Prostate cancer is the second leading cause of death among men. In 2002 it is estimated
that 30,200 men will die from prostate cancer and 189,000 men will be diagnosed
(American Cancer Society Facts & Figures 2002). The incidence of prostate cancer
increases with age with 75% of all prostate cancers being diagnosed in men over
the age of 65.
The symptoms of prostate cancer may be similar to those of prostate infection or
enlargement. Many times there are no symptoms, even when prostate cancer is advanced.
They include inability to urinate, a weak or halting urinary flow, difficulty starting
or stopping urination, frequency of urination especially at night, blood in the
urine, pain or burning on urination, and/or chronic pain in the low back, pelvis
or upper thighs. It is important to see your physician if you have these symptoms
but it is equally important to undergo prostate cancer screening annually even if
you don't have symptoms.
The importance of screening and early detection is key for long-term survival. Screening
for prostate cancer consists of a prostate-specific antigen (PSA) blood test and
a digital rectal examination. Men should start being screened for prostate cancer
at the age of 50. Screening should start earlier, at age 40, for men with the following
- All men regardless of race if there is a family history of prostate cancer
in either the mother or father's side
An elevated prostate-specific antigen and/or an irregular feeling prostate or nodule
in the prostate found on digital rectal examination may be suspicious for prostate
cancer. The diagnosis of prostate cancer is made on the basis of a prostate biopsy
performed under ultrasound guidance generally in the physician's office.
Once the diagnosis of prostate cancer is made the physician will review all treatment
options available to the patient. Further studies to evaluate the extent or stage
of disease may be necessary to assist in making a decision about treatment.
There are many different treatment options and combinations of treatments depending
on the stage of disease and the age and health of the patient. Generally the treatments
available for prostate cancer are:
Radical prostatectomy: The surgical removal of the prostate. The best cure rate
for localized prostate cancer is with the use of radical prostatectomy. Prostate
cancer is said to be localized when the cancer is confined to the prostate.
Radiation: This involves the application of an external beam of radiation directed
to the prostate and the prostate bed.
Brachytherapy: Radioactive seed implantation. This procedure involves the insertion
and removal of needles into the perineum to place radioactive seeds into the prostate.
The seeds deliver a controlled and pre-determined amount of radiation to the prostate
Cryotherapy: Cryotherapy involves the insertion of probes into the prostate and
the introduction of liquid nitrogen to produce an ice ball within the prostate.
This effectively destroys both prostate cancer and healthy prostatic tissue.
Hormone therapy: Medication or surgery to inhibit the production of testosterone
and therefore slow the growth of prostate cancer.
For more information on the diagnosis of prostate cancer and the treatment options
available visit the American Cancer
Society's web site.
Recent journal articles and research have suggested that diet may have an influence
on the prevention of prostate cancer. A diet low in animal fat along with a daily
intake of vitamin E 50 mg/day, Selenium 200 mcg/day, and a diet high in soy protein
may be beneficial in the prevention of prostate cancer (Journa of Urology, Vol.
161, 1748-1760, June 1999).
Cancer Support Groups
An organization called US TOO International sponsors support groups for men with
the diagnosis of prostate cancer. The organization has support groups throughout
the country. Most of the support groups meeting monthly.
To find out more about this organization go to the
US TOO web site.
Cancer Risk Reduction
It has not been proven that any particular diet, dietary supplement or medication
will prevent prostate cancer. A number of studies have shown some potential risk
reduction for the development of prostate cancer (especially in previous or current
smokers) from the use of vitamin E, selenium, and soy protein. The optimal dosage
for these substances remains to be determined. These substances are available in
tablet form at the health food store but many researchers believe the best source
for these substances is from dietary foods. Suggestions for reducing the risk of
developing prostate cancer are:
1) Maintain a healthy diet consisting of:
at least five servings of fruits and vegetables per day
limit the intake of red meat and fat
2) Suggested daily intake of vitamin E, selenium, soy protein and lycopene:
Vitamin E 400 IU per day as a supplement taken with meals.
Selenium 200 mcg per day as a supplement taken with meals.
Soy Isoflavones 40 to 50 mg per day (specifically the isoflavones genistein
and daidzen). As a supplement or in diet.
Lycopene 10 mg/day. As a supplement or in diet.
3) Regular physical activity of 30 to 45 minutes on five or more
days a week. Men over the age of 40 who have not been physically active should be
evaluated by their physician before beginning an exercise program and they should
gradually increase the intensity, duration and frequency of exercise.
