A 27-year-old woman with a history of uncontrolled asthma and a prior mild SARS-CoV-2 infection presented 48 hours after completing oral phenoxymethylpenicillin 1,000,000 IU daily for five days, administered for a peritonsillar abscess, with new-onset facial edema and trismus. Physical examination revealed hemodynamic stability, absence of respiratory distress, and a palpable, homolateral, tender cervical adenopathy consistent with regional lymphadenopathy. Laboratory findings demonstrated leukocytosis, thrombocytopenia, and elevated acute-phase reactants, with no significant abnormalities in other parameters. Imaging studies included a head and neck CT, which revealed a large thrombus involving both the internal and external carotid arteries, consistent with a potentially infectious or inflammatory etiology triggering vasculopathy. A chest CT scan identified bilateral pulmonary septic emboli, indicating the dissemination of infectious material via venous thromboembolism from the head and neck region. Arterial Doppler ultrasound of the neck vessels was unremarkable, and cardiac Doppler ultrasound excluded cardiac vegetations, suggesting a non-cardiac source of embolic material. Initial empiric intravenous therapy consisted of ceftriaxone 1 g every 12 hours and clindamycin 300 mg every 6 hours to cover both gram-negative and gram-positive pathogens, including potential anaerobes. Concurrent anticoagulation was initiated with enoxaparin, dosed at 60 mg subcutaneously every 12 hours, adjusted for body weight and renal function, to manage the thrombotic burden. Over the subsequent 72 hours, the patient developed a fever of 38.5 °C and further leukocytosis, prompting repeat imaging and hemocultures. Hemocultures remained negative, and pharyngeal exudate culture was obtained. Given the clinical progression and lack of microbial growth in cultures, the antibiotic regimen was escalated to piperacillin-tazobactam 4.5 g every 6 hours intravenously to enhance coverage against multidrug-resistant or extended-spectrum pathogens. The patient responded favorably to this regimen, with resolution of fever and clinical signs of infection, and by day 14, chest CT showed complete absence of pulmonary embolic lesions. At that point, oral clindamycin 300 mg every 6 hours was transitioned to continue coverage for anaerobic flora, and anticoagulation was switched to acenocumarol, adjusted to body weight, to maintain therapeutic anticoagulation levels. The patient was discharged without residual complications. The clinical course reflects a rare but serious complication of odontogenic infection—namely, infectious thrombophlebitis of the carotid arteries leading to septic pulmonary embolism—likely mediated by a systemic inflammatory response and endothelial activation due to bacterial endotoxin exposure, potentially exacerbated by underlying immunological vulnerabilities such as uncontrolled asthma and prior viral infection. The thrombotic event may represent a direct effect of bacterial toxins on vascular endothelium or a hypercoagulable state induced by acute inflammation, with subsequent embolic seeding of the pulmonary circulation. This case underscores the importance of early recognition of systemic complications in odontogenic infections, particularly in patients with comorbidities or immunological predispositions, and highlights the need for prompt initiation of broad-spectrum antibiotics and anticoagulation in the setting of suspected septic embolism.


A 5-year-old child swallowed a toxic substance called chlorpyrifos, which hurt his body badly. He also breathed in a mix of charcoal and palm oil, which made his lungs worse. He started with fast breathing, sweating, shaking, and couldn’t breathe properly. He fell into a deep sleep (coma) and had very weak limbs. His breathing was so bad that he needed help right away. Doctors gave him breathing support at home (like a mask), medicine to stop the poison, and drugs to help his heart and blood pressure. He also had blood changes that needed fixing — they replaced part of his blood to clean it. His body slowly got better, he woke up fully, and stopped having trouble breathing. After 10 days, he was strong enough to go home. He didn’t have any serious late problems like some other kids with this poison might. But he didn’t come back for check-ups after leaving the hospital.


A 5-year-old child suffered severe poisoning from chlorpyrifos, a type of organophosphate pesticide, after swallowing it. Shortly after, the child also inhaled a mixture of charcoal and palm oil, which worsened the condition. The poisoning caused serious symptoms including fast breathing, excessive sweating, vomiting, muscle jerks, and eventually coma. At the time of arrival at the emergency department, the child had a very low level of consciousness, pinpoint pupils, weak limbs, and dangerously low oxygen levels in the blood. The heart was beating very fast, and blood pressure was low.

The child was diagnosed with severe organophosphate poisoning and lung damage from aspiration. Treatment included non-invasive breathing support (using bubble CPAP), intravenous atropine to help with the poisoning, antibiotics for the lung infection, and steroids to reduce inflammation. Because the family could not afford intensive care, the treatment was managed with available resources. The child received two blood exchange transfusions to help remove toxic substances from the blood.

Over the next few days, the child’s breathing improved, consciousness returned, and symptoms slowly went away. Blood sugar levels were unstable at first but stabilized with treatment. The child was able to regain full awareness by the 39th hour and started eating regular food again. After 10 days of hospitalization, the child was discharged home, though no follow-up care was arranged afterward. The child did not develop a known complication called intermediate syndrome and responded well to treatment.


{
  "proficient_health_literacy": "A 5-year-old child presented to the pediatric emergency department (ED) 13 hours after ingestion of chlorpyrifos, a potent organophosphate pesticide, followed by aspiration of a charcoal-palm oil mixture. The clinical presentation included acute cholinergic crisis characterized by abnormal muscle jerks, tachypnea (respiratory rate of 48 breaths per minute with intermittent sighing), dyspnea, excessive sweating, polyuria, increased secretions, and involuntary limb movements. The patient lapsed into coma prior to arrival, with presentation parameters including a core temperature of 38.3°C, Glasgow Coma Scale (GCS) of 3, pinpoint pupils, and global hypotonia. Vital signs at presentation revealed tachycardia (pulse 180 beats per minute), normotensive blood pressure (120/80 mmHg), and hypoglycemia (random blood glucose 14 mg/dL). Physical examination noted severe respiratory distress with oxygen saturation of 88% and widespread bilateral crackles on auscultation, indicative of pulmonary edema and aspiration-related pneumonitis.\n\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. Given the lack of ICU resources and affordability constraints, non-invasive ventilation (NIV) was initiated using bubble continuous positive airway pressure (b-CPAP), which successfully improved oxygenation to 99–100%. Hypoglycemia was promptly corrected with a dextrose bolus, and tachycardia was managed with 20 mL/kg of normal saline. Empirical intravenous antibiotics were administered to address suspected aspiration pneumonia. Intravenous atropine was administered at a dose of 0.02 mg/kg/dose to counteract excessive parasympathetic stimulation, with the first dose leading to a significant tachycardic response, prompting discontinuation due to risk of arrhythmia. Dexamethasone and mannitol were administered for cerebral protection and intracranial pressure control, respectively.\n\nDue to the severity of the cholinergic crisis and ongoing respiratory compromise, the patient underwent two episodes of fresh-whole-blood exchange blood transfusion (FWB-EBT), each involving 500 mL of blood, within the first 30 hours of admission. This intervention was likely aimed at rapidly removing circulating organophosphate metabolites and potentially mitigating neuromuscular and metabolic toxicity, though the exact mechanism remains under investigation in the context of acute OPP.\n\nOver the course of the first 30 hours, the patient’s neurological status improved, with GCS rising from 3 to 9/15, and respiratory distress gradually resolving. By day 2, rhonchi developed, managed with nebulized salbutamol and budesonide, and the patient transitioned to nasal prong oxygen therapy with sustained saturation at 97%. A chest radiograph confirmed bilateral pulmonary infiltrates consistent with pneumonia, likely secondary to aspiration and possible secondary infection.\n\nConsciousness was fully restored by the 39th hour of admission. Antioxidant therapy was initiated with intravenous vitamin C and B complex, and oral vitamin E and zinc to counteract oxidative stress induced by organophosphate toxicity and inflammation. A graded dietary reintroduction was implemented over the subsequent 48 hours. The patient’s clinical course remained stable, with progressive recovery of physiological parameters. He was discharged home after 10 days of hospitalization, though subsequent follow-up was lost to contact.\n\nPathophysiologically, chlorpyrifos inhibits acetylcholinesterase (AChE) in synaptic and neuromuscular junctions, leading to accumulation of acetylcholine, resulting in overstimulation of muscarinic and nicotinic receptors. This manifests as the classic cholinergic symptoms (e.g., bronchorrhea, bradycardia, miosis, sweating) and neuromuscular effects (e.g., fasciculations, paralysis). In this case, the severe respiratory failure and type I paralysis (flaccid paralysis) reflect profound neuromuscular blockade due to AChE inhibition. The development of intermediate syndrome, which typically occurs 24–96 hours post-exposure with delayed neuromuscular weakness, was absent, suggesting either a rapid clinical response to treatment or a possible protective effect of early exchange transfusion. The absence of pralidoxime administration (an oxime reactivator of AChE) due to unavailability may have limited the potential for early enzyme reactivation, though the patient’s favorable outcome suggests that supportive care and timely intervention were sufficient to prevent progression to irreversible neurological damage. Serum cholinesterase levels, which are typically suppressed in OPP, were not measured due to institutional limitations, limiting direct biochemical confirmation of enzyme


A 19-year-old woman came to the hospital with a fast, irregular heartbeat and signs that her heart wasn't pumping well. Tests showed her heart was working poorly, and the doctors thought it might be because of a birth defect in her heart. They checked her heart with different scans: one ruled out a heart attack, another didn’t find heart muscle damage, and a special scan (CCTA) found that the main blood vessel to her right side of the heart was missing at the start. Instead, a small blood vessel grew around it to supply the heart. The doctors found the problem spot on a part of the heart muscle called the posteromedial papillary muscle, which was causing the fast heartbeat. They fixed it with a procedure that stops the abnormal heartbeat. Since then, she hasn’t had any symptoms and is feeling fine.


A 19-year-old woman came to the emergency department with sudden palpitations and signs of cardiogenic shock. Her electrocardiogram showed a fast heart rhythm and other abnormal patterns, and her blood tests showed elevated markers of heart stress. A 12-lead ECG ruled out a heart attack, and cardiac MRI did not show signs of heart muscle disease. Because of this, doctors performed a cardiac CT scan (CCTA) to look for a possible congenital heart problem. The scan revealed that the opening of the right coronary artery was missing, and the heart was relying on a collateral blood vessel to supply blood to that area. This is a rare congenital condition. She was referred to a specialist center for congenital heart disease. There, an electrophysiological study found that the arrhythmia was originating from the posteromedial papillary muscle, and this area was successfully treated with radiofrequency ablation. Since the procedure, she has not had any symptoms and is doing well with regular follow-up.


