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.

Food sources

1. Prostatitis is inflammation of the prostate gland. There are three types of prostatitis:
   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).
2. 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.
3. 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 that the proper treatment may be initiated.

Diagnosis
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 re ctal exam. This fluid is examined for white blood cells and bacteria, sometimes a culture is done.

Treatment
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 improved 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 historic evidence of BPH. 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 were estimated to 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.

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.

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 BPH.

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.

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.

Treatment
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 with BPH.

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.

1. Thermotherapy: 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.

 

Mechanical Therapies

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 symptoms 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.

 

Laser Technology

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.

 

Conclusion

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.

 

Bibliography

BPH Phytotherapy

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.

 

Thermal Therapy

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

BOOKS

1) PROSTATE & CANCER: A FAMILY GUIDE TO DIAGNOSIS, TREATMENT & SURVIVAL
Authors: Sheldon Marks, M.D. Publisher: Fisher Books. Revised 1999. www.fisherbooks.com

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.

 

INTERNET

1) Urology Clinics of North Texas Web site at www.urologyclinics.com

2) 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 www.ustoo.com

3) National Institutes of Health, National Cancer Institute Web site at www.cancer.gov.

 

FOUNDATIONS SUPPORTING PROSTATE CANCER RESEARCH

1. American Foundation for Urologic Disease www.afud.org
2. Foundation for Urology Research and Education, Pat Fulgham, M.D., Director, 214-345-5030
3. CaP Cure, Michael Milken, Director, www.capcure.org

 

PROSTATE 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 meet monthly.

Dallas area support groups:

Presbyterian Hospital of Dallas: 214-345-5030
2nd Tuesday of the month, 7:00 p.m. in Haggar Hall in the Fogelson Forum Building

Baylor University Medical Center, Dallas: 214.820.2608

To find out more about this organization, go to the US TOO Web site.

 

VIDEOS
(Available for check-out through Urology Clinics of North Texas)

1. Prostate Cancer: Treatment Options. Dr. Pat Fulgham, Urology Clinics of North Texas Run time 27 minutes
2. Presbyterian’s Comprehensive Cancer Center . Dr. Pat Fulgham received the 2000 Communicator Award for this video which provides general information regarding prostate cancer and the treatment facilities available at Presbyterian Hospital of Dallas. Run time: 15 minutes.

 

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