4) Maintain ideal body weight.
||Wheat germ oil
||Almonds & other nuts
|Barley, oats, whole wheat, bran, wheat
||Soybean oil, sunflower oil, corn oil, olive
||Vegetable juice (V8)
|Fish, meat, poultry
IMPORTANT: There are potential adverse side effects from taking more than
the recommended doses of vitamins. Also, when you are asked by a health care provider
to list the current medications you take on a regular basis be sure to mention the
vitamins and supplements that you take and the amounts.
SOME POTENTIAL SIDE EFFECTS:
• Increasing the effect of
blood thinners (i.e. Coumadin, aspirin)
• Pathological changes to nails
• Brittle hair or hair loss
Potentially interferes with the absorption
of thyroid hormone replacement. If you are on
Synthroid or other thyroid hormone replacement
do not take a soy supplement at the same time
as the thyroid replacement. Take them at different times such as one
in the morning and the other in the evening.
Prostatitis is inflammation of the prostate gland. There are three types of
Acute (severe) infectious prostatitis: This may be caused by a bacteria or virus.
The symptoms come on suddenly and may be severe. They include fever and chills,
low back pain, frequent and painful urination, decreasing or less forceful urinary
stream and urinary retention (the bladder does not empty urine completely).
Chronic (long-lasting) infectious prostatitis: This also may be caused by a
bacteria. Stress, caffeine, nicotine, or alcohol may worsen the condition. Symptoms
may include repeat bladder infections, frequent urination, and pain in the lower
abdomen or low back.
Noninfectious prostatitis: This form of prostatitis is not caused by a bacteria
and therefore antibiotics are not helpful. This is the most common type of prostatitis.
It may be exacerbated by stress and/or irregular sexual activity. Stress may
cause the pelvis muscles to tighten and cause pain. Increased pressure during
voiding may cause urine to back up into the ducts resulting in a form of chemical
prostatitis. The prostate gland produces fluid for semen and infrequent ejaculation
may cause the ducts to become clogged with secretions.
Prostatitis is not contagious to your sexual partner. The symptoms of prostatitis
are similar to those of benign prostatic hyperplasia (enlargement of the prostate)
or urethritis (inflammation of urethra). It is important to see your physician for
a prostate examination so the proper treatment may be initiated.
Your physician will need to perform a urinalysis to check for infection or blood
cells. He will also perform a digital rectal exam to palpate the prostate. He may
collect a sample of prostatic fluid which is obtained by pressing on the prostate
during the digital rectal exam. This fluid is examined for white blood cells and
bacteria, sometimes a culture is done.
The infectious form of prostatitis may be treated with antimicrobial medication.
Acute prostatitis may be treated with antimicrobial medication for 7-14 days while
chronic prostatitis may require 4 to 12 weeks of medication before the prostatitis
is cleared. The non-infectious form of prostatitis may be helped by taking hot baths,
drinking more fluids, changing your diet, and ejaculating frequently (to drain the
prostate gland and relax the muscles). If muscle relaxation improves your symptoms
your physician may prescribe alpha blockers, drugs that relax the muscle tissue
in the prostate and allows urine to flow more freely.
Follow your physician's recommendations and be sure to follow-up in the office with
your physician as instructed to make sure your prostatitis has been completely cleared,
even if your symptoms have disappeared.
Benign enlargement of the prostate gland is a common but incompletely understood
consequence of aging. The clinical symptoms of frequency, urgency and decreased
force of urinary stream, also known as lower urinary tract symptoms (LUTS) are also
associated with advancing age.
That an enlarging prostate and the development of LUTS are both age dependent, is
indisputable. Autopsy studies have demonstrated that up to 80% of 80 year old men
will have histologic evidence of BPH (Figure 1). Approximately 40% of those same
men will demonstrate an enlarged prostate on physical examination; however, only
25-30% of 80 year old men will have symptomatic BPH and pursue treatment.
The economic consequences of BPH in an aging population are profound. Historically,
the primary treatment has been transurethral resection of the prostate (TURP) which
is a highly effective form of management, and still the standard against which all
other therapies are evaluated.
In 1992, 400,000 prostatectomies were performed in the U.S. This amounted to 38%
of the major surgery performed by urologists in this country at an annual cost of
approximately $4 billion to the healthcare system. At that time, transurethral resection
of the prostate was second only to cataract surgery for men over the age of 65.
