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Review
. 2016 Apr;26(4):874-81.
doi: 10.1007/s11695-016-2092-5.

Insulinoma After Bariatric Surgery: Diagnostic Dilemma and Therapeutic Approaches

Affiliations
Review

Insulinoma After Bariatric Surgery: Diagnostic Dilemma and Therapeutic Approaches

Christopher M Mulla et al. Obes Surg. 2016 Apr.

Abstract

Hypoglycemia is increasingly recognized as a complication of bariatric surgery. Typically, hypoglycemia does not appear immediately postoperatively, but rather more than 1 year later, and usually occurs 1-3 h after meals. While rare, insulinoma has been reported after bariatric surgery. Clinical factors which should raise suspicion for insulinoma and the need for comprehensive clinical and biochemical evaluation include hypoglycemia occurring in the fasting state, predating bariatric surgery, and/or worsening immediately postoperatively, and lack of response to conservative therapy. Localization and successful resection of insulinoma can be achieved using novel endoscopic ultrasound and surgical approaches. In summary, hypoglycemia presenting shortly after gastric bypass or with a dominant fasting pattern should be fully evaluated to exclude insulinoma. Additionally, evaluation prior to gastric bypass should include screening for history of hypoglycemia symptoms.

Keywords: Bariatric surgery; Gastric bypass; Hypoglycemia; Insulinoma; Minimally invasive surgery.

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Conflict of interest statement

CONFLICT OF INTEREST DISCLOSURE STATEMENT

Authors CMM, AS, EUY, DL, MSS, and AJM declare no conflict of interest. MEP reports grants from American Society for Metabolic and Bariatric Surgery, Medimmune, Nuclea Biosciences, Bristol-Myers Squibb, Astra-Zeneca, Novo-Nordisk Foundation, and Sanofi outside the submitted work. In addition, Dr. Patti has a submitted patent “Methods and Compositions for Treating Hypoglycemia.”

Figures

Figure 1
Figure 1
Suggested approach to evaluating hypoglycemia in otherwise healthy appearing individual with history of gastric surgery *Whipple’s triad includes:1) symptoms, 2) plasma glucose < 55 mg/dl, and 3) improvement of symptoms with normalization of blood glucose **Controlled portions of complex carbohydrates, adequate protein & healthy fats with micronutrient supplements
Figure 2
Figure 2
Endoscopic ultrasonography of the pancreas demonstrating the insulinoma. A. Ill-defined hypoechoic density within the pancreas parenchyma as seen on B-mode ultrasound. B. Image demonstrates contrast-enhanced harmonics and shows rapid uptake of Optison™ contrast (Perflutren Protein-Type A Microspheres Injectable Suspension) seen as multiple hyperechoic foci (marked with arrows) within the lesion. Washout of contrast leaves a hypoechoic lesion without defined borders. C. Computed tomography angiogram (pancreas protocol) demonstrates a subtle hyperattenuating 1.4 ×1.7 cm mass at the pancreatic body-tail junction. Labels: a: portal vein, b: pancreatic body, c: pancreatic tail. Arrow indicates mass. D. Intraoperative inspection of the pancreas. The puncture site on the pancreatic parenchyma from prior biopsy is indicated by the arrow. a: pancreatic body, b: pancreatic tail.
Figure 3
Figure 3
Histopathology of the resected pancreatic sample, including insulinoma (A–C), neuroendocrine microadenoma (D), and background pancreas (E–F). A. Well-differentiated, low grade neuroendocrine tumor showing a well-circumscribed nodule composed of nests of epithelioid cells within fibrous stroma (tumor on right, non-neoplastic pancreas on left), 20× magnification, H&E. B. 400× magnification, H&E. C. 400× magnification, insulin immunostain. D. Neuroendocrine microadenoma. Well-circumscribed nodular proliferation of neuroendocrine cells measuring up to 2.8 mm (right), 40× magnification, H&E. E. Islets showing some variability in distribution and size, 200× magnification, H&E. F. Synaptophysin immunostain, 200× magnification.
Figure 4
Figure 4
Frequency of hypoglycemia occurring in the fasting state, postprandial state, or both in patients with insulinoma discovered following gastric surgery.

References

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