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Protein C or S Deficiency

Protein-ribbon Cat and Snake
Protein C and Protein S deficiency are autosomal dominant inherited disorders characterized by an inability to inactivate coagulation factors V and VIII. Because normal levels of protein C and S help to inhibit these clotting factors, those with a deficiency are in a hypercoagulable state. Patients display recurrent DVTs, or DVTs that arise at a young age. This disorder can also be unmasked when warfarin is given to a patient, as they develop warfarin necrosis. To circumvent this, patients needing anticoagulation are initially started on heparin, and slowly bridged to warfarin.
Autosomal Dominant

Protein C and Protein S deficiency are inherited in an autosomal dominant pattern.

Inability to Inactivate Factor Va and VIIIa
Inability to kill the 5-rabbit and 8-beaver building clots

Protein C and S normally work to inactivate Factor Va and VIIIa, decreasing coagulability. When patients are born with a deficiency of these proteins (C and S), they are unable to inactivate the clotting pathway effectively.

Hypercoagulable State
Hiker-clog State

Being unable to effectively inhibit clotting factors Va and VIIIa, patients with protein C or S deficiency are in a hypercoagulable state.

Recurrent DVTs or DVTs at Young Age
DVT with redness and swelling

Due to their hypercoagulable state, patients can develop recurrent DVTs (deep vein thromboses). Often, protein C or S deficiency can be diagnosed when a child presents with DVTs at a young age.

Begin Heparin

In order to prevent warfarin necrosis, patients should be started on heparin initially. Heparin inhibits factor Xa, which is not affected by proteins C or S. Furthermore, heparin is an IV medication which has an immediate effect on anticoagulation, which is why it is recommended to use this drug while "bridging" to warfarin.

Slowly Bridge to Warfarin
Snail Bridge to War-fairy

Patients who will be chronically anticoagulated should be bridged to oral warfarin. Warfarin does not have an immediate effect on anticoagulation, and patients taking this medication transiently develop a hypercoagulable state.

Hemorrhagic Skin Necrosis
Hemorrhage-hammer Necrosis-crow

Warfarin inhibits production clotting factors II, VII, IX X, protein C and protein S. Protein C and protein S have a shorter half-lives than the other factors and are depleted faster. Thus, when patients take warfarin, the initial depletion of protein C and S makes them hypercoagulable for a short period of time. It is during this time period that patients with protein C and S deficiency are further depleted, leading to warfarin necrosis.

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