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Correspondence response
Response to: ‘COVID-19 in patients with rheumatological diseases treated with Anti-TNF’ by Brito et al and ‘Clinical characteristics and outcomes of patients with COVID-19 and rheumatic disease in China ‘hot spot’ versus in US ‘hot spot’: similarities and differences’ by Zhao et al
  1. Kristin M D’Silva1,
  2. Naomi Serling-Boyd1,
  3. Rachel Wallwork1,
  4. Tiffany Hsu2,
  5. Jeffrey A Sparks2,
  6. Zachary Scott Wallace1
  1. 1 Division of Rheumatology, Allergy, and Immunology, Harvard Medical School, Boston, Massachusetts, USA
  2. 2 Division of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, Massachusetts, USA
  1. Correspondence to Dr Zachary Scott Wallace, Rheumatology Unit, Massachusetts General Hospital, Boston, MA 02114, USA; zswallace{at}partners.org

https://doi.org/10.1136/annrheumdis-2020-218196

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    We appreciate the comments by Brito et al,1 and Zhao et al,2 in response to our manuscript evaluating outcomes among a cohort of patients with rheumatic diseases and COVID-19.3 We were interested to read the reports of their patients during the COVID-19 pandemic and would like to reply to some of their queries.

    Brito et al raised the important point that the risk of severe infections may vary with therapeutic class of immunosuppressive therapy. We agree that further studies are needed to assess this important question, and we plan to investigate this by therapeutic class for our cohort in future studies as our sample size grows. We agree that studies of therapeutic class will have to account for potential confounding factors, including glucocorticoid exposure, in their design. A recent report performed among patients with rheumatic diseases suggested lower odds of hospitalised infection for biological/targeted disease-modifying antirheumatic drugs (DMARDs) and higher …

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    Footnotes

    • Handling editor Josef S Smolen

    • Twitter @jeffsparks

    • Correction notice This article has been corrected since it published Online First. The title and reference 2 have both been corrected.

    • Contributors All authors contributed to the conception and drafting of the article. All listed authors provided critical revision for important intellectual content and final approval.

    • Funding KMD and NS-B are supported by the National Institutes of Health Ruth L. Kirschstein Institutional National Research Service Award (T32-AR-007258).

    • Competing interests JAS reports grants from NIH/NIAID/Autoimmune Centers of Excellence, the Rheumatology Research Foundation, the Brigham Research Institute, and the R. Bruce and Joan M. Mickey Research Scholar Fund as well as personal fees from Bristol-Myers Squibb, Gilead, Inova, Janssen, and Optum. ZSW reports grants from NIH/NIAMS (K23AR073334 and L30 AR070520) and Bristol-Myers Squibb.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

    • Provenance and peer review Commissioned; internally peer reviewed.

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