Comparative analysis observes liver cell characteristics post-COVID-19, indicating potential liver damage mechanisms.
Objective. Comparative analysis of liver subpopulations of lymphocytes and cells of the system of mononuclear phagocytes on the material of autopsies in deaths from acute period of COVID-19, without its previous diseases and bacterial/mycotic superinfection, as well as from noninfection diseases in the distant future after the new coronavirus infection. Material and methods. Study of morphological changes of the liver in 47 deaths from COVID-19, confirmed by a PCR test, and noninfection diseases within 40 to 300 days after a new coronavirus infection. The study did not include those who died with previous liver diseases and comorbid diseases accompanied by liver damage, and in the first two groups of observations — also with bacterial/mycotic superinfection, and after hepatotoxic therapy. 1 group consisted of 10 observations (average age — 75.2 years) with the exudative phase of diffuse alveolar damage (DAD), 2nd group — 27 observations (average age — 71.7 years) with the proliferative or exudative-proliferative phases of DAD, 3d group — 10 observations (average age — 84.7 years), died from cardiovascular diseases in the period from 40 to 300 days after the transfer COVID-19. Imunohistochemical (IHC) reactions with antibodies to CD3, CD4, CD8, CD20, CD56 and CD68 were used with statistical analysis. Results. In portal tracts and perisinusoid spaces, the total number of CD3+, CD4+, CD8+, CD56+ and CD20+ lymphocytes and CD68+ cells are not higher in the acute period COVID-19, and in perisinusoid spaces are even less than in observations after a new coronavirus infection in patients died from cardiovascular diseases. The number of intraepithelial CD3+, CD4+, CD8+, CD56+ lymphocytes of the bile ducts of portal tracts was increased, which also infiltrate the walls of small vessels. Number of CD4+ lymphocytes in the stroma and liver parenchyma, ratio CD4+/CD8+ lymphocytes and proliferation of Kupfer cells are most increased in the exudative phase of DAD in COVID-19. Conclusion. The study confirms that the morphological substrate COVID-19-associated liver damage may be ischemic hepatitis and COVID-19-associated cholangiopathy and microangiopathy give it a certain specificity. The revealed changes do not allow to exclude that the pathogenesis of liver damage can be also associated, including with other factors the direct action of SARS-CoV2 or immune disorders associated with COVID-19.
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Krasnenkova et al. (2026) studied this question.
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