J Urol. 2004 Sep;172(3):839-45.
Mechanisms in prostatitis/chronic pelvic pain syndrome.

Pontari MA, Ruggieri MR.

Department of Urology, Temple University School of Medicine, 3401 N.
Broad Street, Philadelphia, PA 19140, USA.

PURPOSE: We reviewed the current literature on mechanisms involved in
the pathogenesis of prostatitis/chronic pelvic pain syndrome (CPPS).
MATERIALS AND METHODS: A literature review for the years 1966 to 2003
was performed using the MEDLINE database of the United States National
Library of Medicine. RESULTS: National Institutes of Health categories
I and II prostatitis result from identifiable prostatic infections,
whereas patients with category IV are asymptomatic. The majority of
symptomatic cases are category III or chronic prostatitis (CP)/CPPS.
The etiology of CP/CPPS is unknown. The traditional marker of
inflammation, namely white blood cells in prostatic fluids, does not
correlate with the predominant symptom of pelvic pain. An imbalance
toward increased proinflammatory and decreased anti-inflammatory
cytokines has been implicated and a few studies have shown some
correlation of this with pelvic pain. The imbalance in some men may
result from polymorphisms at the cytokine loci. An autoimmune process
may be involved and experimental evidence indicates that this can be
under hormonal influence. Recent findings include possible defects in
the androgen receptor. The prostate may not even be the source of the
symptoms. 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 influence the other processes. The role of
normal prostatic bacterial flora in inciting the inflammatory response
has also been reconsidered. CONCLUSIONS: The symptoms of CP/CPPS
appear to result from an interplay between psychological factors and
dysfunction in the immune, neurological and endocrine systems.