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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 ...
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 ]
Dietary deficiencies: Folate deficiency and vitamin B12 deficiency are common causes of anemia in pregnancy. Folate deficiency occurs due to diets low in leafy green vegetables, and animal sources of protein. [10] B12 deficiency tends to be more common in individuals with Crohn's disease or gastrectomies. [11]
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.
Protein S (also known as PROS) is a vitamin K-dependent plasma glycoprotein synthesized in the liver. In the circulation, Protein S exists in two forms: a free form and a complex form bound to complement protein C4b-binding protein (C4BP). In humans, protein S is encoded by the PROS1 gene. [5] [6] Protein S plays a role in coagulation.
Hypoprothrombinemia can be the result of a genetic defect, may be acquired as the result of another disease process, or may be an adverse effect of medication.For example, 5-10% of patients with systemic lupus erythematosus exhibit acquired hypoprothrombinemia due to the presence of autoantibodies which bind to prothrombin and remove it from the bloodstream (lupus anticoagulant ...
Pregnancy-induced hypercoagulability is probably a physiologically adaptive mechanism to prevent post partum hemorrhage. [1] Pregnancy changes the plasma levels of many clotting factors, such as fibrinogen, which can rise up to three times its normal value. [2] Thrombin levels increase. [3] Protein S, an anticoagulant, decreases
The last category, alterations in the constitution of blood, [6] has numerous possible risk factors such as hyperviscosity, coagulation factor V Leiden mutation, coagulation factor II G2021A mutation, deficiency of antithrombin III, protein C or S deficiency, nephrotic syndrome, changes after severe trauma or burn, cancer, late pregnancy and ...