Estimation of glucose utilization in a type 2 diabetes mellitus patient on insulin analogs with tumor hypoglycemia induced by IGF-II

• Published in: Growth hormone & IGF research Vol. 26; pp. 8 - 10
• Main Authors: Chode, Suresh, Albert, Stewart G, Shoemaker, James D, Green, Aileen L
• Format: Journal Article
• Language: English
• Published: Scotland Elsevier Ltd 01.02.2016
• Subjects: 18-Fluorodeoxyglucose (FDG) positron emission tomography/computerized tomography (PET/CT) scan; Adult; Advanced Basic Science; Diabetes Mellitus, Type 2 - drug therapy; Diabetes Mellitus, Type 2 - metabolism; Endocrinology & Metabolism; Glucose - pharmacokinetics; Humans; Hypoglycemia; Hypoglycemia - etiology; Hypoglycemia - metabolism; Hypoglycemic Agents - therapeutic use; IGF-II; Insulin - analogs & derivatives; Insulin-Like Growth Factor II - adverse effects; Insulin-Like Growth Factor II - secretion; Male; NICTH; Non-islet cell tumor hypoglycemia; Retroperitoneal Neoplasms - complications; Retroperitoneal Neoplasms - metabolism; Tumor induced hypoglycemia; Tumor induced hypoglycemia; NICTH; Non-islet cell tumor hypoglycemia; Hypoglycemia; 18-Fluorodeoxyglucose (FDG) positron emission tomography/computerized tomography (PET/CT) scan; IGF-II
• ISSN: 1096-6374; 1532-2238
• DOI: 10.1016/j.ghir.2015.11.004

Abstract We present a 38-year-old male patient with insulin requiring type 2 diabetes mellitus (DM) who had fasting hypoglycemia caused by a non-pancreatic-islet-cell mesenchymal tumor producing IGF-II. The evaluation was confounded in that there was pre-existing DM being treated with insulin analogs. Insulin levels were assessed with an immunoassay with cross reactivity with the insulin analogs. An 18-Fluorodeoxyglucose (FDG) positron emission tomography/computerized tomography (PET/CT) scan localized the 19.7 × 18.0 × 17.8 cm retroperitoneal mass. A 3.25 kg tumor was resected. Post-operatively insulin treatment was resumed and circulating IGF-II levels returned to normal. The maximum standardized uptake values of FDG (SUVmax ) along with a steady state glucose infusion of 17.5 g/h were used to determine the components of glucose utilization due to IGF-II induced muscle glucose uptake (utilization, 62%) whereas the tumor itself was responsible for approximately 22% of measurable glucose uptake. Whereas tumor induced hypoglycemia has been ascribed to preferential glucose utilization by the tumor, the predominant hypoglycemic effect was due to hormonal IGF-II induced total body glucose uptake.