Ibrahim Kulac1, Berrak Gumuskaya1, Charles G Drake2,3,4, Beverly Gonzalez5, Kathryn B Arnold6, Phyllis J Goodman6, Alan R Kristal7, M Scott Lucia8, Ian M Thompson9,10, William B Isaacs3,4, Angelo M De Marzo11,12,13, Elizabeth A Platz14,15,16. 1. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland. 2. Department of Immunology, Johns Hopkins University School of Medicine, Baltimore, Maryland. 3. Department of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland. 4. Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland. 5. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. 6. SWOG Statistical Center, Fred Hutchinson Cancer Research Center, Seattle, Washington. 7. Cancer Prevention Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington. 8. Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado. 9. Department of Urology, University of Texas Health Science Center at San Antonio, San Antonio, Texas. 10. Department of Cancer Therapy and Research Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas. 11. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland. ademarz@jhmi.edu. 12. Department of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland. ademarz@jhmi.edu. 13. Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland. ademarz@jhmi.edu. 14. Department of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland. eplatz1@jhu.edu. 15. Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland. eplatz1@jhu.edu. 16. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. eplatz1@jhu.edu.
Abstract
BACKGROUND: Intraprostatic inflammation has been associated with lower urinary tract symptom (LUTS) progression. However, prior studies used tissue removed for clinical indications, potentially skewing inflammation extent or biasing the association. We, therefore, evaluated inflammation and LUTS incidence and progression in men who underwent biopsy of the prostate peripheral zone irrespective of indication. MATERIALS AND METHODS: We developed nested case-control sets in men in the placebo arm of the Prostate Cancer Prevention Trial who were free of clinical BPH and had a protocol-directed year 7 biopsy. Cases had baseline IPSS <15 and year 7 IPSS of 8-14 (low, N = 47), 15-19 (incident moderate, N = 42), or ≥20 (incident high, N = 44). Controls had baseline and year 7 IPSS <8 (N = 41). For progression from IPSS <8, cases had baseline to year 7 IPSS slope >75th percentile (N = 46) and controls had a slope <25th percentile (N = 45). For progression from IPSS = 8-14, cases had a slope >75th percentile (N = 46) and controls had a slope <25th percentile (N = 46). We reviewed three H&E-stained biopsy cores per man to determine prevalence of ≥1 core with inflammation and mean extent (%) of tissue area with inflammation. RESULTS: Inflammation prevalence in low cases (64%) was similar to controls (66%), but higher in moderate (69%) and high (73%) cases (P-trend = 0.4). Extent did not differ across LUTS categories (P-trend = 0.5). For progression from IPSS < 8, prevalence (65%, P = 0.9) and extent (2.5%, P = 0.8) in cases did not differ from controls (64%, 2.7%). For progression from IPSS 8-14, prevalence in cases (52%) was lower than in controls (78%, P = 0.009), while extent was higher in cases (5.3%) than controls (3.6%), especially in men with ≥1 core with inflammation (10.1% versus 4.6%, P = 0.06). CONCLUSION: Peripheral zone intraprostatic inflammation is not strongly associated with LUTS incidence or progression. Prostate 76:1399-1408, 2016.
BACKGROUND:Intraprostatic inflammation has been associated with lower urinary tract symptom (LUTS) progression. However, prior studies used tissue removed for clinical indications, potentially skewing inflammation extent or biasing the association. We, therefore, evaluated inflammation and LUTS incidence and progression in men who underwent biopsy of the prostate peripheral zone irrespective of indication. MATERIALS AND METHODS: We developed nested case-control sets in men in the placebo arm of the Prostate Cancer Prevention Trial who were free of clinical BPH and had a protocol-directed year 7 biopsy. Cases had baseline IPSS <15 and year 7 IPSS of 8-14 (low, N = 47), 15-19 (incident moderate, N = 42), or ≥20 (incident high, N = 44). Controls had baseline and year 7 IPSS <8 (N = 41). For progression from IPSS <8, cases had baseline to year 7 IPSS slope >75th percentile (N = 46) and controls had a slope <25th percentile (N = 45). For progression from IPSS = 8-14, cases had a slope >75th percentile (N = 46) and controls had a slope <25th percentile (N = 46). We reviewed three H&E-stained biopsy cores per man to determine prevalence of ≥1 core with inflammation and mean extent (%) of tissue area with inflammation. RESULTS:Inflammation prevalence in low cases (64%) was similar to controls (66%), but higher in moderate (69%) and high (73%) cases (P-trend = 0.4). Extent did not differ across LUTS categories (P-trend = 0.5). For progression from IPSS < 8, prevalence (65%, P = 0.9) and extent (2.5%, P = 0.8) in cases did not differ from controls (64%, 2.7%). For progression from IPSS 8-14, prevalence in cases (52%) was lower than in controls (78%, P = 0.009), while extent was higher in cases (5.3%) than controls (3.6%), especially in men with ≥1 core with inflammation (10.1% versus 4.6%, P = 0.06). CONCLUSION: Peripheral zone intraprostatic inflammation is not strongly associated with LUTS incidence or progression. Prostate 76:1399-1408, 2016.
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