Alpha2-Antiplasmin deficiency as a risk factor for bleeding from esophageal varices

ABSTRACT

The coagulation state and alpha [2] antiplasmin level and their relation to the degree of hepatic dysfunction were evaluated in 16 patients with bleeding esophageal varices and 10 healthy controls. Prothrombin time [P.T.], partial thromboplastin time [P.T.T.] and thrombin clotting time were significantly prolonged in bleeders compared to controls [P<0.01], P.T.T prolongation was more pronounced in ascitic than non-ascitic bleeders. Fibrinogen was normal in both bleeders and controls but its level was significantly lower in ascitic than non-ascitic bleeders [P<0.01]. Alpha [2] antiplasmin level was significantly lower in bleeders than controls [P<0.01] and within the bleeder group, it was significantly lower in ascitic than non-ascitic bleeders [P<0.01]. This low level was associated with positive fibrin degradation products and normal platelet count in 6 patients [4 with ascites] pointing to its responsibility for the hyperfibrinolytic state occurring in such patients. Alpha [2] antiplasmin level and fibrinogen were inversely correlated with liver function tests [SGOT, SGPT, alkaline phosphatase and total bilirubin]. It is concluded that hepatic dysfunction adversely affects blood coagulation resulting in aggravation of bleeding from esophageal varices. The decrease of synthesis of alpha [2] antiplasmin may be responsible for aggravating bleeding. When associated with positive FDP's and normal platelet count, antifibrinolytic agents may be considered as potential therapeutic agents