ANTITHROMBIN III

Antithrombin III is a serine protease inhibitor that regulates blood coagulation by inactivating thrombin (factor IIa) and other activated clotting factors—especially factor Xa. It prevents excessive fibrin formation and limits clot propagation. Heparin and heparan sulfate accelerate antithrombin’s activity. Inherited or acquired antithrombin deficiency impairs this regulation and increases the risk of venous thrombosis.

Antithrombin III (AT III or antithrombin) is not a clotting factor; it’s a natural anticoagulant plasma protein produced by the liver. It neutralizes thrombin (factor IIa) and several activated coagulation factors (IXa, Xa, XIa), and its activity is potentiated by heparin. Deficiency increases venous thrombosis risk and can reduce heparin effectiveness.

Antithrombin III deficiency often causes a tendency to form blood clots. Symptoms include recurrent deep vein thromboses (leg pain, swelling, redness), pulmonary embolism (sudden breathlessness, chest pain, cough, sometimes coughing blood), and clots in unusual sites (brain, liver, gut). It can cause pregnancy loss and neonatal severe clotting in homozygous cases; some people remain asymptomatic until a first thrombotic event.

High antithrombin activity means increased circulating antithrombin function — a stronger natural anticoagulant effect. Common causes include recent heparin or other anticoagulant therapy, sample contamination with heparin, or transient acute‑phase changes. It’s often a laboratory artifact or temporary finding; rarely congenital. Clinically it may imply higher bleeding tendency or altered clotting tests, so interpret with clinical context and consider repeat testing.

Antithrombin III deficiency is treated by preventing and treating blood clots: acute thrombosis is managed with heparin (often with antithrombin concentrate if levels are very low) followed by long-term oral anticoagulation (warfarin or direct oral anticoagulants). Prophylactic anticoagulation is used during high-risk situations (surgery, pregnancy). Management includes individualized anticoagulation duration, monitoring, and family screening/genetic counseling.

Antithrombin III deficiency is rare. Estimates suggest it occurs in roughly 0.02–0.2% of the general population (about 1 in 5,000 to 1 in 500 people). It’s more commonly detected among people with venous thromboembolism, where prevalence may reach about 1–5%. Familial (congenital) forms are less common; heterozygous cases carry the most clinical significance.