An Atypical Presentation of a Patient With Postprandial Hypoglycemic Induced Seizures

Abstract

Abstract Background: Insulinomas are exceptionally uncommon pancreatic islet cell neuroendocrine tumors. Typically, insulinoma induced hypoglycemia occurs exclusively in the fasting state in 73 percent, reported in a retrospective analysis of 237 patients, whereas 6 percent reported only postprandial symptoms. Clinical Case: A 53-year-old female with a history of rheumatoid arthritis, obesity, and prediabetes initially admitted for new onset seizures and recurrent spontaneous hypoglycemic episodes. She experienced recurrent, symptomatic, post-prandial, hypoglycemia daily for the past 8 years. Each episode was closely associated with a high carbohydrate meal, inducing a post-prandial hypoglycemia more consistently and more profoundly than intermittent fasting. Symptoms of lightheadedness, shakiness, and seizure were exacerbated by each carbohydrate meal. Initial labs revealed serum glucose of 35 mg/dl. After recovery with dextrose infusion, a brief fasting trial less than 24 hours was performed with no recurrence of hypoglycemia. However, a mixed meal study utilizing watermelon resulted in a postprandial serum hypoglycemia of 28 mg/dl, provoking a seizure within 30 minutes. During her hospitalization, recurrent hypoglycemia was found during the postprandial period rather than intermittent fasting periods requiring dextrose infusion and octreotide. A Hypoglycemia panel sent during the initial episode was consistent with endogenous hyperinsulinism (Serum glucose=35, Insulin level=24, Proinsulin=166, C-peptide=0.9, BHB=undetectable, Sulfonurea=negative). A subsequent CT of the abdomen/pelvis revealed a mass associated with the pancreatic tail, measuring 4.1 x 4.4 x 5.2 cm concerning for pancreatic malignancy. A fine needle aspiration followed by a distal pancreatectomy and splenectomy with histopathological and immuno-histochemical evaluation confirming a well differentiated (grade 1), 5.0 x 4.5 x 3.0 cm, neuroendocrine tumor (insulinoma). Her recovery, post-operatively, was complicated by an intraabdominal abscess, left pleural effusion, necessitating insulin therapy for hyperglycemia believed to be secondary to morbid obesity, weight gain, and insulin resistance. Hypoglycemic symptoms resolved, blood glucose normalized, and insulin therapy was weaned over the following 3 months and she remains on metformin to date with no evidence of recurrence. Conclusion: Although rare, an insulinoma should be considered in the differential diagnosis of any individual with recurrent episodes of frequent symptomatic hypoglycemia. The classical clinical manifestation of an insulinoma is a fasting hypoglycemia, with distinct episodes of autonomic symptoms. However, postprandial symptoms have been reported with increasing frequency. Here we present a case of surgically confirmed insulinoma with predominantly post-prandial hypoglycemia.