The Pharmacokinetic data on the absorption metabolism and elimination of carbimide in humans are incomplete. Since nausea, headache, and vomiting occur because of the rapid absorption of carbimide, for treatment purposes it is formulated as a slow-release tablet. Peak plasma concentrations of carbimide following oral administration in experimental animals occur at 60 minutes; the drug is then metabolized at a relatively rapid rate so that half disappears about every 90 minutes (i.e., an apparent elimination half-life of 92.4 minutes). In humans, an alcohol challenge reaction will occur on an average of 12 to 24 hours after drinking.

Alcohol (ethanol) is normally metabolized first to acetaldehyde, which is then quickly metabolized further so that levels of acetaldehyde are ordinarily quite low in the body (acetaldehyde is toxic). Carbimide produces competitive inhibition of hepatic (liver) aldehyde-NAD oxidoreductase dehydrogenase (ALDH), the enzyme from the liver responsible for oxidation of acetaldehyde into acetate and water. Within two hours of taking carbimide by mouth, ALDH inhibition occurs. If alcohol is then ingested, blood acetaldehyde levels are increased; also mild facial flushing, rapid heartbeat, shortness of breath, and nausea occur with just one drink. As more is drunk, the severity of the reaction increases, with rising discomfort and apprehension. severe reactions can pose a serious medical risk that requires immediate attention.

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