人凝血复合物诱发血栓形成的病理机制及其评估方法分析

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。

Analysis of pathological mechanism coagulant complex induced thrombosis and its assessment methods

Objective To analyze the pathological mechanism of human coagulation complexes induced thrombosis and its assessment methods. Metheds Chose our hospital from July 2009 to July 2010 cerebral arterial thrombosis, deep vein thrombosis and myocardial infarction patients, 50 patients for group A, group B and group C, another 50 healthy volunteers as controls group D. Application saturated salting of human genomic DNA was extracted the prothrombin gene fragments amplified by polymerase chain reaction （PCR） method and DNA amplification instrument observed parting and recorded. Results Of group A patients 20210A with group D compared to the control group there was significant differ- ence, RR = 6. 8768 （ u = 2. 6543, P 〈 0. 01 ） ; Group B patients 20210A compared with the control group there was sig- nificant difference, RR =0. 9765 （u = 1. 6422, P 〉 0. 05） ; Group C patients 20210A compared to the control group, there was significant difference, RR = 4. 1265 （ u = 5. 8546, P 〈 0. 01 ）. Conclusions Thrombin original 20210G / A gene mutation may be an important reason to cause coagulation hyperthyroidism caused thrombosis, dose, purity and ac- tivation of human coagulation complexes and their thrombogenicity, evaluation methods, including a variety of in vivo and in vitro methods, non - stagnation model test is the best evaluation method.