Introduction

Patients with gastric intestinal metaplasia (GIM) can be stratified into non-extensive and extensive GIM. In patients with extensive GIM surveillance is recommended based on a higher risk of neoplastic progression. The updated Sydney protocol is the most widely accepted biopsy system to identify extended GIM, and includes, besides biopsies of the corpus and antrum also biopsies of the incisura angularis (IA). However, data on the added value of additional biopsies of the IA in patients with premalignant gastric lesions is scarce. Our aim is to evaluate the yield and added value of the updated Sydney protocol in a low incidence gastric cancer region.

Aims & Methods

This prospective cohort study included patients with GIM who underwent follow-up endoscopies. Biopsies were taken according to the updated Sydney protocol.

Results

In total 177 patients with GIM were included. Median age was 62 (IQR 20) and 55.9% was male. During follow-up seven (4.0%) patients developed gastric neoplasia after a median follow-up of 37 months (IQR 38). At baseline 50 patients were classified as extensive GIM (28.2%), of which only one patient showed neoplastic progression. The other six patients that showed progression were classified as non-extensive GIM. At baseline, angular GIM was found in 97 (54.8%) patients of which six showed neoplastic progression; two patients had GIM in antrum and IA, two patients had GIM in IA and corpus, one patient had GIM in antrum, IA and corpus and in one patient there was GIM in the IA only.

Conclusion

In patients with gastric intestinal metaplasia angular GIM might be a better risk factor for neoplastic progression than the extension of GIM.

Introduction

Diarrhea after cholecystectomy is a well-known complication that worsens the quality of life of the patient and may become a real challenge for the doctor.
Both changes in the bile acids spectrum (BAsS) and possible changes in microbiota and Small Intestinal Bacterial Overgrowth (SIBO) may have a major impact. What is primary in this circle is not fully understood.

Aims & Methods

The aim was to assess BAsS and SIBO in patients prior to cholecystectomy, three and twelve months after cholecystectomy.
Methods: Initially, the bile of the patients was obtained directly from the gallbladder after it was removed during the surgery. For the second and third time, the bile of the same patients after cholecystectomy was obtained in 3 and 12 months postoperatively, after the intubation of the duodenum under ultrasound control. The spectrum of BA was assessed using photocalorimetry. To assess the possible influence of SIBO, all the patients underwent a hydrogen breath test before cholecystectomy, and if SIBO was confirmed, they were not included in the study. Successive hydrogen breath tests were performed 3 and 12 months after cholecystectomy to all the patients who were included. The data were analyzed using parametric and non-parametric methods of evaluating the results through the Statistica program (StatSoft Inc, USA).

Results

14 patients, predominantly women (71.4%) were enrolled in the study. The spectrum of BA three months after cholecystectomy showed a tendency for secondary BA (deoxycholic acid) to predominate over primary BA (cholic acid) (P>0.05). After 12 months, the BAs pool returned to the baseline in most of the patients (P>0.05). SIBO was not registered in patients 3 months after cholecystectomy, but it was detected in 50% of cases (P>0.05) after 12 months.

Conclusion

The predominance of secondary BA in the early postoperative period probably indicates an increase in the number of bacteria, for the transformation of primary BA in the ileum, but the breath test is not sensitive enough to determine this.
Over time, if the equilibrium in a complex mechanism of BA homeostasis is not achieved (the amount of bile in the ileum, bacteria, FXR, etc.), this may lead to the SIBO development.

Introduction

Managment of functional hepatobillary pain remains a significant challenge for physicians. Botulinum toxin injection of the ampulla of vatter and endoscopic sphincterotomy has been shown to be an effective treatment with diagnostic and prognostic benefit, however, it has a relatively high complication rate.

