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What is rheumatoid arthritis? Considering consequences of changed classification criteria
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  1. Annette H M van der Helm-van Mil1,2,
  2. Angela Zink3,4
  1. 1Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands
  2. 2Department of Rheumatology, Erasmus Medical Center, Rotterdam, The Netherlands
  3. 3Epidemiology Unit, German Rheumatism Research Centre, Berlin, Germany
  4. 4Department for Rheumatology and Clinical Immunology, Charité University Medicine, Berlin Germany
  1. Correspondence to Professor Dr Annette H M van der Helm-van Mil, Department of Rheumatology, Leiden University Medical Center, P.O. Box 9600, RC Leiden 2300, The Netherlands; AvdHelm{at}lumc.nl

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Changes in classification criteria

Rheumatoid arthritis (RA) was recognised as a separate disease entity in the middle of the 20th century. Since then several sets of classification criteria were developed for use in clinical studies. The 1987 American College of Rheumatology (ACR) criteria1 have been criticised as they are fulfilled rather late in the disease. Consequently, trials that included patients with RA based on the 1987 criteria studied patients with relatively long-standing arthritis. The aim of the American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) expert panel was therefore to develop novel criteria without the features of long-standing disease such as erosions or nodules. Indeed the hitherto developed 2010 ACR/EULAR classification criteria for RA2 are fulfilled earlier in the disease course than the 1987 criteria.3 ,4 Thus, the major objective of the new criteria was achieved.

The study of Nordberg et al5 makes us think about the consequences of the novel criteria for the phenotype of RA. According to the 1987 criteria, the characteristic phenotype of RA consists of symmetric polyarthritis of small joints with morning stiffness (ignoring the features of long-standing disease nodules and erosions). Symmetry and morning stiffness are no longer included in the 2010 criteria. There is less emphasis on clinical elements in the 2010 criteria, and this is paralleled by an emphasis on the results of additional investigations: anti-citrullinated peptide antibodies (ACPA) and acute phase responses were introduced (table 1). The majority of the six points required to fulfil the 2010 criteria can be achieved either by the presence of autoantibodies or on the number of swollen joints. Nordberg et al showed that patients with ACPA-positive RA fulfilling the 2010 criteria have less inflamed joints (measured with either physical examination or with ultrasound) than patients with ACPA-negative RA. This finding is not surprising if we …

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