JACC. Case reports · 2026
Fulminant Eosinophilic Myocarditis After Sequential Biologic Therapy in Ulcerative Colitis.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lee Jinyoung, Kim Darae, Hong David, Cha Ji Hyun, Noeul Kang, Kim Jung-Sun, Yang Jeong Hoon, Choi Jin-Oh
Аннотация
BACKGROUND: Eosinophilic myocarditis has heterogeneous presentations and may cause fulminant cardiogenic shock.
CASE SUMMARY: A 35-year-old man with ulcerative colitis and eosinophilia developed cardiogenic shock after sequential biologic therapy (most recently vedolizumab) and corticosteroid withdrawal. He rapidly deteriorated with severe biventricular dysfunction (left ventricular ejection fraction 10%) and hypereosinophilia (eosinophil count 2,154/μL). Coronary angiography showed no obstructive disease, and cardiac magnetic resonance suggested diffuse myocardial involvement. Endomyocardial biopsy confirmed eosinophilic myocarditis. He required veno-arterial extracorporeal membrane oxygenation and high-dose intravenous methylprednisolone. Recurrent eosinophilia during tapering prompted use of mepolizumab, followed by recovery of left ventricular function.
DISCUSSION: Biologic exposure with corticosteroid withdrawal was temporally associated with systemic eosinophilic activation, and histologic confirmation by biopsy enabled escalation to targeted therapy.
TAKE-HOME MESSAGES: In patients with inflammatory bowel disease receiving biologics, hypereosinophilia with acute heart failure should prompt evaluation for eosinophilic myocarditis. Early biopsy may enable timely escalation to targeted immunomodulatory therapy.
CASE SUMMARY: A 35-year-old man with ulcerative colitis and eosinophilia developed cardiogenic shock after sequential biologic therapy (most recently vedolizumab) and corticosteroid withdrawal. He rapidly deteriorated with severe biventricular dysfunction (left ventricular ejection fraction 10%) and hypereosinophilia (eosinophil count 2,154/μL). Coronary angiography showed no obstructive disease, and cardiac magnetic resonance suggested diffuse myocardial involvement. Endomyocardial biopsy confirmed eosinophilic myocarditis. He required veno-arterial extracorporeal membrane oxygenation and high-dose intravenous methylprednisolone. Recurrent eosinophilia during tapering prompted use of mepolizumab, followed by recovery of left ventricular function.
DISCUSSION: Biologic exposure with corticosteroid withdrawal was temporally associated with systemic eosinophilic activation, and histologic confirmation by biopsy enabled escalation to targeted therapy.
TAKE-HOME MESSAGES: In patients with inflammatory bowel disease receiving biologics, hypereosinophilia with acute heart failure should prompt evaluation for eosinophilic myocarditis. Early biopsy may enable timely escalation to targeted immunomodulatory therapy.