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The efficacy of treatment with TSH suppressive doses of L-thyroxine was evaluated by echography in 35 patients with euthyroid nodular goiter. Patients have been subdivided in two groups comparable for sex age and size of the goiter. Sixteen patients were treated for nine months with suppressive doses of thyroxine and nineteen were followed without therapy as control. Patients in treatment were then followed up for additional 9 months without therapy. The mean decrease of thyroid volume at nine months was 25% (27 +/- 10 ml vs 20 +/- 8 ml; p < 0.01). After discontinuation of treatment thyroid volume increased and had returned to base line values after nine months of follow up. In the control group mean thyroid volume had increased by 17.7% at nine months (28 +/- 17 vs 33 +/- 19 ml; p < 0.001). Thyroid nodules in response to thyroid hormone treatment showed a variable behaviour: 30.7% (4/13) of the nodules responded to the therapy with a reduction > to 25% at the ninth month; the remaining nodules were insensitive to the therapy. In conclusion suppressive thyroxine treatment is effective in reducing the goiter, nodules instead are only in part sensitive to the treatment. Thyroxine therapy of euthyroid nodular goiter must be followed for long term since upon thyroxine discontinuation there is a prompt reappearance of the goiter.

The influence of estradiol and of two electron donors (succinate and malate) on testosterone metabolism was studied in vitro. In presence of estradiol the metabolic pattern of testosterone in male liver was changed to a female pattern. On the contrary, addition of malate or succinate to the female liver incubate gave origin to polar metabolites of testosterone which are typical of the male metabolic pattern.

Distribution and metabolism of testosterone were studied in male and female rats. While no differences between sexes were observed in the hormone distribution to liver, kidney, spleen, heart, adipose tissue, muscle, brain and adrenal, male liver was found to metabolize testosterone mainly to polar compounds; female liver mainly to A-ring reduced compounds.

Previous work has shown NADPH to be a necessary cofactor in adrenal production of steroids. Synthesis is, in effect, a function of dehydrogenase activity and the adrenals are particularly rich in these enzymes. The present paper deals with an appraisal of the importance of G 6-PD as a source of NADPH for mitochondrial hydroxylation. 11-beta-hydroxylation was used as parameter. It was found that the activity of this enzyme, and hence NAPDH production, was stimulated by the administration of ACTH; no parallel increase in 11-beta-hydroxylase activity was noted.

Chronic administration of oestradiol has several times been reported as leading to stimulation of in vitro adrenal hydroxylative activity in the rat. It is now shown that acute stimulation is also possible, provided ACTH is present in the system. Synthetic oestrogens with metabolic activity equivalent to that of oestradiol, however, are incapable of stimulating steroid production. It is clear that the mechanism of action of oestrogens is extremely complicated as far as the adrenal glands are concerned.