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Introduction

The IBD-Disk is a widely used, self-administered visual analogue tool for measuring disability in patients with inflammatory bowel disease (IBD). However, it does not capture key aspects of daily life, particularly diet and nutrition, which are critical for IBD patients and may significantly influence disability.

Aims & Methods

This cross-sectional study explored the prevalence of moderate to severe disability in young adults with IBD and evaluated the use of a modified IBD-Disk (mIBD-Disk) to screen for eating disorders and food avoidance. Patients previously diagnosed with IBD during childhood and adolescence (<18 years old), and currently followed at two adult IBD academic centers, were consecutively enrolled. All participants were assessed for disability and screened for eating disorders (ED) and avoidant restrictive food intake disorder (ARFID). Restrictive eating behaviours were evaluated using the Nine Item ARFID Screen (NIAS), which assesses three domains: picky eating, low appetite, and food-related fear with a score >23 suggesting probable ARFID. The Eating Attitudes Test (EAT-26) was used to screen for ED, with a score ≥20 indicating a positive result. Disability was measured using the IBD-Disk with a score >40 indicating moderate to severe disability) and the modified IBD-Disk (mIBD-Disk)¹, which consisted of the original 10 items plus an additional question on dietary habits, for a total of 11 items

Results

A total of 144 patients (50.7% with Crohn’s disease) were included, with a median age of 24 years (range: 21–28), and 54.2% were female. One-third (34.7%) had clinically active disease, and the median BMI was 21.8 (range: 20.1–24.2). Moderate to severe disability, as assessed by the IBD-Disk, was observed in 38.9% (56/144) of the cohort, and the median mIBD-Disk score was 33 (IQR: 16–61). ARFID risk was identified in 24 participants (16.7%), with food-related fear being the most frequent domain (13.2%). The median EAT-26 score was 5 (range: 3–12), with ED present in 17 patients (11.8%). In both univariate and multivariate analyses, moderate to severe disability (OR: 4.03; 95% CI: 1.23–13.17; p = 0.02) and a score greater than 4 on question 11 of the mIBD-Disk related to dietary habits (OR: 3.49; 95% CI: 1.06–11.47; p = 0.04) were independently associated with ARFID risk. ROC curve analysis showed that the mIBD-Disk Q11 had an 82% diagnostic accuracy (95% CI: 0.73-0.91) for predicting ARFID.

Conclusion

Patients diagnosed with IBD in childhood and adolescence have an increased prevalence of moderate to severe disability. Integrating the mIBD-Disk into clinical practice could provide an effective tool to identify patients at risk for eating behaviours and food avoidance, supporting timely referrals for nutritional and psychological interventions

References

Nardone OM, et al. Dig Liver Dis. 2025 Mar;57(3):753-761. doi: 10.1016/j.dld.2024.11.004. . PMID: 39617658.

REAL-WORLD USE OF THE MODIFIED IBD DISK TOOL FOR EVALUATION OF EATING DISORDERS IN YOUNG ADULTS WITH INFLAMMATORY BOWEL DISEASE

Olga Maria Nardone 1, Ferdinando D'Amico 2, Giulio Calabrese 1, Tommaso Lorenzo Parigi 2, Alessia La Mantia 1, Sarah Bencardino 2, Flavia Palumbo 1, Alessia Dalila Guarino 1, Antonio Rispo 1, Anna Testa 1, Silvio Danese 2, Fabiana Castiglione 1

1 University of Naples Federico II, Naples, Italy

2 IRCCS San Raffaele Hospital and Vita-Salute, Milan, Italy

Conference

UEG Week Berlin 2025

Topics

IBD

Submission format

Abstract

Session

IBD (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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PEGOZAFERMIN DEMONSTRATED ROBUST HISTOLOGICAL IMPROVEMENT AND BENEFIT IN HEPATIC AND METABOLIC BIOMARKERS: RESULTS FROM A 48-WEEK MULTI-CENTER, RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED PHASE 2B TRIAL (ENLIVEN)

