Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 22 P472

Institute od Endocrinology, Diabetes and Metabolic Disorders, Clinical Center of Serbia and University of Belgrade School of Medicine, Belgrade, Serbia.

Objectives: Besides well known increased adrenal androgen production, an enhanced peripheral cortisol metabolism was also observed in polycystic ovary syndrome (PCOS). This could induce a compensatory rise of ACTH secretion, tending to maintain normal plasma cortisol concentration at the expense of adrenal androgen excess. On the other hand, obesity is associated with a hyperactivity of the hypothalamic–pituitary–adrenal (HPA) axis and impaired androgen balance. In this study we examined HPA axis sensitivity in obese women with PCOS.

Methods: Thirty-eight obese women with PCOS (age: 26.0±5.8 years, BMI: 32.3±4.7 kg/m2) and sixteen age and BMI matched obese healthy controls were examined. PCOS was diagnosed using ESHRE/ASRM criteria. In all subjects serum concentrations of glucose, insulin (with HOMA-IR calculation), C-peptide, testosterone, SHBG (with FAI calculation), DHEAS, leptin, adiponectin and basal cortisol were determined. Overnight dexamethasone supression test (0.5 mg) was performed in all women: 0.5 mg of dexamethasone was taken orally at 2300 h and blood samples for determination of cortisol were obtained at 0800 h the following day.

Results: There was no difference in glucose (P=0.95), insulin (P=0.30), HOMA-IR (P=0.45), C-peptide (P=0.23), leptin (P=0.40), adiponectin (P=0.09) and DHEAS (P=0.06) concentrations between groups. SHBG concentration (P=0.005) was significantly lower and testosterone (P=0.001), FAI (P<0.001) and androstenedion (P=0.046) concentrations were significantly higher in obese PCOS women than in obese controls. Obese PCOS had significantly higher basal cortisol concentrations then obese controls (452.8±151.5 vs 347.5±107.1 nmol/l; P=0.01). The percentage of cortisol suppression in response to 0.5 mg of dexamethasone was similar between obese PCOS and obese controls (81 vs 83%; P=0.31). Only in PCOS group, there was modest but statistically significant correlation between testosterone and cortisol concentrations (ρ=0.33, P=0.04).

Conclusion: Our results showed an increased basal cortisol concentration in obese PCOS in comparison to controls, and a possible alteration in the sensitivity of the adrenal glands to ACTH in obese woman with PCOS.

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