血管紧张素转换酶、血管紧张素Ⅱ受体Ⅰ型基因多态性与脑梗死关系的横断面研究

目的 研究血管紧张素转换酶(ACE)基因、血管紧张素Ⅱ受体I型(ATⅠR)基因多态性和多种危险因素与脑梗死的相关性。方法 采用整群抽样的方法选取开滦矿业集团职工1351人。所有样本均清晨空腹抽取静脉血测定肿瘤坏死因子（TNF—-α)，白介素(IL-6、IL-8、IL-l0，C反应蛋白（CRP)，血浆纤维蛋白原(Fg)浓度，纤维蛋白单体的聚合速度(FMPV)，纤维蛋白单体的聚合速率与最大光密度之比(FMPV/Amax)等炎性因子和ACE、ATⅠR基因型及相关生化指标，并进行体检和问卷调查。结果 ACE基因各基因型分布及脑梗死患病率无明显差异，ATⅠR基因AA基因型分布在脑梗死组高于对照组，且AA型人群脑梗死患病率高于其他基因型，但两种基因各联合基因型脑梗死患病率无差异。在与脑梗死有关的各种危险因素存在条件下，仅不吸烟人群和有高血压病人群中脑梗死组ATIR基因AA基因型频率分布高于对照组。logistic回归发现IL-6、ATⅠR基因多态性、性别、FMPV／Amax与脑梗死有明显相关性。脑梗死组IL-6水平明显高于对照组。结论 在具有高血压病的ATⅠR的AA基因型人群发生脑梗死的危险性明显增加；同时脑梗死病例中IL-6显著增高，提示局部炎症和免疫反应可能是其病因之一，说明脑梗死的发病可能是“基因与环境”因素共同作用的结果。

A cross-sectional study on angiotensin-converting enzyme and angiotensin Ⅱ type Ⅰ receptor gene polymorphism and cerebral infarction

OBJECTIVE: To explore the relation of angiotensin-converting enzyme (ACE) gene polymorphism, angiotensin II type I receptor (ATIR) gene polymorphism and other factors on cerebral infarction. METHODS: One thousand three hundred fifty-one subjects from Tangshan coalmine were enrolled with study method of cluster sampling. Face to face interviews were conducted to fill in questionnaires by trained interviewers. ACE gene, ATIR gene and inflammation factors including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-8, IL-10, C reactive protein (CRP), fibrinogen (Fg), fibrin monome polymerized velocity (FMPV), absorbance maximum (A(max)), FMPV/A(max), were measured. RESULTS: No different prevalence rates of ACE genotype were found on cerebral infarction. The distributions of AA genotype of ATIR gene in the cerebral infarction was higher than that of the controls. The prevalence of AA genotype was higher than other groups, but the prevalence of combined genotype did not show much difference. Under the existence of factors that related to cerebral infarction, AA genotype frequencies were higher than those of non-smoking and with hypertension. IL-6, ATIR gene polymorphism, sex, FMPV/A(max) were strongly related to cerebral infarction. The level of IL-6 was higher than the normal ones. CONCLUSIONS: The prevalence of cerebral infarction obviously increased in the hypertensive groups having AA genotype of ATIR gene. In the cerebral infarction groups, the level of IL-6 was higher than that in the normal population, indicating that these can be resulted from local inflammation and immunity reactivity. Environmental and genetic factors in the pathogenesis of cerebral infarction might have coordinating functions.