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THE EFFICACY OF MAINTENANCE TREATMENT WITH GUSELKUMAB IN PATIENTS WITH MODERATELY TO SEVERELY ACTIVE ULCERATIVE COLITIS: PHASE 3 QUASAR MAINTENANCE STUDY RESULTS AT WEEK 44 BY BIOLOGIC/JANUS KINASE INHIBITOR HISTORY

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Introduction

The Phase 3 QUASAR Maintenance Study evaluated the efficacy of maintenance treatment with subcutaneous (SC) guselkumab (GUS), a dual-acting IL-23p19 subunit inhibitor, in patients (pts) with ulcerative colitis (UC) who achieved clinical response following IV GUS induction treatment. Here, we report Week(Wk) 44 efficacy and safety results for GUS treatment compared with withdrawal (placebo) and by history of treatment with biologics/Janus kinase (JAK) inhibitors.

Aims & Methods

At maintenance baseline, clinical responders to 12 weeks of GUS IV induction from QUASAR Phase 2b and Phase 3 induction studies (NCT04033445) were randomized 1:1:1 to GUS 200 mg SC q4w, GUS 100 mg SC q8w, or PBO (GUS withdrawal). The primary analysis population included randomized and treated pts in the Maintenance Study with a modified Mayo score of 5-9 at induction baseline. Key clinical, symptomatic, histologic, and endoscopic efficacy endpoints and safety events were evaluated through Wk 44.

Results

Of the 568 pts included, 240 (42.3%) had a history of inadequate response or intolerance to biologics/JAK inhibitors, 309 (54.4%) were biologic/JAK inhibitor naïve, and 19 (3.3%) were biologic/JAK inhibitor experienced without documented inadequate response or intolerance. Among pts with inadequate response or intolerance to biologics/JAK inhibitors (anti-TNFs [87.9%], vedolizumab [49.2%], or tofacitinib [20.0%]), 48.3% had inadequate response or intolerance to two or more biologic/JAK inhibitor therapies. At induction baseline, pts with a history of inadequate response or intolerance to biologics/JAK inhibitors had longer disease duration (mean 9.94 vs 6.25 yrs) and more severe endoscopic disease (Mayo endoscopy subscore=3, 79.6% vs 56.7%) compared with pts with no such history.

Results for key efficacy endpoints are included in Table 1. At Wk 44, clinical remission was achieved by 40.0% of GUS-treated pts (vs 8.0% of withdrawal pts, nominal p<0.001) who had inadequate response or intolerance to biologics/JAK inhibitors, and 54.2% of biologic/JAK inhibitor naïve pts who were treated with GUS (vs 25.9% of withdrawal pts, nominal p<0.001). The proportions of pts who met the key endpoints were generally higher in the biologic/JAK inhibitor naïve subpopulation compared with the subpopulation of pts with prior inadequate response or intolerance to biologics/JAK inhibitors across treatment groups, however, the treatment differences were generally greater in pts with prior inadequate response or intolerance to biologics/JAK inhibitors. Through Wk 44, adverse events for these subpopulations were consistent with the overall population, and no new safety concerns were identified.