A 19-year-old woman presented to the emergency department with acute onset of palpitations. Initial 12-lead electrocardiogram (ECG) revealed ventricular tachycardia with right branch bundle block and left posterior hemiblock, accompanied by T-wave inversion in inferior and precordial leads. Laboratory findings demonstrated elevated serum troponin (27 ng/L; normal <14 ng/L) and NT-pro BNP (2225 pg/mL; normal <130 pg/mL), indicating myocardial injury and volume overload consistent with cardiogenic shock. She was admitted to the coronary care unit.

Five years prior, she had presented with cardiogenic shock secondary to fascicular ventricular tachycardia. Subsequent evaluation included cardiac magnetic resonance (CMR) and transesophageal electrophysiological study, both of which were inconclusive. She was diagnosed with tachycardiomiopathy and initiated standard medical therapy comprising angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and beta-blockers, with routine follow-up scheduled. Her clinical course remained stable thereafter.

During the current admission, no additional episodes of hyperkinetic arrhythmias were observed. Baseline 12-lead ECG and echocardiography revealed diffuse hypokinesia of both ventricles, consistent with global systolic dysfunction. CMR remained inconclusive for underlying cardiomyopathy. Given the persistence of symptoms despite exclusion of acute myocardial infarction and structural cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed to evaluate for undiagnosed congenital coronary anomalies. The CCTA was conducted using a GE Lightspeed scanner (GE HealthCare, Chicago, USA) with retrospective gating, at 100 kVp, 696 mAs, gantry rotation time of 0.35 s, and 0.625 mm slice thickness, with intravenous administration of 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).

Differential diagnosis of cardiogenic shock includes myocardial infarction, arrhythmias, and various forms of cardiomyopathy. In otherwise healthy adult patients, undiagnosed congenital heart disease represents a significant and often underrecognized etiology. When acute myocardial infarction is excluded by 12-lead ECG and cardiomyopathy is not confirmed by CMR, CCTA becomes the preferred imaging modality to differentiate between obstructive coronary disease and congenital coronary anatomical variants.

CCTA findings demonstrated a regular origin of the left main coronary artery, with a well-developed left anterior descending (LAD) artery exhibiting a wide ramus intermedium, two diagonal branches, and a thin, non-dominant left circumflex artery. No obstructive lesions were identified in any of these vessels. However, the ostium and proximal segment of the right coronary artery (RCA) were completely absent. Instead, the mid and distal RCA was supplied by a large collateral branch originating from the distal LAD, which encircles the lateral wall of the right ventricle, traverses the distal atrioventricular groove, and gives rise to thin posterior interventricular and posterolateral arteries. Additionally, a fine branch arising from the mid-LAD was observed to supply the sinoatrial node, potentially contributing to autonomic instability.

Based on these findings, the patient underwent stress echocardiography, which confirmed inducible myocardial ischemia in the inferior wall—consistent with the anatomical location of the arrhythmic focus. She was subsequently transferred to a specialized center for congenital cardiovascular disease. There, she underwent transcatheter radiofrequency ablation targeting the sustained ventricular tachycardia originating from the posteromedial papillary muscle. Post-procedural follow-up revealed complete suppression of arrhythmias. At 6-month follow-up, she remains asymptomatic with no recurrence of ventricular tachycardia. Medical therapy post-ablation includes acetylsalicylic acid and verapamil for antiplatelet and rate control, respectively. The case underscores the importance of advanced imaging in diagnosing rare congenital coronary anomalies that may present with phenotypes mimicking acquired cardiomyopathy or acute coronary syndromes, particularly in young patients with recurrent arrhythmias and elevated biomarkers despite negative acute infarction workup.


A 17-year-old boy was found to have a small metal button stuck in his nose during a dental check-up. He had no symptoms like nose blockage, bleeding, or pain. The button had been there for over 10 years, probably since he was 7 years old when he put it in. It was hidden in the bottom part of his nose, covered with mucus and dirt, and looked shiny — that’s how doctors knew it was metal. X-rays showed the button clearly, and doctors confirmed it was safe and not hurting any bones or sinuses. The family had ignored earlier advice to remove it, thinking it would fall out on its own. The button was safely taken out in the clinic with local numbing spray and a small tool, with no serious bleeding. After removal, the nose healed well, and the boy is now doing fine with regular nose rinses.


{
  "proficient_health_literacy": "An 18-year-old Hispanic male with no significant past medical history presented to the emergency department (ED) with acute onset of substernal, non-radiating chest pain, orthopnoea, dry non-productive cough, and subjective fevers lasting 3–4 days. Family history is notable for paternal grandfather with non-ischaemic cardiomyopathy and pacemaker implantation at age 86. The patient lives with both parents, denies smoking, alcohol use, recreational drug use, or abuse. He works at an auto parts shop and plans to begin college. Initial workup revealed elevated serum troponin I, diffuse ST-segment elevation on electrocardiogram (ECG), and an enlarged cardiac silhouette with mild pulmonary oedema on chest X-ray. Transthoracic echocardiography (TTE) demonstrated a left ventricular ejection fraction (LVEF) of 40%, severe left ventricular (LV) concentric hypertrophy (septal thickness 1.9 cm, inferolateral wall 2.2 cm), and mild posterior pericardial effusion. Coxsackie virus A and B titres were elevated, prompting initial consideration of viral myopericarditis. Symptoms initially improved with ibuprofen and colchicine, and cardiac catheterization confirmed absence of coronary artery disease. Repeat TTE showed LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral walls, and elevated LV end-diastolic pressure consistent with diastolic dysfunction. Chest CT angiogram revealed pneumonitis and pericardial effusion, supporting a diagnosis of Coxsackie virus-induced myopericarditis. On day 4 of admission, the patient developed diaphoresis, tachycardia, and hypotension with undetectable blood pressure. Repeat TTE revealed large pericardial effusion with signs of impending cardiac tamponade, necessitating emergent pericardiocentesis. During the procedure, the patient experienced pulseless electrical activity (PEA) cardiac arrest, requiring 30 minutes of advanced cardiovascular life support. He was intubated, placed on veno-arterial extracorporeal membrane oxygenation (VA ECMO), and initiated vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min). Significant bleeding from ECMO cannulae necessitated multiple transfusions (9 packed red blood cells, 10 platelets, 10 cryoprecipitate, 4 fresh frozen plasma). The patient was transferred to a tertiary center for endomyocardial biopsy (EMB) due to concern for fulminant myocarditis or infiltrative cardiomyopathy. EMB showed no evidence of inflammatory or infiltrative process. Repeat Coxsackie serology confirmed positivity for Coxsackie A9, B2, and B6, and quantitative PCR for Epstein-Barr virus (EBV) DNA was elevated at 133,000 IU/mL. A subsequent TTE revealed a severely reduced LVEF of 10%–15% with persistent severe concentric LV hypertrophy. Intravenous immunoglobulin (IVIG) was initiated for suspected Coxsackie myocarditis, broad-spectrum antibiotics were administered for worsening leucocytosis without identifiable focus, and colchicine was discontinued due to concern for rhabdomyolysis (serum creatine kinase elevated to 2874 U/L). Vasopressors were discontinued and the patient was extubated. He subsequently developed flushing, fever, dyspnoea, and hypoxaemia with chest X-ray showing congested lung parenchyma suggestive of acute respiratory distress syndrome (ARDS), leading to IVIG discontinuation. Despite initial decompensation, cardiac function improved with a subsequent TTE showing LVEF of 25%–30%, prompting consideration of ECMO removal—this was unsuccessful. The patient remained on VA ECMO and was evaluated for left ventricular assist device (LVAD) placement, which was deemed contraindicated due to extensive global concentric LV hypertrophy. A multidisciplinary team concluded that emergency listing for heart transplantation was appropriate, with consideration of transition to intra-aortic balloon pump and inotrope support. During evaluation for transplantation, an incisional biopsy of a 1×1 inch, painless, rubbery, mobile lesion in the right upper extremity was performed. Pathology revealed aggressive EBV-positive natural killer/T-cell lymphoma (ENKTCL) with cytotoxic immunophenotype (positive for CD2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1, and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybrid


A 50-year-old man who smoked a lot and had bad cholesterol levels for years got a serious problem in one eye. The eye swelled fast, caused constant double vision (diplopia), and the eye movement got very weak. Even though his thyroid was normal, the eye tissue in one muscle (the right inferior rectus) turned hard and stiff, like fibrous tissue. This made the double vision worse and stayed bad even after steroid shots. The doctor tried medicine first, then surgery to open up the eye socket, which helped a little. The biopsy showed the muscle was completely filled with scar tissue. This case is rare and shows how serious eye problems can be in people with no thyroid issues.


A 50-year-old man with a long history of smoking and high cholesterol developed a rare eye condition called euthyroid single muscular Graves' ophthalmopathy. He had no family or personal history of thyroid disease. Over several months, his right eye swelled rapidly, causing severe pain and constant double vision (diplopia) that made daily activities difficult. His vision was normal, but he could no longer move his eye properly, especially upward, which worsened his quality of life. Tests showed mild signs of thyroid autoimmunity, but his thyroid function was normal. Inflammation in the eye area was moderate, and imaging showed significant swelling only in the right inferior rectus muscle, while other eye muscles were unaffected. A biopsy confirmed massive fibrosis (scarring) in that muscle. Initial treatment with high-dose steroid injections helped reduce inflammation but did not improve double vision or eye movement. Two surgeries to relieve pressure in the eye socket were needed. The scarring in the muscle was the main reason the symptoms didn’t improve. This case highlights a rare form of eye disease that can cause serious vision problems even when the thyroid is healthy.


