Postprandial hypoglycemia in islet beta cell hyperplasia with adenomatosis of the pancreas

Joseph M. Tibaldi, Daniel Lorber, Steven Lomasky, J. J. Steinberg, Robert Reisman, Harry Shamoon

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Organic hyperinsulinism causing hypoglycemia in adults is caused by insulinoma, islet hyperplasia, or a combination of adenomata and hyperplasia. We present a patient with long‐standing symptoms of postprandial hypoglycemia occurring within 15 minutes of meals in the absence of fasting hypoglycemic symptoms. An intravenous glucagon stimulation test resulted in a rise of plasma insulin from 194 to 21,883 pmol/L at 7.5 minutes. Blood glucose simultaneously rose from 4.9 to 5.9 mmol/L. A glucose tolerance test revealed an exuberant insulin response. A euglycemic hyperinsulinemic clamp demonstrated incomplete suppression of plasma C‐peptide. At surgery, three nodules were found and a 50–60% distal pancreatectomy was performed. The pancreas revealed a combination of multiple β‐cell islet adenomata and islet hyperplasia with no evidence of nesidioblastosis. The coexistence of islet adenomata with hyperplasia must be considered in the differential diagnosis of postprandial hypoglycemia. © 1992 Wiley‐Liss, Inc.

Original languageEnglish (US)
Pages (from-to)53-57
Number of pages5
JournalJournal of Surgical Oncology
Volume50
Issue number1
DOIs
StatePublished - May 1992

Keywords

  • differential diagnosis
  • glucagon stimulation test
  • hyperinsulinemia
  • hyperinsulinemic clamp
  • hypoglycemia
  • pancreatectomy
  • pancreatic adenomatosis

ASJC Scopus subject areas

  • Surgery
  • Oncology

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