As a testimony to the changing climate of healthcare in general, and the significant
advances in the medical management of BPH, the number of prostatectomies performed
in 1998 will be less than half that in 1992. The ultimate economic consequences
of less invasive and medical therapies for BPH remains to be evaluated since prolonged
bladder outlet obstruction may have secondary consequences when incompletely treated.
A better understanding of the pathophysiology of BPH and specifically a better understanding
of the genesis of LUTS has stimulated the development of medical therapies for BPH
and a host of innovative technologies aimed at reducing these symptoms.
Prostate Anatomy and Physiology
The prostate is a secondary sexual organ located at the base of the bladder. It
encircles the urethra and serves the function of contributing fluid to the ejaculate.
Approximately 50% of the total fluid in the ejaculate is of prostatic origin and
is manufactured by apocrine excretion from epithelial cells. The prostate is one
of the most phylogenetically consistent organs in the animal kingdom being present
from invertebrates through mammals. A newborn typically has a prostate which weighs
1 gm. There is a rapid increase in prostatic size following puberty with a continuing
more gradual increase in size thereafter. The average prostatic weight in a 70 year
old man is 30-60 gm. Since the specific gravity of prostatic tissue is near that
of water, prostatic volume can typically be related to prostatic weight. Two conditions
are necessary for the development of BPH; namely, aging and the presence of testes.
It is well known that human males who are castrated prior to the time of puberty
never develop BPH.
A. The hypothalamic-pituitary-testis-prostate-hormonal axis:
The development of BPH requires the presence of testosterone. The cascade of
hormonal events leading to this phenomenon begins with the release of luteinizing-releasing
hormone (LHRH) by the hypothalamus. LHRH acts on the anterior pituitary gland to
stimulate the production of luteinizing hormone (LH). LH circulates in the bloodstream
and induces the testicular Leydig cells to produce testosterone. Testosterone, in
turn, acts on individual prostatic epithelial cells where it binds at the cell membrane
with a surface receptor and is a substrate for the enzyme 5a -reductase. The primary
product of 5a -reductase activity on testosterone is the metabolite, 5a -dihydrotestosterone
(DHT). DHT binds with a receptor in the cytosol and becomes a hormone-receptor complex
which is then transported to the nucleus. It is DHT which seems to be critical for
the development of BPH.
B. Zonal and Histologic Anatomy of the Prostate:
A helpful concept in considering the affects of an enlarged prostate on the lower
urinary tract is to consider the zonal anatomy of the prostate. McNeill introduced
the concept of three distinct zones in prostatic anatomy. The periurethral tissue
which primarily consists of short branching epithelial glands is called the transition
zone. It is this zone which experiences a disproportionate nodular growth in the
process of BPH. The outer portion of the prostate, or peripheral zone, is composed
of long branching epithelial glands which are typically compressed by the enlarging
transition zone. This constitutes what is called the surgical capsule of the prostate
and is the zone most likely to demonstrate prostate cancer. The central zone of
the prostate is that portion at the base of the gland which encircles the seminal
vesicles. Why the transition zone should be disproportionately involved with BPH
is unknown. There is a combination of stromal and glandular hyperplasia which results
in nodular growth so characteristic of BPH. How and whether BPH mechanically obstructs
the urethra is a matter of some conjecture. Clearly in some cases mechanical encroachment
and obstruction of the urethra occurs by virtue of enlarging lateral prostatic lobes.
In other cases it may be that distortion of the bladder neck by the adenoma prevents
the appropriate relaxation of the bladder neck. In any case, the size of the prostate
does not correlate well with either the degree of symptomatology or objective parameters
of bladder outlet obstruction, including intravesical pressure. It has been postulated
that the development of BPH may be on the basis of a lack of cellular apoptosis,
the process of natural cell death. This may be mediated through the protease members
of the capsase family. A final component of prostatic histology which is often overlooked
is the presence of smooth muscle cells in the prostatic capsule. This so-called
fibromuscular stroma may play a role in the tone of the prostatic urethra. This
observation has been exploited in some forms of BPH management.
