BILATERAL PROSTATIC HYPERPLASIA
OVERVIEW: Benign prostatic hyperplasia (BPH),
benign prostatic hypertrophy or, benign
enlargement of the prostate (BEP),
are descriptive terms for the enlargement of the prostate that men develop
with aging. Technically, the cells that line the urethra multiply
(hyperplasia) not enlarge (hypertrophy), but the result is the same:
When the nodules enlarge enough there is a relative to complete
obstruction of urine flow. The process begins in the 30's and by age 80,
75% of men have symptoms. For half, the symptoms are significant enough to
take medication or have surgery[.]2
Men experience voiding symptoms including:
(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
International Prostate Symptom Score (IPSS)
questionnaire, designed to assess the severity of BPH.
CAUSE: [from Wikipedia]
A study published in 2008 in the journal of andrology "Andrologia" reports
on a newly discovered venous route by which free (active) testosterone
reaches the prostate in extremely high concentrations, promoting the
accelerated proliferation of prostate cells, leading to the gland's
enlargement. The study suggests that BPH is caused by malfunction of the
valves in the internal Spermatic
veins manifesting as varicocele,
a phenomenon which has been shown to increase rapidly with age, roughly
equal to the 10% per year increasing prevalence of BPH. The 6- to 8-fold
elevated hydrostatic pressure then leads to retrograde venous drainage,
allowing free communication with the prostatic circulation. Having
measured a concentration of free testosterone of some 130-fold above serum
level in the internal spermatic vein (the testes being the main source and
the blood being undiluted in systemic circulation), the authors conclude
that the elevated venous pressure causes hypertrophy and exposure to high
concentrations of free testosterone causes hyperplasia in the prostate.
The study also proposes a treatment method (GatGoren Technique) similar
to that used in treating varicocele,
which restores normal pressure in the venous drainage system, effectively
reducing the volume of the prostate and clinical manifestation of BPH.
Androgens (testosterone and
related hormones) are
considered to play a permissive role in BPH by most experts. This means
that androgens have to be present for BPH to occur, but do not necessarily
directly cause the condition. This is supported by the fact that castrated boys
do not develop BPH when they age. On the other hand, 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, those
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 epithelial
cells. In both of these cell types, DHT binds to nuclear androgen
receptors and signals the transcription of growth
factors 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 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.PMID:
Testosterone promotes prostate cell proliferation, but
relatively low levels of serum testosterone are found in patients with BPH. One
small study has shown that that medical castration lowers the serum and
prostate hormone levels unevenly, having less effect on testosterone and
dihydrotestosterone levels in the prostate.
While there is some evidence that estrogen may play a role in the etiology
of BPH, this effect appears to be mediated mainly through local conversion
of estrogen to androgens in the prostate tissue rather than a direct
effect of estrogen itself. In
canine in vivo studies
castration, which significantly reduced androgen levels but left estrogen
levels unchanged, caused significant atrophy of the prostate. Studies
looking for a correlation between prostatic hyperplasia and serum estrogen
levels in humans have generally shown none.
On a microscopic level, BPH can be seen in the vast majority of men as
they age, in particular over the age of 70 years, around the world.
However, rates of clinically significant, symptomatic BPH vary
dramatically depending on lifestyle. Men that lead a western lifestyle
have a much higher incidence of symptomatic BPH than men that 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
Much work remains to be done to completely clarify the causes of BPH.
The initial medical treatmente, if
symptomatic, is a 5-alpha reductase medication, whether
Flomax or Avadart.
is associated with a 20% incidence of arthralgia (muscle aches and pains)
and headaches. Avadart
interferes with blood donations. When medication fails, there are a
number of office/ out-patient surgial procedures that apply heat/radiation
to the prostatic tissue that surrounds the urethra. The resulting
tissue damage causes shrinkage of the BPH and relief of symptoms, although
a urethral catheter or similar device may be necessary for a number of
days. If this fails, the 'tired-and-true" surgery called TURP
(Transurethral Resection of the Prostate) can be performed in an
If BPH is caused by the local effects of testosterone
or testosterone's conversion to either estrogen or dihydro-testosterone,
then changing the principal androgen from testosterone to nandrolone
should relieve symptoms while lowering estradiol and DHT levels.
Although spirolactone is a 5-alpha reductase, it's use in BPH has not been
While no clinical studies have been performed to date,
personal experience has found this to be at least temporarily helpful and
discontinuation of 5-alpha reductase medications was well tolerated.
CLINICALLY, TESTOSTERONE REPLACEMENT CAN BE BENEFICIAL.
Purpose. We performed a randomised controlled study regarding the effects
of androgen replacement therapy (ART) on lower urinary tract symptoms (LUTS)
in hypogonadal men with benign prostate hypertrophy (BPH).
Methods. Fifty-two patients with hypogonadism and BPH were randomly
assigned to receive testosterone (ART group) as 250 mg of testosterone
enanthate every 4 weeks or to the untreated control group. We compared
International Prostate Symptom Score (IPSS), uroflowmetry data,
post-voiding residual volume (PVR) and systemic muscle volume at baseline
and 12 months after treatment. Results. Forty-six patients (ART group,
n = 23; control, n = 23) were included in the analysis. At the 12-month
visit, IPSS showed a significant decrease compared with baseline in the
ART group (15.7 ± 8.7 vs. 12.5 ± 9.5; p < 0.05). No significant changes
were observed in the control group. The ART group also showed improvement
in maximum flow rate and voided volume (p < 0.05), whereas no significant
improvements were observed in the controls. PVR showed no significant
changes in either group. In addition, the ART group showed significant
enhancement of mean muscle volume (p < 0.05), whereas no significant
changes were seen in the controls. Conclusion. ART improved LUTS in
hypogonadal men with mild BPH.
ICD 9 CPT CODE 600.
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