A 5-year-old drank a farm bug killer called chlorpyrifos. Some charcoal and palm oil were later breathed into the lungs. The child got very sick. Breathing failed. The body went into shock. The child was in a coma. There was an early kind of paralysis (type 1). In the emergency room, a mask machine helped with breathing. Doctors swapped out some blood and put in new blood more than once. They gave atropine through a vein. They used a drip to help the heart and blood pressure. They also gave antibiotics and steroids. The child got better quickly. The child did not get the delayed muscle weakness that can happen later. The child went home after 10 days in the hospital.


A 4‑month‑old indigenous infant from a remote rural area of Panama (about three hours by canoe from the nearest health subcenter) with protein‑calorie malnutrition presented with acute diarrhea and moderate‑to‑severe dehydration. She had limited prior health care, had not received routine vaccinations, and was initially given Enterogermina (Bacillus clausii spores) and oral rehydration before being transferred to higher‑level hospitals because local facilities lacked supplies. On arrival at a third‑level hospital she had respiratory distress and signs of shock and was admitted to the pediatric intensive care unit, intubated, and treated with fluids, blood products, and multiple antibiotics. Initial blood culture grew methicillin‑resistant Staphylococcus aureus (MRSA); a gastrointestinal panel later detected Clostridioides difficile. Subsequent serial blood cultures from both peripheral blood and the central venous catheter repeatedly grew Bacillus clausii. Despite changes to antibiotic therapy to cover MRSA, C. difficile, and B. clausii, she developed worsening multisystem organ failure, including cardiac and kidney dysfunction, and died twelve days after admission.


This story is about a 62-year-old white North African woman. She was diagnosed in 2021 with a rare condition called Von Hippel–Lindau disease. This condition caused growths in several parts of her body. She had a tumor in a bone near her left ear. She had a tumor in the left adrenal gland, which sits above the kidney. She had cancer in her left kidney. Her right kidney had many cysts. She also had growths in her pancreas. She received several treatments. She had radiation treatment. She had surgery to remove the left adrenal gland. She had surgery to remove the left kidney. She had major surgery on the pancreas and nearby small intestine. Later, ultrasound and MRI scans showed a lump with both fluid and solid parts near the left ovary and tube. Keyhole surgery looked inside the pelvis. It found cyst-type tumors in the thin support tissue next to both fallopian tubes. Doctors then removed the uterus and both ovaries and tubes. The lab checked the tissue. It showed tumors of the same type on both sides in the thin support tissue around the tubes and the uterus. These findings fit with Von Hippel–Lindau disease.


A 36-year-old woman with ulcerative colitis developed a week of worsening chest pressure with autonomic symptoms (such as sweating and nausea). Her electrocardiogram showed ST-segment elevation in the inferior leads, consistent with an inferior-wall heart attack. She also reported several months of fatigue and night sweats.

Urgent coronary angiography found severe two-vessel coronary artery disease. The right coronary artery was the culprit lesion and was opened successfully with a stent. Because the interventional team suspected inflammation of the aorta (aortitis), additional workup was done. Inflammatory markers were mildly elevated, and CT angiography showed fibrotic thickening around the aorta with significant narrowing in multiple arteries, pointing to Takayasu arteritis.

She started treatment with prednisone and methotrexate. After stabilization, she underwent delayed coronary bypass surgery and did well.


A 36-year-old woman had dysphagia due to a congenital right aortic arch with mirror-image branching.
In this rare pattern, the aorta runs to the right, wraps around the right main bronchus, and the head-and-arm arteries branch in the reverse order of normal.
Most people have no symptoms unless the aorta or an associated bulge compresses the esophagus or trachea.
Surgery is considered for major airway or esophageal compression, aneurysmal disease, thoracic aortic dissection, or a Kommerell diverticulum larger than 2 cm.
There is no standard operation; treatment is tailored to the person’s anatomy and symptoms.
In this case, imaging showed external compression of the upper esophagus with a small Kommerell diverticulum (about 1.3 cm), so no intervention was performed and her symptoms improved.


A 75-year-old postmenopausal woman from Western Ethiopia had a Lippes loop IUD retained for 40 years and came in with pelvic pain. On speculum exam, part of the loop was seen at the external opening of the cervix. The device was removed easily with spongy forceps. She was discharged with pain medication and doxycycline twice a day for 3 days. Additional context: She reported no fever, bleeding, or vaginal discharge; her exam and pelvic ultrasound were otherwise unremarkable. She was observed for a few hours after removal, then sent home. On follow-up, her pelvic pain resolved.


An 18-year-old Hispanic male with no prior medical history presented with 3–4 days of substernal, nonradiating chest pain, orthopnoea, dry cough, and subjective fevers. Initial ED workup showed elevated troponin I and diffuse ST-segment elevation. Chest X-ray demonstrated an enlarged cardiac silhouette with mild pulmonary oedema. TTE revealed LVEF 40% with severe LV concentric hypertrophy and a mild posterior pericardial effusion. Coxsackie A and B titres were elevated. Symptoms transiently improved on ibuprofen and colchicine. Coronary angiography showed no CAD. Repeat TTE showed LVEF 40–45%, anteroapical and inferolateral hypokinesis, and elevated LVEDP consistent with diastolic dysfunction. Chest CT angiography showed pneumonitis and a pericardial effusion. Working diagnosis was Coxsackie myopericarditis. On hospital day 4 he acutely decompensated (diaphoresis, tachycardia, undetectable BP). Emergent TTE showed a large pericardial effusion with impending tamponade; pericardiocentesis was performed but was complicated by PEA arrest requiring ~30 minutes of ACLS. He was intubated, cannulated to VA-ECMO, and started on vasopressors (norepinephrine 5 mcg/min, vasopressin 0.05 units/min) with substantial transfusion requirements (9 PRBC, 10 platelets, 10 cryoprecipitate, 4 FFP) due to cannula site oozing. At the receiving centre, EMB was obtained for suspected fulminant myocarditis/infiltrative disease and was negative for inflammatory or infiltrative pathology. Repeat serology showed Coxsackie A type 9 and Coxsackie B2/B6 positivity and EBV DNA PCR 133,000 IU/mL. TTE now showed EF 10–15% with persistent severe LV concentric hypertrophy (septum 1.9 cm, inferolateral wall 2.2 cm). He was started on IVIG for presumed Coxsackie myocarditis and broad-spectrum antibiotics for worsening leucocytosis without a clear source; colchicine was stopped for concern of rhabdomyolysis (CK 2874 U/L). He subsequently developed flushing, fever, dyspnoea, and hypoxaemia with CXR consistent with pulmonary congestion/concern for ARDS, and IVIG was discontinued. Vasopressors were weaned off and he was extubated. Attempted ECMO decannulation failed; due to global concentric LV hypertrophy he was not an LVAD candidate. Emergency heart transplant listing and possible transition to IABP with inotropes were discussed. During transplant evaluation, an incisional biopsy of a 1×1 inch, painless, mobile right arm mass disclosed aggressive EBV(+) NK/T-cell lymphoma with a cytotoxic immunophenotype (CD2+, CD3+, CD56+, BCL2+, granzyme B+, TIA1+, MUM1+, diffuse EBER positivity). In situ hybridisation of the prior EMB was negative for EBV-RNA. Cardiac MRI demonstrated inferolateral and anterolateral hypokinesis with subendocardial to transmural LGE in those territories with relative septal sparing, marked pericardial thickening with avid enhancement, and a loculated pericardial effusion; no discrete mass was identified. Differential included Coxsackie myopericarditis and EBV myocarditis (noting EBV PCR is more sensitive than serology), but the absence of myocardial inflammation on EMB, marked concentric hypertrophy, and atypical LGE pattern argued against primary viral myocarditis. Amyloidosis was considered, but Congo red staining on EMB was negative. The overall picture—pericardial effusion refractory to initial therapy, acute heart failure with concentric hypertrophy, and the new diagnosis of EBV(+) NK/T-cell lymphoma—favoured pericardial/myocardial involvement by ENKTCL. Given ENKTCL without marrow involvement and concern for third spacing, a modified SMILE was planned (excluding methotrexate). Because of haemodynamic instability and concerns about tolerating cytotoxic therapy, induction was initiated with carboplatin (days 1–3), etoposide (days 1–5), and dexamethasone; peg-asparaginase was added (days 7–21). This regimen led to rapid improvement in LV function and haemodynamic stability, after which two cycles of modified SMILE were administered, followed by two cycles of DDGP (dexamethasone, gemcitabine, carboplatin, peg-asparaginase). Whole-body PET was negative. The treatment plan is to complete six total cycles and consider radiotherapy and possible stem cell transplantation. He is on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation. Outcome: after initiation of chemotherapy and optimisation of HF therapy, TTE showed recovery of LVEF to 55%, normal wall motion, and normal myocardial wall thickness, with resolution of the pericardial effusion and regression of hypertrophy. He continues multidisciplinary follow-up with cardiology/heart failure and oncology. Pathophysiologic context: cardiotropic RNA viruses such as Coxsackie can trigger receptor-mediated endocytosis and replication, leading to myocyte dysfunction and apoptosis; in susceptible hosts, maladaptive immune activation (persistent T-cell activation and antibody-mediated myocyte injury) can precipitate fulminant myocarditis. In this case, however, the lack of myocardial inflammation on EMB and the imaging phenotype supported lymphoma-associated cardiac involvement rather than primary viral myocarditis.


A 59-year-old man with long-standing type 1 diabetes presented with acute heart failure. An echocardiogram showed large vegetations on the mitral and aortic valves. Blood cultures were positive for Staphylococcus warneri, a coagulase‑negative staphylococcus commonly found on the skin. He was diagnosed with native valve endocarditis. After medical stabilization, he ultimately underwent replacement of both the mitral and aortic valves. In retrospect, mild laboratory abnormalities and several months of weight loss beginning about four months earlier were likely early signs of endocarditis. He had no history of immunosuppressive therapy and no implanted medical devices.


A 36-year-old female with ulcerative colitis (well controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares) presented with 1 week of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, the ECG was in sinus rhythm with ST-segment elevation in the inferior wall. She endorsed a 6-month history of general malaise, fatigue, and night sweats, and had experienced exertional precordial pain that progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.

Emergency coronary angiography demonstrated severe 2-vessel coronary disease: a severe 90% ostial lesion in the left coronary trunk (left main) and a severe 99–100% subocclusive ostial lesion in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful placement of a drug-eluting stent. The hemodynamicist noted possible aortitis given arch involvement and vessel friability during balloon advancement and recommended an inflammatory/etiologic evaluation prior to definitive management of the left main lesion.

Laboratory testing showed mild anemia (hemoglobin 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated ESR 42 mm/h, CRP 4.9 mg/L (normal <1), and elevated high-sensitivity troponin. Autoimmunity panel: normal complement C3/C4, negative ANA, anti-DNA, and ENA profile; non-reactive VDRL. Cardiac MRI with contrast demonstrated acute non-transmural infarction of the left ventricular inferior wall and subendocardial ischemia in the anteroseptoapical region at rest, with mild aortic and mitral insufficiency and preserved biventricular systolic function.

