{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,1,29]],"date-time":"2025-01-29T05:34:35Z","timestamp":1738128875858,"version":"3.33.0"},"reference-count":12,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2017,4,4]],"date-time":"2017-04-04T00:00:00Z","timestamp":1491264000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Urologia"],"published-print":{"date-parts":[[2017,7]]},"abstract":"<jats:sec><jats:title>Introduction<\/jats:title><jats:p> The aim of this study was to analyze the significance of an increase in total prostate-specific antigen (PSA) serum levels despite dutasteride treatment as a predictor of prostate cancer (PC) at biopsy. We focused our attention on the rate of the first PSA increase and on the influence of prostatic inflammation. <\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p> From 2011 to 2016, 365 men with a previous negative prostate biopsy and persistent elevated PSA levels received dutasteride treatment. The population was followed for a range of 12-48 months. <\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p> One hundred twelve cases with a confirmed PSA increase &gt;0.5 ng\/ml over the nadir value during the follow-up were included in Group A and underwent a new prostate biopsy. In Group A, the PSA increase was associated with PC at the re-biopsy in 66% of cases. The percentage of PSA reduction after 6 months of treatment was not a significant indicator of the risk for PC. The distribution of inflammatory infiltrates significantly (p&lt;00.01) varied from positive to negative prostate biopsies. The relative risk for PC at biopsy significantly increased according to PSA level during dutasteride. <\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p> Treatment with dutasteride can help to analyze PSA kinetic. A persistent prostatic inflammation is a factor able to reduce the performance of PSA kinetic during dutasteride treatment. <\/jats:p><\/jats:sec>","DOI":"10.5301\/uj.5000227","type":"journal-article","created":{"date-parts":[[2017,4,21]],"date-time":"2017-04-21T12:50:06Z","timestamp":1492779006000},"page":"158-164","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":1,"title":["Prostate-Specific Antigen Increase during Dutasteride to Indicate the Need for Prostate Biopsy: Influence of Prostatic Inflammation"],"prefix":"10.1177","volume":"84","author":[{"given":"Alessandro","family":"Sciarra","sequence":"first","affiliation":[{"name":"Department of Urology, Sapienza University, Rome - Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martina","family":"Maggi","sequence":"additional","affiliation":[{"name":"Department of Urology, Sapienza University, Rome - Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrea","family":"Fasulo","sequence":"additional","affiliation":[{"name":"Department of Statistic, Istituto Superiore di Sanit\u00e0, Rome - Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefano","family":"Salciccia","sequence":"additional","affiliation":[{"name":"Department of Urology, Sapienza University, Rome - Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vincenzo","family":"Gentile","sequence":"additional","affiliation":[{"name":"Department of Urology, Sapienza University, Rome - Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susanna","family":"Cattarino","sequence":"additional","affiliation":[{"name":"Department of Urology, Sapienza University, Rome - Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alessandro","family":"Gentilucci","sequence":"additional","affiliation":[{"name":"Department of Urology, Sapienza University, Rome - Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2017,4,4]]},"reference":[{"key":"bibr1-uj.5000227","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2010.09.011"},{"key":"bibr2-uj.5000227","doi-asserted-by":"publisher","DOI":"10.1016\/j.juro.2006.04.024"},{"key":"bibr3-uj.5000227","doi-asserted-by":"publisher","DOI":"10.1093\/jnci\/djj307"},{"key":"bibr4-uj.5000227","doi-asserted-by":"publisher","DOI":"10.1016\/j.eururo.2010.10.040"},{"key":"bibr5-uj.5000227","unstructured":"HeidenreichA BastianPJ BellmuntJ BollaM JoniauS MasonMD Prostate cancer. 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