A 10-year-old boy from Ethiopia came to the hospital with sudden weakness in his legs and trouble controlling his bladder and bowels for 10 days. He had pain in his stomach area for a long time but no fever or injury. Tests showed his liver was damaged and had a very high level of a protein called AFP, which is a sign of liver cancer. A needle test from the liver and imaging showed tumors in his liver and that the cancer had spread to his spine. This means he had liver cancer with cancer in his spine. The doctors told his parents about the serious outcome, and they chose to go home and care for him at home instead of continuing treatment.


A 10-year-old Ethiopian boy arrived at a hospital in Addis Ababa with sudden weakness in his legs and loss of control over his bladder and bowels, which had been going on for 10 days. He also had long-standing pain in his upper abdomen. He did not have a fever, cough, or any recent injury. He had not been exposed to someone with a chronic cough. Because he was born before the national hepatitis B vaccine program started, he never received the hepatitis B vaccine. His temperature was slightly high, and his liver was enlarged and painful. Neurological tests showed that his spinal cord damage was at the level of T10, with no muscle strength in his legs and no reflexes. Blood tests showed elevated liver enzymes and a very high level of alpha-fetoprotein (AFP), which is a marker for liver cancer. Imaging scans showed multiple liver tumors and a collapsed vertebra with swelling around the spine, pressing on the spinal cord. The doctors suspected either tuberculosis or cancer spreading to the spine. Further tests found solid liver masses and involvement of the portal vein. The fine needle biopsy of the liver confirmed the presence of hepatocellular carcinoma (HCC) with spread to the spine. The family was given information about the serious prognosis and chose to stop treatment and go home for palliative care.


{
    "proficient_health_literacy": "A 10-year-old Ethiopian male presented to Tikur Anbessa Specialized Hospital, Addis Ababa, with a sudden onset of lower extremity weakness beginning 10 days prior, associated with urinary and fecal incontinence. He had a history of chronic epigastric pain. No fever, diarrhea, cough, altered mental status, abnormal movements, or trauma was reported. No exposure to individuals with chronic cough was documented. He had received all routine childhood vaccinations, including four doses of oral polio vaccine, but was not vaccinated against hepatitis B due to the timing of his birth—prior to the implementation of a routine three-dose hepatitis B vaccination schedule in Ethiopia (which began in 2015), leading to a delayed exposure window. The patient presented in 2016.\n\nPhysical examination revealed an axillary temperature of 38.0 °C and tachycardia (115 beats per minute). Hepatomegaly was noted, measuring 16 cm in total span (10 cm below the right costal margin), described as hard and tender. Neurological assessment demonstrated a sensory level at T10, bilateral lower extremity muscle power of 0/5, areflexia, and hypotonic anal tone.\n\nLaboratory findings included a normal complete blood count and erythrocyte sedimentation rate (25 mm/hr). Liver function tests showed elevated alanine aminotransferase (160 U/L) and aspartate aminotransferase (136 U/L), with markedly elevated alkaline phosphatase (761 U/L) and low serum albumin (3.4 mg/dL). Coagulation profile, renal function, serum electrolytes, blood and urine cultures, human immunodeficiency virus (HIV), and hepatitis C virus (HCV) serologies were all negative. Hepatitis B surface antigen (HBsAg) was positive, confirming active hepatitis B infection. Further serologic characterization of the hepatitis B viral state (e.g., HBV DNA load, HBeAg status) was not available due to limited diagnostic access.\n\nThoracolumbar magnetic resonance imaging (MRI) revealed collapse of the T9 vertebral body with abnormal marrow signal characteristics: T1 isointensity and T2 heterogeneous hyperintensity, indicating intravertebral pathology. Extensive epidural and par


A 28-year-old man with no prior health problems started having bad headaches and neck pain 2 months ago after lifting a heavy object. His symptoms got worse after a neck therapy session at a chiropractor he didn’t know was not trained properly. He began acting strangely and felt sick, with nausea and vomiting. When he finally went to the hospital, a brain scan showed blood buildup (SDH) on both sides of his brain. He had surgery to drain the blood, and right after, his headaches and neck pain went away. A follow-up scan 8 months later showed no blood left and no return of symptoms. He’s now fully better and back to normal.


A 28-year-old healthy man developed severe headaches and neck pain about 2 months ago after lifting a heavy object. His symptoms worsened after visiting a chiropractor for neck pain. He then started experiencing nausea, vomiting, and behavioral changes over the past two days. He went to the emergency department, where a brain CT scan showed bilateral subdural hematomas (SDHs) — collections of blood between the brain and the tissues covering it. He had no history of trauma, seizures, bleeding disorders, or drug use. After surgery, which involved small incisions in the skull to drain the blood, his symptoms improved quickly. The surgery was successful with no complications. A follow-up brain CT scan eight months later showed no remaining blood or signs of recurrence. He has been fully recovered and is back to normal without any ongoing symptoms.


{
    "proficient_health_literacy": "A 28-year-old fit male soldier presented to the Emergency Department with a chronic history of severe headache, neck pain, nausea, and vomiting, accompanied by behavioral changes over the past two days. The headache and neck pain began two months prior following the lifting of a heavy object, with progressive worsening of symptoms. Prior to this episode, he had visited the ED twice, during which cervical spine X-rays were performed without brain imaging; he was discharged on analgesics and referred for outpatient follow-up, with no improvement in symptoms. Subsequently, he received a neck therapy session from an uncertified chiropractor, after which his headache and neurological symptoms significantly exacerbated. The headache became refractory and unbearable, prompting further evaluation with brain computerized tomography (CT), which revealed bilateral subdural hematomas (SDHs). There was no history of traumatic brain injury, loss of consciousness, seizures, or systemic conditions such as hematological disorders, coagulopathies, or bleeding tendencies. The patient denied smoking, alcohol, or illicit drug use, and had a negative family history of intracranial aneurysms or inherited bleeding disorders. Physical examination revealed stable vital signs, normal temperature, and alertness with orientation, though the patient exhibited signs of depression and agitation. A notable neurological finding was the onset of bilateral, involuntary, repetitive extension movements involving the little fingers, which began two days prior to presentation. The remainder of the neurological examination was unremarkable. All routine laboratory investigations, including complete blood count, coagulation profile (Factor VIII and XIII, vWF cofactor and antigen), and blood smear, were within normal limits. Advanced imaging studies—computed tomography angiography (CTA), magnetic resonance angiography (MRA), and whole-spine magnetic resonance imaging (MRI)—were performed to exclude underlying vascular pathology, arteriovenous malformations, or spinal cord compression, but no identifiable etiology was found. The patient underwent bilateral mini-craniotomies with placement of bilateral subdural drains for evacuation of the hematomas. Histopathological examination of the external membrane of the SDH demonstrated typical features consistent with subdural hematoma formation, including fibrin deposition, erythrocyte clots, and organized fibrous tissue, confirming the diagnosis. The surgical procedure was successful with no intraoperative complications or significant bleeding. Clinical symptoms improved immediately postoperatively. During hospitalization, additional hemostatic workup was completed and


A 14-year-old boy got hurt when a baseball hit his right middle finger. At first, he wore a splint, but didn’t go back for check-ups. Five months later, his finger still hurt and couldn’t move well. Doctors saw that a piece of bone and cartilage was missing from the joint, and it was misaligned. They fixed it with surgery. A small hole was made in the finger’s joint, and a piece of bone and cartilage taken from the boy’s knee was put in the hole and pressed in place. The knee piece was taken from a part that doesn’t carry weight, so it didn’t hurt. After surgery, he started moving his finger right away and used a tape to help it heal. After 3 months, he stopped using the tape and went back to playing baseball. One year later, his finger no longer hurt, moved freely from straight to bent, and the joint looked smooth on a scan. The knee where the piece came from is still healthy, and the finger is back to normal.


A 14-year-old boy injured his right middle finger with a baseball hit. Initially, he was treated with a splint, but he didn’t follow up properly. Five months later, he still had pain and trouble moving his finger. X-rays and a CT scan showed a bony and cartilage defect in the joint of the finger, which meant the fracture had not healed properly. This condition was diagnosed as a malunited intra-articular fracture of the PIP joint. The boy had surgery to fix it. A small piece of bone and cartilage (osteochondral plug) was taken from his left knee, where the joint doesn’t bear much weight, and inserted into the damaged area of the finger. The plug was pressed into place using a drill hole. After surgery, he wore a splint for one day and then started gentle finger exercises. He continued buddy taping for three months and gradually returned to playing baseball. One year later, he has no pain, can fully bend and straighten his finger, and the joint looks healthy on MRI. The bone has healed well, and there is no damage to the knee donor site. A small amount of finger misalignment still remains, but it has improved significantly.


{
    "proficient_health_literacy": "A 14-year-old right-handed male presented with persistent pain and restricted range of motion (ROM) in the right middle finger five months following a traumatic baseball impact. Initial management at the treating hospital included splint fixation for a fracture of the middle phalanx, but the patient discontinued follow-up care. Clinical examination at presentation revealed swelling and ulnar deviation of the proximal interphalangeal (PIP) joint at extension, with a limited ROM of 0° extension to 60° flexion. Radiographic evaluation—including posterior-anterior and lateral views—demonstrated a bony defect on the articular surface of the middle phalanx, with ulnar displacement of the digit. Lateral X-ray showed a depressed articular surface, and computed tomography (CT) confirmed a 5 × 6.5 × 2 mm bony defect localized to the PIP joint articular surface of the middle phalanx. Additional imaging revealed a 1 × 2 mm cartilage defect on the palmar aspect of the proximal phalanx articular surface. Based on these findings, a diagnosis of malunited intra-articular fracture of the PIP joint was established, prompting surgical intervention. A palmar incision was used to expose the PIP joint, and a columnar-shaped recipient hole was created at the site of the osteochondral lesion in the middle phalanx. A cylindrical autogenous osteochondral plug measuring 4.5 mm in diameter was harvested via the mosaicplasty autogenous osteochondral grafting system (Acufex, Smith & Nephew, Andover, MA, USA) from the upper lateral femoral condyle of the left knee—a non-weight-bearing site—using an obliquely angled cartilage surface aligned with the long axis to optimize insertion geometry. The osteochondral plug was press-fitted into the recipient site to achieve mechanical and biological integration. The proximal phalanx cartilage defect, measuring 1 × 2 mm, was left untreated due to its minimal size and lack of functional impact. Postoperatively, the patient underwent immediate splint fixation followed by early mobilization initiated the next day via buddy taping, which was maintained for up to three months. After removal of buddy taping, the patient gradually resumed athletic activity, including baseball. At one-year follow-up, the patient reported complete resolution of pain and restoration of PIP joint ROM to 0


A 65-year-old woman came to the emergency room with severe belly pain, nausea, and vomiting. She had a history of diabetes and prior belly problems. A scan showed a blockage in her small intestine, near the part called the jejunum, and enlarged lymph nodes in her pelvis. Doctors thought it could be cancer, scar tissue, or inflammation. Her condition got worse quickly, so they had to surgically remove part of her small intestine. After checking the tissue, doctors found cells that looked like cancer, especially T-cells that were growing fast and were all part of the same group. This matched a rare type of cancer called jejunal EATL. Five weeks later, she started having brain problems — her mind changed and she lost strength on her left face and arm. A brain scan showed a tumor in the right front part of her brain, with swelling around it. She had surgery to remove it, and the tissue tested confirmed the tumor was from the same type of cancer that had spread to her brain. This means the cancer started in her small intestine and spread to her brain.


