Health and Prostate

Benign prostatic hyperplasia (BPH) is the most common cause of voiding dysfunction, and one of the most frequent causes of disability in aging men. BPH is a nonmalignant neoplasm of prostatic epithelial and stromal tissue. Often inappropriately termed “benign prostatic hypertrophy,” the disease process involves hyperplasia rather than hypertrophy. Benign prostatic hyperplasia is a rare occurrence in men less than 40 years of age. After age 40 the prevalence of BPH is age-dependent and approximately 50% of men greater than 50 years of age have moderate urinary difficulties due to the disease process. By age 85, approximately 90% of men will have BPH. Men of all races and cultures are afflicted, suggesting the etiology of BPH may not be environmentally or genetically influenced.

Often benign prostatic hyperplasia (BPH) is present prior to the fifth decade of life; however, it is benign and unnoticed since patients are usually asymptomatic. Generally BPH becomes symptomatic commencing with the fifth decade of life. Identified risk factors for BPH are aging and normal testicular function. Since the prostate surrounds the urethra, urinary symptoms are the signs of prostatic hyperplasia. Although benign prostatic hyperplasia (BPH) and prostate cancer often coexist, there is no evidence that men with BPH are more likely to develop prostate cancer.

Pathogenesis of benign prostatic hyperplasia (BPH)

Aging and androgens are all that is required for the development of benign prostatic hyperplasia (BPH). The disease is not seen in men who are castrated early in life, and castration actually promotes regression of BPH. Testosterone, the major circulating androgen, diffuses into the prostate cells, and is predominantly converted to dihydrotestosterone (DHT) by the enzyme 5-alpha reductase. More than 90% of testosterone in the prostate is of testicular origin with the remainder produced by the adrenal glands. Testosterone and DHT bind to androgen receptors and result in increased protein biosynthesis and hyperplasia. Thus, prostatic hyperplasia is dependent directly on androgen stimulation.

Prostatic obstruction consists of two elements: the static and dynamic components. The static component is related to enlargement of the prostate gland, which requires the presence of dihydrotestosterone (DHT). Thus, the use of antiandrogens and more recently the 5-alpha reductase inhibitor finasteride (Proscar), approved in 1992 by the Food and Drug Administration (FDA) to treat BPH, are therapeutic options. The dynamic component originates from the tone of the prostatic smooth muscle and is under the influence of the sympathetic nervous system. Smooth muscle contraction in the urethra, prostate and bladder neck contribute to the voiding symptoms of benign prostatic hyperplasia (BPH). Research in the animal model demonstrated that the rat prostate contracts in the presence of norepinephrine, an adrenergic agonist. Alpha-adrenergic receptors are abundant in the prostatic adenoma, prostatic capsule, and bladder neck, and these adrenergic receptors are primarily the alpha-1 type. On the basis of these findings, the nonselective alpha-adrenergic antagonist phenoxybenzamine was studied as an agent to decrease muscular resistance to urinary outflow, and proved to be beneficial in the treatment of BPH. Consequently, the selective alpha-1 adrenergic antagonists (prazosin, terazosin and doxazosin) have been advocated for use in patients with benign prostatic hyperplasia (BPH).