greatly improved. CT scans showed that the pneumonia was getting better. He was diagnosed with a mild liver issue possibly caused by the virus, and received treatment to protect his liver. To prevent long-term lung damage, he took a medication to support lung healing. By February 12, his lungs showed clear signs of recovery, and he was discharged from the hospital fully recovered.


{
    "proficient_health_literacy": "A 46-year-old male from Yili Development Zone, Xinjiang, China, was admitted to the University of Hong Kong-Shenzhen Hospital on 19 January 2020 with an 11-day history of fever (38 °C), dry cough, muscle ache, and fatigue. He reported close contact with an individual from Wuhan on 10 January and traveled from Yili to Shanghai (16 January), Shanghai to Ningbo (17 January), and Ningbo to Shenzhen (19 January), with no exposure to Wuhan. On 18 January, symptoms progressed to chest tightness without chest pain or hemoptysis. Initial testing excluded influenza A/B, respiratory syncytial virus (RSV), Mycoplasma pneumoniae, Cryptococcus haemolyticus, Aspergillus, Epstein-Barr virus (EBV) IgM and DNA, and Cytomegalovirus (CMV) DNA/antigen. Blood gas analysis on admission revealed a pH of 7.445, PaCO₂ of 4.72 kPa, and PaO₂ of 7.82 kPa, indicating hypoxemia. The patient was isolated in a single ward and initially treated with levofloxacin for suspected bacterial pneumonia. On 22 January, BALF testing was negative for Aspergillus, Legionella, Pneumocystis carinii, acid-fast bacilli, and Mycobacterium tuberculosis, leading to a diagnosis of severe bilateral community-acquired pneumonia (not excluding COVID-19) with hypoxemia. Levofloxacin was discontinued and replaced with a combination of amoxicillin-clavulanate and doxycycline for broad-spectrum coverage. On 23 January, the patient was transferred to the Third People’s Hospital of Shenzhen for further management. He had no comorbidities, allergies, or gastrointestinal or renal abnormalities.\n\nDuring hospitalization, the patient received a multimodal therapeutic regimen. Interferon-alpha-1b (60 μg via inhalation, administered twice daily) was used for antiviral activity against RNA viruses. Bio-Three tablets (0.4 g orally, three times daily) and Bifid-triple viable capsules (420 mg, three times daily) were administered to modulate intestinal microbiota. Mucosolvan (


A 60-year-old woman from Eritrea had a lump coming out of her left eye for 3 months, and her vision in that eye got worse. When doctors checked her, her left eye was bulging out a lot, her vision was very poor, and the back of her eye was swollen. Blood tests were normal, and a scan showed a fluid-filled cyst in her eye socket, which looked like a hydatid cyst. She took medicine for 2 weeks to help shrink it. Then, the doctors cut into her eye socket to remove the cyst. During surgery, the cyst broke and clear fluid came out, and the lining was taken out carefully. The tissue was tested and confirmed it was a hydatid cyst. After surgery, she had some swelling and trouble moving her eye slightly, but these improved over a week. Her vision and eye swelling got better. However, she moved back to Eritrea and we couldn’t check on her after that.


A 60-year-old Eritrean woman had a 3-month history of painless swelling in her left eye, along with slowly worsening vision. On exam, her left eye was noticeably bulging, her vision was very poor, and there was swelling in the back of the eye (papilledema). Blood tests were normal, and a CT scan showed a fluid-filled cyst in her orbital area, which is typical of a hydatid cyst. She was treated with two weeks of oral albendazole, a medication that helps fight the cyst. After that, she had surgery where the cyst was removed through an incision in the eye socket. During surgery, the cyst ruptured and was carefully removed, and the tissue was sent for testing. The biopsy confirmed it was a hydatid cyst. After surgery, she had mild swelling of the eyelid and some difficulty moving her eye inward (adduction), but these improved over time. Her vision and eye swelling also improved. However, she moved back to Eritrea and we were unable to monitor her condition further.


{
    "proficient_health_literacy": "A 60-year-old female sheep herder from Eritrea presented to the St. Paul’s Hospital Millennium Medical College ophthalmology department with a three-month history of painless left eye proptosis accompanied by progressive decline in left eye visual acuity. Right eye visual acuity was 6/18, while left eye acuity was reduced to counting fingers at the front of the eye. Physical examination demonstrated a 4 mm exophthalmometric discrepancy between the eyes, with a proptosis measurement of 21 mm on the left side. Fundus examination revealed a tortuous temporal arcade and grade 4 papilledema in the left eye, indicating significant intracranial pressure due to optic nerve compression. Laboratory investigations, including a complete blood count, were within normal limits. A computed tomography (CT) scan of the brain and orbit demonstrated a well-defined, thin-walled, non-enhancing cystic lesion measuring 2.6 cm × 2.0 cm × 1.9 cm located in the left orbital cavity, exhibiting compression and lateral displacement of the globe and stretching of the optic nerve. The left medial rectus muscle was not distinctly delineated from the lesion, suggesting intimate adhesion. No osseous lytic or sclerotic changes were observed in the bony orbit, further supporting a non-invasive, soft-tissue origin. The imaging findings were consistent with a hydatid cyst of the orbit, a parasitic infection caused by *Echinococcus granulosus*. Abdominal ultrasound and chest X-ray were unremarkable, excluding extra-orbital hydatid disease or pulmonary involvement.\n\nThe patient was initiated on oral albendazole 400 mg twice daily for two weeks, a standard antihelminthic regimen targeting the larval stage of *Echinococcus*, with the goal of reducing cyst viability and preventing further growth. Following this medical phase, she underwent anterior medial orbitotomy for surgical excision of the cystic mass. Intraoperatively, a cystic lesion attached to the inferior aspect of the medial rectus muscle was identified. During manipulation, the cyst ruptured, releasing a clear fluid. The cyst wall, described as paper-white and laminated, was removed in piecemeal fashion, with careful preservation of the medial rectus muscle to avoid functional compromise. The external capsule was excised with meticulous dissection to prevent irreversible damage to the extraocular


