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In a 46 year old man, who arrived at our observation suffering for three months from considerable increasing weakness and progressive impairment of libido, we documented a condition of secondary hypocorticism due to an isolated ACTH deficiency associated with a reduced somatotropin reserve, the last improved after treatment with corticosteroids. We found low serum levels of ACTH and cortisol, good response of adrenal glands to corticotropin depot, normalization of the clinical board during glucocorticoid replacement. Stimulating test with CRH (corticotropin releasing hormone) did not cause a response in ACTH, suggesting the presence of primitive damage of the hypophyseal corticotroph cells.

A 34-year man was admitted to the hospital with symptoms of hypoglycemia. The endocrine investigations indicated adrenocortical insufficiency secondary to isolated ACTH deficiency: low ACTH and cortisol plasma levels, significant increase of cortisol following prolonged stimulation with depot tetracosactrin, normal secretory reserve of other anterior pituitary hormones. The absence of ACTH-response after corticotropin releasing hormone and insulin tolerance tests suggested a primary impairment of corticotropin cells.

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.