A chronic alcoholic presents after 3 days of binge drinking with minimal food intake. He has vomiting, abdominal pain, and a high anion gap metabolic acidosis with glucose of 130 mg/dL. Laboratory studies show a beta-hydroxybutyrate to acetoacetate ratio far higher than that seen in typical diabetic ketoacidosis. This altered ratio is best explained by:

• A Enhanced activity of mitochondrial HMG-CoA synthase by ethanol
• B High cytosolic and mitochondrial NADH shifting acetoacetate toward beta-hydroxybutyrate ✓
• C Inhibition of acetoacetate decarboxylation to acetone by acetaldehyde
• D Increased renal clearance of acetoacetate relative to beta-hydroxybutyrate

Explanation

Alcohol metabolism via ADH and ALDH generates excess NADH. Because the interconversion of acetoacetate and beta-hydroxybutyrate is catalyzed by an NADH-dependent dehydrogenase, the redox state drives equilibrium toward beta-hydroxybutyrate, producing ratios much higher than in DKA. Ethanol does not stimulate HMG-CoA synthase, acetaldehyde does not inhibit decarboxylation, and differential renal handling does not explain the ratio shift.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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Written and medically reviewed by the StethoPrep medical team.