[Physiopathological aspects of the treatment of benign prostatic hypertrophy. Role of prostatic stroma and estrogens].

The hypothesis of the etiopathogenesis of Benign Prostatic Hypertrophy (BPH) on the basis of stroma-epithelium interaction is presented. The fetal prostate has its origin in the urogenital sinus depending on the dehydrotestosterone stimulating the stromal cells having androgenic receptors. This stroma hyperplasia is considered to be the initial factor in the BPH formation. The inequality in growth factors is also relevant for its formation. Stimulating factors, especially the epidermal growth factor (EGF) prevail on involution factors. The stromal cell has estrogenic receptors. The estrogens from the testosterone aromatization are the first stimulus on the prostatic stroma on the transitional and periurethral area stimulating the glandular epithelium causing BPH. The knowledge of BPH etiopathogenesis will make its rational medical treatment possible, and eventually slow or stop its growth when therapy in its early evolutive stages is prescribed.