Antoni Stadnicki Pages 659 - 669 ( 11 )
Inflammatory bowel diseases (IBD), Crohn’s disease and ulcerative colitis (UC) are idiopathic, intestinal and systemic inflammatory disorders which are immunologically mediated with the activation of plasma proteolytic cascades. The activation of coagulation in IBD is related to the activity and colonic extension of the disease, but may still be persistent in a quiescent stage. Factor XIII seems to be as much a coagulation factor as a connective tissue factor which may contribute to intestinal healing. Fibrinolytic capacity is reduced in systemic circulation of IBD patients. Platelets activation is a feature of IBD which contributes to a pathogenic inflammatory sequel. There is evidence that coagulation activation may in turn mediate and amplify inflammatory cascades in IBD, especially via activating PARs related pathways. The etiology of thromboembolism in IBD seems to be multifactorial but is largely attributable to the coagulation activation and platelet aggregation during systemic inflammation. Thromboembolic (TE) complications in both Crohn’s disease and UC appear to have at least 3-4 fold increased risk of developing compared to control patients. Currently, no single TE laboratory marker has a predictive value, but a recently developed endogenous thrombin potential test may have a potentially predicative value in IBD. At present, no interaction between IBD and inherited factors of thrombophilia has been found. An efficacy of heparin treatment in UC is still controversial, although heparin is safe in UC flare. Prophylactic anticoagulation against TE is currently not fully defined, however, high - risk patients should be considered for using a moderate dose of heparin.
Coagulation, Crohn’s disease, fibrinolysis, heparin, inflammatory bowel disease, platelets, risk factors, thromboembolic complications, ulcerative colitis, thrombin
Department of Basic Biomedical Sciences, Medical University of Silesia, Ul. Kasztanowa 3, 41 - 200 Sosnowiec, Poland.