4.3 Article

The association between circulating high-sensitivity C-reactive protein concentration and pathologic measures of colonic inflammation

期刊

CANCER CAUSES & CONTROL
卷 25, 期 4, 页码 409-418

出版社

SPRINGER
DOI: 10.1007/s10552-014-0343-0

关键词

C-reactive protein; Inflammation; Colorectal cancer; Obesity

资金

  1. Seraph Foundation
  2. Frederik B. Bang Award for Student Research in Pathobiology, Johns Hopkins Bloomberg School of Public Health
  3. Maryland Cigarette Restitution Fund at Johns Hopkins
  4. National Cancer Institute [T32 CA009314]

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C-reactive protein (CRP), an inflammation marker, is associated with colorectal cancer (CRC) risk in some prospective studies. Whether increased CRP is indicative of colonic inflammation, a possible CRC cause, or of other sources of inflammation (e.g., adiposity), is unknown. Thus, we evaluated the association between CRP and colonic mucosal measures of inflammation. 151 adults undergoing colonoscopy provided a blood sample and random left- and right-side colonic mucosal biopsies. Height and weight were measured, and lifestyle information was collected. High-sensitivity C-reactive protein (hsCRP) was measured by immunoturbidometric assay. A gastrointestinal pathologist evaluated biopsies for seven colonic inflammation measures. Of 119 participants with complete information, 24 had an inflammatory bowel disease (IBD) history and were analyzed separately. We calculated the number of colonic inflammation measures present in both biopsies, and separately for right and left biopsies. Adjusted geometric mean hsCRP was calculated using linear regression, overall, by demographic and lifestyle factors, and inflammation measures. Most participants had a parts per thousand yen1 colonic inflammation measure (0: 21 %, 1: 39 %, a parts per thousand yen2: 40 %). Adjusted mean hsCRP did not increase with increasing number of inflammation measures (0: 1.67; 1: 1.33; a parts per thousand yen2: 1.01 mg/L; p trend = 0.21). Obese (2.03 mg/L) and overweight (1.61 mg/L) participants had higher adjusted mean hsCRP than normal-weight participants (0.62 mg/L; p trend < 0.0001). Patterns were similar for participants with a history of IBD. hsCRP concentration was not associated with colonic inflammation, although hsCRP increased with adiposity. The hsCRP-CRC association may be explained by residual confounding by other risk factors, such as adiposity, rather than by CRP marking colonic inflammation.

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