BACKGROUND AND AIMS:The British Society of Gastroenterology recommend use of structured transition programs to improve control of chronic gastrointestinal disease in adolescents. We sought to determine the impact of attending a structured transition program on engagement of patients with inflammatory bowel disease (IBD) services and disease outcomes. METHODS:We performed a retrospective multicenter study of patients with IBD prior to and post-transfer to adult services. Patients were grouped into those who attended a structured transition program and those who received standard care, transferred with a referral letter. RESULTS:A total of 282 patients were included: 155 patients in our structured transition program cohort and 127 patients in the standard care cohort. Patients who took part in a structured transition program had significantly better engagement with adult IBD services with significantly lower rates of nonattendance at outpatient clinics 1-year post-transfer (12.3% vs 27.2%, P = .002) and significantly lower rates of disengagement with services (4.2% vs 13.1%, P = .015). There were no significant differences seen in rates of biologic failure, need for steroid/surgery or median fecal calprotectin levels between either group. Attending a structured transition program was the only factor that positively impacted engagement with IBD services in a multivariate analysis (OR 4.08, confidence interval 1.41-11.91, P = .01). CONCLUSION:Structured transition programs in IBD can improve engagement of patients with IBD services with significantly lower rates of disengagement with IBD services seen in our study. Large prospective studies are needed in this field to further investigate this and the impact of these programs on disease outcomes.

Abstract Background Standard biological therapy for moderate-severe cases of UC consists in the use of Infliximab (IFX), an anti-tumour necrosis factor α (anti-TNF-α) targeting agent. However, approximately 40% of the patients do not respond to IFX. While transcriptional alterations have been widely associated with non-response to IFX, the precise factors that regulates this altered gene expression remains poorly understood. The aim of this study was perform a robust in silico analysis to identify master transcriptional regulators (MTRs) which regulate gene expression changes in IFX non-responsive UC patients, followed by perturbation in vitro to establish their functional role in UC pathogenesis. Methods Differentially expressed genes (DEGs) identified from four independent public datasets were applied to the GeneXplain platform to identify transcription factors (TFs) enriched for the DEG’s. This was followed by an upstream analysis to identify MTR’s which regulate expression of these genes through the TFs. We next explored the role of these MTRs in driving UC-associated phenotype, using siRNA-mediated knock-down in a novel IBD-like in vitro system comprising of normal rectal epithelial cells treated with TNFa. Results Over 200 TFs were identified in both upregulated and downregulated genes in IFX non-responders across all data sets. RELA, NANOG, FOSJUN were the top 3 TF’ enriched for upregulated genes in three out of the four datasets. Using the TF data, the upstream analysis identified CXCL8, SELE, PTGS2, FCGR3, TFPI2 as the top five MTRs. Next, we showed that of the 5 MTRs, only TFPI2 (tissue factor pathway inhibitor 2) were significantly upregulated in an IBD-like in vitro model (normal rectal epithelial cell line: CRL1831 +TNFa). siRNA-mediated knock-down of TFPI2 in this model resulted in a significant decrease in genes including TNFAIP6, TNFAIP3, FCGR3B, BIRC3 and CXCL5, all of which were predicted in silico to be upregulated by TFPI2 during the upstream analysis. Intriguingly, we showed that downregulation of TFPI2 resulted in significant amelioration of pro-inflammatory cytokines including IL1β, IFNγ, IL10, IL13, IL6 and IL8. Conclusion Our study for the first time identifies key MTRs such TFPI2 which acts as a master regulator of genes whose upregulation drives poor response to IFX. Therefore, these results warrant further in vitro/ex vivo investigation to rationalise their role of TFPI2 as a potential therapeutic target, whose perturbation in UC patient would likely result in improved response to IFX.

