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January 1978

Treatment of Alcoholic Acidosis: The Role of Dextrose and Phosphorus

Author Affiliations

From the Department of Medicine, University of Rochester (NY) School of Medicine and Dentistry. Dr Miller is now with the Renal Divison, University of Colorado Medical Center, Denver.

Arch Intern Med. 1978;138(1):67-72. doi:10.1001/archinte.1978.03630250043015

We have made serial metabolic observations in 18 acute episodes of alcoholic ketoacidosis in ten patients. Data from patients treated with only saline initially were compared to data from patients who received modest amounts of intravenous dextrose (7.0 to 7.5 gm/hr). More rapid improvement in the acidotic state was seen in the latter group (P <.001). The quicker decline in absolute levels and ratio of β-hydroxybutyrate to acetoacetate when glucose was given suggests that this treatment induced mitochondrial oxidation of the reduced form of nicotinamide adenine dinucleotide (NADH). Since phosphorus is a critical cofactor necessary for NADH oxidation and the glucose-induced correction of the acidosis was associated with a rapid decline in serum phosphorus from an initial mean of 6.79 ±.82 mg/100 ml SEM to 0.96 ± 0.12 mg/100 ml in 24 hours, we propose that glucose enhanced the mitochondrial capacity to oxidize NADH by increasing hepatocyte phosphorus. This effect combined with decline in free fatty acid levels results in reversal of acidosis. Our data suggest that glucose provides the safest, most effective treatment for this disorder; addition of either insulin or bicarbonate is usually unnecessary.

(Arch Intern Med 138:67-72, 1978)