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The normal prostate is walnut-sized organ
composed of glandular tissue that makes ejaculatory fluid, its only known function.
Benign Prostatic hyperplasia (BPH) is
nonmalignant adenomatus overgrowth of the periurethral prostate gland. Using size (. 30mL & urinary score) the prevalence
of BPH in men aged 55-74 is 19%, but only 4% of them have urinary problems. Based
on autopsy studies BPH is found in 8% of the men aged 31-40; 40-50% for men 51-60, and > 80% in men over 80. 38% of men
40-79 experience moderate to severe symptoms, and one in 4 men in their 8th decade will require treatment for BPH. On rectal examination the prostate usually is enlarged and has a rubbery consistency,
and in many cses has lost the median furrow. BPH causes elevated PSA in 30-50%
of the time.
Multiple fibroadenomatous nodules develop
in the periurtheral region of the prostate rather than in the fibromuscular prostate, which is displaced by progressive growth
of the peripheral nodules growth. Overgrowth that obstructs the flow of urine
will increase the risk of calculus formation in the bladder, infection in the bladder, prostate, and upper urinary tract,
and hydronephrosis and compromised renal function.
*
accumulation of urine in the kidney because of an obstruction in the ureter.
PATHOPHYSIOLOGY:
BPH first develops in the transitional zone of the prostate. The transitional
zone lies immediately external to the preprostatic sphincter. The Prostatic stromal
{supporting framework or matrix of a cell} and epithelial cells maintain a paracrine* type of communication whereby the growth
of the Prostatic epithelium can be regulated by cellular interaction with the basement membrane and stromal cells. There is strong evidence that stromal cell production of an excretory protein regulates epithelial cell
differentiation. BPH may therefore be due to defect in a stromal component that
normally inhibits epithelial proliferation. Androgens play a permissive role
in BPH; thus castrated boys, when they age, do not develop BPH. However, administering
exogenous testosterone is not associated with a significant increase in BPH. Dihydrotestosterone
(DHT), a metabolite of testosterone and a critical mediator of prostatic growth is synthesized in the prostate from circulating
testosterone by the action of the enzyme 5α-reductase, type 2. The enzyme
is localized principally in the stromal cells. DHT binds to the androgen receptors
and signals the transcription of growth factors for the stromal cells, and in a paracine* fashion by diffusion to epithelial
cells. mitogenic to the epithelial and stromal cells. The importance of DHT in causing nodular hyperplasia is supported by the clinical observations that an
inhibitor of 5α-reductase, which reduces DHT content, is given for BPH, and it reduces the prostate volume and in many
cases relieves BPH symptoms.
An additional vector is probably estrogen. This is based on the fact that BPH occurs when men generally have elevated estrogen
levels and relatively reduced free testosterone levels, and when prostate tissue becomes more sensitive to estrogens and less
responsive to DHT.
*
Paracrine: Of, relating to promoted by, or being a substance secreted
by a cell and acting on adjacent cells.
DIANGNOSIS:
Rectal examination (palpation
of the prostate through the rectrum) may reveal a markedly enlarged prostate.
Often, blood tests are performed
to rule out prostatic malignancy: elevated prostate specific antigen (PSA) levels needs further investigations such as reinterpretation
of PSA results, in terms of PSA density and PSA free percentage, rectal examination and transrectal ultrasonography. These
combined measures can provide early cancer detection.
Ultrasound examination of
the testicles, prostate and kidneys is often performed, again to rule out malignancy and hydronephrosis.
TREATMENT:
Various medical interventions including
5α reductase inhibitors and α-adrenergic blockers and a combination of both have been tried with modest success. Industry sponsored studies of α-adrenergic blockers show a 20-30% increase in
urinary flow rate and a 20-50% improvement in symptom scores. 5α-reductase
inhibitors (Finasteride) inhibits the conversion of testosterone to dihydrotestosterone in the prostate. A 1-year placebo-controlled study of 1229 men with BPH demonstrated no improvement in IPSS (questionnaire)
and flow rate over placebo, and only a small improvement in volume of prostate (Cronn 701).
Transuretheral resection of the prostate (TURP) is standard. TURP results
in Erectile dysfunction in 5-35%; incontinence 1%; and retrograde ejaculation in 5-10%.
Less invasive procedures include intraurethral stents, balloon dilation, microwave thermotherapy, high-intensity focused
ultrasound thermotherapy, laser ablation, electrovaporization, and radiofrequency vaporization. The choices among these less invasive treatments have not been firmly established, and long-term ability
to alter the natural history of BPH is under study.
In a study of 556 men with moderate symptoms
of BHP a comparison of treatment with transurethral resection of the prostate (TURP) to that of watchful waiting. During a 3-year follow up, 8% of the TURP & 17 of the watchful waiting failed treatment.
Saw Palmetto (Serenoa repens) is the most
common herbal treatment for health of prostate and bladder. However, a randomized,
placebo-controlled study showed that saw palmento was associated with epithelial cell contraction, especially in the transition
zone. However, no significant improvement in symptom score or flow rate was observed
(Cronn 701).
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