Michael A Matthay and B Taylor Thompson1 have very nicely summarised the evidence-based role of dexamethasone in hospitalised patients with COVID-19. Their pertinent analysis is based on the background of the RECOVERY trial, 2 which concluded that therapy with dexamethasone at a dose of 6 mg once daily for up to 10 days decreased 28-day mortality in patients with COVID-19 on respiratory support. Patients not requiring oxygen showed no benefit but had a possibility of harm with corticosteroid therapy. 2 One crucial feature of corticosteroid therapy is its duration, particularly in patients with COVID-19 with sustained persistence of ground-glass opacities. Currently, an extended course of corticosteroids beyond 10 days is considered only in select cases of severe COVID-19. 3 One rationale for prolonged treatment is the prevention of post-disease fibrosis in patients with COVID-19 for whom risk factors for pulmonary fibrosis might be established.

However, in COVID-19, such a long-lasting course of corticosteroids can inadvertently lead to poor treatment outcomes. The possible effect of steroids in the procoagulant environment of patients with COVID-19, in whicheven anticoagulant treatment does not sufficiently shield from the thrombotic complications found in deceased patients, should be considered. A hypercoagulable state with profound endothelial injury following infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has an essential role in thrombosis. In autopsy studies of patients with COVID-19, diffuse alveolar disruption with large vessel