Updated: Jun 8, 2009
Benign prostatic hyperplasia (BPH), also known as benign prostatic hypertrophy, is a histologic diagnosis characterized by proliferation of the cellular elements of the prostate. Cellular accumulation and gland enlargement may result from epithelial and stromal proliferation, impaired preprogrammed cell death (apoptosis), or both. BPH involves the stromal and epithelial elements of the prostate arising in the periurethral and transition zones of the gland. The hyperplasia presumably results in enlargement of the prostate that may restrict the flow of urine from the bladder.
BPH is considered a normal part of the aging process in men and is hormonally dependent on testosterone and dihydrotestosterone (DHT) production. An estimated 50% of men demonstrate histopathologic BPH by age 60 years. This number increases to 90% by age 85 years; thus, increasing gland size is considered a normal part of the aging process.
The voiding dysfunction that results from prostate gland enlargement and bladder outlet obstruction (BOO) is termed lower urinary tract symptoms (LUTS). It has also been commonly referred to as prostatism, although this term has decreased in popularity. These entities overlap; not all men with BPH have LUTS, and, likewise, not all men with LUTS have BPH. Approximately half of men diagnosed with histopathologic BPH demonstrate moderate-to-severe LUTS. Clinical manifestations of LUTS include urinary frequency, urgency, nocturia (getting up at night during sleep to urinate), decreased or intermittent force of stream, or a sensation of incomplete emptying. Complications occur less commonly but may include acute urinary retention (AUR), impaired bladder emptying, or the need for corrective surgery.
Prostate volume may increase over time in men with BPH. In addition, peak urinary flow, voided volume, and symptoms may worsen over time in men with untreated BPH. The risk of AUR and the need for corrective surgery increases with age.
The prostate is a walnut-sized gland that forms part of the male reproductive system. It is located in front of the rectum and just below the urinary bladder. It is in continuum with the urinary tract and connects directly with the penile urethra. It is therefore a conduit between the bladder and the urethra. The gland is composed of several zones or lobes that are enclosed by an outer layer of tissue (capsule). These include the peripheral, central, anterior fibromuscular stroma, and transition zones. BPH originates in the transition zone, which surrounds the urethra. Microscopically, BPH is characterized as a hyperplastic process. The hyperplasia results in enlargement of the prostate that may restrict the flow of urine from the bladder, resulting in clinical manifestations of BPH. The prostate enlarges with age in a hormonally dependent manner. Notably, castrated males (ie, who are unable to make testosterone) do not develop BPH.
The traditional theory behind BPH is that, as the prostate enlarges, the surrounding capsule prevents it from radially expanding, potentially resulting in urethral compression. However, obstruction-induced bladder dysfunction contributes significantly to LUTS. The bladder wall becomes thickened, trabeculated, and irritable when it is forced to hypertrophy and increase its own contractile force. This increased sensitivity (detrusor instability), even with small volumes of urine in the bladder, is believed to contribute to urinary frequency and LUTS. The bladder may gradually weaken and lose the ability to empty completely, leading to increased residual urine volume and, possibly, acute or chronic urinary retention.
The main function of the prostate gland is primarily secretory; it produces alkaline fluid that comprises approximately 70% of the seminal volume. The secretions produce lubrication and nutrition for the sperm. The alkaline fluid in the ejaculate results in liquefaction and helps to neutralize the acidic vaginal environment. The prostatic urethra is a conduit for semen and prevents retrograde ejaculation (ie, ejaculation resulting in semen being forced backwards into the bladder) by closing off the bladder neck during sexual climax. Ejaculation involves a coordinated contraction of many different components, including the smooth muscles of the seminal vesicles, vasa deferentia, ejaculatory ducts, and the ischiocavernosus and bulbocavernosus muscles.
As many as 14 million men in the United States have symptoms of BPH.
Worldwide, approximately 30 million men have symptoms related to BPH.
In the past, chronic end-stage BOO often led to renal failure and uremia. Although this complication is much less common now, chronic BOO secondary to BPH may lead to urinary retention, renal insufficiency, recurrent urinary tract infections, gross hematuria, and bladder calculi.
The prevalence of BPH in white and African-American men is similar. However, BPH tends to be more severe and progressive in African-American men, possibly because of higher testosterone levels, 5-alpha-reducatase activity, androgen receptor expression, and growth factor activity in this population. The increased activity leads to an increased rate of prostatic hyperplasia and subsequent enlargement and its sequelae.
