What is K-Vitamin Deficiency Factors?
The development of this pathology is due to impaired synthesis in liver cells (hepatocytes), as well as a decrease in plasma concentration of factors VII, X, II and IX.
Pathogenesis during Defecit K-Vitamin-dependent Factors
According to the mechanism of development, the following types of this syndrome are distinguished:
- due to insufficient formation of vitamin K in the intestine (hemorrhagic disease of the newborn, K-hypovitaminosis with enteropathy and intestinal dysbacteriosis of drug origin);
- forms associated with insufficient absorption of this fat-soluble vitamin due to the lack of bile in the intestine, for example, with obstructive jaundice;
- in case of competitive displacement of vitamin K from the metabolic chain by its functional antagonists, such substances are: coumarins, warfarins, phenylins;
- forms caused by damage to the liver parenchyma (acute dystrophy of the liver, parenchymal hepatitis, cirrhosis and parasitic lesions).
Forms characterized by vitamin K deficiency, including the effect of “indirect” anticoagulants, differ from the lesions of the liver parenchyma in that they do not violate all stages of the synthesis of factors II, VII, X and IX, but only its final phase.
Incomplete antecedents of Factors II, VII, X, and IX are abbreviated as PIVKA (Proteins Induced by Vitamin Absence, i.e., proteins induced by a lack of vitamin K).
In order to properly understand the mechanisms of hemorrhagic syndrome development, it is necessary to take into account the importance and dynamics of the development of depression of individual K-vitamin-dependent factors.
Of all the factors, the most severe bleeding (hematomal type) is deficiency of factor IX, the less pronounced mixed type is deficiency VII, and the deficit of factors X and II is less dangerous, leading to the development of bleeding of the Sinyachkov type.
Depression of factors VII, X, IX, and II arises in K-hypovitaminosis, not simultaneously, but sequentially.
It should be noted that this fact is explained by the time of circulation of these factors in the blood.
The half-life of factor VII is 2-6 h, and therefore it first decreases with K-hypovitaminosis and treatment with coumarins. Further, there is a decrease in factors IX and X, the half-life of which is about 30-36 and 48 hours respectively. Prothrombin decreases much later (the half-life is about 4 days). The restoration of the level of factors takes place in the same order after the abolition of anticoagulants and the elimination of K-hypovitaminosis: factor VII is quickly normalized, later factors IX and X, and then only prothrombin is deficient for several more days.
Diagnosis of Defetsit K-vitamin-dependent Factors
One of the most common methods for diagnosing the deficiency of K-vitamin-dependent coagulation factors and monitoring anticoagulant therapy is the prothrombin test.
This test registers a pronounced deficiency of factors of the prothrombin complex. Also, the test controls depression of only 3 of 4 K-vitamin-dependent factors (VII, X and II), whereas the level of factor IX, which participates only in the internal mechanism of coagulation, does not affect it.
It should be noted that the most severe hematoma-type bleedings are directly associated with factor IX deficiency.
In some patients with K-vitamin deficiency, especially when taking fast-acting anticoagulants, the level of factor IX can decrease early, and in this situation, bleeding sometimes occurs with a still quite high prothrombin index.
In this regard, for all types of deficiency of K-vitamin-dependent factors, as well as to control therapy with indirect anticoagulants, not only the prothrombin test is used, but also a test sensitive to factor IX depression (activated partial thromboplastin time, or autocoagulation test).
The advantage of this test is that its implementation does not require the use of special reagents.