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.