[Pathogenetic therapy of metabolic syndrome at the stage of visceral lesions].

Insulin resistance and oxidative stress play an important role in the pathogenetic mechanism of non-alcoholic fatty liver disease. Hepatoprotective therapy that blocks the second phase of pathogenesis (oxidative stress) is a promising modality for the treatment of non-alcoholic steatohepatitis (NACH). An alternative approach is the use of medicines recovering the mitochondrial membrane, lipid bi-layer of the plasma membrane, oxidative phosphorilation, and cellular metabolism. In this context, succinic acid-based remaxol showing antioxidative, antihypoxic and cytoprotective activities can be regarded as a promising metabolic hepatoprotector for the treatment of non-alcoholic fatty liver disease. The present original study demonstrated the clinical efficacy of remaxol in pathogenetic therapy of NACH in patients with metabolic syndrome. Its introduction in the combined treatment of NACH increased functional capacity of the liver by decreasing the severity of cytolysis, cholestasis, hepatomegalia, and steatosis (ultrasonic study), improved lipid metabolism, reduced cholesterol level, triglyceridemia, and atherogenic index. Remaxol exerted nephroprotective action in patients with diabetic nephropathy at stage 1 of chronic renal insufficiency (increased glomerular filtration rate and decreased blood creatinine level). The study demonstrated the advantage of medications with antihypoxic properties over traditional therapy of NACH.