The dissertation by Lyzanets N.V., "Clinical and Immunological Features and Rationale for the Treatment of Patients with Chronic Hepatitis C Combined with Non-Alcoholic Fatty Liver Disease and Obesity," explores the clinical and immunological aspects of diagnosing and treating patients with chronic hepatitis C (CHC) who also suffer from non-alcoholic fatty liver disease (NAFLD) and obesity. The primary goal of this research is to improve treatment efficacy through an analysis of the relationships between body composition, immunoendocrine homeostasis, angiogenesis, fibrogenesis, lipid metabolism, and morphological changes in the liver. The objectives include investigating correlations between adipose tissue hormones and lipid metabolism indicators, as well as identifying predictors of fibrosis regression following antiviral therapy.
The study revealed that CHC patients with a normal body mass index (BMI) exhibit an increased fat mass, predominantly due to visceral obesity, which is associated with an imbalance of adipose tissue hormones, including adiponectin and leptin. The observed correlations between adiponectin, leptin, total cholesterol, and lipoproteins suggest that, even with a normal BMI, visceral obesity can significantly impact lipid metabolism disorders and the hormonal status of CHC patients.
Antiviral treatment provided a sustained virological response in 95.1% of patients; however, lipid metabolism disorders and elevated levels of angiopoietin-2 (Ang-2) and transforming growth factor (TGF-β1) persisted in some patients, necessitating additional therapy. It was shown that the inclusion of rosuvastatin, ademetionine, and ursodeoxycholic acid (UDCA) improved lipid metabolism markers, reduced the degree of steatosis, and enhanced quality of life by decreasing anxiety and depression. Elevated Ang-2 and TGF-β1 levels after viral elimination were associated with higher degrees of fibrosis and steatosis in patients with NAFLD and increased body mass.
The novelty of this research lies in the substantiation of additional therapy with rosuvastatin and UDCA, which supports fibrosis regression, normalizes lipid profiles, and reduces liver steatosis severity in patients after antiviral therapy. This study expands scientific knowledge regarding the factors influencing fibrosis progression in CHC+NAFLD patients with increased body mass following the complete elimination of hepatitis C virus, identifying factors such as higher baseline fibrosis stage, elevated Ang-2 and TGF-β1 levels, high leptin levels, and elevated LDL levels before antiviral therapy.
The research demonstrates that CHC patients with concurrent NAFLD and obesity continue to experience lipid metabolism disorders post-virus elimination, promoting fibrotic liver changes that require ongoing correction and monitoring. The practical significance of this work lies in developing recommendations for diagnosing and managing CHC patients, incorporating complex therapy with hepatoprotectors and lipid-correcting agents, and including body composition assessments for early NAFLD detection. This study refines treatment strategies for CHC patients comorbid with NAFLD, obesity, and dyslipidemia, advocating for the use of rosuvastatin, ademetionine, and UDCA after completing direct-acting antiviral therapy, particularly in patients with advanced liver fibrosis (F3-4) and significant liver steatosis (S2-3), to address cytokine imbalances and prevent fibrosis progression.
Key words: chronic hepatitis C, non-alcoholic fatty liver disease, steatosis, liver fibrosis, bioimpedance, obesity, cytokines, dyslipidemia, angiopoietin-2, rosuvastatin, antiviral therapy, hepatoprotectors.
