ECE2013 Poster Presentations Female reproduction (47 abstracts)
1Clinic for Endocrinology, Diabetes and Metabolic Diseases, Clinical Center of Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia; 2Clinical-Hospital Center Bežanijska kosa, Belgrade, Serbia; 3Institute for Biologic Investigations, Siniša Stanković, Belgrade, Serbia.
Introduction: It has been shown that most women with polycystic ovary syndrome (PCOS) have increased adrenal androgen production, enhanced peripheral metabolism of cortisol and elevated in urinary excretion of its metabolites. Simultaneously, this increased cortisol clearance in PCOS was shown to be followed by a compensatory overdrive of the hypothalamopituitaryadrenal (HPA) axis. The aim of this study was to determine HPA axis sensitivity in women woth PCOS.
Methods: We studied 65 non-obese women with PCOS (group PCOS; 24.7±4.0 years; 22.5±3.5 kg/m2) aged 20 years and BMI matched healthy women (group controls; 27.3±5.3years; 21.9±1.9 kg/m2). PCOS was diagnozed using ESHRE/ASRM criteria. In all subjects during follicular faze of menstrual cycle levels of cortisol, ACTH, DHEAS, testosterone, androstenedione and 17-OH-progesterone were determined. Overnight dexamethasone test with 0.5 mg was performed with subsequent determination of morning cortisol.
Results: PCOS and controls significantly differed in SHBG (40.9±22.9 vs 65.9±31.2 nmol/l, P=0.021) and FAI (9.1±8.1 vs 3.6±1.4%, P=0.018), while DHEAS, 17-OH-progesterone, androstenedione, basal cortisol, ACTH did not differe between groups. PCOS supressed cortisol less than controls after 0.5 mg of dexamethasone (85.0±16.9% vs 93.3±3.2%, P=0.001).
Conclusion: Lower HPA axis sensitivity women with PCOS with simultaneously normal basal cortisol and ACTH levels could be a mechanism for compensatory overdrive of HPA axis in this patients.