Abstract
Coronavirus disease 2019 (COVID-19) is a multi-systemic disease caused by Severe acute respiratory syndrome coronavirus 2, SARS-CoV-2. Since the onset of the pandemic, understanding the pathophysiological mechanisms of this disease has posed a significant challenge, with the intent to determine its progression and implement appropriate treatment strategies. The heightened severity and mortality associated with SARS-CoV-2 infection can be attributed, in part, to a phenomenon known as cytokine storm. This refers to an uncontrolled systemic inflammatory response characterized by elevated proinflammatory cytokines and chemokines, leading to an overproduction of free radicals. The aforementioned cytokine storm is accompanied by the excessive generation of reactive oxygen species and affects the virus and directly damages the host's cells. Given that the SARS-CoV-2 virus primarily targets respiratory cells, pneumonia is a common manifestation of the disease. Consequently, chest multidetector computed tomography (MDCT) plays a crucial role in evaluating lung tissue inflammation, determining disease severity, making decisions regarding hospitalization, and assessing the necessity of intensive care unit treatment. Assessing the level of oxidative stress can be accomplished by measuring the products resulting from damage to lipids, proteins, and DNA - whereas the inflammatory and multiorgan impairment biomarkers can be procured from routine laboratory practice. Due to the established association of a cytokine storm with a free radical storm, it might be postulated that during the acute phase of COVID-19 pneumonia the redox biomarkers might correlate with inflammatory and multiorgan impairment biomarkers, as well as chest MDCT findings.
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