“…Aggregation (Ag) and activation of platelets play a crucial role in myocardial infarction, unstable angina pectoris, and stroke [ 33 ]. Moreover, elevated proinflammatory cytokines in patients with IBD, such as TNF-α and IL-1, can induce changes in endothelial cells, monocytes, macrophages, and platelets, such as upregulation of tissue factor, which binds plasma factor VIIa, resulting in procoagulant activity [ 34 , 35 , 36 ]. In addition, in patients with IBD, decreased levels of protein C and protein S, increased plasma levels of PAI-1, and reduced plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI) were found, indicating the imbalance of fibrinolysis in IBD [ 35 , 37 ].…”