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The causes of acquired antithrombin deficiency are easier to find than the hereditary deficiency. [3] The prevalence of antithrombin deficiency is estimated at ~0.02 to 0.2% of the general population, and 1-5% of patients with venous thromboembolism. [6] There is an elevated risk of thrombosis, whereby 50% patients with AT deficiency were found ...
Antithrombin (AT) is a small glycoprotein that inactivates several enzymes of the coagulation system. It is a 464-amino-acid protein produced by the liver.It contains three disulfide bonds and a total of four possible glycosylation sites. α-Antithrombin is the dominant form of antithrombin found in blood plasma and has an oligosaccharide occupying each of its four glycosylation sites.
Anti-thrombin antibodies can react with both types of thrombin in the antithrombin-thrombin complex. [1] Antibodies (IgG) against thrombin can strongly inhibit its activity. [ 2 ] Inhibitory anti-thrombin antibodies can be divided into 2 groups, those that inhibit coagulation activity and those the inhibit coagulation and amidase activity. [ 3 ]
Thrombin demonstrates a high level of allosteric regulation. [2] Allosterism in thrombin is regulated by the exosites 1 and 2 and the sodium binding site. A recent patent review has shown that the general consensus among researchers is that allosteric inhibitors may provide a more regulatable anticoagulant. [3]
There have also been cases in patients with other deficiency, including protein S deficiency, [6] [7] activated protein C resistance (Factor V Leiden) [8] and antithrombin III deficiency. [ 9 ] Although the above hypothesis is the most commonly accepted, others believe that it is a hypersensitivity reaction or a direct toxic effect.
Reptilase time (RT) is a blood test used to detect deficiency or abnormalities in fibrinogen, [1] [2] especially in cases of heparin contamination. Reptilase, an enzyme found in the venom of Bothrops snakes, has activity similar to thrombin. Unlike thrombin, reptilase is resistant to inhibition by antithrombin III.
In people without a detectable thrombophilia, the cumulative risk of developing thrombosis by the age of 60 is about 12%. About 60% of people who are deficient in antithrombin will have experienced thrombosis at least once by age 60, as will about 50% of people with protein C deficiency and about a third of those with protein S deficiency.
Heparin cofactor II (HCII), a protein encoded by the SERPIND1 gene, is a coagulation factor that inhibits IIa, and is a cofactor for heparin and dermatan sulfate ("minor antithrombin"). [ 5 ] The product encoded by this gene is a serine protease inhibitor which rapidly inhibits thrombin in the presence of dermatan sulfate or heparin.