Blood Fatty Acids Profile in MIS-C Children.

Elvira Verduci,Angelo Sala,Patrizia Risé,Elena Zoia,Christian Pinna,Dario Dilillo,Elisabetta Di Profio,Valeria Calcaterra,Sara Vizzuso,Savina Mannarino,Gianvincenzo Zuccotti,Laura Fiori

doi:10.3390/metabo11110721

Elvira Verduci, Angelo Sala + Show 10 more

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https://doi.org/10.3390/metabo11110721

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MIS-C (multisystem inflammatory syndrome in children) linked to SARS-CoV-2 infection, is a pathological state observed in subjects younger than 21 years old with evidence of either current SARS-CoV-2 infection or exposure within the 4 weeks prior to the onset of symptoms, the presence of documented fever, elevated markers of inflammation, at least two signs of multisystem involvement, and, finally, lack of an alternative diagnosis. They share with adult COVID-19 patients the presence of altered markers of inflammation, but unlike most adults the symptoms are not pulmonary but are affecting several organs. Lipid mediators arising from polyunsaturated fatty acids (PUFA) play an important role in the inflammatory response, with arachidonic acid-derived compounds, such as prostaglandins and leukotrienes, mainly pro-inflammatory and ω3 PUFA metabolites such as resolvins and protectins, showing anti-inflammatory and pro-resolution activities. In order to assess potential alterations of these FA, we evaluated the blood fatty acid profile of MIS-C children at admission to the hospital, together with biochemical, metabolic and clinical assessment. All the patients enrolled showed altered inflammatory parameters with fibrinogen, D-dimer, NT-proBNP, ferritin, aspartate aminotransferase (AST), C-reactive protein (CRP) and TrygIndex levels over the reference values in all the subjects under observation, while albumin and HDL-cholesterol resulted below the normal range. Interestingly, linoleic acid (LA), arachidonic acid (AA) and the ω3 PUFA docosahexaenoic acid (DHA) results were lower in our study when compared to relative amounts reported in the other studies, including from our own laboratory. This significant alteration is pointing out to a potential depletion of these PUFA as a result of the systemic inflammatory condition typical of these patients, suggesting that LA- and AA-derived metabolites may play a critical role in this pathological state, while ω3 PUFA-derived pro-resolution metabolites in these subjects may not be able to provide a timely, physiological counterbalance to the formation of pro-inflammatory lipid mediators. In conclusion, this observational study provides evidence of FA alterations in MIS-C children, suggesting a significant contribution of ω6 FA to the observed inflammatory state, and supporting a potential dietary intervention to restore an appropriate balance among the FAs capable of promoting the resolution of the observed inflammatory condition.

Highlights

During the COVID-19 pandemic, children appeared to be less affected than adults, and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infections were in most cases asymptomatic or had mild symptoms [1,2,3]
While sharing common features with Kawasaki Disease, toxic shock syndrome, and secondary hemophagocytic lymphohistiocytosis/macrophage activation syndrome [19], MIS-C importantly shares with COVID-19 the presence of laboratory evidence of inflammation, and it has been hypothesized that viral replication affects the production and release of inflammatory mediators, leading to a severe inflammatory reaction both in MIS-C and in COVID-19
Lipid mediators play a critical role in the physiological evolution of the acute inflammatory reaction: oxygenated metabolites arising from ω6

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Introduction

During the COVID-19 pandemic, children appeared to be less affected than adults, and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infections were in most cases asymptomatic or had mild symptoms [1,2,3]. High concentrations of D-dimer have been associated with increased mortality from COVID-19, and evidence in the literature suggest that COVID-19 coagulopathy is largely determined by the host inflammatory response, which in turn causes a pro-thrombotic status [15], leading to severe pulmonary manifestations similar to acute respiratory distress syndrome (ARDS) [16], even if non pulmonary organ damage was present in the most severe cases [17]

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