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Benign prostatic hyperplasia—gaining insight and potential new treatment identified in mice

Two recent studies explored the role of fibrosis in benign prostatic hyperplasia (BPH). The prostate is a male gland about the size and shape of a walnut. It surrounds the urethra just below the bladder, where it adds fluid to semen before ejaculation. The prostate gland commonly becomes enlarged as a man ages. This condition is called benign prostatic hyperplasia (BPH) and is caused by the non-cancerous (benign) growth (hyperplasia) of two different cell types—epithelial and smooth muscle—in regions of the prostate called nodules. As the prostate enlarges, it may squeeze the urethra and affect the flow of the urinary stream. The lower urinary tract symptoms (LUTS) associated with the development of BPH rarely occur before age 40, but more than half of men in their sixties, seventies, and eighties have some LUTS. The most common symptoms vary but involve changes or problems with urination, such as a hesitant, interrupted, weak stream; urgency and leaking or dribbling; more frequent urination, especially at night; and urge incontinence. Previous studies have suggested that formation of fibrosis in the prostate gland contributes to the development of BPH and LUTS. During pathological fibrosis, normal structures are replaced by scar tissue, which is characterized by excess production and deposition of proteins such as collagen—thus collagen is often used as a marker of fibrosis.

One group of researchers sought to evaluate the contribution of fibrosis, specifically collagen, to the development of BPH in men. Normal prostate tissue was obtained from patients undergoing prostatectomy for surgical management of prostate cancer. BPH nodule tissue was obtained from patients during prostate resection surgery (a procedure to remove part of the prostate gland in order for urine to more easily flow through the urethra). Total collagen content was determined to be similar between normal and BPH tissue samples. However, a significant increase in a type of collagen pattern called “thicker collagen bundles” was noted in BPH tissue compared to normal tissue—suggesting that these bundles may play a role in BPH. Medical management of LUTS due to BPH includes the use of prescription medications called α-blockers (e.g., tamsulosin) and 5α-reductase inhibitors (e.g., finasteride). Collagen levels in BPH prostate samples obtained from patients treated with either α-blockers or 5α-reductase inhibitors were compared to BPH prostate samples from patients not treated with medications. Collagen levels in tissue samples were found to be similar in medication-treated men compared to men not taking either of the two medications, suggestive that these medications do not lead to a decrease in fibrosis within the prostate.

Using a mouse model of bacterial-induced prostate inflammation, a second group of investigators examined the reversibility of fibrosis after eliminating the infection and inflammation with an antibiotic treatment. In this model, uropathogenic E. coli bacteria (a leading cause of urinary tract infections) are placed in the urethra in close proximity to the ejaculatory ducts of the prostate, whereas saline was placed in the urethra in close proximity to the ejaculatory ducts of mice that served as controls. Mice whose prostates were infiltrated with E. coli produced more collagen in their prostates compared to control animals. The investigators further showed that antibiotic treatment completely eliminated the bacterial infection and partly reduced the accompanying collagen build-up in the prostate.

These studies provide new information on the potential role of fibrosis in BPH. A better understanding of fibrosis, in general, could yield insights into how this process unfolds in other tissues (i.e. kidney), potentially opening new avenues to therapy for a range of conditions and diseases.


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