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Journal of Clinical Endocrinology & Metabolism Vol. 72, No. 2 426-431
doi:10.1210/jcem-72-2-426
Copyright © 1991 by the Endocrine Society.
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High Testosterone Levels of Ovarian Origin Affect Adrenal Steroidogenesis?

FRANCA FRUZZETTI, GIAN BENEDETTO MELIS, VALERIO MAIS, DANIELA BECONCINI, ANNA MARIA PAOLETTI, GIOVANNI CRISTIANI, ENEO MIAN and PIERO FIORETTI

Department of Obstetrics and Gynecology (F.F., P.F.) and Department of Dermatology (D.B., G.C., EM.), University of Pisa Pisa, Italy
Department of Obstetrics and Gynecology (G.B.M., V.M., A.M.P.), University of Cagliari Cagliari, Italy

Address all correspondence and requests for reprints to: Dr. F. Fruzzeti, Clinica Ginecologica e Ostetrica, Universita' di Pisa, Via Roma 67, 56100 Pisa, Italy.

Androgens of ovarian origin have been suggested to affect adrenal enzymatic activity. To investigate this possibility, the 17-hydroxyprogesterone (17-OH P) and cortisol (F) responses to an ACTH stimulation test (0.25 mg iv, bolus) were evaluated in 10 normal women and in 39 hyperandrogenic women with normal (14 subjects) or high (25 subjects) testosterone (T) levels. The 17-OH P release and the ratio between 17-OH P and F release in response to the ACTH stimulation test were significantly higher (P < 0.05) in hyperandrogenic women with high T levels than in normal subjects. Eight hyperandrogenic women with high T received intranasal GnRH agonist (Buserelin, 1200 µg/day) for 4 weeks, and the 17-OH P and F release in response to the ACTH stimulation was reassessed after agonist treatment. At the end of GnRH agonist administration the mean circulating lev sis of T were significantly reduced (P < 0.05). The F response to the ACTH test was not modified by pretreatment with the GnRH agonist. The 17-OH P response to the ACTH stimulation test after the GnRH agonist was unchanged in comparison w.th control tests, as well as the ratio between 17-OH P and F responses to the ACTH test. These data do not seem to confirm, as previously suggested, that high T levels of ovarian origin affect adrenal steroidogenesis.

Received November 7, 1989.







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Copyright © 1991 by The Endocrine Society