Objective The Inflammatory Bowel Disease Disability Index (IBD-DI) was developed according to WHO standards and has been validated in population-based cohorts. However, there are limited data on its relationship to various psychosocial and economic variables or its relevance to hospital clinical practice. The study aims were to determine the validity and reliability of the IBD-DI in an English-speaking hospital out-patient population and to evaluate its association with short and long-term disease activity. Design/Methods 329 subjects were enrolled in a cross-sectional and longitudinal study assessing the IBD-DI and a range of quality of life, work impairment, depression, anxiety, body image, interpersonal, self-esteem, disease activity, symptom scoring scales in addition to long-term outcome. Results The IBD-DI had adequate structure, was internally consistent and demonstrated convergent and predictive validity and was reliable in test–retest study. Disability was related to female sex (p=0.002), antidepressant use (p<0.001), steroid use (p<0.001) and disease activity (p<0.001). Higher IBD-DI scores were associated with long-term disease activity and need for treatment escalation in univariate (p<0.001) and multivariate (p=0.002) analyses. Conclusion The IBD-DI is a valid and reliable measure of disability in English-speaking hospital populations and predicts long-term requirement for treatment escalation.

Colonoscopy following a positive FIT test in an average risk population is effective in reducing CRC incidence and mortality. While lower gastrointestinal symptoms remain a common cause for referral for colonoscopy, symptoms are poor predictors of clinically significant disease. The study was performed to compare neoplasia detection FIT +ve individuals and age-matched symptomatic cohorts. A single centre retrospective observational study was performed including all index colonoscopies performed on patients aged 60-70 from January 2015 to September 2021. Diagnostic yield was reported as adenoma detection rate, SSL detection rate, detection of high risk finding or adenocarcinoma. 8,106 colonoscopies were performed on patients aged 60-70 years. 3,695 (45.6%) originated from screening (FIT +ve). With exclusion criteria applied, 2,640 (59.9%) for screening and 1,767 (40.1%) for symptomatic patients were included. Median age in screening was 65 years (IQR 62-67) and 64 years in the symptomatic group (IQR 62-68), with male predominance in both groups (n=1,536, 58.1%, n=944, 53.4%). There were significant differences in both the ADR (56% vs 26.3%, p<0.01) and the SSLDR (10.4% vs. 8.1%, p=0.05) in the screening cohort compared to the symptomatic group. High risk findings (21.3% vs. 7.5%, p<0.01) were significantly more prevalent in the screening group with a considerably higher colorectal cancer (4.7% vs. 0.9%, p=<0.001) detection rate. FIT based triage significantly outperforms symptom based investigation for individuals in the 60-70 age group. Patients should be preferentially referred to organised colorectal cancer screening. FIT can be performed on symptomatic patients, to identify low risk individuals.

Abstract Background Hand grip strength (HGS) is a recognised tool for diagnosis / screening of muscle impairment and sarcopenia, however it remains underutilised in IBD cohorts. The aim of the study was to measure the prevalence of muscle impairment by HGS and association with quality of life in a cohort of UC patients in disease remission. Methods Potential subjects were prospectively identified for selection from the Gastroenterology Department in St. Vincent’s University Hospital Outpatient Department. All patients had a confirmed diagnosis of UC for >3 month with stable, quiescent disease (no escalation of medical therapy in the previous 3 months with a documented Faecal Calprotectin (FCP) <100 μg/g). Along with anthropometry data, HGS measurements were performed using the Jamar®Plus+Dynamometer. Quality of life scores were measured using 36-item Short Form Survey (SF-36), Short Inflammatory Bowel Disease Questionnaire (SIBDQ), and Short Health Scale questionnaires were measured. Linear regression was used to calculate standardised β-coefficients for correlation analysis. Non-parametric data was analysed using algorithms including Kruskal-Wallis and Wilcoxon rank-sum test. Results 60% (n=18) of subjects had a HGS outside the lower limit of the 95% confidence interval of age and sex matched normative values, indicative of impaired grip strength. This was significantly more prevalent in subjects with normal BMI than BMI>30 (p=0.035). Prevalence of fatigue was 43.3% according to SIBDQ question 2a and ’Energy/Fatigue’ scores of SF-36 were significantly lower compared to normal Irish population data (51.0 v 64.8, p = 0.0002). Composite scores of fatigue in both SIBDQ (question 2a) and SF-36 were compared, resulting in a standardized β-coefficient of 0.52 of statistical significance (p value = 0.003).Significant correlation was demonstrated between predicted HGS and ’Energy/Fatigue’ SF-36 scores (standardised β-coefficient = 0.4, p value = 0.027). Conclusion HGS is a convenient means of measuring muscle function in an IBD population and correlates significantly with ’Energy/fatigue’ SF-36 scores. These results suggest sarcopenia as a potentially important contributor to fatigue in patients with IBD and suggest HGS is an objective, easily applied objective measure which merits validation as an outcome measure for intervention studies to improve fatigue in patients with IBD.

