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We appreciate the interest of Lo et al in our opinion piece and thank them for the data presented in their letter.1 2 Several reports of QT prolongation and torsades de pointes in patients with COVID-19 receiving antimalarials have been published.3–5 These and other reports have indirectly raised questions regarding the arrhythmogenic potential of hydroxychloroquine (HCQ) when used to treat rheumatic disease.
Lo et al used the unique resource of the National Health Insurance Research Database of Taiwan. Through propensity scores, they matched patients who used HCQ and who did not use HCQ for the treatment of newly diagnosed rheumatoid arthritis (RA). Data about other disease-modifying antirheumatic drugs used by the patients was not reported. Therefore, it is unclear if the groups were similar in their RA disease severity, although they seemed similar related to comorbidities. The authors did not find differences in the cumulative risk of arrhythmia between the two groups after 1 year of follow-up. However, a prior meta-analysis on reported cardiotoxic events of antimalarials found that cardiac conduction abnormalities were the most common cardiac adverse events and were associated with higher cumulative doses (median cumulative HCQ dose of 1235 …
Footnotes
AHK and JAS are joint senior authors.
Handling editor Josef S Smolen
Twitter @MaxKonigMD, @alhkim, @jeffsparks
AHK and JAS contributed equally.
Contributors AD-G, ERG, JWL, MFK, 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 JWL reports grant funding from Pfizer, unrelated to this manuscript. MFK was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) of the National Institutes of Health (NIH) under award no. T32AR048522 and received personal fees from Bristol-Myers Squibb and Celltrion, unrelated to this manuscript. AHK reports grants from Rheumatology Research Foundation, support from NIH/NIAMS, 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.
Provenance and peer review Commissioned; internally peer reviewed.