A 43-year-old man from Asia had cancer in his penis that had been growing for 3 years. The cancer spread to his right eye, where it damaged the inside of the eye and made him lose his vision. Doctors saw signs of cancer in the eye using scans — the cancer looked bright on one type of scan and dark on another. Because the eye pain was severe and vision couldn't be saved, they removed the entire right eye. After checking the tissue from the eye, they found it was cancer that started in the penis and had spread to the eye. This cancer was not very aggressive but still dangerous. The man got treatment with chemo and radiation, but later the cancer spread to his brain and he passed away.


A 43-year-old Asian man with a 3-year history of penile cancer developed cancer that spread to his right eye. He had been diagnosed with advanced cancer (stage T4N3M1) and had already lost vision in his right eye more than a month before. Imaging tests showed that the cancer had spread to the inside of his right eye, including the retina, optic nerve, and surrounding structures. On MRI, the tumor appeared bright on T1-weighted images and dark on T2-weighted images, which are signs of metastatic cancer. After removing the affected eye (enucleation) due to severe pain and no chance of recovery, pathologist tests confirmed it was metastatic, moderately differentiated penile squamous cell carcinoma. The cancer had spread into the eye's layers, including the sclera, choroid, and retina. He received chemotherapy and radiation for six months, but eventually died from brain metastasis.


{
    "proficient_health_literacy": "A 43-year-old Asian male with a three-year history of progressively invasive penile carcinoma (PC) presented on January 31, 2015, with acute pain in the right eye and irreversible vision loss, with best-corrected visual acuity of no light perception in the right eye and 20/20 in the left eye. The patient was previously staged as T4N3M1 according to the TNM classification, indicating advanced local invasion (T4), regional lymph node involvement (N3), and distant metastasis (M1). Prior to ocular metastasis, he had developed bilateral inguinal lymph node and ipsilateral iliac node metastases, followed by systemic dissemination to the liver and lungs. His medical history included multiple prior surgical interventions, with no reported family history of hereditary disorders or psychiatric conditions.\n\nOphthalmological examination revealed mild proptosis and intact ocular motility in all directions. The right eye demonstrated a dilated pupil (5 mm) with absent pupillary reflex, and fundus examination showed post-equatorial retinal detachment with a black eminence and a pale optic disc. B-scan ultrasonography confirmed retinal detachment with intraretinal hemorrhage. Orbital magnetic resonance imaging (MRI) demonstrated thickening and structural strengthening of the right lateral orbital wall, consistent with metastatic tumor infiltration. The internal rectus and lateral rectus muscles were also thickened and hardened, with a 2-cm-long optic nerve exhibiting significant thickening and invasion at its stump. MRI sequences revealed hyperintensity on T1-weighted imaging and hypointensity on T2-weighted imaging, indicative of tumor-associated signal characteristics. Contrast-enhanced MRI showed inhomogeneous enhancement of the posterior orbital wall, supporting active tumor vascularity and cellular infiltration. Histopathological evidence confirmed invasion of the optic nerve, choroid, sclera, retina, and external intraocular structures by metastatic cells.\n\nIntraoperative evaluation of the enucleated right eye revealed complete tumor involvement of the globe. Histopathological analysis, performed using hematoxylin-and-eosin (H&E) staining, identified keratin pearls and sheets of keratinized squamous carcinoma cells with intercellular bridges, consistent with moderately differentiated penile squamous cell carcinoma. The tumor demonstrated infiltrative growth patterns, with extensive spread into the deep layers of the eye, including the choroid, which is a


A 33-year-old man had belly pain and vomiting. Doctors found a 45-mm lump in his small intestine (ileum) that had some calcium inside it. The lump wasn’t blocking or twisting, so they didn’t think it was an emergency. After checking it with a scan, they knew it was a tumor. They did a small surgery through just one spot on his belly to remove part of the small intestine. The tumor looked like a soft, white growth with lots of thick, stiff tissue and tiny calcium spots. It had some immune cells inside. Tests showed that a certain protein (factor XIIIa) was present, but other tumor markers were missing. This pattern matched a type of rare tumor called CFT. The man got better after the surgery and hasn’t had any problems in 6 months. No signs of it coming back.


A 33-year-old man came in with abdominal pain and vomiting. His physical exam showed lower abdominal tenderness, but blood tests and imaging like ultrasound and X-ray were normal. A CT scan found a 45-mm mass in the ileum (a part of the small intestine) with some calcification, but no signs of blockage or twisting. The tumor was suspected, and after further testing with MRI, doctors considered several possibilities, including a gastrointestinal stromal tumor (GIST), a chronic hematoma, a leiomyoma, or a CFT (cystic fibrosis-related tumor — actually, in this case, a CFT refers to a specific type of tumor called IgG4-related fibrosis). The patient underwent laparoscopic surgery using a single small incision in the belly button. During the procedure, a white, pedunculated tumor was found in the ileum, and only that tumor was seen. A partial resection (removal) of the ileum was done, and the ends were reconnected. Pathology showed a tumor made up of spindle-shaped cells, dense collagen, and scattered calcifications, with some lymphoplasmacytic cells present. Key test results showed that factor XIIIa was positive, while other markers for common tumors were negative. Over 40% of the immune cells in the tumor were IgG4 positive, which is a key sign of CFT. Based on these findings, the tumor was finally diagnosed as a CFT. The patient recovered well, was discharged on day 7, and has had no signs of recurrence in the 6 months since surgery.