Background and Aims:Primary sclerosing cholangitis (PSC) is a progressive cholestatic disease with up to 80% of patients also suffering from ulcerative colitis (PSC-UC). The difficulty in the diagnosis along with the increased risk for developing cancer represents a clinical challenge. Furthermore, the precise molecular factors regulating the phenotype of this disease subtype remain unknown. Methods:We applied methyl-capture sequencing and mRNA sequencing to colonic mucosal biopsies from 3 groups of treatment-naïve children at diagnosis from the Determinants and Outcomes in CHildren and AdolescentS study: UC (n = 10), PSC-UC (n = 10), and healthy controls (n = 10). Results:Differential gene expression between UC and PSC-UC showed significantly higher gene expression changes in PSC-UC patients when compared to UC. Specifically, expression of these genes was regulated by master transcriptional regulators (NLRP3, DLL1) and transcription factors (RELA, Myogenin, and FOXO1), which are shown to regulate expression of inflammatory response and immune-associated genes in PSC-UC patients exclusively. Differential methylation analysis between PSC-UC and UC demonstrated >2000 differentially methylated regions with a large proportion of them enriched in gene promoter and enhancer regions. We further show no difference in epigenetic age between PSC-UC and UC. Finally, we identify KLHL17 as hypomethylated and upregulated in PSC-UC patients. Conclusion:Our study, for the first time, identifies distinct gene expression and DNA methylation alterations that differentiate UC from PSC-UC at diagnosis in treatment-naïve pediatric patients. We show the gene expression differences observed between PSC-UC and UC are modulated by intricate molecular mechanisms involving master transcriptional regulator-mediated signaling through transcription factors. These findings suggest the potential utility of these molecular markers as predictive biomarkers for PSC development in UC at an early stage of development. Further validation in larger patient cohorts is warranted.

Abstract Background Primary sclerosing cholangitis (PSC) is a progressive choleostatic disease and up to 80% of patients also have ulcerative colitis (PSC-UC). This presents a clinical challenge owing to difficulty in diagnosis and increased risk for developing cancer. While several multifactorial processes including inflammation and microbial dysbiosis have been associated with PSC-UC pathogenesis, the precise molecular factors that regulate the phenotype of this disease subtype remain unknown. Methods We applied methyl-capture sequencing and mRNA sequencing to colonic mucosal biopsies derived from the DOCHAS study (GEN-193/11), to identify transcriptomic and epigenetic differences between treatment naïve paediatric UC (n=10), PSC-UC (n=10) and healthy controls (n=10) samples. Results Differential gene expression between UC and PSC-UC identified 9 up-regulated genes - ADMTS14, PNCK, NLRP3, SLC6A19, DLL1, FCGR2C, KLHL17, APOB, EHBP1L1 and 5 downregulated - SLC37A2, SLC14A2, RPL27, RPS25, SLC38A4 in PSC-UC relative to UC. Importantly, we show that expression of these genes was intricately regulated by master transcriptional regulators (pro-caspases, IL7RA) and transcription factors (TFs) :AR, p53, JUND, CEBPA. Similarly, differential methylation analysis between PSC-UC and UC identified 22 differentially methylated regions (DMRs) relative to controls, where 5 were hypermethylated and 8 hypomethylated. Intriguingly, in general we show that these DMRs are largely localised in gene promoter regions as opposed to enhancers. Importantly, we show that these DMR’s identified between PSC-UC vs UC is enriched for binding sites for the TF: ASCL1, suggesting its activity likely is effected due to the altered methylation of its binding site in PSC-UC patients. Collectively, these results highlight the importance of TF’s in driving molecular differences between PSC-UC and UC paediatric patients in a treatment naïve setting. Conclusion In summary, for the first time this study provides a critical insight into the transcriptional differences between treatment naïve children with PSC-UC vs UC as well as highlights the intricate regulatory processes involving master transcriptional regulators, transcription factors and DNA methylation. These processes thus warrant further examination in larger cohorts to rationalise their role as diagnostic/therapeutic targets.

