Dysfibrinogenemia in a Patient with Primary Hepatoma

In a female patient with hepatoma and a prolonged thrombin time, the coagulation defect was shown to be localized in the phase of fibrin monomer aggregation. The defect fulfilled all the preliminary laboratory criteria of the congenital dysfibrinogenemias. Exogenous inhibitors and fibrinolysis were excluded. Since no evidence for inheritance of the abnormality was found, it is suggested that the defect was acquired and that an abnormal fibrin monomer fraction was interfering with the aggregation of normal fibrin monomers. The abnormal fibrinogen is most probably synthesized by the hepatoma.