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机构地区:[1]广州医学院附属二院,广州510260 [2]深圳宝安医院,深圳518101
出 处:《血栓与止血学》2005年第4期159-161,共3页Chinese Journal of Thrombosis and Hemostasis
基 金:广东省医学科研课题(A 2003317)
摘 要:目的研究肝脏疾病患者血浆中组织因子途径抑制物(TFPI)与抗凝血酶(AT)的改变及其临床意义。方法 TFPI抗原(TFPI:Ag)采用双夹心ELISA抗原测定法。TFPI活性(TFPI:A)采用发色底物法。AT:Ag采用免疫浊度法。AT:A采用发色底物法。结果急性中毒性肝炎14例,急性病毒性肝炎20例,慢性乙型肝炎48例,肝硬化50例,共132例肝病患者:TFPI:Ag与TFPI:A均高于正常值(P<0.05,P<0.01),仅失代偿期肝硬化TFPI:Ag降低(P<0.05)。AT:Ag除失代偿期肝硬化外,均接正常值。AT:A除慢性乙肝与肝硬化低于正常值外,其他组接近正常值。结论肝病患者TFPI上调,表明组织受损与炎症存在,而AT正常或降低,表明肝细胞合成AT减少。而失代偿期肝硬化除TFPI:A保持高水平外,其余多项指标均降低,表明肝组织毁损严重,抗凝蛋白合成功能减退。Objective To investigate the chang of tissue factor pathway inhibitor (TFPI) and antithrombin (AT) in the plasma of patients with hepatic disease. Methods TFPI: Ag by ELISA assay. TFPI : A by colored substrate method. AT: Ag by immune furbidimetry. AT: A by colored substrate method. Results The plasma level of TFPI : Ag ( except for decompensatory phase of cirrhosis ) and TFPI: A all increased than control group. The level of AT: Ag( except for decompensatory phase of cirrhosis ) all consistent with normol value. AT:A except for chronic hepaitis B and hepatocirrhosis lower than normol value , other groups close to control group. Conclusion The elevation of TFPI in hepatic inflammatory disease indication of tissue injury and inflammation . The lower level of AT are expression decreased of symtheic proteins in liver. Hepatocirrhosis on the part of syntheic proteins lower preforable to other hepatic disease.
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