BACKGROUND AND AIMS:Patients with inflammatory bowel disease [IBD] have an attenuated response to initial COVID-19 vaccination. We sought to characterize the impact of IBD and its treatment on responses after the third vaccine against SARS-CoV-2. METHODS:This was a prospective multicentre observational study of patients with IBD [n = 202] and healthy controls [HC, n = 92]. Serological response to vaccination was assessed by quantification of anti-spike protein [SP] immunoglobulin [Ig]G levels [anti-SPIgG] and in vitro neutralization of binding to angiotensin-converting enzyme 2 [ACE2]. Peripheral blood B-cell phenotype populations were assessed by flow cytometry. SARS-CoV-2 antigen-specific B-cell responses were assessed in ex vivo culture. RESULTS:Median anti-SP IgG post-third vaccination in our IBD cohort was significantly lower than HCs [7862 vs 19 622 AU/mL, p < 0.001] as was ACE2 binding inhibition [p < 0.001]. IBD patients previously infected with COVID-19 [30%] had similar quantitative antibody response as HCs previously infected with COVID-19 [p = 0.12]. Lowest anti-SP IgG titres and neutralization were seen in IBD patients on anti-tumour necrosis factor [anti-TNF] agents, without prior COVID-19 infection, but all IBD patients show an attenuated vaccine response compared to HCs. Patients with IBD have reduced memory B-cell populations and attenuated B-cell responses to SARS-CoV-2 antigens if not previously infected with COVID-19 [p = 0.01]. Higher anti-TNF drug levels and zinc levels <65 ng/ml were associated with significantly lower serological responses. CONCLUSIONS:Patients with IBD have an attenuated response to three doses of SARS-CoV-2 vaccine. Physicians should consider patients with higher anti-TNF drug levels and/or zinc deficiency as potentially at higher risk of attenuated response to vaccination.

Objective To evaluate the impact of British Society of Gastroenterology/Association of Coloproctology of Great Britain and Ireland/Public Health England (BSG/ACPGBI/PHE) 2019 polypectomy surveillance guidelines within a national faecal immunochemical test-based bowel cancer screening (BS) cohort on surveillance activity and detection of pathology by retrospective virtual application.Design A retrospective review of BS colonoscopies performed in 2015-2016 with 5 years prospective follow-up in single institution. Index colonoscopies were selected. Incomplete colonoscopies were excluded. Histology of all resected polyps was reviewed. Surveillance intervals were calculated according to BSG/ACPGBI/PHE 2019 guidelines and compared with pre-existing 'European Guidelines for Quality Assurance in Colorectal Cancer Screening and Diagnosis' (EUQA 2013). Total number of colonoscopies deferred by virtual implementation of BSG/ACPGBI/PHE 2019 guidelines were calculated. Pathology identified on procedures that would have been deferred was reviewed.Results Total number of index BS colonoscopies performed in 2015-2016 inclusive was 890. 115 were excluded (22 no caecal intubation, 51 inadequate bowel preparation, 56 incomplete polyp clearance). N=509 colonoscopies were scheduled within a 5-year interval following index colonoscopy surveillance rounds based on EUQA guidelines. Overall, volume of surveillance was significantly reduced with retrospective application of BSG/ACPGBI/PHE 2019 guidelines (n=221, p<0.0001). No cancers were detected within the 'potentially deferred' procedures who attended for follow-up (n=330) with high-risk findings found in<10% (n=30) of colonoscopies within the BSG/ACPGBI/PHE cohort.Conclusion BSG/ACPGBI/PHE 2019 guidelines safely reduce the burden of colonoscopy demand with acceptable pathology findings on deferred colonoscopies.

