Hypercoagulability observed in patients with inflammatory bowel diseases(IBD)may lead to thromboembolic events(TE),which affect the venous and arterial systems alike and are an important factor in patients’morbidity and mortality.The risk of TE in IBD patients has been demonstrated to be approximately threefold higher as compared to the general population.The pathogenesis of thrombosis in IBD patients is multifactorial and not fully explained.The most commonly listed factors include genetic and immune abnormalities,disequilibrium between procoagulant and anticoagulant factors,although recently,the role of endothelial damage as an IBD-triggering factor is underlined.Several studies report that the levels of some coagulation enzymes,including fibrinogen,factorsⅤ,Ⅶ,Ⅷ,active factorⅪ,tissue factor,prothrombin fragment 1+2and the thrombin-antithrombin complex,are altered in IBD patients.It has been demonstrated that there is a significant decrease of tissue plasminogen activator level,a marked increase of plasminogen activator inhibitor type 1 and thrombin-activable fibrinolysis inhibitor,a significantly lower level of antithrombinⅢand tissue factor pathway inhibitor.IBD patients have been also observed to produce an increased amount of various anticoagulant antibodies.Hyperhomocysteinemia,which is a potential risk factor for TE was also observed in some IBD patients.Further studies are necessary to assess the role of coagulation abnormalities in IBD etiology and to determine indications for thromboprophylactic treatment in patients at high risk of developing TE. Hypercoagulability observed in patients with inflammatory bowel diseases (IBD) may lead to thromboembolic events (TE), which affect the venous and arterial systems alike and are an important factor in patients’morbidity and mortality. The risk of TE in IBD patients has been demonstrated to be approximately threefold higher as compared to the general population. The pathogenesis of thrombosis in IBD patients is multifactorial and not fully explained. the most regularly listed factors include genetic and immune abnormalities, disequilibrium between procoagulant and anticoagulant factors, although recently, the role of Endothelial damage as an IBD-triggering factor is underlined. Seral studies report that the levels of some coagulation enzymes, including fibrinogen, factors V, VII, VIII, active factor XI, tissue factor, prothrombin fragment 1 + 2 and the thrombin-antithrombin complex, are in IBD patients. Having has been been demonstrated that there is a significant decrease of tissue plasminogen activator le vel, a marked increase of plasminogen activator inhibitor type 1 and thrombin-activable fibrinolysis inhibitor, a significantly lower level of antithrombin III and tissue factor pathway inhibitor. IBD patients have been also observed to produce an increased amount of various anticoagulant antibodies. Hyperhomocysteinemia, which is a potential risk factor for TE was also observed in some IBD patients. Future studies are necessary to assess the role of coagulation abnormalities in IBD etiology and to determine indications for thromboprophylactic treatment in patients at high risk of developing TE.