The role of endothelial dysfunction in the development and progression of liver fibrosis in children with chronic viral hepatitis B and C
DOI:
https://doi.org/10.32782/2415-8127.2024.69.11Keywords:
endothelial dysfunction, marker of fibrogenesis (arginase-1), children, chronic viral hepatitis B and C, liver fibrosisAbstract
The article presents scientific data about modern mechanisms of endothelial dysfunction, as well as features of the level of Arg-1 as a marker of liver fibrosis in children with chronic viral hepatitis B and C. The role of Arg-1 as a marker of endothelial dysfunction was studied. The purpose of the study: to determine the level of Arg-1, as a marker of endothelial dysfunction, in children with chronic viral hepatitis B and C depending on the degree of fibrous changes of the liver parenchyma. Material and methods: 30 patients with diagnosed of chronic viral hepatitis B and C were examined (mean – 12,26±0,69 years). All patients underwent anamnesis collection, general clinical examination, determination of the degree of liver fibrosis using Fibrotest. The level of Arg-1 was determined by the ELISA. Data analysis was performed using the software “Statistica 8.0”, “DataTab”, “R-Studio”. The reliability of the data difference was established using the Student’s paired t-test. The difference was considered significant at p<0.05. Results: in the examined patients of the main group, the level of Arg-1 was significantly higher (101,03±4,52 ng/ml) compared to the children of the control group (71,34±7,91 ng/ml) (p<0,01). The level of Arg-1 in children of the main group with oncological diseases was higher (107,62±6,08 ng/ml), compared to children without this factor (92,4±6,23 ng/ml). The level of Arg-1 was significantly higher in patients of the main group with fibrotic liver changes at the level of F0-1 (112,37±7,07 ng/ml; p<0,001), ≥F2 (94,03±5,23 ng/ml; p<0,05) compared to the control group (71,34±7,91 ng/ml). The level of Arg-1 was significantly higher in children with the degree of fibrotic changes F0-1 compared with patients with changes ≥F2 (p<0,05). In I group of patients, a correlation between the level of Arg-1 and the degree of liver fibrosis was detected (R=-0,54; p=0,002). Conclusion: Arg-1 is an innovative marker that reveals and characterizes the role of endothelial dysfunction as an additional mechanism of the occurrence and progression of liver fibrosis in children with chronic viral hepatitis B and C.
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