eMedicine Specialties > Urology > Benign Prostatic Hypertrophy
Prostate Hyperplasia, Benign: Differential Diagnoses & Workup
Updated: Jun 8, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Differential Diagnoses
Other Problems to Be Considered
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:
- Cystitis
- Prostatitis
- Prostatodynia
- Prostatic abscess
- Overactive bladder (OAB)
- Carcinoma of the bladder
- Foreign bodies in the bladder (stones or retained stents)
- Urethral stricture due to trauma or a sexually transmitted disease
- Prostate cancer
- Neurogenic bladder
- Pelvic floor dysfunction
Excluding these entities based on findings from a thorough history and appropriately directed diagnostic studies is essential.
Workup
Laboratory Studies
- Urinalysis: Examine the urine using dipstick methods and/or via centrifuged sediment evaluation to assess for the presence of blood, leukocytes, bacteria, protein, or glucose.
- Urine culture: This may be useful to exclude infectious causes of irritative voiding and is usually performed if the initial urinalysis findings indicate an abnormality.
- Prostate-specific antigen
- Although benign prostatic hyperplasia (BPH) does not cause prostate cancer, men at risk for BPH are also at risk for prostate cancer and should be screened accordingly. The American Cancer Society recommends that annual prostate-specific antigen (PSA) testing and DRE for prostate cancer screening be offered at the following ages:2
- Starting at age 50 years in men who are expected to live at least 10 more years
- Starting at age 45 years in men at high risk for prostate cancer (African-Americans and men with a close relative with prostate cancer)
- Starting at age 40 years in men with multiple close relatives with prostate cancer
- A physician should discuss the risks and benefits of PSA screening with the patient.
- Notably, men with larger prostates may have slightly higher PSA levels.
- Although benign prostatic hyperplasia (BPH) does not cause prostate cancer, men at risk for BPH are also at risk for prostate cancer and should be screened accordingly. The American Cancer Society recommends that annual prostate-specific antigen (PSA) testing and DRE for prostate cancer screening be offered at the following ages:2
- Electrolytes, BUN, and creatinine: These evaluations are useful screening tools for chronic renal insufficiency in patients who have high postvoid residual (PVR) urine volumes. A routine serum creatinine measurement is not indicated in the initial evaluation of men with lower urinary tract symptoms (LUTS) secondary to BPH.
Imaging Studies
- Ultrasonography (abdominal, renal, transrectal) and intravenous urography are useful for helping determine bladder and prostate size and the degree of hydronephrosis (if any) in patients with urinary retention or signs of renal insufficiency. Generally, they are not indicated for the initial evaluation of uncomplicated LUTS.
- TRUS of the prostate is recommended in selected patients. The success of certain minimally invasive treatments (see Surgical Care) may depend on the anatomical characteristics of the gland.
- In patients with elevated PSA levels, TRUS-guided biopsy may be indicated.
- Imaging of the upper tracts is indicated in patients who present with concomitant hematuria, a history of urolithiasis, an elevated creatinine level, high PVR volume, or history of upper urinary tract infection.
- Other diagnostic studies, such as CT scanning and MRI, have no role in the evaluation and treatment of uncomplicated BPH.
Other Tests
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
- Medical history: A medical history should be taken to qualify and quantify voiding dysfunction. Identification of other causes of voiding dysfunction and medical comorbidities are essential to properly assess the condition and to determine conditions that may complicate treatment.
- Physical examination: The physical examination consists of a focused physical examination and a neurologic examination. The physical examination includes a DRE to measure prostate size and to assess for abnormalities. The neurological examination is geared toward lower-extremity neurologic and muscular function, as well as anal sphincter tone. Examination of the phallus and foreskin occasionally reveals meatal stenosis, unretractable foreskin, penile ulcers, or foreign bodies such as warts.
- PSA testing: PSA testing should be offered to any patient with a 10-year life expectancy in whom the diagnosis of prostate cancer would change management.
