Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
SARS-CoV-2 vaccines reduce the risk of COVID-19.1–3 However, some disease-modifying anti-rheumatic drugs (DMARDs), particularly glucocorticoids, methotrexate, mycophenolate mofetil and rituximab, may blunt the immunological response to COVID-19 vaccination.4 Little is known about the clinical efficacy of these vaccines at preventing COVID-19 infection in patients with systemic autoimmune rheumatic diseases (SARDs).
Mass General Brigham (MGB) is a large multicentre healthcare system in the Boston, Massachusetts, USA area. Patients with SARDs with a positive SARS-CoV-2 PCR or antigen test between 30 January 2020 and 30 July 2021 at MGB were identified using diagnostic billing codes or were referred by physicians, as previously described.5 From this cohort, we identified breakthrough infections in fully vaccinated patients, defined as a positive test ≥14 days after the final vaccine dose.6
Of 786 SARD patients with COVID-19, 340 occurred after the initial emergency use authorisation for COVID-19 vaccination in the USA. Of these, 16 (4.7%) were breakthrough infections (online supplemental figure 1). Among the breakthrough infections, 12 (75%) were female, 11 (69%) were white, the median age was 50 years and 12 (75%) had ≥1 comorbidity (table 1). The most common SARDs included rheumatoid arthritis (6, 38%), inflammatory myositis (3, 19%) and systemic lupus erythematosus (3, 19%). Rituximab (5, …
Handling editor Josef S Smolen
Contributors All authors made substantial contributions to the conception or design of the work and in the acquisition, analysis and interpretation of the data. All authors drafted or revised the work for critically important intellectual consent. All authors provided final approval of the version to be published.
Funding NJP and KMD are supported by the National Institutes of Health Ruth L. Kirschstein Institutional National Research Service Award (T32-AR-007258). KMD is supported by the Rheumatology Research Foundation Scientist Development Award. TY-TH is supported by the National Institutes of Health Ruth L. Kirschstein Institutional National Research Service Award (T32-AR-007530). 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 R03AR078938).
Competing interests JAS reports research support from Bristol-Myers Squibb and consultancy fees from Bristol-Myers Squibb, Gilead and Pfizer. ZSW reports research support from Bristol-Myers Squibb and Principia/Sanofi and consulting fees from Viela Bio and MedPace. All other authors report no competing interests.
Provenance and peer review Not commissioned; externally peer reviewed.
Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.