s Benign Prostatic Hyperplasia (BPH) —Viquepedia


Pathology and Management of Benign Prostatic Hyperplasia (BPH)/Lower Urinary Tract Symptoms (LUTS)

Benign Prostatic Hyperplasia or BPH is a common noncancerous condition affecting nearly all aging men and a very common cause of urinary retention.

The term prostatic hyperplasia can be defined in terms of microscopic changes in the prostate gland, or clinical manifestations produced by the changes in the prostate gland.

Microscopically, BPH is manifest by proliferation (hyperplasia) of the stromal and epithelial cells within the periurethra zone of the prostate gland. This cellular hyperplasia causes glandular enlargement and the typical symptoms commonly known as prostatism, although size of the prostate, degree of urethral resistance, and severity of symptoms are not strongly correlated.

Some clinicians argue that the term benign prostatic hyperplasia should be used to describe histologic evidence of cellular hyperplasia and that benign prostatic enlargement is a more appropriate term for description of macroscopic prostatic enlargement; however, BPH is the commonly used term and the one recommended by the International Consultation on BPH.

The Fourth International Consultation on BPH also recommended the use of standardized terminology to describe lower urinary tract voiding symptoms. In the past, the term prostatism was used to refer to symptoms associated with voiding difficulty, such as hesitancy, intermittency, and weak urinary stream; however, these symptoms occur in women as well as men, and to date a cause and effect relationship has not been adopted to describe symptoms of voiding difficulty and to replace the old term prostatism.


The etiology and pathogenesis of BPH are not clearly understood, and the true incidence has not yet been established. Several population studies suggest that the overall incidence is 15 per 1000 man-years and that the incidence increases from a rate of 3 per 1000 man-years in men less than 49 years of age to 38 per 1000 man-years in men aged 75 or more.

Indeed, as many as 50% of 60-year old men and 80% of 80-year old men suffer voiding dysfunction and lower urinary tract symptoms (LUTS) related to BPH. Severe LUTS have a significant impact on health and well-being, and the number of men affected by this condition will continue to rise as a result of longer life expectancies.

Data regarding risk factors for BPH are inconclusive and sometimes contradictory. For example, one study of Asian men found that alcohol use and smoking appeared to reduce the risk of BPH, whereas several other population surveys found these behaviors to be associated with increased risk.

Smoking stimulates the sympathetic nervous system and theoretically may increase smooth muscle tone at the bladder neck and sphincter, thus, smoking seems more likely to act as a risk factor than a protective factor.

Studies supporting this hypothesis include a study conducted in the United States of African-American men in which the following factors were associated with increased risk for LUTS: history of smoking or current tobacco use, heavy alcohol consumption, history of hypertension or heart disease, and diabetes.

Similarly, a study of Finnish men found a higher prevalence of LUTS among those who smoked as compared with those who did not. Race appears to affect the rate at which symptoms develop; African-American men develop symptoms earlier than white men, whereas Asian men develop symptoms later than white men. Comorbidities associated with LUTS include neurologic disease, arthritis, and constipation or fecal impaction.


Factors currently believed to be important in the development of BPH include growth factors, stromal-epithelial cell interaction (signaling), hormonal factors (production of dihydrotestosterone and relative proportion of estrogens), and nonandrogenic factors produced by the testes.

Growth factors are known to affect cell growth and cell death and are believed to function synergistically with androgens (dihydrotestosterone) to stimulate stromal cell hyperplasia.

The growth factors most relevant to BPH include epidermal growth factor, keratinocyte growth factor, and basic fibroblast growth factor. A synergistic effect involving androgens and growth factors helps to explain stromal cell hyperplasia; however, it does not explain epithelial cell hyperplasia, because these cells are unresponsive to androgens.

The mitotic response of epithelial cells is believed to be mediated by stromal-epithelial cell interactions. Although epithelial cells are unresponsive to androgenic stimulation, they are very responsive to growth factors produced by the stromal cells, and these growth factors are produced in greater quantities when the stromal cells are stimulated by androgens.

Thus, androgenic stimulation may indirectly affect epithelial hyperplasia. In addition, the testes may produce a nonandrogenic substance that acts to sensitize the prostatic tissues to the effects of androgens. Finally, estrogen is believed to play some type of supportive or synergistic role in the development of BPH.

