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  • Response to: ‘Correspondence on ‘SARS-CoV-2 antibody response after COVID-19 in patients with rheumatic disease’’ by C et al

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Correspondence response
Response to: ‘Correspondence on ‘SARS-CoV-2 antibody response after COVID-19 in patients with rheumatic disease’’ by C et al
  1. Kristin M D’Silva1,
  2. Naomi Serling-Boyd1,
  3. Tiffany Y-T Hsu2,
  4. Jeffrey A Sparks2,
  5. 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-2021-220166

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    We appreciate the comments by Shanoj et al 1 in response to our letter regarding the SARS-CoV-2 antibody response after COVID-19 in patients with rheumatic disease.2 Examining whether patients treated with CD20 inhibitors have antibody responses to SARS-CoV-2 is a question of great clinical importance in the management and vaccination of patients taking these medications during the COVID-19 pandemic.

    Shanoj et al describe anti-spike and anti-nucleocapsid antibody test results among five patients with PCR-confirmed COVID-19 and prior exposure to rituximab.1 Among these patients, one patient developed neither anti-spike nor anti-nucleocapsid antibodies.1 This patient had been treated with rituximab for several years and had no detectable CD19+ B cells shortly before the onset of COVID-19.1 One patient developed anti-spike but not anti-nucleocapsid antibodies; although the duration of rituximab treatment is not provided, …

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    Footnotes

    • Handling editor Josef S Smolen

    • Twitter @jeffsparks

    • Contributors KMD’S, NS-B, TY-TH, JAS and ZSW contributed to the conception and drafting of the article. All listed authors provided critical revision for important intellectual content and final approval.

    • Funding KMD’S and NS-B are supported by the National Institutes of Health Ruth L. Kirschstein Institutional National Research Service Award (T32-AR-007258). KMD’S is supported by the Rheumatology Research Foundation Scientist Development Award. JAS is funded by NIH/NIAMS (grant numbers K23 AR069688, R03 AR075886, L30 AR066953, P30 AR070253 and P30 AR072577), the Rheumatology Research Foundation R Bridge Award, the Brigham Research Institute, and the R. Bruce and Joan M. Mickey Research Scholar Fund. ZSW is funded by NIH/NIAMS (K23AR073334 and L30 AR070520).

    • Competing interests JAS reports research support from Amgen and Bristol-Myers Squibb and consultancy fees from Bristol-Myers Squibb, Gilead, Inova, Janssen, Optum, and Pfizer. ZSW reports research support from Bristol-Myers Squibb and Principia and consulting fees from Viela Bio and MedPace.

    • 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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