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Christopher-Stine L.
Department of Medicine, Division of Rheumatology, Johns Hopkins
University School of Medicine, Baltimore, Maryland, USA.
PURPOSE OF REVIEW: 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.
RECENT FINDINGS: 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.
SUMMARY: 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. |