Computed tomographic angiography of the chest/abdomen/pelvis showed periaortic fibrotic wall thickening involving the aortic root, arch, and abdominal aorta, with severe left coronary trunk stenosis, mild left subclavian and left vertebral artery stenoses, and severe inferior mesenteric artery stenosis. The differential included IgG4-related disease versus Takayasu arteritis. Total IgG was 1,600 mg/dL (ref 700–1,600) with IgG1 1,024 mg/dL (elevated) and normal IgG2 456 mg/dL, IgG3 98.8 mg/dL, and IgG4 13.6 mg/dL, findings not supportive of IgG4-related aortitis. Takayasu arteritis was diagnosed clinically and by imaging.

Immunosuppression was initiated with prednisone 60 mg daily and methotrexate 20 mg weekly (parenteral) with folic acid 1 mg daily. After 3 weeks of therapy, she underwent myocardial revascularization surgery using the left internal mammary artery graft to the descending anterior artery (LAD) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta appeared healthy. She was discharged home in good general condition and remains under ambulatory follow-up.

Context: Takayasu arteritis is a large-vessel granulomatous vasculitis affecting the aorta and its major branches that can produce aorto-ostial coronary lesions (as in this case, involving the left main and right coronary ostia), leading to myocardial ischemia/infarction. The mildly elevated inflammatory indices, periaortic fibrotic thickening, and multifocal arterial stenoses on CTA are characteristic, and the lack of IgG4 elevation argues against IgG4-related aortitis. The staged approach—urgent culprit-vessel PCI followed by immunosuppression and delayed CABG—is consistent with management principles aiming to control vascular inflammation before definitive surgical revascularization.


A 17-year-old boy felt fine. A routine dental x-ray found something in his right nose by accident. He did not have a stuffy nose, nosebleeds, or pain. The pictures showed a bright spot in his right nose. It was a small metal snap button, like one on clothing. It was stuck low on the floor of the right side of his nose. It had probably been there for more than 10 years.


A 57-year-old patient had asthma and nose allergies. She kept having stomach pain. Her blood showed very high levels of allergy-fighting white cells. A certain immune protein (IgG4) was also high. The doctors checked for blood cancers and other causes and did not find them. They gently took tiny samples from the lining of her large intestine. The samples showed too many of those allergy cells sitting in the tissue. This meant she had eosinophilic colitis, which is swelling of the colon from a build-up of allergy cells. She took a steroid medicine to calm the swelling. Then she stayed on montelukast to keep the problem quiet. Her pain went away and did not come back for three months.


A 19-year-old man was admitted with an 8-month history of a painful left scrotal mass. He underwent an orchidectomy, and pathology favored epididymal tuberculosis. Imaging then revealed additional TB sites: lymph nodes, lungs, the chest wall (parietal), and the bones and joints (osteoarticular). Standard anti-tuberculosis therapy was started. In the fourth month of treatment he developed generalized seizures, and brain MRI showed tuberculomas. Treatment was continued along with an anticonvulsant, leading to good clinical and radiologic improvement.


This 54-year-old man had long-term kidney disease. He took steroids and other medicines that weaken the body’s defenses for a long time. He came to the lung department with fever, cough with mucus, and trouble breathing. A scan showed many cloudy spots in both lungs, like frosted glass. Blood tests showed a lot of inflammation. This suggested an infection from germs such as bacteria, a virus, or a fungus. A blood test was positive for RSV antibodies. Tests for other germs were not positive. His immune system was weak. His antibody level (IgG) was low. His infection-fighting T cells (CD4 and CD8) were also low. Doctors gave strong medicines for infection and support to help his breathing. His illness got worse quickly. He died from breathing failure.


A 4-year-old boy had blood in his pee and swelling for 5 days. He then had headaches, nausea, and vomiting. He came to the hospital with seizures and very high blood pressure. Blood tests showed a low level of a protein called C3 and signs of a recent strep infection. This meant his kidney filters were inflamed after strep. His brain was affected by the very high blood pressure. Doctors suspected a problem called PRES, which is brain swelling from high pressure. A brain MRI confirmed this. His immune system also attacked his red blood cells. This made his blood level drop very low, to 5 g/dL. He was treated with medicines to lower his blood pressure, steps to protect his brain, and steroid medicines. He left the hospital after 31 days. Six months later, he had no symptoms.


A 78-year-old man from the Amhara region, Ethiopia, with a permanent pacemaker placed for complete heart block was scheduled for retropubic prostatectomy. The anesthesia and cardiology teams recommended switching his dual-chamber, rate‑modulated pacemaker to an asynchronous mode perioperatively to reduce the risk of electromagnetic interference during surgery. He could not afford reprogramming and chose to proceed with the existing plan after informed consent; permission to publish the case was obtained after the operation. He received combined spinal–epidural anesthesia at L3–L4 using 0.5% isobaric bupivacaine 2.5 ml (12.5 mg) plus fentanyl 50 µg. Standard ASA monitoring was applied with special attention to cardiac stability. Intraoperatively, he remained stable with minimal changes in vital signs; blood pressure was supported with isotonic saline as needed. Postoperatively, he was monitored in the PACU, received analgesia at 4 hours with an epidural top‑up, and was transferred to the ward about 6 hours after surgery in stable condition. Epidural analgesia was continued for 72 hours. He was discharged at the 88th postoperative hour in good condition.


A 65-year-old woman with no relevant personal or family history had a posterior mediastinal tumour detected incidentally during preoperative assessment for knee surgery (August 2022). On admission, physical examination was noncontributory and laboratory studies were within normal parameters. Chest CT demonstrated a tumour in the posterior right mediastinum measuring 6.5 × 4.2 cm with well-defined borders and mixed fat and solid density, without bone erosion or infiltration of surrounding tissues. An image-guided biopsy was obtained via a posterior approach using an 18G × 250 mm semiautomatic cutting needle. Histopathology showed a benign neoplasm composed of mature adipose tissue with areas of haemorrhage alternating with haemopoietic elements, predominantly erythroid precursors, along with myeloid elements at varying stages of maturation and megakaryocytes, establishing the diagnosis of primary mediastinal myelolipoma (MPM). Given the diagnosis and lesion characteristics, conservative management was chosen. The patient had an uncomplicated course and was discharged in good condition.


A 52-year-old male with no prior medical history was transferred from a lower-level facility for a tonic–clonic seizure secondary to alcohol withdrawal and a non-reduced right LFGHP. He was evaluated by traumatology 24 hours after admission: he was conscious, with bilateral shoulder ecchymosis and severe limitation of passive external rotation bilaterally. At that time, he was physically restrained (both feet and the left hand) due to intermittent psychomotor agitation. Admission radiographs reviewed at our center showed a right LFGHP and a simple posterior dislocation of the left shoulder that had been missed at the referring facility; the left-sided posterior dislocation was diagnosed approximately 48 hours after arrival. CT of both shoulders was then obtained and demonstrated interval progression of the left injury from a simple posterior glenohumeral dislocation on the initial radiographs to an LFGHP on CT 48 hours later, possibly related to the period of physical restraint, i.e., intrahospital aggravation.

Preoperative planning: On the right, the glenoid was intact; humeral head articular surface involvement was 40% with a large fragment continuous with the lesser tuberosity, amenable to osteosynthesis using a 4.0 mm partial-thread spongy screw plus high-strength sutures. On the left, there was no significant glenoid defect and the humeral head defect was 20%; the plan was to fill the defect using the lesser tuberosity fragment at the time of osteosynthesis (McLaughlin-type strategy).

Surgical technique: A single-session bilateral open reduction and internal fixation with locked plates was performed. The patient was positioned in a beach-chair position. For the right shoulder, a classic deltopectoral approach was used. A posterior mini-open incision (arthroscopy portal size) permitted digital maneuvering to reduce the posterior humeral head fragment. Provisional reduction was achieved with high-strength sutures and needles. Definitive fixation employed a partial 4.0 mm spongy screw and high-strength sutures to secure humeral head fragments, followed by a Philos (Depuy Synthes) locked plate to achieve stable reduction; rotator cuff tendons were tied to the plate with high-strength sutures. The wound was closed in layers and the arm immobilized. The left shoulder was addressed immediately afterward via the same deltopectoral approach with an accessory posterior portal for digital manipulation and reduction; fixation mirrored the right but without a spongiosa screw, as the anterior fragment was adequately stabilized with high-strength sutures alone.

Postoperative course: Bilateral shoulder immobilizers were used for four weeks. From the second postoperative week, elbow pendulum flexion–extension and hand exercises were started to pain tolerance. At the one-month radiographic control, loss of reduction of the greater tuberosity on the left was observed; revision surgery achieved stable fixation with high-strength sutures. The left shoulder was re-immobilized for an additional four weeks, then the home exercise program was restarted from week two post-revision. Six weeks after the revision, supervised kinesiologic therapy was initiated twice weekly; after 30 sessions, the patient returned to work five months after the initial injury. At one year, the right shoulder had recovered strength and mobility, whereas the left had marked ROM limitations, especially external rotation; arthroscopic capsular release and hardware removal were performed on the left. At two years post-trauma, evolution was favorable and consistent with functional scales: QuickDASH 5% and Constant scores of 72 (left) and 76 (right).


A 27-year-old woman developed facial swelling and trismus 48 hours after finishing phenoxymethylpenicillin for a dental infection. A head and neck CT showed a large blood clot in the internal jugular vein. A chest CT showed septic emboli in the lungs. She was treated promptly with intravenous broad-spectrum antibiotics and anticoagulation. She improved with care and continued treatment after discharge.


A 62-year-old white North African woman with Von Hippel–Lindau (VHL) disease diagnosed in 2021 developed several VHL-related tumors: a left petrous bone tumor, a left pheochromocytoma, left renal cell carcinoma, a multicystic right kidney, and pancreatic masses. She was treated with radiotherapy to the petrous bone lesion, left adrenalectomy, left nephrectomy, and cephalic duodenopancreatectomy for the pancreatic tumors. During surveillance, ultrasound and MRI showed a solid–cystic mass in the left adnexal (ovary/tube) region. Laparoscopy then identified cystic tumors in the mesosalpinx on both the right and left sides. She underwent hysterectomy with removal of both adnexa. Pathology confirmed bilateral clear-cell papillary cystadenomas of the mesosalpinx and broad ligament, a pattern consistent with VHL.


A 4‑month‑old Indigenous infant from Urracá, rural Panama (approximately 3 hours by canoe from the nearest health subcenter), with protein‑calorie malnutrition and no prior healthcare or vaccinations, presented with 4 days of non‑bloody diarrhea and vomiting, progressing to moderate–severe dehydration. At the initial health center she received oral fluids and 4 doses of Enterogermina (Bacillus clausii: two billion spores/5 mL), but due to supply limitations was transferred to a second‑level facility and then to a tertiary hospital in Panama City with a working diagnosis of acute gastroenteritis and severe dehydration.

On arrival to the ED she had altered mental status, signs of shock (tearless cry, dry mucosa, cold extremities, capillary refill >2 s, filiform pulse, mottling), tachycardia 170 bpm, tachypnea 55/min, BP 91/37 mmHg, SpO2 99%, generalized edema (+++) of hands, feet, abdomen, and face, and skin changes suggestive of pellagroid dermatosis. Anthropometrics: weight 4.7 kg, length 56 cm, H/A Z −2.52 (W/H and W/A not quantifiable due to severe dehydration). Chest exam had fine basal crackles. Initial management included LR 10 mL/kg bolus, followed by 5% dextrose/0.33% saline then 5% dextrose/0.9% saline; empiric ceftriaxone 50 mg/kg/day for suspected sepsis. CBC showed leukocytosis 39×10^3/µL, severe anemia Hgb 5.6 g/dL, thrombocytosis 502×10^3/µL. She received 50 mL filtered, leukoreduced PRBCs and 40 cc FFP for coagulopathy. Enteral feeds were started via NGT; fluids were titrated with ongoing negative balance.

