"Menstrual irregularities in PCOS. Does it matter when it starts?".

BACKGROUND: PCOS is presented by a broad spectrum of menstrual irregularities appearing often at puberty or later on during the reproductive years in women suffering from this multifaceted syndrome. To our knowledge, there is no evidence to suggest whether the time of onset of menstrual irregularities (peri or post pubertal) indicates a differential metabolic and/or hormonal profile as well as ovarian ultrasonographic findings, in adulthood in women with PCOS. AIM OF THE STUDY: To compare anthropometric, hormonal-metabolic profile and ultrasound findings in PCOS women with peripubertal onset of menstrual disorders with the corresponding data obtained from PCOS patients with post pubertal onset of menstrual irregularities, matched for BMI and age. PATIENTS-METHODS: 89 PCOS women were evaluated cross-sectionally at the age of 25 years. In 49 subjects menstrual irregularities were present from menarche, whereas in 40 women the irregularities appeared at least 3 years post menarche. RESULTS: Anthropometric parameters were comparable between the 2 groups. The 2 groups did not differ on metabolic and hormonal profile as well as ovarian ultrasound findings. CONCLUSIONS: These data indicate that the timing of menstrual irregularities, do not appear to have an impact, on hormonal/metabolic profile and ovarian ultrasound morphology in patients diagnosed with PCOS, later in life.

Pancreatic beta-cells dysfunction in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a major risk factor for impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2D). Several studies have examined possible mechanisms related to glucose metabolism and insulin secretion that may be responsible for the high prevalence of disorders of glucose metabolism in women with PCOS. The actual pathogenic mechanisms appear to be complex and multifactorial, possibly characterized by the lack of uniformity between patients, thus reflecting the heterogeneity of PCOS. Impaired insulin action and/or beta-cell dysfunction and/or decreased hepatic clearance of insulin have been implicated so far. This article focuses on the role of beta-cell function in the increased predisposition to GDM and T2D in PCOS and the possible genetic basis of defects in insulin secretion. Conditions, like pregnancy and exogenous glucocorticoid administration, aggravate insulin resistance ,thereby placing additional strains upon beta-cells, which may be inherently prone to dysfunction in women with PCOS. The aggravation of insulin resistance amplifies the demands for insulin secretion by beta-cells. The resultant unfavourable state unmasks potential latent defects of beta-cell function, thereby possibly precipitating the development of T2D or of gestational diabetes (GDM) in pregnant women with PCOS. In addition to metabolic sequelae, insulin resistance and compensatory hyperinsulinemia contribute to ovarian dysfunction,manifested by hyperandrogenemia and anovulation, characterizing PCOS. The role of ovarian androgen excess in metabolic aberrations,specifically insulin action and secretion remains unclears.