Recurrent Hypoglycemia Following Total Pancreatectomy and Islet Autotransplantation.

Abstract

Total pancreatectomy and Islet autotransplantation (TP-IAT) is a treatment modality for chronic pancreatitis after therapies have been exhausted. The aim to prevent surgical diabetes in these patients is achieved in approximately one third of cases. In another third, autograft function is insufficient to achieve insulin independence while still improving glucose management. We report a case of an insulin independent islet autograft recipient, experiencing frequent hypoglycemia. The patient developed symptoms of abdominal pain her early thirties, leading to the diagnosis of idiopathic pancreatitis and subsequent Whipple resection of the pancreatic head in 2003 followed by a symptom free interval. Obstruction of the pancreaticojejunostomy necessitated a surgical revision and Roux-en-Y reconstruction of the gastrojeujunostomy in 2008. An episode of acute on chronic pancreatitis and recurring symptoms culminated in the indication of completion pancreatectomy and splenectomy, followed by IAT in 2012. The islet Isolation from the pancreas remnant (29 g) yielded a total Islet equivalents (IEQ) of 267,000 (5650,000 IEQ/kg BW). Islets were infused into the liver via the splenic vein stump under systemic heparinization. Post-operative blood glucose (BG) levels did not exceed 160 mg/dl. Following the discontinuation of protective exogenous insulin therapy 3 months postoperatively, the patient experienced hypoglycemia with increasing frequency and intensity, especially postprandial, following physical exercise and at night. Supportive treatment with a diet of Carbohydrates with low Glycemic index and Acarbose were initiated but failed to prevent hypoglycemia. Extensive workup and metabolic testing revealed a relative lack of glucagon response to hypoglycemia, reduced first phase insulin secretion, impaired Cortisol response to hypoglycemia and impaired postprandial incretin release. In conclusion, we report the rare case of Hypoglycemia complicating the outcome of IAT. Mechanisms of post IAT hypoglycemia remain elusive despite some evidence for impaired Glucagon action. Treatment thus far is limited to glycemic management with continuous glucose monitoring and therapeutic glucose intake.