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  • Obstructive or irritative voiding symptoms.

  • Enlarged prostate size on rectal examination.

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


Benign prostatic hyperplasia (BPH) is extremely common, and its incidence rises with increasing age. The prevalence of histologic BPH in autopsy studies rises from approximately 20% in men aged 41–50 years, to 50% in men aged 51–60, and to greater than 90% in men over 80 years of age. Bothersome urinary symptoms related to BPH also increase with age. 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 BPH 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 BPH 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.


The etiology of lower urinary tract symptoms is multifactorial. Benign prostatic enlargement is a common component of this symptom complex. 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 BPH. Each element may be targeted in medical management schemes.

Laboratory and clinical studies have identified two necessary factors for development of BPH: the effect of endocrine compounds (eg, dihydrotestosterone [DHT]) on prostate growth, and the impact of aging. The main mechanism of action seems to be stromal-epithelial interactions (stromal cells regulating growth of epithelial cells or other stromal cells by paracrine or autocrine signaling or by secreting growth factors such as basic fibroblast growth factor or transforming growth factor beta). Studies have also demonstrated that BPH is under endocrine control and that castration results in the regression of established disease and improvement in urinary symptoms. Administration of a luteinizing hormone–releasing hormone (LHRH) analog in men reversibly shrinks established BPH, resulting in objective improvement in urinary flow rate and subjective improvement in symptoms.


BPH is truly a hyperplastic process, resulting from an increase in cell numbers. Microscopic evaluation reveals a nodular growth pattern consisting of stroma or epithelium. Stroma is composed of varying amounts of collagen and smooth muscle. The differential representation of various histologic components of BPH in part explains the potential variable responsiveness to medical therapy. Thus, alpha-blocker therapy may result in excellent responses in patients with BPH when there is a significant component of smooth muscle, while hyperplasia composed predominantly of epithelium might respond better to 5-alpha-reductase inhibitors. Patients ...

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