Protein C is a vitamin K–dependent anticoagulant produced by the liver. When activated by the thrombin–thrombomodulin complex on endothelial cells, activated protein C (APC), with protein S as a cofactor, inactivates clotting factors Va and VIIIa, reducing thrombin formation. APC also has anti-inflammatory and cell-protective effects and promotes fibrinolysis. Protein C deficiency raises venous thrombosis risk.

High protein C levels are uncommon and usually not harmful. They often reflect lab variation, recent therapy (e.g., protein C concentrate), or transient changes from inflammation, pregnancy, or certain medications. Isolated elevations rarely indicate disease; clinicians typically repeat the test, review medications and clinical context, and investigate further only if there are symptoms or other clotting abnormalities.

Protein C is a vitamin K–dependent serine protease made in the liver that, when activated by the thrombin–thrombomodulin complex, degrades clotting factors Va and VIIIa to limit coagulation. Protein S is a vitamin K–dependent nonenzymatic cofactor for activated protein C; only its free form supports APC activity (much is bound to C4b‑binding protein). Deficiencies raise venous thrombosis risk.

Treating low protein C depends on cause and risk: acute thrombosis requires prompt anticoagulation (heparin then oral anticoagulants); severe congenital deficiency or purpura fulminans may need protein C concentrate or fresh frozen plasma. Long-term anticoagulation is often recommended for recurrent events, with specialist hematology input and family testing. Correct reversible causes (vitamin K deficiency, liver disease) and discuss pregnancy prophylaxis with clinicians.

Protein C is a natural anticoagulant that, when activated, inactivates clotting factors Va and VIIIa to limit thrombus formation. It also has anti-inflammatory and cytoprotective effects on the endothelium, helps maintain vascular integrity, and reduces cell apoptosis. Adequate protein C levels lower risk of venous thrombosis and severe clotting complications; deficiency raises risk of recurrent clots and purpura fulminans.

Yes. Inherited protein C deficiency is uncommon: heterozygous defects affect roughly 0.2–0.5% of people (about 1 in 200–1 in 500), while the severe homozygous form is extremely rare and can cause neonatal purpura fulminans. Prevalence is higher among people with unexplained venous clots. Protein C levels may also fall secondarily with liver disease, vitamin‑K deficiency, warfarin use, or sepsis.