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Diagnosis of osteoporosis in statin-treated patients is dose-dependent

机译:诊断他汀类药物治疗患者的骨质疏松症是剂量依赖性的

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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. 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. 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 (0–10?mg 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 40?mg threshold for simvastatin (OR: 1.64, 95%?CI 1.31 to 2.07, p<0.01), and the exceeding of a 20?mg 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 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.
机译:目的是HMG-COA还原酶抑制,他汀类药物的主要机制起在骨质疏松症的发病机制中起作用,到目前为止并不完全已知。因此,本研究旨在调查不同种类和剂量与骨质疏松症的关系的关系,假设抑制胆固醇的合成可以影响性激素,从而抑制骨质疏松症的诊断。方法医疗权利要求2006年至2007年的所有奥地利人的数据用于鉴定用他汀类药物治疗的所有患者,以计算六种不同类型的他汀类药物的日常定义的剂量平均值。我们应用了多元逻辑回归,分析了单独为每种他汀类药物被诊断患有骨质疏松症的剂量依赖性风险。结果在一般性研究人群中,他汀类药物治疗与诊断骨质疏松症的夸张相关(或3.62,95%?CI 3.55至3.69,P <0.01)有关。他汀类药物剂量与骨质疏松症或骨质疏松症的高度不普遍依赖。骨质疏松症在低剂量毒素治疗(每天0-10毫克)(包括洛伐他汀(或:0.39,CI 0.18至0.84,P <0.05),普伐他汀(或:0.68,95%?CI 0.52至0.89, P <0.01),辛伐他汀(或:0.70,95%?CI 0.56至0.86,P <0.01)和罗萨伐他汀(或:0.69,95%?CI 0.55至0.87,P <0.01)。然而,超过40?Mg的辛伐他汀阈值(或:1.64,95%?CI 1.31至2.07,P <0.01),以及阿托伐他汀的超过20?Mg阈值(或:1.78,95%?CI 1.41至2.23,P <0.01)和罗苏瓦司汀(或:2.04,95%?CI 1.31至3.18,P <0.01)与骨质疏松症的过度陈述有关。结论我们的研究结果表明,患者治疗患者骨质疏松症的诊断是依赖剂量的。因此,骨质疏松症在低剂量和高剂量调毒毒素治疗中经历了超过,证明了在调查他汀类药物和骨质疏松症之间的关系时,将来的研究进入剂量依赖的重要性。

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