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Journal of Clinical Endocrinology & Metabolism, Vol 75, 536-539, Copyright © 1992 by Endocrine Society

ARTICLES

Corticoid-induced growth hormone (GH) secretion in GH-deficient and normal children

P Martul, J Pineda, C Dieguez and FF Casanueva
Pediatric Endocrinology Section, Hospital de Cruces, Spain.

Acute administration of corticoids is a potent stimulus of GH secretion in man. To ascertain their mechanism and point of action as well as the suitability of this novel test in the diagnosis of GH-deficient states, normal controls and GH-deficient children were studied. They were selected based on auxological criteria and the GH response to provocative stimuli. The GH-deficient children presented a blunted GH (mean +/- SEM; microgram/L) discharge after insulin-induced hypoglycemia (2.9 +/- 0.4), propranolol-exercise (7.4 +/- 1.5), and clonidine (6.5 +/- 0.8) compared with values in the normal children (7.2 +/- 2.2, 15.8 +/- 2.4, and 15.6 +/- 1.8, respectively). As expected, GH-releasing hormone (GHRH)-induced GH discharge in GH- deficient children (33.2 +/- 4.9) was similar to that in the control children (35.1 +/- 6.0). Administration of 2 mg/m2 body surface dexamethasone, iv, to normal children induced, 3 h later, a mean GH peak of 14.1 +/- 1.2 micrograms/L. This was significantly higher that the corticoid-induced GH peak in GH-deficient children (6.7 +/- 1.1 micrograms/L). The corticoid-induced areas under the secretory curve were 1130 +/- 55 and 616 +/- 54 for the control and GH-deficient children, respectively. GH release in children after dexamethasone administration followed the pattern previously described for adults, i.e. there were no modifications of basal GH levels in the first 2 h, the GH peak appeared around the third hour, and the GH levels remained increased until the fourth hour after dexamethasone administration. Individually considered, practically all control children, but only 2 of 12 GH-deficient children, presented a dexamethasone-induced GH peak over the 10 micrograms/L level. In both normal and GH-deficient patients, corticoids appeared just as potent a stimulus as propranolol- exercise and clonidine, and more potent than hypoglycemia. This new stimulus showed a pattern similar to that of the hypothalamic stimuli, but clearly different with respect to the pituitary one (GHRH), suggesting that corticoids activate GH secretion by acting at hypothalamic level. In conclusion, acute administration of corticoids could be a suitable test in the diagnostic armamentaria of GH-deficient states.


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