The typical symptoms associated with BPH (diminished urinary stream, hesitancy, intermittency, nocturia, terminal dribbling, frequency, and urgency) are thought to be caused by the gradual increase in size of the prostate gland.

These symptoms may or may not be associated with significant outlet obstruction. In nonobstructed men, LUTS are thought to be caused by a complex interplay of poorly understood factors, including some degree of urethral obstruction, impaired detrusor contractility (overactive bladder), and sensory urgency.

Approximately two-thirds to three-fourths of patients with clinical signs of BPH are found to have some degree of obstructed voiding and urinary retention; however, these patients do not necessarily progress to complete inability to void. Potential predictors of complete retention include prostate size, poor uroflow, and clinical symptoms.

The primary risk factors for complete obstruction are increasing level of symptoms as measured by the AUA Symptom Score, the sensation of incomplete emptying, urinary frequency (urge to void every 2 hours or more often), and a weak urinary stream. In North America, serious complications of BPH are rare; therefore, treatment should be guided by the patient’s perceptions of symptom severity and the impact on his quality of life, as opposed to prostate size per se.

–Pathology of Outlet Obstruction Secondary to Benign Prostatic Hyperplasia

As noted, BPH may or may not progress to the point of significant outlet obstruction. When outlet obstruction does occur, it is thought to develop as a result of both static (structural) and dynamic (functional) factors.

  1. Static Factor

The static factor is the size of the prostate gland and the degree to which it compresses the urethral lumen. Men whose prostate glands are larger than 30 mL are three times more likely to progress to obstruction than men with smaller prostates (less than 30 mL).

Enlargement of the median lobe of the prostate is of particular importance; median lobe hypertrophy can cause significant urethral compression even if the overall size of the prostate appears nonsignificant. This is partly because of the effect of the nonelastic prostatic capsule, which restricts the direction in which the prostate can spread.

Prostatic ultrasound scanning can delineate both overall gland enlargement and median lobe enlargement, and the formula obtained by ultrasound (transition zone volume/total prostatic volume) appears to accurately predict patients at high risk for acute retention.

The importance of median lobe enlargement (transition zone volume) and total prostate enlargement is supported by the observation that 5-alpha-reductase inhibitors reduce both transition zone volume and overall prostatic volume and also improve symptoms of voiding dsyfunction.

  1. Dynamic Factor

Dynamic factors contributing to outlet obstruction include smooth muscle tone and alpha-adrenergic receptors.

Prostatic hyperplasia appears to cause both an increased volume of smooth muscle and increased sympathetic tone, both of which contribute to increased resistance at the level of the prostatic urethra. This has major implications for management, because pharmacologic agents can be used to increase or reduce sympathetic tone; for example, sympathomimetic agents such as pseudoephedrine increase smooth muscle tone and urethral resistance, whereas blockade of the sympathetic receptors by alpha-adrenergic antagonists produces smooth muscle relaxation and reduced resistance at the bladder neck and prostatic urethra.

Clinically, the introduction of alpha-adrenergic antagonists has radically changed the management of patients with BPH, because these drugs are highly effective in improving urinary flow rates and reducing obstructive symptoms. There is some controversy about the precise mechanism underlying the dynamic obstruction associated with increased prostatic smooth muscle tone. For example, the benefits provided by alpha-adrenergic antagonists could be explained by the reduction of resistance at the bladder neck (as opposed to the prostatic urethra) or by inhibition of various neurologic reflexes affectivn vesicourethral function.

–Phases of Prostatic Obstruction

Tanagho identified two major phases in the development of outlet obstruction caused by BPH:

  1. the compensatory phase, during which the bladder wall hypertrophies in an attempt to overcome the increased urethral resistance; and
  2. the decompensation phase, during which contractility is significantly diminished and residual urine volumes rise significantly (Table X1)
Table X1 | Phases of Bladder Response to Benign Prostatic Hypertrophy
Stage of Bladder ResponsePathologic Changes in Bladder
Compensatory phaseTrabeculation of bladder wall, hypertrophy of the trigone, detrusor overactivity
Decompensation phaseChanges in muscle function and loss of contractility, resulting in elevated postvoid residual urine volume, loss of bladder wall compliance resulting in elevated intravesical pressures and increased resistance at ureterovesical junction; the end result consists of ureteral dilation, hydronephrosis, and potential for urinary tract infection, pyelonephritis, and impaired renal function
Data from Tangho EA. Urinary obstruction and stasis. In: Tangho EA, McAninch JW, editors: Smith’s general urology, ed 16, New York, 2004, Lange Medical Books/McGraw-Hill, pp 175-187.

