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COMPARATIVE RISK OF ADVANCED BIOLOGICAL AGENTS FOR CARDIOVASCULAR AND THROMBOTIC EVENTS IN PATIENTS WITH INFLAMMATORY BOWEL DISEASE: DATA FROM A REAL WORLD COHORT

Dhruv Ahuja 1, Kuan-Hung Yeh 2, Claudia Dziegielewski 2, Soo-Kyung Park 3, Sagar B. Patel 2, Shane W. Goodwin 4, Christopher Ma 5, Ashwin N. Ananthakrishnan 6, Namrata Singh 7, Ronghui Xu 2, Siddharth Singh 2

Affiliations

1 University of California, San Diego, United States|||Indira Gandhi Hospital, New Delhi, India

2 University of California, San Diego, United States

3 University of California, La Jolla, San Diego, United States|||Samsung Kangbuk Hospital, Sungkyunkwan University School of Medicine, Seoul, None

4 Western University, Ontario, Canada

5 University of Caglary, Calgary, Canada

6 Harvard Medical Schools, Boston, United States

7 University of Washington, Seattle, United States

Summary

AI Generated

A retrospective U.S. claims database analysis of 21,675 IBD patients initiating advanced biological therapies from 2013 to 2023 found no difference in risk of major adverse cardiovascular events or venous thromboembolism between any biological agent or small molecule compared to TNF antagonists.

The study included 12,245 Crohn's disease patients and 9,430 ulcerative colitis patients who were incident users of TNF antagonists, IL-12/23 antagonists, IL-23 antagonists, vedolizumab, JAK inhibitors, or S1PR modulators.
In ulcerative colitis, VTE incidence rates ranged from 1.69 to 2.01 per 100 person-years and MACE rates from 0.52 to 0.99 per 100 person-years; in Crohn's disease, VTE rates ranged from 0.89 to 2.33 and MACE rates from 0.68 to 1.73 per 100 person-years.
Hazard ratios for all therapies compared to TNF antagonists showed no statistically significant differences, with confidence intervals crossing 1.0 for both VTE and MACE in both diseases.
Stabilized inverse probability of treatment weighting using multinomial propensity scores was applied to account for baseline confounding, including differences in comorbidity burden across treatment groups.
Clinicians managing IBD patients may find this real-world comparative safety data useful when selecting advanced biological therapies.

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Abstract

Introduction

We conducted a retrospective analysis of a large U.S. based administrative claims database comparing the risk of major adverse cardiovascular events (MACE) and venous thromboembolism (VTE) among patients with inflammatory bowel disease (IBD) initiating advanced biological therapies.

Aims & Methods

Patients with CD and UC who were incident users of advanced biological agents from 2013 to 2023 were identified within the Optum Labs® database. The therapeutic agents included either tumor necrosis factor-α (TNF) antagonists (infliximab, adalimumab, and certolizumab pegol), IL-12/23 antagonists (ustekinumab), IL-23 antagonists (risankizumab), anti-integrin agents (vedolizumab), Janus kinase (JAK) inhibitors (tofacitinib and upadacitinib), or S1PR modulators (ozanimod). Eligible patients were required to have continuous insurance coverage for at least one year before and after treatment initiation. We estimated incidence rates (IRs) and compared risks for VTE and MACE (myocardial infarction and stroke). Fatal cardiovascular outcomes were excluded due to limited specificity and data constraints.
To account for baseline confounding, we applied stabilized inverse probability of treatment weighting (IPTW) using multinomial propensity scores. Hazard ratios were estimated using Cox proportional hazard models.

