Ashwin N Ananthakrishnan1, Andrew Cagan2, Tianxi Cai3, Vivian S Gainer2, Stanley Y Shaw4, Susanne Churchill5, Elizabeth W Karlson6, Shawn N Murphy7, Katherine P Liao6, Isaac Kohane8. 1. Division of Gastroenterology, Massachusetts General Hospital, Boston, Massachusetts; Harvard Medical School, Boston, Massachusetts; Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts. Electronic address: aananthakrishnan@mgh.harvard.edu. 2. Research Information Services and Computing, Partners HealthCare, Charlestown, Massachusetts. 3. Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. 4. Harvard Medical School, Boston, Massachusetts; Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts; Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts. 5. Department of Biomedical Informatics, Harvard Medical School, Boston, Massachusetts. 6. Harvard Medical School, Boston, Massachusetts; Division of Rheumatology, Allergy and Immunology, Brigham and Women's Hospital, Boston, Massachusetts. 7. Harvard Medical School, Boston, Massachusetts; Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts. 8. Harvard Medical School, Boston, Massachusetts; Department of Biomedical Informatics, Harvard Medical School, Boston, Massachusetts; Children's Hospital Boston, Boston, Massachusetts.
Abstract
BACKGROUND & AIMS: Inflammatory bowel diseases (IBDs) such as Crohn's disease and ulcerative colitis are associated with an increased risk of colorectal cancer (CRC). Chemopreventive strategies have produced weak or inconsistent results. Statins have been associated inversely with sporadic CRC. We examined their role as chemopreventive agents in patients with IBD. METHODS: We collected data from 11,001 patients with IBD receiving care at hospitals in the Greater Boston metropolitan area from 1998 through 2010. Diagnoses of CRC were determined using validated International Classification of Diseases, 9th revision, Clinical Modification codes. Statin use before diagnosis was assessed through analysis of electronic prescriptions. We performed multivariate logistic regression analyses, adjusting for potential confounders including primary sclerosing cholangitis, smoking, increased levels of inflammation markers, and CRC screening practices to identify an independent association between statin use and CRC. We performed sensitivity analyses using propensity score adjustment and variation in the definition of statin use. RESULTS: In our cohort, 1376 of the patients (12.5%) received 1 or more prescriptions for a statin. Patients using statins were more likely to be older, male, white, smokers, and have greater comorbidity than nonusers. Over a follow-up period of 9 years, 2% of statin users developed CRC compared with 3% of nonusers (age-adjusted odds ratio, 0.35; 95% confidence interval, 0.24-0.53). On multivariate analysis, statin use remained independently and inversely associated with CRC (odds ratio, 0.42; 95% confidence interval, 0.28-0.62). Our findings were robust on a variety of sensitivity and subgroup analyses. CONCLUSIONS: Statin use was associated inversely with the risk of CRC in a large IBD cohort. Prospective studies on the role of statins as chemopreventive agents are warranted.
BACKGROUND & AIMS:Inflammatory bowel diseases (IBDs) such as Crohn's disease and ulcerative colitis are associated with an increased risk of colorectal cancer (CRC). Chemopreventive strategies have produced weak or inconsistent results. Statins have been associated inversely with sporadic CRC. We examined their role as chemopreventive agents in patients with IBD. METHODS: We collected data from 11,001 patients with IBD receiving care at hospitals in the Greater Boston metropolitan area from 1998 through 2010. Diagnoses of CRC were determined using validated International Classification of Diseases, 9th revision, Clinical Modification codes. Statin use before diagnosis was assessed through analysis of electronic prescriptions. We performed multivariate logistic regression analyses, adjusting for potential confounders including primary sclerosing cholangitis, smoking, increased levels of inflammation markers, and CRC screening practices to identify an independent association between statin use and CRC. We performed sensitivity analyses using propensity score adjustment and variation in the definition of statin use. RESULTS: In our cohort, 1376 of the patients (12.5%) received 1 or more prescriptions for a statin. Patients using statins were more likely to be older, male, white, smokers, and have greater comorbidity than nonusers. Over a follow-up period of 9 years, 2% of statin users developed CRC compared with 3% of nonusers (age-adjusted odds ratio, 0.35; 95% confidence interval, 0.24-0.53). On multivariate analysis, statin use remained independently and inversely associated with CRC (odds ratio, 0.42; 95% confidence interval, 0.28-0.62). Our findings were robust on a variety of sensitivity and subgroup analyses. CONCLUSIONS: Statin use was associated inversely with the risk of CRC in a large IBD cohort. Prospective studies on the role of statins as chemopreventive agents are warranted.
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