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Benign prostatic hyperplasia: a new metabolic disease?
L Vignozzi1, G Rastrelli, G Corona
1Sexual Medicine and Andrology Unit, Department of Experimental and Clinical Biomedical Sciences, University of Florence, Viale Pieraccini 6, 50139, Florence, Italy.
Journal of Endocrinological Investigation
|January 25, 2014
Summary
Benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS) in aging men are linked to inflammation, dyslipidemia, and hormonal changes. These factors interact to promote prostate enlargement and urinary issues.
Area of Science:
- Urology
- Andrology
- Pathophysiology
Background:
- Benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS) are highly prevalent in aging males.
- The role of androgens in BPH/LUTS pathogenesis is debated, but low testosterone and high estradiol may promote disease progression.
- Metabolic syndrome and prostate inflammation are emerging factors in BPH/LUTS development.
Purpose of the Study:
- To review evidence on the pathogenesis of BPH/LUTS.
- To specifically examine the metabolic influences contributing to BPH/LUTS.
Main Methods:
- A comprehensive literature review was conducted using the Medline database.
Main Results:
- A "three-hit hypothesis" for BPH/LUTS pathogenesis emerged: 1) prostatic inflammation (infection-induced), 2) altered metabolism (e.g., hypercholesterolemia), and 3) hormonal imbalance (hypogonadism/hyperestrogenism).
- Combined hits lead to TLR overexpression, prostatic cell activation, and growth factor overproduction, causing prostate remodeling and enlargement.
- Mechanical obstruction and unfavorable metabolic/hormonal factors contribute to LUTS.
Conclusions:
- Prostate inflammation, dyslipidemia, and altered sex-steroid milieu are key, interacting factors in the development of BPH/LUTS.
- These elements mutually contribute to the pathophysiology of benign prostatic hyperplasia and lower urinary tract symptoms.
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