Hyperinsulinemic Hypoglycemia with Nesidioblastosis after Gastric-Bypass Surgery

TLDR

Gastric bypass may increase beta‑cell trophic factors, leading to pancreatic islet hyperfunction without obesity. Six post‑Roux‑en‑Y gastric bypass patients with postprandial neuroglycopenia underwent selective arterial calcium‑stimulation testing to guide partial pancreatectomy. Histology revealed nesidioblastosis in all resected specimens, multiple insulinomas in one case, and post‑operative hypoglycemic symptoms resolved, despite no radiologic insulinoma evidence in most patients.

Abstract

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.