The pathogenesis of benign prostatic hyperplasia.

Development of prostatic hyperplasia is an almost universal feature of the aging man and dog, and in both species the process develops only in males with intact testes. As the result of studies of plasma hormone levels as a function of age, measurements of the concentration of androgen and of androgen receptor proteins within the prostate, and studies of the effects of the administration of various hormones on growth of the prostate in the castrated dog, it is possible to provide a working hypothesis as to the pathogenesis. Dihydrotestosterone accumulation within the gland serves as the hormonal mediator for the hyperplasia in both species; the accumulation probably occurs in part because of decreased catabolism of the molecule and in part because of enhanced intracellular binding of the molecule. The process is accelerated by estrogen, which enhances the level of the androgen receptor in the gland; increase in the androgen receptor allows for androgen-mediated growth even in the face of declining androgen production in advanced age. On theoretic grounds the therapeutic implications of this model are exciting; several potential medical treatments may be feasible that do not involve a chemical castration.