{
    "proficient_health_literacy": "A 33-year-old man with no prior medical or surgical history presented with acute abdominal pain and vomiting. Physical examination revealed localized tenderness in the lower abdomen, while laboratory investigations were unremarkable: C-reactive protein at 0.16 mg/dL, white blood cell count of 9600 /μL, neutrophil percentage 91.3%, and lymphocyte count 5.4%. Initial imaging with ultrasonography and radiography failed to identify a source of pain. Contrast-enhanced computed tomography (CT) revealed a 45-mm-sized mass in the ileum with partial calcification, showing no signs of invagination, obstruction, or volvulus, and no other radiological findings suggestive of underlying pathology. The patient was clinically diagnosed with an ileal tumor, and his symptoms resolved spontaneously. Subsequently, magnetic resonance imaging (MRI) was performed to characterize the lesion, demonstrating hypointensity on both T1-weighted and T2-weighted images, with isointense enhancement on gadolinium-enhanced T1WI, which supported a differential diagnosis including gastrointestinal stromal tumor (GIST), chronic distending hematoma, leiomyoma, and carcinoid tumor of the gastrointestinal tract (CFT).\n\nLaparoscopic surgical intervention was performed for both diagnostic and therapeutic purposes using a single-port technique via a vertical 4-cm umbilical incision with EZ access and Lap Protector (Hakko Medical, Nagano, Japan), employing two 5-mm ports. Intraoperatively, a white-colored tumor was identified in the ileum at 100 cm from the terminal ileum. No additional tumors, lymph node metastases, or evidence of systemic dissemination were detected in the abdominal cavity. The tumor was extracorporeally retrieved and a partial resection of the ileum was carried out, followed by a functional end-to-end anastomosis. Macroscopically, the tumor was pedunculated and located on the antimesenteric side. Microscopically, it extended from the muscularis propria to the subserosa, exhibiting a hypocellular architecture composed of spindle cells embedded in dense hyalinized collagen with interspersed calcification and focal infiltration of lymphoplasmacytic cells. Immunohistochemical analysis showed negative or nearly negative staining for CD34, c-kit, DOG-1, desmin, S100


A 24-year-old man from Somalia had a fever, headache, stomach pain, nausea, vomiting, and lost weight over two months. He had been treated before with medicine and a blood transfusion, but it didn’t help. When he came to the hospital, he looked very weak and pale, and his belly was swollen. His blood tests showed very low red blood cells, white blood cells, and platelets — this means his body wasn’t making enough blood cells. The test for malaria was positive, but after three days of anti-malarial medicine, his symptoms didn’t go away and his belly got worse. Other tests ruled out HIV, hepatitis, and infections like Brucella or Leishmania. Blood and bone marrow checks showed no infection or cancer. A small piece of the spleen was taken and tested — it confirmed the cause was visceral leishmaniasis. He was given a special medicine mix (sodium stibogluconate and paromomycin) for 17 days. After a few weeks, his symptoms got better, and by the end, he was fully back to normal. A second test of his spleen showed no more signs of the disease, and he was sent home.


A 24-year-old man from a rural area in Somalia, who recently moved from Yemen, came to the hospital with a two-month history of fever, headache, abdominal pain, nausea, vomiting, and weight loss. He had previously been treated at a local clinic with antibiotics, fever-reducers, and a blood transfusion, which gave only temporary relief. When he returned with worsening symptoms, he was found to be pale, weak, and had an enlarged spleen and liver. Blood tests showed low levels of red blood cells, white blood cells, and platelets (a condition called pancytopenia), and a rapid test for malaria was positive. However, after three days of anti-malarial treatment, his symptoms did not improve and his spleen continued to grow larger. Other tests for infections like HIV, hepatitis, and Brucella were negative, and blood and bone marrow exams showed no signs of infection or cancer. A biopsy of the spleen confirmed the diagnosis of visceral leishmaniasis, a serious parasitic infection. The patient was treated with a combination of sodium stibogluconate and paromomycin for 17 days. After four weeks, his symptoms improved significantly, and by the fifth week, he was fully recovered. A follow-up spleen biopsy showed normal results, and he was discharged.


