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

Coagulopathy is a well recognised complication of peritoneovenous shunting for ascites. The relative contributions of primary fibrinolysis and disseminated intravascular coagulation remain controversial. Plasminogen activating activity was significantly lower in malignant ascites (n=10, median <0.02 (range <0.02-1.26) IU/ml) than in alcoholic ascites (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 plasminogen activator inhibitor-1. There was no significant difference between the two groups in the concentration of tissue plasminogen activator (34 (12-64) ng/ml in malignant ascites v 29 (12-43) ng/ml in alcoholic 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 ascites 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 plasminogen activator inhibitor-2 (33 (<6-140) ng/ml v 9 (<6-28) ng/ml alcoholic ascites). The plasminogen activating activity of alcohol ascites may lead to primary fibrinolysis after peritoneovenous shunting. The considerably lower activity found in malignant ascites may explain why coagulopathy after shunting is less pronounced in this group of patients.