Benign prostatic hyperplasia

From Wikipedia, the free encyclopedia
  (Redirected from Enlarged prostate)
Jump to: navigation, search
For other uses of the acronym BPH, see BPH (disambiguation).
Benign prostatic hyperplasia
Classification and external resources

Diagram illustrating normal prostate (left) and benign prostatic hyperplasia (right).
ICD-10 N40
ICD-9 600
DiseasesDB 10797
eMedicine med/1919
MeSH D011470

Benign prostatic hyperplasia (BPH), benign enlargement of the prostate (BEP), adenofibromyomatous hyperplasia and incorrectly referred to benign prostatic hypertrophy, is an increase in size of the prostate.

BPH involves hyperplasia (an increase in the number of cells) rather than hypertrophy (a growth in the size of individual cells), but the two terms are often used interchangeably, even amongst urologists.[1] It involves hyperplasia of prostatic stromal and epithelial cells, resulting in the formation of large, fairly discrete nodules in the periurethral region of the prostate. When sufficiently large, the nodules compress the urethral canal to cause partial, or sometimes virtually complete, obstruction of the urethra, which interferes with the normal flow of urine. It leads to symptoms of urinary hesitancy, frequent urination, dysuria (painful urination), increased risk of urinary tract infections, and urinary retention. Although prostate specific antigen levels may be elevated in these patients because of increased organ volume and inflammation due to urinary tract infections, BPH does not lead to cancer or increase the risk of cancer.[citation needed]

Adenomatous prostatic growth is believed to begin at approximately age 30 years. An estimated 50% of men have histologic evidence of BPH by age 50 years and 75% by age 80 years. In 40-50% of these patients, BPH becomes clinically significant.[2]

Contents

[edit] Signs and symptoms

Benign prostatic hyperplasia symptoms are classified as storage or voiding.

Storage symptoms include urinary frequency, urgency (compelling need to void that cannot be deferred), urgency incontinence, and voiding at night (nocturia).

Voiding symptoms include urinary stream, hesitancy (needing to wait for the stream to begin), intermittency (when the stream starts and stops intermittently), straining to void, and dribbling. Pain and dysuria are usually not present. These storage and voiding symptoms are evaluated using the International Prostate Symptom Score (IPSS) questionnaire, designed to assess the severity of BPH.[3]

BPH can be a progressive disease, especially if left untreated. Incomplete voiding results in stasis of bacteria in the bladder residue and an increased risk of urinary tract infection. Urinary bladder stones are formed from the crystallization of salts in the residual urine. Urinary retention, termed acute or chronic, is another form of progression. Acute urinary retention is the inability to void, while in chronic urinary retention the residual urinary volume gradually increases, and the bladder distends. This can result in bladder hypotonia. Some patients that suffer from chronic urinary retention may eventually progress to renal failure, a condition termed obstructive uropathy.

[edit] Diagnosis

[edit] Management

[edit] Lifestyle

Patients should decrease fluid intake before bedtime, moderate the consumption of alcohol and caffeine-containing products, and follow timed voiding schedules.

[edit] Medications

The two main medications for management of BPH are alpha blockers and 5α-reductase inhibitors.

  • The 5α-reductase inhibitors finasteride[12] and dutasteride[13] are another treatment option. These medications inhibit 5a-reductase, which in turn inhibits production of DHT, a hormone responsible for enlarging the prostate. Effects may take longer to appear than alpha blockers, but they persist for many years.[14] When used together with alpha blockers, a reduction of BPH progression to acute urinary retention and surgery has been noted in patients with larger prostates.[15] Side effects include decreased libido and ejaculatory or erectile dysfunction.[12]

Antimuscarinics such as tolterodine may also be used, especially in combination with alpha blockers.[16] They act by decreasing acetylcholine effects on the smooth muscle of the bladder, thus helping control symptoms of an overactive bladder.[citation needed]

Sildenafil citrate shows some symptomatic relief, suggesting a possible common etiology with erectile dysfunction.[17]

[edit] Herbal remedies

People often seek herbal remedies for BPH.[18] Several are approved in European countries, but none in the USA. Saw palmetto extract from Serenoa repens is one of the most extensively studied. It showed promise in early studies,[19] though later trials of higher methodological quality indicated no difference from placebo.[20][21][22] There are no known negative effects of saw palmetto, so if taking the supplement relieves symptoms, there is no harm in taking it. The quality of saw palmetto products varies.[23]

