Hypoglycemia pathogenesis in children with dumping syndrome.Pediatrics. 1987 Dec; 80(6):937-42.Ped
Three children with severe hypoglycemic reactions secondary to dumping syndrome were studied to discern the mechanism by which hypoglycemia occurred. Symptoms in patient 1 developed after fundoplication, generalized autonomic dysfunction occurred in patient 2, and dumping syndrome developed in patient 3 after malplacement of a feeding gastrostomy tube. Average blood glucose levels studied during and after two to seven meals in each child were 375 +/- 97 mg/dL (mean +/- SD) 30 minutes postprandially and 35 +/- 10 mg/dL greater than 120 minutes later. Swings in glucose values were proportional to the volume of meals. Insulin and glucagon levels were followed during a single meal challenge test in each patient; the average glucose concentration increased to 356 +/- 59 mg/dL 30 minutes postprandially and decreased to 32 +/- 11 mg/dL at 150 +/- 30 minutes. Hormonal analyses indicated (1) inappropriate early release of glucagon (300 pg/mL at 15 minutes) in patient 1, (2) exuberant early release of insulin (maximum 190 +/- 15 microU/mL) resulting in rapid decrease in glucose concentration in all patients, (3) development and/or persistence of hypoglycemia after the decline in circulating insulin to undetectable levels, and (4) inadequate glucagon response to hypoglycemia resulting in sustained hypoglycemia. These data indicate that gross disturbances of the insulin-glucagon axis attend childhood dumping syndrome.