A 65-year-old woman came to the emergency room with severe abdominal pain, nausea, and vomiting. She had a history of type 2 diabetes and previous intestinal problems. A CT scan showed a blockage in her small intestine, specifically in the jejunum, and enlarged lymph nodes in her pelvis. Doctors considered possible causes like a tumor, scar tissue, or inflammation.

Her condition quickly got worse, so she needed emergency surgery to remove part of her small intestine. Examining the removed tissue showed signs of both benign T-cells (which can happen in celiac disease) and abnormal lymphocytes with unusual features. These abnormal cells were positive for CD-3, had a high rate of cell growth (90% stained positive for Ki-67), and showed a clonal pattern in T-cell gene testing — all signs of a rare type of lymphoma called jejunal extranodal T-cell lymphoma (EATL).

Five weeks after diagnosis, she started having new neurological symptoms, including confusion and weakness on her left side. A brain MRI found a single abnormal area in the right front and parietal part of her brain, surrounded by swelling. She had surgery to remove this brain lesion, and the tissue sample confirmed it was metastatic EATL — meaning the cancer had spread from her intestine to her brain.


{
    "proficient_health_literacy": "A 65-year-old female presented to the emergency room with uncontrolled abdominal pain, nausea, and vomiting. Her medical history included Type 2 diabetes mellitus, a prior history of intestinal intussusception, and chronic moderate abdominal pain. Initial abdominal computed tomography (CT) scan revealed a small bowel obstruction with a transition point localized in the jejunal region, accompanied by mildly enlarged lymph nodes in the right pelvic region. The differential diagnosis considered small bowel neoplasm, postoperative adhesions, or a reactive intestinal inflammatory process, such as celiac disease. Histological examination of the resected jejunal segments demonstrated small intestinal mucosa with intraepithelial and mucosal infiltrates of benign CD3-positive T-cells, consistent with celiac sprue, suggesting a prior immune-mediated enteropathy. In addition, the tissue showed medium-sized infiltrating lymphocytes exhibiting pleomorphic nuclei and prominent nucleoli, indicative of a proliferative lymphoid process. Immunohistochemical staining revealed tumor cells positive for CD-3, with weak positivity for BCL-2, and negative staining for CD5, CD20, CD10, and cyclin-D1—findings that exclude B-cell lymphoma and support a T-cell origin. Ki-67 immunoreactivity demonstrated a markedly elevated proliferative index, with 90% of the lymphocytes showing positive staining, reflecting a high rate of cell division and aggressive biological behavior. Polymerase chain reaction (PCR) analysis of the T-cell receptor-gamma (TCRγ) gene revealed clonal rearrangement, confirming the presence of a monoclonal population of T-cells, a hallmark of malignancy in T-cell lymphoproliferative disorders. The integrated morphological and immunophenotypic profile of the jejunal lesion is consistent with extranodal T-cell lymphoma, enteropathy type (EATL), specifically involving the small intestine. Systemic workup, including blood chemistry, imaging, and serologic markers, was non-contributory, supporting the localization of the primary disease to the gastrointestinal tract. The patient was discharged and initiated chemotherapy for the primary EATL. Three weeks after diagnosis, a whole-body positron emission tomography-CT (PET-CT) scan of the skull to mid-thigh demonstrated no hypermetabolic lesions suggestive of active malignancy in the cranial base or neck, indicating a clinically quiescent systemic disease at that time. However, five


A 24-year-old woman has had muscle pain for many years, starting when she was 7. The pain comes and goes, used to happen every 1–2 years, but now happens up to four times a year. Each time, it starts with a sore throat, cough, or urinary tract infection. When the pain comes, her muscles hurt a lot, but it goes away quickly when she takes a medicine called prednisolone. She had her tonsils removed in 1992 because of frequent sore throats. No other health problems were found. This pattern — muscle pain starting with infections — has never been seen before in someone her age and with this frequency.


A 24-year-old Caucasian woman has had recurring muscle pain, especially in her legs, for over 18 years. The pain usually comes after infections like sore throats, coughs, or urinary tract infections, and has occurred up to four times a year in recent years. This pattern — frequent muscle inflammation triggered by infections — has not been seen before. When she had these episodes, her muscle enzymes (CK) were elevated, and the pain improved quickly with oral steroids. She had a tonsillectomy in 1992 due to repeated sore throats, but no other major health issues. Tests showed no evidence of common viruses like strep, flu, or EBV in active form, and no signs of immune deficiency. Muscle biopsies showed inflammation, especially from a type of white blood cell called CD4 lymphocytes, suggesting a specific immune reaction. Despite extensive testing, no clear cause was found, and the condition appears to be rare and unique to her case.


{
    "proficient_health_literacy": "A 24-year-old Caucasian female presented with a 17-year history of recurrent lower limb myositis, initially occurring every 1–2 years since age seven, with a marked increase in frequency to four episodes annually starting in 2005. Each episode was preceded by upper respiratory tract infections (e.g., sore throat, cough) and, more recently, by urinary tract infections (dysuria). During active attacks, serum creatine kinase (CK) levels ranged from 89 to 700 U/litre (normal <175 U/litre), reflecting muscle damage, and normalized between episodes. Oral prednisolone provided rapid symptomatic relief, indicating a reversible inflammatory myopathy. A tonsillectomy was performed in 1992 based on a history of recurrent sore throats and elevated antistreptolysin O (ASOT) titre, with no other significant medical or drug history.\n\nDuring a detailed investigation in September 2005, a myositis episode was preceded by a productive cough with green sputum. Physical examination revealed mild pharyngeal injection and tenderness in the calves and anterior compartment muscles. Muscle biopsy of the right tibialis anterior demonstrated mild fiber atrophy of uncertain clinical significance. Laboratory findings included elevated erythrocyte sedimentation rate (ESR: 39 mm/hour), leukocytosis (16.6 × 10⁹/litre), with neutrophilia (13.6 × 10⁹/litre, 81.9%) and monocytosis (1.06 × 10⁹/litre, 6.4%). All other laboratory parameters—including lymphocyte, eosinophil, basophil counts, CK, renal, and hepatic function—were within normal limits.\n\nSerological testing was negative for influenza A/B, respiratory syncytial virus (RSV), Mycoplasma pneumoniae, Chlamydia, Q fever, adenovirus, enterovirus, and ASOT. Epstein-Barr virus (EBV) serology showed positive EBNA IgG, VCA IgG, and VCA IgM, which may reflect either a false-positive VCA IgM, a recent primary EBV infection (within 3–12 months), or EBV reactivation. Convalescent serology performed five months later revealed


An 85-year-old woman who uses her left hand mostly had a lump on her thumb side of the hand that grew fast over six weeks. The lump was big, soft, and could move around — about 5 inches by 4 inches and covered the whole thumb area. Doctors first thought it might be cancer, but X-rays showed weak bones and damage near the thumb joint. A scan showed a fluid-filled sac near the joint. During surgery, they saw a lump with a neck that went into the thumb joint. Lab tests confirmed it was a ganglion cyst, a common type of fluid-filled bump. She recovered well and hasn’t had the lump come back.


An 85-year-old woman who uses her left hand mostly had a lump on the thumb side of her hand that grew quickly over six weeks. The lump was large, not painful, and could move around. It measured 5 by 4 centimeters and covered the entire thenar area. At first, doctors thought it might be a sarcoma, a type of cancer. X-rays showed weak bones and damage to the joint at the base of the thumb, along with a soft tissue swelling near a bone spur. MRI showed a cyst-like structure connected to the thumb joint, with signs of active joint inflammation. During surgery, the doctors saw a multilobulated lump that extended into the thumb joint. Lab tests confirmed it was a ganglion cyst, a common benign (non-cancerous) cyst that forms near joints. The patient recovered well after surgery and has not had any signs of the lump coming back.


An 85-year-old left hand-dominant female presented with a six-week history of a rapidly enlarging lump at the thenar eminence. Clinical examination identified a non-tender, large, lobulated, mobile swelling measuring 5 × 4 cm that involved the entire thenar region. Initial differential diagnosis included sarcoma due to the size, rapid growth, and location. Plain radiography demonstrated severe osteopenia with erosive changes at the first carpometacarpal (CMC) joint, along with a soft tissue mass adjacent to a detached osteophyte originating from the base of the first metacarpal. Magnetic resonance imaging (MRI) revealed a septate, thin-walled, cystic lesion extending from the first CMC joint space, occurring against a background of diffuse active synovitis, suggesting chronic joint inflammation and possible mechanical irritation. In the operating theater, a multilobulated lesion with a well-defined neck extending into the first CMC joint was observed, consistent with a complex cystic structure. Histological evaluation of a 3.4 g specimen previously excised confirmed a ganglion cyst, specifically a thenar ganglion arising from the synovial membrane of the first CMC joint, with characteristic features including a cystic lumen, fibrous septa, and associated synovial proliferation. The lesion was fully resected with clear margins. Post-operative course was uncomplicated, with no evidence of recurrence at follow-up. The pathogenesis is likely attributable to mechanical stress and joint instability, leading to synovial cyst formation via fluid accumulation in the joint capsule and surrounding connective tissue, a process amplified by age-related degenerative joint changes and osteopenia. The presence of active synovitis on MRI supports the inflammatory component of the cystic lesion, which may contribute to its growth and expansion over time.