We present a rare case of euthyroid unilateral Graves' ophthalmopathy (GO) characterized by early and massive mono-muscular fibrosis involving the right inferior rectus muscle in a 50-year-old male patient. The patient has a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no personal or familial history of thyroid autoimmune disorders. He is a long-term smoker (20 cigarettes/day since age 30) and has had chronic dyslipidemia for several years, with laboratory findings showing total cholesterol of 220 mg/dL, triglycerides of 297 mg/dL, and low high-density lipoprotein cholesterol (HDL) of 38 mg/dL—indicating a pro-atherogenic lipid profile. Since June 2020, the patient developed rapid and progressive soft tissue swelling in the right orbit, moderate pain during ocular movements, eyelid redness, and persistent diplopia. Visual acuity remained normal (16/17 and 17/17 in right and left eyes, respectively), and color vision was preserved. Ocular motility evaluation revealed severe depression of elevation and persistent primary position depression of the right globe, as quantified by the Gorman score, with constant diplopia. Clinical Activity Score (CAS) was 3/7, indicating moderate active inflammation, and Hertel measurements were 24 mm (right) and 18 mm (left), with a right orbital muscle orbit area ratio of 0.25 (in-house Autocad-based method; normal threshold vn ≤ 0.20±0.03), confirming significant enlargement of the inferior rectus muscle. CT imaging (1.25 mm contiguous slices, 200 mA, 120 kV, pitch 0.5) demonstrated marked expansion of the lower rectus body to the level of its tendon insertion, while all other extraocular muscles in both orbits exhibited normal morphology. Thyroid function tests were within normal limits, with only a slight elevation in thyroid-stimulating hormone receptor antibody (TSH-R-Ab) levels at 1.75 mU/L (normal <1.5 mU/L), consistent with subclinical autoimmune thyroid stimulation. Thyroid ultrasound revealed a thyroiditis-like pattern, suggestive of non-autoimmune thyroid inflammation. Electrophysiological assessment showed a slight reduction in the amplitude of the p100 wave in the right eye, indicating early neuro-ocular dysfunction. Routine systemic laboratory evaluations were unremarkable, excluding hematological or systemic diseases. Initial treatment with intravenous corticosteroid pulse therapy (Solumedrol, 4500 mg cumulative dose over 12 weeks) resulted in resolution of inflammatory signs and symptoms, but failed to improve ocular motility, Hertel measurements, or quality of life as measured by the Graves’ Ophthalmopathy Quality of Life Questionnaire (GO-QOL), where functional subscale scores (12.5) remained significantly lower than appearance subscale (50), despite normal visual acuity. Notably, electrophysiological parameters and visual function deteriorated during this period. As a result, second-line therapy with two-wall orbital surgical decompression combined with continued parenteral glucocorticoids was initiated. Histopathological examination of the right inferior rectus muscle biopsy revealed extensive fibrosis with significant adipose tissue infiltration, confirming the presence of early, severe, and isolated mono-muscular fibrotic change. This case highlights the potential for rapid progression of unilateral, euthyroid GO with prominent fibrotic transformation, even in the absence of significant thyroid autoimmunity, and underscores the importance of early surgical intervention in patients with persistent diplopia and progressive muscle enlargement despite medical therapy. The observed fibrosis may reflect a dysregulated fibroproliferative response to chronic inflammation, possibly driven by local cytokine milieu and metabolic factors such as dyslipidemia and smoking-related oxidative stress, which are known contributors to extracellular matrix remodeling in orbital tissues.


A 15-year-old boy had stomach pain and vomiting for four days. Doctors first thought it was a stomach bug, but it didn’t go away. His belly was swollen, and tests showed his intestines were blocked. A scan found a piece of intestine stuck in a small opening in his belly, called the Winslow hiatus. This caused the blockage. The doctors tried a small surgery first, but couldn’t see clearly, so they did a bigger cut in the middle of his belly to fix it. They pulled the stuck piece of intestine back into place and found it was just a small part of the small intestine that had slipped through the opening. No part of the intestine had to be cut off. They didn’t do any extra steps to prevent it from happening again. After surgery, he had a small pocket of fluid in his pelvis, which was treated with medicine and didn’t get worse. He’s now recovering at the pediatric surgery clinic and doing well.


A 15-year-old boy with no prior medical issues came in with vomiting and abdominal pain that had lasted four days. At first, doctors thought it was gastroenteritis, but the symptoms didn’t go away. He was admitted to the hospital after tests showed signs of intestinal obstruction.

An abdominal CT scan found that a loop of small intestine had gotten stuck at the Winslow hiatus — a key opening in the abdomen — causing a blockage. The doctors tried to fix it with laparoscopy (a minimally invasive surgery), but poor visibility made it difficult. They switched to a larger open surgery (supraumbilical midline laparotomy) to safely see and treat the problem.

During the surgery, they found a section of the ileum (part of the small intestine) that had herniated through the Winslow hiatus. The loop was about 5 centimeters long and was causing the blockage. The area around the opening looked normal, so no extra steps were taken to prevent it from coming back.

After surgery, the boy had a temporary stop in bowel movement (paralytic ileus), which resolved after five days. He started eating again and did well. He also developed a small fluid collection in his pelvis, which was treated with antibiotics and improved over time. He was discharged ten days after surgery and is now being followed up in outpatient paediatric surgery. No further surgery is planned to prevent recurrence.


We present a clinical case of a 15-year-old male with no prior medical history or surgical interventions, who presented to the paediatric emergency department with a four-day history of vomiting and epigastric abdominal pain, remaining afebrile throughout. Initial evaluation was consistent with gastroenteritis, but symptoms persisted, including biliary vomiting and ongoing epigastric discomfort, prompting admission for further investigation.

Physical examination revealed an otherwise stable general condition, afebrile status, and mild signs of dehydration. The abdomen was distended, with absent peritoneal signs and diminished bowel sounds. Laboratory findings were non-contributory. Abdominal radiography demonstrated features consistent with small bowel obstruction.

Urgent computed tomography (CT) was performed, revealing ascites and significant dilatation of small intestinal loops, with a focal change in caliber at the level of the Winslow hiatus, indicating interposition of a small intestinal loop within the trans-cavity of the epiploic foramen. The CT findings suggested a mechanical obstruction due to internal herniation of a segment of the ileum.

Surgical management began with exploratory laparoscopy. Intraoperatively, dilated loops of the small intestine, including the terminal ileum, cecum, and ascending colon, were observed in the right hypochondrium. The cecum was noted to be highly mobile without adhesions to the right parietocolic space. Proximal to the terminal ileum, small intestinal loops were identified in the region corresponding to the theoretical location of the Winslow hiatus. Attempts to mobilize the cecum and terminal ileum toward the right iliac fossa were unsuccessful due to obstruction by the lower edge of the liver and the distended bowel loops. Percutaneous puncture of a dilated loop to decompress gas was attempted but did not improve visualization or facilitate reduction.

Due to poor visualization and failure to identify the precise site of caliber change, a conversion to supraumbilical midline laparotomy was performed. In the open laparotomy, a clear change in intestinal caliber was observed approximately 40 cm distal to the ileocecal valve, confirming a herniation of a 5-cm segment of ileum through the Winslow hiatus. The herniated loop exhibited characteristic congestive imprints at both ends, consistent with compression and ischemic changes due to entrapment. The normal anatomical caliber of the Winslow hiatus was confirmed, and no preventive surgical technique (e.g., hernia repair or reinforcement) was performed to reduce the risk of recurrence.

Postoperatively, the patient developed a paralytic ileus, which resolved over five days, allowing for nasogastric tube removal and initiation of oral intake with good tolerance. Concurrently, a pelvic collection was identified and managed conservatively with antibiotic therapy, with favorable clinical evolution. The patient was discharged ten days after surgery with preserved bowel transit, absence of fever, and stable general condition. He is currently under outpatient follow-up in the paediatric surgery clinic.

This case highlights the diagnostic challenge of internal hernias in adolescents, particularly those involving the Winslow hiatus, which may present with nonspecific gastrointestinal symptoms and mimic other conditions such as gastroenteritis or acute appendicitis. The anatomical complexity of the trans-cavity epiploic foramen, combined with the distension and mobility of bowel loops, contributes to the difficulty in both preoperative diagnosis and intraoperative identification. Internal hernias are often missed on routine imaging and require high index of suspicion, especially in young patients with prolonged abdominal pain and obstructive features. The lack of preventive intervention in this case underscores the potential for recurrence, although the absence of recurrence in the current follow-up suggests a favorable outcome in the absence of anatomical reinforcement.


A 75-year-old woman from Western Ethiopia had a small birth control device (IUD) put in her uterus 40 years ago. Since then, she never checked it or saw a doctor. Now, she has pain in her lower belly and vagina, which started 3 years ago and got worse. The doctor found the old IUD still inside, near the opening of her cervix. It was easy to pull out using simple tools. She was given pain medicine and doxycycline to help her feel better and get rid of any infection. She went home after being watched for 4 hours and her pain went away.


A 75-year-old woman from Western Ethiopia, who had her last period 25 years ago, came to the hospital with ongoing lower abdominal pain and discomfort in her vagina. She had been using an intrauterine device (IUD), specifically a Lippes loop, since she was 18 years old — meaning it had been in place for 40 years. She had never had a gynecological checkup since then and didn’t know it was still inside her. During a pelvic exam, doctors found part of the IUD at the opening of her cervix. It was easily removed using special forceps. The patient was given pain relief and doxycycline for 3 days to prevent infection. She was discharged after being observed for 4 hours and her pain went away after treatment.


A 71-year-old man had a long-time skin condition called vitiligo and started losing vision in his right eye six months before hospital visit. He also lost hearing in both ears, worse on the right side. He had bad headaches, fever, and lost weight without trying. When doctors checked his eyes, the right eye was very sensitive to light and had redness, while the left eye could only see blurry shapes. The right eye’s back part had dark spots and the optic nerve was damaged (atrophied), and the left eye had swelling around the nerve and early nerve damage (optic neuritis). Doctors checked for infections and diseases like TB, herpes, or autoimmune problems, but none were found. A spinal fluid test showed normal pressure but a bit high protein, which could mean nerve issues. Nerve tests showed damage to nerves in arms and legs, worse in the legs. Brain and eye scans didn’t show tumors, but showed signs of infection in the sinuses and lining of the brain. Sarcoidosis was ruled out with blood and scan tests. Because of the eye and nerve damage, doctors started high-dose steroid pills to reduce inflammation. After a few weeks, the man’s vision and headaches got better, and he started feeling stronger. He’s now being followed up in the clinic for ongoing care.


A 71-year-old man with long-standing vitiligo had lost vision in his right eye six months before hospitalization, along with hearing loss in both ears, worse on the right side. He also had chronic headaches, fever, and lost a lot of weight without trying. On eye exams, his right eye had very poor vision, was sensitive to light, and showed signs of damage including a swollen optic nerve and pigment spots. His left eye had good vision (20/200), but the optic nerve was swollen and there was early nerve damage. The right eye also showed signs of nerve degeneration. Tests were done to check for conditions like tuberculosis, infections, or autoimmune diseases, and none were found. A spinal fluid test showed normal pressure but slightly high protein levels. Nerve tests showed damage to multiple nerves, especially in the legs. Brain and eye MRI scans found no tumors, but showed signs of sinus infection and inflammation around the brain lining. Sarcoidosis was ruled out with normal blood and imaging tests. After further eye evaluation, the doctor confirmed ongoing eye nerve damage, including optic atrophy on the right and optic neuritis on the left. The patient started high-dose steroid treatment, which was slowly reduced over time. He improved over time, with better vision and less nerve-related symptoms, and was referred for ongoing follow-up care.


