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London Center for Pediatric Endocrinology and Metabolism, Great Ormond Street Hospital for Children, National Health Service Trust, London WC1N 3JH, United Kingdom; and Institute of Child Health, University College London, London WC1N 1EH, United Kingdom
Address all correspondence and requests for reprints to: Dr. K. Hussain, Department of Biochemistry, Endocrinology, and Metabolism, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, United Kingdom. E-mail: k.hussain{at}ich.ucl.ac.uk.
Hypoglycemia is a potent stimulus for GH and cortisol secretion. The insulin tolerance test (ITT) is the gold standard for assessing GH and cortisol responses from the hypothalamic-pituitary-adrenal axis. The serum GH and cortisol responses to spontaneous hypoglycemia in 22 children were compared with those of 16 children undergoing an ITT for diagnostic purposes. The mean serum GH and cortisol concentrations 1 h before spontaneous hypoglycemia were 6.9 ± 1.1 mU/liter and 424 ± 51 nmol/liter, respectively, and at the time of spontaneous hypoglycemia they were 6.7 ± 1.3 mU/liter and 601 ± 66 nmol/liter, respectively. The mean serum GH and cortisol values at +10, +20, +30, +40, and +50 min from the time of hypoglycemia were 5.4 ± 1.0, 4.7 ± 0.7, 4.6 ± 1.0, 5.4 ± 1.4, and 5.5 ± 1.3 mU/liter and 633 ± 69, 645 ± 71, 668 ± 70, 680 ± 72, and 662 ± 77 nmol/liter, respectively. There was no significant difference between any of these means for GH secretion. In contrast, in the ITT the mean serum GH concentration before hypoglycemia was 5.1 ± 1.3 mU/liter, and at the time of hypoglycemia it was 29.2 ± 7.30 mU/liter. The difference between these means was highly significant (P < 0.01, by t test). There was no significant difference between the cortisol response to spontaneous hypoglycemia and that to the ITT. Physiological changes in the serum nonesterified fatty acid concentration had no significant effect on serum GH secretion. In conclusion, the mechanism(s) of the serum GH response to spontaneous hypoglycemia is different from that due to the ITT. A low GH level detected at the time of spontaneous hypoglycemia does not necessarily imply GH deficiency or GH as a cause of the hypoglycemia.
Some of this work was undertaken by Great Ormond Street Hospital for Children National Health Service Trust, which received a proportion of its funding from the National Health Service Executive. The views expressed in this publication are those of the authors and are not necessarily those of the National Health Service Executive.
Abbreviations: CoA, Coenzyme A; HI, hyperinsulinism of infancy; ITT, insulin tolerance test; NEFA, nonesterified fatty acid; SS, somatostatin.
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