BPH occurs only in males. Women do not have prostate glands.
BPH is a common problem that affects the quality of life (QOL) in approximately one third of men older than 50 years. BPH is histologically evident in up to 90% of men by age 85 years.
The diagnosis of benign prostatic hyperplasia (BPH) can often be suggested based on history alone. Special attention to the onset and duration of symptoms, general health issues (including sexual history), fitness for any possible surgical intervention, severity of symptoms and how they are affecting QOL, medications, and previously attempted treatments is essential to making the correct diagnosis. Symptoms often attributed to BPH can be caused by other disease processes, and a history and physical examination are essential in ruling out other etiologies of LUTS (See Other Problems to be Considered).
When the prostate enlarges, it may act similar to a "clamp on a hose," constricting the flow of urine. Nerves within the prostate and bladder may also play a role in causing the following common symptoms:
Epidemiologic studies have identified LUTS as an independent risk factor for erectile dysfunction and ejaculatory dysfunction.1
Conduct a focused physical examination to assess the suprapubic area for signs of bladder distention and a neurological examination for sensory and motor deficits.
The digital rectal examination (DRE) is an integral part of the evaluation in men with presumed BPH.
| Bladder Cancer | Prostatitis, Tuberculous |
| Bladder Stones | Radiation Cystitis |
| Bladder Trauma | Urethral Strictures |
| Chronic Pelvic Pain | Urinary Tract Infection, Males |
| Interstitial Cystitis | |
| Neurogenic Bladder | |
| Prostatitis, Bacterial |
The differential diagnoses of benign prostatic hyperplasia (BPH), in which bladder outlet obstruction (BOO) must be differentiated from lower urinary tract symptoms (LUTS), include the following:
Excluding these entities based on findings from a thorough history and appropriately directed diagnostic studies is essential.
The American Urological Association (AUA) has developed rigorous clinical practice guidelines for BPH based on the 1994 Agency for Healthcare Research and Quality clinical practice guidelines for BPH. In 2006, The AUA Practice Guidelines Committee updated the 1994 evidence-based guidelines for the diagnosis and treatment of BPH originally created under the auspices of the United States Department of Health and Human Services Agency for Health Care Policy and Research.3,4 These panels have established the following categories to classify diagnostic tests and studies. A recommended test is one that should be performed on every patient, whereas an optional test is of proven value in selected patients.
Recommended tests
Optional tests
Tests that are not recommended
Endoscopy of the lower urinary tract (cystoscopy)
BPH is characterized by a varying combination of epithelial and stromal hyperplasia in the prostate. Some cases demonstrate an almost pure smooth-muscle proliferation, although most demonstrate a fibroadenomyomatous pattern of hyperplasia. Prostatic enlargement depends on the potent androgen DHT. In the prostate gland, type II 5-alpha-reductase metabolizes circulating testosterone into DHT (works locally, not systemically). DHT binds to androgen receptors in the cell nuclei, potentially resulting in BPH.
In vitro studies have shown that large numbers of alpha-1-adrenergic receptors are located in the smooth muscle of the stroma and capsule of the prostate, as well as in the bladder neck. Stimulation of these receptors causes an increase in smooth-muscle tone, which can worsen LUTS. Conversely, blockade of these receptors (see Treatment) can reversibly relax these muscles, with subsequent relief of LUTS.
In the bladder, obstruction leads to smooth-muscle-cell hypertrophy. Biopsy specimens of trabeculated bladders demonstrate evidence of scarce smooth-muscle fibers with an increase in collagen. The collagen fibers limit compliance, leading to higher bladder pressures upon filling. In addition, their presence limits shortening of adjacent smooth muscle cells, leading to impaired emptying and the development of residual urine.
Since BPH is a nonmalignant condition, no formal staging systems apply.
Patients with mild symptoms (IPSS/AUA-SI score <7) or moderate-to-severe symptoms (IPSS/AUA-SI score >8) of benign prostatic hyperplasia (BPH) who are not bothered by their symptoms and are not experiencing complications of BPH should be managed with a strategy of watchful waiting. In these situations, medical therapy is not likely to improve their symptoms and/or QOL. In addition, the risks of treatment may outweigh any benefits. Patients managed expectantly with watchful waiting are usually re-examined annually.