A 32-year-old woman had a lump in the area where the rectum and vagina meet for 9 years. It grew quickly in the last year, from 4 cm to 9.7 cm, and started causing problems like stool getting stuck. A doctor saw the lump with a special tube (endoscopy) and thought it might be a type of tumor or a fibroid. But when they tried to take a small piece of tissue from the lump with a needle (biopsy), they got too little tissue and also had bleeding from the vagina, so they couldn’t make a clear diagnosis. After talking with a team of doctors, they decided to try again using a better method: a needle guided by ultrasound to find the right spot. This time, they got enough tissue and found it was a rectal tumor called a GIST. The doctors recommended a drug called imatinib to shrink it first. After the tumor got smaller, they removed it through the back of the vagina. After surgery, they gave extra treatment to help prevent it from coming back. As of December 2019, the tumor hasn’t come back or spread anywhere.


A 32-year-old woman had a mass in the area between her rectum and vagina for 9 years. It didn’t grow much until the past year, when it enlarged from 4.0 cm to 9.7 cm and started causing symptoms like difficulty passing stool due to pressure. An endoscopy showed a growth under the rectal lining, but repeated biopsies only found inflammation, not actual tumor tissue — which didn’t match her symptoms. She came to our hospital for a clearer diagnosis.

Initial tests, including blood work and imaging, were normal. A CT scan and ultrasound showed a large, irregular mass in the rectovaginal space, which could be either a gastrointestinal stromal tumor (GIST) or an uterine fibroid growing outward.

A first biopsy was done using a needle through the abdomen, but it failed because the tissue collected was too small and the procedure caused vaginal bleeding, which stopped the biopsy early. Pathologists could not make a definite diagnosis from that sample.

After discussion among doctors from different specialties, a second biopsy was planned using a more precise method. This involved using ultrasound guidance — first with endoscopic ultrasound (ERUS) and then with contrast-enhanced ultrasound (CEUS) — to see exactly where the active, living parts of the tumor were, avoiding the dead (necrotic) areas. This helped ensure the needle would reach the right part of the tumor.

The second biopsy was done through the perineum (the area between the vagina and anus) under local anesthesia, with real-time ultrasound guidance. The doctors successfully collected tissue from the active part of the tumor. Pathology confirmed it was a rectal gastrointestinal stromal tumor (GIST).

The medical team recommended imatinib as the first-line treatment, which helped shrink the tumor. Once it was small enough, the tumor was removed through the back of the vagina. After surgery, additional treatment was given to reduce the risk of coming back. As of December 13, 2019, the patient has not had any recurrence or spread of the cancer.


{
    "proficient_health_literacy": "A 32-year-old female presented with a progressively enlarging mass in the rectovaginal space, initially detected during a routine examination 9 years prior. No significant growth was observed in annual follow-ups until a 12-month period of rapid expansion, during which the mass increased from a maximum diameter of 4.0 cm to 9.7 cm, resulting in symptomatic compression of the rectal lumen and the development of stool-related dents. Endoscopic evaluation at an external facility revealed a submucosal protrusion, yet repeated endoscopic biopsies over the preceding two years yielded only inflammatory findings—lacking definitive tumor tissue—contradicting the clinical suspicion of a neoplastic process. This discrepancy prompted referral to our institution for definitive diagnosis.\n\nThe patient had no significant comorbidities, no personal or familial history of malignancy, and preserved general health parameters, including normal mental status, appetite, sleep, weight, and absence of abdominal distension, tenesmus, rectal prolapse, diarrhea, or constipation. Digital rectal examination demonstrated a plump anterior rectal wall without tenderness or visible blood on the digit.\n\nLaboratory investigations, including complete blood count, coagulation profile, carcinoembryonic antigen (CEA), α-fetoprotein (AFP), carbohydrate antigen (CA) 19-9, and CA125, were within normal limits, excluding systemic malignancy or infection.\n\nContrast-enhanced computed tomography (CECT) revealed a heterogeneous mass within the rectovaginal space with central liquefaction necrosis (low-density region) and indistinct margins. Transabdominal ultrasound (US) identified a heterogeneous hypoechoic lesion measuring 9.7 cm in maximum diameter, consistent with either a rectal gastrointestinal stromal tumor (GIST) or an exophytic uterine fibroid.\n\nA transabdominal core needle biopsy (CNB) was performed using the MG1522 BARD MAGNUM Biopsy Instrument (16 G, 16 cm, disposable, Tempe, AZ, USA), with prior written informed consent obtained. Preoperative laboratory workup was unremarkable. However, spontaneous vaginal hemorrhage occurred during the procedure, terminating the biopsy prematurely. The retrieved tissue consisted of fragmented greyish material with a maximum diameter of less than 0.3 cm. Hist


A 68-year-old woman had pain in her left leg for 3 weeks. At first, she went to urgent care for redness and swelling on her shin, and was given antibiotics for a possible infection, but it didn’t get better. When she came to the emergency room, she wasn’t feverish and was stable. Her leg was still red, swollen, and painful, especially when walking. Tests showed her body was fighting an infection. A scan (ultrasound) found a hole in her bone and fluid moving back and forth through it, which means the bone is infected. Doctors diagnosed it as bone infection (osteomyelitis) and treated her with strong antibiotics and surgery to drain the pus from the soft tissue. The surgery helped, and she’s now getting antibiotics for 6 weeks to make sure the infection is fully gone.


A 68-year-old woman came to the emergency department with 3 weeks of increasing pain in her left lower leg. She first visited urgent care, where her left shin was red and swollen, and she was given antibiotics for a suspected skin infection (cellulitis) with ceftriaxone. The pain didn’t improve. At the emergency department, she was not feverish and her blood pressure was normal. Her left shin remained red, swollen, and tender, and the swelling stopped before reaching her knee. Blood tests showed high levels of inflammation. An ultrasound scan revealed a fluid collection near the bone, with a break in the bone surface and fluid flowing back and forth—this is a sign of bone infection. The imaging also showed a large fluid-filled area near the tibia, with connections to the inside of the bone. A CT scan confirmed a large abscess near the tibia, with signs of both skin and bone infection. She was diagnosed with osteomyelitis, an infection of the bone. She was started on strong antibiotics and had surgery to drain the abscess. No bacteria were found in the wound or blood samples. Her treatment continued with antibiotics for 6 weeks under the guidance of specialists.


{
    "proficient_health_literacy": "A 68-year-old female with a history of hypertension, hyperlipidemia, type 2 diabetes mellitus, gout, rheumatoid arthritis, and bilateral knee replacements—on clindamycin prophylaxis due to prior joint infections—presented to the emergency department with a three-week history of progressive left lower extremity pain. Initial evaluation at urgent care revealed erythema and swelling of the left shin, with plain radiographs showing no osseous abnormalities. She was empirically treated for cellulitis with intramuscular ceftriaxone for 10 days, but symptoms persisted without resolution. On presentation, she was afebrile and hemodynamically stable, with persistent erythema, swelling, and tenderness localized to the left pretibial soft tissues. The area of involvement extended distal to the knee joint, with no joint effusion or objective limitation in range of motion; pain was exacerbated by ambulation, though she maintained partial weight-bearing capacity. Repeat plain radiographs demonstrated focal soft tissue swelling overlying the anterior tibia. Point-of-care ultrasound, performed using orthogonal transverse and longitudinal scanning with a linear probe, revealed a large heterogeneous fluid collection adjacent to the tibial cortex. A focal defect in the cortical bone was identified, with pulsatile fluid communicating directly with the medullary cavity. Bidirectional flow of fluid was confirmed via color Doppler and pulsed-wave spectral Doppler, indicating active communication between the soft tissue collection and the intramedullary space. Laboratory findings included a normal white blood cell count (7.7 × 10³/μL), but markedly elevated systemic inflammatory markers: C-reactive protein (CRP) at 38 mg/dL and erythrocyte sedimentation rate (ESR) at 91 mm/hr. Computed tomography (CT) imaging revealed a 5.7 × 2.4 × 7.1 cm fluid collection adjacent to the tibial cortex, with well-defined sinus tracts extending into the medullary cavity, consistent with an abscess complicated by adjacent cellulitis and osteomyelitis. The patient was initiated on vancomycin and piperacillin/tazobactam, and orthopedic surgery was consulted. She was admitted to the internal medicine service and underwent incision and drainage of the left pretibial abscess. Neither wound nor blood cultures yielded growth. Infectious Diseases reviewed the


A 71-year-old man had knee surgery 18 months ago and started having bad knee pain a few weeks after. The surgery went well, but the pain got worse over time. Doctors checked and found no problems with the knee or infection. The pain was sharp, spread to his ankle, and made his knee feel tingly. He had trouble with touch and pain in his knee, but his leg strength was normal. After trying medicine and other treatments, the pain didn’t go away. A short test with a nerve block helped a little, but only for about a month. Then he tried a pain device called a spinal cord stimulator, which works by sending gentle signals to his nerves. The device was placed successfully and worked great. Right after, his pain stopped completely. Six months later, he still has no pain and no longer needs pain pills.


A 71-year-old man who had knee surgery 18 months ago now suffers from chronic left knee pain that worsened over time. After the surgery, he did well initially, but started having increasing pain around the third week after surgery. His knee was working properly, and there was no sign of infection or hardware problems. The pain was sharp, rated 7 out of 10, and spread to his ankle, with numbness or tingling in the same area. He also had increased sensitivity to touch (allodynia) and sharp pain from light touch (hyperesthesia) on the front of his knee. His strength was normal, and his wound was healing well. After trying physical therapy and several pain medications with little success, he had a temporary improvement with a sympathetic nerve block, lasting about a month. He then had a trial of a spinal cord stimulator (SCS), which successfully reduced his pain. He received two 16-contact leads with a Boston Scientific SCS system, which delivers different types of electrical stimulation to block pain signals. After the first follow-up, he reported complete relief from pain. At his 6-month check-up, his pain was still fully gone, and he was able to stop using opioid pain medication entirely.


