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TRYPTOPHAN DEFICIENCY IS FREQUENT IN THE WESTERNIZED POPULATION AND INSTIGATES SEVERE COURSE OF INTERNAL-MEDICINE DISEASES

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TRYPTOPHAN DEFICIENCY IS FREQUENT IN THE WESTERNIZED POPULATION AND INSTIGATES SEVERE COURSE OF INTERNAL-MEDICINE DISEASES

Lina Welz 1, Jeanette Franzenburg 1, Sascha Thielke 2, Katrin Franzpötter 3, Sarah Meier 3, Corina Maetzler 2, Olaf Schneider 4, Jan Heyckendorf 2, Thomas Bahmer 2, Domagoj Schunk 2, Stefan Schreiber 5, Konrad Aden 1

Affiliations

1 University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany|||University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany

2 University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany

3 Christian-Albrechts-Universität zu Kiel, Kiel, Germany

4 Cerascreen, Leipzig, Germany

5 University Hospital Schleswig-Holstein, Kiel, Germany|||University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany

Summary

AI Generated

Tryptophan deficiency is frequent in the western population (39.3% of healthy controls, 30.2% of GI disease patients) and associates with longer hospitalisations, more procedures, and higher mortality in internal-medicine and gastrointestinal diseases.

In 15,188 healthy controls, 39.3% had tryptophan deficiency (lowest quartile), which inversely correlated with self-reported symptoms including gastrointestinal symptoms.
Among 4,349 emergency-ward patients, tryptophan deficiency was present in 26.6% overall and 30.2% of the 516 gastrointestinal disease patients (ICD-10 K00-K93), versus 1.4% of healthy controls.
In gastrointestinal diseases, patients in the lowest versus highest tryptophan quartile had 3.91 days longer hospitalisation, 0.48 days longer ICU stays, and 3.3 more in-hospital procedures.
Baseline tryptophan showed low-to-moderate predictive value (AUROC 0.54–0.62) for complicated outcomes in GI diseases, including hospitalisation longer than 7 days, ICU admission, and death.
Tryptophan reduction was pronounced even when C-reactive protein was below 5 mg/L, suggesting tryptophan may reflect chronic low-grade inflammation not captured by standard markers.
The authors propose that tryptophan degradation along the de novo NAD synthesis pathway is an overarching metabolic hallmark of chronic low-grade inflammation and a risk factor for severe disease courses.

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Abstract

Introduction

Micronutrient deficiency is an underestimated problem in the westernized population with unclear effects on the manifestation of acute or chronic disease. Westernized lifestyle instigates disrupted gut-microbial crosstalk and chronic low-grade inflammation¹. Tryptophan (Trp) is an essential amino acid used for de novo synthesis of cellular nicotinamide adenine dinucleotide (NAD). We have previously shown increased Trp degradation in several chronic inflammatory disorders, including IBD^2,3. Whether Trp deficiency is a widespread phenomenon in the western population is unknown. Here, we tested the hypothesis that Trp deficiency is frequent in the western population and associates with increased overall disease severity in internal-medicine and especially gastrointestinal (GI) diseases.

Aims & Methods

To screen the micronutrient status of the healthy population, we assessed quantitative amino acid levels in n=15.188 healthy controls (HC) with a commercially available home-care dry blood spot test for targeted metabolomics (cohort 1). Self-reported symptoms were assessed with a digital questionnaire. To validate Trp deficiency (defined as the lowest Trp quartile) in acute internal-medicine diseases (cohort 2), we measured serum Trp by HPLC in HC (n=291) and patients presenting in the emergency ward of the University Hospital Schleswig-Holstein, Kiel (n=4349, categorized by ICD10; thereof GI diseases n=516 (K00-K93: diseases of the digestive system); 10/2023-09/2024). Next to laboratory and clinical assessment at presentation, disease courses were followed up digitally for at least 6 months. Statistical analyses were performed with linear mixed models (LMM) and logistic regression correcting for age and sex at birth; predictive performance was evaluated via area under the receiver-operating-characteristic (AUROC; R version 4.4.1).