Results

We included 12,245 patients with CD (mean age: 44.5 ± 17.5 years; 54.2% female; 30.9% using concomitant steroids), and 9,430 patients with UC (mean age: 47.5 ± 17.7 years; 49.2% female; 50% on concomitant corticosteroids). Patients receiving JAK inhibitors and vedolizumab were more likely to have higher comorbidity burden than others for CD while those receiving IL-23 antagonists had the most comorbid burden for UC patients, when assessed through proportion of patients with Charlson comorbidity index of ≥ 5. In UC patients, VTE incidence rates ranged from 1.69 to 2.01 for VTE and MACE rates from 0.52 to 0.99 per 100 person-years. For CD, VTE incidence rates ranged from 0.89 to 2.33 and for MACE, 0.68 to 1.73. Hazard ratios comparing the risk of events across therapies is presented in table 1.

Table 1: Hazard ratios for risk of VTE and MACE in patients with Crohn’s disease and Ulcerative colitis receiving advanced biological therapies and small molecules

	Hazard Ratio using stabilized IPW weights (95% CI)
Therapies	Ulcerative Colitis (UC)		Crohn’s disease (CD)
	VTE	MACE	VTE	MACE
TNF antagonists (reference)	1.0 (reference)	1.0 (reference)	1.0 (reference)	1.0 (reference)
Vedolizumab	1.08 [0.81; 1.44]	0.90 [0.57; 1.39]	1.04 [0.73; 1.49]	1.11 [0.75; 1.62]
JAK inhibitors	0.72 [0.40;1.30]	0.73 [0.29; 1.85]	0.42 [0.07; 2.42]	--
IL-12/23 antagonists*	0.97 [0.65; 1.45]	1.23 [0.70; 2.16]	1.05 [0.76; 1.45]	0.94 [0.63; 1.38]
S1PR modulators	0.54 [0.13; 2.23]	--	--	--
IL23 antagonists			1.26 [0.64; 2.48]	1.37 [0.56; 3.31]

* For UC analysis, this group included 67 patients receiving IL-23 antagonists

Conclusion

In this large real-world IBD cohort, there was no difference in risk of adverse cardiovascular and thrombotic events between any biological agent or small molecule, in compairosn to TNF antagnoists.

Disclosure

CM: Consulting fees from AbbVie, Alimentiv, Amgen, AVIR Pharma Inc, Bristol Myers Squibb, Celltrion, Eli Lilly, Ferring, Forte Biosciences, Fresenius Kabi, Gilead, Janssen, McKesson, Mirador Therapeutics, Mylan, Pendopharm, Pfizer, Prometheus Biosciences Inc., Roche, Sanofi, Takeda, Tillotts Pharma; speaker's fees from AbbVie, Amgen, AVIR Pharma Inc, Alimentiv, Bristol Myers Squibb, Eli Lilly, Ferring, Fresenius Kabi, Janssen, Merck, Organon, Pendopharm, Pfizer, Sanofi, Takeda, Tillotts Pharma; royalties from Springer Publishing; research support from AbbVie, Eli Lilly, Ferring, Pfizer.
VJ: Consulting/advisory board fees from AbbVie, Alimentiv Inc, Arena pharmaceuticals, Asahi Kasei Pharma, Asieris, Astra Zeneca, Bristol Myers Squibb, Celltrion, Eli Lilly, Ferring, Flagship Pioneering, Fresenius Kabi, Galapagos, GlaxoSmithKline, Genentech, Gilead, Janssen, Merck, Mylan, Pandion, Pendopharm, Pfizer, Protagonist, Prometheus, Reistone Biopharma, Roche, Sandoz, Second Genome,Takeda, Teva, Topivert, Ventyx, Vividion; speaker’s fees from, Abbvie, Ferring, Galapagos, Janssen Pfizer Shire, Takeda, Fresenius Kabi
SS: Research grants from Pfizer

Conference

UEG Week Berlin 2025

Topics

IBD

Submission format

Abstract

Session

Tackling IBD with epidemiology (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Hao Chen

SPATIALLY DIFFERENTIATED MEASUREMENT OF INFLAMMATORY CELLS WITH DEEP LEARNING REVEALS THE HETEROGENEITY OF CHANGES IN ULCERATIVE COLITIS

