Prostate Histopathology and the Chronic Prostatitis/Chronic Pelvic Pain Syndrome: A Prospective Biopsy Study

True, Lawrence D.; Berger, Richard E.; Rothman, Ivan; Ross, Susan O.; Krieger, John N.

doi:10.1016/s0022-5347(05)68090-1

Cited by 137 publications

(78 citation statements)

References 18 publications

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“…In 97 patients showing symptoms of CP/CPPS, only 5% showed moderate or severe histological findings of inflammation in a total of 368 biopsies (17). These data apparently exclude a close relationship between clinical and histological prostatitis.…”

Section: Clinical and Epidemiological Studiesmentioning

confidence: 80%

Inflammation, prostatitis, proliferative inflammatory atrophy: ‘Fertile ground’ for prostate cancer development?

Perletti¹,

Montanari

Vral³

et al. 2009

Mol Med Rep

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Abstract. Inflammatory processes caused by chemical, physical or biological agents are known to be important cofactors in the pathogenesis of human cancer. In the prostate, epithelial tissue damage followed by cell regeneration in the presence of inflammation is believed to be a key event in neoplastic transformation. According to the 'injury and regeneration' model, inflammatory cells infiltrating the prostate release reactive species in response to bacterial/viral infection, uric acid, or dietary prostate carcinogens. Besides inducing inflammation, tissue injury by these and other agents would promote the appearance of proliferative inflammatory atrophy (PIA). A subset of proliferating atrophic cells -possibly showing stemcell features -may be exposed to the genotoxic insult of free radicals and to an increased rate of mutations and chromosomal aberrations, ultimately leading to neoplastic initiation, promotion and progression. In the last decade, the link between inflammation and cancer and the hypothesis pointing to PIA as a risk lesion for prostate cancer have been extensively investigated at the pre-clinical, clinical, morphological, cellular and molecular levels. In this article, recent reports describing supportive or negative evidence on the link between prostate inflammation, atrophy and cancer are schematically reviewed.

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Section: Clinical and Epidemiological Studiesmentioning

confidence: 80%

Inflammation, prostatitis, proliferative inflammatory atrophy: ‘Fertile ground’ for prostate cancer development?

Perletti¹,

Montanari

Vral³

et al. 2009

Mol Med Rep

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“…Two large biopsy studies have studied prostatic histological inflammation in patients with chronic prostatitis. True and coworkers [27] found prostatic inflammation in only 33% of patients with 29% having mild inflammation and 4% moderate inflammation. This group examined 124 biopsies taken from 97 men.…”

Section: Discussionmentioning

confidence: 96%

Autoimmune T cell responses to seminal plasma in chronic pelvic pain syndrome (CPPS)

Batstone

Doble

Gaston

2002

Clinical and Experimental Immunology

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INTRODUCTIONChronic abacterial prostatitis and prostatodynia (now referred to as CPPS types IIIa and IIIb, respectively, in the NIH classification [1]) are poorly understood conditions, which are insufficiently recognized [2]. They are surprisingly common and account for approximately 8% of visits to urologists in the United States. They affect men in all age groups but primarily those in the age group 36-50 years [3]. It has been documented that the impairment to quality of life from chronic prostatitis compares with that due to myocardial infarction, angina and Crohn's disease [4].Controversy exists concerning the aetiology of this condition. Current investigation has focused largely on a microbial or an autoimmune cause, though the two are not mutually exclusive. To investigate a microbial cause, investigators have used PCR to amplify microbial 16S rRNA genes from prostatic biopsies. Kreiger et al. demonstrated microbial 16S rRNA in 77% of the prostates of men with chronic prostatitis but did not investigate a control group [5]. A subsequent paper by Keay et al. found the 16S rRNA in the prostates of 8/9 men with prostate cancer (although this group had previously had trans-rectal biopsies) [6]. Hochreiter [7] found no 16S rRNA gene product in the stored prostates of 18 men whose prostates had been preserved at the time of organ donation and in whom there was no information on whether they had any prostatitis symptoms ante-mortem. In a subsequent study Kreiger found the 16S rRNA gene product in 20% of 107 patients with prostate cancer as compared to 46% of 170 men with chronic prostatitis. The median age of the men with prostate cancer was 64 and the median age of the men with prostatitis was 38 [8]. Essentially it is difficult to obtain aged matched controls to undergo a prostatic biopsy.The autoimmune hypothesis suggests that types IIIa and IIIb prostatitis (CPPS) are caused by autoimmune mediated injury to the genital tract (including the prostate), which is precipitated by genitourinary inflammatory events such as urinary tract infection (UTI), acute bacterial prostatitis, urethritis and repetitive trauma. The male genital tract is an immune privileged site [9], and seminal plasma is highly immunosuppressive due to high concentrations of PGE 2 [10] in the semen. The seminal plasma is also capable of being recognized by the immune system. Halpern first described seminal plasma allergy in 1967 [11] in a woman who experienced postcoital anaphylaxis. Other authors have reported similar findings and suggested that the allergic component was a protein(s) in the range of 20-40 KD [12,13]. An antigen does not need to be produced by the prostate for the prostate to be affected as intraprostatic spermatozoa have been found on postmortem analysis [14] mainly in the peripheral zone.The finding of increased levels of IgA and IgG in the expressed prostatic secretion of patients with abacterial prostatitis, compared to controls, supports an autoimmune aetiology for this condition, since this Ig was not specific for know...

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“…When present, prostatitis was subclassified using previously described criteria [2]. Separate evaluations of the degree and extent of inflammation in biopsy cores free of cancer and in cancerous biopsy cores were undertaken.…”

Section: Methodsmentioning

confidence: 99%

“…In most cases it is impossible to make a definitive diagnosis of bacterial vs. viral vs. noninfectious prostatitis and patients are frequently treated empirically with antibiotics with mixed results. Cultures of patients' urine or prostatic secretions are typically negative and prostatic biopsies show inflammation in only about one-third of patients [1,2].…”

Section: Introductionmentioning

confidence: 99%

Preexisting histologic evidence of prostatitis is unrelated to postimplant urinary morbidity

et al. 2001

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Prostate Histopathology and the Chronic Prostatitis/Chronic Pelvic Pain Syndrome: A Prospective Biopsy Study

Abstract: The finding of moderate or severe inflammation in only 5% of 97 patients argues for the need to reevaluate current concepts of the pathophysiology of the chronic prostatitis/chronic pelvic pain syndrome.

Cited by 137 publications

References 18 publications

Inflammation, prostatitis, proliferative inflammatory atrophy: ‘Fertile ground’ for prostate cancer development?

Inflammation, prostatitis, proliferative inflammatory atrophy: ‘Fertile ground’ for prostate cancer development?

Autoimmune T cell responses to seminal plasma in chronic pelvic pain syndrome (CPPS)

Preexisting histologic evidence of prostatitis is unrelated to postimplant urinary morbidity

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