Dae Sung Kim, Won Moon
Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is associated with a hypercoagulable state that increases thromboembolic complication risk. The interaction between inflammation and coagulation increases risk by upregulating coagulation factors, downregulating natural anticoagulants, and impairing fibrinolysis. Patients with IBD exhibit elevated levels of prothrombotic markers, including thrombin-antithrombin complexes, von Willebrand factor, and tissue factor, reflecting persistent coagulation activation. Furthermore, platelet abnormalities, such as thrombocytosis, enhanced platelet reactivity, and increased platelet-leukocyte aggregates, contribute to the prothrombotic state. Impaired fibrinolysis, characterized by elevated plasminogen activator inhibitor-1 (PAI-1) and decreased urokinase plasminogen activator (uPA) levels, results in reduced clot degradation and prolonged thrombus stability. Endothelial dysfunction and immune-mediated disruptions in anticoagulant pathways also exacerbate coagulation abnormalities. The thromboembolic risk in patients with IBD is influenced by disease activity, hospitalization, immobility, and specific therapeutic agents. Certain treatments, such as JAK inhibitors, increase the risk, whereas anti-TNF agents may offer protective effects. Given the notable impact of coagulation and platelet dysfunction on IBD pathophysiology and patient outcomes, a comprehensive understanding of these abnormalities is essential to optimize clinical management and reduce critical thromboembolic complications.