Results

In cohort 1, 39.3% of HC presented with Trp deficiency. Trp deficiency significantly inversely correlated with the amount of self-reported symptoms, such as e.g. GI symptoms. Validating these findings in internal-medicine and a subgroup of GI diseases in cohort 2, we found significantly reduced serum Trp compared to HC (mean Trp 56.58±10.84µM vs. 45.06±16.65 (all disease groups), 45.21±20.69 (GI diseases)), especially when the serum inflammation marker C-reactive protein was not elevated (<5 mg/l). Here, Trp deficiency was observed in 1.4% of HC, while it was strongly increased in all disease groups (26.6%) and GI diseases (30.2%). Using LMM, we found that patients that were hospitalized, admitted to the ICU or died within the follow-up period had a significantly lower Trp compared to patients with favourable outcomes (outpatient/no ICU/alive). Patients with Trp at the lowest compared to the highest quartile underwent longer hospitalisation and ICU treatment (all diseases: 3.17/0.37 days (d) longer; GI diseases: 3.91/0.48d longer) as well as a higher number of in-hospital procedures (all diseases: 1.47 more; GI diseases: 3.3 more). The predictive value of Trp for complicated outcomes (hospitalisation, hospitalisation >7d, ICU treatment, death) as assessed by AUROC was low-moderate (all diseases: AUC 0.69, 0.67, 0.61, 0.72; GI diseases: AUC 0.61, 0.6, 0.54 and 0.62, respectively).

Conclusion

We report that Trp deficiency is frequent in the westernized population and associates with more severe disease courses. Our data suggests Trp degradation along the de novo NAD synthesis pathway as an overarching metabolic hallmark of chronic low-grade inflammation and a risk factor for severe disease courses of internal-medicine and GI diseases.

References

1. Christ, A. & Latz, E. The Western lifestyle has lasting effects on metaflammation. Nature Reviews Immunology vol. 19 267–268 Preprint at https://doi.org/10.1038/s41577-019-0156-1 (2019).
2. Harris, D. M. M. et al. Tryptophan degradation as a systems phenomenon in inflammation – an analysis across 13 chronic inflammatory diseases. EBioMedicine 102, 105056 (2024).
3. Nikolaus, S. et al. Increased Tryptophan Metabolism Is Associated With Activity of Inflammatory Bowel Diseases. Gastroenterology 153, (2017).

Event

UEG Week Berlin 2025

Topics

Gut Microbiota Small Intestine & Nutrition

Submission format

Abstract

Session

The gut ecosystem: From pathogenesis to treatment

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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UEG Presentation

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Specific key function of gut microbiota

Marius Vital 1

Affiliations

1 Deutsches Zentrum für Infektionsforschung, Braunschweig, Germany

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Abstract

Event

UEG Week Berlin 2025

Topics

Gut Microbiota Primary Care

Session

The art of making clinical research precise: Can we unlock the microbiome?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Marius Vital

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D. Nageshwar Reddy

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Jian Qi

ENDO-HISTO FOUNDATIONAL FUSION MODEL: A NOVEL ARTIFICIAL INTELLIGENCE APPROACH FOR PREDICTING HISTOLOGIC REMISSION AND EARLY RESPONSE TO THERAPY IN A PHASE 2 ULCERATIVE COLITIS CLINICAL TRIAL

Valery Naranjo

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Valerie Paradis

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Salvatore Oliva

UEG Presentation

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

IMPACT OF TIMING OF PREMEDICATION ON MUCOSAL VISIBILITY DURING ENDOSCOPY-A RANDOMIZED CONTROLLED TRIAL

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IMPACT OF TIMING OF PREMEDICATION ON MUCOSAL VISIBILITY DURING ENDOSCOPY-A RANDOMIZED CONTROLLED TRIAL

Zaheer Nabi 1, MARAGONI RAJESH GOUD 2, Preeti Sudha 1, D. Nageshwar Reddy 1

Affiliations

1 Asian Institute of Gastroenterology, Hyderabad, India

2 Asian Institute of gastroenterology,Hyderabad, Hyderabad, India

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Abstract

Introduction

Gastric mucosal visibility is essential for high-quality upper gastrointestinal (GI) endoscopy. While simethicone and N-acetylcysteine (NAC) have been shown to improve mucosal visibility, the optimal time interval between preparation and endoscopy remains undefined.

