Molecular and functional resemblance of dexamethasone and quercetin: A paradigm worth exploring in dexamethasone‐nonresponsive COVID ‐19 patients
Abstract
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is continuously expanding in morbidity and mortality, with 22 million confirmed cases and 0.77 million deaths worldwide as of August 20, 2020 (WHO Coronavirus Disease (COVID-19) Dashboard). Major clinical manifestations of SARS-CoV-2 involve respiratory failure caused by virus-induced pulmonary injury and/or a hyperactive host immune response involving an inflammatory response and secondary "cytokine storm," leading to acute respiratory distress syndrome (ARDS) in patients (von der Thüsen & van der Eerden, 2020; Xu et al., 2020). In addition to antiviral therapy, immunomodulatory drugs are also being used as treatment strategies to suppress hyperinflammation and to reduce death among COVID-19 patients (Mehta et al., 2020). Corticosteroids have a long history of use in severe cases of coronavirus disease, including SARS, MERS, and COVID-19, as immunomodulatory drugs (Arabi et al., 2018; Huang et al., 2020; So et al., 2003). Recently, dexamethasone (a synthetic adrenal corticosteroid), whose demand has surged suddenly after publication of the preprint paper of the RECOVERY trial (https://www.medrxiv.org/content/10.1101/2020.06.22.20137273v1.full.pdf), was found to be the first drug, which successfully reduced deaths in approximately one-third of critically ill COVID-19 patients, who were on invasive mechanical ventilation support and by one-fifth in noninvasive…
How strong is the evidence?
Evidence Hub reads this as a randomized trial, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence. Reported size: 19 participants or records.
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