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.
- Author:
Xi-run WU
1
;
Qi WANG
;
Shui-sheng SHI
;
Ming-he LU
;
Wen-dong GUO
Author Information
- Publication Type:Journal Article
- MeSH: Female; Hepatitis B, Chronic; complications; Humans; Liver Cirrhosis; blood; Male; Middle Aged; Plasminogen Activator Inhibitor 1; blood; Receptors, Cell Surface; blood; Receptors, Urokinase Plasminogen Activator; Urokinase-Type Plasminogen Activator; blood
- From: Chinese Journal of Hepatology 2004;12(2):82-84
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVESTo 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.
METHODS72 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.
RESULTSWith 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.
CONCLUSIONIn 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.