{
    "proficient_health_literacy": "A 71-year-old Caucasian non-Hispanic male presented with chronic left knee pain persisting 18 months following total knee arthroplasty (TKA). His preoperative medical history included well-controlled hypertension, hyperlipidemia, and gastroesophageal reflux disease, with no significant comorbidities or prior surgical interventions. He measured 70 inches in height and weighed 215 lbs, with a normal body mass index (BMI) consistent with overweight status. He was retired, previously maintained an active lifestyle involving regular physical activity and daily functional mobility, and had no history of tobacco use; his social history included moderate social alcohol consumption. Post-TKA, he initially reported good recovery during the acute postoperative phase, but developed progressively worsening left knee pain beginning around the third postoperative week. The pain was described as sharp, with a visual analog scale (VAS) intensity of 7/10, poorly localized, radiating to the left ankle, and associated with paresthesias in a dermatomal distribution consistent with anterior lower extremity innervation. Physical examination revealed hyperesthesia and allodynia specifically along the anterior knee region, with intact motor function: lower left leg strength was 5/5 in both flexion and extension, and full strength (5/5) was observed in all lower extremity myotomes, including hip flexion, inversion, eversion, plantar flexion, and dorsiflexion. The surgical incision was well-healed, without signs of erythema, swelling, or tissue compromise. Orthopedic imaging and clinical assessment ruled out hardware loosening, infection, or mechanical joint pathology, supporting the exclusion of primary orthopedic causes of pain. Given the constellation of symptoms—including sensory hyperexcitability, allodynia, preserved motor function, and absence of structural or inflammatory joint pathology—a diagnosis of complex regional pain syndrome (CRPS) type I of the left lower extremity was established. Initial conservative management with physical therapy, non-steroidal anti-inflammatory drugs (NSAIDs), muscle relaxants, neuropathic agents (e.g., gabapentin, pregabalin), and low-dose opioids provided minimal to no symptomatic relief. A lumbar sympathetic block was performed, resulting in transient pain reduction to a VAS of 3/10, which lasted approximately one month, suggesting a sympathetic-mediated component to the pain pathway. This response prompted further intervention. The patient


A 46-year-old woman had a long-term thyroid problem where her body wasn’t making enough thyroid hormone. She was taking a medicine called levothyroxine every day to fix it. For years, her thyroid tests looked normal, so her doctor kept the dose the same. Eight years later, her test showed very high levels of a hormone called FT4, but she had no signs of being overactive — like fast heartbeats or weight loss. This didn’t make sense. The lab checked again using a different testing method, and found the real level was actually low. The reason? Her body made antibodies that messed up the test. These antibodies thought the hormone was there when it wasn’t. This is called anti-T4 autoantibodies. The test that measures free T4 is not always accurate when these antibodies are present. After testing, her doctor gave her the original dose of medicine again, and her thyroid levels became normal. She doesn’t have any symptoms of overactive thyroid, and the problem was only caught because of the wrong test results.


A 46-year-old woman with long-term hypothyroidism, treated with levothyroxine, was seen eight years after her diagnosis. Her routine blood tests showed a high level of free thyroxine (FT4) and a slightly high TSH, but she had no symptoms of an overactive thyroid, like rapid heartbeat or weight loss. This was confusing because her thyroid function was stable for years, and she didn’t feel any different. Tests using two different lab methods showed a big difference: one method showed a very high FT4, while the other showed a low FT4. This inconsistency raised suspicion that her blood test was being affected by antibodies in her blood that react with thyroxine, specifically anti-T4 autoantibodies. These antibodies interfered with the test results, making the FT4 appear higher than it actually was. The problem was confirmed through special lab tests that showed the antibodies were causing the false high reading. The patient did not have symptoms of hyperthyroidism, and her other thyroid markers were normal. After confirming the interference, her levothyroxine dose was restored to the original level. This case shows that sometimes lab results can be misleading due to antibodies, and it’s important to use multiple testing methods when there’s a mismatch in results, especially in patients with long-standing thyroid conditions.


{
    "proficient_health_literacy": "We report a case of a 46-year-old female with autoimmune hypothyroidism managed on chronic levothyroxine replacement, who presented eight years after diagnosis with a serum thyrotropin (TSH) of 7.393 µUI/mL (normal range: 0.5–5 µUI/mL) and a markedly elevated free thyroxine (FT4) level of 51.7 pg/mL (normal range: 8–18 pg/mL), alongside a normal free triiodothyronine (FT3) level of 2.8 pg/mL (normal range: 2.3–4.2 pg/mL). The patient exhibited no clinical signs of hyperthyroidism, including tremor, palpitations, sweating, insomnia, diarrhea, or visual disturbances, and had no family history of thyroid disease. Her body mass index was 35 kg/m², blood pressure was 129/88 mmHg, and heart rate was 98 bpm. She had recently gained 7 kg over six months, but denied symptoms consistent with hyperthyroidism. Given the absence of hyperthyroidism symptoms and the normal FT3 level in the context of high FT4, interference in FT4 quantification was suspected. The diagnosis of thyroid hormone resistance was ruled out due to normal FT3 levels and absence of familial thyroid disease.\n\nInitial testing was performed using the Siemens Healthcare Reagents Kit on the Advia Centaur platform, which reported a high FT4 value of 51.7 pg/mL. To evaluate potential assay interference, a parallel FT4 measurement was conducted in a second immunoassay platform, the Roche Cobas e 411, using a Roche Diagnostics reagent kit. The test was performed on serum collected 20 days after the initial sample, following overnight fasting and 24 hours post-levothyroxine administration. Serum samples were processed with 20-minute room temperature incubation, centrifuged at 3000g for 15 minutes, and either analyzed immediately or stored at −70°C for seven days. Quality control was maintained using freeze-dried human-based controls: Biorad Immunoassay Plus Control (Advia Centaur) and Roche Precinorm U (Cobas e 411), with intra- and inter-run coefficients of variation (CV) of <


A 26-year-old man with no serious health problems before suddenly got weak in both legs after getting a shot of dexamethasone. He had muscle cramps earlier, which went away, but then woke up weak and couldn't stand. His legs were very weak, and he fell, hurting his arms. His blood showed very low potassium, which is a key mineral for muscles. Doctors gave him potassium shots, and within hours his legs started getting stronger. He could walk again after his potassium levels went back to normal. Tests showed he wasn’t losing potassium through his urine or stool, and no other medicines were causing it. The weak muscles came back fast when potassium was fixed, so doctors thought it was hypokalemic periodic paralysis. This condition is not hereditary in his family, and it was likely caused by the steroid shot. Later, he had another episode after eating a big meal with lots of carbs. Now he knows to avoid steroid shots and high-carb foods to stay safe.


A 26-year-old Asian man suddenly developed weakness in both legs after receiving an injection of dexamethasone, a steroid medication. He had no prior medical problems, except for a long-time history of aseptic meningitis that did not cause lasting issues. He worked as a construction worker and had been experiencing muscle cramps in his right shoulder and back for a week. He visited a traditional medicine practitioner who gave him anti-inflammatory drugs and another unknown injection. The cramps went away, but the next morning he woke up with sudden leg weakness, making it hard to stand and causing him to fall and get bruises on his arms.

At the emergency department, his temperature was slightly elevated, but his blood pressure and other vital signs were normal. His mental state was clear, and he was well-nourished. Examination showed that his leg muscles were weak, especially in the upper parts of the legs, with strength dropping from 2/5 to 1/5. His arms and reflexes were normal, and there was no sign of nerve damage. Blood tests showed low potassium levels (1.7 mEq/L), which is a key factor in muscle weakness. His ECG showed changes typical of low potassium, and after receiving potassium supplements, his muscle strength improved by the afternoon. His potassium levels returned to normal (4.0 mEq/L), and he was able to walk again.

His urine tests showed he wasn’t losing potassium through his urine, and he had not taken any medications known to cause potassium loss, such as diuretics or insulin. His hormone levels were mostly normal, except for a slightly high TSH, which may have played a role. The doctors believed the weakness was caused by hypokalemia (low potassium), and since it improved quickly after potassium was restored, they did not perform further tests like electromyography.

It was later found that the dexamethasone injection had triggered the condition. This type of hypokalemic periodic paralysis (HPP) is not inherited and is often triggered by certain medications or high-carbohydrate meals. The patient was advised to avoid corticosteroids and large meals high in carbohydrates to prevent future episodes. A year later, he had another episode after eating a large carbohydrate meal, confirming the pattern.

The final diagnosis was non-familial hypokalemic periodic paralysis, likely caused by the dexamethasone injection.


{
    "proficient_health_literacy": "A 26-year-old Asian male presented to the emergency department with an acute onset of bilateral proximal lower limb weakness, initially manifesting as difficulty standing and subsequent falls resulting in upper limb contusions. The patient had no significant medical history beyond a prior episode of aseptic meningitis over a decade ago, which was asymptomatic. He was a construction worker engaged in heavy physical labor and reported intermittent muscle cramping in the right shoulder radiating to the back for one week. Prior to presentation, he received intramuscular injections of non-steroidal anti-inflammatory drugs (NSAIDs) and an unknown agent from a traditional medicine practitioner, after which the cramping resolved. However, upon waking in the morning, he developed acute, symmetric lower limb weakness, with initial muscle strength in both legs measured at 2/5, progressing to 1/5, while upper limb strength remained preserved. Neurological examination revealed intact deep tendon reflexes (knee jerks) and lower limb sensation, with no Babinski sign bilaterally, indicating no upper motor neuron involvement.\n\nVital signs were stable, with a tympanic temperature of 38.1°C, normotension, and no signs of systemic infection or shock. Laboratory investigations revealed a normal complete blood count, blood glucose, and urinalysis; however, serum potassium was markedly low at 1.7 mEq/L, with a mild elevation in creatine phosphokinase (178 U/L), consistent with myopathic changes. Electrocardiography demonstrated flattened T waves and prominent U waves in precordial leads V1–V3, which are characteristic of hypokalemia and reflect decreased cardiac membrane stability. Oral and intravenous potassium supplementation (initially 40 mEq) was administered, with serum potassium remaining at 2.0 mEq/L the following morning. A second bolus of 60 mEq was given, leading to a gradual improvement in lower limb muscle strength to 4/5 by afternoon. The patient was admitted and received an additional 20 mEq of intravenous potassium (total 120 mEq), resulting in normalization of serum potassium to 4.0 mEq/L and full recovery of ambulation.\n\nUrinary potassium excretion was low (urine potassium/creatinine ratio of 1.5 mmol/mmol), excluding significant renal potassium wasting. There was no evidence of gastrointestinal potassium loss, and


A 32-year-old man felt pain in his chest that spread to his back and left shoulder, like a heart attack, but tests showed no heart damage. His heart was sitting too far to the left, and X-rays showed lung tissue pushing between the aorta and the main lung artery. A special heart scan (MRI) found that the left layer of the heart's outer sac was missing — this is called left pericardial agenesis. The heart moves a lot and is twisted, which causes the lung tissue to push into places where it shouldn’t. He doesn’t need surgery right now and is just being watched closely. He should avoid lifting heavy things to prevent more pain.


