摘要
目的:探讨多因素强化干预条件下,血管紧张素转换酶(ACE)基因多态性对新诊断T2DM患者颈总动脉内中膜厚度(CCA-IMT)进展的预测作用。方法:采用限制性片段长度多形态多聚酶链式反应(PCR-RFLP)技术检测100例新诊断T2DM患者ACE基因内含子16 I/D多态性,利用B超检测新诊断T2DM患者CCA-IMT,并对其进行多因素强化干预治疗,探讨ACE基因多态性对新诊断T2DM患者CCA-IMT进展的预测作用。结果:携带ACE DD基因型者CCA-IMT、hs-CRP高于携带II及ID基因型者(P<0.05);强化干预后,携带ACE DD基因型者CCA-IMT、hs-CRP与携带II及ID基因型者差异无显著性(P>0.05),干预前后自身比较CCA-IMT值、hs-CRP水平较干预前显著下降(P<0.05),CCA-IMT非进展组与进展组患者ACE基因型、等位基因携带者比例均差异无显著性(P>0.05);Logistic回归分析显示,ACE DD基因型不是新诊断T2DM患者CCA-IMT进展的危险因素。结论:多危险因素强化干预条件ACE DD基因型不能预测CCA-IMT的进展,多危险因素强化干预延缓了携带ACE DD基因型者CCA-IMT的进展。
Objective：To investigate the predicting effects of angiotensin 1-converting enzyme（ACE）gene polymorphism on the common carotid artery intima-media thickness （CCA-IMT） in newly diagnosed type 2 diabetes mellitus （T2DM） after the multifactorial intervention. Methods：The polymorphisms of ACE （I/D） gene were determined by polymerase chain reaction-restriction fragment length polymorphism （PCR-RFLP） in 100 T2DM. CCA-IMT was compared among the groups with different genotypes of ACE. Then the 100 newly diagnosed type 2 diabetics （duration≤1 year） received the multifactorial targeted intervention ,including taking aspirin and controlling blood glucose ,blood pressure ,blood lipid and body weight. The predicting effects of ACE gene polymorphism on CCA-IMT in T2DM was investigated. Results ：Patients with ACE DD genotypes had higher CCA-IMT than those with ACE-II or ACE ID genotypes; After the multifactorial intervention There were no differences in ACE genotypes between CCA-IMT increasing group and non-increaslng group. Logistic regression analysis showed that ACE DD genotypes were not closely correlated with CCA-IMT, Conclusions： After the muitifactorial intervention ACE DD genotypes may not predict the progression of CCA-IMT in patients with newly diagnosed T2DM and CCA-IMT was delayed in T2DM with ACE DD genotypes.
出处
《中国误诊学杂志》
CAS
2008年第12期2776-2779,共4页
Chinese Journal of Misdiagnostics
关键词
肽基二肽酶A/遗传学
多态性
限制性片段长度
糖尿病
2型/病理学
颈动脉/病理学
人类
Peptidyl-Dipeptidase A/genetics
Polymorphism, Restriction Fragment Length
Diabetes Mellitus, Type 2/pathology
Carotid Arteries/pathology
Humans
