{
  "proficient_health_literacy": "A 70-year-old white male with severe symptomatic aortic regurgitation secondary to healed infective endocarditis was managed with transcatheter aortic valve implantation (TAVI) via an apical approach. The procedure was indicated due to his high surgical risk, assessed using a logistic EuroSCORE I of 24.36%, compounded by secondary pulmonary hypertension, severely impaired left ventricular function (left ventricular ejection fraction [LVEF] of 20%), chronic renal insufficiency (serum creatinine 2.1 mg/dL), and comorbidities including chronic kidney disease and systemic hypertension. Pre-TAVI medical therapy included torasemide 20 mg daily, ramipril 5 mg daily, bisoprolol 2.5 mg twice daily, and spironolactone 12.5 mg daily. On admission, the patient presented with cardiac decompensation and dyspnea (temperature 36.7 °C, pulse 99/min, blood pressure 109/48 mmHg), with no evidence of active infection (normal C-reactive protein and leukocyte count), and no microbiological workup performed. Laboratory findings revealed mild hepatocellular dysfunction (aspartate aminotransferase 59 U/L, alanine aminotransferase 67 U/L) and mild anemia (hemoglobin 10.7 g/dL), with no urine analysis conducted. Coronary angiography, performed prior to TAVI, was normal, supporting the exclusion of coronary artery disease as a contributing factor.\n\nThe initial TAVI was performed with a JenaValve 27 mm self-expandable bioprosthesis. Post-procedural imaging demonstrated minimal transvalvular central insufficiency and stable hemodynamics, indicating initial procedural success. However, despite this, the patient experienced recurrent cardiac decompensation due to persistent left ventricular dysfunction, leading to a repeat interdisciplinary evaluation. Four weeks after the initial TAVI, the patient underwent implantation of a left ventricular assist device (LVAD) system (Thoratec® HeartMate II) to support ventricular function. The postoperative course was uneventful, and the patient remained asymptomatic for one year.\n\nDuring this period, the LVAD system generated recurrent high-flow alarms, prompting further evaluation. Serial echocardiographic assessments revealed a progressive worsening of transvalvular central aortic insufficiency to a severe level, with no evidence of structural leaflet damage or prosthetic thrombosis in the JenaValve. This suggested a functional impairment of the aortic outflow due to hemodynamic alterations, likely related to the high flow dynamics generated by the LVAD and the inherent geometry of the existing prosthesis. Given the persistent regurgitation and lack of improvement in ventricular function, a valve-in-valve strategy was adopted.\n\nThe subsequent TAVI procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm self-expanding valve, without prior valvuloplasty. Hemodynamic management during implantation included reduction of LVAD flow to minimum and maintenance of cardiac pacing at 140 beats per minute to optimize ventricular filling and reduce flow-induced turbulence. Positioning was guided by real-time fluoroscopy and transesophageal echocardiography (TEE), with specific attention to placing the ventricular strut end of the CoreValve Evolut R between the ventricular end and the 'cusp feelers' of the existing JenaValve prosthesis. This positioning was informed by individualized CT imaging, which confirmed optimal alignment of the JenaValve's ventricular edge within the left ventricular outflow tract (LVOT). The initial positioning was successful without repositioning, and the valve was released in the planned anatomical position after final fluoroscopic confirmation. Post-implantation, rapid pacing was discontinued, and LVAD flow was gradually increased to ensure adequate hemodynamic stability.\n\nThe postoperative course was uneventful, and follow-up TEE at 12 months demonstrated no significant aortic regurgitation, with only marginal residual insufficiency. The patient reported no symptoms and demonstrated significant functional improvement, with a 6-minute walk distance increasing from 148 meters on admission to 381 meters at 12-month follow-up. Echocardiography also revealed an improvement in left ventricular function, with LVEF rising to 33%. This case illustrates the complex interplay between prosthetic valve dynamics, LVAD-induced hemodynamics, and the risk of transvalvular regurgitation in patients with pre-existing severe aortic regurgitation and severely compromised left ventricular function. The valve-in-valve approach, when carefully planned with precise positioning and optimized hemodynamic support, can


A 12-year-old boy came in with sudden headaches and drinking a lot of water, urinating a lot. Doctors found he had a small cyst in his brain that had burst, but it wasn’t pressing on any parts of his brain or causing serious problems. His hormones were mostly normal, except for a small problem with water balance, which got better with medicine. No surgery was needed because the cyst stayed the same size and didn’t get worse over three years. He grew up normally, started puberty on time, and had no vision issues. But his growth slowed down a bit, so doctors tested him and found he had a little missing growth hormone. After starting treatment, his growth sped up. The cyst stayed stable and didn’t get bigger or smaller much over time.


A 12-year-old male presented with acute onset of headache and polyuria-polydipsia, which began one week prior to evaluation. He had no significant past medical history. Physical examination revealed a height of 146.5 cm (−1.4 SD) and weight of 30 kg. No signs of adrenal insufficiency or hypothyroidism were observed. He was at the early stages of puberty, with bilateral gonadal volumes of 3.2 cm and penile length of 6.2 cm (male standard). The polyuria-polydipsia was severe, with urinary fluid excretion reaching up to 113 ml/kg/day, nocturnal enuresis, and excessive fluid intake of 3.8 liters/m². Ophthalmologic assessment, including optical coherence tomography (OCT), showed normal visual function and retinal structure, with no evidence of optic nerve or retinal pathology.

Endocrine evaluation revealed diabetes insipidus (DI), characterized by a serum sodium of 140 mEq/L, plasma osmolality of 287 mosm/kg, and urine osmolality of 179 mosm/kg—indicating a profound inability to concentrate urine. All other endocrine markers, including insulin-like growth factor-1 (IGF-1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH), were within normal reference ranges, suggesting intact hypothalamic-pituitary axis function except for the specific deficiency of antidiuretic hormone (ADH) action.

Magnetic resonance imaging (MRI) with and without contrast demonstrated apoplexy of a Rathke cleft cyst (RCC), showing spontaneous hyperintensity on both T1 and T2-weighted sequences with dimensions of 15 × 6 × 11 mm. The anterior pituitary exhibited homogeneous contrast enhancement, consistent with normal vascularization and structural integrity. Notably, the posterior pituitary showed loss of typical hyperintensity on T2 sequences, which is a key radiological finding in RCC apoplexy and suggests hemorrhage or disruption of neurohypophyseal tissue. No evidence of craniopharyngioma or other structural lesions was identified. The RCC apoplexy remained stable over a nine-month follow-up period, with size reduction to 12 × 11 × 10 mm, and subsequent imaging at 2 and 3 years revealed progressive stabilization, ultimately measuring 7 × 10 × 6 mm, indicating a non-progressive, possibly self-limiting hemorrhagic event.

A multidisciplinary team comprising an endocrinologist, neurosurgeon, and radiologist reviewed the case. Given the absence of compressive neurologic symptoms, normal neuroimaging progression, and stable hormonal profiles (excluding DI), a conservative management strategy was adopted, involving regular clinical, biochemical, and radiological monitoring. Over a three-year follow-up, the patient achieved normal pubertal development without significant endocrine deficiencies, except for a partial growth hormone (GH) deficiency, which emerged later as a secondary finding.

Growth velocity declined from −0.8 SD to −1.1 SD, prompting further investigation. At age 14 years and 9 months, two GH stimulation tests—propranolol-glucagon test and insulin tolerance test—were performed, yielding GH peak values of 19.3 µUI/ml and 10.0 µUI/ml, respectively, both below the threshold for normal pubertal growth, confirming a partial GH deficiency. Following initiation of recombinant human growth hormone (rhGH) therapy, growth velocity improved significantly, increasing from −1.1 SD to +0.2 SD over one year, indicating effective hormonal replacement.

Radiological follow-up was conducted at a single center with consistent interpretation by the same radiologist, ensuring longitudinal reliability and minimizing inter-observer variability. The stability of the RCC apoplexy over time, coupled with the absence of expansion or mass effect, supports the conclusion that the lesion is benign and non-encroaching, with no indication for surgical intervention. The case underscores the importance of long-term monitoring in pediatric patients with RCC apoplexy, particularly when initial endocrine and neurologic findings are non-compressive and within normal limits, and highlights the potential for delayed emergence of secondary endocrine deficiencies, such as partial GH deficiency, despite otherwise normal early puberty and hormonal function.


A 67-year-old male with no significant comorbidities presented with a six-month history of progressive dysphonia and dysphagia, culminating in a marked deterioration of general condition accompanied by a 15 kg weight loss over six months. Initial clinical examination revealed a conscious patient with a Glasgow Coma Scale of 15/15, normothermia, blood pressure of 12/8 mmHg, oxygen saturation of 100%, heart rate of 80 beats per minute, and normal conjunctival color. A large mass was identified in the nasopharyngeal cavity, with no evidence of hepatomegaly, splenomegaly, or lymphadenopathy. Physical examination remained otherwise unremarkable.

Cervico-thoraco-abdomino-pelvic CT imaging demonstrated a 70 mm × 40 mm nasopharyngeal mass extending to 60 mm in size. Laboratory investigations, including complete blood count, renal and hepatic function tests, lactate dehydrogenase, and serologies for HIV, HCV, and HBV, were within normal limits. Histopathological and immunohistochemical analysis of the nasopharyngeal biopsy, performed in two independent laboratories, confirmed a grade 1–2 follicular B-cell non-Hodgkin lymphoma (NHL) characterized by CD20+, CD19+, CD79a+, and CD10+ expression, consistent with a follicular lymphoma subtype. Bone marrow biopsy and pre-therapeutic work-up were normal, excluding hematologic involvement.

The patient received four cycles of R-CHOP chemotherapy (rituximab 375 mg/m² intravenously, cyclophosphamide 750 mg/m² intravenously, oncovin 2 mg intravenously, prednisolone 100 mg orally, doxorubicin 50 mg/m² intravenously), which yielded no clinical or radiological response. Subsequently, three cycles of R-DHAOX chemotherapy (rituximab 375 mg/m² intravenously on day 1, high-dose aracytine 2 g/m² intravenously on day 2 administered over two days, dexamethasone 40 mg intravenously daily from day 1 to day 4, oxalipatin 100 mg/m² intravenously on day 1) were administered, also without response. Persistent growth of the nasopharyngeal mass necessitated tracheostomy due to airway compromise.

Repeat biopsy of the nasopharyngeal lesion revealed a complete absence of B-cell lymphoid infiltration and the presence of AL-type amyloid deposits, specifically kappa light chain–associated amyloidosis, suggesting a clonal plasma cell disorder. Immunoelectrophoresis of plasma proteins demonstrated elevated immunoglobulin M (IgM) with kappa light chain specificity, although light chain free light chain quantification was not performed due to institutional resource limitations. Myelogram and a second bone marrow biopsy remained normal, excluding overt multiple myeloma or plasma cell dyscrasia.

