Rapid Changes in Urinary Symptoms Linked to CRP
Jennifer L. St. Sauver, PhD, of Mayo Clinic in Rochester, Minn., and colleagues analyzed data from a population-based cohort of 2,115 men in Olmsted County, Minnesota.
The researchers examined the association between levels of C-reactive protein (CRP)—a nonspecific marker of systemic inflammation—and rapid increases in irritative LUTS, prostate volume, and PSA levels and rapid decreases in peak urinary flow rate.
Investigators assessed CRP measurements using serum samples provided by men in 1996. Four rounds of biennial follow-up encounters were subsequently completed. A previously validated questionnaire analogous to the American Urological Association symptom index was used to evaluate LUTS. Researchers used a urometer to measure peak urinary flow rates and transrectal ultrasonography to measure total prostate volume.
After adjustments for age, BMI, hypertension, and smoking history, men with CRP levels of 3 mg/L or higher were twice as likely as men with lower CRP levels to have rapid increases in LUTS and rapid decreases in peak flow rate, according to data published in the American Journal of Epidemiology (2009;169:1281-1290).
The associations between CRP levels and rapid changes in irritative LUTS and peak urinary flow rates strengthened as CRP levels increased.
Elevated CRP levels were not associated with rapid increases in prostate volume, obstructive LUTS, or PSA levels.
“While elevated CRP levels are currently used primarily as a marker for risk of heart disease, our data suggest that elevated levels may also indicate when a man is at increased risk of rapidly worsening urinary symptoms,” the authors concluded.
The absence of a significant association between CRP levels and rapid increases in prostatic growth and obstructive LUTS, the authors pointed out, “do not discount the possibility that inflammatory processes in the prostate are associated with prostatic growth; however, they do suggest that rapid growth in the prostate is not necessarily reflected in systemic levels of CRP.”
In an accompanying commentary (pp.1291-1293), Stephen J. Freedland, MD, of Duke University Medical Center in Durham, N.C., and William J. Aronson, MD, of the University of California in Los Angeles, observed: “Given that clinical trials of anti-inflammatory drugs for LUTS have been largely unsuccessful, the role of inflammation as a contributor to LUTS remains an interesting hypothesis that requires further study.”