title: Eosinophilic myocarditis due to Churg-Strauss syndrome with markedly elevated eosinophil cationic protein.
abstract: A 67-year-old woman with asthma visited our hospital with increasing dyspnea and new-onset paresthesia and purpura in her legs. Physical examination showed a wheeze, pretibial edema, and surrounding purpura. Chest X-rays showed cardiac decompensation and an electrocardiogram revealed a new ST-T change. Laboratory data showed leukocytosis, hypereosinophilia (10,450/μL), troponin T(+), elevated  BNP, and markedly elevated eosinophil cationic protein (ECP) (> 150 ng/mL). Echocardiography revealed diffuse left ventricular hypokinesis (ejection fraction 30%) with increased wall thickness. Coronary angiography was normal. Cardiac magnetic resonance imaging implied diffuse myocardial edema and subendocardial late gadolinium enhancement. Skin biopsy of purpura showed superfi cial perivascular dermatitis with remarkable eosinophilic infiltrations. No evidence of drug allergies, parasitic infection, or myeloproliferative disorder was detected. Based on these findings, a diagnosis of eosinophilic myocarditis due to Churg-Strauss syndrome was considered. She was administered prednisolone at a dose of 1 mg/kg, cyclophosphamide, and diuretics. Several markers of eosinophilic myocarditis and heart failure gradually improved, including ECP. She was discharged 30 days later with no cardiac event. Eosinophilic myocarditis is characterized by predominantly eosinophilic infi ltration. Eosinophilic granule proteins, such as ECP and major basic protein, play important roles in the pathogenesis of eosinophilic myocarditis. We experienced a rare case of eosinophilic myocarditis due to Churg-Strauss syndrome. Markedly elevated ECP played an important role in the early diagnosis and subsequent reduction in ECP served as a marker of monitoring. In an asthmatic patient with dyspnea, hypereosinophilia, and vasculitis, Churg-Strauss syndrome with eosinophilic myocarditis should be considered.
authors: Department of Cardiovascular Medicine, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
authors: Tomoya
authors: T
authors: Hara
authors: Koji
authors: K
authors: Yamaguchi
authors: Takashi
authors: T
authors: Iwase
authors: Muneyuki
authors: M
authors: Kadota
authors: Mika
authors: M
authors: Bando
authors: Kozue
authors: K
authors: Ogasawara
authors: Sachiko
authors: S
authors: Bando
authors: Takayuki
authors: T
authors: Ise
authors: Toshiyuki
authors: T
authors: Niki
authors: Yuka
authors: Y
authors: Ueda
authors: Noriko
authors: N
authors: Tomita
authors: Yoshio
authors: Y
authors: Taketani
authors: Hirotsugu
authors: H
authors: Yamada
authors: Takeshi
authors: T
authors: Soeki
authors: Tetsuzo
authors: T
authors: Wakatsuki
authors: Masataka
authors: M
authors: Sata
mesh_terms: D000368:Aged; D001249:Asthma / Q000150:complications; D001706:Biopsy; D015267:Churg-Strauss Syndrome / Q000150:complications*; D003520:Cyclophosphamide / Q000008:administration & dosage*; D004232:Diuretics / Q000008:administration & dosage*; D004452:Echocardiography / Q000379:methods; D004562:Electrocardiography / Q000379:methods; D047091:Eosinophil Granule Proteins / Q000097:blood; D004802:Eosinophilia / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D005260:Female; D006333:Heart Failure / Q000503:physiopathology; D006334:Heart Function Tests / Q000379:methods; D006801:Humans; D007166:Immunosuppressive Agents; D008279:Magnetic Resonance Imaging / Q000379:methods; D009205:Myocarditis / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D011239:Prednisolone / Q000008:administration & dosage*; D011693:Purpura / Q000150:complications / Q000473:pathology
chemical_list: D004232:Diuretics; D047091:Eosinophil Granule Proteins; D007166:Immunosuppressive Agents; D003520:Cyclophosphamide; D011239:Prednisolone