Clinical-nutritional and metabolic disorders in the formation of non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) encompasses a range of diseases, including non-alcoholic fatty liver and non-alcoholic steatohepatitis (NASH), potentially leading to cirrhosis and hepatocellular carcinoma. Globally, approximately 30% of the population suffers from NAFLD, with recent data indicating an increasing prevalence. The increasing incidence of NAFLD and its complex relationship with metabolic dysfunction highlight the risk of liver cirrhosis in patients with different BMIs who are not provided with timely diagnosis and therapy. Therefore, it is critical to prioritize prevention and screening measures for NAFLD. The purpose of our work was to determine risk factors for the development of NAFLD with and without obesity. Materials and methods. A one-time study was carried out with a comprehensive assessment of nutritional status, including anthropometry, bioimpedansometry and assessment of actual nutrition, as well as a study of the level of biochemical and hormonal indicators on the basis of the Regional Clinical Hospital of War Veterans No. 3 in Novosibirsk. A total of 349 people took part in the study. Of these: 113 patients with NAFLD without obesity, 122 patients with NAFLD with obesity according to BMI and 114 apparently healthy people. Results and its discussion. In the course of multivariate regression analysis, models were identified that combine a set of factors influencing the development of non-alcoholic fatty liver disease in patients with different nutritional status. For patients with NAFLD without obesity, the factors for the development of the disease are: excess dietary cholesterol intake EXP(B) = 1.004 95CI [1.001-1.008], HOMA -IR index EXP(B) = 20.535 95CI [5.893-71.551], total cholesterol level EXP (B) = 5.092 95CI [2.226-11.649], gamma-glutamyl transpeptidase (GGTP) EXP(B) = 1.282 95CI [1.155-1.423] and visfatin EXP(B) = 1.117 95CI [1.067-1.107]. In patients with NAFLD in combination with obesity, the risk factor model consisted of total fat mass according to bioimpedance measurements EXP(B) = 1.288 95CI [1.123-1.477], HOMA-IR index EXP(B) = 13.318 95CI [3.045-58.242], level GGT EXP(B) = 1.388 95CI [1.185-1.626] and visfatin EXP(B) = 1.193 95CI [1.063-1.338]. Conclusion. Thus, patients with NAFLD, depending on BMI, have a different combination of risk factors, the model of which includes both important features of nutritional status and metabolic and hormonal disorders that underlie the formation of the disease as a whole. The resulting combinations of factors can be used for early diagnosis of NAFLD in patients with both obesity and normal body weight as an expanded screening.