Adrenal cortex and type II polycystic ovary syndrome

The aim of this study was to investigate whether the adrenal gland participates in the pathogenesis of type II polycystic ovary syndrome (PCO), and, if so, to see if an altered pattern of ACTH secretion might be responsible. Circadian secretion and pulsatility (morning and evening) of ACTH, and adrenal and pituitary responsiveness to exogenous ACTH and GnRH, respectively, were evaluated in 10 women with type II PCO and 10 normally menstruating women. After the patients had been administered oral dexamethasone (0.5 mg each night) for 3 months, studies were repeated. Mean plasma values of PRL, testosterone, DHA-S and 17-OH progesterone (17-P) measured by RIA were significantly higher (p less than 0.05) in patients than in controls. FSH and sex hormone binding globulin (SHBG) were significantly lower (p less than 0.05). Cortisol and 17-P responses to ACTH, and the LH/FSH ratio (both in basal conditions and after GnRH stimulation) were significantly higher (p less than 0.05) in patients. ACTH circadian secretion and pulsatility were similar in both groups. Treatment with dexamethasone significantly reduced plasma values of testosterone, DHA-S, androstenedione (adione), cortisol and the LH/FSH ratio (basal and after GnRH), but adrenal hyperresponsiveness to ACTH was maintained. ACTH pulsatility and secretion were significantly (p less than 0.05) reduced in the morning. Our results suggest that there are abnormalities at the adrenal level in type II PCO. Given that ACTH secretion appears to be normal and that adrenal hyperresponsiveness is still observed after treatment with dexamethasone, it is tempting to speculate that excessive trophic stimulation of the gland by a factor other than ACTH could exist in such patients.