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Mothers who are Rh negative (A−, B−, AB−, or O− blood types) and have anti-D antibodies (found on the antibody screen) need to determine the fetus's Rh antigen. If the fetus is also Rh negative (A−, B−, AB−, or O− blood types) then the pregnancy can be managed like any other pregnancy.
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 ...
The minor ("type 2") thrombophilias are much more common. Factor V Leiden is present in 5% of the population of Northern European descent, but much rarer in those of Asian or African extraction. In people with thrombosis, 10% have factor V Leiden. In those who are referred for thrombophilia testing, 30–50% have the defect.
Hypercoagulability in pregnancy is the propensity of pregnant women to develop thrombosis (blood clots). Pregnancy itself is a factor of hypercoagulability (pregnancy-induced hypercoagulability), as a physiologically adaptive mechanism to prevent post partum bleeding . [ 1 ]
It is estimated that less than 1ml of fetal blood is lost to the maternal circulation during normal labour in around 96% of normal deliveries. [1] [2] The loss of this small amount of blood may however be a sensitising event and stimulate antibody production to the foetal red blood cells, an example of which is Rhesus disease of the newborn.
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.
Hemolytic disease of the newborn, also known as hemolytic disease of the fetus and newborn, HDN, HDFN, or erythroblastosis fetalis, [1] [2] is an alloimmune condition that develops in a fetus at or around birth, when the IgG molecules (one of the five main types of antibodies) produced by the mother pass through the placenta.
The disorder was first described by Egeberg in 1965. [5] 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]
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