Platelet aggregation and coagulation and fibrinolysis parameters in both portal and systemic circulations in patients with cirrhosis and hepatocellular carcinoma

A tendency to bleed and local vasodilation in the portal circulation are ex acerbatory clinical factors in patients with liver cirrhosis. Esophageal va riceal bleeding, in particular, is a frequent complication in these patient s. Cirrhotic patients have been reported to show impairment of platelet agg regation and an activated fibrinolytic state, possibly with consequential l engthening of the bleeding time. Our previous study has demonstrated enhanc ed generation of PGI,, a vasodilating and anti-platelet aggregating hormone , ill the portal circulation of cirrhotic patients. In the present study, w e compared the platelet aggregation and coagulation and fibrinolytic profil es in portal circulation with those in systemic circulation in twenty cirrh otic patients complicated with hepatocellular carcinoma. A portal blood sam ple was collected through a fine needle inserted percutaneously and guided ultrasonographically to the intrahepatic portal vein. Simultaneously, venou s blood was drawn from a forearm vein as the systemic blood sample. Coagula tion and fibrinolytic profiles were assessed by examining the extrinsic fib rinolytic system (tissue plasminogen activator (tPA), t-PA-plasminogen acti vator inhibitor complex), fibrinogen degeneration product, fibrinogen euglo bulin lysis time, platelet count, and platelet aggregation elicited by ADP and collagen. Although fibrinolytic factors were activated in patients in t he present study, there were no significant differences between the portal and systemic blood samples in all the coagulation and fibrinolytic paramete rs examined except for platelet aggregation. The curve of platelet aggregat ion response to collagen (1, 2, 10 mug/ml), but nor that to ADP, shifted si gnificantly more to the right in the portal blood compared to the systemic blood (P < 0.05). This result suggested that the difference in prostaglandi n generation reported previously, may cause the dissociation between collag en and ADP elicitation of platelet response in portal blood while there is no effect on other parameters in the coagulation and fibrinolytic profiles. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.