Abstract
The current pandemic emergence of novel coronavirus disease (COVID-19) poses a relevant threat to global health. SARS-CoV-2 infection is characterized by a wide range of clinical manifestations, ranging from absence of symptoms to severe forms that need intensive care treatment. Here, plasma-EDTA samples of 30 patients compared with age- and sex-matched controls were analyzed via untargeted nuclear magnetic resonance (NMR)-based metabolomics and lipidomics. With the same approach, the effect of tocilizumab administration was evaluated in a subset of patients. Despite the heterogeneity of the clinical symptoms, COVID-19 patients are characterized by common plasma metabolomic and lipidomic signatures (91.7% and 87.5% accuracy, respectively, when compared to controls). Tocilizumab treatment resulted in at least partial reversion of the metabolic alterations due to SARS-CoV-2 infection. In conclusion, NMR-based metabolomic and lipidomic profiling provides novel insights into the pathophysiological mechanism of human response to SARS-CoV-2 infection and to monitor treatment outcomes.
Highlights
The World Health Organization announced coronavirus disease 2019 (COVID-19) outbreak a pandemic in March 2020 [1,2]
The current COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is markedly affecting the world population
We analyzed via 1H nuclear magnetic resonance (NMR) spectroscopy the metabolomic and lipidomic profiles of plasmaEDTA samples obtained from 30 patients affected by COVID-19
Summary
The World Health Organization announced coronavirus disease 2019 (COVID-19) outbreak a pandemic in March 2020 [1,2]. About 20% of patients, the older ones and those affected by chronic comorbidities such as hypertension, diabetes mellitus, renal and heart diseases, may develop interstitial pneumonia and respiratory distress requiring oxygen therapy or mechanical ventilation [4]. In addition to interstitial pneumonia and acute respiratory distress syndrome (ARDS), COVID-19 is associated with other life-threatening complications such as sepsis, thromboembolism and multi-organ failure [5]. Patients with the highest rate of morbidity and mortality following SARS-CoV-2 infection develop a hyperinflammatory syndrome due to the overproduction of early response proinflammatory cytokines (such as IL-1β, IL-6, TNFα, MCP-1)–the so called “cytokine storm”–leading to an increased vascular permeability, activation of coagulation pathways, dysregulation of T cells with associated lymphopenia, multiorgan injury and rapid clinical deterioration [6,7,8,9]
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