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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.

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

1 Hospital Universitario Virgen de las Nieves, Granada, Spain

2 Hospital Virgen de las Nieves, Granada, Spain

Conference

UEG Week Berlin 2025

Topics

Pancreas

Submission format

Abstract

Session

PANCREAS (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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THE RESISTANT MICROBIOME: INSIGHTS FROM POUCHITIS AND HEALTHY ILEAL POUCHES

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Introduction

Chronic pouchitis is a common complication following ileal pouch-anal anastomosis (IPAA), with limited effective treatment options.¹ Antibiotics remain the first-line therapy; however, in cases of chronic pouchitis, prolonged antibiotic use contributes to increased antimicrobial resistance within the ileal pouch microbiome.² Fecal microbiota transplantation (FMT) has been proposed as a means of restoring microbial balance. Nevertheless, randomized placebo-controlled trials have demonstrated that, although FMT can alter the microbiome, it does not confer clinical benefits compared to placebo.^3–5

Aims & Methods

Given the lack of efficacy of FMT using stool from healthy donors, the present study aims to characterize the microbiome of a healthy ileal pouch and to evaluate the impact of high antibiotic exposure in patients with chronic pouchitis.
In this cohort study, stool samples were collected from four groups: patients with a normally functioning IPAA, patients with chronic pouchitis, patients with ulcerative colitis, and healthy controls. Microbiome composition and antibiotic resistance genes were analyzed across these groups. Fecal samples underwent metagenomic sequencing, and metagenome-assembled genomes (MAGs) were reconstructed. For Escherichia coli MAGs, the antibiotic resistance gene (ARG) profiles and plasmid content were specifically examined.

Results

This study included 197 participants. A clear pattern emerged in the microbial composition, revealing that reduced alpha diversity is directly associated with declining gut function and clinical health. Both species richness and Shannon diversity were lowest in patients with chronic pouchitis and highest in healthy individuals, with intermediate levels observed in the other groups. Notably, the ileal pouch microbiome of many chronic pouchitis patients was dominated by E. coli. Given the potential clinical implications of high E. coli abundance, we further investigated the ARG profiles and plasmid content of E. coli MAGs. E. coli MAGs from chronic pouchitis patients exhibited a significantly higher frequency of single nucleotide polymorphisms (SNPs) associated with resistance to fluoroquinolones—an antibiotic uniformly used among this patient group—compared to MAGs from the normally functioning IPAA and healthy control cohorts. Furthermore, E. coli MAGs from chronic pouchitis patients harbored a greater number of plasmids, with an increased presence of plasmid-borne ARGs conferring resistance to antibiotics commonly administered in this group, relative to the other cohorts.

Conclusion

These findings demonstrate that the composition of the ileal pouch microbiome—both in chronic pouchitis and normally functioning IPAA—differs significantly from that of individuals with normal gut physiology. This suggests that the microbiome of a normally functioning IPAA may serve as a more appropriate baseline for comparative studies than the healthy gut microbiome. Additionally, our results indicate that antibiotic use exerts increased selective pressure on E. coli strains carrying antibiotic resistance genes, directly correlating with the types of antibiotics administered.

References

1. Hata K, Ishihara S, Nozawa H, et al. Pouchitis after ileal pouch-anal anastomosis in ulcerative colitis: Diagnosis, management, risk factors, and incidence. Dig Endosc 2017;29:26–34.
2. Shen B, Kochhar GS, Rubin DT, et al. Treatment of pouchitis, Crohn’s disease, cuffitis, and other inflammatory disorders of the pouch: consensus guidelines from the International Ileal Pouch Consortium. Lancet Gastroenterol Hepatol 2021;7:69–95.
3. Herfarth H, Barnes EL, Long MD, et al. Combined Endoscopic and Oral Fecal Microbiota Transplantation in Patients with Antibiotic-Dependent Pouchitis: Low Clinical Efficacy due to Low Donor Microbial Engraftment. Inflamm Intest Dis 2019;4:1–6.
4. Karjalainen EK, Renkonen-Sinisalo L, Satokari R, et al. Fecal Microbiota Transplantation in Chronic Pouchitis: A Randomized, Parallel, Double-Blinded Clinical Trial. Inflamm Bowel Dis 2021;27:1766–1772.
5. Kousgaard SJ, Cold F, Halkjær SI, et al. The effect of non-pooled multi-donor faecal microbiota transplantation for inducing clinical remission in patients with chronic pouchitis: Results from a multicentre randomised double-blinded placebo-controlled trial (MicroPouch). J Crohn’s Colitis 2024;18:1753–1766.

