Journal
PROSTATE
Volume 77, Issue 13, Pages 1325-1334Publisher
WILEY
DOI: 10.1002/pros.23392
Keywords
C-reactive protein; infection; infectious mononucleosis; prostate cancer; prostate-specific antigen; sexually transmitted infection
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Funding
- NCI [P30 CA006973]
- Fund for Research and Progress in Urology, Johns Hopkins University School of Medicine
- Barnes-Jewish Hospital Foundation
- Alvin J. Siteman Cancer Center
- Patrick C. Walsh Prostate Cancer Research Fund
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BackgroundTo investigate mechanisms underlying our previous observation of a large rise in serum prostate-specific antigen, a marker of prostate pathology, during both sexually transmitted and systemic infections, we measured serum high-sensitivity C-reactive protein (hsCRP), a marker of systemic inflammation, in our previous case-control study of young, male US military members and compared our findings to those for PSA. MethodsWe measured hsCRP before and during infection for 299 chlamydia, 112 gonorrhea, and 59 non-chlamydial, non-gonococcal urethritis (NCNGU) cases; before and after infection for 55 infectious mononucleosis (IM) and 90 other systemic/non-genitourinary cases; and for 220-256 controls. ResultsOnly gonorrhea cases were significantly more likely to have a large hsCRP rise (1.40mg/L or 239%) during infection than controls (P<0.01). However, gonorrhea, IM, and other systemic/non-genitourinary cases were more likely to have a rise of any magnitude up to one year post-diagnosis than controls (p=0.038-0.077). ConclusionsThese findings, which differ from those for PSA, suggest distinct mechanisms of elevation for hsCRP and PSA, and support both direct (eg, prostate infection) and indirect (eg, systemic inflammation-mediated prostate cell damage) mechanisms for PSA elevation. Future studies should explore our PSA findings further for their relevance to both prostate cancer screening and risk.
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