Benign prostatic hyperplasia (BPH), a nearly ubiquitous condition,

is the most common benign neoplasm of American men

Clinical benign prostatic hyperplasia (BPH) is one of the most

common diseases in ageing men which can lead to lower urinary
tract symptoms (LUTS)
Age
• The peak incidence of clinical BPH occurs at 63 to 65
years of age.
• Symptomatic disease is uncommon in men younger
than 50 years, but some urinary voiding symptoms
are present by the time men turn 60 years of age.
• The Boston Area Normative Aging Study estimated
that was 78% in patients at age 80 years.
• Similarly, the Baltimore Longitudinal Study of Aging
projected that approximately 60% of men at least
60 years old
RACE
• No clear patterns have emerged with respect to
BPH risk and race.
• Observational studies comparing black, Asian and
white men have produced variable results.
• Large analyses of the US Prostate, Lung,
Colorectal and Ovarian (PLCO) Cancer Screening
Trial and the Health Professionals Follow-Up
Study observed no differences in clinical BPH risk
between black and white men.
• Some data have suggested a decreased risk of
clinical BPH in Asian compared with white men
Genetics
• A case control analysis, in which men below 64 years
underwent surgery for BPH, noted that male relatives
and brothers had a 4-fold and 6-fold increase
Diet
• Increased total energy intake, energy-adjusted total
protein intake, red meat, fat, milk and dairy products,
cereals, bread, poultry and starch all potentially
increase the risks of clinical BPH and BPH surgery
• Vegetables, fruits, polyunsaturated fatty acids, linoleic
acid and vitamin D potentially decrease the risk of BPH
• Higher circulating concentrations of vitamin E,
lycopene, selenium and carotene have been inversely
associated with BPH
Physical activity
• A meta-analysis of 11 published studies indicated that
moderateto-vigorous physical activity reduced the risk
of BPH by as much as 25% relative to a sedentary lifestyl
Metabolic syndrome
• Obesity increases the risks of BPH surgery, urinary
symptom progression and initiation of BPH medical
therapy
• Physician-diagnosed diabetes, increased serum insulin
and elevated fasting plasma glucose have been
associated with increased prostate size and increased
risk of prostate enlargement, clinical BPH and BPH
surgery
Inflammatory cytokines are over-expressed in BPH tissues
• The prostate gland comprises three types of tissue:
epithelial tissue, stromal tissue, and the capsule
• The role of intraprostatic DHT and type II 5α-
reductase in the development of BPH is evidenced
by several observations:
 BPH does not develop in men who are castrated
before puberty.
 Patients with type II 5α-reductase enzym
deficiency do not develop BPH.
 Administration of testosterone to orchiectomized
dogs of advanced age produces BPH.
 Anatomic enlargement
of the prostate gland_ a
physical block at the
bladder neck and
thereby obstructs
Static urinary outflow
factors Enlargement of the gland
depends on androgen
stimulation of epithelial
tissue and estrogen
Pathogenesis stimulation of stromal
of BPH tissue in the prostate
Excessive α-adrenergic
tone of the stromal
Dynamic component of the prostate
gland, bladder neck, and
factors posterior urethra, which
results in contraction of
the prostate gland
• Patients experience urinary hesitancy, urine
dribbles out of the penis, and the bladder feels
full even after voiding.
• Irritative signs and symptoms are common and
result from long-standing obstruction at the
bladder neck.
• Patients experience urinary frequency, urgency,
and nocturia.
• BPH progression may produce complications
including chronic kidney disease, gross hematuria,
urinary incontinence, recurrent urinary tract
infection, bladder diverticula, and bladder stones.
 TREATMENT

Goals of Treatment: The goals are to control

symptoms, prevent progression of complications, and
delay need for surgical intervention.

Management options include watchful waiting, drug

therapy, and surgical intervention.
watchful waiting Reassessed at 6 to 12
month intervals

Educated about behavior modification_

such as fluid restriction before bedtime,
avoiding caffeine and alcohol, frequent
emptying of the bladder, and avoiding
drugs that exacerbate symptoms

Drugs_ testosterone, α-adrenergic agonists (eg,

decongestants), and anticholinergic effects (eg,
antihistamines, phenothiazines, tricyclic anti- depressants,
antispasmodics, and antiparkinsonian agents).
Patients with a prostate gland more than 40 g and
PSA of 1.4 ng/mL or more (1.4 mcg/L) (consider
combination therapy)
 α-Adrenergic Antagonists
• Function relax smooth muscle in the prostate and
bladder neck, increasing urinary flow rates by 2 to 3
mL/sec in 60% to 70% of patients and reducing PVR
urine volumes.
• Do not decrease prostate volume or PSA levels.
• Prazosin, terazosin, doxazosin, and alfuzosin are
second-generation α1-adrenergic antagonists. They
antagonize peripheral vascular α1-adrenergic receptors
in addition to those in the prostate.
• Adverse effects include first-dose syncope, orthostatic
hypotension, and dizziness.
• Alfuzosin is less likely to cause cardiovascular adverse
effects than other second-generation agents.
• Tamsulosin and silodosin, third-generation α1-adrenergic
antagonists, are selective for prostatic α1A-receptors
• Tamsulosin is a good choice for patients who cannot
tolerate hypotension
 5α-Reductase Inhibitors
• 5α-Reductase inhibitors interfere with the stimulatory effect of
testosterone.
• Compared with α1-adrenergic antagonists, disadvantages of
5α-reductase inhibitors include 6 months of use to maximally
shrink prostate, less likely to induce objective improvement
and more sexual dysfunction.
• Dutasteride inhibits types I and II 5α-reductase, whereas
finasteride inhibits only type II.
• Dutasteride more quickly and completely suppresses
intraprostatic DHT (vs 80%–90% for finasteride) and decreases
serum DHT by 90% (vs 70%).
• 5α-Reductase inhibitors may be preferred in patients with
uncontrolled arrhythmias, poorly controlled angina, use
multiple antihypertensives, or cannot tolerate hypotensive
• Measure PSA at baseline and again after 6 months of therapy, If
does not decrease by 50% after 6 months of therapy in a compliant
patient, evaluate the patient for prostate cancer.
• in FDA pregnancy category X and are therefore contraindicated in
pregnant women. Pregnant and potentially pregnant women
should not handle the tablets or have contact with semen from
men taking 5α-reductase inhibitors.
Phosphodiesterase Inhibitors
• Increase in cyclic GMP by phosphodiesterase inhibitors (PI) may relax smooth
muscle in prostate and bladder neck.
• Effectiveness may be result of direct relaxation of detrusor muscle of bladder.
• Tadalafil 5 mg daily improves voiding symptoms but does not increase urinary flow
rate or reduce PVR urine volume.
• Combination therapy with α-adrenergic antagonist results in significant
improvement in lower urinary tract symptoms, increased urinary flow rates, and
decreased PVR volume.

Anticholinergic Agents
• Oxybutynin and tolterodine to α-adrenergic antagonists relieves irritative voiding
symptoms including urinary frequency, urgency, and nocturia.
• Start with lowest effective dose to determine tolerance of CNS adverse effects and
dry mouth.
• Measure PVR urine volume before initiating treatment (should be less than 250 mL).
• If systemic anticholinergic adverse effects are poorly tolerated, consider transdermal
or extended-release formulations or uroselective agents (eg, darifenacin or
solifenacin).