Table 1. Endpoints at maintenance Week 44 by history of biologic/JAK inhibitor therapy: Primary analysis population	History of Inadequate Response/Intolerance to Biologics/JAK Inhibitors			Biologic/JAK Inhibitor Naïve
	GUS Withdrawal (Placebo) (N=75)	GUS 100mg SC q8w (N=77)	GUS 200 mg SC q4w (N=88)	GUS Withdrawal (Placebo) (N=108)	GUS 100mg SC q8w (N=105)	GUS 200mg SC q4w (N=96)
Clinical remission, ^a1,bn (%) Adjusted treatment difference (95%CI)	6 (8.0%)	31 (40.3%) 30.4% (18.7%, 42.1%) P<0.001	35 (39.8%) 32.4% (21.1%, 43.7%) P<0.001	28 (25.9%)	53 (50.5%) 24.3% (12.0%, 36.5%) P<0.001	56 (58.3%) 28.8% (16.5%, 41.1%) P<0.001
Maintenance of clinical remission, ^a2,bn/N (%) Treatment difference (95%CI)	4/15 (26.7%)	12/20 (60.0%) 33.3% (-0.9%, 62.1%) P=0.087	10/18 (55.6%) 28.9% (-5.9%, 59.0%) P=0.158	14/41 (34.1%)	28/43 (65.1%) 31.0% (9.3%, 50.6%) P=0.008	38/48 (79.2%) 45.0% (24.9%, 62.2%) P<0.001
Maintenance of clinical response, ^a3,b n (%) Adjusted treatment difference (95%CI)	21 (28.0%)	54 (70.1%) 40.8% (27.4%, 54.2%) P<0.001	59 (67.0%) 39.4% (25.8%, 53.0%) P<0.001	58 (53.7%)	87 (82.9%) 29.0% (17.2%, 40.8%) P<0.001	78 (81.3%) 26.3% (14.0%, 38.6%) P<0.001
Symptomatic remission,^a4,b n (%) Adjusted treatment difference (95%CI)	18 (24.0%)	50 (64.9%) 39.1% (25.9%, 52.2%) P<0.001	53 (60.2%) 36.8% (23.4%, 50.2%) P<0.001	50 (46.3%)	78 (74.3%) 27.6% (15.1%, 40.1%) P<0.001	73 (76.0%) 28.2% (15.4%, 41.0%) <0.001
Endoscopic improvement,^a5,b n (%) Adjusted treatment difference (95%CI)	6 (8.0%)	35 (45.5%) 35.8% (23.8%, 47.8%) P<0.001	37 (42.0%) 34.6% (23.1%, 46.0%) P<0.001	28 (25.9%)	56 (53.3%) 27.2% (15.0%, 39.5%) P<0.001	57 (59.4%) 30.0% (17.6%, 42.4%) P<0.001
Histo-endoscopic mucosal improvement,^a6,bn (%) Adjusted treatment difference (95%CI)	6 (8.0%)	29 (37.7%) 27.7% (16.0%, 39.5%) P<0.001	34 (38.6%) 31.2% (19.8%, 42.5%) P<0.001	25 (23.1%)	52 (49.5%) 26.1% (14.0%, 38.2%) P<0.001	54 (56.3%) 29.5% (17.3%, 41.7%) P<0.001
Endoscopic normalization (remission)^a7,b n (%) Adjusted treatment difference (95%CI)	6 (8.0%)	24 (31.2%) 21.4% (10.0%, 32.7%) P<0.001	21 (23.9%) 16.3% (6.4%, 26.1%) P=0.005	22 (20.4%)	40 (38.1%) 17.3% (5.6%, 29.1%) P=0.005	40 (41.7%) 17.5% (6.0%, 29.0%) P=0.004
*Biologic/JAK inhibitor experienced without documented inadequate response or intolerance to biologics/JAK inhibitors: placebo, n=7 ; GUS 100 mg, n=6; GUS 200 mg, n=6. All p-values were nominal.* P-values were based on the CMH test, stratified by clinical remission status at maintenance baseline and induction treatment, except for the maintenance of clinical remission, which was based on the Fisher’s exact test . Adjusted treatment difference was based on the Wald statistic with CMH weight. ^a1Clinical remission: A Mayo stool frequency subscore of 0 or 1 and not increased from induction baseline, a Mayo rectal bleeding subscore of 0, and a Mayo endoscopy subscore of 0 or 1 with no friability. ^a2Maintenance of clinical remission: Clinical remission at Wk 44 among pts in clinical remission at maintenance baseline. ^a3Maintenance of clinical response: Clinical response at Wk 44 among pts in clinical response at maintenance baseline. ^a4 Symptomatic remission: A stool frequency subscore of 0 or 1 and not increased from induction baseline, and a rectal bleeding subscore of 0. ^a5Endoscopic improvement: An endoscopy subscore of 0 or 1 with no friability present on the endoscopy.^a6Histo-endoscopic mucosal improvement: Achieving a combination of histologic improvement (neutrophil infiltration in <5% of crypts, no crypt destruction, and no erosions, ulcerations or granulation tissue per Geboes grading system) and endoscopic improvement. ^a7Endoscopic normalization: An endoscopy subscore of 0. ^b Pts who had a prohibited change in UC medication, an ostomy or colectomy, a dose adjustment (including a sham dose adjustment) , or discontinued study agent due to lack of efficacy or an adverse event of worsening of UC or other reasons except for COVID-19 related reasons (excluding COVID-19 infection) or regional crisis in Russia and Ukraine prior to the Wk 44 visit were considered not to have achieved the endpoint. Pts who were missing one or more components pertaining to a specified endpoint at Wk 44 were considered not to have achieved the endpoint.

