Biliary tract dysfunctions: Possibilities of combined drugs of plant origin as advantage therapy

Abstract

Introduction. Non-alcoholic fatty liver disease (NAFLD) is caused by excess accumulation of fats in hepatocytes. An increasing percentage of adipose tissue is associated with chronic inflammation and developing oxidative stress. These pathological conditions can lead to the progression of steatosis to steatohepatitis with the further development of fibrosis and cirrhosis.Aim. To evaluate the indicators of lipid peroxidation and antioxidant defence factors in steatosis and steatohepatitis in patients with NAFLD.Materials and methods. During the work, 116 patients with NAFLD were examined, of which 65 had steatosis, and 51 had steatohepatitis. The study of biochemical markers of metabolism of proteins, fats and carbohydrates was performed on a Mindray BS-380 biochemical analyzer. The indicators of the LPO-AOD system (MDA, SOD, catalase, ceruloplasmin) were assessed using spectrophotometric methods. Statistical data processing was carried out in the STATISTICA and SPSS 26 programs using nonparametric tests.Results. Patients with steatohepatitis had more severe dyslipidemia, blood triglyceride, total cholesterol levels and LDL were significantly higher (p > 0.05). Impaired cholesterol metabolism was reflected by a high atherogenic index of 3.46. In patients with steatosis, changes in the lipid profile were less pronounced. No disturbances in protein and carbohydrate metabolism were detected. Increased levels of liver markers were noted only in patients with steatohepatitis. The change in the balance in the LPO- AOD system was more pronounced in patients with steatohepatitis; they had a high level of MDA, a high concentration of catalase; in patients with steatosis, only a decrease in the level of MDA and an increase in the level of ceruloplasmin were noted.Conclusion. Dyslipidemia, hepatocyte cytolysis and liver fibrosis are detected in patients with steatohepatitis. Disturbances in the LPO-AOD system have been identified in both forms of NAFLD, but in steatosis they are compensated. In steatohepatitis, disturbances in “LPO-AOD” in the form of an increase in pro-oxidants and a decrease in antioxidants cause the development of oxidative stress.