THE RESISTANT MICROBIOME: INSIGHTS FROM POUCHITIS AND HEALTHY ILEAL POUCHES

Sabrina Kousgaard 1, Alberte Holm Møllekær 2, Sebastian Mølvang Dall 2, Lone Larsen 3, Mads Albertsen 2, Ole Thorlacius-Ussing 4

1 Aalborg University Hospital, Aalborg, Denmark|||Aalborg University Hospital, Aalborg, Denmark

2 Aalborg University, Aalborg, Denmark

3 Aalborg University Hospital, Aalborg, Denmark|||Aalborg University, Copenhagen, Denmark

4 Aalborg University Hospital, Aalborg, Denmark

Event

UEG Week Berlin 2025

Topics

Colorectal Gut Microbiota Mechanisms & Personalised Medicine IBD

Submission format

Abstract

Session

Dissecting the microbiome in gut inflammation

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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TARGETED PHAGE INTERVENTION IMPROVES BACTERIAL-DRIVEN COLITIS AND RESPONSE TO TOPICAL CORTICOSTEROIDS BY ATTENUATING VIRULENCE OF CROHN’S DISEASE-ASSOCIATED BACTERIA

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Introduction

Current therapies for inflammatory bowel disease (IBD) suppress inflammation rather than inhibiting underlying microbial drivers. Treatment failures of frontline interventions, including corticosteroids, can lead to dose escalation and risk of adverse effects.^1,2 Bacteria with pro-inflammatory potential, like adherent-invasive Escherichia coli (AIEC), have been postulated as a possible microbial driver in Crohn’s disease (CD), however, targeting these bacteria with precision in IBD remains challenging.^3,4 Most antibiotics have broad-spectrum activity and disturb the background microbiome, which may exacerbate inflammation.⁵ Attention has shifted towards bacteriophages, yet their underlying mechanisms of treating IBD, and how they may work as an adjunctive therapy, remains elusive.

Aims & Methods

We aimed to assess whether and how phage therapy, specific for a CD-associated bacterium, reduces colitis severity using gnotobiotic mouse models.
In vitro kill curves and biofilm challenges were used to identify lytic phage candidates. Adult germ-free C57BL/6 mice were colonized with altered Schaedler-flora (ASF) and E. coli NRG857c (NRG), a CD-associated isolate. After 3 weeks, mice were treated with an NRG-specific lytic phage (1x10⁹ PFU/dose; daily or TIW) or vehicle (PBS) for 2 weeks (n=6/group) and then exposed to 1 cycle of dextran sulfate sodium (2%; DSS) in drinking water. PBS-treated mice (n=6) not exposed to DSS served as controls. Phage treatment was also tested in a spontaneous model of colitis using C57BL/6NTac-Il10^em8Tac (IL-10^-/-) mice, treated weekly. Mice were monitored daily for weight, stool consistency, and occult blood. Fecal contents were cultured to determine bacterial load, and the expression of NRG fimS was quantified using qPCR as an assessment of virulence. At endpoint, colon tissues were collected for histological and immunohistochemistry analysis to quantify colitis severity and NRG infiltration, respectively. Additional C57BL/6 mice were colonized and treated as previously described. During colitis induction, mice received a low-dose of budesonide (2μg/day)⁶ (n=5) or vehicle (n=5) until endpoint. Mice were monitored daily for disease activity and colon tissues were collected for histological analysis. HPLC was used to determine active budesonide levels.

