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A cyclooxygenase-2 inhibitor reduces serum prostatic-specific antigen levels in men with benign prostatic hyperplasia and lower urinary tract symptoms and helps differentiate chronic inflammation from prostate cancer

Jing-Liang Chen, Hann-Chorng Kuo

Department of Urology, Buddhist Tzu Chi General Hospital and Tzu Chi University, Hualien, Taiwan

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Abstract
Emerging evidence indicates that prostatic inflammation may contribute to prostatic growth in benign prostatic hyperplasia (BPH) and neoplastic changes (prostate cancer). The Medical Therapy of Prostatic Symptoms study showed that men with inflammation had a significantly higher risk of BPH progression and acute urinary retention. Evidence also shows that a cyclooxygenase-2 (COX-2) inhibitor can increase apoptotic activity in human BPH tissue. COX-2 inhibitors in combination with alpha-adrenergic blockers may increase the effectiveness of therapy for lower urinary tract symptoms (LUTS) secondary to BPH without significant side effects. COX-2 inhibitors may decrease the serum prostatic-specific antigen level and act as a biomarker to differentiate chronic inflammation from prostate cancer in patients with LUTS suggestive of BPH who do not have a palpable prostate nodule but have a serum prostatic-specific antigen level higher than 4 ng/mL. The results might provide a simple way to initially differentiate chronic inflammation from prostatic cancer. If chronic inflammation of the prostate can be reduced by COX-2 inhibitor treatment, bothersome LUTS as well as voiding conditions might be improved.

Keywords
Benign prostatic hyperplasia; Cyclooxygenase-2 inhibitor; Inflammation; Prostate cancer; Prostatic-specific antigen


 

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