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Mesalamine, but Not Sulfasalazine, Reduces the Risk of Colorectal Neoplasia in Patients with Inflammatory Bowel Disease: An Agent-specific Systematic Review and Meta-analysis

O'Connor, Anthony MD, MRCPI*,†; Packey, Christopher D. MD, PhD*; Akbari, Mona MD, MPH*; Moss, Alan C. MD, FACG, AGAF, FRCPI*

doi: 10.1097/MIB.0000000000000540
Original Clinical Articles

Background: In some studies, 5-aminosalicylates as a class have been associated with protective effects against colorectal cancer in inflammatory bowel disease. In practice, only mesalamine at doses greater than 1.2 g per day is currently widely in this setting. The specific impact of mesalamine at these doses has not has not previously been determined.

Methods: We performed a systematic review and meta-analysis of the effect of mesalamine on risk of colorectal neoplasia (CRN) from prior cohort and case–control studies. Sensitivity analyses for study setting and case definition were performed. A quality assessment was made of all included studies.

Results: Mesalamine was associated with a modest reduction in the odds ratio (OR) of CRN (OR = 0.6, 95% confidence interval, 0.4–0.9, P = 0.04). This effect was only noted in hospital-based studies and only in the reduction of all CRN (not cancers alone). Patients prescribed doses >1.2 g per day had a lower risk of CRN (OR = 0.5, 95% confidence interval, 0.3–0.9, P = 0.02) than lower doses. This effect was also only present in the hospital-based studies. In contrast, there was no reduction in the risk of CRN in patients prescribed sulfasalazine (OR = 0.8, 95% confidence interval, 0.5–1.2, P = 0.3), regardless of study setting.

Conclusions: Mesalamine, particularly at doses >1.2 g per day, produces a modest reduction in the risk of CRN in inflammatory bowel disease patient populations from referral centers. Sulfasalazine does not seem to reduce the risk. No benefit was noted in population-based studies.

Article first published online 20 August 2015.Supplemental Digital Content is Available in the Text.

*Center for Inflammatory Bowel Diseases, Beth Israel Deaconess Medical Center, Boston, Massachusetts; and

Leeds Gastroenterology Institute, St James's University Hospital, Leeds, United Kingdom.

Reprints: Alan C. Moss, MD, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215 (e-mail:

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (

Alan C. Moss is the principal investigator on grants from Salix and Shire (to BIDMC) for unrelated projects.

The authors have no conflict of interest to disclose.

Received June 5, 2015

Accepted June 17, 2015

© Crohn's & Colitis Foundation of America, Inc.
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