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

Re-live UEG Week 2026 on Gutflix Gut Guide online What's new on Gutflix

Trending on Gutflix

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

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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

INCREASED RISK OF GASTROINTESTINAL CANCERS IN COELIAC DISEASE: A NATIONWIDE COHORT STUDY

Georgia Malamut 1, Yannick Girardeau 2, Stanislas Chaussade 1, Romain Coriat 1, Nadine Cerf-Bensussan 3, Anne-Sophie Jannot 2

Affiliations

1 Université Paris Cité APHP Centre Hôpital Cochin, Paris, France

2 Université Paris Cité APHP Centre, Paris, France

3 Imagine Institute INSERM France, Paris, France

Summary

AI Generated

A French nationwide cohort study of 27,244 coeliac disease patients found increased risks of multiple gastrointestinal cancers beyond the well-known lymphoma and small bowel cancer associations, with further elevation of risk in those with concurrent inflammatory or autoimmune digestive conditions.

Coeliac patients had substantially increased risk of small bowel cancer (OR=13.9), non-Hodgkin's lymphoma (OR=4.1), and 104 cases of Enteropathy Associated T cell Lymphoma versus none in matched controls.
Increased risks were also observed for pancreatic cancer (OR=2.4), colonic cancer (OR=1.7), esophageal cancer (OR=1.7), and gastric cancer (OR=1.5), but not for rectal cancer or hepatocellular carcinoma.
Coeliac patients showed elevated risks of pernicious anaemia (OR=11.3), microscopic colitis (OR=4.5), Crohn's disease (OR=4.2), ulcerative colitis (OR=3.3), and non-alcoholic chronic pancreatitis (OR=1.7).
When coeliac patients had concurrent pernicious anaemia, non-alcoholic chronic pancreatitis, or microscopic colitis, their risks of gastric, pancreatic, and colonic cancers respectively were further increased.
The authors conclude these findings argue for early and regular screening of digestive cancers and inflammatory or autoimmune digestive diseases in coeliac patients.

Download PDF

Was this helpful?

Thanks for your feedback.

This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

Abstract

Introduction

Patients with coeliac disease have well-known increased risks of non-Hodgkin’s lymphoma and small bowel cancer but risks of other digestive cancers remain controversial. The objective of this study was to assess the risks of gastrointestinal cancers in coeliac patients and possible favoring conditions.

Aims & Methods

We performed an exposed-non-exposed cohort study comparing coeliac patients with non-exposed control individuals (with a diagnosis of cutaneous superficial burn or sprained ankle) for risk of malignant gastrointestinal diseases using the French nationwide hospitalization database covering all the inpatient admissions during a 9-years follow-up (2011-2019).

Results

27244 patients with coeliac disease were compared to the same number of non-exposed age and sex matched patients. 104 cases of Enteropathy Associated T cell Lymphoma were recorded in the group of coeliac patients and none in control group. In addition to non-Hodgkin’s lymphoma (OR=4.1 [95% CI 2.8; 6.2]) and small bowel cancer (OR=13.9 [95% CI 7.5; 29.6]), coeliac patients had increased risk of pancreatic cancer (OR=2.4 [95% CI 1.8; 3.3], esophageal cancer (OR=1.7 [95% CI 1.1; 2.8]), gastric cancer (OR=1.5 [95% CI 1.1; 2.2]) and colonic cancer (OR=1.7 [95% CI 1.4; 2.1]) but neither of rectal cancer (OR=1.1 [95% CI 0.8; 1.4]) nor of hepatocellular carcinoma (OR=0.8 [95% CI 0.54; 1.21]). Regarding possible favoring conditions, we also noted an increased risk of pernicious anaemia (OR=11.3 [95%CI 7.3; 18.4]), Crohn’s disease (OR=4.2 [95%CI 3.4; 5.1]), ulcerative colitis (OR=3.3 95%CI 2.7; 4.0]), microscopic colitis (OR=4.5 [95%CI 4.1; 5]) and non-alcoholic chronic pancreatitis (OR=1.7 [95% CI 1.2; 2.3]) in coeliac group. Coeliac patients with non-alcoholic chronic pancreatitis, pernicious anaemia and microscopic colitis had a more increased risk of pancreatic (OR=5.9 [95%CI 1.4;15.9]; p=0.003), gastric ((OR=9 [95%CI 3.1;20.4]; p<0.001) and colonic cancers (OR=1.8 [95%CI 1.3;2.6]; p<0.001), respectively.

