α2antiplasmin and disseminated intravascular coagulation in liver cirrhosis

Abstract

Subnormal concentrations of α 2 Antiplasmin ( α 2AP) in liver cirrhosis may be due to an impaired hepatic synthesis and/or to a fibrinolysis activation in disseminated intravascular coagulation (DIC).In order to clarify this problem, in 26 cirrhotic patients (15 compensated and 11 decompensated) α 2AP plasma activity and plasma Fibrinopeptide A (FPA) were measured. Serum albumin, p-Cholinesterase (p-CHE), Fibrinogen and Fibrinogen Degradation Products (FDP) were also carried out. Our data show that α 2AP and FPA were equally abnormal in compensated and decompensated cirrhosis.The significant negative correlation obtained between α 2AP and FPA as well as the lack of correlation between α 2AP and albumin, α 2AP and p-CHE in both groups suggests that, in our patients, α 2AP decrease may be due to a fibrinolysis activation induced by a DIC which appears chronic since Fibrinogen and FDP were normal.These findings are in agreement with the results obtained in the four subgroups a posteriori selected on the basis of FPA levels: α 2AP in subgroups with high FPA was significantly different from con trols while it did not differ in subgroups with normal FPA.