The association of GATM polymorphism with statin-induced myopathy: a systematic review and meta-analysis
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PHARMACOGENETICS
The association of GATM polymorphism with statin-induced myopathy: a systematic review and meta-analysis Mengyuan Liu 1 & Fangfang Fan 1 & Yan Zhang 1 & Jianping Li 1 Received: 16 June 2020 / Accepted: 7 October 2020 # The Author(s) 2020
Abstract Purpose Statin-induced myopathy (SIM) is the commonest reason for discontinuation of statin therapy. The aim of this present meta-analysis is to assess the relationship between glycine amidinotransferase gene (GATM) polymorphism and risk of SIM. Methods MEDLINE, EMBASE, Web of Science, and Cochrane Library databases were searched systematically for case-control studies investigating the relationship between GATM polymorphism and SIM. Retrieved articles were carefully reviewed and assessed according to the inclusion criteria. Associations were assessed in pooled data by calculating odds ratio with 95% confidence intervals. Subgroup analysis was performed according to comedications and severity of SIM. Results Six studies with 707 cases and 2321 controls were included in this meta-analysis. GATM rs9806699 G>A was associated with decreased risk of SIM (OR = 0.80, 95% CI 0.68–0.94, P = 0.006). This association remained significant in the subgroup with fibrates or niacin excluded. However, the association of rs9806699 G>A with severe SIM was not significant. In addition, another two variations at GATM, rs1719247 C>T, and rs1346268 T>C were also associated with declined risk of SIM. Conclusions GATM polymorphism including rs9806699 G>A, rs1719247 C>T, and rs1346268 T>C may be protective factors of SIM. GATM rs9806699 G>A may only exert protective effect on mild SIM cases. Our meta-analysis indicates that GATM polymorphism may represent a pharmacogenomics biomarker for predicting incidence of SIM, which contributes to risk stratification and optimizing statin adherence. Keywords Glycine amidinotransferase gene . Statin-induced myopathy . Single nucleotide polymorphism . Meta-analysis
Introduction Statin-induced myopathy (SIM) is the most frequently reported adverse effect of statins and is the commonest cause for discontinuation of statin therapy [1]. Symptoms of SIM can vary from mild myalgia to rare but life-threatening rhabdomyolysis [2]. The high prevalence of statin use made the absolute number of SIM became more substantial. Unfortunately, the underlying mechanisms of SIM have not been fully understood. Risk factors of SIM have been investigated in the past,
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00228-020-03019-3) contains supplementary material, which is available to authorized users. * Jianping Li [email protected] 1
Department of Cardiology, Peking University First Hospital, No. 8 Xishiku St, Xicheng District, Beijing 100034, China
such as high statin doses, older age, hypothyroidism, hepatic, and renal insufficiency [3–5]. Recently, genetic predisposition was found to play a crucial role in SIM [6]. It is now well established that a single nucleotide polymorphism (SNP) of solute carr
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