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Clinical science
Diagnosis of osteoporosis in statin-treated patients
is dose-dependent
Michael Leutner et al. Department of Internal Medicine. University of Vienna.
Ann Rheum Dis 2019;78:1706–1711.
Key messages
What is already known about this subject?
► There is a relationship between statins and
osteoporosis.
What does this study add?
► Osteoporosis is underrepresented in low-dose
statin treatment.
► There is an overrepresentation of osteoporosis
in high-dose statin treatment.
How might this impact on clinical practice or
future developments?
► In clinical practice, high-risk patients for
osteoporosis under high-dose statin treatment
should be monitored more frequently.
Abstract
Objective: Whether HMG-CoA-reductase inhibition,
the main mechanism of statins, plays a role in the
pathogenesis of osteoporosis, is not entirely known so
far. 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.
Methods Medical 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.
Results: In 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, p<0.01). There was a highly
non-trivial dependence of statin dosage with the ORs
of osteoporosis. Osteoporosis was underrepresented
in low-dose statin treatment (0–10mg per day),
including lovastatin (OR: 0.39, CI 0.18 to 0.84, p<0.05),
pravastatin (OR: 0.68, 95%CI 0.52 to 0.89, p<0.01),
simvastatin (OR: 0.70, 95%CI 0.56 to 0.86, p<0.01) and
rosuvastatin (OR: 0.69, 95%CI 0.55 to 0.87, p<0.01).
However, the exceeding of the 40mg threshold for
simvastatin (OR: 1.64, 95%CI 1.31 to 2.07, p<0.01),
and the exceeding of a 20mg threshold for atorvastatin
(OR: 1.78, 95%CI 1.41 to 2.23, p<0.01) and for
rosuvastatin (OR: 2.04, 95%CI 1.31 to 3.18, p<0.01)
was related to an overrepresentation of osteoporosis.
Conclusion: Our results show that the diagnosis
of osteoporosis in statin-treated patients is dosedependent.
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.
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