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Content of some redox homeostasis parameters in blood of patients with liver cirrhosis, depending on its severity according to the criteria of C. H. Child-R. N. Pugh and their connection with endothelial dysfunction development

Maryana Abrahamovych, Orest Abrahamovych, Oksana Fayura, Solomiya Tolopko
Minerva Gastroenterologica e Dietologica 2020 March 24
32218418

BACKGROUND: Liver is one of the first organs to be exposed to reactive oxygen species (ROS). But the data about the levels of redox homeostasis parameters in the patients with liver cirrhosis (LC) are contradictory. We hypothesized that the levels of malondialdehide and catalase should change in accordance with the LC severity causing the endothelial dysfunction.

METHODS: In a randomized way with the preliminary startification by the presence of LC 81 patients and 20 healthy volunteers were examined. To determine the contents of catalase, malondialdehide, cyclic guanosine monophosphate, endothelin-1, renin, aldosterone, natriuretic peptide, the routine standartized methods were used. The results were processed in Statistica 6.0, RStudio v. 1.1.442 and R Commander v.2.4-4.

RESULTS: Patients with LC revealed the statistically significant increase of malondialdehide and decrease of catalase levels in parallel with the increase of cyclic guanosine monophosphate, endothelin-1, renin, aldosterone, natriuretic peptide contents and disease course worsening according to C. H. Child-R. N. Pugh criteria. It testifies the huge oxidative stress impact on the organism. Initially, at the stage of LC compensation, it slightly stimulates the activation of antioxidant system, followed by its gradual suppression at the stages of sub- and decompensation. Disorders of redox homeostasis lead to the endothelial dysfunction that becomes the background of extrahepatic comorbid disorders.

CONCLUSIONS: The cirrhotic patients have the significant abnormalities in the redox homeostasis that becomes the background of the endothelial dysfunction - common trigger mechanism for the syntropic comorbid diseases and early pathophysiologic symptom of the unfavorable prognosis for such patients.

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