Why initially couple of days warfarin behaves opposite effect like coagulant effect.
Warfarin inhibits vitamin K epoxide reductase, reducing the production of vitamin K-dependent clotting factors: II, VII, IX, X, and also protein C and protein S.
Here is the answer...
Protein C and Protein S are natural anticoagulants (they help prevent clotting).
Protein C has a very short half-life (~8 hours), much shorter than the clotting factors like II (prothrombin), which has a half-life of ~60-72 hours.
So, early in warfarin therapy:
Protein C levels drop quickly.
Clotting factors take longer to decrease.
This creates a temporary imbalance, where the body's natural anticoagulant effect is reduced before the full anticoagulant effect of warfarin kicks in.
Result: a transient hypercoagulable state (blood is more prone to clotting).
Clinical Implication:
This is why patients are often "bridged" with a rapid-acting anticoagulant (like heparin or enoxaparin) when starting warfarin, especially if there's a high clot risk (e.g., in DVT, PE, or atrial fibrillation with stroke risk).
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