The role of vitamin K in coagulation

As mentioned above, vitamin K not only participates in the synthesis of coagulation factors Ⅱ (i.e prothrombin) ⅶ, ⅸ and Ⅹ, but also is a promoter for maintaining the transformation of prothrombin into fibrin in the process of coagulation Therefore, when vitamin deficiency, the most obvious symptom is coagulation dysfunction, the above factors in the blood content decreased, coagulation time prolonged In clinical practice, prothrombin time is the most widely used indicator of vitamin K deficiency and therapeutic effect When the prothrombin index in the blood drops below 35% (normal 80-100%), the area suffering from trauma (new surgical wound, contusion, delivery, etc.) is at risk of serious bleeding If the prothrombin index is less than 20%, it can develop into severe hemorrhagic quality with hematuria, vomit, nosebleed, hematoma and hematocele There are many arguments about the theory of vitamin K on the formation of coagulation factors The hypothesis that vitamin K is a component of prothrombin has not been confirmed up to now It has been suggested that vitamin K may also be involved in the biosynthesis of the above coagulation factors by the formation of galloferment from unidentified enzyme proteins It is also believed that the mechanism of vitamin K is related to the effect of oxidative phosphorylation, but it has not been generally recognized It is also believed that vitamin K is involved in the synthesis of polypeptides on the ribosome of hepatocytes and can promote the synthesis of corresponding mRNA according to DNA It is also believed that vitamins are involved in the later stage of prothrombin and other coagulation factors synthesis, that is, the stage of promoting liver microsomes to synthesize prothrombin and other coagulation factors from various coagulation factors In the 1950s, it was proposed that vitamin K is a cofactor that catalyzes the biosynthesis of some coagulation factors in the liver into the whole enzyme This theory has been widely paid attention to The lack of vitamin K can lead to the disorder of enzyme system and slow down or stop the formation of coagulation factors The mechanism of action of dicoumarin, an indirect anticoagulant, is that they are the same type of vitamin K and can competitively replace vitamin K in the enzyme system of prothrombin synthesis Because vitamin K and dicoumarin have similar naphthoquinone structure and tend to accumulate in the liver, the action site of vitamin K on the oxidation pathway of cytochrome in the liver is easily occupied by antagonists, which hinders the normal synthesis of vitamin K-dependent coagulation factors These are the first antagonistic mechanisms that have been used in the past to explain vitamin K and oral anticoagulants In recent years, it has been pointed out that in the plasma of patients taking dicoumarins, the four normal vitamin K-dependent factors are significantly reduced, and there are four corresponding abnormal proteins, whose structures are similar to those of normal vitamin K-dependent coagulation factors Ⅱ, Ⅶ, ⅸ, Ⅹ, but not exactly the same These proteins are called "protein caused by vitamin K antagonists" (prot Ein induced by vitamin K antoniost), take the initials of each word as "PIVKA" What are the differences between coagulation factors Ⅱ, Ⅶ, ⅸ, Ⅹ and PIVKA Ⅱ, Ⅶ, ⅸ, Ⅹ? Taking PIVKA Ⅱ as an example, it is identical with prothrombin (i.e coagulation factor Ⅱ) in antigenicity and chemical structure, but it has no biological activity and can not combine calcium ion with barium sulfate It has been found that the terminal of some peptide fragments of PIVKA Ⅱ is γ - hydroxy amino acid, which has more hydroxyl than the former, so it has the ability to absorb calcium ion, but glutamic acid is not Have this ability The hydroxylation process of glutamic acid must involve the participation of vitamin K when vitamin K is deficient or its antagonist dicoumarins are used, the hydroxylation process of glutamic acid is blocked and normal hydroxylation cannot be formed, so PIVKA Ⅱ is formed In the process of coagulation, the role of calcium ion is indispensable When coagulation factor II is activated, calcium ion is required to act as a bridge first, so that coagulation factor II can be adsorbed on the phospholipid membrane (PL) of platelets, then XA can change coagulation factor II into IIA with the participation of factor v Since PIVKA Ⅱ can't combine with calcium ion, it can't participate in the coagulation process At present, it has been proved that the glutamic acid residues of PIVKA ⅸ, Ⅹ are not hydroxylated, so they can not be combined with calcium ions, so the coagulation process is blocked The above is a new theory on the relationship between vitamin K and PIVKA Ⅱ, ⅸ, Ⅹ.