ESPE Abstracts (2016) 86 P-P1-556

ESPE2016 Poster Presentations Perinatal Endocrinology P1 (24 abstracts)

Pancreatic Glucagon Secretion is Severely Impaired and Somatostatin Secretion Unchanged in Patients with Hyperinsulinaemic Hypoglycaemia

Pratik Shah a, , Sofia Rahman a , Clare Gilbert b , Kate Morgan b , Louise Hinchey b , Paul Bech c , Rakesh Amin a, & Khalid Hussain a,


aUCL Institute of Child Health, London, UK; bGreat Ormond Street Hospital for Children, London, UK; cGut Hormone Laboratory, Imperial College London, London, UK

Background: Hyperinsulinaemic hypoglycaemia (HH) is a common cause of hypoglycaemia in children. Glucagon is an important counter-regulatory hormone and the role of somatostatin is not known in children with HH.

Objective and hypotheses: To understand the roles of glucagon and somatostatin in children with HH.

Method: Children admitted for management of HH in our hospital were included in the study. Plasma insulin, glucagon and somatostatin were collected at the start and end of the fast or at the time of hypoglycaemia. Glucagon and somatostatin were measured by radioimmunoassay. Descriptive statistics mean, S.D. and three quartiles (Q1, Q2 and Q3) were obtained to check normality assumptions for patients with HH and control group respectively.

Results: There were 26 children with HH and seven children as controls included in the study. Both mean and median were different and hence 50th centile (Q2 or median) is considered for calculation. Among HH patients, median insulin concentration was significantly increased at the start of fast compared to end of fast (P value = 0.001). There was no significant change in glucagon and somatostatin concentration at the start and at the end of the fast (at the time of hypoglycaemia) (P value > 0.05). Among control group, median insulin concentration was significantly decreased and glucagon concentration was significantly increased (P value < 0.05) at the end of the fast respectively. However, there was no significant change in somatostatin concentration at the start and end of the fast (P value > 0.05).

Conclusion: This study suggests that in HH glucagon secretion is severely impaired from the alpha-cell whereas somatostatin secretion from the delta-cell is unaffected. The mechanisms that lead to impaired glucagon secretion in HH are unknown. Somatostatin does not seem to have any significant role as a glucoregulatory hormone in patients with HH.

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