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ACCEPTABILITY OF FECAL CALPROTECTIN IN PATIENTS WITH INFLAMMATORY BOWEL DISEASE: IMPACT OF AN ALTERNATIVE COLLECTION DEVICE FOR STOOL SAMPLING (THE ACCALMI STUDY)

Giulia Pasi 1, Amale Antari 1, Damien Masson 1, Hélène Caillon 1, Thomas Dejoie 1, Marie Anne Vibet 1, Michael Collins 1, Arnaud Bourreille 1, Catherine Le Berre 1

Affiliations

1 CHU Nantes, Nantes, France

Summary

AI Generated

The ACCALMI study found that an alternative stool collection device similar to FIT test devices significantly improved acceptability of fecal calprotectin testing among IBD patients compared to standard containers.

In a randomized study of 156 IBD patients, the alternative device (Procise Stool Collection Device with spiral-shaped probe) significantly improved acceptability with an odds ratio of 2.69 (p < 0.001) on ordinal scale assessment.
Acceptability scores were higher with the alternative device: 86.1% rated it good or very good versus 46.4% for standard containers, and mean VAS scores were 7.9/10 versus 6.1/10.
Among patients previously tested, 55% preferred the alternative device compared to 7.2% preferring conventional containers, with the alternative device alleviating embarrassment and discomfort.
Compliance remained similarly high in both groups at 92%, with long home-to-hospital distance and use of the alternative device being the only factors associated with better acceptability in multivariate analysis.
This patient-centered innovation may improve monitoring adherence in IBD patients who require routine fecal calprotectin testing.

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Abstract

Introduction

Fecal calprotectin (FC) is a key non-invasive biomarker used to monitor inflammatory bowel disease (IBD). Despite its clear clinical value, patient adherence to the test remains suboptimal, mainly due to reluctance related to stool collection. The objective of the ACCALMI study was to compare the acceptability of a new stool collection device, similar to the one used for fecal immunochemical tests (FIT), with a standard stool container, and to evaluate its impact on patient compliance.

Aims & Methods

In this prospective, single-center study, 156 patients with an established diagnosis of IBD and who had been prescribed an FC test as part of their routine care, were randomly assigned to either the standard container group or the alternative device group (Procise Stool Collection Device™), which includes a collection tube with a thin spiral-shaped probe facilitating stool collection. Acceptability was assessed using a 4-category ordinal scale (from "poor" to "very good") and a visual analog scale (VAS, from 0 to 10). Analyses were conducted in both per-protocol and intention-to-treat (ITT) populations, with missing data handled using the maximum bias method. Factors associated with improved FC acceptability, and compliance with FC testing, were analyzed.

Results

The alternative collection device significantly improved acceptability as measured by the ordinal scale (odds ratio [OR] 2.69; p < 0.001). In the alternative group, acceptability ratings were significantly higher with only 1.4% versus 7.0% rating it as ‘poor’, 12.5% versus 46.6% as ‘average’, 66.7% versus 40.8% as ‘good’, and 19.4% versus 5.6% as ‘very good’. Measured using the VAS, the average acceptability was 7.9/10 in the group using the alternative device compared to 6.1/10 in the standard group, with a significant difference of 30.4% (95% CI [19.7 - 44.7%], p < 0.001), although it did not reach the threshold of 30% that was set a priori. The ITT analysis led to the same conclusions. Among the patients who had already undergone FC testing and were randomized to the "alternative device" group, 55% indicated a preference for the alternative device, compared to 7.2% for the conventional device, while 37.7% found them similar. Embarrassment and discomfort associated with the standard container were alleviated by the alternative device. A long home-to-hospital distance (> 50 km) and the use of the alternative device were the only factors associated with better acceptability in the multivariate analysis. Compliance was similar between both groups and remarkably high (92%).

Conclusion

The ACCALMI study demonstrated that the alternative stool collection device, similar to the one used in FIT for colorectal cancer screening, is more accepted by IBD patients than the standard container, thus improving the acceptability of FC testing. These findings support the integration of patient-centered innovations in diagnostic and follow-up testing to improve the monitoring of IBD.

Disclosure

Acknowledgments: Collaboration with Biosynex®.

