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Antithrombin III deficiency (abbreviated ATIII deficiency) is a deficiency of antithrombin III.This deficiency may be inherited or acquired. [1] It is a rare hereditary disorder that generally comes to light when a patient suffers recurrent venous thrombosis and pulmonary embolism, and repetitive intrauterine fetal death (IUFD). [2]
The study included women admitted to hospital for one or more days for reasons other than delivery or venous thromboembolism. [5] Pregnancy after the age of 35 augments the risk of VTE, as does multigravidity of more than four pregnancies. [2] Pregnancy in itself causes approximately a five-fold increased risk of deep venous thrombosis. [6]
Direct factor Xa inhibitors (xabans) are anticoagulants (blood thinning drugs), used to both treat and prevent blood clots in veins, and prevent stroke and embolism in people with atrial fibrillation (AF).
Results are given in units/mL of anti-factor Xa, such that high values indicate high levels of anticoagulation and low values indicate low levels of anticoagulation in the plasma sample. [ 17 ] LMWHs have a targeted therapeutic window of approximately 0.6–1.2 IU/ml. LMWH has a potency of 70 units/mg of anti-factor Xa activity and a ratio of ...
Factor Xa also plays a role in other biological processes that are not directly related to coagulation, like wound healing, tissue remodelling, inflammation, angiogenesis and atherosclerosis. Inhibition of the synthesis or activity of Factor X is the mechanism of action for many anticoagulants in use today.
Antiphospholipid syndrome is known for causing arterial or venous blood clots, in any organ system, and pregnancy-related complications.While blood clots and pregnancy complications are the most common and diagnostic symptoms associated with APS, other organs and body parts may be affected like platelet levels, heart, kidneys, brain, and skin.
A person needs to inherit a defective gene from both parents. People who have only one defective gene usually do not exhibit the disease, but can pass the gene on to their offspring. Different genetic mutations have been described. [citation needed] In persons with congenital FX deficiency the condition is lifelong.
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 ...