Pharmacogenomic insights into treatment and management of statin-induced myopathy

Bas Jm Peters,Frank L Visseren,Olaf H Klungel,Anthonius De Boer,Anke-Hilse Maitland-Van Der Zee

doi:10.1186/gm120

Bas Jm Peters, Frank L Visseren + Show 3 more

Open Access

https://doi.org/10.1186/gm120

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Abstract

Although statins are generally well tolerated, the most common adverse drug reaction from statin therapy is myopathy. This article reviews the current pharmacogenomic knowledge of statin-induced myopathy. Furthermore, we will discuss the importance of recent pharmacogenetic advances for the treatment and management of statin-induced myopathy. Variation in the SLCO1B1 gene is associated with increased incidence of statin-induced myopathy, particularly with simvastatin and less so with other statins. If different pharmacokinetic enzymes and transporters are responsible for susceptibility to myopathy, this may explain differences in the occurrence of statin-induced myopathy in individual patients. Genotyping in patients suffering from statin-induced myopathy may help to personalize the choice of statin for the lowest chance of developing myopathy.

Highlights

To reduce the morbidity and mortality associated with heart disease, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) inhibitors are used by millions of patients worldwide
The primary mechanism by which statins reduce the risk of coronary artery disease (CAD) involves lowering low-density lipoprotein cholesterol (LDLc) in plasma
The most common adverse drug reaction (ADR) from statin therapy is myopathy, symptoms of which can range from myalgia (mild fatigue and muscle pain without raised creatine kinase (CK) [1]) to life-threatening rhabdomyolysis

Summary

Introduction

To reduce the morbidity and mortality associated with heart disease, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) inhibitors (statins) are used by millions of patients worldwide. In contrast to the incidence of minor muscle pains in clinical trials, observational studies have reported considerably higher numbers of statin-associated myalgia cases [4,5]. Several studies have been conducted to investigate the contribution of genetic variability to the risk of SIM.

Results

Conclusion