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Introduction

Patients with eosinophilic esophagitis (EoE) commonly face diagnostic delays, often due to misdiagnosis of conditions with similar symptoms such as gastroesophageal reflux disease (GERD).^1-3 Diagnostic delay in EoE has been associated with stricture formation, food impaction, persistent symptoms with impaired quality of life, and potentially a decrease in response to treatment.

Aims & Methods

This study examined the path from first symptoms to EoE diagnosis from both physician and patient perspectives and the impact of misdiagnosis. Data were from the Adelphi EoE Disease Specific Programme™ (DSP), a real-world, cross-sectional survey of physicians and their patients with confirmed diagnosis of EoE in the US, UK, and EU (France, Germany, Italy, Spain) from July to December 2023, including clinical data abstracted from medical records.⁴ Physicians reported if patients had been misdiagnosed prior to EoE diagnosis and the timing of key milestones, such as first symptoms, first medical consultation, and referral. Patients also reported timings of key milestones. We completed a descriptive analysis and presented results for the subset of patients who completed the survey and had clinical data abstracted.

Results

Physicians (n=190; 73% gastroenterologists, 18% allergists, 4% internal medicine, 4% pediatric gastroenterologists, 1% pediatric allergists) abstracted data on 1141 patients with EoE (93% adults, 89% White), of which 285 also completed a survey (25% response rate). For 967 patients, physicians assessed if the patient was previously misdiagnosed; 28% (n=272) were misdiagnosed, and the majority (81%) were misdiagnosed with GERD prior to the EoE diagnosis. Physicians reported that those who were misdiagnosed had a longer time from (1) first documented symptoms to patient’s first medical consultation (mean days [SD]: 368.7 [671.0] vs 175.6 [611.8]) and (2) first consultation to EoE diagnosis (mean days [SD]:332.3 [503.2] vs 78.9 [149.9]) when compared with patients who were not misdiagnosed (n=695). Misdiagnosed patients themselves also reported longer time from first symptoms to first medical consultation (mean days [SD]:622.2 [1161.3] vs 327.1 [1154.2]) (Table).

Conclusion

Diagnostic delay is a known challenge in the management and care of EoE. Not only is clinical presentation underrecognized, but patients with EoE are commonly misdiagnosed, often with GERD, and experience prolonged diagnostic delay. Patients with a physician-confirmed misdiagnosis prior to their EoE diagnosis had longer time from their first symptoms to diagnosis due to both patient delay in seeking medical care and diagnostic delay. These findings highlight the significant unmet need for physician and patient education regarding EoE symptoms in order to facilitate timely diagnosis of EoE, which could aid in appropriate treatment strategies and improve both short- and long-term outcomes for patients with EoE.

Table.

	Total (n=1141)	Misdiagnosed^a (n=272)	Not misdiagnosed^a (n=695)	Unknown^a (n=174)
Age, mean [SD], years	36.6 [14.7]	36.8 [14.7]	35.7 [14.0]	40.1 [16.7]
Female, %	34	34	34	32
White/Caucasian, %	89	86	90	89
BMI, mean [SD]	24.1 [3.5]	24.2 [3.3]	24.0 [3.6]	24.2 [3.4]
Conditions that were misdiagnoses, %		GERD (81) Achalasia (8) Esophageal candidiasis (3) Hypereosinophilic syndrome (1) Connective tissue disease (1) Don’t know (5)
Physician-reported time from first symptom to first medical consultation,^b n mean [SD], days median min–max IQR	n=214 248.9 [876.2] 61.0 0–11,688 153.2	n=50 367.6 [516.9] 198.0 0–2556 275.0	n=150 211.5 [994.3] 38.0 0–11,688 84.0	n=14 225.9 [410.2] 92.0 0–1595 186.8
Patient-reported time from first symptom to first medical consultation,^c n mean [SD], days median min–max IQR	n=269 378.3 [1122.8] 91.2 1–10,950 304.2	n=58 566.1 [1191.3] 197.7 20–8030 501.9	n=171 339.6 [1213.3] 60.8 1–10,950 154.4	n=40 271.4 [318.30] 152.1 1–1460 307.7
Physician-reported time from first medical consultation to EoE diagnosis,^d, n mean [SD], days median min–max IQR	n=236 168.1 [351.0] 59.0 0–2256 102.8	n=57 442.0 [595.5] 183.0 0–2256 398.5	n=161 73.1 [126.3] 36.0 0–1350 53.0	n=18 149.9 [218.8] 58.5 0–911 197.7
IQR=interquartile range ^aPhysicians were asked “Was this patient misdiagnosed with any other condition(s) to explain their symptoms prior to a confirmed diagnosis of EoE? (Yes, No, Don’t know). ^bPhysician reported for patients that have abstracted clinical data and the subset that completed a survey (n=285). N is based on those with non-missing data. ^cOnly a subset of patients (n=285) for which physician abstract data completed a survey. N is based on non-missing patient survey data. ^dPatients were not asked to report on the time from first medical consultation to EoE diagnosis.

