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It has been demonstrated that activated factor XIII may catalyze the formation of covalent cross-links between fibrin and collagen. This is shown by the disappearance of the gamma-gamma dimer band in PAA-SDS gel electrophoresis when fibrinogen is clotted in presence of collagen, factor XIII and Ca ions, and by the binding of labeled fibrinogen. This reaction may explain the outstanding physiological importance of factor XIII.
The fibrin-stabilizing factor (XIII factor of the hemostasis system) was studied in 101 patients with unresolved mechanical jaundice. It was first shown that this disease is characterized by a statistically significant decrease of the FSF to 56-68%. The decrease of the XIII factor is prognostically unfavourable and points to the development of hepatic insufficiency. The experience has shown that in critical patients with the content of FSF lower than 30% it is expedient to perform decompressive procedures such as cholecystostomy, percutaneous transhepatic cholangiostomy, endoscopic papillotomy etc. as well as transfusion of fresh frozen plasma and hemosorption if there is no contraindications. In patients with FSF lower than 50% before operation it is sufficient to perform hemosorption and transfusion of fresh frozen plasma.
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Fibrinogen, the major structural precursor of blood clots, was deglycosylated by peptide-N-(N-acetyl-beta-glucosaminyl)asparagine amidase without denaturation of the polypeptide chains. Deglycosylated fibrinogen behaved normally in clinical coagulation assays, although it is less soluble than normal fibrinogen. However, the turbidity of clots formed from deglycosylated fibrinogen always rose faster and higher than that of clots from normal fibrinogen. Scanning and transmission electron microscopy demonstrated that fibrin made from clots of deglycosylated fibrinogen consisted of thicker, less-branched fiber bundles in a more porous network. Moreover, the degree of lateral aggregation was directly related to clot turbidity and inversely related to branching. Deglycosylation promoted turbidity development, lateral aggregation, and porosity of clots under all conditions tested. All other steps in the coagulation pathways appeared to be unaffected by the absence of carbohydrate. These results suggest that carbohydrate constitutively affects the behavior of deglycosylated fibrinogens by 1) contributing a repulsive force that promotes fibrinogen solubility and limits fibrin assembly and 2) sensitizing fibrin to conditions that influence assembly and clot structure.
Three coagulation tests available in the emergency department are described in this article. Methods, results, and implications in the bleeding patient are reviewed.
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In vitro and in vivo formed fibrin clots were investigated by SDS-PAA gel electrophoresis in regard to the amount and distribution of fibrin subunits. It was found that with decreasing factor XIII levels fewer and shorter alpha-polymers were formed in vitro and more so in the exterior than in the core of a clot. Inversely the concentrations of residual alpha-chains rose. These structural changes already began at factor XIII levels of 50%. gamma-dimer formation was not influenced. Nearly all in vivo thrombi, either arterial or venous, consisted of a normal distribution of subunits, but alpha-polymerization was more extensive in the core than in the exterior parts. A significant impairment of alpha polymerization was found in extravasal clots, but not in thrombi formed during anticoagulant therapy.
A therapeutic concentrate of factor XIII containing both A and B sub-units has been prepared from 300 kg pools of human plasma. The process starts from a cold-ethanol fraction from cryoprecipitate supernatant and therefore does not interfere with the recovery of other clinically valuable plasma proteins. Factor XIII is purified approximately 600-fold from plasma by precipitation with sodium citrate and by the removal of fibrinogen by brief heating. The product has been pasteurised in sorbitol solution to inactivate blood-borne viruses, ultrafiltered to remove sorbitol, adsorbed with bentonite and freeze-dried in a formulation meeting requirements for intravenous injection.
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Thromboembolic diseases are frequent sequelae of surgical interventions. On account of the possible severe effects an aimed prophylaxis of thrombosis in operative medicine is necessary. The classical anticoagulants may be used in surgery, if the adequate possibilities of control are present. The use of heparin in low dosage reduces the expenditure of control. Experiences with an own variant of the heparin treatment are reported in which heparin is applied intravenously. The use of tetracyclines as well as the control of the factor XIII level and, if necessary, substitution of the factor XIII are recommended. When thrombosis in the venous system appeared the conservative methods in comparison to operative thrombectomy are preferred.
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