Whither "chronic prostatitis"?

I t is nearly a decade since the National Institutes of Health (NIH) sponsored international consensus conference on chronic prostatitis led to the development of a productive multicentre collaboration in North America (Chronic Prostatitis Collaborative Research Network) and stimulated research initiatives around the world. A modified classification for prostatitis was proposed, with a new name and clinical definition for the largest category, chronic pelvic pain syndrome (CPPS), to replace chronic non-bacterial prostatitis and prostatodynia. Subsequently, development of a validated Chronic Prostatitis Symptom Index (NIH-CPSI) provided an outcome measure for treatment trials that is now almost universally adopted and allows comparison between studies. Although not intended to be a diagnostic instrument, and therefore requiring caution in its use as a means of detecting the condition, numerous studies using the same instrument have suggested a high population prevalence of CPPS. Significant advances have been made in our understanding of the prevalence and impact of this condition, its natural history, and to some extent, the pathogenesis, although the aetiology remains a mystery and advances in therapy have been disappointing. Nearly 10 years on, the time has come for greater clarity in our diagnostic labelling and a frank acceptance of the limitations of historical diagnostic approaches. The time has come to drop the term ‘‘chronic prostatitis’’ and to avoid misleading and imprecise use of ‘‘prostatitis’’ (box). The NIH classification signalled a conceptual shift in approach, and its four categories (acute bacterial prostatitis, chronic bacterial prostatitis, CPPS, and asymptomatic inflammatory prostatitis) are distinct entities. It now becomes arguable whether these conditions should feature in the same classification. Use of the unvalidated four glass test in diagnosis and classification led to confusion; recent work confirmed that results do not correlate with symptoms, and white cells in expressed prostatic secretions are a regular feature in symptomless controls. 6 This adds to the evidence for lack of clinical value in subclassifying CPPS into inflammatory and non-inflammatory categories. In the light of developments, the current classification should, logically, be dismantled, and a greater focus placed on each of its components. In particular, CPPS (NIH category III) may encompass a heterogeneous group of causes of chronic genital or pelvic pain. Better understanding of the aetiology or aetiologies will be essential for development of reliable diagnostic techniques and effective treatment. In theory, CPPS may be caused by bladder, pelvic floor, prostate, or seminal vesicle pathology. Urodynamic studies suggested a neuromuscular basis for CPPS (pelvic floor or bladder neck dysfunction) that provided the rationale for treatment with a blockers. Current interest is focused on explaining observed elevations in proinflammatory cytokines in the genital tract in men with CPPS, especially infective triggers, autoimmunity, or neurogenic inflammation. Recently, increased perineal pain sensitisation was reported in men with CPPS. CPPS also has the features of a somatoform disorder. Despite the high prevalence of this condition, which is regularly seen by GPs, urologists, and genitourinary physicians, a recent review did not include CPPS in a long list of functional somatic syndromes by specialty (although chronic pelvic pain in women was included). Treatment of the condition remains frustrating. We have a clearer picture of what doesn’t work or should no longer be used, such as very prolonged courses of antibiotics. Otherwise, none of the treatments used is supported by good evidence. This position hasn’t improved much since publication of a systematic review in 2000, except that recent small controlled trials have strengthened the case for a blockers (such as tamsulosin) in severe CPPS. 17 The range of other possible therapies under recent evaluation remains unfocused, and includes anti-inflammatory approaches (cyclooxygenase-2 selective inhibitors; corticosteroids), ‘‘phytotherapy’’ (quercetin), hormonal methods (finasteride; mepartricin), physical therapies (electrostimulation; transurethral needle ablation), complementary therapies (acupuncture), and biofeedback. Controlled studies examining possible psychological factors reported elevated scores for depression, anxiety, and somatisation in men with CPPS. 28 In one study, more intense patterns of psychological distress were demonstrated in approximately 40% of men, many of whom were depressed. This highlighted the need to consider undiagnosed depression and anxiety states in men presenting with severe refractory CPPS, and the importance of evaluating mental health interventions. In this issue of STI (p 147), Lee and colleagues report interesting preliminary findings from their trial of the antidepressant sertraline, a selective serotonin reuptake inhibitor (SSRI), in men with CPPS. Improvement in symptoms was demonstrated for sertraline 50 mg daily taken for 13 weeks. However, it would be premature to recommend use of sertraline in men with CPPS on the basis of the study, because of failure to reach significance in the placebo controlled substudy (possibly owing to small numbers and lack of power) and use of a symptom index that predates the NIH-CPSI. Concerns about possible suicide risk associated with SSRIs might also be a barrier in their use, although the risk seems linked to depression rather than a separate drug effect. SSRIs might influence symptoms in CPPS by treating underlying depression Modernisation of chronic prostatitis