Does prostatic inflammation lead to later prostate cancer?

A question that comes up all the time is whether there is any direct (i.e., cause and effect) association between prostate “inflammation” and a subsequent diagnosis of prostate cancer.

A new review article by De Nunzio et al. has attempted to address this question.

Over the years there have been numerous suggestions that “prostatic inflammation” is a potentially underlying cause of both prostate cancer (the most common form of cancer in males) and of benign prostatic hyperplasia or BPH (the most common condition diagnosed in aging men). De Nunzio et al. have tried to carry out a careful evaluation of the available evidence related to this theoretical possibility and to discuss the potential clinical implications for the management, prevention, and treatment of the two diseases.

After a careful literature search encompassing data published over the past decade and earlier data referenced in that literature, the authors report as follows:

  • The histologic signature of chronic inflammation is a common finding in benign and malignant prostate tissue.
  • The inflammatory cell types indentifiable are
    •  CD3(+) T lymphocytes (70-80 percent, mostly CD4)
    • CD19 or CD20 B lymphocytes (10-15 percent)
    • Macrophages (15 percent).
  • Bacterial infections, urine reflux, dietary factors, hormones, and autoimmune response have all been considered as capable of  causing inflammation in the prostate.
  • Tissue damage associated with inflammatory response and subsequent chronic tissue healing may result in the development of BPH nodules and proliferative inflammatory atrophy (PIA).
  •  The loss of glutathione S-transferase P1 (GSTP1) may be responsible for the transition of PIA into high-grade intraepithelial neoplasia (HG-PIN) and prostate cancer in genetically predisposed patients.
  • There is no proof at this time that targeting prostate inflammation with a pharmacologic agent results in a lower incidence and progression or regression of either BPH or prostate cancer.

In the context of this report, it is worth noting that Krongrad and Lai, in a recent article giving early data from a Phase II trial of the treatment of men with severe, chronic, treatment-refractory patients with laparoscopic radical prostatectomy, stated that two of the first six patients treated in this pilot study were found to have identifiable foci of prostate cancer. However, we again have no evidence at this time of a cause-and-effect relationship between prostatic inflammation (even when it leads to severe, chronic prostatitis) and prostate cancer or BPH.

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