ASSOCIATION BETWEEN LOW-GRADE DISSEMINATED INTRAVASCULAR COAGULATION AND ENDOTOXEMIA IN PATIENTS WITH LIVER-CIRRHOSIS

Background and Aims: Hyperfibrinolysis may complicate the clinical cou rse of liver cirrhosis. The aim of this study was to evaluate if, in c irrhosis, hyperfibrinolysis is primary or secondary to intravascular c lotting activation and if endotoxemia is associated with activation of clotting and/or the fibrinolytic system. Methods: Clotting, fibrinoly tic indexes, and endotoxemia were studied in 41. cirrhotic patients an d 20 healthy subjects. Results: Twenty-seven cirrhotic patients (66%) had high plasma levels of prothrombin fragment F1+2, a marker of throm bin generation. Nineteen patients had elevated Values of D-dimer, a ma rker of fibrinolysis in vivo. All patients with high values of D-dimer also had high values of prothrombin fragment F1+2. Endotoxemia was el evated in patients with severe liver failure and significantly correla ted to prothrombin fragment F1+2. Thirty patients were treated for 7 d ays either with standard therapy (n = 15) or with standard therapy plu s nonabsorbable antibiotics (n = 15). Although standard therapy did no t significantly change laboratory indexes, a significant reduction of endotoxemia, prothrombin fragment F1+2, and D-dimer was found in those patients who received the combined treatment. Conclusions: This study shows that, in cirrhotic patients, hyperfibrinolysis is not a primary phenomenon but occurs as a consequence of clotting activation and tha t endotoxemia might play a pathophysiological role.