Conclusion

Maintenance treatment with both GUS dosing regimens resulted in greater improvements compared with placebo withdrawal across key clinical, symptomatic, endoscopic, and histologic endpoints at Wk 44 regardless of prior history with biologics/JAK inhibitors. Safety results for both GUS maintenance dose regimens were comparable across subpopulations by treatment history and consistent with the known safety profile of GUS.

Disclosure

JRA: consultant for Finch Therapeutics, Artugen, Pfizer, Takeda, Janssen, and Iterative Scopes; research support from Merck; consultant and speaker for BMS.
JP: received consultancy fees/honorarium from AbbVie, Alimentiv, Athos, Atomwise, Boehringer Ingelheim, Celsius, Ferring, Galapagos, Genentech/Roche, GlaxoSmithKline, Janssen, Mirum, Nimbus, Pfizer, Progenity, Prometheus, Protagonist, Revolo, Sanofi, Sorriso, Surrozen, Takeda, and Wasserman, and has served on a data safety monitoring board for Alimentiv, Mirum, Sorriso, Sanofi, and Surrozen.
LPB: personal fees from AbbVie, Allergan, Alma, Amgen, Applied Molecular Transport, Arena, Biogen, Boehringer Ingelheim, BMS, Celgene, Celltrion, Enterome, Enthera, Ferring, Fresenius, Genentech, Gilead, Hikma, Index Pharmaceuticals, Janssen, Lilly, MSD, Mylan, Nestlé, Norgine, Oppilan Pharma, OSE Immunotherapeutics, Pfizer, Pharmacosmos, Roche, Samsung Bioepis, Sandoz, Sterna, Sublimity Therapeutics, Takeda, Tillots and Vifor; grants from AbbVie, MSD and Takeda; stock options from CTMA.
BES: consulting fees from Abbvie, Alimentiv, Amgen, Arena Pharmaceuticals, Artugen Therapeutics, Astra Zeneca, Boehringer Ingelheim, Boston Pharmaceuticals, Calibr, Celgene, Celltrion, ClostraBio, Equillium, Enthera, Evommune, Fresenius Kabi, Galapagos, Genentech (Roche), Gilead Sciences, GlaxoSmithKline, Gossamer Bio, Index Pharmaceuticals, Innovation Pharmaceuticals, Inotrem, Kaleido, Kallyope, Merck, Morphic Therapeutics, MRM Health, Progenity, Prometheus Biosciences, Prometheus Laboratories, Protagonist Therapeutics, Q32 Bio, Sun Pharma, Surrozen, Target RWE,Teva, TLL Pharmaceutical, Ventyx Biosciences; consulting and speaking fees from Abivax; consulting and speaking fees and other support from Lilly; research grants, consulting and speaking fees and other support from Bristol Myers Squibb, Janssen, Pfizer, Takeda; research grants and consulting fees from Theravance Biopharma; and stock options from Ventyx Biopharma.
SY, KGH, MG, JZ and HZ: employees of Johnson & Johnson and own company stock/stock options.
