FIBRINOLYTIC-ACTIVITY OF ASCITES CAUSED BY ALCOHOLIC CIRRHOSIS AND PERITONEAL MALIGNANCY

Coagulopathy is a well recognised complication of peritoneovenous shun ting for ascites. The relative contributions of primary fibrinolysis a nd disseminated intravascular coagulation remain controversial. Plasmi nogen activating activity was significantly lower in malignant ascites (n=10, median <0.02 (range <0.02-1.26) IU/ml) than in alcoholic ascit es (n=10, 1-07 (0.30-1.49) IU/ml) (p<0.05). Fibrinolytic activity was determined by a balance between tissue plasminogen activator and plasm inogen activator inhibitor-1. There was no significant difference betw een the two groups in the concentration of tissue plasminogen activato r (34 (12-64) ng/ml in malignant ascites v 29 (12-43) ng/ml in alcohol ic ascites), but the concentration of plasminogen activator inhibitor- 1 was significantly higher in malignant ascites (736 (213-1651) ng/ml) than in alcohol ascites (29 (12-43) ng/ml) (p<0.05). Malignant ascite s contained significantly higher concentrations of urokinase (0.7 (<0. 1-1.3) ng/ml v 0.2 (<0.1-0.6) ng/ml in alcoholic ascites) and plasmino gen activator inhibitor-2 (33 (<6-140) ng/ml v 9 (<6-28) ng/ml alcohol ic ascites). The plasminogen activating activity of alcohol ascites ma y lead to primary fibrinolysis after peritoneovenous shunting. The con siderably lower activity found in malignant ascites may explain why co agulopathy after shunting is less pronounced in this group of patients .