Spontaneous Hypoglycemia in Childhood Is Accompanied by Paradoxically Low Serum Growth Hormone and Appropriate Cortisol Counterregulatory Hormonal Responses
Author(s) -
Khalid Hussain,
Peter C. Hindmarsh,
A AynsleyGreen
Publication year - 2003
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2003-030137
Subject(s) - hormone , endocrinology , hypoglycemia , medicine , hydrocortisone , growth hormone , insulin
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.
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