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

Melissa Milbrandt, Anke C. Winter, Remington L. Nevin, Ratna Pakpahan, Gary Bradwin, Angelo Michael Demarzo, Debra J. Elliott, Charlotte A Gaydos, William B Isaacs, William G Nelson, Nader Rifai, Lori J Sokoll, Jonathan Mark Zenilman, Elizabeth A Platz, Siobhan Sutcliffe

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)1325-1334
Number of pages10
JournalProstate
Volume77
Issue number13
DOIs
StatePublished - Sep 15 2017

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Prostate-Specific Antigen
C-Reactive Protein
Gonorrhea
Prostate
Infectious Mononucleosis
Infection
Inflammation
Urethritis
Chlamydia Infections
Infection Control
Sexually Transmitted Diseases
Serum
Early Detection of Cancer
Case-Control Studies
Prostatic Neoplasms
Observation
Pathology

Keywords

  • C-reactive protein
  • infection
  • infectious mononucleosis
  • prostate cancer
  • prostate-specific antigen
  • sexually transmitted infection

ASJC Scopus subject areas

  • Oncology
  • Urology

Cite this

Insight into infection-mediated prostate damage : Contrasting patterns of C-reactive protein and prostate-specific antigen levels during infection. / Milbrandt, Melissa; Winter, Anke C.; Nevin, Remington L.; Pakpahan, Ratna; Bradwin, Gary; Demarzo, Angelo Michael; Elliott, Debra J.; Gaydos, Charlotte A; Isaacs, William B; Nelson, William G; Rifai, Nader; Sokoll, Lori J; Zenilman, Jonathan Mark; Platz, Elizabeth A; Sutcliffe, Siobhan.

In: Prostate, Vol. 77, No. 13, 15.09.2017, p. 1325-1334.

Research output: Contribution to journalArticle

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title = "Insight into infection-mediated prostate damage: Contrasting patterns of C-reactive protein and prostate-specific antigen levels during infection",
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.",
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author = "Melissa Milbrandt and Winter, {Anke C.} and Nevin, {Remington L.} and Ratna Pakpahan and Gary Bradwin and Demarzo, {Angelo Michael} and Elliott, {Debra J.} and Gaydos, {Charlotte A} and Isaacs, {William B} and Nelson, {William G} and Nader Rifai and Sokoll, {Lori J} and Zenilman, {Jonathan Mark} and Platz, {Elizabeth A} and Siobhan Sutcliffe",
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T1 - Insight into infection-mediated prostate damage

T2 - Contrasting patterns of C-reactive protein and prostate-specific antigen levels during infection

AU - Milbrandt, Melissa

AU - Winter, Anke C.

AU - Nevin, Remington L.

AU - Pakpahan, Ratna

AU - Bradwin, Gary

AU - Demarzo, Angelo Michael

AU - Elliott, Debra J.

AU - Gaydos, Charlotte A

AU - Isaacs, William B

AU - Nelson, William G

AU - Rifai, Nader

AU - Sokoll, Lori J

AU - Zenilman, Jonathan Mark

AU - Platz, Elizabeth A

AU - Sutcliffe, Siobhan

PY - 2017/9/15

Y1 - 2017/9/15

N2 - 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.

AB - 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.

KW - C-reactive protein

KW - infection

KW - infectious mononucleosis

KW - prostate cancer

KW - prostate-specific antigen

KW - sexually transmitted infection

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