Physiology of Micturition
Bladder Anatomy and Physiology: The function of the urinary
bladder is the low pressure storage and periodic complete emptying of urine. The
process of urination, or micturition, requires an intact detrusor muscle, an intact
bladder and urethra and coordinated relaxation of the bladder neck and external
striated sphincter. This complex process of detrusor contraction and sphincteric
relaxation results in low pressure emptying of urine. It is mediated by the central
nervous system. An understanding of the physiology of micturition is essential to
understanding the strategies aimed at managing LUTS and BPH. As the urinary bladder
fills from continuous urine production from the upper urinary tracts, bladder wall
tension decreases. The bladder is the only solid viscus which demonstrates decreasing
wall tension with increasing volume. This phenomenon allows for the low pressure
storage of urine. The sensation of bladder fullness is transmitted to the CNS via
the pelvic nerves. The process of voiding commences with efferent signals stimulating
detrusor contraction and concomitant relaxation of the pelvis floor and external
striated sphincter. The detrusor muscle is smooth muscle. Alpha receptors in the
bladder are concentrated near the bladder neck and proximal urethra. Stimulation
of these alpha receptors results in contraction of the bladder outlet increasing
the resistance to urine flow. Conversely, alpha blockade facilitates bladder emptying.
While the development of LUTS in the aging male population is often attributed to
BPH the differential diagnosis of obstructive and irritative voiding symptoms is
extensive. The etiology of LUTS in the aging male population may include both urologic
and non-urologic conditions. Parkinson's disease, cerebrovascular accident, diabetes
mellitus, congestive heart failure, bladder cancer, prostate cancer, urinary tract
infection, urethral stricture and bladder neck hypertrophy may cause symptoms indistinguishable
from those caused by BPH. A thorough history and physical examination evaluating
other potential sources of lower urinary tract obstructive symptoms should be undertaken
before empiric treatment for BPH is begun.
Once bladder outlet obstruction has been confidently diagnosed it is helpful to
think of this concept as being attributable to both static and dynamic factors.
The static component of bladder outlet obstruction may be attributed to the physical
enlargement of the prostate as it encroaches on the prostatic urethra and bladder
outlet. The dynamic portion of the obstruction is more likely related to the relative
tension of prostatic and bladder neck smooth muscle. It is particularly useful when
formulating a strategy for the treatment of bladder outlet obstruction to consider
whether the detrusor itself is intact. A variety of conditions, most notably diabetes
mellitus, may result in a detrusor muscle that is ineffective in generating pressures
high enough to overcome even normal resistance at the bladder outlet.
The litany of symptoms classically associated with BPH is well known to everyone
who cares for older men. Frequency of micturition is often one of the first manifestations
of BPH. The patient often also complains of an urgent need to urinate and the inability
to delay urination for any significant time. These symptoms are often exacerbated
by stimulants of the prostate and urethra; particularly caffeine, nicotine, and
alcohol. As the natural history of BPH progresses one begins to see the mechanical
effects of bladder outlet obstruction which are the decreased forcefulness of urinary
stream, post-void dribbling and spraying of the urinary stream. Progression of this
situation may lead to incomplete bladder emptying which results in an exacerbation
of urinary frequency owing to the decreased functional capacity of the bladder.
In severe cases the patient may complain of continuous dribbling which is secondary
to overflow incontinence. The symptom of nocturia or increased frequency of voiding
at night deserves special consideration. While nocturia may be a consequence of
BPH there are a number of other potential explanations. It is thought that patients
who sequester fluid in their lower extremities during the day may mobilize that
fluid and actually produce greater volumes of urine at night. It has been suggested
that there is an increased diuresis on the basis of decreased activity of ADH (antidiuretic
hormone) during the nighttime hours. It is also thought that long-standing bladder
outlet obstruction with detrussor hypertrophy may up-regulate neurologic receptors
in the bladder wall creating a sensation of needing to void. Decreased sensory stimulation
during the night may heighten a patient's awareness of his bladder so that although
the total volume of urine excreted over an 8-hour period does not truly increase,
the frequency of voiding does.
The severity of symptoms associated with bladder outlet obstruction tends to wax
and wane over time. It is not uncommon for patients to have episodic exacerbation
of their symptoms only to have them improve spontaneously without therapy. The AUA
Symptom Index Score is an attempt to quantify the degree of bladder outlet obstruction
based on symptoms. This questionnaire consisting of 14 questions attempts to quantify
obstructive and irritative voiding symptoms and then determine to what degree they
affect the patient's lifestyle. Although this information is not particularly useful
in making clinical decisions on a one-time basis, the trend over time may be important.
