Purpose of review To examine the recently recognized association between bariatric surgery-induced weight loss and postprandial hyperinsulinemic hypoglycemia. Recent findings Postprandial hypoglycemia following gastric bypass for obesity is generally considered a late manifestation of the dumping syndrome and can usually be managed with dietary modification. A rare syndrome characterized by more severe postprandial hypoglycemia and hyperinsulinemia, accompanied by diffuse pancreatic islet hyperplasia and expansion of beta-cell mass, however, has recently been identified. In our experience, the therapeutic approach to these patients is guided by the severity and frequency of hypoglycemia, and includes nutritional modification to reduce postprandial glycemic excursion and stepped medical management, including acarbose, octreotide and diazoxide. Other therapeutic agents previously used to inhibit insulin secretion or action, including calcium channel blockade, β-blockers and anticholinergics, have been minimally effective. For life-threatening hypoglycemia refractory to medical management, partial pancreatectomy may be necessary, but hypoglycemia has recurred in some patients. These findings suggest that gastric bypass-induced weight loss may unmask an underlying beta-cell defect or contribute to pathologic islet hyperplasia. Summary Severe postprandial hyperinsulinemic hypoglycemia may be regarded as a rare, late complication of bariatric surgery. Management of these patients may require nutritional, pharmacological and, on occasion, surgical intervention. The pathophysiology remains incompletely understood.
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Goldfine et al. (2006) studied this question.
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