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肝硬化患者血浆中尿激酶型纤溶酶激活物的检测及其意义
引用本文:武希润,王琦,师水生,吕敏和,郭文栋. 肝硬化患者血浆中尿激酶型纤溶酶激活物的检测及其意义[J]. 中华肝脏病杂志, 2004, 12(2): 82-84
作者姓名:武希润  王琦  师水生  吕敏和  郭文栋
作者单位:1. 山两医科大学第二医院消化科工作,030001
2. 山西医科大学第二医院
3. 250012,济南,山东大学
摘    要:
目的 探讨肝硬化患者血浆尿激酶型纤溶酶激活物(uPA)、尿激酶型纤溶酶激活物受体(uPAR)、纤溶酶原激活物抑制剂-1(PAI-1)的变化及其意义。 方法 确诊的72例乙型肝炎后肝硬化患者,Child-pugh分级A级23例(A组),B级29例(B组),C级20例(C组)。6例健康志愿献血者为正常对照组。酶联免疫吸附实验测定血浆uPA、uPAR、PAI-1的变化。并同时检测血透明质酸(HA)、Ⅳ型胶原(C Ⅳ)、Ⅲ型前胶原(PC Ⅲ)、血浆白蛋白、胆红素、凝血酶原时间及其活动度改变。 结果 随着肝硬化的进展,血浆uPA、uPAR、PAI-1逐渐增加,HA、PC Ⅲ也明显增加。Child C组患者血浆uPA、uPAR、PAI-1水平(μg/L)分别为1.88±0.64、4.82±2.02和52.60±16.87,A组分别为1.36±0.43、3.03±1.48和24.09±7.14,B组分别为1.79±0.62、4.80±2.22和41.40±17.52,C组与A、B组比较,t值为2.81~7.38,P值均<0.01。A组血浆uPA与PC Ⅲ呈负相关(r=-0.4785,P<0.05);C组PAI-1与HA呈正相关(r=0.5447,P<0.01)。 结论 肝硬化晚期,虽然血浆uPA、PAI-1增加,但总的效应表现为uPA相对不足,肝基质纤维降解受抑制,血浆uPA、PAI-1与肝硬化发展密切相关。

关 键 词:肝硬化 血浆 尿激酶型纤溶酶激活物 检测 尿激酶型纤溶酶激活物受体 纤溶酶原激活物抑制剂-1
修稿时间:2003-03-21

The plasma levels of urokinase plasminogen activator and urokinase plasminogen activator receptor and plasminogen activator inhibitor-1 in patients with different stages of liver cirrhosis following chronic hepatitis B
WU Xi-run,WANG Qi,SHI Shui-sheng,LU Ming-he,GUO Wen-dong. The plasma levels of urokinase plasminogen activator and urokinase plasminogen activator receptor and plasminogen activator inhibitor-1 in patients with different stages of liver cirrhosis following chronic hepatitis B[J]. Chinese journal of hepatology, 2004, 12(2): 82-84
Authors:WU Xi-run  WANG Qi  SHI Shui-sheng  LU Ming-he  GUO Wen-dong
Affiliation:The medical college, Shangdong University, Jinan 250012, China.
Abstract:
OBJECTIVES: To measure the plasma levels of urokinase plasminogen activator (uPA), urokinase plasminogen activator receptor (uPAR) and plasminogen activator inhibitor-1 (PAI-1), and study the relationship between the plasma levels of uPA, PAI-1 and the serum albumin (Alb), collagen type IV (CIV), the serum hyaluronic acid (HA), prothrombin time (PT) and prothrombin activity (PTA) in patients with different stages of liver cirrhosis following chronic hepatitis B. METHODS: 72 cases with liver cirrhosis of different stages were classified according to child-pugh's categories A, B, C, in which there were 23 cases in child A, 29 cases in child B, and 20 cases in child C. The plasma levels of uPA, uPAR, PAI-1 and the serum levels of HA, CIV were detected by ELISA. The serum PCIII concentration was determined by radioimmunoassay. RESULTS: With the progression of hepatic fibrosis, the plasma levels of uPA, uPAR and PAI-1 were (1.36+/-0.43) microg/L, (3.03+/-1.48) microg/L and (24.09+/-7.14) microg/L respectively in group A, (1.79+/-0.62) microg/L, (4.80+/-2.22) microg/L and (41.40+/-17.52) microg/L respectively in group B. The highest levels were in child C, whose levels were (1.88+/-0.64) microg/L, (4.82+/-2.02) microg/L and (52.60+/-16.87) microg/L respectively, compared with group A and group B, t value were from 2.81 to 7.38, all of P value were less than 0.01. There was negative correlation between the plasma levels of uPA and the serum PCIII (r=-0.4785, P<0.05) in child A, but, positive correlation between the plasma PAI-1 and the serum HA (r=0.5447, P<0.01) in child C. The value of PAI-1/uPA was significantly decreased in child A, but increased in child B and child C. CONCLUSION: In the late of liver cirrhosis, increased PAI-1 together with uPA, uPAR are associated with overall inhibition of matrix degradation. The plasma levels of uPA and PAI-1 were correlation to the progression of liver cirrhosis.
Keywords:Hepatitis B  Liver cirrhosis  Urokinase plasminogen activator
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