纤维蛋白原Bβ链-148C/T基因多态性及血小板膜糖蛋白VIT13254C基因多态性与冠心病的关系

A Study on Bβ-Fibrinogen -148C/T Polymorphism and Platelet Membrane Glycoprotein Ⅵ T13254C Polymorphism of Coronary Heart Disease

目的 探讨纤维蛋白原 (Fib)Bβ链 14 8C/T基因多态性及血小板膜糖蛋白Ⅵ (GpⅥ )T132 5 4C基因多态性在血栓形成中的作用及其与冠心病的关系。方法 采用Clauss法测定 15 4例经选择性冠状动脉造影检查 ,确诊为冠心病的患者及 12 1例经冠状动脉造影证实无冠脉病变的对照者血浆Fib水平 ,以多聚酶链式反应 限制性内切酶片段长度多态性 (PCR RFLP)分析血小板膜糖蛋白基因多态性及纤维蛋白原Bβ链 14 8C/T基因多态性。结果 急性心肌梗死组 (AMI组 )和不稳定心绞痛组(UAP组 )血浆Fib水平均明显高于对照组 (P <0 0 0 1) ,AMI组血浆Fib水平较UAP组明显增高 (P <0 0 0 1) ;三组间FibBβ 14 8C/T的基因型和等位基因频率分布无显著性差异 (分别为 χ2 =1 78,P >0 0 5 ;χ2 =0 5 6 7,P >0 0 5 ) ;急性心肌梗死患者中 ,两组基因型间血浆Fib水平具有显著差异 (P <0 0 5 )。GpⅥT132 5 4C的C等位基因频率为 0 0 33;冠心病组与对照组GpⅥT132 5 4C的基因型和等位基因频率分布无显著性差异 (分别为 χ2 =0 6 17,P >0 0 5 ;χ2 =0 14 8,P >0 0 5 )。结论 Fib是冠心病的一个独立危险因素 ,FibBβ 14 8C/T基因多态性与AMI组血浆Fib水平明显相关 ,与冠心病的发生无直接关系。本地人群的GpⅥT132 5 4C等位基?

Objective To investigate the function of platelet membrane glycoprotein Ⅵ （GPⅥ） T13254C polymorphism and B β-fibrinogen-148C/T polymorphism in arterial thrombosis and the association with coronary heart disease. Methods In a case-control study, the fibrinogen levels were detected by Clauss in 154 subjects with angiographically documented coronary artery disease and 121 subjects without CHD （ CHD was excluded by coronarography）. Restriction fragment length polymorphism （RFLP） analysis was performed to screen the GPⅥ T13254C polymorphism and B β-fibrinogen-148C/T polymorphism. Results Mean plasma Fib levels were significantly higher in patients with coronary heart disease than that in controls （p 〈 0. 01 ）. In CHD patients, Fib levels in AMI group were remarkably higher in patients with coronary heart disease than those in UAP group （p 〈0.001 ）. Patients carrying the 148 T alleles showed higher plasma Fib levels compared with those carrying 148CC genotype in AMI group, （P 〈 0.05 ）. The frequencies of Bβ-fibrinogen -148C/T genotype and alleles had no difference in UAP,AMI and control group （x^2 = 1.78, P 〉0. 05; x^2 =0. 567,P 〉0. 05 respectively）. The frequenciys of GPⅥ T13254C C alleles is 0.033 in all of subjects. No significant difference was found in the frequencies of GPⅥ T13254C genotype and alleles between controls and CHD patients （x^2 =0.617,P〉0.05;x^2 =0. 148, P〉0.05 respectively）. Conclusion The level of fibrinogen was an independent risk factor of CHD. There was obvious relationship between the Bβ-fibrinogen-148C/T mutation and high fibrinogen level in AMI group. The BIS-fibrinogen-148C/T polymorphism was not correlated with the risk of CHD. In this study the rate of GPⅥ T13254C mutation was quite low, GPⅥ T13254C polymorphism was not associated with an increased risk of CHD.