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Abstract
Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) in the absence of any identifiable pathology such as cancer, curable infection, or anatomic abnormalities is defined as “urologic pain or discomfort in the pelvic region, associated with urinary symptoms and/or sexual dysfunction, lasting for at least 3 of the previous 6 months”. However, etiologic factors of CP/CPPS remain unknown. The traditional marker of inflammation, namely white blood cells in prostatic fluids, dose not correlate with the predominant symptom of pelvic pain. The role of normal bacterial flora in prostate in inciting the inflammatory response has also been reconsidered. Nanobacterial infection might be an important etiologic factor of type III prostatitis. An imbalance toward increased proinflammatory and decreased anti-inflammatory cytokines has been implicated, and its correlation with pelvic pain has also been observed to some extent. Pelvic pain also correlates with the neurotrophin (nerve growth factor) implicated in neurogenic inflammation and central sensitization. Finally, psychological stress may produce measurable biochemical changes and affect other processes. Here, the author reviewed the existing literature on etiology involved in the mechanisms of CP/CPPS.
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Fig. 1.
Interplay of immunological, endocrine, neurological and psychological factors in development of CP/CPPS and proposed mechanisms. CP/CPPS: chronic prostatitis/chronic pelvic pain syndrome, NGF: nerve growth factor, IFN-γ: interferon-γ, IL: interleukin, TNF-α: tumor necrosis factor (adapted from Pontari and Ruggieri. J Urol 2008;179(5 Suppl):S61-7, with permission of Elsevier).6
Table 1.
Cytokines levels in → chronic prostatitis/chronic pelvic pain syndrome type IIIB vs. asymptomatic controls
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