OBJECTIVE: To reevaluate the clinical significance of elevations of adrenal androgens in polycystic ovary syndrome (PCOS). METHODS: Thirty women with PCOS and ten ovulatory controls were evaluated. Serum dehydroepiandrosterone (DHEA) sulfate and 11 beta-hydroxyandrostenedione were measured before and after 3 and 6 months of GnRH agonist (GnRH-A) therapy. All controls and 15 women with PCOS received intravenous ACTH before and after GnRH-A therapy. RESULTS: Twenty-one (70%) of the women with PCOS had elevations of DHEA sulfate, and 16 (53%) had elevations in 11 beta-hydroxyandrostenedione. Only two women with PCOS had normal values of both adrenal androgens. After GnRH-A therapy, only 11 subjects (37%) had elevated values of DHEA sulfate. Four of 16 women had reductions in 11 beta-hydroxyandrostenedione. Only those with elevated baseline DHEA sulfate levels had reductions after GnRH-A therapy. The reduction of DHEA sulfate with GnRH-A correlated with the reduction in androstenedione. Of the subjects who had reductions in DHEA sulfate with GnRH-A therapy, there was a blunted response of DHEA to ACTH after treatment. CONCLUSION: Our findings suggest that the ovary may influence the prevalence and magnitude of adrenal androgen excess in PCOS.
OBJECTIVE: To reevaluate the clinical significance of elevations of adrenal androgens in polycystic ovary syndrome (PCOS). METHODS: Thirty women with PCOS and ten ovulatory controls were evaluated. Serum dehydroepiandrosterone (DHEA) sulfate and 11 beta-hydroxyandrostenedione were measured before and after 3 and 6 months of GnRH agonist (GnRH-A) therapy. All controls and 15 women with PCOS received intravenous ACTH before and after GnRH-A therapy. RESULTS: Twenty-one (70%) of the women with PCOS had elevations of DHEA sulfate, and 16 (53%) had elevations in 11 beta-hydroxyandrostenedione. Only two women with PCOS had normal values of both adrenal androgens. After GnRH-A therapy, only 11 subjects (37%) had elevated values of DHEA sulfate. Four of 16 women had reductions in 11 beta-hydroxyandrostenedione. Only those with elevated baseline DHEA sulfate levels had reductions after GnRH-A therapy. The reduction of DHEA sulfate with GnRH-A correlated with the reduction in androstenedione. Of the subjects who had reductions in DHEA sulfate with GnRH-A therapy, there was a blunted response of DHEA to ACTH after treatment. CONCLUSION: Our findings suggest that the ovary may influence the prevalence and magnitude of adrenal androgen excess in PCOS.