OUTCOMES OF GP OUTREACH PROGRAMME OFFERING COLONOSCOPIC SURVEILLANCE FOR IBD PATIENTS MANAGED IN PRIMARY CARE

12-months of diagnosis is associated with a reduced risk of disease progression in CD

Introduction Colonoscopic surveillance in IBD patients can reduce the development of colorectal cancer (CRC) and the rate of CRC-associated death.We recently reported that 27% of IBD patients living in East Devon are managed exclusively in primary care of whom about 23% maybe eligible for colonoscopic surveillance.We devised an outreach programme, whereby we invited primary care physicians to enrol these patients in a colonoscopic surveillance programme.Methods In December 2017 we contacted 37 general practices, where 161 patients with UC who were eligible for surveillance had been identified.Each practice was sent a letter explaining the goals of the project, a link to the National Institute for Healthcare and Clinical Excellence (NICE) guidance for CRC surveillance in IBD patients and patient information booklets.We informed the practices of their eligible patients and asked them to refer patients for secondary care IBD consults if appropriate.We included an outcome form that captured whether the patient was referred, was deemed inappropriate for surveillance, had surveillance elsewhere, had declined surveillance, or was no longer registered at the practice.
Results Sixty-five percent of practices (24/37) responded and we received responses for 57 of 161 (35%) potentially eligible patients.Thirty-five (61%) patients were referred to our IBD service; 7 (12%) patients declined surveillance; 7 (12%) patients were deemed by their GP to be unfit for surveillance and 5 (10%) were no longer registered at the identified GP practice; 2 (4%) had surveillance arranged elsewhere and 1 (2%) patient had died.Amongst the 35 patients referred to secondary care; 22 (63%) underwent surveillance colonoscopy, 12 (34%) declined surveillance after discussion or did not attend their booked appointments and one is awaiting colonoscopy.Half of patients who had a colonoscopy had active inflammation.We diagnosed one CRC He was an elderly man with a locally invasive signet ring caecal tumour, without distant metastases, who went onto to have a curative right hemicolectomy without complication.Conclusions Patients with longstanding IBD are frequently managed exclusively in primary care and maybe overlooked for colonoscopic CRC surveillance.There is a need to implement processes to facilitate identification and recall of patients eligible for surveillance across primary and secondary care.
Based on b-diversity dispersion analysis, estimated using Bray-Curtis distance, EEN induced clear alterations to the microbiome.Permutation ANOVA was used to identify significant changes to the microbiome during EEN.Most of the change that occurred was apparent within the first 4 weeks of treatment with R2: 4.7%, (p=0.001) and by the end of EEN R2: 3.2%, (p=0.001).
In patients to enter remission using EEN, we observed a quick reversion in the microbiome composition to that of pretreatment (p=0.23).
Assessing the metabolic activity of the microbiome we observed a significant decrease in the concentration of acetate (start: 423.6 [183.6]Christopher A Lamb*,3 Bingbing Dai, 3 Ryan Ichikawa, 1,2 Meghan Acres, 1 Gillian Hulme, 1,2 Christopher D Carey, 1 Jeremy Palmer, 2 Claire J Jones, 2 Anna K Long, 1,2 John C Mansfield, Introduction Targeting integrins that mediate adhesion and migration of lymphocytes to the gastrointestinal (GI) tract is an effective therapy in inflammatory bowel disease (IBD).a4b7 and a4b1 are expressed on circulating lymphocytes that may mediate inflammation, while aEb7 integrin is expressed primarily on a subset of T cells within the mucosa.
Etrolizumab is a humanized monoclonal antibody that selectively binds the b7 subunit of the a4b7 and aEb7 integrin heterodimers.The relative role of individual integrin heterodimers in lymphocyte migration and retention in the GI tract remains to be characterized.Methods pSMAD3, MAdCAM, VCAM and ICAM levels were measured in colonic and ileal biopsies.a4b7+ and a4b7human T cells were induced to express aE integrin by TGF-b 1 stimulation followed by qPCR array gene expression analysis.A murine photo-convertible reporter system was used to determine the effect of blockade of a4b7 and/or aEb7 integrins on lymphocyte migration and retention.T cell-epithelial cell interactions were evaluated using intravital two-photon microscopy.Results pSMAD3 was observed in the epithelium and lamina propria in IBD biopsies, suggesting active TGF-b signalling.Adhesion molecule expression was increased in inflamed biopsies.TGF-b1 stimulation induced aE integrin expression on both a4b7+ and a4b7circulating T cells.aEb7+ cells derived from a4b7+ and a4b7progenitors had similar cytokine, chemokine, transcription factors and effector molecule gene expression.In a mouse model of T cell migration, combined blockade of both a4b7 and aEb7 with anti-b7 (etrolizumab surrogate) led to a greater reduction of T cell accumulation in the intestinal mucosa and epithelium compared to single blockade of either a4b7 or aEb7.Further intravital two-photon microscopy and photo-specific labelling experiments revealed that blockade of aEb7 reduces T cell:epithelial cell interactions, increases the migratory speed of activated T cells in the intestinal mucosa, and facilitates effector T cell egress from the intestinal mucosa through lymphatic vessels.Conclusions aEb7 is induced by TGF-b1 on both a4b7+ or a4b7-T cells.Co-blockade of a4b7 and aEb7 together leads to greater inhibition of T cell accumulation in gastrointestinal tissues through a stepwise inhibition of T cell migration and subsequent tissue retention.Introduction There is an unmet need for blood-based biomarkers that help predict disease and its course at inception to allow tailoring of treatments, achieve early mucosal healing and improve clinical outcomes.In our study, we explore the clinical utility of miRNAs in Inflammatory bowel disease (IBD).Methods A 2-stage prospective multi-centre case control study was performed.Small RNA sequencing was performed on a discovery cohort of immunomagnetically separated leucocytes (90 CD4+ & CD8+ T-lymphocytes and CD14+ monocytes) , end: 224.9 [101.5];p< 0.001), propionate (start: 93.8 [50.6], end: 55.7 [27.3]; p< 0.001) and butyrate (start: 95.0 [64.2], end: 41.0 [50.7]; p< 0.001).During FR, there was a rapid reversion in levels of acetate and propionate (acetate EEN end: 224.9 [101.5]vs 17d FR: Amy Buck, 2 Jack Satsangi. 1 MRC Centre for Inflammation Research, University Of Edinburgh, Edinburgh, UK; 2 Nuffield Department of Medicine, University of Oxford, Oxford, UK; 3 Institute of Immunology and Infection Research and Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh, UK; 4 LifeArc, Edinburgh, UK; 5 Centre for Genomic and Experimental Medicine, Edinburgh, UK; 6 Exeter IBD and Pharmacogenetics group, University of Exeter, Exeter, UK;