Recent news indicates that Dexamethasone may reduce mortality of severe COVID-19 patients only. COVID-19 infection has been shown to cause multi organ disease caused by autoimmune degradation of the lungs. This lung damage is caused by uncontrolled release of proinflammatory cytokines. In order for the body to best the infection, a coordinated attack from T and B cells is required. However, Dexamethasone is an immunosuppressant that would limit the damage from inflammation but inhibit the protective effect from B and T cells. It would prevent them from making antibodies and potentially lead to a greater viral load. Similarly, it inhibits the activity of macrophages. This drug may be helpful temporarily for severe patients, but continued use in recovery could inhibit the production of antibodies and be dangerous.
Currently there is no clinical evidence or data to support the researchers' claims about Dexamethasone. Dexamethasone decreases inflammation while inhibiting B, T, macrophage, and natural killer cells. The use of corticosteroids in COVID-19 patients was associated with increased viral load that persists after a patient survives SARS. If the goal of Dexamethasone is to decrease inflammation, then the targeting of Mast cells would be a good alternative. Mast cells release a majority of inflammatory cytokines, and thus, they would be a good target to downregulate. The neutral flavonoid luteolin is safer than corticosteroids and is a potent inhibition of mast cells. It is also shown to have anti-viral properties as well. Dexamethasone should not be touted as the solution to all the issues. Clinical data must be acquired and analyzed.