Statin myopathy: an update.
OBJECTIVE
Statin therapy has become the mainstay of treatment for lipid lowering, demonstrating cardiovascular risk reduction. Associated with statin popularity are misconceptions and fears of untoward side effects on muscle. This review clarifies the terminology relating to statin-related muscle disease; explores potential pathogenic mechanisms; reviews current estimates of statin myopathy prevalence; and examines diagnosis and management.


RESULTS
The fundamental mechanism of statin myopathy remains elusive but is believed to be a class effect. The most common explanation for the cause of toxic muscle injury invokes the deficiency of one of three main synthetic products in the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway. Recent studies have revealed several patients with statin-induced rhabdomyolysis who also have metabolic muscle defects, indicating that statin use may unmask presymptomatic metabolic myopathies. Although statin-related myotoxicity is believed to be a noninflammatory, toxic myopathy, experimental evidence suggests that it may be triggered by an autoimmune reaction or, conversely, initiate an autoimmune process. The precise mechanism is uncertain.


CONCLUSIONS
As a class, statins appear to be usually safe, well tolerated agents with an excellent risk: benefit profile. The etiology and pathogenesis of statin myopathy are poorly understood owing to the relative rarity of its existence.
Christopher-Stine
Lisa
L
Department of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA. LChrist4@jhmi.edu
D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000009:adverse effects*; D009135:Muscular Diseases / Q000175:diagnosis* / Q000209:etiology*; D012219:Rheumatology / Q000639:trends*; D009626:Terminology as Topic
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors