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[Alcohol and drug biotransformation].

Authors: W, Klinger;

[Alcohol and drug biotransformation].

Abstract

Alcohol is partly degraded by the same enzyme system which also metabolizes drugs. The competition with impairment of the biotransformation and prolongation of the half-life period of elimination for drugs was not yet proved human-pharmacologically. Alcohol is an enzymes inductor in relative small doses: the activity of enzymes of biotransformation increases also in man. In alcohol-induced enlargement of the liver and only slight (reversible) fat deposition the capacity of biotransformation is increased, the elimination accelerated. With increasing degree of severity of the liver defect by alcohol an increasing impairment of drug biotransformation and a clinically significant prolongation of the half-life periods of elimination develop. If in the multifactorial genesis of chronic liver diseases alcohol is not in foreground, so there is no enzyme induction effecting against the liver defect and restriction of the biotransformation and elimination of drugs become measurably already in liver defects of lower degree.

Keywords

Ethanol, Liver, Pharmaceutical Preparations, Solubility, Chronic Disease, Humans, Lipids, Liver Diseases, Alcoholic, Biotransformation, Protein Binding

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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
0
Average
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Average