Adrenal and ovarian steroid hormone responses to gonadotropin-releasing hormone agonist treatment in polycystic ovary syndrome

Frank Gonzalez, Denise A. Hatala, Leon Speroff

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

It has been postulated that in polycystic ovary syndrome ovarian steroids can influence adrenal steroidogenesis. To test this hypothesis, basal and dexamethasone-suppressed-corticotropin-stimulated steroid hormone responses were compared among three groups of women before, during, and after gonadotropin-releasing hormone agonist treatment for 3 months. The groups were characterized as follows: (1) women with polycystic ovary syndrome with high dehydroepiandrosterone sulfate levels (>400 μg/dl), (2) women with polycystic ovary syndrome with normal dehydroepiandrosterone sulfate levels (<300 μg/dl), and (3) normal ovulatory women. In response to gonadotropin-releasing hormone agonist, basal serum luteinizing hormone, follicle-stimulating hormone, estradiol, estrone, 17-hydroxyprogesterone, androstenedione, and testosterone in all three groups were suppressed to similar levels. Basal serum dehydroepiandrosterone sulfate levels in the group with high levels declined, but they did not reach the normal, unaltered concentrations in the other two groups. Two subjects with polycystic ovary syndrome in this group with high levels, who showed the greatest declines in basal serum dehydroepiandrosterone sulfate levels (34%, 40%), also had evidence of 3β-hydroxysteroid dehydrogenase deficiency before treatment, which was resolved by the end of treatment. In both groups with polycystic ovary syndrome, the increase in maximum incremental rise of dehydroepiandrosterone and dehydroepiandrosterone sulfate levels in response to a pharmacologic dose of corticotropin from a dexamethasone-suppressed baseline (adrenal androgen capacity) remained unaltered during gonadotropin-releasing hormone agonist administration. We conclude that ovarian steroids may promote excessive adrenal androgen secretion in women with polycystic ovary syndrome, may induce 3β-hydroxysteroid dehydrogenase deficiency as a mechanism for adrenal involvement in some women with polycystic ovary syndrome, and do not influence adrenal androgen capacity.

Original languageEnglish (US)
Pages (from-to)535-545
Number of pages11
JournalAmerican Journal of Obstetrics and Gynecology
Volume165
Issue number3
DOIs
StatePublished - Sep 1991

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Keywords

  • 3β-hydroxysteroid dehydrogenase deficiency
  • Polycystic ovary syndrome
  • dehydroepiandrosterone sulfate
  • gonadotropin-releasing hormone agonist

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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