Free testosterone levels during the menstrual cycle in obese versus normal women.

In a group of seven normally ovulating moderately obese women, testosterone parameters were studied throughout the menstrual cycle and compared with values obtained in normal-weight control women. Plasma T, percent free T (unbound), and free T concentrations were higher and exhibited little variation during the phases of the cycle compared with the normal-weight controls. Testosterone production and its parameters thus are higher in even moderately obese women.

The source(s) of estrogen production in hirsute women with polycystic ovarian disease as determined by simultaneous adrenal and ovarian venous catheterization.

To determine the significant source(s) of estrogen production in women with polycystic ovarian disease (POD), 12 women underwent selective adrenal and ovarian vein catheterization, with simultaneous peripheral blood samplings for determination of cortisol, androstenedione (delta 4A), testosterone, estrone (E1), and estradiol (E2). Ovarian vein E2 gradients were observed in 11 of the 12 patients with a mean of 13.4, whereas adrenal blood samples did not demonstrate significant E2 gradients. Seven of 8 patients exhibited ovarian secretion of E1, with a mean gradient of 13.6 times that of peripheral blood, whereas 4 of the 8 adrenal samples showed E1 gradients. The mean value was 1.4 times peripheral levels. No significant correlations were found between peripheral E1 levels and body weight or degree of adiposity, nor was there a relationship between obesity and E1/delta 4A molar ratio in peripheral blood. The subjects with the highest ovarian delta 4A levels had a significant correlation between peripheral delta 4A and E1. Therefore, our data indicate a significant contribution of ovarian E1 secretion to the peripheral E1 pool in addition to the extraglandular conversion of delta 4A to E1. There was general lack of correlation between peripheral E1 concentrations and plasma E2, and these relationships versus body size suggest that the major source of E2 in women with POD was ovarian secretion.

Determination of the source(s) of androgen overproduction in hirsutism associated with polycystic ovary syndrome by simultaneous adrenal and ovarian venous catheterization. Comparison with the dexamethasone suppression test.

To determine the source(s) of the excessive androgen production in patients with the polycystic ovary syndrome (PCOS), 12 hirsute women with PCOS underwent selective left adrenal and left ovarian venous catheterization. Blood samples were collected simultaneously for determination of cortisol, 17-hydroxy-progesterone, androstenedione (delta), testosterone (T), dehydroepiandrosterone, and dehydroepiandrosterone sulfate. The relative contributions of adrenal secretion rates of T and delta in each patient were estimated by relating their adrenal gradients to those of cortisol. From such calculations we found that in all patients the major source of androgens was the ovary (direct ovarian secretion and/or ovarian secretion of prehormones which then were converted to androgen in the peripheral circulation). After catheterization, 11 of the 12 patients underwent a 5-day dexamethasone suppression test (2 mg/day). In 7 patients studied, plasma delta and/or T levels decreased significantly. Our results indicate that in hirsutism associated with the PCOS, the predominant source of androgens is the ovaries and that glucocorticoid suppression cannot assign adrenal origin as the site of excessive androgens.

Suppression and stimulation of mineralocorticoid hormones (MCH) in the simple virilizing form of congenital adrenal hyperplasia (CAH) evaluated by the quantitation in adrenal venous blood.

Four untreated female patients with the nonsalt-losing form of congenital virilizing adrenal hyperplasia (21-hydroxylase deficiency) (21-OHD) maintained on a daily sodium intake of 120 m-equiv were studied by bilateral adrenal vein catheterization. Simultaneous right and left adrenal and peripheral blood samples were collected for determination of cortisol (F), progesterone (P), 17-hydroxyprogesterone (17-OHP), aldosterone (Aldo), and deoxycorticosterone (DOC). All patients were studied during sequential ACTH suppression (30 min after intravenous administration of 4 mg of dexamethasone) and stimulation (5 min after intravenous administration of 250 micrograms beta-ACTH [cosyntropin]). Basal peripheral concentrations of Aldo, DOC, P and 17-OHP were increased, whereas F concentrations were in the lower limit of the normal range. Dexamethasone suppressed adrenal secretion in all subjects. Subsequent adrenal stimulation by ACTH increased P, 17-OHP and DOC, whereas F returned to only control levels. DOC responses to ACTH in the adrenal vein effluents correlated significantly with Aldo responses but not with the 17-OHP increments, suggesting that the adrenal responses of Aldo and DOC to ACTH are events that probably occur in the same zone.

Evaluation of the gonadotropic responsiveness of the pituitary to acute and prolonged administration of LH/FSH-releasing hormone (lhrh) in untreated patients with congenital adrenal hyperplasia.

The pituitary gonadotropic responsiveness to acute and prolonged administration of LH/FSH-releasing hormone (LHRH) were assessed in 6 patients with untreated congenital virilizing adrenal hyperplasia (partial 21-hydroxylase deficiency). The oldest subjects had normal response in comparison to females at the midfollicular phase, to the acute infusion of 25 ug LHRH regarding both gonadotropins whereas LH secretory area was decreased during the prolonged (100 ug LHRH in 8 hours) infusion with normal FSH secretion. The two youngest subjects, with higher steroid levels in our series, were either unresponsive on both ways of testing or presented pre-pubertal response.

Oestrogen dynamics in adrenal venous effluents in congenital virilizing adrenal hyperplasia.

Four patients with untreated congenital virilizing adrenal hyperplasia (partial 21-hydroxylase deficiency) were studied by bilateral adrenal vein catheterization. Simultaneous right and left adrenal and peripheral blood samples were collected for determination of oestrone (E1) and oestradiol (E2). The concentrations of both were higher in the adrenal effluents than in the peripheral blood samples, indicating their secretion by the adrenals. All patients were also studied during a sequential test of suppression (0.5 h after i.v. administration of 4 mg dexamethasone) and stimulation (5 min after i.v. administration of 250 microgram ACTH 1-24; Synacthen). Mean peripheral E2 concentrations did not change significantly whereas E1 increased above control levels after stimulation. In contrast, suppression of adrenal venous blood concentrations with dexamethasone, and stimulation with ACTH, was demonstrated for every patient. The results indicate that in congenital adrenal hyperplasia the adrenal glands secrete significant amounts of E1 and E2.