Glucocorticoids (GC) have stimulatory effects on GH secretion in vitro and suppressive effects when administered in pharmacological amounts in vivo. We studied six patients with ACTH deficiency and severely impaired serum GH responses to insulin tolerance tests and arginine infusion tests. All patients underwent the same tests during GC replacement while receiving cortisone acetate in doses ranging from 12.5-25 mg/day. The three patients with idiopathic ACTH deficiency and no evidence of pituitary mass lesions had impaired GH secretion, which returned to normal during GC replacement. In contrast, the three patients with ACTH deficiency and hypothalamo-pituitary mass lesions detected by a computed tomography scan had impaired GH secretion during GC replacement therapy. Our data indicate that in patients with idiopathic ACTH deficiency, an impaired GH response to stimuli reversible during GC replacement therapy may be the functional consequence of the low levels of circulating cortisol. We conclude that physiological serum cortisol levels are necessary for normal serum GH responses to provocative stimuli in man.
A 45-year-old man with type I diabetes mellitus of 25-yr duration and well controlled by conventional insulin therapy developed an isolated adrenocorticotropic hormone (ACTH) deficiency. He presented with a 3-month history of weight loss, weakness, anorexia and persistent tendency to hypoglycemia that he had never experienced before. Basal and dynamic endocrine testing disclosed absent cortisol secretion caused by an isolated ACTH deficiency due to a primary pituitary defect. Corticosteroid replacement therapy allowed again a good glycometabolic control. The possible causes of hypoglycemia in insulin-treated diabetes and the pathogenetic basis of the reported association are discussed.
We examined the effects of the acute administration of salmon calcitonin on phosphate metabolism in tumoral calcinosis. On two different days, 200 MRC U of the synthetic hormone were administered sc to a 38-year-old patient, either as twice daily 100 MRC U injections, or as a continuous sc infusion via a portable pump. Both ways of calcitonin administration elicited a phosphaturic effect and a lowering of serum phosphate level comparable with that observed after an iv infusion of calcitonin. 1,25 dihydroxyvitamin D level, which was in the normal range during a control study, increased after calcitonin administration. In our patient, long term therapy with diet, a phosphate-binding agent and calcitonin prevented the occurrence of new ectopic calcifications. Owing to its phosphaturic activity, synthetic salmon calcitonin may be a useful adjunct to diet and aluminium-containing antacids in long-term management of tumoral calcinosis.
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