A 32-year-old man came in with chest pain that spread to his back and left shoulder, which reminded doctors of a heart attack. However, his ECG and heart enzymes were normal, and his overall exam was unremarkable. His heart rate was high (164 beats per minute), but his blood pressure and other tests were normal. A chest X-ray taken two days apart showed the heart shifted to the left side, with a bulging left border and a clear space between the aorta and pulmonary artery. This suggested something unusual about the heart's structure. A cardiac MRI confirmed that the patient had left pericardial agenesis — a rare condition where the protective sac around the left side of the heart is missing. This causes lung tissue to push between the aorta and pulmonary artery, and the heart rotates abnormally. The left atrial appendage also sticks out abnormally. There’s a small hole in the heart wall allowing blood to flow from the left side to the right side. The patient’s symptoms, especially during heavy lifting or exertion, are likely linked to this structural issue. He was treated with regular follow-up and advised not to lift heavy weights or do strenuous exercise.


{
    "proficient_health_literacy": "A 32-year-old male professional driver presented with episodic chest discomfort and radiating pain to the back and left shoulder, which exacerbated following four days of weight training. The symptoms began at age 10 and have recurred in association with physical exertion, including heavy lifting and uphill climbing. There is no history of comorbidities, surgical interventions, substance abuse, or familial history of ischemic heart disease. Clinical examination was unremarkable, with normal vital signs: heart rate of 164 bpm (indicating sinus tachycardia), blood pressure of 130/84 mmHg, respiratory rate of 24 breaths per minute (tachypnea), and normal blood glucose. Electrocardiography (ECG) was normal, and cardiac biomarkers (troponins, CK-MB) were within normal limits, ruling out acute myocardial infarction.\n\nInitial imaging via chest radiography revealed a normal cardiac apex and left heart border, but a lucent area—interpreted as lung tissue—was observed between the aorta and the pulmonary artery, as well as between the left hemidiaphragm and the base of the heart. The repeat chest X-ray, taken 24 hours later, demonstrated a leftward displacement of the cardiac apex (wandering cardiac apex), consistent with significant cardiac levorotation. Echocardiography confirmed marked levorotation of the heart, with normal left ventricular size, preserved systolic function (ejection fraction of 60%), and substantial cardiac mobility—defined as apex displacement exceeding 1.5–2 mm, indicating increased myocardial excursion. No pericardial or pleural effusion was detected, and ventricular wall motion was normal.\n\nCardiac MRI further delineated the anatomical abnormalities: significant anterior interposition of lung tissue between the main pulmonary artery and the descending aorta, and between the left ventricle and the diaphragm. The left atrial appendage was abnormally protruding along the lateral aspect of the aortic arch. A 6-mm defect in the middle atrial septum was identified, consistent with a secundum type of atrial septal defect (ASD), leading to left-to-right shunting. The left inferior pulmonary vein exhibited restricted caliber due to compression between the descending aorta and the left atrium, a consequence of the pronounced levorotation. Pulmonary vein diam


A 71-year-old woman started feeling weak, lost weight, had diarrhea, and her skin turned yellow over two years. She had been checked regularly for liver problems, but nothing was clear. When she got really sick, she had very low blood pressure and her heart was barely working. She needed to be in the hospital’s intensive care unit because her body was failing. Tests showed damage in her liver, stomach, spleen, and brain. A second liver test finally found the cause: a rare condition that affects many parts of the body, called multisystem LCH, which caused her bile ducts to become scarred and blocked. This is known as secondary sclerosing cholangitis. She was given medicine to help her hormones and a special drug to stop the disease from getting worse. But she had many other health problems, like pancreatitis and diabetes, and after being in the hospital several times, she chose comfort care to focus on feeling better, not fighting the illness.


A 71-year-old woman came to the hospital with worsening weakness, weight loss, diarrhea, and yellowing of the skin (jaundice). She had been seeing her doctor for high liver enzymes over the past two years, but treatments like ursodiol and low-dose steroids didn’t help. When she arrived, she was very low on blood pressure and had a slow heart rate. Her blood tests showed high white blood cell counts, high liver enzymes, and signs of inflammation. Her thyroid function was also abnormal, with no active thyroid hormone levels.

Imaging scans showed damage in multiple organs, including the liver, gastrointestinal tract, spleen, and brain. The liver biopsy, which was previously inconclusive, now showed signs of a rare condition called multisystem Langerhans cell histiocytosis (LCH). This condition affects several organs and caused the liver disease in the form of secondary sclerosing cholangitis — a type of bile duct damage.

She needed intensive care because she developed severe shock, requiring medications to support her blood pressure and heart function. Brain imaging showed inflammation of the pituitary gland, which affects hormone production. She also had pancreatitis, blood sugar issues, and developed central diabetes insipidus.

Treatment started with hormone replacement to fix her low hormone levels. After discussion with a team of specialists, she was given a drug called vemurafenib, which targets a specific mutation found in LCH cells. Despite treatment, she had repeated hospitalizations and eventually chose comfort care to focus on quality of life.


{
    "proficient_health_literacy": "A 71-year-old female with a history of gastroesophageal reflux disease presented to the emergency department following a syncopal episode, accompanied by progressive diarrhea, unexplained weight loss, worsening jaundice, and fatigue. She had been undergoing outpatient evaluation for chronically elevated liver enzymes over the preceding two years. Prior therapeutic trials with ursodiol and low-dose prednisone were ineffective. On admission, her vital signs demonstrated hypotension (blood pressure 72/53 mm Hg) and a nadir heart rate of 62 beats per minute. Physical examination revealed jaundice and cachexia. Laboratory findings included leukocytosis (27.7 × 10⁹/L; normal 3.4–9.6 × 10⁹/L) with neutrophilic predominance. Hepatic function tests showed elevated aspartate aminotransferase (85 U/L; normal 8–43 U/L), alanine aminotransferase (85 U/L; normal 7–45 U/L), bilirubin (9.3 mg/dL; normal <1.2 mg/dL), and markedly elevated alkaline phosphatase (2262 U/L; normal 35–104 U/L) and gamma-glutamyl transferase (494 U/L; normal 5–36 U/L). C-reactive protein was elevated at 52 mg/L (normal <8 mg/L), and thyroid function tests revealed hyperthyroidism with elevated TSH (22.8 mIU/L; normal 0.3–4.2 mIU/L), undetectable free T3 and T4, consistent with panhypopituitarism. A prior 6-month liver biopsy demonstrated periportal fibrosis with lymphocytic and scattered neutrophilic infiltrates in portal tracts, but no evidence of histiocytic infiltration. Imaging studies included contrast-enhanced computed tomography (CT) of the abdomen and pelvis, which revealed diffusely heterogeneous liver parenchymal enhancement without ductal dilatation, duodenitis, and diffuse colonic thickening suggestive of pancolitis. CT chest showed bilateral centrilobular ground-glass opacities with mild pulmonary edema. Echocardiography was normal, excluding cardiac etiology. Brain magnetic resonance


A 21-year-old woman from northern Tanzania, who had been breastfeeding for 8 months after having a baby by C-section, came in with belly pain, swelling, fever, and unusual discharge from her vagina. She had a hard lump in her lower belly that was tender and about the size of a 16-week pregnancy. A scan showed a possible infection in her pelvis, but after surgery, doctors found a large, swollen uterus with hair, oily stuff, and pus inside. They removed the whole uterus and tested the tissue. The test showed it was a type of growth called a mature teratoma, which is like a skin cyst that can grow and get infected. She recovered well, had no more symptoms, and has stayed healthy for 8 months after surgery.


A 21-year-old woman from the northern region of Tanzania, who is of Sukuma ethnicity, came to the hospital with abdominal pain, swelling, fever, and abnormal vaginal discharge that had lasted for three weeks. She had been breastfeeding for eight months after having a child via cesarean section. During her exam, doctors found a large, tender mass in her abdomen and signs of infection in her pelvic area. A pelvic ultrasound suggested a pelvic abscess, but after surgery, they found a different cause: a mature uterine teratoma, which is a type of benign tumor that contains skin-like tissue, hair, and sebaceous material. The tumor was infected and had pus inside. The surgery involved removing the entire uterus (total hysterectomy), and the tissue was tested under a microscope, confirming the diagnosis. The patient recovered well, received blood and antibiotics, and has not had any signs of the disease returning for eight months.


{
    "proficient_health_literacy": "A 21-year-old female of Sukuma ethnicity from the northern region of Tanzania presented to the Bugando Medical Centre (BMC) outpatient clinic in Mwanza with a three-week history of abdominal pain, distension, fever (approximately 38.5 °C), and abnormal vaginal discharge. She was lactating for eight months following a previous cesarean section delivery. On physical examination, she exhibited signs of systemic illness, including weakness, fever, and a blood pressure of 110/70 mmHg. Her blood group was A, Rh-positive, with a hemoglobin level of 6.3 g/dL, indicating significant anemia. Abdominal examination revealed a sub-umbilical midline surgical scar and a palpable suprapubic mass corresponding to a uterus of approximately 16 weeks' gestational size, described as soft, tender, and mobile. Digital pelvic and vaginal examination demonstrated a closed cervix with tenderness on cervical mobility, tenderness in the posterior fornix, and gloved finger staining with pus-like discharge. Pelvic ultrasound imaging suggested the presence of a pelvic abscess.\n\nThe patient was referred for emergency laparotomy. Intraoperatively, the uterus was found to be markedly bulky with a discharging sinus located on the left fundal aspect. Both ovaries appeared normal in morphology and structure, with no evidence of adnexal pathology or fluid in the pouch of Douglas. A transverse incision was made at the level of the sinus tract. The uterine cavity contained yellowish, mucinous, tenacious material intermixed with hairy tissues and sebaceous debris. A decision was made to proceed with total hysterectomy, during which the excised uterus was observed to contain abundant hair and sticky sebaceous material within the uterine cavity.\n\nPostoperatively, the patient received one unit of packed red blood cells to correct her anemia and was administered intravenous antibiotics: ceftriaxone, gentamicin, and metronidazole, with concurrent prophylactic heparin therapy to prevent thromboembolic complications. The patient recovered uneventfully.\n\nHistopathological evaluation of the resected uterus, which measured 18 cm × 9 cm × 4 cm and contained no adnexal structures, revealed a cystic lesion measuring 10 cm in diameter located within the myometrium at the left fundal


A 64-year-old woman had a filter put in her leg vein 3 months ago to stop a blood clot. The filter didn’t come out easily, and the doctor tried to pull it back but failed. Then, 3 months later, she got sudden, bad pain on her right side of the belly. Her urine was red, and she had swelling in her right leg. The filter’s hook went too far and cut into her right leg artery, causing a bulge (like a balloon) in the artery. This blocked her urine pipe, so her kidney swelled up. Both her leg veins and part of her main vein were completely blocked. The doctors did emergency surgery to remove the filter, the bulge, and the blocked parts. They fixed the artery and fixed her veins. The surgery found a bacteria called Staphylococcus aureus in the tissue, which was treated with antibiotics. After surgery, she stayed in the hospital for 12 days and started taking medicine to prevent clots and fight infection. Six months later, a scan showed the artery was open and her kidney swelling was only mild. She’s doing better now.


