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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.
The increase in APC resistance is much greater with oral estrogens than with transdermal estradiol. [14] Increased APC resistance with both the aPTT-based and ETP-based tests has been observed with feminizing hormone therapy in transgender women, which involves higher doses of estradiol than are used in other contexts.
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.
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.
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.
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.
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 ...