Other herbal medicines that have research support in systematic reviews include beta-sitosterol[24] from Hypoxis rooperi (African star grass) and pygeum (extracted from the bark of Prunus africana),[25] while there is less substantial support for the efficacy of pumpkin seed (Cucurbita pepo) and stinging nettle (Urtica dioica) root.[26] There is weak evidence that pollen extracts frp, rye grass (Secale cereale) may also correlate with modest symptomatic relief.[27]

[edit] Minimally invasive therapies

Medication is often prescribed as the first treatment option, there are many patients who do not achieve success with this line of treatment. Those patients may not achieve sustained improvement in symptoms or they may stop taking the medication because of side-effects.[28] There are options for treatment in a urologist's office before proceeding to surgery. The two most common types of office-based therapies are transurethral microwave thermotherapy (TUMT) and transurethral needle ablation (TUNA). Both of these procedures rely on delivering enough energy to create sufficient heat to cause cell death (necrosis) in the prostate. The goal of the therapies is to cause enough necrosis so that, when the dead tissue is reabsorbed by the body, the prostate shrinks, relieving the obstruction of the urethra. These procedures are typically performed with local anesthesia, and the patient returns home the same day. Some urologists have studied and published long-term data on the outcomes of these procedures, with data out to five years. The most recent American Urological Association (AUA) Guidelines for the Treatment of BPH in 2003 lists minimally invasive therapies including TUMT and TUNA as acceptable alternatives for certain patients with BPH.[29]

Transurethral microwave therapy (TUMT) was originally approved by the FDA in 1996, with the first generation system by EDAP Technomed. Since 1996, other companies have received FDA approval for TUMT devices, including Urologix, Dornier, Thermatrix, Celsion, and Prostalund. Multiple clinical studies have been published on TUMT. The general principle underlying all the devices is that a microwave antenna that resides in a urethral catheter is placed in the intraprostatic area of the urethra. The catheter is connected to a control box outside of the patient's body and is energized to emit microwave radiation into the prostate to heat the tissue and cause necrosis. It is a one-time treatment that takes approximately 30 minutes to 1 hour, depending on the system used. It takes approximately 4 to 6 weeks for the damaged tissue to be reabsorbed into the patient's body. Some of the devices incorporate circulating coolant through the treatment area with the intent of preserving the urethra while the microwave energy heats the prostatic tissue surrounding the urethra.

Transurethral needle ablation (TUNA) operates with a different type of energy, radio frequency (RF) energy, but is designed along the same premise as TUMT devices, that the heat the device generates will cause necrosis of the prostatic tissue and shrink the prostate. The TUNA device is inserted into the urethra using a rigid scope much like a cystoscope. The energy is delivered into the prostate using two needles that emerge from the sides of the device, through the urethral wall and into the prostate. The needle-based ablation devices are very effective at heating a localized area to a high enough temperature to cause necrosis. The treatment is typically performed in one session, but may require multiple sticks of the needles depending on the size of the prostate.

[edit] Surgery

If medical treatment fails, and the patient elects not to try office-based therapies or the physician determines the patient is a better candidate for transurethral resection of prostate (TURP), surgery may need to be performed. In general, TURP is still considered the gold standard of prostate interventions for patients that require a procedure. This involves removing (part of) the prostate through the urethra. There are also a number of new methods for reducing the size of an enlarged prostate, some of which have not been around long enough to fully establish their safety or side-effects. These include various methods to destroy or remove part of the excess tissue while trying to avoid damaging what remains. Transurethral electrovaporization of the prostate (TVP), laser TURP, visual laser ablation (VLAP), ethanol injection, and others are studied as alternatives.

Newer techniques involving lasers in urology have emerged in the last 5–10 years, starting with the VLAP technique involving the Nd:YAG laser with contact on the prostatic tissue. A similar technology called Photoselective Vaporization of the Prostate (PVP) with the GreenLight (KTP or LBO crystal) laser have emerged very recently. This procedure involves a high-power 180-watt 532nm wavelength laser with a 650-micrometre laser fiber inserted into the prostate. This fiber has an internal reflection with a 70-degree deflecting angle. It is used to vaporize the tissue to the prostatic capsule. GreenLight 532nm lasers target haemoglobin as the chromophore and typically have a penetration depth of 0.8mm (two times deeper than holmium).

