Management of Post Gastric Bypass Noninsulinoma Pancreatogenous Hypoglycemia (nesidioblastosis)

Introduction: Post gastric bypass hyperinsulinemic 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. The primary surgical therapy is distal or subtotal pancreatectomy. Here we describe our surgical experience for the management of this rare condition.

Materials and methods: A retrospective study was done at tertiary care center. 15 patients were identified with symptomatic post gastric bypass hypoglycemia between 2004-2008. All patients were initially treated with maximal medical therapy for hypoglycemia. Nine refractory patients eventually underwent surgical treatment. The preoperative workup included triple-phase contrast islet cell protocol CT scan of abdomen, endoscopic ultrasound of pancreas, 72-hr fast, and calcium stimulated selective arteriography. Splenic, gastroduodenal, superior mesenteric and hepatic arteries were selectively cannulated and serial sampling for insulin level was done from hepatic vein. At surgery, intraoperative ultrasound was also performed. Patients then underwent thorough abdominal exploration, lysis of adhesions, exploration of the whole pancreas and extended distal pancreatectomy.

Results: Nine patients underwent surgery. Eight were female and one was male. The age range was from 28 to 62 years. The median age was 33 years. The onset of symptoms ranged from 1 month after Roux-en-Y gastric bypass to 4.5 years. The mean duration of symptoms was 14 months. Symptoms were those of severe neuroglycopenia and included dizziness, shakiness, confusion, syncope and blurring of vision. The 72-hr fast was negative in 7 patients (as expected). It was positive in 2 patients. Triple-phase contrast CT scan of the abdomen was negative in all patients. Endoscopic ultrasound showed 1 cm lesion in head of pancreas in one patient. The final pathology on that was mucinous cystadenoma (which was present in addition to nesidioblastosis). Calcium-stimulated arteriography showed elevated insulin secretion with stimulation of splenic and gastroduodenal arteries. Some patients showed elevated insulin on stimulation of SMA also, in addition to above indicating more diffuse involvement of the pancreas. Extended distal (80%) pancreatectomy was performed in all nine patients. The spleen was spared in seven patients. The procedure was done laparoscopically in 8 patients, but converted to open in three. One patient had an open procedure from start to finish. Three patients had pancreatic leak, which was managed with drain. Pathology showed islet cell hyperplasia consistent with nesidioblastosis with varying degrees of hyperplasia of islet cells. No insulinoma was identified in any patient.

Follow-up: Follow-up ranged from 2 – 48 months (median 24 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 a month) not requiring any medication; three patients developed more frequent symptoms (more than twice a month), controlled with medications; and one patient had severe symptoms refractory to maximal medical therapy (calcium channel blockers, diazoxide, octreotide). She underwent repeat preoperative work-up evaluation and subsequently underwent near total (95%) pancreatectomy with marked, but not complete, resolution of symptoms.

Discussion: Postprandial hypoglycemia after gastric bypass surgery with endogenous hyperinsulinemia is being increasingly recognized. It is associated with diffuse hyperplasia of islet cells but the exact cause is not understood. It must be distinuished from insulinoma. Various diagnostic tests aim to differentiate between the two. Sometimes they can coexist, as reported in some case reports. There are very few series and some case reports noted in the literature about post gastric bypass hyperinsulinemic hypoglycemia. Our present series will be one of the largest after the Mayo Clinic series. 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 for islet cell hypertrophy. There is no gold standard treatment but varying degrees of pancreatectomy to debulk the islet cells is the main surgical modality.

Session: Podium Presentation

Program Number: S010

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