Transurethral resection of the prostate (TURP) has long been accepted as the criterion standard for relieving bladder outlet obstruction (BOO) secondary to BPH. In current clinical practice, most patients with BPH do not present with obvious surgical indications; instead, they often have milder lower urinary tract symptoms (LUTS) and, therefore, are initially treated with medical therapy.
The era of medical therapy for BPH dawned in the mid 1970s with the use of nonselective alpha-blockers such as phenoxybenzamine. The medical therapeutic options for BPH have evolved significantly over the last 3 decades, giving rise to the receptor-specific alpha-blockers that comprise the first line of therapy.
Rationale for alpha-1-receptor blockade in benign prostatic hyperplasia
A significant component of LUTS secondary to BPH is believed to be related to the smooth-muscle tension in the prostate stroma, urethra, and bladder neck. The smooth-muscle tension is mediated by the alpha-1-adrenergic receptors; therefore, alpha-adrenergic receptor–blocking agents should theoretically decrease resistance along the bladder neck, prostate, and urethra by relaxing the smooth muscle and allowing passage of urine. BPH is predominantly a stromal proliferative process, and a significant component of prostatic enlargement results from smooth-muscle proliferation. The stromal-to-epithelial ratio is significantly greater in men with symptomatic BPH than in those with asymptomatic BPH.
The 3 subtypes of the alpha-1 receptor include 1a, 1b, and 1c. Of these, the alpha-1a receptor is most specifically concentrated in the bladder neck and prostate. Provided that the alpha-1a subtype is predominant in the prostate, bladder neck, and urethra, but not in other tissues, drugs that are selective for this receptor (ie, tamsulosin) may have a potential therapeutic advantage.
Tamsulosin is considered the most pharmacologically uroselective of the commercially available agents because of its highest relative affinity for the alpha-1a receptor subtype. Recently, a new alpha-1a receptor selective blocker, silodosin (Rapaflo) was approved. It is indicated for treatment of the signs and symptoms of BPH.
The efficacy of the titratable alpha-blockers doxazosin and terazosin (Hytrin) is dose-dependent. Maximum tolerable doses have not been defined for any alpha-blocker; however, the higher the dose, the more likely the adverse events (orthostatic hypotension, dizziness, fatigue, ejaculatory disorder, nasal congestion).
An approximately 4- to 6-point improvement is expected in IPSS/AUA-SI scores when alpha-blockers are used. Interestingly, alpha-blocker therapy has not been shown to reduce the overall long-term risk of acute urinary retention (AUR) or BPH-related surgery.5
Rationale for 5-alpha-reductase inhibitors in benign prostatic hyperplasia
Hormonal medical management emerged from the discovery of a congenital form of pseudohermaphroditism secondary to DHT deficiency (due to a lack of 5-alpha-reductase activity). This deficiency produced a hypoplastic prostate. The two types of 5-alpha-reductase include type 1 (predominantly located in extraprostatic tissues, such as skin and liver) and type 2 (predominant prostatic reductase).
Prostatic enlargement depends on the potent androgen DHT. In the prostate gland, type II 5-alpha-reductase metabolizes circulating testosterone into DHT (works locally, not systemically). DHT binds to androgen receptors in the cell nuclei; this can result in BPH. DHT promotes growth of prostatic tissue. Inhibition of 5-alpha-reductase type 2 blocks the conversion of testosterone to DHT, resulting in lower intraprostatic levels of DHT. This leads to inhibition of prostatic growth, apoptosis, and involution. The exact role of 5-alpha-reductase type 1 in normal and abnormal prostatic development is undefined. 5-Alpha-reductase inhibitors improve LUTS by decreasing prostate volumes; thus, patients with larger prostates may achieve a greater benefit. Further, maximal reduction in prostate volume requires 6 months of therapy.
Rationale for combination therapy with alpha-1-receptor blockade and 5-alpha-reductase inhibitors in benign prostatic hyperplasia
Landmark clinical trials
Numerous phase II and phase III trials of drugs used in the treatment of BPH have been conducted. A few landmark studies are selected below.
