SARS-CoV-2 accesses host cells via the enzyme ACE2[1][2]
On March 11 a correspondence[3] in the Lancet claimed that “the increased expression of ACE2 would facilitate infection with COVID-19” and “ACE2 can also be increased by thiazolidinediones and ibuprofen”
While the first claim seems sensical the authors did not provide a reference for the second claim.
I am not an expert in this area and a search if ibuprofen or NSAIDs[4] really increase ACE2 expression revealed just articles like [5] “Ibuprofen could ameliorate the cardiac fibrosis in diabetic rats by reduction of the ACE/AngII/AT1-R axis and enhancement of the ACE2/Ang(1-7)/Mas-R axis …” which does not really answer my question.
[1] https://en.wikipedia.org/wiki/Coronavirus_disease_2019
[2] https://www.cell.com/cell/fulltext/S0092-8674(20)30229-4
[3] https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30116-8/
[4] https://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drug
[5] https://www.ncbi.nlm.nih.gov/pubmed/25896805
On the other hand in Germany there were several articles, e.g. https://www.deutschlandfunk.de/covid-19-coronavirus-warnunge... warning about fake whatapp messages (seems it was forwarded voice messages) regarding Ibuprofen.
If your research points to University of Vienna, they issued a denial https://twitter.com/MedUni_Wien/status/1238782938344554496
There has simply been a correlation between hypertensive/diabetic patients and graver Covid-19 symptoms. The article speculates that ACE2 inhibitors could be the cause. And Ibuprofen is not an ACE2 inhibitor in the real sense of the term.
If there really were a link, then common blood pressure and diabetes medication would be far more risky than ibuprofen.
However, it should also be noted that women express ACE2 more than men do. And yet women are known to have a lower mortality rate than me with respect to SARS-COV-2.
Correlation does not imply causality and the article is simply an unconfirmed hypothesis.