Conclusion

In addition to small bowel cancer and lymphoma, coeliac patients have increased risk of pancreatic, gastric and colonic cancers. Coeliac patients have also increased risks of inflammatory and/or autoimmune gastrointestinal diseases which major risks of corresponding digestive cancers. These results argue for an early and regular screening of digestive cancers and inflammatory/autoimmune digestive diseases in coeliac patients.

Disclosure

none

Conference

UEG Week Copenhagen 2023

Topics

Small Intestine & Nutrition

Submission format

Abstract

Session

Coeliac disease (Posters)

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

More Like This:

Is nutrition the missing link in long-term IBD management?

Charlie W. Lees

UPPER GASTROINTESTINAL CROHN’S DISEASE DOES NOT CONFER INTRINSIC BIOLOGIC RESISTANCE BUT REMAINS ASSOCIATED WITH INCREASED INTESTINAL SURGERY DESPITE BIOLOGIC THERAPY

Esther García-Planella

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior

MICROBIOTA‑ORIENTED DIETARY PATTERN, PROTEOMIC MEDIATORS, AND INCIDENT INFLAMMATORY BOWEL DISEASE: A UK BIOBANK PROSPECTIVE COHORT STUDY

Rui Ji

Introduction: Mistakes in… Upper GI

Henriette Heinrich

THE OBESITY-LITERACY CASCADE: WHAT PATIENTS WITH OBESITY DON'T KNOW — FROM DISEASE CONCEPT TO ENDOSCOPIC SLEEVE GASTROPLASTY

Cem Simsek

UEG Presentation

New

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

Is nutrition the missing link in long-term IBD management?

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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

Is nutrition the missing link in long-term IBD management?

Charlie W. Lees 1

Affiliations

1 Institute of Genetics & Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Abstract

Event

UEG Week Barcelona 2026

Topics

Surgery Small Intestine & Nutrition IBD

Session

IBD nutrition matters

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

More Like This:

Is nutrition the missing link in long-term IBD management?

Charlie W. Lees

UPPER GASTROINTESTINAL CROHN’S DISEASE DOES NOT CONFER INTRINSIC BIOLOGIC RESISTANCE BUT REMAINS ASSOCIATED WITH INCREASED INTESTINAL SURGERY DESPITE BIOLOGIC THERAPY

Esther García-Planella

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior

MICROBIOTA‑ORIENTED DIETARY PATTERN, PROTEOMIC MEDIATORS, AND INCIDENT INFLAMMATORY BOWEL DISEASE: A UK BIOBANK PROSPECTIVE COHORT STUDY

Rui Ji

Introduction: Mistakes in… Upper GI

Henriette Heinrich

THE OBESITY-LITERACY CASCADE: WHAT PATIENTS WITH OBESITY DON'T KNOW — FROM DISEASE CONCEPT TO ENDOSCOPIC SLEEVE GASTROPLASTY

Cem Simsek

UEG Presentation

New

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

UPPER GASTROINTESTINAL CROHN’S DISEASE DOES NOT CONFER INTRINSIC BIOLOGIC RESISTANCE BUT REMAINS ASSOCIATED WITH INCREASED INTESTINAL SURGERY DESPITE BIOLOGIC THERAPY

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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

UPPER GASTROINTESTINAL CROHN’S DISEASE DOES NOT CONFER INTRINSIC BIOLOGIC RESISTANCE BUT REMAINS ASSOCIATED WITH INCREASED INTESTINAL SURGERY DESPITE BIOLOGIC THERAPY

