论文部分内容阅读
目的：对尿毒症患者的血浆中抗凝物质－组织因子途径抑制物（ＴＦＰＩ）与抗凝血酶Ⅲ（ＡＴ－Ⅲ）进行测定以研究其病理改变与凝血机理的关系，以及透析治疗对它的影响。方法：ＴＦＰＩ抗原（ＴＦＰＩ：Ａｇ）测定采用酶联免疫（ＥＬＩＳＡ）方法，ＡＴ－Ⅲ活性（ＡＴ－Ⅲ：Ａ）测定采用发色底物法。结果：尿毒症组（２０例）ＴＦＰＩ：Ａｇ为１７７３５±４６５８ｎｇ／ｍｌ，较正常组（３０例）为高（Ｐ＜００１）；ＡＴ－Ⅲ：Ａ为７３１１０±１７０１，较正常组为低（Ｐ＜００１）。尿毒症组（１０例）透析前后比较：ＴＦＰＩ：Ａｇ从１８２９１±３１２０降至１３１５５±３６５１（Ｐ＜００１）；ＡＴ－Ⅲ：Ａ从８４２６±１６１９升至１１０００±２６５１（Ｐ＜００１）。结论：尿毒症患者ＴＦＰＩ：Ａｇ增高，ＡＴ－Ⅲ：Ａ降低，表明其组织病理损伤明显而致ＴＦ过度表达，从而呈现一定程度的高凝状态。透析治疗可使此病理过程得到一定程度的矫正。
OBJECTIVE: To determine the relationship between the pathological changes and coagulation mechanism in plasma of patients with uremia and the relationship between coagulation mechanism and dialysis therapy Impact. Methods: TFPI antigen (TFPI: Ag) was determined by enzyme-linked immunosorbent assay (ELISA) and AT-Ⅲ activity (AT-Ⅲ: A) Results: TFPI: Ag was 17735 ± 4658ng / ml in uremia group (20 cases), higher than that in normal group (30 cases) (P <001); ATⅢ: A was 73110 ± 17 01, lower than the normal group (P <0 01). Uremic group (n = 10) compared before and after dialysis: TFPI: Ag decreased from 18291 ± 3120 to 13155 ± 3651 (P <001); AT-Ⅲ: A from 8426 ± 16 19 to 11000 ± 2651 (P <001). Conclusion: TFPI: Ag increased and AT-Ⅲ: A decreased in patients with uremia, indicating that its histopathological damage was significantly over-expression of TF, leading to a certain degree of hypercoagulable state. Dialysis treatment can make this pathological process to a certain degree of correction.