JB received grant support from AbbVie, Janssen, Pfizer and Ferring. Consulting fees from Janssen, Pfizer, Abbvie, Takeda, Ferring, Microba, Anatara, DrFalk, Bristol Meyers Squibb, Glaxo Smith Klein and Chieisi, and lecture fees from AbbVie, Janssen, Pfizer, Takeda, and Ferring.
JK reports personal fees from Bristol-Myers Squibb, Celltrion, Ferring, Fresenius, Janssen, Lilly, Nestlé.
TK served as an investigator for Janssen.
TH: grant support from AbbVie, Daiichi-Sankyo, EA Pharma Co, Ltd. JIMRO, Mitsubishi Tanabe Pharma Corporation, Mochida Pharmacuetical Co., Ltd., Nippon Kayaku Co., Ltd., Pfizer Inc., Takeda Pharmaceutical Co., Ltd., consulting fees from EA Pharma Co, Ltd., Janssen Research & Development, LLC., and lecture fees from AbbVie, EA Pharma Co, Ltd, Mitsubishi Tanabe Pharma Corporation, Takeda Pharmaceutical Co., Ltd.
DTR: research funding from Takeda, and has served as a consultant to AbbVie, Altrubio, Allergan, Inc., Arena Pharmaceuticals, Aslan Pharmaceuticals, Athos Therapeutics, Bellatrix Pharmaceuticals, Boehringer Ingelheim, Ltd., Bristol Myers Squibb, Celgene Corp/Syneos, Connect BioPharma, GalenPharma/Atlantica, Genentech/Roche, InDex Pharmaceuticals, Ironwood Pharmaceuticals, Iterative Scopes, Janssen Pharmaceuticals, Eli Lilly, Materia Prima, Pfizer, Prometheus Biosciences, Reistone, Takeda, Techlab, Inc and is a co-founder of Cornerstones Health, Inc.
BB: advisor/speaker for Abbvie, BMS, Ferring, Janssen, Merck, Novartis, Organon, Pfizer, Sandoz, Takeda; advisor for Alimentiv, Allergan, AMT, Bausch Health, BMS, Celgene, Celltrion Healthcare, Eupraxia, Fresenius Kabi, Genentech, Gilead, Iterative Scopes, Jamp Pharma, Merck Amgen, Microbiome Insights, Mylan, Pendopharm, Protagonist, Viatris; received research support from Abbvie, Amgen, BI, BMS, Genentech, GSK, Janssen, Merck, Qu Biologic; and reports stock options for Qu Biologic.
AD: fees for clinical trials, data monitoring boards, statistical analysis and end point committees from Abivax, AbbVie, BMS, Dr Falk Foundation, Galapagos, Gilead, Janssen, and Pfizer; consultancy fees from AbbVie, Amgen, Arena Pharmaceuticals, Biogen, Boehringer Ingelheim, BMS, Celltrion, Dr Falk Foundation, Ferring Pharmaceuticals, Fresenius Kabi, Galapagos, Janssen, Lilly, MSD, Pfizer, Pharmacosmos, Roche, Sandoz,; Stada, Takeda, Tillotts, and Vifor Pharma; payment for lectures from AbbVie, Biogen, CED Service GmbH, Celltrion, Falk Foundation, Ferring, Galapagos, Gilead, High5MD, Janssen, Materia Prima, MedToday, MSD, Pfizer, Sandoz, Takeda, Tillotts, and Vifor Pharma; payment for manuscript preparation from Abbvie, Falk Foundation, Janssen, Takeda, Thieme, and UniMed Verlag.

