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Histological insights into the pathogenesis of post‐Roux‐en‐Y hyperinsulinaemic hypoglycaemia
Author(s) -
Lash R. W.,
Giordano T. J.,
Moraitis A. G.,
Hodish I.
Publication year - 2014
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/dme.12571
Subject(s) - medicine , pathogenesis , nesidioblastosis , hyperinsulinism , pancreatitis , gastroenterology , hypoglycemia , roux en y anastomosis , hyperplasia , diabetes mellitus , gastric bypass , pancreas , etiology , islet , histopathology , insulin , endocrinology , pathology , weight loss , obesity , insulin resistance
Background β‐cell hyperplasia has been implicated in the aetiology of post Roux‐en‐Y gastric bypass hyperinsulinaemic hypoglycaemia, but the pathogenesis of this condition is still unclear. Case report We report a case of a 52‐year‐old man with post‐Roux‐en‐Y gastric bypass hyperinsulinaemic hypoglycaemia who underwent distal pancreatectomy to alleviate his symptoms. Pancreatic histopathology showed chronic pancreatitis with a corresponding loss of exocrine tissue and islet retention. Amyloid deposition was found in pancreatic islets. These features are more typically associated with Type 2 diabetes. Discussion This case highlights the potential multifactorial pathogenesis of symptomatic hypoglycaemia after Roux‐en‐Y gastric bypass.