Potentiation of Warfarin-Induced Hypoprothrombinemia by Chloral Hydrate

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Abstract
During therapy with chloral hydrate one of its major metabolites, trichloroacetic acid, accumulates in plasma to more than 80 mg per liter. Trichloroacetic acid is highly protein-bound and displaces warfarin from binding sites on plasma albumin at 3 and 37°C. The resulting increase in the concentration of free plasma warfarin leads to a 25 per cent shortening of the biologic half-life of warfarin. During chronic warfarin therapy the trichloroacetic acid-induced increase in free plasma warfarin also potentiates the depression of vitamin-K-sensitive clotting-factor synthesis in the liver.