Benign prostatic hyperplasia (BPH) is the nonmalignant enlargement of the prostate gland occurring in >50% of men over 60 years of age, most of whom have lower urinary tract symptoms (LUTS).1, The two most well established causative factors of BPH include age and normal androgenic functions.1 The prevalence of LUTS due to BPH increases with increasing age with moderate to severe symptoms occurring in 40 and 80% of men after the age 60 and by 80 years, respectively.3 Clinically, BPH may be manifested as irritative LUTS such as urgency, frequency, nocturia and obstructive LUTS such as hesitancy, a weak and interrupted urinary stream, straining to initiate urination, and a sensation of incomplete bladder emptying. Prolonged obstructions may eventually lead to acute urinary retention (AUR), recurrent urinary tract infection (UTI), hematuria, bladder calculi, and renal insufficiency.3 BPH is characterized by stromal and glandular epithelial hyperplasia that occurs in the periurethral transition zone of the prostate.3 Symptoms of BPH arise through two mechanisms i.e. static, in which the hyperplastic prostatic tissue leads to urethral compression and dynamic, wherein increased adrenergic nervous system and prostatic smooth muscle tone promotes obstruction of urinary flow (Figure 1). Additionally, both mechanisms increase resistance to urinary flow at the level of the bladder outlet.