Abstract
Summary and ConclusionsIn man as in the rat, salicylate in adequate dosage induces prothrombinopenia which can be prevented by vitamin K compounds, if liver function is adequate. The effect on the prothrombin level (or activity) is detected most readily by the use of 12.5% plasma. The dietary intake particularly of vitamin K appears to play a significant role in determining the extent and duration of the prothrombinopenia. Cirrhosis of the liver and pre-existing prothrombinopenia augment the effect of salicylate. Acetyl salicylic acid appears to be a more potent agent than sodium salicylate. The action of salicylate is apparently identical with that of the anticoagulant dicumarol, but less effective. The two drugs can complement each other. This may be useful in the clinical application of dicumarol and should be realized to avoid excess prothrombinopenia.
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