Abstract
The aim of the study was to evaluate the dynamics of changes in 13C-metacetin breath test in patients with non-alcoholic fatty liver disease and healthy individuals. Material and methods. 30 people with hepatic steatosis and 17 apparently healthy volunteers were examined. The complete clinical examination included anthropometric characteristics (height, body weight, body mass index), determination of hepatic transaminases, lipid profile, ultrasound investigation of the liver and 13C-metacetin breath test. Results. At careful inspection of patients with NAFLD overweight or obesity, signs of a metabolic syndrome, dyslipidemia, increase in concentration of ALT and AST are most often found. According to the results of ultrasound diagnostic in 80% of the examined patients with steatosis showed hepatomegaly, hyperechogenicity and heterogeneity of liver structure. According to the results of 13C-MDT, it was found that the rate of metabolism is maintained at a high level in apparently healthy individuals, which provides sufficient accumulation of 13C-metacetin and corresponds to approximately 100% of functioning hepatocytes. Under steatosis, the slowing of the metabolic rate and, accordingly, a significant reduction in the cumulative dose is due to a reduction in the functional activity of hepatocytes to 30-40 min instead of 60 min compared to apparently healthy individuals. Conclusions. The diagnostic value of 13C-MDT is in non-invasive dynamic assessment of metabolic rate and changes in liver metabolic capacity in vivo at an early stage of NAFLD. It was found that in the presence of hepatic steatosis there is a slowing of metabolic rate and a reliable reduction of the cumulative dose, due to reduced functional activity of hepatocytes. The above changes in test parameters allow to estimate the condition of the liver and are reasonable causes to recommend such patients to make lifestyle modifications and prescribe early treatment. Using of 13C-MDT in medical practice will deepen the knowledge of scientists on the pathogenesis of steatosis, improve its diacrisis and approaches to treatment.
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