References

Murray FR, Kreienbuehl AS, Greuter T, Nennstiel S, Safroneeva E, Saner C, Schindler V, Schlag C, Schoepfer AM, Schreiner P, Straumann A, Biedermann L. Diagnostic delay in patients with eosinophilic esophagitis has not changed since the first description 30 years ago: diagnostic delay in eosinophilic esophagitis. Am J Gastroenterol. 2022 Nov 1;117(11):1772-1779. doi: 10.14309/ajg.0000000000001950. Epub 2022 Aug 12. PMID: 35971224.
Schoepfer AM, Safroneeva E, Bussmann C, Kuchen T, Portmann S, Simon HU, Straumann A. Delay in diagnosis of eosinophilic esophagitis increases risk for stricture formation in a time-dependent manner. Gastroenterology. 2013 Dec;145(6):1230-6.e1-2. doi: 10.1053/j.gastro.2013.08.015. Epub 2013 Aug 13. PMID: 23954315.
Schoepfer AM, Safroneeva E, Bussmann C, Kuchen T, Portmann S, Simon HU, Straumann A. Delay in diagnosis of eosinophilic esophagitis increases risk for stricture formation in a time-dependent manner. Gastroenterology. 2013 Dec;145(6):1230-6.e1-2. doi: 10.1053/j.gastro.2013.08.015. Epub 2013 Aug 13. PMID: 23954315.
Anderson P, Higgins V, Courcy J, Doslikova K, Davis VA, Karavali M, Piercy J. Real-world evidence generation from patients, their caregivers and physicians supporting clinical, regulatory and guideline decisions: an update on Disease Specific Programmes. Curr Med Res Opin. 2023 Dec;39(12):1707-1715. doi: 10.1080/03007995.2023.2279679. Epub 2023 Dec 15. PMID: 37933204.

Disclosure

LB has received consulting/advisory board fees from AbbVie, Amgen, Bristol Myers Squibb, MSD, Vifor, Falk, Esocap, Janssen, Lilly, Calypso, Ferring, Pfizer, Takeda Pharmaceuticals, Janssen, and Sanofi. KD and JM are employees of and shareholders in Bristol Myers Squibb. CZ is a contractor to Bristol Myers Squibb. DM and TP are employees of Adelphi Real World. JWC has received fees for consulting from Sanofi-Regeneron and Takeda Pharmaceuticals.

MISDIAGNOSIS IS COMMON ON THE PATH TO EOSINOPHILIC ESOPHAGITIS

Luc Biedermann 1, Kiran Dave 2, Carla Zema 3, Daniel Mascia 4, Tia Pennant 4, Joy W. Chang 5

1 Department of Gastroenterology and Hepatology, Universitäts Spital Zürich, Zürich, Switzerland

2 Bristol Myers Squibb, Uxbridge, United Kingdom

3 Bristol Myers Squibb, Princeton, NJ, United States

4 Adelphi Real World, Bollington, United Kingdom

5 Division of Gastroenterology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, United States

Conference

UEG Week Vienna 2024

Topics

Oesophagus

Submission format

Abstract

Session

Clinical presentation and impact on treatment in EoE (Posters)

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Which advanced therapy should you choose in patients with fistulising Crohn's disease?

