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To the Editor: Dr Meier and colleagues¹ suggest that statins may lower the risk of fracture. Their results are consistent with the finding that statins increase bone morphogenetic protein-2 (BMP-2) in rodent and human cells and increase the rate of bone formation in rodents by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase.² However, pravastatin has recently been shown to be ineffective at increasing BMP-2 or stimulating bone formation.³ This may be due to the different physicochemical properties and relative hepatoselectivity of pravastatin.⁴ Indeed, pravastatin binds less strongly to plasma proteins than do lovastatin, simvastatin, or fluvastatin.⁴ Excluding pravastatin from the analysis may increase the association between statins and decreased risk of fracture. Although Meier et al indicate that each of the statins was individually associated with a decreased fracture risk it would be of interest to know how the reduction in risk by pravastatin compares with the other statins.

Meier et . . . [Full Text of this Article]

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