Fasting Hypoglycemia after Ethanol
During the postabsorptive state, normal plasma glucose is maintained by hepatic glucose output derived from both glycogenolysis and gluconeogenesis. With prolonged starvation, glycogen reserves become depleted within 18-24 hours and hepatic glucose output becomes totally dependent on gluconeogenesis.
Under these circumstances, a blood concentration of ethanol as low as 45 mg/dL can induce profound hypoglycemia by blocking gluconeogenesis. Neuroglycopenia in a patient whose breath smells of alcohol may be mistaken for alcoholic stupor.
Prevention consists of adequate food intake during ethanol ingestion. Therapy consists of glucose administration to replenish glycogen stores until gluconeogenesis resumes.
Postethanol Reactive Hypoglycemia
When sugar-containing soft drinks are used as mixers to dilute alcohol in beverages (gin and tonic, rum and cola), there seems to be a greater insulin release than when the soft drink alone is ingested and a tendency for more of a late hypoglycemic overswing to occur 3-4 hours later. Prevention would consist of avoiding sugar mixers while ingesting alcohol and ensuring supplementary food intake to provide sustained absorption.
- Differential Diagnosis
- Hypoglycemia due to Pancreatic B cell tumors
L General Considerations
L Clinical Findings
- Persistent Islet Hyperplasia
- Hypoglycemia Due to Extrapancreatic Tumors
- Postprandial Hypoglycemia (Reactive Hypoglycemia)
L Postgastrectomy Alimentary Hypoglycemia
L Functional Alimentary Hypoglycemia
L Late Hypoglycemia (Occult Diabetes)
- Alcohol-Related Hypoglycemia
L Fasting Hypoglycemia after Ethanol
L Postethanol Reactive Hypoglycemia
- Factitious Hypoglycemia
- Immunopathologic Hypoglycemia
- Drug-Induced Hypoglycemia