nonneoplastic glandular and stromal hyperplasia of the transition zone of the prostate.

demographics: increases with age (present in ∼ 50% of men > 50 years and more than 80% of men > 80 years).

Aetiology:

The aetiology is not fully understood. The following factors play a role in prostatic hyperplasia and growth:

• Androgens
  • Dihydrotestosterone (DHT) is a potent prostatic growth factor.
  • Gene amplification of androgen receptors (present in the glandular epithelial cells and stromal cells) → increased androgen receptor sensitivity to androgens → prostatic hyperplasia
• Estrogens: Estrogens (mainly estradiol) are potent stimulators of prostatic hyperplasia.
• Androgen-estrogen imbalance: As men age, testosterone levels decline, but estrogen levels remain the same, which results in a higher estrogen/testosterone ratio.
• Stem cell proliferation and longevity: abnormal proliferation and longer prostatic stem cell life-span
• Genetic susceptibility: Genes involved in the development of BPH include growth factor genes, androgen-regulator genes, apoptosis genes, and androgen-regulated genes.

Pathophysiology

• Hormonal factors, stem cell proliferation and genetic susceptibility → glandular and stromal hyperplasia in the transition zone → formation of smooth, elastic, firm hyperplastic nodule → slit-like prostatic urethral compression → BOO (bladder outlet obstruction) → obstructive symptoms of BPH
• Bladder outlet obstruction leads to:
  • Detrusor overactivity (involuntary detrusor contractions during bladder filling) → irritative symptoms of BPH
  • Weakening of the bladder wall → incomplete voiding → urinary stasis → predisposition to urinary tract infections, acute/chronic urinary retention, and formation of bladder stones
  • Increased intracystic pressure while voiding → detrusor muscle hypertrophy → bladder trabeculation and pseudodiverticula formation

Risk factors: Obesity, diabetes, physical activity and alcohol intake

Clinical Features