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目的探讨血清抵抗素与动脉粥样硬化的关系及其可能在糖尿病大血管并发症中所起的作用。方法病例选自2004年9月至2005年3月北京军区总医院的行冠状动脉造影的患者共88例,分为单纯冠心病组、糖尿病合并冠心病组、单纯糖尿病组以及正常对照组。受试者空腹采血,行生化检查及血清抵抗素、高敏C反应蛋白(hs-CRP)、可溶性肿瘤坏死因子受体2(sTNF-R2)的测定。结果各组患者血清抵抗素以及hs-CRP、sTNF-R2均高于正常对照组(P<0·05);抵抗素与sTNF-R2呈正相关(r=0·24,P=0·025),而与hs-CRP无显著相关性(P=0·613);多元回归分析显示,性别(b=0·194,P=0·029)及冠状动脉病变支数(b=0·155,P=0·001)是影响血清抵抗素水平的因素;随着冠脉病变支数的增加,血清抵抗素呈增高的趋势(P=0·004)。结论冠心病患者,特别是糖尿病合并冠心病患者,血清抵抗素水平增高;冠脉病变支数是影响血清抵抗素的重要因素;血清抵抗素水平与炎症标志呈正相关,提示抵抗素可能作为炎症因子在动脉粥样硬化以及糖尿病大血管并发症的发病机制中发挥作用。
Objective To investigate the relationship between serum resistin and atherosclerosis and its possible role in the macrovascular complications of diabetes mellitus. Methods A total of 88 patients undergoing coronary angiography at the Beijing Military Region General Hospital from September 2004 to March 2005 were enrolled in this study. They were divided into simple coronary heart disease group, diabetes mellitus combined coronary heart disease group, simple diabetes mellitus group and normal control group. Fasting blood samples were collected for biochemical tests and serum resistin, hs-CRP and sTNF-R2. Results The levels of serum resistin, hs-CRP and sTNF-R2 in all groups were significantly higher than those in normal control group (P <0.05). The resistin level was positively correlated with sTNF-R2 (r = 0.24, P = , But no significant correlation with hs-CRP (P = 0. 613) .Multivariate regression analysis showed that gender (b = 0.194, P = 0.0292) and coronary artery lesions (b = P = 0.001) were the factors influencing the level of serum resistin. The serum resistin showed an increasing trend with the increase of coronary lesion count (P = 0.004). Conclusion The level of serum resistin is elevated in patients with coronary heart disease, especially in patients with diabetes mellitus and coronary heart disease. The number of coronary lesions is an important factor affecting serum resistin. The level of serum resistin is positively correlated with inflammation markers, suggesting that resistin might be an inflammatory factor Play a role in the pathogenesis of atherosclerosis and diabetic macrovascular complications.