On hospital day (HD) 2, the initial peripheral blood culture signaled Gram‑positive cocci in clusters; oxacillin 200 mg/kg/day was added and ceftriaxone increased to 75–100 mg/kg/day. Hypocalcemia (Ca 6.38 mg/dL) was corrected. On HD3 she lost peripheral access; a central venous catheter (CVC) was placed. She remained hypovolemic with worsening work of breathing; LR 20 mL/kg was given. ABG: pH 7.26, HCO3− 13 mmol/L, pCO2 28.4 mmHg, pO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to PICU for mechanical ventilation. Management included total fluids ~100 mL/kg, epinephrine infusion, low‑salt albumin, 10% calcium gluconate; analgesia/sedation was switched from fentanyl to remifentanil due to elevated transaminases.

The admission blood culture grew methicillin‑resistant Staphylococcus aureus (MRSA); oxacillin was discontinued and clindamycin 40 mg/kg/day was added. A subsequent blood culture smear showing Gram‑negative bacilli prompted a change from ceftriaxone to ceftazidime 150 mg/kg/day. On PICU day 1 there was a marked rise in cardiac injury biomarkers; echocardiogram showed mild MR/TR, LV dilation, LVEF 58%, without thrombi, vegetations, or pericardial effusion, consistent with acute myocarditis. She received milrinone 0.4 mcg/kg/min, furosemide, and IVIG 1 g/kg once.

By HD4–5, the second‑day blood culture identified Bacillus clausii via VITEK 2; no susceptibility profile was generated (no interpretive breakpoints). Considering it was not a contaminant, antimicrobial therapy was adjusted: ceftazidime was changed to ciprofloxacin 30 mg/kg/day and ceftaroline 8 mg/kg q8h was added, with clindamycin continued for MRSA coverage. Three subsequent blood cultures at 48‑hour intervals remained positive for B. clausii from both peripheral blood and the CVC. On HD6, a GI panel (Maripoc) detected Clostridioides difficile toxin A/B; tests for Campylobacter jejuni, Norovirus GI/GII.4, Adenovirus, and Rotavirus were negative. Therapy was escalated to IV vancomycin 60 mg/kg/day plus oral metronidazole; ceftaroline, clindamycin, and ciprofloxacin were discontinued to streamline coverage for MRSA, B. clausii, and C. difficile. HIV, Chagas serology, and SARS‑CoV‑2 antigen (FIA) were negative; immunoglobulins were within reference ranges.

On HD7, arterial hypertension developed and spironolactone was initiated. By HD8, coagulopathy worsened and azotemia with 12 hours of anuria was documented; vancomycin dosing was adjusted and vitamin K administered. Due to clinical instability, peritoneal dialysis catheter placement was deferred. She progressed to anasarca and sustained hypotension; norepinephrine was added. Despite intensive care and multiple antibiotic regimens, she developed refractory septic shock and multisystem organ failure. She died 12 days after admission. No autopsy was performed due to family cultural objections.

Key microbiologic findings were: (1) initial MRSA bacteremia; (2) GI panel positive for C. difficile toxin; and (3) persistent Bacillus clausii bacteremia documented in serial peripheral and CVC cultures after prior administration of Enterogermina. The clinical course was marked by severe malnutrition, shock, myocarditis, evolving renal failure with anuria, coagulopathy, and ultimate multiorgan failure despite escalated antimicrobial and organ support.


A 65-year-old man had a cough, trouble breathing, and lost weight. A chest scan showed a spot in the right lung. A needle test of the spot showed it was a kind of lung cancer. Under the microscope, the cancer cells were large and sat among many infection-fighting cells. Lab tests fit this cancer type and ruled out other common lung cancers. A virus called Epstein–Barr was found inside the tumor cells. Another test showed a protein called PD-L1 was very high on the cancer cells. He was treated with strong chemotherapy and an immune therapy (gemcitabine, cisplatin, and durvalumab). The cancer kept growing. He died 9 months after diagnosis.


A 2 years 6 months old female with genetically confirmed NF1 (heterozygous pathogenic variant c.5606_5627del [p.Gly1869Valfs*28]) presented with 4 weeks of blood-streaked diarrhea (5–10/day). Initial ED evaluation showed rotavirus positive, low inflammatory markers, negative coproculture, and a normal abdominal ultrasound; she was hospitalized 3 days for dehydration and discharged with persistent semi-liquid stools. Ten days later she recurred with blood-streaked diarrhea, decreased intake, and ~1 kg weight loss, prompting admission for further workup after outpatient GI pathogen and C. difficile PCR panels were negative. There was no fever, abdominal pain, vomiting, respiratory/urinary symptoms, arthralgia, pet exposure, travel, or dietary changes. NF1 phenotype included café-au-lait macules and osseous involvement; she underwent ankle arthrodesis at 18 months for tibial bowing; no family history of NF1 or IBD. Exam: soft, non-tender abdomen with increased bowel sounds; perianal exam normal; multiple café-au-lait macules. Labs: microcytic–hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (13,900/µL), CRP 1.37 mg/dL (ULN 0.5).

Index colonoscopy evaluated rectum, sigmoid, and colon to cecum; distal ileum was also inspected. The colonic mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency; the cecal mucosa itself appeared normal; no lesions in the anal canal or cecum. Biopsies: ileal mucosa with preserved villous architecture, adequate epithelial differentiation, and non-inflamed lamina propria. Colonic mucosa showed mild architectural distortion, adequate epithelial differentiation, lamina propria edema with a mild mixed inflammatory infiltrate, lymphoid follicular hyperplasia, and isolated crypt microabscesses—consistent with mild colitis with features suggesting chronicity. CMV PCR on colon biopsy was positive. Additional virology: CMV IgG positive, IgM negative; plasma CMV viral load 79.7 IU/mL. Stool GI pathogen panel and C. difficile PCR were negative. Biopsy microbiology: Gram stain +++ leukocytes without bacteria; culture with very low S. gallolyticus/equinus interpreted as flora; acridine orange, Ziehl–Neelsen, Koch culture, and adenovirus PCR were negative. Clinical impression: endoscopy and histology suggestive of ulcerative colitis (UC) in the setting of moderate activity (PUCAI 50). Mesalazine 70 mg/kg/day tid initiated; fecal calprotectin >600 µg/g. Immunology workup for suspected PID: normal lymphocyte subsets and immunoglobulins; HIV negative; memory T-cell abnormalities attributed to CMV viremia; lymphoproliferation normal. Invitae PID panel (429 genes; 68 monogenic IBD) returned 7 VUS, none in monogenic IBD genes.

Treatment with IV ganciclovir for 15 days led to clinical improvement; CMV PCR was undetectable prior to discharge. She achieved PUCAI 0 at discharge with normalized stool frequency/consistency and no rectal bleeding, nocturnal stools, or abdominal pain. Two months later she had an IBD flare with bloody diarrhea (PUCAI 35); CBC normal, GI pathogen panel negative, C. difficile PCR positive, and CMV load undetectable. She received oral metronidazole but persisted with blood-streaked diarrhea and was re-hospitalized. Repeat colonoscopy showed diffuse erythematous mucosa from rectum to cecum with nodularity and loss of vascular transparency, more prominent in the left and transverse colon; no focal lesions; ileum and anal canal without lesions. Histology (terminal ileum, right and left colon): ileal architecture preserved without inflammation; colon with mild architectural distortion and epithelial dedifferentiation; lamina propria expanded by mixed inflammatory infiltrate with transmucosal distribution; foci of cryptitis and crypt abscesses; reactive lymphoid follicular hyperplasia; no granulomas or viral/parasitic cytopathic changes. She was treated with oral vancomycin and prednisone 1 mg/kg/day with good response and was discharged with reduced stool frequency. At outpatient follow-up she has mild residual symptoms (PUCAI 5); corticosteroids are being tapered and mesalazine maintained.

Overall, this case represents pediatric UC in an NF1 patient with tissue CMV positivity at presentation and low-level viremia, responsive to ganciclovir and 5-ASA, followed by a subsequent flare associated with C. difficile infection that improved with vancomycin and corticosteroids; CMV remained undetectable thereafter.


She had a heart transplant because her heart got very weak after pregnancy. Later, her kidneys—the body’s filters—were hurt by a germ called BK virus. A small kidney sample showed long‑lasting irritation and damage from this virus. A blood test also showed a high amount of BK virus (log 4.5). Her doctors turned down her anti‑rejection medicines to help. After about two years, her kidney numbers stayed steady. Her creatinine was 2.5 mg/dL and her GFR was 23.4 mL/min/1.73m2.


A 65-year-old woman had a lump in the back part of the space between her lungs. A chest scan showed it was oval like an egg, had smooth edges, and measured about 6.5 by 4.2 centimeters. Doctors took a small sample with a needle through the chest. Under the microscope, it had fat and blood-making cells. This means the lump was a myelolipoma in the area between the lungs.


A 65-year-old woman was found to have an incidental mass in the back part of the chest between the lungs (posterior mediastinum). Chest CT showed an oval, well-defined tumor measuring 6.5 × 4.2 cm. A transthoracic needle biopsy was performed. Microscopy revealed mature fat and blood-forming tissue, confirming a primary mediastinal myelolipoma. Imaging showed no invasion of nearby structures, and the lesion was managed conservatively with a good outcome.


A 78-year-old man from the Amhara region of Ethiopia had a permanent heart pacemaker because of a complete heart block. He was scheduled for prostate surgery. Before surgery, the anesthesia and heart doctors advised switching his pacemaker to a steady, fixed beat to lower the chance of problems. He could not afford that change. He chose to go ahead with the operation. He signed consent for the plan. After surgery, he also gave permission to share his case. For anesthesia, he got a numbing injection in the lower back (a combined spinal–epidural). The team used 2.5 ml of strong numbing medicine (0.5% bupivacaine) and a tiny dose of fentanyl (50 micrograms). Standard monitors were used, and his heart was watched closely. His vital signs stayed steady, with only small changes. His blood pressure stayed good with IV salt water. After surgery, he went to the recovery room. He got pain medicine after 4 hours and an extra dose through the epidural. Six hours after surgery, he moved to the ward in stable condition. The epidural pain control continued for 72 hours. He went home in stable condition about 88 hours after surgery.


A 52-year-old woman had burning when she peed and had to pee very often for a long time. She tried many treatments for bladder infections, but the problem did not go away. Regular scans and lab tests looked normal. A camera test that looked inside her bladder showed the lining was red and irritated, with tiny bits floating in the urine. Later, the lab saw a live larva (a baby insect) in her urine under the microscope. That finding explained her symptoms. She was told to keep very clean. She was also told to drink plenty of water every day.