- International Prostate Symptom Score (IPSS)/American Urological Association Symptom Index (AUA-SI) for BPH and the IPSS disease-specific QOL question
- Developed to quantitate and validate responses to the questions asked, this set of 7 questions has been adopted worldwide and yields reproducible and quantifiable information regarding symptoms and response to treatment.
- Each question allows the patient to choose 1 of 6 answers indicating increasing severity of symptoms on a scale of 0-5; the total score ranges from 0-35. Questions concern incomplete emptying, frequency, intermittency, urgency, weak stream, straining, and nocturia. The eighth question is known as the bother score and pertains to the patient's perceived QOL. Scores can range from 0 (delighted) to 6 (terrible). After calculating the total score for all 8 eight questions, patients are classified as 0-7 (mildly symptomatic), 8-19 (moderately symptomatic), or 20-35 (severely symptomatic).
- Specific IPSS/AUA-SI questions are as follows (adapted from the recommendations of the International Scientific Committee, 2000, and the AUA Guideline, 2003/updated 2006):
- Incomplete emptying: Over the past month, how often have you had the sensation of not emptying your bladder completely after you have finished urinating? (Not at all = 0, less than 1 time in 5 = 1, less than half the time = 2, about half the time = 3, more than half the time = 4, almost always = 5)
- Frequency: Over the past month, how often have you had to urinate again less than 2 hours after you finished urinating? (Not at all = 0, less than 1 time in 5 = 1, less than half the time = 2, about half the time = 3, more than half the time = 4, almost always = 5)
- Intermittency: Over the past month, how often have you stopped and started again several times when urinating? (Not at all = 0, less than 1 time in 5 = 1, less than half the time = 2, about half the time = 3, more than half the time = 4, almost always = 5)
- Urgency: Over the past month, how often have you found it difficult to postpone urination? (Not at all = 0, less than 1 time in 5 = 1, less than half the time = 2, about half the time = 3, more than half the time = 4, almost always = 5)
- Weak stream: Over the past month, how often have you had a weak urinary stream? (Not at all = 0, less than 1 time in 5 = 1, less than half the time = 2, about half the time = 3, more than half the time = 4, almost always = 5)
- Straining: Over the past month, how often have you had to push or strain to begin urination? (Never = 0, once = 1, twice = 2, thrice = 3, 4 times or more = 4, 5 times or more = 5)
- Nocturia: Over the past month, how many times did you most typically get up to urinate from the time you went to bed until the time you got up in the morning? (Not at all = 0, less than 1 time in 5 = 1, less than half the time = 2, about half the time = 3, more than half the time = 4, almost always = 5)
- Bother score: The IPSS uses the same 7 questions as the AUA-SI, with the addition of the following disease-specific QOL question: How would you feel if you were to spend the rest of your life with your urinary condition just the way it is now? (Delighted = 0, pleased = 1, mostly satisfied = 2, mixed = 3, mostly dissatisfied = 4, unhappy = 5, terrible = 6) This helps assess perceived QOL due to urinary symptoms, and the score ranges from 0 (delighted) to 6 (terrible).
Optional tests
- Flow rate
- Flow rate is useful in the initial assessment and to help determine the response to treatment. It may be performed prior to embarking on any active treatments, including medical treatment.
- A maximal flow rate (Qmax) is the single best measurement, but a low Qmax does not help differentiate between obstruction and poor bladder contractility. For more detailed analysis, a pressure flow study is required. A Qmax value of greater than 15 mL/s is considered by many to be normal. A value of less than 7 mL/s is widely accepted as low.
- The results of flow rate measurements are somewhat effort- and volume-dependent; therefore, the best plan to make a reasonable determination of significance is to obtain at least 2 tracings with at least 150 mL of voided volume each time.
- Postvoid residual urine
- Obtain this value after the patient voids in order to gauge the severity of bladder decompensation.
- It can be obtained invasively with a catheter or noninvasively with a transabdominal ultrasonic scanner.
- A high PVR (ie, 350 mL) may indicate bladder dysfunction and may predict a negative response to treatment.
