THE ROLE OF SIALIC-ACID IN THE DYSFIBRINOGENEMIA ASSOCIATED WITH LIVER-DISEASE - DISTRIBUTION OF SIALIC-ACID ON THE CONSTITUENT CHAINS

  • 1 January 1983
    • journal article
    • research article
    • Vol. 61  (6) , 1196-1202
Abstract
To further evaluate the role of sialic acid in the dysfibrinogenemia associated with liver disease, the effect of removal of excess sialic acid residues from the fibrinogen of 5 patients with liver disease on the thrombin time and fibrin monomer aggregation was studied. Patient fibrinogens containing 1.4-3.4, residues of sialic acid per molecule in excess of normal controls, with thrombin times 12-22 are longer than normal and with abnormal fibrin monomer aggregation, were stripped of their excess sialic acid by incubation with Vibrio cholerae neuraminidase, followed by rapid removal of the enzyme by antineuraminidase antibody affinity chromatography. These partially desialylated patient fibrinogens, with a normal number of sialic acid residues remaining, exhibited normal thrombin times and normal fibrin monomer aggregations. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis reduced normal, patient and partially desialylated patient (sialyl-3H)-fibrinogen exhibited 60% of the radioactivity in the B.beta. chain and 40% in the .gamma. chain. There was no radioactivity detectable in the A.alpha. chain. These studies provide additional evidence that the increased sialic acid content of the acquired dysfibrinogenemia of liver disease is responsible for its functional defect and that the excess sialic acid is distributied on the B.beta. chain and .gamma. chains of the fibrinogen.

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