Introduction

Artificial Intelligence (AI) is rapidly evolving in the field of gastrointestinal (GI) endoscopy. However, the prevailing perceptions and attitudes of endoscopists towards AI remain poorly understood.

Aims & Methods

This review aims to provide a summary on the current views and perspectives covering the incorporation of AI into GI endoscopy, as well as to identify any obstacles hindering its adoption. Electronic databases including MEDLINE, PubMed, and Scopus were searched from inception to 25th March 2024 to identify qualitative studies, such as questionnaires or surveys, conducted on endoscopists regarding the use of AI in GI endoscopy. The Joanna Briggs Institute (JBI) critical appraisal checklist was used to assess study quality. Qualitative synthesis of included studies was conducted by employing thematic analysis classified into the following five domains: 1) Knowledge and attitudes towards AI, 2) Perception on the ability of AI to improve accuracy and quality of endoscopy, 3) Impact of AI on endoscopists, 4) Impact of AI on patients and 5) Barriers towards the implementation of AI. This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and was registered with the International Platform of Registered Systematic Review and Meta-analysis Protocols (Registration ID: INPALSY202430064).

Results

Included Studies Wadhwa et al. (2020)	Country USA	Sample size n = 124	Domains covered:	1) Awareness and knowledge X	2) Improving endoscopic performance X	3) Impacts on Endoscopists X	4) Impacts on patients -	5) Barriers to implementation X
Kochhar et al. (2021)	USA	n = 165		X	X	-	X	X
Leenhardt et al. (2021)	UK	n = 333		X	X	X	X	X
Van der Zander et al. (2022)	Netherlands	n = 80		X	X	X	X	X
Tian et al. (2022)	China	n = 210		X	X	X	X	X
Tham et al. (2022)	Singapore	n = 16		X	X	X	X	X
Kader et al. (2022)	UK	n = 104		X	X	-	-	X
Nehme et al. (2023)	USA	n = 16		X	X	X	-	X
Goh et al. (2023)	Singapore	n = 165		X	X	X	X	X
Leggett et al. (2024)	USA	n = 374		X	X	X	X	X

Table 1. Study characteristics of included studies

Ten studies were included in this systematic review comprising of 1587 endoscopists across Europe (32.6%), North America (42.8%), and Asia (24.6%). Domain 1: Most endoscopists (69–100%) reported having basic knowledge of AI. Furthermore, the majority (79.5–87.5%) expressed interest and optimism regarding the use of AI in endoscopy. Domain 2: Most respondents (62.5–97%) supported the notion that AI would positively impact endoscopic performance and quality. Domain 3: There were mixed perceptions regarding the extent of operator dependence on AI (6.2–62.8% agreement), and whether AI would prolong procedural time (21–81.3% in agreement). Most endoscopists (71–100%) disagreed that AI would replace them at work. Domain 4: A substantial proportion of respondents (81.3%) felt that AI would lead to an increase in the quality of patient care. Only a minority of endoscopists (6.2–24%) felt that AI could improve the patient-physician relationship and provide empathetic care. Domain 5: A significant proportion of endoscopists (75.2–91%) identified costs as a potential barrier to the implementation of AI in endoscopy. Opinions on ethical concerns and the lack of regulation varied (12.5–100% and 35–88%, respectively), with many endoscopists feeling that there was need for clear guidelines and regulations when integrating AI into clinical practice.

Conclusion

Overall, there is a positive attitude towards the use of AI in endoscopy. However, concerns regarding impact on clinical practice, costs and medicolegal considerations remain. The establishment of robust regulatory frameworks is imperative to ensure successful integration of AI into clinical practice.

Disclosure

Nothing to disclose.

Introduction

Budesonide orodispersible tablet (BOT) is the only approved topical steroid available in Europe for the induction and maintenance of remission in patients with eosinophilic esophagitis (EoE). Available randomized controlled trials have demonstrated that, following induction of histological remission with BOT 1mg twice daily (bid), patients can be maintained in remission with BOT 0.5mg bid. It is currently unknown whether a dose of 1mg once daily (od) has comparable efficacy to 0.5mg bid.