A 64-year-old woman was admitted with sudden, severe pain on the right side of her abdomen. She had previously had an IVC filter placed three months ago to prevent blood clots after a deep vein thrombosis in her left leg. The filter was placed through her right femoral vein and was meant to be removed later, but a previous attempt to retrieve it failed. Since then, imaging was stopped due to the pandemic.

She developed severe abdominal pain and noticed red urine, but no fever or other signs of infection. On exam, her abdomen was tender, her right leg was swollen, and her right femoral pulse was weak. Blood tests showed high white blood cells, indicating inflammation or infection.

A CT scan revealed that the hook part of the filter had pierced into her right iliac artery, causing a bulge (pseudoaneurysm) in that artery. This also blocked her right ureter, leading to swelling of the kidney on that side. Both iliac veins and the lower part of her IVC were completely blocked, which affects blood flow.

She underwent emergency open surgery to remove the IVC filter, the pseudoaneurysm, and the damaged parts of the iliac veins and IVC. Her right iliac artery was reconstructed to restore blood flow. Bacteria (Staphylococcus aureus) were found in the tissue sample, and she was treated with antibiotics and anticoagulation therapy.

She was discharged on day 12. Six months later, a follow-up CT showed that her right iliac artery was open and flowing properly, and only mild kidney swelling remained. Her condition has improved, but ongoing care is needed.


{
    "proficient_health_literacy": "A 64-year-old female presented to our institution with a 1-day history of severe right abdominal pain following a 3-month history of inferior vena cava (IVC) filter placement. The initial indication for IVC filter placement was deep venous thrombosis (DVT) of the left lower extremity, managed with anticoagulation. A double-basket retrievable IVC filter (Visee WXF-32, Shandong Visee Medical Devices Company Limited, China) was inserted infrarenally via the right femoral vein. Ten days later, endovascular retrieval of the filter using standard femoral venous access failed, and subsequent imaging follow-up was discontinued due to the COVID-19 pandemic. Three months later, the patient presented with acute right lower quadrant pain, no fever or chills, and reddish urine consistent with hematuria. She had a history of scoliosis, poorly controlled type 2 diabetes mellitus, and chronic substance use including tobacco and alcohol. On admission, vital signs were stable: heart rate 97 bpm, respiratory rate 23 breaths/min, blood pressure 126/73 mmHg. Physical examination revealed diffuse abdominal tenderness with rebound tenderness, mild right lower limb swelling, and a weak femoral artery pulse. Laboratory findings showed normal hepatic and renal function, hemoglobin 101 g/L, leukocyte count 14.74 × 10⁹/L, and neutrophilic granulocyte percentage of 91.0%, indicating a significant inflammatory response. During surgical intervention, a partial pseudoaneurysmal lesion was excised for tissue culture, yielding isolation of Staphylococcus aureus, which demonstrated sensitivity to moxifloxacin. Computed tomography angiography (CTA) revealed that the retrieval hook of the IVC filter had penetrated the right common iliac artery (CIA), resulting in a 52 mm × 48 mm × 55 mm pseudoaneurysm in the right iliac artery. This pseudoaneurysm was associated with complete right ureteral obstruction leading to ipsilateral hydronephrosis. Bilateral iliac veins and the distal segment of the IVC were completely occluded, with extensive pelvic varicosities observed. Emergency open surgical repair was performed, including complete removal of the IVC filter, the right


A 32-year-old woman felt越来越 short of breath, had no appetite, and woke up sweating every night for two weeks. Doctors found a big tumor in her left kidney that had grown into her main vein and reached her heart. The tumor was very large and pushed into her heart, which is a serious problem. She had surgery to remove the kidney and the tumor from her vein and heart. The tumor was found to be a rare cancer called Ewing's sarcoma, which started in the kidney and spread through the blood vessels. This cancer was confirmed by a test that looked for a specific gene change. After surgery, she started chemotherapy to kill any remaining cancer cells. She still takes blood thinners to prevent new clots because both the cancer and treatment can cause blood clots. Her scans show no more cancer, and she is doing well.


A 32-year-old Iranian woman came in with worsening shortness of breath, loss of appetite, and night sweats over the past two weeks. Tests showed a tumor in her left kidney that had spread into the veins leading to her heart, including the inferior vena cava and into the right atrium. This was a rare and serious condition. She had surgery to remove the kidney and the tumor from the veins. During the surgery, the tumor was found extending into her right atrium and was diagnosed as Ewing's sarcoma, a type of cancer that starts in the kidneys and spreads. Pathology tests confirmed the presence of a genetic change (EWSR1 rearrangement) that is typical of this cancer. She started chemotherapy after surgery, with adjustments made to reduce side effects. Her follow-up scans showed no signs of cancer recurrence, and she is doing well with ongoing treatment and monitoring.


{
    "proficient_health_literacy": "A 32-year-old Iranian female presented with progressive dyspnea at rest, accompanied by anorexia, fever, chills, and night sweats over a two-week period prior to admission. Initial evaluation at Rajaei Hospital Cardiac Center included echocardiography and computed tomography (CT) angiography, which revealed pulmonary thromboembolism (PTE) consistent with a massive tumor thrombus. The diagnosis of PTE was confirmed, and she was initiated on heparin followed by transition to oral rivaroxaban for anticoagulation, with subsequent stable discharge under close follow-up.\n\nTwo weeks later, she returned with worsening dyspnea and systemic symptoms. Abdominal ultrasound and contrast-enhanced abdominopelvic CT demonstrated a solid, heterogeneously enhancing mass in the mid-to-lower pole of the left kidney measuring 70 mm × 75 mm × 105 mm, with tumor thrombus extending from the left renal vein through the inferior vena cava (IVC) to the right atrium over a craniocaudal length of approximately 23 cm. Mild hypodense fluid was noted in the pelvic cavity. CT findings also revealed filling defects in the right main pulmonary artery and its segmental branches, consistent with pulmonary thromboembolism, and a 7 mm ground-glass nodule in the left lower lobe superior segment. No signs of acute abdominal pathology, such as appendicitis, cholecystitis, pancreatitis, hydronephrosis, or free air, were identified.\n\nEchocardiography showed normal left ventricular systolic function (ejection fraction = 55%), with mild to moderate tricuspid regurgitation, mitral regurgitation, and pulmonary insufficiency. Mean pulmonary artery pressure was 27 mmHg, and peak instantaneous pressure gradient was 17 mmHg. A large, rope-like, hyperechoic mass was observed in the IVC measuring 14 cm × 2.7 cm, protruding into the right atrium, strongly suggestive of extensive intracardiac tumor thrombosis.\n\nGiven the clinical suspicion of a primary renal malignancy with extensive venous invasion, the patient underwent a combined surgical approach: open radical nephrectomy for the left kidney, followed by IVC thrombectomy under cardiopulmonary bypass. During surgery,


A 53-year-old man had a broken hip and started having seizures after surgery. Doctors found a lump in his brain that was not in the normal brain area — it was on the outside of the brain, attached to the lining. This lump looked like a brain tumor, but it wasn’t a regular tumor. It was made of special cells that were not part of the brain. The doctors had to cut into the brain to remove it, and during the surgery, they had to cut some small blood vessels on the brain’s surface. Because of that, the man lost some movement on his left side. After surgery, a scan showed a bleed and a spot in his brain that was likely from those cut blood vessels. The doctors found this lump was not just in the brain — it was also in the nervous system, and it was the only place it was found. The man has not had seizures since, and his movement is slowly getting better. No other parts of his body showed signs of this condition.


A 53-year-old man with diabetes and a broken hip was admitted to the hospital. He had a seizure after surgery, and was referred for further evaluation. Brain imaging showed a mass on the right side of his brain, specifically in the parietal area, that was consistent with a type of tumor called meningioma en plaque. This tumor was attached tightly to the brain surface and had many small blood vessels running through it. To remove the tumor completely, these blood vessels had to be cut, which led to complications. The surgery was done through a frontotemporal craniotomy. After the procedure, the patient developed incomplete weakness on his left side and a bleeding area in the right frontal lobe, likely due to the damaged blood vessels. A biopsy showed unusual immune cells in the tumor, and the findings matched a rare condition called isolated central nervous system RDD (extranodal RDD), meaning the tumor started in the brain but is not spread to other parts of the body. The patient has been seizure-free since surgery and has slowly recovered from his weakness over six months. No signs of the disease spreading to other organs were found.


{
    "proficient_health_literacy": "A 53-year-old homeless man was admitted for a right femoral neck fracture; his medical history included noninsulin-dependent diabetes mellitus. Physical examination at admission was unremarkable, with no fever, lymphadenopathy, or baseline neurological deficits. Laboratory findings showed white blood cell count of 4330 cells/mL, hemoglobin of 9.2 g/dL, and platelet count of 29,900 platelets/mL, consistent with normochromic-normocytic anemia; C-reactive protein was negative, indicating no active systemic inflammation. The orthopedic surgery for the fracture was successfully performed. However, during the postoperative course, the patient developed an episode of generalized seizures, for which phenytoin was administered. Subsequently, he was referred to our neurosurgical department for further evaluation.\n\nNon-contrast head computed tomography (CT) revealed a high-density, extraaxial mass in the right parietal convexity, with prominent peritumoral brain edema. Enhanced magnetic resonance imaging (MRI) demonstrated a dural-based, extraaxial, homogeneously enhancing lesion with well-defined borders, consistent with a meningioma en plaque. On T1-weighted imaging, the lesion was iso- to hyperintense; on fluid-attenuated inversion recovery (FLAIR) and T2-weighted sequences, it was iso- to hypointense. The imaging characteristics, combined with the dural attachment and vascular architecture, strongly supported the diagnosis of meningioma en plaque.\n\nThe tumor was resected via a right frontotemporal craniotomy. Microscopic examination revealed a firm, xanthochromic, nonaspiratable mass with high vascularity and dural origin. The tumor was tightly adherent to the adjacent cerebral cortex and was extensively infiltrated by pial arteries and veins of the brain surface. This intimate vascular integration rendered the preservation of these pial vessels during complete resection highly improbable, necessitating their sacrifice to achieve total tumor removal. Postoperatively, the patient developed incomplete left hemiparesis, likely secondary to ischemic injury from the disruption of pial arterial supply.\n\nA postoperative non-contrast brain CT demonstrated a hemorrhagic lesion and a low-density area in the right frontal lobe, which is believed to result from the surgical sacrifice of pial arteries at the tumor-brain interface. The


A woman in her 80s had a knee infection after a surgery she had seven years ago. Her knee was swollen, painful, and had pus coming out. Doctors found a type of yeast called Cy. fabianii in her knee during surgery. At first, they thought it was a different yeast called Candida utilis, but later testing proved it was really Cy. fabianii. This yeast can cause serious infections in joints, and the right treatment was needed to fix it. She got antibiotics to fight the infection and is now recovering at home.


