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A clinical suspicion for antithrombin deficiency can be made in patients with: 1. recurrent venous thromboembolic disease, 2. childhood thrombosis, 3. thrombosis in pregnancy. Testing for antithrombin activity can confirm deficiency if the levels are less than 70%.
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.
Inhibitory anti-thrombin antibodies can be divided into 2 groups, those that inhibit coagulation activity and those the inhibit coagulation and amidase activity. [3] Autoimmune anti-thrombin was also found to inhibit the binding of antithrombin III to thrombin. [4] Such activities are more often found with primary biliary cirrhosis.
In human adults, the normal blood level of antithrombin activity has been measured to be around 1.1 units/mL. Newborn levels of thrombin steadily increase after birth to reach normal adult levels, from a level of around 0.5 units/mL 1 day after birth, to a level of around 0.9 units/mL after 6 months of life. [12]
TAT levels are increased with pregnancy [6] and by ethinylestradiol-containing birth control pills. [7] They have also been reported to be increased by menopausal hormone therapy, although findings are mixed, [3] [8] and with high-dose parenteral estradiol therapy for prostate cancer. [9] [10] [11]
There is also an increased activity of another form of Antithrombin, Beta Antithrombin in newborns compared to older children and adults. [6] alpha-2-Macroglobulin (A2M): is also a major inhibitor of thrombin. It is present in 2-3 fold higher concentration during childhood, approaching adult levels in late teenage years.
[1] [3] They may also be useful in the assessment of hypercoagulability and venous thromboembolism risk. [4] [5] [6] Levels of coagulation activation markers are increased with pregnancy, [7] with estrogen-containing birth control pills, [8] with menopausal hormone therapy, [9] [6] and with high-dose parenteral estradiol therapy for prostate ...
Human Chr 3. In terms of the cause of protein S deficiency it can be in inherited via autosomal dominance.A mutation in the PROS1 gene triggers the condition. The cytogenetic location of the gene in question is chromosome 3, specifically 3q11.1 [6] [7] Protein S deficiency can also be acquired due to vitamin K deficiency, treatment with warfarin, liver disease, kidney disease, chemotherapy ...