Protein C | Activity

General Information

Protein C is a glycoprotein synthesized in the liver (with the participation of vitamin K), circulates in plasma and participates in the prevention of thrombosis. Its anticoagulant function is manifested by the inactivation of factors V and VIII. It also acts as a pro-fibrinolytic (fibrin-breaking) agent.

Protein C is activated by thrombin. The acceleration of activation is mediated by the interaction between thrombin and thrombomodulin on endothelial cells.

Activated protein C removes activated factors V and VIII by proteolytic cleavage, thereby reducing the coagulation activity of plasma. The inactivation of coagulation factors requires the presence of the cofactor protein S, as well as calcium and phospholipids on the surface of the cell membrane. Activated protein C is neutralized by alpha-2-antiplasmin and alpha-2-macroglobulin.

Protein C deficiency can be congenital or acquired. In the case of congenital deficiency, the severity of clinical manifestations depends on the homozygous or heterozygous status of the gene alleles.

Heterozygous Individuals present with deep vein thrombosis, with or without pulmonary embolism, at a young age.

Homozygous In some cases, massive thrombosis occurs immediately after birth, causing neonatal purpura and death.

Acquired protein C deficiency occurs in liver disease, disseminated intravascular coagulation syndrome, insulin-dependent diabetes mellitus, essential hypertension, sickle cell anemia, malignancies, and treatment with oral anticoagulants or L-asparaginase.

When is the survey conducted?

• For the diagnostics of unexplained thromboembolic complications, especially in patients over 50 years of age with a family history of thrombotic events.
• Before prescribing oral contraception, in patients with thrombotic episodes or a family history of thrombosis.

Patient preparation

The study is performed on an empty stomach. Oral anticoagulants should be discontinued 2 weeks prior to the study.

Research material – Venous blood

Protein C Reference boundaries

70-140%

Interpretation of results

Decreased protein C activity is associated with the following conditions:

• Severe thrombotic episode in the neonatal period
• Increased risk of venous thrombosis
• Warfarin-induced skin necrosis (characteristic of the heterozygous form of protein C deficiency, at the beginning of warfarin treatment)
• Thrombophlebitis and pulmonary thrombosis, especially in young people.

The risk of developing thrombosis in individuals who are heterozygous for protein C is approximately 7 times higher than in the general population.

Protein C activity is practically undetectable in homozygous individuals.

Protein C deficiency is characterized by the development of stroke and myocardial infarction at a young age.

Protein C deficiency is also associated with pregnancy loss beyond 28 weeks of gestation.

Important information

Protein C activity is low in newborns

Pregnancy, oral contraception, and postoperative conditions are also associated with decreased protein C activity.

The impact of anticoagulant therapy on protein C activity determination

• Unfractionated heparin Does not affect the determination of protein C by the chromogenic method, however, since this drug is prescribed in acute conditions, the study is not recommended against the background of treatment
• Low molecular weight heparin It does not affect the study, although it is recommended to collect the test sample within 12 hours of taking the last dose of the medication.
• Oral anticoagulants Reduces protein C activity, therefore, the medication should be discontinued 2 weeks before taking Nimish.
• Activated factor X direct inhibitors Does not affect chromogenicity When determining protein C activity by the method.