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• Clustering and seroconversion in juvenile-onset SLE
  Ufuk Ilgen
  Published on: 6 June 2023

• Published on: 6 June 2023

  Clustering and seroconversion in juvenile-onset SLE

  • Ufuk Ilgen, Rheumatologist Ankara University

  Ufuk Ilgen
  Rheumatology, Ankara University, Ankara, Turkey

  On behalf of all co-authors: Ufuk Ilgen, Mucteba Enes Yayla, Askin Ates, Ilyas Ercan Okatan, Emine Uslu Yurteri, Murat Torgutalp, Ayse Bahar Dincer Kelesoglu, Tahsin Murat Turgay, and Gulay Kinikli

  Dear Editor,

  We read the article by Bao S et al1 with interest. The authors cited our previous work2 by stating: “Prior research of aPL analysis in patients with JSLE did not include the other autoantibodies, and thus the results may not be convincing enough because the impact of the other autoantibodies was neglected in the disease course.” We have some concerns about the interpretation of our results:

  1. Our study did not include patients with juvenile-onset SLE. As clearly stated in Methods, all were adult patients. Disease duration did not either date back to childhood (Table 1).

  2. Potential impact of other autoantibodies on disease course was not neglected. As stated in Methods, all patients had a panel of 16 autoantibodies (against Sm, nucleosome, histone, PCNA, PO, SS-A 60 kDa, SS-A 52 kDa, SS-B, CENP-B, Scl-70, U1-RNP, Jo-1, PM/Scl, Mi-2, Ku, and dsDNA). However, none were found to be associated with antiphospholipid antibody status.

  3. The aim of our study was not to determine a relationship between a general autoantibody profile and SLE manifestations at all. Patients with serial antiphospholipid antibody measurements were included in the study.
  Some additi...

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  Ufuk Ilgen
  Rheumatology, Ankara University, Ankara, Turkey

  On behalf of all co-authors: Ufuk Ilgen, Mucteba Enes Yayla, Askin Ates, Ilyas Ercan Okatan, Emine Uslu Yurteri, Murat Torgutalp, Ayse Bahar Dincer Kelesoglu, Tahsin Murat Turgay, and Gulay Kinikli

  Dear Editor,

  We read the article by Bao S et al1 with interest. The authors cited our previous work2 by stating: “Prior research of aPL analysis in patients with JSLE did not include the other autoantibodies, and thus the results may not be convincing enough because the impact of the other autoantibodies was neglected in the disease course.” We have some concerns about the interpretation of our results:

  1. Our study did not include patients with juvenile-onset SLE. As clearly stated in Methods, all were adult patients. Disease duration did not either date back to childhood (Table 1).

  2. Potential impact of other autoantibodies on disease course was not neglected. As stated in Methods, all patients had a panel of 16 autoantibodies (against Sm, nucleosome, histone, PCNA, PO, SS-A 60 kDa, SS-A 52 kDa, SS-B, CENP-B, Scl-70, U1-RNP, Jo-1, PM/Scl, Mi-2, Ku, and dsDNA). However, none were found to be associated with antiphospholipid antibody status.

  3. The aim of our study was not to determine a relationship between a general autoantibody profile and SLE manifestations at all. Patients with serial antiphospholipid antibody measurements were included in the study.
  Some additional concerns are:
  a. If patients with juvenile-onset SLE in the study by Bao S et al are divided into two groups based solely on the anti-U1-RNP status, the generated groups will exactly be the same as the cluster analysis results provided in Table 2. If a cluster analysis by just a single variable, the anti-U1-RNP status, is run, one will also have exactly the same result. Similar to antiphospholipid antibodies, the inclusion of autoantibodies other than the anti-U1-RNP to clustering would not have any impact on the results. So, the results provided in Table 3 may be interpreted as “clinical features associated with anti-U1-RNP antibodies”.
  b. Some autoantibodies such as anti-dsDNA, anti-Sm, and anti-RNP have been known to have strong clinical associations, whereas some have little impact on disease phenotype and activity. Moreover, each may have somewhat differential impact on disease manifestation domains. As an example, positivity (including positive seroconversion) of anti-dsDNA has been known to be associated with nephritis which strongly contributes to disease activity, whereas anti-La positivity (including positive seroconversion) is associated with sicca which is not considered as a component of SLE disease activity in widely used disease activity indices such as SLEDAI. Putting all seroconversions in a single pool may cause losing fine clinical associations of particular autoantibodies. High rate of lupus nephritis in seroconverters in this study is not necessarily related to seroconversion itself, rather this may be related to high prevalence of baseline anti-Sm/RNP in the seroconverter group (Table 1). This point requires further analysis.
  In conclusion, clustering based solely on autoantibody profile may not have a clinical translation other than established clinical associations of particular autoantibodies. Clinical associations of seroconversion should be interpreted for each particular autoantibody.

  References
  1. Bao S, Huang H, Jin Y, et al. Autoantibody-based subgroups and longitudinal seroconversion in juvenile-onset systemic lupus erythematosus. Lupus Science & Medicine 2023;10:e000834. doi:10.1136/ lupus-2022-000834
  2. Ilgen U, Yayla ME, Ateş A, et al. Antiphospholipid antibodies and non-thrombotic manifestations of systemic lupus erythematosus. Lupus 2018;27:665-9. doi: 10.1177/0961203317734924

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  Conflict of Interest:
  None declared.

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