Benign Prostatic Hyperplasia : Symptom, Cause, and Treatment

Saturday, June 10th 2017. | Disease

Benign prostatic hyperplasia (BPH), a nearly ubiquitous condition, is the most common benign neoplasm of American men and occurs as a result of hormone-driven prostate growth.


  • The prostate gland comprises three types of tissue: epithelial or glandular, stromal or smooth muscle, and capsule. Both stromal tissue and capsule are embedded with α1-adrenergic receptors.
  • The precise pathophysiologic mechanisms that cause BPH are not clear. However, both intraprostatic dihydrotestosterone (DHT) and type II 5 Îreductase are thought to be involved.
  • BPH commonly results from both static (gradual enlargement of the prostate) and dynamic (agents or situations that increase Îadrenergic tone and constrict the gland’s smooth muscle) factors. Examples of drugs that can exacerbate symptoms include testosterone, Îadrenergic agonists (e.g., decongestants), anticholinergics (e.g., antihistamines, phenothiazines, tricyclic antidepressants, anticholinergic antispasmodics, and anticholinergics for Parkinson’s disease).

benign prostatic hyperplasia


  • Patients with BPH can present with a variety of signs and symptoms. Symptoms vary over time and can improve, remain stable, or worsen spontaneously.
  • Obstructive signs and symptoms result when dynamic and/or static factors reduce bladder emptying. Patients experience urinary hesitancy; urine dribbles out of the penis, and the bladder feels full even after voiding.
    Irritative signs and symptoms result from long-standing obstruction at the bladder neck. Patients experience frequency, urgency, and nocturia.
  • Complications include chronic kidney disease, gross hematuria, urinary incontinence, recurrent urinary tract infection, bladder diverticula, and bladder stones.


Diagnosis of BPH requires a careful medical history, physical examination, objective measures of bladder emptying (e.g., peak and average urinary flow rate, postvoid residual urine volume), and laboratory tests (e.g., blood urea nitrogen [BUN] and prostate-specific antigen [PSA]).
Medication history should include all prescription and nonprescription medications as well as dietary supplements.
On digital rectal examination, the prostate is usually, but not always, enlarged (more than 20 g), soft, smooth, and symmetric.
BPH treatment is aimed primarily at relieving manifestations of the disease that are bothersome for the patient. A secondary, but controversial, aim is to prevent serious complications in selected patients.
Management options for BPH include watchful waiting, drug therapy, and surgical intervention.
The choice depends on the severity of signs and symptoms (Table 80-1), with an emphasis on the patient’s perception.


Watchful waiting is appropriate for patients with mild disease, and for those with moderate disease with only mildly bothersome symptoms and without complications.
Watchful waiting involves reassessment at regular 6- to 12-month intervals. Patients should be educated about behavior modification such as fluid restriction before bedtime, avoiding caffeine and alcohol, frequent emptying of the bladder, and avoiding drugs that exacerbate symptoms.


Pharmacologic therapy is appropriate for patients with moderately severe BPH and as an interim measure for patients with severe BPH.
Pharmacologic therapy interferes with the stimulatory effect of testosterone on prostate gland enlargement (reduces the static factor) or relaxes prostatic smooth muscle (reduces the dynamic factor) (Table 80-2).
Two approaches are frequently used in the United States and merit separate consideration in this chapter. In general, reductase inhibitors have the advantage of decreasing prostate volume. ÎAdrenergic antagonists have faster onset and are more likely to relieve symptoms. Combination therapy with both approaches is ideal for patients with severe symptoms and a prostate gland of 40 to 50 g or more.

Agents that interfere with androgen stimulation of the prostate are not popular in the United States because of adverse effects. The luteinizing hormone-releasing hormone agonists leuprolide and goserelin cause decreased libido, erectile dysfunction, gynecomastia, and hot flashes. The antiandrogens bicalutamide and flutamide cause nausea, diarrhea, and hepatotoxicity.
Reductase Inhibitors

Reductase inhibitors are the only agents approved for BPH by the Food and Drug Administration (FDA) that interfere with the stimulatory effect of testosterone. These agents slow disease progression and decrease the risk of complications.
Compared with Îadrenergic antagonists, reductase inhibitors have the disadvantages of requiring 6 months to maximally shrink an enlarged prostate, being less likely to induce objective improvement, and causing more sexual dysfunction.
Whether the pharmacodynamic advantages of dutasteride confer clinical advantages over finasteride is unknown. Dutasteride inhibits types I and II 5 Îreductase, whereas finasteride inhibits only type II. Dutasteride more quickly and completely suppresses intraprostatic DHT (versus 80% to 90% for finasteride) and decreases serum DHT by 90% (versus 70%).
The ideal candidate has a prostate gland of 50 g or more. reductase inhibitors might also be preferred in patients with uncontrolled arrhythmias, poorly controlled angina, use of multiple antihypertensives, or inability to tolerate hypotensive effects of Îadrenergic antagonists.
Reductase inhibitors reduce serum PSA levels by 50%. Therefore, PSA should be measured at baseline and, for monitoring purposes, subsequent measurements should be doubled.
Reductase inhibitors are in FDA pregnancy category X and are therefore contraindicated in pregnant females. Pregnant and potentially pregnant women should not have contact with semen from men receiving reductase inhibitors.
Adrenergic Antagonists
Adrenergic antagonists relax the smooth muscle in the prostate and bladder neck, thereby increasing urinary flow rates by 2 to 3 mL/s in 60% to 70% of patients and reducing postvoid residual urine volumes. Terazosin and tamsulosin produce durable responses for 3 to 4 years.
Adrenergic antagonists do not decrease prostate volume or PSA levels.
Terazosin, doxazosin, and alfuzosin are second-generation adrenergic antagonists. They antagonize peripheral vascular α1-adrenergic receptors in addition to those in the prostate. Therefore, their adverse effects include first-dose syncope, orthostatic hypotension, and dizziness. Alfuzosin is less likely to cause cardiovascular adverse effects than other second-generation agents.
To minimize orthostatic hypotension and first-dose syncope with terazosin and doxazosin, patients should be slowly titrated to a maintenance dose and should take these drugs at bedtime.
Tamsulosin, the only third-generation adrenergic antagonist, is selective for prostatic α1A receptors. Therefore, tamsulosin does not cause peripheral vascular smooth muscle relaxation.
Tamsulosin is a good choice for patients who cannot tolerate hypotension; have severe coronary artery disease, volume depletion, cardiac arrhythmias, severe orthostasis, or liver failure; or are taking multiple antihypertensives. Tamsulosin is also suitable for patients who want to avoid the delay of dose titration or to avoid dosing only at bedtime.
Caution is needed to avoid potential drug interactions. Tamsulosin decreases metabolism of cimetidine and diltiazem. Carbamazepine and phenytoin increase catabolism of adrenergic antagonists.


Prostatectomy, performed transurethrally or suprapubically, is the gold standard for treatment of patients with moderate or severe symptoms of BPH and for all patients with complications.
Prostatectomy does not relieve irritative voiding symptoms of BPH. These patients may benefit from anticholinergic agents (see Chapter 82).


Although widely used in Europe for BPH, phytotherapy with products such as saw palmetto berry (Serenoa repens), stinging nettle (Urtica dioica), and African plum (Pygeum africanum) should be avoided. Studies of these herbal medicines are inconclusive, and the purity of available products is questionable.