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目的研究尿酸异常与纤维蛋白原(fibrinogen,Fg)Bβ链-854G/A、-455G/A、-249C/T、-148C/T、448G/A和Bcl-1G/A位点基因多态性及其血浆Fg含量和聚合功能表达的关系。方法选取开滦集团离退休职工1386人,均抽取清晨空腹静脉血测定血生化、尿酸(UA)、血浆Fg浓度和纤维蛋白单体聚合反应速率(FMPV)、FMPV/Amax等反映Fg聚合功能的指标,并检测FgBβ链6个位点基因多态性。依据尿酸值将人群分为高尿酸血症组与正常尿酸组,探讨尿酸异常与Fg的关系。结果高尿酸与否人群FgBβ各多态性位点等位基因和基因型频率分布差别无统计学意义(P>0.05);在-854GG型、-455GG型、Bcl-1GG型人群中FMPV/Amax,-249CT+TT型人群中Fg浓度、FMPV、FMPV/Amax,-148CC型、448GG型人群中Fg浓度、Amax均为高尿酸血症组低于正常尿酸组(P<0.05);以有无高尿酸为因变量的Logistic回归分析,依次筛选出肌酐、性别、高血压病、体重指数、年龄、FMPV/Amax等指标。结论尿酸可以影响FgBβ链6个基因多态性位点对于血浆Fg含量和分子活性功能表达的调控作用;高尿酸血症与脂代谢异常及其引发的慢性炎症反应等因素共同作用可导致脑梗死的发病。
Objective To investigate the relationship between uric acid abnormality and fibrinogen (Fg) Bβ chain -854G / A, -455G / A, -249C / T, -148C / T, 448G / A and Bcl- And its plasma Fg content and polymerization function of the relationship. Methods A total of 1386 retired workers from Kailuan Group were enrolled in this study. Fasting venous blood samples were collected for determination of blood biochemistry, uric acid (UA), plasma Fg concentration and fibrin monomer polymerization rate (FMPV), FMPV / Amax Indicators, and detect FgBβ chain 6 locus gene polymorphisms. According to the uric acid value, the population was divided into hyperuricemia group and normal uric acid group to explore the relationship between uric acid abnormality and Fg. Results There was no significant difference in allele and genotype distribution between FgBβ polymorphisms and loci in high-uric acid group (P> 0.05). In F-type, -455GG and Bcl-1GG groups, FMPV / Amax Fg concentration, FMPV, FMPV / Amax, -148CC type in -249CT + TT group, Fg concentration in Amagatan 448GG group and Amax were lower in hyperuricemia group than in normal uric acid group (P <0.05) Hyperuricemia as a dependent variable Logistic regression analysis, followed by screening of creatinine, gender, hypertension, body mass index, age, FMPV / Amax and other indicators. Conclusions Uric acid can influence the regulatory effect of six genetic polymorphisms of FgBβ chain on the functional expression of Fg and molecular activity in plasma. Hyperuricemia, combined with abnormal lipid metabolism and chronic inflammatory response, may lead to cerebral infarction The incidence.