Hypoglycemia after ingestion of ethanolic beverages has been reported (1-4). In some cases (1, 2), hypoglycemia was attributed to the nonethanol ingredients in such mixtures as "smoke" and "solox" (methyl alcohol, and gasoline and ethyl acetate). Cummins, however, suggested that hypoglycemia might be caused by ethanol itself (3). He described a 6-year-old boy who had convulsions and hypoglycemia after ingestion of gin. Neame and Joubert also ascribed hypoglycemia observed in their patients to ethanol rather than other ingredients (4). They also emphasized the inadequate dietary intake before the ethanolic ingestion and the development of hypoglycemia.Recently, we studied a chronic alcoholic patient who had several documented episodes of hypoglycemia and minimal evidence of abnormal liver function. Our findings indicated that his hypoglycemia was probably induced by ethanol consumption in combination with a poor dietary intake. Studies were also performed with normal control subjects which indicated that ethanol ingestion after a 2-day fast caused hypoglycemia. During ethanol-induced hypoglycemia, conversion of fructose to glucose was normal, but glycogen synthesis appeared to be inhibited, from the failure of an adequate hyperglycemic response to glucagon. Animal studies suggested that ethanol caused hypoglycemia by interfering with gluconeogenesis as well as glycogen synthesis. Recent studies reported in abstract form have also proposed that the mechanism of ethanol-induced hypoglycemia might be an interference in gluconeogenesis (5).
MATERIALS AND METHODSThe patient C.P. was a white, 52-year-old, male plumber. He had a long history of ethanol ingestion averaging approximately one pint of whiskey daily. His dietary habits were variable and he would frequently miss one or two meals a day. His first episode of hypoglycemia came 10 years ago when he suddenly felt dizzy and collapsed after a 24-hour fast. He denied any ethanolic intake just before this episode. He was treated with iv glucose and made a prompt recovery. His next attack came 6 years later under similar circumstances; blood sugar was 28 mg per 100 ml, and he responded rapidly to 25 g iv glucose. One year later, another episode of hypoglycemia with a blood glucose of 28 mg per 100 ml was documented; a 6-hour glucose tolerance test was normal, and a 3-day fast did not cause hypoglycemia. Two years before admission, he was seen at home by his physician for another, similar, but somewhat milder, attack. He gave a history then of heavy alcoholic consumption for the 2 preceding days and no food intake for the 24 hours just before the attack. He was treated with glucose and responded promptly. The recurrence of a similar episode with a blood glucose of 25 mg per 100 ml led to the patient's hospitalization at the Clinical Center of the National Institutes of Health. Physical examination was unremarkable, except for severe, symmetrical, subcutaneous lipomatosis limited to the upper half of the body and bilateral, sensory, peripheral neuropathy of the legs. He...