Usala Rachel L, Fernandez Stephen J, Mete Mihriye, Shara Nawar M, Verbalis Joseph G
Graduate Medical Education, Department of Medicine, MedStar Georgetown University Hospital, Washington, District of Columbia.
Department of Biostatistics and Bioinformatics, MedStar Health Research Institute, Washington, District of Columbia.
J Endocr Soc. 2019 Jan 4;3(2):411-426. doi: 10.1210/js.2018-00320. eCollection 2019 Feb 1.
Patients with diabetes mellitus are at increased risk for bone fragility fracture secondary to multiple mechanisms. Hyperglycemia can induce true dilutional hyponatremia. Hyponatremia is associated with gait instability, osteoporosis, and increased falls and bone fractures, and studies suggest that compromised bone quality with hyponatremia may be independent of plasma osmolality. We performed a case-control study of patients with diabetes mellitus matched by median glycated hemoglobin (HbA1c) to assess whether hyponatremia was associated with increased risk of osteoporosis and/or fragility fracture.
Osteoporosis (n = 823) and fragility fracture (n = 840) cases from the MedStar Health database were matched on age of first HbA1c ≥6.5%, sex, race, median HbA1c over an interval from first HbA1c ≥6.5% to the end of the encounter window, diabetic encounter window length, and type 1 vs type 2 diabetes mellitus with controls without osteoporosis (n = 823) and without fragility fractures (n = 840), respectively. Clinical variables, including coefficient of glucose variation and hyponatremia (defined as serum [Na] <135 mmol/dL within 30 days of the end of the diabetic window), were included in a multivariate analysis.
Multivariate conditional logistic regression models demonstrated that hyponatremia within 30 days of the outcome measure was independently associated with osteoporosis and fragility fractures (osteoporosis OR 3.09; 95% CI, 1.37 to 6.98; fracture OR, 6.41; 95% CI, 2.44 to 16.82).
Our analyses support the hypothesis that hyponatremia is an additional risk factor for osteoporosis and fragility fracture among patients with diabetes mellitus.
糖尿病患者因多种机制导致骨脆性骨折风险增加。高血糖可诱发真性稀释性低钠血症。低钠血症与步态不稳、骨质疏松以及跌倒和骨折风险增加有关,研究表明低钠血症导致的骨质受损可能与血浆渗透压无关。我们进行了一项病例对照研究,对糖化血红蛋白(HbA1c)中位数相匹配的糖尿病患者进行评估,以确定低钠血症是否与骨质疏松和/或脆性骨折风险增加有关。
来自MedStar Health数据库的骨质疏松症患者(n = 823)和脆性骨折患者(n = 840),根据首次HbA1c≥6.5%的年龄、性别、种族、从首次HbA1c≥6.5%到诊疗窗口结束的时间段内的HbA1c中位数以及糖尿病诊疗窗口时长,以及1型与2型糖尿病,分别与无骨质疏松症(n = 823)和无脆性骨折(n = 840)的对照进行匹配。临床变量,包括血糖变异系数和低钠血症(定义为糖尿病窗口结束后30天内血清[Na]<135 mmol/dL),纳入多变量分析。
多变量条件逻辑回归模型显示,在结局测量指标的30天内出现的低钠血症与骨质疏松症和脆性骨折独立相关(骨质疏松症的比值比为3.09;95%置信区间为1.37至6.98;骨折的比值比为6.41;95%置信区间为2.44至16.82)。
我们的分析支持以下假设,即低钠血症是糖尿病患者骨质疏松症和脆性骨折的一个额外风险因素。