Introduction: Therapy-related acute myeloid leukemia (t-AML) is a recognized complication of leukemia-directed cytotoxic therapy. However, the emergence of therapy-related monocytic AML shortly after successful CD19-directed chimeric antigen receptor T-cell (CAR-T) therapy for relapsed Pro-B acute lymphoblastic leukemia (B-ALL) raises important questions regarding clonal evolution, lineage plasticity, and treatment-related leukemogenesis. Case Description: We describe a 73-year-old man diagnosed with Philadelphia chromosome-negative Pro-B ALL with hyperdiploidy/tetraploidy, whose initial presentation posed a diagnostic challenge due to expression of immature and partial myeloid-associated markers, initially suggesting minimally differentiated AML. Repeat immunophenotyping clarified the diagnosis as Pro-B ALL. The patient achieved complete remission with the GMALL Elderly protocol despite severe infectious and treatment-related complications. Following relapse during maintenance therapy, he received salvage treatment with inotuzumab ozogamicin followed by CD19-directed CAR-T therapy, achieving marrow remission. Five months later, he developed secondary monocytic AML with no immunophenotypic evidence of residual B-ALL. Conclusion: This case underscores the importance of precise immunophenotypic characterization in diagnostically ambiguous acute leukemias and illustrates the complex biologic evolution that may follow sequential chemotherapy and modern immunotherapeutic approaches, including the emergence of secondary myeloid neoplasms after CAR-T therapy.
Introduction: Oxymetazoline is a widely used over-the-counter topical nasal decongestant that is generally perceived as safe. Although systemic cardiovascular adverse effects have been reported, clinically significant arrhythmias remain rare. Case description: A 64-year-old man with diabetes and hypertension developed new-onset atrial fibrillation with a rapid ventricular response up to 180 bpm. This arrhythmia was refractory to pharmacological and synchronized electrical cardioversion, necessitating intensive care unit admission for refractory arrhythmia and hypoxic respiratory failure. Further history revealed oxymetazoline nasal spray use for several days prior to presentation. Following discontinuation of oxymetazoline, sustained conversion to sinus rhythm occurred and was maintained at 6-month follow-up. Discussion: This case underscores the potential for serious cardiovascular effects of topical nasal decongestants that may be underrecognized because of their over-the-counter availability. While atrial fibrillation has been reported with other imidazoline-containing nasal decongestants, oxymetazoline-associated atrial fibrillation refractory to standard pharmacologic and electrical cardioversion requiring intensive care unit admission has not been previously reported, to our knowledge. Conclusion: This case highlights a rare but potentially severe arrhythmogenic complication of oxymetazoline nasal spray. Clinicians should consider over-the-counter topical medications as potential contributors in patients presenting with unexplained or refractory atrial fibrillation.
Introduction: Coronary artery disease (CAD) is a multifactorial condition influenced by both genetic predispositions and environmental exposures. Case description: We present a pair of male monozygotic twins diagnosed with identical critical left anterior descending artery stenosis, suggesting a possible hereditary susceptibility involving this coronary segment. One twin presented with acute coronary syndrome while the other was diagnosed with CAD during screening prompted by his sibling’s diagnosis. Conclusion: This report underscores the importance of early screening among genetically related individuals and contributes to the understanding of phenotypic variability in genetically identical patients with CAD.
Introduction: BRASH syndrome – bradycardia, renal failure, AV nodal blockade, shock and hyperkalaemia – is a self-amplifying pathophysiological loop. Its association with severe amiodarone-induced hypothyroidism is rarely described in detail. Case description: A 79-year-old woman with permanent atrial fibrillation on long-term amiodarone and bisoprolol presented after prolonged unwitnessed floor immobilisation with extreme bradycardia (24–30 bpm), haemodynamic instability, KDIGO stage 3 acute kidney injury, hyperkalaemia (5.5 mmol/l), metabolic acidosis, rhabdomyolysis and profound hypothyroidism (TSH 68.5 mUI/l; free T4 4.62 pmol/l) against a normal thyroid baseline 13 months prior. The Popoveniuc myxoedema coma score was 45 (high-risk zone). High-sensitivity troponin T showed flat kinetics consistent with type 2 myocardial injury. Isoproterenol was required for bradycardia refractory to initial metabolic correction, achieving a ventricular rate of 62–68 bpm with QTc shortening from 0.62 s to 0.38 s. The patient was discharged on day 8 with renal recovery and improving thyroid function. Thyroid antibody negativity at 30-day follow-up was consistent with an amiodarone-induced rather than autoimmune aetiology. Conclusion: This case illustrates BRASH syndrome presenting with only mild hyperkalaemia in the context of severe amiodarone-induced hypothyroidism, which may have potentiated the pathophysiological loop. Systematic thyroid monitoring during long-term amiodarone therapy and multi-target metabolic correction, including isoproterenol as a pharmacological bridge, may avert invasive pacing.
Introduction: Hypertrophic pachymeningitis is a rare inflammatory thickening of the dura mater, complicating an estimated 1–3% of ANCA-associated vasculitis (AAV), usually PR3-ANCA disease with systemic involvement. Isolated meningeal disease with normal inflammatory markers is exceptional and easily mistaken for a non-inflammatory or ischaemic optic neuropathy. Case description: An independent 82-year-old woman presented with 48 hours of bilateral visual loss after nine days of severe, non-postural occipital headache. She had no light perception, non-reactive pupils and optic disc pallor, without renal, pulmonary, cutaneous or sinonasal manifestations. Chest computed tomography, erythrocyte sedimentation rate and creatinine were normal. Contrast-enhanced magnetic resonance imaging showed diffuse pachymeningeal thickening with intense dural enhancement. Cerebrospinal fluid was acellular, with elevated protein and negative microbiology, including two Mycobacterium tuberculosis PCR assays. Anti-MPO exceeded 400 RU/ml, with negative anti-PR3, low C3 and C4, and normal IgG4, consistent with microscopic polyangiitis. Intravenous methylprednisolone 500 mg/day, started four days after blindness onset, was followed by recovery to counting fingers at 30 cm in the right eye by day 9. Discussion: MPO specificity, isolated blindness and an absent acute-phase response made this presentation atypical. Visual loss probably reflected dural compression and hypoperfusion of the optic nerves rather than infarction, possibly explaining partial recovery. An ejection fraction of 30% favoured rituximab over cyclophosphamide. Conclusion: MPO-ANCA-associated vasculitis may be confined to the dura, with normal acute-phase reactants. ANCA testing should accompany rather than follow the work-up for dural enhancement, and glucocorticoids should not await the result: functional reserve, not age, determines treatment intensity.
