A Case of Profound Hypoglycemia in the Setting of Starvation and Beta-Adrenergic Blockade in a Patient with Hyperthyroidism

ABSTRACT Objective: The objectives of this case report are to describe an unusual presentation of Graves disease presenting with life-threatening hypoglycemia and to discuss rarely considered physiological mechanisms involved in this patient's hypoglycemia. Methods: Clinical evaluation in this case report involved multiple laboratory assays directed towards the confirmation and further evaluation of the potential etiology of the hypoglycemia. Insulin-mediated etiologies of hypoglycemia, hypoglycemia secondary to ingestion of sulfonylureas and glinides, and the patient's hypothalamic-pituitary-adrenal axis were evaluated through assessment of serum insulin, C-peptide, proinsulin, ACTH-stimulated cortisol, and insulin secretagogue serum concentrations. Results: Hypoglycemia associated with thyrotoxicosis is a rare phenomenon. We excluded insulin-mediated causes of hypoglycemia (given undetectable serum proinsulin, insulin, and C-peptide in the setting of concomitant hypoglycemia), oral hypoglycemic agents (given negative serum screen for sulfonylureas and glinides), and adrenal insufficiency (given a normal cosyntropin stimulation test result). Given the negative workup for common causes of hypoglycemia, more esoteric etiologies of hypoglycemia were considered leading to our working hypothesis of hypoglycemia due to a combination of thyrotoxicosis, hepatic glycogen depletion, and β-blocker-induced impaired glucoregulation. Conclusion: We report a rare case of hypoglycemia that serves as a lesson in physiology and underscores the need to consider atypical combined etiologies for hypoglycemia and judicious use of therapeutic agents. Under certain conditions, hyperthyroidism may contribute to hypoglycemia, demonstrating the possible physiological interplay between hyperthyroidism and severe hepatic glycogen depletion, followed by the additional pharmacological insult of β-blockade therapy, resulting in further impairment in peripheral glucose mobilization.