fibrinopeptide-a and Ascites

Ascitic fluid reinfusion in severe cirrhosis has frequently been associated with intravascular coagulation (DIC). A low-grade DIC has been postulated to be present in liver cirrhosis. PT, APTT, fibrinogen, plasminogen, antiplasmin, fibrin degradation producers (FDP), euglobulin lysis time, tissue plasminogen activator, and fibrinopeptide A were investigated both in the plasma and ascitic fluid of cirrhotic patients before and after the concentration-reinfusion technique. Our results indicate that increased thrombin formation associated with hyperfibrinolysis is present in the plasma of cirrhotic patients. In ascitic fluid very high levels of thrombin and fibrinolysis activation were found. We conclude that (1) a DIC-like picture exists in ascites and (2) after ascites reinfusion procedures, ascitic fluid is the principal factor in the pathogenesis of DIC. During ascitic fluid reinfusion heparin treatment could be used successfully.

Topics: Aged; Ascites; Disseminated Intravascular Coagulation; Female; Fibrin; Fibrinogen; Fibrinopeptide A; Humans; Liver Cirrhosis; Male; Middle Aged; Partial Thromboplastin Time; Plasminogen; Prothrombin Time; Reference Values; Tissue Plasminogen Activator

Ascitic fluid from patients with ovarian cancer contains high levels of fibrin(ogen) degradation products (FDP). Crosslinked fibrin derivatives were isolated by precipitation and separated by PAA-gel-electrophoresis. In order to evaluate the submolecular structure the total precipitate and single derivatives were investigated after cleavage of the disulfide bonds. The findings are related to the radioimmunological measurements of certain fibrinopeptides. Tumor ascites contains approximately ten times higher levels of crosslinked fibrin derivatives than cirrhosis ascites. The fibrinopeptide A content is similar, whereas the levels of plasmin-induced alpha-chain fragment are significantly higher in tumor ascites. The findings suggest a catabolism of fibrinogen in ascitic fluid via coagulation and fibrinolysis. In tumor ascites fibrinogen is catabolized to a significantly higher degree via the degradation of crosslinked fibrin. Crosslinked fibrin derivatives may therefore be usable as non-carcinoembryogenic tumor markers.

Topics: Ascites; Ascitic Fluid; Female; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinopeptide A; Humans; Liver Cirrhosis; Ovarian Neoplasms