The decision to treat patients who have symptoms of bladder outlet obstruction is
highly dependent on their perception of those symptoms. Since the physical size
of the prostate is poorly correlated to the outcomes of therapy, a thorough history
may be the single most important diagnostic tool in the management of patients with
Beyond clinical symptoms the pathophysiological consequences of bladder outlet obstruction
may be profound. With incomplete bladder emptying there is an increased risk of
urinary tract infection and the development of bladder stones. Secondary changes
in the bladder muscle include trabeculation (which is a manifestation of hypertrophy)
followed by the development of cellulae and diverticula. Although high intravesical
pressures are probably not directly transmitted to the upper urinary tract, changes
in the intramural ureter may result in secondary obstruction of the ureters and
hydronephrosis. In severe cases of longstanding bladder outlet obstruction secondary
changes in the ureters including dilatation, tortuosity, and elongation. The ultimate
outcome may be renal insufficiency and even renal failure.
Bladder Outlet Obstruction Secondary to BPH
Because symptoms often correlate poorly with prostatic size it may be valuable to
have quantitative information regarding bladder outlet obstruction. The urinary
flow rate recorded in cc/second has long been used as a measure of bladder outlet
obstruction. The normal urinary bladder will hold approximately 400 cc of urine
comfortably and can be emptied completely within 15 to 30 seconds.
A normal flow rate shows a rapid increase in flow with a slower decrease in flow
but in general has a parabolic profile. In cases where bladder outlet obstruction
exists it is common to see a much slower increase in the rate of flow, a lower peak
flow rate, and intermittency of the stream. Complete bladder emptying often requires
2-3 minutes. There are two significant problems with using flow rates to make clinical
decisions about bladder outlet obstruction: 1) The detrusor muscle is not very efficient
at low volumes. This means that if the patient has less than 150 cc of voided volume,
the flow rate may not represent his true detrusor function or the degree of bladder
outlet obstruction he is experiencing. 2) If the same patient voids on three different
occasions on the same day vastly different patterns may be seen. These results may
be related not only to bladder fullness but patient motivation and extrinsic environmental
factors as well. Therefore, flow rate, although it may be useful in certain situations,
is a poor clinical predictor of the severity of bladder outlet obstruction or the
consequences of treatment.
A second measure which is possibly useful in the evaluation of patients with bladder
outlet obstruction is the post-void residual. This has historically been measured
by performing an in-and-out catheterization on a patient after spontaneous micturition.
In recent years this practice has been supplanted by evaluating the post-void residual
by suprapubic ultrasound. In any case the post-void residual is poorly correlated
with the degree of mechanical bladder outlet obstruction and is also highly dependent
on patient motivation and external factors. In general, a post-void residual of
>60 cc is thought to be clinically important.
The most sophisticated measure of lower urinary tract function is the urodynamic
evaluation. This study involves the use of perineal patch electrodes to measure
muscular activity of the pelvic floor with simultaneous measurement of intravesical
pressures during filling and intravesical pressures during voiding are obtained.
This study provides valuable information regarding the bladder capacity, the compliance
of the bladder wall and the coordination between detrusor function and external
sphincter function. Perhaps the most useful parameter in evaluating bladder outlet
obstruction is the pressure flow study whereby intravesical pressures are recorded
along with the flow rate. The critical issue here is how high the intravesical pressure
must be to overcome resistance at the bladder outlet. Using nomograms it is, in
this way, possible to make a quantitative determination of the presence of bladder
outlet obstruction. Such a determination does not reliably indicate the etiology;
that is, it does not differentiate between the static and the dynamic component
of bladder outlet obstruction.
The management of bladder outlet obstruction and BPH can be conveniently separated
into four categories: observation, medical therapy, minimally invasive therapy,
and ablative therapy.
A. Observation: If a patient complains of symptoms of bladder outlet
obstruction which are mild, observation is certainly a reasonable alternative. In
the initial evaluation of patients with BPH, especially those over the age of 40,
a prostate-specific antigen (PSA) should be obtained. It is often useful to do a
microscopic urinalysis as well as a urine culture to determine that the patient
is uninfected. Physical examination including evaluation of the urethral meatus,
palpation of the penile shaft and perineum, and digital rectal examination are essential.
A neurologic exam should demonstrate any gross abnormality which might be responsible
for symptoms of bladder outlet obstruction. A serum creatinine is a useful baseline
value. Follow-up at 6 to 12-month intervals seems reasonable. Unfortunately, progression
of secondary structural abnormalities may be relatively silent in the BPH population.
