Endocrine Abstracts

Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder present in 5–10% women of the reproductive period. The endocrine manifestations of PCOS include excess androgen production of ovarian and/or adrenal origin and arrested follicular development leading to chronic oligo- or anovulation. As a consequence, PCOS is associated with increased risk of infertility, and in long term to type 2 diabetes, and possibly cardiovascular disease. The ovary is generally considered the principal source of androgens, but many patients with PCOS also have increased adrenal androgen secretion. Previous works on this issue showed possible androgen hyperresponsivity to direct (ACTH) or indirect (CRH) stimulation of the adrenal cortex. Increased urinary free cortisol (UFC) has also been reported in PCOS patients. This alteration has been attributed to enhanced cortisol metabolism, followed by a compensatory overdrive of the hypothalamic–pituitary–adrenal (HPA) axis and hence increased androgen production. It was supposed an abnormal P450c17 function in PCOS that is principally responsible for the adrenal androgen excess, as well as increased peripheral metabolism of cortisol, either through enhanced 5α-reductase or impaired 11β-HSD1 activities. Known role of glucocorticoids (GCs) in the development of components of the metabolic syndrome (MS) led to the examination of possible hormonal dysregulation of HPA, by analyzing indices of glucocorticoid receptor (GR) binding in peripheral mononuclear leucocytes of women with PCOS. Although differences in some of the GR binding indices were not shown, it seems that number of the receptors and its affinity depends of the source of the androgens, namely adrenal DHEA-S, and its concentrations. Presence of several GR gene polymorphisms can modulate GCs effects. It seems that BClI polymorphism of the GR gene, could be related to the components of the metabolic syndrome in women with PCOS.