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-mu-g/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 levels 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 with 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.
High testosterone levels of ovarian origin affect adrenal steroidogenesis?
MELIS, GIAN BENEDETTO;MAIS, VALERIO;PAOLETTI, ANNA MARIA;
1991-01-01
Abstract
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-mu-g/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 levels 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 with 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.
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