Aims & Methods

In this prospective study conducted at two tertiary referral centers for EoE, we enrolled consecutive patients with EoE undergoing clinical, endoscopic, and histologic re-assessment while on maintenance treatment for EoE with BOT 0.5mg bid or BOT 1mg od. All included patients had achieved histological remission (i.e., <15 eosinophils/high-power field, eos/HPF) following induction of remission with BOT 1mg bid. At the end of the induction of remission period (T0), all patients were assessed using the dysphagia symptom questionnaire (DSQ), the EoE endoscopic reference score (EREFS), and peak eosinophil counts (PEC). At re-assessment while on maintenance treatment (T1), all patients underwent 1) assessment of dysphagia and adaptive behaviors with the DSQ and the Pisa EoE Adaptation Questionnaire v1.0 (PiEAQ). Clinical remission was defined as DSQ not increasing >30% compared to T0. 2) upper endoscopy (EGDS) with assessment of EREFS score and at least six esophageal biopsies, and 3) histological assessment using the EoE Histology Scoring System (EoEHSS). In addition, a comprehensive global assessment of clinical, endoscopic, and histologic findings was performed using the validated index of severity for EoE (I-SEE score). Kruskal-Wallis Rank Sum Test and Pearson’s Chi-squared were used for comparisons. Significance threshold was p<0.05.

Results

Fifty-six patients were included (46 males and 10 females). Following histological remission with BOT 1mg bid, 28 (50%) initiated maintenance treatment with BOT 1mg od and 28 (50%) with BOT 0.5 bid. At the end of induction of remission (T0), the two groups had achieved similar outcomes, with comparable median DSQ [0 (0-28) vs 0 (0-28)], EREFS [1 (0-2) vs 1 (0-1)], and PEC [1 (0-7) vs 1.5 (0-4)] (all p>0.3) (Table 1). At the end of the maintenance treatment (T1), the two groups had been taking maintenance treatment for a comparable duration [20 weeks (12 – 36) vs 20 weeks (12 – 32; p=0.7). Persistent histological and clinical remission at T1 was present in 86% of BOT 1mg od versus 93% of BOT 0.5 bid (p=0.7). In addition, EREFS scores were comparable between groups at T1 [1 (0-2) vs 1 (0-2), p=0.8]. Similarly, the EoEHSS stage and grade was comparable between groups, as was the PiEAQ score [1.5 (0.75-2) vs 0.5 (0-2); p=0.06], and the I-SEE score [ 3 (2-4) vs 3 (2-4); p=0.5] (Table 2).

Conclusion

Persistent clinical endoscopic, and histological remission was maintained in most patients treated either with BOT 1mg od or BOT 0.5mg bid for a median of 20 weeks, indicating that the total daily dose of BOT 1mg may be more important that the frequency of administration, at least in the short term.

Patients’ data on maintenance treatment	0.5mg bid (n = 28)	1mg od (n = 28)	p-value
Maintenance treatment duration before biopsy collection (weeks)	20 (12 - 32)	20 (12 - 36)	>0.9
Eosinophil counts per high-power field	0 (0 - 2)	1 (0 - 3)	0.5
EREFS on maintenance treatment	1.00 (0.00 - 2.00)	1.00 (0.00 - 2.00)	0.8
ISEE-Total (0-40)	3.00 (2.00 - 4.00)	3.00 (2.00 - 4.00)	0.5
EOEHSS STAGE	0.50 (0.00 - 1.00)	0.00 (0.00 - 1.00)	0.3
EoEHSS GRADE	0.00 (0.00 - 1.00)	1.00 (0.00 - 1.25)	0.06
PiEAQ on maintenance treatment	0.50 (0.00 - 2.00)	1.50 (0.75 - 2.00)	0.06
Abnormal DSQ post treatment (>30% compared to baseline)	2 (7.1%)	4 (14%)	0.7
Histological recurrence while on maintenance treatment	2 (7.1%)	4 (14%)	0.7

Disclosure

Speaker or Consultancy for Apogee Therapeutics, Alfasigma, Dr Falk Pharma, Sanofi, Malesci, JB Pharmaceuticals

Introduction

Avoidant/restrictive eating is common in people with neurogastroenterology disorders including functional dyspepsia (FD). There is debate on whether avoidant/restrictive food intake disorder (ARFID) is an expected response to severe symptoms or simply a common comorbid disorder. To address this, among adults with FD, we aimed to contrast those with and without ARFID on FD symptoms, quality of life, psychosocial factors, nutrient tolerance, and gut transit.