Results

HER259 was identified as a lytic phage against CD-associated AIEC NRG. In ASF and NRG colonized mice, HER259 reduced clinical symptoms (p< 0.001, p< 0.001) and histological scores (p< 0.0001, p< 0.001) in chemical induced and spontaneous colitis, respectively. A 1-log reduction in NRG bacterial load was observed in HER259-treated mice (p< 0.001). Reisolated NRG exhibited a reduced FimS ON/OFF ratio (p-value < 0.01). Immunohistochemistry revealed reduced infiltration of NRG into the lamina propria following HER259 treatment, with greater accumulation in the epithelium. HER259 treatment increased the efficacy of a sub-therapeutic dosing regimen of budesonide (p< 0.001), which was independent of microbial-based drug metabolism as determined by HPLC.

Conclusion

Our results demonstrate that lytic phage targeting a CD-associated bacterium attenuates colitis in two gnotobiotic mouse models. The intervention did not lead to complete eradication of the disease-driving agent, but instead modulated bacterial virulence mechanisms and enhanced responses to corticosteroid therapy. The data suggests that alternative mechanisms should be considered when translating phage therapy to treat IBD in clinical trials.

References

1. Yan, Y. et al. Commensal bacteria promote azathioprine therapy failure in inflammatory bowel disease via decreasing 6-mercaptopurine bioavailability. Cell Rep Med 4, 101153 (2023).
2. Nagayama, M., Gogokhia, L. & Longman, R. S. Precision microbiota therapy for IBD: premise and promise. Gut Microbes 17, 2489067 (2025).
3. Darfeuille-Michaud, A. et al. High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn’s disease. Gastroenterology 127, 412–421 (2004).
4. A, D.-M. et al. Presence of adherent Escherichia coli strains in ileal mucosa of patients with Crohn’s disease. Gastroenterology 115, 1405–1413 (1998).
5. Nelson, R. L., Suda, K. J. & Evans, C. T. Antibiotic treatment for Clostridium difficile-associated diarrhoea in adults. Cochrane Database Syst Rev 3, (2017).
6. Bercik, P. et al. Chronic gastrointestinal inflammation induces anxiety-like behavior and alters central nervous system biochemistry in mice. Gastroenterology 139, (2010).

TARGETED PHAGE INTERVENTION IMPROVES BACTERIAL-DRIVEN COLITIS AND RESPONSE TO TOPICAL CORTICOSTEROIDS BY ATTENUATING VIRULENCE OF CROHN’S DISEASE-ASSOCIATED BACTERIA

Kyle Jackson 1, Heather Galipeau 2, Amber Hann 2, Marco Constante 2, Megan Zangara 3, Alexandra Fuentas 2, Chiko Shimbori 2, Premysl Bercik 2, Brian Coombes 3, Zeinab Hosseinidoust 1, Elena Verdu 2

1 McMaster University, Hamilton, Canada|||Farncombe Family Digestive Health Research Institute, Hamilton, Canada

2 Farncombe Family Digestive Health Research Institute, Hamilton, Canada

3 McMaster University, Hamilton, Canada

Event

UEG Week Berlin 2025

Topics

Gut Microbiota IBD

Submission format

Abstract

Session

New tales of the gut microbiome: From profiling to new therapies

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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The usefulness of target trial emulations to enhance the field of Gastroenterology

Louise Emilsson 1

1 County Council of Värmland, Värmlands, Sweden

Event

UEG Week Berlin 2025

Topics

Mechanisms & Personalised Medicine Standards & Guidelines

Session

The art of making clinical research precise: Options for study design

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

Anastomotic leaks and fistulae following upper gastrointestinal (GI) surgery remain a serious clinical challenge, carrying high morbidity and mortality. Endoscopic vacuum therapy (EVT) has emerged as a promising minimally invasive treatment option for managing these complications. This study aimed to assess the efficacy and safety of EVT for postoperative anastomotic leaks in a high-volume tertiary referral center.

Aims & Methods

We conducted a retrospective analysis of all patients treated with EVT for anastomotic leakage following upper GI surgery between January 2022 and January 2025. The primary outcome was EVT success, defined as complete leak closure confirmed through both endoscopic and radiologic assessment. Secondary outcomes included procedure-related adverse events and all-cause mortality.

