【摘要】 目的探讨阿托伐他汀治疗对2型糖尿病患者糖代谢、脂代谢、炎症因子水平及颈动脉粥样硬化的作用。方法选取临沂市人民医院2015年1月至2016年12月收治的2型糖尿病患者196例,按治疗方式的不同随机分为对照组与阿托伐他汀组,各98例。2组患者均予降糖、降压及阿司匹林治疗,阿托伐他汀组在此基础上加用阿托伐他汀20 mg治疗,均持续治疗6个月。采用t检验比较2组患者治疗前后糖代谢指标[空腹血糖(FPG)、糖化血红蛋白(Hb A1c)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)]、脂代谢[总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)]、炎症因子[C反应蛋白(CRP)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)、内皮细胞选择蛋白(Selectin)]水平及颈动脉粥样硬化指标[颈动脉内中膜厚度(IMT)、斑块厚度、斑块大小、斑块数量)的差异,采用Logistic回归分析分析IMT的影响因素。结果治疗后,阿托伐他汀组的糖代谢指标FPG、Hb A1c、FINS、HOMA-IR水平与对照组相比差异均无统计学意义[(6.42±1.21)mmol/L vs(6.27±1.05)mmol/L,t=0.406,P=0.572;(6.21±0.65)%vs(6.08±0.73)%,t=0.662,P=0.339;(13.04±1.21)%vs(12.83±1.15)%,t=0.316,P=0.606;(3.75±0.27)vs(3.64±0.35),t=0.283,P=0.692)];脂代谢指标TC、TG、LDL-C的水平低于对照组,HDL-C的水平高于对照组,差异具有统计学意义[(3.18±0.33)vs(4.76±0.39),t=2.738,P=0.009;(1.69±0.14)vs(2.13±0.31),t=3.012,P=0.003;(1.74±0.27)vs(3.08±0.39),t=3.974,P=0.001;(1.26±0.21)vs(1.04±0.15),t=2.458,P=0.014)];炎症因子CRP、IL-6、TNF-α、ICAM-1、VCAM-1、Selectin的水平低于对照组,差异具有统计学意义[(0.83±0.09)vs(0.92±0.11),t=2.576,P=0.036;(1.83±0.25)vs(2.32±0.36),t=3.119,P=0.025;(33.83±4.15)vs(41.92±6.11),t=3.102,P=0.029;(198.83±14.15)vs(210.92±15.11),t=2.583,P=0.035;(457.83±41.15)vs(501.92±38.11),t=2.104,P=0.043;(20.04±1.91)vs(25.83±2.09),t=2.722,P=0.031)];颈动脉粥样硬化指标IMT、斑块厚度、斑块大小、斑块数量低于对照组差异具有统计学意义[(1.05±0.12)mm vs(1.30±0.16)mm,t=3.501,P=0.012;(2.64±0.37)mmvs(3.23±0.55)mm,t=3.164,P=0.019;(0.078±0.021)cm2 vs(0.093±0.025)cm2,t=4.068,P=0.001;(3.54±0.62)个vs(4.23±0.92)个,t=2.083,P=0.042]。服用阿托伐他汀和HDL-C水平是IMT的保护因素,TC、TG、LDL、CRP、IL-6和TNF-α水平是IMT的危险因素。结论阿托伐他汀治疗可有效调节2型糖尿病患者的脂代谢,降低炎症反应和颈动脉粥样硬化。更多还原

【Abstract】 Objective To investigate the effect of atorvastatin intervention on glucose and lipid metabolism, inflammatory cytokine levels, and carotid atherosclerosis in patients with type 2 diabetes mellitus. Methods A total of 196 patients with type 2 diabetes mellitus treated at our hospital between January 2015 and December 2016 were collected and divided into either a control group(n=98) or an atorvastatin group(n=98) according to treatment method. The patients in both groups were treated with basic treatment, and the patients in the atorvastatin group were additionally treated with atorvastatin. The changes of glucose metabolism, lipid metabolism, inflammatory cytokine levels, and carotid artery atherosclerosis-related indexes were analyzed and compared between the two groups. Results After treatment, FPG, Hb A1 c, INS, and HOMA-IR levels were not statistically significant between the two groups of patients [(6.42±1.21) mmol/Lvs(6.27±1.05) mmol/L, t=0.406, P=0.572;(6.21±0.65)% vs(6.08±0.73)%, t=0.662, P=0.339;(13.04±1.21)% vs(12.83±1.15)%, t=0.316, P=0.606;(3.75±0.27) vs(3.64±0.35), t=0.283, P=0.692), respectively]. TC, TG, and LDL-C were significantly lower and HDL-C was significantly higher in the atorvastatin group than in the control group [(3.18±0.33) vs(4.76±0.39), t=2.738, P=0.009;(1.69±0.14)vs(2.13±0.31), t=3.012, P=0.003;(1.74±0.27) vs(3.08±0.39), t=3.974, P=0.001;(1.26±0.21) vs(1.04±0.15), t=2.458, P=0.014), respectively]. CRP, IL-6, TNF-α, ICAM-1, VCAM-1, and Selectin levels were significantly lower in the atorvastatin group than in the control group [(0.83±0.09) vs(0.92±0.11), t=2.576, P=0.036;(1.83±0.25) vs(2.32±0.36), t=3.119, P=0.025;(33.83±4.15) vs(41.92±6.11), t=3.102, P=0.029;(198.83±14.15) vs(210.92±15.11), t=2.583, P=0.035;(457.83±41.15) vs(501.92±38.11), t=2.104, P=0.043;(20.04±1.91) vs(25.83±2.09), t=2.722, P=0.031), respectively]. IMT, plaque thickness, plaque size, and plaque number were significantly lower in the atorvastatin group than in the control group [(1.05±0.12) mm vs(1.30±0.16) mm, t=3.501, P=0.012;(2.64±0.37) mm vs(3.23±0.55) mm, t=3.164, P=0.019;(0.078±0.021) cm2 vs(0.093±0.025) cm2, t=4.068, P=0.001;(3.54±0.62) vs(4.23±0.92), t=2.083, P=0.042, respectively]. In multivariate logistic regression analysis, IMT was significantly associated with atorvastatin, HDL-C, TC, TG, LDL, CRP, IL-6, and TNF-α. Conclusion Atorvastatin can regulate lipid metabolism and reduce inflammatory cytokine levels and carotid atherosclerosis in patients with type 2 diabetes mellitus.更多还原