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GUSELKUMAB, AN IL-23P19 SUBUNIT–SPECIFIC MONOCLONAL ANTIBODY, BINDS CD64 ON THE SURFACE OF IL-23-SECRETING MYELOID CELLS, CAPTURES LOCALLY PRODUCED IL-23, AND DELIVERS IL-23 TO INTRACELLULAR COMPARTMENTS

Raja Atreya 1, Maria T. Abreu 2, James G. Krueger 3, Kilian Eyerich 4,5, Robert Bissonnette 6, Carrie Greving 7, Brian Stoveken 8, Deeper Hammaker 7, Kristen Leppard 8, John Hartman 8, Indra Sarabia 7, Matthew Duprie 8, Joseph Brown 7, M. Merle Elloso 9, Phuc Bao 7, Eilyn Lacy 8, Kacey Sachen 7, Christopher Ritchlin 10, Iain B. McInnes 11, Matthieu Allez 12, Anne Fourie 7

Affiliations

1 Erlangen University Hospital, Erlangen, Germany

2 University of Miami, Miami, FL, United States

3 The Rockefeller University, New York, NY, United States

4 Medical Center, Freiburg, Germany

5 Karolinska Institute, Stockholm, Sweden

6 Innovaderm Research Inc., Montréal, Québec, Canada

7 Janssen Research & Development, LLC, San Diego, CA, United States

8 Janssen Research & Development, LLC, Spring House, PA, United States

9 Janssen Scientific Affairs, LLC, Horsham, PA, United States

10 University of Rochester, Rochester, NY, United States

11 University of Glasgow, Glasgow, United Kingdom

12 Hôpital Saint-Louis, Université Paris Cité, Paris, France

Summary

AI Generated

Guselkumab, but not risankizumab, binds CD64 on IL-23-producing myeloid cells in addition to neutralizing IL-23, which may contribute to therapeutic differences between these anti-IL-23p19 monoclonal antibodies in inflammatory bowel disease.

Guselkumab is a fully human IgG1 antibody with a native Fc region that binds Fcγ receptors, whereas risankizumab has a mutated Fc region designed to prevent Fcγ receptor binding.
Both antibodies displayed comparable picomolar binding affinity for IL-23 and equivalent high potency for inhibiting IL-23-induced STAT3 phosphorylation.
Only guselkumab showed strong binding to CD64 and was able to bind CD64-positive IL-23-producing inflammatory monocytes while simultaneously capturing endogenous IL-23 secreted from those cells.
The guselkumab-IL-23 complex bound to CD64-positive inflammatory macrophages was internalized in a time-dependent manner, mediating delivery of IL-23 to low-pH intracellular compartments.
The authors hypothesize that guselkumab may be locally enriched in inflamed intestinal tissue where CD64-positive IL-23-producing myeloid cells are increased, potentially enabling dual action by neutralizing IL-23 at its source and mediating its removal from tissue.

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Abstract

Introduction

Monoclonal antibodies (mAbs) targeting the interleukin (IL)-23p19 subunit are effective in the treatment of inflammatory bowel diseases (IBD) but have different molecular attributes that may translate to distinctions in clinical efficacy. Guselkumab (GUS) is a fully human immunoglobulin G (IgG) 1 mAb with a native Fc region, whereas risankizumab (RZB) is a humanized IgG1 mAb with a mutated Fc region. The native Fc region enables GUS to bind Fcγ receptors (FcγRs), whereas RZB was designed to prevent binding to FcγRs by virtue of its mutated Fc domain. This is of particular interest because FcγRI (CD64)⁺ IL-23–producing myeloid cells are increased in the inflamed colon in IBD and correlate with endoscopic disease severity (1, 2).

