Epidemiology and Treatment Modalities for the Management of Benign Prostatic Hyperplasia

Soum D. Lokeshwar; Benjamin T. Harper; Eric Webb; Andre Jordan; Thomas A. Dykes; Durwood E. Neal Jr; Martha K. Terris; Zachary Klaassen

Disclosures

Transl Androl Urol. 2019;8(5):529-539. 

In This Article

Epidemiology and Pathophysiology

BPH and its associated symptomatology affect many men worldwide: as of 2010, the prevalence is over 210 million men.[11] Up to 50% of men over the age of 50 and up to 80% of men over the age of 80 experience LUTS from BPH.[12] Furthermore, BPH prevalence is on the rise, due to an increase in modifiable metabolic risk factors, such as obesity.[13] Male obesity has been linked to increased risk of BPH and an increased severity of LUTS in the men affected by BPH.[14] Obesity causes a number of systemic effects including increased inflammatory processes as well as increased intra-abdominal pressures.[15] These systemic affects may be a factor in the increased prevalence of BPH and may increase the reported severity of LUTS. Similar to the inflammatory effects of obesity, infection has also been linked to increased severity of BPH symptoms.[16] The reverse is also true, with BPH leading to unique infectious complications in patients.[17]

Since the late 1800s, BPH, previously known as Benign Prostatic Hypertrophy, has been linked to two factors: age and the presence of testosterone.[18] However, the exact pathophysiology is still yet to be identified. The pathophysiology of BPH has been linked to many factors including sex hormones, neurotransmitters, inflammation, diet, microorganisms and cellular effects on epithelial as well as stromal tissue.[19] Although androgen levels have long been studied as one of the largest influencers on prostatic growth,[20] estrogen may also play a role. It may seem counterintuitive that as men age and testosterone levels fall, the prostate still continues to grow. However, with the help of estrogen, prostatic hyperplasia is allowed to continue even with diminishing androgen levels. Estrogen signaling increases the level of androgen receptors in the prostatic gland leading to signal amplification and stimulation of hyperplasia, even with reducing levels of androgen.[21] Additionally, estradiol has been found to induce epithelial-to-mesenchymal transition in benign prostatic epithelial cells.[22] Epithelial-to-mesenchymal transition causes prostatic hyperplasia, and is evidenced by the loss of E-cadherin, increased pSmad3 and high Snail markers in BPH samples. This affirmed the notion that the accumulation of mesenchymal-like cells derived from prostatic epithelium causes BPH rather than prostatic stromal proliferation.[23] With an understanding of the mechanisms involved in BPH formation and the increasing number of cases of symptomatic BPH, it is imperative to explore the current management of symptomatic BPH.

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