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Chronic pelvic pain syndrome; common and poorly understood; fresh approach needed [BMJ 1999]

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Jun 4, 2017, 9:37:04 PM6/4/17
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Chronic pelvic pain syndrome
Is common and poorly understood—a fresh approach is needed 
Graz Luzzi, Consultant physician and Michael O’Leary, Assistant professor in urological surgery

Additional article information

A syndrome in men, characterised by chronic perineal and penile pain with varying degrees of urinary and sexual dysfunction, is generally recognised without difficulty by clinicians and often labelled chronic prostatitis.1 As the cause of the most prevalent, non-bacterial, forms of the condition remains unknown, and therefore no definitive diagnostic test exists, the diagnosis has relied on a combination of clinical features, exclusion of other diagnoses (such as bladder outlet obstruction), and the results of investigations, especially the four glass (Stamey) test.2 However, there is no generally agreed clinical definition that brings together the symptomatic features and investigative findings, so it is difficult to make reliable comparisons among the many descriptive and therapeutic studies in 30 years of medical literature—or to draw many conclusions.

None the less, the condition is probably highly prevalent. Urologists and primary care physicians diagnose chronic prostatitis regularly, in adult men of all ages.3 Accurate data on incidence and prevalence are not available, but statistics for the United States indicate that there were more physician visits for prostatitis than for benign prostatic hyperplasia or prostate cancer in 1985. The distribution of pain, its severity, and associated symptoms, such as voiding dysfunction, are highly variable; the impact of the disease in patients with the severest symptoms may match that of serious chronic conditions such as ischaemic heart disease.4 Although patients may be symptomatic for years, there are few complications, although in a subgroup genital tract inflammation may be associated with subfertility.5

The National Institutes of Health has taken the initiative in developing a large scale strategic approach to research into prostatitis. Following a workshop in 1995 new diagnostic criteria and a revised classification were proposed (see box). While not substantially different from the existing classification,2 the new one has the advantage of including other evidence for genital tract inflammation in addition to the four glass test, and the new nomenclature (chronic pelvic pain syndrome) is more descriptive and correctly emphasises the central place of pain.6

The aetiology of inflammatory chronic pelvic pain syndrome has proved elusive, and the best studies have not identified an infective cause. In particular, despite recent small series that suggest a role for genital Chlamydia trachomatis, chlamydia has not been shown conclusively to cause chronic prostatic infection.1 Other proposed mechanisms include bladder neck dysfunction with reflux of urine into the prostatic parenchyma, tension myalgia of the pelvic floor, and autoimmunity. Recent work shows that even when prostatic inflammation is not demonstrable by the four glass test (non-inflammatory chronic pelvic pain syndrome), markers of inflammatory activation may be detectable,7 showing that inflammation may be a feature in both forms of chronic pelvic pain syndrome. However, the cause of the inflammatory process remains unknown, and its importance is unclear. No correlation seems to exist between prostatic inflammation and the presence or severity of symptoms, and inflammation is often an incidental histological finding in the prostate. 1 8

The four glass test has several difficulties as a diagnostic method. Central to the test are the microscopy and culture of expressed prostatic secretions obtained by prostatic massage. The presence of leucocytes in the secretions (>10 per high power field (×400 magnification)) is usually taken to signify prostatic inflammation. But secretions are not obtained from many patients, and the alternative of measuring changes in urinary leucocyte and bacterial colony counts before and after prostatic massage is not standardised.

Current classification2 Proposed classification6
Acute bacterial prostatitis Acute bacterial prostatitis
Chronic bacterial prostatitis Chronic bacterial prostatitis
Chronic non-bacterial prostatitis (no demonstrable infection) Chronic pelvic pain syndrome, inflammatory (symptoms; white cells in semen, expressed prostatic secretions, or urine immediately after prostatic massage)
Asymptomatic inflammatory prostatitis (no symptoms; white cells in semen, prostatic secretions, urine immediately after prostatic massage, or prostate tissue)
Prostatodynia (no demonstrable infection) Chronic pelvic pain syndrome, non-inflammatory
In the absence of an agreed definition for chronic prostatitis, the four glass test has not been evaluated against a gold standard, so its sensitivity and specificity (and consequently predictive values) are unknown. The test has not been shown to be of value in managing chronic pelvic pain syndrome, so doing it in men with pelvic pain cannot be regarded as a standard in clinical management. Surveys indicate that urologists perform the investigation infrequently, and some authors have concluded that the test should be confined to research studies.9