Aims & Methods

We compared functional characteristics of the antigen-binding and Fc regions of GUS and RZB and explored the implications of CD64 binding on IL-23 neutralization. IL-23 binding affinities of GUS and RZB were compared in vitro using KinExA. In vitro cellular potency of GUS and RZB was measured by the impact on IL-23–induced STAT3 phosphorylation in human peripheral blood mononuclear cells. Binding of GUS and RZB to FcγRs was assessed in cells transfected with individual FcγRs. In primary human inflammatory monocytes, differentiated with granulocyte-macrophage colony-stimulating factor and interferon-γ followed by toll-like receptor stimulation to induce IL-23 production, binding of GUS and RZB to CD64 and capture of endogenously secreted IL-23 were assessed using flow cytometry. The potential impact of GUS binding to CD64 on these cells was assessed using a human 41-plex cytokine bead assay. To determine the fate of CD64-bound GUS and GUS-captured IL-23, live cell confocal imaging was performed with CD64⁺ inflammatory human macrophages cultured with fluorescently-labeled mAbs and IL-23 labeled with a pH-sensitive fluorophore.

Results

Although GUS and RZB displayed comparable picomolar binding affinity for IL-23 and equivalent high potency for inhibition of IL-23-induced STAT3 phosphorylation, only GUS showed strong binding to CD64 compared with other FcγRs. GUS, but not RZB, was able to bind to the surface of CD64⁺ IL-23-producing inflammatory monocytes and simultaneously capture endogenous IL-23 secreted from the same cells. GUS binding to CD64 did not affect cytokine production by these cells. The GUS–IL-23 complex bound to the surface of CD64⁺ inflammatory macrophages was internalized in a time-dependent manner, mediating the delivery of IL-23 to low-pH intracellular compartments.

Conclusion

GUS, but not RZB, can simultaneously bind CD64⁺myeloid cells relevant in the pathogenesis of IBD (1, 2) and neutralize IL-23 with high affinity and potency. These data support a hypothesis of local GUS enrichment within the inflamed microenvironment of the intestinal tissue, where CD64⁺ IL-23–producing myeloid cell populations are increased. This may enable dual action of GUS against IL-23, whereby GUS can potently neutralize IL-23 at its source of production and mediate its internalization and removal from inflamed tissue, thus potentially contributing to differences in therapeutic profiles between GUS and RZB.

References

Chapuy L, et al. Mucosal Immunol. 2019;12(3):703-719.
Chapuy L, et al. J Crohns Colitis. 2020;14(1):79-95.

Disclosure

RA served as a paid or unpaid consultant for or received honoraria from AbbVie, Amgen, Arena Pharmaceuticals, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Celltrion Healthcare, Dr. Falk Pharma, Ferring, Fresenius Kabi, Galapagos, Gilead, GlaxoSmithKline, InDex Pharmaceuticals, Janssen, Kliniksa Pharmaceuticals, Merk Sharp & Dohme, Novartis, Pfizer, Roche, Samsung Bioepsis, Stelic, Sterna Biologicals, Takeda, and Tillotts. MTA has received consulting and/or speaking fees from AbbVie, Alimentiv, Amgen, Arena Pharmaceuticals, Bristol Myers Squibb, Celsius Therapeutics, Eli Lilly and Company, Gilead Sciences, Janssen Pharmaceuticals, Microba Life Sciences, Pfizer Pharmaceutical, Prometheus Biosciences, Takeda Pharmaceuticals, UCB Biopharma SRL, and WebMD Global LLC. JGK served as a consultant for, received honoraria from, and/or received institutional grant support from AbbVie, Allergan, Amgen, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Janssen, Eli Lilly, Nimbus Lackshmi, Novartis, Pfizer, and UCB; served as a consultant for and/or received honoraria from Aclaris, Almirall, Arena, Aristea, Asana, Aurigene, Escalier, Galapagos, MoonLake Immunotherapeutics, Sanofi, Sienna Biopharmaceuticals, Sun Pharma, Target-Derm, Valeant, and Ventyx; and received institutional grant support from Akros, Avillion, Exicure, Incyte, Innovaderm, Kyowa Kirin, Novan, Parexel, Regeneron, and Vitae Pharmaceuticals. KE received speaker fees from and/or served on an advisory board for AbbVie, Almirall, Boehringer Ingelheim, Bristol Myers Squibb, Hexal, LEO Pharma, Eli Lilly, Janssen, Pfizer, Novartis, Sanofi, and UCB. RB is an advisory board member, consultant, speaker and/or investigator for and received honoraria and/or grants from AbbVie, Alumis, Almirall, Amgen, AnaptysBio, Arcutis, Aristea, Bausch Health, Boehringer-Ingelheim, Boston, Bristol-Myers Squibb, Dermavant, Eli Lilly, Escalier, Janssen, Kyowa Kirin, LEO Pharma, Nimbus, Novartis, Pfizer, Regeneron, Sienna, UCB, VentyxBio and Xencor; and is an employee and shareholder of Innovaderm Research. CR received grant/research support and/or consulting fees from UCB, AbbVie, Amgen, Lilly, Pfizer, Novartis, Gilead, and Janssen. IBM received consultant fees from and/or grant research support from Compugen, AstraZeneca, Bristol Myers Squibb, Amgen, Eli Lilly, GlaxoSmithKline, Janssen, Novartis, Roche, UCB, AbbVie, Cabaletta, Gilead, Pfizer, and Sanofi; is a shareholder and/or sits on a board of directors for Compugen, Evelo, and Causeway Therapeutics; serves as a board member for National Health Service Greater Glasgow and Clyde; and is a trustee for Versus Arthritis. MA has received consulting and/or lecture fees and grant support from Janssen, Takeda, and Genentech/Roche; consulting and/or lecture fees from AbbVie, Amgen, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Celltrion, Eli Lilly, Ferring, Galapagos, Gilead, IQVIA, Novartis, Pfizer, and Tillotts. CG, BS, DH, KL, JH, IS, MD, JB, MME, PB, EL, KS, and AF are current or former employees of Janssen and may hold stock in Johnson & Johnson.

