Thrombin-activatable fibrinolysis inhibitor deficiency in cirrhosis is notassociated with increased plasma fibrinolysis

Background & Aims: The bleeding tendency of patients suffering from cirrhos is is in part ascribed to accelerated fibrinolysis. In this study, the role of the recently discovered inhibitor of fibrinolysis, thrombin-activatable fibrinolysis inhibitor (TAFI) in cirrhosis was examined. Methods: In 64 pa tients with cirrhosis of varying severity, TAFI antigen levels were measure d by enzyme-linked immunosorbent assay and compared with TAFI levels in con trol subjects. Furthermore, a plasma-based fibrinolysis assay was performed in the presence and absence of a specific inhibitor of activated TAFI. Res ults: TAFI levels were decreased in cirrhosis. Mean TAFI levels were 66% in Child's A, 55% in Child's B, 47% in Child's C cirrhosis, and 26% in acute liver failure. Decreased TAFI antigen levels were highly correlated with an tithrombin and alpha (2)-antiplasmin activity levels. Clot lysis times and clot lysis ratio (defined as ratio between clot lysis time in the absence a nd presence of a specific inhibitor of activated TAFI) of cirrhotics were n ot significantly different from healthy controls. Conclusions: Despite decr eased levels of TAFI and other components of the fibrinolytic system, no ev idence of increased plasma fibrinolytic potential in cirrhosis is observed using the plasma-based assay of this study. The reduction of antifibrinolyt ic factors in cirrhosis is compensated by the concomitant reduction in prof ibrinolytics.