What advice can be drawn from the existing literature on treatment? For the few patients with chronic bacterial prostatitis, antibiotic selection should be guided by the sensitivities of the organism cultured from urine or prostatic secretions, and an agent with good prostatic penetration; usually a quinolone such as ciprofloxacin, would be the agent of choice. One month of initial therapy is suggested by existing studies, but up to a third of patients may relapse and need more prolonged courses or suppressive antibiotic treatment.10

The treatment of the non-infective syndrome is more problematic. Although the condition is so common, there are no published large scale randomised treatment trials. The trials that have been published are difficult to compare because of differences in study populations, treatment regimens, and duration of follow up. Small controlled trials and observational studies have suggested a place for selected antibiotics (which may act by non-antimicrobial mechanisms such as anti-inflammatory effects) including doxycycline, erythromycin, and ofloxacin; α blockers such as terazosin; transurethral microwave thermotherapy; and allopurinol.11,12 However, no highly effective therapy has been identified and well designed randomised trials are urgently needed. These should also evaluate new approaches to pain management, including behavioural interventions and use of low dose tricyclic antidepressants.

The National Institutes of Health’s interest and funding in this area of relative clinical ignorance is welcome. The multicentre collaboration in the US will promote a standardised clinical definition, define the epidemiology, validate symptom scoring indices for clinical monitoring, guide research into the aetiology, and conduct high quality trials. Patients with this frustrating and neglected condition should see the benefits over the coming years.

Article information
BMJ. 1999 May 8; 318(7193): 1227–1228.
PMCID: PMC1115628
Graz Luzzi, Consultant physician
(ku.oc.nomed.ugcyw@gzul)
Department of Genitourinary Medicine, Wycombe Hospital, High Wycombe, HP11 2TT
Michael O’Leary, Assistant professor in urological surgery
Harvard Medical School, Cambridge, MA 02115
Copyright © 1999, British Medical Journal
This article has been cited by other articles in PMC.
Articles from The BMJ are provided here courtesy of BMJ Publishing Group
References
1. Roberts RO, Lieber MM, Bostwick DG, Jacobsen SJ. A review of clinical and pathological prostatitis syndromes. Urology. 1997;49:809–821. [PubMed]
2. Drach GW, Meares EM, Fair WR, Stamey TA. Classification of benign diseases associated with prostatic pain: prostatitis or prostatodynia? J Urol. 1978;120:266. [PubMed]
3. McNaughton Collins M, Stafford RS, O’Leary MP, Barry MJ. How common is prostatitis? A national survey of physician visits. J Urol. 1998;159:1224–1228. [PubMed]
4. Wenninger K, Heiman JR, Rothman I, Berghuis JP, Berger RE. Sickness impact of chronic nonbacterial prostatitis and its correlates. J Urol. 1996;155:965–968. [PubMed]
5. Wolff H. The biologic significance of white blood cells in semen. Fertil Steril. 1995;63:1143–1157. [PubMed]
6. Executive summary: chronic postatitis workshop, December 1995. Bethesda, MD: National Institutes of Health-National Institute of Diabetes and Digestive and Kidney Diseases; 1995. www.niddk.nih.gov./health/urolog/pubs/cpwork/cpwork.htm Appendix 1:1-5. ( www.niddk.nih.gov./health/urolog/pubs/cpwork/cpwork.htm) )
7. Joller-Jemelka HI, John H, Hailemariam S, Barghorn A, Sulser T, Hauri D. Immunopathology in noninflammatory chronic pelvic pain syndrome. J Urol. 1998;159:S271.
8. Zhang W, Sesterhenn IA, Connelly RR, Mooneyhan RM, Moul JW. Inflammatory infiltrate (prostatitis) in whole-mounted radical prostatectomy specimens from black and white patients. J Urol. 1998;159:S273. [PubMed]
9. Berger RE, Krieger JM, Kessler D, Ireton RC, Close C, Holmes KK, et al. Case control study of men with suspected chronic idiopathic prostatitis. J Urol. 1989;141:328–331. [PubMed]
10. Andriole VT. Use of quinolones in treatment of prostatitis and lower urinary tract infections. Eur J Clin Microbiol Infect Dis. 1991;10:342–350. [PubMed]
11. Luzzi G. The prostatitis syndromes. Int J STD AIDS. 1996;7:471–478. [PubMed]
12. Nickel JC, Siemens DR, Lundie MJ. Allopurinol for prostatitis: where is the evidence? Lancet. 1996;347:1711–1712. [PubMed]


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