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目的 系统性红斑狼疮患者常并发出血或血栓形成 ,本文首次对其血浆中的组织因子途径抑制物 (TEPI)与抗凝血酶 (AT -Ⅲ )进行研究 ,并探索其病理机制与临床的联系。方法 ①TFPI抗原测定采用双夹心ELISA抗原测定法 ;②AT-Ⅲ活性测定采用发色底物法。结果 SLE(2 2例 )血浆中TFPI:Ag为 195 .73± 19.80 (ng/ml,x±s)与对照组 (30例 ) 144 .80± 2 3.18相比 ,明显增高 (P <0 .0 1) ,其中 5例患者经治疗后TFPI:Ag转为正常。SLE(18)例血浆中AT -Ⅲ :A为 76 .78± 8.30 (% ,x±s)与对照组 (30例 ) 10 0 .5 0± 13.30相比 ,明显降低 (P <0 .0 1)其中 5例患者经治疗后AT -Ⅲ比治疗前更显低值 (P<0 .0 5 )。结论 SLE病理有广泛的组织损伤 ,且多涉及血管内皮 ,故组织因子过度表达、血小板活化 ,致TFPI:Ag反馈性增高 ,治疗后可盼恢复正常。AT -Ⅲ :A受TF抑制故降低 ,治疗后可能系病变血管以血栓形成作修复过程 ,AT -Ⅲ在慢性凝血过程中继续消耗而更为降低。
Objective To investigate the relationship between TEPI and antithrombin (AT-Ⅲ) in plasma and to explore the relationship between the pathogenesis and clinical features of systemic lupus erythematosus . Methods ① TFPI antigen assay using double sandwich ELISA antigen assay; ②AT-Ⅲ activity assay using chromogenic substrate method. Results The plasma TFPI: Ag in SLE group was 195.73 ± 19.80 (ng / ml, x ± s), which was significantly higher than that in control group (30 cases) 144.80 ± 2 3.18 (P <0.05). 0 1). TFPI: Ag turned normal after treatment in 5 patients. Compared with the control group (30 cases), the AT-Ⅲ: A of 76.78 ± 8.30 (%, x ± s) in SLE (18) patients was significantly lower than that in the control group (10.050 ± 13.30, P < 1) 5 cases of patients after treatment, AT-III was significantly lower than before treatment (P <0. 05). Conclusion SLE pathology has a wide range of tissue damage, and more involved in vascular endothelial, tissue factor overexpression, platelet activation, resulting in increased feedback TFPI: Ag, expected to resume normal after treatment. AT-III: A reduced by TF inhibition, after treatment may be the lesion of blood vessels for thrombosis repair process, AT-III in the process of chronic coagulation continue to consume more and more.