Overview of benign prostatic hypertrophy.

Urology
J Geller

Abstract

Pathogenesis and therapy of benign prostatic hypertrophy (BPH) are reviewed. Elevated prostate dihydrotestosterone concentrations, increased 5 alpha-reductase activity in the hypertrophic prostate, and prostate atrophy following castration all suggest a significant role for dihydrotestosterone in the pathogenesis of BPH. An increasing plasma estrogen/testosterone ratio with age, and the presence of estrogen receptors in the prostatic stroma, indicate that estrogen also may be involved in the development of BPH. Symptomatic improvement of BPH with androgen withdrawal therapy (including castration, antiandrogens, GnRH agonists, and 5 alpha-reductase inhibitors), as well as effective estrogen withdrawal with tamoxifen, strongly supports the endocrine pathogenesis of BPH.

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Citations

Aug 1, 1996·The Prostate·D G BostwickA Lopez-Beltran
Jan 1, 1992·Journal of Cellular Biochemistry. Supplement·D G Bostwick
Mar 1, 2006·World Journal of Urology·Murat LekiliCoşkun Büyüksu
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Sep 8, 2006·Ultrasound Quarterly·Hossein Sadeghi-NejadVikram Dogra
Oct 1, 1995·Histopathology·M C Parkinson
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Oct 20, 2009·The Journal of Steroid Biochemistry and Molecular Biology·Kevin ShoularsBarry M Markaverich
Jan 24, 2004·Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc·David G Bostwick, Junqi Qian
Mar 6, 1998·Journal of the Royal Society of Medicine·M R Feneley, C Busch

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