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Oral Advanced Therapies in UC: Are More Options Needed? (Abivax) (Complete Session)

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Oral Advanced Therapies in UC: Are More Options Needed? (Abivax) (Complete Session)

Marla C. Dubinsky 1, Severine Vermeire 2

1 Mount Sinai Hospital, Mount Sinai, New York City, United States of America

2 University Hospital Leuven, Leuven, Belgium

Publisher

Abivax S.A.

Event

UEG Week Vienna 2024

Session

Oral Advanced Therapies in UC: Are More Options Needed? (Abivax)

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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ANTI-TNF TREATMENT WITHDRAWAL IN ULCERATIVE COLITIS, A MULTICENTER, OPEN-LABEL, RANDOMIZED CONTROLLED TRIAL

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Introduction

The BIOSTOP Trial is a prospective, multicenter, randomized, controlled, open-label study conducted in Norway to evaluate the two-year outcomes of tumor necrosis factor-alpha (anti-TNF) antibody withdrawal in patients with ulcerative colitis (UC) in sustained clinical and endoscopic remission. Prior non-randomized studies have suggested that approximately half of such patients maintain remission after anti-TNF discontinuation and that reintroduction of anti-TNF therapy is generally effective and safe in the event of relapse.

Aims & Methods

A total of 174 UC patients in confirmed clinical and endoscopic remission were enrolled across 19 gastroenterology centers between June 2017 and December 2020 and randomized 1:1 to either continue or discontinue anti-TNF therapy. Eligibility criteria included at least 12 months of first-line anti-TNF maintenance treatment, clinical remission, fecal calprotectin <200 µg/g, and endoscopic remission (Mayo endoscopic score 0 or 1). Two-year follow-up data were available for 172 patients (86 in each group). In 156 of the patients endoscopies were available for central reading (77 in the withdrawal group and 79 in the maintenance group). The primary endpoint was sustained endoscopic remission at two years.

Results

At two years, central reading of follow-up colonoscopies confirmed endoscopic remission in 64 of 77 patients (83%, 95% CI 71.8 – 93.1) in the anti-TNF withdrawal group, compared to 77 of 79 patients (96 %, 95 % CI 92.1 – 100.8) in the anti-TNF maintenance group. The non-inferiority primary endpoint of the study was thus not met. During the study period, 48% of patients in the withdrawal group and 88% in the maintenance group remained in sustained clinical and endoscopic remission without relapse. Among the 45 patients in the withdrawal group who experienced endoscopic confirmed relapse, 28 (62%) resumed anti-TNF therapy, with 26 achieving both clinical and endoscopic remission. Additionally, 10 of 13 patients with mild relapses achieved endoscopic remission with optimized non-biologic therapy. There were no difference in serious adverse events between the groups.

Conclusion

After two years, 83% of patients in the anti-TNF withdrawal group and 96% in the maintenance group were in clinical and endoscopic remission, including those who experienced flares and achieved new remission after reintroduction of anti-TNF or optimized non-biologic therapy. Nearly half of the patients maintained remission without anti-TNF, and the majority of relapses were effectively managed. These findings suggest that anti-TNF withdrawal is a safe option for selected UC patients in confirmed remission, provided they are monitored closely.
Trial Registration: ClinicalTrials.gov Identifier: NCT03011268; EudraCT Number: 2016-001409-18. Trial completion date: 31 January 2025.

Disclosure

No disclosures

ANTI-TNF TREATMENT WITHDRAWAL IN ULCERATIVE COLITIS, A MULTICENTER, OPEN-LABEL, RANDOMIZED CONTROLLED TRIAL

Ingrid Prytz Berset 1, Frode Lerang 2, Dag Arne Lihaug Hoff 3, Knut E.A. Lundin 4

1 Gastroenterology Aalesund, Alesund, Norway

2 Central Hosspital of Ostfold, Grålum, Norway

3 Aalesund Hospital, Møre & Romsdal Hospital trust, Aalesund, Norway

4 K. G. Jebsen Coeliac Disease Research Centre, University of Oslo and Oslo University Hospital, Oslo, Norway

Event

UEG Week Berlin 2025

Topics

Endoscopy IBD

Submission format

Abstract

Session

Tackling IBD in clinics

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Will there be pathologists in 2030 or only AI?