Krisztina Barbara Gecse 1

1 Amsterdam University Medical Center, Amsterdam, Netherlands

Event

UEG Week Berlin 2025

Topics

IBD Mechanisms & Personalised Medicine Surgery

Session

Focus on fistulising Crohn’s disease

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Identifying disease trajectories by AI

Florian Tran 1

1 University Medical Center Schleswig-holstein, Campus Kiel, Kiel, Germany

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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IL-23

Laurent Peyrin-Biroulet 1

1 Inserm NGERE and University of Lorraine, Vandœuvre-lès-Nancy, France

Event

UEG Week Berlin 2025

Topics

IBD Mechanisms & Personalised Medicine

Session

What's new in advanced therapies for IBD in 2025?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Optimising success in IBD treatment: Timing surgery and medical treatment

Wilhelmus A. Bemelman 1, Hannah Gordon 2

1 Academisch Medisch centrum Dept. of Surgery - Department of Surgery, Academisch Medisch centrum Dept, Amsterdam, Netherlands

2 Royal London Hospital, London, United Kingdom

Event

UEG Week Berlin 2025

Session

How to optimise success in IBD treatment

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Optimising surgical therapies in fistulising Crohn's disease

Philip J. Tozer 1

1 St Marks Hospital, London, United Kingdom

Event

UEG Week Berlin 2025

Topics

IBD Mechanisms & Personalised Medicine Surgery

Session

Focus on fistulising Crohn’s disease

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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THE EFFICACY AND SAFETY OF ETRASIMOD IN MILDLY TO MODERATELY ACTIVE ULCERATIVE COLITIS: RESULTS FROM THE GLADIATOR TRIAL

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Introduction

Etrasimod is an oral, once-daily, selective sphingosine 1-phosphate (S1P)_1,4,5 receptor modulator for the treatment of moderately to severely active ulcerative colitis (UC), with demonstrated efficacy in patients (pts) with baseline modified Mayo Score (MMS) 4–9.¹ No prior clinical trials of advanced therapies in UC have studied efficacy only in pts with baseline MMS ≤6.

Aims & Methods

GLADIATOR (NCT04607837) was a proof-of-concept, global, randomised, double-blind, placebo-controlled trial to evaluate the efficacy and safety of etrasimod in adults with mildly to moderately active UC (MMS 4–6; endoscopic subscore ≥2; rectal bleeding subscore ≥1) and inadequate response, loss of response or intolerance to ≥1 UC therapy. Pts were randomised 2:1 to etrasimod 2 mg or placebo once daily, stratified by previous biologic/Janus kinase inhibitor exposure and baseline corticosteroid use. GLADIATOR used a treat-through design (12-week [wk] induction period followed by a 40‑wk maintenance period). From Wk 12, pts whose disease had worsened or not improved vs baseline may have been eligible to enrol in an open-label extension trial (NCT03950232). The primary efficacy endpoint was the proportion of pts achieving clinical remission at Wk 52; additional endpoints are shown in the Table. Safety was monitored throughout the study.

Results

In the primary analysis set for efficacy, 127 and 60 pts received etrasimod and placebo, respectively. At Wk 52, 26.0% and 18.3% of pts receiving etrasimod and placebo, respectively, were in clinical remission (p=0.2524; Table). At Wk 12, a greater proportion of pts receiving etrasimod achieved clinical remission, endoscopic improvement (EI) and endoscopic improvement-histologic remission (EIHR) vs placebo (p<0.05; Table). Pts receiving etrasimod were more likely to achieve sustained clinical remission vs placebo (p=0.0104; Table). Etrasimod was generally well tolerated and findings were consistent with the known safety profile.