Aims & Methods

Adults with Rome-IV confirmed FD and healthy controls (HC) from an ongoing study participated. ARFID diagnosis was assigned based on a semi-structured DSM-5 diagnostic interview. Surveys: Patient Assessment of GI Disorders Symptom Severity Index (PAGI-SYM), Short Form Nepean Dyspepsia Inventory (SF-NDI), Nine-Item ARFID Screen (NIAS), Fear of Food Questionnaire (FFQ), Visceral Sensitivity Index (VSI), and Hospital Anxiety/Depression Scale (HADS). Nutrient Drink Test (NDT) measured gastric tolerance—liquid nutrient ingestion at 30mL/minute until subject reported unbearable fullness. Wireless Motility Capsule (WMC) measured gut transit. Height/weight was measured for body mass index (BMI).

Results

Sample (80% female, M_age=37.1±14.4y) included 37 FD+ARFID, 14 FD only, and 18 HC. Groups did not significantly differ in sex or age. Adjusted pairwise comparisons showed small (r=.1-.2) non-significant differences between FD and FD+ARFID on FD symptoms by PAGI-SYM and SF-NDI (Table 1). However, FD+ARFID had significantly worse scores compared to FD with medium effects (r=.3-.4) on: FD-related quality of life by SF-NDI, Fear of Food by NIAS-Fear and FFQ, GI-anxiety by VSI, and anxiety by HADS. FD+ARFID vs FD also had small differences (rs=.2) on: feeling more bothered by FD symptoms on SF-NDI, worse depression by HADS, lower BMI, and less NDT consumption. Compared to HC, FD and FD+ARFID had significantly worse survey scores with large effects for FD+ARFID (r=.6-.8) and medium effects for FD vs HC (r=.3-4). For the NDT, FD+ARFID consumed significantly less than HC with large effect (r=.6) but with a trend medium effect for FD consuming less than HC (r=.3). Groups did not significantly differ in WMC transit times.

Conclusion

Our findings suggest ARFID, when present in FD, does not reflect a response to more severe FD symptoms. Thus, ARFID is a legitimate secondary condition in FD. ARFID may reflect more profoundly altered distress around symptoms (e.g., fear of symptoms, anxiety sensitivity) and greater negative impacts (e.g., FD-related quality of life, lower liquid nutrient tolerance).

Introduction

The diagnosis of Coeliac Disease (CD) in adults still continues to rely heavily on duodenal histology, in spite of several studies demonstrating a positive predictive value (PPV) of 100% for Marsh 3 histology when anti-tissue transglutaminase (TTG) exceeds 10x upper limit of normal. The majority of these studies come from tertiary centres and the slow uptake of the non biopsy approach may be as a result of limited data on the histological outcome of positive serology originating in the primary care setting.

Aims & Methods

To determine the PPV of primary care-based TTG testing with concurrent anti-endomysial antibody (EMA) positivity for histological diagnosis of CD.
The immunology lab in our institution performs reflex EMA testing on all newly positive and newly borderline positive TTG samples from the West of Ireland (TTG≥5U/ml Celikey by Phadia). Over a 6 year period (2018-2023), 1,361 index TTG positive samples also proved positive when tested for EMA. Following electronic medical record review, we excluded all samples from patients who were <16 years old, had a previous diagnosis of CD made elsewhere, lacked biopsy data, or had biopsies that predated the serological test. Patients who had their coeliac serology testing requested by any hospital-based physician were also excluded to ensure that only patients identified by primary care-based screening were included in the outcome analysis. In this manner, 335 adult patients who had serology screening performed by their primary care physician were eligible for further analysis. These eligible patients were then stratified by TTG levels ( ≤20, 21-69, and ≥70 U/ml). PPV was calculated for each stratum. Logistic regression assessed the relationship between TTG values and biopsy results. Additional analyses examined influence of interval between serology and biopsy.