A 20‑year‑old woman had a 12‑year history of idiopathic nephrotic syndrome that initially presented with extensive cerebral venous thrombosis and pulmonary embolism. She was treated with anticoagulation and oral corticosteroids, then mycophenolate mofetil as a steroid‑sparing agent. A comprehensive thrombophilia work‑up was negative. She experienced multiple relapses controlled with steroids until 2017, then remained in remission; anticoagulation and MMF were discontinued. One year later, she developed sudden diffuse abdominal pain with postprandial vomiting and bilateral leg edema. Laboratory tests confirmed a relapse of nephrotic syndrome. Abdominal CT showed acute superior mesenteric artery thrombosis causing acute mesenteric ischemia. At surgery, there was extensive small‑bowel necrosis not compatible with survival. She died 48 hours later.


A 20-year-old Arabic male martial artist (91.5 kg, 180 cm, BMI 28.24) presented with 5 weeks of posterior left thigh pain after a short sprint during soccer, described as an acute “pop,” followed by progressive loss of knee flexibility and inability to fully flex or extend the knee; the knee rested in approximately 15° of flexion. He reported no ecchymosis or significant swelling, could barely weight-bear on the affected limb, and withdrew from all sport. Initial self-management included icing, elevation, a crepe bandage, crutches, and step-to stair negotiation; NSAIDs, cryotherapy, and compression provided little relief. He denied prior lumbar symptoms and had no notable medical comorbidities (no alcohol use, smoking, diabetes, hypertension, or hereditary disease). Examination showed an analgesic gait with reduced heel strike; AROM of the left knee was 10–15° versus 0–130° on the right. Palpation identified tenderness and firmness in the middle third of the semimembranosus and semitendinosus. Manual muscle testing and isometrics were deferred due to discomfort. NPRS was 5/10 at rest and 7/10 with activity. Clinical evaluation ruled out lumbar disc involvement and gluteal/ischial tunnel syndromes. Although the slump test is a standard screen for lower-limb neurodynamic mechanosensitivity, it was negative in this patient. Despite a presentation suggestive of hamstring strain injury, the team implemented a neural glide based on neurodynamic principles and the anatomical/functional proximity of peripheral nerve structures to hamstring flexibility. Technique: seated with arms folded behind the back; knees extended and ankles dorsiflexed; therapist-guided thoracic and cervical flexion with knee extension to the patient’s tolerance, followed by active cervical flexion–extension coordinated with ankle dorsiflexion–plantarflexion (15 repetitions) to facilitate nerve gliding. Three sets were performed daily over 3 consecutive days. The therapist also facilitated progressive thoracic/cervical flexion until knee-area pain was provoked and then repeated the sequence. By day 3, active knee extension improved from approximately 5° to 10° and then to a 15°-bent position, and standing posture improved. Postural re-education included active chin flexion, prone passive stretching of cervical extensors, and progressive scapular retractor strengthening (arm positions T→Y→W) in prone with limb weight. To address kyphotic posture, active pectoral stretches at wall corners were prescribed, progressing hold time from 5 to 10 seconds, 10 repetitions, 3 sets daily. Outcomes: Measured by NPRS and Knee Society Score (KSS). Within 3 treatment days, substantial improvement was observed; pain medication was discontinued. NPRS decreased from 5/10 (rest) and 7/10 (activity) to 2/10 and 4/10, respectively. KSS improved from 22 to 61 (pain domain) and from 30 to 80 (function). After a 2-week home program, the patient achieved full active straight leg raise. At 2-month follow-up, he reported full recovery of knee function and pain resolution and had returned to sport without disruption. This case suggests that, even with a negative slump test, targeted neurodynamic mobilization combined with postural retraining may rapidly improve pain and function in select hamstring strain presentations; proposed mechanisms include reduced intraneural/extraneural adhesions, improved neural excursion, and modulation of nociceptive input.


A 17-year-old male had an asymptomatic nasal foreign body (NFB) found incidentally on routine dental x-rays and cone beam CT during orthodontic planning. He denied any nasal blockage, nosebleeds, or discomfort. His parents recalled that at age seven he had put something in his nose; the family had been advised at the time to remove it under sedation but did not follow up, assuming it had fallen out. Endoscopic exam showed a deviated septum and enlargement of the lower nasal turbinate, with mild redness and swelling of the nasal lining. A shiny object was seen stuck to the floor of the right nasal cavity beneath the inferior turbinate and was partly covered with mucus and crust. X-rays and CBCT confirmed a circular radiopaque object consistent with a metallic snap button about 1 cm across, with mild surrounding inflammation but no damage to the nearby bone or sinuses. With parental consent, the button was removed in the clinic under local anesthesia and nasal decongestion while the patient was semi‑upright to reduce the risk of it moving toward the airway; removal with a hook and forceps was uncomplicated, with only minimal bleeding. The retrieved snap button showed corrosion and biological deposits, consistent with being present for many years. The patient was discharged in stable condition, advised to use saline nasal rinses, and was doing well with a normal exam at two-week follow-up.


A 59-year-old Japanese man with a 28-year history of type 1 diabetes on intensive multiple-dose insulin therapy (BMI 18.4 kg/m2, undetectable C‑peptide, HbA1c ~9.0%) and remote, asymptomatic chronic severe (grade III) aortic regurgitation (diagnosed 16 years earlier without subsequent follow‑up) presented with acute decompensated heart failure. He had never undergone surgery or prosthetic device implantation and had no history of immunosuppressive therapies.

Eight days after a routine visit, he developed dyspnea and fever >38℃. On arrival: BP 192/82 mmHg, HR 118/min, orthopnea, SpO2 80%. Exam: Levine 3/6 systolic murmur; no Osler nodes, Janeway lesions, or conjunctival petechiae. Labs: WBC 20,800/μL, CRP 6.06 mg/dL, CK‑MB 6.0 IU/L, troponin T negative. CXR showed pulmonary congestion with cardiomegaly (CTR 55%). ECG had ST elevation in V1–V4, but emergent echocardiography showed no systolic dysfunction. He was diagnosed with acute heart failure due to valvular disease and treated with non‑invasive positive pressure ventilation and nitrates.

Transthoracic echocardiography demonstrated severe aortic regurgitation and severe mitral regurgitation with a mobile mitral vegetation. Transesophageal echocardiography identified a 16.5×6‑mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5‑mm nonmobile vegetation on the noncoronary cusp of the aortic valve, raising strong suspicion for native valve endocarditis (NVE). Head CT and MRI showed no cerebral infarction or hemorrhage.

Retrospective review revealed subtle abnormalities starting four months pre‑admission: mildly elevated WBC, albumin decreased to 3.0 g/dL the following month, and gradual hemoglobin decline over two months, with a 4‑kg weight loss. EGD and whole‑body CT were unrevealing. He partially regained weight and labs nearly normalized except for a CRP of 0.54 mg/dL. At the last pre‑admission visit (8 days prior), WBC was 9,300/μL, Hb 13.1 g/dL, Alb 3.0 g/dL, CRP 4.18 mg/dL, and diastolic BP had fallen; he remained afebrile and asymptomatic aside from weight loss.

Empiric antibiotics were initiated with ampicillin–sulbactam 12 g/day plus gentamicin 120 mg/day. Three admission blood culture sets all grew Staphylococcus warneri, a coagulase‑negative staphylococcus (CoNS) and resident skin flora (MICs: ABPC/S ≤8 μg/mL; GM ≤1 μg/mL; CEZ ≤2 μg/mL), confirming S. warneri IE. Per Japanese Circulation Society guidance, emergency surgery is generally recommended for NYHA III–IV heart failure or urgent surgery for NVE with mobile vegetation >10 mm and severe valve dysfunction. Because heart failure improved rapidly and appropriate antibiotics were started (reducing embolic risk), and given poorly controlled type 1 diabetes increasing operative risk, elective surgery was planned after stabilization of infection and glycemia. Antibiotics were narrowed to cefazolin 6 g/day; dental evaluation showed no periodontitis.

After four weeks of antibiotics, surgery revealed a bicuspid aortic valve with intact aortic and mitral annuli and no abscess. Large vegetations were exenterated, and both valves were replaced with mechanical prostheses. The postoperative course was uneventful; he was discharged on postoperative day 22 without apparent embolism and has remained recurrence‑free for over two years. This case represents NVE due to the resident CoNS S. warneri in a patient without prosthetic material or immunosuppression, with prodromal laboratory abnormalities and weight loss evident up to four months before presentation.


A 14-year-old treated for non-Hodgkin lymphoma developed hypertriglyceridaemia and pseudohyponatraemia after multiple doses of L-asparaginase with prednisone. Pseudohyponatraemia means the sodium result looks low because very high blood lipids interfere with the lab method; the body’s actual sodium status is not truly low. Clinicians suspected an adverse drug reaction and, using the modified Karch and Lasagna causality algorithm, classified the reaction as definitive for the combination of L-asparaginase and corticosteroids. Management included diet changes (low fat/low refined sugars, high fiber) and lipid-lowering therapy with a fibrate (ciprofibrate 100 mg daily) plus omega-3 fatty acids (4 g daily). Per protocol, L-asparaginase and prednisone were not discontinued because the indicated treatment phase had reached its end; the patient completed the planned doses. Triglycerides fell to 79 mg/dL within 14 days, and the episode resolved without complications.


A 67-year-old patient with no medical history presented with a 6‑month course of dysphagia and dysphonia and deterioration of general condition (15 kg weight loss over 6 months). On examination: GCS 15/15, afebrile, BP 12/07 cmHg, SpO2 100%, HR 80/min, normal conjunctivae, and a large mass in the cavum; no hepatosplenomegaly or peripheral adenopathy; otherwise unremarkable exam. Cervico-thoraco-abdomino-pelvic CT identified a 70 × 40 mm nasopharyngeal mass extending to 60 mm. Laboratory studies were normal (WBC, renal and hepatic function, LDH) with negative HIV, HCV, and HBV serologies. Nasopharyngeal biopsy with histology and immunohistochemistry in two independent readings supported a grade 1–2 follicular B‑cell NHL: CD20+, CD19+, CD79a+, CD10+. Bone marrow biopsy and the pre‑therapeutic work‑up were normal. The patient received 4 cures of R‑CHOP‑21 (rituximab 375 mg/m2 IV, cyclophosphamide 750 mg/m2 IV, oncovin 2 mg IV, prednisolone 100 mg PO, doxorubicin 50 mg/m2 IV) without response, followed by 3 cures of R‑DHAOX (rituximab 375 mg/m2 IV D1, high‑dose aracytine 2 g/m2 × 2 IV D2, dexamethasone 40 mg D1–D4, oxaliplatine 100 mg/m2 D1) with no clinical response. Due to persistence and increase of the nasopharyngeal mass, a tracheotomy was performed. Repeat biopsy of the mass objectified disappearance of lymphoid B infiltration with presence of AL‑type kappa amyloid deposits. Immune electrophoresis of plasma proteins revealed immunoglobulin M kappa; serum free light chains were not dosed due to resource limitations. Myelogram and a second bone marrow biopsy were normal. PET (TEP) showed a hypermetabolic nasopharyngeal process without other anomalies. Cardiac evaluation (ECG, natriuretic peptides, troponin, echocore) and renal assessment were unremarkable. The patient is currently under a bortezomib, prednisone, and bendamustine protocol, with good clinical evolution after the first treatment. This trajectory suggests an IgM‑associated localized AL amyloid process emerging in the site of the prior follicular lymphoma, despite systemic evaluations (including marrow and organ assessments) remaining normal.