- Pressure flow studies
- Although these tests are somewhat invasive, requiring catheterization of the urethra and placement of a transrectal pressure transducer, the findings are invaluable for evaluating for bladder outlet obstruction (BOO), especially prior to any invasive therapy.
- Urodynamic studies are the only way to help distinguish poor bladder contraction ability (detrusor underactivity) from outlet obstruction.
- BOO is characterized by high intravesical voiding pressures (>60 cm water) accompanied by low urine flow rates (Qmax <15 mL/s).
- Urine cytology: Cytologic examination of the urine may be considered in patients with predominantly irritative voiding symptoms. Risk factors for bladder cancer (smoking, previous bladder cancer) should alert the physician to consider this noninvasive test.
- Other validated assessment instruments addressing LUTS in men with BPH
Tests that are not recommended
- Routine measurement of serum creatinine is not indicated in the initial evaluation of men with LUTS secondary to BPH.
Procedures
Endoscopy of the lower urinary tract (cystoscopy)
- This may be indicated in patients scheduled for invasive treatment or in whom a foreign body or malignancy is suspected. In addition, endoscopy may be indicated in patients with a history of sexually transmitted disease (eg, gonococcal urethritis), prolonged catheterization, or trauma. Findings may suggest urethral stricture as the cause of BOO, instead of BPH.
- Flexible cystoscopy can be easily performed in several minutes in an office-based setting using topical gel-based intraurethral anesthesia without sedation.
Histologic Findings
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.
Staging
Since BPH is a nonmalignant condition, no formal staging systems apply.
More on Prostate Hyperplasia, Benign |
| Overview: Prostate Hyperplasia, Benign |
 Differential Diagnoses & Workup: Prostate Hyperplasia, Benign |
| Treatment & Medication: Prostate Hyperplasia, Benign |
| Follow-up: Prostate Hyperplasia, Benign |
| Multimedia: Prostate Hyperplasia, Benign |
| References |
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References
Seftel AD, Rosen RC, Rosenberg MT, Sadovsky R. Benign prostatic hyperplasia evaluation, treatment and association with sexual dysfunction: practice patterns according to physician specialty. Int J Clin Pract. Apr 2008;62(4):614-22. [Medline].
American Cancer Society. 2009. American Cancer Society - Learn About Prostate Cancer. Available at http://www.cancer.org/docroot/lrn/lrn_0.asp. Accessed 1/29/2009.
McConnell JD, Barry MJ, Bruskewitz RC, et al. Benign Prostatic Hyperplasia: Diagnosis and Treatment. Clinical Practice Guideline. No. 8, AHCPR Publication No. 94-0582. Rockville, Md: Agency for Healthcare Policy and Research,. Public Health Service, US Department of Health and Human Services, 1994.
AUA Clinical Guidelines - Management of BPH ('03/Updated '06). Available at http://www.auanet.org/content/guidelines-and-quality-care/clinical-guidelines.cfm?sub=bph. Accessed 1/29/2009.
Emberton M, Cornel EB, Bassi PF, Fourcade RO, Gómez JM, Castro R. Benign prostatic hyperplasia as a progressive disease: a guide to the risk factors and options for medical management. Int J Clin Pract. Jul 2008;62(7):1076-86. [Medline].
Cantrell MA, Bream-Rouwenhorst HR, Steffensmeier A, Hemerson P, Rogers M, Stamper B. Intraoperative floppy iris syndrome associated with alpha1-adrenergic receptor antagonists. Ann Pharmacother. Apr 2008;42(4):558-63. [Medline].
Bell CM, Hatch WV, Fischer HD, Cernat G, Paterson JM, Gruneir A, et al. Association between tamsulosin and serious ophthalmic adverse events in older men following cataract surgery. JAMA. May 20 2009;301(19):1991-6. [Medline]. [Full Text].
Madersbacher S, Marszalek M, Lackner J, Berger P, Schatzl G. The long-term outcome of medical therapy for BPH. Eur Urol. Jun 2007;51(6):1522-33. [Medline].
