We read with interest the article from Drs. Stancik and coworkers on the effects of NIH-IV prostatitis on total PSA, free PSA and free-to-total PSA ratio [1]. Of the 1090 men who underwent prostatic biopsy in their unit, complete biochemical and histological records were available for 404 men of whom 161 (39.8%) with no history of clinical symptoms of prostatitis, were diagnosed as having chronic inflammatory cell infiltrates and of those, 137 with no detectable prostate cancer were included in the study cohort. The presence of inflammatory cell infiltrates in a subpopulation of men with raised PSA and undetectable prostate cancer represents an extremely common histologic finding that can be overestimated by the high incidence of repeated biopsy in some series [2], [3], and [4]. In this respect the authors failed to mention how many of the 404 biopsies evaluated were redo biopsy, this being possibly the cause of prostatitis but at the same time being unrelated to the elevated PSA level that guided the first biopsy. It is well known that acute bacterial prostatitis causes a remarkable elevation of serum PSA but a clear relationship between raise in total and free PSA levels and asymptomatic prostatic inflammation detected either by the evaluation of prostatic secretions or during histological review of prostate biopsies is yet to be clearly demonstrated and seems far from an unanimous consensus. Nearly all the papers published on the relationship between serum PSA and asymptomatic prostatic inflammation (NIH category IV prostatitis) in a subpopulation of men with raised PSA and undetectable prostate cancer have concluded that, prostate volume measured by ultrasound is the most evident determinant of the PSA level [2], [3], [4], and [5]. Unfortunately in the series by Stancik and coworkers the prostatic volume was not reported. Moreover, to test the influence of NIH category IV prostatitis on free and total PSA it would have been interesting to assess the extent and the severity of the inflammatory changes [4] and [6]. In a recently published paper by Kwak and coworkers, while patients with PSA level greater than 2.5 ng/ml were found to have greater inflammation extent and aggressiveness than those with 2.5 ng/ml or less; no statistically significant difference was found using the 4 ng/ml threshold [4], this results indicating that subclinical prostatic inflammation may contribute to a slight elevation of serum PSA that usually stay under 4.0 ng/ml. Accordingly, Carver et al. showed that in a screening population, men with evidence of NIH-IV prostatitis had a mean serum PSA of 2.3 ng/ml that was significantly higher than 1.4 ng/ml reported in men with normal prostatic secretions [7]. Indeed, the evaluation of prostate volume and inflammation extent/aggressiveness as well as the exclusion of repeated biopsy from the reviews seem essential to provide balanced and unbiased data on the possible role of t-PSA, f-PSA and f/t PSA in differentiating prostate cancer and NIH-IV prostatitis. Further studies are needed to clarify the real relationship between inflammatory cell in needle biopsy specimen and total, free PSA and the free-to-total PSA ratio nevertheless we do agree with the authors that, at the state of our knowledge, there is no clinical utility in looking at the prostatic inflammation and at the fPSA/tPSA ratio in patients with negative biopsy findings, especially with regards to whether or not to perform subsequent repeated biopsy.

Re: Stancik I, Luftenegger W, Klimpfinger M, Muller MM, Hoeltl W. Effect of NIH-IV prostatitis on free and free-to-total PSA. Eur Urol 2004;46:760-4 / Minervini A;Serni S;Masieri L;Carini M. - In: EUROPEAN UROLOGY. - ISSN 0302-2838. - STAMPA. - 47:(2005), pp. 720-722. [10.1016/j.eururo.2004.12.012]

Re: Stancik I, Luftenegger W, Klimpfinger M, Muller MM, Hoeltl W. Effect of NIH-IV prostatitis on free and free-to-total PSA. Eur Urol 2004;46:760-4.

MINERVINI, ANDREA;SERNI, SERGIO;MASIERI, LORENZO;CARINI, MARCO
2005

Abstract

We read with interest the article from Drs. Stancik and coworkers on the effects of NIH-IV prostatitis on total PSA, free PSA and free-to-total PSA ratio [1]. Of the 1090 men who underwent prostatic biopsy in their unit, complete biochemical and histological records were available for 404 men of whom 161 (39.8%) with no history of clinical symptoms of prostatitis, were diagnosed as having chronic inflammatory cell infiltrates and of those, 137 with no detectable prostate cancer were included in the study cohort. The presence of inflammatory cell infiltrates in a subpopulation of men with raised PSA and undetectable prostate cancer represents an extremely common histologic finding that can be overestimated by the high incidence of repeated biopsy in some series [2], [3], and [4]. In this respect the authors failed to mention how many of the 404 biopsies evaluated were redo biopsy, this being possibly the cause of prostatitis but at the same time being unrelated to the elevated PSA level that guided the first biopsy. It is well known that acute bacterial prostatitis causes a remarkable elevation of serum PSA but a clear relationship between raise in total and free PSA levels and asymptomatic prostatic inflammation detected either by the evaluation of prostatic secretions or during histological review of prostate biopsies is yet to be clearly demonstrated and seems far from an unanimous consensus. Nearly all the papers published on the relationship between serum PSA and asymptomatic prostatic inflammation (NIH category IV prostatitis) in a subpopulation of men with raised PSA and undetectable prostate cancer have concluded that, prostate volume measured by ultrasound is the most evident determinant of the PSA level [2], [3], [4], and [5]. Unfortunately in the series by Stancik and coworkers the prostatic volume was not reported. Moreover, to test the influence of NIH category IV prostatitis on free and total PSA it would have been interesting to assess the extent and the severity of the inflammatory changes [4] and [6]. In a recently published paper by Kwak and coworkers, while patients with PSA level greater than 2.5 ng/ml were found to have greater inflammation extent and aggressiveness than those with 2.5 ng/ml or less; no statistically significant difference was found using the 4 ng/ml threshold [4], this results indicating that subclinical prostatic inflammation may contribute to a slight elevation of serum PSA that usually stay under 4.0 ng/ml. Accordingly, Carver et al. showed that in a screening population, men with evidence of NIH-IV prostatitis had a mean serum PSA of 2.3 ng/ml that was significantly higher than 1.4 ng/ml reported in men with normal prostatic secretions [7]. Indeed, the evaluation of prostate volume and inflammation extent/aggressiveness as well as the exclusion of repeated biopsy from the reviews seem essential to provide balanced and unbiased data on the possible role of t-PSA, f-PSA and f/t PSA in differentiating prostate cancer and NIH-IV prostatitis. Further studies are needed to clarify the real relationship between inflammatory cell in needle biopsy specimen and total, free PSA and the free-to-total PSA ratio nevertheless we do agree with the authors that, at the state of our knowledge, there is no clinical utility in looking at the prostatic inflammation and at the fPSA/tPSA ratio in patients with negative biopsy findings, especially with regards to whether or not to perform subsequent repeated biopsy.
2005
47
720
722
Minervini A;Serni S;Masieri L;Carini M
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Utilizza questo identificatore per citare o creare un link a questa risorsa: https://hdl.handle.net/2158/687331
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