A 71-year-old male with a history of untreated vitiligo presented with right-sided visual loss six months prior to admission, accompanied by bilateral sensorineural hearing loss with predilection for the right ear. He also reported chronic headaches, intermittent fever, and significant unintentional weight loss, along with generalized weakness and cutaneous thickening. Ophthalmologic examination revealed reduced visual acuity in the right eye (RO) to light perception with impaired color discrimination, and 20/200 visual acuity in the left eye (LO), with an afferent pupillary defect in both eyes. Both eyes exhibited hyperemic bulbar conjunctiva and ciliary injection. Corneal findings included peripheral, nummular, subepithelial infiltrates in both eyes, with aqueous anterior chamber (AAC) clear and no cellular infiltrate. Iris and lens were normal, though both demonstrated nuclear opacities. Fundus examination of the right eye showed a pale ++ papilla with 50% excavation, blunt nasal border, thinned and raised vascular pattern, macular involvement, and scattered pigmentary deposits. The left eye fundus demonstrated vitreous haze 2+, edematous papilla, blurred borders, peripapillary streaked hemorrhages, an unevaluable excavation, thinned vascular pattern, macular changes, and scattered pigment. Notably, the right optic nerve exhibited atrophy, and the left eye showed signs of anterior optic neuritis. Additional neurological evaluation included lumbar puncture, which revealed normal opening pressure and a cerebrospinal fluid (CSF) protein level of 54 mg/dL, consistent with non-inflammatory or mild neuroinflammatory processes. Nerve conduction studies demonstrated a pattern of symmetric polyradiculoneuropathy with moderate to severe axonal degeneration affecting all four extremities, with greater involvement in the lower limbs, suggesting a distal symmetric polyneuropathy. Contrast-enhanced magnetic resonance imaging (MRI) of the skull and orbits showed no evidence of optic nerve enhancement or intracranial tumors, but did reveal sinusitis and meningeal enhancement, indicating possible meningeal inflammation. Sarcoidosis was excluded based on normal angiotensin-converting enzyme (ACE) levels and a whole-body gamma scan without focal or diffuse uptake. Anti-neutrophil cytoplasmic antibody (ANCA)-positive and ANCA-negative vasculitides were also ruled out. The ocular and neurological manifestations progressed over time, confirming persistent disease activity. High-dose pulse corticosteroid therapy was initiated, followed by a stepwise tapering regimen, resulting in clinically and functionally significant improvement in both ophthalmological and neurological parameters. The patient was subsequently referred for ongoing outpatient follow-up. The clinical course supports a diagnosis of a chronic, immune-mediated neuro-ophthalmic disorder, likely involving autoimmune-mediated optic nerve damage, with features consistent with a vasculitic or inflammatory process affecting the optic pathways, possibly related to the underlying vitiligo, which may represent a chronic autoimmune skin condition with systemic immune dysregulation.


A 39-year-old female with peripartum cardiomyopathy underwent heart transplantation in October 2014. Induction therapy consisted of basiliximab and methylprednisolone, with maintenance immunosuppression comprising tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. During the first post-transplant year, she experienced two episodes of acute rejection, both managed effectively with methylprednisolone pulse therapy. No prior history of renal disease was noted, and early post-transplant renal function was stable, with serum creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m². Routine monitoring for polyomavirus infection, including BK virus viral load and urinary cytology, was not performed during follow-up. In 2016, serum creatinine elevated to a peak of 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m². At that time, minimum tacrolimus level was 7.2 ng/mL and everolimus 5.2 ng/mL, prompting suspicion of calcineurin inhibitor toxicity. Tacrolimus was reduced to 4 mg daily, resulting in a partial recovery of renal function (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m²); no renal biopsy was conducted. In March 2017, creatinine rose to 2.69 mg/dL and GFR dropped to 21.4 mL/min/1.73m², necessitating hospitalization despite the absence of clinical symptoms. Physical examination revealed normal general condition, heart rate of 80 bpm, blood pressure 130/90 mmHg, respiratory rate of 15/min, and no fever. Imaging and laboratory studies, including renal ultrasound (normal size, increased echogenicity), urinalysis (negative for hematuria, pyuria, and casts), urine culture, echocardiography (normal cardiac function), and serologic screening for HIV, syphilis, hepatitis B and C (all negative), were unremarkable. Minimum immunosuppressant levels remained within therapeutic range (tacrolimus 5.2 ng/mL, everolimus 5.98 ng/mL). Intravenous hydration and further reduction of tacrolimus to 2 mg daily were initiated, but renal function did not improve, leading to the decision for renal biopsy. The biopsy revealed active chronic tubulointerstitial nephritis with evidence of late-stage BK virus nephropathy. BK virus PCR detected a viral load of 33,800 copies/mL in serum (log 4.5), confirming active viral replication. Tacrolimus was discontinued due to its nephrotoxic potential in the context of BK virus infection. Post-treatment, serum creatinine stabilized between 2.2 and 2.4 mg/dL without further elevation, and the viral load progressively declined to undetectable levels. Over a three-year follow-up period, the patient remained free of cardiac rejection episodes. The most recent serum creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m², indicating stable but significantly reduced renal function consistent with chronic tubulointerstitial injury secondary to BK virus infection. The pathophysiological mechanism involves BK virus-induced tubular epithelial cell damage, leading to interstitial inflammation, fibrosis, and progressive glomerular dysfunction, exacerbated by immunosuppressive therapy that impairs viral clearance. The clinical course highlights the importance of vigilant monitoring for polyomavirus infection in solid organ transplant recipients, particularly in the setting of prolonged immunosuppression and declining renal function, even in the absence of overt symptoms.


A 14-year-old boy who had a cough and breathing trouble was found to have a lump in his chest, likely cancer called non-Hodgkin lymphoma. He was treated with a medicine called L-asp and prednisone. During this treatment, he started having high fat levels in his blood and low sodium levels, which doctors thought might be a side effect of the medicines. They checked this using a special method and found it was definitely caused by the mix of L-asp and prednisone. He was given a low-fat diet, plus medicines to lower his fat levels. His fat levels went back to normal in 14 days. The medicines were not stopped because the cancer treatment was still going. His body got better without any serious problems.


A 14-year-old boy with a history of a nighttime cough was admitted to the hospital after developing severe breathing problems and abdominal pain. Tests showed a mass in the middle of his chest, leading to a suspicion of non-Hodgkin lymphoma. He was treated with chemotherapy, including L-asp and prednisone, as part of a standard protocol. During treatment, he developed high levels of triglycerides in his blood and low sodium levels (a condition called pseudohyponatraemia), which are known to be linked to certain medications. Doctors suspected this was a drug reaction (ADR) caused by the combination of L-asp and prednisone. Using a standard method to evaluate drug reactions, they concluded it was a 'definitive' drug reaction. He was given a low-fat, high-fiber diet and medications to lower his triglycerides, which improved within 14 days. His condition stabilized, and the drug reaction resolved without complications. The medications were not stopped because the treatment for lymphoma was still ongoing, as per the treatment plan.


{
  "proficient_health_literacy": "A 14-year-old previously healthy adolescent presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of nocturnal irritative cough, progressing to dyspnoea and orthopnoea. Upon evaluation at the Osorno Base Hospital (OBH), he was found to have severe respiratory distress, intolerance to supine positioning, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU) in a tachycardic, hypertensive, polypneic state with oxygen saturation of 96% on 35% FiO2, rosy peripheries, adequate hydration, and well-perfused tissues, with flat jugular veins and small bilateral supraclavicular lymphadenopathies. Physical examination revealed no soft tissue retraction, maintained genupectoral posture, decreased pulmonary murmurs in both lung bases, and muffled cardiac tones without breath sounds. Abdominal examination showed non-depressible, tender soft tissue in both hypochondria with doubtful visceral enlargement and no trauma. Chest radiography demonstrated a superior mediastinal mass, atelectasis of the right middle lobe, and ipsilateral pleural effusion. Contrast-enhanced chest imaging was not performed due to contraindication of anaesthesia, as noted in the transfer summary. The patient was transferred to the PICU HBV with a diagnosis of mediastinal compression syndrome and clinical suspicion of non-Hodgkin lymphoma. Multidisciplinary evaluation by paediatric haemato-oncology, surgery, intensive care, imaging, radiotherapy, and oncology teams confirmed a normal pulmonary murmur and muffled cardiac auscultation, with no breath sounds, and persistent abdominal tenderness and suspected visceral enlargement. The chest radiograph remained consistent with a superior mediastinal mass and right middle lobe atelectasis with pleural effusion. A nephrological assessment revealed acute renal failure secondary to tumor lysis syndrome, with serum creatinine of 1.54 mg/dL, phosphoria of 11 mg/dL, and no hypernatremia. No dialysis was required, and the patient was managed with furosemide for volume control and amlodipine for hypertension. Respiratory support was initiated with Venturi mask at 35% FiO2, which was discontinued on day three due to clinical improvement. Episodes of psychomotor agitation, attributed to diagnostic stress, were managed according to institutional protocols with psychological and psychiatric support, resulting in satisfactory clinical course. On day three, a contrast-enhanced CT of the thorax, abdomen, and pelvis was performed, revealing thymic enlargement with homogeneous appearance, suggestive of a lymphoproliferative process, and findings consistent with pulmonary thromboembolism. AngioCT of the thorax confirmed jugular vein thrombosis, extensive bilateral pleural effusion, atelectasis in both lung bases, and signs of bilateral nephrotic syndrome. Anticoagulation with enoxaparin (1 mg/kg every 12 hours) was initiated for 20 days, with follow-up angioCT showing complete resolution of thrombosis. On day four, comprehensive diagnostic workup was completed, including complete biochemical profile (including lipid panel), bone marrow myelogram showing granulopoietic hyperplasia, flow cytometry of bone marrow and peripheral blood, which was negative for clonal or neoplastic haematopoietic immunophenotypes, and cytological analysis of pleural fluid, which was negative for neoplastic cells. Flow cytometry of pleural fluid also failed to detect haematological neoplasia. The patient was referred to the paediatric oncology committee, where, due to the absence of a viable biopsy specimen (as the mediastinal mass resolved with cytoreductive therapy), a diagnosis of lymphoblastic lymphoma was established based on clinical presentation and response to treatment, in accordance with the PINDA 0516 induction protocol. This protocol includes eight doses of L-asp (L-asparaginase) at 10,000 IU/m² in Induction IA. The patient received seven doses of L-asp, accumulating a total of 90,000 IU, in combination with prednisone glucocorticoids. During this period, he developed clinical deterioration with vomiting, abdominal pain, and mild dehydration. Pancreatitis was suspected but ruled out by normal amylase and lipase levels and normal hepatic function tests. Laboratory findings included hyponatraemia (126 mOsm/kg) and hypertriglyceridaemia, with urinary osmolality of 510 mOsm/kg (within normal range), leading to suspicion of a drug-induced metabolic disturbance—specifically, pseudohyponatraemia secondary to hypertriglyceridaemia. This was further supported


