SUMMARY The activities of Hageman factor, high molecular weight kininogen (HMWK), and prekallikrein were studied in patients who had chronic active hepatitis and cirrhosis. Serum HMWK and prekallikrein activities were decreased in chronic active hepatitis and cirrhosis, but Hageman factor activity was low in cirrhosis only. The reduction of prekallikrein, HMWK, and Hageman factor was dependent on the degree of liver failure. Similar prekallikrein values were found in serum samples, activated or not, with an excess of Hageman factor and HMWK, which suggests that the decrease of prekallikrein in liver disease is not influenced by the simultaneous decrease of Hageman factor and HMWK.Prekallikrein, a protein synthesised by liver cells,, is an activator of intrinsic coagulation and fibrinolytic pathways.2 3 A recent investigation showed that prekallikrein plasma activity is a very sensitive marker of liver failure, making it a potentially useful indicator of liver insufficiency.4The functional assay of prekallikrein requires Hageman factor and high molecular weight kininogen (HMWK), two constituents of the initial coagulation phase that can be reduced in liver failure.5`' In fact, at least 25% of normal Hageman factor activity is necessary for prekallikrein to be converted into kallikrein; HMWK seems to be a cofactor in the initial rate of kallikrein formation.5`As low values of prekallikrein in patients with cirrhosis could be due to low Hageman factor and HMWK activities, we studied the relation between prekallikrein, Hageman factor and HMWK in patients affected by chronic liver disease to evaluate the in vitro influence of Hageman factor and HMWK on prekallikrein activation. Analysis of prekallikrein activity was performed with and without a clotting activator containing an excess of Hageman factor and HMWK.
Material and methods