Use of Statins and Risk of Fractures

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Abstract
Synthesis of cholesterol is reduced by inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase in the liver, which catalyzes conversion of HMG-CoA to mevalonic acid. Statins have been shown to be reversible, competitive inhibitors of this enzyme and, thus, are currently used for clinical treatment of hypercholesterolemia.1,2 Mevalonic acid has been found to be a precursor not only of cholesterol but also of proteins such as geranylgeranyl pyrophosphate, which is important in the control of osteoclast-mediated bone resorption. Nitrogen-containing bisphosphonates, such as alendronate and risedronate, may exert their antiresorptive action by suppressing the generation of geranylgeranyl pyrophosphate in the mevalonate pathway.3 Furthermore, recent animal and in vitro research has led to a hypothesis that statins may reduce risk of fractures.4 Some epidemiological studies have reported reductions in fracture risk,5-8 but the preliminary results of a large follow-up study have not confirmed these observations.9 Given the widespread use of statins, the possible effects on fracture is an important clinical issue. We performed a population-based case-control study in which a history of statin use in fracture cases was compared with that among age- and sex-matched control patients.