Year : 2002 | Volume
: 19 | Issue : 1 | Page : 9--15
Chronic prostatitis: Journey from a wastebasket diagnosis to a true clinical entity
Aneesh Srivastava, Nand Kishore Arvind
Department of Urology and Renal Transplantation, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India
Department of Urology and Renal Transplantation. SGPGIMS, Lucknow - 226 014
|How to cite this article:|
Srivastava A, Arvind NK. Chronic prostatitis: Journey from a wastebasket diagnosis to a true clinical entity.Indian J Urol 2002;19:9-15
|How to cite this URL:|
Srivastava A, Arvind NK. Chronic prostatitis: Journey from a wastebasket diagnosis to a true clinical entity. Indian J Urol [serial online] 2002 [cited 2022 May 18 ];19:9-15
Available from: https://www.indianjurol.com/text.asp?2002/19/1/9/21074
The clinical picture of chronic prostatitis has been obscure and understanding of the disease has been poor in part because of limited physical access to -land, uncertain etiology, lack of distinguishing clinical features, nonuniform diagnostic criteria and protracted treatment course.  Contrary to popular belief, epidemiological research during the last decade has indicated prostatitis to be one of the major medical healthcare problems in urology with significant impact on patient and society. Currently advances in basic research are changing the clinical concept of prostatitis, which had been stagnant for last three decades. With appreciation of the myths of this disease, increased understanding of the epidemiology of the syndrome and its ramification on health and resources, and new research initiatives in etiopathogenesis, diagnosis and treatment, prostatitis has become a true clinical entity from its relegation to wastebasket diagnosis.  With ongoing research, urologists and patients diagnosed with prostatitis can hope that this exciting evolution will improve the dismal record for the disease. This article is an attempt to highlight various developments in this field in the last decade and their impact on diagnosis and treatment.
Chronic prostatitis is a common, resource draining, and a very debilitating disease. Various epidemiological studies have revealed it to be a cause for more office visits than BPH or Carcinoma Prostate.  The diagnosis of prostatitis has been responsible for up to 25% of all genitourinary complaint-related office visits.  It is the most common urological diagnosis in men less than 50 years of age and the third most common urological diagnosis in men above the age of 50 years.  A recent state- wide survey in Wisconsin estimated its incidence at 6% and population-based studies in Olmsted county, Minnesota discovered a prevalence rate of over 8%. , The diagnosis is associated with chronic pain, psychological alteration. particularly depression and major sexual disturbances. , It has been clearly demonstrated that patients diagnosed with chronic prostatitis have quality of life impact similar to patients suffering from MI, Angina or Crohn's disease. 
Definition and Classification
Traditionally, prostatitis has been classified into four clinical entities: Acute bacterial prostatitis (ABP) and prostatic abscess as its sequel, Chronic bacterial prostatitis (CBP). Non-bacterial prostatitis (NBP) and Prostatodynia.  Where- as acute prostatitis is an almost established entity, the other three categories are relatively poorly understood and are put together as chronic prostatitis.
This classification system does not address adequately several important problems concerning diagnostic workup of chronic prostatitis. Nickel has highlighted the major problems associated with this classification, and stressed the need to evolve a better system of classification.  In CBP, the role of Enterococci, coagulase negative Staphylococci, Chlamydia and anerobes is not clear, though they have been isolated from prostatic secretion in men with CBP. Further role of bacteria and micro-organisms in recurrent culture prove to be negative for bacterial prostatitis after initial successful treatment is not defined. The broad group of NBP includes men with prostatitis which could result from a variety of different postulated etiologies: autoimmune, immunological or secondary to non-uropathogenic or cryptic micro-organism. The entity Prostatodynia has been criticized because it does not appear to have any relationship to prostate and is being described predominantly as a neuromuscular disorder of pelvic floor/perineal neuromuscular unit. Asymptomatic inflammation of prostate noted histologically in BPH specimen, prostatic biopsy, or detected in expressed prostatic secretions (EPS) during evaluation for other disorders have not been addressed in this classification.