Another procedure termed Holmium Laser Ablation of the Prostate (HoLAP) has also been gaining acceptance around the world. Like KTP, the delivery device for HoLAP procedures is a 550 um disposable side-firing fiber that directs the beam from a high-power 100-watt laser at a 70-degree angle from the fiber axis. The holmium wavelength is 2,140 nm, which falls within the infrared portion of the spectrum and is invisible to the naked eye. Whereas GreenLight relies on haemoglobin as a chromophore, water within the target tissue is the chromophore for Holmium lasers. The penetration depth of Holmium lasers is <0.4 mm, avoiding complications associated with tissue necrosis often found with the deeper penetration and lower peak powers of Nd:YAG lasers used in the 1990's.

HoLEP, Holmium Laser Enucleation of the Prostate, is another Holmium laser procedure reported to carry fewer risks compared with either TURP or open prostatectomy.[30] HoLEP is largely similar to the HoLAP procedure; the main difference is that this procedure is typically performed on larger prostates. Instead of ablating the tissue, the laser cuts a portion of the prostate, which is then cut into smaller pieces and flushed with irrigation fluid. As with the HoLAP procedure, there is little bleeding during or after the procedure.

Both wavelengths, GreenLight and Holmium, ablate approximately one to two grams of tissue per minute.

Post surgery care often involves placement of a Foley catheter or a temporary prostatic stent to permit healing and allow urine to drain from the bladder.

[edit] Epidemiology

Disability-adjusted life year for benign prostatic hyperplasia per 100,000 inhabitants in 2004.[31]
  no data
  less than 20
  20-28
  28-36
  36-44
  44-52
  52-60
  60-68
  68-76
  76-84
  84-92
  92-100
  more than 100

The prostate gets larger in most men as they get older, and, overall, 45% of men over the age of 46 can expect to suffer from the symptoms of BPH if they survive 30 years. Incidence rates increase from 3 cases per 1000 man-years at age 45–49 years, to 38 cases per 1000 man-years by the age of 75–79 years. Whereas the prevalence rate is 2.7% for men aged 45–49, it increases to 24% by the age of 80 years.[32]

For some men, the symptoms may be severe enough to require treatment.

[edit] See also

[edit] Further reading

Christensen, Tyler L.; Andriole, Gerald L. (February 2009). "Benign Prostatic Hyperplasia: Current Treatment Strategies". Consultant 49 (2): 115–22. http://www.consultantlive.com/prostate-cancer/content/article/10162/1376744. 