Conference

UEG Week Copenhagen 2023

Topics

IBD

Submission format

Abstract

Session

IL-23: Many but different? (Posters)

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

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Best of UEG Week 2024 with Thomas Seufferlein on "Oncology for Gastroenterologists"

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

Victoria Úbeda Vargas

Diverticulitis: When not to be worried?

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Salvatore Petta

Sense and non-sense of the new nomenclature

Maria Effenberger

UEG Podcast Episode

UEG Podcast

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Best of UEG Week 2024 with Thomas Seufferlein on "Oncology for Gastroenterologists"

Thomas Seufferlein, Julia Mayerle

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Abstract

Topics

Digestive Oncology

Published

2024

More Like This:

Best of UEG Week 2024 with Thomas Seufferlein on "Oncology for Gastroenterologists"

Thomas Seufferlein

EUS-guided biliary drainage (Complete Session)

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

Victoria Úbeda Vargas

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Salvatore Petta

Sense and non-sense of the new nomenclature

Maria Effenberger

UEG Presentation

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EUS-guided biliary drainage (Complete Session)

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EUS-guided biliary drainage (Complete Session)

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Abstract

Event

UEG Week Berlin 2025

Topics

Endoscopy Hepatobiliary

Session

EUS-guided biliary drainage

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

Best of UEG Week 2024 with Thomas Seufferlein on "Oncology for Gastroenterologists"

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EUS-guided biliary drainage (Complete Session)

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Salvatore Petta

Sense and non-sense of the new nomenclature

Maria Effenberger

UEG Presentation

Share via Email Share on Facebook Share on X Share on LinkedIn Share on Bluesky

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

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

Leticia Rodríguez-Alcolado 1,2, Emilio Jose Laserna-Mendieta 1,3, Victoria Úbeda Vargas 1, Sergio Casabona-Francés 4,5, Edurne Amorena Muro 6, Leonardo Blas 7, Edoardo Vincenzo Savarino 8, Isabel Pérez-Martínez 9,10, Jesús Barrio Andrés 11, Antonio Guardiola Arevalo 12, Danila Guagnozzi 13, Marina Coletta 14, Laura Martín Asenjo 15, Luisa de la Peña Negro 16, Gaia Pellegatta 17, Alejandro García-Díaz 18, Elena Betoré 19, Anne Lund Krarup 20, Susana de la Riva 21, Silvia Carrión Bolorino 3,22, María Pipa 23, Sonia Fernandez-Fernandez 24, Carlos Teruel Sanchez - Vegazo 25, Juan Naves 26, BLANCA BELLOC 27, Salvatore Oliva 28, Mónica Llorente-Barrio 29, Carlo Maria Rossi 30, Juan Armando Rodríguez Oballe 31, Maria Luisa Masiques-Mas 32, Raúl Honrubia-López 33, Raffaella Dainese Plichon 34, Alexis González Almeida 35, Luis Bujanda Fernández de Piérola 36, Juan Khaled Bisso Zein 37, Alba Juan-Juan 38, Sara Feo Ortega 1, Verónica Martín Domínguez 4,5, Jennifer Fernández-Pacheco 4,5, Oscar Nantes Castillejo 6, Julia Nicolay Maneru 6, Marta Álvarez-García 7, Matteo Ghisa 8, Carmen Díaz-Donado 9, Paula Gil Simón 11, Alicia Granja 12, Ronald Llerena Castro 13, Roberto Penagini 14, Cecilio Santander 4,5, Alfredo J. Lucendo 1,3

