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  1. Ambang T, Tan JS, Ong S, Wong KT, Goh KJ
    PLoS One, 2016;11(9):e0162760.
    PMID: 27611456 DOI: 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 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.
    Matched MeSH terms: Muscular Diseases/chemically induced*
  2. Boonmuang P, Nathisuwan S, Chaiyakunapruk N, Suwankesawong W, Pokhagul P, Teerawattanapong N, et al.
    Drug Saf, 2013 Sep;36(9):779-87.
    PMID: 23615756 DOI: 10.1007/s40264-013-0055-5
    HMG-CoA reductase inhibitors [statins], a widely prescribed cholesterol-lowering therapy, are associated with muscle-related adverse events. While characteristics of such events are well documented in Western countries, little data exists for the Thai population.
    Matched MeSH terms: Muscular Diseases/chemically induced*
  3. Li JJ, Liu HH, Wu NQ, Yeo KK, Tan K, Ako J, et al.
    Expert Opin Drug Metab Toxicol, 2020 Sep;16(9):837-851.
    PMID: 32729743 DOI: 10.1080/17425255.2020.1802426
    INTRODUCTION: Statins have been established as the standard of care for dyslipidemia and preventing cardiovascular diseases while posing few safety concerns. However, misconceptions about statin intolerance lead to their underuse, indicating a need to improve the understanding of the safety of this treatment.

    AREAS COVERED: We searched PubMed and reviewed literatures related to statin intolerance published between February 2015 and February 2020. Important large-scale or landmark studies published before 2015 were also cited as key evidence.

    EXPERT OPINION: Optimal lowering of low-density lipoprotein cholesterol with statins substantially reduces the risk of cardiovascular events. Muscle adverse events (AEs) were the most frequently reported AEs by statin users in clinical practice, but they usually occurred at a similar rate with statins and placebo in randomized controlled trials and had a spurious causal relationship with statin treatment. We proposed a rigorous definition for identifying true statin intolerance and present the criteria for defining different forms of muscle AEs and an algorithm for their management. True statin intolerance is uncommon, and every effort should be made to exclude false statin intolerance and ensure optimal use of statins. For the management of statin intolerance, statin-based approaches should be prioritized over non-statin approaches.

    Matched MeSH terms: Muscular Diseases/chemically induced*
  4. C Thambiah S, Meor Anuar Shuhaili MFR, Chew BH, Samsudin IN, Abdul Rahman H, Stanslas J, et al.
    Biomarkers, 2019 Nov;24(7):659-665.
    PMID: 31342800 DOI: 10.1080/1354750X.2019.1648554
    Introduction: Statin, the first-line treatment for dyslipidaemia, may have suboptimal adherence due to its associated muscle adverse events. These data, however, remain limited. Aim: To determine the association of serum creatine kinase (CK) and SLCO1B1 rs4363657 polymorphism with statin-associated muscle adverse events (SAMAE) among dyslipidaemia participants.
    Methods: This was a prospective cohort study at government health clinics involving newly diagnosed adults with dyslipidaemia. SAMAE were recorded based on the patient's complaint after a month on statin. CK was taken at baseline and follow-up. Genetic profiling was performed for SLCO1B1 rs4363657 polymorphism.
    Results: Among 118 participants, majority were Malay (72%) males (61%) with a mean age of 49 ± 12.2 years old and prescribed lovastatin (61.9). There was a significant association between statin types (lovastatin and simvastatin) and SAMAE (p = 0.0327); no significant association noted between CK and SAMAE (p = 0.5637). The SLCO1B1 rs4363657 polymorphism was significantly associated SAMAE (p 
    Matched MeSH terms: Muscular Diseases/chemically induced
  5. Sharma N, Khurana N, Muthuraman A, Utreja P
    Eur J Pharmacol, 2021 Jul 15;903:174112.
    PMID: 33901458 DOI: 10.1016/j.ejphar.2021.174112
    In the present study, we investigated the anti-Parkinson's effect of vanillic acid (VA) (12 mg/kg, 25 mg/kg, 50 mg/kg p.o.) against rotenone (2 mg/kg s.c.) induced Parkinson's disease (PD) in rats. The continuous administration of rotenone for 35 days resulted in rigidity in muscles, catalepsy, and decrease in locomotor activity, body weight, and rearing behaviour along with the generation of oxidative stress in the brain (rise in the TBARS, and SAG level and reduced CAT, and GSH levels). Co-treatment of VA and levodopa-carbidopa (100 mg/kg + 25 mg/kg p.o.) lead to a significant (P 
    Matched MeSH terms: Muscular Diseases/chemically induced
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