Abstract
Abnormal fibrinogen in patients with liver diseases, especially severe liver cirrhosis was studied. In these patients, the prolonged thrombin time, the prolonged reptilase time, and the delayed polymerization of fibrin monomer were observed in plasma. These findings suggested the dysfunction of fibrinogen which was related closely to the disability of polymerization of fibrin monomer.
Similar results were identified by using purifired abnormal fibrinogen. From this results, the involvement of the inhibitors againt coagulation in plasma appeared to be unlikely. The total content of sialic acid in purified abnormal fibrinogen was markedly increased as compared to that in purified nomal fibrinogen. Since the prolonged thrombin time was statistically significantly (p<0.01) correlated with the total content of sialic acid in fibrinogen, it may be suggested that sialic acid plays a great role in the dysfunction of abnormal fibrinogen.
To determine whether sialic acid can block the polymerization of fibrinogen monomer, or not, asialofibrinogen was obtained from the purified fibrinogen treated with neuraminidase. When coagulation time was examined by using asialofibrinogen obtained by neuraminidase treatment, the prolonged coagulation time was partially normalized in 3 patients with liver cirrhosis tested. Thus, it was suggested that sialic acid might block the polymerization of fibrin monomer, resulting in the dysfunction of fibrinogen.
