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REVIEW ARTICLE
Year : 2002  |  Volume : 19  |  Issue : 1  |  Page : 9-15
 

Chronic prostatitis: Journey from a wastebasket diagnosis to a true clinical entity


Department of Urology and Renal Transplantation, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

Correspondence Address:
Aneesh Srivastava
Department of Urology and Renal Transplantation. SGPGIMS, Lucknow - 226 014
India
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Source of Support: None, Conflict of Interest: None


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Keywords: Prostatitis; Chronic Prostatitis; Diagnosis


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 2019 Apr 21];19:9-15. Available from: http://www.indianjurol.com/text.asp?2002/19/1/9/21074



   Introduction Top


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. [1] 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. [2] 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.


   Epidemiology Top


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. [3] The diagnosis of pros­tatitis has been responsible for up to 25% of all genitourinary complaint-related office visits. [4] 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. [5] 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%. [6],[7] The diagnosis is associated with chronic pain, psychological alteration. par­ticularly depression and major sexual disturbances. [8],[9] 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. [10]


   Definition and Classification Top


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. [11] 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. [12] 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. [13] [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. [14]


   Etiopathogenesis Top


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. [15],[16],[17],[18],[19]

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 More Details coli, makes one sus­pect that bacteria might not be primary etiologic factor.[20]

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 Scientific Name Search , 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). [12]


   Management Top


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. [21],[22] 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. [23] 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. [24] 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. [25],[26] Staining procedures sim­plify identification and quantification of leukocytes. Re­cent data indicate an increased sensitivity to detect inflammation when using a counting chamber. [27]

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. [28] Nadler et al in lim­ited study found IL-1 and TNF-alpha to be elevated in prostatic secretion of men with chronic prostatitis. [29] More trials are needed to establish role of these proinflammatory markers as diagnostic and therapeutic markers.


   The Role of Other Modalities Top


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. [30]

TRUS has proven the best sonographic approach to visu­alize the prostate gland in case of acute or chronic inflam­mation. [31] A number of sonographic abnormalities have been used to identify patients with chronic prostatitis in contrast to normal controls. [32] Some authors tried to compare sonographic abnormalities to histological findings obtained by biopsy. [33] 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. [34] 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. [34]

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. [34] 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). [35] 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". [36] 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.


   Treatment Top


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. [37],[38]

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. [39],[40],[41] 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. [42] 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. [43]

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. [44],[45] 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. [46]

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. [47] 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. [48],[49],[50]

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. [51],[52] 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. [53]

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. [54] 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. [55]

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. [56] 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.


   Current Recommendations Top


Category II

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.

Category IV

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.


   Conclusion Top


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.

 
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51.Kumaon H, Ono N et al. Transrectal hyperthermia for treatment of chronic bacterial prostatitis. Nippen Henyokiva Gazkai Zeoshi 1993; 84: 265.  Back to cited text no. 51    
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.  Back to cited text no. 52    
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.  Back to cited text no. 53    
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.  Back to cited text no. 54    
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.  Back to cited text no. 55    
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.  Back to cited text no. 56    



 
 
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    Introduction
    Epidemiology
    Definition and C...
    Etiopathogenesis
    Management
    The Role of Othe...
    Treatment
    Current Recommen...
    Conclusion
    References
    Article Tables

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