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Int J Cancer. 2016 May 1;138(9):2221-30. doi: 10.1002/ijc.29966. Epub 2016 Jan 21.

Infectious mononucleosis, other infections and prostate-specific antigen concentration as a marker of prostate involvement during infection.

Author information

1
Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St. Louis, MO.
2
Alvin J. Siteman Cancer Center, Department of Surgery, Washington University School of Medicine, St. Louis, MO.
3
Department of Mental Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.
4
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD.
5
Division of Epidemiology and Biostatistics, Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, AZ.
6
Department of Urology and the James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD.
7
Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD.
8
Division of Infectious Diseases, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
9
Department of Pharmacology, Johns Hopkins University School of Medicine, Baltimore, MD.
10
U.S. Army Public Health Command (Provisional), Aberdeen Proving Ground, Aberdeen, MD.
11
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.

Abstract

Although Epstein-Barr virus has been detected in prostate tissue, no associations have been observed with prostate cancer in the few studies conducted to date. One possible reason for these null findings may be use of cumulative exposure measures that do not inform the timing of infection, i.e., childhood versus adolescence/early adulthood when infection is more likely to manifest as infectious mononucleosis (IM). We sought to determine the influence of young adult-onset IM on the prostate by measuring prostate-specific antigen (PSA) as a marker of prostate inflammation/damage among U.S. military members. We defined IM cases as men diagnosed with IM from 1998 to 2003 (n = 55) and controls as men without an IM diagnosis (n = 255). We selected two archived serum specimens for each participant, the first collected after diagnosis for cases and one randomly selected from 1998 to 2003 for controls (index), as well as the preceding specimen (preindex). PSA was measured in each specimen. To explore the specificity of our findings for prostate as opposed to systemic inflammation, we performed a post hoc comparison of other infectious disease cases without genitourinary involvement (n = 90) and controls (n = 220). We found that IM cases were more likely to have a large PSA rise than controls (≥ 20 ng/mL: 19.7% versus 8.8%, p = 0.027; ≥ 40% rise: 25.7% versus 9.4%, p = 0.0021), as were other infectious disease cases (25.7% versus 14.0%, p = 0.020; 27.7% versus 18.0%, p = 0.092). These findings suggest that, in addition to rising because of prostate infection, PSA may also rise because of systemic inflammation, which could have implications for PSA interpretation in older men.

KEYWORDS:

epidemiology; infection; infectious mononucleosis; prostate cancer; prostate-specific antigen

PMID:
26678984
DOI:
10.1002/ijc.29966
[Indexed for MEDLINE]
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