Benign prostatic hyperplasia

Hyperplasia of the epithelial and stromal compartments, particularly in the transitional zone, may be attributed to various factors including shifts in age-related hormonal changes creating androgen/oestrogen imbalances. Changes in prostatic stromal-epithelial interactions that occur with ageing and increases in prostatic stem cell numbers are also aetiological considerations. Progression from pathological BPH to clinical BPH (i.e., the presence of symptoms) may require additional factors such as prostatitis, vascular effects, and changes in the glandular capsule.[6]Isaacs JT, Coffey DS. Etiology and disease process of benign prostatic hyperplasia. Prostate. 1989;15(S2):33-50. http://www.ncbi.nlm.nih.gov/pubmed/2482772?tool=bestpractice.com

BPH involves hyperplasia of both epithelial and stromal prostatic components. A key characteristic of BPH is increased stromal:epithelial ratio. Over time, prostatic hyperplasia can result in bladder outlet obstruction. Obstruction has both a prostatic component due to increased epithelial tissue, particularly in a transition zone, and a dynamic component due to increases in stromal smooth muscle tone. A large number of alpha-adrenergic receptors are present in the prostate capsule, stroma, and the bladder neck. The predominant alpha-1 receptor in prostatic stromal tissue is the alpha-1A receptor. Treatment of symptomatic BPH is mainly accomplished via the reduction of the size of the glandular component following inhibition of the formation of dihydrotestosterone by 5-alpha-reductase inhibitors and through relaxation of smooth muscle tone with alpha-blockers.[7]Patel AK, Chapple CR. Benign prostatic hyperplasia: treatment in primary care. BMJ. 2006 Sep 9;333(7567):535-9. http://www.ncbi.nlm.nih.gov/pubmed/16960209?tool=bestpractice.com Select surgical intervention (e.g., transurethral resection) alleviates symptoms of urinary obstruction by reduction of prostatic bulk.