Division of Nephrology and Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Division of Endocrine and Metabolism, Department of Internal Medicine, Taipei Tzu Chi Hospital, The Buddhist Medical Foundation, Taipei, Taiwan.
J Bone Miner Res. 2017 Apr;32(4):743-752. doi: 10.1002/jbmr.3033. Epub 2017 Feb 14.
Primary aldosteronism (PA) is associated with increased urinary calcium excretion and osteoporosis prevalence. We studied the long-term effect of hyperaldosterone on fracture risk and possible risk mitigation via treatments, by comparing PA patients and their essential hypertension (EH) counterparts extracted by propensity score match. We used a longitudinal population database from the Taiwan National Health Insurance, and used a validated algorithm to identify PA patients diagnosed in 1997-2010. Our sample included 2533 PA patients, including 921 patients with aldosterone-producing adenoma (APA). Our methods for assessing excessive fracture risk included multivariable Cox regression and the competing risk regression. The incidence rate of fracture at any site was 14.4 per 1000 person-years for PA, and 11.2 per 1000 person-years for APA. In contrast, the incidence rate of fracture at any site was 8.3 per 1000 person-years in EH controls for PA, and 6.5 per 1000 person-years in EH controls for APA. Mineralocorticoid receptor antagonist (MRA) treatment might be associated with higher risk of osteoporotic fracture in the whole female PA cohort (subdistribution hazard ratio [SHR] = 2.12, p = 0.008) as well as female APA patients (SHR = 1.15, p = 0.049). As to fracture at any site, MRA treatment was also associated with higher risk; the SHR was 1.88 (p < 0.001) in the whole female PA cohort, and 2.17 (p = 0.019) in female APA patients. PA is tightly associated with higher risk of bone fracture, even in the case where the competing risk of death was controlled. Particularly, female PA patients treated with MRA were confronted with significantly higher risk in bone fracture than their EH controls. © 2017 American Society for Bone and Mineral Research.
原发性醛固酮增多症（PA）与尿钙排泄增加和骨质疏松症患病率增加有关。我们通过倾向评分匹配，比较了 PA 患者及其原发性高血压（EH）对照，研究了高醛固酮血症对骨折风险的长期影响以及通过治疗可能降低骨折风险。我们使用来自台湾全民健康保险的纵向人群数据库，并使用经过验证的算法来识别 1997-2010 年诊断出的 PA 患者。我们的样本包括 2533 名 PA 患者，其中包括 921 名醛固酮分泌腺瘤（APA）患者。我们评估过度骨折风险的方法包括多变量 Cox 回归和竞争风险回归。PA 患者任何部位的骨折发生率为 14.4/1000 人年，APA 患者任何部位的骨折发生率为 11.2/1000 人年。相比之下，PA 患者的 EH 对照组任何部位的骨折发生率为 8.3/1000 人年，APA 患者的 EH 对照组任何部位的骨折发生率为 6.5/1000 人年。在整个女性 PA 队列中，醛固酮受体拮抗剂（MRA）治疗可能与骨质疏松性骨折风险增加相关（亚分布危险比[SHR] = 2.12，p = 0.008），也与女性 APA 患者相关（SHR = 1.15，p = 0.049）。对于任何部位的骨折，MRA 治疗也与更高的风险相关；在整个女性 PA 队列中，SHR 为 1.88（p < 0.001），在女性 APA 患者中，SHR 为 2.17（p = 0.019）。PA 与骨折风险增加密切相关，即使在控制死亡竞争风险的情况下也是如此。特别是，接受 MRA 治疗的女性 PA 患者骨折风险明显高于其 EH 对照。 © 2017 美国骨骼与矿物质研究协会。
