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Patients with non-Jo-1 anti-RNA-synthetase autoantibodies have worse survival than Jo-1 positive patients
  1. Baptiste Hervier1,
  2. Hervé Devilliers2,
  3. Olivier Benveniste3
  1. 1Internal Medicine department 2, French Reference Centre for Lupus; Hôpital Pitié-Salpêtrière, APHP & University of Paris VI Pierre & Marie Curie, Paris, France
  2. 2Clinical Investigation Centre, Clinical Epidemiology & Clinical Trials, INSERM CIE1 and Internal Medicine & Systemic Disease Department, University Hospital of Dijon, Dijon, France
  3. 3Internal Medicine department 1, French Reference Centre for Neuromuscular Disorders; Hôpital Pitié-Salpêtrière, APHP & University of Paris VI Pierre & Marie Curie, Paris, France
  1. Correspondence to Dr Baptiste Hervier, Service de Médecine Interne 2, Centre National de référence du Lupus, 47-83 boulevard de l'hôpital, Paris, cedex 13 75651, France; bhervier{at}

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We read with interest the manuscript by Aggarwal et al1 entitled ‘Patients with non-Jo-1 anti-RNA-synthetase autoantibodies have worse survival than Jo-1 positive patients’. This large cohort study provides important information on outcomes for patients with antisynthetase syndrome (ASS), based on the specificity of the anti-RNA-synthetase autoantibody subtypes. Interestingly, the authors decided to include patients with anti-glycyl (EJ), anti-isoleucyl (OJ) and anti-asparagyl (KS)-tRNA-synthetase autoantibodies, something which had not yet been done in the previous studies,2 ,3 due to the rarity of these autoantibodies. The conclusion by Aggarwal et al confirmed our previous data showing a worse prognosis for patients with non-Jo-1 as compared with patients with Jo-1.2 However, this study prompts questions on the following two points:

  1. The authors showed that a longer delay in diagnosing patients with non-Jo1 was a major predictor of poor survival. For this, they used a multivariate Cox model analysis, adjusted for diagnosis delay, as well as for the following parameters: gender, ethnicity, and age at initial and final diagnoses. However, the model was not tested with any of the variables that have clearly been shown to correlate with either poor prognosis (ie, interstitial lung disease1 and pulmonary hypertension1 ,4) or with better survival (ie, the presence of a myositis at ASS diagnosis2). Although the main objective is of course to decrease the diagnosis delay in all patients, it would be quite valuable to know whether this delay is an independent predictor of survival after adjusting for these variables.

  2. The results shown in table 3 and in figure 1 are difficult to interpret since no information is provided about the censored data (overall median patient follow-up <3 years vs survival evaluations >5 years). In table 3, the absolute number of patients evaluated at 5 years and 10 years is not given, which leads to some confusion: do the percentages of patients correspond to the ratio of living patients to total number of patients at diagnosis, or to the probability of survival, as estimated with the Kaplan-Meyer method? Similarly, there are no marks to help identify the censored data in the Kaplan-Meyer curve of figure 1, making it difficult to identify the number of censored patients during the follow-up period.

We thank the authors for addressing these issues and for providing additional data that will be useful for understanding the factors associated with survival of patients with ASS.


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  • Competing interests None.

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