Positron emission tomography (PET) imaging confirmed a hypermetabolic nasopharyngeal lesion with no evidence of systemic metastatic disease. Cardiac evaluation (electrocardiogram, n-terminal pro-B-type natriuretic peptide, troponin, echocardiography) and renal function were unremarkable. The patient is currently receiving a triplet therapy protocol comprising bortezomib, prednisone, and bendamustine, which has demonstrated favorable clinical response following the initial cycle. The clinical course indicates a possible transformation from follicular lymphoma to a concomitant or secondary amyloidosis, potentially driven by clonal B-cell dysregulation and IgM production, with the nasopharyngeal mass serving as a site of extramedullary amyloid deposition. This case highlights the clinical challenge of distinguishing between primary lymphoma and amyloid-related pathology in the setting of a large, non-lymphomatous-appearing extramedullary mass with immunological features of B-cell dyscrasia.


A 46-year-old man from Haiti who now lives in Chile had warty bumps on his right leg for one year. The bumps started small and got bigger, then began to hurt, bleed, and ooze yellow fluid. Doctors saw the bumps and found a type of fungus called chromoblastomycosis. This fungus shows up in skin samples as thick-walled, brown cells (muriform cells) and grows into black, fuzzy spots in the lab. Under a microscope, the fungus looked like tiny branches with small dots, matching a type called Fonsecaea. He was treated with a medicine (itraconazole) taken twice a day for six months, and had cold treatments (cryotherapy) every 6 to 8 weeks on the thick parts of the bumps. After six months, the bumps went away completely. No signs of the disease came back, and only a little dark spot remains, which is normal after cold treatment.


A 46-year-old Haitian man who had been living in Chile for one year presented with warty, skin-like plaques on the front of his right leg that had been growing for about a year. He originally had no symptoms, but three months before coming in for care, the area started to itch, hurt, and developed a small ulcer with yellow discharge. On exam, the plaques were about 1 cm to 3 cm in size and had a rough, warty appearance. Dermatoscopy showed thickened skin with dark spots and red blood vessels. Blood tests were normal, and tests for infections like syphilis, HIV, and tuberculosis were negative. A skin biopsy was done and showed thickened skin with inflammation and special cells called muriform cells, which are a key sign of chromoblastomycosis. Fungal culture grew black, velvet-like colonies, and under the microscope, the fungus had long, branching structures and small spores typical of Fonsecaea species. The diagnosis was confirmed as chromoblastomycosis. The patient was treated for six months with itraconazole (an antifungal medicine) and regular cryotherapy (freezing the affected areas with liquid nitrogen) every six to eight weeks. He also used mupirocin ointment to prevent bacterial infections when the skin broke. After six months, the lesions completely went away, and there has been no return of the disease. The only remaining issue is mild skin lightening in the treated areas, which is expected after cryotherapy.


A 46-year-old Haitian male, residing in Chile for one year, presented with a one-and-a-half-year history of progressive cutaneous lesions originating as a papule on the anterior right tibial region. Initially asymptomatic, the lesion evolved over time to include pruritus, pain, superficial ulceration, and yellowish exudate. Physical examination revealed three well-demarcated warty plaques measuring 1×1 cm, 2×2 cm, and 3×2 cm on the anterior right leg. Dermatoscopic evaluation demonstrated a hyperkeratotic mass with a central ulcerated area, characterized by reddish-black dots and congested hemorrhagic vessels, consistent with chronic inflammatory and proliferative dermal changes. The patient's general laboratory workup, including VDRL, HIV serology, and PPD, was non-reactive, ruling out syphilis, HIV infection, and latent tuberculosis. Tissue sampling via punch biopsy encompassed epidermis, dermis, and subcutaneous tissue, and was subjected to Gram staining, routine bacterial culture, and anaerobic culture—all of which were negative. Bacilloscopy and Koch complex culture of the same specimen also yielded negative results, excluding mycobacterial and bacillary etiologies. Histopathological analysis using hematoxylin and eosin staining revealed pseudoepitheliomatous hyperplasia of the epidermis, with a dense mixed inflammatory infiltrate containing suppurative foci and foreign body giant cells. Within these giant cells, round, muriform cells with thick, brown-walled walls were observed, morphologically consistent with fungal elements; this finding was further confirmed by periodic acid-Schiff (PAS) staining, which highlighted the fungal wall structure. Mycological culture on Sabouraud dextrose agar at 25°C demonstrated after 15 days of incubation the growth of dematiaceous (black-pigmented), elevated, well-defined, velvety colonies, characteristic of darkly pigmented fungi. Direct microscopic examination using 20% potassium hydroxide (KOH) revealed long, branched, occasionally tortuous hyphae and short chains of acropetal conidia, which are pathognomonic for Fonsecaea spp., a known etiological agent of chromoblastomycosis. The patient was initiated on systemic itraconazole at a dose of 100 mg every 12 hours for a duration of six months, in conjunction with regular cryotherapy using liquid nitrogen applied every six to eight weeks to hypertrophic and ulcerated areas. Topical mupirocin ointment was applied frequently to manage bacterial superinfections resulting from local lesion erosion and ulceration. The clinical course was favorable, with complete regression of all visible lesions and no evidence of relapse at the time of follow-up. Persistent mild local hypopigmentation was noted in treated areas, which is a known sequelae of cryotherapy-induced tissue damage and is expected in the context of repeated cold therapy. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in histopathology, dematiaceous fungal colonies in culture, and conidia morphologically compatible with Fonsecaea spp. in direct microscopy, establishing a definitive fungal etiology with a well-documented clinical and pathological profile.


A 19-year-old man had a painful lump in his scrotum for 8 months that didn’t go away with antibiotics. He also had fever, night sweats, loss of appetite, and lost weight. No one in his family had tuberculosis, but he had the TB vaccine. The lump was surgically removed and tested — it showed signs of tuberculosis in the tube-like part of the testicle. X-rays showed TB in his lungs, lymph nodes, and bones. He started TB medicine, but after 4 months, he had seizures. A brain scan found small TB-related lumps in his brain. He started medicine to stop the seizures and kept taking TB medicine. His symptoms got better — he gained weight, the body lumps went away, and he didn’t have more seizures. The brain lumps slowly got smaller, so he kept taking TB medicine for a long time. After 19 years of treatment, he was fully healed with no long-term problems.


A 19-year-old man with no prior medical problems was admitted to the hospital with a painful lump in his left scrotum that had been growing for 8 months. The lump didn't go away with antibiotics, and he also had symptoms like low-grade fever, night sweats, loss of appetite, and unexplained weight loss. He had no history of tuberculosis in his family or personal history, and he was vaccinated at birth. Exam findings showed a large, tender lump in the scrotum and some firm lumps on his chest. His blood tests showed high inflammation markers, and a chest X-ray showed signs of lung infection. After surgery to remove the scrotal lump, the tissue tested positive for tuberculosis in the epididymis, which is a part of the testicle. Tests also found tuberculosis in his lungs, around the abdomen and chest walls, and in his spine and bones. He started standard tuberculosis treatment with several medications. After four months, he had seizures, and a brain scan showed small areas of tuberculosis in the brain, called tuberculomas. He was then given anti-seizure medication along with continuing tuberculosis treatment. His condition improved over time—he regained his weight, the lung and body infections went away, and the seizures stopped. Although the brain tuberculomas slowly shrank, he needed to stay on tuberculosis treatment for a long time, totaling 234 months (about 19 years), before being declared cured with no long-term effects.


A 19-year-old male with no significant medical history presented with a painful left scrotal mass that had persisted for 8 months without improvement following empirical antibiotic therapy for pyogenic infections. He reported intermittent low-grade fever, night sweats, anorexia, and unexplained weight loss since symptom onset, with no history of cough, sputum production, or hemoptysis. There was no personal or familial history of tuberculosis, and he had received standard bacillus Calmette-Guérin (BCG) vaccination at birth. Physical examination revealed a large, tender, slightly warm left scrotal bursa and two elongated, firm, poorly defined subcutaneous masses in the anterior thoracic wall measuring 3–4 cm in length, without audible rales on lung auscultation. The remainder of the systemic examination was unremarkable. Laboratory findings demonstrated a markedly elevated c-reactive protein (CRP) of 90 mg/dL, while complete blood count, serum creatinine, blood glucose, and liver function tests remained within normal limits. Standard chest radiography revealed bilateral reticulonodular infiltrates consistent with pulmonary involvement.

Ultrasound imaging suggested an epididymal mass, prompting a left orchidectomy. Histopathological analysis of the resected specimen revealed granulomatous epithelioid cell necrosis involving the body and tail of the epididymis, with sparing of the head and testicular tissue, strongly suggestive of active epididymal tuberculosis. The intradermal tuberculin skin test (TST) was positive, supporting the diagnosis. Direct microscopy and culture for acid-fast bacilli (AFB) in sputum and urine over three consecutive days were negative, and serological testing for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Wright's stain (to rule out other hematological disorders) were all negative, excluding alternative infectious or hematologic etiologies.

To evaluate for extrapulmonary dissemination, a thoraco-abdomino-pelvic tomodensitometry was performed, which demonstrated miliary tuberculosis, coelo-mesenteric necrotic lymphadenopathy, two parietal collections (right: 33 × 10 mm; left: 45 × 10 mm) arising from the external oblique muscles, and focal osteolytic lesions at D11 and L5, consistent with early spondylodiscitis. Magnetic resonance imaging (MRI) of the spinal cord confirmed spondylodiscitis at the D7, D11, L4, and L5 levels. This constellation of findings led to a definitive diagnosis of disseminated tuberculosis involving the epididymal, pulmonary, parietal, lymphatic, and osteo-articular compartments.

Treatment was initiated with a 2-month intensive phase of quadruple antitubercular chemotherapy consisting of isoniazid, rifampicin, ethambutol, and pyrazinamide, followed by a continuation phase of isoniazid and rifampicin. At the fourth month of therapy, the patient developed generalized tonic-clonic convulsive seizures. Brain MRI revealed multiple nodular lesions located above and below the tentorial membrane, consistent with tuberculomas—focal granulomatous brain lesions caused by Mycobacterium tuberculosis. The patient was promptly started on adjunctive anticonvulsant therapy while continuing anti-tubercular treatment. Clinical and radiological follow-up demonstrated a favorable evolution, including resolution of systemic symptoms, weight gain, and gradual disappearance of thoracic parietal collections, lymphadenopathy, and miliary infiltrates on imaging. However, the tuberculomas showed a slow, progressive reduction in size, necessitating prolonged continuation of antituberculous therapy. The patient was ultimately declared cured at the end of the 234th month of treatment, with a 2-year post-treatment follow-up confirming no recurrence of disease or neurological sequelae. This case illustrates the potential for disseminated tuberculosis to present with extrapulmonary manifestations, including epididymal involvement and central nervous system tuberculomas, and underscores the importance of early diagnosis, comprehensive imaging, and long-term management in young adults with atypical presentations.


