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作 者:刘敏涓[1] 周立红[1] 刘泽霖[1] 谭获[1] 赖毅妍[1]
机构地区:[1]广州医学院第二附属医院
出 处:《广州医药》1999年第1期13-15,共3页Guangzhou Medical Journal
摘 要: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 observe measurement of coagulation Inhibitors-Tissue Factor Pathway Inhibitor (TFPI) and Antithrombin-Ⅲ(AT-Ⅲ)in Patients with Uremia To study the relationship between pathologic change and coagulation mechanism, and its effected by hemodialysis Methods: TFPI Antigen (TFPI:Ag) was determined with an enzyme-linked immunity (ELISA) AT-Ⅲ active (AT-Ⅲ:A) was determined with chromogenic peptide substrate Results: uremia groups (20 cases) plasma levels of TFPI:Ag were 177 35± 46 58 ng/ml, higher than the healthy subjects (30 cases) ( P <0 01); AT-Ⅲ:A were 73 10±17 01, lower than controls ( P <0 01) The 10 cases of uremia compared before hemodialys and after hemodialysis TFPI:Ag from 182 91±31 20 decreases to 131 55± 36 51 ( P <0 005); AT-Ⅲ:A from 84 26±16 19 elevated to 110 00±26 51 ( P <0 01) Conclusion: uremic patients TFPI:Ag increases and AT-Ⅲ:A decreases point to severe lesion on kidney tissue arise from tissue factor obvious elevated; the patients prome to hyper coagulable state and this state were changed to normal levels by hemodialysis
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