[Polycystic ovary syndrome: a hypothalamic or a gonadal anomaly?].

Evidence obtained from the study of polycystic ovarian disease in the female is reviewed. The etiology of this problem remains unknown, in spite of advances achieved by means of biochemical and morphologic studies. No correlation has been observed between histological findings and the pituitary or gonadal hormone production. However, an abnormal hypothalamic-pituitary-gonadal interaction prevails, characterized by a increased LH-FSH ratio associated with high level of androgens, mainly androstenedione. The pituitary reserve test performed with potent GnRH agonists have confirmed the hyper-response of LH along with that of androstenedione, as well as augmentation of 17-hydroxyprogesterone. Since the pattern of gonadotropins and steroid hormone secretion in women with polycystic ovarian disease resembles that seen in normal men, the basic alteration may well consist in a functionally "masculinized" hypothalamus.