2009 Southern Regional Meeting Abstracts
Session: Joint Plenary Poster Session and Reception
Noninsulinoma Pancreatogenous Hyperinsulinemic Hypoglycemia Syndrome in an 18 year old post Gastric Bypass Surgery
Patel S1, Koch C1, Asnani S2. 1University of Mississippi Medical Center, Jackson, MS and 2Jersey Shore University Medical Center, Neptune, NJ.
Case Report: Background: The pandemic of obesity includes teenagers and the pediatric age group as well. Behavioral modification and pharmacotherapy produces modest long term benefits. Gastric bypass surgery is emerging as an alternative treatment for weight loss. Rapid weight loss post gastric bypass surgery has been associated with noninsulinoma pancreatogenous hyperinsulinemic hypoglycemia syndrome due to neo-differentiation of islets of Langerhans. Objective : To illustrate a potentially deadly side effect, hypoglycemia resulting from nesidioblastosis, of/after gastric bypass surgery in an 18-yo obese girl. Case Report: An 18-yo girl with recurrent symptoms of postprandial neuroglycopenia, which could not be controlled with lifestyle modifications. She had history of morbid obesity status post Roux-en-Y gastric bypass surgery and 160 lbs weight loss in 10 months (BMI 48 to 24 kg/m2). After non diagnostic 72 hr fast results, she underwent a mixed meal study with a nadir glucose of 30 mg/dL at 120 min associated with neuroglycopenic symptoms. Concomitant serum insulin was 11 uU/ml and C-peptide 4.3 ng/mL. Helical CT abdomen showed no pancreatic mass. A calcium stimulation test suggested abnormality in splenic artery distribution. She underwent distal pancreatectomy & splenectomy with successful resolution of her hypoglycemic symptoms. Path results confirmed nesidioblastosis showing islet cell hypertrophy. Discussion: To our knowledge, we present here the youngest case of gastric bypass surgery associated with nesidioblastosis. Altered GI transit stimulates gut hormones, notably GLP-1. GLP-1 mediates beta cell neogenesis and proliferation while inhibiting apoptosis. Longterm stimulation of beta cell growth may be involved in the pathogenesis of this disorder. GLP-1 receptor agonist, exenatide, and DPP-IV inhibitor sitagliptin are both approved by the FDA for management of type 2 diabetes. Patients treated with these agents need to be monitored for potential risks of longterm beta cell stimulation which may result in autonomy and inappropriately high insulin levels. Caution is also recommended when treating children with pharmacotherapy and surgery for obesity.
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