Pathogenesis of development and influence of metabolically associated fatty liver disease by correlation analysis

Abstract

Metabolically associated (nonalcoholic) fatty liver disease (MAFLD) has become the most common liver disease worldwidewhich can be effectively treated and prevented only at the stage of steatosis, which is why the pathogenesis of its occurrence and progression should be taken into account. The study aims at establishing the pathogenetic relationship between the occurrence and progression of MAFLD using correlation analysis. Materials and methods. To achieve the research objectives the total of 36 patients with hypertension, compensated hypothyroidism and overweight/obesity have been examined, median age 56.0 years, 92% women.The patients were divided into the main group (n = 23) with sonographically confirmed MAFLD and control (n = 13) without it, which were examined according to the standard protocols with additional determination of cortisol in blood, obesity characteristics (waist-to-hip ratio, total adipose tissue volume; mass of visceral adipose tissue; relative proportion of body fat), adaptive potential according to Baevsky RM (1987). The results were statistically processed for calculating the median (M), the significance was determined by Mann-Whitney U-test; the correlations were estimated using the Kendall rank correlation coefficient; the probability value was assumed to be p<0.05. Results and discussion. The patients withMAFLD were significantly different in all anthropometric characteristics of obesity,characterized by a higher degree of hypertension, an increase in the right lobe of the liver above normal (158.0 [153.0; 170.0] vs. 145.0 [137.0; 150.0] mm) and portal vein dilation (10.0 [10.0; 10.8] vs. 7.5 [5.9; 10.0] mm, both p <0.05). The liver echogenicity correlated with the obesity parameters, degree of hypertension, cardiovascular risk and aortic root diameter.In addition, the increased echogenicity was associated with a decrease in the total blood cholesterol (τ = -0.26; p = 0.032) and an increase in cortisol (τ = 0.63; p = 0.047).The increase in both liver sizes significantly correlated with the increase in the heart rate (τ = 0.28; p = 0.027), which occurred in parallel with the increase in blood cortisol (τ = 0.63; p = 0.047),activation of the sympathetic nervous system according to the Kerdo index (τ = 0.29; p = 0.021) and inflammation according to segmental blood neutrophils (τ = 0.29; p = 0.028) and seromucoid levels (τ = 0.67; p = 0.021). Conclusions: the changes which were described in metabolically associated fatty liver disease constitute the only vicious circle of pathogenesis, each link of which exacerbates the other and makes the pathological process irreversible.