Impact of overnight dexamethasone suppression on the adrenal androgen response to an oral glucose tolerance test in women with and without polycystic ovary syndrome

• Published in: Human reproduction (Oxford) 1997-06, Vol.12 (6), p.1138-1141
• Main Authors: Buyalos, R P, Geffner, M E, Azziz, R, Judd, H L
• Format: Article
• Language: English
• Subjects: Adrenal Cortex - drug effects; Adrenal Cortex - physiopathology; Adult; Androgens - blood; Biological and medical sciences; Blood Glucose - metabolism; Case-Control Studies; Dehydroepiandrosterone - blood; Dehydroepiandrosterone Sulfate - blood; Dexamethasone - administration & dosage; Female; Female genital diseases; Glucose Tolerance Test; Gynecology. Andrology. Obstetrics; Humans; Hydrocortisone - blood; Insulin - blood; Medical sciences; Non tumoral diseases; Polycystic Ovary Syndrome - physiopathology; Stress, Physiological - diagnosis; Stress, Physiological - physiopathology; Stress, Physiological - prevention & control; Testosterone - blood
• ISSN: 0268-1161; 1460-2350
• DOI: 10.1093/humrep/12.6.1138

In order to test the hypothesis that adrenocortical overactivity, possibly related to the stress of testing, may impact on the measurement of circulating androgen concentrations during glucose-induced hyperinsulinaemia, we prospectively screened 10 patients with the polycystic ovary syndrome (PCOS) and nine healthy control women with an oral glucose tolerance test (OGTT), before and after the administration of dexamethasone. Blood sampling was performed at 0, 30, 60, 90, and 120 min following the oral ingestion of 75 g of glucose, before and after the administration of 1.0 mg dexamethasone on the evening prior to testing. Total and free testosterone, androstenedione, dehydroepiandrosterone (DHEA), DHEA sulphate (DHEAS), cortisol, glucose and insulin were assessed during the 2 h OGTT. Women with PCOS had increased basal concentrations of free testosterone, total testosterone, androstenedione, and insulin compared to control women. In women with PCOS an acute decline in circulating concentrations of DHEAS occurred during the OGTT. In PCOS women there were no changes in other ovarian or adrenal androgens during OGTT before or following dexamethasone administration. In control women DHEA concentrations declined during the OGTT. Following overnight dexamethasone suppression in control women, circulating concentrations of DHEAS and testosterone also declined. It is concluded that: (i) in PCOS women only the concentration of circulating DHEAS decreased during glucose-induced hyperinsulinaemia and dexamethasone administration did not further alter androgen responses to an OGTT; (ii) it is possible that, in these hyperandrogenic patients, the insulin-related suppression of adrenocortical testosterone and DHEA is negated by their much greater ovarian secretion of these androgens; (iii) in control women DHEA concentrations acutely declined during the OGTT and the administration of dexamethasone resulted in the acute decline of DHEA, DHEAS, and testosterone; (iv) it appears that the stress related to testing impacts on the androgen response to OGTT, at least in healthy women.