We were fascinated by the reduction in fracture risk with statin therapy reported by the Geelong Osteoporosis Study (odds ratio, 0.40; adjusted odds ratio, 0.45).1 These striking results are in concordance with 3 other published observational studies that found fracture risk reductions of similar magnitudes associated with statin exposure.2- 4 However, they are in conflict with the results of a randomized clinical trial that found no association between pravastatin use and fracture risk.5 The explanation offered for the difference between these results is heterogeneity of effect on bone morphogenic protein-2 production between statins, and this contention is supported by in vitro data showing that pravastatin does not have the same effect as other statins on this biological marker.6 This intriguing hypothesis and its role in the divergence between the observational results and the pravastatin clinical trial results could be supported by presenting a subgroup analysis of effect according to specific statin, and we encourage the authors of the Geelong Osteoporosis Study to present such a subgroup analysis if data on specific statins are available. Since the other observational studies showing substantially reduced fracture risk with statin therapy included some pravastatin exposure, demonstrating that pravastatin is ineffective at preventing fracture would imply that the other statins are even more effective than the combined results would suggest.
Seeger JD, Choi HK. Statin Use and Fracture Risk. Arch Intern Med. 2002;162(20):2381. doi: