[Hemostatic studies on acquired abnormal fibrinogenemia in severe liver diseases and umbilical cord blood].

An abnormal fibrinogen in patients with liver diseases, especially liver cirrhosis and hepatocellular carcinoma was examined. In these patients, delayed polymerization of fibrin monomer, which was useful for detecting abnormal fibrinogen in plasma and also detecting one of liver dysfunctions, was observed. Same results were found by using purified abnormal fibrinogen from these patients. However, according to electrophoretic and immunochemical studies, no difference were shown between purified abnormal fibrinogen and purified normal fibrinogen. The total content of sialic acid in purified abnormal fibrinogen was markedly increased as compared to that in purified normal fibrinogen. When coagulation time was examined by using asialofibrinogen treated with neuraminidase, the prolonged coagulation time was partially normalized even in patients with liver cirrhosis. These findings suggested that sialic acid might affect the polymerization of fibrin monomer. It was reported by Harvey (1978) that an abnormal fibrinogen in liver diseases was similar to the fetal fibrinogen in the content of sialic acid and prolongation of thrombin time. Therefore, purified fibrinogen from umbilical cord blood was also investigated by similar methods. Consequently, it was suggested that a dysfunction of fibrinogen in umbilical cord blood was not related to molecular abnormality, but some inhibitory mechanisms which caused the abnormal pattern of coagulation might be existed.