A 10-year-old boy was getting chemotherapy for a serious type of cancer called leukemia. During the early treatment, he got a brain infection caused by a bacteria named B. cereus. Doctors found it using brain scans and a fluid from around the brain. He had a bad headache that didn’t go away, so they checked his brain and found a spot that looked like an infection. Even though he didn’t have a fever, he started to feel very sick and needed help in the hospital. Doctors gave him strong antibiotics, and the infection went away. After a few weeks, his headache stopped and his brain scans showed the infection was getting smaller. He fully recovered and is back to normal.


A 10-year-old boy was treated for acute lymphoblastic leukaemia, a type of blood cancer, using a standard chemotherapy protocol. During the early stages of treatment, he developed a serious brain infection called a cerebral abscess caused by a bacteria named B. cereus. This was found through brain imaging and by testing the fluid around the brain (cerebrospinal fluid). Although the infection was severe, it responded well to antibiotics. The boy’s symptoms improved, and he made a full recovery with no lasting brain problems. Follow-up scans showed the infection had shrunk, and he was able to continue his treatment safely.


We present a case of a 10-year-old male with high-risk early T-cell acute lymphoblastic leukaemia (ALL), managed according to the LAL SEHOP-PETHEMA 2013 protocol. Two years post-diagnosis, he experienced an early central nervous system (CNS) relapse, prompting intervention under the InteReALL HR 2010 protocol, which included bortezomib. During induction therapy, the patient became neutropenic for four weeks (neutrophil count: 20/μL), receiving prophylactic antimicrobials consisting of cefepime, cotrimoxazole, and fluconazole. Concurrently, he was treated with acyclovir for a documented herpes simplex virus 1 (HSV-1) skin infection. On presentation, he developed a severe, treatment-refractory headache, prompting a cranial computed tomography (CT) scan that revealed a hypodense lesion in the right temporal lobe. Given the infectious etiology hypothesis, a lumbar puncture was performed, and empirical therapy was updated to meropenem and vancomycin.

Despite the absence of fever, the patient rapidly progressed to septic shock on day one of hospitalization, requiring transfer to the paediatric intensive care unit (PICU) for inotropic and vasoactive support. Antimicrobial coverage was broadened to include gentamicin and caspofungin. Laboratory findings demonstrated a progressive rise in inflammatory markers: C-reactive protein (CRP) reached 312 mg/L and procalcitonin (PCT) peaked at 47.58 ng/mL by day three, consistent with a severe bacterial infection, while no other significant biochemical abnormalities were detected. Complete blood count revealed pancytopenia, attributable to chemotherapy-induced bone marrow suppression. Blood cultures were negative for both bacteremia and fungemia; herpesvirus serologies (HSV-1, HSV-2, HHV-6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus) and urine/fecal cultures were also negative, excluding common pathogens.

Cerebrospinal fluid (CSF) analysis showed normal glucose (63 mg/dL), protein (16 mg/dL), and leukocyte count (1/μL), indicating a non-inflammatory, non-lymphocytic CSF profile. However, microbiological culture identified *Bacillus cereus* as the causative organism, which was sensitive to meropenem, vancomycin, linezolid, and ciprofloxacin. All other potential CNS pathogens—including *Neisseria meningitidis*, *Listeria monocytogenes*, *Streptococcus pneumoniae*, *Cryptococcus*, and *Toxoplasma gondii*—were ruled out in CSF. Electroencephalography (EEG) revealed diffuse cerebral slowing without epileptiform discharges, suggesting non-epileptic encephalopathy consistent with metabolic or infectious insult.

On day 4, following stabilization of hemodynamics, cranial magnetic resonance imaging (MRI) demonstrated two hyperintense lesions on T2 and FLAIR sequences involving the subcortical regions of the right temporal and parietal lobes. The parietal lesion exhibited ring enhancement after gadolinium administration, and both lesions displayed peripheral diffusion restriction on apparent diffusion coefficient (ADC) mapping, indicative of restricted water diffusion typical of abscess formation. Additionally, scattered small hemorrhagic foci were observed within the brain parenchyma. These imaging findings, in conjunction with the CSF culture result and clinical course, supported a diagnosis of *Bacillus cereus* cerebral abscess, an atypical and rare cause of CNS infection in the immunocompromised setting.

The patient responded favorably to antibiotic therapy, with resolution of headache and absence of new neurological deficits. Follow-up MRI at two weeks showed significant reduction in lesion size. Vancomycin and acyclovir were discontinued after three weeks, and meropenem was continued for a total of six weeks. This case highlights the diagnostic challenge of atypical bacterial CNS infections in children undergoing intensive chemotherapy, particularly in the context of prolonged neutropenia and prophylactic regimens, and underscores the importance of early imaging, CSF analysis, and broad-spectrum empirical therapy in such high-risk populations.


A 16-year-old girl has a flat, gray spot on her left thigh that's been there since birth. The spot is about 10.5 cm wide and 8.0 cm long, and it's got small blood vessels running around the edge. Over time, the spot turned lighter and became flatter. A scan showed that the spot has extra blood vessels in the skin and layer below it, which is normal for this type of growth. There's no sign that it's affecting her legs differently or spreading into muscles or bones.


16-year-old female presenting with a congenital, depressed gray plaque measuring 10.5 × 8.0 cm located in the lower lateral aspect of the left thigh, characterized by interspersed hypochromic regions and peripheral telangiectatic vessels, including visible superficial veins adjacent to the lesion. The lesion was present at birth and initially exhibited a violaceous hue, evolving over time to become lighter in color and more depressed in elevation. No asymmetry in lower limb length was observed, ruling out significant skeletal or musculoskeletal involvement. Angioresonance imaging revealed a complex vascular malformation involving the dermal and subcutaneous layers, primarily supplied by intermuscular branches of the popliteal artery. Notably, early venous filling was demonstrated both within the lesion and in the surrounding tissue, indicating early venous shunting and possible venous override. No significant dilation of deep draining veins was identified, although a superficial draining vein was observed coursing along the subcutaneous cellular tissue of the anterior thigh. Histopathological and imaging findings confirm thinning of the subcutaneous tissue within the affected region, consistent with chronic vascular remodeling, without evidence of intramuscular or bony extension. The clinical and imaging profile supports a diagnosis of a venous or venous-lymphatic malformation with early venous dominance, likely arising from aberrant vascular development during embryogenesis, involving the popliteal artery-derived vascular plexus.


A 57-year-old woman with a long history of asthma and allergic rhinitis came in with recurring abdominal pain that had been going on for two months. The pain was dull and intermittent, along with nausea, loss of appetite, fatigue, and a 5-kilogram weight loss. She had no fever, no blood or mucus in her stool, and no respiratory symptoms. Tests showed very high levels of a type of white blood cell called eosinophils, and her IgG4 levels were also elevated. After checking for infections, blood disorders, and other conditions that could cause high eosinophils, doctors found no clear cause. A biopsy of her colon tissue showed a large number of eosinophils in the lining of the colon, which confirmed a diagnosis of eosinophilic colitis (EoC). She was treated with corticosteroids and montelukast, and her symptoms improved within two weeks. Her eosinophil levels returned to normal, and after stopping the steroids, she continued on montelukast for three months without any symptoms coming back.


{
  "proficient_health_literacy": "A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, managed on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain initiated two months prior. The pain was intermittent, dull, and associated with nausea, anorexia, malaise, and a 5 kg weight loss. Notably, there were no fever, blood or mucus in stool, respiratory symptoms (rhinorrhea, wheezing, cough), or history of alcohol, tobacco, or herbal medicine use. Six weeks before admission, she was diagnosed with an intestinal infection based on a complete blood count (CBC) showing leukocytosis and marked eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotic therapy and mebendazole, which failed to alleviate symptoms. On presentation, vital signs were stable: blood pressure 110/70 mmHg, temperature 37°C, heart rate 88 bpm, respiratory rate 18 bpm. Body mass index was 16.6 kg/m², consistent with severe underweight, and sarcopenia was present, with no skin rash, lymphadenopathy, or edema. Abdominal examination revealed tenderness in the epigastric and umbilical regions without rebound or guarding. Repeat CBC demonstrated persistent leukocytosis and significant eosinophilia (20.8 G/L total WBC, 77.8% eosinophils), with peripheral blood film showing normal eosinophil morphology. Bone marrow aspiration revealed 48% eosinophils without blasts or atypical cells, suggesting a clonal or reactive process but excluding hematologic malignancy. Fluorescence in situ hybridization (FISH) for CHIC2 deletion, a surrogate marker for FIP1L1-PDGFRA fusion in eosinophilic disorders, was negative, ruling out primary myeloid eosinophilia. Autoimmune and vasculitis screening (ANA, anti-dsDNA, p-ANCA, c-ANCA) remained negative, excluding systemic autoimmune conditions. Serum immunoglobulins showed elevated IgG (2760 mg/dL; normal 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal 3.9–86.4 mg/dL), with a mild elevation in IgE (137.5 IU/mL; normal <100 IU/mL) and elevated rheumatoid factor (RF 144.4 IU/mL; normal <20 IU/mL), though these findings were not sufficient to support an autoimmune etiology. All other laboratory parameters—including aminotransferases, blood urea nitrogen, serum creatinine, complement C3/C4, vitamin B12, serum cortisol, and NT-proBNP—were within normal limits. Electrocardiogram and echocardiogram were unremarkable. Chest CT revealed mild pulmonary fibrosis and bronchiectasis, consistent with chronic airway inflammation. Sputum acid-fast bacilli (AFB) smear and bronchoscopy were negative; bronchoalveolar lavage (BAL) cytology showed 35% neutrophils and no eosinophils, indicating that airway eosinophilia was not the primary driver of systemic eosinophilia. Spirometry demonstrated severe obstructive lung disease with a significant bronchodilator response, and fractional exhaled nitric oxide (FeNO) was 15 ppb, supporting a Th2-mediated inflammatory phenotype. Stool analysis revealed leukocyte presence, but no ova, parasites, or evidence of infectious etiology. Serology testing confirmed positive IgG to Toxocara canis (54.2 NovaTec-Units), suggestive of toxocariasis, but remained negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. Abdominal contrast-enhanced CT showed gallbladder stones without acute cholecystitis and no structural abnormalities in the gastrointestinal tract. Upper endoscopy was unremarkable, while colonoscopy revealed mucosal inflammation in the sigmoid, left, transverse, and right colon, prompting systematic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies demonstrated significant eosinophilic infiltration, with counts exceeding 85 eosinophils/HPF in


A 35-year-old man had a heart problem that got worse over time. At first, he had chest pain and trouble breathing, especially after activity. Doctors found a lump in his heart called a cardiac myxoma, and also saw that his heart was getting bigger and weaker — this is called dilated cardiomyopathy. He had signs of Carney syndrome, a rare condition that affects the heart and skin, like dark spots on his ears and small cysts in his kidney. Doctors tested his genes and confirmed the diagnosis. At first, he was treated with medicine but didn’t have surgery. Later, his symptoms got much worse — he could barely breathe, even when lying down, and his heart was failing badly. His heart function was rated as very poor (NYHA Grade IV). Doctors said he needed a heart transplant. On October 1, 2024, he got a new heart from a donor. The surgery was done by cutting open his chest, removing the damaged heart parts, and putting in the new one. The new heart was connected properly with no leaks. After the surgery, he started recovering fast. By day one, he was urinating well and his heart function improved. His blood tests showed his heart was working better. He took medicine to stop his body from rejecting the new heart and to fight infections. After a week, his recovery was good, and by October 20, 2023, his heart was working normally. All tests were normal, and he’s now doing well and living a healthy life.


