The relevance of the problem of the comorbid course of nonalcoholic steatohepatitis, type 2 diabetes and diabetic kidney disease lies in the rapid progression of all comorbid diseases, decompensation of carbohydrate metabolism processes, and the development of hepatocellular and renal failure. The specified comorbid diseases have a number of mutually burdening mechanisms, the elimination of which will contribute to achieving clinical remission of diseases, compensation of the functional potential of the liver and kidneys. The aim of the study was to find out the probable effect of the complex of metformin, rosuvastatin and bicyclol on the markers of hepatocyte cytolysis in patients with non-alcoholic steatohepatitis and type 2 diabetes with diabetic kidney disease, the degree of hepatocyte steatosis and the stage of liver fibrosis, which are markers of the progression of non-alcoholic steatohepatitis. Materials and methods. Depending on the prescribed treatment, the examined patients were randomly divided into 2 groups: (1 group – control: 28 people) received a hypocaloric diet taking into account the restrictions of diet No. 9, essential phospholipids (Essentiale forte H 300 mg 2 capsules 3 times a day ) for 90 days in order to treat active non-alcoholic steatohepatitis, for type 2 diabetes and hyperlipidemia metformin hydrochloride (Metformin-Teva 1000 mg per day, rosuvastatin (Rosuvastatin-Teva 5 mg once a day) was prescribed for 90 days. Group 2 consisted of patients (32 people), who, in addition to similar dietary recommendations, hypoglycemic and hypolipidemic therapy, instead of essential phospholipids, additionally received the drug Bicyclol 25 mg 3 times a day for 90 days. The average age of the patients was (53,8±3,52) years. Group comparison for the presentation of reference values of homeostasis indicators was made by 30 healthy persons of the appropriate age. Research results and their discussion. The analysis of indicators of cytolytic syndrome activity indicates that the activity of ALT increased before treatment (by 3,6 times, p<0,05) – after treatment it decreased in patients of groups 1 and 2: by 2.2 and 3,7 times, respectively (p<0,05) with the presence of a probable intergroup difference (p<0,05). At the same time, the increased indicator of steatosis of hepatocytes before treatment, which exceeded the reference values by 4,0 times (p<0,05) – under the influence of treatment also probably decreased in patients of 1 and 2 observation groups – by 1.2 and 1.8 times, respectively (p<0,05) with the presence of a probable intergroup difference (p<0,05). Thus, both traditional treatment with essential phospholipids and the drug Bicyclol actively affect and during 90 treatments contribute to the reduction of the main components of the pathological process in the liver in non-alcoholic steatohepatitis – cytolysis and fatty dystrophy of hepatocytes, but Bicyclol as part of complex hypoglycemic and hypolipidemic therapy has a more intense effect. It should also be pointed out that the effect of traditional therapy and the activity of liver fibrosis, according to previous studies, was probably lower than the proposed Bicyclol therapy. Thus, the significantly increased FibroTest indicator before treatment (3,2 times, p<0,05) in patients with non-alcoholic steatohepatitis with comorbid diabetes mellitus and diabetic kidney disease in the dynamics of treatment in patients of group 1 decreased by 10,7% (p< 0,05), and in patients of group 2 – by 40,0% (р<0,05) with the presence of a probable intergroup difference (р<0,05). The obtained data indicate a favorable anti-inflammatory effect of Bicyclol, which is aimed at inhibiting and preventing liver fibrosis. Conclusions from the study. Complex therapy with metformin, rosuvastatin in combination with bicyclol in people with comorbid non-alcoholic steatohepatitis, type 2 diabetes and diabetic kidney disease for 3 months contributed to the elimination of hepatocyte cytolysis syndrome, a significant decrease in steato-test and fibrotest indicators (p<0.05), probable reducing the intensity of liver tissue fibrosis.
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