P026 Investigating Predictors of Antibodies to Infliximab Formation in Inflammatory Bowel Disease – The Importance of Immunomodulators

Abstract

BACKGROUND: Anti-tumor necrosis factor (TNF)-α have revolutionized the treatment of inflammatory bowel diseases (IBD), modifying their natural history. Loss of response to anti-TNFs is a clinical challenge and has been associated with formation of antibodies. AIM: To identify predictive factors of antibodies to infliximab (ATI) formation in IBD patients. METHODS: Retrospective single-center study including all consecutive IBD patients being treated with infliximab with at least one ATI and infliximab level determination and with a minimum follow-up of six months after the first testing. Presence of ATI was considered if at least one determination was positive during the follow-up and infliximab levels at this testing were registered. Clinical and demographic data obtained included disease phenotype, surgical background, duration of infliximab therapy, use of premedication, concomitant immunomodulator therapy at the time of testing, compliance, occurrence of an infusion reaction and biochemical assessment at the time of first induction treatment. RESULTS: 104 patients were included, 56 females (53.8%) with mean age of 38.2 ± 13.1 years. The overall prevalence of detectable ATI was 28.8% (30) and the mean time to its formation was 32.8 ± 24.3 months. Most (66.7%) patients with ATI had simultaneously nontherapeutic levels of infliximab. Patients treated with concomitant immunomodulators were less likely to develop ATI (33% versus 88%, P < 0.001). Additionally, it was found that patients with Ulcerative Colitis (UC) were more likely to have detectable ATI than those with Crohn Disease (CD) (44.4% vs 23.4%, P = 0.04). However, UC patients were less treated with concomitant immunomodulators (48.1% vs 80.5%, P = 0.001). At logistic regression analysis only lack of immunomodulator use (P < 0.001; OR 13.5, CI 95%, 4.63–40.0) was independently associated with ATI formation. CONCLUSION(S): Concomitant immunomodulator therapy was the only protective factor for the ATI formation, supporting its institution to prevent loss of response to anti-TNFs.