Antonio Giordano 1, Guillermo Bastida Paz 2, PILAR VARELA TRASTOY 3, María Dolores Martín-Arranz 4, Carlos Maroto Martín 5, Elena Ricart 6,7, Isabel Pérez-Martínez 8, Eva Iglesias-Flores 9,7, Daniel Sebastian Ceballos Santos 10, Montserrat Rivero 11, Eduard Brunet 7,12, Olivia Belen Galipienso 13,7, Fernando Gomollón 14,7, Pilar Corsino 15, Javier P. Gisbert 7,16, Ángel Febles-González 17, Manuel Barreiro de Acosta 18, Fernando Bermejo 19, Maria Luisa De Castro Parga 20, Iago Rodríguez-Lago 21, Orlando García-Bosh 22, Javier Santos Fernández 23, Lara Arias García 24, Rufo Lorente Poyatos 25, Miriam Mañosa Ciria 26,7, Ángel Ponferrada-Díaz 27, Cristina Rodríguez Gutiérrez 28, Eva Sesé 29, David Rafael de la Cruz Esteban 30, Maria Isabel Vera Mendoza 31, Carlos González-Muñoza 1, Mariana Fe García Sepulcre 32, José Lázaro Pérez-Calle 33, Marta Piqueras Cano 34, Yamile Zabana 7,35, Francisco Mesonero Gismero 36, Esther Estrella 37, Ignacio Marín-Jiménez 38, Mónica Sierra-Ausín 39, Francisco Rodriguez-Moranta 40, Cristina Alejandra Sánchez Gómez 41, Jose Maria Huguet 42, Víctor Merino 43, Oscar Moralejo Lozano 44, Laura Ramos Lopez 45, Carmen Orenga 46, Raquel Camargo Camero 47, Guillem Font 48, Eugeni Domenech Morral 7,26, Esther García-Planella 1

Affiliations

1 Hospital de la Santa Creu i Sant Pau (IR SANT PAU), Barcelona, Spain

2 Hospital Universitari i Politècnic La Fe, Valencia, Spain

3 Hospital Universitario de Cabueñes, Gijón, Spain

4 Hospital Universitario La Paz - Instituto de Investigación Sanitaria del Hospital La Paz (IDIPAZ), Madrid, Spain

5 Hospital Universitario Río Hortega, Valladolid, Spain

6 Hospital Clinic de Barcelona, Barcelona, Spain

7 Centro de Investigación Biomédica en Red – Enfermedades Hepáticas y Digestivas (CIBER-EHD), Madrid, Spain

8 Hospital Universitario Central de Asturias - Diet, Microbiota and Health Group, Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), Oviedo, Spain

9 Hospital Universitario Reina Sofía, Córdoba, Spain

10 Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, Spain

11 Hospital Universitario Marqués de Valdecilla, stituto de Investigación Valdecilla (IDIVAL), Santander, Spain

12 Hospital Universitari Parc Taulí, Sabadell, Spain

13 Hospital General Universitario de Alicante, Alicante, Spain

14 Universidad de Zaragoza, Instituto de Investigación Sanitaria Aragón, Zaragoza, Spain

15 Hospital Universitario Miguel Servet, Zaragoza, Spain

16 Hospital Universitario de La Princesa Centro de Investigación Biomédica en Red en Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain

17 Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain

18 Complexo Hospitalario Universitario de Santiago, Santiago de Compostela, Spain

19 Hospital Universitario de Fuenlabrada, Fuenlabrada, Spain

20 Complexo Hospitalario Universitario de Vigo, SERGAS, IIS Galicia Sur, Vigo, Spain

21 Hospital Universitario de Galdakao - Biobizkaia Health Research Institute, Bilbao, Spain

22 Hospital Sant Joan Despí Moisès Broggi, Barcelona, Spain

23 Complejo Hospitalario de Palencia, Palencia, Spain

24 Hospital Universitario de Burgos, Burgos, Spain

25 Hospital General Universitario de Ciudad Real, Ciudad real, Spain

26 Hospital Universitari Germans Trias i Pujol, Badalona, Spain

27 Hospital Universitario Infanta Leonor, Madrid, Spain

28 Hospital Universitario de Navarra, Instituto de Investigación de Navarra (IdiSNA), Pamplona, Spain

29 Hospital Universitario Arnau de Vilanova, Lleida, Spain

30 Hospital Universitario Doce de Octubre, Madrid, Spain

31 Hospital Universitario Puerta de Hierro, Madrid, Spain

32 Hospital General Universitario de Elche, Elche, Spain

33 Hospital Universitario Fundación Alcorcón, Madrid, Spain

34 Consorci Sanitari Terrassa, Terrassa, Spain

35 Hospital Universitari Mútua Terrassa, Terrassa, Spain

36 Hospital Ramon y Cajal, Los Santos de la Humosa, Spain

37 Hospital Clínico Universitario Virgen de la Arrixaca, Murcia, Spain

38 Hospital General Universitario Gregorio Marañón, Madrid, Spain

39 Complejo Asistencial Universitario de León, León, Spain

40 Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Spain

41 Complexo Hospitalario Universitario de Ourense, Ourense, Spain

42 Consorcio Hospital General Universitario de Valencia, Valencia, Spain

43 Hospital Clínico Universitario de Valencia, Valencia, Spain

44 Complejo Hospitalario de Toledo, Toledo, Spain

45 Hospital Universitario de Canarias, La Laguna, Spain

46 Hospital General de Granollers, Granollers, Spain

47 Hospital Virgen de la Victoria, Málaga, Spain

48 Hospital del Mar, Barcelona, Spain

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Abstract

Introduction

Upper gastrointestinal involvement (UGI) in Crohn’s disease (CD) has been associated with a more aggressive disease course, but whether it confers intrinsic resistance to biologic therapy remains unclear. We aimed to assess biologic treatment effectiveness in patients with UGI and to evaluate their risk of intestinal surgery despite biologic therapy in a large real-world cohort.

Aims & Methods

A retrospective cohort study including biologic-treated patients with CD from the ENEIDA multicenter registry between 2015 and 2025 was performed. UGI was defined according to the Montreal classification (L4), and analyses were restricted to patients with ileal or ileocolonic disease. The primary outcome was treatment persistence, defined as time to discontinuation due to primary non-response or loss of response. The secondary outcome was time to intestinal resection. Inverse probability of treatment weighting (IPTW) was used to balance baseline characteristics between patients with and without L4 phenotype. Cox proportional hazards models adjusted for biologic class were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). Subgroup analyses according to L4 subtypes (L4a, L4b, L4ab) and interaction analyses with biologic class were performed.

Results

Among 9,524 biologic-treated patients, 27.9% had UGI. Median follow-up was 81 months (IQR 36–155). After IPTW and adjustment for biologic class, UGI was not associated with reduced biologic persistence (HR 1.03; 95% CI 0.96–1.10). Causes of treatment discontinuation due to lack of effectiveness were comparable between groups. In contrast, UGI was independently associated with increased intestinal resection (HR 1.19; 95% CI 1.04–1.36). Subtype analysis demonstrated that this risk was primarily driven by patients with combined L4a/L4b involvement (HR 1.47; 95% CI 1.15–1.88), whereas isolated L4a (HR 1.00; 95% CI 0.59–1.67) and L4b (HR 1.14; 95% CI 0.97–1.33) phenotypes were not significantly associated with surgery. Biologic class was independently associated with persistence and intestinal resection, with ustekinumab showing the highest treatment durability and a lower risk of intestinal resection across the overall cohort. However, no significant interaction between drug type and L4 phenotype was observed.

Conclusion

UGI in CD does not confer intrinsic resistance to biologic therapy but remains associated with increased long-term risk of intestinal surgery despite biologic treatment. These findings support that L4 phenotype identifies patients at higher risk of surgical complications rather than impaired pharmacologic responsiveness.