A 45-year-old man was in the hospital with lung infection from the virus that causes COVID-19. He had no past brain or nerve problems. On day 16 in the hospital, he suddenly became less awake. Both eyes pulled to the right. His left face and chest had quick jerks. Then he had a full-body seizure. After that, the left side of his body stayed weak. A lab test on the fluid around his brain and spine found the COVID-19 virus. He slowly got better, and the final result was good.


A 14-year-old with suspected lymphoblastic non-Hodgkin lymphoma on protocolized induction (PINDA 0516) received L-asp E. coli 10,000 IU/m2 plus a glucocorticoid (prednisone). After seven doses of L-asp (cumulative ~90,000 IU) he developed clinical decline with vomiting, abdominal pain, and mild dehydration. Pancreatitis was suspected but excluded (amylase/lipase normal; liver tests normal). Laboratory assessment showed hyponatraemia (reported as 126 mOsm/kg) with urinary osmolality 510 mOsm/kg and concurrent hypertriglyceridaemia, prompting the diagnosis of pseudohyponatraemia secondary to hypertriglyceridaemia associated with L-asp plus corticosteroids. He was managed by Gastroenterology and Endocrinology with a diet low in refined sugars and rich in fiber, fibrates (ciprofibrato/ciprofibrate 100 mg PO daily), and omega-3 fatty acids (4 g PO daily), targeting triglycerides ≤300 mg/dL. Two weeks later triglycerides were 79 mg/dL; ciprofibrato and omega-3 were discontinued with advice for prophylactic use during subsequent corticosteroid/L-asp exposure. The patient ultimately completed 12 total doses of L-asp (cumulative 184,000 IU) for induction; L-asp and prednisone were not discontinued due to the end of indication per protocol. Causality assessment for the adverse drug reaction (ADR) using the modified Karch and Lasagna algorithm (WHO) was Definitive for the association of L-asp plus prednisone. No complications occurred, and the hypertriglyceridaemia resolved within 14 days. Mechanistically, L-asparaginase can reduce lipoprotein lipase activity and increase VLDL, while corticosteroids augment hepatic VLDL production; marked lipaemia then produces pseudohyponatraemia via indirect ion-selective electrode dilutional error, with normalization as triglycerides fall.


A 71-year-old man with long-standing vitiligo reported six months of visual loss in the right eye and hearing loss in both ears, worse on the right. During hospitalization, he had chronic headaches, fever, and marked unintentional weight loss. On eye exam, the right eye was reduced to light perception and the white of the eye was notably red; the left eye had a visual acuity of 20/200. Fundus findings showed scattered pigmentation in the right eye, a swollen optic disc in the left eye, and evidence of optic atrophy on the right.


A 12-year-old boy was admitted with sudden headaches and a week-long history of excessive urination and thirst. Tests showed central diabetes insipidus (low urine concentration with normal blood sodium and plasma osmolality), and MRI identified apoplexy (bleeding or sudden change) in a Rathke cleft cyst measuring about 15 × 6 × 11 mm; the normal bright signal of the posterior pituitary was lost but the anterior pituitary enhanced normally. He had no visual problems and routine pituitary hormone tests were otherwise normal. Because he was early in puberty, had no compressive symptoms, and basic endocrine tests were normal, a multidisciplinary team chose conservative management: clinical, hormonal and MRI follow-up, and treatment of the diabetes insipidus with vasopressin. Over three years the cyst remained stable then decreased in size (about 12 × 11 × 10 mm at nine months, 11 × 12 × 11 mm at two years, and 7 × 10 × 6 mm at three years), puberty progressed normally, and vision stayed normal. During follow-up his growth slowed, and stimulation tests at age 14 years 9 months showed a partial growth hormone deficiency; after starting growth hormone therapy his growth rate improved markedly. Overall, conservative follow-up was effective: the Rathke cleft cyst apoplexy stabilized and shrank, diabetes insipidus was controlled, and the only long-term endocrine issue was a treatable partial GH deficiency.


A 4-year-old male, two weeks post nasal impetigo treated with topical mupirocin and oral cefadroxil (dose/duration/adherence unknown), presented with 5 days of macroscopic glomerular haematuria and lower-extremity oedema, followed by 12 hours of headache, nausea, and vomiting, and arrived to the ED in convulsive status after 20 minutes of generalized tonic–clonic seizures. On ED arrival he was afebrile, with non-evaluable BP, depressed consciousness, generalized hypertonia, and bilateral pretibial oedema. He was intubated and loaded with phenobarbital 10 mg/kg. In the ICU, BP was 134/94 mmHg (p95 for age 108/66; p95+12 120/78), consistent with hypertensive emergency. Initial labs: urinalysis with haematuria (>100 RBC/hpf), proteinuria 3+, leucocyturia 10–25/hpf; creatinine 0.3 mg/dL; anaemia Hct 21%, Hb 7 g/dL with normocytic, normochromic indices; leukocytosis 23,900/mm3; thrombocytosis 756,000/mm3; no elevation of acute-phase reactants; hypocomplementemia with C3 25 mg/dL (VN 80–150) and normal C4. Throat rapid antigen for group A Streptococcus was positive and ASO positive. Non-contrast head CT was unremarkable. Renal ultrasound showed bilateral nephromegaly with increased cortical echogenicity and decreased corticomedullary differentiation. The working diagnosis was nephritic syndrome due to complicated GNAPE with hypertensive emergency and status epilepticus. He required mechanical ventilation and phenobarbital; EEG the next day was normal; CSF was normal. Cefotaxime was started for Streptococcus pyogenes eradication and furosemide for diuresis. By day 2 he developed AKI (creatinine 0.99 mg/dL), hypertension, and 24-hour proteinuria 36.6 mg/m2/h without oliguria. Antihypertensive therapy included amlodipine and IV labetalol with initial control. After extubation at 48 hours, he deteriorated neurologically within 24 hours (GCS 8) with BP > p95+12 despite labetalol infusion up to 3 mg/kg/h, amlodipine 10 mg/day, and furosemide, necessitating reintubation and sodium nitroprusside infusion up to 3 mcg/kg/min with a planned gradual BP reduction of 25% per day to mitigate secondary neurologic injury. Given acute neurologic deficits with severe HTN in GN, PRES was suspected and confirmed by brain MRI on day 5 showing increased subcortical T2/FLAIR signal in bilateral symmetric occipital regions without diffusion restriction, consistent with vasogenic edema. Ophthalmologic exam was normal; repeat EEG showed occasional generalized voltage depression. Enalapril was added. Over 10 days, BP normalized with slow pharmacologic weaning; follow-up MRI on day 12 showed radiologic regression, and he was successfully extubated after 5 days. During the ICU course, Hb fell to 5 g/dL with normocytic, normochromic indices and no thrombocytopenia; hemolytic anemia was diagnosed given a positive direct Coombs test and hemoglobinuria. He required two packed RBC transfusions. Methylprednisolone 1 mg/kg/day was given for 72 hours. Stool culture and urinary antigen for Streptococcus pneumoniae were negative. Serologies for EBV and Parvovirus B19, ENA profile, ANCA, anti-dsDNA, anti-β2 glycoprotein I, anticardiolipin, and lupus anticoagulant were all negative; all cultures (blood, urine, endotracheal aspirate, pharyngeal) were negative. ANA was positive at 1:160. Clinical status improved with BP control, rising complement levels, and resolution of proteinuria and haematuria; the direct Coombs remained positive on hospital day 9. He was discharged on day 31 normotensive, non-anaemic, with preserved renal function, no proteinuria or haematuria, normalized C3, and asymptomatic neurologically. Discharge medications: prednisone, amlodipine, enalapril, and folic acid. He remained asymptomatic with no recurrence at 6 months. Overall, the case represents GNAPE with hypocomplementemia (low C3) and elevated ASO complicated by hypertensive emergency causing encephalopathy and secondary PRES, plus autoimmune hemolytic anemia with Hb nadir 5 g/dL, successfully managed with antihypertensives, neuroprotective measures, and corticosteroids, with full clinical and radiologic recovery.


A 23-year-old man came to the emergency room with a sudden, very bad headache. He also felt sick, threw up, and felt heavy pressure in his chest. His blood pressure was high and he was breathing fast. A quick heart test looked like a major heart attack. He was rushed for a procedure to check and open the heart arteries. The heart arteries looked normal. A head CT scan then showed bleeding in the space around his brain. A team of specialists cared for him, but he got worse quickly. He went into cardiac arrest and died.


A 27-year-old man came to the emergency room with a break at the top of his right thigh bone, near the hip. The break happened after a small fall that twisted his hip and pushed straight down on it. As a child, he had a bone problem in that same area and had surgery to help prevent breaks. The doctors scraped out the weak bone, added graft bone, and used metal to hold it for a time. That metal was removed a year later. To fix the new break for good, the doctors removed the damaged top part of the thigh bone and put in a new artificial hip. They also used metal bands to help hold things steady. They sent a piece of the bone to the lab. The test showed he still had the same bone condition from childhood.


A 19-year-old female presented with a 2-day history of headache plus recurrent nausea/vomiting and a 1-day fever. On admission: T 39.1°C, BP 189/120 mmHg, HR 148 bpm. Laboratory testing showed WBC 14.77×10^9/L and neutrophils 13.55×10^9/L. She received empiric antibiotics and was admitted to the ICU. One year prior she had similar symptoms and was diagnosed with myocarditis; hypertension was diagnosed at that time, but she was nonadherent post-discharge. Family history was notable for her father’s sudden unexplained death.

Chest CT incidentally identified a left adrenal soft-tissue mass measuring 43 × 36 mm; head and chest CT had no other pathologies. ECG showed sinus tachycardia with a shortened PR interval and tall, peaked P waves in II, III, and aVF. Transthoracic echocardiography was without significant abnormalities.

On hospital day 2, BNP and troponin I increased. Cardiology provisionally diagnosed myocarditis of uncertain etiology. She was treated with methylprednisolone 0.25 g daily, furosemide 20 mg q12h, spironolactone 20 mg q12h, perindopril amlodipine (10 mg:5 mg daily), metoprolol tartrate 25 mg q12h, and an esmolol infusion at 0.2 g/h; moxifloxacin was added empirically. Despite high-dose glucocorticoids, she did not develop a catecholamine crisis.

Given the adrenal mass and hypertension, endocrine testing was pursued. In the recumbent position, plasma catecholamines were markedly elevated: dopamine 524.5 pmol/L, norepinephrine 83,975 pmol/L, epinephrine 10,579.3 pmol/L. Twenty-four-hour urine showed free adrenaline 4,368.89 nmol/24 h, free norepinephrine >12,697.60 nmol/24 h, normetanephrine 8,312 nmol/24 h, metanephrines 4,078 nmol/24 h, and vanillylmandelic acid 58.1 mg/24 h, supporting pheochromocytoma. On day 5, glucocorticoids were discontinued and perindopril/amlodipine was changed to terazosin for targeted blood pressure control. Contrast-enhanced abdominal CT confirmed a left adrenal mass highly suggestive of pheochromocytoma.

