Systemic inflammation or low levels of soluble receptors that bind inflammatory cytokines increase the risk of benign prostatic hyperplasia (BPH), according to researchers.

Jeannette M. Schenk, PhD, RD, of the Cancer Prevention Program at Fred Hutchinson Cancer Center in Seattle, and her colleagues analyzed data from the randomized, placebo-controlled Prostate Cancer Prevention Trial, which tested whether finasteride can reduce prostate cancer risk.

The seven-year trial enrolled men who did not have BPH at baseline. Dr. Schenk’s group restricted their analyses to men in the placebo arm of the trial and selected 676 patients in whom BPH developed during the trial and 683 controls who did not. They defined incident BPH as either a report of treatment for or development of significant lower urinary tract symptoms (LUTS).

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After controlling for age, race, and BMI, a high C-reactive protein (CRP) concentration was associated with increased BPH risk. Men in the highest quartile of CRP concentration had a 30% increased risk compared with those in the lowest quartile, according to findings published in the American Journal of Epidemiology (2010; published online ahead of print).

Men in the highest quartile of soluble tumor necrosis factor receptor II (sTNF-RII) concentration had a 39% decreased risk of BPH compared with those in the lowest quartile, after adjusting for age, race, and BMI. Subjects in the highest quartile of interleukin-6 (IL-6) concentration had a 79% increased risk compared with men in the lowest quartile. The associations between sTNF-RII and IL-6 and BPH risk were only in men younger than 65 years, suggesting that the pathogenesis of BPH may differ between younger and older men, the researchers stated.

“This study supports the hypothesis that systemic inflammation plays a role in the development or progression of symptomatic BPH,” the authors concluded.

They pointed out that their findings are supported by multiple lines of evidence implicating inflammation in the development of BPH. They noted, for example, that histologic studies have found acute and/or chronic inflammation in up to 100% of BPH specimens.

Although the prospective design of the PCPT is an important study strength, Dr. Schenk and her group pointed to some limitations. For example, their definition of BPH using LUTS is not specific and cannot distinguish between LUTS related to BPH and LUTS caused by other urologic, neurologic, or bladder conditions.

Nevertheless, the researchers said their results would not be affected substantially by LUTS unrelated to BPH, in part because, by their estimates, the prevalence of other conditions associated with LUTS in the PCPT population would be very low.