In three separate studies involving three different sets of collaborators, elevated levels of 2,3- butanediol have been found in the blood of 80% of chronic alcoholics, but not social drinkers consuming distilled spirits. Two separate methods of gas chromatographic analysis of diols have been developed. One method involving formation of the bromophenylboronate derivative can accurately measure to D-L, or meso-2,3-butanediol to 5uM. In the rat, two pathways of butanediol formation have been demonstrated. The first (Veech RL, et al. Curr Top Cell Regul 1981;18:151-179) involves elevated blood acetaldehyde entering the brain with an active pyruvate dehydrogenase multi-enzyme complex where it condenses with hydroxyethyl thiamine pyrophosphate to form acetoin. The acetoin is subsequently converted in liver to 2,3-butanediol. In a second animal model, 2,3- butanediol in the rat is produced by acetone feeding. Prolonged fasting in man, however, produces only 1,2- propanediol. Whether D/L-2,3-butanediol production is due to expression of an aberrant gene product or is due to some other metabolic change caused by chronic ethanol consumption is not known, but the presence of this compound in approximately 40% of all alcoholics prior to the onset of alcoholic liver disease during periods of ethanol ingestion, and in approximately 25% of all alcoholics with alcoholic cirrhosis in the absence of recent ingestion of ethanol make this compound a useful indicator of alcoholic liver disease.
