Thrombotic mechanism in inflammatory bowel disease patients is complex, multifactorial and not fully understood. Acquired risk factors for thrombosis, often present in inflammatory bowel disease patients, only partially explain increased thrombotic risk. No relevant association has been found regarding genetic pro-thrombotic risk factors in ulcerative colitis or Crohn’s disease patients. Furthermore, many quantitative and qualitative alterations in single components of cascade factors, fibrinolytic system and natural anticoagulants has been found, but none of these were sufficient enough to explain increased thromboembolic risk. It seems to be the case that maintaining pro-thrombotic tendency in this context is multifactorial, thus coagulation components and their inhibitors, as well as hemostatic relevant cells as platelets and endothelial cells, interact in a context of inflamed mucosa that is chronically activated and contributes to maintain chronic inflammation as well. In turn, inflammatory molecules and cytokines have been demonstrated to imbalance the haemostatic system towards hyper-coagulability. The two complex mechanisms of inflammation and coagulation deeply interact in IBD mucosa amplifying and potentiating each other.
Chung, Wei-Sheng, et al. “Inflammatory bowel disease increases the risks of deep vein thrombosis and pulmonary embolism in the hospitalized patients: a nationwide cohort study.” Thrombosis research 135.3 (2015):492-6.
Inflammatory bowel disease affects more than 2 million people in Europe, with almost 20% being diagnosed in pediatric age. Patients with inflammatory bowel disease are at increased risk of thromboembolic complications which may affect patients’ morbidity and mortality. The risk of the most common thromboembolic events, such as deep venous thrombosis and pulmonary embolism, are estimated to be three-fold increased compared to controls. Moreover, patients with ulcerative colitis and Crohn’s disease experience thromboembolic events at a younger age compared to general population. Many factors have been investigated as determinants of the pro-thrombotic tendency such as acquired risk factors or genetic and immune abnormalities, but a unique cause has not been found.
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