{
  "proficient_health_literacy": "A 56-year-old Italian female with β-thalassemia major underwent magnetic resonance imaging (MRI) to quantify myocardial, hepatic, and pancreatic iron deposition. Her clinical history includes transfusion-dependent β-thalassemia with genotype HBB:c.118C>T/HBB:c.93-21G>A, diagnosed at age 7 years, with the first red blood cell transfusion administered at 2 years of age. As a consequence of chronic transfusion and associated bone marrow pathology, she underwent splenectomy and cholecystectomy. At the time of MRI, she was negative for Hepatitis C virus RNA (HCV-RNA), had no evidence of osteoporosis or endocrine, cardiac, or hepatic complications, and maintained stable iron levels despite long-term iron overload. Her current therapy includes deferasirox for iron chelation, vitamin D supplementation, and luspatercept, an erythropoiesis-stimulating agent initiated two years prior to imaging, which demonstrated a 35% increase in transfusion interval duration, indicating a clinically significant response. Transfusion regimen consists of two units of concentrated and filtered red blood cells every 25 days, with pre-transfusion hemoglobin levels maintained between 10–10.5 g/dL.\n\nOn MRI, a solid, lobulated mass with regular contours was identified in the prevascular mediastinum. The lesion exhibited mild hyperintensity on T2-weighted imaging (T2-wi) and isointensity on T1-wi, and was previously detected in a prior MRI performed in 2020 before luspatercept initiation, with marginal enlargement over time. No other mediastinal abnormalities, pleural or pericardial effusions, or neurovascular compression symptoms were observed. Neurological examination was normal, and the patient reported no symptoms of mediastinal syndrome, fever, or weight loss.\n\nFurther evaluation via 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) revealed mild FDG uptake in the mediastinal mass (SUVmax = 4.3), with no abnormal radiotracer accumulation in the neck, chest, abdomen, or skeleton. Chest CT with contrast demonstrated a well-defined, solid lesion with mild contrast enhancement, no evidence of invasion into adjacent structures, and absence of lymphadenopathy or extra-thoracic metastases. These imaging features—indolent temporal progression, lack of systemic symptoms, and low metabolic activity—support a diagnosis of thymoma.\n\nHowever, on lung window analysis, multiple symmetric, thin-walled cystic lesions were identified throughout both lungs, with normal intervening parenchyma, no associated nodules, and no pneumothorax. These findings are consistent with lymphangioleiomyomatosis (LAM), a rare cystic lung disease characterized by proliferation of smooth muscle-like cells in the lung interstitium. The patient is a never-smoker and denies chronic cough, recurrent respiratory infections, or cutaneous fibrofolliculomas. Physical examination revealed clear lung fields, normal peripheral capillary oxygen saturation (98%), heart rate of 75 bpm, and significantly reduced diffusing capacity of the lungs for carbon monoxide (DLCO: 42% of predicted), partially attributable to anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of predicted. These pulmonary function abnormalities are consistent with advanced LAM pathology.\n\nFollowing multidisciplinary tumor board review involving a pulmonologist and thoracic surgeon, the patient underwent left thoracoscopic thymectomy with concomitant lingual segment wedge resection. Histopathological analysis confirmed a type B2 thymoma with focal capsule infiltration, no extracapsular extension, and presence at the resection margin, classifying the tumor as stage IIa by the Masaoka–Koga system and stage 1a by the TNM classification (indicating microscopically incomplete resection, R1). The pulmonary lesion demonstrated cysts of variable size lined by spindle cells with a myoid morphology, immunoreactive for actin, estrogen, progesterone receptors, and focal HMB45 positivity, with moderate chronic interstitial inflammation, vascular congestion, and recent blood extravasation—findings consistent with pulmonary LAM.\n\nFinal diagnosis is dual pathology: type B2 thymoma and pulmonary lymphangioleiomyomatosis. Given the R1 resection margin status, adjuvant radiation therapy is indicated for the thymoma to reduce risk of recurrence. For the LAM, which is associated with chronic iron overload in β-thalassemia, sirolimus therapy is recommended due to its ability to inhibit mTOR signaling, thereby suppressing the proliferation of abnormal smooth muscle-like cells in the lung paren


A 49-year-old woman had a long sickness called lupus that started when she was a child. Over time, her kidneys and heart got weaker because of the disease. She needed dialysis for 4 years until she got a new kidney. Before the surgery, her heart was very weak — only pumping 26% of the blood it should — so doctors gave her a medicine called Levosimendan to help her heart work better. The surgery was hard, but she survived. Afterward, her heart got stronger: now it pumps better, and her kidney function is normal. Her ability to walk stairs improved, and her heart problems got much better over time. She is now doing well after the transplant.


{
  "proficient_health_literacy": "We present a case of a 49-year-old woman with chronic renal and cardiac failure secondary to long-standing systemic lupus erythematosus (SLE), spanning from childhood (initiated at age 13). The patient had a history of lupus nephritis (LN), initially class III and later progressing to class IV, managed with early steroid therapy, followed by cyclophosphamide, subsequently replaced by methotrexate and azathioprine. Partial remission of nephrotic syndrome was achieved, and immunosuppressive therapy was discontinued in 2002 due to active hepatitis C virus (HCV) replication. SLE-related vascular involvement manifested as early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at age 20. In 2007, declining renal function (serum creatinine 2.2 mg/dL) and proteinuria (2 g/day) prompted a kidney biopsy, which revealed active and sclerotic focal proliferative lupus nephritis; immunosuppression was withheld due to HCV activity. Over time, renal function progressively deteriorated. Despite percutaneous coronary intervention (PCI) of the right coronary artery (RCA), the patient developed severe post-infarction dilated cardiomyopathy and required implantation of an implantable cardioverter-defibrillator (ICD) for primary prevention in 2009. Subsequently, significant mitral and tricuspid valve regurgitation developed on the background of lupus-related and secondary cardiomyopathic pathology, necessitating mitral and tricuspid valve repair, followed by left ventricular volume reduction surgery in 2014, complicated by low cardiac output syndrome requiring intra-aortic balloon pump (IABP) support. Postoperatively, renal function further declined, leading to initiation of chronic renal replacement therapy (dialysis), which has been sustained for 4 years. During active waiting for kidney transplantation, laboratory markers of lupus entered remission (normal C3: 0.93 g/L, C4: 0.4 g/L, ANA negative), though circulatory insufficiency persisted, evidenced by markedly reduced exercise tolerance (limited to one flight of stairs) and elevated B-type natriuretic peptide (BNP) of 619 pg/mL (normal range: 0–100 pg/mL). Transthoracic echocardiography prior to transplantation demonstrated significant left ventricular and left atrial enlargement, with severely impaired systolic function: left ventricular ejection fraction (LVEF) of 26% and global longitudinal strain (GLS) of −3. Due to mitral ring implantation, left ventricular diastolic function could not be assessed. A high tricuspid regurgitant flow gradient and a widened, poorly respiratory mobile inferior vena cava (IVC) suggested a high probability of pulmonary hypertension. Given the extremely low ejection fraction and complex cardiac pathology, cardioprotective therapy with levosimendan was initiated during pre-transplant preparation. Levosimendan was administered at a dose of 0.1 μg/kg/min immediately after cross-match confirmation and dialysis session, and continued postoperatively for 24 hours. The anesthetic and perioperative management was optimized to ensure adequate transplanted kidney perfusion, avoiding nephrotoxic agents (including those excreted by functional kidneys), and utilizing nephroprotective strategies. Due to recurrent ventricular extrasystoles and risk of circulatory decompensation, and the necessity of ICD disconnection during transplantation, Swan-Ganz catheterization for hemodynamic monitoring was avoided. Anesthesia was monitored via ECG, central venous pressure (CVP) via central catheter, direct radial artery blood pressure, and continuous cardiac ultrasound. CVP was used to guide fluid management during anesthesia, and postoperatively, cardiac ultrasound and inferior vena cava respiratory fill and motility were used to assess hemodynamic stability. Therapy was guided by goal-directed therapy (GDT) principles. Anesthesia included fentanyl, triacrium, propofol, desflurane, standard antibiotic prophylaxis, and immunosuppressive regimens (steroids, tacrolimus, mycophenolate mofetil), with mycophenolate mofetil discontinued due to persistent leukopenia and cytomegalovirus (CMV) infection. Delayed graft function was observed, requiring hemodialysis for nearly 6 weeks, primarily due to fluid overload. BNP levels peaked at 2996 pg/mL and gradually declined. A kidney biopsy performed two weeks post-transplant revealed acute rejection (AR II B, Banff 2015 classification) with acute tubular necrosis (ATN). The


A 42-year-old woman had bad headaches that were very sharp and strong, like a storm inside her head. The pain came on suddenly, lasted about 30 minutes, and happened many times a day when she coughed or lifted things. She tried medicines, but they caused stomach problems and didn’t work. When the pain got too bad, she went to a pain clinic. There, doctors used an ultrasound to guide a needle to block the nerve causing the pain. The medicine used was bupivacaine. After the first block, her pain went from 9 out of 10 to just 2 out of 10. She had this block once a week for a month. After two months, the headaches became much less frequent and weaker. By the sixth month, she didn’t have any more attacks and no side effects.