McConnell JD, Bruskewitz R, Walsh P, et al. The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyperplasia. Finasteride Long-Term Efficacy and Safety Study Group. N Engl J Med. Feb 26 1998;338(9):557-63. [Medline].
McConnell JD, Roehrborn CG, Bautista OM, Andriole GL Jr, Dixon CM, Kusek JW. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl J Med. Dec 18 2003;349(25):2387-98. [Medline].
Roehrborn CG. Alfuzosin 10 mg once daily prevents overall clinical progression of benign prostatic hyperplasia but not acute urinary retention: results of a 2-year placebo-controlled study. BJU Int. Apr 2006;97(4):734-41. [Medline].
Vallancien G, Emberton M, Alcaraz A, Matzkin H, van Moorselaar RJ, Hartung R. Alfuzosin 10 mg once daily for treating benign prostatic hyperplasia: a 3-year experience in real-life practice. BJU Int. Apr 2008;101(7):847-52. [Medline].
Roehrborn CG, Siami P, Barkin J, Damião R, Major-Walker K, Morrill B. The effects of dutasteride, tamsulosin and combination therapy on lower urinary tract symptoms in men with benign prostatic hyperplasia and prostatic enlargement: 2-year results from the CombAT study. J Urol. Feb 2008;179(2):616-21; discussion 621. [Medline].
Gallegos PJ, Frazee LA. Anticholinergic therapy for lower urinary tract symptoms associated with benign prostatic hyperplasia. Pharmacotherapy. Mar 2008;28(3):356-65. [Medline].
Sildenafil [package insert]. New York, NY: Pfizer Inc.; 2002.
Vardenafil [package insert]. Pittsburgh, Pa: Bayer Pharmaceuticals Corporation/GlaxoSmithKline; 2003.
Tadalafil [package insert]. Indianapolis, IN: Lilly ICOS LLC; 2005.
Mulhall JP, Guhring P, Parker M, Hopps C. Assessment of the impact of sildenafil citrate on lower urinary tract symptoms in men with erectile dysfunction. J Sex Med. Jul 2006;3(4):662-7. [Medline].
Sotelo R, Spaliviero M, Garcia-Segui A, et al. Laparoscopic retropubic simple prostatectomy. J Urol. Mar 2005;173(3):757-60. [Medline].
Malek RS, Kuntzman RS, Barrett DM. Photoselective potassium-titanyl-phosphate laser vaporization of the benign obstructive prostate: observations on long-term outcomes. J Urol. Oct 2005;174(4 Pt 1):1344-8. [Medline].
Kuntz RM. Laser treatment of benign prostatic hyperplasia. World J Urol. Jun 2007;25(3):241-7. [Medline].
Elzayat EA, Habib EI, Elhilali MM. Holmium laser enucleation of the prostate: a size-independent new "gold standard". Urology. Nov 2005;66(5 Suppl):108-13. [Medline].
Kristal AR, Arnold KB, Schenk JM, Neuhouser ML, Goodman P, Penson DF. Dietary patterns, supplement use, and the risk of symptomatic benign prostatic hyperplasia: results from the prostate cancer prevention trial. Am J Epidemiol. Apr 15 2008;167(8):925-34. [Medline].
Arai Y, Fukuzawa S, Terai A, Yoshida O. Transurethral microwave thermotherapy for benign prostatic hyperplasia: relation between clinical response and prostate histology. Prostate. Feb 1996;28(2):84-8. [Medline].
Barry MJ, Cockett AT, Holtgrewe HL, et al. Relationship of symptoms of prostatism to commonly used physiological and anatomical measures of the severity of benign prostatic hyperplasia. J Urol. Aug 1993;150(2 Pt 1):351-8. [Medline].
Barry MJ, Fowler FJ Jr, O'Leary MP, Bruskewitz RC, Holtgrewe HL, Mebust WK. The American Urological Association symptom index for benign prostatic hyperplasia. The Measurement Committee of the American Urological Association. J Urol. Nov 1992;148(5):1549-57; discussion 1564. [Medline].