B. Medical Therapy: Medical therapy for BPH is a fascinating field
which is rapidly evolving. Symptoms of BPH are often exacerbated by other medications
which the patient may be taking. Therefore, the medical management of BPH may be
as involved with withdrawing or changing existing medications as adding new ones.
Specifically anticholinergic type medications, narcotic analgesics, and sophorifics
are detrimental to bladder function. Likewise, alpha adrenergic agents may increase
resistance at the bladder neck. Smooth muscle relaxants are another category of
drugs which may be relatively contraindicated in patients with bladder outlet obstruction,
because they adversely affect detrussor function.
C. Alpha blockade: The concentration of alpha adrenergic
receptors at the bladder neck and proximal urethra is responsible for the strategy
of alpha-blocking drugs in the treatment of BPH. These receptors have been characterized
as primarily alpha-1 receptors. Phenoxybenzamine was the first alpha blocker to
be used in the clinical treatment of BPH but it resulted in significant side effects
such as hypotension, nasal stuffiness and dizziness. These side effects were caused
primarily by blockage of alpha-2 receptors outside the urinary tract. In an attempt
to limit these extra-urinary side effects more and more specific alpha-1 blockers
have been developed. Recently, the alpha-1c subtype receptor has been identified
as predominant at the bladder neck. Not unexpectedly, an agent has been designed
to target the alpha-1c receptor. It must be cautioned that pharmacologic uroselectivity
may not translate to better clinical outcomes. Theoretically the selectivity of
the drug may permit increasing its dosage without increasing the severity of vasogenic
side effects. The affect of alpha-1 blockade appears to be smooth muscle relaxation
in the prostatic capsule and at the bladder neck and clearly addresses only the
dynamic component of bladder outlet obstruction. It is also felt that alpha-1 blockade
may ameliorate the symptoms of bladder outlet obstruction by a separate mechanism
which is neurologically mediated. Multiple randomized prospective studies involving
the use of alpha-1 blocking agents have shown a definite improvement in symptom
scores and a marginal improvement in flow rates compared to placebo. These improvements
are lost within a few weeks of discontinuing the medication.
D. Finasteride:The development of finasteride, (5a -reductase inhibitor)
for the management of BPH, is a fascinating story. In the 1960s a clinical syndrome
called "pseudovaginal penoscrotal hypospadias" was described. In this syndrome the
affected subjects had a 46 XY karyotype with normally differentiated testes, normal
male internal ducts and ambiguous genitalia. It was discovered that these patients
had a deficient or defective type 2, 5a -reductase enzyme. Once it was recognized
that a deficiency of this enzyme would produce a clinical syndrome of decreased
secondary sexual development it was reasoned that an 5a -reductase inhibitor might
be used to induce one aspect of this syndrome in an already developed male, which
is involution of the prostate. Since this enzyme has no other known function in
the body except the conversion of testosterone to dihydrotestosterone it was felt
that blockade of the enzyme could be safely accomplished. The use of selective 5a
-reductase inhibitor does not result in decreased sexual activity or breast growth
as is the case with other androgen withdrawal therapies. In fact, the serum testosterone
level in patients treated with finasteride is normal.
The efficacy of finasteride as a treatment for BPH has been questioned. The long-term
use of finasteride may result in as much as a 30% diminution in the volume of the
prostate gland but often requires up to 6 months to achieve that effect. Furthermore,
it has not been shown in prostates less than 60 gm that there is a significant improvement
in either flow rates or urologic symptoms. In patients with large prostate glands
(>60 gm) the use of finasteride may decrease the ultimate risk of developing urinary
retention. Finasteride does decrease the serum PSA level without diminishing the
risk of prostate cancer. Therefore, its extended use may result in a false sense
of security for the clinician who depends on the PSA level for the early diagnosis
of prostate cancer.
E. Androgen blockade: One strategy which may be useful in the management
of elderly or infirm patients with BPH is the use of androgen blockade. GNRH agonists
such as Lupron™ and Zoladex™ may be useful in diminishing prostatic
volume by 30% without the need for surgical intervention. The side effects of this
treatment include hot flashes and in some cases the loss of bone density and muscle
mass. These injections are expensive and may require several months to show any
clinical effect. LHRH agonists are not recommended for the treatment of most patients
F. Phytotherapy: Phytotherapy is a rapidly emerging field.
Patients are well aware of the availability of herbal preparations for the management
of a variety of clinical conditions including BPH. Of the currently available phytotherapies,
saw palmetto, is the most commonly mentioned and probably the most clinically useful.