This study describes a case of infection in a prosthetic knee joint in an 85-year-old woman who had a total knee replacement seven years earlier. She developed pain, swelling, and pus in her right knee over three months. Tests showed signs of joint infection and bone infection (osteomyelitis). She received antibiotics initially, and the infected knee implant was removed. During surgery, fluid from the joint was tested and grew a type of yeast. At first, the yeast was wrongly identified as Candida utilis, but further testing using advanced lab methods correctly identified it as Cy. fabianii. This correct identification was confirmed through DNA analysis and comparison with known yeast samples in a database. The infection was treated with antifungal medications, and the patient recovered after completing a course of oral and intravenous antibiotics.


{
    "proficient_health_literacy": "An 85-year-old Chinese woman with a history of hypertension, dyslipidemia, and a prior right total knee replacement seven years earlier presented with a three-month history of painful right knee swelling and purulent discharge, without recent trauma or surgical intervention. On admission, she was afebrile, with diffuse swelling, erythema, tenderness, and a sinus tract. Laboratory findings revealed a total white blood cell count of 7.8×10³ cells/µL, elevated C-reactive protein, and increased erythrocyte sedimentation rate, indicating active inflammation. Radiographic imaging demonstrated radiolucency in the distal femur and proximal tibia, consistent with osteomyelitis. The patient was diagnosed with prosthetic joint infection (PJI) of the right knee complicated by osteomyelitis, and empiric therapy with intravenous clindamycin and ciprofloxacin was initiated. Surgical intervention included removal of the prosthetic implant and arthrotomy with washout; intraoperative findings were consistent with osteomyelitic changes. Synovial fluid was inoculated into BD Bactec Plus Aerobic/F and BD Bactec Lytic/10 Anaerobic/F vials and incubated using BD BACTECTM FX. After 72 hours, the aerobic bottle yielded a positive culture. Gram staining revealed gram-positive ellipsoidal budding yeast cells. The isolate grew as cream-colored, smooth, glistening colonies on Sabouraud Dextrose Agar and as whitish colonies on CHROMagar. Corn meal agar culture showed only blastoconidia, with no germ tube formation or urease activity, supporting a non-germ tube-forming yeast phenotype. Bone marrow specimens also yielded identical growth. Initial phenotypic identification using the VITEK® 2 yeast identification system assigned the organism to *Candida utilis* with 95% probability. However, subsequent identification via matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF) by Bruker revealed the organism as *Candida fabianii*, a species frequently misidentified as *C. utilis* due to overlapping phenotypic characteristics. This finding was independently confirmed by molecular analysis: DNA was extracted using the Quick-DNA Fungal/Bacterial Miniprep Kit (Zymo Research), and the D1/D2 domain of the large subunit (


A 56-year-old Moroccan woman had a big lump on one side of her face that grew over 4 months. It hurt a lot, made her mouth hard to open, blocked her nose, and she started bleeding from her nose. The lump was deep in her face and spread into her nose, eye area, and sinuses. Doctors saw it with scans and found it was a serious, fast-growing tumor. A small tissue sample showed it was a cancer called malignant schwannoma. Even though they gave her radiation to ease the pain, she passed away 10 days later because of breathing trouble.


A 56-year-old Moroccan woman was hospitalized in 2013 with a large swelling on one side of her face, on the right side, that had been growing over the previous 4 months. She first noticed sharp facial pain, which was initially thought to be a dental issue but didn’t improve. The swelling grew quickly, causing trouble opening her mouth, nasal blockage, and nosebleeds. She had a painful swelling on her right face, her eye appeared slightly bulging, and she had numbness in parts of her face controlled by the trigeminal nerve. A nasal exam found a tumor in her right nose that was fragile and bled easily. Her hard palate was eroded, and her mouth was so tight it was hard to examine. No lymph nodes or other parts of her throat showed signs of disease. Her hearing and ear exam were normal. She was given morphine for pain. CT and MRI scans showed a large, aggressive tumor in her right temple area, maxillary sinus, and around her eye, spreading into nearby structures like the sinuses and nasal passages. The tumor was invasive and had areas of dead tissue. A biopsy of the tumor confirmed it was a malignant schwannoma, a type of cancer that starts in nerve tissue. Tests showed no spread to other parts of her body. Because the cancer was advanced and not curable, the doctors chose palliative radiotherapy to relieve symptoms. The treatment helped a bit, but she passed away 10 days later due to severe breathing problems.


{
    "proficient_health_literacy": "A 56-year-old Moroccan woman with a 38-year history of chronic cigarette smoking (approximately one pack per day) was hospitalized in 2013 presenting with a rapidly progressive right-sided hemifacial swelling that had evolved over four months. Initial symptoms included persistent, unilateral facial neuralgia localized to the trigeminal nerve distribution, initially misdiagnosed as dental in origin and managed without improvement. The pain progressively worsened to a disabling level, accompanied by a significant increase in right maxillary swelling, limitation of mouth opening (trismus), and recurrent nasal obstruction with epistaxis (nosebleeds). Clinical examination revealed a painful, inflammatory right hemifacial mass, right exophthalmos without evidence of visual acuity reduction, and hypoesthesia in the second and third divisions of the trigeminal nerve (V2 and V3), consistent with peripheral nerve involvement. Endonasal examination identified a friable, bleeding tumor mass within the right nasal cavity. Oral examination, severely limited by trismus, demonstrated erosion of the hard palate. Cervical lymphadenopathy was absent, and upper aerodigestive tract endoscopy showed no mucosal lesions. Otoscopy and audiometry were normal, excluding central nervous system or auditory pathway involvement. The patient was immediately initiated on intravenous morphine for pain control.\n\nImaging studies revealed a large, heterogeneous, infiltrative mass involving the right infratemporal fossa, masticator space, and right maxillary sinus. CT findings demonstrated lysis of the maxillary sinus walls, the ascending ramus of the mandible, and the orbital floor, with extension into the ethmoidal, parapharyngeal, and intraorbital compartments. MRI further characterized the lesion as aggressive and invasive, with irregular boundaries, heterogeneous signal intensity on both T1- and T2-weighted sequences, and heterogeneous contrast enhancement with areas of central necrosis. The tumor exhibited infiltrative growth into the jugular and temporozygomatic soft tissues, consistent with a highly destructive, locally advanced process. The radiological pattern supported extensive local invasion without evidence of distant spread.\n\nA nasal endoscopic biopsy was performed, and histopathological evaluation confirmed a poorly differentiated, invasive malignant process. Immunohistochemical analysis demonstrated strong, diffuse cytoplasmic positivity for anti-S100 protein, a hallmark marker of schwannoma lineage, leading to a definitive diagnosis of malignant schwann


A 76-year-old man had been feeling numbness, pain, and weakness in his arms and legs for 7 years. He also had sweating, constipation, and lost weight without knowing why. In the past month, he started having shortness of breath, swelling in his feet and legs, and low blood pressure. His heart tests showed a strange sign: his heart looked bigger than it should, but the electrical signals were weak — this is a clue that his heart might be full of a harmful protein. Tests on his heart showed the same problem: the heart muscle wasn’t working well, and this matches what happens in a disease called cardiac amyloidosis. Blood tests ruled out a common type of amyloid disease (AL). A gene test found a mutation in the TTR gene — this is the same mutation found in people with a family disease called familial amyloid polyneuropathy (FAP) and heart disease from amyloid. This confirms he had hATTR Val30Met disease. His treatment with medicine didn’t work well. After 80 days, he died because his heart stopped working. His son later had the same symptoms and was found to have the same gene problem.


A 76-year-old man had been slowly getting worse over seven years, with numbness, pain, and weakness in his arms and legs, sweating, constipation, and unexplained weight loss. In the past month, he also developed shortness of breath, swelling in his body, and low blood pressure. Tests showed low electrical signals in his heart (low QRS voltage) that didn’t match his thickened heart muscle — this was a key sign pointing to cardiac amyloidosis (CA). Echocardiogram results, especially using advanced imaging, supported the diagnosis. Blood tests ruled out AL amyloidosis, a common type of amyloid disease, because his free light chain levels were normal. A genetic test found a specific mutation (c.148 G-A, Val30Met) in the TTR gene, which confirms the diagnosis of hereditary amyloidosis caused by a faulty protein called transthyretin. This condition is known as hATTR Val30Met, which leads to both nerve damage (familial amyloid polyneuropathy or FAP) and heart problems. His treatment with doxycycline, ursodeoxycholic acid, and tafamidis did not work well — he developed severe intestinal blockage and eventually died from heart failure. His son later developed similar symptoms and was found to have the same genetic mutation. No tissue biopsies were done after death due to family refusal.


