What is the reason for high antithrombin?

Antithrombin is an active factor in human blood. Generally, as the blood coagulates and the protein in the body dissolves, changes will occur in the blood, which can easily cause blood coagulation, etc. It can easily lead to kidney disease and nephritis, etc. It is very harmful to the human body and requires timely and detailed examinations and treatments. Pay attention to changes in the body.

High antithrombin

Antithrombin III (AT III) is the most important inhibitor of active coagulation factors in the blood, which controls blood coagulation and fibrinolysis.

The level of ATⅢ in the blood varies depending on various comorbidities and is reduced in disseminated intravascular coagulation (DIC), liver disease, nephrotic syndrome, etc.

How it works

Antithrombin Ⅲ (AT Ⅲ). AT III is an inhibitor of thrombin and serine-containing proteases such as factors XIIα, XIα, IXα, and Xα. It binds to thrombin via an arginine-serine peptide bond. The AT Ⅲ thrombin complex is formed, which inactivates the enzyme. Heparin can accelerate this reaction by more than a thousand times. Heparin binds to the lysine contained in AT III, causing a conformational change in AT III, making the arginine residue contained in AT III more easily bound to the serine residue of thrombin. Once the heparin-AT III thrombin complex is formed, heparin dissociates from the complex and combines with another AT III molecule again for repeated use. The AT III-thrombin complex is eliminated by the reticuloendothelial system. The inhibitory effect on thrombin activity is related to the length of heparin molecules. The longer the molecule, the greater the enzyme inhibition.

Deficiency

1. Hereditary ATⅢ deficiency can be divided into two types: (1) CRM-type: both antigen and activity are decreased. (2) CRM+ type: normal antigen, decreased activity.

Hereditary ATⅢ deficiency is an autosomal dominant genetic disease with a prevalence of approximately 1/5000. It mostly occurs in patients aged 10-25 years. Patients often develop venous thrombosis after surgery, trauma, infection, pregnancy or delivery, and thrombosis may occur repeatedly. The biological activity and antigenicity of ATⅢ in the plasma of CRM- patients are about 50% of that of normal people. There are many types of ATⅢ structural and functional abnormalities in CRM+, and the common manifestation is a reduced affinity for heparin, thereby significantly weakening the ability to inactivate serine proteases.

2. Acquired ATⅢ deficiency:

(1) Reduced ATⅢ synthesis is seen in liver diseases, liver dysfunction, mainly in cirrhosis, severe hepatitis, and advanced liver cancer. It is often related to the severity of the disease and may be accompanied by thrombosis.

(2) Increased loss of ATⅢ: seen in nephrotic syndrome.

(3) Increased ATⅢ consumption is seen in prethrombotic and thrombotic diseases, such as angina pectoris, myocardial infarction, cerebrovascular disease, DIC, postoperatively, oral contraceptives, deep vein thrombosis, pulmonary infarction, and pregnancy-induced hypertension.

(4) Increased ATⅢ level is seen in hemophilia A and hemophilia B, oral anticoagulants, and the use of progesterone drugs.