Aims & Methods

This randomized controlled trial evaluated the effect of timing on mucosal visibility and explored the upper limit beyond which visibility begins to decline.
In this single-center, randomized controlled trial, adult patients undergoing elective upper GI endoscopy were randomized into four groups: placebo, simethicone + NAC with endoscopy performed after 10–20 minutes, 20–30 minutes, and >30 minutes. The primary outcome was the proportion of patients achieving adequate gastric mucosal visibility (GMV), defined as a score of <7 on a validated visibility scale. A pre-specified subgroup analysis of the >30 minute group was performed by stratifying patients into 20-minute intervals (31–50, 51–70, and 71–90 minutes) to assess the durability of mucosal clarity over time.

Results

Comparison	Adequate gastric mucosal visibility (%)	P
10–20 min vs 20–30 min	27% vs 62%	0.001
10–20 min vs >30 min	27% vs 67%	0.001
10–20 min vs Placebo	27% vs 2.6%	0.001
20–30 min vs >30 min	62% vs 67%	0.174
20–30 min vs Placebo	62% vs 2.6%	0.001

1,140 patients (median age 42years, 63.2% males) were included in the study. Adequate GMV was significantly higher in all preparation groups compared to placebo (p < 0.001). The 20–30 minute and >30 minute groups demonstrated the highest rates of adequate visibility (61.5% and 73.5%, respectively), both significantly superior to the 10–20 minute group (26.9%) and placebo (2.6%). In the >30 minute subgroup analysis, the 31–50 minute interval demonstrated the highest adequacy (73.5%). The 51–70 minute group showed moderate adequacy (52.1%), which was not significantly different from the 20–30 minute group (p = 0.207). However, the 71–90 minute group had reduced adequacy (43.8%) and did not differ significantly from the 10–20 minute group (p = 0.145). No adverse events were reported across study arms.

Conclusion

Endoscopy performed between 20 and 50 minutes after mucosal preparation yields optimal gastric mucosal visibility. A decline in visibility beyond 50 minutes suggests a practical upper limit for endoscopy timing following preparation. These findings support structured, time-sensitive scheduling following mucosal cleansing to enhance procedural quality.

Disclosure

None

Event

UEG Week Berlin 2025

Topics

Endoscopy Oesophagus

Submission format

Abstract

Session

Randomised controlled trials in upper GI endoscopy

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Marius Vital

IMPACT OF TIMING OF PREMEDICATION ON MUCOSAL VISIBILITY DURING ENDOSCOPY-A RANDOMIZED CONTROLLED TRIAL

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Jian Qi

ENDO-HISTO FOUNDATIONAL FUSION MODEL: A NOVEL ARTIFICIAL INTELLIGENCE APPROACH FOR PREDICTING HISTOLOGIC REMISSION AND EARLY RESPONSE TO THERAPY IN A PHASE 2 ULCERATIVE COLITIS CLINICAL TRIAL

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UEG Presentation

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EXOSOMAL CAGA INDUCES MACROPHAGE POLARIZATION AND FERROPTOSIS BY JAK1-2/STAT1 SIGNALING PATHWAY IN HELICOBACTER PYLORI-ASSOCIATED GASTRITIS

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

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EXOSOMAL CAGA INDUCES MACROPHAGE POLARIZATION AND FERROPTOSIS BY JAK1-2/STAT1 SIGNALING PATHWAY IN HELICOBACTER PYLORI-ASSOCIATED GASTRITIS

JIAHUI Lin 1, Yuting Liu 1, Tingting Luo 1, Jian Qi 1

Affiliations

1 The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China

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Abstract

Introduction

Helicobacter pylori (H. pylori) infection is a major cause of gastric diseases, with the virulence factor CagA carried by exosomes playing a crucial role in regulating inflammation. Ferroptosis and M1 polarization are key mechanisms in promoting inflammation, yet the role of CagA in inducing macrophage ferroptosis and M1 polarization to exacerbate gastric mucosal inflammation remains unclear.