Results

Twenty-four patients were included (79.2% male; mean age: 64 ± 12 years). Of these, 16 patients underwent oesophagectomy and 8 total gastrectomy; only two surgeries were performed for benign conditions. EVT achieved leak closure in 20 patients (87%). One patient died due to hemorrhagic shock from a hepatic artery pseudoaneurysm, unrelated to EVT.
Among successful cases, the mean duration of EVT was 30 ± 19 days, with a median of four sponge exchanges (IQR = 5). Median hospital stay was 52 days (IQR = 41). EVT failure occurred in three patients, all of whom had cancer-related surgeries and defect sizes exceeding 30 mm. In these cases, adjunctive endoscopic treatment with self-expanding metallic stents led to successful leak closure.
A larger defect size was associated with a lower likelihood of closure (p = 0.067), suggesting a trend toward reduced efficacy in extensive leaks. Importantly, no EVT-related complications were observed throughout the study period.

Conclusion

EVT demonstrated a high success rate (87%) and an excellent safety profile for managing postoperative anastomotic leaks following upper GI surgery. Larger leak sizes showed a trend toward lower closure rates, highlighting the importance of early diagnosis and timely initiation of EVT when defects are smaller. Given its effectiveness and minimal risk, EVT should be considered a first-line endoscopic treatment for anastomotic leaks. Further studies are warranted to refine treatment protocols and establish standardized indications based on leak characteristics.

References

1. de Moura DTH, et al. Role of endoscopic vacuum therapy in the management of gastrointestinal transmural defects. World JGastrointestEndosc. 2019 May 16;
2. Mastoridis S, et al. Endoscopic vacuum therapy (EVT) in the management of oesophageal perforations and post-operative leaks. Minim Invasive TherAllied Technol. 2022 Mar;
3. Livingstone I, et al. Current Status of Endoscopic Vacuum Therapy in the Management of Esophageal Perforations and Post-Operative Leaks. Clin Endosc. 2021 Nov;
4. Panneerselvam K,et al. Endoscopic vacuum therapy for treatment of spontaneous and iatrogenic upper gastrointestinal defects. Clin Endosc. 2023 Nov.

ENDOSCOPIC VACUUM THERAPY IN POSTOPERATIVE UPPER GI LEAKS: CLINICAL INSIGHTS AND OUTCOMES FROM A TERTIARY REFERRAL CENTER

André Trigo 1, Filipa Vidal Lima 1, Hugo Ribeiro 1, Diogo Feijó 1, Mara Costa 1, Andrea Emília Pereira Silva 1, Mariana Marques da Silva Sant'Anna 1, Marta Gravito-Soares 2, Elisa Gravito-Soares 3, Cláudia Agostinho 1, Mariana Ruão 2, Pedro Narra Figueiredo 3

1 Unidade Local de Saúde de Coimbra, Coimbra, Portugal

2 Unidade Local de Saúde de Coimbra, Coimbra, Portugal|||Faculdade de Medicina da Universidade de Coimbra, Coimbra, Portugal

3 Faculdade de Medicina da Universidade de Coimbra, Coimbra, Portugal|||Unidade Local de Saúde de Coimbra, Coimbra, Portugal

Conference

UEG Week Berlin 2025

Topics

Oesophagus

Submission format

Abstract

Session

OESOPHAGEAL, GASTRIC AND DUODENAL (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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ESOPHAGEAL FUNCTION TESTING IDENTIFIES ASYMPTOMATIC BARRETT’S ESOPHAGUS PATIENTS WITH PATHOLOGICAL ACID EXPOSURE AT RISK FOR NEOPLASIA: A MULTICENTER STUDY

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Introduction

Pathological esophageal acid exposure may persist in patients with Barrett’s esophagus (BE) despite standard proton pump inhibitor (PPI) therapy and symptom control, although current guidelines recommend at least standard-dose PPI for all patients with BE.¹

