When Hyperinsulinemia Is Not Insulinoma: A Case of Recurrent Post-Prandial Hypoglycemia Following Roux-en-Y Gastric Bypass Surgery

Abstract

Introduction: Roux-en-Y gastric bypass (RYGB) surgery is currently one of the most popular procedures to aid weight loss. Recently, hypoglycemia associated with gastric bypass surgery has been described as a potential complication. We present a case of refractory hypoglycemia after RYGB that necessitated partial pancreatectomy. Case presentation: A 44 year old female with past medical history significant for RYGB ten years ago presented to the hospital with recurrent episodes of postprandial dizziness and near-syncope. She denied any flushing or diaphoresis during these spells. Physical examination was unremarkable. Laboratory data revealed serum glucose of 66 mg/dl with intermittent drop down to 37 mg/dl. Serum insulin level was 8 μU/ml and C peptide level was 3.6 ng/ml. Serum sulfonylurea screen was negative. Computed tomographic (CT) abdomen did not show any pancreatic mass. Endoscopic ultrasound to assess pancreatic anatomy was not feasible in the setting of prior gastric bypass surgery. Dietary modification by decreasing carbohydrate content did not ameliorate her symptoms. A trial of acarbose, diazoxide and somatostatin was unsuccessful. The patient's persistent symptoms necessitated readmission and continuous 5 % Dextrose infusion to prevent hypoglycemia. Since all medical options were exhausted, the patient underwent distal pancreatectomy. Histopathology showed hyperplastic pancreatic islets with amyloid deposits (Fig 1,2) that varied in size. Post operatovely, the patient had resolution of hypoglycemia (figure 3).Figure: Histologic examination of the pancreas demonstrating hyperplastic pancreatic islets containing amyloid deposits staining positively with Congo red.Figure: Histologic examination of the pancreas demonstrating hyperplastic pancreatic islets.Figure: A pictorial representation of our patient's serum glucose during the hospital course. Arrow depicts the time of pancreatectomy and discontinuation of dextrose infusion.Discussion: The prevalence of post bariatric surgery hypoglycemia has been reported as < 1%. It was first described by Service et al. in 2005. In contrast to dumping syndrome, which is noted soon after the surgery and improves with time, post RYGB hypoglycemia presents several months to years after surgery. Its hallmark feature is severe postprandial neuroglycopenia, which is characteristically absent in dumping. Current research suggests that after RYGB, food intake and rapid gastric emptying triggers an excessive rise in glucose, which stimulates GLP-1 secretion with subsequent excess insulin secretion. Other potential mechanisms include enhanced beta cell function and dysregulated insulin secretion. Diagnosis requires documentation of Whipple's triad, elevated serum insulin >3 μU/ml, C peptide > 0.6 ng/ml, negative sulfonylurea screen and negative pancreatic imaging. Most patients respond well to low carbohydrate diet. Medications to decrease postprandial hyperinsulinemia including alpha-glucosidase inhibitors, calcium channel blockers, diazoxide and somatostatin, have had inconsistent results. Patients with persistent hypoglycemia that is not responsive to diet and/ or medical treatment may benefit from pancreatectomy (partial or total). Reversal of gastric bypass has been proposed to alleviate resulting hypoglycemia, but results have not been promising. With increasing use of RYGB to treat obesity, physicians may encounter an increasing incidence of post bariatric surgery hypoglycemia. Additional research is needed to further elucidate its pathophysiology that may open up new avenues for management.