Метаболічно-асоційована жирова хвороба печінки у дітей з ожирінням. Погляд педіатра

Objective — to investigate the characteristics of the development and course of metabolic-associated fatty liver disease (MAFLD) in children with obesity. Materials and methods. A total of 64 children with obesity aged 11—17 years were examined. The main group included 31 children with obesity and MAFLD; the comparison group comprised 33 children with obesity without MAFLD; and the control group consisted of 34 children matched for age and sex who had neither obesity nor disorders of carbohydrate metabolism. The clinical and laboratory assessment included medical history taking, physical examination, and bioche­mical blood analysis with measurement of glucose, cholesterol, β-lipoproteins, total bilirubin, thymol test results, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, the ALT/AST ratio, the de Ritis ratio (AST/ALT), and the Hepatic Steatosis Index. The presence and severity of insulin resistance were assessed using the HOMA-IR index and the Caro coefficient, respectively. Serum insulin, leptin, adiponectin, osteopontin, resistin, and aldosterone levels were measured using commercially available enzyme-linked immunosorbent assay (ELISA) kits. Statistical analysis was performed using the licensed software packages Statistica for Windows 13.0 and SPSS 23.0 for Windows. Results and discussion. Children with MAFLD were characterized by abdominal obesity, accompanied by decreased de Ritis and Caro ratios and increased ALT/AST ratio, Hepatic Steatosis Index, and HOMA-IR index (p < 0.05). Inchildren with MAFLD, serum insulin and aldosterone levels were significantly higher (p < 0.05), whereas in children with obesity without MAFLD, the levels of these hormones were within the range observed in the control group. Obesity in children was associated with significantly higher serum osteopontin and leptin levels and lower adiponectin levels, with the most pronounced changes observed in the group with MAFLD (p < 0.01). Serum resistin levels were elevated in both groups of children with obesity (p < 0.05) and were not associated with the presence of MAFLD. The observed changes in adipokine levels were most pronounced in children with signs of insulin resistance. Based on the findings, a schematic representation of the pathogenetic mechanisms underlying the development of MAFLD in children with obesity was developed. Conclusions. The development of MAFLD in the setting of obesity is a factor that aggravates the course of the underlying disease and is characterized by abdominal obesity, hyperlipidemia, insulin resistance, and hepatic steatosis. These changes are accompanied by hormonal disturbances, including hyperaldosteronism and hyperinsulinism, as well as increased serum levels of osteopontin and leptin and a simultaneous decrease in adiponectin levels (p < 0.05), whereas serum resistin levels remain unchanged. The findings provide a basis for developing measures aimed at preventing the development of MAFLD in children with obesity and ensuring timely treatment of this complication.