THE EFFICACY OF MAINTENANCE TREATMENT WITH GUSELKUMAB IN PATIENTS WITH MODERATELY TO SEVERELY ACTIVE ULCERATIVE COLITIS: PHASE 3 QUASAR MAINTENANCE STUDY RESULTS AT WEEK 44 BY BIOLOGIC/JANUS KINASE INHIBITOR HISTORY

Jessica Allegretti 1, Julian Panés 2, Laurent Peyrin-Biroulet 3, Bruce E. Sands 4, Shadi Yarandi 5, Gary KH Huang 5, Matthew Germinaro 5, Jia Zhan 5, Hongyan Zhang 5, Jakob Begun 6, Jaroslaw Kierkus 7, Tetiana Kravchenko 8, Tadakazu Hisamatsu 9, David T. Rubin 10, Brian Bressler 11, Axel Dignass 12

1 Brigham and Women´s Hospital Crohn's and Colitis Center, Boston, United States

2 Hospital Clínic Barcelona, Barcelona, Spain

3 Nancy University Hospital, Nancy, France

4 Icahn School of Medicine at Mount Sinai, New York, United States

5 Janssen Research & Development, LLC, Spring House, United States

6 Mater Hospital Brisbane, South Brisbane, Australia

7 Children’s Memorial Health Institute, Warsaw, Poland

8 National Medical University, Kyiv, Ukraine

9 Kyorin University School of Medicine, Tokyo, Japan

10 University of Chicago Medicine, Chicago, United States

11 University of British Columbia, Vancouver, Canada

12 Agaplesion Markus Krankenhaus, Frankfurt/ Main, Germany

Event

UEG Week Vienna 2024

Topics

IBD

Submission format

Abstract

Session

Expanding treatment response in IBD

Citation

United European Gastroenterology Journal 2024; 12 (Supplement 8)

Published

2024

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Auto-brewery syndrome: A disease model

Gianluca Ianiro 1

1 Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Catholic University of Rome, Rome, Italy

Event

UEG Week Berlin 2025

Topics

Mechanisms & Personalised Medicine

Session

Breath testing and clinical metabolomics: Back to the future

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Biologic drugs

Luc Biedermann 1

1 USZ Zürich, Zürich, Switzerland

Event

UEG Week Berlin 2025

Topics

Mechanisms & Personalised Medicine Small Intestine & Nutrition Oesophagus Paediatrics

Session

Therapy update: EoE

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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Panel discussion: Therapy update - EoE

Event

UEG Week Berlin 2025

Topics

Mechanisms & Personalised Medicine Small Intestine & Nutrition Oesophagus Paediatrics

Session

Therapy update: EoE

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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CONCOMITANT ATOPY INFLUENCES RESPONSE TO PROTON-PUMP INHIBITORS IN EOSINOPHILIC ESOPHAGITIS: AN ANALYSIS OF THE EOE CONNECT REGISTRY

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Introduction

Eosinophilic esophagitis (EoE) is type-2 chronic inflammatory disorder usually accompanied by other atopic conditions including rhinitis, conjunctivitis, bronchial asthma, dermatitis, hives or chronic rhinosinusitis with nasal polyps. The influence of these atopies in the response to the EoE therapy has been barely investigated, with opposite results in small cohorts (1,2).

Aims & Methods

We aim to describe atopic concomitances in European EoE patients and to evaluate its influence on effectiveness of first-line therapy, consisting in proton-pump inhibitors (PPIs), swallowed topical corticosteroids (STCs) and food-elimination diets (FEDs).
A cross-sectional analysis of the multicenter EoE CONNECT registry (3) was performed. Demographic and clinical data from patients recruited at 42 hospitals in 4 European countries were extracted on March 25^th, 2025. Concomitant atopies were classified as seasonal or persistent. Clinico-histological response (CHR) was defined as the simultaneous presence of symptomatic remission and a peak eosinophil count <15 eosinophils per high power field after therapy.

Results

Overall, 3,900 patients (75.6% males, mean age 33.3 ±15.1 years) were analyzed (Table). CHR rate after first-line monotherapy with PPIs, STCs or FEDs was 50.4% (n=2,685). PPIs was the only treatment affected by concomitant atopy: presence of asthma and hives significantly reduced CHR rates to PPIs (42.7% vs 49.7%, p=0.005, and 39.3% vs 48%, p=0.044, respectively), and CHR also tended to be lower in presence of conjunctivitis (43.6% vs 48.4, p=0.067) and dermatitis (43.2% vs 48.3%, p=0.081). Seasonal or persistent presentation of atopy did not influence response to treatment. Taking into account age at diagnosis, the effect of concomitant atopy in reducing CHR to PPIs was exclusively observed in adults (≥18 years old) for asthma (43.8% vs 51.3%, p=0.007) and dermatitis (42.6% vs 50.3%, p=0.026), and in children (<18 years old) for hives (17.4% vs 39.9%, p=0.032).
We next analyzed whether the number of concomitant atopies influenced CHR to first-line therapy. While no differences were found among patients who presented only one atopic condition, the presence of 2 or more atopies reduced PPI effectiveness in adults (45.0% vs 50.7%, p=0.032) and to FEDs in children (23.5% vs 59.3%, p=0.020). A reduction in CHR rate after PPI therapy was even greater in adults with 3 or more atopies concomitant to EoE (39.0% vs 50.4%, p=0.001). Effectiveness of first-line STCs were not affected in any of these comparisons.