Affiliations

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

2 University of Alcalá, Alcalá de Henares, Spain

3 Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain

4 Hospital Universitario de La Princesa, Madrid, Spain

5 Instituto de Investigación Sanitaria La Princesa, Madrid, Spain

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

7 Fundacion Jiménez Díaz, Madrid, Spain

8 Azienda Ospedaliera Università di Padova, Padua, Italy

9 Hospital Universitario Central de Asturias, Oviedo, Spain

10 Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Oviedo, Spain

11 Hospital Universitario Rio Hortega, Valladolid, Spain

12 Hospital Universitario de Fuenlabrada, Fuenlabrada, Spain

13 Hospital Vall d'Hebrón, Barcelona, Spain

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

15 Hospital Universitario de Álava, Vitoria, Spain

16 Hospital de Viladecans, Viladecans, Spain

17 Humanitas Research Hospital, Rozzano, Italy

18 Hospital Universitario Puerta de Hierro, Majadahonda, Spain

19 Hospital Universitario Miguel Servet, Zaragoza, Spain

20 The North Danish Regional Hospital, Hjørring, Denmark

21 Clínica Universidad de Navarra, Pamplona, Spain

22 Hospital de Mataró, Mataró, Spain

23 Hospital Universitario de Cabueñes, Gijón, Spain

24 Hospital Universitario Severo Ochoa, Leganés, Spain

25 Hospital Universitario Ramón y Cajal, Madrid, Spain

26 Hospital del Mar, Barcelona, Spain

27 Hospital General de la Defensa, Zaragoza, Spain

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

29 Hospital Santa Bárbara, Soria, Spain

30 Fondazione IRCCS Policlinico San Matteo, Pavia, Italy

31 Hospital Universitario Santa María, Lérida, Spain

32 Hospital de Granollers, Granollers, Spain

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

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

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

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

37 Hospital Universitario Costa del Sol, Marbella, Spain

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

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Abstract

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.

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

More Like This:

Best of UEG Week 2024 with Thomas Seufferlein on "Oncology for Gastroenterologists"

Thomas Seufferlein

EUS-guided biliary drainage (Complete Session)

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

Victoria Úbeda Vargas

Diverticulitis: When not to be worried?

Johannes Kurt Schultz

COMPARATIVE EFFECTS OF METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE AND METABOLIC AND ALCOHOL-ASSOCIATED STEATOTIC LIVER DISEASE (METALD) ON RISK OF HEPATIC AND EXTRA-HEPATIC OUTCOMES: A META-ANALYSIS

Salvatore Petta

Sense and non-sense of the new nomenclature

Maria Effenberger

UEG Presentation

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Diverticulitis: When not to be worried?

Johannes Kurt Schultz 1

Affiliations

1 Univertsity of Oslo, Oslo, Norway

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Abstract

Event

UEG Week Berlin 2025

Topics

Colorectal Hepatobiliary Pancreas

Session

Predicting disease severity

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

Best of UEG Week 2024 with Thomas Seufferlein on "Oncology for Gastroenterologists"

Thomas Seufferlein

EUS-guided biliary drainage (Complete Session)

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

Victoria Úbeda Vargas

Diverticulitis: When not to be worried?