Phytotherapeutic agents and dietary supplements
Treatment of concomitant overactive bladder in men with benign prostatic hyperplasia
Treatment of concomitant erectile dysfunction in men with lower urinary tract symptoms/ benign prostatic hyperplasia
Data from the Prostate Cancer Prevention Trial was evaluated for dietary risk factors for BPH. The data revealed that a diet low in fat and red meat and high in protein and vegetables may reduce the risk of symptomatic BPH. Additionally, regular alcohol consumption was associated with a reduced risk of symptomatic BPH, but this is to be interpreted cautiously given the untoward effects of excessive alcohol consumption.23
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
These agents block effects of postganglionic synapses at the smooth muscle and exocrine glands.
Nonselective alpha-adrenergic receptor blocker that antagonizes both alpha-1 and alpha-2 receptors. The nonselectivity leads to higher incidence of adverse effects, causing a decrease in use in clinical settings. Induces subjective improvement in urinary flow rates when compared to placebo. May improve daytime and nighttime urinary frequency. Improves symptoms in 75% of patients.
10 mg PO bid
Not established
Used concurrently, alpha-adrenergic agonists decrease effects; beta-blockers increase toxicity
Documented hypersensitivity; patients in whom a fall in blood pressure would be undesirable
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in cerebral or coronary arteriosclerosis and renal impairment; can worsen symptoms of respiratory tract infections; fatigue, dizziness, impaired ejaculation, nasal stuffiness, and difficulty with visual accommodation may occur
Treats prostatic hypertrophy. Improves urine flow rates by relaxing smooth muscle. Relaxation is produced by blocking alpha-1 adrenoreceptors in the bladder neck and prostate. Advantage over nonselective alpha-adrenergic blockers includes lower incidence of adverse effects. Because of availability of longer-acting, once-daily selective agents, clinical utility for BPH has been reduced. Improves urinary flow rate and frequency of micturition. Subjective improvement observed in 82% of patients treated. When increasing dosages, administer first dose of each increment at bedtime to reduce syncopal episodes. Although doses >20 mg/d do not usually increase efficacy, some patients may benefit from up to 40 mg/d.
2 mg PO bid
Not established
Acute postural hypotensive reaction from beta-blockers may worsen; indomethacin may decrease antihypertensive activity; verapamil may increase serum levels and may increase patients' sensitivity to prazosin-induced postural hypotension; may decrease antihypertensive effects of clonidine
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal insufficiency; adverse effects include dizziness, asthenia, peripheral edema, hypotension, reflex tachycardia, miosis, sedation, nasal stuffiness, and erectile dysfunction
Alpha-1 blocker of adrenoreceptors in prostate. Blockade of adrenoreceptors may cause smooth muscles in bladder neck and prostate to relax, resulting in improvement in urine flow rate and reduction in symptoms of BPH.
2.5 mg PO tid or ER (extended release) 10 mg PO qd
Not established
Effects may increase with coadministration of diuretics and antihypertensive medications
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Dizziness, fatigue, and headache may occur; patients should avoid situations in which injury could result if syncope occurs; exclude presence of carcinoma of prostate before beginning therapy
Not available in the United States. Helps treat prostatic hypertrophy. Improves urine flow rates by relaxing smooth muscle. Relaxation produced by blocking alpha-1 adrenoreceptors in the bladder neck and prostate. Advantage over nonselective alpha-adrenergic blockers includes lower incidence of adverse effects. Because of availability of longer-acting, once-daily selective agents, clinical utility for BPH has been reduced. Improves urinary flow rate and frequency of micturition.
20 mg PO bid
Not established
Acute postural hypotensive reaction from beta-blockers may worsen; indomethacin may decrease antihypertensive activity; verapamil may increase serum levels and may increase patients' sensitivity to indoramin-induced postural hypotension; may decrease antihypertensive effects of clonidine
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal insufficiency; adverse effects include dizziness, asthenia, peripheral edema, hypotension, reflex tachycardia, miosis, sedation, nasal stuffiness, and erectile dysfunction
Quinazoline compound that counteracts alpha1-induced adrenergic contractions of bladder neck, facilitating urinary flow in presence of BPH. Effect on voiding symptoms and flow rates is dose-dependent. Improves irritative and obstructive voiding symptoms. Improvement in flow rate is objective. Hytrin starter pack available for easy dosing progression to 5 mg.
