ArticlePloS one2016
Clinicopathological Features of Telbivudine-Associated Myopathy.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Clinical and pathological aspects of toxic myopathies.Journal of neurology · 2024Review
- Creatine kinase elevation in chronic hepatitis B patients with telbivudine therapy: influence of telbivudine plasma concentration and single nucleotide polymorphisms of TK2, RRM2B, and NME4.European journal of clinical pharmacology · 2024Observational
- Mitochondrial mechanisms in the pathogenesis of chronic inflammatory musculoskeletal disorders.Cell & bioscience · 2024Review
- Telbivudine-Induced Myopathy: Clinical Features, Histopathological Characteristics, and Risk Factors.Journal of clinical neurology (Seoul, Korea) · 2023Article
- Respiratory failure as the prominent manifestation of entecavir-associated mitochondrial myopathy: a case report.BMC infectious diseases · 2022Article
- Immunopathological Characterization of Muscle Biopsy Samples from Immune-Mediated Necrotizing Myopathy Patients.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Case report: lactic acidosis and rhabdomyolysis during telbivudine and tenofovir treatment for chronic hepatitis B.BMC gastroenterology · 2018Article
- Clevudine Induced Mitochondrial Myopathy.Journal of Korean medical science · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 serum creatine 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-associated myopathy is characterized by necrotizing myopathy 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.
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