Therefore, in order to acquire a better definition and understanding of prostatitis syndrome, a new classification system has recently been proposed by a meeting of the National Institute of Diabetic Digestive Kidney Diseases, which focuses on the clinical and diagnostic problems concerning chronic prostatitis and has become the reference standard for research studies on these diseases and disorders.  [Table 1]
This new classification system for chronic prostatitis describes three main categories (II, III and IV), which at first glance looks similar to the older traditional system but acknowledges the lack of an etiologic basis of the former while remaining flexible enough for use in scientific studies and clinical practice. According to this system, most patients fall in the chronic pelvic pain syndrome,which is further subdivided into inflammatory or non-inflammatory groups. This latter differentiation has not yet been validated but is useful for developing treatment strategies. The NIH sponsored First International Prostatitis Collaborative Network Workshop in November 1998 reviewed the first 3 years experience with this classification system, both in clinical practice and research studies, and reaffirmed its usefulness. 
The pathogenesis of various forms of chronic prostatitis syndrome may be associated with infection and prostatic inflammation, clinically observed as the presence of bacteria and leukocytes in prostate specific secretion, that is EPS, post prostatic massage urine (Post-M), or traditional VB 3 urine sample after prostatic massage or in ejaculate. Chronic prostatitis can also exist in absence of evidence of infection or inflammation of prostate. Several mechanisms seem to be involved in the etiology and pathogenesis of different forms of chronic prostatitis like dysfunctional high-pressure voiding, chemical, neuromuscular, auto-immune and intraprostatic ductal reflux. ,,,,
Micro-organism based Etiology: Bacteria have been demonstrated in prostatic secretions (EPS, VB3 /Post-M, and ejaculate) in higher concentration than in the initial stream urine (VB 1 ) and midstream urine (VB 2 or pre-massage urine (Pre-M). They can also be demonstrated in prostatic biopsy specimen and by molecular biologic testing. The actual relevance of bacteria within prostate has never been demonstrated. The variable response to any microbial therapy even in prostatitis, with acknowledged uropathogens such as Escherichia coli, makes one suspect that bacteria might not be primary etiologic factor.
Currently, it is important to differentiate whether prostatic inflammation is associated with uropathogenic bacteria. The problem lies in the fact that other bacteria or micro-organisms can also be associated with prostatic inflammation, the exact relevance of which is unknown. Nickel et al have grouped organisms found as the acknowledged prostate pathogens gram negative uropathogens (i.e., Enterobacteriaceae such as E.coli, Kleibsiella spp., pseudomonas spp.), probable prostate pathogens gram positive (Enterococci and Staphylococcus aureus), possible prostate pathogens (coagulase negative Staphylococcus Chlamydia, Ureaplasma, Anaerobes. Candida and Trichomonas), acknowledged (?) prostate nonpathogenes (Diphtheroids, Lactobacilli, Corynebacterium spp.) and cryptic nonculturable organism ("biofilm bacteria", viruses, cell wall deficient bacteria). 
Most individuals with chronic prostatitis present with vague symptoms and it is difficult to differentiate various categories on the basis of symptomatology alone, regardless of whether the bacteria is localized to prostate or whether inflammatory cells are present in the prostate specific fluid specimens (EPS and urine). Although episodic and fluctuating, the symptoms are usually present for a long period of time (by definition, at least 3 months) and consist of genitourinary pain and variable irritative and obstructive voiding symptoms.
Traditional Meares-Stamey four-glass test has been in use for decades, and all urologists are familiar with it. Yet surveys have shown that very few employ it consistently in evaluation of prostatitis. , The test is considered cumbersome, expensive, and not predictive of symptomatic treatment response with high false positive and false negative rates.
Recently, Nickel has proposed a modification of bacterial localization of prostate in which pre- and post-prostatic massage urine samples are compared instead of four-glass test.  With limited comparison of the two tests, it has the same predictive value and false negative rates as MearesStamey test, with a higher false positive rates. Authors have recommended VB, to rule out urethritis in doubtful cases. Nevertheless, until proven otherwise, MearesStamey four-glass tests remains a gold standard by which all other techniques must be measured.
The four-glass urine test is based on sequential quantitative bacteriological cultures of urethral (VB 1 ), bladder urine (VB 2 ) and prostatic secretion both in EPS and urine after prostatic massage (VB 3 ). The diagnosis is confirmed when quantifiable pathogenic bacteria can be clearly ascribed to the prostate gland. The growth of only small numbers of bacteria of prostatic fluid is pathognomonic in CBP. There exists no absolute count in cfu/ml to diagnose CBP; instead, the counts of bacteria in above-mentioned specimens must be compared. Demonstration of bacteria in EPS or VB 3 , when the urethra and midstream urine specimen show no growth, is highly suggestive of CBP. Alternatively a significant increase of a log or more in the bacterial count in the prostatic specimen when compared to the urethral and bladder specimen is considered diagnostic.