Aims & Methods

Aim was to evaluate the role of esophageal function testing in assessing acid exposure in BE patients on PPI therapy and in predicting neoplastic progression. We conducted a multicenter retrospective study including asymptomatic BE patients (defined by GerdQ total score <8 and a score of 0 on the first GerdQ item) who underwent high-resolution manometry and 24-hour pH impedance monitoring while on various PPI regimens. Maximal PPI therapy included esomeprazole 40 mg, pantoprazole 40 mg, rabeprazole 20 mg, or lansoprazole 30 mg, all administered twice daily. All other regimens were considered standard dosing. Index upper endoscopy with biopsies was performed under the same therapeutic regimen. Histologically, presence and degree of neoplasia (all confirmed by a second pathologist) was recorded. Acid exposure time (AET) <4% was defined as adequate acid control; AET >6% as pathological reflux. Predictors of pathological reflux and neoplasia were assessed using logistic regression analysis.

Results

A total of 135 patients (2016-2025) were included (mean age 58 ± 15 years; 73% male). Median BE length was C1 (range 0–3 cm) and M2 (range 1–5 cm), with 41% (n=56) classified as having long-segment BE. Sixty-seven patients (50%) were on standard-dose PPI. Pathological reflux was identified in 37 patients (27%), of whom 25 (67%) were on standard-dose therapy. Fourteen patients (10%) had borderline AET values (4–6%). Among the 84 patients (62%) with adequate acid control, 33 (39%) were taking standard-dose PPI. On multivariable analysis, standard-dose PPI (OR 3.04; 95% CI 1.34–6.89; p=0.008) and type III esophagogastric junction morphology (OR 2.52; 95% CI 1.01–5.01; p=0.047), consistent with manometric hiatal hernia, were independently associated with pathological reflux. Non-dysplastic BE was found in 112 patients, while 13 (10%) had neoplasia at index endoscopy (8 low-grade dysplasia, 3 high-grade dysplasia, 2 intramucosal adenocarcinoma). Pathological reflux was the only independent predictor of neoplasia (OR 10.41; 95% CI 2.65–41.26; p<0.001).

Table 1. Logistic regression analysis for factors associated with neoplasia on index endoscopy.

	Univariable analysis		Multivariable analysis
	OR (95% CI)	p-value	OR (95% CI)	p-value
Age, years	1.01 (0.96-1.05)	0.695	-	-
BMI, kg/m²	0.95 (0.83-1-10)	0.957	-	-
Male gender	0.71 (0.19-2.54)	0.783	-	-
PPI standard dose vs maximal	0.85 (0.27-2.69)	0.792	-	-
Long-segment BE vs short	1.70 (0.53-5.52)	0.371	-	-
Ineffective/absent contractility vs normal	0.96 (0.30-3.03)	0.939	-	-
EGJ type III morphology vs I/II	3.98 (1.16-13.71)	0.028	3.18 (0.86-11.78)	0.082
AET >6% vs <6%	11.72 (3.01-45.65)	0.001	10.41 (2.65-41.26)	<0.001

Conclusion

Nearly one-third of asymptomatic BE patients exhibit pathological reflux on pH-monitoring despite PPI treatment, predominantly among those on standard-dose and with manometric hiatal hernia. Nonetheless, adequate acid control is achieved in over one-third of patients on standard PPI therapy. Pathological reflux is associated with a 10-fold increased risk of neoplasia.

References

1. Shaheen NJ, Falk GW, Iyer PG, et al. Diagnosis and Management of Barrett's Esophagus: An Updated ACG Guideline. Am J Gastroenterol. 2022;117(4):559-587.

