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.
Keywords: Coagulation, Crohn’s disease, fibrinolysis, heparin, inflammatory bowel disease, platelets, risk factors, thromboembolic complications, ulcerative colitis, thrombin
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