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  • Obstructive or irritative voiding symptoms.

  • Enlarged prostate size on rectal examination.

  • Absence of UTI, neurologic disorder, stricture disease, prostatic or bladder malignancy.


Benign prostatic hyperplasia (BPH) is the most common benign tumor in men, and its incidence is age related. 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. 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 BPH are poorly understood. Studies have shown that genetic and hereditary factors play a role in some patients. Investigation has also demonstrated insulin resistance and metabolic syndrome as independent risk factors for developing BPH. Other research involving chronic inflammation, growth factor–mediated disease progression, as well as androgen- and estrogen-mediated pathways have shed some insight into the pathophysiology of the disease.


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 ...

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