Abstract Background Corticosteroids are used in Crohn’s disease (CD) and ulcerative colitis (UC) to induce remission. We aimed to assess the impact of corticosteroid use during induction therapy on advanced therapy (AT) persistence. Methods We interrogated the Persistence Australian National IBD Cohort (PANIC5) registry from 2007-2021, covering all AT prescribing data for CD and UC in Australia. Non-persistence was defined as 6 months without dispensing. Induction corticosteroids were defined as systemic corticosteroids within three months leading up to or after AT initiation. Kaplan-Meier survival curves were compared using the log-rank test. Cox proportional hazards models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI), P 0.05 was considered significant. Results 19,087 CD and 9,671 UC patients underwent 31,967 and 14,784 lines of AT respectively, totaling 103,025 patient-years follow up. 16.3% of CD and 18.2% of UC patients had induction corticosteroids. In CD, induction corticosteroids were associated with significantly reduced persistence for both tumour necrosis factor inhibitors (TNFi) (median 28.0 vs 40.0 months, HR = 1.20 95%CI: 1.15-1.26, P 0.001) and ustekinumab (median survival 52 months; HR = 1.28 95%CI: 1.12-1.46 P0.001). Corticosteroid use was not associated with vedolizumab persistence in CD (29.0 vs 36.0 months, HR = 1.08 95%CI: 0.94-1.25, P = 0.26). In UC, induction corticosteroids were associated with significantly reduced persistence of TNFi (18.0 vs 24.0 months, HR = 1.13 95%CI: 1.05-1.22, P = 0.001), vedolizumab (28.0 vs 53.0 months, HR = 1.44 95%CI: 1.29-1.60, P 0.001) and tofacitinib (median survival 8 months, HR = 2.91 95%CI: 1.36-6.23, P = 0.003). There was no difference between patients who received one vs multiple courses of corticosteroids for either CD (HR 1.02, 95%CI: 0.94-1.12, P = 0.58) or UC (HR = 0.96, 95%CI: 0.83-1.11, P = 0.57). Conclusion Corticosteroid use during induction is associated with decreased AT persistence across all drug classes. This may be a surrogate marker for patients with increased disease severity, with sicker patients more likely to be given corticosteroids at induction. Conflict of interest: Dr. Gu, Bonita: Dr Bonita Gu has received sponsorship for conference attendance from Johnson & Johnson and Ferring. Chetwood, John: Speaker fees: Novartis, Eli Lilly, Dr Falk Pharma, Johnson & Johnson Pudipeddi, Aviv: Aviv Pudipeddi has received speaker honoraria or advisory board fees from AbbVie, Dr Falk Pharma, Ferring, Johnson & Johnson, Pfizer and Takeda. Yau, Yunki: No conflict of interest Kariyawasam, Viraj: Educational grants or research support – Ferring, Janssen, AbbVie, Takeda, Shire, WSLHD Research and Education network, Crohn’s and Colitis USA Speaker fees – Janssen, AbbVie, Ferring, Takeda, Pfizer, Shire, Chiesi, Celltrion, GSK, Eli-Lilly, Research Review, Limbic Advisory boards – Janssen, Takeda, Ferring, AbbVie Board director- IBD Sydney organisation (not for profit) Paramsothy, Sudarshan: SP has served as a consultant for Vedanta Biosciences and has received speaker / advisory board fees from AbbVie, Dr Falk Pharma, Ferring, Janssen and Takeda. Leong, Rupert: advisory board: AbbVie, Aspen, BMS, Celgene, Celltrion, Chiesi, Ferring, Glutagen, Hospira, Janssen, Lilly, MSD, Novartis, Pfizer, Prometheus Biosciences, Takeda, Spyre, Roche research grants: Joanna Tiddy USYD, McCusker Charitable Foundation, Celltrion, Shire, Janssen, Takeda, Gastroenterological Society of Australia, NHMRC, Gutsy Group, Pfizer
Gu et al. (Thu,) studied this question.