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Response to: ‘Antimalarial use and arrhythmias in COVID-19 and rheumatic patients: a matter of dose and inflammation?’ by Erre et al
  1. Elizabeth R Graef1,
  2. Jean W Liew2,
  3. Alfred HJ Kim3,
  4. Jeffrey A Sparks4
  1. 1 Division of Rheumatology and Clinical Immunology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
  2. 2 Department of Medicine, Division of Rheumatology, University of Washington, Seattke, Washington, USA
  3. 3 Medicine/Rheumatology, Washington University in Saint Louis School of Medicine, Saint Louis, Missouri, USA
  4. 4 Department of Medicine, Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital, Boston, Massachusetts, USA
  1. Correspondence to Dr Jeffrey A Sparks, Department of Medicine, Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 63110, USA; jsparks{at}bwh.harvard.edu; Dr Alfred HJ Kim; akim{at}wustl.edu

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We read the comment by Erre et al to our correspondence about hydroxychloroquine (HCQ) use during the COVID-19 with great interest.1 2 As also highlighted by others, antimalarial use such as HCQ during the COVID-19 pandemic has the potential for cardiotoxicity.3 4 Patients with COVID-19 and those with rheumatic disease represent distinct populations with different dosing strategies. We agree that the potential for cardiotoxicity from antimalarials may also be different related to these issues.

The authors present interesting data on QTc intervals in patients with rheumatoid arthritis (RA) on maintenance HCQ, drawn from an established cohort of patients without known significant underlying cardiovascular disease. While these patients had statistically significant higher QT intervals on HCQ compared with those on other disease-modifying antirheumatic drugs (DMARDs), the mean remained within normal limits so this difference is unlikely to have a …

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Footnotes

  • AHK and JAS are joint senior authors.

  • ERG and JWL are joint first authors.

  • Twitter @alhkim, @jeffsparks

  • AHK and JAS contributed equally.

  • ERG and JWL contributed equally.

  • Contributors All authors contributed to the conception and drafting of the article. All 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 AHK reports grants from NIH/NIAMS and Rheumatology Research Foundation and personal fees from Exagen Diagnostics and GlaxoSmithKline. JAS reports grants from NIH/NIAID/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.

  • 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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