During the compensatory phase, the detrusor muscle gradually adapts and thickens in response to the increasing resistance caused by the prostate. Urodynamic studies during this phase demonstrate high voiding pressures and decreased compliance; voiding pressures rise to two to four times the normal values, that is, from 30 cm H2O to as high as 120 cm H2O.

The elevated intravesical pressures cause formation of cellules, small pockets that are created when segments of the bladder lining are pushed between bundles of superficial muscle fibers. If the pressures within the bladder remain high, the cellules eventually push through the entire thickness of the bladder wall to form diverticula; the diverticular sacs fail to empty effectively, thus creating pools of stagnant urine that act as a reservoir for bacterial proliferation and calculi formation.

The elevated pressures within the bladder wall also promote collagen deposition and hypertrophy of the smooth muscle fibers, resulting in bladder wall trabeculation. Hypertrophy of the smooth muscle fibers is particularly pronounced in the trigonal region; this causes distortion of the ureteric orifices, which results in progressive obstruction of the ureters, reflux, and hydronephrosis. (Catheterization and bladder decompression temporarily relieve the trigonal distension and reduce distortion and obstruction of the ureteral orifices.)

In addition to detrusor hypertrophy, the early phases of outlet obstruction cause detrusor overactivity, as evidenced by the classic symptoms of urgency, frequency, nocturia, and possibly urge incontinence Opens in new window. Finally, on a microscopic level, the bladder wall is infiltrated with plasma cells, lymphocytes, and polymorphonuclear celles.

Unrelieved obstruction eventually results in bladder decompensation. The decompensation phase is characterized by progressive reduction in bladder contractility and ability to empty the bladder. As contractility declines, PVR volumes and the incidence of urinary tract infections rise. If treatment is not initiated, the bladder eventually becomes totally acontractile.


This section addresses the assessment parameters of particular relevance to the patient with BPH.

  1. History

In obtaining patient history, the nurse must remember that LUTS and urinary retention can be caused by many factors and conditions other than BPH; even in the patient with known BPH, there may be neurologic or pharmacologic factors contributing to the degree of retention and severity of symptoms. Therefore, a complete history is always essential; this must include medical conditions, past surgical procedures, all prescription and over-the counter medications, and a thorough discussion of urologic symptoms.

Because the treatment of BPH is affected in large part by the degree of “bother” associated with LUTS, the nurse should query the patient regarding symptom onset, the degree of bother, any diagnostic procedures that have been completed in relation to the problem, and any past or current treatment.

A validated tool should be used to assess symptom severity; the AUA Symptom Score Opens in new window (also known as the International Prostrate Symptom Score) is a validated tool that provides an objective index of symptom severity and can also contribute to the prediction of risk for urinary retention. See here Opens in new window. (The range of scores is from 0, for no symptoms, to 35, extreme symptoms; a score greater than 7 is associated with increased risk for retention.)

It is also helpful to query the patient about any problems with erectile function, especially if treatment with 5-alpha-reductase inhibitors is being considered; the nurse should discuss the potential effects of these drugs on sexual function.

  1. Physical Examination

The most critical element of the physical examination for the patient with BPH is the digital rectal exam; the prostate gland should be carefully assessed for size, shape, consistency, and masses. In addition, the clinician should note tone and contractility of the anal sphincter and the presence and consistency of stool in the rectal vault. Other factors to be assessed include abdominal exam and evidence of neurologic dysfunction.

  1. Diagonostic Studies

As is true of all patients with known or suspected urinary retention, measurement of PVR urine volume and uroflowmetry provide very valuable data. Urodynamic studies should be done when there is concern regarding detrusor contractility and the patient is contemplating TURP, and transurethral ultrasound is indicated when it is important to accurately delineate prostate size (situations in which minimally invasive procedures are being considered).

Prostate-specific antigen (PSA) is not recommended as a routine test for all men with BPH and LUTS; however, is recommended for men with a life expectancy of more than 10 years and for situations in which PSA results may alter treatment. For example, several trials have shown that PSA is a proxy for prostate volume and can be used to predict symptom progression and response to therapies such as 5-alpha-reductase inhibitors.

