Immunochemical characterization of a human antibody to factor XIII.

Antibodies to factor XIII have not been Antisera to ‘yG2, i G3, ‘yG4, ‘yA, ‘yM, previously characterized in detail. An ac‘yD, ‘yE, and k light-chains had no detectquired inhibitor to factor XIII, which develable effect. Preparative zone electrooped in a patient following thrombectomy phoresis revealed the inhibitor to be in for a femoral artery occlusion, has been the cathodal portion of the gamma peak, characterized as to immunoglobulin cornwith moderately restricted electrophoretic position. A highly sensitive monodansylmobility. The factor XIII inhibitor is thus cadaverine assay for factor XIII was characterized as a ‘yGl, X immunoglobulin employed.The inhibitorwas completelyneuand resembles other human antibodies to tralized by antisera specific for the ‘yG clotting factors that are restricted in immuclass, ‘yGl subclass, and X light-chain type. noglobulin composition. F ACTOR XIII, when activated by thrombin, stabilizes the fibrin clot by catalyzing formation of y-glutamyl-c-lysine bridges between fibrin units.1’2 Fibrin, cross-linked by factor XIII, is stable and is insoluble in solutions of 1% monochioroacetic acid and 5 M urea. Fibrin not stabilized by factor XIII is unstable and is soluble in such solutions. Unstable fibrin clots occur in patients with hereditary factor XIII deficiency3 and may be found in patients with liver disease and various hematologic malignancies.4 Recently, acquired inhibitors to factor XIII have been discovered in patients with and without congenital factor XIII deficiency.5’#{176} Some of these inhibitors appear to be specific antibodies to factor XIII,6 although one acquired factor XIII inhibitor has been thought to represent an unusual metabolite of isonicotinic acid hydrazide (INH).7 Factor XIII inhibitors that behave as antibodies have not been characterized in detail as to immunoglobulin content. The characterization of factor XIII inhibitors as antibodies is important from the standpoint of understanding the pathogenesis of their development, the bleeding syndrome resulting from their occurrence, and the possible modes of therapy. Human antibodies to clotting factors, including antibodies to fibrinogen8 and factors V,9 VIII,’#{176}IX,” and XIII,5’6”2 have been described. Many of the acquired human antibodies to clotting factors have been restricted in