Alcoholism, clinical and experimental research
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We prospectively studied 23 episodes of suspected alcoholic ketosis in order to learn whether there was objective evidence of the patients having stopped drinking ethanol a few days before admission, and of being starved. Eight patients had moderate ketosis (plasma 3-hydroxybutyrate 4.1-7.8 mmol/liter); seven patients had mild ketosis (2-4 mmol/liter); and eight had little or no ketosis (less than 2 mmol/liter). The latter eight patients had mainly lactic acidosis (plasma lactate 2.0-13.3 mmol/liter). ⋯ The presence of starvation was supported by the finding of subnormal plasma triiodothyronine levels (less than 90 micrograms/dl) in six of seven ketotic patients (average 60 micrograms/dl for all seven). The ketotic patients usually had low-normal plasma insulin levels (3- 16 microU/ml), as is common in starvation. Our findings support the previously undocumented belief that most patients with alcoholic ketosis did stop drinking ethanol some time before admission, and that starvation is a major pathogenetic factor in the disorder.
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Alcohol. Clin. Exp. Res. · Nov 1984
Alcoholism in Vietnam and Korea veterans: a long term follow-up.
The prevalence of alcoholism was assessed in veterans of the Vietnam and Korean wars. In addition, the role played by exposure to combat in excessive alcohol consumption was evaluated. One-third of patients attending clinics that were not devoted to the treatment of alcoholism had alcohol-related problems. ⋯ Close to 60% of a group of veterans exposed to combat drank excessively at the time of our study versus only 25% of a group of veterans of the Vietnam and Korean eras. An association between alcoholism and war experiences had already been observed by others in the early postwar era. Our data show that the effects of combat exposure can persist for more than a decade after the stressful events.
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Can brain metabolize ethanol? We present data demonstrating that brain catalase in conjunction with endogenous H2O2 will oxidize ethanol in vivo. The method is based on an H2O2-dependent inhibition of brain catalase in vivo by 3-amino-1,2,4-triazole and its prevention by ethanol. The irreversible inhibition of catalase by aminotriazole is known to proceed via the reaction of (catalase-H2O2) compound I with aminotriazole. ⋯ The catalase content of the tissues represented catalase in the brain parenchyma, from which erythrocytes and capillaries had been excluded. Ethanol did not alter the levels of aminotriazole in brain. These results constitute the first demonstration of ethanol oxidation by living brain.