[Relation of prolactin with nodular hyperplasia and carcinoma of the prostate]

The relationship between prolactin in NH and prostate carcinoma has several aspects: under normal conditions, prolactin enhances androgens output, increasing the Leydig cell susceptibility to LH. At the prostate level, it increases testosterone binding to the prostate epithelium and stimulates the conversion of testosterone to dihydrotestosterone. On its own, it decreases prostatic protein degradation and increases the DNA synthesis index. With regard to Nodular Hyperplasia, once its hormone dependency is rated, it also appears to be stimulated by high levels of prolactin. The NH cell cultures with human prostate increase their growth, cell division, as well as the DNA synthesis. The aspects of the prolactin-prostate carcinoma interaction involve considering this hormone as a possible carcinogenic agent, emphasizing the existence of high plasma levels of this hormone in individuals with prostate carcinoma, where any androgen excess is considered a major factor at the genesis of this tumour, and prolactin increases indirectly its testicular synthesis. Also, prolactin itself stimulates the growth and development of carcinomatous human cell lines, increasing its effect in the presence of testosterone. For this reason, controlling this hormone levels becomes an element to have into consideration in the treatment and follow-up of these patients; also, the reevaluation of any drug therapy that, besides the initial goal pursued, does not maintain baseline prolactin levels. The association of anti-prolactin drugs has to be understood as a co-adjuvant therapy when there is androgenic deprivation, never as a single treatment.