PURPOSE: Although inflammation and cell damage due to STIs are hypothesized to contribute to the later development of prostate disease, few clinical studies have been done to investigate the extent to which sexually transmitted agents infect and induce an inflammatory immune response in the prostate. We indirectly investigated this question by measuring serum PSA, a possible marker of prostatic inflammation and cell damage, in men with documented STIs. MATERIALS AND METHODS: Archived serum specimens from young men with laboratory confirmed exudative STIs, including gonorrhea, chlamydia and trichomonosis, and young men with no STI diagnoses were identified in 2 prospective studies of patients at Baltimore City STI clinics, that is 84 in the STI Transmission and Acquisition Study, and 61 in the Mucosal Immunity Study. Serum specimens from visits before, during and after STI diagnoses in men with at least 1 exudative STI diagnosis and from all visits in men with no STI diagnoses were tested for total PSA concentration. RESULTS: After combining the studies patients with STIs were more likely to have a 40% or greater increase in PSA than patients with no STI diagnoses (32% vs 2%, p <0.01). CONCLUSIONS: These findings suggest that STIs may contribute to prostatic inflammation and cell damage in a subset of infected men. Further studies are warranted to replicate study findings and determine host and infection characteristics associated with large PSA increases.
PURPOSE: Although inflammation and cell damage due to STIs are hypothesized to contribute to the later development of prostate disease, few clinical studies have been done to investigate the extent to which sexually transmitted agents infect and induce an inflammatory immune response in the prostate. We indirectly investigated this question by measuring serum PSA, a possible marker of prostatic inflammation and cell damage, in men with documented STIs. MATERIALS AND METHODS: Archived serum specimens from young men with laboratory confirmed exudative STIs, including gonorrhea, chlamydia and trichomonosis, and young men with no STI diagnoses were identified in 2 prospective studies of patients at Baltimore City STI clinics, that is 84 in the STI Transmission and Acquisition Study, and 61 in the Mucosal Immunity Study. Serum specimens from visits before, during and after STI diagnoses in men with at least 1 exudative STI diagnosis and from all visits in men with no STI diagnoses were tested for total PSA concentration. RESULTS: After combining the studies patients with STIs were more likely to have a 40% or greater increase in PSA than patients with no STI diagnoses (32% vs 2%, p <0.01). CONCLUSIONS: These findings suggest that STIs may contribute to prostatic inflammation and cell damage in a subset of infected men. Further studies are warranted to replicate study findings and determine host and infection characteristics associated with large PSA increases.
Authors: Melissa Milbrandt; Anke C Winter; Remington L Nevin; Ratna Pakpahan; Gary Bradwin; Angelo M De Marzo; Debra J Elliott; Charlotte A Gaydos; William B Isaacs; William G Nelson; Nader Rifai; Lori J Sokoll; Jonathan M Zenilman; Elizabeth A Platz; Siobhan Sutcliffe Journal: Prostate Date: 2017-07-12 Impact factor: 4.104
Authors: Siobhan Sutcliffe; Cathee Till; Charlotte A Gaydos; Frank J Jenkins; Phyllis J Goodman; Ashraful M Hoque; Ann W Hsing; Ian M Thompson; Jonathan M Zenilman; William G Nelson; Angelo M De Marzo; Elizabeth A Platz Journal: Cancer Causes Control Date: 2012-07-19 Impact factor: 2.506
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