Author Affiliations: Department of Medicine, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, Ill (Dr Pasche). Dr Pasche is a Contributing Editor, JAMA. Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative, and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass (Dr Serhan).
Colorectal cancer is a leading cause of cancer-related morbidity and
mortality in the Western world. A personal history of inflammatory bowel disease
(IBD) is a well-established risk factor for colorectal cancer. Recent data
suggest that the risk of colorectal cancer for individuals with IBD increases
by 0.5% to 1.0% yearly, 8 to 10 years after diagnosis.1 The
magnitude of colorectal cancer risk increases with early age at IBD diagnosis,
longer duration of symptoms, and extent of the disease.1 In
addition, a wealth of experimental, epidemiological, and randomized trial
evidence suggests that long-term use of aspirin and other nonsteroidal anti-inflammatory
drugs (NSAIDs) can reduce the risk of colorectal adenoma and cancer.2- 4 In both instances, the
duration of either the inflammatory process or the use of anti-inflammatory
agents is emerging as a key predictor of increased and decreased colorectal
cancer risk, respectively.
Pasche B, Serhan CN. Is C-Reactive Protein an Inflammation Opsonin That Signals Colon Cancer Risk?. JAMA. 2004;291(5):623-624. doi:10.1001/jama.291.5.623