A 42-year-old female with a history of menstrual migraine, Hashimoto thyroiditis, familial Mediterranean fever (FMF), and dyspepsia was evaluated for refractory headache. She was on stable therapy including 75 mg daily levothyroxine, 30 mg daily lansoprazole, and 1.5 mg daily colchicine. In February 2023, she developed acute bronchitis treated with antibiotics and bronchodilators, followed by the onset of daily headache episodes manifesting as more than ten brief, self-limiting attacks per day, each lasting approximately 30 minutes, provoked by coughing, straining, or lifting. The pain was bilaterally distributed from the neck to the vertex of the skull, described as sharp and severe, with a characteristic sensation of 'storm-like fluid movement' within the head. Pain intensity was quantified using a 0–10 numeric rating scale (NRS), consistently reaching 9/10 during attacks, which frequently required emergency department visits. Neurological and physical examinations were normal, and laboratory evaluations—including thyroid function, electrolytes, hepatic and renal function, and serological markers—were negative. Brain MRI with and without contrast, cervical spinal MRI, magnetic resonance venography (MRV), and magnetic resonance angiography (MRA) were all unremarkable. Lumbar puncture was not performed due to patient refusal. Prior to presentation to the pain clinic, she was on 25 mg of indomethacin daily; her headache attacks ceased after increasing lansoprazole to 60 mg and raising indomethacin to 150 mg, but gastrointestinal adverse effects led to discontinuation of indomethacin on day three. Concomitant medications, including topiramate and propranolol, were not initiated due to intolerance. Fifteen days after initial evaluation, she presented with a recurrent attack of NRS 9/10 and was taken to the local operating room for ultrasound-guided proximal greater occipital nerve block (PGONB). The procedure was performed using a GE Healthcare Voluson™ E6 ultrasound system with a linear 13–5 MHz probe. The patient’s neck was in a position of flexion, and the probe was initially transversely placed over the occipital protuberance, then advanced caudally to visualize the C2 spinous process, which was observed to have a bicondylar appearance resembling two horns. Lateral probe movement allowed identification of the inferior fibers of the obliquus capitis and semispinalis capitis muscles. The greater occipital nerve (GON) was localized superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle. A 22-gauge spinal needle was inserted at this site, and 3 cc of 0.5% bupivacaine was injected. Within 20 minutes of injection, the headache intensity dropped from 9/10 to 2/10. The procedure was repeated weekly for one month. By the second month, the frequency of attacks reduced to two per month, with an average intensity of 4/10. By the sixth month, no attacks were reported, and no adverse effects were observed. This case demonstrates the efficacy of ultrasound-guided PGONB in managing refractory, non-migraine-like headaches with a distinct mechanical trigger profile, particularly in patients with comorbidities and intolerance to conventional pharmacologic therapies.


A 20-year-old male martial artist had pain in the back of his left thigh for 5 weeks. The pain started after a short sprint in soccer, and he heard a pop. He couldn’t move his knee well and had to stop all sports. Even with pain medicine, ice, and bandages, the pain didn’t go away. The doctor checked and ruled out other serious problems. He couldn’t bend or straighten his knee properly and walked with a limp. His pain was 5 out of 10 at rest and 7 during activity. A special treatment was done: a gentle movement technique to help the nerve slide smoothly, done 3 times a day for 3 days. He also learned how to stand and move better. After 3 days, his pain dropped to 2 out of 10 at rest and 4 during activity. His knee could move much better. At 2 months, he was pain-free and could go back to martial arts without any trouble.


A 20-year-old male Arabic martial artist had a left hamstring strain that lasted for 5 weeks. He tried medications and physical therapy, but his pain didn’t improve. He stopped all sports activities because the pain was severe. After checking with a doctor, other causes like nerve problems or back issues were ruled out. The patient was treated with a modified slump mobilization technique, done four times a day for three days, along with postural retraining. Before treatment, his pain was 5 out of 10 at rest and 7 out of 10 during activity. After three days, pain dropped to 2 out of 10 at rest and 4 out of 10 during activity. His knee function also improved significantly: the Knee Society score went from 22 to 61 for pain and from 30 to 80 for movement. At a 2-month follow-up, he had fully recovered and was able to return to sports without any problems.


A 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, BMI 28.24) presented with a left hamstring strain with a five-week history of persistent pain in the posterior left thigh, initially precipitated by a sudden sprint during soccer play, during which he reported a 'pop' sensation. The pain was severe enough to cause immediate cessation of activity and was rated at 5/10 at rest and 7/10 during activity. There was no associated bruising or significant swelling, and the patient denied prior lower back or leg injuries. Clinical examination revealed a progressive loss of knee joint mobility, with active range of motion (AROM) limited to 10–15° in the left knee versus 0–130° in the contralateral right knee. The patient exhibited an analgesic gait pattern with reduced heel strike and was unable to fully extend or flex the knee when maintained at a 15° flexion position. Palpation identified tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles, consistent with hamstring muscle strain or fascial tightness. Manual muscle testing and isometric assessments were contraindicated due to persistent pain. The patient reported using crutches for ambulation, stair climbing via single-step ascents, and avoiding direct pressure on the thigh, including sitting at the edge of a chair. Despite adherence to nonsteroidal anti-inflammatory drugs (NSAIDs), cryotherapy, and compression bandaging, symptoms worsened over time, leading to referral for specialized evaluation. Diagnostic workup excluded lumbar disc pathology, gluteal tunnel syndrome, and ischial nerve entrapment based on clinical and neurodynamic screening, including a negative slump test for peripheral nerve tension. The clinical picture was consistent with hamstring strain syndrome (HSI), though conventional treatments had failed to yield improvement. The therapeutic intervention consisted of a modified slump mobilization technique involving sequential spinal and joint mobilization under controlled neurodynamic conditions. The protocol included three sets of daily sessions, each comprising thoracic and cervical spine flexion, maximal knee extension under tolerable pain thresholds, and dynamic neck and ankle movements (15 repetitions) to facilitate neural glide. The patient was also instructed to progressively mobilize the mid- and upper back until pain was elicited in the knee region, followed by repetition of the sequence. This neurodynamic approach was based on the biomechanical proximity of the tibial nerve and sciatic nerve to the hamstring musculature and the functional interplay between neural tension and lower limb joint mechanics. By the third day of intervention, active knee extension improved from 5° to 15°, and standing posture normalized. Concurrently, the patient was introduced to a structured postural retraining program including active chin flexion, passive stretching of cervical extensors in prone position, and dynamic shoulder retraction exercises (T-to-Y, Y-to-W) performed with limb weight bearing. Additional interventions included active chest stretches at wall corners to correct kyphotic posture, with exercise duration increased from 5 to 10 seconds, performed in 10 repetitions across three sets daily. Outcomes were quantified using the Numeric Pain Rating Scale (NPRS) and the Knee Society Score (KSS). Pre-intervention NPRS scores were 5/10 at rest and 7/10 during activity; post-intervention (on day 3) these improved to 2/10 at rest and 4/10 during activity. KSS scores increased from 22 to 61 in the pain domain and from 30 to 80 in the functional domain. Pain medication was discontinued following clinical improvement. At the end of a two-week home exercise program, the patient achieved full active straight leg raise (SLR). At the two-month follow-up, the patient reported complete resolution of symptoms, regained full functional mobility, and resumed participation in martial arts without limitations. The intervention demonstrates the efficacy of a neurodynamic mobilization approach in addressing chronic hamstring-related pain when conventional treatments fail, particularly in patients with structural and functional neural-tissue interactions affecting joint mechanics and posture.


{
  "proficient_health_literacy": "A male infant was delivered via emergency cesarean section at 40 weeks' gestation due to fetal distress. The mother was 33 years old, gravida 1, para 1, with no family history of congenital anomalies, aortic disease, or sudden cardiac death. Prenatal ultrasonography revealed a femur length 1–3 weeks above the expected gestational age, suggesting disproportionate growth. Fetal echocardiography demonstrated cardiomegaly with a fetal cardiothoracic circumference ratio of ≥0.5, a larger-than-normal foramen ovale, and left aortic constriction adjacent to the subclavian artery basin; no other structural abnormalities were identified.\n\nAt birth, the infant weighed 3560 g (75th percentile), measured 56.5 cm (above 90th percentile), and had a head circumference of 36 cm (above 90th percentile). Apgar scores were 4 at 1 minute and 6 at 5 minutes. The newborn exhibited absent spontaneous breathing, bradycardia, and cyanosis upon delivery, necessitating immediate neonatal intensive care unit (NICU) admission.\n\nPhysical examination revealed multiple severe musculoskeletal manifestations consistent with Marfan syndrome (MFS), including bilateral arachnodactyly, camptodactyly, flat feet, joint contractures at the elbows and knees, malar hypoplasia, a senile facial appearance, deep-set eyes with down-slanting palpebral fissures, hypoplastic and crumpled external ear cartilage, a sagging mouth, prominent coronal suture, and brachycephaly. Ophthalmologic evaluation confirmed bilateral ectopia lentis with lens subluxation. The musculoskeletal severity was assessed using the Ghent criteria, yielding a total score of 11 points, supporting a diagnosis of severe MFS.\n\nCardiac evaluation revealed a grade V/VI systolic murmur at the upper and left lower sternal borders, accompanied by a parasternal heave. Echocardiography demonstrated poor left ventricular contractility, severe pulmonary hypertension, a dilated aortic sinus (20.2 mm), with Z-scores of 8.08 (Boston), 6.37 (Detroit), and 5.97 (Halifax), indicating extreme dilation. Multiple valvular abnormalities were present: moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation. These findings are consistent with progressive valvular degeneration due to impaired extracellular matrix integrity.\n\nGenetic analysis via Sanger sequencing and polymerase chain reaction (PCR) of the fibrillin-1 (FBN1) gene identified a novel heterozygous mutation at nucleotide position c.3964 + 1G > T, located in intron 32 of the FBN1 gene. This mutation affects the splice site of exon 32 and is classified as a pathogenic variant based on the 2015 ACMG/AMP guidelines. The mutation lies within the previously defined 'neonatal region' of the FBN1 gene (exons 24–32), which is associated with a more severe, early-onset phenotype of MFS, including neonatal cardiac involvement and rapid progression of valvular and musculoskeletal pathology.\n\nOn postnatal day 1, refractory hypoxemia was observed despite >60% oxygen supplementation, indicating inadequate cardiac output and pulmonary perfusion. Medical management was initiated to address low cardiac output secondary to severe mitral and aortic regurgitation. Therapeutic interventions included milrinone (an inodilator) for afterload reduction, continuous fentanyl sedation to suppress myocardial oxygen demand, and diuretic therapy to manage oliguria and fluid overload. Despite these measures, the infant developed progressive respiratory failure, worsening pulmonary hypertension, and deteriorating cardiac contractility. Echocardiographic follow-up confirmed progressive worsening of aortic and mitral regurgitation, with sustained severe pulmonary hypertension.\n\nMultidisciplinary team consultations with the family and clinical staff concluded that surgical intervention—such as valve repair or replacement—was not feasible given the rapid disease progression and poor prognosis. Palliative care was initiated instead. Over the following weeks, the infant developed hepatic and pulmonary congestion, pulmonary hemorrhage, and ultimately progressed to multiple organ dysfunction syndrome (MODS). The patient died 32 days after birth. This case exemplifies the severe, early-onset form of Marfan syndrome associated with a novel FBN1 mutation in the neonatal region, characterized by profound cardiac dysfunction, valvular deterioration, and multisystem involvement, underscoring the critical need for early genetic diagnosis and the limitations of medical therapy


