ISSN 1470-3947 (print)
ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology

Published by BioScientifica
Endocrine Abstracts (2003) 5 P243 
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Insulin sensitivity and hypoglycaemic susceptibility in children with endocrinopathies reflects the underlying hormone deficiency and treatment regimen

HC Johnstone, K Bartlett & TD Cheetham

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Introduction
Children with growth hormone (GH) deficiency and primary/secondary hypoadrenalism are susceptible to hypoglycaemia pre-treatment but little is known about insulin sensitivity and hypoglycaemic susceptibility post-diagnosis.
Methods
12 children (10.1 plus/minus 4.2y; mean plus/minus 1SD) with pituitary hormone deficiency (5 GHD, 7 GH/cortisol insufficient - GHCD) and 7 (8.2 plus/minus 3.8y) with congenital adrenal hyperplasia (CAH) were studied after obtaining ethical approval. Treatment was administered on one night with evening GH and/or morning hydrocortisone omitted on the other. Children fasted from 2200h. Blood glucose (BG) and insulin were measured from 0700 until 1200h. Insulin sensitivity was assessed using HOMA.
Results
There was no difference in age/BMI between groups. CAH patients received more hydrocortisone than the GHCD (12.2 vs 8.8 milligrams per meter 2; p=0.001). GH omission in children with PHD resulted in a lower BG at 0700h (4.1 plus/minus 6 vs 4.9 plus/minus 0.6 millimoles per litre; n=12, p=0.01) and during the morning after omission of hydrocortisone (n=7; p=0.01). GHCD children had lower BG concentrations than the GHD when medication was omitted (p=0.006). 3 of the 7 GHCD patients became hypoglycaemic (BG < 3.5 millimoles per litre). Omitting medication did not change BG or insulin sensitivity in CAH patients (logS% AUC 14.2 on v 14.1 off; p=0.92) in contrast to the GHCD (15.7 on v 19.8 off; p=0.003). There was no change in insulin sensitivity in those with GHD when GH was omitted (logS% AUC 14.7 v 15.7; p=0.23).
Conclusions
Omission of a single dose of GH and hydrocortisone in children with MPHD increases insulin sensitivity and susceptibility to hypoglycaemia in contrast to those with CAH. We suspect that this difference reflects the higher cortisol dose used to treat CAH and that the associated biochemical picture is a precursor of obesity and hypertension seen in later life in these patients.

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