Conference

UEG Week Berlin 2025

Topics

IBD

Submission format

Abstract

Session

IBD (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

DISCOVERY OF A NOVEL, SELECTIVE SIK3 INHIBITOR FOR THE TREATMENT OF ULCERATIVE COLITIS, CROHN'S DISEASES AND OTHER AUTOIMMUNE DISEASES

Pierre Raboisson

ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Xuemei Liu

Guiding diagnosis and therapy using proteomics

Knut E.A. Lundin

Building a bile duct: What can structural tissue patterning tell us about liver disease?

Luke Boulter

ACUTE PANCREATITIS: HAS THE EPIDEMIOLOGICAL PROFILE CHANGED OVER THE PAST TEN YEARS?

Eduardo Redondo-Cerezo

LONG TERM RISK OF ACUTE PANCREATITIS IN PATIENTS WITH CED: A NATIONWIDE POPULATION-BASED, SIBLING-CONTROLLED COHORT STUDY

Jonas F Ludvigsson

UEG Presentation

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DISCOVERY OF A NOVEL, SELECTIVE SIK3 INHIBITOR FOR THE TREATMENT OF ULCERATIVE COLITIS, CROHN'S DISEASES AND OTHER AUTOIMMUNE DISEASES

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DISCOVERY OF A NOVEL, SELECTIVE SIK3 INHIBITOR FOR THE TREATMENT OF ULCERATIVE COLITIS, CROHN'S DISEASES AND OTHER AUTOIMMUNE DISEASES

Fabrice KOLB 1, John-Paul Gallivan 1, Steve De Vos 2, Nicolas Desroy 2, David Moreno 2, Michael Torok 2, Anouk Blauw 2, Christian Seemayer 2, Emmanuel Karouzakis 2, Chantal Tasset 2, Christophe Peixoto 3, Didier Merciris 3, Catherine Jagerschmidt 3, Adrien Cosson 3, Stéphanie Lavazais 3, Wulf-Otto Boucher 2, Pierre Raboisson 1

Affiliations

1 Onco3R Therapeutics, Leuven, Belgium

2 Galapagos NV, Mechelen, Belgium

3 Novalix, Romainville, France

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Abstract

Introduction

Current treatment options for IBD are limited by low clinical remission rates and loss of response. Most therapies target single pathogenic pathways and while combinations of biologics targeting different pathogenic cytokines can increase clinical remission rates, dosing schedules are inconvenient. JAK inhibitors, target multiple cytokine pathways, but are limited by safety concerns.
Salt-inducible kinases (SIKs) are a subfamily of serine/threonine kinases in the AMP-activated protein kinase (AMPK) family and act as key regulators of immune cell signaling. SIK inhibitors have been shown to target multiple cytokine pathways.
Three SIK isoforms exist: SIK1, SIK2 and SIK3. SIK inhibitors targeting multiple isoforms have been investigated in clinical trials. Although there have been signals of activity in patients with ulcerative colitis and psoriasis, limited efficacy and safety concerns related to SIK1 and 2 inhibition have hampered their development.

Aims & Methods

We performed structure based drug design to identify highly potent and selective SIK3 inhibitors that could offerbest in class efficacy and safety for the treatment of various auto-immune diseases. Our effort led to to the discovery of 100s of compounds spanning SIK3 binding sites. Compounds were tested in protein and cell-based assays to evaluate potency and selectivity against SIK3 and in a phenotypic human whole blood TNFα assay. Lead optimization involving rigorous testing in safety and pharmacology panels, resulted in the selection of lead candidates that were tested in a variety of translational models to identify the most efficacious compounds. Human PK predictions were performed using non-clinical in vivo PK assessments and allometric scaling leading to the selection of the drug candidate, which entered GLP toxicology studies.