Inflammatory Chronic Pelvic Pain Syndrome (CPPS) and CBP are differentiated from noninflammatory CPPS on the basis of demonstration of lipid-laden macrophages and leukocytes in prostatic secretion in former. Controversies exist on the criterion number of white blood cells indicative of inflammation. The cut-off point for inflammatory disease has been suggested at greater or equal to 10 and 15 white blood cells per high power field, respectively.  When insufficient or no EPS is obtained for analysis, the presence of greater than 10 leukocytes/high power field in urine after prostatic massage has been proposed to be indicative of inflammation. , Staining procedures simplify identification and quantification of leukocytes. Recent data indicate an increased sensitivity to detect inflammation when using a counting chamber. 
Alexander et al has shown pro-inflammatory cytokines TNFα and IL-β to be present in semen in men with CP/ CPPS but not in that of normal men.  Nadler et al in limited study found IL-1 and TNF-alpha to be elevated in prostatic secretion of men with chronic prostatitis.  More trials are needed to establish role of these proinflammatory markers as diagnostic and therapeutic markers.
The Role of Other Modalities
The evaluation of the bladder emptying process is accepted to be a mandatory diagnostic step in patients with prostatitis-like symptoms. However, discrepancies exist about the prevalence of urodynamic abnormalities in these patients. Where Gissen prostatitis study group found urodynamic changes in approximately 33-45% of patients following the analysis of urinary flow pattern, other authors demonstrated a significant bladder outlet obstruction in only a few patients as assessed by a complete urodynamic evaluation. In our study in 1998, we found urodynamic evaluation an important adjunct in treating patients of CP/CPPS having persistent symptoms. 
TRUS has proven the best sonographic approach to visualize the prostate gland in case of acute or chronic inflammation.  A number of sonographic abnormalities have been used to identify patients with chronic prostatitis in contrast to normal controls.  Some authors tried to compare sonographic abnormalities to histological findings obtained by biopsy.  However, most of these studies have been performed with old 3.5-4 MHz scanners, which cannot match the images of today's high-resolution transducers. The Gissen prostatitis study group demonstrated a significantly higher prevalence of prostatic calculi, particularly diffuse calcifications, in patients with inflammatory vs. non inflammatory CPPS.  These results gain importance, because infected prostatic stones, similar to kidney stones, may be impregnated with pathogens that are shielded from antibacterial agents and thereby lead to recurrent prostatitis as well as relapsing urinary tract infection. Ludwig et al have described echo-poor periurethral zones, heterogeneous internal echo pattern, irregularity of the prostatic capsules and the periprostatic venous plexus as other TRUS signs that indicate prostatic inflammation. 
As there are multidimensional associations in patients with prostatitis to physical and mental health status, a comprehensive symptomatic evaluation appears necessary using appropriate questionnaires with the aim of providing the possibility to ask for typical true prostatitis symptoms and to quantify symptoms severity. First experience with different scoring system is available, these include the University of Washington Symptom Score, the Prostatitis Symptoms Severity Index, and the Gissen Prostatitis Symptoms Score.  These symptoms scores are useful to determine, the severity of disease, its progression over time and for evaluation of the results of various therapies. NIH-sponsored Chronic Prostatitis Clinical Research Network following a structured literature review, extensive focus group (patient and experts) evaluation followed by cognitive and validation studies, has developed a specific NIH-Chronic Prostatitis Symptoms Index (NIH-CPS I).  This new index of 9 questions addresses the 3 most important domains of chronic prostatitis: pain (location, severity and frequency), voiding (irritative and obstructive symptoms) and, impact on the quality of life.
Chronic prostatitis has a severe impact on the quality of life of patients. The single question from the AUA-BPH symptoms index "If you were to spend rest of your life with your (genitourinary) condition just the way it is now, how would you feel about that?" allows patients to describe how distressed or happy they are with their symptoms by rating the answers from "terrible" to "delighted".  The question has been validated for chronic prostatitis as a part of the process in developing the NIH-CPSI and is useful in recording and quantification of quality of life aspects of disease.