A 35-year-old man was diagnosed with heart failure caused by a rare condition called Carney syndrome. This condition leads to the growth of a non-cancerous tumor (called a cardiac myxoma) in the heart and weakens the heart muscle, leading to a condition known as dilated cardiomyopathy. Three years ago, he first had chest tightness and shortness of breath after physical activity. An ultrasound of his heart showed a tumor, and further tests confirmed Carney syndrome. He was treated with medications, but did not have surgery at the time. Over time, his symptoms worsened, and he could no longer lie down without breathing difficulty. His heart function was severely weakened (NYHA Class IV), and new tests showed both the tumor and a weakened heart. Because the heart was no longer able to pump effectively, doctors decided on a heart transplant. On October 1, 2024, he received a new heart from a donor. The surgery involved opening the chest, removing the damaged heart tissue, and connecting the new heart to the major blood vessels. The procedure was successful, and the new heart began working properly. After surgery, he received medicines to prevent his body from rejecting the new heart and to fight infection. His recovery was good, and by October 20, 2024, his heart function was normal, with no signs of problems. He is now doing well and has been followed up regularly since discharge.


{
  "proficient_health_literacy": "A 38-year-old male presented with recurrent episodes of chest tightness and dyspnea, initially occurring post-exertion three years prior. Outpatient echocardiography revealed a left atrial echogenic mass suggestive of a cardiac myxoma, prompting hospital admission for comprehensive evaluation. Physical examination identified characteristic cutaneous pigmentation in the ears, manifesting as multiple small brown and black macules, consistent with cutaneous manifestations of Carney Complex (CNC). Abdominal computed tomography (CT) demonstrated multiple hepatic lesions and small cystic formations in the left kidney, further supporting the diagnosis. Genetic analysis revealed biallelic pathogenic mutations in both the TTN (titin) and PRKAR1A genes, confirming the diagnosis of Carney syndrome (CNC) through integration of clinical, imaging, and molecular findings. The patient underwent symptomatic management with no surgical intervention, which was voluntarily declined despite the presence of a cardiac myxoma. On September 20, 2023, he presented with worsening dyspnea, including orthopnea and paroxysmal nocturnal dyspnea, necessitating rehospitalization. Physical examination revealed jugular venous distension, leftward and inferior cardiac border displacement, irregular cardiac rhythm (auscultated as atrial fibrillation), a mitral valve murmur of intensity 2/6–3/6 at the fourth intercostal space along the left sternal border, and bilateral wet rales in the middle and lower lung zones. Palpation demonstrated hepatomegaly extending three fingers below the xiphoid process and two fingers below the costal margin, with bilateral lower limb pitting edema. Echocardiography confirmed global left ventricular (LV) dilation, with a left ventricular ejection fraction (LVEF) of 23.1% and fractional shortening (FS) of 10.9%, indicative of severe systolic dysfunction. Additional findings included moderate mitral regurgitation, dilation of the aortic sinus and pulmonary artery, and a well-defined, irregular echogenic mass measuring 54 mm × 43 mm attached to the atrial septum. Electrocardiography revealed atrial fibrillation with an average ventricular rate of 150 beats per minute and abnormal Q waves in leads V1–V3, suggesting prior myocardial injury or infarction. The clinical picture was consistent with both Carney syndrome and dilated cardiomyopathy (DCM), with concomitant cardiac myxoma. Given the progression to end-stage heart failure and the presence of a large, non-resectable myxoma, heart transplantation was deemed the optimal therapeutic strategy to address both the structural and functional cardiac deterioration. A suitable donor heart was available for immediate transplantation on October 1, 2024. The surgical procedure involved a median sternotomy with layer-by-layer dissection of the skin and subcutaneous tissues. The sternum was longitudinally opened using a saw, and bleeding was controlled with electrocoagulation and bone wax. Extracardiac exploration revealed global cardiac enlargement, with marked left ventricular dilation and diminished contractile function. The aorta and main pulmonary artery (PA) were dissected from the supravalvular region. Diseased atrial and ventricular tissues—including the right atrium, left atrium (LA), right ventricle, and left ventricle—were excised, with preservation of portions for anastomotic reconstruction. The excised mass was described as greyish-white and mucoid in consistency, consistent with a myxoma. The donor and residual recipient left atria were sutured using double continuous 3/0 Prolene sutures, with meticulous inspection for bleeding. End-to-end anastomosis of the donor ascending aorta to the recipient pulmonary artery was performed with continuous 5/0 Prolene sutures, and no significant hemorrhage was observed. The donor and recipient left atria were closed with double continuous 5/0 Prolene sutures, and the inferior vena cava of both hearts was similarly sutured with 5/0 Prolene, with multiple inspections confirming hemostasis. Following deflation of the left heart, rewarming was initiated, oxygenation was restored, the ascending aorta was unclamped, and spontaneous return to sinus rhythm was achieved. Continuous 5/0 Prolene sutures were applied to the superior vena cava of both donor and recipient, with careful inspection for bleeding. After successful discontinuation of extracorporeal circulation, venous cannulae were decannulated. Tissue specimens from the patient’s left ventricle and cardiac gray matter were collected for histopathological analysis, confirming the presence of both dilated cardiomyopathy and cardiac myxoma. Postoperatively, the patient exhibited a robust early recovery: on postoperative


A 2.5-year-old girl with a known condition called NF1 has been having diarrhea with blood in it for several weeks. The doctor looked inside her colon with a special tool and saw red, swollen lining from the bottom of the rectum all the way to the start of the colon. A small tissue sample showed long-term inflammation, and tests found a virus called CMV that was causing the problem. This combination of red lining and virus infection means she has a type of chronic colitis, similar to ulcerative colitis. She is being treated with medicine to reduce inflammation and is still having some symptoms, but they are getting better.


{
  "proficient_health_literacy": "A 2-year-6-month-old female pre-schooler with a prior diagnosis of neurofibromatosis type 1 (NF1), confirmed by genetic testing at 8 months of age via detection of a heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28), presented with a 4-week history of bloody diarrhea, with 5 to 10 episodes of blood-streaked stools per day. Initial evaluation in the emergency department revealed rotavirus infection (positive), with normal inflammatory markers, negative coproculture, and normal abdominal ultrasound. The patient was hospitalized for 3 days to manage dehydration and discharged without active bleeding, though persistent semi-liquid stools remained. Ten days post-discharge, she developed recurrent bloody diarrhea associated with reduced oral intake and a 1 kg weight loss, prompting referral to a pediatric gastroenterologist. A polymerase chain reaction (PCR) panel for gastrointestinal pathogens and PCR for Clostridium difficile were both negative, leading to hospitalization for further investigation.\n\nThe clinical history was non-specific for systemic infection: no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions were reported. No pet exposure, recent travel, or dietary changes were noted. The patient has documented skin manifestations (café au lait spots) and bone involvement (requiring ankle arthrodesis at 18 months due to tibial curvature), with no family history of NF1 or inflammatory bowel disease (IBD).\n\nPhysical examination revealed a soft, non-distended abdomen with increased air-bubble murmurs, no masses or visceral enlargement. Perianal examination was normal. Multiple brown-coffee-colored stains were observed on the lower extremities and back, consistent with café au lait spots. Laboratory findings included moderate microcytic-hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and mildly elevated inflammatory markers (CRP 1.37 mg/dL, above the normal threshold of ≤0.5 mg/dL).\n\nColonoscopy was performed from the anal margin to the cecum, including inspection of the ileocecal valve and appendicular orifice, with the distal ileum also evaluated. The mucosa from the anal margin to the cecum demonstrated erythema and loss of vascular transparency, a feature not observed in the cecal mucosa, which appeared normal. No focal lesions were identified in the anal canal or cecum.\n\nHistopathological analysis of biopsies revealed preserved villous architecture and adequate epithelial differentiation in the ileal mucosa with a non-inflamed lamina propria. In the colonic mucosa, there was mild architectural distortion, preserved epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate, and hyperplasia of reactive lymphoid follicles. Isolated microabscesses were identified, consistent with a diagnosis of mild chronic colitis. A PCR assay for cytomegalovirus (CMV) on colonic biopsy was positive. Additional serological testing confirmed positive CMV IgG, negative IgM, and a blood viral load of 79.7 IU/mL, supporting active, recent CMV viremia. Stool PCR for gastrointestinal pathogens and C. difficile were negative. Gram stain of the biopsy showed +++ leukocytes without bacterial presence; culture yielded low-level growth of S. gallolyticus/equinus complex, interpreted as normal commensal flora; acridine orange, Ziehl-Neelsen, Koch culture, and adenovirus PCR were all negative.\n\nEndoscopic and histological findings were consistent with ulcerative colitis (UC), with moderate clinical activity (PUCAI score of 50). The patient was initiated on mesalazine (70 mg/kg/day, three times daily), and fecal calprotectin was measured, yielding a value >600 µg/g, confirming active intestinal inflammation. An immunological workup was conducted to evaluate for potential immunodeficiency: lymphocyte subpopulations, immunoglobulin levels, HIV status, memory T-cell populations (showing expected alterations in the context of CMV viremia), and lymphoproliferation test were all within normal limits. A comprehensive genetic panel for primary immunodeficiencies (Invitae, comprising 429 genes, including 68 associated with monogenic inflammatory intestinal disease) was performed, yielding seven variants of uncertain significance, none of which were classified within the monogenic IBD panel.\n\nThe patient was treated with intravenous ganciclovir for CMV infection, administered for 15 days, with subsequent PCR monitoring showing undetectable viral load prior to discharge. Clinical


