DECREASED CONTACT FACTOR-MEDIATED FIBRINOLYSIS IN CIRRHOSIS

We studied extrinsic and intrinsic fibrinolysis in 20 patients with ci rrhosis (nine mild/moderate, group 1; 11 severe, group 2) and 19 norma l controls to define the role of intrinsic (contact factor mediated) f ibrinolysis in cirrhosis. Global plasma fibrinolytic activity (fibrin plate lysis) was similar in all groups. Dextran sulphate activated con tact factor mediated fibrinolysis was decreased in group 2 (median 95. 2%) compared with group 1 (121.0%) and controls (131.7%). Tissue plasm inogen activator antigen (t-PA Ag) levels were increased in group 2 (2 8.2 ng/ml) compared both with group 1 (8.5 ng/ml) and controls (5.9 ng /ml). Plasma t-PA activity was raised in group 2 (5.50 IU/ml) and grou p 1 (5.25 IU/ml) versus controls (0.82 IU/ml). Plasminogen activator i nhibitor-1 (PAI-1 Ag) levels were raised in group 2 (28.0 IU/ml) versu s controls (8.5 IU/ml) but PAI activity was similar in all groups. Fac tor XH activity was decreased in group 2 (48.76 u/dl), but not group 1 , versus controls (89.1 u/dl). Prekallikrein activity was decreased bo th in group 2 (27.27 u/dl) and group 1 (33.01 u/dl) versus controls (1 08.59 u/dl) and was lower in group 2 than group 1. C1-esterase inhibit or chromogenic activity was decreased in group 1 (102.30 u/dl) and gro up 2 (58.76 u/dl) versus controls (116.24 u/dl). The normal global fib rinolytic activity despite increased t-PA activity may be due to a con comitant increase in PAI. The decreased intrinsic fibrinolysis in seve re cirrhosis, unaccompanied by a rise in C 1 -esterase inhibitor, may be explained by the decreased factor XII and prekallikrein activity. T hese changes are probably due to reduced liver cell mass.