A Clinical Review of Statin-Associated Myopathy

Abstract

Objective: To review the epidemiology, clinical features, proposed mechanisms, risk factors, and management of statin-associated myopathy. Data Sources: Literature searches were conducted in PubMed (1948 to April 2013), TOXLINE, International Pharmaceutical Abstracts (1970 to April 2013, and Google Scholar using the terms statin, hydroxymethylglutaryl-coenzyme A reductase inhibitors, myopathy, myalgia, safety, and rhabdomyolysis. Results were limited to English publications. Study Selection and Data Extraction: All relevant original studies, guidelines, metaanalyses, and reviews of statin-associated myopathy and safety of statins were assessed for inclusion. References from selected articles were reviewed to identify additional citations. Data Synthesis: The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors remain one of the most effective medications for reducing low-density-lipoprotein cholesterol. Statins are well tolerated by most patients; however, it is estimated that 10% to 15% of patients develop statinrelated muscle adverse effects known as statin-associated myopathy. Although clinicians may be aware of statin-associated myopathy, they may not be aware of its clinical presentation. Providers should assess individual patient risk factors before choosing the appropriate statin. A variety of skeletal muscle aches that may not present as a danger to the patient, may affect patient adherence and quality of life. There are several steps that providers can take to properly treat and manage patients with myalgia complaints. Conclusions: Statin-associated myopathy is a clinical problem that contributes to statin therapy discontinuation. Patients who are statin intolerant may be treated with alternative treatment options such as lowdose statins, switching statins, using alternative dosing strategies in statins with longer half-lives, non-statin lipid-lowering agents, and complementary therapies.

Assessment of bee venom therapy in animal model of statin-induced myopathy

“…Regarding CK, the present study reports that simvastatin induces CK elevation for more than 4 folds. These findings are in agreement with several other reports both in humans and animals [25][26][27][28]. Co-administration of the bee venom with simvastatin is found to partially reduce CK elevation to 2 folds only, which was still significantly high.…”

Colchicine triggered severe rhabdomyolysis after long-term low-dose simvastatin therapy: a case report

“…These may range from mild myalgia, may lead to manifest myopathy and myositis-mimicking symptoms, and may culminate in severe rhabdomyolysis. The latter may – when not recognized early enough – induce crush kidney with consecutive renal failure and death [11]. …”

“…Several theories exist ranging from membrane destabilization due to decreased cholesterol content of skeletal muscle plasma membrane, impaired mitochondrial function due to coenzyme Q10 depletion, disturbed calcium metabolism, and vitamin D deficiency [11]. Also, there are various co-medications that increase the risk of SAM, mostly by interference of the metabolizing cytochrome p450 system (CYP3A4, CYP2C).…”

Coenzyme Q10 and statin-related myopathy

“…The mechanism underlying statin-induced muscle damage is unclear 1,5,7,9. Proposed mechanisms include decreased cholesterol in skeletal muscle membrane or depletion of isoprenoids including coenzyme Q10 through inhibition of the mevalonate pathway (see Figure) leading to impaired mitochondrial function, vitamin D deficiency, induction of apoptosis, and disturbed calcium metabolism 5,7…”