AUA: Management of LUTS Attributed to BPH (2021)

Background

Definition of benign prostatic hyperplasia (BPH): histologic diagnosis that refers to the proliferation of glandular epithelial tissue, smooth muscle, and connective tissue within the prostatic transition zone.

Multifactorial process, exact etiology unknown
Requires testosterone
- 5-alpha reductace converts testosterone to its active metabolite, dihydrotestosterone (DHT).
- DHT, which has a higher affinity for the androgen receptor and is considered the more potent androgenic steroid hormone, forms a complex that is then transported to the nucleus. The T/DHT-androgen receptor complex within the nucleus of the prostate cells initiates transcription of DNA and translation, with subsequent normal development, growth, and hyperplasia of the prostate. BPH develops due to an imbalance between growth and apoptosis (cellular death) in favor of growth, subsequently causing an increase in cellular mass.

Prevalence of BPH increases with age
- Prevalence by age 60 is 60%, by age 80 is 80%
Prevalence and severity of lower urinary tract symptoms increases with age

BPH can lead to benign prostatic enlargement (BPE), which can cause obstruction at the level of the bladder neck, termed benign prostatic obstruction (BPO).

Classification: storage vs. voiding/empything
Male LUTS may be caused by a variety of conditions, including BPE and BPO.
- BPE contributes to LUTS via at least two routes:
  - Direct BOO/BPO from enlarged tissue (static component)
  - Increased smooth muscle tone and resistance within the enlarged gland (dynamic component).
In men, overactive bladder (OAB) storage symptoms may be the result of primary detrusor overactivity (DO), underactivity, or from obstruction induced by BPE and BPO.
The most important motivations for men seeking treatment are severity and degree of bother associated with symptoms.4 While LUTS/BPH is rarely lifethreatening, the impact on QoL is significant and should not be underestimated