Clevudine Induced Mitochondrial Myopathy.
10.3346/jkms.2017.32.11.1857
- Author:
Soo Hyun PARK
1
;
Kyung Seok PARK
;
Nam Hee KIM
;
Joong Yang CHO
;
Moon Soo KOH
;
Jin Ho LEE
Author Information
1. Department of Neurology, Dongguk University Ilsan Hospital, Goyang, Korea. nheekim8@hanmail.net
- Publication Type:Clinical Trial ; Original Article
- Keywords:
Clevudine;
Antiviral Agent;
Hepatitis B;
Mitochondrial Myopathy;
Myopathy
- MeSH:
Biopsy;
Creatine Kinase;
Electromyography;
Extremities;
Female;
Hepatitis B;
Hepatitis B virus;
Humans;
Lower Extremity;
Male;
Mitochondrial Myopathies*;
Muscular Diseases;
Neck;
Virus Replication
- From:Journal of Korean Medical Science
2017;32(11):1857-1860
- CountryRepublic of Korea
- Language:English
-
Abstract:
Clevudine was approved as an antiviral agent for hepatitis B virus, which showed marked, rapid inhibition of virus replication without significant toxicity. However, several studies have reported myopathy associated with clevudine therapy. Also, we experienced seven patients who suffered from myopathy during clevudine therapy. To characterize clevudine-induced myopathy, we collected previously reported cases of clevudine myopathy and analyzed all the cases including our cases. We searched electronic databases that were published in English or Korean using PubMed and KoreaMed. Ninety-five cases with clevudine myopathy, including our seven cases, were selected and analyzed for the demographic data, clinical features, and pathologic findings. The 95 patients with clevudine-induced myopathy comprised 52 women and 43 men aged 48.9 years (27–76 years). The patients received clevudine therapy for about 14.2 months (5–24 months) before the development of symptoms. Weakness mainly involved proximal extremities, especially in the lower extremities, and bulbar and neck weakness were observed in some cases (13.7%). Creatine kinase was elevated in the majority of patients (97.9%). Myopathic patterns on electromyography were observed in most patients examined (98.1%). Muscle biopsy presented patterns compatible with mitochondrial myopathy in the majority (90.2%). The weakness usually improved within about 3 months after the discontinuation of clevudine. Though clevudine has been known to be safe in a 6-month clinical trial, longer clevudine therapy for about 14 months may cause reversible mitochondrial myopathy. Careful clinical attention should be paid to patients with long-term clevudine therapy.