{
    "proficient_health_literacy": "A 24-year-old male patient from Sa’ada, northwest Yemen, recently relocated to Burhakaba, Somalia, was referred to our hospital with a complaint of a left upper hypochondrial mass. He presented with a two-month history of high-grade fever, headache, abdominal pain, nausea, vomiting, anorexia, and progressive weight loss. He reported a prior episode of similar symptoms three months earlier. Prior to hospital admission, he had been evaluated at a local health facility where he received symptomatic management with antipyretics, broad-spectrum antibiotics, and two units of whole blood transfusion, resulting in transient clinical improvement. However, symptoms recurred two months later, now accompanied by generalized weakness and further weight loss.\n\nOn presentation, the patient exhibited signs of chronic illness: pallor, fever (temperature 38.9°C), tachycardia (pulse 110 beats/minute), and splenomegaly. Vital signs included blood pressure 110/78 mmHg, respiratory rate 16 breaths/minute, blood glucose 110 mg/dL. Laboratory findings revealed profound pancytopenia: white blood cell count of 1.03 × 10⁹/L (normal 4.00–10.00 × 10⁹/L), hemoglobin 6.6 g/dL (normal 12.0–16.0 g/dL), hematocrit 0.203 (normal 0.400–0.540), and platelet count 70 × 10⁹/L (normal 100–300 × 10⁹/L). Inflammatory markers were elevated: C-reactive protein 45.73 mg/L (normal 2.5–10 mg/L), with significant hepatocellular enzyme elevation—ast 104.5 U/L (normal 6–38 U/L) and alt 112.5 U/L (normal 6–40 U/L). Renal function parameters were mildly impaired: serum creatinine 1.4 mg/dL (normal 0.4–1.4 mg/dL) and serum urea 54.3 mg/dL (normal 10–50 mg/dL).\n\nA rapid diagnostic


A 34-year-old man felt short of breath when walking, had swelling in his legs, lost 50 pounds without trying, and was tired all the time. He had small spots in his lungs and fluid building up around his heart and lungs. Tests showed fluid pressing on his heart, which made it hard to pump blood. A drain was put in to remove the fluid, and after a while, the fluid came back and his heart stopped working properly. Doctors did an emergency surgery to open up the space around his heart to let the fluid go out. Later, scans showed the tissue around his heart was stiff and not moving right, which means his heart was being squeezed. Tests confirmed this was due to a disease called sarcoidosis, which causes small lumps in the lungs, lining of the lungs, and the sac around the heart. The surgery removed the stiff tissue, and the tissue tested showed small lumps, proving the disease was in the heart sac. Now he’s doing better, no more swelling, no shortness of breath, and he’s on medicine to keep it from coming back.


A 34-year-old man with a five-month history of shortness of breath when active, swelling in his legs, unexplained weight loss, and fatigue was evaluated. He had a cough and felt tired easily. Tests showed lung nodules, especially in the upper lungs, and fluid buildup in his lungs and around his heart. His heart was showing signs of pressure problems due to fluid around it, which led to a temporary drain being placed. After the drain was removed, the fluid returned and caused a serious heart condition called cardiogenic shock, requiring an emergency procedure to relieve the pressure. Imaging tests showed that the fluid around the heart was thickening and not moving normally, which is a sign of constrictive pericarditis. A procedure called pericardiectomy was done, and the tissue samples showed small, non-necrotizing granulomas, confirming that the condition was sarcoidosis affecting his lungs, pleura, and heart. He was started on steroids and later switched to a lower dose with methotrexate. Over time, his symptoms improved, his breathing got better, and his heart function returned to normal. Follow-up tests showed no ongoing issues and he was able to return to a stable condition.


{
    "proficient_health_literacy": "A 34-year-old Caucasian male presented with a five-month history of progressive exertional dyspnea, productive cough, lower extremity edema, unintentional 50-pound weight loss, fatigue, and early satiety. His medical history included controlled hypertension managed with hydrochlorothiazide and carvedilol, with recent initiation of furosemide for peripheral edema. He was a non-smoker with no recent travel or environmental exposures. Physical examination revealed diaphoresis, pallor, diminished cardiac sounds, markedly reduced breath sounds in the right thorax, and 2+ pitting edema of the lower extremities. Vital signs showed oxygen saturation of 92% on 2 L/min supplemental oxygen and mild tachycardia.\n\nPulmonary function testing revealed an intrinsic restrictive ventilatory defect: forced vital capacity (FVC) of 4.03 L (59% of predicted) and diffusion capacity of the lung for carbon monoxide (DLCO) of 23.3 mL/min/mmHg (55% of predicted). Arterial blood gas analysis demonstrated hypoxemia with a partial pressure of oxygen (PaO₂) of 60 mmHg. High-resolution chest computed tomography (HRCT) showed diffuse pulmonary nodules with upper lobe predominance and perilymphatic distribution, diffuse partially calcified mediastinal and hilar lymphadenopathy, moderate to large right pleural effusion, and moderate to large pericardial effusion with pericardial thickening.\n\nTransthoracic echocardiography revealed preserved left ventricular systolic function, a large circumferential pericardial effusion, and evidence of respiratory variation in mitral and tricuspid inflow, along with paradoxical septal shift—findings consistent with early tamponade physiology. The patient was admitted and underwent urgent pericardiocentesis, during which 500 mL of serosanguinous fluid was removed, resulting in immediate clinical improvement. The fluid was monocyte-dominant, culture-negative, and showed no evidence of infection or malignancy. The pericardial drain was removed after several days of minimal output.\n\nDiagnostic workup included thoracentesis, fiberoptic bronchoscopy with bronchoalveolar lavage (BAL), transbronchial biopsy, and endobronchial ultrasound-guided


A 62-year-old woman had high CA125 levels in her blood for a year. At first, doctors thought it was a harmless cyst called a chocolate cyst, but after checking with ultrasound and special imaging, they saw signs of a serious tumor. A test using contrast ultrasound showed the tumor had solid parts and blood flow, which made doctors think it might be cancer. The final test on the tumor tissue confirmed it was high-grade serous adenocarcinoma, a type of ovarian cancer. She had surgery to remove the tumor and then received chemotherapy, which worked well. Her CA125 levels went back to normal, and she is now doing well.


