Factor II Deficiency

What is Deficiency Factor II?

The disease is extremely rare. It combines various molecular defects of factor II, in which the ability of this factor to transform into active thrombin and cause blood coagulation is more or less reduced.

Symptoms of Deficit Factor II

Bleeding of the bruise type is characteristic of factor II deficiency. The severity of hemorrhagic syndrome corresponds to the severity of the deficiency. Spontaneous bleeding is pronounced at the level of factor II up to 5% (at an average rate of 100%), but it is also possible at a concentration of 10-15%. Post-traumatic and postoperative bleeding reliably stop and prevent with an increase in the concentration of prothrombin to 40% or more.

Diagnosis of Deficit Factor II

The heterogeneity of the molecular defects of factor II in hereditary hypo- and / or dysprothrombinemia (reduced prothrombin content in the blood) determines some significant differences in the indications of individual laboratory tests in different patients. In some patients, the prothrombin time is relatively moderately prolonged, while in others, tests reflecting the internal mechanism of blood coagulation are less disturbed.

Disorders of the prothrombin time, as well as the altered indications of all other coagulation tests, are not eliminated by either the old serum or plasma, but are compensated by the old normal plasma.

Another group of tests to diagnose factor II deficiency is based on the use of snake venoms. They convert prothrombin to thrombin without the participation of factors VII, X and V of blood coagulation. These properties are possessed by the Australian snake poisons taipan and sandy efa. With a prothrombin deficiency, the plasma clotting time is prolonged under the influence of these poisons, and the longer, the greater the deficiency of factor II.

The diagnosis is clarified after quantifying the level of factor II in the plasma of the patient being examined. This approach allows us to differentiate the true deficiency and molecular anomalies of prothrombin.

Deficit Factor II Treatment

Replacement therapy of hypoprothrombinemia is carried out either with normal or fresh frozen donor plasma, or with concentrates. Plasma transfusions are used to prevent and relieve small bleeding, in which hemostasis can be achieved by increasing the concentration of factor II in the plasma to 15–20%. Supporting transfusions in a dose of 20-40 U / kg of body weight can be done once every 2-4 days, since the half-life of prothrombin in the bloodstream of the patient is 3-5 days.

Vitamin K preparations for hereditary hypoprothrombinemia do not have any noticeable effect and do not improve the testimony of laboratory tests.