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Ketoacidosis Associated with Alcoholism in Nondiabetic Subjects

[+] Article, Author, and Disclosure Information

Supported in part by U.S. Public Health Service Research Grant #AM-12404, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Md. Dr. Gordon is a Career Scientist of the Health Research Council of the City of New York under contract I-551.

Presented in part 19 April 1972, 53rd Annual Session of the American College of Physicians, Atlantic City, N.J.

▸Requests for reprints should be addressed to Edwin E. Gordon, M.D., New York University Medical Center, 550 First Ave., New York, N.Y. 10016.

New York, New York

Ann Intern Med. 1973;78(2):213-219. doi:10.7326/0003-4819-78-2-213
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Six episodes of metabolic acidosis in five nondiabetic, chronically alcoholic patients have been documented. All patients had a history of chronic alcoholism and appreciable alcohol intake before admission. Protracted vomiting and prolonged abstention from food were common features. The acidosis resulted from the accumulation of β-hydroxybutyrate, acetoacetate, and lactate in the blood plasma. The acidotic state was promptly corrected with intravenous fluids containing glucose, NaCl, and modest amounts of NaHCO3. Analysis of the plasma at admission showed low concentrations of insulin and extremely elevated free fatty acid and cortisol concentrations. It is postulated that increased ketone body synthesis in these patients is a direct consequence of enhanced release of free fatty acids from adipose tissue stores. Exaggerated lipolysis could be secondary to low levels of circulating insulin, to increased concentrations of plasma cortisol and growth hormone, or to the response of other lipolytic hormones.





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