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학술저널
저자정보
Ruben J. Colman (The University of Chicago Medicine Chicago IL) David T. Rubin (The University of Chicago Medicine Chicago IL)
저널정보
대한장연구학회 Intestinal research Intestinal research Vol.14 No.3
발행연도
2016.1
수록면
202 - 210 (9page)

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Background/Aims: Ulcerative colitis (UC) patients are at greater risk for the development of colorectal neoplasia. Severalindividual studies have demonstrated associations between severity of histologic inflammation and colorectal neoplasia. However, a comprehensive systematic review has not been completed. We performed a systematic review and meta-analysisto explore the relationship between histologic inflammation and risk for neoplasia among available observational studies. Methods: Three databases (EMBASE, MEDLINE and the Cochrane Library) were systematically searched. Studies wereincluded if they included UC patients who underwent colonoscopic assessment and when histologic inflammation andcolorectal neoplasia were both reported. Colorectal neoplasia rates were compared. Quantitative meta-analysis was attempted. Results: Four of 1,422 records found were eligible. Results from 2 case-control studies reported a 3.5-fold increased risk forcolorectal neoplasia associated with a single point increase in histologic inflammation. This result was further corroboratedby one cohort study that demonstrated increased hazard ratios. The second cohort study reported outcomes for patients withnormal gross endoscopy, but had increased histological inflammation when neoplasia was assessed. Finally, this study reportedincreased risk for neoplastic progression by histological inflammation among patients who were normal by gross endoscopicevaluation. Quantitative meta-analysis was unsuccessful due to heterogeneity between study measures. Conclusions: There isstrong evidence that histologic inflammation among patients with UC increases the risk of colorectal neoplasia. The depth andnature of assessment of additional clinical variables was varied and may have resulted in greater outcome discrepancy. Additionalstudy related to mechanisms of inflammation-related neoplasia and therapeutic modification is needed.

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