Benign Prostatic Hyperplasia (BPH) in Men

An age related, non-malignant enlargement of the prostate gland, benign prostatic hyperplasia is a common disorder of men as they get older. The prostate, very small at birth, grows during puberty and reaches adult size around the age of 20. Benign hyperplasia, which is an increase in the number of cells, normally starts to occur at 40 to 45 years of age, and continues slowly through the rest of life. Of all men over the age of 55 it is estimated that one-fourth will have symptoms while one-half of men over the age of 75 will exhibit symptoms. Most men first find out they have this condition when they visit their doctor complaining of urinary dysfunction.

The cause of benign prostatic hyperplasia is unknown, but risk factors include age, family history, race, ethnicity, and hormonal factors. The incidence, which increases with age, is highest in African Americans and lowest in Japanese men. Those with a family history of BPH have an increased chance of getting it.

The two necessary preconditions for BPH are the age of 50 or greater and the presence of testicles. Men who are castrated before puberty do not develop benign prostatic hyperplasia. Dihydrotestosterone (DHT) which is formed in the prostate from testosterone is the androgen that is responsible for prostate growth. Although androgen levels decrease in aging men, the aging prostate appears to become more sensitive to available DHT. Estrogen, which is produced is small amounts in males, appears to sensitize the prostate gland to the effects of DHT as well. Increasing estrogen levels associated with aging or a relative increase in estrogen related to testosterone levels may contribute to prostatic hyperplasia.

BPH begins as small nodules in the periurethal glands, which are the inner layers of the prostate. The prostate enlarges through formation and growth of nodules (hyperplasia) and enlargement of glandular cells (hypertrophy). These changes occur over a long period of time. The pathophysiologic effects result from a combination of factors, including urethral resistance to the effects of BPH, intravesical pressure during voiding, detrusor muscle strength, neurologic functioning, and general physical health.

The expanding prostatic tissue compresses the urethra and causes partial or complete obstruction of the flow of urine from the bladder. The detrusor muscles hypertrophy to compensate for increased resistance to urinary flow; eventually decreased bladder compliance and bladder instability result. As a result of this the signs and symptoms of BPH begin to appear and include weak urinary stream, increased time to void, hesitancy, incomplete bladder emptying post void dribbling. There is also irritation which can manifest as increased frequency urinating, urgency, incontinence, nocturia, dysuria, and bladder pain.

Urinary retention can become chronic, resulting in overflow incontinence with any increase in intra-abdominal pressure. There is little correlation between the size of the prostate gland and the urinary manifestations.

Unless the enlarging prostate is reduced multiple complications may occur. As urine is retained in the bladder, increasing bladder distention occurs. Diverticula, which are outpouchings on the bladder wall result from distension. The distension may also obstruct the ureters. Infection, more common in retained urine and in Diverticula, may ascend from the bladder to the kidneys, which can cause kidney infections.