A 40-year-old HIV-positive male with sustained antiretroviral therapy adherence—documented viral load of 4500 copies/mm³ and CD4 count of 70/mm³ from the prior year—presented with a two-year history of intermittent febrile episodes that lacked a consistent temporal pattern and responded only transiently to non-steroidal anti-inflammatory drugs (NSAIDs). Over the preceding two months, he developed progressive diffuse abdominal pain, with a predominant localization in the upper right quadrant, accompanied by the emergence of a tree-in-bud pulmonary opacification pattern on imaging and bilateral pleural effusions. Abdominal imaging revealed marked hepatosplenomegaly and ascites. Laboratory evaluation demonstrated pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute-phase reactants, indicative of systemic inflammation. Computed tomography (CT) of the thorax, abdomen, and pelvis confirmed generalized lymphadenopathy, hepatosplenomegaly, and the pulmonary tree-in-bud pattern. Multiple microbiological investigations were conducted, including culture-based detection of Mycobacterium species from various specimens, all of which were negative, except for a positive result via RT-PCR for Human Herpesvirus 8 (HHV-8). A left iliac ganglion biopsy was performed, yielding histopathological findings consistent with multicentric Castleman’s disease, a lymphoproliferative disorder characterized by abnormal proliferation of lymphoid tissue and cytokine overproduction, particularly interleukin-6. Despite re-initiation of antiretroviral therapy, clinical deterioration progressed, necessitating the administration of corticosteroids and ganciclovir to address potential HHV-8-driven immune activation. However, within one week, the patient developed multi-organ failure and anasarca, rendering further pharmacologic intervention contraindicated. A repeat chest CT demonstrated worsening pulmonary infiltrates with persistent tree-in-bud morphology and progressive hepato-splenomegaly and ascites. He was transferred to the intensive care unit (ICU) 48 hours after symptom onset, where he rapidly deteriorated and succumbed to fulminant hepatic failure within hours. Postmortem analysis of a tracheal aspirate culture yielded a positive identification of Mycobacterium tuberculosis, confirming latent or active pulmonary tuberculosis as a contributing pathogen. Additionally, a percutaneous liver biopsy revealed non-necrotizing granulomas, consistent with a tuberculous etiology, while the parenchymal architecture remained largely preserved, suggesting a chronic, non-destructive inflammatory process. This case highlights the clinical complexity of HIV-associated lymphoproliferative disorders, particularly Castleman’s disease, in the context of overlapping opportunistic infections and immune dysregulation, and underscores the importance of timely microbiological diagnostics and immune reconstitution in such patients. The study was conducted in accordance with the ethical principles outlined in the World Health Organization’s Declaration of Helsinki.


{
  "proficient_health_literacy": "A 4-month-old indigenous lactating infant from the rural interior of Panama, specifically from Urracá, approximately 3 hours by canoe from the nearest health subcenter, presented with acute diarrhea and moderate-severe dehydration due to protein-caloric malnutrition. The infant was the fourth daughter, born via vaginal home delivery by a relative without prenatal care; birth weight, height, and Apgar score are unknown. The infant did not receive breast milk and was exclusively fed powdered milk formula with iron (3 ounces every 4 hours), which is inconsistent with recommended infant feeding guidelines for infants under 6 months of age. The household consisted of six members (parents and four children), living in a two-room structure with board walls and palm roof, lacking electricity and relying on kerosene lamps for illumination, well water for hydration, open defecation in a river, and open burning of waste. Household economic activity was based on subsistence agriculture, and the infant received no vaccinations as part of the national expanded programme of immunization. Parents reported normal neurodevelopment prior to hospitalization.\n\nThe infant presented to a primary health center with a 4-day history of diarrhea without mucus or blood, accompanied by vomiting of food content; the mother substituted milk with tea due to intolerance. The infant was afebrile and without respiratory symptoms. Initial management included oral rehydration with lactate Ringer's solution (10 ml/kg) and four doses of Enterogermina® (2 billion spores/5 mL), a probiotic containing *Bacillus clausii*. Due to lack of intravenous access (no catheters or intraosseous access), the infant was transferred to a second-level hospital in the provincial capital and subsequently to a tertiary care facility in Panama City, diagnosed with acute gastroenteritis and severe dehydration.\n\nOn emergency department admission, the infant exhibited signs of consciousness compromise, profound dehydration (tearless cry, dry oral mucosa), and signs of shock: capillary refill time >2 seconds, cold extremities, filiform pulse, marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. Physical examination revealed +++ edema in hands, feet, abdomen, and face. Anthropometric data: weight 4.7 kg, height 56 cm; height/age Z-score of -2.52, with unquantifiable weight/height and weight/age Z-scores due to severe dehydration. Segmental examination revealed fine crepitus in both lung bases suggestive of pulmonary interstitial involvement, and erythematous-squamous skin lesions with desquamation, as well as hypopigmented patches on trunk and upper limbs, interpreted as pellagroid dermatosis, likely secondary to vitamin B3 deficiency.\n\nInitial resuscitation included lactate Ringer's bolus (10 ml/kg), followed by 5% dextrose in 0.33% saline (500 mL) infused at 29 mL/h over 6 hours without KCL until diuresis was achieved. Empirical antibiotic therapy was initiated with ceftriaxone 50 mg/kg/day for suspected sepsis. After stabilization, the patient was transferred to the ward and maintained on 500 mL of 5% dextrose in 0.9% saline at 20 mL/h. Laboratory findings included leukocytosis (39.0 × 10³/μL), severe anemia (5.6 g/dL), and thrombocytosis (502 × 10³/μL). The patient received a transfusion of 50 mL of filtered, leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to coagulopathy. Enteral feeding was initiated via nasogastric tube, and fluid infusion was reduced to 15 mL/h of 5% dextrose in 0.9% saline (500 mL), with a negative water balance maintained.\n\nOn day 2, initial peripheral blood culture yielded Gram-positive cocci in clusters, interpreted as *Staphylococcus aureus*. Oxacillin was administered at 200 mg/kg/day, and ceftriaxone was escalated to 75–100 mg/kg/day. Total fluid replacement was increased to 120 mL/kg/day, and calcium was corrected (to 6.38 mg/dL). On day 3, venous access was lost, necessitating placement of a central venous catheter (CVC). The patient remained hypovolemic with subhydrated oral mucosa, increased respiratory effort, cold extremities, and capillary refill time of 3–4 seconds. A rapid Ringer's lactate infusion (


A 2-year-old girl had a big lump inside her eye socket that made her eye stick out and move inward and upward. The lump was soft, not painful, and grew slowly over a year. Doctors saw it on a scan and found it was a type of tumor called a teratoma. They removed it through a small cut in the lower eyelid, and during surgery, they saw parts of brain, skin, and cartilage inside the lump. After the surgery, the child’s eye started to sink back in (enophthalmos), her eyelid became red, and her cornea got inflamed because the space in her eye was too small. To fix this, doctors placed a piece of donor eye tissue (sclera) into the socket to fill the space and help the eye sit properly again. One year later, the tumor didn’t come back, and her eye looked better. She still has a little bit of eye sinking and a small eyelid issue, but her vision is the same as before. The eye is now stable and no other problems were seen.


A 2-year-old female presented with a 1-year history of painless, progressive left-sided proptosis, without systemic comorbidities or familial predisposition. Ophthalmologic evaluation revealed preserved light perception as the sole visual input in the left eye, accompanied by marked proptosis, inward and upward displacement of the globe, and restricted downward and outward extraocular muscle movements. A palpable, irregularly shaped, well-circumscribed soft mass was identified in the inferior left orbit, associated with left lower eyelid ectropion. The pupil measured 4 mm in diameter and exhibited absent pupillary reaction. Anterior segment examination was otherwise unremarkable, though fundus assessment was compromised due to the child’s small size. Hertel exophthalmometry demonstrated a right eye measurement of 10.5 mm and a left eye measurement of 18 mm, indicating significant orbital expansion. Magnetic resonance imaging (MRI) revealed a well-defined orbital mass with hypointense signal intensity on T1-weighted images (T1WI) and hyperintense signal intensity on T2-weighted images (T2WI), consistent with a cystic or mixed tissue composition. Contrast-enhanced MRI showed no significant enhancement, suggesting a non-vascularized or low-vascularity lesion. A transconjunctival approach via the inferior fornix was employed, with concomitant canthotomy and cantholysis to facilitate access. Surgical exploration revealed a grayish-white, cystic mass with a distinct interface from surrounding orbital tissues. Posterior dissection encountered tight adhesion between the mass and the optic nerve, indicating prior extensive orbital expansion and tissue deformation. Given the substantial size of the lesion and limited surgical field, volume reduction was necessary; approximately 12.5 mL of intralesional fluid was aspirated prior to complete excision. Histopathological analysis confirmed a fibrous capsule lined with squamous and glandular epithelium, with the presence of brain-derived tissue and a cartilaginous matrix, pathologically consistent with an orbital teratoma. One month postoperatively, the patient developed enophthalmos, conjunctival hyperemia, and keratitis. This sequelae was attributed to the preoperative orbital cavity enlargement, leading to postoperative orbital volume collapse and corneal exposure, resulting in inflammation due to inadequate eyelid coverage. With informed consent from the patient’s guardian, a second surgical intervention was performed involving the implantation of allogeneic sclera into the orbital cavity to restore orbital volume, correct fossal pitting, and re-establish corneal apposition. Follow-up over one year demonstrated no recurrence of teratoma or other complications. Persistent minor enophthalmos and outer canthus deformity remained, though visual acuity remained unchanged from preoperative levels. Repeat Hertel exophthalmometry showed a right eye measurement of 10.5 mm and a left eye measurement of 8 mm, indicating partial correction of proptosis. The anterior segment remained clinically stable, with no evidence of recurrent inflammation or structural compromise. The findings support the diagnosis of a complex orbital teratoma with significant orbital expansion, and highlight the importance of surgical volume management and postoperative orbital reconstruction in pediatric cases with large, adherent teratoma masses.


A 78-year-old woman was feeling very tired, weak, dizzy, and confused for months. This made it hard for her to leave her house or walk around. She was taking many medicines, and one of the problems might have been her blood pressure medicines. Her kidneys weren’t working as well as they should, which means her body can’t clear some medicines as easily. The doctors checked her kidney function and found it was low. Based on this, they decided to lower the dose of two blood pressure medicines — losartan and manidipine — so her blood pressure wouldn’t go too low. They also switched her pain medicine from pregabalin to gabapentin, which is safer for her kidneys. After two months, her tiredness, dizziness, and confusion went away. Her blood pressure improved, and she felt much better.