Anti-microbial therapy remains the mainstay for treatment of acute bacterial prostatitis, but, its role in chronic prostatitis remains under scrutiny. Trimethoprim-sulfamethoxazole or trimethoprim alone were the agents of choice for many years for patients with chronic prostatitis in whom the cause was (or was thought to be) bacterial uropathogens. Recent clinical trials and long-term results (cure rates between 15% and 60%) do not support its earlier effectivity as seen in animal pharmacological studies. ,
The results of quinolone therapy including norfloxacin, ciprofloxacin, and ofloxacin seem to be better and the eradication (of bacteria) rate impressive; however, the long-term results in regards to recurrence and symptoms eradication are unknown. ,, Limited data exists in regards to empiric antibiotic therapy for possible infections by chlamydia, ureaplasma, yeast, and other cryptic noncultured organisms.
Analgesics are used empirically for most categories of prostatitis, but there is scant evidence of their long-term efficacy. Anecdotal experience suggests that adding tricyclic antidepressants is helpful in controlling the symptoms associated with prostatitis syndromes.
Nonsteroidal anti-inflammatory drugs such as nimusulide and indomethacin may be lead to favorable results in some patients with non-specific inflammation but longterm results are still awaited.  Muscle relaxants such as diazepam and baclofen are helpful in patients with category IIIb chronic pelvic pain syndrome, especially if sphincter dysnergia or pelvic floor/perineal muscle spasm is confirmed as shown by Osborn et al in 1981 although they have not been subjected to clinical scrutiny in terms of prospective clinical trials. 
Small poorly controlled studies with alpha blockers such as phenoxybenzamine, alfuzosin and terrazosin suggest that clinical improvement is seen in 48% to 80% of patients especially those in categories III CPPS having dysfunctional voiding. , Barbalias et al in 1998 in prospective study on 134 patients of chronic prostatitis in which terrazosin or alfuzocin was used in combination with antibiotics, found that recurrence of bacterial prostatitis was significantly reduced while in abacterial prostatitis there was a lower rate of symptoms recurrence. 
5-Alpha-Reductase inhibitors are postulated to promote the regression of ductal and glandular tissue in the prostate, improve flow parameters, reduce intraprostatic reflux, and perhaps even influence inflammation.  Finesteride has been found to favorably influence inflammation, voiding, and pain associated with category Illa chronic pelvic pain syndrome in double blind placebo-controlled small pilot studies conducted by Perrson, Holm and Galio et al. ,,
Favorable results have been reported with transrectal hyperthermia and transurethral thermotherapy in patients with chronic prostatitis, but the problem lies in identifying these select groups of patients who will benefit maximally from this invasive treatment. , Heat therapy accelerates the natural healing process and tends to have effect of intraprostatic sympathectomy by destroying the nerve fibers of prostate.
Repetitive prostatic massage helps in draining occluded prostatic ducts, improving circulation, and antibiotic penetration has recently regained its old popularity because of limitation of standard medical therapy in patients of chronic prostatitis. 
The role of surgery in patients of chronic prostatitis is limited to certain specific conditions. Transurethral incision of bladder neck is effective in patients with urodynamically proven bladder neck obstruction.  Radical transurethral resection of prostate and even radical prostatectomy (especially with infected calculi) have been advocated by some, but there is no significant experience employing this type of invasive therapy in chronic prostatitis. 
A recent addition in treatment of men with CP/CPPS is phytotherapy, but there are few well-designed clinical trials in support of extravagant claim of efficacy.  In chronic prostatitis, the only placebo-controlled, double blind trial has been for the bioflavanoid quercetin. In trial, patients taking placebo had mean improvement in NIH symptoms score from 20.2 to 18.8, while those taking the bioflavonoid had mean improvement from 21.0 to 13.1 (p=.003). 20% of patients taking placebo and 67% of patients taking the bioflavonoids had an improvement of symptoms of at least 25%.
Supportive therapy, including biofeedback, relaxation exercise, massage therapy, chiropractic therapy, meditation and lifestyle changes (like discontinuing bike riding, diet changes etc) are some of the ways to ameliorate patients' symptoms and cope with this disease.
