Severe hypoglycaemia post-gastric bypass requiring partial pancreatectomy: evidence for inappropriate insulin secretion and pancreatic islet hyperplasia

TY - JOUR

T1 - Severe hypoglycaemia post-gastric bypass requiring partial pancreatectomy

T2 - evidence for inappropriate insulin secretion and pancreatic islet hyperplasia

AU - Patti, M E

AU - McMahon, G

AU - Mun, E C

AU - Bitton, A

AU - Holst, Jens Juul

AU - Goldsmith, J

AU - Hanto, D W

AU - Callery, M

AU - Arky, R

AU - Nose, V

AU - Bonner-Weir, S

AU - Goldfine, A B

PY - 2005/11

Y1 - 2005/11

N2 - 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.

AB - 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.

KW - Adult

KW - Aged

KW - Diazoxide

KW - Diet Therapy

KW - Dumping Syndrome

KW - Female

KW - Gastric Bypass

KW - Humans

KW - Hyperplasia

KW - Hypoglycemia

KW - Insulin

KW - Islets of Langerhans

KW - Male

KW - Middle Aged

KW - Octreotide

KW - Pancreas

KW - Pancreatectomy

U2 - 10.1007/s00125-005-1933-x

DO - 10.1007/s00125-005-1933-x

M3 - Journal article

C2 - 16195867

SN - 0012-186X

VL - 48

SP - 2236

EP - 2240

JO - Diabetologia

JF - Diabetologia

IS - 11

ER -