Surgical Endoscopy

, Volume 24, Issue 10, pp 2547-2555

First online:

Management of postgastric bypass noninsulinoma pancreatogenous hypoglycemia

  • Viney K. MathavanAffiliated withDepartment of Surgery, St Vincent Hospital Email author 
  • , Maurice ArreguiAffiliated withDepartment of Surgery, St Vincent Hospital
  • , Chad DavisAffiliated withDepartment of Surgery, St Vincent Hospital
  • , Kirpal SinghAffiliated withDepartment of Surgery, St Vincent Hospital
  • , Anand PatelAffiliated withDepartment of Surgery, St Vincent Hospital
  • , James MeachamAffiliated withClarian Diabetes and Endocrinology

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Postgastric bypass noninsulinoma hyperinsulinemic pancreatogenous hypoglycemia defines a group of patients with postprandial neuroglycopenic symptoms similar to insulinoma but in many cases more severe. There are few reports of patients with this condition. We describe our surgical experience for the management of this rare condition.


A retrospective study was performed at St. Vincent Hospital, Indianapolis. Fifteen patients were identified with symptomatic postgastric bypass hypoglycemia for the period 2004–2008. All patients were initially treated with medical therapy for hypoglycemia. Nine patients eventually underwent surgical treatment. The preoperative workup included triple-phase contrast CT scan of the abdomen, endoscopic ultrasound of the pancreas, a 72-h fast followed by a mixed meal test, and calcium-stimulated selective arteriography. Intraoperative pancreatic ultrasound also was performed in all patients. Patients then underwent thorough abdominal exploration, exploration of the entire pancreas, and extended distal pancreatectomy.


Nine patients underwent surgery. The mean duration of symptoms was 14 months. The 72-h fast was negative in eight patients (as expected). Triple-phase contrast CT scan of the abdomen was negative in eight patients and showed a cyst in the head of pancreas in one patient. Extended distal (80%) pancreatectomy was performed in all nine patients. The procedure was attempted laparoscopically in eight patients but was converted to open in three. One patient had an open procedure from start to finish. Pathology showed changes compatible with nesidioblastosis with varying degrees of hyperplasia of islets and islet cells. Follow-up ranged from 8–54 (median, 22) months. All patients initially reported marked relief of symptoms. Over time, two patients had complete resolution of symptoms; three patients developed occasional symptoms (once or twice per month), which did not require any medication; two patients developed more frequent symptoms (more than twice per month), which were controlled with medications; and two patients had severe symptoms refractory to medical therapy (calcium channel blockers, diazoxide, octreotide).


Postprandial hypoglycemia after gastric bypass surgery with endogenous hyperinsulinemia is being increasingly recognized and reported in the literature. Our experience with nine patients is one of the largest. The etiology of this condition is not entirely understood. There may be yet unknown factors involved but increased secretion of glucagon-like peptide 1 and decreased grehlin are being implicated in islet cell hypertrophy. There is no “gold standard” treatment—medical or surgical—but distal pancreatectomy to debulk the hypertrophic islets and islet cells is the main surgical modality in patients with severe symptoms refractory to medical management.


Islet cell hyperplasia Nesidioblastosis Postgastric bypass Noninsulinoma pancreatogenous hypoglycemia