Aims & Methods

CagA-positive (CagA+) and CagA-negative (CagA-) H. pylori strains were co-cultured with gastric epithelial cells, and their supernatants were collected. Exosomes were isolated using ultracentrifugation to obtain CagA+Exo and CagA-Exo. Changes in macrophage M1/M2 polarization markers and ferroptosis markers were analyzed under CagA+Exo and CagA-Exo treatment. The activation of the JAK/STAT1 signaling pathway was assessed by Western blot, and STAT1 expression in the nucleus was evaluated using a nuclear protein extraction kit. Chromatin immunoprecipitation (ChIP) was used to identify the binding site of STAT1 on the SLC7A11 promoter. Biopsy samples from the gastric mucosa of gastritis patients infected with CagA+ or CagA- H. pylori were analyzed for macrophage polarization and ferroptosis markers.

Results

Exosomal CagA was found to induce macrophage M1 polarization and ferroptosis, with the ferroptosis inhibitor SLC7A11 playing a key role in CagA-induced ferroptosis. Exosomal CagA activated the JAK/STAT1 signaling pathway, leading to M1 polarization and ferroptosis. Additionally, CagA+Exo increased nuclear STAT1 expression, which subsequently bound to the SLC7A11 promoter to regulate its transcription. In gastric mucosa biopsies from CagA+ H. pylori-infected gastritis patients, increased levels of iNOS (a marker of M1 polarization) and decreased expression of SLC7A11 were observed.

Conclusion

Our findings indicate that exosomal CagA promotes macrophage M1 polarization and ferroptosis through the JAK/STAT1 signaling pathway. This study provides new insights and potential therapeutic targets for H. pylori-associated gastritis.

Event

UEG Week Berlin 2025

Topics

Mechanisms & Personalised Medicine Stomach & H. Pylori

Submission format

Abstract

Session

H. pylori: Between bench and bedside

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

Specific key function of gut microbiota

Marius Vital

IMPACT OF TIMING OF PREMEDICATION ON MUCOSAL VISIBILITY DURING ENDOSCOPY-A RANDOMIZED CONTROLLED TRIAL

D. Nageshwar Reddy

EXOSOMAL CAGA INDUCES MACROPHAGE POLARIZATION AND FERROPTOSIS BY JAK1-2/STAT1 SIGNALING PATHWAY IN HELICOBACTER PYLORI-ASSOCIATED GASTRITIS

Jian Qi

ENDO-HISTO FOUNDATIONAL FUSION MODEL: A NOVEL ARTIFICIAL INTELLIGENCE APPROACH FOR PREDICTING HISTOLOGIC REMISSION AND EARLY RESPONSE TO THERAPY IN A PHASE 2 ULCERATIVE COLITIS CLINICAL TRIAL

Valery Naranjo

Will there be pathologists in 2030 or only AI?

Valerie Paradis

The pan-enteric assessment of IBD: Is this the future of mucosal healing?

Salvatore Oliva

UEG Presentation

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

ENDO-HISTO FOUNDATIONAL FUSION MODEL: A NOVEL ARTIFICIAL INTELLIGENCE APPROACH FOR PREDICTING HISTOLOGIC REMISSION AND EARLY RESPONSE TO THERAPY IN A PHASE 2 ULCERATIVE COLITIS CLINICAL TRIAL

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

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ENDO-HISTO FOUNDATIONAL FUSION MODEL: A NOVEL ARTIFICIAL INTELLIGENCE APPROACH FOR PREDICTING HISTOLOGIC REMISSION AND EARLY RESPONSE TO THERAPY IN A PHASE 2 ULCERATIVE COLITIS CLINICAL TRIAL

Marietta Iacucci 1, Giovanni Santacroce 1, Pablo Meseguer 2, Rocio Del Amor 3, Alejandro Diéguez 3, Bisi Bode Kolawole 4, Ujwala Chaudhari 4, Irene Zammarchi 1, Brian Hayes 5, Rory Crotty 5, Davide Zardo 6, Yasuharu Maeda 1, Ilaria Ditonno 1, Valentina Vadori 4, Louise Burke 5, Klaus Gottlieb 7, Charles Owen 7, William J. Eastman 7, Subrata Ghosh 1, Enrico Grisan 4, Valery Naranjo 3

Affiliations

1 University College Cork, Cork, Ireland

2 Universitat Politècnica de València, Valencia, Spain|||valgrAI – Valencian Graduate School and Research Network of Artificial Intelligence, Valencia, Spain

3 Universitat Politècnica de València, Valencia, Spain

4 London South Bank University, London, United Kingdom

5 Cork University Hospital, Cork, Ireland

6 San Bortolo Hospital, Vicenza, Italy

7 Eli Lilly and Company, Indianapolis, United States

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Abstract

Introduction

Artificial Intelligence (AI)- enabled endoscopy and histology offer accurate, objective, and rapid assessment of disease activity in Ulcerative Colitis (UC). Emerging multi-source AI models integrating diverse datasets may enhance standardised disease evaluation and outcome prediction.

