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Anti-CCP is also very useful in the early diagnosis of rheumatoid arthritis in high-risk groups, such as relatives of RA patients, [19] although Silman and co-workers found that the concordance rate of developing RA was 15.4% among identical (monozygotic) twins and was 3.6% among fraternal (dizygotic) twins.
Anti-MCV antibodies are a member of the ACPA family, a group of the so-called antibodies to citrullinated protein/peptide antigens. Rheumatoid arthritis is an autoimmune disorder. Detection of specific autoantibodies (antibodies directed against the body’s own tissue) such as rheumatoid factors and ACPAs may provide indication of the disease.
The presence of anti-citrullinated protein antibody is a standard test for rheumatoid arthritis, and it is associated with more severe disease. Citrullinated proteins are also found in the cellular debris accompanying the destruction of cells in alzheimer disease , and after smoking cigarettes.
The by far most common clinical test for ACPAs is the anti-cyclic citrullinated peptide (anti CCP) ELISA. In 2008 a serological point-of-care test for the early detection of RA combined the detection of RF and anti-MCV with a sensitivity of 72% and specificity of 99.7%. [79] [better source needed] [80]
Rheumatoid factor is part of the 2010 ACR/EULAR classification criteria for rheumatoid arthritis. RF positivity combines well with anti-CCP and/or 14-3-3η to inform diagnosis. [9] RF positivity at baseline has also been described as a good prognostic marker for future radiographic damage. [10]
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Anti-centromere antibodies (ACAs; often styled solid, anticentromere) are autoantibodies specific to centromere and kinetochore function. They occur in some autoimmune diseases , frequently in limited systemic scleroderma (formerly called CREST syndrome ), and occasionally in the diffuse form of scleroderma .
Anti-histone antibodies are autoantibodies that are a subset of the anti-nuclear antibody family, which specifically target histone protein subunits or histone complexes. [1] They were first reported by Henry Kunkel , H.R. Holman, and H.R.G. Dreicher in their studies of cellular causes of lupus erythematosus in 1959–60.