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Second COVID-19 infection in a patient with granulomatosis with polyangiitis on rituximab
  1. Marcia A Friedman1,
  2. Kevin L Winthrop1,2
  1. 1 Department of Medicine, Oregon Health & Science University, Portland, Oregon, USA
  2. 2 School of Public Health, Oregon Health & Science University, Portland, Oregon, USA
  1. Correspondence to Dr Marcia A Friedman, Department of Medicine, Oregon Health & Science University, Portland, OR 97239-3098, USA; friedmam{at}ohsu.edu

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Introduction

Observational data suggest there may be an association between rituximab and severe COVID-19 outcomes.1–3 Anti-CD20 therapies impair humoral response, theoretically increasing the risk of prolonged SARS-CoV-2 infection and shedding, as well as subsequent reinfection. Here, we report a patient with granulomatosis with polyangiitis (GPA) being treated with rituximab who appears to have developed recurrent SARS-CoV-2 infections in the setting of high-risk employment and on recovery ultimately had no detectable SARS-CoV-2 IgG antibodies. This case highlights a potential risk of rituximab in patients with rheumatic disease, which will become especially relevant as rituximab may impair the immunogenicity of SARS-CoV-2 vaccines.

Case

A woman in her 30s with a history of limited GPA on rituximab developed COVID-19 twice (figure 1). GPA manifestations have included erosive sinusitis, otitis, saddle nose deformity and orbital pseudotumour. She started rituximab in February 2019. The most recent dose of rituximab 1000 mg was given on 28 September 2020. On 14 August, a disease flare was treated with a 3-week prednisone taper, which completed approximately 4 weeks before COVID-19 infection. She works in an assisted living facility with ongoing staff and resident …

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors MAF and KW substantially contributed to the conception or design of the work. MAF acquired the data and drafted the work, and both authors revised it critically for important intellectual content. Both authors approve the final version of this manuscript. Both authors agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

  • Funding MAF is funded by NIH/NCATS KL2TR002370 and the OHSU WheelsUp program. KLW is funded by research grants from BMS and Pfizer.

  • Competing interests KLW receives consulting fees from Pfizer, AbbVie, Union Chimique Belge (UCB), Eli Lilly & Company, Galapagos, GlaxoSmithKline (GSK), Roche, Gilead, BMS, Regeneron, Sanofi, AstraZeneca and Novartis.

  • 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 Not commissioned; externally peer reviewed.