Barry MJ, O'Leary MP. Advances in benign prostatic hyperplasia. The developmental and clinical utility of symptom scores. Urol Clin North Am. May 1995;22(2):299-307. [Medline].
Berry SJ, Coffey DS, Walsh PC, Ewing LL. The development of human benign prostatic hyperplasia with age. J Urol. Sep 1984;132(3):474-9. [Medline].
Bihrle R, Foster RS, Sanghvi NT, et al. High intensity focused ultrasound for the treatment of benign prostatic hyperplasia: early United States clinical experience. J Urol. May 1994;151(5):1271-5. [Medline].
Bolmsjo M, Wagrell L, Hallin A, et al. The heat is on--but how? A comparison of TUMT devices. Br J Urol. Oct 1996;78(4):564-72. [Medline].
Bruskewitz R, Girman CJ, Fowler J, Rigby OF, Sullivan M, Bracken RB. Effect of finasteride on bother and other health-related quality of life aspects associated with benign prostatic hyperplasia. PLESS Study Group. Proscar Long-term Efficacy and Safety Study. Urology. Oct 1999;54(4):670-8. [Medline].
Cohen MS, Steiner MS. Interstitial laser coagulation techniques: local anesthesia techniques. World J Urol. Apr 2000;18 Suppl 1:S18-21. [Medline].
Danielli L, Kaver I, Fintsi Y, et al. Water induced thermotherapy (WIT) for benign prostatic hypertrophy (BPH), one year clinical experience and histopathological studies. Eur Urol. 1996;30(S2):222.
Girman CJ, Epstein RS, Jacobsen SJ, et al. Natural history of prostatism: impact of urinary symptoms on quality of life in 2115 randomly selected community men. Urology. Dec 1994;44(6):825-31. [Medline].
Girman CJ, Jacobsen SJ, Guess HA, et al. Natural history of prostatism: relationship among symptoms, prostate volume and peak urinary flow rate. J Urol. May 1995;153(5):1510-5. [Medline].
International Scientific Committee. The evaluation and treatment of lower urinary tract symptoms (LUTS) in older men. Proceedings of the 5th International Consultation on BPH; Paris, France;. 2000;519-32.
Issa MM. Transurethral needle ablation of the prostate: report of initial United States clinical trial. J Urol. Aug 1996;156(2 Pt 1):413-9. [Medline].
Jacobsen SJ, Jacobson DJ, Girman CJ, et al. Natural history of prostatism: risk factors for acute urinary retention. J Urol. Aug 1997;158(2):481-7. [Medline].
Kaplan SA, Chiou RK, Morton WJ, Katz PG. Long-term experience utilizing a new balloon expandable prostatic endoprosthesis: the Titan stent. North American Titan Stent Study Group. Urology. Feb 1995;45(2):234-40. [Medline].
Kirby R, Lepor H. Evaluation and Non-surgical Management of Benign Prostatic Hyperplasia. In: Wein A, Kavoussi L, Novick A, Partin A, and Peters C, eds. Campbell-Walsh Urology. 9th ed. Philadelphia, PA: WB Saunders Co; 2007:2766-2802.
Le Duc A, Gilling PJ. Holmium laser resection of the prostate. Eur Urol. Feb 1999;35(2):155-60. [Medline].
Lepor H, Sypherd D, Machi G, Derus J. Randomized double-blind study comparing the effectiveness of balloon dilation of the prostate and cystoscopy for the treatment of symptomatic benign prostatic hyperplasia. J Urol. Mar 1992;147(3):639-42; discussion 642-4. [Medline].
Lepor H, Williford WO, Barry MJ, Haakenson C, Jones K. The impact of medical therapy on bother due to symptoms, quality of life and global outcome, and factors predicting response. Veterans Affairs Cooperative Studies Benign Prostatic Hyperplasia Study Group. J Urol. Oct 1998;160(4):1358-67. [Medline].
McCullough DL. Minimally invasive treatment of benign prostatic hyperplasia. In: Walsh PC, Retik AB, Vaughan ED, Wein AJ, eds. Campbell's Urology. 7th ed. Philadelphia, Pa: WB Saunders; 1998:1479-1509.