Whole-exome sequencing identified a heterozygous missense RET mutation, c.1900T > C: p.Cys634Arg, prompting MEN2 evaluation. Thyroid Doppler ultrasound showed a 6 × 4 mm hypoechoic nodule in the left lobe with mildly elevated calcitonin; no other significant abnormalities were detected.

As her condition improved, plasma cortisol and ACTH normalized. She was discharged on metoprolol tartrate 100 mg q12h and ivabradine 5 mg q12h. Three months later, she underwent resection of a 50 × 40 × 30 mm left adrenal tumor. Immunohistochemistry was positive for Vim, CD56, Syn, CgA, and NSE; S-100 was positive in Sertoli cells; CKpan, CD10, MART-1/Melan-A, and Melan-A were negative. Ki-67 was 1%. The final diagnosis was adrenal pheochromocytoma. She was discharged without medications and remained asymptomatic on follow-up.

Over 15 months postoperatively, she had persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium progressively increased. 99mTc-MIBI parathyroid scintigraphy was negative for parathyroid adenoma.

Context and implications: Glucocorticoids are recognized precipitants of hypertensive crisis in pheochromocytoma, yet no crisis occurred here despite a significant tumor and high-dose methylprednisolone. The RET c.1900T > C (p.Cys634Arg) variant is classically associated with MEN2A, which confers high penetrance of medullary thyroid carcinoma and pheochromocytoma and variable primary hyperparathyroidism. The rising PTH and serum calcium with a negative MIBI scan are compatible with early or multigland parathyroid disease, which is common in MEN2A and may be scintigraphically occult when glands are small or hyperplastic.


A 56-year-old woman was diagnosed in 2013 with Sjogren’s syndrome, an autoimmune disease that also caused scarring in her lungs (interstitial lung disease). She developed pulmonary arterial hypertension, which means high blood pressure in the blood vessels of her lungs. Over the years she took many medicines for her lung pressure and autoimmune disease, including sildenafil, bosentan, macitentan, iloprost, and steroid drugs, but her condition got worse. In 2020 she had very bad shortness of breath and her heart began to fail, a life-threatening problem called cardiogenic shock. In May 2023 she started taking one hydrogen capsule each day as an extra treatment. After she began the hydrogen capsules, tests showed she had more of a calming immune cell called CD127+ regulatory T cells. The tests also showed lower levels of anti-Ro antibodies, which are harmful antibodies linked to Sjogren’s syndrome. The tests showed fewer B cells, which are the immune system’s antibody-making cells. Her symptoms became stable and she did not have any side effects from the hydrogen capsules.


A 4‑month‑old male from central Mexico with two apparently healthy older male siblings presented with a painful tumor in the left axilla while living with his hypothyroid mother in a crowded prison cell. He was born appropriate for gestational age, was breast‑fed, and had received BCG without scarring. On admission he was below the 3rd percentile for weight (4,190 g) and length (58 cm), with oxygen saturation of 70%, fever, cough, and a tender, erythematous, warm left axillary mass. CBC: hemoglobin 8.8 g/dL (11.0–12.6), leukocytes 29.3 × 10^9/L (6.0–17.5), neutrophils 18.4 × 10^9/L (1.0–8.5), lymphocytes 7.0 × 10^9/L (4.0–13.5), monocytes 3.5 × 10^9/L, platelets 459 × 10^9/L (150–350), CRP 16 mg/L (< 3.0). Chest radiography showed images suggestive of rib fractures, prompting concern for child abuse and admission. Thoracoabdominal CT demonstrated a left axillary abscess, lytic lesions of ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Biopsy of the axillary lesion showed myositis and suppurative panniculitis. BAL bacterial culture was negative, and PCR for Mycobacterium tuberculosis complex was negative. He received ceftriaxone–clindamycin, then cefepime–vancomycin, and was discharged after 41 days.

At 8 months, he was readmitted with fever, irritability, and a suppurating abscess over the left scapula. CBC: hemoglobin 10.8 g/dL (10.5–12), leukocytes 21.2 × 10^9/L (6–17), neutrophils 12.2 × 10^9/L (1.5–8.5), lymphocytes 7.5 × 10^9/L (4–10.5), monocytes 1.2 × 10^9/L (~0.6), platelets 583 × 10^9/L (150–350); HIV serology was negative. Chest imaging showed left apical consolidation, bronchiectasis, lytic lesions in ribs 2–7 and thoracic vertebrae T2–T7, and a multilocular fluid collection; ultrasound identified a fistula linked to the scapular abscess. Initial piperacillin–tazobactam was switched to voriconazole when Aspergillus fumigatus grew from abscess secretion culture, establishing invasive aspergillosis. Given the recurrence and severity, an innate immune defect was suspected. Dihydrorhodamine (DHR) testing demonstrated absent reactive oxygen species production with absent gp91phox expression in neutrophils, confirming X‑linked chronic granulomatous disease. Next‑generation sequencing identified CYBB c.80_83del/Y (p.Val27Glyfs*33); the mother was a heterozygous carrier (c.80_83del/WT). The patient was discharged after 65 days of hospitalization, including 28 days of voriconazole, and was started on prophylaxis with daily trimethoprim–sulfamethoxazole and fluconazole twice weekly.

At 12 months, he was readmitted with multifocal pneumonia requiring mechanical respiratory assistance. Serum galactomannan was positive, and A. fumigatus was recovered from lavage fluid; voriconazole was re‑initiated. Despite therapy, he developed multiple organ failure and died one month after admission.

Context: CGD is caused by NADPH oxidase dysfunction in phagocytes, leading to impaired oxidative burst and susceptibility to catalase‑positive organisms, especially Aspergillus spp. X‑linked CYBB variants frequently present in infancy with invasive aspergillosis and osteolytic lesions; A. fumigatus remains a leading cause of mortality in CGD.


A 28-year-old man presented to dermatology with a 48-hour history of two red patches with central blisters and shallow ulcers on the inner (flexor) side of his right arm and forearm. He described burning and itching at the sites, had no other systemic symptoms, and had not self‑medicated. He reported being on vacation in the coastal region of Ecuador when the lesions appeared. A skin biopsy showed changes consistent with an acute inflammatory reaction, and, together with the clinical picture and recent travel, the diagnosis of Paederus dermatitis (skin injury caused by contact with certain rove beetles) was made. He was treated with oral antihistamines, topical corticosteroids and cold compresses. After 8 days the lesions resolved, leaving post‑inflammatory hyperpigmentation.


This case report describes a 9-year-old girl who was diagnosed with developmental dyslexia alongside high abilities (giftedness). The team compared her phonological processing, reading and writing before and after a program of 20 weekly phonological remediation sessions. Before intervention (age 8y2m) she showed weak phonological processing, reading at an alphabetic level, and writing in transition between syllabic-alphabetic and alphabetic stages. The remediation targeted phonological awareness, working memory, rapid naming and reading practice. After treatment (age 9y6m) phonological skills improved (notably phonemic awareness), phonological working memory reached age-appropriate levels, and rapid naming times improved for letters, objects and colors (digits stayed below expectation). Her reading advanced from an alphabetic to an orthographic level: oral reading rate rose from about 20 words per minute to about 94 words per minute, with better prosody and comprehension. Writing also showed gains and was classified at the alphabetic phase, but remained imprecise with letter reversals, omissions and segmentation errors that reflect persistent dyslexic features. In summary, phonological remediation produced clear gains in phonology and reading fluency, and helped consolidate alphabetic writing, but some difficulties in lexical access and accurate spelling persisted.


A 78-year-old woman using a prefilled blister pack service (SPD) reported several months of tiredness, weakness, dizziness, and confusion that limited her usual walks. The pharmacy team suspected medication-related low blood pressure and reviewed her treatment, focusing on drugs cleared by the kidneys and on her blood pressure medicines. Her kidney function (eGFR) was about 30, so doses that depend on kidney clearance needed reassessment. The pharmacist prepared a report for the primary care physician recommending lowering the doses of losartan and manidipine according to renal dosing guidance. The physician reduced the doses of these antihypertensives. With follow-up, her blood pressure improved and the earlier symptoms resolved.


This is about a 2-day-old newborn boy. He was born at full term by C-section at a private hospital. He came to the children’s hospital because the right side of his scrotum (the sack that holds the testicles) was swollen since birth. In the emergency room, he looked well. His skin was pink and warm. His blood flow looked good. On exam, the right testicle was big and tight. It was not sore when touched. The skin was red and looked rubbed. A light test did not shine through the right side. The light did shine through the left side. There were no signs of a hernia. An urgent ultrasound scan was done. The scan showed the right testicle was larger and looked uneven inside. No blood was flowing to it. The doctors took him quickly to surgery to look inside the scrotum. In surgery, the right testicle was dead because it had twisted, like a kinked hose that stops flow. There was a small amount of fluid. They removed the right testicle. They fixed the left testicle in place to help prevent twisting.


This report describes the first known case of heatstroke occurring together with SARS‑CoV‑2 infection in a 52‑year‑old man. He had a recent cold and a positive self-test for COVID‑19, then returned to work and lost consciousness after five hours outdoors in 35°C heat. On arrival at the hospital his core temperature was 40°C and he was comatose with breathing problems and gastrointestinal bleeding; clinicians diagnosed heatstroke. He was admitted to the ICU, placed on a ventilator, given IV fluids, antibiotics, blood‑pressure support, and continuous renal replacement therapy when his kidneys failed. Laboratory tests showed severe infection, low platelets and a severe clotting disorder (disseminated intravascular coagulation), plus liver, kidney and heart injury. Sputum and airway cultures later grew several pathogens (including Stenotrophomonas, Candida, MRSA, Acinetobacter and Aspergillus), and he was treated with broad antibiotics, antifungals, plasma and blood products, and anticoagulation as needed. After these treatments his fever subsided and he regained consciousness by about day 13 and was briefly taken off the ventilator. Several days later he suddenly worsened with respiratory failure, high fever and a return to coma; brain imaging showed an ischemic stroke and a hemorrhagic infarct. Despite further intensive care, he developed a large cerebral hemorrhage with brain herniation; surgery was not performed and his condition progressed to multiple organ dysfunction syndrome (MODS). The combination of multi‑pathogen pulmonary infection and an intractable coagulopathy ultimately led to MODS and death on day 29.


A 36-year-old woman had a long-term bowel disease (ulcerative colitis). She came in with chest pain that kept getting worse. She also had shortness of breath, sweating, and felt sick to her stomach. For months she had felt very tired and had night sweats. Her heart test (EKG) showed signs of a heart attack in the lower part of the heart. Doctors did a dye X-ray to look at the heart arteries. It showed bad blockages in two heart pipes. They opened the most blocked pipe right away with a balloon and a tiny mesh tube (stent). While looking, the team worried the main body artery (aorta) was swollen. Blood tests showed mild inflammation. A special CT scan showed the aorta wall looked thick and scarred, with tight narrow spots in several arteries. This pointed to a rare illness that causes swollen big arteries, called Takayasu arteritis. She started strong anti-inflammatory and immune medicines (prednisone and methotrexate). Later she had heart bypass surgery to improve blood flow. She did well after treatment.


