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Background/AimsUlcerative colitis (UC) patients are at greater risk for the development of colorectal neoplasia. Several individual 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-analysis to explore the relationship between histologic inflammation and risk for neoplasia among available observational studies.MethodsThree databases (EMBASE, MEDLINE and the Cochrane Library) were systematically searched. Studies were included if they included UC patients who underwent colonoscopic assessment and when histologic inflammation and colorectal neoplasia were both reported. Colorectal neoplasia rates were compared. Quantitative meta-analysis was attempted.ResultsFour of 1,422 records found were eligible. Results from 2 case-control studies reported a 3.5-fold increased risk for colorectal neoplasia associated with a single point increase in histologic inflammation. This result was further corroborated by one cohort study that demonstrated increased hazard ratios. The second cohort study reported outcomes for patients with normal gross endoscopy, but had increased histological inflammation when neoplasia was assessed. Finally, this study reported increased risk for neoplastic progression by histological inflammation among patients who were normal by gross endoscopic evaluation. Quantitative meta-analysis was unsuccessful due to heterogeneity between study measures.ConclusionsThere is strong evidence that histologic inflammation among patients with UC increases the risk of colorectal neoplasia. The depth and nature of assessment of additional clinical variables was varied and may have resulted in greater outcome discrepancy. Additional study related to mechanisms of inflammation-related neoplasia and therapeutic modification is needed.

Background & Aims Patients with primary sclerosing cholangitis (PSC) and ulcerative colitis (UC) have a high risk of colonic neoplasia. Neoplasia frequently develops in the proximal colon in patients with PSC. Histologic inflammation is an independent risk factor for the development of neoplasia; we investigated whether patients with UC and PSC have more subclinical disease activity than patients with UC alone. Methods We performed a retrospective analysis of data from 143 patients (205 examinations) with ulcerative pancolitis who were in clinical remission and treated at a tertiary medical center from May 2011 through May 2016. Endoscopic and histologic activity were compared between patients with PSC (from 36 examinations) and without PSC (from 169 examinations). Disease activity was scored per colonic segment using a modified Mayo endoscopic subscore and histologic assessment. In each colonic segment, differences in disease activity and the degree of discordance between endoscopic and histologic inflammation among UC patients with and without PSC were compared. Results Patients with UC-PSC had significantly more subclinical endoscopic (odds ratio [OR], 4.21; 95% CI, 1.67–10.63) and histologic activity (OR, 5.13; 95% CI, 2.25–11.68) in the right colon, as well as greater degree of histologic than endoscopic inflammation in the proximal colon (OR, 3.14, 95% CI, 1.24–7.97), compared with patients without PSC. Patients with UC-PSC had significantly less histologic activity in the rectum on multivariate analysis (OR, 0.24; 95% CI, 0.08–0.72). Conclusions Patients with UC and PSC who are in clinical remission are significantly more likely to have endoscopic and histologic inflammation in the right colon than patients with UC without PSC. Our findings provide insight into cause of colorectal cancer in UC patients with PSC. [ABSTRACT FROM AUTHOR]

Background/Aims: Ulcerative colitis (UC) patients are at greater risk for the development of colorectal neoplasia. Several individual 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-analysis to 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 were included if they included UC patients who underwent colonoscopic assessment and when histologic inflammation and colorectal 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 for colorectal neoplasia associated with a single point increase in histologic inflammation. This result was further corroborated by one cohort study that demonstrated increased hazard ratios. The second cohort study reported outcomes for patients with normal gross endoscopy, but had increased histological inflammation when neoplasia was assessed. Finally, this study reported increased risk for neoplastic progression by histological inflammation among patients who were normal by gross endoscopic evaluation. Quantitative meta-analysis was unsuccessful due to heterogeneity between study measures. Conclusions: There is strong evidence that histologic inflammation among patients with UC increases the risk of colorectal neoplasia. The depth and nature of assessment of additional clinical variables was varied and may have resulted in greater outcome discrepancy. Additional study related to mechanisms of inflammation-related neoplasia and therapeutic modification is needed. [ABSTRACT FROM AUTHOR]

PURPOSE: This study was designed to examine postoperative change of mucosal inflammation at strictureplasty segment in Crohn's disease mainly by cytokine measurements. METHODS: Patients who underwent strictureplasty for Crohn' s disease in the terminal ileum were investigated. Mucosal samples at the strictureplasty site were obtained during operation. At 3, 6, and 12 months after operation, biopsy specimens were taken from the strictureplasty site and macroscopic ally normal ileum at endoscopy. Mucosal cytokine concentrations were measured by enzyme-linked immunosorbent assay. RESULTS: The mucosal concentrations of proinflanimatory cytokines (interleukin- 1 [3, interleukin-6, interleukin-8, and tumor necrosis factor-a) and anti-inflammatory mediator (interleukin-1 receptor antagonist) at the strictureplasty segment greatly increased at the time of operation. Interleukin-1 [3, interleukin-1 receptor antagonist, interleukin-6, interleukin-8, and tumor necrosis factor-a concentrations at the strictureplasty segment decreased during a 12-month period after operation. Twelve months after operation there was no significant difference in each cytokine concentration between the strictureplasty and macroscopically normal segments. The mucosal interleukin-1 receptor antagonist/interleukin-1 [3 ratio at the strictureplasty segment increased during a 12-month period after operation. Twelve months after operation there was no significant difference in the ratio between the stricture- plasty and macroscopically normal segments. The endoscopic and histologic seventies of mucosal inflammation at the strictureplasty site also decreased; however, their findings were not normalized during the study. CONCLUSIONS: During one year after strictureplasty for Crohn's disease, cytokine production at the strictureplasty segment was decreased to the level of the macroscopically normal ileum and an imbalance between pro inflammatory and anti- inflammatory cytokines was corrected. [ABSTRACT FROM AUTHOR]