Aims & Methods

This study aimed to develop a novel AI model fusing endoscopic and histological findings to improve the assessment of disease remission and predict early response to therapy in UC clinical trials. A novel multimodal AI fusion algorithm was developed by integrating paired endoscopic videos and histological whole-slide images (WSIs) from the phase 2 clinical trial of Mirikizumab in UC (NCT02589665). The endoscopy branch of the model was trained with 291 white-light videos, using a convolutional neural network to select informative frames and the BioMedCLIP foundational model to extract features. The histology branch utilised the CONCH foundational model and was fine-tuned on 291 WSIs to obtain patch-level features. Features from both modalities were aggregated and fused using multi-head self-attention. The model’s ability to assess histological remission and response to therapy at weeks 12 and 52 was evaluated. Histological remission was defined as Geboes ≤2B.0, while a response to therapy at different time points was based on histological remission or improvement (Geboes <3.1).

Results

The fusion model outperformed single-modality assessments for histological remission, achieving a sensitivity of 89.72% (95% CI: 82.35–94.76), specificity of 89.67% (95% CI: 84.34–93.67), and accuracy of 89.69% (95% CI: 85.61–92.94). It demonstrated remarkable performance in assessing response to therapy at 12 and 52 weeks, with sensitivity of 97.96% (95% CI: 89.15–99.95), specificity of 86.84% (95% CI: 71.91–95.59) and accuracy of 93.10% (95% CI 85.59 – 97.43) for histological remission at week 52. Substantial agreement was observed between the AI fusion model and central readout.

	Histologic remission			Response to therapy
	Endoscopy-only	Histology-only	Endo-Histo fusion	Histologic improvement week 12	Histologic improvement week 52	Histologic remission week 12	Histologic remission week 52
Sensitivity (95% CI)	75.80% (66.46 – 83.47)	85.98% (77.93 – 91.94)	89.72% (82.35 – 94.76)	86.54% (74.21 – 94.41)	93.88% (88.13 – 98.72)	79.59% (65.66 – 89.76)	97.96% (89.15 – 99.95)
Specificity (95% CI)	73.91% (66.94 - 80.10)	88.59% (83.08 – 92.79)	89.67% (84.34 – 93.67)	76.00% (61.83 – 86.94)	81.58% (65.67 – 92.26)	73.58% (59.67 – 84.74)	86.84% (71.91 – 95.59)
PPV (95% CI)	62.79% (53.84 - 71.14)	81.42% (73.01 – 88.11)	83.48% (75.41 – 89.75)	78.95% (66.11 – 88.62)	86.79% (74.66 – 94.52)	73.58% (59.67 – 84.74)	90.57% (79.34 – 96.87)
NPV (95% CI)	83.95% (77.37 – 89.24)	91.57% (86.48 – 95.21)	93.75% (89.09 – 96.84)	84.44% (70.54 – 93.51)	91.18% (76.32 – 98.14)	79.59% (65.66 – 89.76)	97.06% (84.67 – 99.93)
Accuracy (95% CI)	74.57% (69.16 – 79.47)	87.63% (83.29 – 91.18)	89.69% (85.61 – 92.94)	81.37% (72.45 – 88.40)	88.51% (79.88 – 94.35)	76.47% (67.04 – 84.31)	93.10% (85.59 – 97.43)
F1 Score (95% CI)	68.64% (62.31 – 74.51)	83.64% (78.07 – 88.27)	86.49% (81.27 – 90.69)	82.57% (74.13 – 89.17)	90.20% (82.71 – 95.20)	76.47% (67.04 – 84.31)	94.12% (87.64 – 97.81)

Abbreviations: CI, confidence interval; NPV, negative predictive value; PPV, positive predictive value.

