Detection of Functional Ovarian Hyperandrogenism in Women with Androgen Excess

David A. Ehrmann*, Robert L. Rosenfield, Randall B. Barnes, Deborah F. Brigell, Zubie Sheikh

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

314 Scopus citations


Distinguishing between ovarian and adrenal causes of androgen excess may be difficult. We have found that women with the polycystic ovary syndrome have supranormal plasma 17-hydroxyprogesterone responses to the gonadotropin-releasing hormone agonist nafarelin. We determined the usefulness of testing with nafarelin to distinguish ovarian causes of hyperandrogenism in women. We studied 40 consecutive women with hyperandrogenism who had oligomenorrhea, hirsutism, or acne. All 40 underwent testing with nafarelin, dexamethasone, and corticotropin with measurement of circulating concentrations of gonadotropins and steroid hormones, and 19 underwent ovarian ultrasonography. The plasma 17-hydroxyprogesterone response to nafarelin was supranormal in 23 of the 40 women (58 percent), and the plasma androgen response to corticotropin was elevated in 23; 13 women had both abnormalities. Only one woman had conclusive evidence of a steroidogenic block; she had nonclassic adrenal 21-hydroxylase deficiency. Of the 23 women with abnormal responses to nafarelin, only 11 (48 percent) had elevated base-line serum luteinizing hormone concentrations. Of the 13 women with abnormal responses to nafarelin who underwent ultrasonography, 7 (54 percent) had polycystic ovaries. Peak plasma 17-hydroxyprogesterone concentrations after nafarelin administration correlated closely with plasma free testosterone concentrations after dexamethasone administration (r = 0.75, P<0.001). Approximately half of women with oligomenorrhea, hirsutism, or acne have an abnormal response to the gonadotropin-releasing hormone agonist nafarelin, suggesting an ovarian cause of their androgen excess. (N Engl J Med 1992;327:157–62.), THE association of polycystic ovaries, amenorrhea, hirsutism, and obesity was reported by Stein and Leventhal in 1935.1 Abnormalities subsequently found to be characteristic of what is now called the polycystic ovary syndrome include hyperandrogenemia and increased concentrations of serum luteinizing hormone (LH) or an increase in the ratio of LH to follicle-stimulating hormone (FSH) in serum.2 3 4 5 However, the syndrome is clinically, histologically, and biochemically heterogeneous6; some women have the clinical syndrome but not polycystic ovaries or abnormalities of gonadotropin secretion.7 8 9 10 11 12 13 Several lines of evidence suggest that the polycystic ovary syndrome is a form of functional ovarian hyperandrogenism.14 Typically, androgen…

Original languageEnglish (US)
Pages (from-to)157-162
Number of pages6
JournalNew England Journal of Medicine
Issue number3
StatePublished - Jul 16 1992

ASJC Scopus subject areas

  • Medicine(all)


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