Patients with inflammatory bowel diseases (IBD) have an increased risk of thrombosis, possibly due to changes in blood cells and molecules involved in hemostasis. They have increased platelet counts and reactivity as well as increased platelet-derived large extracellular vesicles. Coagulation is continuously activated in patients with IBD, based on measured markers of thrombin generation, and the anticoagulant functions of endothelial cells are damaged. Furthermore, fibrinogen is increased and fibrin clots are denser. However, pathogenesis of thrombosis in patients with IBD appears to differ from that of patients without IBD. Patients with IBD also take drugs that might contribute to risk of thrombosis, complicating the picture. We review the features of homeostasis that are altered in patients with IBD and possible mechanisms of this relationship.

炎症性肠病 (IBD) 患者血栓形成的风险增加，这可能是由于参与止血的血细胞和分子发生了变化。它们具有增加的血小板计数和反应性以及增加的血小板衍生的大细胞外囊泡。根据测量的凝血酶生成标志物，IBD 患者的凝血功能持续激活，内皮细胞的抗凝功能受损。此外，纤维蛋白原增加，纤维蛋白凝块更密集。然而，IBD 患者血栓形成的发病机制似乎与非 IBD 患者不同。IBD 患者还服用可能导致血栓形成风险的药物，从而使情况复杂化。我们回顾了 IBD 患者体内平衡改变的特征以及这种关系的可能机制。