Pituitary-Ovarian Responses to Nafarelin Testing in the Polycystic Ovary Syndrome

R. B. Barnes*, R. L. Rosenfield, S. Burstein, D. A. Ehrmann

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

259 Scopus citations

Abstract

To investigate the basis of polycystic ovary syndrome, we examined the responses of patients to nafarelin, a specific gonadotropin-releasing-hormone agonist, given to stimulate pituitary and gonadal secretion. We compared 16 normal women in the follicular phase, 5 normal men, 8 women with polycystic ovary syndrome, and 1 woman with polycystic ovary syndrome caused by a 3β-hydroxysteroid dehydrogenase deficiency. After 100 μg of nafarelin was given subcutaneously, serum follicle-stimulating hormone and luteinizing hormone increased rapidly to peak levels within four hours. The women with polycystic ovary syndrome had a pattern similar to that of the men, with greater early luteinizing-hormone responses (30 minutes to 1 hour) and lower peak follicle-stimulating-hormone responses than normal women (P<0.05). Patients with polycystic ovary syndrome responded to gonadotropin stimulation with normal to increased production of plasma estrogens and increased levels of androstenedione at 16 to 24 hours (P<0.05). Elevated production of 17α-hydroxyprogesterone was found in all the women with polycystic ovary syndrome and in the men. These abnormal responses were unchanged by pretreatment with dexamethasone to suppress adrenal function. In the patient with the 3β-hydroxysteroid dehydrogenase deficiency, both basal and stimulated plasma levels of Δ5-3β-hydroxysteroids before the enzymatic block were elevated, whereas plasma levels of 17α-hydroxyprogesterone and androstenedione — the steroids immediately beyond the block — were low. We conclude that women with polycystic ovary syndrome have masculinized pituitary and ovarian responses to stimulation by nafarelin. Our findings suggest that the regulation of the ovarian 17-hydroxylase and C-17,20-lyase activities is abnormal in such women. THE cause of polycystic ovary syndrome is the subject of intense controversy.1 The most widely accepted hypothesis is that it is the result of a complex cycle in which the peripheral formation of estrone from androstenedione, which originates in part from the adrenal glands, is central. According to this theory, the elevation in estrone levels sensitizes the pituitary to secrete excess luteinizing hormone, which initiates or maintains the cycle. However, not all patients with polycystic ovary syndrome have elevated levels of luteinizing hormone.2 Consequently, another school of thought holds that the common denominator in polycystic ovary syndrome is functional ovarian…

Original languageEnglish (US)
Pages (from-to)559-565
Number of pages7
JournalNew England Journal of Medicine
Volume320
Issue number9
DOIs
StatePublished - Mar 2 1989

ASJC Scopus subject areas

  • Medicine(all)

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