A 27-year-old woman with a long-term blood condition called beta thalassemia has been having swollen, bleeding gums and bad breath since she became pregnant. She is 16 weeks pregnant and has not seen a dentist before or since. Her gums are red, soft, and bleed easily, and her lips are dry and peeling. This is common when you have both thalassemia and are pregnant. She also has a weak body and was once diagnosed with knee pain from thalassemia-related arthritis. Her blood tests show signs of infection and anemia, which is why she needs regular blood transfusions — but she stopped them during pregnancy. The doctors treated her gums with a special mouth rinse (chlorine dioxide), a hydrogen peroxide swab, antibiotics, and cleaning of her teeth. They also gave her instructions to brush gently and use a small toothbrush between her teeth. After three months of care, her gums healed, the bleeding stopped, and she no longer has bad breath or swollen gums. She is now doing well and keeps her mouth clean with daily care. The team of doctors, dentists, and nurses worked together to fix her problem.


A 27-year-old woman with beta thalassemia major, a condition that requires monthly blood transfusions and iron-lowering drugs, is now pregnant at 16 weeks. Because of her pregnancy, she stopped her blood transfusions and iron treatments. She has been experiencing swollen, bleeding gums, bad breath, and dry, peeling lips. She has never seen a dentist before or since. During her check-up, her dentist found that her gums were red, soft, and swollen with bleeding, and there were deep pockets in her mouth — signs of gum disease. Her blood tests showed anemia and signs of infection, which are common in beta thalassemia. The doctors diagnosed her with gum enlargement and chronic periodontitis (gum disease) linked to both her pregnancy and beta thalassemia.

To treat her condition, she received a combination of care: her gums were cleaned with a 3% hydrogen peroxide solution, she used a chlorine dioxide mouthwash (Oxyfresh®) three times a day, and took antibiotics for a short time. Her dentist also removed tartar and gave her instructions on how to brush and floss properly. Blood transfusions were given monthly during treatment. After three months of care from an oral medicine specialist, a periodontist, and an internist, her symptoms improved greatly. By the end of the treatment, her gums had healed, she no longer had bleeding or bad breath, and she was able to brush without pain. She is now following a routine at home, including using mouthwash, applying petroleum jelly to her lips, and using an interdental brush to keep her mouth clean. The overall outcome was positive because she followed the treatment plan and stayed consistent with her care.


A 38-year-old woman named A.P. was diagnosed with dilated cardiomyopathy at age 17, after having a severe case of tonsillitis that may have led to heart inflammation (myocarditis), though this was never proven. She developed serious heart failure symptoms and was hospitalized for 10 months and 9 days. At the time, her heart was not pumping effectively — her ejection fraction was only 10%, and she was at high risk of dying. She received treatment to support heart function, prevent dangerous heart rhythms, and reduce blood clots. Over time, her heart function improved, and by age 21, her ejection fraction reached 48–57%, marking a period of remission. This improvement lasted for 4 years, after which her condition worsened, and her ejection fraction dropped to 25%. She was hospitalized again for two months and then stabilized with adjusted treatment. By 2006, her heart function had recovered to 50%.

At age 27, she had a successful first pregnancy. After giving birth, her heart function remained stable at around 40%, and she continued with heart medications. In 2015, she became pregnant again. During the second trimester, at 35 weeks, she was hospitalized due to shortness of breath and inability to walk. Her ejection fraction dropped to 18%, and her heart failure worsened. Despite this, her doctors decided to continue the pregnancy. She had a C-section at 39 weeks, and her condition improved within 20 days.

In October 2016, her treatment was updated to include medications like ramipril, metoprolol, spironolactone, and ivabradine, along with a daily fluid limit of 1.5 liters. She also wore a life-saving device called a LifeVest defibrillator from December 2016 to February 2017, when it was removed. After removal, her ejection fraction was 44%, and doctors found no need for a permanent defibrillator. She is now stable on medication, can do normal daily activities, and is a mother of two children. She is not working, but her heart condition is well-controlled with regular check-ups, weight management, and monitoring of kidney function and electrolytes. Her diagnosis remains dilated cardiomyopathy with heart failure stage II, and no further device is needed at this time.


A 13-year-old boy was brought to the hospital after finding a noticeable lump in his left groin area. He had no fever, weight loss, or other general symptoms. The lump was soft, movable, and not painful. His medical history included a past spinal surgery six years ago that left him with limited movement and sensation in his legs, and he had developed pressure sores from being in bed for a long time. Blood tests showed a slightly high inflammation marker (ESR), but all other blood and organ function tests were normal. A CT scan found enlarged lymph nodes in the groin area, the largest being about 3.5 cm in size, but no other abnormalities were seen. Since the lump could have been a sign of serious conditions like lymphoma or leukemia, surgery was done to remove the lymph nodes for testing. The tissue sample showed changes consistent with a rare form of Castleman’s disease called plasma cell type, which is very uncommon in children. This case is the first reported instance of unicentric Castleman disease (UCD) in the groin area. After 12 months of follow-up, the boy had no new symptoms, no further lymph node swelling, and all test results remained normal. He was given a short course of prednisolone and continues to be monitored every three months with regular check-ups and imaging.


A 28-year-old man developed two red, raised patches on his right arm and forearm, each with small blisters and a shallow ulcer, about halfway between the elbow and the wrist. The areas were painful and itchy, but he had no fever or other systemic symptoms. He had been on vacation in a coastal area of Ecuador when the rash appeared. A small skin sample was taken and examined under a microscope, which showed signs consistent with a skin condition caused by exposure to a type of beetle found in tropical regions. The diagnosis was Paederus dermatitis, a rash caused by contact with the beetle’s secretion. He was treated with antihistamines, a topical steroid cream, and cold compresses. After 8 days, the rash went away, though the skin remained slightly darker in those areas as a result of the inflammation.


A 77-year-old woman had repeated episodes of vomiting blood (haematemesis). She had high blood pressure and high cholesterol, but no other major health problems. When she first came to the emergency room, she was shaky and had low blood pressure, and her blood tests showed anaemia, which pointed to bleeding in her upper digestive tract.

A CT scan was done to check the cause. It showed that the third part of the duodenum (a section of the small intestine) bent sharply to the right side of the aorta and went downward without crossing in front of it. The duodenal-jejunal junction (where the duodenum meets the jejunum) and the jejunum were also on the right side. This raised concern that she might have intestinal malrotation — a condition where the intestines are abnormally positioned.

However, seven days later, a repeat CT scan showed that the intestines had moved back to the normal position on their own. This didn’t match typical malrotation, which is usually permanent. Instead, it suggested a different problem: dysplasia of the ligament of Treitz — a condition where the ligament that normally holds the small intestine in place is abnormally formed or weak.

A few months later, she had another episode of vomiting blood. The CT scan again showed the duodenum and jejunum on the right side. Endoscopy (a procedure to look inside the stomach) found a tear at the gastric cardia (the area where the stomach meets the esophagus), which is a known cause of bleeding called Mallory-Weiss syndrome.

Later, during surgery (laparotomy), doctors found that the ligament of Treitz was present but not properly fixed to the jejunum. It was only attached to the duodenum, so it could move easily and caused the intestine to shift to the right side. The rest of the intestines were in normal position, and there was no malrotation.

The surgery fixed the upper jejunum to the back of the abdomen, and the patient recovered well and has not had any further bleeding since.

In short, the repeated, temporary shifts of the small intestine were not due to malrotation, but to a weak or abnormal ligament of Treitz, which allowed the intestine to move freely and cause symptoms during vomiting.


A 12-year-old boy with Down Syndrome and movement problems was referred to the Oral Medicine Department. He had a distinctive facial appearance and dry, cracked lips. Because he wore a cervical collar, doctors could not check his lymph nodes. Inside his mouth, there was a 1×0.7 cm ulcer on the right side of his tongue, with a hard edge and a white-yellow base. The ulcer looked like oral cancer (OSCC) at first, but doctors found it was actually a chronic traumatic ulcer caused by sharp teeth. The tooth at the back of the upper jaw (tooth 55) was sharp and was rubbing against the tongue, causing the injury. The patient also had damaged teeth and tooth remnants on several teeth, which were recommended to be removed and replaced with a space maintainer to prevent shifting of other teeth.

The boy had low sodium levels and higher lymphocyte counts, and an MRI showed dislocation in his neck spine. He was given treatments including salt water (0.9% sodium chloride), povidone-iodine mouthwash (1%) to clean and reduce inflammation, and petroleum jelly to keep his lips moist. His mother was taught how to care for his mouth at home: using gauze soaked in salt water, applying the mouthwash three times a day to the ulcer, and using petroleum jelly on his lips.

After a few days, the ulcer and lip condition improved. By the 10-day follow-up, the ulcer had greatly reduced. Two days after that, the boy had surgery on his neck spine. He was then admitted to the Pediatric Intensive Care Unit, where he later developed respiratory failure and passed away after two weeks of care.


A 19-month-old boy was brought to the emergency room after falling from his highchair. He hit his head and started vomiting, became very irritable, and had fast breathing and heart rate. His oxygen levels were low, and he showed signs of serious breathing difficulty, including pulling in his stomach muscles and weak breath sounds on the left side of his chest. Despite treatment with a breathing tube and oxygen, his oxygen levels kept dropping, so doctors decided to insert a tube into his windpipe to help him breathe. A lung ultrasound showed signs of lung collapse, and a chest CT scan revealed that the entire left lung was collapsed, with a sudden blockage in the main airway of the left lung, about 12 mm from the main branch. This raised suspicion of a foreign object — an almond — being stuck in the airway. The mother reported that the child had had a sudden, intense cough a few days before that went away on its own. A rigid bronchoscopy was performed, and a 2 cm almond was found and removed. The boy had never eaten almonds before and likely swallowed it by accident. After recovery, his breathing improved, and he was able to breathe on his own again within 24 hours. He was then moved to a regular pediatric ward for further care and full recovery.