We report the first case of heatstroke (HS) comorbid with SARS-CoV-2 infection in a 52-year-old male. He self-tested positive for SARS-CoV-2 after a cold, then lost consciousness while working outdoors (ambient 35°C for 5 h). On ED arrival, core temperature was 40°C with persistent coma, dyspnea, and gastrointestinal hemorrhage. HS was diagnosed based on hyperpyrexia, coma, and multiorgan injury. Initial management at the local ICU included mechanical ventilation; fluid resuscitation with Lactated Ringer’s and normal saline at 2.5 mL/kg·h; piperacillin–tazobactam; vasoactive support; and continuous renal replacement therapy (CRRT) for anuria. He received plasma transfusion and tranexamic acid on day 5, but clinical worsening prompted transfer on day 7.

On admission to our medical ICU, nasopharyngeal RT-PCR was positive for SARS-CoV-2, meeting criteria for severe COVID-19 (respiratory failure requiring mechanical ventilation, shock, and multiorgan failure requiring ICU). He had no in-hospital exposures, consistent with community-acquired infection. Examination: GCS 3/15 with bilaterally nonreactive, symmetric pupils; HR 106 bpm; BP 126/77 mmHg on norepinephrine 0.4 µg/kg·min. Laboratory data showed severe infection, anemia, thrombocytopenia, DIC, and acute hepatic and renal injury: WBC 3.55→3.13×10^9/L, lymphocytes 0.25→0.1×10^9/L, N% 85.3%, procalcitonin 2.81 ng/mL, CRP 32.6 mg/L. Microbiology: sputum grew Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture grew Staphylococcus epidermidis; serial blood cultures were negative. CT demonstrated bilateral frontal subdural effusion; lower-lobe consolidation and atelectasis; right upper lobe inflammation; bilateral pleural effusions; and small-volume ascites.

ICU course included SIMV with PEEP 5 mmH2O and FiO2 0.80; continuous norepinephrine and pituitrin for hemodynamic support; hepatic/renal support with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration; antimicrobial escalation to meropenem; Thymalfasin for 20 days; mannitol for 3 days for intracranial pressure; and coagulopathy management with plasma and cryoprecipitate transfusions, continuous IV heparin 6000 U/day, and CRRT with sodium citrate anticoagulation 8 g/day (day 7). Platelet transfusion was given on day 9. Tc fluctuated between 36–38.5°C. CRRT was continued without anticoagulation on day 8. On day 9 he developed GI hemorrhage and fever; EGD showed no active bleeding. He received RBC transfusion, hemostatic therapy, and acid suppression. Teicoplanin was added after MRSA was isolated from sputum. By day 13 he regained consciousness (GCS 14/15) with moderate fever; GI bleeding had ceased; he was extubated. Creatinine rose after CRRT was stopped on day 12.

On day 17 he acutely deteriorated with dyspnea, SpO2 <85%, and fever to 39.3°C, necessitating reintubation. Bronchoscopy showed scant sputum. Coma recurred (GCS 3/15). Labs: WBC 14.94×10^9/L, NEU 13.77×10^9/L; total bilirubin 235.2 µmol/L; creatinine 441 µmol/L. Brain CT: right frontal ischemic stroke and right occipital hemorrhagic infarction. Cooling was provided via CRRT with ice-cold replacement fluid. Meropenem and teicoplanin were continued. Carpofungin was started on day 18 for elevated serum Aspergillus galactomannan, Aspergillus IgG, and Candida mannan. SARS-CoV-2 RT-PCR subsequently turned negative.

By day 20, fever and infection indices improved, but he developed cerebral hemorrhage with herniation (bilateral fixed dilated pupils). Dehydration therapy for intracranial hypertension was given; neurosurgery was declined. On day 22, infection markers and AST/creatinine rose again; BALF cultured carbapenem-resistant Acinetobacter baumannii and Aspergillus fumigatus. Combination therapy with meropenem, teicoplanin, and Carpofungine was continued. Despite comprehensive antimicrobial therapy, organ support, and repeated attempts to correct a refractory coagulopathy, he progressed to multi-pathogen pulmonary infection, intractable coagulopathy, MODS, and died on day 29.


A 15-year-old male with no medical history or prior interventions presented to the pediatric emergency department with 4 days of epigastric abdominal pain and bilious vomiting; he remained afebrile. Examination showed mild dehydration, abdominal distension without peritonism, and decreased hydroaeric sounds. Laboratory tests were unremarkable. An abdominal radiograph was suggestive of intestinal obstruction. Urgent CT demonstrated ascites and marked dilation of small-intestinal loops, with interposition of a small-intestinal loop at the entrance to the transcavity of the epiplons and a caliber change at the level of the hiatus (foramen) of Winslow—compatible with small-bowel obstruction due to an internal hernia.

Urgent exploratory laparoscopy was performed. Intraoperatively, dilated small-bowel loops were seen; the terminal ileum, cecum, and ascending colon were of normal caliber but located in the right hypochondrium, with a very mobile cecum and no adhesions to the right parietocolic space. Following the terminal ileum proximally revealed small-bowel loops of differing caliber arising from the depth of the theoretical location of the hiatus of Winslow. Traction on the cecum and terminal ileum allowed displacement toward the right iliac fossa, but the point of caliber change could not be identified due to the interposition of the inferior hepatic edge and small-bowel distension. Percutaneous puncture of a dilated loop for gas decompression did not improve visualization. To ensure definitive management, conversion to a supraumbilical midline laparotomy was undertaken. On entering the cavity, a caliber change in the ileum was evident ~40 cm from the ileocecal valve, with findings consistent with herniation of an approximately 5-cm ileal segment through the hiatus of Winslow; both ends of the herniated loop bore a congestive imprint from the hiatus. The hiatus of Winslow was of normal caliber; no preventive technique (e.g., narrowing or closure) was performed to reduce recurrence risk. The herniated loop was reduced; it appeared viable, and intestinal resection was not necessary.

Postoperatively, the patient developed a paralytic ileus; the nasogastric tube was removed on postoperative day 5, and oral intake was initiated with good tolerance. A pelvic collection occurred and was managed conservatively with antibiotics, with favorable evolution. He was discharged on postoperative day 10 with preserved transit, afebrile, and in good general condition. He is being followed in the outpatient pediatric surgery clinic.

Context: Internal herniation through the foramen of Winslow is an uncommon cause of small-bowel obstruction; CT identification of a transition at the foramen supports prompt operative reduction, and bowel viability often permits avoidance of resection.


A 46-year-old Haitian male, residing in Chile for one year, presented with a one-and-a-half-year history of a lesion that began as a papule on the anterior aspect of the right leg, with progressive enlargement. Initially asymptomatic, pruritus, pain, superficial ulceration, and yellowish discharge developed three months prior to consultation. On examination (phototype V), there were warty plaques measuring 1 × 1 cm, 2 × 2 cm, and 3 × 2 cm on the anterior right leg. Dermatoscopy revealed a hyperkeratotic mass with an ulcerated center, reddish-black dots, and congested hemorrhagic vessels. General laboratories were normal; VDRL, HIV, and PPD were non-reactive. Punch biopsy including epidermis, dermis, and subcutis was performed; Gram stain, routine bacteriological culture, and anaerobic culture were negative. Bacilloscopy and Koch culture were also negative. Histopathology (hematoxylin and eosin) showed pseudoepitheliomatous epidermal hyperplasia with irregular hyperplasia; the dermis contained abundant mixed inflammatory infiltrate with suppurative foci and foreign body-type giant cells, some containing round, thick-walled brown cells compatible with muriform (sclerotic) cells; these were more evident with PAS stain. Fungal culture on Sabouraud dextrose agar at 25°C demonstrated, after 15 days, growth of black/dematiaceous, elevated, well-defined, velvety colonies. Direct microscopic examination with 20% KOH showed long, branched, sometimes tortuous hyphae and short chains of acropetal conidia, suggestive of Fonsecaea spp. The diagnosis was chromoblastomycosis. Treatment included itraconazole 100 mg every 12 hours for six months, combined with physical measures consisting of cryotherapy (liquid nitrogen) applied to hypertrophic areas every 6–8 weeks. Due to local complications (erosion/ulceration), frequent wound care was provided, with topical mupirocin for signs of bacterial superinfection. The patient had a favorable evolution, with regression of lesions and no evidence of relapse to date, remaining with mild local hypopigmentation expected after cryotherapy. Contextual note: Chromoblastomycosis is a chronic cutaneous and subcutaneous mycosis caused by dematiaceous fungi (classically Fonsecaea, Cladophialophora, and Phialophora), with muriform cells being pathognomonic; combined antifungal therapy and cryotherapy are standard strategies, with itraconazole commonly dosed at 200 mg/day as used here.


A 2.5-year-old girl with a known diagnosis of neurofibromatosis type 1 (NF1) developed four weeks of watery diarrhea that became bloody. She was initially treated for dehydration after a rotavirus infection but continued to have bloody stools and weight loss. Colonoscopy showed red, inflamed mucosa from the anal margin through the colon up to the cecum, with loss of the normal visible blood vessels. Biopsies of the colon showed chronic inflammation with cryptitis and microabscesses, findings consistent with ulcerative colitis (UC). A PCR test on the colon tissue was positive for cytomegalovirus (CMV); blood testing showed past CMV exposure (IgG positive), no IgM, and a low CMV viral load. Blood tests showed mild anemia, a raised white count, and slightly increased CRP; faecal calprotectin was >600 µg/g, supporting active intestinal inflammation. Immunology testing and a broad genetic panel for monogenic immune causes were essentially normal. She was treated with mesalazine and received 15 days of intravenous ganciclovir for CMV, with clinical improvement and undetectable CMV on repeat testing at discharge. Two months later she had a flare with bloody diarrhea; stool testing showed Clostridioides difficile and CMV was undetectable. She was treated with antibiotics and prednisone, improved, and is maintained on mesalazine with only mild ongoing symptoms.


A 23-month-old boy with hypoxic-ischemic encephalopathy at birth but normal psychomotor development had restrictive cardiomyopathy and was listed for cardiac transplantation at 16 months. At 20 months he required implantation of an external Berlin Heart biventricular support device; to prevent embolic events he was maintained on dual antiplatelet therapy plus full-dose heparin anticoagulation. At 23 months he presented with disconnection and right hemiparesis. CT demonstrated a hyperdense left middle cerebral artery (M1) sign and a chronic right parietotemporal infarction. Laboratory studies showed RBC 4.16 × 10^6/µL, hemoglobin 11.4 g/dL, APTT 93 s, and INR 1.08. Intravenous thrombolysis was contraindicated, so intra-arterial mechanical thrombectomy was undertaken. Despite his age, he weighed 10 kg (3rd percentile). Under general anesthesia, the right femoral artery was accessed and an 11 cm 4F sheath (Cordis, Ireland) was placed. A 4F vertebral Radiofocus catheter (Glidecath, Terumo, Belgium) confirmed occlusion of the M1 segment of the left MCA. Recanalization was achieved with a stentriever, using the 4F vertebral catheter as a tutor positioned in the petrous internal carotid artery. A 3 mm × 20 mm Trevo XP Pro Vue device (Stryker, The Netherlands) was delivered via a straight Rapid Transit microcatheter (Codman Neurovascular, UK), reopening the artery in a single pass; the tutor catheter, microcatheter, and stent retriever were removed simultaneously. The control run revealed an iatrogenic dissection of the left internal carotid artery without clinical repercussions, as the left hemisphere was perfused through the anterior communicating artery. One month later, cardiac transplantation was performed successfully. The only long-term neurological sequel was right upper-limb spasticity.


