The cytokeratin 18, adiponectin and leptin levels in patients with non-alcoholic steatohepatitis and coronary heart disease

• Main Authors: Oksana S. KHUKHLINA, Olha B. KUZMINSKA, Alona A. ANTONIV, Tamara H. KOPCHUK, Svitlana P. MELNYCHUK
• Format: Article
• Language: English
• Published: Balkan Medical Union 2019-09-01
• Series: Archives of the Balkan Medical Union
• Subjects: non-alcoholic steatohepatitis; coronary heart disease; cytokeratin 18; adiponectin; leptin
• Online Access: https://umbalk.org/wp-content/uploads/2019/09/09.THE-CYTOKERATIN-18-ADIPONECTIN-AND-LEPTIN.pdf

The aim of the study was to determine the level of cytokeratin 18, adiponectin and leptin in plasma of the patients with nonalcoholic steatohepatitis (NASH) and coronary heart disease (CHD) and their association with the degree of cytolysis, disorders of carbohydrate and lipid metabolism. Materials and methods. We examined 60 patients with NASH, who were divided into 2 groups: group 1 – 30 patients with NASH on the background of obesity of 1st-2nd degree, group 2 – 30 patients with NASH and CHD (the 1st and 2nd functional classes of stable angina pectoris) and obesity of 1st-2nd degree. The mean age of patients was 55.13±6.34 years. The control group consisted of 20 practically healthy persons (PHP). Serum CK18, adiponectin and leptin levels were determined by the immunoassay analysis. Results. Our research showed that NASH is closely associated with disorders of adipocytokine homeostasis. In patients with NASH, comorbid CHD, and obesity of 1st-2nd degree, there is an increase level of CK 18, proinflammatory adipokine leptin and a decrease in the level of adiponectin. Conclusions. The significant increase of liver aminotransferases activity and the level of CK 18 in patients with NASH, their close positive correlation relationship suggest that the leading pathophysiological mechanism of progression of NAFLD is the necrosis and apoptosis of hepatocytes. The determination of serum fragments of CK 18 can be used as a non-invasive test for diagnosis of NASH and liver steatosis.