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Wiley InterScience | ||||||||
  Alcoholism: Clinical and Experimental ResearchVolume 24 Issue 7, Pages 958 - 964 Published Online: 30 May 2006 © 2010 Research Society on Alcoholism
Abstract | References | Full Text: PDF (Size: 768K) | Related Articles | Citation Tracking  Disulfiram Treatment Increases Plasma and Red Blood Cell Acetaldehyde in Abstinent Alcoholics This research was supported by Grants AA-03508 and AA-05934 from the Department of Health and Human Services, the Department of Veterans Affairs, and the Kingsbridge Research Foundation. Portions of this research were presented at the 44th Annual Scientific Meeting of the American Association for the Study of Liver Diseases on November 6, 1993, Chicago, IIIinois, and appeared in abstract form in Hepatology 1993; 18:125A Copyright 2000 The Research Society on Alcoholism KEYWORDS Alcoholics • Cirrhotics • Disulfiram • Acetaldehyde • Transaminases ABSTRACTBackground: Much of alcohol's toxicity is due to its product, acetaldehyde. The role of acetaldehyde derived from endogenous sources was assessed in alcoholic patients administered disulfiram, an inhibitor of aldehyde dehydrogenase. Methods: The first part of the study included 23 subjects without biochemical or clinical evidence of chronic liver disease who were abstinent for 2 weeks; 11 patients were started on disulfiram (250 mg/day), whereas the other 12 were not given disulfiram and served as controls. The second part of the study included 13 alcoholic patients with clinical or pathological evidence of cirrhosis who also were administered disul firam for 2 weeks. Plasma and red blood cell (RBC) acetaldehyde as well as serum transaminases were measured at baseline and after 1 and 2 weeks of treatment. Results: In the disulfiram-treated group of alcoholics without known cirrhosis, RBC acetaldehyde levels increased from the pretreatment value of 2.98 ± 0.18 μM to 4.14 ± 0.33 μM after 1 week and to 4.14 ± 0.26 μM after 2 weeks of treatment (p < 0.001). Compared with the pretreatment values (2.07 ± 0.24 μM), plasma acetaldehyde levels also increased after 1 week (3.18 ± 0.32 μM) and 2 weeks (3.15 ± 0.26 μM) of disulfiram treatment (p < 0.001). There were no significant differences in sequential levels measured in either plasma or RBC acetaldehyde levels in patients who were not administered disulfiram. In the group of cirrhotic patients, the mean baseline RBC acetaldehyde value (3.60 ± 0.22 μM) was significantly higher than in noncirrhotics. Disulfiram therapy increased the RBC acetaldehyde after 1 week (4.63 ± 0.27 μM, p < 0.001) and 2 weeks of treatment (4.06 ± 0.28 μM, p < 0.05). Compared with baseline values, plasma acetaldehyde levels were significantly higher after 1 week but not after 2 weeks of disulfiram. There were no significant differences among serum transaminases in alcoholics administered disulfiram, although three cirrhotic patients did have clinically significant elevations. Conclusions: In abstaining subjects given disulfiram, acetaldehyde concentrations increase, possibly due to diminished catabolism of endogenously generated acetaldehyde. Disulfiram should be given cautiously, especially in patients with cirrhosis. Received for publication December 6, 1999; accepted April 28, 2000 | 
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