Vitamin K deficiency results in prolonged prothrombin time, and eventually hemorrhagic disease, as a result of the impairment of synthesis of the vitamin K-dependent blood clotting proteins. Although osteocalcin synthesis is similarly impaired, the effects on blood clotting predominate, and effects of vitamin K deficiency on bone mineralization can only be demonstrated in experimental animals if they are transfused with preformed blood clotting factors. Otherwise, they suffer fatal hemorrhage before there is any detectable effect on osteocalcin and bone metabolism. However, there is some evidence that undercarboxylated osteocalcin is formed in subjects withmarginal intakes of vitamin K with no evidence of impaired blood clotting (Binkley et al., 2000)
The coumarin anticoagulants act as vitamin K antimetabolites, inhibiting vitamin K quinone reductase and epoxide reductase, and hence cause functional vitamin K deficiency. As discussed in Section 5.3.1, the inhibition of vitamin K quinone reductase does not prevent the formation of the hydroquinone for epoxidase activity, because a warfarin-insensitive enzyme also catalyzes the reaction. Provision of high intakes of vitamin K will overcome the inhibition of glutamate carboxylation caused by anticoagulants by permitting more or less stoichiometric utilization of the vitamin, with excretion of metabolites of the epoxide. This may cause problems with patients receiving anticoagulant therapy who take supplements of vitamin K. High dietary intakes of vitamin K, rather than supplements, may also affect anticoagulant action. Although daily consumption of 250 g of a vitamin K-rich vegetable, such as spinach or broccoli, is required to affect prothrombin time, some of the vegetable oils in common use have a high vitamin K content (Karlson et al., 1986; Bolton-Smith et al., 2000).
The response of deficient animals to repletion with vitamin K, or the administration of the vitamin after anticoagulants, is more rapid than might be expected. There is a considerable intracellular accumulation of preprothrom-bin, which is immediately available for carboxylation when vitamin K becomes available.
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