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Comment on: ‘Idiopathic inflammatory myopathies and antisynthetase syndrome: contribution of antisynthetase antibodies to improve current classification criteria’ by Greco et al
  1. Johannes Knitza1,
  2. Lorenzo Cavagna2,
  3. Georg Schett1,
  4. Jörg H W Distler1
  1. 1 Department of Internal Medicine 3, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany
  2. 2 Department of Rheumatology, University and IRCCS Foundation Policlinico S. Matteo, Pavia, Italy
  1. Correspondence to Dr Johannes Knitza, Department of Internal Medicine 3, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen D-91054, Germany; johannes.knitza{at}uk-erlangen.de

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With great interest, we read the letter titled ‘Idiopathic inflammatory myopathies and antisynthetase syndrome: contribution of antisynthetase antibodies to improve current classification criteria’ by Greco et al 1 published in the Annals of the Rheumatic Diseases.

The authors analysed if the detection of anti-aminoacyl transfer RNA synthetase (ARS) autoantibodies other than anti-Jo1 could improve the European League Against Rheumatism/Amercian College of Rheumatology (EULAR/ACR) classification criteria2 for adult and juvenile idiopathic inflammatory myopathies (IIM) and classification of antisynthetase syndromes (ASSD). These analyses were performed retrospectively assessing a cohort of 37 patients with clinical suspicion of IIM or ASSD and positive ARS using myositis immunoblots. The authors observed that all patients with clinically objectified muscle weakness and positivity for non-anti-Jo1 ARS did not fulfil EULAR/ACR IIM criteria but could be re-classified as IIM, if assigning non-anti-Jo-1 ARS the same weight as anti-Jo1 ARS.

We appreciate the effort of Greco et al to highlight the importance of ARS autoantibodies. We believe, however, that careful interpretation of ARS autoantibody status is necessary as various autoantibody assays are currently used, often resulting in misleading results. Furthermore, in a recent analysis3 at our centre, we could show that only 27/160 (17%) individuals with ARS autoantibodies (using immunoblot technique) had clinical evidence for ASSD presenting with at least one of the triad findings: arthritis, myositis and interstitial lung disease. It would, therefore, be interesting to know if ARS autoantibody status was validated. In an effort to improve and harmonise the classification of ASSD, the CLASS (classification criteria of ASSD) project has recently been funded by the American College of Rheumatology and the European League Against Rheumatism. It will be interesting to see if similar results can be repeated using a large and carefully selected cohort.

Acknowledgments

We thank Greco et al for their important work emphasising the need for further improvement of current IIM and AASD classification criteria.

References

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Footnotes

  • Contributors JK, LC, GS and JHWD wrote the letter.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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