{"title":"Recurrent multiterritorial ischemic stroke with persistent moderate hypereosinophilia: A case report with focused literature review.","authors":"Yu Wang, Na Liu, Ju Zhu","doi":"10.1177/03000605261491519","DOIUrl":null,"url":null,"abstract":"<p><p>Persistent hypereosinophilia may be overlooked during stroke evaluation when conventional vascular risks coexist. We report the case of a man in his late 50s who had hypertension, type 2 diabetes, continued active smoking, and eight clinically apparent magnetic resonance imaging-confirmed strokes in multiple bilateral territories over 29 months. Before systemic glucocorticoid exposure, absolute eosinophil counts ranged from 1.87 to 3.23 × 10<sup>9</sup>/L on repeated measurements. Bone marrow morphology and flow cytometry revealed eosinophil expansion without aberrancy, and common tested clonal drivers were negative. Transthoracic echocardiography, two 24-h Holter recordings, and a bubble study identified no intracardiac source. Aortic computed tomography angiography in April 2026 demonstrated thoracic aortic atherosclerosis with calcified plaques and focal ulceration; transesophageal echocardiography and prolonged rhythm monitoring were not performed. A new left pontine infarct occurred in April 2026 while he was on oral prednisone (20 mg/day). In August 2026, after systemic glucocorticoid withdrawal despite continued inhaled budesonide/formoterol, a new right temporal infarct occurred, with an absolute eosinophil count of 2.66 × 10<sup>9</sup>/L. Worsening wheeze suggested possible eosinophilic airway inflammation; however, emphysema alone did not explain systemic eosinophilia, and eosinophilic granulomatosis with polyangiitis remained unproven. The available evidence favored a multifactorial interpretation; eosinophilia provides biological plausibility, whereas conventional vascular risks and an incompletely characterized thoracic aortic abnormality remain competing explanations. Persistent eosinophilia should prompt repeated etiological reassessment without inferring causality based on blood count or imaging pattern alone.</p>","PeriodicalId":16129,"journal":{"name":"Journal of International Medical Research","volume":"54 9","pages":"3000605261491519"},"PeriodicalIF":1.8000,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of International Medical Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/03000605261491519","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/9/28 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
Abstract
Persistent hypereosinophilia may be overlooked during stroke evaluation when conventional vascular risks coexist. We report the case of a man in his late 50s who had hypertension, type 2 diabetes, continued active smoking, and eight clinically apparent magnetic resonance imaging-confirmed strokes in multiple bilateral territories over 29 months. Before systemic glucocorticoid exposure, absolute eosinophil counts ranged from 1.87 to 3.23 × 109/L on repeated measurements. Bone marrow morphology and flow cytometry revealed eosinophil expansion without aberrancy, and common tested clonal drivers were negative. Transthoracic echocardiography, two 24-h Holter recordings, and a bubble study identified no intracardiac source. Aortic computed tomography angiography in April 2026 demonstrated thoracic aortic atherosclerosis with calcified plaques and focal ulceration; transesophageal echocardiography and prolonged rhythm monitoring were not performed. A new left pontine infarct occurred in April 2026 while he was on oral prednisone (20 mg/day). In August 2026, after systemic glucocorticoid withdrawal despite continued inhaled budesonide/formoterol, a new right temporal infarct occurred, with an absolute eosinophil count of 2.66 × 109/L. Worsening wheeze suggested possible eosinophilic airway inflammation; however, emphysema alone did not explain systemic eosinophilia, and eosinophilic granulomatosis with polyangiitis remained unproven. The available evidence favored a multifactorial interpretation; eosinophilia provides biological plausibility, whereas conventional vascular risks and an incompletely characterized thoracic aortic abnormality remain competing explanations. Persistent eosinophilia should prompt repeated etiological reassessment without inferring causality based on blood count or imaging pattern alone.
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