[edit] References

  1. ^ Bostwick, D. G. (2002). "The Pathology of Benign Prostatic Hyperplasia". In Kirby, Peter; McConnell, John D.; Fitzpatrick, John M. et al. Textbook of Benign Prostatic Hyperplasia. London: Isis Medical Media. ISBN 978-1-901865-55-4. [page needed]
  2. ^ Rubenstein, Jonathan; McVary, Kevin T. (February 6, 2008). "Transurethral Microwave Thermotherapy of the Prostate (TUMT)". eMedicine. http://emedicine.medscape.com/article/449623-overview. 
  3. ^ Barry MJ, Fowler FJ, O'Leary MP, et al. (November 1992). "The American Urological Association symptom index for benign prostatic hyperplasia. The Measurement Committee of the American Urological Association". The Journal of Urology 148 (5): 1549–57; discussion 1564. PMID 1279218. 
  4. ^ Roehrborn, Claus G.; Nuckolls, James G.; Wei, John T.; Steers, William; BPH Registry and Patient Survey Steering Committee (2007). "The Benign Prostatic Hyperplasia Registry and Patient Survey: study design, methods and patient baseline characteristics". BJU International 100 (4): 813–9. doi:10.1111/j.1464-410X.2007.07061.x. PMID 17822462. 
  5. ^ Black, L; Naslund, MJ; Gilbert Jr, TD; Davis, EA; Ollendorf, DA (2006). "An examination of treatment patterns and costs of care among patients with benign prostatic hyperplasia". The American journal of managed care 12 (4 Suppl): S99–S110. PMID 16551208. http://www.ajmc.com/pubMed.php?pii=3096. 
  6. ^ Hutchison, A; Farmer, R; Verhamme, K; Berges, R; Navarrete, R (2007). "The Efficacy of Drugs for the Treatment of LUTS/BPH, A Study in 6 European Countries". European Urology 51 (1): 207–15 discussion 215–6. doi:10.1016/j.eururo.2006.06.012. PMID 16846678. 
  7. ^ MacDonald, Roderick; Wilt, Timothy J.; Howe, R. William (2004). "Doxazosin for treating lower urinary tract symptoms compatible with benign prostatic obstruction: a systematic review of efficacy and adverse effects". BJU International 94 (9): 1263–70. doi:10.1111/j.1464-410X.2004.05154.x. PMID 15610102. 
  8. ^ MacDonald, Roderick; Wilt, Timothy J. (2005). "Alfuzosin for treatment of lower urinary tract symptoms compatible with benign prostatic hyperplasia: A systematic review of efficacy and adverse effects". Urology 66 (4): 780–8. doi:10.1016/j.urology.2005.05.001. PMID 16230138. 
  9. ^ Roehrborn, Claus G (2001). "Efficacy and safety of once-daily alfuzosin in the treatment of lower urinary tract symptoms and clinical benign prostatic hyperplasia: a randomized, placebo-controlled trial". Urology 58 (6): 953–9. doi:10.1016/S0090-4295(01)01448-0. PMID 11744466. 
  10. ^ Djavan, Bob; Marberger, Michael (1999). "A Meta-Analysis on the Efficacy and Tolerability of α1-Adrenoceptor Antagonists in Patients with Lower Urinary Tract Symptoms Suggestive of Benign Prostatic Obstruction". European Urology 36 (1): 1–13. doi:10.1159/000019919. PMID 10364649. 
  11. ^ Aua Practice Guidelines, Committee (2003). "AUA Guideline on Management of Benign Prostatic Hyperplasia (2003). Chapter 1: Diagnosis and Treatment Recommendations". The Journal of Urology 170 (2 Pt 1): 530–47. doi:10.1097/01.ju.0000078083.38675.79. PMID 12853821. 
  12. ^ a b Gormley, Glenn J.; Stoner, Elizabeth; Bruskewitz, Reginald C.; Imperato-Mcginley, Julianne; Walsh, Patrick C.; McConnell, John D.; Andriole, Gerald L.; Geller, Jack et al (1992). "The Effect of Finasteride in Men with Benign Prostatic Hyperplasia". New England Journal of Medicine 327 (17): 1185–91. doi:10.1056/NEJM199210223271701. PMID 1383816. 
  13. ^ Roehrborn, C; Boyle, P; Nickel, JC; Hoefner, K; Andriole, G; ARIA3001 ARIA3002 and ARIA3003 Study Investigators (2002). "Efficacy and safety of a dual inhibitor of 5-alpha-reductase types 1 and 2 (dutasteride) in men with benign prostatic hyperplasia". Urology 60 (3): 434–41. doi:10.1016/S0090-4295(02)01905-2. PMID 12350480. 
  14. ^ Roehrborn, C; Bruskewitz, R; Nickel, J; McConnell, J; Saltzman, B; Gittelman, M; Malek, G; Gottesman, J et al (2004). "Sustained Decrease in Incidence of Acute Urinary Retention and Surgery With Finasteride for 6 Years in Men With Benign Prostatic Hyperplasia". The Journal of Urology 171 (3): 1194–8. doi:10.1097/01.ju.0000112918.74410.94. PMID 14767299. 
  15. ^ Kaplan, S; McConnell, J; Roehrborn, C; Meehan, A; Lee, M; Noble, W; Kusek, J; Nybergjr, L et al (2006). "Combination Therapy With Doxazosin and Finasteride for Benign Prostatic Hyperplasia in Patients With Lower Urinary Tract Symptoms and a Baseline Total Prostate Volume of 25 Ml or Greater". The Journal of Urology 175 (1): 217–20; discussion 220–1. doi:10.1016/S0022-5347(05)00041-8. PMID 16406915. 
