Hyperinsulinemic Hypoglycemia with Nesidioblastosis after Gastric-Bypass Surgery
Geoffrey J. Service, Geoffrey B. Thompson, F. John Service, James C. Andrews, Maria L. Collazo–Clavell, Ricardo V. Lloyd
Abstract
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Geoffrey J. Service, Geoffrey B. Thompson, F. John Service, James C. Andrews, Maria L. Collazo–Clavell, Ricardo V. Lloyd
Abstract
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We describe six patients (five women and one man; median age, 47 years; range, 39 to 54) with postprandial symptoms of neuroglycopenia owing to endogenous hyperinsulinemic hypoglycemia after Roux-en-Y gastric bypass surgery. Except for equivocal evidence in one patient, there was no radiologic evidence of insulinoma. Selective arterial calcium-stimulation tests, positive in each patient, were used to guide partial pancreatectomy. Nesidioblastosis was identified in resected specimens from each patient, and multiple insulinomas were identified in one. Hypoglycemic symptoms diminished postoperatively. We speculate that hyperfunction of pancreatic islets did not lead to obesity but that beta-cell trophic factors may have increased as a result of gastric bypass.
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We describe six patients (five women and one man; median age, 47 years; range, 39 to 54) with postprandial symptoms of neuroglycopenia owing to endogenous hyperinsulinemic hypoglycemia after Roux-en-Y gastric bypass surgery. Except for equivocal evidence in one patient, there was no radiologic evidence of insulinoma. Selective arterial calcium-stimulation tests, positive in each patient, were used to guide partial pancreatectomy. Nesidioblastosis was identified in resected specimens from each patient, and multiple insulinomas were identified in one. Hypoglycemic symptoms diminished postoperatively. We speculate that hyperfunction of pancreatic islets did not lead to obesity but that beta-cell trophic factors may have increased as a result of gastric bypass.
Key concepts: Nesidioblastosis, Medicine, Hyperinsulinemic hypoglycemia, Gastric bypass surgery, Insulinoma, Hypoglycemia, Hyperinsulinemia, Hyperinsulinism