Results

O3R-5671 is a highly potent and specific SIK3 inhibitor with sub-nanomolar potency for SIK3 and low activity against SIK1 and 2 and over all human kinases. It demonstrated potent activity in a panel of human primary phenotypic cell assays inhibiting TNFα, IL-12, and IL-23 release in LPS-stimulated myeloid cells, and inhibiting TNFa release in LPS-stimulated human whole blood. O3R-5671 also inhibited activation of TCR-stimulated human primary T cells and induced IL-10 secretion from myeloid cells.
In vivo, O3R-5671 demonstrated dose-dependent activity in a mouse LPS challenge model, dose-dependent efficacy in two distinct mouse models of IBD, and dose-dependent efficacy in mouse models of IL-23-induced psoriasis and psoriatic arthritis. Cross-species PK and allometric scaling were used to predict O3R-5671’s human PK profile- which is expected to be conducive to potent SIK3 inhibition and clinical efficacy in patients with IBD.
O3R-5671 demonstrated a highly attractive profile in ADME and in vitro safety panels. Six-week GLP toxicity studies in rats and dogs established no observed adverse effect levels (NOAELs) which support dosing in humans with doses that are predicted to be pharmacologically active with a large safety margin.

Conclusion

O3R-5671 is a highly specific and potent SIK3 inhibitor that is predicted to have a flat PK profile in humans. These properties should allow O3R-5671 to apply strong drug pressure on SIK3 while sparing SIK1 and 2. This is expected to result in the inhibition of multiple pathogenic cytokines including TNFa and IL-23, both of which have been validated as IBD targets. A clinical trial is ongoing to establish the safety and PK profile of O3R-5671 and understand its effect on pharmacodynamic biomarkers.

Disclosure

All authors were employed by Galapagos who discovered O3R-5671 or Novalix, a CRO that was employed by Galapagos. Some authors are employed by Onco3R therapeutics, who are currently developing O3R-5671

Event

UEG Week Berlin 2025

Topics

Endoscopy IBD Mechanisms & Personalised Medicine

Submission format

Late-Breaking Abstract

Session

Hot off the press: IBD treatment

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

DISCOVERY OF A NOVEL, SELECTIVE SIK3 INHIBITOR FOR THE TREATMENT OF ULCERATIVE COLITIS, CROHN'S DISEASES AND OTHER AUTOIMMUNE DISEASES

Pierre Raboisson

ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Xuemei Liu

Guiding diagnosis and therapy using proteomics

Knut E.A. Lundin

Building a bile duct: What can structural tissue patterning tell us about liver disease?

Luke Boulter

ACUTE PANCREATITIS: HAS THE EPIDEMIOLOGICAL PROFILE CHANGED OVER THE PAST TEN YEARS?

Eduardo Redondo-Cerezo

LONG TERM RISK OF ACUTE PANCREATITIS IN PATIENTS WITH CED: A NATIONWIDE POPULATION-BASED, SIBLING-CONTROLLED COHORT STUDY

Jonas F Ludvigsson

UEG Presentation

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ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

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ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Shuhui Liu 1, Zhiyuan Ma 1, Bei Ji 1, SHUN YAO 1, Taolang Li 1, Biguang Tuo 1, Xuemei Liu 1

Affiliations

1 Affiliated Hospital of Zunyi Medical University, Zunyi, China

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Abstract

Introduction

Spasmolytic polypeptide expressing metaplasia (SPEM) is a cell repair lineage and is a very important phenotype of gastric mucosal injury and precancerous lesion.
Previously, parietal cells loss is considered as the first step and followed with chief cells transdiffernation to induce SPEM. But whether chief cells initial loss cause SPEM
needs to be further investigation. Acidic mammalian chitinase (CHIA) belongs to the 18 glycosidase family and is highly expressed in the chief cells. Our previous study showed that CHIA deficiency in the chief cells is the key event to induce SPME to progress to gastric cancer (Liu et al., DDW 2023 and 2024). However, the molecular role of CHIA in the development of SPEM is need further investigated.

Aims & Methods

Electron microscopy, qRT-PCR and single-cell sequencing (scRNA-seq) technology, as well as histopathological and immunofluorescence (IF) stainning with specific markers were performed in chief cells specific CHIA knockout mouse model (CHIA^rox/rox-GIF-Dre) and wild-type mice(CHIA^rox/rox), and in CHIA over - expression mice (CHIA ^rox/rox - GIF - Dre + rAAv - CHIA) and the control group (CHIA ^rox/rox - GIF - Dre + rAAv - control).

