Rheumatoid Factor and Anti-CCP Autoantibodies in Rheumatoid Arthritis: A Review

Ashley Nicole Lee; Carolyn E Beck; Margot Hall

doi:10.29074/ascls.21.1.15

This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.

Ashley Nicole Lee, MS CLS (NCA)⇑
Carolyn E Beck, EdD MT (ASCP) SBB
Margot Hall, PhD FAIC (CPC) FACB FRACI (CChemA) MRSC (CChem)

are of The University of Southern Mississippi, Hattiesburg MS

Address for correspondence: Ashley Nicole Lee, PO Box 1937, Ocean Springs MS 39566-1937. (601) 266-4908. starsweeper18{at}hotmail.com.

Extract

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).²

RA 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.