Ibuprofen and COVID-19 disease: separating the myths from facts

ABSTRACT

Introduction: The Coronavirus disease 2019 (COVID-19) poses novel challenges in the healthcare systems around the world. Concern about the role of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) and, in particular, ibuprofen has led to significant speculation.

Areas covered: A literature search was conducted to evaluate ibuprofen’s potential benefits and harms in the COVID-19 disease. Angiotensin-Converting Enzyme 2 (ACE-2) is crucial entry receptor for Severe Acute Respiratory Syndrome coronavirus-2 (SARS-CoV-2) in host cells. We found no scientific evidence linking ibuprofen use and an ACE-2 overexpression. Ibuprofen suppresses the production of various pro-inflammatory cytokines that are implicated in the ‘cytokine storm’ and subsequent ARDS in COVID-19 disease. Nevertheless, the exact role of ibuprofen in the immune response in COVID-19 disease is still unknown. There are no double-blind, placebo-controlled studies assessing the effect of ibuprofen on COVID-19 disease progression.

Expert opinion: The studies that have been performed so far demonstrate no association between ibuprofen use and increased mortality rates or an increased risk for respiratory support. Accordingly, we recommend ibuprofen to be used for managing COVID-19 symptoms.

KEYWORDS:

• COVID-19
• SARS-CoV-2
• ibuprofen
• ACE-2
• NSAIDs

Article highlights

• Concern about the role of ibuprofen in the management of COVID-19 symptoms has led to significant speculation.

• ACE-2 downregulation may be the etiologic factor of the severe lung injury observed in COVID-19 disease.

• Ibuprofen has a beneficial effect or no effect in ACE-2 dependent viral entry into host cells.

• COX inhibition may have a role in preventing the inflammation-driven damaging phase of SARS-CoV-2 that leads to ARDS.

A recommendation for discontinuation of ibuprofen in patients with COVID-19 disease is not supported scientifically.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.