UEG's educational platform for gastroenterology education bringing recordings, courses, guidelines, and more together in one place.

UEG Week Berlin 2025 Recordings Gut Guide online

Rate for better recommendations!

Your feedback helps us show you more of what you like and less of what you dislike!

More of this!

We will show you more similar content.

Not for me!

We won't suggest this again.

Bookmark!

Save this content for later!

New to myUEG? Create an account! Log In with myUEG account

UEG Poster

Standard Poster

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

Free for all myUEG account holders. Your access level is set automatically based on your occupation. Medical professionals get full access to all content. If you are a non-medical user, you can only access UEG Week content from congresses you attended.

Not sure what you can access? Learn more about account types.

Introduction

Modern lifestyles have increased the demand for convenience and extended shelf life, contributing to the rising consumption of ultra-processed foods (UPFs). This trend has been linked to adverse health outcomes, including obesity and inflammatory bowel disease (IBD). IBD encompasses multifactorial digestive disorders characterized by disrupted intestinal homeostasis, resulting in immune dysregulation, impaired nutrient absorption, systemic inflammation, and a marked reduction in quality of life, often associated with chronic fatigue and decreased physical activity. These factors contribute to the activation of muscle protein catabolism and inhibition of skeletal muscle protein synthesis, increasing the risk of sarcopenia in IBD patients.

Aims & Methods

To evaluate ultra-processed food consumption and body composition in patients with IBD. A cross-sectional study was conducted with 105 patients diagnosed with Crohn’s disease or ulcerative colitis at the IBD outpatient clinic of Hospital das Clínicas, Botucatu Medical School (HC-FMB). Assessments included handgrip strength using a dynamometer, bioelectrical impedance analysis, anthropometric measurements, and dietary intake evaluation using a food frequency questionnaire (FFQ).

Results

The sample included 61 patients with ulcerative colitis and 44 with Crohn’s disease, with a mean age of 41.5 ± 15.1 years; 70% were female. Mean disease duration was 11.2 ± 7.6 years. The average BMI was 25.9 ± 5.2 kg/m², with 52.4% classified as overweight. Mean body fat percentage assessed by skinfold measurements was 28.5 ± 7.5%, with 85% exceeding the reference values. Additionally, 18.3% were classified as malnourished based on mid-arm muscle circumference. According to bioelectrical impedance, 86.4% had low muscle mass. Mean handgrip strength was 27.4 ± 8.7 kgf, with 7% presenting inadequate values. Dietary data showed that 22% reported weekly fast food consumption, 30.5% consumed sweets, and 13% drank artificial juices daily. Daily intake of fruits and vegetables was reported by 48% of participants, and 36% reported daily meat consumption.

Conclusion

Patients with IBD are at increased risk of sarcopenia due to inflammatory burden and dietary restrictions. This study identified reduced muscle mass and high intake of certain processed and ultra-processed foods. Regular consumption of UPFs may worsen disease outcomes and negatively affect body composition by increasing fat mass and decreasing muscle mass. Further analyses will explore associations between UPF intake and changes in body composition.

References

Narula N, Wong ECL, Dehghan M, et al. Association of ultra-processed food intake with risk of inflammatory bowel disease: prospective cohort study. BMJ. 2021;374:n1554.
Racine A, Carbonnel F, Chan SS, et al. Dietary Patterns and Risk of Inflammatory Bowel Disease in Europe: Results from the EPIC Study. Inflamm Bowel Dis 2016;22:345-54. 10.1097/MIB.0000000000000638
SUGIHARA, Kohei; KAMADA, Nobuhiko. Diet–microbiota interactions in inflammatory bowel disease. Nutrients, v. 13, n. 5, p. 1533, 2021.
WANG, Yun et al. Encyclopedia of fecal microbiota transplantation: a review of effectiveness in the treatment of 85 diseases. Chinese Medical Journal, v. 135, n. 16, p. 1927-1939, 2022.
Whelan K, Bancil AS, Lindsay JO, Chassaing B. Ultra-processed foods and food additives in gut health and disease. Nat Rev Gastroenterol Hepatol. 2024;21(6):406-27.
World Health Organization (WHO). Prevalence of obesity among adults, BMI (crude estimate). Disponível em: https://www.who.int/data/gho/data/indicators/indicator-details/GHO/prevalence-of-obesity-among-adults-bmi--30-(crude-estimate). Acesso em 28 dez. 2024.
Meyer A, Dong C, Casagrande C, Chan SSM, Huybrechts I, et al. Food Processing and Risk of Crohn's Disease and Ulcerative Colitis: A European Prospective Cohort Study. Clin Gastroenterol Hepatol. 2023 Jun;21(6):1607-1616.e6.