Table. Proportions of pts (n [%]) achieving endpoints at Wk 12 and Wk 52 in GLADIATOR (nonresponder imputation)^a	Endpoint	Placebo (N=60)	Etrasimod 2 mg (N=127)	% difference from placebo^b (95% CI)	Difference from placebo p value^c
Wk 12 Wk 12 completers: Placebo: 56 (93.3)^d Etrasimod: 122 (96.1)^e	Clinical remission^f	7 (11.7)	36 (28.3)	15.6 (4.3, 26.9)	0.0068
	EI^g	12 (20.0)	56 (44.1)	23.3 (9.8, 36.9)	0.0007
	EIHR^h	8 (13.3)	37 (29.1)	15.0 (3.2, 26.8)	0.0128
Wk 52 Wk 52 completers: Placebo: 28 (46.7)ⁱ Etrasimod: 76 (59.8)^j	Clinical remission^f	11 (18.3)	33 (26.0)	7.4 (-5.2, 19.9)	0.2524
	EI^g	14 (23.3)	41 (32.3)	8.2 (-5.2, 21.7)	0.2302
	EIHR^h	9 (15.0)	32 (25.2)	9.6 (-2.1, 21.3)	0.1089
	CS-free clinical remission^k	10 (16.7)	32 (25.2)	8.5 (-3.7, 20.7)	0.1726
Wk 12 and Wk 52	Sustained clinical remission^l	3 (5.0)	21 (16.5)	11.2 (2.6, 19.8)	0.0104
^aAll randomised pts who received ≥1 dose of study treatment with baseline MMS 4–6, baseline ES ≥2 and baseline RBS ≥1 were included in the primary analysis set for efficacy analysis. All pts with missing data were treated as nonresponders in the primary analysis. ^bEstimated common risk difference using the Mantel–Haenszel weighted method, stratified by naïve to biologic/JAKi therapy at trial entry (yes/no) and baseline CS use (yes/no). ^cFrom Mantel–Haenszel test and not adjusted for multiplicity. ^dIn the placebo group, prior to Wk 12, the following reasons for discontinuation were reported: AE (n=2 [3.3%]); withdrawal by pt (n=2 [3.3%]). ^eIn the etrasimod group, prior to Wk 12, the following reasons for discontinuation were reported: AE (n=3 [2.4%]); withdrawal by pt (n=1 [0.8%]); disease worsening (n=1 [0.8%]). ^fClinical remission was defined as SFS=0 or 1 (and no greater than baseline), RBS=0 and ES ≤1 (excluding friability). ^gEI was defined as ES ≤1. ^hEIHR was defined as ES ≤1 with histologic remission measured by Geboes Index score <2.0. ⁱIn the placebo group, after Wk 12, the following reasons for discontinuation were reported: disease worsening (n=26 [43.3%]); withdrawal by pt (n=2 [3.3%]). ^jIn the etrasimod group, after Wk 12, the following reasons for discontinuation were reported: disease worsening (n=33 [26.0%]); withdrawal by pt (n=5 [3.9%]); AE (n=4 [3.1%]); physician decision (n=2 [1.6%]); lack of efficacy (n=1 [0.8%]); study termination by sponsor (n=1 [0.8%]). ^kCS-free clinical remission was defined as clinical remission at Wk 52 and CS free for ≥12 wks immediately prior to Wk 52. ^lSustained clinical remission was defined as clinical remission at both Wk 12 and Wk 52. AE, adverse event; CI, confidence interval; CS, corticosteroid; EI, endoscopic improvement; EIHR, endoscopic improvement-histologic remission; ES, endoscopic subscore; JAKi, Janus kinase inhibitor; MMS, modified Mayo score; N, number of pts in cohort; pt, patient; RBS, rectal bleeding subscore; SFS, stool frequency subscore; wk, week.

Conclusion

In pts with mildly to moderately active UC, etrasimod demonstrated higher rates of clinical remission, EI and EIHR at Wk 12, as well as sustained clinical remission at Wk 52, vs placebo. However, the primary endpoint of clinical remission at Wk 52 was not met. Etrasimod demonstrated efficacy in pts with UC with an MMS 4–9, including those with an MMS 4–6, in the ELEVATE UC clinical programme.¹ The proof-of-concept GLADIATOR trial further supports etrasimod’s efficacy in active UC and provides important insights on studying pts with mildly to moderately active UC.