A 4-month-old boy lived in a prison cell with his mom and two other people. He had a painful lump in his armpit and X-rays showed broken ribs and lung problems. Doctors thought it might be abuse, so he went to the hospital. He was very sick — low oxygen, fever, and swelling — and had a big abscess. Tests showed his body couldn’t fight off infections well. Bacteria were not found, but a fungus called Aspergillus fumigatus was found in the abscess. He got antibiotics and then antifungal medicine (voriconazole) for 28 days. A test showed he had a rare immune problem called chronic granulomatous disease, caused by a gene fault passed from his mom. At 8 months, the infection got worse and spread to his shoulder. He had more lung damage and needed more medicine. At 12 months, he got sick again with the same fungus, even after treatment, and died.


A 25-year-old man had painful sores on his lips and inside his mouth. The sores started a few days ago, got worse when he ate or talked, and he tried using petroleum jelly but it didn’t help. He started using a medicine ointment (triamcinolone) on his lips, and the pain got better, but the sores didn’t go away. He had a fever before the sores came, didn’t eat well for a long time, and often licked his lips. He had chickenpox as a child. The sores were red, bumpy, and bled easily. A test showed he had a virus called HSV-1, which means the sores were caused by a common virus. The doctor said it was HAEM — a condition where the body reacts to stress and poor diet with mouth sores. To fix it, he took vitamins, used an antiviral medicine (acyclovir), and used a salt water rinse. He was also told to brush his teeth and tongue gently, avoid spicy or sour foods, stop licking his lips, and eat better. After a few days, his sores healed completely and he felt much better. Now he needs to keep going to the dentist for more care.


A 25-year-old man came to the dental clinic with painful sores on his lips that started about four days ago and spread to his upper and lower lips two days later. The sores were painful, especially when eating or talking, and didn't improve with self-treatment like petroleum jelly. He tried using triamcinolone ointment, which helped a little, but the sores didn’t fully heal.

He had a fever a week before the sores appeared and had been under a lot of stress with poor nutrition for about a month. He didn’t have any medical conditions, allergies, or habits like smoking or drinking alcohol. However, he often licked his lips, which may have worsened the sores. He also had chickenpox as a child.

On examination, his lips had red, painful sores with crusts that bled easily. His tongue had white patches, and there were other minor oral issues like tooth decay and poor hygiene. A blood test for herpes virus (HSV-1) came back positive, which confirmed the diagnosis of HAEM — a condition caused by herpes virus that affects the mouth and lips, especially in people under stress or with poor nutrition.

Treatment included applying a topical ointment (triamcinolone) to the lips, taking oral multivitamins, and using acyclovir tablets to fight the virus. He was also advised to improve his diet, avoid spicy or acidic foods, stop licking his lips, and keep his mouth clean by brushing teeth and tongue daily.

After a few days, his pain improved and the sores began to heal. By the second follow-up, all the sores had healed completely. His quality of life improved significantly, and he was referred to continue regular dental care. The case was reviewed and approved for publication, following ethical guidelines.


A 29-year-old woman had heavy vaginal bleeding for a month and was living with HIV. Her immune cells (CD4) were very low at 26, meaning her body was weak. A biopsy showed a serious cancer in her cervix that spread beyond the cervix, called extra-nodal BL. This cancer was stage 3B, meaning it had reached her kidneys and pelvic walls. Doctors said she needed chemo and radiation, but it took her 43 days to get treatment because of a long waiting list. That delay was too long — doctors say treatment should start within 48 hours. She died 43 days after diagnosis, before getting treatment. During those days, no more scans could be done because the machines were broken. She got blood transfusions and pain relief, but still passed away. The main reason she died was likely the fast-spreading cancer, especially since she had weak immunity and high virus levels. But her body also failed in many ways — her kidneys and blood system stopped working. Doctors couldn’t do a final test after she died, but they believe the cancer was the main cause, with organ failure as the final result.


A 56-year-old woman was diagnosed in 2013 with Sjogren’s syndrome, a condition that affects dryness in the mouth and eyes, and which also led to lung disease (interstitial lung disease) and pulmonary arterial hypertension (PAH). She was treated with several medications, including sildenafil, bosentan, macitentan, iloprost, and corticosteroids, but her condition continued to worsen. By 2020, she was experiencing severe shortness of breath, cough, and signs of heart failure, including low oxygen levels and high levels of a heart-related marker (BNP), which led to cardiogenic shock. She was hospitalized, treated in the ICU, and stabilized, but her condition remained serious and required frequent hospital visits.

In May 2023, she started a new treatment called molecular hydrogen therapy, taking one capsule per day. This therapy involved hydrogen-rich capsules made from coral calcium. After starting the treatment, tests showed an increase in certain immune cells (CD127+ Treg cells) and a decrease in harmful autoantibodies (anti-Ro) and B cell activity. Her symptoms, such as shortness of breath, stabilized without any side effects. Blood tests confirmed these changes in her immune system. This treatment is being used as an added support, not a replacement for standard care, and so far, it has helped improve her health without causing harm.


A 12-year-old boy was admitted because he had recently started getting headaches and was drinking and urinating a lot. He had no other medical problems. Tests showed he had diabetes insipidus (DI), a condition where the body can't properly regulate water balance, causing excessive urination and thirst. MRI scans found a rare condition called Rathke cleft cyst apoplexy, which is a sudden bleeding or swelling in a cyst in the pituitary area, but it wasn't pressing on any brain parts or causing serious issues. His hormone levels were mostly normal, and there were no signs of other endocrine problems. Because the cyst was stable and not causing harm, the doctors chose a watchful approach — regular check-ups with blood tests, physical exams, and MRI scans instead of surgery. Over three years, the boy developed normally, including puberty, with no major hormone problems except for a small deficiency in growth hormone. His growth slowed slightly, and after testing, it was found he had a partial growth hormone deficiency. He started treatment with growth hormone, and his growth improved over the next year. The cyst on the MRI stayed stable and even slightly decreased in size over time. The team of doctors, including endocrinologists and neurosurgeons, agreed that ongoing monitoring was safe and effective.


A 67-year-old man with no prior medical problems started having trouble swallowing, a hoarse voice, and a general decline in health over six months. He developed a large mass in his neck that was confirmed by biopsy to be a slow-growing type of lymphoma called grade 1 and 2 follicular non-Hodgkin lymphoma. Imaging showed the mass was 70 mm by 40 mm and had spread into nearby areas. Blood tests and bone marrow checks were normal at the start of treatment. The patient received four courses of chemotherapy (rituximab plus CHOP — a combination of drugs including cyclophosphamide, doxorubicin, prednisone, and oncovin) with no improvement. He then had three more courses of a different chemotherapy (rituximab plus DHAOX) with no response either. During follow-up, the biopsy of the mass showed that the lymphoma cells had disappeared and were replaced by AL amyloid deposits, which are a sign of abnormal protein buildup. Blood tests found high levels of immunoglobulin M, a type of antibody. A PET scan showed the mass was very active (hypermetabolic), which is a sign of ongoing disease. The patient is now on a new treatment plan with bortezomib, prednisone, and bendamustine, and is showing improvement after the first dose.


A 16-year-old girl has a flat, grayish patch on her left thigh that has been there since birth. The patch is about 10.5 cm wide and 8.0 cm long, and it has darkened and become depressed over time. It has small blood vessels running around the edge, and the area shows signs of abnormal blood flow. Imaging tests (angioresonance) found that the patch is caused by a vascular malformation in the skin and layer beneath the skin, fed by branches of the popliteal artery. The blood flow shows early signs of shunting, meaning blood is taking an unusual path. There is a small visible vein running under the skin, but no blood vessels have spread into the muscle or bone. The patch does not affect the length of her legs.


A 57-year-old woman with asthma and allergies had stomach pain that came and went for two months. She lost weight and felt tired, but had no fever or diarrhea. Blood tests showed a high number of a type of white blood cell called eosinophils, and her IgG4 levels were high. Doctors checked for infections and other causes, but nothing was found. A tissue sample from her colon showed too many eosinophils, which confirmed a condition called eosinophilic colitis. She was treated with steroids and a medicine called montelukast. Her symptoms went away in two weeks, and after that, she stayed on montelukast for three months with no pain coming back.


A 2.5-year-old girl with a history of neurofibromatosis type 1 (NF1) was brought in with bloody diarrhea that had lasted for several weeks. She had been having 5 to 10 episodes of diarrhea per day, with blood streaks, and had lost some weight. Tests initially showed a rotavirus infection, but that didn’t explain the ongoing symptoms. After being hospitalized for dehydration, her symptoms returned with blood in the stool, low appetite, and weight loss.

An endoscopy exam showed red, inflamed lining in her colon from the anus all the way to the beginning of the large intestine (the cecum), with loss of normal blood vessel visibility. Biopsies of the colon tissue showed signs of chronic inflammation, which is consistent with ulcerative colitis. Additionally, a test for cytomegalovirus (CMV) found a positive result, meaning the child had an active CMV infection.

The child was treated with antiviral medication (ganciclovir) for the CMV, which helped reduce the virus load. Her symptoms improved during hospitalization, and she stopped having bloody stools and abdominal pain. However, after two months, the inflammation returned, with bloody diarrhea again. A repeat endoscopy confirmed ongoing inflammation throughout the colon. She was treated with antibiotics and corticosteroids, which worked well, and she now has mild, ongoing symptoms.

She continues to be managed with a medication called mesalazine to help control the inflammation and is being monitored regularly. Her condition is stable, but she needs long-term care due to the chronic nature of the disease and her underlying NF1.


A 40-year-old man with HIV who was taking his medicine regularly came in with fevers that came and went for two years. Recently, he started having bad pain in his belly, especially on the right side, and his organs — liver and spleen — got bigger. He also had swollen lymph nodes all over. Lab tests showed his blood was weak, his body was fighting off infections, and his proteins were low. X-rays showed big liver and spleen, swollen lymph nodes, and a tree-like pattern in his lung, plus fluid in his lungs and belly. He got worse fast, had liver failure, and ended up in the ICU. He died a few hours later. After he died, doctors found tuberculosis in his lung sample and saw small, harmless spots in his liver that didn’t destroy tissue. This case shows how HIV can lead to serious infections when the body is weak.