Abstract
COVID-19 is a pandemic disease that causes severe pulmonary damage and hyperinflammation. Vitamin A is a crucial factor in the development of immune functions and is known to be reduced in cases of acute inflammation. This prospective, multicenter observational cross-sectional study analyzed vitamin A plasma levels in SARS-CoV-2 infected individuals, and 40 hospitalized patients were included. Of these, 22 developed critical disease (Acute Respiratory Distress Syndrome [ARDS]/Extracorporeal membrane oxygenation [ECMO]), 9 developed severe disease (oxygen supplementation), and 9 developed moderate disease (no oxygen supplementation). A total of 47 age-matched convalescent persons that had been earlier infected with SARS-CoV-2 were included as the control group. Vitamin A plasma levels were determined by high-performance liquid chromatography. Reduced vitamin A plasma levels correlated significantly with increased levels of inflammatory markers (CRP, ferritin) and with markers of acute SARS-CoV-2 infection (reduced lymphocyte count, LDH). Vitamin A levels were significantly lower in hospitalized patients than in convalescent persons (p < 0.01). Of the hospitalized patients, those who were critically ill showed significantly lower vitamin A levels than those who were moderately ill (p < 0.05). Vitamin A plasma levels below 0.2 mg/L were significantly associated with the development of ARDS (OR = 5.54 [1.01–30.26]; p = 0.048) and mortality (OR 5.21 [1.06–25.5], p = 0.042). Taken together, we conclude that vitamin A plasma levels in COVID-19 patients are reduced during acute inflammation and that severely reduced plasma levels of vitamin A are significantly associated with ARDS and mortality.
Highlights
Coronavirus disease 2019 (COVID-19) is a novel infectious disease that has been spreading worldwide [1]
Disease severity was defined as critical, severe or moderate
Our cohort characteristics showed significantly higher levels of inflammatory markers (CRP, IL-6, ferritin) and lower lymphocyte counts in patients with critical disease cases compared to moderately and severely ill and convalescent patients. These data are in line with other studies as both increased inflammatory parameters and decreased lymphocyte counts are well-defined markers of active disease and predictive of a severe course of COVID-19 [21]
Summary
Coronavirus disease 2019 (COVID-19) is a novel infectious disease that has been spreading worldwide [1]. The clinical manifestation of COVID-19 can range from asymptomatic infection to critical illness with severe pneumonia, respiratory failure, and death [2]. Worse clinical outcomes are related to dysregulated immune responses in the host, leading to the uncontrolled release of proinflammatory cytokines such as interleukin-6 (IL-6). This cytokine storm mediates the progression of lung damage and respiratory failure in a relevant number of cases [3]. The RNA-polymerase inhibitor remdesivir and the immunosuppressive corticosteroid dexamethasone are the only Food and Drug Administration (FDA) approved drugs for COVID-19 therapy with demonstrated effects on mortality and disease outcome [4,5]. The lethality of hospitalized, mechanically ventilated patients remains high [6]
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