Age at diagnosis (n=3,705)	<18 years: 19.4%; ≥18 years: 80.6%
Rhinitis (n=3,558)	49.4 %; Seasonal 77.3 %; Persistent 22.7%
Conjunctivitis (n=3,499)	23.8%; Seasonal 88.5%; Persistent 11.5%
Asthma (n=3,526)	28.6%; Seasonal 63.8%; Persistent 36.2%
Dermatitis (n=3,507)	18.7%; Seasonal 43.4%; Persistent 56.6%
Hives (n=3,403)	7.1%; Seasonal 50.7 %; Persistent 49.3%
Chronic rhinosinusitis with nasal polyps (n=3,461)	2.1%; Persistent: 100%
Number of allergies (n=3,353)	At least 1 allergy: 64.7%; ≥2 allergies: 39.1%; ≥3 allergies: 17.4%
Response to 1st treatment option in monotherapy evaluated (n=3,266)	PPI: 82.6%; STC: 11.9%; FED: 5.5%

Conclusion

The coexistence of asthma, dermatitis and hives determined lower response to PPI therapy for EoE. Association of 2 or more atopic condition further decreased effectiveness of PPIs in adults and of FEDs in children.

References

1. Ancellin M, Ricolfi-Waligova L, Clerc-Urmès I, et al. Management of eosinophilic esophagitis in children according to atopic status: a retrospective cohort in northeast of France. Arch Pediatr. 2020;27(3):122-127.
2. Reed WD, Ocampo AA, Xue Z, et al. Eosinophilic esophagitis patients with multiple atopic conditions: clinical characteristics and treatment response to topical steroids. Ann Allergy Asthma Immunol. 2023;131(1): 109-115.e2.
3. Lucendo AJ, Santander C, Savarino E, et al. EoE CONNECT, the European Registry of Clinical, Environmental, and Genetic Determinants in Eosinophilic Esophagitis: rationale, design, and study protocol of a large-scale epidemiological study in Europe. Therap Adv Gastroenterol. 2022;15:17562848221074204.

CONCOMITANT ATOPY INFLUENCES RESPONSE TO PROTON-PUMP INHIBITORS IN EOSINOPHILIC ESOPHAGITIS: AN ANALYSIS OF THE EOE CONNECT REGISTRY

Leticia Rodríguez-Alcolado 1, Emilio Jose Laserna-Mendieta 2, Victoria Úbeda Vargas 3, Sergio Casabona-Francés 4, Edurne Amorena Muro 5, Leonardo Blas 6, Edoardo Vincenzo Savarino 7, Isabel Pérez-Martínez 8, Jesús Barrio Andrés 9, Antonio Guardiola Arevalo 10, Danila Guagnozzi 11, Marina Coletta 12, Laura Martín Asenjo 13, Luisa de la Peña Negro 14, Gaia Pellegatta 15, Alejandro García-Díaz 16, Elena Betoré 17, Anne Lund Krarup 18, Susana de la Riva 19, Silvia Carrión Bolorino 20, María Pipa 21, Sonia Fernandez-Fernandez 22, Carlos Teruel Sanchez - Vegazo 23, Juan Enrique Naves 24, BLANCA BELLOC 25, Salvatore Oliva 26, Mónica Llorente-Barrio 27, Carlo Maria Rossi 28, Juan Armando Rodríguez Oballe 29, Maria Luisa Masiques-Mas 30, Raúl Honrubia-López 31, Raffaella Dainese Plichon 32, Alexis González Almeida 33, Luis Bujanda Fernández de Piérola 34, Juan Khaled Bisso Zein 35, Alba Juan-Juan 36, Sara Feo Ortega 3, Verónica Martín Domínguez 4, Jennifer Fernández-Pacheco 4, Oscar Nantes Castillejo 5, Julia Nicolay Maneru 5, Marta Álvarez-García 6, Matteo Ghisa 7, Carmen Díaz-Donado 37, Paula Gil Simón 9, Alicia Granja 10, Ronald Llerena Castro 11, Roberto Penagini 12, Cecilio Santander 4, Alfredo J. Lucendo 2

