Benign prostatic hyperplasia: Difference between revisions

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{{Benign prostatic hyperplasia}}
{{Benign prostatic hyperplasia}}
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==Etiology==
[[Androgen]]s ([[testosterone]] and related [[hormone]]s) are considered to play a permissive role in [[BPH]] by most experts. This means that [[androgen]]s have to be present for BPH to occur, but do not necessarily directly cause the condition. This is supported by the fact that [[castration|castrated]] boys do not develop BPH when they age, unlike intact men. Additionally, administering exogenous testosterone is not associated with a significant increase in the risk of BPH symptoms. [[Dihydrotestosterone]] ([[DHT]]), a [[metabolite]] of testosterone is a critical mediator of prostatic growth. DHT is synthesized in the prostate from circulating testosterone by the action of the enzyme 5α-reductase, type 2. This enzyme is localized principally in the stromal cells; hence, these cells are the main site for the synthesis of [[DHT]]. 
DHT can act in an [[autocrine]] fashion on the stromal cells or in [[paracrine]] fashion by diffusing into nearby [[epithelium|epithelial cells]]. In both of these cell types, DHT binds to nuclear [[androgen receptor]]s and signals the [[Transcription (genetics)|transcription]] of [[growth factor]]s that are mitogenic to the epithelial and stromal cells. DHT is 10 times more potent than testosterone because it dissociates from the androgen receptor more slowly. The importance of DHT in causing [[nodule (medicine)|nodular]] hyperplasia is supported by clinical observations in which an [[inhibitor]] of 5α-reductase is given to men with this condition. Therapy with 5α-reductase inhibitor markedly reduces the DHT content of the prostate and in turn reduces prostate volume and, in many cases, BPH symptoms.
There is growing evidence that [[estrogen]]s play a role in the [[etiology]] of BPH. This is based on the fact that [[BPH]] occurs when men generally have elevated estrogen levels and relatively reduced free testosterone levels, and when prostate tissue becomes more sensitive to estrogens and less responsive to [[DHT]]. Cells taken from the prostates of men who have [[BPH]] have been shown to grow in response to high [[estradiol]] levels with low androgens present. [[Estrogen]]s may render cells more susceptible to the action of [[DHT]].
On a microscopic level, BPH can be seen in the vast majority of men as they age, particularly over the age of 70 years, around the world. However, rates of clinically significant, symptomatic BPH vary dramatically depending on lifestyle. Men who lead a western lifestyle have a much higher incidence of symptomatic BPH than men who lead a traditional or rural lifestyle. This is confirmed by research in China showing that men in rural areas have very low rates of clinical BPH, while men living in cities adopting a western lifestyle have a skyrocketing incidence of this condition, though it is still below rates seen in the West.
Much work remains to be done to completely clarify the causes of BPH.


==Diagnosis==
==Diagnosis==

Revision as of 19:36, 30 September 2012

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Benign prostatic hyperplasia
ICD-10 N40
ICD-9 600
DiseasesDB 10797
MeSH D011470

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Diagnosis

Rectal examination (palpation of the prostate through the rectum) may reveal a markedly enlarged prostate.

Often, blood tests are performed to rule out prostatic malignancy: elevated prostate specific antigen (PSA) levels needs further investigations such as reinterpretation of PSA results, in terms of PSA density and PSA free percentage, rectal examination and transrectal ultrasonography. These combined measures can provide early cancer detection.

Ultrasound examination of the testicles, prostate and kidneys is often performed, again to rule out malignancy and hydronephrosis.

Epidemiology

More than half of the men in the United States between the ages of 60 and 70 and as many as 90% between the ages of 70 and 90 have symptoms of BPH. For some men, the symptoms may be severe enough to require treatment.

Treatment

Lifestyle

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

Medications

Alpha blockers (α1-adrenergic receptor antagonists) provide symptomatic relief of BPH symptoms. Available drugs include doxazosin, terazosin, alfuzosin and tamsulosin. Older drugs, phenoxybenzamine and prazosin are not recommended for treatment of BPH [1]. Alpha-blockers relax smooth muscle in the prostate and the bladder neck, and decrease the degree of blockage of urine flow. Alpha-blockers may cause ejaculation back into the bladder (retrograde ejaculation).

The 5α-reductase inhibitors (finasteride and dutasteride) are another treatment option. 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.[2]

There is also extensive evidence of the efficacy of Serenoa repens (saw palmetto) fruit extracts in alleviating mild-to-moderate BPH symptoms; a systematic review of evidence found comparable efficacy to finasteride.[3] Other herbal medicines that have solid research support in systematic reviews include beta-sitosterol from Hypoxis rooperi (African star grass) and pygeum (extracted from the bark of Prunus africana), while there is less substantial support for the efficacy of Cucurbita pepo (pumpkin) seed and Urtica dioica (stinging nettle) root.[4] At least one double-blind trial has also supported the efficacy of rye flower pollen.[5]

Sildenafil shows some symptomatic relief, suggesting a possible common etiology with erectile dysfunction[6].

Surgery

If medical treatment fails, transurethral resection of prostate (TURP) surgery may need to be performed. 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's left. Transurethral electrovaporization of the prostate (TVP), laser TURP, visual laser ablation (VLAP), TransUrethral Microwave ThermoTherapy (TUMT), TransUrethral Needle Ablation (TUNA), 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) laser have emerged very recently. This procedure involves a high powered 80 Watt KTP laser with a 550 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. KTP lasers target haemoglobin as the chromophore and have typically have a penetration depth of 2.0mm (four 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 550um disposable side-firing fiber that directs the beam from a high powered 100 Watt laser at a 70degree from the fiber axis. The holmium wavelength is 2,140nm, which falls within the infrared portion of the spectrum and is invisible to the naked eye. Where KTP relies on haemoglobin as a chromophore, water within the target tissue is the chromophore for Holmium lasers. The pentration depth of Holmium lasers is <0.5mm avoiding complications associated with tissue necrosis often found with the deeper penetration and lower peak powers of KTP.

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

Related chapters

References

  1. ↑ AUA Practice Guidelines Committee.AUA guideline on management of benign prostatic hyperplasia (2003). Chapter 1: Diagnosis and treatment recommendations. J Urol 170(2 Pt 1): 530-47. PMID 12853821
  2. ↑ Kaplan SA, McConnell JD, Roehrborn CG, 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. J Urol 175(1): 217-20. PMID 16406915.
  3. ↑ Wilt TJ, Ishani A, MacDonald R, (2002). Serenoa repens for benign prostatic hyperplasia. Cochrane Database Syst Rev 2002 (3), CD001423. (Medline abstract)
  4. ↑ Wilt TJ, Ishani A, Rutks I, MacDonald R (2000) Phytotherapy for benign prostatic hyperplasia Public Health Nutr 3(4A):459-72 (Medline abstract)
  5. ↑ Buck AC, Cox R, Rees RWM, et al. (1990) Treatment of outflow tract obstruction due to benign prostatic hyperplasia with the pollen extract, Cernilton. A double-blind placebo-controlled study Br J Urol 66:398-404 (Medline abstract)
  6. ↑ McVary KT, Monnig W, Camps JL Jr, et al (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. J Urol 177(3) :1071-7. PMID 17296414

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