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Department of Internal Medicine, Chair of Patologia Speciale Medica, University of Brescia 25125 Brescia, Italy
Address all correspondence and requests for reprints to: Andrea Giustina, M.D., Cattedra di Patologia Speciale Medica, c/o II Divisione di Medicina Generale-Spedali Civili di Brescia, Piazzale Spedali Civili 1, 25125 Brescia, Italy.
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. Incontrast, the three patients with ACTH deficiency and hypothalamo- pituitary mass lesions detectedby 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 levelsof circulating cortisol. We conclude that physiological serum cortisol levels are necessary for normal serum GH responses to provocative stimuli in man.
Received April 21, 1988.
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