Fibrinolytic activity ofascites caused byalcoholic cirrhosis andperitoneal malignancy

isa wellrecognised complica- tionofperitoneovenous shunting forascites. Therelative contributions ofprimary fibrino- lysis anddisseminated intravascular coagula- tionremaincontroversial. Plasminogen activating activity was significantly lowerin malignant ascites (n=10, median<0.02(range <0-02-1-26) IU/ml) thaninalcoholic 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 andplasminogen activator inhibitor-i. There was no significant difference between thetwo groupsintheconcentration oftissue plasmin- ogen activator (34(12-64) ng/ml inmalignant ascites v29(12-43) ng/ml inalcoholic ascites), buttheconcentration ofplasminogen activator inhibitor-i was significantly higher inmalig- nantascites (736(213-1651) ng/ml) thanin alcohol ascites (29(12-43) ng/ml) (p<0-05). Malignant ascites contained significantly higher concentrations ofurokinase (07(<01- 1.3) ng/ml v 02(<0.1-0.6) ng/ml inalcoholic ascites) andplasminogen activator inhibitor-2 (33(<6-140) ng/ml v9(<6-28) ng/ml alcoholic ascites). Theplasminogen activating activity ofalcohol ascites may lead toprimary fibrino- lysis after peritoneovenous shunting. Thecon- siderably loweractivity foundinmalignant ascites may explain whycoagulopathy after shunting islesspronounced inthis group of patients. (Gut 1993; 34:1120-1122)