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Impact of vaccination on postacute sequelae of SARS CoV-2 infection in patients with rheumatic diseases
  1. Naomi J Patel1,
  2. Claire Cook1,
  3. Kathleen Vanni2,
  4. Xiaoqing Fu1,
  5. Xiaosong Wang2,
  6. Yumeko Kawano2,
  7. Grace Qian2,
  8. Buuthien Hang1,
  9. Shruthi Srivatsan1,
  10. Emily P Banasiak2,
  11. Emily Kowalski2,
  12. Katarina Bade2,
  13. Yuqing Zhang1,
  14. Jeffrey A Sparks2,
  15. Zachary S. Wallace1
  1. 1Rheumatology Unit and Clinical Epidemiology Program, Division of Rheumatology, Allergy, and Immunology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA
  2. 2Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA
  1. Correspondence to Dr Zachary S. Wallace, Clinical Epidemiology Program and Rheumatology Unit, Massachusetts General Hospital, Boston, Massachusetts, USA; zswallace{at}mgh.harvard.edu

Abstract

Objective Vaccination decreases the risk of severe COVID-19 but its impact on postacute sequelae of COVID-19 (PASC) is unclear among patients with systemic autoimmune rheumatic diseases (SARDs) who may have blunted vaccine immunogenicity and be vulnerable to PASC.

Methods We prospectively enrolled patients with SARD from a large healthcare system who survived acute infection to complete surveys. The symptom-free duration and the odds of PASC (any symptom lasting ≥28 or 90 days) were evaluated using restricted mean survival time and multivariable logistic regression, respectively, among those with and without breakthrough infection (≥14 days after initial vaccine series).

Results Among 280 patients (11% unvaccinated; 48% partially vaccinated; 41% fully vaccinated), the mean age was 53 years, 80% were female and 82% were white. The most common SARDs were inflammatory arthritis (59%) and connective tissue disease (24%). Those with breakthrough infection had more upper respiratory symptoms, and those with non-breakthrough infection had more anosmia, dysgeusia and joint pain. Compared with those with non-breakthrough COVID-19 infection (n=164), those with breakthrough infection (n=116) had significantly more symptom-free days over the follow-up period (+21.4 days, 95% CI 0.95 to 41.91; p=0.04) and lower odds of PASC at 28 and 90 days (adjusted OR, aOR 0.49, 95% CI 0.29 to 0.83 and aOR 0.10, 95% CI 0.04 to 0.22, respectively).

Conclusion Vaccinated patients with SARDs were less likely to experience PASC compared with those not fully vaccinated. While we cannot rule out the possibility that findings may be due to intrinsic differences in PASC risk from different SARS-CoV-2 variants, these findings support the benefits of vaccination for patients with SARDs and suggest that the immune response to acute infection is important in the pathogenesis of PASC in patients with SARDs.

  • Covid-19
  • Vaccination
  • Autoimmune Diseases

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Data are available on reasonable request. Data are available on reasonable request to the corresponding author and appropriate ethical approvals.

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Data availability statement

Data are available on reasonable request. Data are available on reasonable request to the corresponding author and appropriate ethical approvals.

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Footnotes

  • JAS and ZSW are joint senior authors.

  • Handling editor Josef S Smolen

  • Twitter @jeffsparks

  • Contributors NJP, JAS and ZSW had access to the study data, developed the figures and tables and vouch for the data and analyses. XF and YZ performed the statistical analyses and contributed to data quality control, data analysis and interpretation of the data. CC, KV, XF, XW, YK, GQ, SS, EPB, EK and KB contributed to data collection, data analysis and interpretation of the data. ZSW and JAS directed the work, designed the data collection methods, contributed to data collection, data analysis and interpretation of the data and had final responsibility for the decision to submit for publication. All authors contributed intellectual content during the draft and revision of the work and approved the final version to be published. ZSW accepts full responsibility for the finished work and/or the conduct of the study, had access to the data and controlled the decision to publish. JAS and ZSW contributed equally as last authors. ZSW assumes overall responsibility for the content as the guarantor.

  • Funding NJP is funded by the Rheumatology Research Foundation (Scientist Development Award). YK is funded by the National Institutes of Health Ruth L. Kirschstein Institutional National Research Service Award (grant number T32 AR007530). ZSW is funded by NIH/NIAMS (grant numbers K23 AR073334 and R03 AR078938) and the Rheumatology Research Foundation (K Supplement). JAS is funded by NIH/NIAMS (grant numbers R01 AR077607, P30 AR070253, and P30 AR072577), the R. Bruce and Joan M. Mickey Research Scholar Fund, and the Llura Gund Award for Rheumatoid Arthritis Research and Care.

  • Disclaimer The funders had no role in the decision to publish or preparation of this manuscript. The content is solely the responsibility of the authors and does not necessarily represent the official views of Harvard University, its affiliated academic health care centers, or the Rheumatology Research Foundation, or the National Institutes of Health.

  • Competing interests ZSW reports research support from Bristol-Myers Squibb and Principia/Sanofi and consulting fees from Zenas Biopharma, Horizon, Sanofi, Shionogi, Viela Bio, and MedPace. JS reports research support from the R. Bruce and Joan M. Mickey Research Scholar Fund, the Llura Gund Award for Rheumatoid Arthritis Research and Care, and Bristol-Myers Squibb. JS reports consulting fees from AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Gilead, Inova Diagnostics, Janssen, Optum, and Pfizer. NJP reports consulting fees from FVC Health and LLC.

  • 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.

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