Melissa Milbrandt1, Anke C Winter1,2, Remington L Nevin3, Ratna Pakpahan1, Gary Bradwin4, Angelo M De Marzo5,6,7, Debra J Elliott5, Charlotte A Gaydos8, William B Isaacs6,7, William G Nelson5,6,7,9, Nader Rifai4, Lori J Sokoll5,6,7, Jonathan M Zenilman8, Elizabeth A Platz6,7,10, Siobhan Sutcliffe1,2. 1. Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri. 2. Alvin J. Siteman Cancer Center, Washington University School of Medicine, St. Louis, Missouri. 3. Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. 4. Department of Laboratory Medicine, Harvard Medical School and Children's Hospital, Boston, Massachusetts. 5. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland. 6. Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland. 7. Department of Urology and the James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland. 8. Division of Infectious Diseases, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland. 9. Department of Pharmacology, Johns Hopkins University School of Medicine, Baltimore, Maryland. 10. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
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.
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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Authors: Siobhan Sutcliffe; Jonathan M Zenilman; Khalil G Ghanem; Rosemary A Jadack; Lori J Sokoll; Debra J Elliott; William G Nelson; Angelo M De Marzo; Stephen R Cole; William B Isaacs; Elizabeth A Platz Journal: J Urol Date: 2006-05 Impact factor: 7.450
Authors: Siobhan Sutcliffe; Remington L Nevin; Ratna Pakpahan; Debra J Elliott; Marvin E Langston; Angelo M De Marzo; Charlotte A Gaydos; William B Isaacs; William G Nelson; Lori J Sokoll; Patrick C Walsh; Jonathan M Zenilman; Steven B Cersovsky; Elizabeth A Platz Journal: Int J Cancer Date: 2016-01-21 Impact factor: 7.396
Authors: J Bergh; I Marklund; C Gustavsson; F Wiklund; H Grönberg; A Allard; O Alexeyev; F Elgh Journal: Br J Cancer Date: 2006-11-21 Impact factor: 7.640
Authors: 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 Journal: Prostate Date: 2018-05-30 Impact factor: 4.104