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Sustained influence of infections on prostate-specific antigen concentration: An analysis of changes over 10 years of follow-up

  • Marvin E. Langston
  • , Ratna Pakpahan
  • , Remington L. Nevin
  • , Angelo M. De Marzo
  • , Debra J. Elliott
  • , Charlotte A. Gaydos
  • , William B. Isaacs
  • , William G. Nelson
  • , Lori J. Sokoll
  • , Jonathan M. Zenilman
  • , Elizabeth A. Platz
  • , Siobhan Sutcliffe

Research output: Contribution to journalArticlepeer-review

Abstract

Background: To extend our previous observation of a short-term rise in prostate-specific antigen (PSA) concentration, a marker of prostate inflammation and cell damage, during and immediately following sexually transmitted and systemic infections, we examined the longer-term influence of these infections, both individually and cumulatively, on PSA over a mean of 10 years of follow-up in young active duty U.S. servicemen. Methods: We measured PSA in serum specimens collected in 1995-7 (baseline) and 2004-6 (follow-up) from 265 men diagnosed with chlamydia (CT), 72 with gonorrhea (GC), 37 with non-chlamydial, non-gonococcal urethritis (NCNGU), 58 with infectious mononucleosis (IM), 91 with other systemic or non-genitourinary infections such as varicella; and 125-258 men with no infectious disease diagnoses in their medical record during follow-up (controls). We examined the influence of these infections on PSA change between baseline and follow-up. Results: The proportion of men with any increase in PSA (>0 ng/mL) over the 10-year average follow-up was significantly higher in men with histories of sexually transmitted infections (CT, GC, and NCNGU; 67.7% vs 60.8%, P = 0.043), systemic infections (66.7% vs 54.4%, P = 0.047), or any infections (all cases combined; 68.5% vs 54.4%, P = 0.003) in their military medical record compared to controls. Conclusions: While PSA has been previously shown to rise during acute infection, these findings demonstrate that PSA remains elevated over a longer period. Additionally, the overall infection burden, rather than solely genitourinary-specific infection burden, contributed to these long-term changes, possibly implying a role for the cumulative burden of infections in prostate cancer risk.

Original languageEnglish
Pages (from-to)1024-1034
Number of pages11
JournalProstate
Volume78
Issue number13
DOIs
StatePublished - Sep 15 2018

Keywords

  • epidemiology
  • infectious mononucleosis
  • prostate cancer
  • sexually transmitted infection

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