Endocrine Abstracts

Background: Obesity pandemic continues to grow and currently bariatric surgery is the only interventional method proved to induce significant long-term weight reduction. The number of bariatric surgery has doubled in USA over the past decade. We present a case of adult onset nesidioblastosis, post gastric bypass.

Case Summary: A 50 years old female who is 2 years status post Roux-en-Y gastric bypass was admitted to the hospital with a documented hypoglycemia (blood glucose 2.5 mmol/l) and apparent neuroglycopenic symptoms which resulted in road traffic accident. Her obesity history dates back to childhood with BMI 50.0 kg/m². Her post operative course was unremarkable. Over the course of 1 year when BMI stabilized at 25 kg/m², she developed postprandial neuroglycopenia hypoglycaemic symptoms. No symptoms of diarrhoea, flushing or abdominal cramps were detected and dietary interventions were unresponsive. During her hospital course, blood glucose was fluctuating requiring multiple treatments with dextrose 50%. Physical examination revealed no abnormal findings. Endocrine examination excluded hypopituitarism and adrenal sufficiency. Blood sampling during documented hypoglycemic episode (blood glucose 1.6 mmol/l) revealed inappropriately high fasting insulin 55 uIu/ml, with increased proinsulin 10.1 and C peptide 6.5 ng/ml. Anti insulin antibody and sulphonyurea screen were negative. Abdominal computed tomography excluded pancreatic mass lesions.

Due to recurrent refractory hypoglycemia she underwent exploratory laprotomy. Intraoperative ultrasonography revealed pancreatic mass lesion, subtotal 95% pancreatectomy with cholecytectomy was performed. Histopathology and immunohistochemical study of the resected pancreas revealed diffuse islets cells hyperplasia and nesidioblastosis.

Conclusions: The above case highlights the enhanced insulin secretion post gastric bypass with severe neuroglycopenic hypoglycemia which is related to a new pathology rather than dumping syndrome. This rare side event must be considered as a cause of hypoglycemia. Further investigations are critical for elucidation of beta cell expansions mechanisms.