The clinical significance of insulin resistance in non-diabetic patients with early forms of non-alcoholic fatty liver disease

Aim. To assess the presence of insulin resistance (IR) in non-diabetic patients with early forms of non-alcoholic fatty liver disease (NAFLD) - liver steatosis (LS) and steatohepatitis (SH) of mild activity and the influence of IR on the clinical course of these diseases. Materials and methods. 134 patients with NAFLD were examined: 54 with LS and 80 with SH. The control group consisted of 37 healthy donors. Anthropometric parameters (body mass index (BMI), waist circumference (WC)), clinical and biochemical blood indices, including the blood level of cytokeratin-18 fragments (CK-18), TNF-alpha and IL-6 cytokines, insulin were evaluated. The HOMA index and the fibrosis index (NAFLD FS) were calculated. Patients were divided into groups: I - with the absence of IR (HOMA-index <2.7), II - with the presence of IR (HOMA-index> 2.7). Results and discussion. Indicators of hepatic injury, inflammation, cholestasis, fibrosis and atherogenic dyslipidemia are higher in patients with LS of group II (with IR) than in group I patients (without IR). BMI, WC, Y-glutamil transpeptidase, CK-18 and fibrosis index are significantly higher in group II patients with SH compared with group I, there is no significant difference in the level of cytolysis, inflammation and dyslipidemia indices. A high incidence of IR in non-diabetic patients with LS (37.0%) and SH (55.0%) was found and the effect of IR on the clinical course of these diseases was revealed. Conclusion. Insulin resistance in non-diabetic patients with NAFLD was detected in SH (55.0%) with higher frequency than in LS (37.0%). In LS, IR is associated with impaired hepatic cell damage, intrahepatic cholestasis, atherogenic dyslipidemia and fibrosis. In SH, IR is combined with reliable growth in indicators of hepatocyte apoptosis, cytokine proinflammatory status and fibrosis. IR determines the progressing course of NAFLD, promoting the transformation of steatosis into steatohepatitis and steatohepatitis into fibrosis and liver cirrhosis.