Results

Compared with CHIA^rox/rox mice, histological analysis and scRNA-seq technology data showed that loss of chief cells with increased M2 macrophage infiltration and final SPEM formation, but remaining of parietal cells in CHIA^rox/rox-GIF-Dre mice. Electron microscopy showed CHIA deficiency in mice resulted in endoplasmic reticulum was dilated and swollen, as well as the mitochondrial membrane was discontinuous of chief cells, followed with the accumulation of endoplasmic reticulum stress marker, including PERK, XBP-1, eIF2α/P-eIF2α, and GRP78, together with upregulation of pyroptosis-related marker, including NLRP3, ACS, GSDMD, NEK7, Caspase1, Caspase11, IL-1β, and IL-18, which was detected by qRT-PCR. These data indicating that target CHIA deletion caused chief cells pyroptosis. Furthermore, qRT-PCR analysis showed that CHIA deficiency caused the activation of IL33/IL-13 circuit in the mucosa of mice. Moreover, double immunofluorescence staining confirmed that upregulation and colocalization of IL-33 induced M2 macrophage polarization markers, including F4/80 and CD163⁺ with NLRP3 in the base of gastric mucosal of CHIA^rox/rox-GIF-Dre mice when compared with CHIA^rox/rox mice.Notably, CHIA^rox/rox - GIF - Dre + rAvv - CHIA mice reversed the above process compared with controls.

Conclusion

Chief cells specific CHIA deficiency resulted in endoplasmic reticulum stress mediate NLRP3 inflammasome activation to induce chief cells proptosis.
Chief cells initial loss is sufficient and the key step to activate IL-33/ST2-M2 macrophage polarization axis to induce SPEM, which is independent of parietal cells loss.

Event

UEG Week Berlin 2025

Topics

Immunology Neurogastroenterology & Motility Small Intestine & Nutrition Oesophagus Stomach & H. Pylori

Submission format

Abstract

Session

Complexity and diversity in upper GI

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

DISCOVERY OF A NOVEL, SELECTIVE SIK3 INHIBITOR FOR THE TREATMENT OF ULCERATIVE COLITIS, CROHN'S DISEASES AND OTHER AUTOIMMUNE DISEASES

Pierre Raboisson

ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Xuemei Liu

Guiding diagnosis and therapy using proteomics

Knut E.A. Lundin

Building a bile duct: What can structural tissue patterning tell us about liver disease?

Luke Boulter

ACUTE PANCREATITIS: HAS THE EPIDEMIOLOGICAL PROFILE CHANGED OVER THE PAST TEN YEARS?

Eduardo Redondo-Cerezo

LONG TERM RISK OF ACUTE PANCREATITIS IN PATIENTS WITH CED: A NATIONWIDE POPULATION-BASED, SIBLING-CONTROLLED COHORT STUDY

Jonas F Ludvigsson

UEG Presentation

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

Guiding diagnosis and therapy using proteomics

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Guiding diagnosis and therapy using proteomics

Knut E.A. Lundin 1

Affiliations

1 Norwegian Coeliac Disease Research Centre, University of Oslo and Oslo University Hospital, Oslo, Norway

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Abstract

Event

UEG Week Berlin 2025

Topics

Mechanisms & Personalised Medicine

Session

The art of making clinical research precise: Biomarkers of the future - Is it liquid gold?

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

DISCOVERY OF A NOVEL, SELECTIVE SIK3 INHIBITOR FOR THE TREATMENT OF ULCERATIVE COLITIS, CROHN'S DISEASES AND OTHER AUTOIMMUNE DISEASES

Pierre Raboisson

ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Xuemei Liu

Guiding diagnosis and therapy using proteomics

Knut E.A. Lundin

Building a bile duct: What can structural tissue patterning tell us about liver disease?

Luke Boulter

ACUTE PANCREATITIS: HAS THE EPIDEMIOLOGICAL PROFILE CHANGED OVER THE PAST TEN YEARS?

Eduardo Redondo-Cerezo

LONG TERM RISK OF ACUTE PANCREATITIS IN PATIENTS WITH CED: A NATIONWIDE POPULATION-BASED, SIBLING-CONTROLLED COHORT STUDY

Jonas F Ludvigsson

UEG Presentation

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

Building a bile duct: What can structural tissue patterning tell us about liver disease?

