Colchicine as a potent anti-inflammatory treatment in COVID-19: can we teach an old dog new tricks?

Abstract

The recent pandemic has called for urgent treatment solutions for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)-infected patients. Undeniably, the pathophysiological process of coronavirus disease-19 (COVID-19) is yet to be revealed. Although the clinical life-threatening hallmark is acute respiratory distress syndrome (ARDS) and acute lung injury (ALI), systemic COVID-19 complications may also develop. Myocardial injury appears to be a major adverse development even in the absence of pre-existing cardiovascular disease.¹ While the most apparent mechanism of myocardial injury would be an imbalance of oxygen supply and demand due to ARDS/ALI, histologically diagnosed myocarditis by SARS-CoV-2 has been described,² while a cytokine storm, vascular inflammation/endothelial dysfunction, increased sympathetic activity/stress cardiomyopathy, or even true type I acute coronary events as a result of plaque disruption by the aforementioned factors could also play a role. While awaiting data regarding the exact mechanism of action of SARS-CoV-2, data for SARS-CoV are implicating NLRP3 inflammasome activation initiated by viroporin E, a SARS-CoV-2 component.³