Disclosure

AG has received eductation funding from Lilly, FAES Pharma, Falk, Kern Pharma, Johnson&Johndson, and Ferring. ER has received support for congress and conference attendance, speaker fees, research support or consulting fees from MSD, Abbvie,Ferring, Janssen, Otsuka, Pfizer, Takeda, Faes Farma, Galapagos/Alphasigma, Kern Pharma, Lilly, Falk Pharma, Johnson&Johnson, and Fresenius-Kabi. EIF has served as speaker, consultant, and advisory member for or has received research funding fromMSD, Abbvie, Takeda, Janssen, Galapagos/Alfasigma, Lilly, Ferring, Dr. Falk Pharma, Pharma, and Adacyte. MR has served as a speaker or advisory member from Lilly, TaKeda, Janssen, Abbvie, Galapagos, Ferring and Pfizer. EB has served as a speaker and consultant for Janssen, Lilly, Tillotts Pharma, Chiesi, Kern, Takeda, and Alfasigma. FG has served as a speaker and has received research or education funding from Abbvie, Johnson&Johnson, Takeda and Lilly. JG has served as a speaker, consultant, and advisory board member for or has received research funding from the following companies: MSD, AbbVie, Pfizer, Kern Pharma, Biogen, Mylan, Takeda, Janssen, Roche, Sandoz, Celgene/Bristol Myers, Gilead/Galápagos, Lilly, Ferring, Faes Farma, Shire Pharmaceuticals, Dr. Falk Pharma, Tillotts Pharma, Chiesi, Casen Fleet, Gebro Pharma, Otsuka Pharmaceutical, Norgine, and Vifor Pharma. AFG has received research and education funding from ABBVIE, Alfa sigma, and Ferring. FB has been speaker, consultant and advisory member, or has received research funding from Abbvie, Takeda, Janssen, Pfizer, MSD, Biogen, Amgen, Galapagos, Ferring, Faes Farma, Tillotts Pharma, Chiesi, Vifor Pharma, and Lilly. IRL has received financial support for traveling and educational activities from or has served as an advisory board member for Abbvie, Adacyte, Alfasigma, Biogen, Faes Farma, Ferring, Galapagos, Johnson&Johnson, Eli Lilly, Mirum Pharmaceuticals, Merck,Pfizer, Roche, Takeda, and Tillotts Pharma. Research support from AbbVie and Alfasigma LAG has served as speaker or has received research or education funding from MSD; Abbvie; Kern Pharma; Ferring; Faes Farma;Pfizer; Takeda; Johnson and Johnson, and Lilly. RLP has served as a speaker, or has received research or education funding from Abbvie, Pfizer, Johnson and Johnson, Faes Farma,Alfasigma, and Lilly. MMC has served as a speaker, consultant and advisory member for or has received research funding from AbbVie, Janssen, MSD, Kern, Pfizer, Lilly, Adacyte, Faes, Ferring, Falk, Takeda and Tillots. CGM has served as a speaker or received educational funds and grants from Johnson&Johnson, Tillotts Pharma, Takeda, Lilly, and Galápagos. YZ has served as a speaker, or has received research or education funding or advisory fees from: AbbVie, Adacyte Therapeutics, Alfa-Sigma, Amgen, Boehringer Ingelheim, Dr Falk Pharma, FAES Pharma, Fresenius Kabi, Ferring, Galapagos, Johnson&Johnson, Kern Pharma, Lilly,MSD, Pfizer, Sanofi, Sandoz, Takeda, Tillots Pharma, and PSI. FRM has served as a speaker and has received research or education funding or advisory fees from Lilly, Takeda, Johnson&Johnson, FAES Pharma, Falk, AbbVie, Pfizer, Ferring, and Kern Pharma.
JH has performed research projects, scientific meetings or advisory boards sponsored by MSD, Ferring, Abbvie, Johnson & Johnson, Biogen, Sandoz, Kern Pharma, Faes Farma, Lilly, Tillots, and Takeda. CO ha received education funding from Tillots, Alfasigma, Eli Lilly, Johnson&Johnson, Pfizer, and Fresenius. ED has served as a speaker or has received research and educational funds or advisory fees from AbbVie, Adacyte Therapeutics, Biogen, Celltrion, Galapagos, Gilead, GoodGut, Imidomics, Janssen, Kern Pharma, Lilly, MSD, Pfizer, Roche, Samsung, Takeda, and Tillots. EGP has served as a speaker and has received research or educational funds from MSD, Abbvie, Kern, Gebro, Pfizer, Takeda, Jansen, Ferring, Shire Pharmaceuticals, Faes, Tillotts Pharma, and Pfizer. All other authors have no conflicts of interest to declare. All other authors have no conflict of interest to declare.

Event

UEG Week Barcelona 2026

Topics

Mechanisms & Personalised Medicine Immunology IBD

Submission format

Abstract

Session

Abstract session: Hot topics in IBD

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

More Like This:

Is nutrition the missing link in long-term IBD management?

Charlie W. Lees

UPPER GASTROINTESTINAL CROHN’S DISEASE DOES NOT CONFER INTRINSIC BIOLOGIC RESISTANCE BUT REMAINS ASSOCIATED WITH INCREASED INTESTINAL SURGERY DESPITE BIOLOGIC THERAPY

Esther García-Planella

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior

MICROBIOTA‑ORIENTED DIETARY PATTERN, PROTEOMIC MEDIATORS, AND INCIDENT INFLAMMATORY BOWEL DISEASE: A UK BIOBANK PROSPECTIVE COHORT STUDY

Rui Ji

Introduction: Mistakes in… Upper GI

Henriette Heinrich

THE OBESITY-LITERACY CASCADE: WHAT PATIENTS WITH OBESITY DON'T KNOW — FROM DISEASE CONCEPT TO ENDOSCOPIC SLEEVE GASTROPLASTY

Cem Simsek

UEG Presentation

New

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

Evidence of disordered eating in disorders of gut–brain interaction

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior 1

Affiliations

1 Rouen University Hospital, INSERM U1073, CIC-CRB-1404, Rouen, France

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Abstract

Event

Postgraduate Teaching Programme Barcelona 2026

Topics

Neurogastroenterology & Motility Small Intestine & Nutrition

Session

Eating disorders and unexplained weight loss

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

More Like This:

Is nutrition the missing link in long-term IBD management?

