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ObjectiveWhether HMG-CoA-reductase inhibition, the main mechanism of statins, plays a role in the pathogenesis of osteoporosis, is not entirely known so far. Consequently, this study was set out to investigate the relationship of different kinds and dosages of statins with osteoporosis, hypothesising that the inhibition of the synthesis of cholesterol could influence sex-hormones and therefore the diagnosis of osteoporosis.MethodsMedical claims data of all Austrians from 2006 to 2007 was used to identify all patients treated with statins to compute their daily defined dose averages of six different types of statins. We applied multiple logistic regression to analyse the dose-dependent risks of being diagnosed with osteoporosis for each statin individually.ResultsIn the general study population, statin treatment was associated with an overrepresentation of diagnosed osteoporosis compared with controls (OR: 3.62, 95% CI 3.55 to 3.69, pConclusionOur results show that the diagnosis of osteoporosis in statin-treated patients is dose-dependent. Thus, osteoporosis is underrepresented in low-dose and overrepresented in high-dose statin treatment, demonstrating the importance of future studies’ taking dose-dependency into account when investigating the relationship between statins and osteoporosis.

We have read with great interest the correspondence of Burden and Weiler1 referring to our previously published manuscripts.2 3 First, they sharply observe that the crude OR between the statin group and the matched cohort shows no effect and therefore inquire as to how exactly we adjust for age. In our original study, we grouped patients according to their medications, computed mean age and sex within these medication groups as covariates, and performed a weighted multivariate regression on the risk of osteoporosis within the different medication groups (one ‘observation’ corresponds to one medication group, weighted proportionally to the patients in that group). This grouping by medication was performed for computational convenience due to our large cohort. We confirmed that our results do not qualitatively change if instead of grouping the patients we evaluate a regression model in which each observation is one patient. In response to the correspondence by Burden and Weiler, we have now additionally performed a multivariate regression as reported in the original paper, except that we used the ‘matched …

We read with interest the correspondence of Lai .1 Whether statin therapy impacts the risk of osteoporosis is still a matter of debate. We have recently shown that there is a dose-dependent relationship between statins and diagnosis of osteoporosis; while low-dose statin treatment was related to an underrepresentation of diagnosed osteoporosis when compared with non-statin-treated patients, we found in patients on higher dosages of statins an overrepresentation of diagnosed osteoporosis in the general Austrian population.2 Although osteoporosis is often underdiagnosed until incident fractures, our data are based on diagnoses derived from in-patient treatment. Even though there are data available suggesting that some statins could have protective effects on osteoporosis,3 in the JUPITER trial, an international, randomised, double-blind and placebo-controlled study in which 17 802 patients were investigated, it has been shown that high-potency statin treatment did not reduce the risk of fractures.4 The fact that statin treatment might not only have positive …