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Encainide-induced diabetes: analysis of islet cell function.
W E Winter1, M Funahashi, J Koons
1University of Florida, Department of Pathology and Laboratory Medicine, Gainesville.
Research Communications in Chemical Pathology and Pharmacology
|June 1, 1992
Summary
Encainide-induced diabetes in a patient showed relative insulinopenia and insulin resistance, resembling type II diabetes. This drug-induced condition is a bihormonal disorder, not autoimmune.
Area of Science:
- Endocrinology and Metabolism
- Pharmacology and Drug-Induced Conditions
Background:
- Investigating the mechanisms of encainide-induced diabetes is crucial for understanding drug-related metabolic disturbances.
- Differentiating between type I and type II diabetes metabolic profiles in drug-induced cases is essential for accurate diagnosis and management.
Observation:
- A 65-year-old male patient developed diabetes after 6 months of encainide treatment.
- Islet function tests revealed delayed C-peptide secretion and a low C-peptide/glucose ratio, indicating relative insulinopenia.
- Glucagon levels were initially depressed but showed an exaggerated rise post-meal, unlike controls.
Findings:
- Encainide-induced diabetes presented with normal C-peptide secretion but persistent hyperglycemia, suggesting relative insulinopenia.
- The metabolic profile more closely resembled type II diabetes than type I, with no autoimmune markers present.
- The condition was characterized as a bihormonal disorder involving both insulin and glucagon dysregulation.
Implications:
- Encainide-induced diabetes management may require strategies similar to those for type II diabetes, focusing on insulin resistance.
- Understanding the specific mechanisms of drug-induced diabetes can inform the development of safer medications.
- This case highlights the importance of monitoring metabolic function during antiarrhythmic drug therapy.