Sexual medicine reviews · 2019
Testosterone and Benign Prostatic Hyperplasia.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
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Rastrelli Giulia, Vignozzi Linda, Corona Giovanni, Maggi Mario
Аннотация
INTRODUCTION: Benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS) are frequent in aging. Nonetheless, their pathogenesis is largely unknown. The androgen dependence of the first phases of prostate development have inspired the historical view that higher testosterone (T) may be involved in BPH occurrence; however, recent evidence suggests a different scenario.
AIM: To review the available knowledge on the pathogenesis of BPH particularly concerning the role of T and the possible connections with metabolic impairments.
METHODS: Relevant records were retrieved by an extensive search in Medline, including the following keywords ("testosterone"[MeSH Terms] OR "testosterone"[All Fields]) AND ("prostatic hyperplasia"[MeSH Terms] OR ("prostatic"[All Fields] AND "hyperplasia"[All Fields]) OR "prostatic hyperplasia"[All Fields] OR ("benign"[All Fields] AND "prostatic"[All Fields] AND "hyperplasia"[All Fields]) OR "benign prostatic hyperplasia"[All Fields]). There were no limitations in terms of publication date or study design.
MAIN OUTCOME MEASURES: Preclinical and clinical studies have been reported, with special emphasis on our contribution and interpretation.
RESULTS: Inflammation is a key aspect of BPH development. Along with infectious agents, prostate inflammation can be triggered by metabolic stimuli, such as dyslipidemia, an important component of metabolic syndrome (MetS). Low T and hyperestrogenism frequently occur in MetS. Mounting evidence shows that low, rather than high, T and hyperestrogenism may favor prostate inflammation. Considering these data as a whole, we postulate that BPH is the result of the action of multiple factors, which reinforce their mutual detrimental effects.
CONCLUSION: T is not detrimental for the prostate, and treating hypogonadism could even produce relief from LUTS and limit prostatic inflammation, which generates and maintains the process leading to BPH. Rastrelli G, Vignozzi L, Corona G, et al. Testosterone and Benign Prostatic Hyperplasia. Sex Med Rev 2019;7:259-271.
AIM: To review the available knowledge on the pathogenesis of BPH particularly concerning the role of T and the possible connections with metabolic impairments.
METHODS: Relevant records were retrieved by an extensive search in Medline, including the following keywords ("testosterone"[MeSH Terms] OR "testosterone"[All Fields]) AND ("prostatic hyperplasia"[MeSH Terms] OR ("prostatic"[All Fields] AND "hyperplasia"[All Fields]) OR "prostatic hyperplasia"[All Fields] OR ("benign"[All Fields] AND "prostatic"[All Fields] AND "hyperplasia"[All Fields]) OR "benign prostatic hyperplasia"[All Fields]). There were no limitations in terms of publication date or study design.
MAIN OUTCOME MEASURES: Preclinical and clinical studies have been reported, with special emphasis on our contribution and interpretation.
RESULTS: Inflammation is a key aspect of BPH development. Along with infectious agents, prostate inflammation can be triggered by metabolic stimuli, such as dyslipidemia, an important component of metabolic syndrome (MetS). Low T and hyperestrogenism frequently occur in MetS. Mounting evidence shows that low, rather than high, T and hyperestrogenism may favor prostate inflammation. Considering these data as a whole, we postulate that BPH is the result of the action of multiple factors, which reinforce their mutual detrimental effects.
CONCLUSION: T is not detrimental for the prostate, and treating hypogonadism could even produce relief from LUTS and limit prostatic inflammation, which generates and maintains the process leading to BPH. Rastrelli G, Vignozzi L, Corona G, et al. Testosterone and Benign Prostatic Hyperplasia. Sex Med Rev 2019;7:259-271.