Results

Chi-square analysis confirmed significant association between TTG levels and biopsy results (p<0.00001). For each 10 U/ml increase in TTG, odds of positive biopsy increased by 18% (OR 1.18, 95% CI: 1.10-1.26). For TTG 21-69 U/ml, PPV declined with longer serology-to-biopsy intervals: 100% for ≤47 days versus 45.2% for >203 days. High TTG values maintained excellent PPV regardless of interval. Long-term follow-up of initially biopsy-negative patients revealed subsequent CD diagnosis in 19/40 (47.5%) in the low titre group, 11/30 (36.7%) in the intermediate group, and 7/11 (63.6%) in the high titre group.

TTG Group	Biopsy +	Biopsy -	Total	PPV (%)
TTG ≤ 20U/ml (<3xULN)	66	40	106	62.3
TTG 21-69U/ml (3-9.9xULN)	84	30	114	73.7
TTG ≥ 70U/ml (10xULN)	104	11	115	90.4

Conclusion

TTG titre significantly predicts biopsy-confirmed CD, with TTG ≥70 U/ml having 90.4% PPV. The predictive value of intermediate TTG diminishes with increasing interval between serology and biopsy. A substantial portion of initially biopsy-negative patients across all TTG strata were subsequently diagnosed with CD during follow-up. These findings support TTG in risk-stratifying CD patients, suggest prompt biopsies for intermediate TTG values, and highlight the importance of long-term monitoring even in patients with negative initial biopsies.

References

1. Husby S, et al. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac disease. J Pediatr Gastroenterol Nutr. 2012;54(1):136-60.
2. Penny HA, et al. Accuracy of a no-biopsy approach for the diagnosis of coeliac disease across different adult cohorts. Gut. 2021;70(5):876-883.

Introduction

Incidence of sporadic ductal pancreatic adenocarcinoma (PDAC) in the Czech Republic is the third highest in Europe (23.1/100,000 population). New-onset diabetes mellitus with weight loss (> 5% within < 6 months) in patients over sixty can be an early sign of PDAC. New-onset diabetes mellitus was recorded in 12.2% subjects three years prior to the diagnosis of PDAC (in the 60-74+ age group:13.8%) in the Czech Republic in the period 2017-2021 [ref. 1].

Aims & Methods

The aim of this study was to evaluate the standardized incidence ratio (SIR) of PDAC in patients with diabetes mellitus with and without previous history of any other malignancy within a 12-year period.
Methods: The analysis was based on individual population data from the Czech National Registry of Reimbursed Health Services, the National Cancer Registry, and the Death Certificate Information System in the period 2010 - 2021. Patients were divided into two groups: the first one included subjects with diabetes mellitus who had a history of any malignancy prior to the diagnosis of diabetes (follow-up 865,956 person-years); the second cohort consisted of people with diabetes mellitus who had no history of malignancy prior to the diagnosis of diabetes (7,971,090 person-years). The calculated person-years at risk were stratified by sex, age and time periods (2010-2013; 2014-2017; 2018-2021). Subgroup analyses were performed considering follow-up and age at diagnosis of diabetes. The first report of any antidiabetic drug (ATC group A10) was the determinant for the diagnosis of diabetes mellitus in a particular individual. SIR was calculated as the ratio of observed to expected (estimated from incidence in the general population) cases of PDAC.

Results

Selected SIRs stratified according to age and follow-up are displayed in Table 1.
A significantly higher risk of PDAC in diabetes mellitus with a history of previous malignant diseases (compared to the general population) was found for the following: head and neck cancer (SIR 2.54), gastric cancer (2.12), colorectal cancer (1.38), laryngeal cancer (2,51), malignant melanoma (1.65), breast cancer (1.61), cervical cancer (2.22), uterine cancer (1.72), prostate cancer (1.59), testicular cancer (3.1), kidney cancer (1.75), urinary bladder cancer (1.74), thyroid cancer (2.13), Hodgkin lymphoma (2.74), non-Hodgkin lymphoma (2.15) and leukaemias (1.93).

