ClinicopathologicalFeatures of telbivudine-associated myopathy

• Main Authors: Ambang, T., Tan, J.S., Ong, S., Wong, Kum Thong, Goh, Khean Jin
• Format: Article
• Published: Public Library of Science 2016
• Subjects: R Medicine
• Online Access: http://eprints.um.edu.my/18271/; https://doi.org/10.1371/journal.pone.0162760

Telbivudine, a thymidine nucleoside analog, is a common therapeutic option for chronic hepatitis B infection. While raised serum creatine kinase is common,myopathy associated with telbivudine is rare. Reports on its myopathological features are few and immunohistochemical analyses of inflammatory cell infiltrates have not been previously described.We describe the clinical,myopathological and immunohistochemical features of four patients who developed myopathy after telbivudine therapy for chronic hepatitis B infection. All four patients presented with progressive proximal muscle weakness, elevation of serumcreatine kinase and myopathic changes on electromyography. Muscle biopsies showed myofiber degeneration/necrosis, regeneration, and fibers with cytoplasmic bodies and cytochrome c oxidase deficiency. There was minimal inflammation associated with strong sarcolemmal overexpression of class I major histocompatibility complex (MHC class I). Upon withdrawal of telbivudine,muscle weakness improved in all patients and eventually completely resolved in three. In our series, telbivudine-associatedmyopathy is characterized by necrotizingmyopathy which improved on drug withdrawal. Although the occasional loss of cytochrome c oxidase is consistent with mitochondrial toxicity, the overexpression of MHC class I in all patients could suggest an underlying immune-mediated mechanism which may warrant further investigation.