It is thought that saw palmetto has a mechanism of action similar to finasteride.
Although few, if any, good randomized prospective studies exist, the few data which
are available suggest that saw palmetto is probably not harmful and may be helpful.
It does not appear that saw palmetto materially affects serum PSA levels. Thus far,
it does not appear that ginseng, gingko, or other herbal preparations have a significant
affect on BPH or its symptom complex.
Minimally Invasive Therapy
One strategy for the management of BPH and the resultant lower urinary tract symptoms
involves the use of heat provided by various generators. The common sources of heat
are currently focused-ultrasound, high-energy radiofrequency, laser, and microwave
devices. Transurethral microwave therapy (TUMT) makes it possible to obtain high
temperatures in the lateral lobes of the prostate while preserving the urethral
mucosa. The theoretical advantage of this therapy is that it can be undertaken with
local analgesia and sedation only. It does not require the removal of any tissue
and because the urethral mucosa is maintained there is a much lower incidence of
urinary bleeding and post-therapy obstruction. Clinical studies of the effectiveness
of this form of therapy have shown only marginal increases in flow rates but the
majority of patients reported an improvement in their symptoms and quality of life.
Complications in general were mild but included hematospermia and in the early phases
of the development of microwave therapy, thermal injury to both the urethra and
the rectum. Part of the value of this and other "heat therapies" may be destruction
of sensory nerves in the prostate and urethra.
2. TUNA: Another variation on the administration of heat to prostatic
tissue is the transurethral needle ablation of the prostate procedure (TUNA). The
instrument consists of a pair of retractable needles which are advanced into the
prostatic adenoma. Taking advantage of the high resistance of prostatic tissue to
electrical current, heat is generated as current is passed between the needles which
results in tissue destruction. This is another therapy which has a theoretical advantage
of preserving the urethral
mucosa and allows some measure of control regarding the extent of tissue destruction.
As with other heat related therapies there is necrosis and edema of tissue, creating
a moderate probability of urinary retention postoperatively.
At least two mechanical therapies for management of BPH deserve mention.
1. Expandable intraurethral prostatic stent. This apparatus
can be introduced through a standard cystoscope under assisted local anesthesia
and then can be expanded merely by removing it from a sheath. The initial result
is a 36-French lumen in the prostatic urethra which greatly facilitates voiding.
Because this metal mesh causes little tissue reaction, infection and rejection are
unlikely. However, there is an ingrowth of prostatic epithelium over time so that
the wire mesh is ultimately covered by polypoid appearing collections of epithelial
cells. The obvious potential complications of the use of this technology are transmigration
of the stent into the bladder or through the prostate by direct pressure and erosion.
A second risk is encrustation of the device over a long period of time. This treatment
is generally reserved for patients who are poor surgical risks and who otherwise
would require chronic indwelling urethral catheters.
2. Balloon dilation of the prostate. This was one of the
earliest forms of minimally invasive therapy for BPH. This strategy involved placing
an inflatable balloon across the bladder neck in the prostatic urethra and then
expanding it to 36-French. This results in a fracture of the adenoma which must
then heal spontaneously. Clinically the procedure was well tolerated but the results
were not durable. This procedure is currently seldom utilized.
Incisional / Ablative therapies
1. TUIP: Intermediate in effectiveness between the heat
therapies and ablative therapies for BPH is transurethral incision of the prostate.
This procedure is performed through a cystoscope and involves the use of an electrical
device for dividing the bladder neck and prostate to the level of the veru montanum.
This is accomplished by passing current through a cutting wire and then incising
the bladder neck musculature, prostatic adenoma, and prostatic capsule. Because
only a single incision is utilized there is minimal bleeding. No prostatic tissue
is removed. In selected patients this has been a very useful procedure and reduces
the risk associated with a standard transurethral resection of the prostate. Those
patients most likely to benefit from TUIP are young patients with small lateral
lobes and elevated bladder necks.
2. TURP: The most effective surgical procedure for managing BPH
is transurethral resection of the prostate (TURP). This classic procedure is performed
through a cystoscope and involves the use of a cutting loop. The prostate is excavated
from the level of the bladder neck to the veru montanum. This results in debulking
of the lateral adenoma. TURP has resulted in the most objective improvement in flow
rate and the best subjective improvement in symptoms. Patients with irritative voiding
will often be unimproved by TURP. Morever, TURP is subject to a number of potential
complications. Bleeding is a common problem and may occasionally be severe. The
development of scar tissue at the bladder neck (bladder neck contracture) can result
in significant obstruction post surgery. Because of the proximity of the external
striated sphincter damage incurred during a TURP can result in continuous urinary
incontinence. Up to 15% of men report erectile dysfunction or frank impotence following
TURP, although the mechanism of the impotence in this setting is not well understood.