Long-term, full dose antibiotic therapy is the treatment of choice in this category. The best antibiotics are one of the fluoroquinolones. The optimum duration of therapy should be 12 weeks and if the symptoms do not respond. repetitive prostatic massage in conjunction with antibiotics should be used. If the symptoms remain unabated during antibiotic therapy, a suppressive dose of antibiotics needs to be continued for a long period of time. Prophylactic low-dose antibiotic is needed in those having recurrence. Surgery is always the last resort and is indicated in etiological precipitating factors such as bladder neck problems and stricture urethra, documented repetitive prostatic infection with prostatic calculi or when standard antimicrobial therapy has failed.
Category III A
These groups of patients should be initially treated with a course of antibiotics for 6 weeks, which should be continued for another period of 6 weeks if there is a favorable response. The same antibiotics as used in category II are used in addition to coverage for chlamydia and ureaplasma. If patients fail to respond, alpha blockade (for patients with obstructive voiding symptoms), anti-inflammatory agents and repetitive prostatic massage are used as second line therapy. Finesteride, phytotherapy, pentosanpolysulfate, and lifestyle changes may also benefit these patients.
Transurethral microwave therapy may be offered as last resort to patients, if they are willing to accept the potential morbidity of the procedure and the fact that it may not lead to symptoms alleviation.
Category III B
These groups of patients must be subjected to one course of antibiotic (4 weeks) before attempting another form of therapy. When there is no response to standard antibacterial therapy, triple therapy consisting of high dosages of alpha-blockers, analgesics, and muscle relaxants (i.e.. diazepam) should be started and during this period patients should take rest for a period of 2 weeks. If the symptoms respond favorably to this therapy, narcotics are changed to NSAID, diazepam is tapered and discontinued, and the alpha-blockers are continued for 3 months. Supportive therapy in form of biofeedback, relaxation exercises, psychotherapy, and lifestyle changes (e.g., diet, discontinuing bike ride, sitting on soft cushions) are useful in patients not responding to triple therapy. The aim of treatment should be alleviation of patients' symptoms and improvement of quality of life and not cure.
Most of these patients with asymptomatic inflammation of prostate do not need any therapy. The indications are, documented prostatic inflammation in men with BPH or carcinoma prostate before being subjected to endoscopic therapy or surgery, patients with prostatic infection on biopsy undergoing repeat prostatic biopsy and inflammation noted in ejaculate specimen in infertile but otherwise asymptomatic men. All these patients should be given a course of antibiotics.
The prostatitis syndrome is of great significance for urologists as has been demonstrated in recent studies dealing with epidemiological data. A new classification has been suggested which appears promising. A detailed standardized diagnostic procedure remains mandatory to differentiate the various forms of prostatitis. Though new insights into pathogenic factors have been achieved, the genesis of chronic prostatitis still remains uncertain. Treatment options must be considered according to the diagnostic results; however, they are often limited and aimed at improving symptoms. It is hoped that evolution in new management strategies of prostatitis, will eventually benefit majority of patients.
|1||Thin RN. The diagnosis of prostatitis: a review. Genitourin Med 1991:67:279.|
|2||Nickel JC. Prostatitis : Myth and realities. Urol 1998: 51: 326.|
|3||National Kidney and Urological Disease Advisory Board. Long range plan window on the 21" century. Bethesda, Maryland, United States Department of Health and Human Services, NIH Publication 1990: No 90-583, p. 20.|
|4||National Centre for Health Statistics. Advance data from vital and health statistics. Vital Health Stat 1993: 16(7) No. 61-70.|
