Rheumatoid arthritis

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation of the synovial joints, which leads to joint swelling, progressive joint erosion and ultimately lead to cartilage and bone destruction. The disease is often disabling and significantly affects quality of life.

Rheumatoid arthritis is prevalent in all ethnic groups, affecting approximately 0.4-1.0% of the population of the western world. As is often the case with autoimmune diseases, there is a female overrepresentation.

Onset is most frequent between the ages of 40 and 50, but people of any age can be affected. While rheumatoid arthritis primarily affects joints, problems involving other organs of the body are known to occur.

Extra-articular manifestations are clinically evident in about 15–25% of individuals with rheumatoid arthritis.


Disease outcome may vary from mild clinical symptoms to severe systemic disease when joint destruction is accompanied with these extra-articular manifestations.


So far, no therapy has been developed that cures the disease. Current therapies may, however, slow down the extent of swelling and erosive damage. To achieve the greatest therapeutic potential and effect it is essential to initiate treatment at an early stage of the disease.

An early and accurate diagnosis

Early and accurate diagnosis is therefore of outmost importance and presence of autoantibodies to citrullinated proteins/peptides (anti-CCP) has an important prognostic value for the disease and antibodies can be detected even before the onset of clinical symptoms. The anti-CCP2 test has a very high specificity and sensitivity and is a reliable and accurate toolset for the early diagnosis and follow-up of RA. Due to its great clinical use, anti-CCP is included in the ACR/EULAR criteria for diagnosing RA.

Relevant Literature

  1. Aletaha D, et al. "2010 rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative". Ann. Rheum. Dis. 2010; 69: 1580–1588.
  2. Bizzaro N et al. Analytical and diagnostic characteristics of 11 2nd- and 3rd-generation immunoenzymatic methods for the detection of antibodies to citrullinated proteins. Clin Chem 2007; 53: 1527-1533.
  3. de Vries-Bouwstra JK, Goekoop-Ruiterman YP, Verpoort KN, et al. Progression of joint damage in early rheumatoid arthritis: association with HLA-DRB1, rheumatoid factor, and anti-citrullinated protein antibodies in relation to different treatment strategies. Arthritis Rheum 2008; 58:1293-1298.
  4. Finckh A, Liang MH. Anti-cyclic citrullinated peptide antibodies in the diagnosis of rheumatoid arthritis: bayes clears the haze. Ann Intern Med 2007; 146:816-817.
  5. Finckh A. Early inflammatory arthritis versus rheumatoid arthritis Curr Opinion Rheumatology 2009; 21: 118-123
  6. Guillemin F et al Prognostic factors for joint destruction in rheumatoid arthritis: a prospective longitudinal study of 318 patients. J Rheumatol. 2003;30: 2585–2589.
  7. Goekoop-Ruiterman YP, de Vries-Bouwstra JK, Allaart CF, et al. Comparison of treatment strategies in early rheumatoid arthritis: a randomized trial. Ann Intern Med 2007; 146:406-415.
  8. Klareskog L, Catrina AI, Paget S. Rheumatoid arthritis. Lancet 2009; 373:659.
  9. Lee DM, Weinblatt ME. Rheumatoid arthritis. Lancet 2001; 358:903-911.
  10. Levesque M, Zhou Z, Moreland L. Anti-cyclic citrullinated peptide testing for the diagnosis of rheumatoid arthritis and the quest for the improved sensitivity and predictive value. Arthritis Rheum 2009; 60: 2211-2215.
  11. McQueen FM et al. What is the fate of erosions in early rheumatoid arthritis? Tracking individual lesions using x-rays and magnetic resonance imaging over the first two years of disease. Ann Rheum Dis. 2001;60: 859–868.
  12. Pruijn G, Wiik A, van Venrooij W. The use of citrullinated peptides and proteins for the diagnosis of rheumatoid arthritis. Arthritis Research & Therapy 2010; 12: 203
  13. Quinn MA, Emery P. Window of opportunity in early rheumatoid arthritis: possibility of altering the disease process with early intervention. Clin Exp Rheumatol. 2003; 21(5 suppl 31):S154–7.
  14. Russell AS, Devani A, Maksymowych WP. The role of anti-cyclic citrullinated peptide antibodies in predicting progression of palindromic rheumatism to rheumatoid arthritis. J Rheumatol 2006; 33:1240-1242.
  15. Smolen JS et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs. Ann Rheum Dis 2010; 69:964-975.
  16. St Clair EW et al. Combination of infliximab and methotrexate therapy for early rheumatoid arthritis: a randomized, controlled trial. Arthritis Rheum. 2004;50: 3432–3443.
  17. van der Linden M, et al. Value of anti-modified citrullinated vimentin and third-generation anti-cyclic citrullinated peptide compared with second-generation anti-cyclic citrullinated peptide and rheumatoid factor in predicting disease outcome in undifferentiated arthritis and rheumatoid arthritis. Arthritis Rheum 2009; 60: 2232-2241.
  18. van Venrooij W., van Beers J., Pruijn G  Anti-CCP antibodies: the past, the present and the future. Nature Reviews Rheumatology 2011; 7: 391-398
  19. Whiting PF, et al. Systematic review: accuracy of anti-citrullinated Peptide antibodies for diagnosing rheumatoid arthritis. Ann Intern Med. 2010; 152: 456-464.
  20. Wild N et al. Diagnosis of rheumatoid arthritis: multivariate analysis of biomarkers. Biomarkers 2008; 13: 88-105.