Incomplete Fibrin Formation and Highly Elevated Factor XIII Activity in Multiple Myeloma

Abstract

Bleeding is a common complication in patients suffering from multiple myeloma. In some cases a defect in fibrin formation may be a possible cause of hemorrhagic tendency. The defect in fibrin formation, ascertained using polyacrylamide gel electrophoresis, is due to a lack of .alpha.-chain polymerization of fibrin monomers in 5/11 patients with IgG myeloma and in 2/5 patients with IgM paraproteinemia. No disturbed fibrin polymerization could be observed in IgA myeloma (n = 6). Factor XIII concentrations of subunit A and to a lesser extent of subunit S (Laurell technique) were highly elevated in all cases with regular fibrin formation. Comparable values were obtained by measuring the transamidase activity of factor XIII by incorporation of 14C-labeled purtrescin into casein. Levels up to 600% of normal could be recorded. All patients with a lack of .alpha.-chain polymerization had a factor XIII activity within the normal range. Addition of factor XIII concentrate to plasma from patients with defective fibrin formation led in 5/8 cases to a partial cross-linking of .alpha.-monomers. In some cases paraproteins can inhibit the factor XIII and prevent its action on fibrin.