Men with LUTS who have a PSA greater than 1.5 ng/mL are more likely to have a prostate volume of at least 30 mL and are at higher risk for complete obstruction than men whose PSA is less than 1.5 ng/mL. Thus, men whose PSA is elevated and who are symptomatic should undergo therapy designed to reduce prostate gland volume, that is, 5-alpha-reductase inhibitors (possibly in combination with alpha-adrenergic blockers to improve voiding symptoms).

Conversely, men whose PSA is less than 1.5 ng/mL are much less likely to progress to outlet obstruction; in these patients, treatment is determined by symptom severity and bother and is designed to reduce voiding difficulty, as opposed to reducing prostate volume. These patients are best managed with alpha blockers as opposed to 5-alpha-reductase inhibitors.

  1. Risk Factors for Retention

In considering treatment options for the patient with BPH, one consideration is risk for progression to significant retention.

Factors that have been identified as predictive of risk for retention include the following: age; prostate size larger than 30 mL, urinary low rate less than 12 mL/second, AUA Symptom Score greater than 7, and PVR volumes greater than 150 mL.


The introduction of new pharmacologic agents for treatment of BPH and the development of minimally invasive procedures for prostatic resection have led to significant changes in the treatment options for men with clinically significant BPH and LUTS.

Men are now offered a variety of options, depending on symptom severity and potential for obstruction; these include

  • watchful waiting,
  • alpha-adrenergic blocking agents,
  • 5-alpha-reductase agents,
  • transurethral microwave heat treatment (TMT), transurethral needle ablation (TUNA),
  • interstitial laser therapy,
  • stent placement,
  • TURP, and
  • suprapubic prostatectomy.

Patients who are relatively asymptomatic may be managed with “watchful waiting” as well as with reassurance and education regarding behavioral strategies (fluid management, restriction of caffeine and alcohol intake, and routine toileting).

Treatment decisions should be guided by patient preference. The AUA Consensus Guidelines note that even men with moderate or severe symptoms do not necessarily require further diagnostic tests or active therapy if they are not bothered by their symptoms (and if they are relatively low risk for retention).

  1. Management of Irritative Voiding Symptoms

As noted earlier, obstruction may produce bladder overactivity and irritative voiding symptoms (urgency, frequency, nocturia, and possibly urge incontinence), and relief of the obstruction may or may not resolve the symptoms.

Indeed, relief of the obstruction may actually cause worsening of any incontinence, because the “protective mechanism” provided by the obstruction has been removed. If the obstruction has not been prolonged, the symptoms may gradually resolve; in addition, numerous treatment strategies may be of benefit for these individuals, such as fluid management, restriction of caffeine intake, bladder restraining strategies, and anticholinergics.

  1. Management of Obstructive Voiding Symptoms: Alpha-Adrenergic Blockers

As has been stated, medical management of obstructive voiding symptoms related to BPH has been revolutionized by the introduction of alpha-adrenergic antagonists (alpha blockers). (Table X3 outlines the currently available pharmacologic agents for treatment of obstructive voiding symptoms.)

Table X3 | Alpha-I-Adrenergic Receptors in Lower Urinary Tract
Receptors subtypeDistributionEffects of Receptor Blockade
Alapha IAProstatic stroma and capsule, bladder neckDecreases tone in prostate and bladder neck
Alpha IBProstatic epithelium, vascular smooth muscleRelaxes blood vessels
Alpha IDProstatic stroma, vascular smooth muscleDecreases tone in prostate, relaxes blood vessels
From Kaplan SA: Use of alpha adrenergic inhibitors in treatment of benign prostatic hyperplasia and implications on sexual function, Urology 63(3):428-434, 2004.

This means that many men who would formerly have required surgery can now be managed medically; it also means that patients who do require surgery are generally more symptomatic, with larger prostate glands, and are therefore at higher risk for complications.

Alpha-adrenergic receptors mediate catecholaminergic actions in the sympathetic nervous system and alpha blockers bind to these receptors to “block” the effects of sympathetic neurotransmitters such as norepinephrine. At least three alpha-receptor subtypes have been identified in humans; alpha-1a, alpha-1b, and alpha-1d.

In the urinary tract, the most significant alpha-receptor subtypes seem to be alpha-1a and alpha-1d, and the alpha-1d receptors have a much higher affinity for norepinephrine and epinephrine than either the alpha-1a or alpha-1b receptors. The alpha-1d receptors predominate in the detrusor and are less common in the prostatic stroma and capsule; the reverse is true of the alpha-1a receptors.

