Recent evidence suggests that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) re-ductase inhibitors (statins) may stimulate osteoblast activity. However, it is unclear whether a possible increase in bone mineral density is clinically meaningful or associated with fewer fractures. Wang and colleagues conducted a case-control study to determine whether the risk of hip fracture is decreased in elderly patients taking statins.
Data on patients were drawn from the New Jersey Medicaid Program, the New Jersey Pharmacy Assistance for the Aged and Disabled Program and New Jersey Medicare. Patients younger than 65 years and those who had recently been hospitalized were excluded. All patients with a diagnosis of hip fracture were included and were matched (by age and sex) with four randomly selected control patients who had not had a hip fracture (1,222 cases and 4,888 controls). Patients who had filled any statin prescription in the previous six months were classified as having been exposed to a statin, and non-statin lipid-lowering prescriptions were also recorded. The number of days that a patient had been exposed to lipid-lowering therapy was calculated.
Unadjusted analysis of statin use in the previous 180 days showed a 50 percent reduction in hip fracture risk; an adjusted analysis showed the same percentage of reduction. No decrease in the risk of hip fracture was evident in patients receiving non-statin lipid-lowering agents. Any statin use in the previous three years was associated with a 43 percent decrease in the risk of hip fracture. The improved risk was still observed when the patients analyzed were those who had not been in a nursing home and did not die in the year following the fracture (e.g., were presumably healthier).
The authors conclude that the use of a statin lipid-lowering agent is associated with a 50 percent reduction in hip fracture risk in elderly patients. Randomized, controlled trials are needed.
editor's note: In a related editorial, Cummings and Bauer caution that study results showing a reduction in the risk of fracture are observational studies, not randomized, placebo-controlled trials and, as such, should not be used to support statin use as a means of preventing or treating osteoporosis. The studies published so far (including Meier CR, Schlienger RG, Kraenzlin ME, Schlegel B, Jick H. HMG-CoA reductase inhibitors and the risk of fractures. JAMA 2000;282:3205–10) have not included the measurement of bone mineral density. They remind the reader of previous observational studies of sodium fluoride, in which results seemingly indicated a large decrease in the risk of vertebral fracture. However, randomized trials showed an increase in bone mineral density, but an actual increase in the risk of peripheral fractures and no effect on vertebral fractures. Statins, of course, should still be used to treat patients with hyperlipidemia, and randomized controlled trials may ultimately support their use in prevention of fractures.—g.b.h.