A 78-year-old woman who was taking several medications reported feeling tired, weak, dizzy, and confused for months. These symptoms were making it hard for her to leave her home. She was evaluated at a community pharmacy as part of a personalized medication program. The team checked her medications, especially those processed by the kidneys, using her estimated glomerular filtration rate (eGFR), which was 30 ml/min/1.73 m² — a sign of reduced kidney function. Based on this, they found that her doses of losartan and manidipine, which are blood pressure medicines, needed to be lowered to prevent low blood pressure. The pharmacy sent a report to her primary care doctor, who agreed to reduce losartan to 50 mg per day and manidipine to 10 mg per day. The doctor also switched her pregabalin to gabapentin, which is safer for her kidney function. After two months of follow-up, her blood pressure improved, and the symptoms of tiredness, weakness, dizziness, and confusion went away. The change in medication was successful and her condition stabilized.


{
  "proficient_health_literacy": "A 78-year-old female patient, enrolled in a Personalised Medication Dosage System (PDS), presented with persistent symptoms of fatigue, weakness, dizziness, and confusion over several months, significantly impairing her ability to perform ambulatory activities. Upon clinical evaluation, she was referred to a personalised care setting to assess medication knowledge, adherence, and potential drug-related adverse effects. A comprehensive medication review was conducted, with particular focus on pharmacokinetic parameters relevant to renal function, specifically the estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, which yielded an eGFR of 30 ml/min/1.73 m²—indicative of stage 3 chronic kidney disease (CKD).\n\nThe patient's pharmacological regimen includes multiple agents: doxazosin (2 mg/24 h), losartan (100 mg/24 h), manidipine (20 mg/24 h), simvastatin (40 mg/24 h), acetylsalicylic acid (100 mg/24 h), omeprazole (20 mg/24 h), pregabalin (100 mg/12 h), torasemide (10 mg/24 h), dulaglutide (1.5 mg/week), insulin glargine (74 IU/24 h), insulin lispro (20 IU/24 h), and brimonidine (1 drop/12 h). Among these, losartan, manidipine, torasemide, and pregabalin were identified as agents requiring dose adjustment in the context of impaired renal function due to altered pharmacokinetics—specifically, reduced clearance via the kidneys.\n\nLosartan, an angiotensin II receptor blocker (ARB), and manidipine, a dihydropyridine calcium channel blocker (DCCB), are primarily eliminated by renal excretion. In patients with eGFR <60 ml/min/1.73 m², their clearance is diminished, increasing the risk of accumulation and adverse effects, including hypotension. According to product monographs and the consensus guidelines developed by the University of Barcelona Faculty of Pharmacy’s practical pharmacy teaching and research group—based on real-world dispensing data and ATC-based therapeutic categorisation—dose reductions are recommended: for losartan, a reduction to 50–75% of the original dose (i.e., 50 mg/24 h) is advised when eGFR ranges from 30 to 59 ml/min/1.73 m²; for manidipine, the recommended dose is adjusted to 10 mg/24 h when eGFR is between 15 and 30 ml/min/1.73 m². These adjustments are grounded in pharmacodynamic and pharmacokinetic evidence showing dose-dependent hypotensive effects in renal impairment.\n\nTorasemide, a loop diuretic, also influences blood pressure regulation and may contribute to hypotension when used in patients with reduced renal function due to decreased volume excretion and potential for electrolyte imbalance. Pregabalin, used for neuropathic pain, is metabolised via hepatic pathways but may exhibit increased systemic exposure in renal impairment due to secondary effects on clearance; however, its primary route of elimination is hepatic, and thus, dose adjustment is less critical in this context, though monitoring is advised.\n\nAn initial intervention was proposed, recommending a reduction of losartan to 50 mg/24 h and manidipine to 10 mg/24 h, with the option to evaluate pregabalin dose modification post-adjustment of antihypertensives. The patient was informed of the rationale, and a detailed report was submitted to her Primary Care Physician (PCP), outlining the pharmacological basis for the proposed changes. The PCP implemented the recommended dose reductions and substituted pregabalin 100 mg/12 h with gabapentin 300 mg/12 h, a non-narcotic alternative with a more favorable renal clearance profile.\n\nA two-month follow-up demonstrated significant clinical improvement: blood pressure values normalized (systolic 128–135 mmHg, diastolic 75–80 mmHg), and the patient reported complete resolution of fatigue, dizziness, and confusion. The gabapentin dose of 300 mg/12 h was confirmed to be within the recommended range for eGFR 30–60 ml/min/1.73 m² (total daily dose: 300–900 mg), indicating appropriate dosing without risk


This story is about a 9-year-old girl who has very smart brain skills but struggles with reading and writing because of dyslexia. Before help, she could only read simple letters and had a hard time with sounds and words. She wrote in a messy way, mixing up letters and skipping parts. After getting special reading and sound practice (like playing games to learn how sounds work), she got better. Now she reads faster and more clearly, and her writing is more organized. She still has some trouble with some letters and sounds, but she’s making progress. The help focused on her sound skills, which helped her read and write better, even though she’s still smart and has special abilities.


{
  "proficient_health_literacy": "This case study reports a longitudinal evaluation and targeted phonological remediation intervention in a 9-year-old female child diagnosed with developmental dyslexia (DD) and high abilities/giftedness (AH/S). The study was approved by the Research Ethics Committee (CEP) under protocol number 1.012.635, with informed consent obtained from both parents and the participant via Free and Informed Consent (TCLE and TALE). The participant, enrolled in the third year of elementary school, was initially assessed at 8 years and 2 months (T1, 2018) and re-evaluated at 9 years and 6 months (T2, 2019), with the interval attributed to public service constraints, weekly appointment scheduling, and school holidays. The child was born at term with typical neuropsychomotor and linguistic development; she was raised in a French-speaking environment until age 2, after which her primary language at home became Brazilian Portuguese, though her first words were in French. Upon return to Brazil, she attended two private schools, initially experiencing communication difficulties due to language mismatch, leading to a transition into a French school at age 3. Over time, she exhibited persistent difficulties in reading and writing, resulting in a repetition of the first year of elementary school. At age 6, she entered a bilingual Portuguese-English school. At age 8, she underwent an interdisciplinary assessment in speech therapy and neuropsychology, leading to a formal diagnosis of developmental dyslexia with concomitant high cognitive abilities. She was subsequently referred to the Laboratory of Written Language, Interdisciplinarity and Learning (LEIA/UFRN) for comprehensive written language evaluation.\n\nThe intervention consisted of 20 weekly sessions (60 minutes each) of phonological remediation, conducted during the second semester of 2018, with limited parental engagement due to work commitments. Assessments were administered individually over one hour and included standardized tasks measuring phonological processing, reading, and writing. The following protocols were employed:\n\n- **Phonological Awareness**: Evaluated using the Consciência Fonológica Instrumento de Avaliação Sequencial (CONFIAS). This instrument includes tasks assessing syllabic and phonemic awareness (synthesis, segmentation, rhyme, alliteration, initial/final syllable identification, exclusion, transposition). Syllabic awareness comprises 9 items (max 40 points), phonemic awareness 7 items (max 30 points), totaling 70 points. Normative values derived from Ferreiro and Teberosky were used: for syllabic-alphabetic writing hypothesis, expected scores of 27 (syllabic), 12 (phonemic), and 39 (total); for alphabetic writing hypothesis, 31 (syllabic), 15 (phonemic), and 46 (total).\n\n- **Phonological Working Memory**: Assessed via the Phonological Working Memory Test. The protocol includes a non-word repetition task (40 invented words), with scoring: 2 points for first correct repetition, 1 point for second, 0 for third. A digits test in direct and reverse order follows, scored similarly. Age-specific norms were applied: for T1 (age 8 years 2 months), expected scores of 69 (pseudo-words), 13 (direct digits), and 6 (reverse digits).\n\n- **Mental Lexicon Access**: Evaluated using the Rapid Automatic Naming Test (RAN) at T1 and the Automatic Naming Test (TENA) at T2. Both assess naming speed of visual stimuli (colors, objects, letters, digits) using a left-to-right, top-to-bottom reading movement. For T1 (age 8 years 2 months), RAN normative values were 28 (digits), 29 (letters), 52 (objects), 46 (colors). For T2 (age 9 years 6 months), TENA norms were 35 (digits), 32 (letters), 50 (objects), 53 (colors).\n\n- **Reading**: Assessed via two protocols. First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated (LPI), comprising 19 regular words, 20 irregular words, and 20 pseudowords in Arial 24pt font. Correct responses are scored individually (max 59 points). Second, the Assessment of Expository Texts evaluates reading comprehension through directed questions and measures silent and oral reading speed, enabling calculation of words per minute (wpm).\n\n- **Writing**: Evaluated through a free narrative task on a topic of interest, followed by oral reading of the written text and a dictation of LPI words and pseudowords. Qualitative analysis was conducted using orthographic criteria


A 65-year-old woman found a lump in the middle of her chest during a knee surgery check-up. Doctors saw it on a chest scan and found it was a round, clear lump, about 6.5 cm long and 4.2 cm wide, sitting in the back part of the chest. The lump didn’t hurt or spread to nearby areas. They took a small sample and looked at it under a microscope. It showed fat and blood-filled areas, along with some blood cell parts that were normal and mature. This told them it was a harmless tumor, called a myelolipoma. Since it wasn’t dangerous, they chose not to remove it and just watched it. She got better and went home without any problems.


A 65-year-old woman was found to have a tumor in the middle of her chest, specifically in the posterior mediastinum, during a preoperative check-up for knee surgery. The tumor measured 6.5 × 4.2 cm, had clear borders, and was made up of fat and solid tissue with no signs of spreading to nearby structures. A biopsy was done using imaging guidance, and the results showed that the tumor contained mature fat tissue along with blood cells and early blood cell precursors, which is consistent with a benign condition called primary mediastinal myelolipoma. Because the tumor was not dangerous and did not show signs of growth or spread, the doctors chose not to treat it surgically. The patient recovered well and was discharged without any complications.


A 65-year-old woman with no significant personal or familial medical history presented in August 2022 with a posterior mediastinal tumor identified during preoperative imaging for knee surgery, prompting referral for evaluation. Physical examination at admission was unremarkable, and all laboratory investigations remained within normal limits. A chest computed tomography (CT) scan revealed a well-defined, ovoid lesion measuring 6.5 × 4.2 cm in the posterior right mediastinum, exhibiting mixed fat and solid densities, with no evidence of bone erosion, soft tissue infiltration, or vascular involvement. The tumor was characterized by distinct borders and homogeneous attenuation consistent with adipose tissue intermixed with solid components. A trans-thoracic biopsy was performed using a 18G × 250 mm semiautomatic cutting needle under image guidance via a posterior approach, ensuring precise lesion sampling. Histopathological analysis demonstrated a benign neoplasm composed of mature adipose tissue interspersed with areas of hemorrhage and hematopoietic elements, including erythroid precursors (primarily proerythroblasts and basophilic erythroblasts) and myeloid lineage cells at various stages of differentiation, including promyelocytes, myelocytes, metamyelocytes, and mature granulocytes. Additionally, megakaryocytic elements were observed, indicating active hematopoiesis within the adipose matrix. These findings are consistent with primary mediastinal myelolipoma (MPM), a rare benign tumor of the mediastinum characterized by coexistence of mature adipose tissue and hematopoietic elements, typically arising from a primitive mesenchymal precursor that retains hematopoietic potential. The presence of hematopoietic components, particularly in the context of mature adipose stroma, supports the classification as a myelolipoma rather than a hematologic malignancy. Given the benign histological profile, lack of malignant transformation, and absence of local or systemic signs of disease progression, conservative management was elected. The patient demonstrated stable clinical course, with no evidence of tumor growth, complications, or systemic symptoms, and was discharged without adverse events. This case underscores the importance of accurate imaging interpretation and histopathological characterization in distinguishing benign mediastinal masses from malignant counterparts, particularly in the context of hematopoietic tissue coexistence within adipose stroma.


A 52-year-old man got sick with both a bad fever and a COVID-19 virus. He worked outside in very hot weather and suddenly lost consciousness. His body temperature reached 104°F, and he fell into a deep coma. Doctors found he had a serious lung infection, damaged liver and kidneys, and a blood problem that made clots form easily. Even with medicine, fluids, and breathing support, he started having trouble breathing and a brain bleed later. He also had a lung infection from other germs, and his body couldn’t fight it well. After days of treatment, his fever and coma went away, but he got worse — he couldn’t breathe properly and had a brain bleed. The damage to his organs, caused by the fever and infections, eventually led to his death.


{
  "proficient_health_literacy": "A 52-year-old male presented with a community-acquired SARS-CoV-2 infection confirmed by reverse-transcription polymerase chain reaction (RT-PCR) of a nasopharyngeal swab, following a self-reported cold. He returned to work after a two-day rest without fever but lost consciousness while working outdoors in an ambient temperature of 35°C for five hours. Upon emergency department admission, his core temperature (Tc) was 40°C, consistent with hyperpyrexia. He presented with persistent coma, dyspnea, and gastrointestinal hemorrhage, with no known comorbidities or family history of disease. Clinical features—including hyperpyrexia, coma, and multi-organ dysfunction—led to a diagnosis of heatstroke (HS). He was admitted to the emergency intensive care unit (ICU) and required mechanical ventilation due to respiratory failure. Initial laboratory findings revealed severe systemic infection, with leukopenia (WBC: 3.13×10⁹/L), profound lymphopenia (lymphocytes: 0.1×10⁹/L), neutrophilic shift (N%: 85.3%), elevated procalcitonin (2.81 ng/mL) and C-reactive protein (32.6 mg/L), indicating a strong bacterial component. Sputum culture identified Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture revealed Staphylococcus epidermidis, while blood cultures remained negative, suggesting a polymicrobial pulmonary infection with possible nosocomial or community-acquired origin. CT imaging demonstrated bilateral frontal subdural effusions, lower lobe consolidation and atelectasis, right upper lobe inflammation, bilateral pleural effusion, and minimal ascites, consistent with severe pulmonary infection and secondary pulmonary edema.\n\nThe patient received initial resuscitation with intravenous rehydration using lactated Ringer’s solution and normal saline at 2.5 mL/kg·h, vasoactive support with norepinephrine (0.4 µg/kg·min) to maintain blood pressure (126/77 mmHg), and broad-spectrum antibiotics including piperacillin-tazobactam, later switched to meropenem due to resistance concerns. Immune modulation with thymalfasin was administered for 20 days. Hepatic and renal dysfunction were managed with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and continuous renal replacement therapy (CRRT) for anuria. Coagulopathy was characterized by thrombocytopenia, disseminated intravascular coagulation (DIC), and elevated D-dimer levels, managed with plasma and cryoprecipitate transfusions, continuous intravenous heparin (6000 U/day), and CRRT with sodium citrate anticoagulation (8 g/day). Platelet transfusion was initiated on day 9. Intracranial pressure was managed with mannitol for three days. Despite initial improvement, the patient developed recurrent dyspnea and fever on day 17 (Tc: 39.3°C), requiring reintubation. Bronchoscopy showed reduced sputum volume, and GCS dropped to 3/15, with elevated WBC (14.94×10⁹/L) and neutrophils (13.77×10⁹/L). Laboratory markers worsened: serum total bilirubin increased to 235.2 µmol/L, creatinine to 441 µmol/L. Brain CT revealed ischemic stroke in the right frontal lobe and hemorrhagic infarction in the right occipital lobe, suggesting both vascular injury and microangiopathic damage. Cooling therapy via ice-cold CRRT was initiated. Fungal infection was suspected based on elevated serum Aspergillus galactomannan, Aspergillus IgG, and Candida mannan, leading to addition of carpofungin on day 18. SARS-CoV-2 RT-PCR became negative on day 18, indicating viral clearance or assay limitations.\n\nOn day 20, fever and infection resolved, but the patient developed cerebral hemorrhage and brain herniation with bilateral dilated pupils. Dehydration therapy was used to reduce intracranial pressure, but surgical intervention was declined by family. On day 22, inflammatory markers, liver enzymes (aspartate aminotransferase), and creatinine worsened again, with bronchoalveolar lavage fluid cultures positive for carbapenem-resistant Acinetobacter baumannii and Aspergillus fumigatus. Anti-infective therapy was intensified with meropenem, teicoplanin


{
  "proficient_health_literacy": "A 19-year-old female presented to the emergency department with a two-day history of headache, recurrent nausea, vomiting, and one-day fever. On admission, she had a high fever of 39.1°C, severe hypertension (189/120 mmHg), and tachycardia (148 beats per minute). Laboratory findings revealed a leukocytosis (14.77×10^9/L) with neutrophilia (13.55×10^9/L), suggestive of systemic inflammation or infection. Empirical antibiotic therapy with moxifloxacin was initiated, but symptoms persisted, prompting admission to the intensive care unit for close monitoring. A year prior, she had been diagnosed with myocarditis at a local hospital, along with hypertension, for which antihypertensive therapy was prescribed; however, she discontinued adherence to medication and failed to monitor blood pressure regularly. Notably, her father had a history of sudden, unexplained death, raising concerns for a hereditary endocrine disorder.\n\nA chest CT scan incidentally revealed a left adrenal mass measuring 43 mm × 36 mm with soft tissue density. Head and chest CTs showed no other pathological abnormalities. Electrocardiography demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF, consistent with volume overload or myocardial stress. Transthoracic echocardiography was unremarkable.\n\nOn day two of admission, biomarkers including brain natriuretic peptide (BNP) and cardiac troponin I (TnI) increased, supporting a provisional diagnosis of myocarditis of uncertain etiology. Treatment included methylprednisolone (0.25 g/day) for presumed myocardial inflammation, furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) for fluid management, and perindopril amlodipine (10 mg: 5 mg daily) for blood pressure control and afterload reduction. Metoprolol tartrate (25 mg every 12 hours) and esmolol (0.2 g/hour IV infusion) were used to control heart rate and reduce myocardial oxygen demand.\n\nGiven the presence of an adrenal mass and sustained hypertension, endocrine workup was initiated, including assessment of aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines and metabolites. In the recumbent position, plasma catecholamines were markedly elevated: dopamine (524.5 pmol/L), norepinephrine (83,975 pmol/L), and epinephrine (10,579.3 pmol/L). Urinary excretion levels included free adrenaline (4,368.89 nmol/24 h), free norepinephrine (>12,697.60 nmol/24 h), normetanephrine (8,312 nmol/24 h), metanephrines (4,078 nmol/24 h), and vanillylmandelic acid (58.1 mg/24 h). These findings are consistent with pheochromocytoma and supported the clinical diagnosis.\n\nOn day five post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was replaced with terazosin to provide more precise blood pressure control in the setting of catecholamine excess. An enhanced abdominal CT confirmed the left adrenal mass, highly suggestive of pheochromocytoma. Whole-exome sequencing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), resulting in substitution of cysteine by arginine at codon 634. This mutation is pathogenic and associated with multiple endocrine neoplasia type 2A (MEN2A), prompting further endocrine evaluation of the thyroid and parathyroid glands.\n\nThyroid color Doppler ultrasound identified a hypoechoic nodule measuring 6 mm × 4 mm in the left thyroid lobe, with mildly elevated serum calcitonin levels. Parathyroid function tests showed normal serum calcium, phosphate, and parathyroid hormone (PTH) levels. No other significant endocrine abnormalities were detected.\n\nFollowing clinical stabilization, plasma cortisol and ACTH levels normalized. The patient underwent surgical resection of the left adrenal tumor, which measured 50 mm × 40 mm × 30 mm. Immunohistochemical analysis confirmed positive staining for vimentin (


A 36-year-old man had a painful lump on the inside of his penis and scrotum for 5 years. The lump was not causing trouble with urination or weight loss. Doctors found it was a hard, cyst-like growth, about 2 cm big, with lots of blood flow. Imaging showed it was attached to the tube that carries sperm and was deep in the area, not near the testicle or cord. After surgery, the doctors found it was a type of cancer called synovial sarcoma — a kind of tumor that grows in the tissue around joints. The tumor had signs that matched this cancer, and tests confirmed it had a genetic change known in this type of cancer. The first surgery removed the lump, but the cancer came back. The patient had a second surgery to remove more tissue, and even after that, the cancer spread to his liver and spine. He tried several chemotherapy treatments, but none worked. He had more surgeries on his liver, then got a lung tumor. He tried more medicines and radiation, but the cancer kept growing. Eventually, he was moved to palliative care and stopped seeing doctors because the disease was no longer treatable.


