Link between serum lipid signature and prognostic factors in COVID-19 patients

Michele Dei Cas,Gabriella Roda,Sara Ottolenghi,Camillo Morano,Rocco Rinaldo,Stefano Centanni,Rita Paroni,Davide Chiumello,Michele Samaja

doi:10.1038/s41598-021-00755-z

Michele Dei Cas, Gabriella Roda + Show 7 more

Open Access

https://doi.org/10.1038/s41598-021-00755-z

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Journal: Scientific Reports	Publication Date: Nov 4, 2021
Citations: 29	License type: open-access

Affiliation: University of Milan, Ospedale San Paolo

Abstract

Although the serum lipidome is markedly affected by COVID-19, two unresolved issues remain: how the severity of the disease affects the level and the composition of serum lipids and whether serum lipidome analysis may identify specific lipids impairment linked to the patients' outcome. Sera from 49 COVID-19 patients were analyzed by untargeted lipidomics. Patients were clustered according to: inflammation (C-reactive protein), hypoxia (Horowitz Index), coagulation state (D-dimer), kidney function (creatinine) and age. COVID-19 patients exhibited remarkable and distinctive dyslipidemia for each prognostic factor associated with reduced defense against oxidative stress. When patients were clustered by outcome (7 days), a peculiar lipidome signature was detected with an overall increase of 29 lipid species, including—among others—four ceramide and three sulfatide species, univocally related to this analysis. Considering the lipids that were affected by all the prognostic factors, we found one sphingomyelin related to inflammation and viral infection of the respiratory tract and two sphingomyelins, that are independently related to patients' age, and they appear as candidate biomarkers to monitor disease progression and severity. Although preliminary and needing validation, this report pioneers the translation of lipidome signatures to link the effects of five critical clinical prognostic factors with the patients' outcomes.

Highlights

The serum lipidome is markedly affected by COVID-19, two unresolved issues remain: how the severity of the disease affects the level and the composition of serum lipids and whether serum lipidome analysis may identify specific lipids impairment linked to the patients’ outcome
Laboratory findings in the sera obtained from severely ill COVID-19 patients often display high levels of biomarkers, e.g. C-reactive protein (CRP), D-dimer (DD) and excessive cytokines release, linked to systemic hyper-inflammation, some of which are commonly found in patients with acute respiratory distress syndrome (ARDS)[3]
By ranking the disease progression through the engagement of a few clinical variables predicted to influence the outcome, the identified markers were assumed to recapitulate the development of inflammation, hypoxia, coagulation, and kidney function, as well as the independent effects of the patients’ age

Summary

Introduction

The serum lipidome is markedly affected by COVID-19, two unresolved issues remain: how the severity of the disease affects the level and the composition of serum lipids and whether serum lipidome analysis may identify specific lipids impairment linked to the patients’ outcome. Patients were clustered according to: inflammation (C-reactive protein), hypoxia (Horowitz Index), coagulation state (D-dimer), kidney function (creatinine) and age. Considering the lipids that were affected by all the prognostic factors, we found one sphingomyelin related to inflammation and viral infection of the respiratory tract and two sphingomyelins, that are independently related to patients’ age, and they appear as candidate biomarkers to monitor disease progression and severity. Laboratory findings in the sera obtained from severely ill COVID-19 patients often display high levels of biomarkers, e.g. C-reactive protein (CRP), D-dimer (DD) and excessive cytokines release ( known as cytokine storm), linked to systemic hyper-inflammation, some of which are commonly found in patients with acute respiratory distress syndrome (ARDS)[3]. Many viruses can profoundly alter the host lipidome and exploit the host energy resources to support their replication, thereby causing marked changes in the plasma/serum lipidome[8,9]

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