1-5 mg PO qhs; may titrate to maximal dose of 10 mg based on tolerability and symptomatic improvement
Not established
Effects decrease with coadministration of NSAIDs; effects increase with coadministration of diuretics and antihypertensive medications
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal impairment; may cause marked hypotension following first dose and coadministration with beta-blockers; adverse effects include dizziness, headache, asthenia, peripheral edema, hypotension, reflex tachycardia, miosis, sedation, nasal stuffiness, and erectile dysfunction; incidence of erectile dysfunction is lower compared to other antihypertensive agents
Inhibits postsynaptic alpha-adrenergic receptors, resulting in vasodilation of veins and arterioles and decrease in total peripheral resistance and blood pressure. Long-acting alpha1-blocking agent with similar profile to terazosin. Improves irritative and obstructive voiding symptoms.
1 mg PO qhs; may titrate to maximal dose of 8 mg based on tolerability and symptomatic improvement
Not established
Effects decrease with coadministration of NSAIDs; effects increase with coadministration of diuretics and antihypertensive medications
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal impairment; may cause marked hypotension following first dose and with coadministration of beta-blockers; adverse effects include dizziness, headache, asthenia, peripheral edema, hypotension, reflex tachycardia, miosis, sedation, nasal stuffiness, and erectile dysfunction; incidence of erectile dysfunction is lower compared to other antihypertensive agents
Alpha-adrenergic blocker specifically targeted to alpha-1 receptors. Has advantage of relatively less orthostatic hypotension and requires no gradual up-titration from initial introductory dosage. Inhibits postsynaptic alpha-adrenergic receptors, resulting in vasodilation of veins and arterioles and decrease in total peripheral resistance and blood pressure. Improves irritative and obstructive voiding symptoms.
0.4 mg PO qd initially; may increase to 0.8 mg PO qd; no dose titration needed
Not established
Cimetidine may significantly increase plasma concentrations; may increase toxicity of warfarin
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Not for use as antihypertensive drug; may cause orthostasis; avoid situations that may result in injuries if syncope occurs; exclude presence of carcinoma or cancer before initiating treatment; adverse effects include increased rate of retrograde ejaculation and rhinitis
Selectively antagonizes postsynaptic alpha1-adrenergic receptors in prostate, bladder base, prostatic capsule, and prostatic urethra. This action induces smooth muscle relaxation and improves urine flow. Indicated for signs and symptoms of BPH.
8 mg PO qd with food
CrCl 30-50 mL/min: 4 mg PO qd
Not established
Coadministration with strong CYP3A4 inhibitors (eg, itraconazole, clarithromycin, ritonavir) or P-glycoprotein inhibitors (eg, cyclosporine) increases serum levels; concurrent use with other alpha-blockers may increase effect; coadministration with antihypertensive agents may increase incidence of dizziness and orthostatic hypotension
Documented hypersensitivity; severe renal impairment (ie, CrCl <30 mL/min); severe hepatic impairment (ie, Child-Pugh score >10); coadministration with strong CYP3A4 inhibitors
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Risk of postural hypotension and resulting symptoms (eg, dizziness, syncope); caution with moderate renal impairment; may cause intraoperative floppy iris syndrome during cataract surgery; may cause retrograde ejaculation
Inhibit the conversion of testosterone to DHT, causing DHT levels to drop, which, in turn, may decrease prostate size.
Inhibits conversion of testosterone to DHT, causing serum DHT levels to decrease. Beneficial in men with prostates >40 g. Improves symptoms and reduces prostatic size by 20-30%. Reduction in prostate size sustained 5 y following treatment. Improves urinary flow rate by 2 mL/s.
5 mg PO qd; minimum of 6 mo treatment necessary to determine response
Not established
None reported
Documented hypersensitivity; lactation, children
X - Contraindicated; benefit does not outweigh risk
Caution in liver function abnormalities; monitor patients with severely diminished urinary flow for obstructive uropathy (may not be candidates for this therapy); generally well tolerated with few adverse effects; rare headache, loss of libido, and impotence may occur; lowers serum PSA level by 50% after 6 mo of therapy
Used to treat symptomatic BPH in men with an enlarged prostate. Improves symptoms, reduces urinary retention, and may decrease need for BPH-related surgery. Inhibits 5alpha-reductase isoenzymes types I and II. Suppresses >95% conversion of testosterone to DHT, causing serum DHT levels to decrease.
