Glucocorticoid Therapy in COVID-19

Abstract

Coronavirus disease 2019 (COVID-19) pneumonia caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in significant mortality in pandemic proportions. Inflammation in response to the infection contributes to the pathogenesis of pneumonia. This review will discuss prior studies on the use of glucocorticoids to treat respiratory infections, the rationale for the use glucocorticoids in COVID-19, and review of existing data. We will also highlight outstanding research questions for future studies.

Fig.1

Immune pathogenesis of SARS-CoV-2 infection and possible therapeutic targets for the rationale of glucocorticoids employment. A type I IFN response is elicited by SARS-CoV-2 and contributes to viral clearance, leading to mild forms of the infection. In patients with a low type I IFN response, NF-kB activation predominates, culminating in the production of great amounts of inflammatory cytokines (i.e., IL-6, IL-1, and TNF-α) which in turn amplify the mechanism of NF-kB-mediated inflammation. This exuberant inflammatory response leads to hyperinflammatory syndrome, severe COVID-19, and cytokine storm. Glucocorticoids inhibit NF-kB activation, thus attenuating this harmful and dysregulated inflammatory response (Dashed arrows stand for inhibition). COVID-19, coronavirus disease 2019; IFN, interferons; IL, interleukin; MAS, macropahge activating syndrome; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2.