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* = Presenting author

P097 The Thromboembolism in Inflammatory Bowel Disease - apropos of 28 cases

S. Campos*, A. Oliveira, F. Portela, C. Sofia

Centro Hospitalar Universitário Coimbra, Gastroenterology, Coimbra, Portugal

Background

Patients with Inflammatory Bowel Disease (IBD) have an increased risk of thromboembolism (TE). Estimating the magnitude of this risk is important in the decision to start thromboembolic prophylaxis in patients who are already naturally predisposed to bleeding events.

Objective: Characterization of TE in IBD.

Methods

Retrospective study including all patients with IBD and hospitalization between 01-08-2006 and 31-05-2013 with episodes of thromboembolism, venous/arterial. Characterization of the population by the variables: IBD (diagnosis age, type, location, behavior, therapy), thromboembolic event (diagnosis age, type, location, associated risk factors - surgery / trauma, smoking, hypertension, diabetes mellitus, dyslipidaemia; prophylaxis), complications (recurrence, death to 30days).

Results

We recorded 774 admissions of patients with IBD, 28 (3.6%) with thromboembolic episode - 57% male; mean age 58 ± 17 years (21 % <40 years); average duration IBD 13 ± 13years; Ulcerative Colitis 57% (E1-21%, E2-43% and E3-36%) and 39% with Crohn's disease (L1-70%, L2-10%, L3-20 %, B1-25%, B2-42% , B3-33%). Medication: 5-ASA (57%), thiopurines (23%), corticosteroids (15%), anti-TNF (12%). 17 showed arterial complications (10-ischemic stroke, 6-myocardial ischemia, 1-peripheral arterial ischaemia); 7 had pulmonary thromboembolism, 3 deep vein thrombosis, 1 superior mesenteric vein thrombosis. At least 39% of these patients had active IBD. Six venous complications (54%) and 8 arterial complications (47%) had other concomitant risk factors. One case recurred. No deaths were registered.

Conclusion

The TE in IBD is not uncommon, and arterial events seem to be more frequent. However, the concomitant presence of other risk factors requires further study to ascertain the true role of IBD in the pathogenesis of TE.