Racial differences in prostate inflammation: results from the REDUCE study
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Adriana C. Vidal1, Zinan Chen2, Lauren E. Howard2, Daniel M. Moreira3, Ramiro Castro-Santamaria4, Gerald L. Andriole5, Emanuela Taioli6, Jay H. Fowke7, Beatrice Knudsen8, Charles G. Drake9, J. Curtis Nickel10 and Stephen J. Freedland1
1 Department of Surgery, Division of Urology, Cedars Sinai Medical Center, Los Angeles, CA, USA
2 Department of Biostatistics and Bioinformatics, Duke University School of Medicine, Durham, NC, USA
3 Department of Urology, Mayo Clinic, Rochester, MN, USA
4 GlaxoSmithKline Inc., R&D, King of Prussia, PA, USA
5 Washington University School of Medicine in St. Louis, St. Louis, MO, USA
6 Institute for Translational Epidemiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
7 Department of Medicine and Urologic Surgery, Vanderbilt University Medical Center, TN, USA
8 Department of Medicine, Cedars-Sinai Biobank, Cedars Sinai Medical Center, Los Angeles, CA, USA
9 Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, and the Brady Urology Institute, John Hopkins University, Baltimore, MD, USA
10 Department of Urology, Queen’s University, Kingston, ON, Canada
Adriana C. Vidal, email:
Keywords: prostate biopsy, inflammation, race, prostate cancer, acute inflammation
Received: May 27, 2016 Accepted: July 07, 2016 Published: July 18, 2016
Prostate cancer (PC) risk differs between races, and we previously showed prostate inflammation in benign prostate tissue was linked with a lower future PC risk. However, whether prostate tissue inflammation varies by race is unknown. We analyzed baseline acute and chronic prostate inflammation by race in REDUCE, a 4-year, multicenter, placebo-controlled study where all men had a negative prostate biopsy prior to enrollment. We included 7,982 men with standardized central pathology review to determine the presence or absence of chronic or acute inflammation in baseline prostate biopsy tissue. Logistic regression was used to compare prostate inflammation by race, adjusting for confounders. Of 7,982 men, 7,271 were white (91.1%), 180 (2.3%) black, 131 (1.6%) Asian, 319 (4.0%) Hispanic and 81 (1%) unknown. A total of 78% had chronic and 15% had acute inflammation. On multivariable analysis relative to white men, black men were less likely (OR = 0.65, 95%CI: 0.41-1.03, p = 0.07) and Asian men more likely to have acute inflammation (OR = 1.74, 95%CI: 1.14-2.65, p = 0.001). Hispanic men had similar levels of acute inflammation as white men. Chronic inflammation did not significantly differ across races. We identified racial differences in acute inflammation, particularly in Asian men, in benign prostate tissue that inversely mirrored population-level data on PC race disparity. As we showed in REDUCE that acute inflammation is linked with lower future PC risk, if validated in future studies, these data suggest racial differences in prostatic acute inflammation may contribute in part to race differences in PC risk, especially among Asian men.
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