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to alter anticoagulant status, and there are few data on the extent to which long-term differences in dietary vitamin K intake modulate the response to warfarin. Lubetsky and coworkers (1999) studied a population of 46 patients with an estimated (by food frequency recall) median intake of 179 μg/day of phylloquinone. Patients with intakes greater than 250 μg/day were maintained at the targeted international normalized ratio with 5.8 mg/day warfarin, while patients with an intake of less than 250 μg/day of phylloquinone were maintained on a lower warfarin intake of 4.4 mg/day. These data suggest that alterations in vitamin K intake might influence warfarin dosage. As an effective warfarin dose varies widely within individuals, patients are closely monitored. Once a dose has been established, patients can avoid any complications resulting from variations in vitamin K intake by continuing to follow their normal dietary patterns.

Nutrient-Nutrient Interactions

The ability of elevated intakes of vitamin E to antagonize vitamin K action has been clearly established. Woolley (1945) first demonstrated that increased dietary or parenteral α-tocopherol or α-tocopherol quinone could induce a hemorrhagic syndrome in the rat, and vitamin K administration was demonstrated to reverse this response (Rao and Mason, 1975). Studies of the microsomal vitamin K-dependent carboxylase have demonstrated that the enzyme can be inhibited by α-tocopherol and that it is even more sensitive to α-tocopherol quinone (Bettger and Olson, 1982; Dowd and Zheng, 1995).

Increased intakes of vitamin E have not been reported to antagonize vitamin K status in healthy humans. However, in one study, oral supplementation of anticoagulated patients (50 percent plasma prothrombin concentrations) with approximately 360 mg/day (400 IU/day) of α-tocopherol resulted in nonstatistically significant decreases in prothrombin concentrations over a 4-week period, and a statistically significant decrease in the ratio of biologically active prothrombin to prothrombin antigen (Corrigan and Ulfers, 1981). More sensitive measures of vitamin K status are now available and should be used to assess the potential impact of vitamin E supplementation in anticoagulated patients or subjects with low vitamin K intakes.

The metabolic basis for vitamin E antagonism of vitamin K function has not been completely elucidated. Recent data from a study using a rat model have demonstrated an adverse effect of dietary α-



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