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.

Building a bile duct: What can structural tissue patterning tell us about liver disease?

Luke Boulter 1

Affiliations

1 University of Edinburgh, Edinburgh, United Kingdom

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Abstract

Event

UEG Week Berlin 2025

Topics

Hepatobiliary Mechanisms & Personalised Medicine

Session

The art of making clinical research precise: Narrowing the gap between the bench and bedside

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

DISCOVERY OF A NOVEL, SELECTIVE SIK3 INHIBITOR FOR THE TREATMENT OF ULCERATIVE COLITIS, CROHN'S DISEASES AND OTHER AUTOIMMUNE DISEASES

Pierre Raboisson

ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Xuemei Liu

Guiding diagnosis and therapy using proteomics

Knut E.A. Lundin

Building a bile duct: What can structural tissue patterning tell us about liver disease?

Luke Boulter

ACUTE PANCREATITIS: HAS THE EPIDEMIOLOGICAL PROFILE CHANGED OVER THE PAST TEN YEARS?

Eduardo Redondo-Cerezo

LONG TERM RISK OF ACUTE PANCREATITIS IN PATIENTS WITH CED: A NATIONWIDE POPULATION-BASED, SIBLING-CONTROLLED COHORT STUDY

Jonas F Ludvigsson

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ACUTE PANCREATITIS: HAS THE EPIDEMIOLOGICAL PROFILE CHANGED OVER THE PAST TEN YEARS?

Raúl Mendoza-Rodriguez 1, Francisco Valverde-López 1, Ana Lancho Munoz 1, Elisabet López-González 1, Juan Gabriel Martínez-Cara 2, Eduardo Redondo-Cerezo 1

Affiliations

1 Hospital Universitario Virgen de las Nieves, Granada, Spain

2 Hospital Virgen de las Nieves, Granada, Spain

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Abstract

Introduction

The available evidence on the epidemiology of acute pancreatitis (AP) is primarily based on older studies conducted in other countries, limiting its applicability to local settings. This study aims to provide updated data on the clinical characteristics and outcomes of patients with AP in our region thereby improving understanding and management of the disease.

Aims & Methods

A retrospective analysis was conducted on a prospective database comprising a cohort of 526 patients with acute pancreatitis (AP), consecutively included between March 2017 and June 2019 at a tertiary care hospital. Systematic laboratory testing was performed at admission and again at 48 hours. Clinical management followed standard practice guidelines, including routine abdominal ultrasound after admission and abdominal CT scan in cases of diagnostic uncertainty, clinical deterioration, or lack of improvement. Diagnosis and classification were based on the revised 2012 Atlanta classification.

Results

The most frequent etiology of AP in our setting was biliary lithiasis (65.9%), followed by idiopathic (15.4%) and alcohol-related causes (8.4%). Severe AP accounted for 9% of cases, while 14.3% were classified as moderately severe. Up to 20.2% of patients developed local complications; however, only 4.9% presented with pancreatic necrosis. SIRS was observed in 18.7% of patients at admission, decreasing to 8.7% at 48 hours. Only 3.7% of patients required ICU admission (Table 1). Factors such as smoking, ERCP, antibiotic therapy, acute cholangitis, and SIRS showed significant differences across different etiological groups.

	Biliary	Alcohol	Hypertriglyceridemia	Pot-ERCP	Idiopathic	Total
Frequency	304 (65.9%)	39 (8.5%)	8 (1.7%)	5 (1.1%)	71 (15.4%)	461
Severe pancreatitis	28 (9.2%)	2 (5.1%)	0	1 (20%)	8 (12.7%)	42 (9%)
Local complications	24 (7.9%	6 (15.4%)	2 (25%)	1 (20%)	11 (15.5%)	106 (20.2%)
Transient organ failure (<48h)	46 (16.2%)	3 (8.1%)	2 (28.6%)	1 (20%)	14 (20.3%)	72 (16.3%)
Persistent organ failure (>48h)	28 (9.2%)	3 (7.7%)	0	0	9 (12.7%)	42 (9%)
SIRS at admission	46 (15.2%)	12 (30.8%)	1 (12.5%)	1 (20%)	16 (22.5%)	86 (18.5%)
Acute cholangitis (suspected and/or confirmed)	138 (45.5%)	7 (15.4%)	0	3 (60%)	17 (23.9%)	173 (37.6%)
Antibiotic therapy	123 (41.3%)	9 (23.7%)	1 (12.5%)	4 (80%)	19 (27.1%)	165 (36.1%)
ERCP performed	42 (14.1%)	0	0	2 (40%)	2 (2.9%)	49 (10.9%)

