Bleeding Risks with Vitamin K Deficiency
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Vitamin K deficiency
Clotting factor
This is a protocol for a Cochrane Review (Intervention). The objectives are as follows: To assess whether concomitant supplementation of oral vitamin K can significantly improve anticoagulation control in patients on warfarin.
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Warfarin, an oral vitamin K antagonist, is used to prevent arterial and venous thromboembolism in patients suffering from a multitude of diseases. In 2004, 31 million warfarin prescriptions were dispensed in the United States. Warfarin inhibits the activation of the vitamin K–dependent clotting factors (Factors II, VII, IX, and X) and regulatory proteins (proteins C, S, and Z). It is one of the leading drugs implicated in emergency room visits for adverse drug reactions. Annually the frequency of bleeding complications associated with overanticoagulation is 15% to 20%, with fatal bleeds measuring as high as 1% to 3%. The most effective method of warfarin reversal involves the use of Four Factor Prothrombin Complex Concentrate (PCC), which is widely used throughout Europe but is unavailable in the United States. The current therapies available to emergency room physicians in the United States are fresh frozen plasma, recombinant Factor VIIa (rFVIIa), Factor Eight Inhibitory Bypassing Activity, or Three Factor PCC concomitantly administered with vitamin K. We review the advantages and disadvantages of these therapies and recommend Three Factor PCC with small doses of rFVIIa and with vitamin K in life-threatening situations if Four Factor PCC is unavailable. [West J Emerg Med. 2011;12(4):386–392.]
Vitamin K antagonist
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Factor IX
Recombinant Factor VIIa
Factor VII
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Vitamin K deficiency
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Warfarin has been successfully used in the medical management of thromboembolic disease for nearly six decades. It is widely assumed that a dietary vitamin K–warfarin interaction exists. To avoid this potential interaction, patients typically receive instructions to consume a constant dietary intake of vitamin K, and sufficient data exist to suggest that a constant dietary intake of vitamin K that meets current dietary recommendations of 65 to 80 mg/day is the most acceptable practice for patients on warfarin therapy. Data concerning the vitamin K content of commonly consumed foods, however, are not readily accessible to clinicians and patients. An understanding of the dietary vitamin K‐warfarin interaction, and dietary sources and usual intakes of vitamin K may facilitate successful anticoagulation for patients being treated with warfarin. ▪ Key Words: vitamin K, warfarin, anticoagulant phylliquinone
Dietary management
Anticoagulant Therapy
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Administration of warfarin to rats induced not only the well-known anticoagulant effect, but also an impairment of primary hemostasis as reflected by a significant prolongation of the “template” bleeding time. This effect was very closely associated with lowering of the prothrombin complex level and was reversed by administration of vitamin K. It is suggested that some of the clotting factors known to be vitamin K-dependent also play a role in primary hemostasis; alternatively, a putative vascular “bleeding factor” could be modulated by vitamin K availability.
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To the Editor.—
In our experience, and that of others,1acute vitamin K deficiency is a common occurrence in patients who are on no oral intake and receiving antibiotics, as is likely to occur in patients in intensive care units. This deficiency may appear in a period as brief as 48 hours after admission if the patient was nutritionally impaired. This occurrence manifests mainly in a prolongation of the prothrombin time, and it can lead to serious bleeding. Since we instituted routine replacement with parenteral vitamin K, this picture has become a rarity. Those patients still having prolonged prothrombin times were studied in detail (assaying their clotting factors II, V, VII/X, and VIII). As expected, it was found that those patients who failed to respond to intravenous vitamin K had underlying liver disease, and, accordingly, their factor V was decreased (not a vitamin K-dependent factor also synthesized by theClotting factor
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THE PRESENT REPORT concerns the nature and functions of natural vitamin K compounds and of some synthetic naphthoquinone derivatives, referred to as vitamin K analogues. The report emphasizes the use of these compounds in pediatrics, especially for prevention and treatment of hemorrhagic disease of the newborn. The demonstration that water-soluble analogues of vitamin K may be toxic for the newborn infant makes it imperative that these substances be used judiciously. FUNCTIONS AND REQUIREMENT OF VITAMIN K Table I provides information concerning characteristics, sources, available preparations and routes of administration of natural and synthetic compounds with vitamin K activity. Functions Vitamin K is required for synthesis of prothrombin and proconvertin (stable factor, factor VII), and it probably is involved also in synthesis of Stuart-Prower factor (factor X) and PTC (plasma thromboplastic factor, factor IX) since clotting defects due to deficiencies of these factors as well as to deficiencies of prothrombin and proconvertin occur in states of vitamin K deficiency. Requirement and Usual Source of Supply Available evidence indicates that vitamin K compounds cannot be synthesized by the animal organism. However, vitamin K1 is widely distributed in nature, being present in greatest concentrations in green leafy vegetables and in somewhat lesser concentrations in seeds, tubers and fruit. Although it has long been believed that bacterial synthesis of vitamin K2 in the intestine is another important source of the vitamin, recent studies with rats indicate that vitamin K2 formed in this manner is unavailable if coprophagy is prevented. Whether bacterial synthesis of vitamin K2 in the human intestine can contribute to satisfying the requirements for this vitamin is not known, and it is therefore uncertain whether suppression of growth of intestinal micro-organisms by prolonged oral administration of antibiotics or sulfonamides is of practical importance.
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A randomised clinical trial was conducted to establish the effects of oral and intramuscular administration of vitamin K at birth on plasma concentrations of vitamin K1, proteins induced by vitamin K absence (PIVKA-II), and clotting factors. Two groups of about 165 healthy breast fed infants who received at random 1 mg vitamin K1 orally or intramuscularly after birth were studied at 2 weeks and 1 and 3 months of age. Although vitamin K1 concentrations were statistically significantly higher in the intramuscular group, blood coagulability, activities of factors VII and X and PIVKA-II concentrations did not reveal any difference between the two groups. At 2 weeks of age vitamin K1 concentrations were raised compared with reported unsupplemented concentrations and no PIVKA-II was detectable. At 3 months vitamin K1 concentrations were back at unsupplemented values and PIVKA-II was detectable in 11.5% of infants. Therefore, a repeated oral prophylaxis will be necessary to completely prevent (biochemical) vitamin K deficiency beyond the age of 1 month.
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Hypoprothrombinemia
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A randomized, blinded study in 30 patients was undertaken. This study found that low dose oral vitamin K was more effective than placebo when used to correct the INR in patients who are discontinuing warfarin. Larger studies will be required to determine if the use of oral vitamin K, for example in patients who are temporarily discontinuing warfarin to undergo interventional procedures, is safe and effective.
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