2型糖尿病患者餐后高脂血症与颈动脉粥样硬化病变及纤溶活性关系的研究

Relationship between post-prandial hyperlipidemia and carotid ather oscerosis and blood rheology in type 2 diabetic patients

目的:观察2型糖尿病患者餐后甘油三酯水平对动脉粥样硬化形成的影响。方法:2型糖尿病患者90例,按空腹甘油三酯(TG)和脂肪餐后4 h TG水平分为空腹高脂组、餐后正常组、餐后增高组,所有患者均测空腹血糖(FBG)、餐后2 h血糖(PBG2 h)、空腹胰岛素(FINS)、糖化血红蛋白(HbA1C)、总胆固醇(TC)、TG、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、体重指数(BMI)、腰臀比(WHR)、全血粘度、纤维蛋白原、血浆粘度、血浆组织型纤溶酶原激活物(t-PA)及其抑制物-1(PAI-1)活性、D-二聚体(D-D)水平、C反应蛋白(CRP)、肿瘤坏死因子α(TNF-α),并行颈动脉彩色多普勒检查。结果:餐后增高组、空腹高脂组颈动脉内膜中层厚度(IMT)、颈动脉斑块发生率、大血管病变发生率、颈动脉斑块总积分均明显高于餐后正常组(P<0.01),而餐后增高组与空腹高脂组颈动脉IMT无明显差异;餐后增高组、空腹高脂组患者全血的高切粘度、中切粘度、低切粘度,血浆粘度,红细胞压积,纤维蛋白原,血沉均显著高于餐后正常组(P<0.01),餐后增高组与空腹高脂组比较无统计学意义;CRP与TNF-α水平按餐后正常组、餐后增高组与空腹高脂组的顺序依次增高(P<0.05);餐后增高组、空腹高脂组患者血浆PAI-1、D-D水平活性明显高于餐后正常组(P<0.05),血浆t-PA活性明显低于餐后正常组(P<0.01),餐后增高组与空腹高脂组比较,差异无统计学意义。结论:空腹TG正常伴餐后TG增高者与空腹TG增高对动脉粥样硬化有同样的危害性,对促进糖尿病大血管病变的发生有相同的危险性。

Objective： To study the influence of post-prandial hypertriglyceridemia on atherosclerosis in type 2 diabetic patients. Methods： Ninety type 2 diabetics were enrolled in this study, and they were divided into three groups： group Ⅰ （fasting blood triglyceride ≤ 1.7 mmol/L,TG4h≤2.0 mmol/L）, group Ⅱ（fasting blood triglyceride ≤ 1.7 mmol/L,TG4h 〉 2.0mmol/L）, and group Ⅲ （fasting blood triglyceride level≥ 1.7 mmol/L ）. The levels of fasting blood glucose, blood glucose of two hours post-prandial（PBG2 h）, fasting blood insulin, HbAlc, total cholesterol （TC）, total triglyeeride（TG）, HDL-cholesterol, whole blood viscosity, fibrinogen, plasma viscosity, and the levels of ESR, t-PA, PAI, DD, CRP and TNF-α were determined, also the LDL-cholesterol（LDL-C）, BMI, WHR, systolic blood pressure（ SBP） and diastolic blood pressure（DBP） were determined. The carotid color Doppler ultrasonography was applied in all the patients. Results： The carotid artery intima-media thickness（IMT）, the rate of carotid artery plaque and of great vessel complications and carotid artery plaque scores in groups Ⅱ and Ⅲ were significantly higher than those in group Ⅰ. The IMT was not significantly different between groups Ⅱ and Ⅲ. Whole blood viscosity, fibrinogen, plasma viscosity and ESR in groups Ⅱ and Ⅲ were significantly higher than those in group Ⅰ , whereas there were no significant differences between groupsⅡ and Ⅲ. The levels of CRP and TNF-a were gradually increased in the three groups, which produced a significant difference among the three groups. PAI-1 and D-D of groups Ⅱ and Ⅲ were significantly higher than those in group Ⅰ , but there were no differences between groups Ⅱ and Ⅲ. Conclusions： Postprandial hyperlipidemia is at the same risk of causing atherosclerosis as fasting hyperlipidemia, and it is at the same risk of enhancing the development of diabetic great vessel complications as fasting hyperlipidemia.