Aims To evaluate the impact of BSG 2019 and ESGE 2020 polypectomy surveillance guidelines within a national FIT-based bowel cancer screening (BS) cohort on surveillance activity and detection of pathology by retrospective virtual application.

Abstract Background Novel medications including the introduction of biologic therapies in the last decade have expanded treatment options for patients with ulcerative colitis (UC). Large studies in the USA and Europe have shown colectomy rates in UC patients are reducing over the past two decades. Methods We performed a single-centre retrospective study of our prospectively maintained IBD database. Our aim was to look at changes in colectomy rates in patients with UC over the past three decades and need for biologic therapy. Basic demographics, need for biologic therapy and colectomy rates were collected. Need for colectomy and biologic therapy within, 10 years of diagnosis was determined across three groups dependent on decade of diagnosis. Results 2229 patients with confirmed UC were included in our study. Median age at diagnosis was, 37 years [range, 4.9 -92.6]., 1210 [54.28%] were male., 595 patients were diagnosed between, 1990–2000, 795 between, 2000–2010 and, 790 between, 2010–2020. A total of, 366 (16.4%) patients had a colectomy during follow-up and, 363 (16.3%) were treated with biologic therapies. We found rates of colectomy within, 10 years of diagnosis have significant dropped over the past three decades. From, 1990 -2000, 595 patients were diagnosed with UC and, 131 [22%] patients had colectomies, in, 2000-2010, 794 patients were diagnosed with UC and, 135 [17%] had a colectomy and between, 2010-2020, 784 patients were diagnosed with UC and, 55 [7%] had a colectomy [p = <, 0.001]. We found a significant increase in use of biologic therapy within the first, 10-years of diagnosis over the last three decades increasing from, 0.2% to, 5.3% to, 22.7% over the past decade [p = <, 0.001]. Conclusion Management of UC has changed over the past three decades including the introduction of multiple biologic therapies and the use of therapeutic drug monitoring has allowed a more personalised approach to management of UC. We can see from this study changes in the management of UC over the past decade have resulted in significant reduction in need for colectomy and an increase in the use of biologics.

Abstract Background Anti-TNF agents are effective treatments for Inflammatory Bowel Disease (IBD), however, a significant proportion of patients require second-line biologic therapy. Real-world data on the outcome of second line biologic therapy can inform clinical decision-making. Methods To evaluate prescribing practice and second-line biologic therapy persistence in IBD patients. IBD patients, who had received one prior anti-TNF agent and commenced a second-line biologic, at participating centres, were identified. Baseline demographic data, concomitant medication and biologic therapy history were characterised by retrospective review of patients records. Adalimumab(ADA) and golimumab(GOL) were considered subcutaneous(SC) anti-TNF agents. Date of commencement and discontinuation of therapies were documented. Kaplan-Meier survival curves were constructed for time based analyses. P values < 0.05 were considered significant in analyses. Results N=395 IBD patients were included; 30%, 68% and 2% had UC, CD and IBD-U respectively; age (median[IQR]) 26[18–35] years; 56% female; 35% receiving a concomitant immunomodulator (IMM); follow-up time (median [IQR]) 1.5[0.7–3.3] years. Second-line biologic therapy with SC anti-TNF, infliximab(IFX), vedolizumab(VDZ), and ustekinumab(USTK) was used in 36%(n=143), 38%(n=151), 10%(n=38), and 16%(n=63) of patients respectively. Follow-up time (median[IQR]) was significantly longer for SC anti-TNF and IFX compared with VDZ and USTK groups: 1.7 [0.7–3.6], 1.7 [0.7–3.5], 1.1[0.3–2.5], 1.3[0.5–2.3] years respectively, p=0.03. A greater proportion of patients receiving anti-TNF therapy versus alternate class biologic therapy received a concomitant IMM: 42%, 34%, 18% and 29% of SC anti-TNF, IFX, VDZ and USTK treated patients respectively, p=0.03. In a univariate survival analysis there was no significant difference in survival-free of drug discontinuation comparing second-line biologic agents, p=0.8. In a multivariate analysis, including second-line biologic agent type, concomitant IMM use, gender and IBD phenotype the only factor significantly associated with time to drug discontinuation was UC phenotype, Hazard ratio (95%CI): 1.5 (1.1 – 2.1), p=0.007. Conclusion While follow-up time was shorter for VDZ and USTK treated patients, the durability of response to second-line biologic therapy, assessed by drug persistence, appeared similar between agents. UC phenotype was associated with a shorter time to therapy discontinuation.

