Protein C and Warfarin in Blood Clotting

Why does warfarin decrease biological activity of protein C?

Warfarin is an anticoagulant medication that works by inhibiting the synthesis of vitamin K-dependent clotting factors, including factors II, VII, IX, and X. However, it also inhibits the synthesis of other vitamin K-dependent proteins, such as protein C.

Protein C is primarily synthesized in the liver and plays a crucial role in the regulation of blood coagulation. It functions as an anticoagulant by inhibiting the activity of factors Va and VIIIa, which are essential for the clotting process. Protein C relies on vitamin K for its activation, and this is where warfarin comes into play

Vitamin K is necessary for the carboxylation of specific amino acids within the proteins that are involved in blood clotting. These carboxylated residues enable the proteins to bind to calcium ions and phospholipids on the surface of activated platelets, forming the clot. Warfarin acts by interfering with the recycling of oxidized vitamin K back to its reduced form. This disruption, in turn, impairs the synthesis of functional vitamin K-dependent clotting factors and proteins

Since protein C is also a vitamin K-dependent protein, its synthesis and activation are affected by warfarin. As a result, warfarin decreases the biological activity of protein C. The reduced levels of functional protein C lead to an imbalance in the coagulation system, making the blood more prone to clotting

It is important to closely monitor patients on warfarin therapy to avoid excessive anticoagulation, as the decreased activity of protein C can potentially increase the risk of blood clots. Regular blood tests, such as the international normalized ratio (INR) test, are performed to assess and adjust the dosage of warfarin accordingly

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