Non-steroidal anti-inflammatory drugs (NSAIDs)4,14,23,24,25
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The use of ibuprofen (or other NSAIDs) in COVID-19 patients has been raised as a potential concern.
The virus that causes COVID-19 binds to its target cells via angiotensin-converting enzyme 2 (ACE2), which is expressed by the epithelial lining of blood vessels, the kidneys, the intestines, and the lungs. Ibuprofen is one of the drugs that increases ACE2 expression through upregulation, which could theoretically accelerate COVID-19 infection.
As yet, there is no scientific evidence to support the complete dismissal of the drug in COVID-19 patients.
However, the current recommendation is to strongly favour the use of paracetamol in the management of COVID-19 related pain and fever, to be used at the recommended dosage levels to avoid any possible liver damage.
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Angiotensin-converting enzyme inhibitors (ACE-inhibitors) and angiotensin receptor blockers (ARBs)4,14
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Recent work suggests that patients on angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), as well as the thiazolidinediones, as part of their treatment regimen for hypertension, heart disease and/or diabetes mellitus, may also display an upregulation of ACE2.
This might place these patients at risk of worse outcomes when they contract COVID-19.
For the moment, this remains theoretical, with no direct evidence of a linkage to poor clinical outcomes.
In addition, discontinuing or switching such patients’ ACE-inhibitor or ARB therapy to alternative agents may be deleterious to their care.
Pending further evidence, it is therefore not recommended that patients be switched from their ACE-inhibitors or ARBs, unless there are other medical reasons for doing so.
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