Objective The second iteration of the Selecting Therapeutic Targets in Inflammatory Bowel Disease (STRIDE-II) initiative recommends use of the Simple Endoscopic Score for Crohn’s disease (SES-CD) as a treatment target for patients with CD. We aimed to assess whether the STRIDE-II endoscopic endpoints are achievable and whether the degree of mucosal healing (MH) affects long-term outcomes.
Design/method We performed a retrospective observational study between 2015 and 2022. Patients with CD who had baseline and follow-up SES-CD scores after biological therapy initiation were included. The primary outcome was treatment failure, defined as the need for: (1) change of biological therapy for active disease (2) corticosteroid use (3) CD-related hospitalisation or (4) surgery. We compared rates of treatment failure with the degree of MH achieved. Patients were followed up until treatment failure or study end (August 2022).
Results 50 patients were included and followed up for median 39.9 (34.6–48.6) months. Baseline characteristics: 62% male, median age 36.4 (27.8–43.9) years, disease distribution (L1: 4, L2: 11, L3: 35, perianal: 18). The proportion of patients achieving STRIDE-II end-points were: SES-CD ≤ 2–25 (50%) and >50% reduction in SES-CD—35 (70%). Failure to achieve SES-CD ≤ 2 (HR 11.62; 95% CI 3.33 to 40.56, p=0.003) or >50% improvement in SES-CD (HR 30.30; 95% CI 6.93 to 132.40, p<0.0001) predicted treatment failure.
Conclusion Use of SES-CD is feasible in real-world clinical practice. Achieving an SES-CD ≤ 2 or a greater than 50% reduction, as set out by STRIDE-II, is associated with reduced rates of overall treatment failure including CD-related surgery.
- Crohn's disease
- endoscopic procedures
Data availability statement
Data are available upon reasonable request. Data will be shared upon reasonable request to the authors.
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Contributors SM guarantor; MAS, SM, JM and SZ conception, design; SM, ER, SZ data collection, SM and MAS data analysis and interpretation; MAS, SM and ER manuscript drafting, SM, ER, ES, SH, SZ, SR, SHCA, JS, JM, PMI and MAS review, editing and final approval.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests SM has received an educational grant from Pfizer and speaker fees from Dr Falk Pharma. SH received lecture fees from Pfizer, Janssen, and Takeda. JM has received advisory fees from Janssen, Galapagos, Abbvie and lecture fees from Janssen and Pfizer. PMI has received lecture fees from Abbvie, Warner Chilcott, Ferring, Falk Pharma, Takeda, MSD, Johnson and Johnson, Shire and Pfizer. Financial support for research: MSD, Takeda and Pfizer. Advisory fees: Abbvie Warner Chilcott, Takeda, MSD, Vifor Pharma, Pharmacosmos Topivert, Genentech, Hospira, Samsung Bioepis. MAS has served as a speaker, a consultant and/or advisory board member for Sandoz, Janssen, Takeda, MSD, Falk, Samsung Bioepis. MAS has received advisory fees from Bristol-Myers Squibb, Janssen, Takeda, Sandoz, Samsung Bioepis, Galapagos, AbbVie, and has received lecture fees from Bristol-Myers Squibb, Janssen, Takeda, MSD, Falk, AbbVie, Galapagos.
Provenance and peer review Not commissioned; externally peer reviewed.
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