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Introduction

Metabolic dysfunction-associated steatohepatitis (MASH) is often associated with metabolic disorders such as obesity, metabolic syndrome, and/or diabetes. FGF21 analogs are promising therapies for MASH due to their direct anti-fibrotic effects as well as additional hepatic and extrahepatic benefits. Pegozafermin (PGZ), an FGF21 analog, was evaluated for safety and efficacy in a Phase 2b trial (ENLIVEN) with either weekly (QW) or every two-week (Q2W) dosing versus matching placebo in MASH patients with biopsy-proven F2/F3 fibrosis. Primary histology endpoints and non-invasive tests (NITs) were assessed at week 24, followed by additional NIT evaluation at the end of a 24-week blinded extension for a total of 48 weeks.

Aims & Methods

Patients were randomized to PGZ 15mg QW, 30mg QW, or 44mg Q2W or placebo for 24 weeks (histology-based primary endpoints). During the 24-week extension, most patients continued their assigned treatment with the exception of a subset of placebo patients who were re-randomized to receive PGZ 30mg QW. The full analysis set includes F2/F3 patients with NAFLD activity score (NAS) ≥4 at baseline (n=192).

Results

At 24-weeks, PGZ 30mg QW or 44mg Q2W led to statistically significant and clinical meaningful improvement in both primary histological endpoints (one stage of fibrosis improvement without worsening of MASH and MASH resolution without worsening of fibrosis) compared to placebo. Non-invasive testing at weeks 24 and 48 demonstrated that PGZ treatment was associated with robust and sustained reductions in liver fat content (MRI-PDFF), biomarkers of fibrosis (VCTE, ELF, PRO-C3) and liver injury (ALT, AST). PGZ also improved metabolic parameters such as lipids and HbA1c at both 24 and 48 weeks. PGZ was generally safe and well tolerated with the most common treatment emergent adverse events (TEAEs) being mild/moderate nausea and diarrhea. No deaths occurred; six early terminations for TEAEs including one drug-related serious AE occurred.

Conclusion

At 24 weeks, treatment with PGZ in MASH patients with F2/F3 fibrosis led to significant fibrosis regression and MASH resolution, which was corroborated by improvement across a variety of non-invasive tests including liver fat, inflammation, fibrosis, and metabolic markers. Benefits on NITs were sustained over the full 48-weeks of the study, with favorable safety and tolerability. PGZ is the first therapy to achieve fibrosis regression and MASH resolution with a Q2W dosing regimen. Phase 3 studies in noncirrhotic (ENLIGHTEN-Fibrosis) and cirrhotic (ENLIGHTEN-cirrhosis) patients are currently underway to confirm these results.