Johannes Kurt Schultz

COMPARATIVE EFFECTS OF METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE AND METABOLIC AND ALCOHOL-ASSOCIATED STEATOTIC LIVER DISEASE (METALD) ON RISK OF HEPATIC AND EXTRA-HEPATIC OUTCOMES: A META-ANALYSIS

Salvatore Petta

Sense and non-sense of the new nomenclature

Maria Effenberger

UEG Poster

Standard Poster

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COMPARATIVE EFFECTS OF METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE AND METABOLIC AND ALCOHOL-ASSOCIATED STEATOTIC LIVER DISEASE (METALD) ON RISK OF HEPATIC AND EXTRA-HEPATIC OUTCOMES: A META-ANALYSIS

Ciro Celsa 1, Grazia Pennisi 2, Adele Tulone 1, Giacinta Ciancimino 1, Marco Vaccaro 1, Fabiana Pecorella 1, Gabriele Di Maria 1, Marco Enea 1, Calogero Camma 1, Salvatore Petta 1

Affiliations

1 University of Palermo, Palermo, Italy

2 Policlinico Paolo Giaccone, Palermo, Italy

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Abstract

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction with alcohol-related steatotic liver disease (MetALD) are two separate entities within the spectrum of steatotic liver disease (SLD).

Aims & Methods

This meta-analysis aims to compare the risks of hepatic and extrahepatic outcomes between MASLD and MetALD. We systematically searched for observational cohort studies published up to March 1, 2025, comparing clinical outcomes between individuals with MASLD and MetALD. The primary outcome was liver-related events, while secondary outcomes included hepatocellular carcinoma (HCC), liver-related mortality, cardiovascular events, extrahepatic cancers, and all-cause mortality. We used random-effect models to calculate pooled hazard ratios (HRs) with 95% confidence intervals (95% CI).

Results

Twenty-four studies involving 11,396,962 individuals were analyzed (9,622,716 with MASLD and 1,774,246 with MetALD). Individuals with MetALD had significantly higher risks of liver-related events (HR 1.62, 95% CI 1.16-2.25, p=0.02) and HCC (HR 1.33, 95%CI 1.00-1.77, p=0.04) than those with MASLD. The risk of extrahepatic cancers was also increased in MetALD (HR 1.03, 95% CI 1.01-1.06, p<0.001), while the rates of cardiovascular events (HR 0.96, 95% CI 0.85-1.09, p=0.48), extrahepatic cancer-related mortality (HR 1.44, 95% CI 0.97-2.15, p=0.07), and all-cause mortality (HR 1.08, 95% CI 0.97-1.19, p=0.14) did not differ between these two conditions.

Conclusion

MetALD confers a higher risk of liver-related outcomes, HCC, and extrahepatic cancers than MASLD, while all-cause mortality and cardiovascular risk are similar between the two conditions. These findings emphasize the need for distinct clinical strategies for these related yet different entities within the SLD spectrum and highlight the importance of conducting pharmacological clinical trials in this context.

Disclosure

Nothing to disclose

Conference

UEG Week Berlin 2025

Topics

Hepatobiliary

Submission format

Abstract

Session

MASLD: Clinical aspects, experimental and pathology (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Sense and non-sense of the new nomenclature

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Sense and non-sense of the new nomenclature

Maria Effenberger 1

Affiliations

1 Medical University of Innsbruck, Innsbruck, Austria

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Abstract

Event

UEG Week Berlin 2025

Topics

Hepatobiliary Mechanisms & Personalised Medicine

Session

Challenges in metabolic liver diseases

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

Best of UEG Week 2024 with Thomas Seufferlein on "Oncology for Gastroenterologists"

Thomas Seufferlein

EUS-guided biliary drainage (Complete Session)

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

Victoria Úbeda Vargas

Diverticulitis: When not to be worried?

Johannes Kurt Schultz

COMPARATIVE EFFECTS OF METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE AND METABOLIC AND ALCOHOL-ASSOCIATED STEATOTIC LIVER DISEASE (METALD) ON RISK OF HEPATIC AND EXTRA-HEPATIC OUTCOMES: A META-ANALYSIS

Salvatore Petta

Sense and non-sense of the new nomenclature

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