Polycystic ovary syndrome (PCOS) is heterogeneous disorder leading to infertility. The introduction of Rotterdam criteria creates different PCOS phenotypes, i.e. hyperandrogenic anovulatory with (A) and without (B) polycystic ovaries (PCO) morphology in ultrasonography (usg), hyperandrogenic ovulatory with PCO morphology in usg (C), non-hyperandrogenic anovulatory with PCO morphology in usg (D). In PCOS insulin resistance might be involved in the development of endocrine and metabolic abnormalities. It is suggested that low-grade chronic inflammation is related to the pathogenesis of insulin resistance. The aim of the present study was to asses inflammatory markers, adiponectin and insulin sensitivity in hyperandrogenic anovulatory PCOS (A) in comparison to non-hyperandrogenic anovulatory PCOS (D) and control group. We studied 129 PCOS women (phenotype A, n=69, phenotype D, n=60) and 62 healthy controls. Antropomethric parameters, euglycemichyperinsulinemic clamp and estimation of adiponectin, interleukin 18 (IL-18), hsCRP, sex hormone binding globuline (SHBG) and sex hormones were performed. BMI, waist, % of body fat and insulin sensitivity was not different between A and D phenotypes, however hyperandrogenic anovulatory PCOS women had significantly higher systolic blood pressure (P=0.03). Comparison of both PCOS phenotypes with controls revealed significantly lower insulin sensitivity (P=0.036 versus phenotype A, P=0.003 versus phenotype D), lower SHBG serum concentration (P=0.004 versus phenotype A, P<0.0001 versus phenotype D), higher LH (P<0.0001 for both phenotypes) and higher free androgen index (FAI) (P<0.0001 versus phenotype A and P=0.0018 versus phenotype D). Serum adiponectin, hsCRP, IL-18 did not differ between A and D phenotypes. We concluded that non-hyperandrogenic anovulatory PCOS women have similar metabolic and inflammatory profile like hyperandrogenic anovulatory PCOS.
Prague, Czech Republic
24 - 28 Apr 2010
European Society of Endocrinology