1 Hospital General de Tomelloso, Instituto de Investigación Sanitaria de Castilla-La Mancha (IDISCAM), Tomelloso, Spain|||University of Alcalá, Alcalá de Henares, Spain

2 Hospital General de Tomelloso, Instituto de Investigación Sanitaria de Castilla-La Mancha (IDISCAM), Tomelloso, Spain|||Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain

3 Hospital General de Tomelloso, Instituto de Investigación Sanitaria de Castilla-La Mancha (IDISCAM), Tomelloso, Spain

4 Hospital Universitario de La Princesa, Madrid, Spain|||Instituto de Investigación Sanitaria La Princesa, Madrid, Spain

5 Hospital Universitario de Navarra. Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona, Spain

6 Fundacion Jiménez Díaz, Madrid, Spain

7 Azienda Ospedaliera Università di Padova, Padua, Italy

8 Hospital Universitario Central de Asturias, Oviedo, Spain|||Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Oviedo, Spain

9 Hospital Universitario Rio Hortega, Valladolid, Spain

10 Hospital Universitario de Fuenlabrada, Fuenlabrada, Spain

11 Hospital Vall d'Hebrón, Barcelona, Spain

12 Fondazione IRCCS Cà Granda - Ospedale Maggiore Policlinico, Milan, Italy

13 Hospital Universitario de Álava, Vitoria, Spain

14 Hospital de Viladecans, Viladecans, Spain

15 Humanitas Research Hospital, Rozzano, Italy

16 Hospital Universitario Puerta de Hierro, Majadahonda, Spain

17 Hospital Universitario Miguel Servet, Zaragoza, Spain

18 The North Danish Regional Hospital, Hjørring, Denmark

19 Clínica Universidad de Navarra, Pamplona, Spain

20 Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain|||Hospital de Mataró, Mataró, Spain

21 Hospital Universitario de Cabueñes, Gijón, Spain

22 Hospital Universitario Severo Ochoa, Leganés, Spain

23 Hospital Universitario Ramón y Cajal, Madrid, Spain

24 Hospital del Mar, Barcelona, Spain

25 Hospital General de la Defensa, Zaragoza, Spain

26 University Hospital Umberto I - Sapienza University of Rome, Roma, Italy

27 Hospital Santa Bárbara, Soria, Spain

28 Fondazione IRCCS Policlinico San Matteo, Pavia, Italy

29 Hospital Universitario Santa María, Lérida, Spain

30 Hospital de Granollers, Granollers, Spain

31 Hospital Universitario Infanta Sofía, San Sebastián de los Reyes, Spain

32 Centre Hospitalier d’Antibes Juan-les-Pins, Antibes, France

33 Complejo Hospitalario Universitario Insular Materno Infantil, Las Palmas de Gran Canaria, Spain

34 Hospital Universitario de Donostia-Instituto Biodonostia, San Sebastián, Spain

35 Hospital Universitario Costa del Sol, Marbella, Spain

36 Hospital Sant Joan Despí Moisès Broggi, Sant Joan Despí, Spain

37 Hospital Universitario Central de Asturias, Oviedo, Spain

Event

UEG Week Berlin 2025

Topics

Histopathology Mechanisms & Personalised Medicine Oesophagus

Submission format

Abstract

Session

EoE: From gene to clinic

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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Established and novel targets for breath testing

Christian Schulz 1

1 Ludwig Maximilian University, Munich, Germany

Event

UEG Week Berlin 2025

Topics

Mechanisms & Personalised Medicine

Session

Breath testing and clinical metabolomics: Back to the future

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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From Adiposity to Hepatic Health: Exploring the Pleiotropic Clinical Impact of Semaglutide (Novo Nordisk) (Complete Session)

Naim Alkhouri 1, Gema Frühbeck 2

1 Transplant Hepatology Arizona Liver Health Phoenix, AZ, None, United States of America

2 Clínica Universidad de Navarra, Pamplona, Spain

Publisher

Novo Nordisk A/S

Event

UEG Week Berlin 2025

Session

From Adiposity to Hepatic Health: Exploring the Pleiotropic Clinical Impact of Semaglutide (Novo Nordisk)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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