A 62-year-old woman had rising CA125 levels in her blood for one year, which raised concern for ovarian cancer. At a local hospital, her ultrasound showed a large mass in her pelvis, but the doctors initially thought it was a chocolate cyst—a common type of benign ovarian cyst. To get a clearer picture, she was referred to our hospital for further testing. Contrast CT and MRI scans showed a complex cystic mass in her right ovary, with features that could suggest either a benign or malignant condition. A transvaginal ultrasound combined with contrast-enhanced ultrasound (CEUS) revealed signs of a malignant tumor, leading doctors to suspect cystadenocarcinoma. After surgery, the tumor was found to be a high-grade serous adenocarcinoma, a type of aggressive ovarian cancer. Pathology confirmed the diagnosis, and the patient underwent chemotherapy with carboplatin and paclitaxel. Her CA125 levels dropped to normal after treatment, and she is now doing well with no signs of recurrence.


{
    "proficient_health_literacy": "A 62-year-old woman presented with a progressively rising serum CA125 level, initially elevated to 50 U/ml (normal < 35 U/ml) in November 2018, which increased to 75 U/ml by November 2019. Her serum CEA and CA19-9 levels remained within normal limits, and initial transvaginal ultrasound (TUS) revealed no obvious abnormalities. Subsequent TUS at the local hospital demonstrated a large pelvic mass, prompting referral to our institution for further evaluation. Laboratory investigations, including tumor markers, reproductive hormone assays, and routine blood work, were within normal ranges. The patient was asymptomatic, with no palpable abdominal mass on physical examination. A positive family history was noted, as her mother had died of ovarian cancer.\n\nAbdominal computed tomography (CT) revealed a well-circumscribed, hypodense mass in the right adnexa. Contrast-enhanced CT demonstrated mild enhancement of the lesion and a fluid–fluid level sign. Magnetic resonance imaging (MRI) showed a well-defined, lobulated, cystic mass measuring 4.9 × 4.8 cm in the right pelvic cavity. On T2-weighted imaging (T2WI) and T1-weighted imaging (T1WI), the mass exhibited mixed signal intensity, with nodular hypointensity observed on both sequences. Diffusion-weighted imaging (DWI) revealed severe hyperintensity, consistent with restricted diffusion, and a fluid–fluid level sign was present. Based on these imaging features, the lesion was initially suspected to represent a chocolate cyst (endometriotic cyst), a benign condition commonly associated with endometriosis.\n\nPreoperative TUS revealed a right adnexal mass measuring approximately 5.6 × 4.4 × 5.5 cm, characterized by a well-defined cystic structure with mural and septal nodules. The largest internal papillary excrescences measured 3.0 × 1.4 × 1.7 cm. Doppler ultrasound detected blood flow within the internal septations, cystic wall, and papillary projections, with a resistive index of 0.9—indicative of vascular resistance consistent with a neoplastic process. Given the presence of papillary structures and abnormal vascularity, a primary diagnosis of malignant neoplasm was established.\n\nTo further characterize


A 63-year-old woman had very bad kidney disease and couldn’t walk or move. She was confused for 5 days and had been on dialysis for months. She also had liver problems, high blood sugar, and a lung infection. A type of fungus called Candida guilliermondii was found in her blood and in the tube that goes into her vein. Even after changing her medicine, the fungus stayed in her blood. A small lump was found on her heart valve, but the family said no surgery because she had too many serious health problems. She was given medicine for the fungus, but it didn’t work. After 8 weeks, her condition got worse — the lump grew bigger and she had lung and spleen problems. She was given hospice care and sent home on a daily antifungal pill. She died a few weeks later from liver problems and being in a deep sleep.


A 63-year-old woman with end-stage kidney disease was admitted to the hospital after being confused for 5 days. She had been on dialysis since 2014 and had several serious health problems, including liver disease, tuberculosis-related lung issues, and an abnormal protein condition in her blood. She was permanently bedridden and did not use intravenous drugs. She was treated with dialysis through a catheter in her vein. Her first blood culture showed a type of fungus called Candida guilliermondii, and this fungus was found again in later blood tests and in the catheter tip, even after changing her antifungal medicine. A 1.2-cm mass was seen on her pulmonary valve, which is a sign of possible infection. Surgery was suggested, but the family refused due to her many health problems. She was given fluconazole as a long-term treatment, but she eventually died from liver-related confusion and coma.


{
    "proficient_health_literacy": "A 63-year-old woman with end-stage renal disease (ESRD) was admitted to the hospital on June 3, 2015, following a 5-day course of disorientation. She had been undergoing maintenance hemodialysis (HD) since December 2014, initially initiated due to acute on chronic kidney disease secondary to pneumonia. The patient also had a history of hepatitis B-related liver cirrhosis (Child-Pugh class B with hepatic encephalopathy), Mycobacterium tuberculosis-related pleuritis, and an IgGλ monoclonal gammopathy, which remained untreated due to her permanent bedridden status. Hemodialysis was administered via a tunneled-cuffed catheter placed in the right subclavian vein, first inserted on December 8, 2014. She denied active intravenous drug use. On physical examination, she exhibited drowsy consciousness and splenomegaly; no lung crackles or skin track marks were observed. Laboratory findings included a white blood cell count of 2.86 × 10³/uL, absolute neutrophil count of 2116/mm³, platelet count of 14,000/uL, total bilirubin of 3.54 mg/dL, C-reactive protein of 2.31 mg/dL, and serum glucose of 992 mg/dL, without evidence of metabolic acidosis. Given the hyperglycemic hyperosmolar state, blood cultures were obtained and empiric therapy with vancomycin and cefuroxime was initiated. The initial blood culture yielded Candida guilliermondii without concomitant bacterial growth. Intravenous fluconazole 200 mg once daily was administered. The tunneled-cuffed catheter was removed on June 30 due to persistent fungemia, and subsequent catheter tip culture confirmed C. guilliermondii. Blood cultures drawn on July 14 and August 10 and 28 remained positive for C. guilliermondii, even after switching from caspofungin to fluconazole on July 28. No positive cultures were detected in sputum or urine during the 8-week hospitalization period. Transthoracic echocardiography performed on July 20 and August 21 showed no vegetations or congenital val


