Abstract
Objective — to establish intensity of the oxidative and nitrosative stress at the comorbid course of nonalcoholic steatohepatitis (NASH) and chronic kidney disease (CKD) of the 1st and 2nd stages. Materials and methods. Investigation involved 105 patients (48 men and 57 women) with NASH, form them 52 had 1st degree obesity (group 1), and in 53 patients NASH was combined with 1st degree obesity and І - ІІ stages CKD (group 2). The average age of patients was (45.8 ± 3.81) years. The control group consisted of 30 practically healthy age- and sex-matched subjects. The functional endothelium state was studied by the blood levels of stable nitrogen monoxide (NO) metabolites (nitrites, nitrates) by L. C. Green et al. The number of desquamated endothelial cells in blood was determined by the method of J. Hladovec in the modification of N.N Petrischev et al. The state of the antioxidant protection system (AOP) was studied based on the erythrocyte levels of the restored glutathione (GSH), glutathione peroxidase (GPx), glutathione-S-transferase (GSTs), catalase, superoxide dismutase (SOD), ceruloplasmin (CP). Results. It has been established that in case of comorbidity of NASH and І - ІІ stages CKD, the oxidative stress intensity increased with accompanying accumulation of not only intermediate, but also final products of free radical lipid oxidation in all observation groups, testifying presence of the decompensated oxidative stress in this category of patients. The latter fact is an undeniable evidence of the involvement of oxidative stress in the NASH pathogenesis, and its intensity increases with the CKD comorbidity. The obtained results showed the significant increase in blood NO levels of NASH patients vs indices of practically healthy people. The raised number of desquamated endothelial cells in 1.9 times (p < 0.05) evidenced about the expressed endothelial dysfunction in NASH patients. Conclusions. The investigation showed that in case of comorbid course of NASH and І - ІІ stages CKD, the oxidative stress intensity increased with accompanying accumulation of the intermediate and final products of free radical lipid oxidation, early development of the endothelial dysfunction (increased blood number of desquamated endothelial cells and blood levels of the stable NO metabolites) against the background of the activity of the factors of antiradical defense (the decreased erythrocytic levels of the restored glutathione, superoxide dismutase activity, glutathione-dependent enzymes).
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