Clinical and Pathological Features of Clevudine Induced Myopathy

J Korean Neurol Assoc > Volume 31(1); 2013 > Article

Journal of the Korean Neurological Association 2013;31(1): 26-31.

클레부딘(clevudine)유발근병증의 임상과 병리특성

석정임, 김대성 a 박민수 b 남태승 c 송현석 d 박영은 a 김선영 e 김영수 f 허소영 a 이동국 조희영 a 이창훈 g

대구가톨릭대학교 의과대학 신경과학교실, 부산대학교 의학전문대학원 신경과학교실 a , 영남대학교 의과대학 신경과학교실 b , 전남대학교 의학전문대학원 신경과학교실 c , 경북대학교 의학전문대학원 신경과학교실 d , 울산대학교 의과대학 신경과학교실 e , 경상대학교 의학전문대학원 신경과학교실 f , 부산대학교 의학전문대학원 병리학교실 g

Clinical and Pathological Features of Clevudine Induced Myopathy

Jung Im Seok

Department of Neurology, Catholic University of Daegu School of Medicine, Daegu, Korea Department of Neurology a , Pusan National University School of Medicine, Busan, Korea Department of Neurology b , Yeungnam University College of Medicine, Daegu, Korea Department of Neurology c , Chonnam National University School of Medicine, Gwangju, Korea Department of Neurology d , Kyungpook National University School of Medicine, Daegu, Korea Department of Neurology e , University of Ulsan College of Medicine, Seoul, Korea Department of Neurology f , Gyeongsang National University School of Medicine, Jinju, Korea Department of Pathology g , Pusan National University School of Medicine, Busan, Korea

Abstract

Background: Clevudine (Revovir ? ) is a recently introduced antiviral drug, and clinical trials have demonstrated its potent, sustained antiviral activity without specific adverse events. However, several studies have found severe myopathy during clevudine therapy. Our study aimed to summarize the clinical and pathological features of clevudine-induced myopathy.
Methods: We analyzed the demographic data, clinical features, and pathologic findings of 18 consecutive hepatitis-B patients who developed skeletal myopathy during clevudine therapy.
Results: The 18 patients comprised 11 women and 7 men aged 48.2±14.0 years (mean±standard deviation; range 28-74 years). Each of the 18 patients was treated with clevudine for at least 5 months (range 5-20 months) before the development of symptoms. In all patients the main symptom was proximal muscular weakness that progressed slowly over several months. Elevated creatine kinase and myopathic patterns on electromyography were found. Muscle biopsies revealed severe myonecrosis associated with numerous ragged red fibers and cytochrome-c-oxidase-negative fibers, mitochondrial proliferation, and predominant type-II fiber atrophy. The muscle weakness gradually improved within 20 weeks after discontinuation of clevudine.
Conclusions: Clevudine therapy can induce myopathy associated with mitochondrial toxicity. Careful clinical and laboratory monitoring of the skeletal muscle dysfunction is required in patients receiving clevudine therapy. Clevudine, Hepatitis, Myopathy