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A 52 year old man is described in whom the simultaneous occurrence of isolated adrenocorticotrophin (ACTH) deficiency and primary hypothyroidism was documented by the determination of six anterior pituitary hormones by specific radioimmunoassays after suitable stimulations. The urinary 17-hydroxycorticosteroids excretion was persistently reduced and was increased by repeated ACTH injections. The low basal metabolic rate, reduced serum thyroid hormones and elevated serum thyrotrophic hormone were consistent with primary hypothyroidism. After resumption of euthyroidism, secretory reserves of growth hormone and ACTH were assessed. The growth hormone reponse to insulin-induced hypoglycaemic was normal. No rise in plasma cortisol and ACTH was observed following insulin-induced hypoglycaemia. Plasma ACTH was not augmented by iv infusion of metyrapone. The pathogenesis of two co-existent endocrine deficiencies was discussed.

Urinary excretion of 17-ketosteroids was measured during dexamethasone substitution followed by ACTH (Synacthen Depot, 1 mg daily) in 10 non-virilized adrenalectomized women. No significant changes could be demonstrated indicating ovarian androgenic dependence of ACTH in non-virilized females.

A patient with a thymic carcinoid tumour causing ectopic ACTH syndrome is presented. The case illustrates the rapid development of the clinical and laboratory findings often associated with ectopic secretion of ACTH, including severe proximal myopathy, emotional lability, and hypokalaemic alkalosis. Interpretation of conventional tests of pituitary-adrenal function was complicated by intermittent secretion of ACTH by the tumour. The results of selective venous sampling for ACTH ruled out pituitary ACTH hypersecretion and were suggestive of a thymic source; computerized tomography of the chest localized the tumour. In vivo and in vitro investigations confirmed excessive ACTH production by the tumour, and surgical resection plus radiotherapy has resulted in resolution of the syndrome. The diagnostic problems created by intermittent secretion of ACTH by these tumours and the pre-operative and post-operative medical management of these patients are discussed.

The mean basal plasma testosterone level in 28 patients with chromatin positive Klinefelter's syndrome was significantly lower than in 58 healthy male controls. In 12 of the patients the hormone levels were in the normal range. In both the eugonadal males and the Klinefelter patients the plasma testosterone levels spontaneously decreased throughout the day, the relative decrease in both groups being of the same order of magnitude. Short term ACTH infusion and the administration of dexamethasone did not significantly influence the plasma testosterone concentration in the Klinefelter patients. These findings do not support the view that the adrenal cortex plays a major role in contributing to the circulating plasma testosterone levels in this syndrome.