! CAC cap-assisted colonoscopy CRC colorectal cancer EMR endoscopic mucosal resection ESGE European Society of Gastrointestinal Endoscopy FAP familial adenomatous polyposis FICE Fujinon intelligent color enhancement, flexible spectral imaging enhancement FAP familial adenomatous polyposis GRADE grading of recommendations assessment, development and evaluation HD-WLE high definition white-light endoscopy i-SCAN Pentax virtual chromoendoscopy system MAP MUTYH-associated polyposis NBI narrow band imaging PICO population, intervention, comparator, outcome PIVI preservation and incorporation of valuable endoscopic innovations RCT randomized controlled trial SD-WLE standard definition white-light endoscopy TER third eye retroscope WLE white-light endoscopy

OBJECTIVES:The aim of this study was to identify risk factors associated with development of high-grade dysplasia (HGD) or colorectal cancer (CRC) in ulcerative colitis (UC) patients diagnosed with low-grade dysplasia (LGD).METHODS:Patients with histologically confirmed extensive UC, who were diagnosed with LGD between 1993 and 2012 at St Mark's Hospital, were identified and followed up to 1 July 2013. Demographic, endoscopic, and histological data were collected and correlated with the development of HGD or CRC.RESULTS:A total of 172 patients were followed for a median of 48 months from the date of initial LGD diagnosis (interquartile range (IQR), 15–87 months). Overall, 33 patients developed HGD or CRC (19.1% of study population; 20 CRCs) during study period. Multivariate Cox proportional hazard analysis revealed that macroscopically non-polypoid (hazard ratio (HR), 8.6; 95% confidence interval (CI), 3.0–24.8; P<0.001) or invisible (HR, 4.1; 95% CI, 1.3–13.4; P=0.02) dysplasia, dysplastic lesions ≥1 cm in size (HR, 3.8; 95% CI, 1.5–13.4; P=0.01), and a previous history of “indefinite for dysplasia” (HR, 2.8; 95% CI, 1.2–6.5; P=0.01) were significant contributory factors for HGD or CRC development. Multifocal dysplasia (HR, 3.9; 95% CI, 1.9–7.8; P<0.001), metachronous dysplasia (HR, 3.5; 95% CI, 1.6–7.5; P=0.001), or a colonic stricture (HR, 7.4; 95% CI, 2.5–22.1; P<0.001) showed only univariate correlation to development of HGD or CRC.CONCLUSIONS:Lesions that are non-polypoid or endoscopically invisible, large (≥1 cm), or preceded by indefinite dysplasia are independent risk factors for developing HGD or CRC in UC patients diagnosed with LGD.

ObjectiveUlcerative colitis (UC) is a dynamic disease with its severity continuously changing over time. We hypothesised that the risk of colorectal neoplasia (CRN) in UC closely follows an actuarial accumulative inflammatory burden, which is inadequately represented by current risk stratification strategies.DesignThis was a retrospective single-centre study. Patients with extensive UC who were under colonoscopic surveillance between 2003 and 2012 were studied. Each surveillance episode was scored for a severity of microscopic inflammation (0=no activity; 1=mild; 2=moderate; 3=severe activity). The cumulative inflammatory burden (CIB) was defined as sum of: average score between each pair of surveillance episodes multiplied by the surveillance interval in years. Potential predictors were correlated with CRN outcome using time-dependent Cox regression.ResultsA total of 987 patients were followed for a median of 13 years (IQR, 9-18), 97 (9.8%) of whom developed CRN. Multivariate analysis showed that the CIB was significantly associated with CRN development (HR, 2.1 per 10-unit increase in CIB (equivalent of 10, 5 or 3.3 years of continuous mild, moderate or severe active microscopic inflammation); 95% CI 1.4 to 3.0; P<0.001). Reflecting this, while inflammation severity based on the most recent colonoscopy alone was not significant (HR, 0.9 per-1-unit increase in severity; 95% CI 0.7 to 1.2; P=0.5), a mean severity score calculated from all colonoscopies performed in preceding 5 years was significantly associated with CRN risk (HR, 2.2 per-1-unit increase; 95% CI 1.6 to 3.1; P<0.001).ConclusionThe risk of CRN in UC is significantly associated with accumulative inflammatory burden. An accurate CRN risk stratification should involve assessment of multiple surveillance episodes to take this into account.

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BackgroundDistal feeding (DF) describes the insertion of a feeding tube into a fistula or stoma to administer a liquid feed into the distal bowel. It is currently used clinically in patients who are unable to absorb enough nutrition orally. This systematic review investigates DF as a therapeutic measure across a spectrum of patients with stomas and fistulae.MethodsA total of 2825 abstracts and 44 full-text articles were screened via OVID. Fifteen papers were included for analysis. Randomised controlled trials, cohort and observational studies investigating DF as a therapeutic measure were included.ResultsThree feeds were used across the studies—reinfusion of effluent, infusion of prebiotic or a mixture. The studies varied the length of feeding between 24 hours and 61 days, and the mode of feeding, bolus or continuous varied.DF was demonstrated to effectively wean patients from parenteral nutrition in two papers. Two papers demonstrated a significant reduction in stoma output. Three papers demonstrated improved postoperative complication rates with distal feeding regimens, including ileus (2.85% vs 20% in unfed population, p=0.024). One paper demonstrated a reduction in postoperative stool frequency.ConclusionsThis review was limited by study heterogeneity and the lack of trial data, and in the patient groups involved, the variability in diet and length of regimen. These studies suggest that DF can significantly reduce stoma output and improve renal and liver function; however, the mechanism is not clear. Further mechanistic work on the immunological and microbiological action of DF would be important.