ULTRA-PROCESSED FOOD CONSUMPTION IN PATIENTS WITH INFLAMMATORY BOWEL DISEASE

Amanda Spiller 1, Beatriz Gabriela Costa 1, Ryan Nunes Yoshio Yoshihara 1, Enya Zucari Nogueira 2, Natália Salvador Castelhano 1, Giedre Soares Prates Herreira 1, Daniela Salate Biagioni Vulcano 1, Lígia Yukie Sassaki 1

1 São Paulo State University (Unesp), Botucatu, Brazil

2 São Paulo State University, Botucatu, Brazil

Conference

UEG Week Berlin 2025

Topics

Small Intestine & Nutrition

Submission format

Abstract

Session

NUTRITION (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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

JAK2 INHIBITION ATTENUATES PORTAL HYPERTENSION IN METABOLIC DYSFUNCTION-ASSOCIATED LIVER

Not sure what you can access? Learn more about account types.

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.

JAK2 INHIBITION ATTENUATES PORTAL HYPERTENSION IN METABOLIC DYSFUNCTION-ASSOCIATED LIVER

Yifei Liu 1, Shiyao Chen 1

1 Zhongshan Hospital, Fudan University, Shanghai, China

Event

UEG Week Berlin 2025

Topics

Gut Microbiota Hepatobiliary Mechanisms & Personalised Medicine

Submission format

Abstract

Session

MASLD: Inflammatory mechanisms

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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

Not sure what you can access? Learn more about account types.

Future trends in diagnosis and management of coeliac disease

Fabiana Zingone 1

1 University of Padua, Padua, Italy

Event

UEG Week Berlin 2025

Topics

Immunology Small Intestine & Nutrition

Session

Coeliac or non-coeliac enteropathy?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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

Not sure what you can access? Learn more about account types.

Getting out of the block early in Crohn´s disease: Gastroenterologist vs surgeon perspective

Joline de Groof 1, Nurulamin Noor 2

1 Haaglanden Medical Center, The Hague, Netherlands

2 Cambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom

Event

UEG Postgraduate Teaching Programme Berlin 2025

Session

The Crohn´s disease journey

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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

Not sure what you can access? Learn more about account types.

Innovations in IBD Therapy: The Story of TL1A - from Discovery to Potential Future Care (F. Hoffmann-La Roche Ltd) (Complete Session)

Jean-Frédéric Colombel 1, Beatriz Gros 2, Remo Panaccione 3

1 Icahn School of Medicine at Mount Sinai, USA, United States of America

2 Hospital Universitario Reina Sofia, Cordoba, Spain

3 University of Calgary, Calgary, Canada

Publisher

F. Hoffmann La Roche

Event

UEG Week Berlin 2025

Session

Innovations in IBD Therapy: The Story of TL1A - from Discovery to Potential Future Care (F. Hoffmann-La Roche Ltd)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Presentation

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

LINERIXIBAT SIGNIFICANTLY IMPROVES CHOLESTATIC PRURITUS IN PRIMARY BILIARY CHOLANGITIS: RESULTS OF THE PIVOTAL PHASE 3 GLISTEN TRIAL

Not sure what you can access? Learn more about account types.

Introduction

Cholestatic pruritus is common, debilitating and undertreated in patients with primary biliary cholangitis (PBC). Here, we describe the results of GLISTEN (NCT04950127), a Phase 3 study investigating the efficacy and safety of the ileal bile acid transporter inhibitor linerixibat for pruritus in PBC.

Aims & Methods

In this double-blind, randomised, placebo-controlled study, patients with PBC and moderate-to-severe pruritus received oral linerixibat 40 mg or placebo twice daily. Pruritus severity and pruritus-related sleep interference were assessed using a 0–10 numerical rating scale. The primary endpoint was change from baseline in worst itch over 24 weeks. Secondary endpoints included: at Week 2, change in worst itch; over 24 weeks, change in sleep interference; at Week 24, proportion of responders (≥ 2-, ≥ 3-, ≥ 4-point reduction in worst itch) and analysis of responses to 2 patient global impression items (itch severity and change). Safety endpoints included adverse event (AE) reporting.

Results

238 patients were randomised; 95% were female, itch severity was mean (standard deviation [SD]) 7.34 (1.54), 52% had alkaline phosphatase < 1.67 times upper limit of normal, and 47% were receiving stable therapy for pruritus. Pruritus improvement over 24 weeks was significantly greater with linerixibat than placebo: least-squares (LS) mean change -2.86 versus -2.15, adjusted mean difference -0.72; p = 0.001. At Week 24, the observed mean (SD) difference from baseline in pruritus was -3.66 (2.50) with linerixibat and -2.82 (2.32) with placebo. The effect of linerixibat was rapid and superior to placebo at Week 2: LS mean change -1.78 versus -1.07, adjusted mean difference -0.71; p < 0.001. Linerixibat also significantly improved pruritus-related sleep interference over 24 weeks versus placebo: LS mean change ‑2.77 versus -2.24, adjusted mean difference -0.53; p = 0.024. At Week 24, more patients on linerixibat than placebo achieved a ≥ 2-point (68% vs 64%), ≥ 3-point (56% vs 43%) or ≥ 4-point (41% vs 29%) reduction in pruritus and a higher proportion of linerixibat than placebo-treated patients reported their pruritus was very much improved (55% vs 37%) or absent (21% vs 9%). AEs reported more frequently with linerixibat than placebo were predominantly gastrointestinal (GI), including diarrhoea (61% vs 18% of patients) and abdominal pain (18% vs 3% of patients); 4% of patients in the linerixibat group discontinued treatment due to diarrhoea.

