Since the first reported case of the novel coronavirus (SARS-CoV-2) in humans at the end of 2019 in Wuhan, the virus had infected approximately 100 million individuals. One year later, coronavirus disease (COVID-19) was estimated to have affected nearly 30% of the global population, with a case fatality rate of approximately 2%. In the early stages of the pandemic, numerous questions emerged regarding this novel viral agent, including its pathogenic mechanisms, associated vulnerabilities, risk factors, and potential treatment strategies. A wide spectrum of clinical conditions-including chronic diseases, infectious agents, autoimmune disorders, and even genetic or post-therapeutic alterations-can trigger inflammatory syndromes in the human body. A central component of these processes is the dysregulation of cytokine signaling, which may provoke excessive immune cell activation, leading to a self-perpetuating inflammatory loop with potentially life-threatening consequences. Notably, both SARS-CoV-2 infection and elevated C-reactive protein (CRP) levels have been consistently observed during active disease states. Furthermore, vitamin E is well known as an antioxidant that prevents the peroxidation of lipid molecules, as ferroptosis. A well-established phenomenon is that lipid peroxidation levels are higher in COVID-19 patients, while antioxidant capacity is diminished. Therefore, the aim of this study is to evaluate CRP levels in COVID-19 patients administered high doses of vitamin E (alpha-tocopherol)-a lipid-soluble antioxidant-compared to those receiving a placebo.
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Vitamin E reduce CRP levels in COVID-19 patients
Timeframe: Baseline (Day 0) and after 3 months of treatment.