Polycystic ovary syndrome (PCOS) is a heterogeneous syndrome characterized by persistent anovulation, oligomenorrhea or amenorrhea, and hyperandrogenism in the absence of thyroid, pituitary, or adrenal disease and is the most common cause of anovulation in adult women.<sup>21 Chang R.J. Polycystic Ovarian Syndrome   Serono Symposia USA Boston: Springer (1996). 

Cliquez ici pour aller à la section Références</sup> In the ovary, follicles grow to the small antral stage; however, there is no selection of a dominant preovulatory follicle. This results in the accumulation of multiple, small, antral follicles characteristic of the disorder.<sup>42 Fauser B.C.J.M., Pache T.D., Lamberts S.W. , et al. Serum bioactive and immunoreactive luteinizing hormone and follicle-stimulating hormone levels in women with cycle abnormalities, with or without polycystic ovarian disease J Clin Endocrinol Metab 1991 ;  73 : 811-817  [cross-ref]

Cliquez ici pour aller à la section Références</sup> There is also evidence of thecal hyperfunctioning and relative hypofunctioning of the granulosa. Although many, but not all, women with PCOS have relatively high circulating levels of luteinizing hormone (LH) compared with follicle-stimulating hormone (FSH), this does not totally account for the observed increase in thecal androgen production or the relative quiescence and FSH resistance of the granulosa. PCOS most likely has its origins both within, as well as outside, the hypothalamic-pituitary-ovarian axis. In addition to the potential role of gonadotropins, intraovarian autocrine and paracrine regulators seem to be major factors in PCOS. Outside the reproductive axis, metabolic, neuroendocrine, and endocrine regulators also contribute to the pathogenesis of this disorder.<sup>72 Kazer R.R., Unterman T.G., Glick R.P. An abnormality of the growth hormone/insulin-like growth factor-I axis in women with polycystic ovary syndrome J Clin Endocrinol Metab 1990 ;  71 : 958-962  [cross-ref]

Cliquez ici pour aller à la section Références, 85 Morales A.J., Laughlin G.A., Butzow T. , et al. Insulin, somatotropic, and luteinizing hormone axes in lean and obese women with polycystic ovary syndrome: Common and distinct features J Clin Endocrinol Metab 1996 ;  81 : 2854-2864  [cross-ref]

Cliquez ici pour aller à la section Références</sup> This article focuses on insulin-like peptides because insulin and insulin-like growth factors (IGFs) integrate endocrine and metabolic axes relevant to PCOS. In addition, intraovarian IGFs and relatedproteins and peptides most likely have a role in hyperandrogenemia and the arrest of follicular development observed in this disorder.