Adrenal androgen production is frequently abnormal in women with hyperandrogenic oligo-ovulation (HO). A number of investigators, including ourselves, have noted that AA excess may result from a generalized adrenocortical hyper-reactivity to adrenocorticotropic hormone (ACTH) or pituitary over-response to corticotropin releasing hormone (CRH). This adrenocortical dysfunction may represent an acquired defect secondary to excessive ovarian secretion of androgens, such as testosterone. This proposal aims to establish the sensitivity and responsivity to ACTH and CRH in HO patients with and without adrenocortical dysfunction. To achieve this specific aim the adrenocortical sensitivity and responsivity to incremental doses of ACTH, and to ovine CRH, will be determined in 10 HO patients with and 10 without adrenocrotical hyperreactivity and in 10 control women. The above studies may identify a role for pituitary hyper-responsivity to oCRH, and/or adrenocortical hypersensitivity to ACTH, in HO may suggest that the adrenocortical dysfunction evident in at least 50% of HO patients is primary. Furthermore, it may suggest molecular mechanisms, either in the form of abnormalities of common secondary messengers or ACTH receptor abnormalities. If this were to be the case, further testing would be needed to confirm that this finding is independent of the patient's hormonal milieu. Furthermore, these findings may justify (or discourage) the use of glucocorticoid suppression in these women.
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