|5||Collins MM, Stafford RS, O'Leary P and Barry MJ. How common is prostatitis ? A national survey of physicians' visits. J Urol 1997; 157: 243A.|
|6||Moon TD. Diagnostic and treatment practices for prostatitis by urologist and primary care physician visits. J Urol 1997; 157: 242A.|
|7||Roberts RO, Jacobsen SJ, Rhodes T et al. A community-based study on the prevalence of prostatitis. J Urol 1997: 157: 242A.|
|8||Krieger JN, Egman KJ, Ross SO et al. Chronic pelvic pain represents the most prominent urogenital symptom of 'chronic prostatitis'. Urol 1996; 48: 715.|
|9||De la Rosetle, Ruijork MC, Jeukan JM et al. Personality variables involved in chronic prostatitis. Urol 1993; 42: 654.|
|10||Wesimenger K, Heiman JR, Rothman f et al. Sickness impact on chronic non-bacterial prostatitis and its correlate. J Urol 1996; 155: 965.|
|11||Drach GW, Fair WR, Meares EM et al. Classification of benign disease associated with prostatic pain, prostatitis or prostatodynia. J Urol 1978: 120: 266.|
|12||Nickel JC. Prostatitis : Evolving management strategies. Urol Clin North Am 1999; 26: 737.|
|13||Executive summary : NIH Workshop on chronic prostatitis. Bethesda, Maryland, 1995.|
|14||National Institute of Health Summary statement, Presented at the first NIH Institutional Prostatitis collaborative network workshop on prostatitis. Bethesda, Maryland, Nov 1998.|
|15||Blacklock NJ. Urodynamic and psychometric observation and their implication in the management of prostatodynia. In Wiedner M, Brumer H (eds.). Therapy of prostatitis. Munich, Zuckerwerdt Urologie 1986: p. 26.|
|16||Person BE, Ronquist G, Ekbloom M. Amelioration effects of allopurinal on nonbacterial prostatitis : A parallel double blind study. J Urol 1996; 155: 961.|
|17||Anderson JT. Treatment of prostatodynia. In Nickel JC (ed). Textbook of Prostatitis. London 1998; 1813.|
|18||Alexander RB, Brady F, Ponniah S. Autoimmune prostatitis : Evidence of T cell reactivity with normal prostatic proteins in men with history of prostatitis. J Urol 1997; 157S: 934.|
|19||Kirby RS, Lowe D, Bultitude MI et al. Intraprostatic urinary reflux : An etiological factor in bacterial prostatitis. Brit J Urol 1982; 121: 729.|
|20||Nickel JC. Prostatitis. In Mulholland SG (ed.). Antibiotic therapy in urology. Philadelphia, Lippen Cott Raven 1995; 57.|
|21||Meares EM, Stamey TA. Bacteriologic localization patterns in bacterial prostatitis and urethritis. Invest Urol 1968; 5: 492.|
|22||Moon TD. Questionnarire survey of urologist and primary care physicians, diagnostic and treatment practices for prostatitis. Urol 1997; 50: 543.|
|23||Nickel JC. The Pre and Post massage test (PPMT) : A simple screen for prostatitis. Tech Urol 1997; 3: 38.|
|24||Weidner W, Ludwig M. Patient assessment in chronic prostatitis. Curr Opin Urol 1998: 5:51.|
|25||Kreiger JN, Roberta JR, Sussan RO. Does the chronic prostatitis/ pelvic pain syndrome differ from nonbacterial prostatitis and prostatodynia ? J Urol 2000; 164: 1554.|
|26||Weidner W. Prostatitis - diagnostic criteria, classification of patients and recommendation for therapeutic trials. Infect 1992; 20S: 5227.|
|27||Muller H, Mohr L, Berger RE et al. Evaluation of microscopic methods for detection of inflamed expressed prostatic secretions. J Urol 1997; 157 supp: 943.|
|28||Alexander RB, Ponniah S, Hasday J et al. Elevation of proinflammatory cytokines in semen of patients with chronic prostatitis/ chronic pelvic pain syndrome. Urol 1998; 52: 744.|
|29||Nadler RB, Koch AE, Calhoun M et al. IL-1 beta and TNF-alpha in prostate secretions are indicators in evaluation of men with chronic prostatitis. J Urol 2000; 164: 2114.|
|30||Srivastava A, Rao TV, Rao HSGT et al. Non-bacterial prostatitis/ prostatodynia - A urodynamic spectrum. IJ Urol 1998; 15: 272.|
|31||Clements R. Griffith GI, Peeling WB et al. Ultrasonographic features of prostatitis. In Weidner W, Madsen PD, Schaefer HG (eds.). Prostatitis, Berlin. Springer, 1994; p.66.|
