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

• Published in: The Prostate 2018-09, Vol.78 (13), p.1024-1034
• Main Authors: Langston, Marvin E., Pakpahan, Ratna, Nevin, Remington L., De Marzo, Angelo M., Elliott, Debra J., Gaydos, Charlotte A., Isaacs, William B., Nelson, William G., Sokoll, Lori J., Zenilman, Jonathan M., Platz, Elizabeth A., Sutcliffe, Siobhan
• Format: Article
• Language: English
• Subjects: Aged; Antigens; Chlamydia Infections - blood; epidemiology; Follow-Up Studies; Gonorrhea; Gonorrhea - blood; Humans; Infections; Infectious diseases; Infectious mononucleosis; Male; Medical records; Mononucleosis; Non-specific urethritis; Prostate cancer; Prostate-Specific Antigen - blood; sexually transmitted infection; Urethritis; Urethritis - blood; Varicella; Young Adult
• ISSN: 0270-4137; 1097-0045
• DOI: 10.1002/pros.23660

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.