Charlie W. Lees

UPPER GASTROINTESTINAL CROHN’S DISEASE DOES NOT CONFER INTRINSIC BIOLOGIC RESISTANCE BUT REMAINS ASSOCIATED WITH INCREASED INTESTINAL SURGERY DESPITE BIOLOGIC THERAPY

Esther García-Planella

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior

MICROBIOTA‑ORIENTED DIETARY PATTERN, PROTEOMIC MEDIATORS, AND INCIDENT INFLAMMATORY BOWEL DISEASE: A UK BIOBANK PROSPECTIVE COHORT STUDY

Rui Ji

Introduction: Mistakes in… Upper GI

Henriette Heinrich

THE OBESITY-LITERACY CASCADE: WHAT PATIENTS WITH OBESITY DON'T KNOW — FROM DISEASE CONCEPT TO ENDOSCOPIC SLEEVE GASTROPLASTY

Cem Simsek

UEG Presentation

New

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

MICROBIOTA‑ORIENTED DIETARY PATTERN, PROTEOMIC MEDIATORS, AND INCIDENT INFLAMMATORY BOWEL DISEASE: A UK BIOBANK PROSPECTIVE COHORT STUDY

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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

MICROBIOTA‑ORIENTED DIETARY PATTERN, PROTEOMIC MEDIATORS, AND INCIDENT INFLAMMATORY BOWEL DISEASE: A UK BIOBANK PROSPECTIVE COHORT STUDY

Xingyan Zhou 1, Ya Zheng 1, Rui Ji 1

Affiliations

1 The First Hospital of Lanzhou University, Lanzhou, China

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Abstract

Introduction

Gut dysbiosis is widely recognized as a pivotal trigger in the pathogenesis of inflammatory bowel disease (IBD). As a key determinant of the gut microenvironment, dietary patterns profoundly influence the composition of the microbiota, mucosal barrier integrity, and host immunity. Consequently, diet has gained increasing attention as a target for IBD prevention and management. Nevertheless, the optimal strategies for microbiota-oriented dietary interventions remain unclear, and the underlying mechanisms linking diet-microbiota interactions to IBD risk are poorly understood.

Aims & Methods

To evaluate the role of diet-microbiota interactions in IBD etiology, we examined the association between a microbiota-oriented dietary pattern (quantified by the Dietary Index for Gut Microbiota, DI-GM) and incident IBD in a prospective cohort (n = 208,143). Furthermore, we integrated high-throughput plasma proteomic data in a subset (n = 21,919) to identify diet-associated circulating proteins and performed mediation analyses to identify candidate biomarkers underlying the diet-microbiota-IBD axis.

Results

Over a median follow-up of 10.8 years, higher adherence to the microbiota-oriented dietary pattern was associated with a 16% lower risk of incident IBD (hazard ratio, 0.84; 95% CI, 0.72–0.98). Proteomic profiling identified 429 plasma proteins associated with the microbiota-oriented dietary pattern, with functional enrichment primarily in immune-inflammatory responses, cytokine-mediated signaling, and tissue repair pathways. Following selection of 57 candidate proteins by LASSO regression, mediation analysis identified 9 that significantly mediated the association between the microbiota-oriented dietary pattern and IBD risk, individually accounting for 13%–36% of the total effect, including OXT (oxytocin-neurophysin 1), SLC39A5 (solute carrier family 39 member 5), CGREF1 (cell growth regulator with EF hand domain protein 1), IGDCC4 (immunoglobulin superfamily DCC subclass member 4), MMP8 (matrix metalloproteinase 8), IL19 (interleukin-19), ALPP (alkaline phosphatase, placental type), AREG (amphiregulin), and IL15 (interleukin-15). Notably, OXT demonstrated the highest proportion mediated, whereas IGDCC4 exhibited a protective effect, in contrast to the risk-increasing effects of the other 8 mediators.
Table 1. Associations between the microbiota-oriented dietary pattern and incident IBD in the main cohort (n = 208,143)^a.