Valerie Paradis 1

1 INSERM - Hôpital Beaujon, Clichy, France

Event

UEG Week Berlin 2025

Topics

Histopathology IBD Nurses

Session

The art of making clinical research precise: AI – friend or foe?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Managing IBD in a patient with new or recent cancer

Hannah Gordon 1

1 Royal London Hospital, London, United Kingdom

Event

UEG Postgraduate Teaching Programme Berlin 2025

Topics

Digestive Oncology IBD

Session

Cancer and IBD: Mitigating risk among uncertainty

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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EXOPHIALA DERMATITIDIS EXACERBATES COLITIS THROUGH THE SYK-CARD9 SIGNALING PATHWAY

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Introduction

As a small but important component of the intestinal microbiota, the fungal community (mycobiota) has received increasing attention for its involvement in the pathogenesis of Crohn's disease (CD)¹. In our previous study, we identified a significantly increased relative abundance of Exophiala dermatitidis (E. dermatitidis) in the gut of patients with CD, particularly those with active disease². Caspase recruitment domain family member 9 (CARD9), a key adaptor molecule in antifungal immune responses³, has also been strongly associated with CD susceptibility⁴. In this study, we aimed to explore the potential role and underlying mechanisms of E. dermatitidis in intestinal inflammation.

Aims & Methods

To evaluate the impact of E. dermatitidis on intestinal inflammation, we generated Card9-knockout (KO) (Card9^-/-) mice and constructed a dextran sulfate sodium (DSS)-induced colitis model colonized by E. dermatitidis. The underlying molecular mechanisms were investigated by a range of biochemical approaches. Flow cytometry was performed to analyze the proportions of myeloid cells, including CX3CR1⁺ macrophages, in the colonic lamina propria (LP).

Results

Compared to mice with DSS-induced colitis alone (WT-DSS group), the DSS-treated mice colonized by E. dermatitidis (WT-DSS + Ed group) showed a significant weight loss, a worsening of disease activity, a shorter length of the large intestine, and more severe intestinal inflammation characterized by increased inflammatory cell infiltration and crypt destruction in the histological examination of colon hematoxylin and eosin (H&E) staining. Card9^-/- mice were used to further investigate whether E. dermatitis-mediated inflammation was dependent on the CARD9 signaling pathway. We observed that CARD9 deficiency protected against E. dermatitidis-exacerbated colitis, as measured by a higher trend of body weight, longer colon lengths, and amelioration of disease activity in the KO-DSS + Ed group. In addition, flow cytometric analysis of the colonic lamina propria revealed a higher percentage proportion of CX3CR1+ macrophages in the WT-DSS + Ed group and a markedly reduced proportion in the KO-DSS + Ed group. Furthermore, we identified the Mincle-Syk-CARD9-nuclear factor kappa-B (NF-κB) signaling pathway as playing an important role in mediating the inflammatory immune responses to E. dermatitidis.

Conclusion

E. dermatitidis exacerbates the DSS-induced colitis in mice through the Mincle-Syk-CARD9-NF-κB pathway with the participation of CX3CR1+ macrophages, providing a novel therapeutic strategy for CD targeting specific intestinal fungi.

References

1. Sokol H, Leducq V, Aschard H, et al. Fungal microbiota dysbiosis in IBD. Gut 2017;66:1039-1048.
2. Zeng L, Feng Z, Zhuo M, et al. Fecal fungal microbiota alterations associated with clinical phenotypes in Crohn's disease in southwest China. PeerJ 2022;10:e14260.
3. Hu A, Hu Z, Zou H, et al. CARD9 in host immunity to fungal, bacterial, viral, and parasitic infections: An update. Frontiers In Microbiology 2022;13:1021837.
4. Franke A, McGovern DPB, Barrett JC, et al. Genome-wide meta-analysis increases to 71 the number of confirmed Crohn's disease susceptibility loci. Nature Genetics 2010;42:1118-1125.