Laboratory confirmed cases of COVID-19 are millions of people worldwide with hundreds of thousands fatalities (Johns Hopkins University). Most of these fatalities are induced by acute respiratory syndrome (ARDS) and those who survive, might suffer from long term complications of severe pulmonary inflammation. The purpose of this letter is to propose that aldosterone antagonists might improve the outcome of ARDS.
It has been proved by multiple studies on cell lines, animal model, and also human subjects that aldosterone induces collagen synthesis in different tissues [1], [2], and that aldosterone antagonists (e.g. spironolactone) can inhibit collagen synthesis in different tissues including heart, muscle, kidney, and lung [3], [4], [5]. There has been a few studies done on ARDS and it has been shown that spironolactone improves the outcome in this condition as well [6].
Studies have shown that expression of ACE2 might facilitate infection by SARS-CoV-2, but it was demonstrated that aldosterone antagonists (which increase expression of ACE2) can protect against ARDS in animal models [7].
Based on the previous evidence and also pathophysiology of ARDS it seems reasonable to consider spironolcatone for improvement of ARDS outcome if started early in the course of the disease. Now that we have a surge in ARDS cases caused by COVID-19 and since there is not effective treatment or vaccine available yet, we need to decrease mortality and morbidity it seems that early initiation of aldosterone antagonist early in the course of COVID-19 might improve the outcome by decreasing fibrosis in lung tissue.
Sources of support in the form of grants
We had no source of funding and no conflict of interest.
Footnotes
Supplementary data to this article can be found online at https://doi.org/10.1016/j.mehy.2020.109830.
Appendix A. Supplementary data
The following are the Supplementary data to this article:
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