Abstract
Epidemiologic studies have identified a positive association between obesity and colorectal neoplasia. Adiposity induces systemic low-grade inflammation, which is commonly assessed with a sensitive biomarker, C-reactive protein (CRP). To understand the molecular mechanisms of obesity in the etiology of colorectal neoplasia, the present study was conducted in 782 adenoma cases and 738 controls who underwent total colonoscopy, and their plasma CRP level was evaluated in relation to colorectal adenoma prevalence. A logistic regression model was used to compute odds ratios (OR) and 95% confidence intervals (CI) of adenoma according to quartile of plasma CRP. Plasma CRP level was positively associated with higher adenoma prevalence in all subjects (OR 1.30; 95% CI 0.94–1.79 for the highest versus lowest quartile; P trend = 0.031). Further analysis by adenoma size and number revealed a pronounced association with a larger size (≥5 mm) and multiple numbers (≥2). These positive associations were reduced to non-significance following further adjustment for body mass index, and OR for the highest versus lowest quartile of plasma CRP became 1.12 (95% CI 0.80–1.56; P trend = 0.25) in all subjects. In conclusion, this study suggests that obesity-related systemic low-grade inflammation may play an important role in the early stages of colorectal carcinogenesis.
Highlights
Overweight and obesity are consistently associated with an increased risk of colorectal cancer and adenoma[1,2,3,4]
We observed a positive association between plasma C-reactive protein (CRP) concentration and the prevalence of colorectal adenoma
Given that CRP is a preferable biomarker of systemic inflammation and that a highly sensitive method can evaluate low-grade inflammation, our present finding of a positive association between higher CRP levels and an increased prevalence of adenoma supports the hypothesis that the development/growth of colorectal neoplasia likely involves a systemic, low-grade inflammatory state
Summary
Overweight and obesity are consistently associated with an increased risk of colorectal cancer and adenoma[1,2,3,4]. Previously considered to be a passive storage organ, is known to secrete a variety of inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6)[7,8,9]. Excessive secretion of these cytokines from hypertrophic adipocytes following obesity is postulated to induce and maintain a systemic, low-grade inflammatory state, which may contribute to the initiation and progression of carcinogenesis[7,8,9]. We quantified plasma concentrations of CRP using a highly sensitive method which enables the assessment of even low-grade inflammation, and evaluated the association between CRP level and the prevalence of colorectal adenoma
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