Cortisol, androstenedione, testosterone, dehydroepiandrosterone sulphate (DHAS) and free dehydroepiandrosterone (DHA) were measured in plasma of ten women affected by amenorrhoea with hyperprolactinaemia and eleven women affected by secondary hypothalamic amenorrhoea; twelve normal women at the second day of the menstrual cycle were used as controls. All subjects were hospitalized and 17-ketosteroids, 17OH-corticosteroids and total dehydroepiandrosterone were also measured in urine. Plasma DHAS was increased in all subjects affected by amenorrhoea with hyperprolactinaemia, while plasma DHA and urinary DHA were significantly increased in this group in comparison to other groups. Plasma cortisol, androstenedione and testosterone and urinary 17-oxosteroids and 17OH-corticosteroids were not significantly differnt in the three groups. In subjects affected by amenorrhoea with hyperprolactinaemia treated with bromocriptine a clear decrease of DHAS correlating with a decrease of plasma prolactin was observed. Since in wome DHAS sems to be almost exclusively secreted by the adrenal gland and most of the circulating DHA is dervied from adrenal secretion, these data suggest that human prolactin can stimulate DHAS production by the adrenal cortex.

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Plasma testosterone (T), dihydrotestosterone (DHT), 17 beta-estradiol (E2), 17-hydroxyprogesterone (17-OHP), androstenedione (delta), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS), 5-androstene-3 beta-17 beta-diol (A-diol) and cortisol (F) have been measured in a group of normal males and in a group of patients with Klinefelter's syndrome (KS) before and after hCG stimulation. Significantly lower baseline levels of T and DHT and significantly higher baseline levels of E2 were found in patients with KS. No significant differences were found between baseline levels of 17-OHP, delta, DHEA, DHEAS, A-diol, and F. After hCG stimulation between T, DHT, E2 and 17-OHP levels showed a significant increase in the two groups of subjects. The percentage variation of T and DHT, however, was much less important in Klinefeiter patients, while E2 and 17-OHP did not show a significantly different pattern from that of normal controls, hCG administration did not produce any significant variation of delta, DHEA, DHEAS, and F in the two groups of subjects, while A-diol levels increased significantly in normal subjects, but not in Klinefelter patients. Our data may be consistent with the hypothesis that testicular steroidogenesis in Klinefelter patients is impaired below the 21-C-steriod level not only at delta 4 but also at the delta 5 pathway.

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Plasma dehydroepiandrosterone sulphate (DHEAS), cortisol (F) and prolactin (PRL) were measured in seventeen premenopausal women with primary hypothyroidism and in fifteen normal premenopausal women. Significantly lower (P < 0.001) DHEAS levels were found in hypothyroid women while F and PRL were in the range of normal controls. No significant relation was found between DHEAS and total thyroxine (T4) and TSH. Our results support the hypothesis that DHEAS secretion is impaired in some women with primary hypothyroidism.