Table 1
Risk of PDAC in diabetes mellitus

Diabetes mellitus with history of previous malignant disease n = 144,946 individuals		Diabetes mellitus with no history of malignant disease n = 1,123,065 individuals
Age at diagnosis of diabetes mellitus	SIR (95% C.I.)	Age at diagnosis of diabetes mellitus	SIR (95% C.I.)
60 - 69 years	3.13 (2.84 - 3.45)	60 - 69 years	2.12 (2.04 - 2.19)
70 - 79 years	1.58 (1.45 - 1.73)	70 - 79 years	1.05 (1.01 - 1.10)
≥ 80 years	0.79 (0.68 - 0.91)	≥ 80 years	0.63 (0.58 - 0.68)
Follow-up	SIR (95% C.I.)	Follow-up	SIR (95% C.I.)
up to 3 months	5.49 (4.62 - 6.49)	up to 3 months	4.82 (4.46 - 5.20)
3 months to 1 year	2.79 (2.41 - 3.20)	3 months to 1 year	2.49 (2.34 - 2.65)
from 1 to 2 years	1.74 (1.48 - 2.04)	from 1 to 2 years	1.62 (1.52 - 1.74)

C.I.: Confidence Intervals

Conclusion

Risk of PDAC in patients with diabetes mellitus was higher in subjects with a history of various malignant diseases compared to those with no previous history of any malignancy. Particular attention should be paid to new-onset diabetes (diagnosis made within one last year). History of a malignancy, as an important risk factor for PDAC, should be taken into account when surveilling patients with diabetes mellitus.

Funding: Research projects MO1012 (DZVRO) and MH CZ-DRO (UHHK, 00179906).

References

Ref. 1: UEG Journal 2024; 12 (Suppl S8): 565.

Disclosure

There is conflict of interest.

Introduction

There is currently lack of published data on the use of ustekinumab (UST) in routine care setting in Greece. REASSURE study aimed to generate real-world evidence (RWE) on treatment persistence, and patient-reported outcomes (PROs) in patients with Crohn’s Disease (CD).

Aims & Methods

This was an observational, prospective study of adult (18-80 years old) patients with confirmed diagnosis of CD, who commenced therapy with UST as 1^st, 2^nd, or 3rd line biologic treatment, according to physician’s decision, local standards of clinical practice and as per label indication. Data were collected by routine assessments, including Harvey-Bradshaw Index (HBI), and PROs at baseline (start of UST) and follow-up visits every 6-months. Last visit was done at month 24 (±2 months) or at treatment discontinuation (whichever occurred first). Drug persistence, disease activity and safety outcomes over the 24-month observation period are presented herein.

Results

A total of 169 eligible patients were enrolled in 19 Gastroenterology Clinics in Greece between April 2019 and February 2021. At baseline, median age was 45.0 years, 50.9% (86/169) of patients were females, 43.4% (72/166) were employed, and 68.5% (113/165) were former or current smokers. UST was the 1st, 2^nd, and 3rd biologic treatment in 35.5% (60/169), 35.5% (60/169), and 29.0% (49/169) of patients, respectively. The median duration of study participation was 23.9 months (median number of injections received: 13.0). At 24 months, 21.9% (37/169) of patients had discontinued UST after a mean of 10.2 months due to lack/loss of response (15/37), safety issues (10/37), lost at follow-up (6/37), patient’s wish (2/37), death (2/37; both unrelated to UST), pregnancy (1/37) and patient issues (1/37). The Kaplan-Meier (KM)-estimated median drug survival (i.e., time to treatment discontinuation) was not reached in the overall population or subgroups by treatment line, with no statistically significant differences in the risk of UST discontinuation between subgroups of interest [2L vs 1L: hazard ratio (HR)=1.07, 95% confidence interval (CI)=0.48-2.39; 3L vs 1L: HR=1.54, 95% CI=0.70-3.40; 3L vs 2L: HR=1.42, 95% CI=0.65-3.11). The KM-estimated UST treatment-persistence rates for the overall population s were 86.7%, 80.5%, and 78.0%, at 12-, 18-, and 24-months, respectively. The baseline median total ΗΒΙ (8.0) significantly improved (P<0.001) at 12, 18, and 24 months, with a median 4-point reduction at each timepoint, among paired observations. Significant improvements were also noted based on imputed data and in the subgroups per treatment line. The adverse event (AE), serious AE, and UST-related AE rates were 63.9% (108/169), 18.9% (32/169), and 19.5% (33/169), respectively. Each UST-related AE was reported in <4.0% of the patients. Further details on baseline characteristics, 12/18/24-month outcomes, and UST-related AEs are presented in Table 1.