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UEG Presentation

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LARGE-SCALE GENOME-WIDE ASSOCIATION ANALYSIS OF IRRITABLE BOWEL SYNDROME IN 1,099,880 ADULTS REVEALS NEW GENETIC AETIOLOGY

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LARGE-SCALE GENOME-WIDE ASSOCIATION ANALYSIS OF IRRITABLE BOWEL SYNDROME IN 1,099,880 ADULTS REVEALS NEW GENETIC AETIOLOGY

Yajie Zhang 1, Zuodi Liang 2, Weihong Sha 1, Hao Chen 1

Affiliations

1 Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guang Zhou, China

2 School of Medicine of South China University of Technology, Guang Zhou, China|||Department of Gastroenterology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guang Zhou, China

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Abstract

Introduction

Irritable bowel syndrome (IBS), the most prevalent gastrointestinal disorder globally, has a significant impact on the quality of life of 10 - 15% of the population, with a higher prevalence among women than men. Despite the identification of certain contributing factors, the pathophysiology of IBS remains largely unknown.

Aims & Methods

We firstly performed Genome-wide association study (GWAS) on the IBS cohort from the All of Us Research Program and adjusted for sex, age, and top 10 principal components. We conducted GWAS meta-analyses of IBS and its subtypes in 80,737 IBS cases and 1,019,143 asymptomatic control subjects from five independent cohorts (All of Us Research Program, UK Biobank, Bellygenes, Genetic Epidemiology Research on Aging, FinnGen). IBS risk loci were functionally annotated to identify candidate genes. Systematic variant-level analysis, including variants annotation, functional genomics and expression quantitative trait loci, prioritized potential causal variants. Gene-level analyses, including transcriptome-wide association study, colocalization analysis and Mendelian randomization, nominated the potential causal genes.

Results

We identified two independent IBS susceptibility loci at genome-wide significance (P < 5 × 10⁻⁸) in All of Us Research Program cohort totaling 14,897 cases and 245,388 controls. GWAS-meta analysis identified 12 novel independent (P < 5×10^-8) signals and 5 unreported loci (rs143348218, rs3748618, rs6432674, rs9536395, rs976714). Subtype-specific (P < 5×10^-8) findings based on subtype-specific GWAS meta-datasets included 3 loci for subtype IBS-C (3 novel independent loci) , 44 loci for IBS-M (2 novel independent loci). By integrating evidence from layers of different analyses, we prioritized the most plausible causal genes for IBS including CADM2, PCLO, PHF2 and SHISA6. Notably, PCLO (associated with bipolar disorder and major depressive disorder) and SHISA6 (overexpression in Platelet and T-lymphocyte) have been previously unreported in association with IBS.

Conclusion

Our study not only showed the power of the last large-scale GWAS in deciphering the genetic aetiology of IBS, but also uncovered 5 new genetic risk variants, potential unreported causal variants, genes and therapeutic targets for IBS.

References

1 Chey WD, Kurlander J, Eswaran S. Irritable bowel syndrome: a clinical review. JAMA. 2015;313:949–58. doi: 10.1001/jama.2015.0954
2 Soubieres A, Wilson P, Poullis A, et al. Burden of irritable bowel syndrome in an increasingly cost-aware National Health Service. Frontline Gastroenterology. 2015;6:246–51. doi: 10.1136/flgastro-2014-100542
3 Eijsbouts C, Zheng T, Kennedy NA, et al. Genome-wide analysis of 53,400 people with irritable bowel syndrome highlights shared genetic pathways with mood and anxiety disorders. Nat Genet. 2021;53:1543–52. doi: 10.1038/s41588-021-00950-8
4 Bonfiglio F, Zheng T, Garcia-Etxebarria K, et al. Female-Specific Association Between Variants on Chromosome 9 and Self-Reported Diagnosis of Irritable Bowel Syndrome. Gastroenterology. 2018;155:168–79. doi: 10.1053/j.gastro.2018.03.064
5 DeBoever C, Tanigawa Y, Aguirre M, et al. Assessing Digital Phenotyping to Enhance Genetic Studies of Human Diseases. Am J Hum Genet. 2020;106:611–22. doi: 10.1016/j.ajhg.2020.03.007
6 Venner E, Muzny D, Smith JD, et al. Whole-genome sequencing as an investigational device for return of hereditary disease risk and pharmacogenomic results as part of the All of Us Research Program. Genome Med. 2022;14:34. doi: 10.1186/s13073-022-01031-z
7 Weeks EM, Ulirsch JC, Cheng NY, et al. Leveraging polygenic enrichments of gene features to predict genes underlying complex traits and diseases. Nat Genet. 2023;55:1267–76. doi: 10.1038/s41588-023-01443-6

