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Journal of Clinical Endocrinology & Metabolism, Vol 62, 197-201, Copyright © 1986 by Endocrine Society
ARTICLES |
MD Gross, J Wortsman, B Shapiro, LC Meyers, MC Woodbury and JW Ayers
The polycystic ovary syndrome (PCO) is frequently associated with elevated plasma levels of adrenal androgens and/or abnormal adrenal androgen responses to hormonal stimulation and suppression. Because of the overlap in the output of hormones between the adrenal glands and the ovaries, we measured adrenal iodocholesterol accumulation as an index of adrenocortical function in 11 women with PCO confirmed by laparoscopy or culdoscopy. All patients had normal dexamethasone suppression of plasma cortisol or urinary 17-hydroxycorticosteroid excretion. 6 beta-[131I]Iodomethylnorcholesterol (NP-59) adrenal scintiscans showed bilateral and excessive adrenal cortical uptake in PCO patients [0.46 +/- 0.08% (+/- SE) of the administered dose compared to 0.21 +/- 0.01% in a group of normal women; P less than 0.05]. The elevation of adrenal cortical NP-59 uptake in PCO was quantitatively similar to that in women with ACTH-dependent Cushing's syndrome (0.64 +/- 0.11%; P greater than 0.1). These data support the presence of abnormal adrenal cortical function in patients with PCO. The adrenal dysfunction of PCO most likely represents abnormal control of adrenal androgen production/secretion.
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A. Rodin, H. Thakkar, N. Taylor, and R. Clayton Hyperandrogenism in Polycystic Ovary Syndrome -- Evidence of Dysregulation of 11{beta}-Hydroxysteroid Dehydrogenase N. Engl. J. Med., February 17, 1994; 330(7): 460 - 465. [Abstract] [Full Text] |
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