Conclusion

Acute pancreatitis (AP) is a common condition that imposes a significant healthcare burden. Determining the etiology of AP at admission is important not only from an epidemiological standpoint but also due to its profound implications for patient prognosis.
Contrary to what has been reported in the literature, the second most frequent cause of AP in our cohort was idiopathic, surpassing alcohol-related cases. In line with other studies, we observed significant differences between biliary and alcohol-related etiologies regarding smoking habits, development of acute cholangitis, need for ERCP, and use of antibiotic therapy. Patients with alcohol-related AP were significantly more likely to present with SIRS at admission. However, we did not find statistically significant differences in other key clinical outcomes, although patients with alcohol-related AP appeared to have a higher, but not statistically significant, risk of developing local complications, pancreatic necrosis, and SIRS at 48 hours.
This study highlights the importance of tailoring management strategies according to etiology to optimize clinical outcomes.

References

1. Wang, G. J., Gao, C. F., Wei, D., Wang, C., & Ding, S. Q. (2009). Acute pancreatitis: etiology and common pathogenesis. World journal of gastroenterology, 15(12), 1427–1430.
2. Petrov, M. S., & Yadav, D. (2019). Global epidemiology and holistic prevention of pancreatitis. Nature reviews. Gastroenterology & hepatology, 16(3), 175–184.
3. Iannuzzi, J. P., King, J. A., Leong, J. H., Quan, J., Windsor, J. W., Tanyingoh, D., Coward, S., Forbes, N., Heitman, S. J., Shaheen, A. A., Swain, M., Buie, M., Underwood, F. E., & Kaplan, G. G. (2022). Global Incidence of Acute Pancreatitis Is Increasing Over Time: A Systematic Review and Meta-Analysis. Gastroenterology, 162(1), 122–134.

Conference

UEG Week Berlin 2025

Topics

Pancreas

Submission format

Abstract

Session

PANCREAS (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

More Like This:

DISCOVERY OF A NOVEL, SELECTIVE SIK3 INHIBITOR FOR THE TREATMENT OF ULCERATIVE COLITIS, CROHN'S DISEASES AND OTHER AUTOIMMUNE DISEASES

Pierre Raboisson

ACIDIC MAMMALIAN CHITINASE DEFICIENCY RESULTS IN CHIEF CELLS PYROPTOSIS AND GASTRIC REGIONAL IMMUNITY REMODELING IS THE NEW CELLULAR ORIGIN OF SPEM

Xuemei Liu

Guiding diagnosis and therapy using proteomics

Knut E.A. Lundin

Building a bile duct: What can structural tissue patterning tell us about liver disease?

Luke Boulter

ACUTE PANCREATITIS: HAS THE EPIDEMIOLOGICAL PROFILE CHANGED OVER THE PAST TEN YEARS?

Eduardo Redondo-Cerezo

LONG TERM RISK OF ACUTE PANCREATITIS IN PATIENTS WITH CED: A NATIONWIDE POPULATION-BASED, SIBLING-CONTROLLED COHORT STUDY

Jonas F Ludvigsson

UEG Presentation

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

LONG TERM RISK OF ACUTE PANCREATITIS IN PATIENTS WITH CED: A NATIONWIDE POPULATION-BASED, SIBLING-CONTROLLED COHORT STUDY

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

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LONG TERM RISK OF ACUTE PANCREATITIS IN PATIENTS WITH CED: A NATIONWIDE POPULATION-BASED, SIBLING-CONTROLLED COHORT STUDY