Disclosure

Jörn Schattenberg: Consultant: Akero, Alentis Therapeutics, Astra Zeneca, 89Bio, Boehringer Ingelheim, GSK, Ipsen, Inventiva Pharma, Madrigal, MSD, Northsea Therapeutics, Novartis, Novo Nordisk, Pfizer, Roche, Sanofi, Siemens Healthineers; Speaker: Gilead Sciences, Advanz, Echosens, MedPublico GmbH; Grants: Boehringer Ingelheim, Siemens Healthcare GmbH; Stock Options: AGED diagnostics, Hepta Bio
Arun J Sanyal: Consulting: Genefit, Gilead, Malinckrodt, Pfizer, Salix, Boehringer Ingelheim, Novartis, Bristol Meyers Squibb, Merck, Hemoshear, Lilly, Novo Nordisk, Terns, Albireo, Jannsen, Poxel, 89bio, Siemens, AstraZeneca, NGM Bio, Amgen, Regeneron, Genentech, Alnylam, Roche, Madrigal, Inventiva, Covance, Prosciento, HistoIndex, PathAI; Grants: Gilead, Malinckrodt, Boehringer Ingelheim, Novartis, Bristol Meyers Squibb, Merck, Lilly, Novo Nordisk, Fractyl, Madrigal, Inventiva; Stock holder: Exhalenz, GenFit, Hemoshear, Durect, Indalo, NorthSea, Tiziana, Rivus
Naim Alkhouri: Research funding: 89Bio, AbbVie/Allergan, Akero, Better Therapeutics, Boehringer Ingelheim, Bristol-Myers Squibb, Corcept, DSM, Galectin, Genentech, Genfit, Gilead, Hepagene, Healio, Intercept, Inventiva, Ionis, Madrigal, Merck, NGM, Noom, NorthSea, Novo Nordisk, Perspectum, Pfizer, Poxel, Viking, and Zydus; Speaker bureau: AbbVie/Allergan, Alexion, Echosens, Eisai, Exelixis, Gilead, Intercept, Perspectum, Salix, and Theratechnologies; Consultant: 89Bio, AbbVie/Allergan, Echosens, Fibronostics, Gilead, Intercept, Madrigal, Novo Nordisk, Perspectum, Pfizer, and Zydus.
Rohit Loomba: Consultant: Aardvark Therapeutics, Altimmune, Anylam/Regeneron, Amgen, Arrowhead Pharmaceuticals, AstraZeneca, Boston Pharmaceuticals, Bristol-Meyers Squibb, CohBar, Eli Lilly, Galmed, Gilead, Glympse Bio, Hightide, Inipharma, Intercept, Inventiva, Ionis, Janssen Inc., Madrigal, Metacrine, Inc., NGM Biopharmaceuticals, Novartis, Novo Nordisk, Merck, Pfizer, Sagimet, Theratechnologies, 89bio, Terns Pharmaceuticals and Viking Therapeutics; Grants: Arrowhead Pharmacetuicals, AstraZeneca, Boegringer-Ingelheim, Bristol-Meyers Squibb, Eli Lilly, Galectin Therapeutics, Galmeed Pharmaceuticals, Gilead, Hanmi, Intercept, Inventiva, Ionis, Janssen, Madrigal Pharmaceuticals, Merck, NGM Biopharmaceuticals, Novo Nordisk, Pfizer, Sonic Incytes and Terns Pharmaceuticals; Stockholder: Co-founder LipoNexus, Inc
Mildred D Gottwald, Shibao Feng, Germaine D Agollah, Cynthia L Hartsfield, Hank Mansbach, Maya Margalit: 89bio employee and stock holder

PEGOZAFERMIN DEMONSTRATED ROBUST HISTOLOGICAL IMPROVEMENT AND BENEFIT IN HEPATIC AND METABOLIC BIOMARKERS: RESULTS FROM A 48-WEEK MULTI-CENTER, RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED PHASE 2B TRIAL (ENLIVEN)

Jörn Schattenberg 1, Arun J Sanyal 2, Naim Alkhouri 3, Mildred D. Gottwald 4, Shibao Feng 4, Germaine D. Agollah 4, Cynthia L Hartsfield 4, Hank Mansbach 4, Maya Margalit 5, Rohit Loomba 6

1 Universitätsklinikum des Saarlandes und Medizinische Fakultät der Universität des Saarlandes, Homburg, Germany

2 Virginia Commonwealth University School of Medicine, Richmond, United States

3 Arizona Liver Health, Phoenix, United States

4 89bio, San Francisco, United States

5 89bio, Rehovot, Israel

6 University of California San Diego MASLD Research Center, San Diego, United States

Event

UEG Week Berlin 2025

Topics

Hepatobiliary

Submission format

Abstract

Session

Lifestyle management and therapy in MASLD

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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How to boost wound healing in- and outside

Ailsa L Hart 1

1 St Mark’s Hospital and Academic Institute, Harrow, United Kingdom

Event

UEG Week Berlin 2025

Topics

IBD Primary Care Surgery

Session

Disease primer: From inflammation to restoration - wound healing in IBD

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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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

UEG Presentation

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JAK2 INHIBITION ATTENUATES PORTAL HYPERTENSION IN METABOLIC DYSFUNCTION-ASSOCIATED LIVER

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Introduction

Portal hypertension (PHT) most commonly due to cirrhosis, but non-cirrhotic portal hypertension (NCPH) related to metabolic dysfunction, specifically metabolic dysfunction-associated steatotic liver disease (MASLD), necessitates further clarification of its mechanisms and identification of therapeutic targets.

