The genetics of statin-induced myopathy

被引:88
作者
Ghatak, Abhijit [2 ]
Faheem, Osman [1 ]
Thompson, Paul D. [1 ]
机构
[1] Hartford Hosp, Div Cardiol, Henry Low Heart Ctr, Hartford, CT 06102 USA
[2] Univ Connecticut, Dept Internal Med, Farmington, CT 06032 USA
关键词
Genetics; Organic anion transporter; Inherited; COA REDUCTASE INHIBITORS; RIPPLING MUSCLE DISEASE; MALIGNANT-HYPERTHERMIA SUSCEPTIBILITY; MYOADENYLATE DEAMINASE DEFICIENCY; SKELETAL-MUSCLE; SLCO1B1; POLYMORPHISM; MITOCHONDRIAL-DNA; SARCOPLASMIC-RETICULUM; LACTIC-ACIDOSIS; EPISODES MELAS;
D O I
10.1016/j.atherosclerosis.2009.11.033
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Objective: Our goal was to use genetic variants to identify factors contributing to the muscular side effects of statins. Background: Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are usually well tolerated medications, but muscle symptoms, ranging from mild myalgia to clinically important rhabdomyolysis are an important side effect of these drugs and a leading cause of noncompliance. Recent results suggest that genetic factors increase the risk of statin-related muscle complaints. We performed a systematic review of the medical literature to determine genetic factors associated with statin myopathy. Methods: We identified English language articles relating statin myopathy and genetic diseases and gene variants via a PubMed search. Articles pertinent to the topic were reviewed in detail. Results/Conclusions: Our review suggests that some patients are susceptible to statin myopathy because of pre-existing subclinical inherited muscular disorders, or genetic variation in statin uptake proteins encoded by SLCO1B1 or the cytochrome P enzyme system. Variations in genes affecting pain perception and polymorphism in vascular receptors may also contribute to statin myopathy. None of the variants identified in this review suggested novel metabolic mechanisms leading to statin myopathy. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:337 / 343
页数:7
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