[Fibrinogen Bern I and fibrinogen Bern II: 2 hereditary fibrinogen variants with diverse biochemical properties].

Two inherited fibrinogen variants, fibrinogen Bern I and fibrinogen Bern II, have been partially characterized. The markedly prolonged thrombin clotting times observed with both variants result from impaired fibrin monomer aggregation. Complete correction of this polymerization defect at physiological calcium concentrations has been achieved for fibrinogen Bern I. This variant also exhibits a charge abnormality in the gamma-polypeptide chain, an increased sialic acid content and defective calcium binding by the C-terminal part of the molecule. Fibrinogen Bern II, on the other hand, exhibits a defect which, although located at a site important for polymerization, is not influenced by the binding of calcium ions.