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We read the comment on our article by López-González et al with great interest.1 2 The authors detail the presentation of four cases of acute arthritis in patients hospitalised with COVID-19 and underlying gout (three cases) or recurrent arthritis of unknown origin (one case). Although we await further reports, there have been anecdotes of newly diagnosed inflammatory arthritis in the context of COVID-19 infection, perhaps representing either a viral-associated arthritis or a reactive arthritis.3 4 However, as the authors note, common causes of acute inflammatory arthritis must continue to be considered in the differential diagnosis—these include crystal-associated arthritis, such as gout or pseudogout. Acute illnesses, including infection, are well-established risk factors for gout and pseudogout flares; inpatient gout flares are known to complicate admissions for heart failure, pneumonia and acute kidney injury.5 These comorbidities are either associated with or features of severe COVID-19 infection and so may explain the presentations of acute inflammatory arthritis detailed in their report.6
The thorough workup completed by the authors highlights some of the current gaps in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) testing methods. While reverse transcription (RT)-PCR testing was negative in all three of the synovial fluid samples in these patients with documented COVID-19 infection from nasopharyngeal swab, no molecular testing method has been validated yet to detect SARS-CoV-2 in synovial fluid. Thus, the clinical significance of the synovial fluid cultures and RT-PCR results is currently unknown. Despite these uncertainties, we commend the authors’ efforts in providing the first report of SARS-CoV-2 nucleic acid testing in synovial fluid.
AHK and JAS are joint senior authors.
ERG and JWL are joint first authors.
Handling editor Josef S Smolen
Twitter @alhkim, @jeffsparks
AHK and JAS contributed equally.
ERG and JWL contributed equally.
Contributors ERG, JWL, AHK and JAS contributed to the conception and drafting of the article. All listed authors provided critical revision for important intellectual content and final approval.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests AHJK reports grants from National Institutes of Health (NIH)/National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and Rheumatology Research Foundation and personal fees from Exagen Diagnostics, Inc and GlaxoSmithKline. JAS reports grants from NIH/NIAMS/National Institute of Allergy and Infectious Diseases/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. ERG and JWL have disclosed no conflicts of interest or competing interests.
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.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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