You had a long-lasting cough with mucus. Your right ear hurt and kept leaking pus.
Doctors looked for TB germs. They found these germs in fluid taken from a tube from your stomach and in the pus from your right ear.
You took TB medicine for 6 months, along with other helpful medicines. You got completely better.


A 34-year-old woman had new lower back pain. She saw blood in her urine. She also had a big bruise under the skin on her right buttock. She had never had bleeding problems before. Because these bleeding signs were serious, she was sent to the emergency room. Doctors did blood-clotting tests. One test mixed her blood with normal blood to see how it clotted. Another test looked for a blocker against a clotting protein called factor eight. These tests confirmed the diagnosis.


A 56-year-old Italian female with transfusion-dependent β-thalassemia major (genotype HBB:c.118C > T/HBB:c.93-21G > A), diagnosed at age 7 years with first transfusion at age 2, presented for MRI quantification of myocardial, hepatic, and pancreatic iron. Past history included splenectomy and cholecystectomy. At the time of MRI, HCV-RNA was negative; there were no osteoporosis or other endocrine, cardiac, or hepatic complications; and iron levels were good. Ongoing therapy included deferasirox, vitamin D, and luspatercept started 2 years prior with a good response (approximately 35% increase in transfusion interval). Transfusion regimen was two units of concentrated, filtered RBCs every 25 days with pre-transfusion hemoglobin 10–10.5 g/dL.
On MRI, an incidental solid mass with lobulated, regular contours was identified in the prevascular mediastinum. The lesion was mildly hyperintense on T2-weighted imaging and isointense on T1-weighted imaging. It had been visible on a prior MRI in 2020 (before luspatercept) with marginal enlargement over time. No other mediastinal abnormalities and no pleural or pericardial effusions were present. Neurological examination was unremarkable, and there were no symptoms of mediastinal compression, fever, or weight loss.
Further evaluation with 18F-FDG PET-CT and contrast-enhanced chest CT showed mild FDG uptake of the mediastinal mass (SUVmax 4.3) with no other abnormal uptake in the neck, chest, abdomen, or skeleton. On CT, the mass had regular margins, solid density, mild contrast enhancement, no invasion of adjacent structures, and no lymphadenopathies or extra-thoracic disease. Lung window images revealed multiple, symmetrically distributed, thin-walled cysts with normal intervening parenchyma, without nodules, additional interstitial abnormalities, or pneumothorax. Skeletal findings coherent with thalassemic bone disease included widened ribs and mild platyspondyly. Overall, these findings were consistent with cystic lung disease, most likely lymphangioleiomyomatosis (LAM).
Pulmonary evaluation noted a never-smoker with no respiratory symptoms, no history of chronic cough, recurrent infections, or pneumothorax, and no cutaneous lesions such as facial fibrofolliculomas. Lung fields were clear on exam; SpO2 was 98% and heart rate 75 bpm. Pulmonary function testing showed reduced DLCO at 42% predicted, partially attributable to anemia, with KCO at 73% predicted.
After multidisciplinary tumor board discussion (including a pulmonologist), the patient underwent left thoracoscopic thymectomy with concomitant lingual segment wedge resection. Histopathology demonstrated a type B2 thymoma with focal capsular infiltration, no extracapsular extension, but tumor at the resection margin (R1), corresponding to Masaoka–Koga stage IIa and TNM stage 1a. Lung parenchyma showed cysts of variable size lined by spindle cells with myoid habit and immunohistochemical reactivity for actin, estrogen and progesterone receptors, and focal HMB45 positivity, with modest chronic interstitial inflammation, vascular congestion, and recent blood extravasation, consistent with pulmonary LAM.
Final diagnosis: type B2 thymoma and pulmonary LAM. Management recommendations included adjuvant radiation therapy for the microscopically incomplete thymoma resection (R1) and sirolimus for LAM in the context of concomitant β-thalassemia.
Contextual considerations: B2 thymoma with R1 margins is generally managed with adjuvant radiotherapy to reduce local recurrence risk. LAM is a cystic lung disease characterized by aberrant smooth muscle-like cell proliferation with mTOR pathway activation; sirolimus (an mTOR inhibitor) is standard therapy to stabilize lung function and reduce disease progression. Luspatercept, an erythroid maturation agent, can reduce transfusion burden in transfusion-dependent β-thalassemia, as reflected by the patient’s 35% prolongation of the transfusion interval.


A 35-year-old man developed heart failure due to Carney syndrome, which caused a cardiac myxoma and dilated cardiomyopathy. Three years earlier, he presented with sudden chest tightness and shortness of breath. Echocardiography suggested a myxoma, and the diagnosis of Carney syndrome with cardiac myxoma was confirmed by physical examination and genetic screening. He improved with symptomatic treatment and was discharged; surgery was not performed at that time. His symptoms later worsened, and he returned with severe (New York Heart Association class IV) heart failure. Echocardiography then showed dilated cardiomyopathy accompanied by a cardiac myxoma. He ultimately underwent heart transplantation, which successfully treated his heart failure.


A 42-year-old woman with a history of menstrual migraine, Hashimoto thyroiditis, familial Mediterranean fever, and dyspepsia developed daily, short-lasting headache attacks approximately two weeks after an episode of acute bronchitis treated with antibiotics and bronchodilators. Attacks were provoked by coughing, straining, and lifting; occurred more than ten times per day; lasted about 30 minutes; were bilaterally distributed from the neck to the vertex; and were described as sharp, severe, with a sensation of storm-like fluid movement. She denied prior migraine-associated symptoms (no phonophobia, photophobia, vomiting, or throbbing). Neurological examination and laboratory studies (thyroid hormones, electrolytes, liver/kidney function, serologies) were unremarkable. Brain and cervical spine MRI with and without contrast, MRV, and MRA were normal. She declined lumbar puncture. At initial clinic contact, she was taking indomethacin 25 mg/day; increasing indomethacin to 150 mg/day with lansoprazole 60 mg/day aborted attacks, but gastrointestinal adverse effects led to discontinuation on day 3. She was unable to take topiramate and propranolol due to adverse effects. Fifteen days later she returned with an NRS 9/10 attack and was brought to the local operating room for an ultrasound-guided proximal greater occipital nerve block (PGONB). Using a GE Healthcare Voluson E6 system with a 13–5 MHz linear probe, the patient was positioned prone with neck flexed. The probe was placed transversely at the external occipital protuberance and moved caudally to identify the C2 spinous process (“two horns” appearance). Via lateral probe movement, the obliquus capitis inferior and semispinalis capitis were visualized; the greater occipital nerve was identified superior to the obliquus capitis inferior and beneath the semispinalis capitis. A 22-gauge spinal needle was advanced, and 3 mL of 0.5% bupivacaine was injected for GON blockade. Pain intensity decreased from 9/10 to 2/10 within 20 minutes. The block was repeated weekly for one month. By the second month, attack frequency decreased to two per month with intensity 4/10; no adverse effects were observed. At month six, she reported no further attacks.


A 2-year-old girl had a 1-year history of painless, progressive protrusion of the left eye with the eye displaced inward and upward; vision in that eye was only light perception. MRI showed a well-defined mass in the orbit that was dark on T1-weighted images and bright on T2-weighted images, with no clear contrast enhancement. The mass was removed through the lower eyelid conjunctiva using a transconjunctival approach with canthotomy and cantholysis to widen the surgical field; the tumor was cystic, gray‑white, and tightly adherent to the optic nerve, so about 12.5 mL of fluid was aspirated to reduce its size before complete excision. Histology and immunohistochemistry confirmed an orbital teratoma, showing squamous and glandular epithelium, brain tissue, and cartilage‑like material. One month after the first surgery the child developed enophthalmos (a sunken eye), conjunctival redness, and keratitis because removal of the large mass left reduced orbital volume and the cornea could not fully close. A second operation implanted donor (allogeneic) scleral tissue into the orbit to increase volume, correct the posterior fossa indentation, and allow the cornea to recover. At 1-year follow-up there was no tumor recurrence; vision remained at the preoperative level and the child had only minor residual enophthalmos and an outer canthus abnormality.


This report tells the story of one 9-year-old girl. She is very bright and also has dyslexia. The team tested how she handles speech sounds, how she reads, and how she writes. They tested her before and after sound-based help. Before help, she read by sounding out letters. Her writing was between early sound-by-sound writing and full letter-by-letter writing. She had trouble with tasks that use the sounds in words. After help, her sound skills got better. Her writing became steady at the letter-by-letter stage. Her reading moved up to the next stage, where she could recognize whole words and common spelling patterns.


A 71-year-old man had vitiligo for many years. He lost vision in his right eye about six months before he came to the hospital. He also had hearing loss in both ears, worse on the right. While in the hospital, he had ongoing headaches. He had fevers. He lost a lot of weight without trying. The eye exam showed the right eye could only sense light. The white part of the right eye looked very red. The left eye could see at 20/200, which is very blurry. The back of the right eye had small specks of color. The back of the left eye showed a swollen nerve. The nerve of the right eye looked damaged.


A 70-year-old white man with severe symptomatic aortic regurgitation due to healed endocarditis underwent transapical TAVI because of prohibitive surgical risk (secondary pulmonary hypertension, severely impaired LV function with LVEF 20%, chronic renal failure, logistic EuroSCORE I 24.36%). Home medications included torasemide 20 mg qd, ramipril 5 mg qd, bisoprolol 2.5 mg bid, and an aldosterone antagonist 12.5 mg qd. On admission he had decompensated heart failure with dyspnea (T 36.7 °C, HR 99 bpm, BP 109/48 mmHg). Labs were notable for AST 59 U/L, ALT 67 U/L, creatinine 2.1 mg/dL, and Hb 10.7 g/dL; CRP and leukocyte count were normal; urine was not analyzed; coronary angiography was normal. After multidisciplinary discussion and recompensation, a 27-mm JenaValve self-expandable prosthesis was implanted with a good immediate result and minimal central transvalvular insufficiency. Despite this, he had recurrent cardiac decompensation attributed to severely impaired LVEF; 4 weeks after TAVI, a Thoratec HeartMate II LVAD was implanted, and the postoperative course was uneventful. He remained asymptomatic for 1 year until recurrent significant high-flow alarms occurred on the LVAD. Serial echocardiography over that year demonstrated progressive central transvalvular insufficiency culminating in severe regurgitation without structural leaflet alteration of the JenaValve.

A valve-in-valve TAVI was performed under general anesthesia using a 29-mm CoreValve Evolut R without prior valvuloplasty. During deployment, LVAD flow was reduced to minimum and rapid pacing at 140 bpm was applied. Fluoroscopy and TEE guided positioning targeted placement of the ventricular strut end of the CoreValve Evolut R between the ventricular end and the cusp feelers of the JenaValve, informed by CT showing the JenaValve ventricular edge well positioned in the LVOT. Initial positioning was successful without need for repositioning; after final fluoroscopic confirmation, the device was released, rapid pacing was stopped, and LVAD flow was increased, resulting in stable hemodynamics. The postoperative course was uneventful. Follow-up TEE showed only marginal residual insufficiency. At 12 months, the patient reported no complaints, echocardiography showed no relevant aortic regurgitation, LVEF improved to 33%, and the 6-minute walk distance increased to 381 m from 148 m at admission.