TY - JOUR
T1 - Sustained influence of infections on prostate-specific antigen concentration
T2 - An analysis of changes over 10 years of follow-up
AU - Langston, Marvin E.
AU - Pakpahan, Ratna
AU - Nevin, Remington L.
AU - De Marzo, Angelo M.
AU - Elliott, Debra J.
AU - Gaydos, Charlotte A.
AU - Isaacs, William B.
AU - Nelson, William G.
AU - Sokoll, Lori J.
AU - Zenilman, Jonathan M.
AU - Platz, Elizabeth A.
AU - Sutcliffe, Siobhan
N1 - Funding Information:
Fund for Research and Progress in Urology; Johns Hopkins University School of Medicine; Barnes-Jewish Hospital Foundation; Alvin J. Siteman Cancer Center; National Cancer Institute of the National Institutes of Health, Grant numbers: T32CA190194, P30CA006973; Patrick C. Walsh Prostate Cancer Research Fund
Funding Information:
We thank Dr Angelia A. Eick-Cost and Zheng Hu at the Armed Forces Health Surveillance Center for help with participant selection, and Dr Catherine G. Sutcliffe for help preparing serum specimens for testing and coordinating PSA testing. Effort for the authors was funded by the Fund for Research and Progress in Urology, Johns Hopkins University School of Medicine (SS), the Barnes-Jewish Hospital Foundation and Alvin J. Siteman Cancer Center (MEL, RP, SS), and the National Cancer Institute of the National Institutes of Health under award numbers T32CA190194 (MEL) and P30CA006973 (AMD, WBI, WGN, EAP). This work was funded by the Patrick C. Walsh Prostate Cancer Research Fund. The content of this work is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
Publisher Copyright:
© 2018 Wiley Periodicals, Inc.
PY - 2018/9/15
Y1 - 2018/9/15
N2 - 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.
AB - 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.
KW - epidemiology
KW - infectious mononucleosis
KW - prostate cancer
KW - sexually transmitted infection
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U2 - 10.1002/pros.23660
DO - 10.1002/pros.23660
M3 - Article
C2 - 30133756
AN - SCOPUS:85047832431
SN - 0270-4137
VL - 78
SP - 1024
EP - 1034
JO - Prostate
JF - Prostate
IS - 13
ER -