<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Lee, Ashley Nicole</style></author><author><style face="normal" font="default" size="100%">Beck, Carolyn E</style></author><author><style face="normal" font="default" size="100%">Hall, Margot</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Rheumatoid Factor and Anti-CCP Autoantibodies in Rheumatoid Arthritis: A Review</style></title><secondary-title><style face="normal" font="default" size="100%">American Society for Clinical Laboratory Science</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008-01-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">15-18</style></pages><doi><style  face="normal" font="default" size="100%">10.29074/ascls.21.1.15</style></doi><volume><style face="normal" font="default" size="100%">21</style></volume><issue><style face="normal" font="default" size="100%">1</style></issue><abstract><style  face="normal" font="default" size="100%">For many years, laboratory diagnosis of rheumatoid arthritis has relied on the detection of rheumatoid factor. A new assay that detects antibodies to citrullinated peptides, called the anti-CCP assay, has demonstrated a comparable sensitivity but a much higher specificity than the RF test. This paper reviews RF and anti-CCP in rheumatoid arthritis and examines the usefulness of each autoantibody in RA testing.Rheumatoid arthritis (RA) is a systemic autoimmune disease of unknown etiology that is characterized by chronically inflamed synovial joints and subsequent destruction of cartilage and bone. RA is found in about one percent of the population, making it one of the most common autoimmune diseases in the United States.1 RA is marked by several key characteristics, including synovitis occurring in a symmetrical fashion, polyarthritis, morning stiffness lasting over an hour, periods of disease flare-ups followed by periods of disease remission, and the development of subcutaneous rheumatoid nodules.2 The disease does not affect all patients the same way, and may range from a mild form to one that is very debilitating. RA can present with many symptoms, including pain, swelling, stiffness, joint deformity, and loss of movement. It can have a serious impact on a patient's quality of life, and early intervention is key to minimizing the damaging effects of the disease.1 The standard therapies for RA include analgesic drugs, non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids or prednisone, and disease-modifying anti-rheumatic drugs (DMARDs).2RA can be difficult to diagnose, especially in the early stages of the disease. In 1987, the…ABBREVIATIONS: AFA = antifilaggrin autoantibodies; AKA = antikeratin antibodies; APF = antiperinuclear factor; CCP = cyclic citrullinated peptide; CRP = C-reactive protein; DMARDS = disease-modifying anti-rheumatic drugs; ELISA = enzyme-linked immunosorbent assay; ESR = erythrocyte sedimentation rate; Ig = immunoglobulin; MTX = methotrexate; NSAIDS = non-steroidal anti-inflammatory drugs; PAD = peptidylarginine deiminase; RA = rheumatoid arthritis; RF = rheumatoid factor.</style></abstract></record></records></xml>