Lasers may be used to vaporize tissue resulting in a reduction of prostatic tissue
comparable to TURP. Interstitial laser therapy induces necrosis of the prostatic
tissue while preserving the urethral mucosa. The theoretical advantage of both is
less blood loss.
As with all medical interventions, particularly surgical interventions, the key
to successful outcomes is patient selection. For instance, TURP has a high probability
of retrograde ejaculation and would be a poor selection in a young man for whom
fertility is an issue. In that patient population a less invasive and less aggressive
approach such as microwave therapy or transurethral incision of the prostate would
be more appropriate. Likewise, in older patients or patients in poor health, a laser-induced
prostatectomy or a prostatic stent might be a better choice. Even after appropriate
measures have been taken to exclude alternative causes of LUTS, the prevailing attitude
of most clinicians and patients is that at least a trial of medical therapy should
be tried. After that, a sober evaluation of the risks and benefits of surgical intervention
should be undertaken.
1.Wilt, T J; Ashani, A; Stark, G; MacDonald, R; Lau, J; Mulrow, C. Saw Palmetto
Extracts for Treatment of Benign Prostatic Hyperplasia: JAMA, Vol. 280 (18):1604-1609,
November 11, 1998.
2.Vann, Ana. The Herbal Medicine Boom: Understanding What Patients are Taking. Cleveland
Clinic Journal of Medicine. Vol. 65(3):129-132, March 1998.
3.Gerber, G S.: Phytotherapy in the Treatment of Benign Prostatic Hyperplasia. Mediguide
to Urology. Vol. 11(2):2-8.
Minimally Invasive Treatment:
Laser: 1.Kabalin, J N; Gilling, P J; Fraundorfer, M R: Application of the Holmium:
YAG Laser for Prostatectomy. J of Clinical Laser Medicine & Surgery; Vol 16(1):21-27,1998.
1. Ramsey, E W; Miller P D; Parsons, K: A Novel Transurethral Microwave Thermal
Ablation System to Treat Benign Prostatic Hyperplasia: Results of a Prospective
Multicenter Clinical Trial. J of Urology, Vol. 158:112-119; July 1997.
2. Larson, T R; Collins, J M; Corica, A: Details Interstitial Temperature Mapping
During Treatment with a Novel Transurethral Microwave Thermoablation System in Patients
with Benign Prostatic Hyperplasia. J of Urology, Vol 159:258-264, January 1998.
3. Larson, T R; Bostwick, D G; Corica, A: Temperature-Correlated Histopathologic
Changes Following Microwave Thermoablation of Obstructive Tissue in Patients with
Benign Prostatic Hyperplasia. Urology, 47(4):463-469, 1996.
EDUCATION AND SUPPORT RESOURCES ON PROSTATE CANCER
1) PROSTATE & CANCER: A FAMILY GUIDE TO DIAGNOSIS, TREATMENT & SURVIVAL
Authors: Sheldon Marks, M.D. Publisher: Fisher Books. Revised 1999.
2) THE ABCs OF PROSTATE CANCER
Authors: Joseph E. Oesterling, M.D., Urologist-in-Chief, University of Michigan
and Mark A. Moyad, M.P.H., Public-health educator, University of Michigan. Publisher:
Madison Books, 1997. 365 pages.
3) THE PROSTATE: A GUIDE FOR MEN AND THE WOMEN WHO LOVE THEM.
Authors: Patrick C. Walsh, M.D., Urologist-in-Chief, The Johns Hopkins Hospital
and Janet Farrar Worthington, Science Writer. Publisher: The Johns Hopkins
University Press, 1995. 322 pages.
1) PROSTATE CANCER TREATMENT GUIDELINES FOR PATIENTS: The National Comprehensive
Cancer Network and the American Cancer Society have published guidelines for the
treatment of prostate cancer. These guidelines are available at
American Cancer Society's.
You may also contact the NCCN toll free number (1-888-909-6226) to request a copy.
2) US TOO International, Inc. support group
3) National Institutes of Health, National Cancer Institute web site at