Jamal Sophie A, Arampatzis Spyridon, Harrison Stephanie Litwack, Bucur Roxana C, Ensrud Kristine, Orwoll Eric S, Bauer Douglas C
Women's College Research Institute, University of Toronto, Toronto, ON, Canada.
Department of Nephrology, Hypertension, and Clinical Pharmacology, University Hospital Bern (Inselspital), University of Bern, Bern, Switzerland.
J Bone Miner Res. 2015 Jun;30(6):970-5. doi: 10.1002/jbmr.2383.
Hyponatremia may be a risk factor for fracture. To determine the relationship between hyponatremia and fracture we conducted cross-sectional and longitudinal analyses using data from the Osteoporotic Fractures in Men (MrOS) study. The MrOS study enrolled 5122 community dwelling men aged ≥65 years from six centers across the United States. We excluded men taking bisphosphonates, those with unknown medication history, those without serum sodium measures, or those with out of range assays for serum sodium. Serum sodium was measured at study entry. Subjects were followed for fractures (nonspine [including hip], hip, incident morphometric, and prevalent morphometric) for up to 9 years. We used Cox proportional hazards models to analyze the association between serum sodium levels (<135 mmol/L versus ≥135 mmol/L) and risk of nonspine and hip fractures, with results presented as hazard ratios (HRs) and 95% confidence intervals (CIs). We examined the association between morphometric vertebral fractures and serum sodium using logistic regression models, presented as odds ratios (ORs) and 95% CI. Hyponatremia was observed in 64 men (1.2% of the cohort). After adjusting for age, BMI, study center, and other covariates, we found that, compared to men with serum sodium ≥135 mmol/L, those with serum sodium <135 mmol/L, had an increased risk of hip fracture (HR = 3.04; 95% CI, 1.37 to 6.75), prevalent morphometric spine fracture (OR = 2.46; 95% CI, 1.22 to 4.95), and incident morphometric spine fracture (OR = 3.53; 95% CI, 1.35 to 9.19), but not nonspine fracture (OR = 1.44; 95% CI, 0.85 to 2.44). Adjusting for bone mineral density (BMD) did not change our findings. Our data show that hyponatremia is associated with up to a doubling in the risk of hip and morphometric spine fractures, independent of BMD. Further studies, to determine how hyponatremia causes fractures and if correction of hyponatremia decreases fractures, are needed.
低钠血症可能是骨折的一个风险因素。为了确定低钠血症与骨折之间的关系,我们使用来自男性骨质疏松性骨折(MrOS)研究的数据进行了横断面和纵向分析。MrOS研究纳入了来自美国六个中心的5122名年龄≥65岁的社区男性。我们排除了正在服用双膦酸盐的男性、用药史不明的男性、未测量血清钠的男性或血清钠检测结果超出范围的男性。在研究开始时测量血清钠。对受试者进行长达9年的骨折(非脊柱骨折[包括髋部骨折]、髋部骨折、新发形态计量学椎体骨折和现患形态计量学椎体骨折)随访。我们使用Cox比例风险模型分析血清钠水平(<135 mmol/L与≥135 mmol/L)与非脊柱骨折和髋部骨折风险之间的关联,结果以风险比(HRs)和95%置信区间(CIs)表示。我们使用逻辑回归模型研究形态计量学椎体骨折与血清钠之间的关联,结果以比值比(ORs)和95%CI表示。64名男性(占队列的1.2%)出现低钠血症。在调整年龄、体重指数、研究中心和其他协变量后,我们发现,与血清钠≥135 mmol/L的男性相比,血清钠<135 mmol/L的男性髋部骨折风险增加(HR = 3.04;95%CI,1.37至6.75),现患形态计量学椎体骨折风险增加(OR = 2.46;95%CI,1.22至4.95),新发形态计量学椎体骨折风险增加(OR = 3.53;95%CI,1.35至9.19),但非脊柱骨折风险未增加(OR = 1.44;95%CI,0.85至2.44)。调整骨密度(BMD)并没有改变我们的研究结果。我们的数据表明,低钠血症与髋部骨折和形态计量学椎体骨折风险增加高达两倍相关,且独立于骨密度。需要进一步的研究来确定低钠血症如何导致骨折以及纠正低钠血症是否能降低骨折发生率。