What question did this study set out to answer?

This research aims to investigate the impact of primary sclerosing cholangitis on the therapy response in patients with inflammatory bowel diseases.

January 23, 2026

P0787Reduced Therapy Response Rate to Anti-IL-12/23 Antibodies in Patients with Inflammatory Bowel Disease and concurrent Primary Sclerosing Cholangitis: Results from a Case-Control Study

Key Points

This research aims to investigate the impact of primary sclerosing cholangitis on the therapy response in patients with inflammatory bowel diseases.
Compared therapy responses between PSC/IBD patients and IBD-only patients
Used propensity score matching to control for confounding variables
Evaluated primary outcome as clinical response within 20 weeks
Assessed secondary outcomes including endoscopic response and faecal calprotectin levels
Clinical response rates for Infliximab and Vedolizumab were similar between groups
Approximately 73.9% of patients had a UC diagnosis in both groups
UST treatment yielded significantly lower clinical remission and partial response rates in the PSC/IBD group (p = 0.017)
Mucosal healing rates and decreased faecal calprotectin levels were lower in PSC-IBD patients treated with UST

Abstract

Abstract Background Advanced biological therapies have improved outcomes of patients diagnosed with Inflammatory Bowel Diseases (IBD) such as Ulcerative colitis (UC) and Crohn’s disease (CD). However, nonresponse or loss of response remains a significant challenge1. Primary sclerosing cholangitis (PSC) is associated with IBDs, but the impact of concurrent PSC on response to IBD therapy is not well explored2-4. Methods This study compared the intestinal therapy response to biological therapies in patients with PSC and IBD (PSC/IBD group) versus patients with IBD only (IBD group). Therefore, we identified 46 patients in the PSC/IBD group and 180 in the IBD group treated with Infliximab (IFX), Vedolizumab (VDZ) and/or Ustekinumab (UST) at our IBD outpatient clinic. Propensity score matching was employed to match the groups with a ratio of 1:1 based on age, sex, BMI, smoking status, Charlson Comorbidity Index, IBD subtype, duration of IBD, age at IBD diagnosis and Montreal-Classification (caliper width = 0.2). The primary outcome was clinical therapy response within 20 weeks, defined as remission (partial Mayo Score (pMS) ≤ 1/Harvey-Bradshaw-Index (HBI) 5) or partial response (decrease of pMS ≥ 2/HBI 3). Group differences were compared using Chi-square test. Secondary outcomes included treatment persistence, endoscopic response (mucosal healing defined as no or mild inflammation in colonoscopy and histology) and decreased levels of faecal calprotectin (FC 150mg/g or decrease by ≥ 50%). Only patients achieving clinical remission or partial response were included in the secondary analyses. Results After matching, 46 patients per group were analysed, with a total of 136 treatments administered. The cohort demographics and disease characteristics were balanced between PSC/IBD group and control group (mean age: 39.7 ± 12.4 vs. 39.9 ± 13.9 years; male sex: 31 (67.4%) vs. 24 (52.2%); mean BMI: 23.1 ± 3.9 vs. 23.8 ± 4.8 kg/m2; smokers: 9 (20.0%) vs. 13 (31.7%)). In both groups 34 (73.9%) patients having an UC diagnosis. While clinical response rates did not significantly differ between groups in patients receiving IFX or VDZ, in patients treated with UST clinical remission and partial response rates were significantly lower in the PSC/IBD group (p = 0.017, Table 1). The treatment persistence was not different between groups across all therapies (Figure 1). Mucosal healing rates and decreased FC levels were lower in patients with PSC-IBD treated with UST (Table 1). Conclusion IFX and VDZ appear equally efficient for achieving clinical response in patients with PSC-IBD and IBD only, while the efficacy of UST is significantly lower in patients with PSC-IBD. Future prospective data is needed to strengthen our knowledge of treatment outcomes in this population. References: 1) Raine T, Danese S. Breaking Through the Therapeutic Ceiling: What Will It Take? Gastroenterology. 2022/04/01/ 2022;162(5):1507-1511. doi:https://doi.org/10.1053/j.gastro.2021.09.078 2) van Munster KN, Bergquist A, Ponsioen CY. Inflammatory bowel disease and primary sclerosing cholangitis: One disease or two?J Hepatol. Jan 2024;80(1):155-168. doi:10.1016/j.jhep.2023.09.031 3) Pinnuck B, Lynch KD. Navigating the pharmacotherapeutic management of comorbid inflammatory bowel disease and primary sclerosing cholangitis. Expert Opin Pharmacother. Sep 2024;25(13):1835-1849. doi:10.1080/14656566.2024.2407022 4) Barberio B, Massimi D, Cazzagon N, Zingone F, Ford AC, Savarino EV. Prevalence of Primary Sclerosing Cholangitis in Patients With Inflammatory Bowel Disease: A Systematic Review and Meta-analysis.Gastroenterology. Dec 2021;161(6):1865-1877. doi:10.1053/j.gastro.2021.08.032 Conflict of interest: Mr. Tosse, Robert: No conflict of interest Maibier, Martin: No conflict of interest Fischer, Andreas: No conflict of interest Razpotnik, Marcel: No conflict of interest Kouladouros, Konstantinos: No conflict of interest Sigal, Michael: No conflict of interest Wizenty, Jonas: Jonas Wizenty has received honoraria for consulting from Janssen-Cilag and Alfasigma.

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Cite This Study

Tosse et al. (Thu,) studied this question.

synapsesocial.com/papers/69731022c8125b09b0d1febc https://doi.org/https://doi.org/10.1093/ecco-jcc/jjaf231.968

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