Abstract. Pathogenesis of chronic hepatitis C (CHC) remains to be determined. Mechanisms of liver parenchyma damage in patients with CHC are complex and different. Cytokines play the role of intermediaries in the process of fibrosis development and chronic inflammation. In the present study levels of 27 cytokines in the blood plasma of 14 patients with CHC were tested using multiplex analysis. The liver biopsy was performed in all patients to define the activity of inflammation (histological activity index) and the degree of fibrosis. Nineteen samples of blood plasma obtained from healthy individuals were served as a control group in this study. The following cytokines were measured: IL-1β, IL-1ra, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12 (p70), IL-13, IL-15, IL-17, eotaxin, FGF-2, G-CSF, GM-CSF, IFNγ, IP-10, MCP-1, MIP-1α, MIP-1β, RANTES, PDGF-BB, TNFα and VEGF. In patients with CHC elevated levels of plasma IL-1ra, IL-6, IL-7, IFNγ, IL-12 (p70), IL-4, IL-9, IL-8, IP-10, eotaxin, MCP-1, MIP-1β, TNFα, G-CSF and GM-CSF were found in compare with the control group. At the same time levels of FGF-2 and PDGF-BB were reduced in patients with CHC in compare with controls. Differences in the production of IL-1ra, IL-6, IL-7, IFNγ, IL-12 (p70), IL-4, IL-9, IL-8, IP-10, eotaxin, MCP-1, MIP-1β, TNFα, G-CSF and GM-CSF were depend on the genotype of HCV (3a or 1b), histological activity index in liver tissue and the degree of liver fibrosis. The revealed changes of cytokine production in patients with CHC characterize different orientation of regulatory violations confirming that CHC is an immunopathological process.

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The aim of the study was to assess the possibilities of noninvasive diagnosis of liver fibrosis (FIB-4 and APRI indices) in patients with CHC and abdominal obesity.Materials and methods. 52 men with CHC were examined. Genotype 1 was determined in 24 patients, genotype 3 in 19 patients and genotype 2 in 9 patients. According to the severity of fibrosis, patients with CHC were divided: without fibrosis (F0) - 12 patients, with weak fibrosis (F1) - 17 patients, with moderate fibrosis (F2) - 10 patients, with severe fibrosis (F3) - 8 patients, cirrhosis of the liver (F4) was detected in 5 patients. According to a liver biopsy, steatosis was found in 18 patients with CHC. Abdominal obesity was found in 34 patients with CHC. Non-invasive diagnosis of liver fibrosis was assessed using routine FIB-4 and APRI indices. The interval of values of FIB-4 and APRI, not related to the criteria for assessing the stage of fibrosis F3 and F4, we have conventionally designated as the «gray zone». The presence of insulin resistance was evaluated at HOMA-IR> 2.Results. Key values of the FIB-4 index in patients with CHC and abdominal obesity were found significantly more often than when calculating the APRI index. Insulin resistance in patients with CHC and abdominal obesity was statistically significantly more frequent than in patients with CHC and without abdominal obesity. At stages F3-F4 in patients with CHC, abdominal obesity and insulin resistance, APRI values were recorded more often in the «gray zone»than FIB-4 values.Conclusion. The FIB-4, APRI, HOMA-IR indices can be used in patients with CHC and abdominal obesity during the follow-up and dynamic monitoring of patients with CHC to highlight risk groups. FIB-4 was significantly more informative for determining the stage of fibrosis than APRI in patients with CHC and abdominal obesity with insulin resistance (HOMA-IR> 2).