Prostate enlargement is promoted by autoimmune inflammation

Prostate enlargement—benign prostatic hyperplasia (BPH)—is fundamentally an inflammatory process that can undergo conversion to malignancy and emerge as prostate cancer. The authors of a study just published in The Journal of Urology offer important evidence that autoimmune phenomena drive prostate inflammation and enlargement. They state:

"This study was designed to investigate the association between immune inflammation and androgen receptor (AR) expression in benign prostatic hyperplasia (BPH)."

The authors analyzed 105 prostatectomy specimens to apply an immune inflammation score defined by combining three immunohistochemical markers (CD4, CD8 and CD20). The immunohistochemical markers were CD4 and CD8 for T lymphocytes, CD20 for B lymphocytes and androgen receptor (AR) antibody by which the immune system attacks androgen receptors in prostate tissue. The data showed a strong association between prostate hypertrophy and immune inflammation:

"Rates of CD4, CD8, CD20 and AR expression in BPH were 20 (19.0%), 21 (20.0%), 101 (96.2%) and 48 (45.7%), respectively. Total prostate volume (TPV) was higher in the immune inflammation group than in the non-immune inflammation group (62.7 ml vs. 49.2 ml). Patients in the immune inflammation group had a higher serum prostate-specific antigen (PSA) than those in the non-inflammation group (7.5 ng ml-1 vs. 5.4 ng ml-1). Specifically, the immune inflammation group showed a higher rate of AR expression than the non-inflammation group (56.1% vs. 28.2%)."

Every case of prostate enlargement or elevated PSA should be investigated for an autoimmune component. The authors conclude:

"Our study revealed a strong association between immune inflammation and TPV, serum PSA and AR expression in BPH tissue. Prostate hyperplasia caused by an immune inflammatory process may contribute to BPH progression over time. Therefore, the inflammatory response involved in BPH may be a prime therapeutic target."