| Mitochondrial myopathies caused by prolonged use of telbivudine |
| Jong-Mok Lee1, Jin-Hong Shin1, Young-Eun Park2, and Dae-Seong Kim1,2 |
1Department of Neurology, Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Yangsan, Korea
2Department of Neurology, Pusan National University School of Medicine, Yangsan, Korea |
| Corresponding Author:
Dae-Seong Kim ,Tel: +82-55-360-2450, Fax: +82-55-360-2521, Email: dskim@pusan.ac.kr |
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Received October 13, 2016 Revised: December 8, 2016 Accepted December 12, 2016 |
| Copyright © 2017 The Korean Society of Clinical Neurophysiology |
| This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium,
provided the original work is properly cited. |
| ABSTRACT |
Background: Telbivudine is a nucleoside analogue used for the treatment of chronic hepatitis B, but it often develops mitochondrial toxicity leading to symptomatic myopathy. In this study, three patients with telbivudine induced myopathy were enrolled in order to investigate the nature and pathogenesis of mitochondrial toxicity caused by long-term use of telbivudine.
Methods: Clinical features, laboratory findings, muscle pathology, and quantitation of mitochondrial DNA were studied in three patients.
Results: Patients presented with progressive muscle weakness with high serum creatine kinase levels. Light microscopic findings of muscle pathology showed ragged red fibers that reacted strongly with succinate dehydrogenase stain, but negative for cytochrome c oxidase activities. Electron microscopy revealed abnormal mitochondrial accumulation with rod shaped inclusions. The quantitative peroxidase chain reaction showed a depletion of mitochondrial DNA in skeletal muscle of the patients.
Conclusions: Nucleoside analogues including telbivudine are potent inhibitors of viral DNA polymerases. However, they are not specific for viral DNA and can disturb mitochondrial replication at the same time. All nucleotide analogues should be used with close clinical observation in order to avoid development of mitochondrial myopathy. |
| Key words:
Telbivudine; DNA polymerase gamma; Creatine kinase |
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