Thus, blockade of these two receptor types will theoretically improve bladder contractility while reducing urethral resistance. DeGroat suggested that alpha-adrenergic blockers may also slightly enhance bladder contractility by a direct or indirect effect on the parasympathetic ganglia, thus further explaining their ability to improve bladder emptying.

Sympathetic stimulation of the prostatic smooth muscle, which is mediated by alpha-adrenergic receptors, results in increased muscle tone (the dynamic component of outlet obstruction); the primary neurotransmitter is noradrenaline (norephinephrine).

Alpha-adrenergic antagonists (terazosin, doxazosin, tamsulosin, and alfuzosin) improve voiding function by “blocking” the alpha-adrenergic receptors located in the smooth muscle of the bladder neck, proximal urethra, and prostatic stroma and capsule. This blockade rapidly reverses the effects of alpha-adrenergic agonists such as ephedrine and norepinephrine.

A review of efficacy studies indicates that all these agents improve voiding symptoms to a similar degree, and all involve once-daily dosing. However, tamsulosin and alfuzosin are associated with a lower incidence of side effects, especially postural hypotension (as compared with terazosin and doxazosin).

All these agents are selective for alpha-1 receptors; however, tamsulosin is the most selective for the alpha-1a and alpha-1d receptor subtypes in the prostatic stroma and capsule, which may explain its reduced incidence of cardiovascular side effects. However, doxazosin and terazosin may also contribute to reduction in volume of prostatic smooth muscle through a molecular mechanism that enhances apoptosis (death) of the smooth muscle cells; this may account for the long-term benefit conferred by these particular medications. Research is ongoing into the possible use of alpha anatangoists to promote apoptosis in men with prostate cancer.

Men with advanced BPH and severe LUTS may not benefit from alpha-adrenergic antagonists and may require more invasive treatment. Specific indicators for more aggressive treatment include the following: prostate larger than 40 mL, severe symptoms as measured by the AUA symptom score, uroflow of less than 10 mL/second, and/or urodynamic evidence of outflow obstruction.

  1. Reduction of Prostate Size

Prostate size is the static element contributing to BPH-induced outlet obstruction; the degree of urethral compression is directly related to the size of the prostrate as a whole and the median lobe in particular. Until the introduction of 5-alpha-reductase inhibitors, the only way to reduce the size of the prostate was surgical resection (typically TURP).

However, it is well known that the prostate is an androgen-sensitive organ, and BPH can be viewed as a bulky, testosterone-dependent prostatic adenoma. Thus, reduction in testosterone levels (and prostate size) can be achieved by administration of drugs that block the effects of 5-alpha-reductase, a steroid that is necessary for the conversion of testosterone to dihydrotestosterone (a much more potent androgen).

5-alpha-reductase has two isoforms: Type 1 is expressed in the liver, skin, hair follicles, and the testicles; and Type 2, which is responsible for male virilization, is found in genital skin, hair follicles, and the stromal and epithelial cells of the prostate.

Finasteride and dutasteride are the two 5-alpha-reductase inhibitors currently available, and both achieve reduction in prostate size and subsequent reduction in urethral obstruction. The benefits of finasteride are well documented:

  • reduction in size of the prostate gland,
  • reversal of the disease process (BPH reversal),
  • reduction in voiding symptoms,
  • reduced episodes of urinary retention, and
  • reduced likelihood of invasive surgery such as TURP.

Dutasteride differs from finasteride in that it is capable of inhibiting both isoforms of 5-alpha-reductase. This may result in greater inhibition of dihydrotestosterone production and therefore in more rapid clinical response; however, this has not yet been proven. Clinically, to date the drugs appear comparable, although no head-to-head studies have yet been published. Side effects of 5-alpha-reductase inhibitors include decreased libido, impotence, reduced volume of ejaculate, and occasional breast tenderness. Fortunately, most of these side effects diminish over time.

Men who are most likely to benefit from 5-alpha-reductase inhibitors include those with prostrate glands of 40 mL or more. These drugs have been shown to control BPH-related hamaturia in addition to preventing progression of the disease process; these drugs may also contribute to the prevention of prostrate cancer, although further research is needed in this area.

