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EFFECT OF SOMATOSTATIN INFUSION ON INTERMEDIARY METABOLISM AND ENTERO‐INSULAR HORMONE RELEASE IN INFANTS WITH HYPERINSULINAEMIC HYPOGLYCAEMIA
Author(s) -
AYNSLEYGREEN A.,
BARNES N. D.,
ADRIAN T. E.,
KINGSTON J.,
BOYES S.,
BLOOM S. R.
Publication year - 1981
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.1981.tb06246.x
Subject(s) - somatostatin , medicine , endocrinology , motilin , hyperinsulinism , pancreatic polypeptide , secretin , gastric inhibitory polypeptide , insulin , hormone , glucagon , peptide hormone , pancreas , insulin resistance
. Aynsley‐Green, A., Barnes, N. D., Adrian, T. E., Kingston, J., Boyes, S., and Bloom, S. R. (University Department of Paediatrics, John Radcliffe Hospital, Oxford, Department of Paediatrics, New Addenbrookes Hospital, Cambridge, and Department of Medicine, Hammersmith Hospital, London, England). Effect of somatostatin infusion on intermediary metabolism and enteroinsular hormone release in infants with hyperinsulinaemic hypoglycaemia. Acta Paediatr Scand, 70: 889, 1981.‐The hypoglycaemia of infantile hyper‐insulinism is often exceedingly difficult to control. The use of somatostatin has been advocated recently in such infants because of its effect on inhibiting insulin release, but nothing is known of the wider effects of this potent hormone in the young child. Two infants presenting at 9 weeks and 5 days of age with severe hyperinsulinaemic hypoglycaemia were studied during an infusion of somatostatin. In both infants normoglycaemia was restored with suppression of insulin secretion. An increase in blood ketone bodies occurred, but no change was seen in blood pyruvate, lactate or alanine concentrations. The plasma concentrations of glucagon, Cortisol, growth hormone, motilin.‐pancreatic polypeptide, gastric inhibitory polypeptide, neurotensin, gastrin and vasoactive intestinal peptide decreased markedly during the somatostatin infusion. No consistent change occurred in plasma enteroglucagon or secretin values. We conclude that somatostatin effectively suppresses abnormal insulin secretion in infants, but it has profound effects on the release of nine other hormones. Further studies are needed to define the consequences of suppressing the release of these hormones before somatostatin can be used routinely in the management of infantile hyperinsulinism.