Alimentary hypoglycemia associated with the Zollinger-Ellison syndrome

Abstract

The patient described had clinical and laboratory evidence of Zollinger-Ellison syndrome, hyperparathyroidism and reactive hypoglycemia. From the findings of an “endocrine-like” tumor in the duodenal wall (with diminished plasma gastrin levels after its resection) and chief cell hyperplasia of the parathyroids, she was considered to have multiple endocrine adenomatosis. Excessive insulin release coincided with peak glucose concentrations in plasma after the oral administration of glucose with hypoglycemic episodes at two to three hours. The presence of a pancreatic neoplasm or hyperplasia as a cause of the hyperinsulinism in this patient with multiple endocrine adenomatosis was excluded by normal beta cell responses to the intravenous administration of glucose, tolbutamide and glucagon and the absence of pancreatic disease at laparotomy. The exaggerated insulin secretion and hypoglycemia were attenuated by the intragastric administration of sodium bicarbonate and the oral administration of methscopolamine bromide, both of which delay gastric emptying. Although the factors responsible for the hyperinsulinism cannot be absolutely resolved, from the excessive acid production and hypergastrinemia in this patient, it is inferred that increased gastric emptying may have contributed significantly to her alimentary hypoglycemia. The possible roles of enteric hormones in the postprandial hypoglycemia in this patient are discussed.