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Prostate Biopsy Markers of Inflammation are Associated with Risk of Clinical Progression of Benign Prostatic Hyperplasia: Findings from the MTOPS Study

医学 增生 前列腺 前列腺活检 活检 前列腺疾病 内科学 病理 泌尿科 炎症 癌症
作者
Kathleen C. Torkko,R. Storey Wilson,Elizabeth E. Smith,John W. Kusek,Adrie van Bokhoven,M. Scott Lucia
出处
期刊:The Journal of Urology [Ovid Technologies (Wolters Kluwer)]
卷期号:194 (2): 454-461 被引量:76
标识
DOI:10.1016/j.juro.2015.03.103
摘要

No AccessJournal of UrologyAdult Urology1 Aug 2015Prostate Biopsy Markers of Inflammation are Associated with Risk of Clinical Progression of Benign Prostatic Hyperplasia: Findings from the MTOPS Study Kathleen C. Torkko, R. Storey Wilson, Elizabeth E. Smith, John W. Kusek, Adrie van Bokhoven, and M. Scott Lucia Kathleen C. TorkkoKathleen C. Torkko Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado , R. Storey WilsonR. Storey Wilson Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado , Elizabeth E. SmithElizabeth E. Smith Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado , John W. KusekJohn W. Kusek National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland , Adrie van BokhovenAdrie van Bokhoven Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado , and M. Scott LuciaM. Scott Lucia Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado View All Author Informationhttps://doi.org/10.1016/j.juro.2015.03.103AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract Purpose: Factors associated with worsening of benign prostatic hyperplasia are not well understood. We measured inflammatory markers from prostate biopsies to study if inflammation is related to clinical progression of benign prostatic hyperplasia. Materials and Methods: We measured inflammatory cell markers CD45, CD4, CD8 and CD68 in transition zone biopsies from 859 men in the MTOPS biopsy substudy. Using novel imaging techniques we quantified amounts of moderate/severe inflammation. Benign prostatic hyperplasia clinical progression was defined as a confirmed 4-point or greater increase in the AUA symptom score from baseline, or the occurrence of urinary incontinence or acute urinary retention. Baseline clinical parameters including concomitant medication use were determined. Kaplan-Meier curves and multivariate Cox proportional hazard models were used to determine the risk of progression. Results: Inflammation as measured by CD45, CD4 and CD68 increased the risk of clinical progression of benign prostatic hyperplasia. CD4 showed the highest risk where men in the highest tertile of moderate/severe inflammation were at twice the risk of progression compared to men in the lower 2 tertiles combined (HR 2.03, p=0.001). Inflammation was more strongly associated with progression defined by acute urinary retention or incontinence (HR ranging from 2.39 [CD8, p=0.03] to 3.08 [CD4, p=0.01]) than an AUA symptom score increase (CD4, HR 1.86, p=0.01). Men who reported use of nonsteroidal anti-inflammatory drugs or steroids at baseline tended to be at higher risk for progression. Conclusions: Although our data show that inflammation increases the risk of progression, our findings suggest that inflammation has a greater role in men who have conditions requiring anti-inflammatory medications. References 1 : Prostate development and growth in benign prostatic hyperplasia. Differentiation2011; 82: 173. Google Scholar 2 : The role of chronic prostatic inflammation in the pathogenesis and progression of benign prostatic hyperplasia (BPH). BJU Int2013; 112: 432. Google Scholar 3 : The controversial relationship between benign prostatic hyperplasia and prostate cancer: the role of inflammation. Eur Urol2011; 60: 106. Google Scholar 4 : Prostatic fibrosis, lower urinary tract symptoms, and BPH. Nat Rev Urol2013; 10: 546. Google Scholar 5 : The etiology of benign prostatic hypertrophy. Med Hypotheses1998; 50: 61. 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Google Scholar 13 : Phenotype and function of peripheral and prostatic lymphocytes in patients with benign prostatic hyperplasia. J Urol1994; 151: 480. Link, Google Scholar 14 : Increased expression of lymphocyte-derived cytokines in benign hyperplastic prostate tissue, identification of the producing cell types, and effect of differentially expressed cytokines on stromal cell proliferation. Prostate2002; 52: 43. Google Scholar 15 : Do prostatic infarction, prostatic inflammation and prostate morphology play a role in acute urinary retention?. Eur Urol2005; 48: 277. Google Scholar 16 : Does intraprostatic inflammation have a role in the pathogenesis and progression of benign prostatic hyperplasia?. BJU Int2007; 100: 327. Google Scholar 17 : Lower urinary tract symptoms in benign prostatic hyperplasia patients: orchestrated by chronic prostatic inflammation and prostatic calculi?. Urol Int2013; 90: 144. Google Scholar 18 : The prognostic use of inflammation and tissue necrosis in benign prostatic hyperplasia. Urol Int2013; 91: 19. Google Scholar 19 : CD4+ and CD8+ T-lymphocyte scores cannot reliably predict progression in patients with benign prostatic hyperplasia. BJU Int2011; 108: E43. Google Scholar 20 : Insights into the relationships between prostatic disorders and their potential impact on future urologic practice. Eur Urol Suppl2006; 5: 698. Google Scholar 21 : The impact of acute or chronic inflammation in baseline biopsy on the risk of clinical progression of BPH. Results from the MTOPS study. J Urol2005; 173: 346. abstract 1277. Link, Google Scholar 22 : Risk behaviours and benign prostatic hyperplasia. BJU Int2004; 93: 1241. Google Scholar 23 : Non-steroidal anti-inflammatory drug use and the risk of benign prostatic hyperplasia-related outcomes and nocturia in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. BJU Int2012; 110: 1050. Google Scholar 24 : Protective association between nonsteroidal antiinflammatory drug use and measures of benign prostatic hyperplasia. Am J Epidemiol2006; 164: 760. Google Scholar 25 : Non-steroidal anti-inflammatory drugs for lower urinary tract symptoms in benign prostatic hyperplasia: systematic review and meta-analysis of randomized controlled trials. BJU Int2013; 111: 304. Google Scholar 26 : Indications for and use of nonsteroidal antiinflammatory drugs and the risk of incident, symptomatic benign prostatic hyperplasia: results from the Prostate Cancer Prevention Trial. Am J Epidemiol2012; 176: 156. Google Scholar 27 : Associations of obesity, physical activity and diet with benign prostatic hyperplasia and lower urinary tract symptoms. Curr Opin Urol2014; 24: 10. Google Scholar 28 : Limitations of transition zone needle biopsy findings in the prediction of transition zone cancer and tissue composition of benign nodular hyperplasia. Urology1996; 48: 751. Google Scholar © 2015 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetailsCited byLloyd G, Ricke W and McVary K (2019) Inflammation, Voiding and Benign Prostatic Hyperplasia ProgressionJournal of Urology, VOL. 201, NO. 5, (868-870), Online publication date: 1-May-2019. Volume 194Issue 2August 2015Page: 454-461Supplementary Materials Advertisement Copyright & Permissions© 2015 by American Urological Association Education and Research, Inc.Keywordsdisease progressioninflammationprostatic hyperplasiaanti-inflammatory agentsAcknowledgmentsStaff at the Biorepository Core Facility of the University of Colorado Anschutz Medical Campus provided assistance in completing the project.MetricsAuthor Information Kathleen C. Torkko Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado More articles by this author R. Storey Wilson Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado More articles by this author Elizabeth E. Smith Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado More articles by this author John W. Kusek National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland More articles by this author Adrie van Bokhoven Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado More articles by this author M. Scott Lucia Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado More articles by this author Expand All Advertisement PDF downloadLoading ...
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