{
    "proficient_health_literacy": "A 76-year-old male presented with a seven-year history of progressive peripheral neuropathy characterized by limb numbness, pain, weakness, autonomic dysfunction including sweating and constipation, and unexplained weight loss. Over the preceding month, he developed systemic edema, hypotension, and shortness of breath. Physical examination revealed malnutrition, anemia, lethargy, generalized muscle weakness, decreased muscle tone, diminished tendon reflexes, sacroiliac decubitus necrosis, and severe edema. Laboratory findings included persistent elevation of high-sensitivity troponin I (hs-TnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), indicating myocardial injury; neutrophilic leukocytosis; moderate anemia with reduced erythrocyte count and hematocrit; and mild hypoxemia. Chest X-ray demonstrated bilateral pulmonary inflammation with pleural effusion. Electrocardiography (ECG) showed low QRS voltage in the limb leads, abnormal Q waves in leads II, III, and aVF, and a poor R-wave progression in V1–V6, which is inconsistent with left ventricular hypertrophy and suggestive of cardiac amyloidosis (CA). Echocardiography revealed left ventricular hypertrophy, diastolic dysfunction (grade II), and a small pericardial effusion, with a critical discordance between the low QRS voltage and the presence of hypertrophy—this discordance is a key pathological clue in the diagnosis of CA. Speckle tracking strain analysis demonstrated reduced global longitudinal strain (GLS) with apical sparing, an apical-to-basal strain ratio of 2.7, and an ejection fraction to GLS ratio (EFSR) of 4.4, findings that are consistent with the characteristic ultrasonic phenotype of cardiac amyloidosis. Chest CT scans revealed diffuse pulmonary interstitial changes, cystic lung lesions, and progressive subpleural calcifications, which are hallmark radiographic features of pulmonary amyloid deposition. The presence of pulmonary amyloidosis was further supported by the absence of evidence for active infection or inflammation, as confirmed by normal C-reactive protein and blood cell profile. Despite the critical clinical condition, cardiac magnetic resonance (CMR) and positron emission tomography with pyridyl-1,3-diamine (PYP) were not performed due to the patient's instability. To differentiate between


A 12-year-old boy had belly pain for four days, along with hard stools, watery poop, and a swollen belly. He was very sick, breathing fast, and his heart was beating too fast. When doctors looked with ultrasound, they saw the spleen had twisted like a corkscrew and was stuck in the lower belly, attached to the appendix and small intestine. Part of the spleen was dead because of the twist. The doctors did surgery to remove both the spleen and the appendix. The boy recovered well, stayed in hospital for 7 days, and then went home. He now takes medicine to prevent infections and will get vaccines for meningococcal and pneumococcal diseases to stay healthy.


A 12-year-old boy came in with crampy abdominal pain that had lasted for four days. He had a history of constipation, mucoid diarrhea, and a swollen belly. He was very sick-looking, with a fast heart rate and tender abdomen. On ultrasound, doctors saw a 'whirlpool sign' and found that his spleen was not in its normal place — it was located in the lower abdomen, twisted 720 degrees, and had areas of dead tissue (necrosis). The spleen was stuck to the appendix and the end of the small intestine. During surgery, they removed both the spleen and the appendix. The surgery went smoothly, and he recovered well. After recovery, he received vaccines to protect against meningococcal and pneumococcal infections, and started on antibiotics to prevent future infections.


{
    "proficient_health_literacy": "A 12-year-old male presented with a four-day history of crampy, lower abdominal pain, accompanied by prior episodes of constipation, mucoid diarrhoea, and abdominal distension. He reported no vomiting, and there was no family history of similar gastrointestinal or systemic manifestations. The patient lived with his parents, three siblings, and grandparents, with no known congenital or inherited medical conditions in the family. On physical examination, he appeared acutely ill with marked distress; vital signs revealed tachycardia (heart rate 134 beats per minute), respiratory rate of 22 breaths per minute, normothermia (temperature 36.40°C), and normal blood pressure (110/75 mmHg). There was no sunken eye socket, and buccal mucosa was moist. Abdominal examination demonstrated generalized tenderness, distension that moved with respiration, and a firm, 8 cm × 5 cm mass in the left lower quadrant with its lower border inaccessible, consistent with a fixed, non-fluid-containing lesion. No free fluid was detected. Systemic examination was otherwise unremarkable.\n\nLaboratory findings included a white blood cell count of 10,300/μL with a neutrophilic predominance of 78.5%, moderate anemia (hemoglobin 8.6 g/dL, hematocrit 28%), mean corpuscular volume (MCV) of 86 fL, and platelet count of 775 × 10³/μL. Abdominal ultrasound revealed a 'whirlpool sign' at the splenic hilum, indicating vascular torsion, and demonstrated a wandering spleen located in the lower abdominal cavity, displaced below the level of the umbilicus. The spleen exhibited altered echogenicity, suggestive of focal infarction. The ultrasound diagnosis was confirmed as wandering spleen with multifocal infarction due to splenic volvulus.\n\nThe patient was managed with nil-by-mouth status, intravenous maintenance fluids, broad-spectrum antibiotic coverage, and analgesia. After stabilization, an emergency laparotomy was performed. Intraoperatively, a slightly enlarged spleen was identified within the peritoneal cavity, positioned below the umbilicus. The vascular pedicle was found to be torsioned 720°, with the torsion originating


A 56-year-old man had a stroke that went away on its own. He didn’t have any major heart problems, but later started feeling tired, losing weight, and sweating at night. His body showed signs of inflammation — his blood tests showed high levels of markers that mean the body is fighting something. He had breathing problems and was diagnosed with a condition called ANCA-associated vasculitis, which means his body’s immune system attacked his lungs and heart. This condition made his breathing worse, and his heart wasn’t working well. Tests showed his heart was weak and had a leaking aortic valve, which let blood flow backward. The doctor replaced the faulty valve with a new one. After the surgery, his breathing got better. The tissue from the valve showed signs of swelling, inflammation, and thickening — proof that his immune system was causing damage. He’s now being watched closely by heart, lung, and immune specialists to keep his symptoms under control.


A 56-year-old man was diagnosed with ANCA-associated vasculitis, a type of autoimmune disease that causes inflammation in blood vessels. He first developed respiratory symptoms, including shortness of breath, which got worse over time. Initial tests showed signs of inflammation in his lungs and blood, and he was treated with steroids and methotrexate, which helped control the disease.

After two years, his symptoms returned, especially shortness of breath, and his lung function declined. A heart exam revealed that his heart was not pumping effectively, with a low ejection fraction (30–35%), and he had severe aortic valve insufficiency — meaning the valve wasn't closing properly, allowing blood to leak back into the heart. This was confirmed by imaging and tissue analysis showing inflammation, thickening, and scarring in the aortic valve.

He had surgery to replace the damaged aortic valve with a bioprosthesis, which improved his symptoms. After surgery, his heart function and breathing stabilized. He also had a small heart rhythm issue, which was managed with medication. The condition of his lungs remained under close monitoring, and he continued treatment for his underlying vasculitis. This case shows how heart and lung problems can be linked in vasculitis, and why a full medical evaluation is needed when symptoms persist.


{
    "proficient_health_literacy": "A 56-year-old male with a prior spontaneous cerebral stroke at age 49, which resolved without residual neurological deficit and was not evaluated with magnetic resonance imaging, presented at 56 years of age with evolving respiratory symptoms initially attributed to respiratory tract involvement. He had no traditional cardiovascular risk factors, aside from a family history of ischemic heart disease. Ten weeks after the stroke, he developed third-degree atrioventricular (AV) block, initially suspected to be due to acute Borrelia infection; however, the block persisted despite antibiotic therapy, necessitating dual-chamber pacemaker implantation.\n\nDuring hospitalization, he exhibited fatigue, unintentional weight loss, and night sweats. Laboratory findings revealed a sedimentation rate >100 mm/hr, hemoglobin of 5.0 g/mL (indicating severe anemia), thrombocytosis (615×10⁹/L), and C-reactive protein (CRP) of 95 mg/L, with no leukocytosis. Gastrointestinal bleeding was not suspected due to absence of gastrointestinal symptoms. At 4 months, he was diagnosed with ANCA-associated vasculitis, specifically MPO-ANCA-positive, characterized by systemic inflammation with malaise, low-grade fever, arthritis, sinusitis, interstitial lung disease (confirmed by ground-glass opacities on high-resolution computed tomography [HRCT] of both lungs, without biopsy), and absence of mononeuritis multiplex, asthma, skin, renal, cerebral, or gastrointestinal tract involvement. The Birmingham Vasculitis Activity Score (BVAS) was 15, indicating moderate disease activity.\n\nTreatment with high-dose corticosteroids for six months followed by methotrexate led to clinical remission, with normalization of MPO-ANCA titers. Methotrexate was discontinued after two years of sustained remission. One year later, he developed worsening respiratory symptoms, including dyspnea, with rising MPO-ANCA levels, prompting reinitiation of steroid and methotrexate therapy. Despite this, respiratory symptoms persisted, leading to multidisciplinary evaluation involving cardiology, pulmonology, and rheumatology.\n\nInitial cardiac evaluation via transthoracic echocardiography (TTE) showed preserved left ventricular (LV) function, no pulmonary hypertension, and mild-to-moderate aortic regurgitation. A treadmill exercise


A baby girl, 18 days old, was admitted to the hospital because her heart made a strange noise and her legs had weak pulses. Her blood pressure was much higher in her arms than in her legs. Doctors used an ultrasound to see her heart and found a narrow part in the main artery (aortic coarctation). They also saw that a blood vessel that feeds the heart (LCX) was not getting blood the normal way — it was flowing backward, through a small path from the lung artery instead of going into the heart. The heart was working fine, and the pressure in the lungs was normal. To fix this, doctors did surgery at day 23. They removed the narrow part of the artery and reconnected the heart's blood vessel back into the main artery. They also closed a small hole in the lung artery. After surgery, the baby had a fast heart rhythm that was treated with medicine. A follow-up check showed the heart blood vessel was now working properly. The baby recovered well and went home with normal heart tests.


An 18-day-old girl was admitted to the pediatric intensive care unit because of a heart murmur and weak pulses in her legs. She was otherwise healthy, breathing on her own and with normal blood pressure, except for a 30 mmHg difference in blood pressure between her arms and legs. An echocardiogram confirmed aortic coarctation — a narrowing of the aorta — and showed that the heart’s left coronary artery (LCA) was not flowing into the aorta as it should. Instead, it was being supplied by blood from a nearby artery (the right posterior descending artery) and flowed into the right pulmonary artery instead. A coronary angiogram revealed only one right coronary artery and no left main coronary artery. The left circumflex artery (LCX) was feeding through a bypass path, reaching the wall of the aorta without entering it. At 23 days old, she had surgery to remove the narrowed part of the aorta and reconnected the left coronary artery back into the aorta using a technique that kept the artery safe and intact. The defect in the pulmonary artery was closed with a patch. After surgery, she had a few episodes of fast heart rate, which were treated with medication. Follow-up tests showed normal blood flow in the left coronary artery. She recovered well and was discharged home with normal heart function and no signs of damage.