References

1. Sandborn WJ et al. Lancet 2023; 401: 1159–1171.

Disclosure

SD: Lecture fees: AbbVie, Amgen, Ferring Pharmaceuticals Inc, Gilead, Janssen, Mylan, Pfizer Inc, Takeda; Consultancy fees: AbbVie, Allergan, Amgen, AstraZeneca, Biogen, Boehringer Ingelheim, Celgene, Celltrion, Ferring, Gilead Sciences, Hospira, Janssen, Johnson&Johnson, MSD, Mundipharma, Pfizer Inc, Roche, Sandoz, Takeda, TiGenix, UCB, Vifor; Directorship: Gastroenterology and Endoscopy.
MG, KL: Employees of Pfizer AG; shareholders of Pfizer Inc.
LPB: Consultancy fees: AbbVie, Abivax, Alimentiv, Alma Bio Therapeutics, Amgen, Applied Molecular Transport, Arena, Biogen, BMS, Celltrion, CONNECT Biopharm, Cytoki Pharma, Enthera, Ferring, Fresenius Kabi, Galapagos, Genentech, Gilead, Gossamer Bio, GlaxoSmithKline, HAC-Pharma, IAG Image Analysis, Index Pharmaceuticals, Inotrem, Janssen, Lilly, Medac, Mopac, Morphic, MSD, Norgine, Novartis, OM Pharma, ONO Pharma, OSE Immunotherapeutics, Pandion Therapeutics, Par’Immune, Pfizer Inc, Prometheus, Protagonist, Roche, Roivant, Samsung, Sandoz, Sanofi, Takeda, Theravance, Thermo Fisher, Tigenix, Tillotts, Viatris, Vifor, Vectivbio, Ventyx, Ysopia; Grants: Takeda, Fresenius Kabi, Celltrion; Lectures: AbbVie, Amgen, Arena, Biogen, Celltrion, Ferring, Galapagos, Genetech, Gilead, Janssen, Lilly, Medac, MSD, Pfizer Inc, Sandoz, Takeda, Tillotts, Viatris, Vifor.
AJY: Consultancy fees: AbbVie, Arena, BMS, Celltrion, Pfizer Inc, Takeda; Lectures: AbbVie, BMS.
MCD: Consultancy fees: AbbVie, Abivax, Arena Pharmaceuticals, AstraZeneca, BMS, Eli Lilly, Galapagos, Genentech, Gilead Sciences, Janssen Pharmaceuticals, Johnson&Johnson, Merck, Pfizer Inc, Prometheus Laboratories, Prometheus Biosciences, Sanofi, Sphyre, Takeda, UCB; Shareholder: Trellus Health; Directorship: Trellus Health.
DTR: Consultancy fees: AbbVie, Abivax SA, Altrubio, Avalo Therapeutics, Bausch Health, Bristol Myers Squibb, Buhlmann Diagnostics Corp, Celltrion, ClostraBio, Connect BioPharma, Douglas Pharmaceuticals, Eli Lilly & Co., Foresee, Genentech, Image Analysis Group, InDex Pharmaceuticals, Iterative Health, Janssen Pharmaceuticals, Odyssey Therapeutics, Pfizer Inc, Sanofi, Takeda Pharmaceuticals, Throne, Vedanta; Grants: Takeda.
BGF: Senior Scientific Director of Alimentiv Inc, which provides central reading services. He is not a company employee and has no equity stake in the organisation, which is owned by a medical trust; Speaker fees: AbbVie, Janssen, Takeda; Consultancy fees: AbbVie, AbolerIS, AgomAB Therapeutics, Allianthera, Amgen, AnaptysBio, Applied Molecular Transport Inc, Arena Pharma, Avoro Capital Advisors, Atomwise, BioJamp, Biora Therapeutics, Boehringer Ingelheim, Boxer, Celsius Therapeutics,Celgene/BMS, Connect BioPharma, Cytoki, Disc Medicine, Duality, EcoR1, Eli Lilly, Equillium, Ermium, First Wave, First Word Group, Galapagos, Galen Atlantica, Genentech, Gilead, Gossamer Pharma, GSK, Hinge Bio, Hot Spot Therapeutics, Index Pharma, Imhotex, Immunic Therapeutics, JAKAcademy, Janssen, Japan Tobacco Inc, Kaleido Biosciences, Landos Biopharma, Leadiant, L.E.K. Consulting, Lenczner Slaght, LifeSci Capital, Lument AB, Millennium, MiroBio, Morgan Lewis, Morphic Therapeutics, Mylan, OM Pharma, Origo BioPharma, Orphagen, Pandion Therapeutics, Pendopharm, Pfizer Inc, Prometheus Therapeutics and Diagnostics, Play to Know AG, Progenity, Protagonist, PTM Therapeutics, Q32 Bio, Rebiotix, REDX, Roche, Sandoz, Sanofi, Seres Therapeutics, Silverback Therapeutics, Surrozen Inc, Takeda, Teva, Thelium, Tigenix, Tillotts, Ventyx Biosciences, VHSquared Ltd, Viatris, Ysios, Ysopia, Zealand Pharma; Shareholder: Gossamer Pharma.
GRDH: Advisory fees: AbbVie, AstraZeneca, Alimentiv, BMS, Boehringer Ingelheim, Celltrion, Cosmo, Eli Lilly, Galapagos, GSK, Johnson&Johnson, Takeda, Pfizer Inc, Polpharma, Prometheus Biosciences, Tillotts, Ventyx; Speaker fees: AbbVie, Boehringer Ingelheim, Celltrion, Eli Lilly, Johnson&Johnson, Takeda, Pfizer Inc, Tillotts.
FB: Research/grants: AbbVie, Amgen, Eurogenerics, Janssen, Takeda; Lectures: AbbVie, Arena Pharmaceuticals, Celltrion, Ferring, Galapagos, Janssen, Merck Sharp & Dohme, Pfizer Inc, Takeda; Consultancy fees: AbbVie, Abivax, Amgen, Arena Pharmaceuticals, Celgene, Celltrion, Ferring, Fresenius Kabi, Janssen, Merck Sharp & Dohme, Pfizer Inc, Sandoz.
GG, JY, NL, CZ, WW, SM, EHL, IM, SS, WN: Employees/shareholders of Pfizer Inc.
SV: Lectures: AbbVie, Dr. Falk Pharma, Ferring, Galapagos, Hospira, Janssen, MSD, Takeda, Tillotts; Consultancy fees: AbbVie, AbolerIS Pharma, Alimentiv, Arena, AstraZeneca, Avaxia, Bristol Myers Squibb, Boehringer Ingelheim, Celgene, CVasThera, Dr Falk Pharma, Eli Lilly, Ferring, Galapagos, Genentech/Roche, Gilead, Hospira, Imidomics, Janssen, Johnson&Johnson, Materia Prima, MiroBio, Morphic, MrMHealth, MSD, Mundipharma, Pfizer Inc, Prodigest, Progenity, Prometheus, Robarts Clinical Trials, Second Genome, Shire, Surrozen, Takeda, Theravance Biopharma, Tillotts Pharma AG, Zealand Pharma; Grants: AbbVie, MSD, Pfizer Inc, Galapagos, Janssen, Takeda.

