DOI: https://doi.org/10.22141/2308-2097.52.4.2018.154142

Immunological reactivity in patients with chronic diffuse liver diseases

O.M. Tatarchuk, V.I. Didenko, S.L. Melanich, V.Ye. Kudryavtseva

Abstract


Background. The aim of the study was to assess the state of the main indicators of cellular immunity and the level of cytokines in patients with chronic diffuse liver diseases (CDLD). Materials and methods. Sixty eight patients with CDLD were examined, they were divided into 4 groups depending on the etiological factors of the formation and progression of steatosis and liver fibrosis: group I — 36 patients with non-alcoholic fatty liver disease; group II — 13 persons with chronic viral hepatitis C, group III — 14 patients with alcoholic liver disease, IV group — 5 individuals with toxic hepatitis. We studied the main indicators of cellular immunity and the level of interleukin (IL) 6, IL-10 and tumor necrosis factor (TNF) α. Results. In 83.3 % of patients in group I, 76.9 % — in group II and in a half of patients in group III, there was a significant decrease in the T helper cell subpopulation. Cellular immunodeficiency in patients with CDLD leads to the formation of steatosis. In 69.2 % of patients in group II, immunoregulatory disorders indicate the persistence of hepatitis C virus and, as a consequence, the development of fibrosis. According to the results obtained, the concentration of TNF-α in patients of groups I, II and IV signi­ficantly exceeds the control values — by 6.9, 7.9 and 11.0 times, respectively (p < 0.05). The level of IL-6 is significantly higher (by 3.9 times; p < 0.05) in patients of group I compared with group IV. This indicates the progression of the immunopathological process and is a pathogenetic sign of the inadequacy of the immune system functioning in CDLD. Conclusions. The study shows that the progression of liver steatosis is accompanied by a decrease in cellular immune system and an increase in proinflammatory cytokine levels.


Keywords


chronic diffuse liver diseases; immunity; cytokines

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