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Anti-double stranded DNA (Anti-dsDNA) antibodies are a group of anti-nuclear antibodies (ANA) the target antigen of which is double stranded DNA. Blood tests such as enzyme-linked immunosorbent assay (ELISA) and immunofluorescence are routinely performed to detect anti-dsDNA antibodies in diagnostic laboratories.
Subtypes of antinuclear antibodies include anti-Smith and anti-double stranded DNA antibodies (which are linked to SLE) and anti-histone antibodies (which are linked to drug-induced lupus). Anti-dsDNA antibodies are highly specific for SLE; they are present in 70% of cases, whereas they appear in only 0.5% of people without SLE. [13]
The presence of anti-dsDNA antibodies is also linked with lupus nephritis and there is evidence they are the cause. Some anti-dsDNA antibodies are cross reactive with other antigens found on the glomerular basement membrane (GBM) of the kidney, such as heparan sulphate, collagen IV, fibronectin and laminin.
the degree of modification of the capillaroscopy test (skin blood vessel study technique) of nail fold during follow-up. the presence of antinuclear antibodies. young age. [21] severe vitamin D deficiency. [22] the presence of anti-dsDNA, anti-Sm and anti-cardiolipin autoantibodies correlates with the development of systemic lupus erythematosus ...
For instance, up to 80% of those with SLE will have a positive double strand anti-double stranded DNA (anti-dsDNA) autoantibody test, but only about 25–30% will have a positive RNP. Some individuals who do have an autoimmune disorder will have negative autoantibody test results, but at a later date – as the disorder progresses - the ...
p-ANCA is associated with several medical conditions: [3] It is fairly specific, but not sensitive for ulcerative colitis, so is not useful as a sole diagnostic test. [4] When measured together with anti-saccharomyces cerevisiae antibodies (ASCA), p-ANCA has been estimated to have a specificity of 97% and a sensitivity of 48% in differentiating patients with ulcerative colitis from normal ...
These autoantibodies, none of which are present in all cases of SLE, include the: a) antinuclear (i.e., ANA) and anti-dsDNA antibodies; b) anti-Sm, anti-RNP, anti-SSA, and anti–SS-B antibodies (anti-SSA and anti-SS-B antibodies are associated with less severe forms of cSLE); [30]) c) antiphospholipid autoantibodies including the lupus ...
The "lupus anticoagulant paradox" [6] may be explained by platelet activation as described above, as well as enhancement of activated protein C resistance and suppression of the anticoagulant activity of TFPIα. Another proposed mechanism is the antibody-mediated destruction of Annexin A5 on the membranes of endothelial cells and trophoblast cells.