Table 1: Baseline characteristics, 12/18/24-month outcomes, and UST-related adverse events
	Overall (N=169)		Bio-naïve (1L) (N=60)		UST as 2LT (N=60)		UST as 3LT (N=49)
Time from CD diagnosis to UST initiation, median (IQR), years	7.0 (1.8 – 13.0)		1.3 (0.3 – 6.2)		8.2 (3.8 – 11.7)		12.9 (9.0 – 22.1)
Baseline characteristics Age ≤50 years Females At least 1 comorbidity Prior CD-related surgery Prior systemic treatment for CD Stricturing and/or penetrating disease Extraintestinal manifestations Steroid-dependent/refractory disease Starting UST maintenance dosage: 90 mg SC Q8W UST initiated as monotherapy	N 169 169 169 169 169 162 167 149 169 169	npt (%) 106 (62.7) 86 (50.9) 93 (55.0) 54 (32.0) 158 (93.5) 70 (43.2) 61 (36.5) 24 (16.1) 152 (89.9) 99 (58.6)	N 60 60 60 60 60 57 60 55 60 60	npt (%) 31 (51.7) 25 (41.7) 33 (55.0) 3 (5.0) 49 (81.7) 19 (33.3) 19 (31.7) 10 (18.2) 50 (83.3) 37 (61.7)	N 60 60 60 60 60 57 59 52 60 60	npt (%) 45 (75.0) 30 (50.0) 35 (58.3) 24 (40.0) 60 (100.0) 27 (47.4) 23 (39.0) 5 (9.6) 56 (93.3) 32 (53.3)	N 49 49 49 49 49 48 48 42 49 49	npt (%) 30 (61.2) 31 (63.3) 25 (51.0) 27 (55.1) 49 (100.0) 24 (50.0) 19 (39.6) 9 (21.4) 46 (93.9) 30 (61.2)
No disease activity based on HBI (i.e., score of 0-4 points) At Month 12 At Month 18 At Month 24	N 131 117 114	npt (%) 102 (77.9) 90 (76.9) 100 (87.7)	N 49 43 43	npt (%) 42 (85.7) 37 (86.0) 39 (90.7)	N 49 42 40	npt (%) 37 (75.5) 33 (78.6) 36 (90.0)	N 33 32 31	npt (%) 23 (69.7) 20 (62.5) 25 (80.6)
Kaplan-Meier-estimated persistence to UST treatment 12-month rate 18-month rate 24-month rate	% 86.7 80.5 78.0	95% CI 80.6 – 91.1 73.6 – 85.8 70.8 – 83.6	% 89.9 82.9 81.2	95% CI 78.8 – 95.3 70.6 – 90.4 68.6 – 89.1	% 88.3 83.1 79.4	95% CI 77.1 – 94.3 70.9 – 90.6 66.5 – 87.8	% 80.9 74.3 72.2	95% CI 66.5 – 89.6 59.2 – 84.6 56.9 – 82.8
Safetya UST-related AEs UST-related AEs leading to withdrawal UST-related AEs leading to interruption/dose delay	N 169 169 169	npt (%) 33 (19.5) 8 (4.7) 3 (1.8)	N 60 60 60	npt (%) 6 (10.0) 1 (1.7) .	N 60 60 60	npt (%) 14 (23.3) 3 (5.0) 3 (5.0)	N 49 49 49	npt (%) 13 (26.5) 4 (8.2) .
aExcluding drug ineffective/loss of therapeutic response/off-label use. Abbreviations: 1/2/3L: First/Second/Third Line; AE: Adverse Event; CD: Crohn's Disease; CI, Confidence Interval; HBI: Harvey-Bradshaw Index; IQR: Interquartile Range; IV: intravenous; N: number of patients with available data; npt, number of patients with variable; Q8W: every 8 weeks; SC: subcutaneous; UST: ustekinumab.

