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Plasminogen activators and plasminogen activator inhibitor in malignant and non‐malignant ascitic fluid
Author(s) -
HUBER K.,
WOJTA J.,
KIRCHHEIMER J. C.,
ERMLER D.,
BINDER B. R.
Publication year - 1988
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1988.tb01273.x
Subject(s) - plasminogen activator , ascites , cirrhosis , plasminogen activator inhibitor 1 , urokinase , antigen , medicine , chemistry , endocrinology , cancer research , immunology
. Ascitic fluid from tumour patients (hepatoma, gastric cancer, gallbladder cancer, colorectal cancer, ovarian cancer) and from non‐malignant diseases (liver cirrhosis, congestive heart failure) were compared with respect to their content of determinants of the fibrinolytic system, tissue‐type plasminogen activator antigen (t‐PAag) and activity (t‐PAact), urokinase‐type plasminogen activator antigen (u‐PA) and plasminogen activator inhibitor activity (PAI). Furthermore, SDS‐polyacrylamide slab‐gel electrophoresis (SDS‐PAGE) was performed to evaluate molecular weight distribution of the detectable fibrinolytic parameters. In malignant ascites, PAI activity was three to four times higher, and increased complex formation of PAI with t‐PA could be demonstrated, compared with non‐malignant ascitic fluid. Tissue‐type plasminogen activator antigen and activity showed a similar concentration in ascites of both study groups. Urokinase‐type plasminogen activator antigen was detectable neither in ascites of malignant nor in ascites of non‐malignant origin. It is concluded that t‐PA is the physiological plasminogen activator in ascites and that increased PAI levels followed by increased complex formation between t‐PA and PAI might reflect a reaction of the peritoneum.