Abstract Background Anti-TNF agents are effective therapies for Inflammatory Bowel Disease (IBD), however, a significant proportion of patients lose response over time. Real world data on prescribing practices and outcome of anti-TNF therapy are of utility to practicing clinicians Methods To evaluate Anti-TNF prescribing practice and durability of Anti-TNF response in a large multicentre IBD cohort. IBD patients commencing an anti-TNF agent, as first biologic therapy, at participating academic centres were identified from institutional databases. Baseline demographic data, concomitant medication and biologic therapy history were collected. Adalimumab(ADA) and Golimumab(GOL) were consider subcutaneous(SC) anti-TNF agents. Date of commencement and discontinuation of first and second line anti-TNF therapy was documented. Kaplan-Meier survival curves were constructed for time based analyses. P values less than 0.05 were considered significant in all analyses. Results N=991 patients with IBD were included in the study. 29%, 69% and 2% had UC, CD and IBD-U respectively; median [IQR] age 27 [19–37] years; 50% female. 31%, 63% and 4% received infliximab(IFX), ADA and GOL respectively as first-line anti-TNF therapy. 35% of patients received an immunomodulator in combination with first-line anti-TNF agent. Median [95% CI] survival free of therapy discontinuation for first and second-line anti-TNF agents was 4.6 [3.7 – 5.3] years and 3.0 [2.1 – 3.9] years respectively. Survival free of anti-TNF discontinuation was significantly shorter for IFX monotherapy group compared with IFX combination therapy, SC anti-TNF monotherapy and SC anti-TNF combination therapy groups, p=0.005. Conclusion While anti-TNF therapies are effective a significant proportion of patients discontinue therapy over time. Second line anti-TNF therapy results in a less durable response with a shorter time to drug discontinuation compared with first line anti-TNF therapy. The use of a combination immunomodulator is particularly important with infliximab therapy, however, does not influence durability of response for subcutaneous anti-TNF agents.

