alpha 2 Antiplasmin and disseminated intravascular coagulation in liver cirrhosis.
Subnormal concentrations of alpha 2 Antiplasmin (alpha 2 AP) 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) alpha 2 AP 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 alpha 2 AP and FPA were equally abnormal in compensated and decompensated cirrhosis. The significant negative correlation obtained between alpha 2 AP and FPA as well as the lack of correlation between alpha 2 AP and albumin, alpha 2 AP and p-CHE in both groups suggests that, in our patients, alpha 2 AP 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: alpha 2 AP in subgroups with high FPA was significantly different from controls while it did not differ in subgroups with normal FPA.
D000328:Adult; D002802:Cholinesterases / Q000097:blood; D004211:Disseminated Intravascular Coagulation / Q000097:blood / Q000150:complications*; D005260:Female; D005342:Fibrinolysis; D005344:Fibrinopeptide A / Q000032:analysis; D006801:Humans; D008103:Liver Cirrhosis / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012709:Serum Albumin / Q000032:analysis; D000979:alpha-2-Antiplasmin / Q000032:analysis*
D012709:Serum Albumin; D000979:alpha-2-Antiplasmin; D005344:Fibrinopeptide A; D002802:Cholinesterases