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Growth Horm IGF Res. 2016 Feb;26:8-10. doi: 10.1016/j.ghir.2015.11.004. Epub 2015 Nov 26.

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

Author information

1
Department of Internal Medicine, Division of Endocrinology, Saint Louis University School of Medicine, 1402 South Grand Blvd, St. Louis, MO 63104, United States. Electronic address: sureshchode@gmail.com.
2
Department of Internal Medicine, Division of Endocrinology, Saint Louis University School of Medicine, 1402 South Grand Blvd, St. Louis, MO 63104, United States.
3
Department of Biochemistry, Saint Louis University School of Medicine, 1402 South Grand Blvd, St. Louis, MO 63104, United States.
4
Department of Radiology, Division of Nuclear Medicine, Saint Louis University School of Medicine, 1402 South Grand Blvd, St. Louis, MO 63104, United States.

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 19.7×18.0×17.8cm retroperitoneal mass. A 3.25kg 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 17.5g/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.

KEYWORDS:

18-Fluorodeoxyglucose (FDG) positron emission tomography/computerized tomography (PET/CT) scan; Hypoglycemia; IGF-II; NICTH; Non-islet cell tumor hypoglycemia; Tumor induced hypoglycemia

PMID:
26774399
DOI:
10.1016/j.ghir.2015.11.004
[Indexed for MEDLINE]

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