P303. Anticardiolipin antibodies as potential serologic markers of thrombosis risk in IBD patients; a pilot study in referral IBD center
M. Crncevic Urek1, M. Majerovic1, S. Cukovic-Cavka1, L. Banfic2, R. Zadro3, M. Brinar1, N. Turk1, Z. Krznaric1, B. Vucelic1, 1Department of Internal medicine, Division of Gastroenterology and hepatology, 2Department of Cardiovascular Diseases, 3Department of laboratory diagnostics, Clinical unit for special and molecular hematology, University Hospital Center Zagreb, Zagreb, Croatia
Anticardiolipin antibodies (ACA) are important serologic markers of several autoimmune diseases, but also may be elevated in other chronic inflammatory states. Available studies vary in assessment of ACA in inflammatory bowel disease, but the true prevalence of ACA in IBD patients (pts) remains unclear. In this study we evaluated the prevalence of ACA in IBD pts with thromboembolic complications (TE), frequently associated with IBD.
The clinical background of 49 IBD patients with active disease –32 (65%) with Crohn's disease (CD) and 17 (35%) with ulcerative colitis (UC) were analysed prospectively. The diagnosis of TE was confirmed in 9 pts with color doppler ultrasound or CT angiography. Following serologic and genetic prothrombotic risk factors were evaluated in all patients: ACA IgG class (ELISA), Factor V Leiden (FVL) and prothrombin gene factor 20210A (Fll). ACA were grouped as followed: >15 – high positive level; 10–15 equivocal; <10 negative. Patients were phenotyped according to Montreal classification, and disease activity by Crohn's disease activity index (CDAI) and combined clinical and endoscopic criteria for UC patients.
There were 9 pts (19%) with TE complications in our IBD cohort; among them 7 CD pts (2 pts L2, 4 pts L3, 1 L4) and 2 UC pts with pancolitis. Localisation of TE was as follows: deep vein leg thrombosis had 5 pts and pulmonary TE 4 pts. ACA positivity was defined with a cut off value of 10. ACA IgG was positive in 67% pts with thrombosis, meanwhile in non-thrombosis IBD group ACA was positive in 48%. The level of ACA positivity in IBD-thrombosis group were as follows: high-level positivity was found in 45% pts (3 CD pts, 1 UC patient), equivocal positivity in 22% (1 CD-L4, 1 extensive UC), 3 pts (33%) had negative ACA. In IBD non-thrombosis group (12 CD, 5 UC pts) high level positivity was found in 35% of pts, equivocal positivitiy in 12.5% (5 pts). 53% pts in IBD non-thrombosis group were ACA negative. Only one patient in IBD-thrombosis group had positive Fll. The mean age of TE in high and equivocal ACA group patients was 36 yrs.
The overall positivity of ACA in IBD thrombosis group was 67%. Thrombosis in IBD with ACA positivity was especially present in young patients with serious forms of IBD. There was no association between genetic markers of thrombophilia and risk of IBD-thrombosis. These results suggest the potential role of ACA as a prothromobtic serologic marker of thrombosis risk in IBD, and future investigation in this field should be suggested.