Proteins Induced by vitamin K Absence

Prothrombin normally contains 10 y-carboxyglutamate residues in the amino terminal region. In the presence of high concentrations of warfarin, a completely uncarboxylated precursor, preprothrombin, is released into the circulation. Before the nature of this precursor protein was known, it was called protein induced by vitamin K absence or antagonism (PIVKA), a term that is sometimes still used. 

In the future, this test may be replaced by the proteins induced by vitamin K antagonists absence (PIVKA) concentrations in serum. PIVKAs are coagulation factor precursors, normally not detectable in blood but released into the... 

Also see color figure.) Hepatic vitamin K metabolism. Oral anticoagulant drugs act indirectly on the process of glu carboxylation of the vitamin K dependent proteins. The vitamin K antagonists block the reduction of the reaction intermediate, vitamin K-epoxide, that results in the accumulation of vitamin K-epoxide and other nonfunctional forms of vitamin K. Without cycling of the vitamin K-related reaction intermediates in the cycle shown, a depletion of functional vitamin K occurs. Vitamin K antagonists do not block polypeptide synthesis and formation of noncarboxylated proteins occurs. These noncarboxylated proteins are still secreted from the liver and account for nearly normal levels of each of the vitamin K-dependent proteins that can be detected by immunoassay (sometimes called PIVKA, proteins induced in vitamin K absence). 

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