A 46-year-old man with Malay background had pain in his belly and yellowing of his skin because of a tumor in his duodenum. The doctors found a big tumor and decided to remove it with surgery. Before surgery, he was at high risk because he had low blood, poor liver function, and blocked bile flow. During the surgery, a lot of bleeding happened, so they gave him many blood bags to stay alive. After surgery, he couldn’t make urine properly, which means his kidneys were not working well. So, they started a machine called CRRT right after the problem was found — within 24 hours — to help his kidneys. This machine ran for a few hours and helped his body start working again. His urine came back, his blood sugar went down, and the medicine for blood pressure was slowly stopped. By the sixth day after surgery, he was doing better and was able to leave the ICU. He was awake, breathing on his own, and no longer needed a tube in his nose or strong medicine to keep his blood pressure up.


A 46-year-old Malay man had abdominal pain and yellowing of the skin (jaundice) due to a tumor in the duodenum. Imaging showed large masses in the duodenum and near the bile duct, so surgery was planned. He was considered high risk before surgery because of anemia, jaundice, and poor liver function. During the operation, there was heavy bleeding (2500 cc) due to the size of the tumor, so he needed a large amount of blood transfusions.

After surgery, he developed low urine output, which is a sign of acute kidney injury (AKI). To help his kidneys, we started early continuous renal replacement therapy (CRRT) within 24 hours of diagnosing AKI, using a method called continuous veno-venous hemofiltration (CVVH). This treatment helped remove waste and excess fluid from his blood. After just a few hours, his urine output improved, and his blood pressure and blood sugar levels stabilized. His inflammation markers also dropped over time, showing that his body was healing.

The infection signs that appeared after surgery were managed with a stronger antibiotic. By the fourth day after surgery, his condition had improved enough that he was awake, able to breathe on his own, and was taken off the ventilator. He was discharged from the intensive care unit on the sixth day after surgery.


{
    "proficient_health_literacy": "A 46-year-old male of Malay ethnicity presented with persistent abdominal pain and obstructive jaundice, leading to referral to the digestive surgery service at Fatmawati Central General Hospital. Physical examination revealed abdominal distension and palpable hepatosplenomegaly. Abdominal contrast-enhanced computed tomography (CT) demonstrated lobulated masses involving the duodenum and ampulla of Vater, consistent with a stage IIIb duodenal neoplasm. Given the extent and location of the lesion, total pancreatectomy with splenectomy was performed, with the patient admitted to the intensive care unit (ICU) postoperatively.\n\nPreoperative assessment identified high surgical risk due to significant anemia, obstructive jaundice, and impaired liver function. Intraoperatively, extensive tumor resection resulted in massive hemorrhage of 2500 cc, necessitating substantial blood product transfusion. Upon ICU admission, the patient exhibited oliguria, prompting escalation of vasopressor support to 0.3 µg/kg/minute to maintain mean arterial pressure (MAP) above 65 mmHg and systolic blood pressure (SBP) above 95 mmHg. Laboratory findings included a lactate level of 5.8 mmol/L, C-reactive protein (CRP) of 30 mg/dL, white blood cell count of 26,700/μL, and procalcitonin >32 ng/mL, confirming the presence of systemic inflammatory response syndrome (SIRS) secondary to surgical trauma.\n\nTwelve hours postoperatively, the patient developed postoperative acute kidney injury (AKI), defined by urine output <0.3 cc/kg/hour, meeting KDIGO stage 2 criteria. Early continuous renal replacement therapy (CRRT) was initiated within 24 hours of AKI diagnosis. CRRT was performed via continuous veno-venous hemofiltration (CVVH) with an effluent dose of 27 cc/kg/hour and zero fluid removal. Within three hours of initiation, clinical improvement was observed, including an increase in urine output to 0.5–0.6 cc/kg/hour, allowing for rapid tapering of vasopressor support. Furosemide infusion was administered 18 hours after CVVH initiation, resulting in further improvement in urine output to 1–4 cc/kg


A 27-year-old man with AIDS had sudden belly pain for 4 days and fever for 2 days. He already had AIDS, pneumonia, and likely tuberculosis 2 months before. His immune system was very weak at first, with only 91 healthy immune cells in his blood. He got medicine for pneumonia and TB, and later started treatment for HIV. When doctors checked him, his belly hurt on the left side, but no skin rashes or other signs were seen. A scan showed a small spot on his spleen and swollen lymph nodes inside his belly. Tests found a fungus in his blood and bone marrow, which caused the infection. He got IV antifungal medicine first, but had kidney problems, so they switched to a safer version. After 21 days, he started taking itraconazole pills instead of IV medicine. He stayed in the hospital for 29 days and got better. After that, he went home and kept getting better at follow-up visits. No more symptoms or tests were needed.


