Preliminary results suggesting exaggerated ovarian androgen production early in the course of polycystic ovary syndrome

Gary L. Francis, Alan Getts, J. C. Mcpherson

Research output: Contribution to journalArticlepeer-review

Abstract

Excess ovarian androgen production might be a cause of the polycystic ovary syndrome (PCO). Previous studies have evaluated adult women with long-standing abnormality of the hypothalamic-pituitary gonadal axis. Abnormal ovarian function in such patients could be a primary or even a secondary finding. For that reason, this study was designed to evaluate ovarian androgen production in symptomatic adolescent females. Simultaneous adrenal suppression, by using dexamethasone, and ovarian stimulation, by using gonadotropin-releasing hormone (GnRH), were achieved in 12 patients. Following stimulation, blood was serially obtained over 8 hr to measure gonadotropin, estrogen, and androgen responses. Based on the androgen response, patients could be divided into two groups. Group A (five) had a significant increase (p < 0.01) in free testosterone, whereas group B (seven) had no increase in any androgen, including free testosterone (significantly different from group A, p = 0.01). All patients in group A had enlarged or cystic ovaries, whereas only one-quarter patients in group B had enlarged ovaries (significantly different from group A, p < 0.03). The pituitary and estrogenic response was similar in both groups. These preliminary data suggest that some patients with PCO (group A) have a primary abnormality in ovarian androgen production early in the course of their disease.

Original languageEnglish (US)
Pages (from-to)480-484
Number of pages5
JournalJournal of Adolescent Health Care
Volume11
Issue number6
DOIs
StatePublished - Nov 1990
Externally publishedYes

Keywords

  • Polycystic ovary Androgen GnRH

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Public Health, Environmental and Occupational Health

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