الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Rheumatoid arthritis (RA) is a chronic, inflammatory, autoimmune disease that primarily affects the joints and is associated with autoantibodies that target various molecules. It is a heterogeneous disease, with variable clinical presentations and pathogenetic mechanisms. If uncontrolled, RA can lead to accumulating joint damage and irreversible disability. The disease is complex and involves environmental factors that trigger disease in genetically susceptible individuals. About 0.5 % to 1 % of the population are affected with RA worldwide.
The etio-pathogenesis of RA is not fully elucidated. It is attributed to a complex interaction between genetic and environmental factors and the repeated activation of innate and adaptative immune systems that evolves into the breakdown of immune tolerance, aberrant autoantigen presentation and antigen-specific T and B cells activation. All these events result in synovial hyperplasia and bone destruction leading to joint swelling and deformity and to systemic inflammation.
Early diagnosis and immediate, effective therapy are crucial for the prevention of joint deterioration, functional disability and unfavorable disease outcome. The current, optimal management of RA requires that adequate therapy should be initiated within 3-6 months after the onset of the disease.
Autoantibodies are the most vital biomarkers for RA patients. The 2010 ACR/EULAR classification criteria serological biomarkers include RF, anti-citrullinated protein antibodies (ACPA) among other factors to classify RA. Novel biomarkers to identify early RA are emerging including anti-Carbamylated Protein (anti-CarP) antibodies, which were first described by Shi et al. Carbamylation is a chemical modification that is carried out in the presence of cyanate. Anti-CarP antibodies target proteins that contain homocitrulline, also called carbamylated protein. Anti-CarP antibodies can be present years before disease onset and can predict the development of RA in arthralgia patients independent of anti-CCP antibodies