Endocrine Abstracts

Introduction: Hyperinsulinaemic hypoglycaemia (HH) is characterized by dysregulated insulin secretion and is typically associated with reduced fasting tolerance. We aimed to evaluate the clinical and biochemical characteristics of children presenting with postprandial hyperinsulinaemic hypoglycemia.

Methods: Retrospective data collection on children who presented with symptomatic postprandial hypoglycaemia. Children with postprandial hypoglycaemia secondary to gastrointestinal surgery (such as dumping syndrome) were excluded. Prolonged OGTT was performed as per standard protocol.

Results: We identified six children with a mean age of 6.08 (±2.01) years who presented with symptomatic hypoglycemia occurring typically within 2-3 hours after a meal. The symptoms included lethargy, tiredness, hunger and shakiness. In one child seizures were noted during the hypoglycaemic episode. The family history included type two diabetes in two families, postprandial hypoglycaemia in one family and type one diabetes in another family. All children had a normal fast tolerance for age with a mean fast duration of 17.8 (±1.78) hours and appropriately suppressed insulin levels at the end of the fast (< 2 mU/l). All children were noted to mobilize fatty acids at the end of the fast and also demonstrated normal glucocorticoid response. Metabolic screening did not reveal any abnormality. Prolonged OGTT revealed HH (mean blood glucose 2.78 mmol/l and mean insulin concentration 6.95 mU/l) occurring at an average time length of 170 (±36.3) minutes after the glucose load. Treatment with acarbose was noted to be beneficial in three children, diazoxide improved the glycaemic control in one child and two children were managed with frequent feeds.

Conclusion: We describe a group of children with symptomatic postprandial hypoglycaemia who demonstrated HH between 2-3 hours post glucose load. Prolonged OGTT is necessary to identify these episodes. Acarbose is beneficial in children with postprandial HH who do not respond to dietary modification. Further research is required to understand the molecular basis of this postprandial HH.