0.5 mg PO qd
Contraindicated
CYP450 3A4 substrate; data limited, caution with potent CYP450 3A4 inhibitors (eg, ketoconazole, ritonavir, erythromycin) or inducers (eg, rifampin, phenytoin)
Documented hypersensitivity; pregnancy or lactation; women or children
X - Contraindicated; benefit does not outweigh risk
Unknown whether excreted in breast milk; caution with hepatic disease; establish new baseline PSA level 3 mo after therapy initiation
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benign prostatic hyperplasia, BPH, benign prostatic hypertrophy, benign prostate hyperplasia, benign prostate hypertrophy, prostatism, prostatic hypertrophy, enlarged prostate, bladder outlet obstruction, BOO, testosterone, dihydrotestosterone, DHT, obstruction-induced bladder dysfunction, acute urinary retention, AUR, frequent urination, nocturia, lower urinary tract symptoms, LUTS, prostatectomy, transurethral resection of the prostate, TURP, transurethral incision of the prostate, TUIP, transurethral microwave therapy, TUMT, transurethral needle ablation of the prostate, TUNA, water-induced thermotherapy, WIT, digital rectal examination, DRE, prostate-specific antigen, PSA
Raymond J Leveillee, MD, FRCS(Glasg), Professor of Clinical Urology, Radiology and Biomedical Engineering, Department of Urology, University of Miami Miller School of Medicine; Chief, Division of Endourology/Laparoscopy and Minimally Invasive Surgery, Department of Urology, Jackson Memorial Hospital
Raymond J Leveillee, MD, FRCS(Glasg) is a member of the following medical societies: American Urological Association, Endourological Society, Sigma Xi, and Society of Laparoendoscopic Surgeons
Disclosure: ACMI/Gyrus Honoraria Speaking and teaching; Boston Scientific Honoraria Speaking and teaching; Applied Medical Honoraria Speaking and teaching; Intuitive Surgical Honoraria Speaking and teaching; LMA suisse Grant/research funds Consulting; Pluromed Grant/research funds Consulting
Vipul R Patel, MD, Consulting Surgeon, Global Robotics Institute, Florida Hospital Celebration Health
Vipul R Patel, MD is a member of the following medical societies: American College of Surgeons, American Urological Association, Endourological Society, Ohio State Medical Association, and Society of Laparoendoscopic Surgeons
Disclosure: Intuitive Surgical Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching
Vincent G Bird, MD, Assistant Professor of Clinical Urology, University of Miami, Miller School of Medicine; Consulting Staff, Department of Urology, Division of Endourology/Laparoscopy and Minimally Invasive Surgery, University of Miami Miller School of Medicine/Jackson Memorial Hospital
Vincent G Bird, MD is a member of the following medical societies: American Urological Association, Endourological Society, and Society of Laparoendoscopic Surgeons
Disclosure: Nothing to disclose.
Charles R Moore, MD, Fellow, Department of Urology, University of Miami
Charles R Moore, MD is a member of the following medical societies: Alpha Omega Alpha and American Urological Association
Disclosure: Nothing to disclose.
Edward David Kim, MD, FACS, Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center
Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, and Tennessee Medical Association
Disclosure: Lilly Consulting fee Consulting; Astellas Consulting fee Speaking and teaching; Indevus Consulting fee Speaking and teaching
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Martin I Resnick, MD , Former Lester Persky Professor and Chair, Department of Urology, Former Professor, Department of Oncology, Case Western Reserve University School of Medicine
Martin I Resnick, MD is a member of the following medical societies: American College of Surgeons, American Federation for Medical Research, American Institute of Ultrasound in Medicine, American Medical Association, American Society for Bone and Mineral Research, American Society for Reproductive Medicine, American Society of Andrology, American Surgical Association, American Urological Association, Association for Academic Surgery, Endocrine Society, National Kidney Foundation, Ohio Urological Society, and Pan American Medical Association
Disclosure: Nothing to disclose.
J Stuart Wolf Jr, MD, FACS, David A Bloom Professor of Urology, Director of Division of Minimally Invasive Urology, Department of Urology, University of Michigan
J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology
Disclosure: Terumo Corporation Consulting fee Consulting; Omeros Corporation Consulting fee Consulting
Edward David Kim, MD, FACS, Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center
Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, and Tennessee Medical Association
Disclosure: Lilly Consulting fee Consulting; Astellas Consulting fee Speaking and teaching; Indevus Consulting fee Speaking and teaching