A 27-year-old man with AIDS had sudden abdominal pain for 4 days and a fever for 2 days. He had been diagnosed with AIDS, pneumocystis pneumonia, and suspected tuberculosis two months earlier. His initial CD4 count was 91 cells/mm³. He received treatment for both infections and started anti-retroviral therapy later. On exam, he had tenderness in the left upper part of his abdomen but no skin rashes or other signs of illness. His CD4 count improved to 272 cells/mm³ (19%) during this visit. A CT scan showed a small lesion in the spleen and swollen lymph nodes in his abdomen. Tests showed a high level of a fungal marker (galactomannan), leading doctors to treat him with amphotericin B, which was later switched to a safer version due to kidney issues. Blood and bone marrow cultures confirmed the presence of T. marneffei, a rare fungus. After 21 days of IV treatment, he switched to oral itraconazole. He was discharged after 29 days and continued to improve at his follow-up visit. He remains healthy and symptom-free at 12 months after treatment.


{
    "proficient_health_literacy": "A 27-year-old Thai male with AIDS, originally from Mukdahan Province in Northeastern Thailand and residing in Saraburi Province (200 km south of Bangkok), presented with acute onset of left upper quadrant abdominal pain lasting 4 days and a fever of 2 days' duration, peaking at 38.9 °C. He had been diagnosed with AIDS 2 months prior at another hospital, with an initial CD4 count of 91 cells/mm³ (percentage and viral load unknown), and no comprehensive immune status evaluation was conducted. At that time, he presented with respiratory distress subsequently identified as pneumocystis pneumonia and presumptive smear-negative pulmonary tuberculosis. He received a 3-week course of trimethoprim/sulfamethoxazole and a standard anti-tuberculosis regimen consisting of isoniazid, rifampicin, pyrazinamide, and ethambutol during hospitalization. Anti-retroviral therapy (ART) comprising tenofovir disoproxil fumarate, emtricitabine, and efavirenz was initiated 2 weeks later as an outpatient. The anti-tuberculosis regimen was subsequently modified to isoniazid, rifampicin, ethambutol, and levofloxacin after 4 days, and chest radiographic follow-up demonstrated complete resolution of prior pulmonary opacities after 50 days of therapy. The patient maintained 100% adherence to both anti-tuberculosis treatment and ART, with no additional concomitant medications. His CD4 count 8 weeks prior to admission remained at 91 cells/mm³ (unknown percentage).\n\nOn presentation, abdominal pain was localized to the left upper quadrant, described as a dull ache without radiation to the chest, abdomen, or extremities, and was not associated with meals, physical activity, or changes in position. No gastrointestinal symptoms such as diarrhea, nausea, or vomiting were reported. Two days later, a high-grade fever developed without chills. Emergency department evaluation revealed a blood pressure of 120/75 mmHg, heart rate of 110 beats/min, temperature of 38.7 °C, and respiratory rate of 20 breaths/min. Physical examination showed a soft abdomen with normal bowel sounds, but significant tenderness in the left upper quadrant; the spleen was not palpable. No cutaneous lesions were observed on


A man with a fever got sick in November 2018. Doctors found a big lump on his right side of the chest, filling up the space where the lung should be. Tests showed the cancer was in the lining of the lung (pleura) and had spread there but not to other parts of the body. Because of this, they started treatment with three medicines: pembrolizumab, bevacizumab, and chemo. After 4 rounds, the cancer got a little smaller, and stayed under control for 5 months. But later, the man had a lung problem (pneumonia) that needed medicine to fix. When they tried the medicines again, the cancer came back and spread to many organs. He ended up getting very sick and passed away in October 2019.


A 51-year-old man with stage IIIB pleural mesothelioma received second-line treatment using pembrolizumab, bevacizumab, and chemotherapy after initially getting standard chemotherapy. His treatment was guided by genetic testing (second-generation sequencing) that showed specific mutations in his tumor. After four cycles, he had a partial response, meaning the cancer shrunk somewhat, and lived without disease progression for 5 months. Pembrolizumab was stopped because he developed grade 2 immune-related pneumonia, which improved with oral steroids. However, when immunotherapy was restarted and he was given anlotinib, the cancer progressed. He eventually developed multiorgan dysfunction and died suddenly in October 2019.


{
    "proficient_health_literacy": "A 51-year-old Asian male presented with a three-day history of fever in November 2018, prompting hospital admission. No significant past medical history was identified, including asbestosis, and no notable family history of malignancy was reported. Physical examination revealed diminished breath sounds on the right side, suggesting pleural involvement. Whole blood was obtained for next-generation sequencing (NGS) using a targeted gene panel (Yucebio, Shenzhen, China), which identified a TP53 splicing variant in exon 4 at a frequency of 6.44%, consistent with aberrant mRNA splicing leading to loss of tumor suppressor function. The tumor was classified as microsatellite stable (MSS) and exhibited a moderate tumor mutational burden (TMB) of 2.70 mutations per megabase (Mut/Mb), indicating a relatively high mutational load that may influence immunotherapy response. Due to patient refusal, no repeat biopsy was performed, and PD-L1 expression analysis was not conducted. Chest computed tomography (CT) demonstrated right pleural occupation with pleural effusion, and whole-body CT revealed diffuse involvement of the ipsilateral pleural surfaces, confirming localized pleural dissemination without evidence of distant metastasis. Based on these findings, the patient was initiated on second-line therapy comprising pembrolizumab (a PD-1 inhibitor), bevacizumab (an anti-VEGF monoclonal antibody), and standard chemotherapy regimen. After four cycles, a partial response was observed, with a progression-free survival of 5 months. Pembrolizumab was subsequently discontinued due to the development of grade 2 immune-related pneumonia, which was clinically managed with oral glucocorticoids and resolved without long-term sequelae. However, upon rechallenge with immunotherapy, disease progression was observed, followed by subsequent treatment with anlotinib (a multi-kinase inhibitor targeting VEGFR, PDGFR, and c-KIT), which failed to halt disease advancement. The patient ultimately experienced multiorgan dysfunction syndrome and died suddenly in October 2019. The case underscores the complexity of immunotherapy in mesothelioma, particularly in the absence of PD-L1 expression and biopsy confirmation, and highlights the role of tumor genomic features such as TP53 splicing variants and moderate TMB in guiding therapeutic decisions. Additionally, the observed immune-related adverse events and subsequent progression post-rechallenge suggest potential immune exhaustion or


