What is the role of hormones in the pathophysiology of benign prostatic hyperplasia (BPH)?

Updated: Jan 15, 2019
  • Author: Levi A Deters, MD; Chief Editor: Edward David Kim, MD, FACS  more...
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Answer

Prostatic enlargement depends on the potent androgen dihydrotestosterone (DHT). In the prostate gland, type II 5-alpha-reductase metabolizes circulating testosterone into DHT, which works locally, not systemically. DHT binds to androgen receptors in the cell nuclei, potentially resulting in BPH.

However, the fact that serum testosterone levels decrease with age, yet the development of BPH increases, suggests that other agents play an etiologic role. Possible factors include the metabolic syndrome, hyperinsulinemia, norepinephrine, angiotensin II, and insulin-like growth factors. [3]

In vitro studies have shown that large numbers of alpha-1-adrenergic receptors are located in the smooth muscle of the stroma and capsule of the prostate, as well as in the bladder neck. Stimulation of these receptors causes an increase in smooth-muscle tone, which can worsen LUTS. Conversely, blockade of these receptors (see Treatment) can reversibly relax these muscles, with subsequent relief of LUTS.


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