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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 ...
[2] While the cause of rheumatoid arthritis is not clear, it is believed to involve a combination of genetic and environmental factors. [1] The underlying mechanism involves the body's immune system attacking the joints. [1] This results in inflammation and thickening of the joint capsule. [1] It also affects the underlying bone and cartilage. [1]
High levels of rheumatoid factor (in general, above 20 IU/mL, 1:40, or over the 95th percentile; there is some variation among labs) occur in rheumatoid arthritis (present in 80%) and Sjögren's syndrome (present in 50-70% of primary forms of disease). [11] The higher the level of RF the greater the probability of destructive articular disease.
Factor XII deficiency is a deficiency in the production of factor XII (FXII), a plasma glycoprotein and clotting factor that participates in the coagulation cascade and activates factor XI. FXII appears to be not essential for blood clotting, as individuals with this condition are usually asymptomatic and form blood clots in vivo .
[2] Immune-mediated causes could include transient factors as in Mycoplasma pneumoniae infection (cold agglutinin disease) [14] or permanent factors as in autoimmune diseases like autoimmune hemolytic anemia [15] (itself more common in diseases such as systemic lupus erythematosus, rheumatoid arthritis, Hodgkin's lymphoma, and chronic ...
Hence, there is an interest in developing anti-IL-6 agents as therapy against many of these diseases. [58] [59] The first such is tocilizumab, which has been approved for rheumatoid arthritis, [60] Castleman's disease [61] and systemic juvenile idiopathic arthritis. [62] Others are in clinical trials. [63]
The cause of complement deficiency is genetics (though cases of an acquired nature do exist post infection). The majority of complement deficiencies are inherited as autosomal recessive conditions, while properdin deficiency occurs through X-linked inheritance. MBL deficiency can be inherited by either manner. [2]
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.