Conclusion

Our data provide RWE for high persistence rate of treatment with UST in our series with Greek patients with CD. Treatment with UST demonstrated a highly favorable effect on disease activity, in combination with a predictable safety profile.

Disclosure

Disclosure: This study was sponsored by Janssen - Cilag, Greece.

Giorgos Bamias Advisor/lecturer for Janssen, Pfizer, Takeda, Abbvie, MSD, Mylan, Genesis Pharma, Adacyte Therapeutics, Amgen, Ferring, Cooper, BMS; Funding (Grants/Honoraria): Pfizer, Takeda, Abbvie, Aenorasis; Research/Clinical Trials: Abbvie, Takeda, Janssen.
Gerassimos J. Mantzaris has received consultant and/or speaker fees from AbbVie, MSD, Celtrion,Ferring, Aenorasis, Janssen, Pfizer, Takeda, Falk Pharma, and Vianex and research support from AbbVie, Ferring, MSD, and Vianex
Maria Tzouvala has received clinical research funding from Janssen-Cilag Pharmaceuticals SACI, Takeda HELLAS SA, AbbVie Pharmaceuticals S.A. Consulting and/or speaking fees MSD Sharp& Dohme, Janssen-Cilag Pharmaceuticals SACI, Takeda, AbbVie Pharmaceuticals S.A, Pfizer, Amgen. Advisory boards: Janssen-Cilag Pharmaceuticals SACI, Takeda, AbbVie Pharmaceuticals S.A, Pfizer, Amgen
Dimitrios Christodoulou has received consulting and speaking fees for Janssen, MSD, Galenica. Advisory Board for Galenica
Ioannis Koutroubakis has received clinical research funding: Abbvie, Faran, Ferring, Pfizer, Viatris, Vianex, Vifor, Unipharma. Consulting and/or speaking fees Abbvie, Genesis, Janssen, MSD, Takeda, Vianex. Advisory boards: Abbvie, Janssen, MSD, Pfizer, Takeda, Vianex
Christos Liatsos has received clinical research funding from: Janssen, and consulting and/or speaking fees from: MSD, Pfizer, Boston SCI, Amgen, Galenica.
Georgios Papatheodoridis Clinical research funding: Abbvie, Gilead, Takeda, Vianex. Consulting and/or speaking fees: Abbvie, Astra-Zeneca, BioARS Therapeutics, Elpen, Genesis, Gilead, GlaxoSmithKline, Ipsen, Novo Nordisk, Roche, Sobi. Advisory boards: Abbvie, Astra-Zeneca, Albireo, Amgen, Galenica, Genesis, Gilead, GlaxoSmithKline, Ipsen, Janssen, Novo Nordisk, Roche, Takeda
Dr Katsanos Konstantinos received honoraria for consulting services (educational services, scientific articles, participation in Advisory Boards, clinical trials, lecture fees, other) from the companies as follows:AbbVie, AMGEN, ENORASIS, Epsilon Health, Ferring, Genesis, Grifols S.A., JANSSEN, MSD, Mylan, Shire and Takeda.
Evanthia Zampeli has received clinical research funding: Janssen, TAKEDA, ABBVIE. Consulting and/or speaking fees: Janssen, TAKEDA, BMS, AMGEN, MYLAN. Advisory boards: BMS, GALENICA
Georgios Germanidis has received clinical research funding from Janssen.
Konstantinos Soufleris Consulting and/or speaking fees: AbbVie, Janssen, MSD, Pfizer, Takeda. Clinical research funding:Pfizer. Advisory board: BMS, Galenica.
Matina-Lydia Chatzinikolaou has received consulting fees from Abbvie, Takeda, Amgen, Ferring, Janssen
George Kokkonis has received clinical Research funding from Janssen and speaking fees from Janssen and Amgen
Alexandros Boubonaris has served as advisory board member for Amgen, Takeda
Marios Giakoumis has received clinical research funding from Janssen
Artemis Trikola has received clinical research funding from Janssen
George Michalopoulos has received speaker fees : Takeda, MSD, , Abbvie, Jannsen, Pfizer, Amgen
Vasileios Delis, Konstantina Paraskeva, Theodosios Sdonas, Athanasia Tasovasili, Evgenia Papathanasiou, Maria Palatianou, Andreaddds Nakos, Nikoletta Mathou, George Kalopitas, Panagiotis Giannelis, Kalliopi Foteinogiannopoulou, Konstantina Chalakatevaki, Eleni Beka, Chara Lamouri, Eleftheria Giannakoulopoulou have no conflicts to disclose.
Konstantinos Thomopoulos, Stergios Vradelis, Andreas Protopapas, Ioannis Pachiadakis, Ioannis Goulis, Pantelis Karatzas, George Theocharis, George Tribonias, Angeliki Machaira, Nikolaos Kyriakos, Adonis Protopapas, Konstantinos Fasoulas, Eleni Orfanoudaki and Charilaos Taloumtzis have not disclosed any conflicts.
Spyridon Michopoulos has received clinical research funding from Janssen, Takeda, BMS, consulting and/or speaking fees from Takeda, and has served as advisory board member for Takeda.
Christos Gkamaloutsos, Ioannis Kanistras and Aikaterini Mpartsea are employees of Janssen - Cilag, Greece.

