Clinical, biochemical, and pathological characteristics of clevudine-associated myopathy

Clinical, biochemical, and pathological characteristics of clevudine-associated myopathy
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DOI:
10.1016/j.jhep.2010.03.006
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发表时间:
2010-08-01
影响因子:
25.7
通讯作者:
Sohn, Yoon Kyung
Sohn, Yoon Kyung
中科院分区:
医学1区
文献类型:
--
作者:
Tak, Won Young;Park, Soo Young;Sohn, Yoon Kyung

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背景和目的:本研究的目的是确定克夫定治疗期间发生的肌病的临床、生化和病理特征。方法:我们前瞻性地连续招募了 36 名接受克夫定治疗慢性乙型肝炎 (CHB) 的肌病患者。我们评估了患者的完整病史、神经肌肉疾病问卷神经系统检查、实验室检查、电生理学研究和肌肉活检。结果:克夫定治疗的中位持续时间为 18.0 个月(9 至 24 个月)。主诉为下肢无力30例(83.3%),乏力5例(13.9%)。一名患者(2.8%)仅血清肌酶持续升高,没有任何症状。下肢无力主要累及下肢近端肌群,表现为爬楼梯困难(83.3%)、运动能力下降(75.0%)和行走困难(55.6%)。所有患者的血清肌酸激酶、乳酸脱氢酶和乳酸水平均升高超过两倍。对 23 名患者进行的肌肉活检显示,21 名患者存在肌病特征,其中线粒体异常,两名患者存在非特异性肌炎。停药后运动无力逐渐改善。结论:与克拉夫定相关的肌病的特点是下肢近端肌肉无力,肌酶升高,可能是由线粒体毒性引起的。仔细的医学和血清学检查对于早期发现和处理接受克夫定治疗的慢性乙型肝炎患者的这种潜在不良反应至关重要。 (C) 2010 年欧洲肝脏研究协会。由 Elsevier B.V. 出版。保留所有权利。
Background & Aims: The aim of this study was to define the clinical, biochemical, and pathological characteristics of myopathy developed during clevudine therapy.Methods: We prospectively enrolled 36 consecutive myopathy patients who were receiving clevudine therapy for the treatment of chronic hepatitis B (CHB). We evaluated patients with a complete medical history, neurologic examination with a questionnaire on neuromuscular diseases, laboratory tests, electrophysiology studies, and muscle biopsies.Results:The median duration of clevudine therapy was 18.0 months (ranging from 9 to 24 months). The chief complaint was weakness of the lower extremities in 30 patients (83.3%) and asthenia in five patients (13.9%). One patient (2.8%) had only persistently elevated serum muscle enzyme without any symptoms. Weakness of the lower extremity mainly involved proximal muscle group of the lower extremity, characterized by difficulty in climbing stairs (83.3%), a decrease in exercise capacity (75.0%) and difficulty in walking (55.6%). All patients showed an elevation of more than two of serum creatine kinase, lactate dehydrogenase, and lactate levels. Muscle biopsies performed in 23 patients revealed myopathic features with abnormal mitochondria in 21 patients, and nonspecific myositis in two patients. Motor weakness gradually improved after discontinuation of clevudine.Conclusions: Myopathy associated with clevudine is characterized by a weakness in proximal muscles of the lower extremities with elevated muscle enzymes and presumably caused by mitochondrial toxicities. Careful medical and serologic examinations are essential for the early detection and management of this potential adverse reaction in CHB patients under clevudine therapy. (C) 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.