[HTML][HTML] Severe hypoglycaemia post-gastric bypass requiring partial pancreatectomy: evidence for inappropriate insulin secretion and pancreatic islet hyperplasia
Diabetologia, 2005•Springer
Aims/hypothesis Postprandial hypoglycaemia following gastric bypass for obesity is
considered a late manifestation of the dumping syndrome and can usually be managed with
dietary modification. We investigated three patients with severe postprandial hypoglycaemia
and hyperinsulinaemia unresponsive to diet, octreotide and diazoxide with the aim of
elucidating the pathological mechanisms involved. Methods Glucose, insulin, and C-peptide
were measured in the fasting and postprandial state, and insulin secretion was assessed …
considered a late manifestation of the dumping syndrome and can usually be managed with
dietary modification. We investigated three patients with severe postprandial hypoglycaemia
and hyperinsulinaemia unresponsive to diet, octreotide and diazoxide with the aim of
elucidating the pathological mechanisms involved. Methods Glucose, insulin, and C-peptide
were measured in the fasting and postprandial state, and insulin secretion was assessed …
Aims/hypothesis
Postprandial hypoglycaemia following gastric bypass for obesity is considered a late manifestation of the dumping syndrome and can usually be managed with dietary modification. We investigated three patients with severe postprandial hypoglycaemia and hyperinsulinaemia unresponsive to diet, octreotide and diazoxide with the aim of elucidating the pathological mechanisms involved.
Methods
Glucose, insulin, and C-peptide were measured in the fasting and postprandial state, and insulin secretion was assessed following selective intra-arterial calcium injection. Pancreas histopathology was assessed in all three patients.
Results
All three patients had evidence of severe postprandial hyperinsulinaemia and hypoglycaemia. In one patient, reversal of gastric bypass was ineffective in reversing hypoglycaemia. All three patients ultimately required partial pancreatectomy for control of neuroglycopenia; pancreas pathology of all patients revealed diffuse islet hyperplasia and expansion of beta cell mass.
Conclusions/interpretation
These findings suggest that gastric bypass-induced weight loss may unmask an underlying beta cell defect or contribute to pathological islet hyperplasia, perhaps via glucagon-like peptide 1-mediated pathways.
Springer