论文部分内容阅读
目的 评估脂蛋白 a(LP a)在遗传性凝血酶原缺陷的静脉血栓栓塞 (VTE)病人组中所起的作用。方法 研究对象包括至少发生一次静脉血栓栓塞的病人共 6 85例和 2 6 6例性别和年龄相当 ,并排除存在活化蛋白C(APC)抵抗 ,蛋白C、蛋白S及抗凝血酶缺陷 ,血清LP a升高 ,因子 (F)VG16 91A、二甲基四水叶酸还原酶 (methylenetetrahydrofolatereductase ,MTHFR)C6 77T和凝血酶原 (PT)G2 0 2 10A基因突变等因素的健康人对照组。将其LP a升高及FVG16 91A因子突变作比较。结果 病人组中LP a>0 .30g/L的占 2 0 % ,明显高于对照组 (P <0 .0 0 1,OR3.2 ,95 %CI 1.9～ 5 .3) ;LP a升高 ,同时存在FVG16 91A因子 ,在VTE病人中明显多于对照组 (P <0 .0 0 1,OR9.8,95 %CI2 .4～ 4 0 .7)。结论 LP a >0 .30g/L为VTE的一种常见独立危险因子。此外 ,LP a水平可能与由于受其它凝血因子缺陷 ,如FVG16 91A突变影响的VTE疾病的外显率有关
Objective To evaluate the role of lipoprotein a (LPa) in hereditary prothrombin-deficient patients with venous thromboembolism (VTE). METHODS: Sixty-five patients with at least one venous thromboembolism were enrolled in this study. A total of 266 patients were sexually and age-matched. Exclusion of activated protein C (APC) resistance, protein C, protein S and antithrombin deficiency, serum LPa increased, FGGG 91A, MTHFR C6 77T, and PT2G2102A gene mutations in healthy human controls. The increase in LP a and FVG16 91A mutation were compared. Results The percentage of patients with LP a> 0.30 g / L was 20% higher than that of the control group (P0.01, OR3.2, 95% CI 1.9-5.3) , While the presence of FVG16 91A factor in patients with VTE was significantly more than the control group (P <0.01, OR9.8, 95% CI2 .4 ~ 40.7). Conclusion LP a> 0.30 g / L is a common and independent risk factor for VTE. In addition, LPa levels may be related to the penetrance of VTE disease due to other coagulation factor deficiencies, such as FVG16 91A mutation