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-  2016 

血浆 25-羟维生素D在2型糖尿病动脉硬化损害中的作用

DOI: 10.16118/j.1008-0392.2016.05.014

Keywords: 2型糖尿病 动脉硬化 25-羟维生素D 肾素-血管紧张素-醛固酮
type 2 diabetes mellitus atherosclerosis 25-hydroxyvitamin D renin-angiotensin-aldosterone system

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Abstract:

目的 探讨血浆25-羟维生素D[25(OH)D]在2型糖尿病(T2DM)患者动脉硬化损害中的作用。方法 回顾性分析160例T2DM患者的临床资料,根据动脉硬化(atherosclerosis, AS)检测结果,将T2DM组患者分为单纯T2DM组(69例)和T2DM+AS组(91例),另选取160例同期健康者作为对照组。检测各组血浆25(OH)D、RAAS改变,采用多因素logistic回归对AS的危险因素进行分析。结果 与对照组比较,T2DM+AS组、单纯T2DM组血糖和血脂相关指标、BMI、PRA、AngⅡ、ALD、25(OH)D等差异有统计学意义(P<0.05);与单纯T2DM组比较,T2DM+AS组年龄增大,FBG、HbAlc、PRA、AngⅡ、ALD升高,HDL-C、25(OH)D降低(P<0.05);血浆25(OH)D与PRA、AngⅡ、ALD均呈负相关(r=-0.611、-0.591、-0.639,P<0.05);多因素Logistic回归分析显示,年龄、HbAlc、PRA可能是T2DM患者AS的危险因素,HDL-C、25(OH)D则可能是保护因素(P<0.05)。结论 T2DM患者血浆25(OH)D降低,RAAS水平升高,25(OH)D缺乏可能通过对RAAS的负向调控而参与AS发生。
Objective To investigate the association of plasma 25-hydroxyvitamin D and renin-angiotensin-aldosterone system(RAAS) with atherosclerosis(AS) in type 2 diabetes mellitus(T2DM). Methods Clinical data of 160 diabetic patients were retrospectively analyzed, including 69 cases of simplex T2DM and 91 cases of T2DM+AS; and 160 healthy subjects were included as control group. The plasma 25(OH) D levels and RAAS were detected in both groups, and risk factors of AS was analyzed by multivariate logistic analysis. Results There were significantly differences in blood glucose and lipid-related indicators, BMI, PRA, AngⅡ, ALD, 25(OH)D between T2DM group and control group(P<0.05). Compared with simplex T2DM group, the age was higher, the levels of FBG, HbAlc, PRA, AngⅡ, ALD in T2DM + AS group were increased, the levels of HDL-C and 25(OH)D were reduced(P<0.05). Plasma 25(OH)D was negatively correlated with PRA, AngⅡ, ALD(r=-0.611, -0.591, -0.639, P<0.05). Multivariate logistic regression analysis showed that HDL-C, 25(OH)D were protective factors, and age, HbAlc, PRA were risk factors for AS(P<0.05). Conclusion Plasma 25(OH)D level is decreased and RAAS is up-regulated in T2DM patients, and the deficit of 25(OH)D may promote pathogenesis of AS through negative regulation of RAAS

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