  16. ^ Kaplan, S. A.; Roehrborn, C. G.; Rovner, E. S.; Carlsson, M.; Bavendam, T.; Guan, Z. (2006). "Tolterodine and Tamsulosin for Treatment of Men With Lower Urinary Tract Symptoms and Overactive Bladder: A Randomized Controlled Trial". JAMA: the Journal of the American Medical Association 296 (19): 2319–28. doi:10.1001/jama.296.19.2319. PMID 17105794. 
  17. ^ McVary, Kevin T.; Monnig, William; Camps Jr., Joseph L.; Young, Jay M.; Tseng, Li-Jung; Van Den Ende, Gene (2007). "Sildenafil Citrate Improves Erectile Function and Urinary Symptoms in Men With Erectile Dysfunction and Lower Urinary Tract Symptoms Associated With Benign Prostatic Hyperplasia: A Randomized, Double-Blind Trial". The Journal of Urology 177 (3): 1071–7. doi:10.1016/j.juro.2006.10.055. PMID 17296414. 
  18. ^ Lieber, M M (1998). "Pharmacologic therapy for prostatism". Mayo Clinic Proceedings 73 (6): 590–6. doi:10.4065/73.6.590. PMID 9621869. 
  19. ^ Boyle, P; Robertson, C; Lowe, F; Roehrborn, C (2000). "Meta-analysis of clinical trials of Permixon in the treatment of symptomatic benign prostatic hyperplasia". Urology 55 (4): 533–9. doi:10.1016/S0090-4295(99)00593-2. PMID 10736497. 
  20. ^ Bent, Stephen; Kane, Christopher; Shinohara, Katsuto; Neuhaus, John; Hudes, Esther S.; Goldberg, Harley; Avins, Andrew L. (2006). "Saw Palmetto for Benign Prostatic Hyperplasia". New England Journal of Medicine 354 (6): 557–66. doi:10.1056/NEJMoa053085. PMID 16467543. 
  21. ^ Dedhia, R; McVary, K (2008). "Phytotherapy for Lower Urinary Tract Symptoms Secondary to Benign Prostatic Hyperplasia". The Journal of Urology 179 (6): 2119–25. doi:10.1016/j.juro.2008.01.094. PMID 18423748. 
  22. ^ Wilt, Timothy; Ishani, Areef; MacDonald, Roderick; Tacklind, James (2002). Tacklind, James. ed. "Serenoa repens for benign prostatic hyperplasia". Cochrane Database of Systematic Reviews (3): CD001423. doi:10.1002/14651858.CD001423. PMID 12137626. 
  23. ^ "Enlarged Prostate Gland". http://health.yahoo.net/experts/managinghealthcare/saw-palmetto-help-enlarged-prostate-gland. Retrieved 25 February 2011. 
  24. ^ Wilt, Timothy; Ishani, Areef; MacDonald, Roderick; Stark, Gerold; Mulrow, Cynthia D; Lau, Joseph; Wilt, Timothy (1999). Wilt, Timothy J. ed. "Beta-sitosterols for benign prostatic hyperplasia". Cochrane Database of Systematic Reviews (2): CD001043. doi:10.1002/14651858.CD001043. PMID 10796740. 
  25. ^ Wilt, Timothy; Ishani, Areef; Wilt, Timothy; Rutks, I; Stark, G (1998). Wilt, Timothy J. ed. "Pygeum africanum for benign prostatic hyperplasia". Cochrane Database of Systematic Reviews (1): CD001044. doi:10.1002/14651858.CD001044. PMID 11869585. 
  26. ^ Wilt, Timothy J; Ishani, Areef; Rutks, Indulis; MacDonald, Roderick (2007). "Phytotherapy for benign prostatic hyperplasia". Public Health Nutrition 3 (4A): 459–72. doi:10.1017/S1368980000000549. PMID 11276294. 
  27. ^ Wilt, Timothy; MacDonald, Roderick; Ishani, Areef; Rutks, Indy; Stark, Gerold; Wilt, Timothy (1998). Wilt, Timothy. ed. "Cernilton for benign prostatic hyperplasia". Cochrane Database of Systematic Reviews (2): CD001042. doi:10.1002/14651858.CD001042. PMID 10796739. 
  28. ^ Roehrborn, CG (2008). "Current Medical Therapies for Men With Lower Urinary Tract Symptoms and Benign Prostatic Hyperplasia: Achievements and Limitations". Reviews in urology 10 (1): 14–25. PMC 2312341. PMID 18470272. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2312341. 
  29. ^ AUA Clinical guidelines for management of BPH
  30. ^ Gilling, Peter J.; Aho, Tevita F.; Frampton, Christopher M.; King, Colleen J.; Fraundorfer, Mark R. (2008). "Holmium Laser Enucleation of the Prostate: Results at 6 Years". European Urology 53 (4): 744–9. doi:10.1016/j.eururo.2007.04.052. PMID 17475395. 
  31. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. http://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html. Retrieved November 11, 2009. 
  32. ^ Verhamme, K; Dieleman, JP; Bleumink, GS; Van Der Lei, J; Sturkenboom, MC; Artibani, W; Begaud, B; Berges, R et al (2002). "Incidence and Prevalence of Lower Urinary Tract Symptoms Suggestive of Benign Prostatic Hyperplasia in Primary Care—The Triumph Project". European Urology 42 (4): 323–8. doi:10.1016/S0302-2838(02)00354-8. PMID 12361895. 

[edit] External links
Internal
External
Other

Retrieved from "http://en.wikipedia.org/w/index.php?title=Benign_prostatic_hyperplasia&oldid=481579544"
Personal tools
Namespaces

Variants
Actions
Navigation
Interaction
Toolbox
Print/export
Languages