Protein with
Protein C is a vitamin K-dependent glycoprotein of blood plasma. It is synthesized by the liver in the form of an inactive proenzyme, which under the influence of
by the complex of thrombin-thrombomodulin complex is converted into an active form. Activated protein C is an anticoagulant enzyme that selectively inactivates Va and VIIIa factors by hydrolyzing them in the presence of ionized calcium, phospholipids and its cofactor protein S, thereby preventing the prothrombin from passing to thrombin.
Protein C determination is an additional test for assessing the condition of the anticoagulant system. Protein C deficiency is associated with a high risk of thrombosis, especially venous thrombosis and pulmonary embolism in young people.
Protein deficiency C is a common cause of thromboembolic disease in the elderly, so it is indicated in patients over the age of 50 with thrombosis( in this category, the prevalence of protein C deficiency is 25-40%) [Samana M. et al., 1983;Angelo S. V. et al., 1996].Protein C deficiency can be of two types: quantitative( type I) - low concentration of the protein itself, and qualitative( type II) - protein is present, but it is inactive or little active. In case of congenital heterozygous insufficiency of protein C, its activity is 30-60%, with homozygous - 25% and lower. Further studies have shown that resistance to protein C( inactive protein C) is due to a genetically determined defect of factor V( and factor VIII in other cases) - the Leiden anomaly [Angelo S. V. et al., 1996].The most common reason for the acquired resistance to protein C is a violation in the immune system.
The peculiarity of the anticoagulant effect of protein C is that it has no effect without the presence of cofactor protein S( just like heparin is ineffective without ATH), therefore it is recommended that the protein C be measured together with protein S.
Reducing the concentration of protein C in the bloodobserved in pregnancy, liver disease, vitamin K deficiency, DVS-syndrome, GO-mocysteinuria. With nephrotic syndrome, protein C can be lost in the urine. Indirect anticoagulants, oral contraceptives reduce the concentration of protein C.
For the treatment and prevention of thrombosis in patients with a reduced concentration of C / S proteins, antagonists of vitamin K are used;However, due to the short period of their half-life in the blood, at the initial stage of therapy with oral anticoagulants, a transient state of hypercoagulability is observed, due to a faster drop in the content of these proteins compared to vitamin K-dependent clotting factors. In this regard, in patients with an initially lower concentration of C / S proteins in the blood, the probability of developing skin necrosis caused by coumarins is high. To avoid this effect, such patients are recommended to start treatment with vitamin K antagonists against heparin therapy and to reverse heparin only after reaching the required stable level of anticoagulation [McLaughlin M.A. et al., 1996].