Protein C Other names: APC Autoprothrombin IIA Blood coagulation factor XIV Activated protein C

In patients starting treatment with oral anticoagulants belonging to the class of vitamin K antagonists (e.g. warfarin), a transient hypercoagulable state may arise before the desired anticoagulant effect becomes apparent. This transient effect may be explained by the fact that protein C, itself a vitamin K dependent plasma protein, has a shorter half-life than most of the vitamin K dependent proteins (i.e. II, IX and X). Subsequently, in the initial phase of treatment, the activity of protein C is more rapidly suppressed than that of the procoagulant factors. For this reason, if the patient is switched to oral anticoagulants, protein C replacement must be continued until stable anticoagulation is obtained. Although Warfarin-induced skin necrosis can occur in any patient during the initiation of oral anticoagulant therapy, individuals with congenital protein C deficiency are particularly at risk.

Although protein C has been used safely in the treatment of pregnant protein C-deficient women, its safety for use in human pregnancy has not been established in controlled clinical trials. Therefore, the benefit of using protein C during pregnancy must be judged against the risk for the mother, and should be used only if clearly needed.

No information on excretion of protein C in the milk is available. Therefore, the benefit of using protein C during lactation must be judged against the risk for the baby, and should be used only if clearly needed.

Protein C has no influence on the ability to drive and use machines.