Relation between redox homeostasis blood parameters in cirrhotic patients and endothelial dysfunction development

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 malondialdehyde and catalase should change in accordance with the LC severity causing the endothelial dysfunction.

In a randomized way with the preliminary stratification by the presence of LC 81 patients and 20 healthy volunteers were examined. To determine the contents of catalase, malondialdehyde, cyclic guanosine monophosphate, endothelin-1, renin, aldosterone, natriuretic peptide, the routine standardized methods were used.

Patients with LC revealed the statistically significant increase of malondialdehyde 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 the Child-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.

Cirrhotic patients have significant abnormalities in the redox homeostasis, which become the background of the endothelial dysfunction - common trigger mechanism for the syntrophic comorbid diseases and early pathophysiologic symptom of the unfavorable prognosis for such patients.