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Insight into infection-mediated prostate damage: Contrasting patterns of C-reactive protein and prostate-specific antigen levels during infection

TitleInsight into infection-mediated prostate damage: Contrasting patterns of C-reactive protein and prostate-specific antigen levels during infection
Publication TypeJournal Article
Year of Publication2017
AuthorsMilbrandt, M, Winter, AC, Nevin, RL, Pakpahan, R, Bradwin, G, De Marzo, AM, Elliott, DJ, Gaydos, CA, Isaacs, WB, Nelson, WG, Rifai, N, Sokoll, LJ, Zenilman, JM, Platz, EA, Sutcliffe, S
JournalProstate
Volume77
Pagination1325-1334
Date PublishedMay
ISBN Number0270-4137
Accession Number28703328
Keywords*Prostatitis/blood/diagnosis/etiology, Adult, C-Reactive Protein, C-Reactive Protein/*analysis, Chlamydia Infections/*blood, Gonorrhea/*blood, Humans, infection, infectious mononucleosis, Infectious Mononucleosis/*blood, Male, Middle Aged, prostate cancer, Prostate-specific antigen, Prostate-Specific Antigen/*analysis, sexually transmitted infection, Statistics as Topic, Urethritis/*blood/diagnosis/etiology
Abstract

BACKGROUND: To 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. METHODS: We 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. RESULTS: Only gonorrhea cases were significantly more likely to have a large hsCRP rise (>/=1.40 mg/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). CONCLUSIONS: These 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.

PMCID

PMC5578879