Abstract Background Ulcerative colitis (UC) is a chronic inflammatory condition characterized by significant morbidity and escalating economic costs. Effective patient management is severely hampered by a lack of unambiguous molecular biomarkers that can predict response to anti-TNFα treatment such and/or disease progression. While, both genetic and epigenetic factors have been reported to impact UC pathogenesis, their role in regulating disease progression and treatment response remains unclear. Methods Here, we applied methyl-capture sequencing and RNAsequencing to mucosal biopsies derived from clinical cohorts of patients with mild-to-moderate and severe UC with the aim of identifying various regulatory factors that orchestrate treatment response and disease severity in these patients. Results First, differential gene expression analysis between responders and non-responders to infliximab and vedolizumab (anti-TNFα) enabled identification of disease-associated genes that were either up- or down-regulated in responders to both these anti-TNFα agents. Next, upstream analysis of these differentially expressed genes revealed that both up- and downregulated genes in responders are intricately regulated by “master regulators” (MRs) including chemokine ligands and receptors such as FGFR2 and IL8 respectively. Moreover, we show that these MRs play a pivotal role in regulating gene expression through a complex signalling network mediated by transcription factors (TFs) such as FYN and ICAM1. These results for the first time provide evidence of impact of MRs and TFs on genes involved in differential response to anti-TNFα agents in patients with UC. In parallel, targeted DNA methylation profiling of mucosal biopsies derived from mild-to-moderate (n=85) and severe UC (n=33) patients enabled identification of a wide-spread DNA methylation alterations at regulatory regions such as promoters and enhancers. Moreover, we identified distinct significant methylation differences between UC patients who progress in their disease course leading to treatment with anti-TNFα/immunodulators agents vs. patients who are on 5’Asa maintenance treatment. Indeed, similar differences was also observed between responders and non-responders of anti-TNFαagents. Conclusion Taken together, our preliminary results for the first time highlight the regulatory role of master regulator-mediated signalling networks involving transcription factors that regulate gene expression underpinning response to anti-TNFa in UC patients. In parallel, these results identify specific DNA methylation alterations that impact treatment response and disease severity and therefore could ultimately enact as predictive biomarkers in UC.

Abstract Background The DUBLIN (Degree of Ulcerative colitis Burden of Luminal Inflammation) is a novel simple clinical score of inflammation in patients with Ulcerative Colitis (UC) which can be used easily in outpatients and at the bedside. Methods We sought to validate the clinical utility of scoring UC inflammatory burden at diagnosis in predicting disease outcomes using the DUBLIN score (DS). We performed a multicentre retrospective study of patients recruited to the Genuity medicine IBD research project at three centres. DS at diagnosis was calculated based on disease extent and endoscopic severity. Study outcomes were need for immunomodulators and/or biologic therapy and need for surgery. We also examined the association between DS and FCP, albumin and C-reactive protein. Results 679 patients with confirmed UC were identified. 291 had data allowing calculation of DS at diagnosis (median age 38.9 years, 53% male). Median DS was 4 [1–9]. 122 patients were treated with biologic therapy during follow-up. Median DS at diagnosis was significantly higher in patients requiring biologic therapy compared to those not requiring biologic therapy [4 versus 3, p = < 0.001]. Of patients requiring biologic therapy patients with a DS > 3 had a significantly shorter time on 1st biologic therapy [2.1 versus 3.9 years, p = 0.005]. There was no difference in median DS dependent on immunomodulator use. Similarly median DS at diagnosis was significantly higher in patients requiring colectomy compared to those not requiring colectomy [6 versus 4, p = 0.001]. There was a weak positive correlation between both DS and faecal calprotectin [correlation coefficient 0.27, p = 0.001] and C-reactive protein [correlation coefficient 0.7, p = 0.01] and a weak negative correlation between DS and albumin level [correlation coefficient -0.22, p = 0.04]. Conclusion Our study validates the clinical utility DS is an accurate clinical tool at diagnosis and during a patients’ disease course for identifying disease burden. A higher DS correlates with an increased need for biologic therapy, need for colectomy and increased biomarkers of disease activity. This is a useful tool for day to day use in clinical practise providing personalised management of patients with UC.

Aims To determine the effect of endoscopic management on post orthotopic liver transplant (OLT) anastomotic strictures.

Aims Sessile serrated lesions (SSL) are significant precursors of the alternative serrated neoplasia pathway. Achieving key performance indicators (KPI) in colonoscopy increases the detection of premalignant lesions. The SSL detection rate (SSLDR) is not currently recognised as a KPI, with no agreed minimal SSLDR. Data on the impact of Hyoscine Butylbromide (HB) on adenoma detection is conflicting. This study aimed to report the SSL detection rate over time and identify factors associated with increasing SSL detection.