Men with large volume prostrates who also have severe LUTS may benefit from dual therapy, that is, a combination of 5-alpha-reductase inhibitors (to reduce prostrate volume) and alpha-adrenergic antagonists (to reduce urethral resistance); combination therapy reduces the risk of acute urinary retention more effectively than either drug alone. (See Table X4 for summary of various drugs that can be used to reduce LUTS in men with BPH.)
Table X4 | Medical Therapy for Lower Urinary Tract Symptoms (LUTS)
DrugActionDoseSide Effects
Terazosin (Hytrin)Nonselecive alpha-1 blocker; relaxes smooth muscle of bladder neck1 mg at HS to reduce incidence and severity of side effects; gradually increase dose to 2 mg, 5 mg, 10 mg to achieve desired flow rate; 4 to 6 weeks may be required to achieve benefitNB: All alpha-blockers should be administered cautiously in patients taking antihypertensives. Both terazosin and doxazosin: First-dose syncope; postural hypotension, fatigue, dizziness, headache, nasal stuffness, erectile dysfunction, urinary incontinence, need to monitor blood pressure
Doxazosin (Cardura)Nonselective alpha-1 blocker (very similar to terazosin)1 mg once daily; gradually increase to 2 mg, 4 mg, 8 mg to achieve benefit; each increase should be approximately 2 weeks apart

Table X4 Continues
DrugActionDoseSide Effects
Tamsulosin (Flomax)Selective alpha-1 blocker (alpha-1a, 1d receptor subtypes): reduced cardiovascular side effects because of selectivity0.4 mg once daily, increase dose to 0.8 mg after 2 weeks if necessary 10 mg once dailyBoth tamsulosin and alfuzosin: absorption increased with food; take immediately following same meal each day; ejaculatory dysfunction; contraindicated in men with hepatic insufficiency; potential P450 3A4 inhibitor
Alfuzosin (Uroxatral)
Finasteride (Proscar)5-alpha-reductase inhibitor: inhibits Type II isoenzyme in stromal and basal epithelial cells to prevent conversion of testosterone to dihydrotestosterone5 mg once dailyErectile dysfunction; decreased libido; ejaculatory dysfunction; long-term therapy required; may take 6 months to reach peak efficacy; not effective in men with small prostates
Dutasteride (Avodart)5-alpha-reductase inhibitor; may inhibit both Type I and Type 2 isoenzymes0.5 mgSimilar side effects; dual isoenzyme inhibition should cause more rapid relief of obstructive symptoms
Phytotherapy: saw palmetto, betasitosterols, Pygeum africanum, cernitinActions not completely understood; believed to act as mild 5-alpha-reductase inhibitor and possibly aromatase inhibitor Dosages and benefits vary widely depending on preparationAdvise patient that he should not take phytotherapy when using other medical therapy for obstructed voiding
Adapted from Turkoski BB, Lance BR, Bonfiglio MF: Drug information for advanced practice nursing, ed 4, Hudson, Ohio, 2003, Lexi-Camp, p 171, with permission.
  1. Phytotherapy (Herbal Medications)

Phytotherapy is a common form of self-treatment among men with LUTS, and in Europe, nonprescription herbal agents are recommended at least as often as alpha-blocking agents or finasteride. These agents are thought to “work” by inhibiting aromatase. Commonly used herbal agents include

  1. saw palmetto,
  2. beta-sitosterols (Prostatic Perform),
  3. Pygeum africanum (pygeum bark), and
  4. cernitin (Cernilton).

Saw palmetto is the most widely studied of these agents. Randomized controlled trials conducted to date proved the following guidance in use of herbal agents:

  • Saw palmetto provides improvement in voiding symptoms with low incidence of side effects (comparable with placebo), but the clinical benefit is less than that provided by finasteride.
  • Beta-sitosterols improve symptoms as compared with placebo.
  • Pygeum africanum demonstrates a slight benefit over placebo.
  • Cernitin (rye pollen) provides a slight benefit over placebo and appears equal in effect to Pygeum africanum.

As compared with finasteride, saw palmetto is not effective in relieving pain or improving quality of life in men with chronic prostatitis. In the laboratory, Opuntia (prickly pear) cactus demonstrates 5-alpha-reductase, aromatase, and free radical properties but has not been compared with placebo.

Stinging nettle is associated with relief of LUTS and is associated with a decreased AUA Symptom Score; however, in the studies conducted, there was no significant difference in maximum urinary flow rate or in PVR urine.

