Blutgerinnungsfaktor XIII und Fibrinstabilisierung

Abstract

Coagulation factor XIII (fibrin stabilizing factor, FSF) is detectable in plasma, platelets, placenta and various tissues. In the activated form FSF has the enzymatic properties of a transglutaminase and is capable of stabilizing fibrin by inducing covalent bondings between fibrin monomers. In patients with congenital factor XIII deficiency or acquired immune inhibitors of fibrin stabilization a severe bleeding tendency is evident. There is not yet enough information available concerning the significance of reduced FSF-activity as cofactor in hemorrhagic diathesis and wound healing disturbances in various disease states. There are some indications from experimental studies that there might be an influence of FSF on tumor growth and metastasis as well as arteriosclerosis. The quantitation of the enzyme by radiological and immunological techniques yield reproducible results. Fibrin in its stabilized or non stabilized form can be discriminated in polyacrylamide gel electrophoresis after reduction of fibrin clots.

Low levels of fibrin-stabilizing factor (factor XIII) in human Plasmodium falciparum malaria: correlation with clinical severity.

“…Here we report that severe untreated falciparum malaria is associated with low plasma levels of coagulation factor XIII, which normally stabilizes fibrin clots by cross-linking fibrin monomers. 13,14 The low factor XIII levels observed in falciparum malaria might be due to proteolytic degradation since they correlate inversely not only with parasitemia, TNF␣ serum concentrations, and disease severity, but also with elevated levels of HNE. Although the plasma levels of other clotting factors can also be low in malaria, [1][2][3]27 they do not seem to correlate inversely with HNE levels.…”

“…[9][10][11] In addition to inducing endothelial damage directly, HNE efficiently degrades coagulation factor XIII, 12 which normally stabilizes fibrin clots by cross-linking fibrin monomers. 13,14 Inactivation of factor XIII by HNE may contribute to hemostatic disorders and organ failure in gram-negative bacterial sepsis, 15,16 as well as to vascular leakage in Purpura Schönlein-Henoch and inflammatory bowel diseases, [17][18][19] in which factor XIII substitution may be beneficial. In guinea pigs, administration of factor XIII can protect from experimentally induced vascular damage.…”

Rheological characterization and dissolution kinetics of fibrin gels crosslinked by a microbial transglutaminase

“…1 A large literature has been devoted to the implication of Factor XIII in the obtaining of and the properties of the fibrin clot in the coagulation process. [2][3][4][5][6][7][8] At a molecular scale, the reactions are well known. The FXIII reaction on fibrin chains proceeds through two mechanisms, a random binding of weakly interacting substrate pairs, i.e., soluble ␥-chain peptides or flexible ␣-chains, and the binding of an oriented ␥-chain pair.…”

The influence of factor XIII on the fibrosing of a nerve anastomosis in the rat

“…The fibrin-stabilizing factor has a molecular weight of 320,000 [6,7,14,28,37,53,63]. Its main actions which we interesting for this study are:…”