Conclusion

This innovative multimodal fusion AI model enhances the assessment of histological remission and accurately predicts response to therapy. By potentially standardising central readouts and enabling automated disease assessment, this novel tool marks a significant advancement towards precision medicine in clinical trials.

Disclosure

Marietta Iacucci received research grants and consultant fees from Olympus, Pentax, Eli Lilly, and Janssen. All other authors declare no competing interests.

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

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EXOSOMAL CAGA INDUCES MACROPHAGE POLARIZATION AND FERROPTOSIS BY JAK1-2/STAT1 SIGNALING PATHWAY IN HELICOBACTER PYLORI-ASSOCIATED GASTRITIS

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ENDO-HISTO FOUNDATIONAL FUSION MODEL: A NOVEL ARTIFICIAL INTELLIGENCE APPROACH FOR PREDICTING HISTOLOGIC REMISSION AND EARLY RESPONSE TO THERAPY IN A PHASE 2 ULCERATIVE COLITIS CLINICAL TRIAL

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Will there be pathologists in 2030 or only AI?

Valerie Paradis

The pan-enteric assessment of IBD: Is this the future of mucosal healing?

Salvatore Oliva

UEG Presentation

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

Will there be pathologists in 2030 or only AI?

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

Will there be pathologists in 2030 or only AI?

Valerie Paradis 1

Affiliations

1 INSERM - Hôpital Beaujon, Clichy, France

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Abstract

Event

UEG Week Berlin 2025

Topics

Histopathology IBD Nurses

Session

The art of making clinical research precise: AI – friend or foe?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

Specific key function of gut microbiota

Marius Vital

IMPACT OF TIMING OF PREMEDICATION ON MUCOSAL VISIBILITY DURING ENDOSCOPY-A RANDOMIZED CONTROLLED TRIAL

D. Nageshwar Reddy

EXOSOMAL CAGA INDUCES MACROPHAGE POLARIZATION AND FERROPTOSIS BY JAK1-2/STAT1 SIGNALING PATHWAY IN HELICOBACTER PYLORI-ASSOCIATED GASTRITIS

Jian Qi

ENDO-HISTO FOUNDATIONAL FUSION MODEL: A NOVEL ARTIFICIAL INTELLIGENCE APPROACH FOR PREDICTING HISTOLOGIC REMISSION AND EARLY RESPONSE TO THERAPY IN A PHASE 2 ULCERATIVE COLITIS CLINICAL TRIAL

Valery Naranjo

Will there be pathologists in 2030 or only AI?

Valerie Paradis

The pan-enteric assessment of IBD: Is this the future of mucosal healing?

Salvatore Oliva

UEG Presentation

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

The pan-enteric assessment of IBD: Is this the future of mucosal healing?

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 pan-enteric assessment of IBD: Is this the future of mucosal healing?

Salvatore Oliva 1

Affiliations

1 University Hospital Umberto, Sapienza University of Rome, Rome, Italy

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Abstract

Event

UEG Week Berlin 2025

Topics

IBD Mechanisms & Personalised Medicine Surgery

Session

How to optimise success in IBD treatment

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Specific key function of gut microbiota

Marius Vital

IMPACT OF TIMING OF PREMEDICATION ON MUCOSAL VISIBILITY DURING ENDOSCOPY-A RANDOMIZED CONTROLLED TRIAL

D. Nageshwar Reddy

EXOSOMAL CAGA INDUCES MACROPHAGE POLARIZATION AND FERROPTOSIS BY JAK1-2/STAT1 SIGNALING PATHWAY IN HELICOBACTER PYLORI-ASSOCIATED GASTRITIS

Jian Qi

ENDO-HISTO FOUNDATIONAL FUSION MODEL: A NOVEL ARTIFICIAL INTELLIGENCE APPROACH FOR PREDICTING HISTOLOGIC REMISSION AND EARLY RESPONSE TO THERAPY IN A PHASE 2 ULCERATIVE COLITIS CLINICAL TRIAL

Valery Naranjo

Will there be pathologists in 2030 or only AI?

Valerie Paradis

The pan-enteric assessment of IBD: Is this the future of mucosal healing?

Salvatore Oliva

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