Background and aims. Chronic hyperactivation of the clotting and fibinolytic systems, likely triggered by gut-absorbed bacterial substances, haracterizes patients with advanced cirrhosis. However, it is unknown hether the cause is a decreased liver function or the direct pass of these ubstances into the systemic circulation through portosystemic collaterals. ince collaterals persist years after liver transplantations (LT), whereas liver unction is quickly restored, the haemostatic pattern was investigated after uccessful LT. Patients and methods. In 22 LT recipient free from current infections r rejection, we measured the following parameters at 3–12 months after T: thrombin–antithrombin III complex (TAT), D-dimer levels, antithromin III activity (AT III), tumour necrosis factor (TNF) and lipopolysaccharide LPS) levels, to investigate the presence of a procoagulative state secondary o bacteriemia. Moreover, we evaluated tissue plasminogen activator (tA), t-PA inhibitor 1 (PAI-1) levels and thrombin activable fibrinolysis nhibitor activity (TAFIa) to assess the persistence of an excessive fibriolysis. The same parameters were measured in 53 blood donors (BD) nd 76 cirrhotic patients (36 in Child-Pugh-Turcotte class A, 40 in CPT lass B–C). Results. TAFI, PAI and t-PA levels were significantly higher in LT than n cirrhotic patients (p< 0.01), but in both groups they were lower than in BD p< 0.01). AT III levels were increased in LT compared to the cirrhotic group p< 0.001) and was similar to BD. LPS (p< 0.05) and TNF (p< 0.001), but ot TAT levels, were higher in LT and in decompensated cirrhotics compared o BD, whereas no significant difference was evident for TAT, LPS and TNF evels between LT and decompensated cirrhotics. D-dimer decreased in LT roup compared to cirrhotics (p< 0.01) but still remained higher compared o BD (p< 0.01). Conclusion. The present study provides evidence of a partial correction f the clotting and fibrinolytic state by LT and shows signs of persistent pass f gut-adsorbed material through portosystemic collaterals (i.e. persistent ncreased LPS and TNF circulating levels in LT), which appears therefore o play a role, together with liver failure in the haemostatic derangement of dvanced cirrhosis.