For the first time, it is studied that the course of NASH with concomitant COPD and obesity in comparison with NASH without COPD is characterized by higher levels of postprandial glucose, hyperinsulinemia and IR degree, which correlate with the degree of hepatic steatosis, fibrosis index, cytolysis activity, cholestasis and mesenchymal inflammation and depend on the content of leptin and adiponectin in the blood (p<0.05).
For the first time, it is proved that COPD in patients with NASH and obesity is an additional, potent inducer of lipid distress syndrome with significantly higher (compared with NASH without pulmonary pathology) blood levels of TG, total cholesterol (p<0.05), accompanied by higher levels of hyperleptinemia, adiponectin deficiency, which correlate with the degree of hepatic steatosis, fibrosis index, cytolysis activity, cholestasis and mesenchymal-inflammatory syndromes, markers of systemic inflammatory response and interrelated with hyperleptinemia, hypoadiponectine.
For the first time there has been established a deeper imbalance of connective tissue components due to increased synthesis of type IV collagen, carbohydrate-protein components of the extracellular matrix of the liver, increased degradation of fucoglycoproteins and newly formed collagen in patients with NASH on the background of obesity due to comorbidity with COPD. This imbalance leads to stimulation of both liver fibrosis and the development of pneumosclerosis. The index of liver fibrosis (Fibrotest) in NASH and COPD in a strong inverse relationship correlates with a deficiency in H2S (p<0.05).
For the first time, on the basis of histopathological and histochemical study of liver tissue in comorbidity with COPD in NASH and obesity, there has been found a higher percentage of hepatocytes in steatosis, a higher proportion of hepatocytes in fatty necrosis, oncosis, lipofuscinosis, indicating more significant dysmetabolic disorders and inflammatory activity in hepatocytes, as well as a higher degree of liver fibrosis (increase in connective tissue volume, specific volume of collagen fibers, optical color density of collagen fibers) (p<0,05).
The author proves for the first time that comorbid NASH and obesity contributed to a higher degree of activation of lung fibrosis in patients with COPD (increase in specific volume of connective tissue in the lungs), increase in the number and diameter of lipocytes in the lungs compared with isolated COPD (p<0.05). For the first time it is found that NASH with obesity is characterized by a probable increase in the optical density of collagen fibers in lung tissue compared with healthy individuals (p<0.05).
The author has significantly supplemented the pathogenetic concept of mutual aggravation of NASH with COPD, which consists in increasing the activity of certain clinical, biochemical syndromes of steatohepatitis, the degree of hepatocyte steatosis, the intensity of hepatocyte apoptosis and the intensity of liver fibrosis (p<0.05), due to significantly higher activation of systemic proteolysis, oxidative and nitrosative stress, systemic endotoxicosis, against the background of lack of natural components of the antioxidant defense and detoxification (glutathione), hydrogen sulfide deficiency, significant deepening of lipid distress syndrome and insulin resistance syndrome in comparison with the course of NASH without bronchopulmonary pathology.
For the first time, in the complex therapy of NASH, obesity with COPD (groups B, C, D) there has been proposed and proven the effectiveness of antral and policosanol, which significantly reduced the activity of markers of cytolysis, cholestasis, blood cholesterol, TG, LDL, normalization of blood glucose and insulin level, reducing the intensity of endogenous intoxication, oxidative and nitrosative stresses, systemic proteolysis, as well as restoring blood and H2S (p<0.05), reducing the degree of hepatocyte steatosis, the intensity of liver fibrosis with a probable decrease in collagen anabolism IV, hexosamines, degradation of fucose of extracellular matrix, as well as the degree of broncho-obstructive syndrome (p<0,05).
