P666 Neutropenia in inflammatory bowel disease patients on TNF inhibitors: A single-centre, retrospective cohort study

Abstract Background Tumor necrosis factor-α inhibitors (TNFi) have become the mainstay of treatment in moderate to severe cases of IBD. The haematological safety profile of these agents has been documented in multiple clinical trials and post-marketing registries. Nonetheless, neutropenia has been reported in patients receiving TNFi for IBD and other diseases (Bessissow et al 2012). In this study, we aim to ascertain the relationship between the use of TNFi and the development of neutropenia in IBD patients. Methods This is a retrospective cohort study including all adult IBD patients receiving TNFi at our centre from the year 2007 to 2018. Our primary outcome was the development of any neutropenic episode after starting a TNFi. Neutropenia was defined as circulating absolute neutrophil count (ANC) less than 1500/mm3. For our secondary outcomes, we evaluated the impact of concomitant use of (5-ASA) or an immunomodulator on the risk of developing neutropenia. We also looked at the effect of baseline neutrophil and WBC counts on the subsequent development of neutropenia. Results A total of 292 patients met the inclusion criteria, 11 patients were excluded for not having neutrophil count done. The final analysis included 281 patients. The mean age of patients in this study was 33. Adalimumab was the most frequently prescribed TNFi. Of those included, 96 patients (34.2%) developed at least one episode of neutropenia while on a TNFi. The majority of these episodes (67.7%) were mild with ANC between 1000 and 1500/mm3. There was no significant difference in the age, gender, agent used or type of IBD between those who developed neutropenia and those who did not. On the other hand, baseline neutrophil count and concomitant use of azathioprine and 5-ASA were significant independent predictors of neutropenia after commencing TNFi. (Table 1). Conclusion In this study, mild neutropenia was common amongst IBD patients on TNFi. Patients were more likely to develop neutropenia if they have been on concurrent therapy with an immunomodulator or 5-ASA. Future prospective studies are required to further clarify the significance of neutropenia in IBD patients receiving TNFi. </jats:sec

Biologic therapy for inflammatory bowel disease: Real-world comparative effectiveness and impact of drug sequencing in 13,222 patients within the UK IBD BioResource

BACKGROUND AND AIMS: This study compares the effectiveness of different biologic therapies and sequences in patients with inflammatory bowel disease [IBD] using real-world data from a large cohort with long exposure. METHODS: Demographic, disease, treatment, and outcome data were retrieved for patients in the UK IBD BioResource. Effectiveness of treatment was based on persistence free of discontinuation or failure, analysed by Kaplan-Meier survival analysis with inverse probability of treatment weighting to adjust for differences between groups. RESULTS: In total, 13 222 evaluable patients received at least one biologic. In ulcerative colitis [UC] first-line vedolizumab [VDZ] demonstrated superior effectiveness over 5 years compared to anti-tumour necrosis factor [anti-TNF] agents [p = 0.006]. VDZ was superior to both infliximab [IFX] and adalimumab [ADA] after ADA and IFX failure respectively [p < 0.001 and p < 0.001]. Anti-TNF therapy showed similar effectiveness when used as first-line treatment, or after failure of VDZ. In Crohn's disease [CD] we found significant differences between first-line treatments over 10 years [p = 0.045], with superior effectiveness of IFX compared to ADA in perianal CD. Non-anti-TNF biologics were superior to a second anti-TNF after first-line anti-TNF failure in CD [p = 0.035]. Patients with UC or CD experiencing TNF failure due to delayed loss of response or intolerance had superior outcomes when switching to a non-anti-TNF biologic, rather than a second anti-TNF. CONCLUSIONS: We provide real-world evidence to guide biologic selection and sequencing in a range of common scenarios. Our findings challenge current guidelines regarding drug selection after loss of response to first anti-TNF treatment