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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 ...
There is an association between rheumatoid factor and more persistently active synovitis, more joint damage, greater eventual disability and arthritis. [12] [13] Other than in rheumatoid arthritis, rheumatoid factor may also be elevated in other conditions, including: Systemic lupus erythematosus (SLE) [14] [15] Sjögren syndrome [14] [15]
Other causes of reactive thrombocythemia include: post surgery, iron deficiency, drugs, and rebound effect after bone marrow suppression. [8] Research suggests that thrombocytosis can also occur after physical exercise , and is triggered by hemoconcentration and the release of platelets from the liver , lungs and spleen .
Glanzmann's thrombasthenia is an abnormality of the platelets. [2] It is an extremely rare coagulopathy (bleeding disorder due to a blood abnormality), in which the platelets contain defective or low levels of glycoprotein IIb/IIIa (GpIIb/IIIa), which is a receptor for fibrinogen.
Scott syndrome is a rare congenital bleeding disorder that is due to a defect in a platelet mechanism required for blood coagulation. [1]Normally when a vascular injury occurs (i.e., a cut, scrape or other injury that causes bleeding), platelets are activated and phosphatidylserine (PS) in the inner leaflet of the platelet membrane is transported to the outer leaflet of the platelet membrane ...
Fibrinogen deficiency, also known as factor I deficiency, is a rare inherited bleeding disorder related to fibrinogen function in the coagulation cascade. It is typically subclassified into four distinct fibrinogen disorders : afibrinogenemia, hypofibrinogenemia, dysfibrinogenemia, and hypodysfibrinogenemia.
Heyde's syndrome is a syndrome of gastrointestinal bleeding from angiodysplasia in the presence of aortic stenosis. [1] [2] It is named after Edward C. Heyde, MD, who first noted the association in 1958. [3] It is caused by cleavage of Von Willebrand factor (vWF) due to high shear stress forces from aortic valvular stenosis.
Vos originally described Rh-deficiency syndrome in 1961, when a sample of blood failed to respond with several Rh antisera. However, R. Ceppellini used the term "Rhnull" for the first time. So far, at least 43 people from 14 families have been reported in the literature as having the Rhnull phenotype. [4]
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