McNeal JE. Origin and evolution of benign prostatic enlargement. Invest Urol. Jan 1978;15(4):340-5. [Medline].
McNeal JE. The prostate gland: Morphology and pathobiology. Monogr Urol. 1983;4:3-33.
Mebust WK. Transurethral Surgery. In: Walsh PC, Retik AB, Vaughan ED, Wein AJ, eds. Campbell's Urology. 7th ed. Philadelphia, Pa: WB Saunders; 1998:1511-28.
Muschter R, Hofstetter A. Interstitial laser therapy outcomes in benign prostatic hyperplasia. J Endourol. Apr 1995;9(2):129-35. [Medline].
Narayan P, Starling J. Minimally invasive therapies for the treatment of symptomatic benign prostatic hyperplasia: the University of Florida experience. J Clin Laser Med Surg. Feb 1998;16(1):29-32. [Medline].
Narayan P, Tewari A, Aboseif S, Evans C. A randomized study comparing visual laser ablation and transurethral evaporation of prostate in the management of benign prostatic hyperplasia. J Urol. Dec 1995;154(6):2083-8. [Medline].
[Best Evidence] Nickel JC, Sander S, Moon TD. A meta-analysis of the vascular-related safety profile and efficacy of alpha-adrenergic blockers for symptoms related to benign prostatic hyperplasia. Int J Clin Pract. Oct 2008;62(10):1547-59. [Medline].
Oesterling JE. Retropubic and Suprapubic Prostatectomy. In: Walsh PC, Retik AB, Vaughan ED, Wein AJ, eds. Campbell's Urology. 7th ed. Philadelphia, Pa: WB Saunders; 1998:1529-41.
Oesterling JE, Kaplan SA, Epstein HB. The North American experience with the UroLume endoprosthesis as a treatment for benign prostatic hyperplasia: long-term results. The North American UroLume Study Group. Urology. Sep 1994;44(3):353-62. [Medline].
Reich O, Bachmann A, Siebels M, et al. High power (80 W) potassium-titanyl-phosphate laser vaporization of the prostate in 66 high risk patients. J Urol. Jan 2005;173(1):158-60. [Medline].
Roehrborn C, McConnell JD. Benign Prostatic Hyperplasia: Etiology, Pathophysiology, Epidemiology and Natural History. In: Wein A, Kavoussi L, Novick A, Partin A, and Peters C, eds. Campbell-Walsh Urology. 9th ed. Philadelphia, Pa: WB Saunders; 2007:2727-2765.
Schulman CC. Lower urinary tract symptoms/benign prostatic hyperplasia: minimizing morbidity caused by treatment. Urology. Sep 2003;62(3 Suppl 1):24-33. [Medline].
Steele GS, Sleep DJ. Transurethral needle ablation of the prostate: a urodynamic based study with 2-year followup. J Urol. Nov 1997;158(5):1834-8. [Medline].
Stein BS, Bihrle RB, Issa M, et al. Minimally Invasive Surgeries for BPH. 009826 PG. Presented at AUA 93rd Annual Meeting; San Diego, California, USA. Baltimore, Md: AUA Office of Education; 1998.
Steiner MS, Cohen MS, Conn RL, et al. The armamentarium for BPH. Physicians Dialogue. 1998;1:5-11.
Tewari A, Oleksa J, Johnson C, et al. Minimally invasive therapy of benign prostatic hypertrophy. Hospital Physician. 1999;May:29-68.
[Best Evidence] U.S. Preventive Services Task Force. Screening for prostate cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. Aug 5 2008;149(3):185-91. [Medline].
Watson G, Anson K, Janetschek G, et al. An in-depth evaluation of contact laser vaporization of prostate. J Urol. 1994;151:231A.
Further Reading
Additional resources on benign prostatic hyperplasia (BPH) are available at Medscape's Benign Prostatic Hyperplasia Resource Center.
Keywords
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