Aims & Methods

To assess the effectiveness and complication rate of botox injection and sphincterotomy for treatment of sphincter of oddi dysfunction (SOD). And assess if response to botox injection is predictive of durable response to completion sphincterotomy. Patients were identified from a single centre endoscopy database from January 2014 until October 2024 using the keyword searches “Botox” and “Botulinum”. Studies were included if 100IU botox injection to the ampulla was done at endoscopy for the purpose of treating SOD. SOD was defined as per the ROME IV criteria and classified as per Milwaukee classification. Baseline clinical, demographic, endoscopic, and radiological data were collected. Symptomatic response was assessed through interrogation of clinical notes post procedure. Patients who progressed on to sphincterotomy were identified, and symptomatic response to this was obtained from clinical review of notes at 3 months and 1 year post procedure. For categorical variables Fisher’s exact test was used.

Results

364 duodenoscopies were identified from the database, 74 duodenoscopies from 52 patients were included. 13 patients had more than one botox injection. 77% (40 patients) were female, and the median [range] age at first procedure was 41.2 [21.7 - 66.6] years. 1 (1.9.%), 44 (84.6%), and 7 patients (12.5%) had type I, Type II, and Type III SOD respectively. Diclophenac was given at time endoscopy in 26 (36%) procedures. Four patients were admitted for 24 hours with non-pancreatitis related abdominal pain post procedure. Three patients had no data on response post botox injection. 42 (85%) patients reported improvement in their symptoms following botox injection. 35 of the 44 patients with type II SOD responded. 6 of the 8 patients with type III, and the only type I patient responded. 25 (48%) patients in total progressed on to sphincterotomy (one type I, 22 type II, and 2 Type III). 10 patients with no response to botox progressed on to sphincterotomy. 10 patients had >1 sphincterotomies for treatment of SOD. 36 post botox sphincterotomies were included, 8 (22%) had complications. There were 5 (14%) micro-perforations, there was one (2.8%) pancreatitis and two (5.5%) admissions for abdominal pain without evidence of pancreatitis. No patient had requirement for ICU or surgery. Initial response to sphincterotomy was at 3 months was 72% (18). Twelve (48%) patients (11 type II SOD, and one Type III) had durable response at one year.
There was a trend that patients who responded to botox injection were more likely to have response from sphincterotomy at one year, 10 patients (55%) compared to two (28%) Patients who did not respond to botox injection responded to sphincterotomy at one year. However, this was not statistically significant (p=0.37).

Conclusion

Our data indicated a low incidence of complication to botox injection with no recorded cases of pancreatitis. There was a trend that patients who responded to botox injection may be more likely to respond to sphincterotomy. Further data is required, however there was a trend towards patients who responded to botox injection being more likely to benefit from sphincterotomy.

Disclosure

Nothing the disclose

Introduction

Janus kinase (JAK) inhibitors have emerged as an important therapeutic class for the management of several immune-mediated conditions, including inflammatory bowel disease (IBD), but they are associated with several side effects. A renewed attention to the safety profile of this drug class has been driven by increasing reports of JAK inhibitor-induced acneiform eruptions seen in clinical trials and real-life practice.

Aims & Methods

We aimed to investigate the epidemiology, clinical characteristics, and treatment outcomes of this condition in patients with IBD. This was an international, multicenter, retrospective cohort study that consecutively enrolled patients with IBD who were treated with JAK inhibitors and subsequently developed acne. The primary objective was to evaluate the clinical characteristics of acne presentation. Secondary objectives included determining acne prevalence, assessing its impact on quality of life, and evaluating the effectiveness of treatments.

