Plasma testosterone, androstenedione, oestradiol-17β, follicle stimulating hormone (FSH) and luteinizing hormone (LH) were not significantly different in patients with prostatic cancer, with benign prostatic hyperplasia or in patients without prostatic disease. Plasma prolactin concentrations were significantly lower in the patients with benign disease than those with prostatic carcinoma. Endocrine therapy in the form of stilboestrol administration significantly decreased plasma levels of testosterone, oestradiol-17β, FSH and LH within 7 days of the treatment. After 7 days therapy prolactin levels increased significantly in all patients studied. Changes in growth hormone concentrations were more varied in response to stilboestrol, being elevated in several patients and remaining unchanged in others. Treatment of a few prostatic carcinoma patients who were receiving stilboestrol therapy with CB154, an inhibitor of prolactin secretion, brought an immediate decrease in prolactin levels which was sustained. Plasma testosterone, androstenedione and growth hormone were unchanged in these patients but a significant decrease in plasma oestradiol-17β was noted in two patients during CB154 administration.

The effect of Synacthen (β1–24-corticotrophin) on plasma testosterone and 4-androstene-3,17-dione concentrations in untreated patients with prostatic carcinoma, and in patients receiving endocrine therapy is described. An established specific radioimmunoassay was used for the measurement of testosterone, and a radioimmunoassay for 3-androstene-3,17-dione using thin layer chromatography has been developed. Administration of Synacthen resulted in a fall in testosterone in untreated patients, but a rise in 4-androstene-3,17-dione was observed. The plasma concentration of testosterone in all treated patients increased after administration of Synacthen. An increased concentration of plasma 4-androstene-3,17-dione was also observed in these treated patients after Synacthen, but the magnitude of the response was not significantly different from that of untreated patients. The work provides further evidence that in the patient being treated with oestrogen for carcinoma of the prostate a rise in plasma testosterone concentration will result from an increased secretion of ACTH.

The study describes the effects of ACTH, prolactin and other protein hormones on the synthesis and secretion of steroid hormones by tissue from a feminising adrenocortical carcinoma removed from a post-menopausal female. Steroid production by the tissue was determined by high resolutionmass fragmentography and by radioimmunoassay. Prolactin and ACTH stimulated the synthesis of oestrogens by the tissue whereas GH, LH and ACTH were more effective than prolactin in stimulating androgen synthesis. The effect of protein hormones, other than ACTH, on adenylate cyclase activity of this tumour tissue indicated a lack of specificity of the membrane receptor sites.

Mean plasma cortisol levels were 314 and 553 μg/100ml 1 h after intramuscular hydrocortisone hemisuccinate 12.5 and 25 mg respectively, and significant levels were still present 10 h later. Half-life values in the period 2–8 h after injection range from 116 to 218 min with a mean of 147 min. Mean blood glucose increased by 12 mg/100 ml 2 h after injection.

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