A 43-year-old man got a deep cut on his left forehead and near his ear from a broken lawnmower blade. The cut was bleeding very badly and couldn't be stopped by pressure. His blood pressure was very low and his heart was racing. He lost consciousness quickly and needed a breathing tube. Doctors quickly started giving him blood. They cut open his neck to stop the bleeding by squeezing the outside neck artery (ECA) for 100 minutes. This stopped the massive bleeding. They also used a balloon to plug the wound. Later, a scan showed a metal piece from the blade stuck in his skull, and there were many broken bones on the left side. There was also bleeding inside his brain. The metal piece was removed. The maxillary artery was cut and tied off. After that, the neck artery was released and no more bleeding was seen. He got a lot of blood and plasma. He stayed in the hospital for 10 days. He woke up and could move his body, but his left face stayed paralyzed because the facial nerve was damaged. He also lost vision in his left eye because the optic nerve was badly hurt. The bleeding was stopped, but the damage to his face and eye is permanent.


A 43-year-old man suffered a severe injury to his left forehead and neck area when a broken grass-cutting blade pierced his skin. The wound caused a serious, non-compressible bleed from an artery, which is a life-threatening situation. His blood pressure was very low and his heart rate was extremely high, showing he was in serious danger. He quickly lost consciousness and needed emergency treatment, including intubation and blood transfusions.

Doctors used a tourniquet to temporarily stop the bleeding by squeezing the external carotid artery (ECA), which took 8 minutes from the time the emergency team activated to the start of the procedure. This helped stabilize him. The bleeding was controlled, and the patient was then taken for a CT scan of his brain and neck, which showed a metal piece from the blade, multiple skull fractures, and bleeding in the brain (subarachnoid and subdural hemorrhage), but no direct injury to major brain arteries.

After the scan, the patient returned to surgery. The metal object was removed, and the maxillary artery was completely cut and sealed. The ECA was then released and no active bleeding was found. The total time the tourniquet was applied was 100 minutes. The dura (the protective covering of the brain) was repaired, and a drain was placed.

He received several units of blood products, including red blood cells, plasma, and platelets. He stayed in the ICU for 10 days. After recovery, he had mild brain function issues, with good consciousness (GCS E4V5M6) and normal movement on one side, but he lost vision in his left eye due to damage to the optic nerve. He also has permanent facial paralysis on the left side because the facial nerve was damaged and reconnected to a nearby nerve. The injury was serious, but the team managed to save his life with timely intervention and staged surgery.


{
    "proficient_health_literacy": "A 43-year-old male presented with a severe penetrating injury to the left frontotemporal and preauricular region caused by a broken grass-cutting blade, resulting in a noncompressible, pulsatile arterial hemorrhage. Upon arrival at the trauma center, his vital signs were critically unstable: systolic blood pressure of 60–70 mmHg, tachycardia at 140 beats per minute, and oxygen saturation of 80%. Physical examination identified active arterial bleeding originating from the maxillary artery anterior to the mandibular neck. His neurological status rapidly deteriorated to E1V1M5, prompting immediate endotracheal intubation and initiation of group O red blood cell transfusion.\n\nThe trauma plus protocol was activated, and the patient was rapidly transported to the operating room. A longitudinal incision was made along the anterior margin of the left sternocleidomastoid muscle, with the posterior belly of the digastric muscle dissected to expose the carotid bifurcation. The left common facial vein was divided, and the left common carotid, external carotid (ECA), and internal carotid arteries were exposed and secured with vascular slings. Transient occlusion of the ECA was achieved using a Rumel tourniquet, which successfully controlled the massive arterial bleed. The interval between trauma protocol activation and ECA occlusion was 8 minutes. The preauricular wound tract was tamponaded with a balloon to stabilize the bleeding site.\n\nThe patient was then transferred for computed tomographic angiography (CTA) of the brain and neck, which revealed a metallic foreign body embedded in the left skull with multiple comminuted fractures involving the zygomatic process of the left temporal bone, lateral wall of the left orbit, left orbit apex, left superior orbital fissure, left optic canal, squamous part of the left temporal bone, sphenoid and ethmoid sinus walls, and the greater and lesser wings of the sphenoid bone. Imaging also demonstrated acute subarachnoid hemorrhage along the left Sylvian fissure and acute subdural hemorrhage on the frontotemporal convexity with associated brain swelling. Notably, no intracranial arterial injury was identified.\n\nFollowing CTA, the patient returned to the operating room for foreign body removal. A complete transection of the maxillary artery was identified