Session: FP09-Obesity: Physiologic Responses to Energy Balance Disruption
Bench to Bedside
Room 307 (Moscone Center)
Poster Board SAT-662
Clinical case: Two patients with post-RYGB hypoglycemia were enrolled in the study. One patient is a 35-year woman who developed postprandial hypoglycemia 2 years after the RYGB with one episode of seizure. After failing dietary modification, she underwent RYGB reversal. The second patient is a 62-year woman who developed postprandial hypoglycemia 1 year after the RYGB including two episodes with loss of consciousness. Subsequent endocrine evaluation included normal 72-hour fast and measurement of hormones during an episode of postprandial hypoglycemia showing a glucose of 48 mg/dl with concurrent serum insulin of 43.2 μIU/ml (<29.1 normal) and C-peptide 13.6 ng/ml (1.1-5 normal) consistent with inappropriate endogenous insulin production. CT of abdomen and intra-arterial calcium gluconate stimulation test showed no evidence of localized insulin production within the pancreas. Severe hypoglycemia persisted despite dietary modifications and pharmacologic intervention with octreotide and acarbose. Therefore, she underwent distal pancreatectomy 3 years after her RYGB with no histologic evidence of insulinoma or nesdioblastosis. Given persistent hypoglycemia, she underwent RYGB reversal 5 years after her RYGB. Both patients underwent standardized meal tolerance test (MTT) prior to and 8-18 months after RYGB reversal with measurement of glucagon-like-peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), insulin and glucose concentrations. Both subjects showed persistent evidence of hypoglycemia with marked hyperinsulinemia after the RYGB reversal. GLP-1 concentrations decreased by 76% and 70%, respectively, compared to the concentration of nonhypoglycemic post-RYGB controls. In contrast, GIP concentrations increased after the RYGB reversal in both patients (3 and10-fold the pre-reversal concentrations). Clinical improvement was variable after the reversal of RYGB.
Conclusions: Reversal of RYGB did not alleviate hyperinsulinemic hypoglycemia upon mixed meal challenge in both of our patients thus suggesting its limited clinical benefit as treatment of post-RYGB hypoglycemia. The marked increase in GIP concentrations and concurrent decrease in GLP-1 concentrations in both of our patients suggest the role of GIP in persistent hyperinsulinemic hypoglycemia after the reversal of RYGB.
Nothing to Disclose: CJEL, TTB, OC, JME, DE
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