Exposure	Hazard Ratio (95% CI)	P value
Adherence levels to a microbiota-oriented dietary pattern
Lower (0–4)	1.00 [Reference]	-
Intermediate (5–6)	0.85 (0.74, 0.98)	0.02
Higher (≥7)	0.84 (0.72, 0.98)	0.03
P for trend	-	0.02

ᵃ Fully adjusted for demographic, socioeconomic, lifestyle, and dietary covariates.

Conclusion

These findings underscore the potential preventive role of diet, a highly modifiable factor, in IBD. Proteomic signatures may complement traditional dietary assessments and provide mechanistic insight into diet-IBD associations.

Disclosure

The authors declare that they have no competing interests.

Event

UEG Week Barcelona 2026

Topics

IBD Mechanisms & Personalised Medicine Immunology Gut Microbiota Small Intestine & Nutrition

Submission format

Abstract

Session

On bugs and food: New lessons in microbiomics and dietomics in IBD

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

More Like This:

Is nutrition the missing link in long-term IBD management?

Charlie W. Lees

UPPER GASTROINTESTINAL CROHN’S DISEASE DOES NOT CONFER INTRINSIC BIOLOGIC RESISTANCE BUT REMAINS ASSOCIATED WITH INCREASED INTESTINAL SURGERY DESPITE BIOLOGIC THERAPY

Esther García-Planella

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior

MICROBIOTA‑ORIENTED DIETARY PATTERN, PROTEOMIC MEDIATORS, AND INCIDENT INFLAMMATORY BOWEL DISEASE: A UK BIOBANK PROSPECTIVE COHORT STUDY

Rui Ji

Introduction: Mistakes in… Upper GI

Henriette Heinrich

THE OBESITY-LITERACY CASCADE: WHAT PATIENTS WITH OBESITY DON'T KNOW — FROM DISEASE CONCEPT TO ENDOSCOPIC SLEEVE GASTROPLASTY

Cem Simsek

UEG Presentation

New

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

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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

Introduction: Mistakes in… Upper GI

Henriette Heinrich 1

Affiliations

1 Stadtspital Triemli, Zürich, Switzerland

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Abstract

Event

UEG Week Barcelona 2026

Topics

Small Intestine & Nutrition Surgery Neurogastroenterology & Motility

Session

Mistakes in… Upper GI

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

More Like This:

Is nutrition the missing link in long-term IBD management?

Charlie W. Lees

UPPER GASTROINTESTINAL CROHN’S DISEASE DOES NOT CONFER INTRINSIC BIOLOGIC RESISTANCE BUT REMAINS ASSOCIATED WITH INCREASED INTESTINAL SURGERY DESPITE BIOLOGIC THERAPY

Esther García-Planella

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior

MICROBIOTA‑ORIENTED DIETARY PATTERN, PROTEOMIC MEDIATORS, AND INCIDENT INFLAMMATORY BOWEL DISEASE: A UK BIOBANK PROSPECTIVE COHORT STUDY

Rui Ji

Introduction: Mistakes in… Upper GI

Henriette Heinrich

THE OBESITY-LITERACY CASCADE: WHAT PATIENTS WITH OBESITY DON'T KNOW — FROM DISEASE CONCEPT TO ENDOSCOPIC SLEEVE GASTROPLASTY

Cem Simsek

UEG Poster

New

Standard Poster

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

This content is part of Gutflix. Log in with your myUEG account, or create one free, to watch it.

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

THE OBESITY-LITERACY CASCADE: WHAT PATIENTS WITH OBESITY DON'T KNOW — FROM DISEASE CONCEPT TO ENDOSCOPIC SLEEVE GASTROPLASTY

Alime Sena Kocyigit 1, Muhammet Furkan Çakmak 1, Muhammed bahaddin Durak 1, İbrahim Ethem Güven 1, Hatice yasemin Balaban 1, Cem Simsek 1

Affiliations

1 Hacettepe University Faculty of Medicine, Ankara, Türkiye

Summary

AI Generated

Summary is not available for this content yet.

Download PDF

Was this helpful?

Thanks for your feedback.

Abstract

Introduction

Effective obesity care depends on patients understanding obesity as a chronic disease, recognising its complications, and being informed about the full therapeutic continuum. Prior literacy studies have focused narrowly on surgical attitudes; granular, stepwise mapping of what patients do and do not know — from basic disease concept down to procedure-specific awareness — is lacking, and is the prerequisite for designing targeted patient education.