Event

UEG Week Berlin 2025

Topics

Colorectal

Submission format

Abstract

Session

Lower GI motility I

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Christian Schulz

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

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UEG Presentation

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

SPATIALLY DIFFERENTIATED MEASUREMENT OF INFLAMMATORY CELLS WITH DEEP LEARNING REVEALS THE HETEROGENEITY OF CHANGES IN ULCERATIVE COLITIS

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SPATIALLY DIFFERENTIATED MEASUREMENT OF INFLAMMATORY CELLS WITH DEEP LEARNING REVEALS THE HETEROGENEITY OF CHANGES IN ULCERATIVE COLITIS

Dylan Windell 1, Alastair Magness 1, Rongqi Li 1, Paul Aljabar 1, Eve Fryer 2, Robert D. Goldin 3, Phil Wakefield 1, Caitlin Langford 4, Jonathan Landy 5

Affiliations

1 Perspectum Ltd., Oxford, United Kingdom

2 John Radcliffe Hospital, Oxford, United Kingdom

3 Centre for Pathology, London, United Kingdom

4 Perspectum, Cambridge, United States

5 London North West University Healthcare NHS Trust, London, United Kingdom

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Abstract

Introduction

Histological assessment in Inflammatory Bowel Disease (IBD) is often required with endoscopic diagnoses to establish disease activity. This is evident in patients where histological healing is a major therapeutic goal and when endoscopic healing can also exhibit microscopic disease. IBD can manifest in numerous landmark features which are structural and inflammatory related. Histological activity is determined through erosion/ulceration, architectural changes in tissue morphology, mucin depletion and presence of varied inflammatory cells the colonic crypts, Muscularis Mucosae (MM) and Lamina Propria (LP). Histological scoring systems vary in complexity and methodology and subject to discrepancies in inter-rater consensus. Our model aims to provide accurate measurements of key histological features in Ulcerative Colitis (UC) used in scoring systems as both a decision support tool for improving pathologist scoring alignment and sensitive quantitative metrics of inflammatory cells to evaluate disease activity.

Aims & Methods

We developed an ensemble of convolutional neural networks to identify cell types, tissue foreground, crypts, MM, and haemorrhage in H&E images of IBD biopsy data. Models were trained with expert-labelled annotations comprising 34,289 image-annotation pairs (80% training, 20% validation) from in-house and publicly available data. Model accuracy was assessed with 6,464 held-out image-annotation pairs from 26 Whole Slide Images (WSIs) from all sites of the large intestine commonly sampled during endoscopic investigation, while ground truth annotations were reviewed by GI-trained pathologists to certify accuracy. We used geospatial methods to derive boundaries of the LP from other predicted domains, associate cells to delineated regions, measure architectural changes and derive spatially differentiated metrics of inflammatory burden in 66 patients with confirmed UC.

