COVID-19 Inflammatory Syndrome: Lessons from TNFRI and CRP about the Risk of Death in Severe Disease

<b>Background/Objectives</b>: Cytokine storm in severe COVID-19 is responsible for irreversible tissue damage and death. Soluble mediators from the TNF superfamily, their correlation with clinical outcome, and the use of TNF receptors as a potent predictor for clinical outcome were evaluated. <b>Methods</b>: Severe COVID-19 patients had the levels of soluble mediators from the TNF superfamily quantified and categorized according to the clinical outcome (death versus survival). Statistical modeling was performed to predict clinical outcomes. <b>Results</b>: COVID-19 patients have elevated serum levels from the TNF superfamily. Regardless of sex and age, the sTNFRI levels were observed to be significantly higher in deceased patients from the first weeks following the onset of symptoms. We analyzed hematological parameters and inflammatory markers, and there was a difference between the groups for the following factors: erythrocytes, hemoglobin, hematocrit, leukocytes, neutrophils, band cells, lymphocytes, monocytes, CRP, IL-8, IFN-γ, IL-10, IL-6, IL-4, IL-2, leptin MIF sCD40L, and sTNFRI (<i>p</i> < 0.05). A post hoc analysis showed an inferential capacity over 70% for some hematological markers, CRP, and inflammatory mediators in deceased patients. sTNFRI was strongly associated with death, and the sTNFRI/sTNFRII ratio differed between outcomes (<i>p</i> < 0.001; power above 90%), highlighting the impact of these proteins on clinical results. The final logistic model, including sTNFRI/sTNFRII and CRP, indicated high sensitivity, specificity, accuracy, and an eight-fold higher odds ratio for an unfavorable outcome. <b>Conclusions</b>: The joint use of the sTNFRI/sTNFRII ratio with CRP proves to be a promising tool to assist in the clinical management of patients hospitalized for COVID-19.

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Journal
Biomedicines
Published
2024-09-20
DOI
https://doi.org/10.3390/biomedicines12092138
Citations
1
Primary Topic
COVID-19 Clinical Research Studies
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article
Field-Weighted Citation Impact
0.39
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article

COVID-19 Inflammatory Syndrome: Lessons from TNFRI and CRP about the Risk of Death in Severe Disease

Fabiano Vilela Mundim, Loren Queli Pereira, Sarah Cristina Sato Vaz Tanaka, Guilherme Henrique Machado et al.
1 citations
Biomedicines
COVID-19 Clinical Research Studies
0.39
article

COVID-19 Inflammatory Syndrome: Lessons from TNFRI and CRP about the Risk of Death in Severe Disease

Fabiano Vilela Mundim, Loren Queli Pereira, Sarah Cristina Sato Vaz Tanaka, Guilherme Henrique Machado, Leonardo Eurípedes Andrade-Silva, Malú Mateus Santos Obata, Beatriz Sodré Matos, Marcela Rezende Lemes, Rafaela Miranda Barbosa, Thaís Soares Farnesi-de-Assunção, Wellington Francisco Rodrigues, Hélio Moraes‐Souza, Chamberttan Souza Desidério, Djalma Alexandre Alves da Silva, Denise Bertulucci Rocha Rodrigues, Carlo José Freire Oliveira, Yulsef Moura Ferreira, Ivan Borges Monteiro, Laís Milagres Barbosa, Rafael Obata Trevisan, Anna Victória Bernardes e Borges, Juliana Cristina Costa-Madeira, Fernanda Bernadelli De Vito, Virmondes Rodrigues, Fernanda Rodrígues Helmo, Andrezza Cristina Cancian Hortolani, Ana Carolina de Morais Oliveira-Scussel, Marcos Vinicius da Silva
article en
1 citations

Abstract

<b>Background/Objectives</b>: Cytokine storm in severe COVID-19 is responsible for irreversible tissue damage and death. Soluble mediators from the TNF superfamily, their correlation with clinical outcome, and the use of TNF receptors as a potent predictor for clinical outcome were evaluated. <b>Methods</b>: Severe COVID-19 patients had the levels of soluble mediators from the TNF superfamily quantified and categorized according to the clinical outcome (death versus survival). Statistical modeling was performed to predict clinical outcomes. <b>Results</b>: COVID-19 patients have elevated serum levels from the TNF superfamily. Regardless of sex and age, the sTNFRI levels were observed to be significantly higher in deceased patients from the first weeks following the onset of symptoms. We analyzed hematological parameters and inflammatory markers, and there was a difference between the groups for the following factors: erythrocytes, hemoglobin, hematocrit, leukocytes, neutrophils, band cells, lymphocytes, monocytes, CRP, IL-8, IFN-γ, IL-10, IL-6, IL-4, IL-2, leptin MIF sCD40L, and sTNFRI (<i>p</i> < 0.05). A post hoc analysis showed an inferential capacity over 70% for some hematological markers, CRP, and inflammatory mediators in deceased patients. sTNFRI was strongly associated with death, and the sTNFRI/sTNFRII ratio differed between outcomes (<i>p</i> < 0.001; power above 90%), highlighting the impact of these proteins on clinical results. The final logistic model, including sTNFRI/sTNFRII and CRP, indicated high sensitivity, specificity, accuracy, and an eight-fold higher odds ratio for an unfavorable outcome. <b>Conclusions</b>: The joint use of the sTNFRI/sTNFRII ratio with CRP proves to be a promising tool to assist in the clinical management of patients hospitalized for COVID-19.

BiomedicinesVol. 12(9)
Universidade Federal do Triângulo Mineiro (BR), Universidade de Uberaba (BR), Hospital São Domingos (BR)
Good health and well-being
Openalex Percentile: Top 37%
COVID-19 Clinical Research Studies
0.39
DOIOpen Access PDFOpenAlex
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