We report a rare case of Insulin Autoimmune Syndrome in a 35-year-old woman with prior autoimmune features who developed hypoglycemia after an allergic reaction. Diagnosis was confirmed by insulin autoantibodies. Immunosuppressive therapy yielded significant improvement. This case suggests a broader autoimmune process may underlie seemingly isolated IAS presentations.

Parvovirus B-19 (B19-PV) infection is usually a self-limiting illness that occurs in children, although there have been reported cases affecting older people and presenting with a wide range of symptoms, especially neurological ones. The diagnosis can be tricky and can cost time; therefore, knowledge of this infectious etiology and how it manifests can aid physicians in prompt and timely diagnosis, as time is vital in such cases in order to preserve organ functions and prevent life-threatening complications. Herein, we report Parvovirus B19-associated clinical features and workup in a series of five patients with laboratory-confirmed B19-PV from 2024 to 2025, which, to our knowledge, is the first case series in the West Bank of Palestine. The mean age of our population was 60.5 years, with a sex ratio (male: female) of 3:2, though of note, males were all above 60 and all females were under 50, mainly presenting with neurological manifestations.

Introduction: Low-molecular-weight heparins (LMWHs) are widely used during pregnancy and postpartum to prevent thrombosis and are generally safe. Rarely, they can trigger delayed hypersensitivity reactions causing skin necrosis and infection. Recognizing this complication is important for timely care. Case presentation: A 40-year-old woman developed painful necrotic patches at enoxaparin injection sites on her abdomen and arm one week after cesarean delivery. The lesions were red, tender, and associated with elevated inflammatory markers, while platelet counts were normal, excluding heparin-induced thrombocytopenia. She was diagnosed with LMWH-induced delayed hypersensitivity complicated by cellulitis. Enoxaparin was stopped, and she recovered with apixaban, intravenous antibiotics, wound care, and partial debridement. Discussion: These reactions usually appear 5–14 days after starting LMWH and can mimic infection or thrombosis. They reflect T-cell–mediated vascular injury and require clinical attention. Conclusion: LMWH-induced skin necrosis is rare but serious. Early recognition and switching to alternative anticoagulation are essential for favorable outcomes.

Severe thermal burns involving ≥ 20% of total body surface area (TBSA) initiate a distinct, prolonged physiological cascade extending well beyond the acute phase. This dysregulated response features chronic hypermetabolism, lipid remodeling, and sustained cardiovascular stress. While survival has improved with advances in acute care, the long‐term cardiometabolic effects, particularly the link between lipid abnormalities and cardiovascular risk, remain underexplored. This review highlights the complex pathophysiology of burn‐induced hypermetabolism, including elevated resting energy expenditure, catecholamine‐driven lipolysis, mitochondrial uncoupling, and maladaptive adipose browning. Even in metabolically healthy individuals, these mechanisms promote atherogenic dyslipidemia, characterized by hepatic steatosis, elevated small‐dense LDL, reduced HDL‐C, and persistent hypertriglyceridemia. Emerging lipidomic and clinical data correlate these changes with increased Framingham risk scores, systemic inflammation, and TBSA extent. Simultaneously, cardiovascular vulnerability increases due to myocardial remodeling, autonomic dysfunction, and vascular impairment, particularly in young survivors with prolonged metabolic responses. Imaging and metabolomics reveal endothelial injury, subclinical cardiac dysfunction, and elevated arrhythmogenic risk persisting years after healing. We evaluate current interventions, β ‐blockers, omega‐3 fatty acids, statins, anti‐inflammatory agents, and structured rehabilitation, within a multimodal framework. Additionally, we identify critical gaps, including the need for precision metabolic modulation, omics‐based monitoring, and tailored cardiovascular risk algorithms. Recognizing severe burns as systemic illnesses with delayed but measurable cardiovascular consequences requires a paradigm shift in long‐term care. This review advocates for proactive, multidisciplinary cardiometabolic surveillance as an essential component of postburn recovery. This review follows the TITAN 2025 guideline for transparency in research and reporting. ¹

Background: Tumor necrosis factor-alpha (TNF-α) inhibitors are widely used for immune-mediated inflammatory diseases, including Crohn’s disease. Although generally effective, TNF-α blockade has been linked to uncommon but clinically significant paradoxical immune-mediated neurologic adverse events, including inflammatory demyelinating disorders of the central nervous system (CNS). Case presentation: A 32-year-old woman with Crohn’s disease (perianal fistula) treated with infliximab for one year presented with progressive dizziness, headache, and bilateral lower-limb weakness. Neurologic examination demonstrated ataxic gait, intention tremor, dysarthria, brisk reflexes (right-predominant), and a positive right Babinski sign, with preserved sensation. Initial laboratory testing and head CT were unremarkable. Brain MRI revealed multiple multifocal T2/FLAIR hyperintense lesions involving bilateral periventricular and deep white matter, with plaques affecting the thalami, internal capsule, corpus callosum, cerebellum, and cerebellar peduncles; spinal MRI showed no active lesions. Cerebrospinal fluid studies were normal; infectious testing and autoimmune screening were negative, and oligoclonal bands and serum aquaporin-4 antibodies were negative. Infliximab was discontinued, and high-dose pulse corticosteroids were administered, resulting in mild symptomatic improvement; however, ataxia and dysarthria persisted. At three months, follow-up MRI showed stable lesions without radiologic activity alongside slow clinical improvement with rehabilitation. Conclusion: This case highlights a clinically significant, infliximab-associated CNS demyelinating syndrome with an MS-like radiologic pattern in a patient without prior neurologic history. Prompt recognition, discontinuation of the suspected agent, and early immunotherapy are essential; nonetheless, incomplete recovery may occur, underscoring the need for careful neurologic vigilance in patients receiving anti-TNF therapy.