Results

The AI model spatially differentiates and segments cell types and tissue compartments. This produces metrics for inflammatory cell counts in regions of interest such as crypts, LP, and MM. Goblet cell segmentation within crypts allows for measurement of mucin depletion. This can be visualized for pathologists where each inflammatory cell type across the WSI is represented as density metrics. Automated quantification of inflammatory cells across AI-identified tissue domains throughout the bowels of UC patients revealed large intra- and inter-patient variability.

Conclusion

Our AI model can measure histological healing by detecting architectural change, inflammatory cell number, goblet cell reduction and erosions and ulceration. This allows for metrics and visual overlays to assist with pathologist reading and quantifying changes in mucosal biopsies in a clinical trial setting which requires extremely sensitive tools only AI can provide.

Disclosure

DW/AM/RL/PA/PW and CL are employees at Perspectum Ltd. EF and RG are consultants for Perspectum Ltd. All other co-authors have no conflicts of interest to declare relevant to this work.

Event

UEG Week Berlin 2025

Topics

IBD

Submission format

Abstract

Session

Artificial intelligence in IBD

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

LARGE-SCALE GENOME-WIDE ASSOCIATION ANALYSIS OF IRRITABLE BOWEL SYNDROME IN 1,099,880 ADULTS REVEALS NEW GENETIC AETIOLOGY

Hao Chen

SPATIALLY DIFFERENTIATED MEASUREMENT OF INFLAMMATORY CELLS WITH DEEP LEARNING REVEALS THE HETEROGENEITY OF CHANGES IN ULCERATIVE COLITIS

Jonathan Landy

JAK2 INHIBITION ATTENUATES PORTAL HYPERTENSION IN METABOLIC DYSFUNCTION-ASSOCIATED LIVER

Shiyao Chen

Nutritional management of small intestinal enteropathies

Francisca Joly

Established and novel targets for breath testing

Christian Schulz

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

Nurulamin Noor

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

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JAK2 INHIBITION ATTENUATES PORTAL HYPERTENSION IN METABOLIC DYSFUNCTION-ASSOCIATED LIVER

Yifei Liu 1, Shiyao Chen 1

Affiliations

1 Zhongshan Hospital, Fudan University, Shanghai, China

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Abstract

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.

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

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SPATIALLY DIFFERENTIATED MEASUREMENT OF INFLAMMATORY CELLS WITH DEEP LEARNING REVEALS THE HETEROGENEITY OF CHANGES IN ULCERATIVE COLITIS

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Shiyao Chen

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Francisca Joly

Established and novel targets for breath testing

Christian Schulz

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

Nurulamin Noor

UEG Presentation

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

Nutritional management of small intestinal enteropathies

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Nutritional management of small intestinal enteropathies

Francisca Joly 1

Affiliations

1 Beaujon Hospital, Assistance Publique-Hôpitaux de Paris, Clichy, France

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Abstract

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

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LARGE-SCALE GENOME-WIDE ASSOCIATION ANALYSIS OF IRRITABLE BOWEL SYNDROME IN 1,099,880 ADULTS REVEALS NEW GENETIC AETIOLOGY

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Christian Schulz

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UEG Presentation

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Established and novel targets for breath testing

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Established and novel targets for breath testing

Christian Schulz 1

Affiliations

1 Ludwig Maximilian University, Munich, Germany

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Abstract

Event

UEG Week Berlin 2025

Topics

Mechanisms & Personalised Medicine

Session

Breath testing and clinical metabolomics: Back to the future

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Shiyao Chen

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Francisca Joly

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Christian Schulz

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

Nurulamin Noor

UEG Presentation

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

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

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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

Affiliations

1 Haaglanden Medical Center, The Hague, Netherlands

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

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Abstract

Event

UEG Postgraduate Teaching Programme Berlin 2025

Session

The Crohn´s disease journey

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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LARGE-SCALE GENOME-WIDE ASSOCIATION ANALYSIS OF IRRITABLE BOWEL SYNDROME IN 1,099,880 ADULTS REVEALS NEW GENETIC AETIOLOGY

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

Nurulamin Noor

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

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