COVID-19 and Non-steroidal Anti-Inflammatory Drugs (NSAIDS) – No Increased Risk
By Dr. David Borenstein M.D. updated 10/2020
An ongoing concern involving individuals who suffer from rheumatic diseases including inflammatory and non-inflammatory disorders is whether their illness or their therapy increases the risk of dying from COVID-19 infection. In March 2020, a study from France suggested that the use of NSAIDS in COVID-19 patients was associated with increased mortality As a result of this study, acetaminophen was suggested as a substitute for NSAIDS for symptoms of COVID-19 infection.1 At the time, a suggestion was made that additional investigation was needed to know if NSAIDS were, in fact, more deadly.
In response to the need for additional information, two studies were organized involving a British population of 536,423 current NSAIDS users and 1,927,284 non-users in the general population. In this first study, there was no evidence of difference in risk of COVID-19 related death associated with current NSAIDs use.
In the second study, a population of 1,708,781 people with osteoarthritis or rheumatoid arthritis, of whom, 175,495 were current NSAIDS users were included.2 A higher proportion of people aged 70+ years were included in this population than the general population In this group with rheumatic disease, a lower risk of COVID-19 related death associated with current use of NSAIDS versus non-use.
The mechanisms that may explain this outcome are not self-evident. An unproven possibility is the inhibition of attachment of the virus to cells with angiotensin 2 receptors. It would seem that the benefits of the use of NSAIDS for the control of clinical symptoms of OA and RA do not increase the risk of a poor outcome in the setting of COVID infection.
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References:
- Central Alerting System. Novel Coronavirus – Anti-inflammatory medications. 2020. Available: [Accessed 13 Jul 2020]
- Wong AYS et al. Use of non-steroidal anti-inflammatory drugs and risk of death from COVID-19: and OpenSAFELY cohort analysis based on two cohorts Ann Rheum Dis doi:10.1136/annrheumdis-2020-219517