In three separate studies involving three different sets of collaborators, elevated levels of 2,3-butanediol has been found in 80% of the blood samples taken from chronic alcoholics when consuming distilled spirits, but not in social drinkers consuming distilled spirits. 2,3-butanediol has also been identified in two other abnormal metabolic states, patients with congenital propionic and methylmalonic acid uria (Duran M, et al. Clin Chim Acta 1987;165:197-204) and premature infants (Mills GA, Walker V. Clin Chim Acta 1989;179:51-9).In rat, three experimental models for the production of 2,3-butanediol have been demonstrated. The first involves elevated blood acetaldehyde entering the brain with an active pyruvate dehydrogenase multi-enzyme complex where it condenses with hydroxyethylthiamine pyrophosphate to form acetoin (Veech RL, et al. Curr Top Cell Regul 1981;13:151-79). The acetoin is subsequently converted in liver to 2,3-butanediol. In the second animal model, 2,3-butanediol in the rats is produced by acetone feeding (Casazza JP, et al. J Biol Chem 1984;259:231-6). Prolonged fasting, which results in elevated serum acetone, does not result in 2,3-butanediol production in man. A third model results in the production of 2,3-butanediol after acute administration of short and medium chain fatty acids. The mechanism of production in this case appears to be similar to that observed in acetaldehyde stimulated production of 2,3-butanediol, but in this case pyruvate serves as both the initial substrate and as the acceptor of the hydroxyethyl moiety due to a decreased level of free CoA. Whether 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 D/L diastereomer of this compound during periods of ethanol ingestion in approximately 40% of all alcoholics prior to the onset of alcoholic liver disease and approximately 25% of all alcoholics with alcoholic cirrhosis in the absence of recent ingestion of ethanol makes this compound a useful indicator of alcoholic liver disease.