Aims & Methods

We aimed to construct a granular obesity-literacy cascade in adults with obesity by quantifying, in successive steps, the proportion who (i) frame obesity as a medical disease, (ii) can name an obesity-related complication, (iii) recognise each of the four treatment modalities (diet, exercise, pharmacotherapy, endoscopy/surgery), (iv) claim accurate efficacy and side-effect knowledge per modality, and (v) are aware of EBMT and ESG specifically. Patients completed a structured Turkish-language questionnaire covering disease conceptualisation, comorbidity knowledge, treatment awareness (existence, efficacy, side-effects for each modality), EBMT awareness, ESG-specific awareness, willingness, barriers, and 1–5 Likert ratings of decision drivers. Fisher's exact, Mann–Whitney U, and Spearman ρ were applied; α = 0.05.

Results

Twenty-five consecutive adults with obesity (BMI 36.1 ± 6.9 kg/m²; 56% female; 48% MASH; 40% with ≥2 metabolic comorbidities) were included. The literacy cascade revealed a progressive, stepwise deficit. Only 8% (2/25) framed obesity in medical/disease terms and only 16% (4/25) could name an obesity-related complication. Treatment-modality recognition fell steeply: diet 100%, exercise 92%, pharmacotherapy 68%, bariatric surgery 32%. A striking inversion emerged for surgery — 44% claimed to know its side-effects while only 32% acknowledged it as a treatment option, suggesting negative beliefs without factual grounding. Within EBMT, 68% had any prior awareness, 80% recognised intragastric balloon, yet only 28% knew ESG and 0% knew small-bowel therapies. Among 13 ESG-candidate patients (BMI ≥27 with ≥ 1 comorbidities), 77% did not know ESG and 69% were unwilling or unsure. Literacy correlated positively with education (ρ=0.64, p=0.001) and inversely with BMI class (ρ=−0.42, p=0.046). The top-ranked hesitation drivers were side-effects (83%) and invasiveness (56%); the top-ranked decision drivers were long-term outcomes (4.33/5) and other patients' experience (4.30), both outranking doctor's recommendation (4.08).

Conclusion

Obesity literacy is deficient at every level of the cascade — starting with the disease concept itself and narrowing sharply as treatments become more specialised. Patients most under-informed about surgical and endoscopic options are also those with the highest BMI — i.e. the strongest clinical candidates for EBMT. These granular, step-resolved findings map the specific literacy gaps a structured patient-education programme must close, and justify a prospective multi-centre intervention trial.

Granular literacy cascade

Literacy step	% (n/N)
Step 1 — Frames obesity as a medical disease	8% (2/25)
Step 2 — Names ≥1 obesity-related disease	16% (4/25)
Step 3 — Knows all 4 treatment modalities exist	28% (7/25)
Step 4 — Knows bariatric surgery exists	32% (8/25)
Step 5 — Knows anti-obesity pharmacotherapy exists	68% (17/25)
Step 6 — Aware of any EBMT	68% (17/25)
Step 7 — Knows intragastric balloon	80% (20/25)
Step 8 — Knows ESG specifically	28% (7/25)
Step 9 — Knows small-bowel endoscopic therapy	0% (0/25)

Conference

UEG Week Barcelona 2026

Submission format

Abstract

Session

OTHER (Posters)

Citation

2026: United European Gastroenterology Journal 2026; 14 (S1)

Published

2026

More Like This:

Is nutrition the missing link in long-term IBD management?

Charlie W. Lees

UPPER GASTROINTESTINAL CROHN’S DISEASE DOES NOT CONFER INTRINSIC BIOLOGIC RESISTANCE BUT REMAINS ASSOCIATED WITH INCREASED INTESTINAL SURGERY DESPITE BIOLOGIC THERAPY

Esther García-Planella

Evidence of disordered eating in disorders of gut–brain interaction

Chloé Melchior

MICROBIOTA‑ORIENTED DIETARY PATTERN, PROTEOMIC MEDIATORS, AND INCIDENT INFLAMMATORY BOWEL DISEASE: A UK BIOBANK PROSPECTIVE COHORT STUDY

Rui Ji

Introduction: Mistakes in… Upper GI

Henriette Heinrich

THE OBESITY-LITERACY CASCADE: WHAT PATIENTS WITH OBESITY DON'T KNOW — FROM DISEASE CONCEPT TO ENDOSCOPIC SLEEVE GASTROPLASTY

Cem Simsek