Results

Of the 2,183 JAK inhibitor-treated patients with IBD screened, 272 developed acne and were included in the study. The crude prevalence rates of acne were 15.9% for upadacitinib, 4.3% for tofacitinib, and 1.9% for filgotinib, with dose-dependent relationships observed for upadacitinib and tofacitinib. Acne predominantly affected patients aged 30–50 years, with most cases being mild to moderate in severity. Acneiform eruptions most frequently involved the face (89%), followed by the back (33%) and chest (27%). Lesion characteristics were documented in 159 patients; papules (82%), pustules (52%), and comedones (42%) were the most frequently reported. In contrast, nodules (19%) and cysts (18%) – features associated with more severe disease – were less commonly observed. Among the 213 patients with available time-to-onset data, the median time to acne onset following JAK inhibitor initiation was 47 days (IQR: 28–98 days). Patients with a previous history of acne vulgaris were significantly more likely to develop severe drug-induced acne (p<0.0001). Although corticosteroids are known to contribute to acne, our data did not demonstrate an association between concomitant steroid use and increased acne severity. There was also no difference in time to onset or resolution of acne between the steroid-treated and non-steroid treated groups. A third of patients reported a negative impact on psychosocial well-being, and 40% required pharmacological intervention. Topical therapies were required for 106 patients (39%), with 52 (49%) showing acne improvement or resolution. Systemic oral agents were required for 38 patients (14%), including 25 patients who did not respond or had a partial response to topical therapies. Antibiotics were prescribed to 29 patients (most commonly from the tetracycline class), leading to acne improvement or resolution in 14 patients (48%). Oral isotretinoin was required for 8 patients (3%) and was effective in all but one patient. Eighteen percent of patients who developed acne (2.2% of total cohort) required a JAK inhibitor dose reduction or discontinuation, although most did not have severe disease.

Conclusion

This study is the first to characterise this adverse event in JAK inhibitor-treated patients with IBD and presents the largest cohort of JAK inhibitor-induced acne cases to date across all immune-mediated diseases. JAK inhibitor-induced acne is a common adverse effect resulting in significant psychological burden. Early identification, proactive counselling, and timely interventions, such as dose reduction or referral to dermatology, are crucial in managing this side effect.

Introduction

Interleukin (IL) inhibitors are monoclonal antibodies that have been shown to be effective in inducing and maintaining remission in moderate to severe ulcerative colitis (UC).
Ustekinumab (UST) was approved in the EU for the treatment of UC in 2019 and binds specifically to the p40 protein subunit of IL-12 and IL-23. Mirikizumab (MIRI) was approved 4 years later and selectively binds to the p19 subunit of the IL-23 cytokine. By binding to the IL subunits, the interaction with the IL-23 receptor is inhibited.
In this study, we compared the response rate to induction therapy with UST and MIRI in patients with moderately to severe UC.

Aims & Methods

All patients with active UC who began induction therapy with UST or MIRI at our outpatient clinic between 2019 and 2024 were analyzed retrospectively with a follow-up period until April 2025. Patients who received the IL-23 inhibitor due to a disease other than UC or following a prednisolone therapy exceeding 20 mg and patients with pouchitis were excluded from the study.
We determined the response to IL-23 therapy 8 to 24 weeks after the start of treatment and documented this either as clinical remission (Mayo-Score ≤1), improvement (Mayo-Score reduction by at least 3 points), inadequate response (Mayo-Score reduction between 0 and 2) or no response (lack of benefit, switch to another medical class or colectomy).
We examined the levels of calprotectin in the stool 0 to 24 weeks before the start of IL-23 therapy up to 24 weeks after initial administration.
Our study included 40 patients treated with UST and 23 patients treated with MIRI, in the latter group 26% have previously been treated with UST. Patients in both groups were similar in age (mean age, 47.75 vs. 44.59 y; P 0.28), gender, disease duration (mean duration, 11 vs. 9 y; P 0.32), and extent of disease (pancolitis, 40% vs. 48%).

Results

After completion of induction, 25% in the UST group and 57% in the MIRI group reached clinical remission. MIRI after UST achieved clinical remission in 67%. Improvement was shown in 20% vs. 30%, UST vs. MIRI. For UST, 5% were non-responder. For MIRI, no non-responder was noted. In general, the difference between the pre- and post-induction Mayo-Score is significantly higher for MIRI, indicating a better response to the newly started drug (mean Mayo-Score difference, UST vs. MIRI, 2.95 vs 4.5; P 0.0003)
The mean calprotectin level before treatment was not significantly different (mean calprotectin, UST vs. MIRI, 1652 vs. 2452 mg/kg; P 0.17). The post-treatment calprotectin level was significantly higher for UST vs. MIRI (mean calprotectin, 1092 vs. 278 mg/kg; P 0.0083).

Conclusion

Mirikizumab is an effective induction treatment for patients with active ulcerative colitis, including those who previously did not respond adequately to Ustekinumab therapy.