MedWire News: Prostate cancer is not predicted by inflammation on initial and subsequent biopsy, say US researchers who nevertheless caution that a role for inflammation in prostate cancer pathogenesis cannot be dismissed.
Previous epidemiologic studies have revealed correlations between prostate cancer and sexually transmitted infections, and antioxidant and anti-inflammatory drug intake. Nevertheless, the role of chronic inflammation in the development of prostate cancer is unclear.
To examine associations between chronic periglandular inflammation on prostate needle biopsy and subsequent prostate cancer development, William Bassett, from Brigham and Women’s Hospital in Boston, Massachusetts, and team studied 655 patients from a prostate/needle biopsy registry.
All participants presented with prostate-specific antigen (PSA) >4 ng/ml or abnormal digital rectal examination (DRE) between 1990 and 2004. The team gathered information on PSA density, prostate volume, histology, and age to determine clinical and pathologic correlations with inflammation, which was defined as an inflammatory cell infiltrate composed predominantly of lymphocytes in a periglandular distribution.
The median age of the participants was 62 years, while the median PSA level was 5.2 ng/ml, the median prostate volume was 49 ml, and the proportion with positive DRE was 25.7%. Overall, 14% of patients had inflammation on initial biopsy, the team notes in the journal Urology.
On initial biopsy, chronic inflammation was significantly associated with prostate volume, PSA, and DRE, although the association for PSA and DRE was no longer significant after taking into account prostate volume.
In a follow-up subset analysis of 308 patients with four biopsies, of whom 23% had chronic inflammation, the team found that chronic inflammation was predicted by prostate volume and DRE, although the latter was no longer significant after accounting for prostate volume.
Kaplan-Meier analysis revealed that inflammation did not predict subsequent prostate cancer, while Cox regression analysis demonstrated that time to positive biopsy was not predicted by inflammation at initial biopsy, inflammation at last biopsy, or inflammation on any previous biopsy, with the evidence potentially indicating a nonsignificant reduced risk with chronic inflammation.
“Although chronic periglandular inflammation on initial and subsequent biopsy does not predict prostate cancer in this cohort, we cannot dismiss its role in prostate cancer pathogenesis,” the team concludes. “Additional research is necessary to explore the relationship between chronic prostatic inflammation and the pathogenesis of prostate cancer.”