DYSFIBRINOGENEMIA ASSOCIATED WITH HEPATOMA - INCREASED CARBOHYDRATE CONTENT OF FIBRINOGEN MOLECULE

Abnormal coagulation studies indicative of a dysfibrinogen were found in the plasma of four of seven patients with malignant hepatoma. The abnormal fibrinogen was characterized by prolonged prothrombin, thrombin and reptilase times and inhibition of the coagulation of normal plasma. Purified fibrinogen revealed abnormalities similar to those in plasma. The functional defect was one of delayed polymerization of the fibrin monomer. The carbohydrate content of the abnormal fibrinogen was increased, and this change was related to the abnormal fibrinogen function. Enzymatic cleavage of sialic acid from the abnormal fibrinogen restored fibrinogen function to normal. This hepatoma-associated dysfibrinogen (acquired dysfibrinogenemia) is similar in many respects to fetal fibrinogen and may represent the presence of a fetal form of fibrinogen in hepatoma. (N Engl J Med 299:221–226, 1978) CONGENITAL dysfibrinogenemia is a well recognized disorder, but acquired dysfibrinogenemia has only recently been recognized. Acquired dysfibrinogenemia has been reported with primary hepatoma, 1 2 3cancer metastatic to the liver4 and acute and chronic hepatic disease.5 6 7 8 It is not clear from previous reports whether the acquired dysfibrinogenemia in these states is related to proteolysis of fibrinogen and the presence of fibrinogen degradation products, to increased inhibitors to fibrinogen-fibrin conversion other than degradation products, or to the presence of an abnormal fibrinogen molecule. We report below on the dysfibrinogenemia found in four of seven patients with primary hepatoma, and present evidence that the. © 1978, Massachusetts Medical Society. All rights reserved.