Fibrinogen-bound sialic acid levels were determined in 75 normal controls and 80 patients with liver disease. Patients with abnormal fibrin monomer polymerisation (FMP) had sialic acid levels significantly higher than controls or patients with normal FMP. Enzymatic removal of sialic acid from the abnormal fibrinogens corrected the abnormal FMP and thrombin-clotting times to the range of desialated controls. The accelerating effects of calcium ions, protamine sulphate and Polybrene were largely abolished by desialation, suggesting that these cations accelerate FMP by neutralising the negativity charged sialic acid residues.