Abstract

Hypoglycemia among non-diabetics is rare. The etiologies range from drugs, critical illnesses, hormone deficiencies, autoimmune or insulinomas. Diagnosis of symptomatic hypoglycemia includes the evaluation for Whipples Triad: symptoms of hypoglycemia, plasma glucose concentration less than 55 mg/dl, and resolution of symptoms after plasma glucose is increased. This case report details symptomatic hypoglycemia secondary to concurrent illicit drugs use. A 32 year-old Caucasian female with a history of homelessness and polysubstance abuse was admitted for dizziness and lethargy for several days. There was no known history of diabetes. Initial labs were significant for hemoglobin A1C was 5.3% with glucose level of 31 mg/dL. Glucose improved to 73 mg/dL after 2 intravenous boluses of 50% dextrose. Subsequently, her glucose levels continued to drop to as low as 10 mg/dL prompting additional rounds of D50W boluses and glucagon. ACTH and morning cortisol levels were normal; insulin antibody level, serum and urine ketone, and alcohol level were negative. Urine drug screen was positive for MDMA, marijuana, and cocaine. Her pro-insulin, C-peptide levels and insulin levels were elevated at 19.36 ng/mL and 164.2 mcInt Units/mL, respectively. MRI abdomen was unremarkable for insulinoma or mass. However, a sulfonylurea level came back positive for glimepiride. Given this positive sulfonylurea finding along with her history of illicit drug usage, she was diagnosed with symptomatic hypoglycemia secondary to sulfonylurea and amphetamine usage confounded by marijuana usage. She was safely discharged to a homeless shelter with recommended follow up to the endocrine clinic in two weeks. Glimepiride stimulates pancreatic insulin secretion leading to elevated pro-insulin and C-peptide levels. She denied taking any medication. Given that she experienced hypoglycemic episodes after the ingestion of her illicit drugs, we speculated glimepiride must have been added by her drug supplier. Glimepiride has a half-life of 6-10 hours meaning her hypoglycemic symptoms should have abated within a day. Since her hypoglycemia persisted for several days, this raised suspicions of another contributing factor. A case report by Carrera et al demonstrated amphetamines and THC associated with hyperinsulinemia-induced hypoglycemia. Given the similarity to Carrera et al, the diagnosis of hyperinsulinemia-induced hypoglycemia secondary to sulfonylurea concurrent with amphetamine and THC usage. The pathophysiology of amphetamines and THC-induced insulin secretion is unclear. This case report emphasizes the importance of maintaining a wide differential for hypoglycemia including polysubstance abuse.

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