Jialu Yao 1, Jiangwei Sun 1, Fahim Ebrahimi 1, David Bergman 1, Peter HR Green 2, Benjamin Lebwohl 2, Daniel A. Leffler 3, David Surendran Sanders 4, Björn Lindkvist 5, Jonas F Ludvigsson 1

Affiliations

1 Karolinska Institutet, Stockholm, Sweden

2 Columbia University College of Physicians and Surgeons, New York, United States

3 Takeda Pharmaceuticals International Co., Cambridge, United States

4 Royal Hallamshire Hospital - NHS Trust, Royal Hallamshire Hospital; Sheffield/GB, Sheffield, United Kingdom

5 Sahlgrenska University Hospital, Gothenburg, Sweden

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Abstract

Introduction

Celiac disease (CeD) may affect the interplay between the duodenal mucosa and exocrine pancreatic function as a consequence of intestinal inflammation, and could potentially increase the risk of acute pancreatitis (AP). However, the association between these two conditions remain largely unexplored.

Aims & Methods

This Swedish nationwide cohort study in ESPRESSO aimed to investigate the risk of incident AP in patients with CeD without previous pancreatic disease. Patients with biopsy-confirmed CeD were identified between 1969 and 2023 (n=57,221) and were individually matched with ≤5 general population reference individuals (n= 279,126) by sex, birth year, calendar year, and county of residence. Included individuals were followed until 31 August 2024. The primary outcome was any incident AP. Secondary outcomes included (1) specific AP types (i.e., gallstone-related, non-gallstone-related, potential alcohol-related AP); (2) severe AP, defined as (i) any hospitalization for AP that lasts for ≥14 days or being combined with diagnostic or procedural code implying a complicated episode, or (ii) all-cause death <90 days after being discharged for AP); as well as (3) second episode of any AP that occurred ≥90 days after being discharged for incident AP. Flexible parametric survival models were used to estimate the adjusted hazard ratios (aHRs) for investigated outcomes. Familial risk factors were additionally accounted for in the comparison with CeD-free full siblings (n=70,016).

Results

During a median follow-up of 15.5 years, incident AP was observed in 549 patients with CeD (incidence rate (IR)=59 per 100,000 person-years) and 1,732 reference individuals (IR=38). Patients with CeD had a higher hazard of developing any AP than reference individuals (aHR=1.50, 95% confidence interval:1.35 to 1.67). The hazard elevation remained significant for more than 25 years after the diagnosis of CeD, resulting in one extra AP event per 185 CeD patients until then. CeD was significantly associated with gallstone-related AP (aHR=1.31 [1.12 to 1.54]), non-gallstone-related AP (aHR=1.65 [1.41 to 1.93]), severe AP (aHR=1.68 [1.32 to 2.14]), but not with potential alcohol-related AP (aHR=1.22 [0.89 to 1.67]). The association between CeD and any AP was attenuated but remained significant in the sibling comparison and in sensitivity analyses that respectively accounted for the potential influence of cancer, medications that may induce AP (i.e., steroids, mesalamine, and immunosuppressants), and the COVID-19 pandemic.
Restricting our data to patients who had experienced a first AP, the risk of second-time AP was not higher in patients with CeD (aHR=0.81 [0.61 to 1.07]) than in reference individuals.

Conclusion

Patients with CeD were at an increased risk of incident AP, especially non-gallstone-related AP, for more than 25 years after diagnosis. However, the risk was no longer elevated beyond the first AP episode. Further research is needed to investigate the underlying mechanism linking CeD to AP.

Disclosure

All authors have completed the ICMJE uniform disclosure form and declare:
FE has served as an advisory board member for Boehringer Ingelheim.
DAL is an employee of Takeda Pharmaceuticals and owns stock in this company.
JFL has coordinated a study on behalf of the Swedish IBD quality register (SWIBREG). That study received funding from Janssen Corporation. JFL has also received financial support from MSD/Merck developing a paper reviewing national healthcare registers in China, and for a collaboration on inflammatory bowel disease. JFL also has a research collaboration on celiac disease with Takeda.
The other authors report no disclosures relevant to the manuscript.

Event

UEG Week Berlin 2025

Topics

Mechanisms & Personalised Medicine Small Intestine & Nutrition

Submission format

Abstract

Session

Coeliac disease: From screening to new drugs

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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