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目的分析人凝血复合物诱发血栓形成的病理机制及其评估方法。方法选择2009年7月至2010年7月河源市人民医院诊治的脑动脉血栓、下肢深静脉血栓及心肌梗死患者各50例为组A、组B及组C,另选择50例健康志愿者为对照组组D。应用饱和盐析法提取人基因组DNA,聚合酶链反应(PCR)法及DNA扩增仪器扩增凝血酶原基因片段,观察其分型并记录。结果组A患者20210A与对照组组D相比存在统计学差异,RR=6.8768(u=2.6543,P<0.01);组B患者20210A与对照组相比存在统计学差异,RR=0.9765(u=1.6422,P>0.05);组C患者20210A与对照组相比存在统计学差异,RR=4.1265(u=5.8546,P<0.01)。结论凝血酶原20210G/A基因突变可能是导致凝血功能亢进,引起血栓形成的重要原因,人凝血复合物的剂量、纯度及激活程度与其致血栓性相关,其评价方法包括体内及体外多种方法,其中非停滞模型试验为目前最佳的评价方法。
Objective To analyze the pathological mechanism of thrombosis induced by human coagulation complex and its assessment method. Methods Fifty patients with cerebral arterial thrombosis, deep venous thrombosis and myocardial infarction in Heyuan People’s Hospital from July 2009 to July 2010 were selected as group A, group B and group C, and 50 healthy volunteers Control group D. Saturated salting-out method was used to extract human genomic DNA. PCR amplification and DNA amplification were used to amplify the prothrombin gene fragment. The genotypes were observed and recorded. Results There was a statistically significant difference between group A and control group 20210A (RR = 6.8768, u = 2.6543, P <0.01). There was a significant difference between group A and group B 1.6422, P> 0.05). There was a significant difference between group C and control 20210A, RR = 4.1265 (u = 5.8546, P <0.01). Conclusions The mutation of prothrombin 20210G / A gene may be an important cause of thrombogenesis induced by hyperthyroidism. The dosage, purity and activation of human coagulation complex are related to thrombosis. The evaluation methods include in vitro and in vivo methods , Of which non-stagnant model test is the best method of evaluation.