Systemic Thromboembolism in Inflammatory Bowel Disease: Mechanisms and Clinical Applications

Abstract

Systemic thromboembolism is an extraintestinal manifestation of inflammatory bowel disease (IBD), and an important cause of patient morbidity and mortality. The underlying basis for the hypercoagulable state in IBD is complex, and involves altered activity of all three components that govern hemostasis: platelets, fibrinolysis, and the coagulation cascade. Currently, there are no distinct guidelines for treating or preventing thromboembolic (TE) events in IBD patients compared with the general population. However, the prothrombotic state in IBD stems, at least in part, from several modifiable factors, such as hyperhomocysteinemia and an active inflammatory state. In this review we summarize the mechanisms that favor thrombosis in IBD, and the principles that need to be applied for the primary and secondary prevention of TE in this selected group of patients.

Cerebral venous thrombosis and heparin-induced thrombocytopenia in an 18-year old male with severe ulcerative colitis

“…TE can also occur in the pediatric age group [15] . The potential mechanisms underlying the prothrombotic state in IBD are hypercoagulation (elevated FⅧ, fibrinogen, decrease in antithrombin, protein S and protein C ), hypofibrinolysis [elevated PAI-1 and lipoprotein (a)], platelet abnormalities, endothelial dysfunction (increased von Willebrand factor) and immunological abnormalities (antiphosphlipid antibodies) [14,16] . The common genetic risk factors for TE factor Ⅴ mutation (Factor Ⅴ Leiden) and prothrombin mutation (G20210A) are not overrepresented in patients with TE and IBD compared to other patients with TE [16] .…”

“…The increased risk of thromboembolism (TE) in patients with active IBD is well established [9][10][11][12][13] with a 6.5% incidence of thrombosis or a 3-4 fold higher risk than in the general population [14] . TE can also occur in the pediatric age group [15] .…”

An Unusual Case of Acute Abdominal Pain

“…Portal vein thrombosis often leads to severe sequelae such as portal hypertension, which in turn increases the risk of bleeding because of both esophageal varices and hypersplenism-related thrombocytopenia (Martinelli et al, 2008). Indeed, the decision on the duration of oral anticoagulation should be individually tailored (Kappleman et al, 2011, Twing et al, 2005 according to the risk/benefit ratio due to presence or absence of major risk factors for bleeding or recurrent thrombosis (De Stefano et al, 2010). bleeding risk is low or absent, anticoagulant therapy should be continued until vessel recanalization is documented.…”

“…This extraintestinal manifestation is an important cause of mortality in patients with IBD (Quera et al, 2004, Twing et al, 2005, and Hatoum et al, 2005. This rare condition, at least in noncirrhotic patients, infrequently involves uncommon sites as the splenic-mesentericportal vein system and may be associated with severe morbidity and mortality (Guglielmi et al, 2005).…”

Neurological Manifestations of Inflammatory Bowel Disease

“…Nevertheless, the use of steroids, dehydration, the increase of homocysteine and infections (all of which are associated with relapsing periods) may also contribute to the development of thrombotic complications [10][11][12][13]16]. Furthermore, the presence of mutations in Leiden factor V in IBD patients leads to a higher incidence of thrombotic events [17].…”