Conclusion

In patients with PBC and moderate-to-severe pruritus, linerixibat rapidly and significantly improved pruritus and pruritus-related sleep interference versus placebo. While GI AEs were more common with linerixibat than placebo, they rarely led to treatment discontinuation.

Disclosure

Funded by GSK. Various authors declare conflicts of interest as consultants, employee, recipients of grants and stockholders. These will be reported in full during the presentation.

LINERIXIBAT SIGNIFICANTLY IMPROVES CHOLESTATIC PRURITUS IN PRIMARY BILIARY CHOLANGITIS: RESULTS OF THE PIVOTAL PHASE 3 GLISTEN TRIAL

Gideon M. Hirschfield 1, Christopher L. Bowlus 2, David Jones 3, Andreas E. Kremer 4, Marlyn J. Mayo 5, Atsushi Tanaka 6, Pietro Andreone 7, Jidong Jia 8, Qinglong Jin 9, Ricardo Macias-Rodriguez 10, Alexander R. Cobitz 11, Brooke M. Currie 11, Ciara Gorey 12, Ivana Lazic 12, Danielle J. Podmore 12, Andrea Ribiero 13, Jennifer B. Shannon 14, Brandon Swift 14, Megan M. McLaughlin 11, Cynthia Levy 15

1 Toronto General Hospital, Toronto, Canada

2 University of California Davis School of Medicine, Sacramento, United States

3 Newcastle University, Newcastle Upon Tyne, United Kingdom

4 University Hospital Zurich, Zurich, Switzerland

5 University of Texas Southwestern Medical School, Dallas, United States

6 Teikyo University School of Medicine, Tokyo, Japan

7 Azienda Ospedaliero-Universitaria di Modena and Università di Modena e Reggio Emilia, Modena, Italy

8 Capital Medical University, Beijing, China

9 The First Hospital of Jilin University, Changchun, China

10 Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico

11 GSK, Collegeville, United States

12 GSK, London, United Kingdom

13 GSK, Madrid, Spain

14 GSK, Durham, United States

15 University of Miami, Miami, United States

Event

UEG Week Berlin 2025

Topics

Hepatobiliary Immunology Mechanisms & Personalised Medicine

Submission format

Abstract

Session

Advances in management of immune-mediated biliary disease

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

UEG Poster

Standard Poster

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

Not sure what you can access? Learn more about account types.

Introduction

Prompt initiation of advanced therapy (AT) medications, encompassing biologics and small molecule treatments, is crucial for the effective treatment of inflammatory bowel disease (IBD). The time taken from the decision to start the AT to it’s first administration, or time to advanced therapy (TAT), can vary significantly between individuals negatively impacting upon their disease course. However, our knowledge of the causes for the variation in TAT is poor.

Aims & Methods

We aimed to investigate the impact that different demographic and disease-related factors have on the TAT. A retrospective analysis of electronic patient records, conducted at a tertiary IBD referral centre in London in March 2024, analysed electronic patient records of all those over the age of 18 currently being treated for IBD with an AT and collected data on the TAT for their index AT, defined as the number of days from the documented decision to start an AT to the date of the first administration. Data was also collected on multiple variables which including disease type, type of AT, age, sex, ethnicity and socioeconomic status by analysing patients’ Index of Multiple Deprivation (IMD). A multiple negative binomial regression was performed entering all variables together to assess their relative effect on TAT.

Results

1298 patients were identified and 485 were excluded due to either their index AT being started elsewhere, incomplete data, a positive screening test or because they were enrolled in a clinical trial. The multiple binomial regression found that TAT was significantly longer for those of non-white ethnicity (p=0.039) (table 1). Analysis for patients of black ethnicity found an Incident Rate Ratio (IRR) of 1.46 (95% CI 1.09,1.95), for mixed ethnicity IRR=1.26 (95% CI 0.77,2.05) and for asian ethnicity IRR=1.17 (95% CI 0.96, 1.41) when compared to white patients. Treatment with adalimumab was also associated with a longer TAT (p=<0.001, IRR 1.37, 95% CI 0.95,1.96) but no other factors were statistically significant: IMD p=0.133; age p=0.155; sex p=0.702; disease type p=0.335.

		IRR	95% CI	p-value
Ethnicity	Asian	1.17	0.96, 1.21	0.039
	Black	1.46	1.09, 1.95
	Mixed	1.26	0.77, 2.05
	White	1
Treatment	Adalimumab	1.37	0.95, 1.96	<0.001
	Filgotinib	1.37	0.87, 2.16
	Infliximab	0.97	0.68, 1.40
	Tofacitinib	0.89	0.58, 1.36
	Ustekinumab	0.91	0.61, 1.35

IRR: Incidence Rate Ratio. IMD: Index of multiple deprivation.

Conclusion

Our study has identified that non-white ethnicity is associated with a longer TAT and this may be a contributing factor to worse outcomes in patients with IBD from an ethnic minority background. Further research into the causes for this are required to help address this health disparity.