Endocrine Abstracts

Fasting hypoglycemia in the setting of hyperinsulinemia typically is persistent and often progressive. We present a case where fasting hypoglycemia with hyperinsulinemia was transient in nature over a fortnight. This occurred in the setting of recurrent seizure-like activity. Seizures are a well known sequela of hypoglycemia; however, the reverse is not nearly as well documented. A 20 year old male with a history of developmental delay, chronic PEG tube, and nonverbal at baseline presented for breakthrough seizures after a 17 year seizure-free period. On day 3 of admission, his fasting glucose levels fell to less than 65 mg/dl. He required D10 infusion, and experienced return of hypoglycemia when D10 was stopped. Labs obtained during a hypoglycemic episode showed blood glucose 47 mg/dl, insulin 12 uU/ml, beta-hydroxybutyrate 0.07 mmol/l, C-peptide 7.9/ml, sulfonylurea screen negative, and negative insulin antibodies. Octreotide was started in addition to D10 for persistent hypoglycemia. MRI abdomen did not reveal pancreatic lesions and 68 Gallium-DOTATAE PET scan showed normal pancreatic structure. Over a two week period, octreotide and D10 infusion were slowly weaned off without return of hypoglycemia. During his admission, he underwent EEG assessment, which showed a moderate degree of diffuse or possibly multifocal cerebral dysfunction warranting clinical correlation. True hypoglycemia needs to fulfill Whipple’s Triad: Documented venous hypoglycemia, symptoms consistent with hypoglycemia, and resolution of symptoms with correction of hypoglycemia. In this case, the triad was presumed to be positive based on laboratory evaluation and a report of behavioral changes with hypoglycemia from patient’s parents. Laboratory assessment met criteria for endogenous hyperinsulinemia. Imaging did not reveal a source for excess insulin. He went from requiring D10 and octreotide to being euglycemic off both medications. Critical illness is also implicated in fasting hypoglycemia, particularly in end-organ failure or sepsis. The patient did not have any organ damage to this degree, but there was recurrent seizure-like activity. Status epileptics causes a massive release of catecholamines, which increases serum glucose. The latter then leads to a large insulin release from the pancreas, which can lead to a period of hypoglycemia. Although clear epileptiform activity was not noted on EEG, the patient’s clinical presentation with seizures raises the possibility that the hypoglycemia was related to recurrent seizures. This case highlights the need to consider epiletiform activity as a cause of hyperinsulinemic hypoglycemia.