P350 Induction of antiphospholipid antibodies in patients with inflammatory bowel disease treated with anti-TNFα agents

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Background: Anti-tumor necrosis factor alpha drugs (antiTNFα) can induce the production of autoantibodies, mainly anti-nuclear antibodies (ANAs) and anti-dsDNA. There are limited data on the induction of other antibodies such as antiphospholipid antibodies (APLs) or the development of antiphospholipid syndrome in patients receiving such agents. Our aim was to determine the presence of antiphospholipid antibodies in a cohort of Inflammatory Bowel Disease (IBD) patients receiving treatment with an antiTNFα.

Methods: We performed a longitudinal study in IBD patients that were scheduled to start treatment with an antiTNFα agent. Coagulation tests were determined prior to drug initiation and at each monitoring visit (every 8 to 12 weeks). If activated partial thromboplastin time (aPTT) without prolongation of prothrombin time was identified, the result was confirmed in a second analysis. If prolongation of aPTT was established, then lupus anticoagulant (LAC), anticardiolipin antibodies (aCL) and anti-β2-glycoprotein (aβ2GPI) were determined. Time from start of antiTNFα to the first prolonged aPTT was recorded. Clinical data including a history of thrombosis and abortions were collected. Results were expressed as medians, percentages and percentiles. Fisher's exact test was used for categorical variables, and Mann-Whitney U for quantitative variables. Statistical significance was determined with a double-tailed p-value of <0.05.

Results: Two-hundred and eighty-eight patients with IBD were included. Age at inclusion was 40 years [32–50], 48% were women and 75% had a diagnosis of Crohn's disease. Out of the cohort, we identified 23 patients (8%) with prolongation of aPTT, with a median of 63 months [35–84] from the start of the antiTNFα until the alteration was found. Seventy percent of these patients were women (p=0.048, OR: 2.66, 95% CI: 1.09–6.5), 68% (n=15) had positive LAC, 22% (n=5) were aCL positive and 17% (n=4) had a positive aβ2GPI. Additionally, 80% had positive ANAs and 43% anti-dsDNA. No patient fulfilled criteria for antiphospholipid syndrome. There were no differences in type of IBD, duration, location or behavior of the disease, concomitant treatment and type of antiTNFα agent between patients with or without aPTT prolongation.

Conclusions: Antiphospholipid antibodies can be induced in IBD patients that are receiving treatment with antiTNFα drugs. It would be reasonable to include coagulation studies at the start and follow-up of patients receiving antiTNFα treatment and to evaluate for the presence of antiphospholipid antibodies.

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