腔隙性脑梗死患者FXII CRM^+及其对纤溶酶原活性影响的初步研究

The change of FXII CRM^+ and initial study of its effect on profilorinolysin in cerebral infarction patient

目的 :研究接触启动系统的凝血因子 XII(FXII)在激活纤溶酶和血管病变时对纤溶酶原活性的影响。方法 :分别检测 80例腔隙性脑梗死 (简称腔梗 )患者和 5 9例正常对照者的血浆 PL G:A、α2 AP:A、D-二聚体、FXI-I:Ag和 F1 + 2 水平 ,并比较两组各项指标的差异 ,以了解腔梗患者的纤溶酶原活性及潜在的纤溶酶原功能在血管病变中的作用。结果 :2 8例腔梗患者存在明显的 FXII:C减低 ,和 α2 AP:A升高 ,而 PL G:A、FXII:Ag和 D-二聚体水平与正常对照组差异无显著性意义 (P >0 .0 5 ) ,而血浆 F1 + 2 水平均增高。结论 :部分腔梗患者存在 FXII CRM+可能是引起血栓形成的重要因素 ,并有必要对 FXII基因的多态性作进一步研究。

Objective:To study contact system factor XII activated plasminogen and affected on fibrinolysis when associated vascular disease was present.Method:PLG:A, α 2AP:A,D-Dimer,F 1+2 ,FXII:C and FXII:Ag were determinated in 80 lacunar infarction patients and 59 health controls.The difference was compared between the patients and controls to investigate activity.Result:There is significant decrease in FXII:C and increase in α 2AP:A and plasma F 1+2 level in 28 patients with lacunar infarction. No change of PLG:A,plasma XII:Ag and D-Dimer level the patients and controls.Conclusion:There is a change of FXII CRM+ in lacunar infarction patients.which may be an important factor in inducily thrombosis in hypercoagulant state.It is suggested that further study of FXII gene polymorphism is necessary.