PHT may precede the development of hepatic fibrosis in MASLD, and even serve as a driving factor in the pathogenesis of MASLD. Consequently, metabolic dysfunction-associated PHT might not depend on structural alterations such as hepatic fibrosis or pseudolobule formation, but rather correlate with other factors such as endothelial dysfunction, which has been demonstrated to play a pivotal role in NCPH. Endothelial dysfunction encompasses endothelial injury and endothelial-to-mesenchymal transition (EndMT), the latter being a specific type of epithelial-to-mesenchymal transition (EMT). As reported, the JAK/STAT3 signaling pathway plays a pivotal role in the initiation and progression of EMT. Similarly, patients with NCPH induced by myeloproliferative neoplasms (MPN) often lack pathological features such as hepatic fibrosis or pseudolobule formation. The Janus kinase 2 (JAK2) V617F mutation is highly prevalent in MPN patients. Therefore, targeted inhibition of JAK2 serves as an effective therapeutic strategy for MPN.

Given the shared pathological features between MPN-associated portal hypertension and MASLD-associated portal hypertension, as well as the vital role of JAK2 in both disease, the application of JAK2 inhibitor holds significant therapeutic potential for metabolic dysfunction-associated portal hypertension.

Aims & Methods

This study aims to verify the therapeutic efficacy of JAK2 inhibition in attenuating MASLD-associated PHT, with particular focus on its modulation of EndMT. Mice were fed with a high-fat diet (HFD) diet for 12 weeks to induce MASLD-associated PHT and divided into two groups, the treatment group (Rux) and control (Ctr) group. Ruxolitinib (JAK2 inhibitor) was given as a suspension by gavage (60 mg/kg in 0.2 ml) every two days for 3 weeks, while controls received the same volume of saline, from week 10-12 of feeding. Portal pressure was measured, serological analysis and histopathological staining were performed. RT-PCR and Western Blot were conducted to measure EndMT-related genes expression.

Results

The treatment group (Rux) demonstrated a significant reduction in directly measured portal pressure, with concordant changes observed in the spleen-to-body weight ratio, which served as an indirect indicator of portal pressure. Concurrent improvement was noted in ALT, AST and TC. H&E, Masson and Sirius red staining showed decreased perisinusoidal and perivascular fibrosis in the Rux group. Electron microscopy revealed restoration of endothelial fenestration. Additionally, ruxolitinib treatment led to downregulation of endothelial damage markers, mesenchymal cell markers as well as EndMT-related regulatory factors, indicating an alleviation of EndMT and endothelial dysfunction.

Conclusion

The JAK2 inhibitor demonstrates therapeutic potential for MASLD-associated PHT through modulation of endothelial dysfunction and EndMT. These mechanistic insights position ruxolitinib as a promising candidate for clinical management of NCPH, particularly in the MASLD-associated PHT.

References

[1] European Association for the Study of the Liver; European Association for the Study of Diabetes; European Association for the Study of Obesity. EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD): Executive Summary. Diabetologia. 2024 Jun 13. [2] Song Z, Liu X, Zhang W, et al. Ruxolitinib suppresses liver fibrosis progression and accelerates fibrosis reversal via selectively targeting Janus kinase 1/2. Journal of Translational Medicine. 2022, 20(1): 157.
[3] Zhang XL, Zhang XY, Ge XQ, et al. Mangiferin prevents hepatocyte epithelial-mesenchymal transition in liver fibrosis via targeting HSP27-mediated JAK2/STAT3 and TGF-β1/Smad pathway. Phytotherapy Research. 2022, 36(11): 4167-4182.
[4] Jin W. Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial-Mesenchymal Transition. Cells. 2020;9(1):217.
[5] Hammoutene A, Rautou PE. Role of liver sinusoidal endothelial cells in non-alcoholic fatty liver disease. Journal of Hepatology. 2019, 70(6): 1278–1291.