Pankaj Shah1, Jarek Aniszweski, F John Service. 1. Division of Endocrinology, Diabetes, Metabolism, & Nutrition, Mayo Clinic Rochester, Rochester, Minnesota 55905, USA.
Abstract
OBJECTIVE: To present a case of symptomatic hypoglycemia induced by propoxyphene. METHODS: The historical features, results of laboratory evaluations, and clinical course of a man with end-stage renal disease in whom hypoglycemia developed during treatment with propoxyphene are described. RESULTS: A 54-year-old man with chronic renal failure had recurrent episodes of hypoglycemia (plasma glucose level, 40 mg/dL). While he continued treatment with propoxyphene, 58 hours into a 72-hour fast the plasma glucose concentration was 38 mg/dL, in conjunction with a beta-hydroxybutyric acid level of 0.9 mmol/L and inappropriately elevated plasma insulin, serum C-peptide, and proinsulin levels. A plasma drug screen was negative for sulfonylureas. A selective arterial calcium stimulation test yielded negative results. A 72-hour fast after discontinuation of propoxyphene therapy resulted in no hypoglycemia, and he experienced no hypoglycemic episodes for at least 2 years after withdrawal of the propoxyphene treatment. CONCLUSION: The importance of obtaining a thorough medication history in a patient with renal failure and hypoglycemic episodes is highlighted by this case of propoxyphene-induced hypoglycemia. The mechanism of this effect is not known, although non-micro receptor agonism or noncompetitive N-methyl-D-aspartate receptor antagonism may have a role in causing hypoglycemia.
OBJECTIVE: To present a case of symptomatic hypoglycemia induced by propoxyphene. METHODS: The historical features, results of laboratory evaluations, and clinical course of a man with end-stage renal disease in whom hypoglycemia developed during treatment with propoxyphene are described. RESULTS: A 54-year-old man with chronic renal failure had recurrent episodes of hypoglycemia (plasma glucose level, 40 mg/dL). While he continued treatment with propoxyphene, 58 hours into a 72-hour fast the plasma glucose concentration was 38 mg/dL, in conjunction with a beta-hydroxybutyric acid level of 0.9 mmol/L and inappropriately elevated plasma insulin, serum C-peptide, and proinsulin levels. A plasma drug screen was negative for sulfonylureas. A selective arterial calcium stimulation test yielded negative results. A 72-hour fast after discontinuation of propoxyphene therapy resulted in no hypoglycemia, and he experienced no hypoglycemic episodes for at least 2 years after withdrawal of the propoxyphene treatment. CONCLUSION: The importance of obtaining a thorough medication history in a patient with renal failure and hypoglycemic episodes is highlighted by this case of propoxyphene-induced hypoglycemia. The mechanism of this effect is not known, although non-micro receptor agonism or noncompetitive N-methyl-D-aspartate receptor antagonism may have a role in causing hypoglycemia.