A 36-year-old man had a painful lump in the penis and scrotum for 5 years. The lump was about 20 mm in size, not attached to the spermatic cord, and was tender but not causing urinary problems. Imaging showed a well-defined mass with lots of blood flow, and it was connected to the vas deferens. Blood tests were normal. After surgery, the tissue was examined and found to be a type of cancer called synovial sarcoma. The tumor cells were arranged in a specific pattern and tested positive for markers like TLE-1, CD99, BLC2, cytokeratin, and EMA. A genetic test confirmed a known change in the SS18 gene, which is common in this type of cancer. The first surgery removed the mass completely, but the margins were hard to assess because the sample was fragmented. A second surgery was done with wider margins, and the new tissue sample showed no signs of cancer. However, after 16 months of monitoring, the cancer spread to the liver and spine. Despite multiple treatments—including chemotherapy with Ifosfamide and Doxorubicin, surgery to remove liver tumors, and targeted therapy with Pazopanib and radiation—the cancer continued to grow. He tried several other chemotherapy regimens, including Gemcitabine and Docetaxel, and Dacarbazine, but all failed. Eventually, he was moved to palliative care and stopped treatment due to disease progression.


{
  "proficient_health_literacy": "A 36-year-old male with no significant past medical history presented with a 5-year history of a left-sided penoscrotal mass. The patient reported no lower urinary tract symptoms, trauma, infections, weight loss, anorexia, or fever. Physical examination revealed a smooth, tender, cystic lesion measuring approximately 20 mm × 20 mm located at the penoscrotal junction, attached to the left side of the bulbar urethra, deep in the tissue, without skin tethering or association with the left spermatic cord, and partially mobile. Doppler ultrasonography demonstrated a well-defined hypoechoic mass measuring 2.7 cm × 3.1 cm × 2.0 cm with markedly increased vascularity on the left penoscrotal junction. Pelvic magnetic resonance imaging (MRI) showed a lesion in the left inferolateral base of the penis with a distinct fat plane, isointense to testicular tissue on T2-weighted, T1-weighted, and diffusion-weighted imaging sequences, and with direct connection to the vas deferens; no regional lymphadenopathy was observed. Serum alpha-fetoprotein and beta-human chorionic gonadotropin levels were within normal limits. Given the chronic pain and imaging findings, surgical resection was performed for both diagnostic and therapeutic purposes. Intraoperatively, a mass was identified in the left posterolateral scrotum and completely resected, with the specimen sent for histopathological evaluation.\n\nHistopathological analysis revealed a cellular spindle cell tumor organized in interlacing fascicles, comprising spindle- to oval-shaped cells with vesicular nuclei, evenly distributed chromatin, and inconspicuous nucleoli. The tumor exhibited high mitotic activity, with up to 3 mitotic figures per high-power field. Immunohistochemical staining was positive for TLE-1, CD99, B-cell lymphoma 2 (BCL-2), focal cytokeratin, and focal epithelial membrane antigen (EMA), consistent with synovial sarcoma. Fluorescence in situ hybridization (FISH) analysis confirmed a characteristic rearrangement of the SS18 gene at 18q11.2, a molecular hallmark of synovial sarcoma. Histological assessment of the margins was inconclusive due to fragmentation of the resection specimen.\n\nTwo weeks post-initial surgery, the patient returned for a multidisciplinary review. Based on the histopathology, a second surgical resection with wider margins was proposed and accepted. A positron emission tomography–computed tomography (PET/CT) scan of the head, neck, chest, abdomen, pelvis, and musculoskeletal system was performed, revealing a 29 mm × 27 mm thyroid nodule in the lower pole of the left lobe with moderate hypermetabolism (standardized uptake value [SUV] of 4.9). Thyroid ultrasound demonstrated a solid, isoechoic, well-defined nodule without echogenic foci. The nodule was classified as TIRADS category 3 (TR3), indicating a low risk of malignancy.\n\nA second surgical resection was performed three weeks after the initial procedure. The resection extended bilaterally to the spermatic cords, deepening to the corpus spongiosum and shaving superiorly to the urethra. The final resected specimen measured 6.0 cm × 6.0 cm × 3.0 cm and was histologically negative for residual tumor. The patient then entered active surveillance. At 16 months, metastatic disease was detected in the sixth segment of the liver and the L1 vertebral body. The oncology team initiated a six-cycle regimen of ifosfamide and doxorubicin, which showed no clinical or radiographic response. Subsequent surgical resection of the fifth and sixth liver segments, along with cholecystectomy, was performed. The patient later developed a new pulmonary lesion, prompting initiation of pazopanib and stereotactic body radiation therapy (SBRT). After six months of surveillance, new lesions emerged in both the liver and lungs. A gemcitabine and docetaxel combination chemotherapy regimen was administered for three cycles, followed by progression. The patient then received two cycles of dacarbazine, with further progression. Subsequently, two cycles of pembrolizumab were administered, also resulting in disease progression. Given the lack of response to all available systemic therapies, the patient was transitioned to palliative care and discontinued follow-up. This case highlights the aggressive clinical course of synovial sarcoma, particularly in the penoscrotal region, with early local recurrence, metastatic spread to liver and bone, and resistance to conventional chemotherapy and immunotherapy regimens, underscoring the need for early detection, comprehensive surgical margins, and exploration of novel targeted or immunother


A 13-year-old boy came to the emergency room with sudden chest pain on the sides of his chest, especially when coughing. The pain wasn’t linked to fever or other symptoms, and he didn’t feel short of breath. He had a mild cold and a one-time fever, but no joint pain, weight loss, or fatigue. He still played sports regularly. His chest X-ray from 4 years ago showed a similar lung problem, which was treated with an antibiotic called azithromycin and has stayed quiet since. This time, his new chest scan showed a lot of cloudy areas in both lungs, more than two-thirds of them, which points to a rare lung condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including the coronavirus, came back negative. A lung fluid test showed a milky fluid and a sign that matches PAP. His breathing test showed a slight drop in lung function, but he’s still able to breathe and play. No gene changes were found that cause lung problems. A test for a specific immune protein showed it was missing, which makes it likely this is an autoimmune form of PAP. After 20 months, he’s feeling fine, breathing normally, and still plays sports. No treatment is needed right now — just regular check-ups to keep an eye on his lungs.


{
  "proficient_health_literacy": "A 13-year-old male with no significant prior medical history presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain, associated with mild non-productive cough, mild rhinorrhea, and a single febrile episode (38°C). The chest pain was localized to the costal margin and exacerbated by coughing, without diurnal variation or respiratory distress. Symptoms were partially relieved with paracetamol. There were no reports of joint pain, weight loss, anorexia, fatigue, syncope, or exercise intolerance; he maintained regular physical activity, including weekly canoeing. No history of infectious exposure, environmental exposures (e.g., dust, fumes, mineral oils), or familial cardiopulmonary disease was reported. A prior chest radiograph, obtained four years earlier during an acute illness, demonstrated a marked interstitial infiltrate, which was initially treated with azithromycin and has remained asymptomatic since, with no subsequent follow-up.\n\nOn admission, vital signs were stable: temperature 37.8°C, oxygen saturation 99% on room air, heart rate 93 bpm, respiratory rate 15 breaths per minute, and blood pressure at the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two-thirds of the lung fields without adventitious sounds, respiratory distress, cyanosis, clubbing, or abnormal cardiac murmurs. Chest radiography showed a persistent interstitial infiltrate, morphologically similar to the prior finding. Thoracic computed tomography (CT) revealed multiple bilateral ground-glass opacities involving greater than 65% of lung parenchyma, with areas of 'crazy paving' pattern—findings highly suggestive of pulmonary alveolar proteinosis (PAP).\n\nRespiratory viral testing, including for SARS-CoV-2, was negative. The patient was initially managed with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) for suspected respiratory infection, and symptoms resolved. He was discharged and referred to a pediatric respiratory clinic for further evaluation.\n\nOutpatient workup revealed positive antinuclear antibodies (ANA) at a titer of 1/89 with a fine speckled pattern, while other autoantibodies (e.g., anti-dsDNA, anti-Smith, anti-Ro/SSA) were negative, and immunoglobulin levels were within normal ranges. Bronchoalveolar lavage (BAL) fluid exhibited a milky appearance and demonstrated positive periodic acid-Schiff (PAS) staining, indicating the presence of surfactant proteins and alveolar protein accumulation. Microbiological analysis of BAL, including for mycobacteria, was negative, excluding infectious etiologies. Spirometry showed a mild restrictive pattern: forced vital capacity (FVC) of 2.92 L (77%), forced expiratory volume in 1 second (FEV1) of 3.21 L (69.9%), and a normal FEV1/FVC ratio of 109%, consistent with preserved airflow dynamics. Diffusing capacity of the lungs for carbon monoxide (DLCO, single breath) was reduced to 13.8 ml/min/mmHg (48.6%), indicating impaired gas exchange, consistent with alveolar membrane thickening or protein deposition.\n\nGenetic testing for mutations associated with surfactant dysfunction (e.g., SFTPA1, SFTPB, SFTPC, ABCA3) was negative, ruling out inherited surfactant-related disorders. Testing for anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibodies was strongly positive, supporting a diagnosis of autoimmune pulmonary alveolar proteinosis (AI-PAP), in which the immune system produces autoantibodies that inhibit GM-CSF function, leading to impaired alveolar macrophage clearance of surfactant proteins and subsequent protein accumulation in alveoli.\n\nAt 20-month follow-up, the patient remains asymptomatic and continues to engage in regular physical activity. Repeat spirometry shows normalization of FVC (4.03 L, 81.3%), FEV1 (3.71 L, 87.5%), and FEV1/FVC ratio (91.96%), indicating partial recovery or stabilization of pulmonary function. DLCO has improved to 25.54 ml/min/mmHg (83.7%), suggesting partial restoration of gas exchange. Given the absence of symptoms and stable pulmonary function, treatment was deferred, and the patient is being managed with routine clinical monitoring. The case underscores the clinical and radiological overlap between acute respiratory illness and chronic alveolar proteinosis, particularly in adolescents with recurrent interstitial infiltrates and autoimmune markers,


A 27-year-old woman had swelling on her face and trouble opening her mouth 48 hours after taking antibiotics for a tooth infection. A scan of her neck showed a big blood clot in a vein, and a chest scan found clots in her lungs. She was treated right away with strong antibiotics and medicine to thin her blood to stop the clots from getting worse. She got better after a few days of this treatment.


A 27-year-old woman developed facial swelling and difficulty opening her mouth (trismus) 48 hours after taking phenoxymethylpenicillin for a throat infection. Tests showed a large blood clot in the internal jugular vein of her neck and lung clots from the infection spreading to her lungs (pulmonary septic embolism). She was treated with strong intravenous antibiotics and anticoagulant medication to stop the clot from growing and to fight the infection. Her symptoms improved over several days, and after 14 days of treatment, she was able to go home on oral antibiotics and continued anticoagulation therapy.