In summary, the role of phytotherapeutics is not yet clearly defined, but they are frequently used; thus, the health history must always include inquiries regarding use of these agents.

  1. Aromatase Inhibitors

Estrogen and estradiol are thought to play a role in prostate stromal growth and the resulting BPH, because the relative concentration of estrogens increases with age and the plasma levels of testosterone diminish. Aromatase inhibitors block estrogen biosynthesis, which theoretically should result in reduction of prostate size. However, to date, aromatase therapy has produced no significant difference in voiding symptoms as compared with placebo; this therapy therefore remains investigational.

  1. Anticholinergics/Antimuscarinics

Anticholinergic medications bind to the muscarinic receptors and block the uptake of acetylcholine, which is released by cholinergic nerves in response to parasympathetic stimulation. These agents are the mainstay of pharmacologic therapy for overactive bladder, and it is well established that bladder outlet obstruction caused by prostatic hyperplasia often produces symptoms of overactive bladder.

However, clinicians have been reluctant to prescribe anticholinergics for these patients, because a theoretic side effect is diminished bladder contractility resulting in increased PVRs or in urinary retention. Although this makes sense physiologically, a recent review of the literature suggests that men who receive either tolterodine or oxybutynin for symptoms of urgency, frequency, and nocturia do obtain symptom relief and are at no greater risk of elevated PVRs or urinary retention than men who receive placebo.

Surgical Intervention: Transurethral Resection of the Prostate and Minimally Invasive Procedures (TURP)

TURP is the most common approach to surgical resection of the prostate is considered to be gold standard in terms of treatment efficacy. Before undertaking surgical resection, it is important to determine accurately whether the patient’s voiding symptoms are caused by urethral obstruction, because prostatic resection is of benefit only in these patients.

LUTS in unobstructed patients are usually caused either by detrusor instability or by compromised contractility; prostatic resection does not correct detrusor instability and may actually cause worsening of the symptoms and onset of urinary incontinence, and prostatic resection is of little benefit in the case of reduced contractility because it fails to address the underlying pathologic features.

These issues point to the value of urodynamic studies before surgical intervention, because pressure-flow data can provide the information needed to differentiate between outlet obstruction and impaired contractility; however, routine use of urodynamic testing for all patients with prostatic obstruction remains controversial.

Risk factors for poor voiding function following TURP include the following: age more than 80 years, retention of more than 1500 mL urine, absence of detrusor instability, poor sensation, and maximal detrusor pressure lower than 28 cm H2O. These factors should be taken into consideration when considering a patient’s candidacy for surgery.

Minimally Invasive Procedures

Recent advances in the field of prostate surgery include the development of minimally invasive procedures: TMT, water-induced thermotherapy, TUNA, and high-energy TMT. All these procedures use an energy source to heat the obstructing prostatic tissue, which results in coagulation tissue necrosis.

Energy sources include microwave thermotherapy, water-induced thermotherapy, radiofrequency, and laser. These procedures are generally recommended for men with less severe obstructive symptoms, who have not responded to medical management with alpha blockers and/or 5-alpha-reductase inhibitors, and who do not wish to undergo more invasive surgery (or who are not candidates for more invasive procedures.)

Noninvasive procedures are usually attractive to patients and payors because they can usually be done in day surgery or the physician’s office, and they are less costly than TURP. Outcomes vary as compared with TURP, but all appear effective in the short term.


In summary, the pathology of BPH is complex and not well understood. Of note is that pathology studies on resected prostatic (predominantly stromal hyperplasia, predominantly glandular hyperplasia, and mixed hyperplasia), which suggests distinct phatologic conditions that may affect treatment.

Currently, the mechanisms believed to account for the clinical symptoms include static outlet obstruction caused by the enlarging prostate gland, dynamic outlet obstruction related to sympathetic tone in the prostate and bladder neck, and factors such as changes in sensory input and altered detrusor stability and contractility.

Current treatment options include medical or surgical reduction of prostatic volume, medical inhibition of sympathetic tone, and strategies to reduce overactive bladder symptoms. It is likely that future management of patients with BPH will be based on a much clearer understanding of the specific pathologic mechanisms and a broader choice of treatment options.

    Adapted from: Urinary & Fecal Incontinence: Current Management Concepts Authored by Dorothy B. Doughty. References as cited include:
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