Protein C

Reference values (norm) for protein C concentration in plasma are 70-130%.

Protein C is a vitamin K-dependent glycoprotein of blood plasma. It is synthesized by the liver as an inactive proenzyme, which under the influence of the thrombin-thrombomodulin complex is converted into an active form. Activated protein C is an anticoagulant enzyme that selectively inactivates factors Va and VIIIa by hydrolyzing them in the presence of ionized calcium, phospholipids and its cofactor, protein S, thereby preventing the conversion of prothrombin to thrombin.

Protein C determination is an additional test to assess the state 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 C deficiency is a common cause of thromboembolic diseases in the elderly, so its determination is indicated in patients over 50 years of age suffering from thrombosis (in this category of patients, the prevalence of protein C deficiency is 25-40%). Protein C deficiency can be of two types: quantitative (type I) - low concentration of the protein itself, and qualitative (type II) - the protein is present, but it is inactive or slightly active. In congenital heterozygous protein C deficiency, its activity is 30-60%, in homozygous - 25% and lower. Further studies have shown that resistance to protein C (inactive protein C) is explained by a genetically determined defect of factor V (and factor VIII in other cases) - Leiden anomaly. The most common cause of acquired resistance to protein C is disorders in the immune system.

The peculiarity of the anticoagulant action of protein C is that it has no effect without the presence of a cofactor - protein S (just as heparin is ineffective without antithrombin III), therefore it is recommended to determine protein C together with protein S.

A decrease in the concentration of protein C in the blood is observed during pregnancy, liver disease, vitamin K deficiency, DIC syndrome, homocystinuria. In nephrotic syndrome, protein C can be lost in the urine. Indirect anticoagulants, oral contraceptives reduce the concentration of protein C.

Vitamin K antagonists are used to treat and prevent thrombosis in patients with low protein C/S levels; however, due to their short half-life in the blood, a transient hypercoagulation state is observed at the initial stage of oral anticoagulant therapy, caused by a more rapid decrease in the content of these proteins compared to vitamin K-dependent coagulation factors. In this regard, patients with initially low protein C/S levels in the blood are at high risk of developing coumarin-induced skin necrosis. To avoid this effect, such patients are recommended to begin treatment with vitamin K antagonists while receiving heparin therapy and to discontinue heparin only after achieving the required stable level of anticoagulation.

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