|32||Ludwig M, Weidner W, Schroeder-Printen I et al. Transrectal Prostatic sonography as useful diagnostic means in patients with chronic prostatitis/prostatodynia. Brit J Urol 1994; 73: 664.|
|33||Double A, Thomas BJ, Walker MM et al. The role of Chlamydia trichomatis in chronic abacterial prostatitis : A study using US guided Biopsy. J Urol 1991; 141: 332.|
|34||Ludwig M, Weidner W. Prostatitis and Urethritis. Eur Urol 1999; 35: Currie Urol 2:1.|
|35||Letwin MS, McNaughton-Collins M, Fowler FJ et al. The NIH chronic prostatitis symptom index development and validation of new outcome measures. J Urol 1999: 162: 369.|
|36||Barry MJ, Fowler FJ. O'Leavy MP et al : The AUA symptom index for BPH: The Measurement Committee of the American Urological Association. J Urol 1992; 148: 1549.|
|37||Meares EM. Long-term therapy of chronic bacterial prostatitis with trimethoprim-sulphamethoxazole. Can Med Assoc J 1975; 112: 22 Spec.|
|38||Nickel JC. The role of the animal model in study of prostatitis. In Bergen (ed.): UTI. Karger Basel, 1997, p. 89.|
|39||Schaeffer AL Darras FS. The efficacy of norfloxacin in the treatment of chronic bacterial prostatitis refractory to trimethoprimsulphamethoxazole and/or carbencillin. J Urol 1999; 144: 690.|
|40||Childs SJ. Ciprofloxacin in treatment of chronic bacterial prostatitis. Urol 1990; 35: 5.|
|41||Remy G, Rouger C, Clavant P et al. Use of ofloxacin for prostatitis. Rev Infect Dis 1988 Suppl; 10: 173.|
|42||Canall D, Turche P, Giroge PM et al. Treatment of a bacterial prostato-vasculitis with nimuleside. Drugs 1993; 46: 147.|
|43||Osborn DE, George NJR, Rao PN. Prostatodynia - physiological characteristics and rational management with muscle relaxants. Brit J Urol 1981; 156: 1668.|
|44||De la Rosset JS, Kirthous HF, van Karrebrock PF et al. Research in `prostatitis syndromes'. The use of alphazucin (a new alpha-1 receptor-blocking agent) in patients mainly presenting with micturation complaints of an irritative nature and confirmed urodynamic abnormalities. Eur Urol 1992: 22: 222.|
|45||Neal DEJ, Moon TD. Use of terrazosin in prostatodynia and validation of a symptom score questionnaire. Urol 1994; 43: 460.|
|46||Barbalias GA, Nekifordis G, Liatsikos EN. Alpha blockers for the treatment of chronic prostatitis in combination with antibiotics. J Urol 1998; 159-883.|
|47||Nickel JC. 5-Alpha reductase inhibitor therapy for chronic bacterial prostatitis. In Nickel JC (ed.). Textbook of Prostatitis. London ISIS, 1999.|
|48||Galio G. The use of finesteride in the treatment of chronic bacterial prostatitis. Abstract of the 49 th Annual Meeting of Northeastern section of American Urological Association, Phoenix, AZ, 1997 p.128.|
|49||Holm M, Mehoff HH. Chronic prostatitis pain : A new treatment with finesteride? Scand J Urol Nephrol 1996; 31: 213.|
|50||Oleavi L, Make L, Imo M. Effects of finesteride in patients with chronic idiopathic prostatitis : A double-blind, placebo-controlled pilot study. Eur Urol 1981; 156: 1668.|
|51||Kumaon H, Ono N et al. Transrectal hyperthermia for treatment of chronic bacterial prostatitis. Nippen Henyokiva Gazkai Zeoshi 1993; 84: 265.|
|52||Nickel JC, Sorensen R. TUMT for non-bacterial prostatitis : A randomized double-blind sham-controlled study using new prostate specific questionnaire. J Urol 1996; 155: 1950.|
|53||Hinnefent Br. Feliciano AE Jr. Changes in white blood count in men undergoing thrice-weekly prostatic massage, microbial diagnosis and antimicrobial therapy for genitourinary complaints. Brit J Urol 1998: 81: 370.|
|54||Kaplsn SA, Te AE, Jacobs BJ et al. Urodynamic evidence of vesical neck obstruction with misdiagnosed chronic nonbacterial prostatitis and the therapeutic role of endoscopic incision of the bladder and neck. J Urol 1997: 155: 2063.|
|55||Sant GR, Heaney JA, Meares EM et al. "Radical" transurethral Prostatic resection in the management of chronic bacterial prostatitis. American Urological Association, J Urol 1984: 131: 690.|
|56||Shoskes DA, Zeitlin SI. Saheed A et al. Quercetin in men with category Ill chronic prostatitis : A preliminary prospective doubleblind placebo-controlled trial. Urol 1999; 54: 960.|