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Proinflammatory cytokines VEGFA, IL-6, IL-8 as markers of hepatotoxicity after COVID-19

https://doi.org/10.15789/1563-0625-PCV-2843

Abstract

The mechanism of hepatocellular liver damage after COVID-19 is a multifactorial process. The most widely discussed causes are cytolytic liver damage due to the inflammatory response after COVID-19, drug-induced hepatotoxicity and direct cytotoxic effect of the virus. There are observations that SARSCoV-2 infection causes hepatitis B virus reactivation, but little has been described about the interaction between hepatitis C virus and SARS-CoV-2. The course of coronavirus infection is associated with marked expression of proinflammatory cytokines, participants in the multisystem inflammatory response, IL-1β, IL-6, IL-8, IL-18, MCP-1, TNFα, which contribute significantly to the observed early and late liver function impairment. The aim of the study was to evaluate the role of proinflammatory cytokines (VEGFA, IL-8, IL-6, MCP-1, TNFα, IL-18) as additional markers of hepatotoxicity after COVID-19. The study was performed between March and August 2022. Patients were divided into 2 groups: Group 1 – with increased aminotransferases against the background of treatment from COVID-19 and/or in the following 3-6 months after the disease without viral liver damage (n = 42), Group 2 – patients with co-infection (chronic viral hepatitis C (HCV) and COVID-19 (n = 26). The levels of cytokines – VEGF-A, IL-6, IL-8, MCP-1, IL-18, TNFα in blood serum were estimated by enzyme immunoassay method. Statistical analysis was performed using StatTech v. 3.1.4. The results of the study revealed a comparable increase in the level of transaminases and C-reactive protein in both groups, significantly different from the reference values. Direct correlations of moderate strength (linear Spearman correlation) were found between the following cytokines: TNFα-MCP-1 (R = 0.559; p = 0.001), TNFα-VEGFA (R = 0.400; p = 0.002), TNFα-IL-6 (R = 0.503; p = 0.001). We diagnosed a significant increase in serum VEGFA levels in group 1 patients (hepatotoxicity after COVID-19) (Me (Q0.25-Q0.75): 522 (250 to 1002), p = 0.001) and in group 2 patients (HCV + COVID-19) (Me 1196, Q0.25-Q0.75: (73 to 432). Similar trend with the level of IL-6, IL-8, exceeding the values of cytokines in healthy donors and significantly higher than in group 2 patients. Identified correlations between inflammatory cytokines prove unidirectional changes in the functioning of the regulatory network controlling immune virus-induced reactions.

About the Authors

M. A. Urevskii
Ulyanovsk State University
Russian Federation

Urevskii M.A., Student, Faculty of Medicine, Institute of Medicine, Ecology, and Physical Education, Research Intern at the S. Kapitza Technological Research Institute 

Ulyanovsk



L. V. Ilmukhina
Ulyanovsk State University
Russian Federation

Ilmukhina L.V., PhD (Medicine), Associate Professor, Department of Dermatovenerology and Infectious Diseases, Faculty of Medicine, Institute of Medicine, Ecology, and Physical Education 

Ulyanovsk



Ya. E. Saranskaya
Ulyanovsk State University
Russian Federation

Saranskaya Ya.E., Senior Lecturer, Department of Dermatovenerology and Infectious Diseases, Faculty of Medicine, Institute of Medicine, Ecology, and Physical Education 

Ulyanovsk



A. A. Lapshin
Ulyanovsk State University
Russian Federation

Lapshin A.A., Student, Faculty of Medicine, Institute of Medicine, Ecology, and a medical student at the Institute of Medicine, Ecology, and Physical Education 

Ulyanovsk



R. R. Gafurova
Ulyanovsk State University
Russian Federation

Gafurova R.R., Student, Faculty of Medicine, Institute of Medicine, Ecology, and a medical student at the Institute of Medicine, Ecology, and Physical Education 

Ulyanovsk



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For citations:


Urevskii M.A., Ilmukhina L.V., Saranskaya Ya.E., Lapshin A.A., Gafurova R.R. Proinflammatory cytokines VEGFA, IL-6, IL-8 as markers of hepatotoxicity after COVID-19. Medical Immunology (Russia). 2023;25(4):803-808. https://doi.org/10.15789/1563-0625-PCV-2843

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ISSN 1563-0625 (Print)
ISSN 2313-741X (Online)