Summary: Inflammatory bowel diseases (IBD), which include Crohn's disease (CD) and ulcerative colitis (UC), are systemic diseases with a predominant intestinal inflammation. Like other diseases with immunological etiology, IBD can coexist with other diseases, including thrombosis. The risk of thromboembolic events (TEEs) is about three times higher in patients with IBD than in the general population. In addition, cardiovascular diseases (CVDs) occur more frequently compared to the general population. The pathogenesis of thrombosis in patients with IBD is multifactorial and not fully understood. Numerous studies have shown qualitative and quantitative abnormalities in the production of prothrombotic, antithrombotic, and fibrinolytic factors in IBD, which favor the occurrence of TEE. In addition, the inflammatory process itself can trigger coagulation, inhibit the fibrinolytic system, and reduce the activity of natural antithrombotic mechanisms. TEEs are often overlooked, as shown by the low diagnosis rate of about 6% in patients with IBD during hospitalization, and are also an important factor in the increased risk of death in these patients. The complexity of the multifactorial mechanisms of TEEs in IBD is the subject of numerous studies, the results of which are presented at regular intervals in consensus reports. The consensus reports aim to define and evaluate the aetiological factors of TEEs in patients with IBD and to provide recommendations for reducing the risk of venous and arterial thrombosis in IBD. Although the international consensus reports recommend antithrombotic prophylaxis in patients with active IBD being hospitalized, many gastroenterologists do not use this prophylaxis, despite studies showing that unfractionated and low-molecular-weight heparin preparations are safe in patients with active IBD. It should be borne in mind that TEEs occur not only in the active phase but also in remission of IBD.