Unexpectedly, inflammation markers do not appear to be involved with the chemopreventative effect of aspirin on colorectal adenomas, according to a brief communication published online October 12 in the Journal of the National Cancer Institute.
Aspirin has been shown to prevent the recurrence of colorectal polyps, but it's not clear how it works. One hypothesis is that it may affect the levels of substances, such as C-reactive protein and others, that are markers of inflammation.
To study this, Gloria Y.F. Ho, Ph.D., of the department of Epidemiology & Population Health, at Albert Einstein College of Medicine in Bronx, N.Y., and colleagues examined changes in plasma levels of five inflammation markers--C-reactive protein, interleukin 6, tumor necrosis factor, soluble TNF receptor type II, and IL-1 receptor antagonist--at baseline and at year 3 of 884 subjects. The trial had three aspirin groups (including an aspirin placebo group) and two folic acid groups (including a folate placebo group).
Changes in levels of all five inflammation markers were not associated with adenoma recurrence. For those who did not receive folic acid, C-reactive protein levels in those in the 325 mg/d aspirin group changed very little, whereas it was statistically significantly increased in the placebo group. For subjects who received folic acid, the reverse association was observed.
"Our data suggest that low dose aspirin has modest effects on stabilizing [C-reactive protein], which may be abrogated by a high level of folate," the authors write. "However, such beneficial effects do not appear to confer protection against colorectal neoplasia. Inflammation markers do not mediate the previously observed effects of aspirin and folic acid on colorectal adenomas."
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