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Key Clinical Updates in Benign Prostatic Hyperplasia

There has been a significant shift toward more minimally invasive therapies due to cost of care and better data from 3- to 5-year (or more) outcomes. Studies have also shown decreased cost of operative treatments compared with medical therapies in as short as 6 months (or as long as 8 years).

ESSENTIALS OF DIAGNOSIS

  • Obstructive or irritative voiding symptoms.

  • May have enlarged prostate on rectal examination.

  • Absence of urinary tract infection, neurologic disorder, stricture disease, prostatic or bladder malignancy.

GENERAL CONSIDERATIONS

Benign prostatic hyperplasia is the most common benign tumor in men, and its incidence is age related. The prevalence of histologic benign prostatic hyperplasia in autopsy studies rises from approximately 20% in men aged 41–50 years, to 50% in men aged 51–60, and to over 90% in men over 80 years of age. Although clinical evidence of disease occurs less commonly, symptoms of prostatic obstruction are also age related. At age 55 years, approximately 25% of men report obstructive voiding symptoms. At age 75 years, 50% of men report a decrease in the force and caliber of the urinary stream.

Risk factors for the development of benign prostatic hyperplasia are poorly understood. Some studies have suggested a genetic predisposition and some have noted racial differences. Approximately 50% of men under age 60 years who undergo surgery for benign prostatic hyperplasia may have a heritable form of the disease. This form is most likely an autosomal dominant trait, and first-degree male relatives of such patients carry an increased relative risk of approximately fourfold.

ETIOLOGY

The etiology is not completely understood but seems to be multifactorial. The prostate is composed of both stromal and epithelial elements, and each, either alone or in combination, can give rise to hyperplastic nodules and the symptoms associated with benign prostatic hyperplasia. Each element may be targeted in medical management schemes.

Laboratory and clinical studies have identified two factors necessary for the development of benign prostatic hyperplasia: dihydrotestosterone (DHT) and aging. Animal studies have demonstrated that the aging prostate becomes more sensitive to androgens. Prostatic growth in aging dogs appears to be related more to a decrease in cell death than to an increase in cell proliferation. Laboratory studies have suggested several theories in this area: (1) stromal epithelial interactions (stroma cell may regulate growth of epithelial cell or other stromal cells via a paracrine or autocrine mechanism by secreting growth factors such as basic fibroblast growth factor or transforming growth factor beta), and (2) aging may result in stem cells undergoing a block in the maturation process, preventing them from entering into programmed cell death (apoptosis). The impact of aging in animal studies appears to be mediated via estrogen synergism. In canines, estrogens induce the androgen receptor; alter steroid metabolism, resulting in higher levels of intraprostatic DHT; inhibit cell death when given ...

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