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目的探讨凝血因子Ⅻ基因(FⅫ)多态性与肺血栓栓塞(PTE)形成的相关性及其影响。方法采用直接测序法检测56例PTE患者和40例对照组的FⅫ基因启动区第46位碱基多态性,并采用一期凝固法、发色底物法及免疫比浊法等测定血浆凝血因子Ⅻ活性(FⅫ∶C)、抗凝血酶活性(AT∶A)、纤溶酶原活性(PLG∶A)及血浆D-二聚体(D-D)含量等各项指标。结果 FⅫ基因多态性46TT型在PTE患者所占比例较对照组明显增高,其多态性在分布上差异有统计学意义(P<0.05)。46TT型血浆FⅫ∶C、AT∶A均明显低于其他型及对照组(P<0.05),但在46CT型及46CC型与对照组之间比较,差异无统计学意义(P>0.05)。与对照组比较,46TT型的D-D含量明显升高(P<0.05)。PLG∶A在各型患者及对照人群之间差异均无统计学意义(P>0.05)。结论肺血栓栓塞患者的FⅫ基因46TT型增多并导致FⅫ活性明显下降,该多态性是引起肺血栓栓塞的潜在因素。
Objective To investigate the relationship between coagulation factor Ⅻ gene (F Ⅻ) polymorphism and the formation of pulmonary thromboembolism (PTE) and its influence. Methods Direct sequencing was used to detect the 46th polymorphism in promoter region of FⅫ gene in 56 PTE patients and 40 control subjects. Plasma coagulation was measured by primary coagulation assay, chromogenic substrate assay and immunoturbidimetric assay Factor Ⅻ activity (F Ⅻ: C), antithrombin activity (AT: A), plasminogen activity (PLG: A) and plasma D-dimer (DD) content and other indicators. Results The percentage of 46TT polymorphism in FⅫ gene was significantly higher in PTE than that in control group, and the distribution of 46TT polymorphism was statistically significant (P <0.05). 46TT plasma F: C, AT: A were significantly lower than other types and control group (P <0.05), but there was no significant difference between 46CT type and 46CC type and control group (P> 0.05). Compared with the control group, the D-D content of 46TT group was significantly increased (P <0.05). PLG: A in all types of patients and control groups, there was no significant difference (P> 0.05). Conclusions Patients with pulmonary thromboembolism have more fibronectin type 46TT and lead to a significant decrease in FⅫ activity. This polymorphism is a potential factor causing pulmonary thromboembolism.