ESOPHAGEAL FUNCTION TESTING IDENTIFIES ASYMPTOMATIC BARRETT’S ESOPHAGUS PATIENTS WITH PATHOLOGICAL ACID EXPOSURE AT RISK FOR NEOPLASIA: A MULTICENTER STUDY

Edoardo Vespa 1, Edi Viale 1, Ernesto Fasulo 1, Alberto Barchi 1, Elisa Marabotto 2, Marcella Pesce 3, Stefania Piccirelli 4, ANDREA PASTA 2, Jacopo Fanizza 1, Maria Caterina Fratto 1, Paola Cesaro 4, Giovanni Sarnelli 3, Francesco Vito Mandarino 1, Sandro Passaretti 1, Silvio Danese 1, Edoardo Vincenzo Savarino 5

1 IRCCS Ospedale San Raffaele, Milano, Italy

2 University of Genoa, Genova, Italy

3 Univers. of Naples ´'Federico II', Naples, Italy

4 Fondazione Poliambulanza Istituto Ospedaliero, Brescia, Italy

5 University of Padua, Division of Gastroenterology, Padua, Italy

Event

UEG Week Berlin 2025

Topics

Neurogastroenterology & Motility Oesophagus

Submission format

Abstract

Session

Burning issues in GERD

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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Introduction

20-25% of ulcerative colitis (UC) patients will experience at least one episode of acute severe colitis (ASUC). Up to 20% of non-responders to medical treatment will require surgery during the index episode. For approximately one third of the patients, ASUC is the first manifestation of the disease, presenting unique challenges.

Aims & Methods

A single-center, retrospective, cohort study. We included adult patients hospitalized in our gastroenterology department with ASUC. We aim to compare the clinical outcomes between patients with new-onset and established UC.

Results

62 (33.5%) patients had new-onset UC, while 123 (66.5%) had established UC. No significant differences were found in demographic and baseline clinical characteristics of the two groups. Patients with new-onset UC experienced longer hospitalizations (19 ± 22 vs. 12 ± 11 days, P = 0.002), longer delay until receiving rescue therapy [11 days (IQR 6) vs. 6 days (IQR 8), (P = 0.014)] and more severe bacterial infections (16% vs. 4%, P = 0.005) compared with patients with established UC. Histological features of chronicity, including architectural distortion, were more frequently observed in patients with established disease. We found no significant differences in steroid response (P = 0.719), need for rescue therapy (P = 0.522), response to rescue therapy (P = 0.234), colectomy (P = 0.655), mortality (P = 0.516) and hospital readmission (P = 0.929) between groups. After one year, colectomy or death occurred in 13.5% of patients. Independent predictors of adverse outcomes included active smoking, extensive colitis, the need for rescue therapy, and severe bacterial infections — but not new-onset disease.

Conclusion

Major clinical outcomes were similar between patients with new onset and established ASUC. These findings support the efficacy of standardized, protocol-driven management in mitigating risks across both groups.

References

Ordás I, Eckmann L, Talamini M, Baumgart DC, Sandborn WJ. Ulcerative colitis. Lancet. 2012;380(9853):1606-1619. doi:10.1016/S0140-6736(12)60150-0
Hindryckx P, Jairath V, D’Haens G. Acute severe ulcerative colitis: from pathophysiology to clinical management. Nat Rev Gastroenterol Hepatol. 2016;13(11):654–664. doi: 10.1038/nrgastro.2016.116
Dhaliwal J, Tertigas D, Carman N, et al. Outcomes Following Acute Severe Colitis at Initial Presentation: A Multi-centre, Prospective, Paediatric Cohort Study. J Crohns Colitis. 2024;18(2):233-245. doi:10.1093/ecco-jcc/jjad143
Spinelli A, Bonovas S, Burisch J, et al. ECCO Guidelines on Therapeutics in Ulcerative Colitis: Surgical Treatment. J Crohns Colitis. 2022;16(2):179-189. doi:10.1093/ecco-jcc/jjab177

OUTCOMES OF ACUTE SEVERE ULCERATIVE COLITIS AT INITIAL PRESENTATION

Diogo Couto Sousa 1, Samuel Raimundo Fernandes 1, Sofia Saraiva 1, Ana Isabel Valente 1, Ana Rita Gonçalves 1, Luis Correia 1

1 ULS Santa Maria, Lisboa, Portugal

Conference

UEG Week Berlin 2025

Topics

IBD

Submission format

Abstract

Session

The value of histology and ancillary tests (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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