Clinical Case Summary

We report the case of a 16-year-old boy followed since age 10 for pancolitis-type ulcerative colitis (UC), resistant to 5-ASA, corticosteroids, immunosuppressants, anti-TNFα, and recently deemed refractory to ustekinumab. The disease was complicated by primary sclerosing cholangitis (PSC), leading to decompensated cirrhosis.
The patient presented with a moderate flare during ustekinumab induction, including diarrhea, rectal syndrome, abdominal pain, intractable vomiting, inflammatory lower-back pain, and new-onset ascites.
Colonoscopy revealed multiple polyps from rectum to cecum, some with irregular, raspberry-like surfaces, arising on normal-appearing mucosa without erythema or ulceration. Upper endoscopy, performed due to vomiting and hematemesis, showed grade III esophageal varices, portal hypertensive gastropathy, and multiple gastric polyps, some with similar irregular surfaces. MR enterography, though limited by suboptimal bowel distension, showed no small bowel polyposis.
These unexpected endoscopic findings introduced new challenges. Management options included treatment of refractory UC, assessment and surveillance of colonic and gastric polyps—raising concern for an underlying polyposis syndrome—and liver transplant evaluation for cirrhosis. The patient was treated with IV corticosteroids, then transitioned to an oral taper after clinical improvement.
Due to the complexity, a combined therapeutic approach (colectomy, gastrectomy, and liver transplantation) was considered unfeasible. The patient and family were counseled and referred to a national transplant and surgical center for sequential management planning: liver transplantation, followed by colectomy and endoscopic resection of gastric polyps.
This rare case highlights the therapeutic and diagnostic complexity of managing refractory pediatric UC with PSC, cirrhosis, and gastrointestinal polyposis, necessitating a highly individualized, multidisciplinary approach.

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Figure 1 showing endoscopic images of the gastric (1a) and colonic (1b) polyposis
Figure 2 showing histological findings of biopsies of some of the gastric (2a) and colonic (2b) polyps
Figure 3 MR enterography of the patient showing no signs of small bowel involvement