THE EFFICACY AND SAFETY OF ETRASIMOD IN MILDLY TO MODERATELY ACTIVE ULCERATIVE COLITIS: RESULTS FROM THE GLADIATOR TRIAL

Silvio Danese 1, Martina Goestch 2, Laurent Peyrin-Biroulet 3, Andres Yarur 4, Marla C. Dubinsky 5, David T. Rubin 6, Brian G. Feagan 7, Geert R. D'Haens 8, Filip Baert 9, Krisztina Lazin 2, Guibao Gu 10, Jin Yu 10, Nervin Lawendy 11, Chuanbo Zang 11, Wenjin Wang 11, Sujatha S. Menon 12, Ernest Law 13, Irene Modesto 13, Sarah Sidhu 13, Wojciech Niezychowski 11, Severine Vermeire 14

1 Division of Gastroenterology and Endoscopy, IRCCS San Raffaele Hospital and Vita Salute San Raffaele University, Milan, Italy

2 Pfizer AG, Zürich, Switzerland

3 Department of Gastroenterology, CHRU Nancy, INSERM NGERE, Université de Lorraine, Vandœuvre-lès-Nancy, France

4 Inflammatory Bowel Disease Center and Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, CA, United States

5 Susan and Leonard Feinstein IBD Center, Icahn School of Medicine, Mount Sinai, New York, NY, United States

6 University of Chicago Medicine Inflammatory Bowel Disease Center, Chicago, IL, United States

7 Division of Gastroenterology, Department of Medicine, Western University, London, ON, Canada|||Alimentiv Inc, London, ON, Canada

8 Department of Gastroenterology and Hepatology, Amsterdam University Medical Centers, Amsterdam, Netherlands

9 Department of Gastroenterology, AZ Delta, Roeselare, Belgium

10 Pfizer Inc, La Jolla, CA, United States

11 Pfizer Inc, Collegeville, PA, United States

12 Pfizer Inc, Groton, CT, United States

13 Pfizer Inc, New York, NY, United States

14 Department of Gastroenterology and Hepatology, University Hospitals Leuven, Leuven, Belgium

Event

UEG Week Berlin 2025

Topics

IBD Mechanisms & Personalised Medicine

Submission format

Abstract

Session

Advanced therapies in ulcerative colitis

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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